Behind The Headlines - Health News from NHS Choices

'Universal' colour-coded food nutrition labels

Wed, 19 Jun 2013 02:33:00 EST

A radical overhaul of how nutritional information is displayed on the front of the packaging of many food products has been announced.

The government, food makers and food retailers have agreed the new standardised front-of-pack labelling to help make it easier for people to make healthier choices about what they buy and eat.

The Department of Health has today set out what the new food labels will look like and outlined how a colour-coding scheme of energy, salt, sugar and fat will look and how their levels are set.

Currently, food and drink labels often differ in the range of nutritional information provided. Currently, there is no law forcing retailers and manufacturers to display such information and manufacturers are currently only required by law to provide nutritional information if the product makes a nutritional claim. For instance, nutritional information must be on a product that claims to be ‘low fat’ or if vitamins or minerals have been added to the product.

Under new European Union rules, manufacturers will be required to provide particular nutritional information by December 2016. But any manufacturer that chooses to provide front-of-pack information will have to comply with the EU regulation by the end of 2014.

What changes are being made to food labels?

Nutrition labels, when they are displayed, are often provided on the back, side or on the front of packaging. The new, standardised food labels will be displayed on the front of food and drink products and they will routinely include the following information per portion of food:

the amount of energy (presented in kilojoules (kJ) and kilocalories (kcal), known as calories)
the amount of fat and saturated fat
the amount of sugar
the amount of salt

These amounts will be shown as ‘Reference Intakes’ (formerly known as ‘Guideline Daily Amounts’). Alongside the amounts listed above, food labels will show how much of the maximum daily intake a portion of food accounts for.

Food labels will also contain red, amber and green colour-coding to visually show the nutritional value of food portions. This will allow people to see at a glance if the food product has high, medium or low amounts of fat, saturated fat, sugars and salt:

red means high
amber means medium
green means low

In short, the more green lights, the healthier the choice.

When are these changes being made?

Standardised front-of-label packaging will be in place by December 2014 by organisations that have signed up to make the changes. Some have already made the changes and some will make changes from today.

Why are food labels being changed?

Research has shown that the different nutrition labels on food are confusing. These different nutrition labels have arisen because companies have responded to their customers’ demand for more nutritional information, but until now there has been no agreement on a consistent format. The new labelling system aims to make it easier for people to make healthier choices, by comparing the same kinds of foods to see if there is a healthier option.

As part of the government’s efforts to improve health through reducing obesity levels, the Department of Health is working with food manufacturers and supermarkets through a programme called the Responsibility Deal. This programme aims to get business to reduce the amount of calories, salt and saturated fat in foods. The standardised front-of-pack label is a new Responsibility Deal pledge that food and drink companies can sign up to. Many companies already have taken this pledge to change their food labels.

Public Health Minister, Anna Soubry, said: “The UK already has the largest number of products using a front-of-pack label in Europe, but we know that people get confused by the variety of labels that are used. Research shows that, of all the current schemes, people like this label the most and they can use the information to make healthier choices.

“We all have a responsibility to tackle the challenge of obesity, including the food industry. By having all major retailers and manufacturers signed up to the consistent label, we will all be able to see at a glance what is in our food – this is why I want to see more manufacturers signing up and using the label.”

The labels are not designed to ‘demonise’ foods with lots of reds, but to have people consider what they are eating and make sure it’s part of a balanced diet. Download the Eatwell plate (PDF, 1.6Mb) for more information about a healthy balanced diet.

Who is changing their labels?

Links To The Headlines

Food packaging 'traffic lights' to signal healthy choices on salt, fat and sugar. The Guardian. June 19 2013

New food labelling system launched. The Daily Telegraph. June 19 2013

Traffic light food labelling introduced by big supermarkets. Daily Mirror. June 19 2013

Food labelling: Consistent system to be rolled out. BBC News. June 19 2013

Major UK Supermarkets Launch New Food Labels. Sky News. June 19 2013

Red labels to warn of unhealthy food: Logos to appear on items considered 'bad' for health in anti-obesity drive. Daily Mail. June 19 2013

Health claims about vitamin D examined

Tue, 18 Jun 2013 13:33:00 EST

Rarely a month goes by without the papers reporting at least one health news story related to vitamin D. In recent weeks the media has reported that vitamin D can help relieve the symptoms of asthma and lower blood pressure.

There have been long-standing claims that vitamin D brings a wide range of benefits, from preventing cancer risk to improving mental health, or even reducing your risk of getting multiple sclerosis.

But is there good evidence to back up the claims? And do you need to change your diet or take vitamin D supplements to reduce your risk of disease?

What is vitamin D?

Vitamin D is a group of related molecules that the body needs to help absorb calcium and phosphate. These are substances that help keep the bones healthy and strong.

Vitamin D is somewhat unusual in that we obtain it from two difference sources:

sunlight
dietary sources

How much sun is needed to get enough vitamin D?

When the skin is exposed to the ultraviolet B contained in sunlight, it generates the production of vitamin D. Most people generate around 90% of the vitamin D in their body from sunlight.

Your sunshine requirements differ depending on factors such as your skin tone and your weight. A 2010 consensus statement on vitamin D (PDF, 126.69kb), released by a combination of charities, recommended a "little and often" approach. It says regularly going out with sunscreen for a few minutes in the middle of the day should provide enough exposure to create sufficient vitamin D.

You certainly don't need to get a suntan, let alone risk sunburn. Overexposure to the sun in this way can increase your risk of skin cancer.

How to get enough vitamin D through your diet

Eating a healthy balanced diet should be sufficient to top up the remaining 10% or so that experts believe we need through our diet. Dietary sources of vitamin D include:

oily fish, such as salmon, sardines and mackerel
eggs
fortified fat spreads
fortified breakfast cereals
powdered milk

What is vitamin D deficiency?

Vitamin D deficiency is when the body does not have enough vitamin D to properly absorb the required levels of calcium and phosphate.

Mild to moderate vitamin D deficiency can lead to bone pain and weakening of the bones (osteoporosis). This could make you more likely to fracture a bone if you had a fall.

More severe levels of deficiency can lead to the development of rickets in children and osteomalacia in adults.

Rickets, osteomalacia and vitamin D

Chronic severe vitamin D deficiency in children can disrupt the normal formation of bones, causing them to become soft and malformed and resulting in the condition known as rickets.

Symptoms of rickets include:

bone pain
deformities
fragile bones vulnerable to fracture

Previously regarded as a disease of the past associated with Victorian slums, rickets is now making a comeback in some parts of England.

In 2012 the Royal College of Paediatrics and Child Health released a statement highlighting the problems of vitamin D deficiency in children, reporting that rates of rickets have risen fourfold in the last 15 years.

Osteomalacia, like rickets, develops because of softening of the bones. The main symptom of osteomalacia is a dull, throbbing and often severe bone pain that usually affects the lower section of the body. Osteomalacia can also result in muscle weakness.

How common is vitamin D deficiency?

Vitamin D is thought to be much more common than most people realise. A 2007 survey estimated that around 50% of all adults have some degree of vitamin D deficiency.

In 2012 the Chief Medical Officer for the United Kingdom wrote to GPs highlighting the issue of vitamin D deficiency in high-risk groups (see below).

An independent advisory committee is also reviewing current recommendations on vitamin D, but the results of this extensive analysis are not expected until 2014.

What are the risk factors for vitamin D deficiency?

Lack of exposure to sunlight

Unsurprisingly, a significant risk factor for vitamin D deficiency is lack of exposure to the sun.

Possible factors that can result in limited exposure to sunlight include:

overuse of sunblock
being housebound or spending long parts of the day inside
wearing clothes that cover up most of your body, often for cultural or religious regions

There are anecdotal reports that children may be more likely to develop vitamin D deficiency these days, as they are less likely to play outside than children did in the past.

Darker skin tone

Having a darker skin tone means you require a greater amount of sunlight exposure to generate vitamin D.

It is estimated that people with a naturally dark skin tone may require three to five times longer sunlight exposure to make the same amount of vitamin D as a white person.

Obesity

Obesity could be an overlooked cause of vitamin D deficiency. A recent study published in February 2013 suggested there is a direct relationship between increasing body mass index (BMI) and falling vitamin D levels.

The authors of the study speculated that vitamin D may become "trapped" inside fat tissue, so there is less available to circulate inside the blood.

How is vitamin D deficiency treated?

Mild to moderate vitamin D deficiency can usually be treated by making lifestyle changes such as getting more sun and eating foods rich in vitamin D. In some cases your GP may also recommend you take vitamin D supplements.

In more severe cases where the deficiency has affected bone growth and density, such as rickets, a vitamin D injection may be recommended.

Foods fortified with vitamin D

Unlike in some other countries, in England staple food items such as milk, flour and cereals are not routinely fortified with vitamin D. Fortified versions of goods such as cereals and milk are available from most supermarkets. You can read the food labels to compare the levels of vitamin D between products.

Some argue that people in the UK, especially in the north of England and Scotland, would benefit from fortification. However, the vitamin D we get from dietary sources is thought to stay in the body longer than the vitamin D we get from sunlight. Fortifying staple foods and drinks could potentially lead to dangerously high levels of vitamin D in a small number of people (vitamin D toxicity).

Other benefits of vitamin D

Links To Science

Avenell A et al. Vitamin D and vitamin D analogues for preventing fractures associated with involutional and post-menopausal osteoporosis. Cochrane Database of Systematic Reviews. April 2009

Bjelakovic G et al. Vitamin D supplementation for prevention of mortality in adults. Cochrane Database of Systematic Reviews. July 2011

Garland CF et al. Vitamin D for Cancer Prevention: Global Perspective. Annals of Epidemiology. July 2009

Holick MF et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology and Metabolism. July 2011

Jagannath VA et al. Vitamin D for the management of multiple sclerosis. Cochrane Database of Systematic Reviews. December 2010

Pearce SH, Cheetham TD. Diagnosis and management of vitamin D deficiency. BMJ. January 2010

Urashima M et al. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. American Journal of Clinical Nutrition. March 2010

Vimaleswaran KS et al. Causal Relationship between Obesity and Vitamin D Status: Bi-Directional Mendelian Randomization Analysis of Multiple Cohorts. PLOS Medicine. Published online February 5 2013

Misguided claims alcohol in pregnancy helps baby

Tue, 18 Jun 2013 13:33:00 EST

“A glass of wine every day in pregnancy could be good for your baby,” is the entirely incorrect headline in The Daily Telegraph today. Other newspapers reported that drinking while pregnant does ‘no harm’, these claims are also misleading.

The news is based on a new study investigating the link between alcohol exposure before birth and childhood balance, which is considered an important sign of children’s development. Previous research has found that alcohol consumption during pregnancy is linked to poorer outcomes on several markers of neurodevelopment, but the effect on balance is uncertain.

Researchers found no evidence of an adverse effect of low-to-moderate maternal alcohol consumption on childhood balance. They also found moderate alcohol exposure seemed to have a beneficial effect compared to no alcohol. However, the researchers say that this positive effect is possibly due to them not being able to fully adjust for the fact that higher alcohol use was linked to social advantage.

This study adds to knowledge about the effects of alcohol in pregnancy on children’s balance. However, uncertainty remains over whether there is a ‘safe’ level of alcohol consumption during pregnancy. For this reason, current guidance suggests that women avoid alcohol completely during the first three months of pregnancy. If women choose to drink after this time, they should not drink more than one to two units of alcohol once or twice per week, and avoid binge drinking altogether. Contrary to media suggestions, this study does not change this advice.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and University Hospital Bristol NHS Foundation Trust and was funded by the UK Medical Research Council, the Wellcome Trust, the University of Bristol and the Alcohol Education and Research Council (AERC). The study was published in the peer-reviewed, open access medical journal, BMJ Open.

The Telegraph’s headline was incorrect and potentially dangerous. While the researchers found a positive effect of alcohol in one measure, they clearly and categorically said that this likely to be a statistical blip. This headline also ignores the fact that the research was into just one aspect of children’s development and that alcohol consumption was measured at only one point in time.

Because of these limitations, women should stick to the existing advice on alcohol in pregnancy. Fortunately, in its online edition, the Telegraph used a more accurate headline. All other newspapers’ headlines suggested that drinking in pregnancy was “OK”, or does “no harm” – and are also misleading.

What kind of research was this?

This was a prospective cohort study that aimed to determine whether there was a link between alcohol exposure during pregnancy and balance in 10-year old children. Although this is the ideal study design to address this question, cohort studies can only show association, and cannot prove a cause-and-effect relationship. This is because other factors (confounders) may be responsible for any association seen.

This problem is demonstrated by this study. Despite the fact that the researchers collected information on a number of socioeconomic factors, and adjusted for them in their analyses, they conclude that the associations seen are probably due to not fully being able to adjust for social advantage.

What did the research involve?

The researchers used information on 6,915 children and their parents, who were participating in the Avon Longitudinal Study of Parents and Children.

This study used children who were born singly (who were not twins or another multiple birth) between April 1991 and December 1992, who had undergone balance assessment at 10 years of age and for whom they had information on the mother’s alcohol intake.

The balance assessment evaluated three types of balance:

dynamic balance: time to cross a 2m balance beam, walking heel to toe
static balance, eyes open: heel to toe balance on a beam, eyes open and standing on one leg, eyes open. Both balances were held for a maximum of 20 seconds
static balance, eyes closed: heel to toe balance on a beam, eyes closed and standing on one leg, eyes closed. Both balances were held for a maximum of 20 seconds

Children were said to have ‘good balance’ if they were in the top 25% fastest times for crossing the balance beam (good dynamic balance), if they maintained the static balances with their eyes open for 20 seconds (good static balance with eyes open), and if they were in the top 25% longest times for holding the static balances with eyes closed (good static balance with eyes closed).

Alcohol exposure was measured by asking mothers and fathers to self-report their alcohol intake at 18 weeks of pregnancy.

At 18 weeks of pregnancy, mothers reported both their current consumption and their consumption prior to pregnancy. For each time point, the mothers reported the total number of glasses (defined as a pub measure of spirits, half a pint of larger or cider, a small glass of wine) consumed per week, categorised into none (0 glasses), low (1-2 glasses), moderate (3-7 glasses), and high (more than 7 glasses) consumption. Mothers were also asked how many days in the previous month they had drunk the equivalent of at least four units of alcohol (binge drinking). Similarly, fathers reported alcohol consumption and binge drinking.

Information on other factors that could explain any association seen (confounders) was also collected. These included marital status, crowding index (number of people in the household and number of rooms), home ownership, parity (the number of previous children the mother has), maternal education, ethnicity, maternal age, maternal social class, smoking, cannabis use, caffeine consumption, number of stressful maternal life events during pregnancy, and maternal depression.

The researchers looked to see whether there was a link between alcohol exposure during pregnancy and the balance ability of 10-year old children after adjusting for these potential confounders.

What were the basic results?

Few mothers reported drinking heavily during pregnancy, with 95.5% of mothers reporting no alcohol consumption to moderate alcohol consumption.

In general, higher total levels of maternal alcohol consumption were associated with higher socioeconomic status and higher maternal age, whereas higher levels of binge drinking were associated with lower socioeconomic status and lower maternal age.

No evidence was found of an adverse effect of maternal alcohol consumption on childhood balance.

There was no association between any level of alcohol consumption during pregnancy and childhood dynamic balance.
Compared to no alcohol consumption at 18 weeks of pregnancy, moderate maternal alcohol consumption was significantly associated with good static balance with both eyes open and eyes closed.
There was no significant difference in static balance (eyes open or eyes closed) between no alcohol, low alcohol or high alcohol (the only significant association seen was for moderate alcohol).

Regular heavy maternal binge drinking (more than 10 times per month) was also associated with good static balance (eyes shut) in children. There was no significant association between any other level of binge drinking, or any other measure of balance.

Paternal drinking during the first three months was associated with good static balance (eyes open) in children, with fathers that reported drinking less than one glass per week, at least one glass per week and at least one glass per day having children with better static balance than those that reported never drinking.

The researchers then analysed the data differently, using a technique called “Mendelian randomisation”. This approach is based on the assumption that a person’s DNA is not linked to socioeconomic status.

It is known from previous research that particular variations in a gene that codes for alcohol dehydrogenase (an enzyme that breaks down alcohol) predisposes people to lower alcohol consumption. The researchers looked at this variant. Mothers carrying this variant consumed less alcohol before, during and after pregnancy.

There was no evidence that mothers carrying this variant had children with poorer balance, which is not what would be expected if alcohol exposure improves balance. The researchers use this result to suggest that the previous association between maternal alcohol consumption and balance outcomes may have been due to the fact that the current analysis could not completely adjust for socioeconomic status.

How did the researchers interpret the results?

The researchers suggest that the most correct interpretation of their results is that they, “provide no strong evidence of an effect, either beneficial or detrimental, of moderate maternal alcohol use during pregnancy on offspring balance.”

Conclusion

This large, well-designed prospective study has found no evidence that moderate maternal alcohol consumption at 18 weeks of pregnancy has an adverse effect on offspring balance at age 10.

The study is limited by the fact that, as a cohort study, it cannot show a cause-and-effect relationship. This is because other confounding factors may be responsible for any association seen.

Despite the fact that the researchers collected information on a number of socioeconomic factors, and adjusted for them in their analyses, they conclude that the small benefits seen for some outcomes with some drinking patterns are probably due to not fully being able to adjust for social advantage.

Also, maternal and paternal alcohol use was self-reported and alcohol use during pregnancy was assessed at only one point in time, which could be subject to bias. The researchers also reported that the balance measures used had low test-retest reliability.

Although the results of this study will add to knowledge about the effects of alcohol in pregnancy on one particular developmental outcome, uncertainty remains over what is a ‘safe’ level of alcohol consumption during pregnancy.

Current guidance suggests that women avoid alcohol completely during the first three months of pregnancy due to increased risk of miscarriage, and if they choose to drink after this time, should not drink more than one to two units of alcohol once or twice per week, and avoid binge drinking altogether. This study does not change this advice.

For more advice, read Can I drink alcohol when pregnant.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

A glass of wine a day in pregnancy could be good for your baby. The Daily Telegraph. June 18 2013

Moderate drinking during pregnancy 'does not harm baby's development'. The Guardian. June 18 2013

Pregnant women told moderate drinking will not harm the baby. The Independent. June 18 2013

Mums-to-be 'CAN have a glass of wine a day without harming their child's development'. Daily Mail. June 18 2013

Glass of wine per day OK during pregnancy, study claims. Daily Mirror. June 18 2013

Glass of wine does no physical harm, pregnant women told. The Times. June 18 2013

Links To Science

Humphriss R, et al. Prenatal alcohol exposure and childhood balance ability: findings from a UK birth cohort study. BMJ Open. Published online June 18 2013

Earlier breast screening in high-risk women shows 'encouraging' results

Mon, 17 Jun 2013 13:33:00 EST

"Women with a family history of breast cancer should be screened in their thirties," says The Daily Telegraph.

The news relates to an ongoing study that aims to look at the effects of mammography screening in women with a family history of breast cancer when they are between the ages of 35 and 39.

National guidelines currently recommend that women identified as being at increased risk of breast cancer because of a family history of the disease are offered annual mammography screening from the age of 40. Women at very high risk, such as those with BRCA1 or 2 mutations, are already offered annual MRI screening from the age of 30.

This report covers the first stage of the study, which looked back at the type of screening offered to women in this category at 33 centres across the UK. It found that the majority of the centres surveyed offered mammography, with most offering it on an annual basis.

In the five centres with the most rigorous follow-up, 47 cancers were identified in women, with almost half identified through screening and about a third identified between mammograms.

Comparison of these cancers with results reported in previous studies in unscreened women suggested that in the women offered screening, the cancers identified were smaller and less likely to have spread to the lymph nodes at the time of diagnosis.

The current study gives a snapshot of existing surveillance measures in the UK for women aged 35-39 who have an increased risk of breast cancer because of their family history. But as the centres surveyed were not specifically collecting information in order to analyse the effectiveness of mammography screening, they did not have enough information for a thorough analysis.

Therefore, the second part of this study plans to follow 2,800 high-risk women offered mammography screening on an annual basis up to 2016. These results will give a better idea of the potential benefits, risks and costs of screening in this younger age group.

Where did the story come from?

The study was carried out by researchers from the Genesis Breast Cancer Prevention Centre at the University Hospital of South Manchester NHS Trust and other hospitals and research centres in the UK.

It was funded by Breast Cancer Campaign and was published in the peer-reviewed medical journal, Familial Cancer.

The Daily Telegraph's headline doesn't convey the preliminary nature of these findings, but it does report later on in the story that a larger study is planned and that changes to recommendations are only likely if the larger study confirms the results.

What kind of research was this?

The researchers were reporting on part of a study of breast cancer screening in younger women with a family history of breast cancer (the FH02 study). The first part of the study was a retrospective analysis of the type of breast cancer surveillance that has been offered to these women in the past and what their outcomes were.

In the UK, all women between the ages of 50 and 70 are currently offered mammography. Women whose family history indicates that they are at increased risk are offered annual mammograms from the age of 40 as a form of "surveillance" for the disease. Women at very high risk, including those who are known to carry mutations in one of the BRCA1/BRCA2/TP53 genes, are offered annual MRI screening from the age of 30.

The researchers report that a previous study looked at mammography for women aged 40-49 in the UK with a significant family history of the disease (the FH01 study), but the effects of mammography in women aged 35-39 has not yet been assessed.

The National Institute for Health and Care Excellence (NICE) has produced guidelines on how doctors should classify breast cancer risk in women with a family history of the disease, and how they should be assessed and treated.

The researchers state that in the second part of this study, they will carry out a prospective study to look at the effects of breast cancer surveillance in these younger women. A previous study suggested that the health professionals caring for these women feel that such surveillance is likely to be of benefit. For this reason, it was decided that it would not be ethical to carry out a randomised controlled trial and that the study would compare the participants' results with those from previous studies instead.

What did the research involve?

Retrospective study

The researchers sent a survey to the 33 centres taking part in the study. The survey asked whether they had previously carried out mammographic surveillance in women under the age of 40 with an increased familial risk of breast cancer.

If they answered yes, the survey then asked about exactly how they selected women for surveillance and what this consisted of. They also asked about the outcomes of this surveillance, including the number and type of cancers identified.

The researchers compared these results with the types of cancer reported in studies published previously looking at women:

aged 40-49 years with a family history of breast cancer who had annual mammography (the FH01 study)
aged 40-49 years with a family history of breast cancer
a series of women aged 30-49 having breast cancer surgery
women aged 35-39 years with a family history of breast cancer who had not been screened

Prospective study

The researchers reported in detail the planned approach for their prospective study. This study aims to identify the likely benefit of annual mammography for women aged 35-39 with a family history of breast cancer.

They will compare the results in this group with results from the preceding study in older women with a family history of the disease (the FH01 study) and the UK Age Trial, a randomised controlled trial that assessed the effects of annual mammography screening in women from the age of 40 (not selected on the basis of family history). This study will also assess the cost of surveillance, so it can estimate its cost effectiveness.

The researchers say they have recruited 2,280 women from 33 centres, and should have reached the target of 2,800 by the end of June 2013. The study is expected to continue until June 2016.

What were the basic results?

In their survey, the researchers found that among the 33 centres:

mammography screening in women aged 35-39 at increased risk of breast cancer was already carried out in 27 centres
almost all of this screening was reported to use film mammography, rather than the newer digital mammography
these 27 centres record a three generation family history and carry out a risk assessment in these women to determine their risk level
25 of the centres record the women's lifetime risk of cancer and 22 record whether they have the known genetic mutations which predispose women to breast cancer (BRCA1, BRCA 2 and TP53)
26 of the centres offered the women annual mammograms and one centre offered them screening every two years
17 centres offered MRI scanning
14 centres offered routine physical examinations
none of the centres routinely offered ultrasound

Five centres had robust systems to reliably identify whether any breast cancers were identified in these women in the period between mammograms (called interval cancers), as well as any detected in the mammogram.

There were 47 breast cancers in the women attending these centres between 1994 and 2010. Ten of these cancers (21%) were already known when the women attended the centres, 22 were new cancers (47%) identified through screening, and 15 (32%) were detected between mammograms.

Compared with two groups of unscreened women with breast cancer – one who had a similar family history and one without a family history – the cancers among the screened women were significantly smaller and less likely to have spread to the lymph nodes.

More of the screened women were alive with no spread of the disease in the screened group than in the two groups of unscreened women with breast cancer. However, the number of deaths from breast cancer was too small to carry out a robust analysis.

How did the researchers interpret the results?

The researchers say that this is the first study to assess the effects of mammography alone in women aged under 40 who are at increased risk of breast cancer.

They say that the results are "encouraging", but that the prospective part of their study is needed to assess the effects of digital mammography in moderate and high-risk women in order to inform cost effectiveness analyses.

Conclusion

The current study gives a snapshot of existing surveillance measures in the UK for women aged 35 to 39 with an increased risk of breast cancer due to their family history.

There are some points to note, which the authors themselves highlight:

As this first part of the study is retrospective, the centres will not have collected all the relevant information that would allow thorough evaluation of the effects of mammography.
The number of cancers in women receiving screening described in detail in the current study is small (just 47). The larger prospective part of the study is needed to get better estimates of the rates of cancer in these women.
Most previous screening in the centres used film mammography, but the newer technique of digital mammography may offer better results.
In addition, the comparisons performed in the current part of the study against results in other studies may be affected by differences between the groups of women other than the screening offered. For example, the studies covered different time periods, and breast cancer management may have differed over these periods and could affect the chances of survival.

Overall, the current study gives some background information, but the second part of the study will shed more light on the potential effects of mammography surveillance in younger women at increased risk of breast cancer.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Family history of breast cancer should mean screening earlier. The Daily Telegraph, June 17 2013

'Screen women aged 30 for breast cancer': Half a million at risk because of family history could be offered mammograms. Daily Mail, June 17 2013

Call for more breast cancer screening. The Times website, June 17 2013

Links To Science

Evans DG et al. Mammographic surveillance in women aged 35–39 at enhanced familial risk of breast cancer (FH02). Familial Cancer. Published online June 4 2013

Baldness drug finasteride 'cuts men's drinking'

Mon, 17 Jun 2013 13:33:00 EST

“Anti-baldness drug can cause men to lose interest in alcohol,” reports the Mail Online.

This report is based on a small survey of young men who had been taking the drug, finasteride, for hair loss. Impotence and decreased libido are recognised side effects of this anti-male-hormone drug, and all 83 men in this study had experienced sexual side effects that lasted at least three months after they stopped taking it.

The survey found that the men reported drinking less at the time of the survey than before they started taking the drug. However, this was on average five years earlier, so it is not clear how well these men could remember what they drank so far in the past.

Also, as the study had no control group who didn’t take the drug, it’s not possible to say that these changes wouldn’t have happened naturally over time as the men aged. The results may also not be representative of what might be seen in older men, men taking the drug for its other use (enlarged prostate), or men who do not experience the sexual side effects of the drug.

Overall, these findings are inconclusive. Larger studies, ideally with a control group, are needed to assess the effects of the drug on alcohol consumption.

Where did the story come from?

The study was carried out by a single researcher from The George Washington University in the US. No sources of funding were reported. It was published in the peer-reviewed journal Alcoholism: Clinical and Experimental Research.

The Mail Online reports the results of the study, but not any of its fairly extensive limitations.

What kind of research was this?

This was a cross-sectional study reporting on the alcohol consumption among men taking the drug finasteride. This anti-male-hormone drug is licensed to treat benign (non-cancerous) enlargement of the prostate and male pattern hair loss.

The recognised side effects of the drug include sexual problems such as decreased libido, impotence and erectile dysfunction. It may also have effects on the nervous system. The researchers reported that finasteride has been shown to reduce alcohol intake in male mice, but no studies have assessed this in humans.

This study relied on men reporting their own alcohol consumption before and after taking the drug in a single survey. This is likely to be less reliable as men may not accurately remember their consumption in the past. Asking the men to keep an alcohol diary before and after they started taking the drug would be a more reliable approach.

The study also didn’t include a comparison group not taking the drug. Therefore, the result cannot conclusively show that the drug itself is definitely causing a change in alcohol consumption.

What did the research involve?

The researchers surveyed the alcohol consumption habits in 83 men aged under 40, who had been taking finasteride to treat or prevent male pattern hair loss. These men had experienced persistent sexual side effects but were otherwise healthy.

The men were reported to be recruited from the author’s previous studies on persistent sexual side-effects of finasteride. These men had side-effects for at least three months despite stopping finasteride. Men who had sexual dysfunction before taking finasteride, had chronic medical conditions, current or past psychiatric conditions, or had taken psychiatric medication were excluded.

The survey asked about their average weekly alcohol consumption before they started taking finasteride, and at the time of the interview. A glass of wine, can of beer, or shot of hard liquor was considered a standard drink.

What were the basic results?

Sixty-three of the men reported drinking at least one alcoholic drink per week before starting finasteride. Among these men, at the time of the survey:

65% reported reduced alcohol consumption
32% reported no change in their alcohol consumption
3% reported an increase in their alcohol consumption

On average, of the men who reported drinking alcohol, the average number of drinks per week reduced significantly – from 5.2 before finasteride to 2.0 after finasteride. As the men had stopped taking finasteride, they were not taking the drug at the time of assessment.

The authors reported that although they were not asked about this specifically, some men volunteered the information that they could not tolerate alcohol as well after starting to take finasteride. Eighteen men reported giving up alcohol entirely.

How did the researchers interpret the results?

The researchers concluded that among men who developed persistent sexual side effects from finasteride and stopped taking the drug, almost two-thirds reported reduced alcohol consumption.

Conclusion

This relatively small study in a very select group of men provides only limited evidence of the effects of finasteride on alcohol consumption in men. Its limitations include:

The study didn’t include a comparison group not taking the drug. Therefore, the result cannot conclusively show that the drug itself is definitely causing a change in alcohol consumption, rather than the men just having changing alcohol tolerance as they got older.
The study asked men to remember what their alcohol consumption was before taking the drug – on average about five years previously. This is likely to be less reliable as men may not accurately remember their consumption in the past. Asking the men to keep an alcohol diary before and after they started taking the drug would be a more reliable approach.
The study only used a crude assessment of the number of drinks consumed, the size and alcohol content of these drinks may vary and this could affect comparison of before and after findings.
The study did not say exactly how men were selected to take part, or whether they knew the purpose of the study. The men’s responses may have altered if they knew that finasteride may have an effect on alcohol consumption.
The men all had persistent sexual dysfunction following taking finasteride for male pattern hair loss. The results may not apply to other men taking the drug, for example those without these side effects, or those taking it for an enlarged prostate.
The author reported that many of the men in the study experienced depressive symptoms, and this may have affected their alcohol consumption.

As the author acknowledges, more research would be needed to determine the effects of finasteride on the nervous system and alcohol consumption.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Anti-baldness drug can cause men to lose interest in alcohol. Mail Online. June 17 2013

Links To Science

Irwig MS. Decreased Alcohol Consumption Among Former Male Users of Finasteride with Persistent Sexual Side Effects: A Preliminary Report. Alcoholism: Clinical and Experimental Research. Published online June 13 2013

Are men's sex drives to blame for the menopause?

Fri, 14 Jun 2013 13:33:00 EST

“'Cradle snatchers' cause menopause, says biologist,” is the bizarre headline in The Guardian today.

The menopause has always been a bit of an evolutionary puzzle. Evolution is about one thing only – reproducing genes. So why would genes that cause a woman to lose fertility halfway through her life survive?

Two main theories have been previously suggested:

one theory suggests the menopause is a trade-off in increased fertility versus prolonged survival
the second theory is known as the “grandmother effect”, whereby older, post-menopausal women are no longer fertile so they can instead help out with raising their grandchildren

A new study has provided a third theory. Humans started off with prolonged fertility, but if men theoretically preferred mating with younger women there would be no pressure to weed out the mutations that cause infertility in later life. According to this theory, over time mutations affecting fertility in older women accumulate – leading to most, and then all, women experiencing menopause.

Researchers used a complicated computer model to run a number of evolutionary cycles and found that the model was consistent with their theory. But it’s not possible to say conclusively that this model accurately represents what has happened in human evolution, and other factors may contribute.

The findings are interesting but they have no direct health implications. Menopause – for whatever reason it may occur – is a natural part of human female life, to which no blame should be attached.

Where did the story come from?

The study was carried out by researchers from McMaster University, Ontario, Canada, and was funded by the Origins Institute and Shared Hierarchical Academic Research Computing Network at McMaster University, and the Natural Sciences and Engineering Research Council of Canada.

The study was published in the peer-reviewed open access scientific journal PLoS Computational Biology.

The media reporting of the theory is broadly accurate but it is just that, a theory. This complex computer modelling research can only suggest certain scenarios that could potentially explain the observations seen. It is not possible to say conclusively that these models do represent what truly happened.

Headlines that suggested men are “to blame for the menopause” are a bit silly. Evolutionary forces are not something anyone has any control over. Blaming men for the menopause is like blaming someone other hereditary conditions that have evolved in humans over time, say, sickle cell anaemia.

A number of the news sources carry a quote from another expert critical of the theory. Dr Maxwell Burton-Chellew, an evolutionary biologist in the department of zoology at the University of Oxford, was quoted as saying: “This [theory] is probably the wrong way round - the human male preference for younger females is likely to be because older females are less fertile.”

What kind of research was this?

This was a computer modelling study trying to determine why women undergo menopause.

As the authors note, survival beyond the menopause is a characteristic that appears almost unique to humans with only odd exceptions (such as whales, and chimps in captivity). Evolutionary theories suggest that natural selection should operate against living beyond reproductive age and it is not clear (theoretically) why women live beyond the menopause.

At least two possibilities have been put forward to explain this phenomenon: a trade-off favouring longer lifespan over reproduction in women (because giving birth when older may increase mortality risk); and that menopause increases the reproductive success of the woman’s offspring (that is, the “grandmother effect” of older women being able to assist their children in rearing their own children).

Other researchers have suggested that living beyond menopause could be down to an influence from males. They suggest that the fact that men remain fertile throughout their lifespan would prevent accumulation of lifespan-shortening mutations, allowing men and women to live longer. However, this does not explain why women undergo menopause.

The current research aimed to test the effect of male mating preference on the evolution of the menopause. In particular, they were interested in the effect a male mating preference for younger females would have.

What did the research involve?

The research involved a complex computer model that looked at the effect on a population of male lifelong fertility and of male mating preference on female fertility.

The researchers modelled a population of a fixed size, which initially had pre-set fertility and survival probabilities. Each individual started the model in one of 18 increasing age classes. Survival probability for each age group (determined by the number and type of mortality-causing mutations introduced) was assessed at five-year intervals.

The different computer models then introduced mutations into the population that separately affected mortality and fertility – mutations that affected fertility did not affect survival, and mutations that affected survival did not affect fertility.

This determined whether any individual in each age group died or went into the next age bracket. All individuals that reached the oldest age class (class 18) died in the model.

Deaths in the model were replaced by new births assigned to the first age category. The births were simulated by randomly selecting a male from the surviving male population, and a female from the surviving female population. Male and female fertility probabilities in the model were influenced by the number and type of fertility-affecting mutations that had been introduced into the population.

The researchers used their model to look at two scenarios.

First scenario

In their first scenario, men retained lifelong fertility, while women underwent menopause. In this scenario men did not have an age-specific mating preference. The researchers looked at the effect of introducing into the population theoretical genetic mutations that reduced lifespan but did not affect fertility.

Second scenario

In their second scenario, the researchers started out with men and women being fertile all their lives. They then introduced mutations that caused reducing fertility, and mutations that affected survival. They looked at the impact on this scenario of men having a preference for mating with younger females.

What were the basic results?

In their first scenario – where men did not have an age-specific mating preference and women underwent menopause – the researchers found that if men retained lifelong fertility this did prevent
mortality-causing mutations from accumulating in females. However, this does not explain why menopause came about.

In their second scenario - where both sexes started with lifelong fertility and men preferred to mate with younger females – over time the mutations reducing female fertility with age accumulated in the population, causing a decline in female fertility with age; effectively the menopause.

However, a similar effect was not seen if male mating preference was not influenced by women’s age.

How did the researchers interpret the results?

The researchers say that their model suggests that male mating preference for younger females could have driven the evolution of menopause. Their model did not need the presence of the other suggested explanations for the menopause to be present in order to work (the trade-off between fertility and lifespan and the “grandmother effect”). Instead they say that these explanations “may be insufficient factors in elucidating the origin of menopause”.

Conclusion

This computer modelling study has suggested that a male preference for mating with younger females could be the reason why menopause evolved in humans. However, whether this is truly the reason, or whether other factors some into play is not possible to say.

While this may be of interest to sociologists and others interested in the possibilities of human evolution, it has no direct health implications.

Unless someone comes up with a working time machine there is little we can do about the genetic cards that evolution has dealt us.

If you are experiencing the menopause, tempting as it may be to start blaming the men in your life, you are better off seeking support from your doctor, who may be able to offer treatment for particular symptoms of menopause.

A commonly used treatment is hormone replacement therapy (HRT), although there are also alternatives for women are not suited to HRT.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

'Cradle snatchers' cause menopause, says biologist. The Guardian, June 13 2013

Men 'to blame for the menopause'. BBC News, June 14 2013

Men may be to blame for the menopause. The Daily Telegraph, June 13 2013

Did man's yearning for young women create the menopause? Research suggests that men's wandering eyes may have caused middle-age loss of fertility in women. Mail Online, June 14 2013

Links To Science

Morton RA, Stone JR, Singh RS. Mate Choice and the Origin of Menopause. PLoS Computational Biology. Published online June 13 2013

Tenofovir halves HIV risk for injecting drug users

Fri, 14 Jun 2013 13:33:00 EST

“New AIDS prevention pill could cut infection rates in IV drug users by 50%,” the Mail Online reports, as the US Centers for Disease Control and Prevention (CDC) is set to approve the medication for injecting drug users.

The drug proved its worth in a large, well-conducted randomised control trial in Thailand. In this study, over 2,000 injecting drug users were given either placebo tablets or the ‘new’ drug tenofovir – which has been used to treat HIV since 2006.

The participants also attended monthly clinics to have blood tests to check for HIV infection, assess adverse events and to give them risk-reduction counselling. They were followed, on average, for four years to see if they contracted HIV.

The trial found that daily oral tenofovir reduced the drug users’ risk of catching HIV during the trial by about half: seven to eight per 1,000 would develop HIV per year without taking tenofovir, reducing to three to four per 1,000 per year if they did take tenofovir. Side effects for tenofovir were tolerable.

These are promising results though there are many other factors that would need to be considered before implementing an effective strategy on a wider scale outside of the context of a clinical trial.

While the obvious message in terms of HIV prevention is to stop injecting drugs, this type of pragmatic harm reduction approach could save many lives.

Where did the story come from?

The study was carried out by researchers from Bangkok Tenofovir Study Group, Bangkok, Thailand, and additional researchers from Centers for Disease Control and Prevention (CDC), Atlanta, and Johns Hopkins University, Baltimore, in the US. Funding was provided by the US CDC and Bangkok Metropolitan Administration.

The study was published in the peer-reviewed medical journal The Lancet.

The Mail Online's reporting of the study is accurate. However, there are additional issues that may need to be considered before the drug is licensed for this use, which the Mail does not describe.

What kind of research was this?

This was a randomised controlled trial that aimed to assess whether daily use of the antiretroviral (anti-HIV) drug, tenofovir, could reduce HIV transmission in injecting drug users.

Injecting drug users are at high risk of getting HIV due to needle sharing. Tenofovir is currently licensed for the treatment of people who have HIV infection, usually taken in combination with other antiretrovirals.

The researchers suggest that use of antiretrovirals to prevent HIV infection could be ‘a promising new strategy to end the HIV/AIDS epidemic’. Previous studies in animals and humans have suggested the drugs can prevent transmission of the virus. They are currently used to reduce the risk of mother-to-child transmission of HIV, and to reduce risk among healthcare workers who may have been exposed to HIV (for example, through a ‘needlestick’ injury).

The current study is a phase III trial, meaning the research has already progressed through the earlier stages of clinical trials. This study investigated tenofovir's effects and safety compared with inactive placebo in a large sample of injecting drug users.

What did the research involve?

The trial assessed whether giving tenofovir to injecting drug users reduced their chances of getting HIV over an average of four years.

It enrolled 2,413 injecting drug users from 17 drug-treatment clinics in Bangkok, Thailand. The clinics offer a wider range of services including HIV counselling and testing, risk-reduction counselling, social services, medical care, methadone treatment, condoms, and materials to clean injecting equipment (clinics cannot provide fresh needles under Thai law).

Participants were eligible if they were aged between 20 and 60 years, were HIV-negative, and reported injecting drugs during the previous year. The researchers excluded those positive for hepatitis B, and pregnant or breastfeeding women.

Participants were given contraception and hepatitis B vaccine, and were randomised to receive either daily oral tenofovir 300mg or identical placebo pills. Participants could choose either to be observed daily taking their treatment (this ensures the participants do actually take their pills), or could just attend the monthly visits. All participants attended monthly clinic visits where they received HIV blood testing, were assessed for adverse effects, and were counselled on risk-reduction and adherence to treatment.

Risk behaviour was assessed in more depth every three months.

The trial was long term, and lasted up to seven years. The average duration of follow-up was four years. The researchers assessed the number who remained in treatment each year.

What were the basic results?

Of the 2,413 randomised participants, 80% were men, 43% were in their 20s, 38% were in their 30s, and the remainder were older. The majority (63%) had injected drugs within the past three months.

Drugs used included heroin (22%), methamphetamine (33%), midazolam – a sedative which can give feelings of euphoria if injected at high doses (23%), and 22% were currently in a methadone programme.

For the first year, the proportion of participants retained in the trial was high (88% of the tenofovir group and 89% of the placebo group). However, this gradually declined each year up to seven years.

Overall, 34% of both groups withdrew from the study during the course of the seven years. Dropout during the course of the trial was for various reasons including loss to follow-up, death, pregnancy and contracting HIV. Participants took the drugs for an average 84% of treatment days, with no difference in adherence between the groups. Overall, 8% of participants reported sharing their drugs in some way.

HIV was acquired by 50 people during the trial:

17 in the tenofovir group – an incidence of 3.5 cases per 1,000 person-years of follow-up (if 1,000 people were followed for one year, three to four would develop HIV while taking tenofovir)
33 in the placebo group – an incidence of 6.8 per 1,000 person-years of follow-up (if 1,000 people who were not taking preventative treatment were followed for one year, six to eight would develop HIV)

This meant that taking tenofovir cut the risk of contracting HIV by about half (48.9% reduction, 95% confidence interval [CI] 9.6 to 72.2%).

There was no significant difference in the risk of any adverse events between groups. The most frequent adverse events were:

abdominal pain
nausea
vomiting
weight loss
diarrhoea
rash
fractures

Between 5% and 20% of people in both groups experienced these events. The only event that was significantly more common with tenofovir was nausea and vomiting, which affected 8% of the tenofovir group and 5% of the placebo group.

How did the researchers interpret the results?

The researchers concluded that daily oral tenofovir reduced the risk of HIV infection in people who inject drugs. They suggest that preventative treatment with tenofovir ‘can now be considered for use as part of an HIV prevention package for people who inject drugs’.

Conclusion

This was a well-conducted trial which has many strengths, including its very large sample size, long duration of follow-up, and regular and thorough assessments of HIV outcomes, adherence to treatment, adverse effects and risk counselling.

It found that daily oral tenofovir, when taken by injecting drug users, causes an almost 50% reduction in their relative risk of contracting HIV. It found that about seven to eight per 1,000 would develop HIV per year without taking tenofovir, reducing to three to four per 1,000 per year if they did take tenofovir.

Although the drug has been demonstrated to be effective, it is not yet licensed by drug regulators for this use. They will need to review a submission from the manufacturer on the evidence of efficacy and safety of the drug in injecting drug users before this can be granted. If tenofovir is licensed for this use, when considering whether it should be widely offered for this purpose, there are many factors to be taken into account. This includes the number of people that would need to be treated and duration of treatment, and the cost of this treatment.

For injecting drug users there are other important considerations. This includes that injecting drug–users’ often chaotic lives mean that they can find it difficult to access health services and may only be in contact with health professionals sporadically. This trial included only those who were currently attending drug treatment clinics. However, there are likely to be many other vulnerable groups of injecting drug users in the community who are not attending clinics, or who attend but then are lost to follow-up. Therefore, ensuring that all drug users are able to access care, and receive continued care and treatment may be issues that would need to be considered.

Another potential concern, is that preventative HIV treatment could possibly give false reassurance that the person is fully protected and would not be harmed by practices such as sharing needles or other injecting equipment, or having unprotected sex. It would still be important to ensure that people receive full information and guidance on the risks of blood borne infections (and other sexually transmitted infections), and the need to follow safe practices such as using single use needles and equipment and using condoms.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New AIDS prevention pill could cut infection rates in IV drug users by 50%. Mail Online, June 13 2013

Links To Science

Choopanya K, Martin M, Suntharasamai P, et al. Antiretroviral prophylaxis for HIV infection in injecting drug users in Bangkok, Thailand (the Bangkok Tenofovir Study): a randomised, double-blind, placebo-controlled phase 3 trial. The Lancet. Published online June 13 2013

Claims angry Lego faces could upset children

Thu, 13 Jun 2013 13:33:00 EST

“Lego characters are getting angrier – and could be harming children's development,” reports the Daily Mail.

Its report is based on a study that asked over 250 adults in the US to rate the emotion on the faces of more than 600 different Lego minifigures (affectionately known as "minifigs"). It found that most faces are happy, but that anger is also a common expression. Initially very different heads were produced, with the first face from 1975 being rated as sad, and the next few produced in the late 1970s and early 80s rated as happy.

Over time, the proportion of happy faces has declined. This increase has been partially driven by an increasing tendency towards cross-branding, such as Star Wars Lego, with some minifigs representing "baddies", rogues and warriors from these films.

Importantly, the study did not look at what impact the faces had on a child’s emotions. It is a great stretch to say that they may be “harming children’s development”.

You could also make the point that children actually enjoy an angry villain. Children’s fiction is full of infamous examples, ranging from Captain Hook to Voldemort.

A final piece of advice, provided by Lego, is that parents who are concerned “can always just switch heads with another figure”.

Where did the story come from?

The study was carried out by researchers from the Human Interface Technology Laboratory New Zealand at the University of Canterbury, and the Industrial Research Institute for Automation and Measurements in Poland. No sources of funding were reported.

The study appears to be a written summary of a presentation to be given at a scientific conference on how humans interact with objects that are designed to represent personalities. It is unclear whether the study has been peer-reviewed.

The media coverage has tended to overinterpret the findings of this research, with the lead researcher’s suggestion that angry faces could affect a child’s emotional development being accepted uncritically.

Also, The Guardian reports that “there were risks involved in exposing children to a variety of emotions, with small fans likely to remember the anger and fear in their figurines' faces, as well as their happier moments”. It is not clear how the paper came to include this statement, as the study did not assess children at all. In fact, only The Daily Telegraph explicitly reported in its text that the study only included adults.

The BBC News coverage includes a balancing comment from the author that it is "hard to derive a causal relationship" between angry toys and children's behaviours.

What kind of research was this?

This was a cross-sectional study looking at people’s perception of the emotion shown on Lego figures’ faces. The researchers were interested in whether the types of faces on Lego figures had changed over the last 35 years, and if perception of the face varies if the whole body of the figure is shown. The researchers are from a laboratory that looks at “developing and commercialising technology that improves human computer interaction”, with the ultimate goal of improving users’ experience.

Therefore, the study did not really focus on health issues or child development as such. It suggested that their study may help other researchers to understand the effect of the figures’ appearance on users over time, and also to inform design of other faces in game and toys.

What did the research involve?

The researchers took a sample of Lego figure faces over the years, and asked people what emotions the face expressed to see if the types of expression changed over time.

The researchers photographed all 3,655 Lego minifigures released between 1975 and 2010. They identified 628 heads with different faces used on these figures, and identified the year in which the head was first introduced. They used all of these faces in their study. They also randomly selected 100 heads and a minifigure with that head for use in their survey. They excluded six heads where the face was largely obscured, for example by a helmet. They also presented one figure (a Harry Potter figure) with two different skin colours – the traditional Lego yellow or a “natural” peach-coloured skin tone.

The researchers recruited 264 adults in the US through a website that enables people and businesses to ask other people to do tasks that computers are not capable of doing (called Human Intelligence Tasks).

They used the website to present the isolated faces and minifigures in a random order, with 30 people asked to rate each face. The participants were asked to rate which of these six emotions each face expressed:

anger
fear
disgust
happiness
sadness
surprise

They were asked to rank on a five-point scale (similar to a Likert scale) how intensely the face showed the emotion, ranging from “weak” to “intense”. The participants could rate as many of the faces as they liked and they were paid one cent per face they rated.

For each face, the researchers identified the dominant emotion for each face by finding which emotion was most commonly reported as being present. The researchers then looked at whether the figures’ faces had changed in the emotions shown over time. They also looked at whether presenting a face with the body of the figure changed perception of the face’s emotion.

What were the basic results?

The researchers found that each face was reported as expressing about four different emotions on average. The dominant emotion on most faces was happiness (324 faces) followed by anger (192 faces).

The number of different faces produced has increased over time, from fewer than five faces each year up to 1988, to more than 90 in 2010. From the early 1990s there was an increase in the variety of facial emotions shown by the minifigures. In 1975, the faces produced were all rated as sad, while in 1978 and 1980 all were rated as happy. However, in these years, only very few faces were produced. The proportion of happy faces released in each year decreased over time as more different and more varied faces were introduced.

If the figure’s body was shown as well as the face, anger tended to be reported more frequently, and disgust, sadness and surprise less frequently.

The minifigure’s skin colour did not affect which emotion was perceived on the face.

How did the researchers interpret the results?

The researchers concluded that “toy design has become a more complex design space in which the imaginary world of play does not only consist of a simple division of good versus evil, but a world in which heroes are scared and villains can have a superior smile”. They suggest that face designers should take care in designing the expressions and to test their effect “since toys play an important role in the development of children”. However, they also say that to appeal to users the faces need to offer a wide range of emotions “that connect to the complex interaction scenarios of today’s users”.

Conclusion

Overall, this research suggests that Lego figures’ faces have changed over time. This is a finding that is unlikely to surprise parents (or big kids of a certain age). The default minifig of old (described in the study as having an “enigmatic smile”) is now just part of a much larger family of minifigs including pirates, Star Wars “imperial stormtroopers” and ninjas.

So, as more faces have been produced it is unsurprising that a larger variety of emotions has been shown on the faces – particularly as minifigs now more commonly represent warriors. This study only assessed adults’ responses to the faces, and children’s perceptions of the faces may differ.

The study did not look at how children perceived the faces’ emotions or what impact the faces had on a person’s own emotions. The study doesn’t tell us anything about how the faces might potentially impact the health or development of children or adults playing with the figures. Therefore, it is a great stretch to say that they may be “harming children’s development” or are a “possible cause for concern”.

As the Lego manufacturer suggested in The Guardian, parents who might be concerned “can always just switch heads with another figure” (however, wary parents may want to consider the emotional effects of decapitating their children’s toys).

There are also studies suggesting that playing with Lego – or other toys designed to stimulate creativity, planning and building skills – can play a positive role in a child’s development.

Read more about why play is important.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Lego faces are getting angrier, study finds. The Guardian, June 12 2013

Do Lego Minifigures' have anger-management issues? Toy's faces are becoming less cheerful and more grumpy, fearful and disdainful, finds study. Daily Mail, June 13 2013

Lego faces are angrier now, study shows. The Daily Telegraph, June 13 2013

Links To Science

Bartneck, C, Obaid, M, Zawieska, K Agents with faces – What can we learn from Lego Minifigures? (PDF 1.7Mb) Proceedings of the 1st International Conference on Human-Agent Interaction. 2013

Childhood obesity-related hospital visits quadruple

Thu, 13 Jun 2013 12:33:00 EST

'Generation XXL' is the headline on the front page of the Metro, as the results of a new study show that hospital admissions related to obesity in children have soared in recent years.

The study looked at English hospital admissions over a 10-year period for obese children and teenagers. It found that hospital admission rates for obesity and obesity-related health problems among children and young people have risen more than fourfold in the last decade, particularly among girls and teenagers.

Most admissions were not for obesity itself but for complications of obesity, including asthma, sleep apnoea (disturbed breathing during sleep), and pregnancy complications. The number of children having weight loss surgery has also risen sharply, with most operations being performed in teenage girls. However, the figures have remained low. There was just one admission in 2000 and 31 in 2009.

As the authors point out, some of this increase could be attributed to greater awareness and improved diagnosis of obesity-related conditions. Nevertheless, this reliable study makes disturbing reading and highlights the possibility that the "obesity epidemic" in children may be leading to health problems far earlier than previously expected.

Where did the story come from?

The study was carried out by researchers from Imperial College London, UK and the University of South Carolina, US. It was published in the peer-reviewed open access journal PLOS ONE. Its authors are funded by a number of public institutions, including the UK National Institute for Health Research.

The research was covered fairly in the media, with several reports including comments from independent experts. Somewhat surprisingly, none of the papers' coverage chose to denigrate the main group identified – obese teenage mums-to-be. The coverage may have been guided by a press release from Imperial College London that sensibly and accurately outlined the research.

What kind of research was this?

This study looked at national trends in hospital admissions associated with obesity and weight loss surgery among children and young people in England between 2000 and 2009.

The authors point out that although the recent steep rise in childhood obesity appears to be levelling off, national surveys suggest that about three in 10 children between the ages of two and 15 are overweight, and 14-20% are obese.

Obese children are at increased risk of conditions such as type 2 diabetes, asthma and sleep apnoea, while emerging evidence suggests they may also be at risk of cardiovascular disease.

The health consequences of childhood obesity could translate into large increases in demand for healthcare services, placing already stretched services under increased financial pressure.

What did the research involve?

The researchers used information from a national database which records all single episodes of NHS hospital admissions in England, including NHS-funded treatment performed in private hospitals. The database is called Hospital Episode Statistics and is freely available for everyone to look at.

For every admission, the database gives the main reason for admission (the primary diagnosis) and other health conditions that may contribute to the condition (the secondary diagnosis) using international disease codes. It also includes information such as gender and the age of the patient, as well as any procedures performed.

The researchers used data on planned or emergency obesity admissions in all children aged 5-19 between 2000 and 2010. The data included admissions for the management of obesity where obesity was the primary diagnosis and admissions for other health problems where obesity was thought to be a contributory factor (secondary diagnosis). They also identified children and young people who underwent weight loss (bariatric) surgery.

Three age bands – 5-9, 10-14 and 15-19 – were created to reflect key stages of childhood development, with children under the age of five excluded. They obtained population estimates for these three age groups for 2000-09 in England, stratified by sex. They then calculated the age- and sex-specific admission rates per million children for all years.

What were the basic results?

Between 2000 and 2009, researchers found that hospital admission rates in 5-19-year-olds for total obesity-related diagnoses increased more than fourfold from 93 (95% confidence interval [CI] 86-100) per million children to 414 (95% CI 410.7-417.5) per million children.

They say the increase was largely due to rising admissions in which obesity was mentioned as a secondary diagnosis. In just over a quarter (26.7%) of admissions, obesity was the main reason for admission (primary diagnosis), while for the remaining three-quarters (73.3%) obesity was a secondary diagnosis (contributing to the condition they were admitted for).

The researchers also found that:

the average age of admission to hospital over the study period was 14 years
admissions were more common in girls than boys (56.2% v 43.8%)
the most common reasons for admission where obesity was a secondary diagnosis were sleep apnoea, asthma and complications of pregnancy
the number of bariatric surgery procedures rose from one per year in 2000 to 31 in 2009, with the majority performed in obese girls (75.6%) aged 13-19 years

How did the researchers interpret the results?

The researchers point out that hospital admissions for obesity in children and young people have increased more than fourfold in the last decade, with more and more NHS resources being used to treat conditions associated with obesity.

They say public health action is needed both to quantify the scale of the problem more clearly and reverse the "obesity epidemic", thereby reducing the number of admissions caused by obesity.

Conclusion

This study is useful for monitoring national trends in the number of child hospital admissions for obesity and obesity-related conditions over the past decade.

However – as the authors point out – the study has some limitations. The quality of the data used relies on the accuracy of disease coding, and it is possible that obesity as a secondary diagnosis may sometimes be omitted. But this would lead to an underestimate of children admitted for obesity-related conditions, rather than the reverse.

Also, the big increase in obesity-related admissions may partly reflect increased awareness and improved diagnosis, rather than rising incidence of obesity.

The authors also point out that compared with admission rates for other common childhood diseases, admission rates for obesity are still small. Nevertheless, the results of this study make disturbing reading, and indicate that some of the health consequences of obesity may be felt in childhood as well as adulthood.

If you are worried that your child is obese, you need to take action now. If you don't, it is highly likely that your child's obesity will persist into adulthood, which can cause a range of serious complications.

Your GP or practice nurse can assess your child's weight and provide further advice on lifestyle changes. They may also be able to refer you to a local weight management programme for children, such as those run by the Weight Management Centre, MEND and Carnegie Weight Management.

These programmes are often free to attend through your local health authority, and typically involve a series of weekly group workshop sessions with other parents and their children. These workshops will teach you more about the diet and lifestyle changes that will help your child achieve a healthy weight.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

NHS swamped by fourfold rise in obese children cases. Metro, June 12 2013

Child obesity hospital admissions quadruple. The Daily Telegraph, June 12 2013

Rise in child obesity-related hospital admissions. BBC News, June 13 2013

Childhood obesity cases up four-fold in a decade: Nearly 21,000 aged five to 19 treated in hospital for weight-related conditions. Daily Mail, June 12 2013

Links To Science

Jones Nielsen JD, Laverty AA, Millett C, et al. Rising Obesity-Related Hospital Admissions among Children and Young People in England: National Time Trends Study. PLOS ONE. Published online June 12 2013

No link between going grey and stress

Wed, 12 Jun 2013 13:33:00 EST

“If you’re worried about going grey – try to relax”, the Daily Mail advises its readers, adding, “scientists have found that too much stress really does turn our hair white”.

However, the claim is simply not true.

The research this story is based on actually involved mice and human scalp cells in a lab. It looked at a group of cells known as melanocyte stem cells (McSCs) – a type of stem cell that produces melanin, a pigment responsible for skin and hair colour.

Stem cells can develop into many different cell types in the body and play a crucial role in maintenance and repair. The researchers wanted to see how McSCs reacted to three types of intervention; injury, exposure to ultraviolet B (UVB) radiation, and stress hormones.

Using both mice and samples of human tissue, the researchers found that a combination of injuries caused some of the McSCs to ‘migrate’ out of hair follicles and into the affected area of tissue.

However, it was also found that stress hormones only increased the ‘migration’ of melanocytes in the skin when the skin was damaged – in this case by exposure to UVB.

When only the stress hormones were present, no skin melanocyte stem cells were produced.

This is an interesting study, but going grey may involve many factors – including the genes we inherit. The theory that stress is a cause has yet to be proved.

One practical application of the research is that it could lead to the development of treatments which manipulate the behaviour of McSCs, which could be used for skin pigmentation disorders such as vitiligo (pale white patches on the skin, caused by lack of melanin) and piebaldism (a condition in which white patches develop on the skin).

Where did the story come from?

The study was carried out by researchers from New York University School of Medicine and Baylor College of Medicine, US. The study had no external funding, but two of the researchers are supported by, or have grants from, a number of public institutions.

The study was published in the peer-reviewed journal Nature Medicine.

Not surprisingly, the study was covered widely in the press, where it was reported with a spin promising ways to avoid going grey. The press coverage focussed on the possibility (presented as fact) that stress hormones have the potential to turn hair grey. However, there is some distance between experiments on mice and human skin cultures and the development of treatments against grey hair.

What kind of research was this?

This was laboratory research using mice and mouse and human skin cultures. Its aim was to look at the behaviour of melanocyte stem cells (McSCs) and whether these can migrate from the hair follicles to the skin.

What did the research involve?

Researchers carried out several studies. These included the following:

Experiments on mice. Mice are different to humans in that the melanocytes in the skin disappear shortly after birth but remain in the hair follicle (presumably because mice have a coat and therefore don’t need them in their skin). The researchers used genetically modified mice with markers allowing them to track the movement of certain cells. The researchers created a small 1cm² cut on the back of mice or exposed an area of skin to UVB and looked at whether melanocytes and melanocyte stem cells moved from the hair follicle to the skin, and what happens after that.
Experiments on human scalp cultures to look at whether the same process happens in human skin. In this experiment, they removed melanocyte cells in the skin and analysed whether melanocytes in the follicles migrated to the skin.
They looked at the role of Mc1r, a stress hormone receptor, in the migration of McSCs from hair follicles to skin – hormone receptors are proteins on the surface of cells that react to the effects of certain hormones. To do this they used genetically modified mice and cultured mouse cells.

What were the basic results?

Researchers found that in mice that had been cut or exposed to UVB, melanocyte stem cells moved from the hair follicle to the skin, where they produced melanocytes.

Normally, stem cells renew themselves as well as producing cells that go on to form new tissue. However, the researchers found that the stem cells moved without replicating, meaning that after damage there were fewer melanocyte stem cells in the hair follicles surrounding the wound.

After a cut, some hair follicles surrounding the wound had no melanocyte stem cells, causing the hairs growing out of that follicle to be white.

After UVB exposure, there were still enough stem cells for the hair to be coloured. The fact that stem cells move suggests that recovery from injury takes precedence over stem cell maintenance.

New hair follicles that developed in patches of repaired skin were coloured if they developed in areas of skin that had melanocytes. This suggests that the melanocyte stem cells that had migrated to the skin could revert back to follicular stem cells.

A similar process occurred in samples from human scalp (once skin melanocytes were removed, they could be replaced by melanocytes originating from the hair follicle).

The researchers then tried to determine how the stem cells were moving. They saw that a receptor on the surface of melanocytes (Mc1r) plays a role – this receptor responds to stress hormones. Fewer stem cells moved in mice that lacked this receptor.

The researchers then did an experiment where they cultured mouse skin in the presence of a stress hormone. The stress hormones increased the production of melanocytes in the skin but only when the skin was damaged – in this case by exposure to UVB.

When only the stress hormone was present, no skin melanocyte stem cells were produced.

How did the researchers interpret the results?

The researchers say that stem cell differentiation due to injury takes precedence over stem cell maintenance. The melanocyte stem cell mechanism could be manipulated they say, to develop therapies for skin pigmentation disorders. They speculate the mechanism could also explain why stress may cause both skin pigmentation and paradoxically, hair greying.

Conclusion

This is an interesting study and its results may eventually lead to the development of treatments for skin pigmentation disorders. Stress hormones also seem to be involved in the movement of melanocyte stem cells from hair follicles to the skin but the relationship appears complicated, involving multiple factors. Whether stress by itself causes hair to go grey is still uncertain.

Still, there is evidence that prolonged stress can damage both your mental and physical health. Visit the NHS Choices Moodzone for more information on stress and methods you can use to relieve or reduce your stress levels.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Could your job be making you grey? Stress can make hair colour disappear, say scientists. Daily Mail, June 11 2013

Stress is to blame for grey hairs. The Daily Telegraph, June 11 2013

Going grey? It’s fifty shades of stress. Daily Express, June 11 2013

Links To Science

Chou WC, Takeo M, Rabbani P, et al. Direct migration of follicular melanocyte stem cells to the epidermis after wounding or UVB irradiation is dependent on Mc1r signalling. Nature. Published online June 9 2013

No proof heading footballs causes brain damage

Wed, 12 Jun 2013 13:33:00 EST

'Headers can damage a footballer's brain, study finds,' is the worrying warning in The Daily Telegraph. Football is one of the world's biggest participation sports, so it's important to know if it has any adverse health consequences. Fortunately for budding Rooneys and Ronaldos, the risks of heading balls may have been hyped in the headlines.

The news is based on a US study that tested whether regular "heading" of a football led to brain changes that could indicate traumatic brain injury, a type of injury usually only seen after a severe blow to the head.

Researchers gave 37 amateur players advanced brain scans that can detect changes in the brain's white matter. They also carried out neurological tests and asked players how often they thought they headed the ball.

The researchers found that more heading was associated with changes similar to those seen in people who suffered traumatic brain injury. Heading was also associated with poorer memory scores.

Despite these results, there is no evidence of a direct casual link between headers and brain damage. The people in the study were only tested at one point in time, so it is uncertain if the current findings represent any new changes, or if the players already had poor memories or abnormal white matter.

Any potential risk of brain injury has to be balanced against the wide range of health benefits from playing football regularly.

Where did the story come from?

The study was carried out by researchers from Albert Einstein College of Medicine of Yeshiva University, US. The US National Institutes of Health and the US National Institute of Neurological Disorders and Stroke funded the study, which was published in the peer-reviewed online edition of the science journal Radiology.

In general, the media headlines that suggest that heading a football can leave you with traumatic brain injury and memory loss are rather alarmist, and do not take account of the important limitations of this small cross-sectional study.

A number of papers highlighted the case of West Bromwich Albion legend Jeff Astle, who died at the age of 59 from a degenerative brain disease. A coroner attributed this disease to many years of heading footballs. However, as the Daily Mirror rightly points out, footballs were much heavier during Astle's playing career (1959-77) than they are now.

What kind of research was this?

This was a cross-sectional study examining the association between football heading and evidence of brain changes that indicate traumatic brain injury.

The researchers say they chose to study footballers as football is one of the most popular sports worldwide and it is unclear whether repetitive heading of the ball causes permanent damage.

This type of research can only indicate possible associations between lifestyle factors (such as heading footballs) and health outcomes (such as brain changes). However, it cannot establish cause and effect.

To reliably assess the effects, researchers would need to regularly image players' brains – with the first assessments ideally before they started playing football – and follow them up over time to see how any changes are related to objective assessments of the number of headers the players had made.

However, for several reasons – including cost (MRI scans are expensive to carry out) – a prospective cohort study is unlikely to be feasible.

What did the research involve?

Thirty-seven football players (28 men and nine women; median age 31 years) were recruited from amateur football leagues in New York City. The players completed a questionnaire that asked them to estimate the amount of footballs they had headed in the previous 12 months. This was so the researchers could rank them into "exposure" groups in order to compare levels of exposure and any related abnormal brain changes. They categorised exposure as:

low exposure (≤276 headings per year) – nine people
medium exposure (277-1,095 headings per year) – 19 people
high exposure (≥1,096 heading per year) – nine people

The questionnaire also asked whether the players had experienced one or more concussions in their lifetime. To determine this, participants were asked a series of questions about any previous head trauma for which they had tried to receive, had received, or were recommended to receive medical attention.

Each player underwent neurological tests supervised by a neuropsychologist to test their:

psychomotor speed (a measurement of the relationship between brain function and physical movement)
attention
executive function (such as planning)
memory

Finally, the players underwent a brain imaging technique called diffusion tensor imaging (DTI). DTI is a specialised type of MRI scan that the researchers used to detect any abnormal changes to the structure of the brain, including evidence of any prior trauma (such as signs of small bleeds).

DTI assesses the movement of water molecules with and along the nerve fibres that make up the brain's white matter. The researchers say the DTI imaging technique allowed them to measure the "uniformity of water movement (called fractional anisotropy, or FA) throughout the brain". They say abnormally low FA within white matter has previously been associated with cognitive impairment in people with traumatic brain injury.

Associations between heading and abnormal brain changes were then determined using statistical analyses.

What were the basic results?

The participants reported having played football for an average of 22 years and an average of 10 months during the previous 12 months.

In total, they reported heading a football between 32 and 5,400 times (median 432 times) in the previous 12 months.

The main findings of the research were:

there were no signs of structural abnormality or bleeds identified among any of the participants
greater heading exposure was associated with significantly lower fractional anisotropy (FA) at three regions in the brain diffusion tensor imaging – the threshold for the amount of headings and an association depended on the region of the brain the changes were seen in (range of heading thresholds was 885-1,550)
there was a significant association between heading exposure and memory function, with an association threshold of 1,800 headings per year identified
there was no association between heading exposure and neurological tests, other than memory
reported concussions over the participants' lifetime and other demographic details were not significantly associated with either brain matter changes or neurological performance

The researchers say these findings are consistent with findings from another study of people with traumatic brain injury.

How did the researchers interpret the results?

The researchers conclude that heading a football is associated with abnormal changes to the white matter (nerve fibres) of the brain, as well as poorer neurocognitive performance. They say this relationship is not explained by a history of reported concussion.

Discussing the study's findings, lead researcher Dr Michael Lipton said: "Our study provides compelling preliminary evidence that brain changes resembling mild traumatic brain injury are associated with frequently heading a soccer ball [football] over many years."

Conclusion

Overall, this research provides no evidence that there is a direct cause and effect between repeated heading of a football and traumatic brain injury. However, there are several important limitations to this study that are worth noting.

One-off tests and scans of players

The people in the study only had brain images and neurological tests at one point in time, and were asked about heading in the previous year and if they had any concussions in their lifetime.

Without having the imaging and neurological tests prior to the year in question – or preferably in early periods of life, before they started playing football – we don't know whether the current findings represent any new changes.

It could be that the white matter always looked the way it did on imaging, or has done so for a long period of time. As such, the study does not prove that one causes the other – there may have been other factors at play not identified in this research that caused the brain changes seen.

Small study sample size

This was a very small study, with only 37 amateur football players participating. Larger prospective studies involving repeat brain imaging and neurological tests from a much larger number of people from more than one area are needed to draw further associations. It would also be interesting to test professional footballers, who are likely to head the ball more but use a better technique.

Amount of heading was self-reported

Heading was determined by self-reporting, and it is possible participants did not accurately report how often they headed the ball in the previous 12 months. This can make the results less reliable. In the rush and confusion of a football match, are players really going to accurately remember how many times they have headed a ball?

Lack of information on heading

The research did not take into account different types of headers, considering the speed, velocity and site of impact. These are all important factors when looking at the repetitive nature of heading.

Real-world outcomes for players

We don't know whether the observed brain structure and memory test performance actually had a significant impact on the person in terms of their everyday life and functioning.

Overall, it is plausible that repeated minor impacts to the head may be associated with changes to the brain similar to those seen in people with traumatic brain injury. However, on its own this small study does not provide proof that heading a ball directly causes brain injury.

On a more positive note, we know regular exercise (such as playing football) can help lower blood pressure and cholesterol levels, which in turn can reduce the risk of heart disease and stroke. These benefits have to be weighed against any theoretical risk of memory problems caused by frequently heading a ball.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Headers can damage a footballer's brain, study finds. The Daily Telegraph, June 11 2013

Footballers can suffer brain damage and memory loss by heading a ball. Daily Mirror, June 11 2013

Footballers beware: Heading a ball can cause traumatic brain injury, research reveals. Daily Express, June 11 2013

Links To Science

Lipton ML, Kim N, Zimmerman ME, et al.Soccer Heading Is Associated with White Matter Microstructural and Cognitive Abnormalities. Radiology. Published online June 11 2013

Breast cancer screening 'may not reduce deaths'

Tue, 11 Jun 2013 14:33:00 EST

The findings of a study examining 39 years of breast cancer death rates have hit the headlines, with The Guardian reporting that, 'Breast cancer screening not shown to reduce deaths.' The value of breast cancer screening has been the subject of debate for many years. Every time it seems the question has been settled – as some presumed was the case after the publication of a 2012 review into screening – new evidence emerges that reignites the debate.

The latest study by researchers at Oxford University found that declines in mortality rates over time were highest in women under the age of 40, who are not normally invited for screening. The researchers also found significant downward changes in trend in women aged between 50 and 64 years old, the age group screening is targeted at.

But this change occurred in 1979 in Oxford and in 1990 throughout England, with the researchers concluding that better treatment for breast cancer is behind the trend, not screening programmes. This is because the downward trend began either before screening was introduced or too soon after the introduction of screening for it to have an effect.

Breast cancer screening is an extremely complex topic and it is difficult to assess the value of screening programmes. It may be possible the benefits of screening have been obscured by other risk factors and improvements in treatment. It is hoped the picture will become clearer as more evidence becomes available.

Where did the story come from?

The study was carried out by researchers from the University of Oxford and was funded by the National Institute for Health Research in the UK.

It was published in the peer-reviewed Journal of the Royal Society of Medicine.

The results of the study were reported well by the media.

What kind of research was this?

This study was a time-trend analysis of mortality (death) data in England to see whether breast cancer screening using mammography reduced deaths from breast cancer.

As this is an observational study, it is possible the benefits of screening programmes may be obscured by changes in both treatment and risk factors that have occurred over time.

Ideally a randomised controlled trial would be performed to assess the benefits of a screening programme. However, it is unlikely that any new randomised controlled trials of breast cancer screening in the UK will be performed.

To perform a randomised controlled trial, women would have to be prepared to be randomised to screening or to no screening. As there is currently a national screening programme in place, it is unlikely that enough women would be prepared to possibly forgo screening.

What did the research involve?

Researchers analysed the number of women who died from breast cancer in the Oxford region between 1979 and 2009. They focused on data from this region because all causes of death are mentioned on death certificates there, not just the underlying cause of death.

The researchers wanted to try to exclude the possibility that ambiguity about the underlying cause of death or changes in reporting practices distort the true picture. A total of 20,987 death certificates where female breast cancer was noted were included.

The researchers also analysed the rate of death from breast cancer between 1971 and 2009 for the whole of England, where only the underlying cause of death is reported on the death certificate.

Researchers compared trends in the rate of death from breast cancer before and after the English National Breast Cancer Screening Programme was introduced in 1988. Three groups of women were included for the same time period:

women who had been screened once
who had been screened several times
unscreened women

The researchers used a statistical technique called joinpoint analysis to estimate the years in which trends changed. Joinpoint analysis makes use of specialist statistical software to track trends over time. Each joinpoint corresponds to the estimated location of a change in a trend – in this case, mortality.

What were the basic results?

In the Oxford region, of the women with breast cancer mentioned on their death certificate, breast cancer was the underlying cause of death in 96% of women aged under 65 at death, 88% of women aged between 65 and 74, 78% aged between 75 and 84, and 66% of women aged 85 or older.

Trends for breast cancer-related deaths were very similar for whether breast cancer was listed as the underlying cause or whether it was mentioned on the death certificate. This suggests that it is unlikely that changes in death certification practices or changes in the rules for selecting the underlying cause of death affect the change in deaths due to breast cancer over time.

For all ages combined, death rates peaked in 1985 (both when breast cancer was the underlying cause and when breast cancer was mentioned) and then started to decline. This occurred prior to the introduction of the screening programme in 1988.

Between 1979 and 2009, for deaths due to breast cancer as the underlying cause, rates declined uniformly (without a detected change in trend over time):

for unscreened women aged 40-49 there was a decline of -2.1% per year, and
for screened women aged 50-64 there was a similar decline of -2.1% per year

There was also a significant change in trend downward in deaths caused by breast cancer in 1987 in women aged 65-74, and in those aged 75 years or older in 1989. These changes occurred before the screening programme was introduced, or before it was likely to have had an effect.

Between 1979 and 2009, rates of breast cancer mentioned on the death certificate also declined uniformly in women aged 40-49 (unscreened) and women aged 50-64 (screened). There was a significant downward change in trend in breast cancer deaths among women aged 65-74 in 1990, and among women aged 75 years or older in 1996.

In England, the first estimated changes in trend occurred prior to the introduction of screening, or before screening was likely to have had an effect (between 1982 and 1989). A second downward change in trend occurred in 2001 in women under the age of 40 (who are not routinely screened) and in 1990 in women aged between 50 and 64.

Most significantly, there was no evidence that declines in mortality rates were consistently greater in women in age groups and cohorts that had been screened, or screened several times, compared with other unscreened women in the same time periods.

How did the researchers interpret the results?

The researchers say that, "mortality statistics do not show an effect of mammographic screening on population-based breast cancer mortality in England."

Conclusion

This study of rates of death caused by breast cancer over a 39-year period has found no evidence of the benefits of breast cancer screening. Age-specific mortality rates for women aged between 40 and 49, 50 and 64, and 64 and 74 years peaked prior to the introduction of breast cancer screening in 1988. Declines in mortality were greatest in women under the age of 40 and smallest among women aged 75 years or older.

The researchers found that there were significant changes in downward trend in women aged between 50 and 64 years old – the age group screening is targeted at – but that these occurred in 1979 in Oxford and in 1990 in England. Both of the changes occurred before the introduction of screening, or too soon after the introduction of screening for it to be likely that screening caused the change.

In addition, significant declines in mortality rates per year were seen in women aged under 40, who would not normally be invited for screening.

As an observational study of population level data, several points are worth noting:

Direct comparisons of individuals who were screened with those who weren't is not possible with this type of study design. Researchers were only able to compare mortality for women in age groups that were likely to have been screened with those who were unlikely to have been screened.
The results do not rule out a benefit at the level of individual women, but the effect is not large enough to be detected at the population level.
"Secular" effects – that is, effects that occur over time independently of screening – can obscure the screening effects. For example, the effect of better drug treatments or changes in risk factors such as childbearing patterns over time might have outweighed smaller improvements thanks to screening.

This study provides additional valuable population data to inform the breast cancer screening debate. There is a great deal of information on both the pros and cons of screening. The 2012 review into breast cancer screening estimated that for every 10,000 women invited for screening from the age of 50 for 20 years:

43 deaths from breast cancer will be prevented
681 breast cancers will be diagnosed
129 of these diagnoses will be "overdiagnosed"

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Breast cancer screening not shown to reduce deaths, say researchers. The Guardian, June 11 2013

Breast cancer screening fails to cut deaths. The Daily Telegraph, June 11 2013

Breast screening 'doesn't cut deaths': Study of 40 years of mammograms show 'no evidence' they reduce chance of dying. Mail Online, June 11 2013

Links To Science

Mukhtar TK, Yeates DRG, Goldacre MJ. Breast cancer mortality trends in England and the assessment of the effectiveness of mammography screening: population-based study. Journal for the Royal Society of Medicine. Published online June 10 2013

'Early death map' shows English health inequality

Tue, 11 Jun 2013 14:33:00 EST

“North and South health divide: Chilling study reveals premature death is 'postcode lottery',” the Daily Mirror reports.

The news is based on a new interactive map showing the variation in premature death rates across England.

The Longer Lives map, created by the new organisation Public Health England, ranks 150 local authorities by their premature death rates (deaths occurring before age 75).

The interactive map also enables users to compare these areas by five common causes of premature (and potentially preventable) deaths:

cancer
heart disease
stroke
lung diseases, such as chronic obstructive pulmonary disease
liver diseases such as cirrhosis

The simple, colour-coded map enables users to see the variations between each local authority at a glance, including a measure of socioeconomic deprivation.

Much of the media coverage of the new map was dominated by the striking contrast between large parts of the north, coloured red (poor health), and the affluent south, mostly coloured green (good health). However, there are also pockets of poor health in some southern cities, boroughs of London, and in the Midlands.

What information is this map based on?

The information provided in Longer Lives is from the Public Health Outcomes Framework. This uses records of deaths from the Office of National Statistics.

The death rates are standardised to account for the fact that death rates are higher in older populations and adjusts for differences in the age make-up of different areas.

What factors could explain the variations?

Links To The Headlines

Early deaths: Regional variations 'shocking' – Hunt. BBC News, June 11 2013

Councils should look at banning fizzy drinks in schools, says Health Secretary. The Daily Telegraph, June 11 2013

The health gap: New mortality rates show how the north loses out to the south. The Independent, June 11 2013

Steer clear of Manchester to avoid an early grave: City has highest rate of people who die prematurely. Daily Mail, June 11 2013

North and South health divide: Chilling study reveals premature death is 'postcode lottery'. Daily Mirror, June 11 2013

Early Death Atlas Shows 'Shocking' Variations. Sky News, June 11 2013

Most deaths in under-75s are potentially avoidable, says health body. The Guardian, June 11 2013

Want a long life? Live in the south of England. Metro, June 11 2013

Decision over e-cigarettes and 'vaping' imminent

Tue, 11 Jun 2013 13:33:00 EST

An announcement is expected soon about whether electronic cigarettes are to be licensed and regulated as an aid to quit smoking.

Medical experts and trading standards officials have urged the government to classify e-cigarettes – battery-operated devices that mimic cigarettes – as a form of nicotine-replacement therapy, which would mean stringent checks by medicine regulator the MHRA.

At the moment, e-cigarettes are only covered by general product safety legislation, meaning they can legally be promoted and sold to children, and we cannot be sure of their ingredients or how much nicotine they contain.

Are e-cigarettes safe?

We don’t really know until they have been thoroughly assessed and monitored in a large population over time. However, compared with regular cigarettes, they are certainly the lesser of two evils.

First, e-cigarettes don’t contain any tobacco – only nicotine, which is highly addictive but much less dangerous. For this reason, smoking e-cigarettes (known as ‘vaping’) is generally regarded a safer alternative to smoking for those unable or unwilling to stop using nicotine.

Also, while the US Food and Drug Administration (FDA) found the liquid and vapour to contain traces of toxins (PDF, 237kb), including cancer-causing chemicals nitrosamines and formaldehyde, the level of these toxins is about one thousandth of that in cigarette smoke.

We cannot be certain that these traces of toxins are harmless, but tests on animals and a small study of 40 smokers are reassuring, providing some evidence that e-cigarettes are well tolerated and only associated with mild adverse effects (slight mouth or throat irritation, a dry cough).

Public health charity Action on Smoking and Health (ASH) is cautiously optimistic, concluding in its January 2013 briefing (PDF, 447kb) that ‘there is little evidence of harmful effects from repeated exposure to propylene glycol, the chemical in which nicotine is suspended.’

Others are more wary. Some health professionals do not recommend them because they believe the potential for harm is significant. It is worth bearing in mind that nicotine is not altogether harmless – for example, it has been linked to anxiety – and research suggests nicotine plays a direct role in the development of blood vessel disease.

E-cigarettes are banned by other countries and by some UK schools concerned about their influence on adolescents (see ‘What are the other concerns?’).

What do e-cigarettes contain, and how do they work?

Most e-cigarettes contain a battery, an atomiser and a replaceable cartridge. The cartridge contains nicotine in a solution of either propylene glycol or glycerine and water, and sometimes also flavourings.

When you suck on the device, a sensor detects the air flow and starts a process to heat the liquid inside the cartridge, so it evaporates to form water vapour. Inhaling this vapour delivers a hit of nicotine straight to your lungs.

Will they help me quit smoking?

We don’t yet know. The evidence so far is promising, but not strong enough to draw any firm conclusions.

A 2011 study and a 2013 survey found that e-cigarettes decreased the number of cigarettes consumed by smokers, and the survey also suggested they reduce cigarette cravings – although participants were recruited from websites of e-cigarette manufacturers, so results may not be representative.

It’s not certain whether e-cigarettes deliver as much nicotine as forms of nicotine replacement therapy such as patches, so they may not be as effective at curbing nicotine cravings.

However, they do have the advantage of looking and feeling like cigarettes: they satisfy the same hand-to-mouth action, give out a smoke-like vapour, and even have an LED light that resembles the burning tip of a cigarette. This could be why a 2010 study found that even placebo e-cigarettes (with no nicotine) relieved the desire to smoke within the first 10 minutes of use.

If you want to try a safer alternative to cigarettes but are concerned about the uncertainties surrounding e-cigarettes, you may wish to consider a nicotine inhalator. This licensed quit-smoking aid, available on the NHS, consists of just a mouthpiece and a plastic cartridge. It’s proven to be safe, but the nicotine vapour only reaches the mouth rather than the lungs, so you don’t get the quick hit of nicotine that comes with e-cigarettes (see box below, which compares e-cigarettes with inhalators).

E-cigarettes vs nicotine inhalators

Is there any risk to others from e-cigarette vapour?

It’s not clear until more studies are done (see ‘Are e-cigarettes safe?’). Research to date has not shown the vapour to be harmful – it largely consists of water.

According to ASH: “Any health risks of secondhand exposure to propylene glycol vapour are likely to be limited to irritation of the throat.” To support this, it cites a 1947 study that exposed animals to propylene glycol for 12-18 months at doses 50 to 700 times the level the animal could absorb through inhalation. Compared to animals living in a normal room atmosphere, no irritation was found, and the kidney, liver, spleen and bone marrow were all found to be normal.

What are the other concerns?

Because e-cigarettes can be smoked in public places such as bars, restaurants and public transport, some people feel they may be normalising what has come to be seen as an unacceptable activity.

Also, some argue that e-cigarettes (with their flavourings and clever marketing) are a ‘gateway to smoking’ for children and teenagers, encouraging them to smoke when they wouldn’t otherwise take up the habit.

If they're not a gateway to smoking, they are at least a gateway to nicotine addiction. Cancer Research UK asks whether smokers who may have otherwise successfully conquered their nicotine addiction may be more likely to stay on e-cigarettes (and thus be addicted to nicotine) long term, if they start using them.

However, these are just theories and questions, which need to be properly researched before we can jump to any conclusions, and their potential influence on children would hopefully not be an issue if e-cigarettes were tightly regulated as a medicine.

Where do I buy e-cigarettes, and how much do they cost?

E-cigarettes are widely available to buy online and from newsagents, supermarkets and even some pharmacies. They are not available on the NHS.

A starter kit costs anything from £17 to £90 (many retail at around £35-£45). For this, you typically get a battery, a charger and two or more replaceable cartridges containing nicotine. When the cartridges run out, a refill will cost you £10-£17. In all, they are estimated to be 20% cheaper than cigarettes.

How long do they last?

E-cigarette manufacturers say that a refill cartridge is equivalent to anything from seven to 25 regular cigarettes, depending on its nicotine content – but these may be overestimates, and its duration obviously depends on how heavily you use the device. The battery is said to last between two and five hours.

Analysis by NHS Choices. Follow Behind the Headlines on Twitter.

Diabetes drugs may be linked to pancreatic cancer

Mon, 10 Jun 2013 14:33:00 EST

A British Medical Journal (BMJ) investigation into two classes of type 2 diabetes drugs has prompted headlines in the Daily Mail. The newspaper claims, 'Diabetes drugs taken by thousands linked to cancer of the pancreas and other serious health problems,' going on to allege that drug manufacturers may be trying to hide potentially harmful side effects.

It is important to stress that there is no evidence of any legal or regulatory wrongdoing by any of the drug companies mentioned in the BMJ article.

The BMJ investigation focused on two relatively new classes of type 2 diabetes drugs collectively known as "incretin mimetics". There are two main types of incretin mimetic:

glucagon-like peptide-1 (GLP-1) agonists, such as exenatide, which help boost insulin production while decreasing blood sugar levels – the drug also has the added benefit of leading to modest weight loss
dipeptidylpeptidase-4 inhibitors (DPP-4), such as sitagliptin, which block the effects of an enzyme that can have a harmful impact on blood sugar levels

Neither of these drugs are first-line treatments for people with type 2 diabetes. Instead, they tend to be used if first-choice drugs are not working well enough by themselves.

As both types of drugs act on the pancreas, concerns have been raised that they may also have adverse effects on the organ. The article discusses these concerns and the evidence behind them.

This evidence includes the results of animal studies and reports from medicines regulatory agencies which suggest that the drugs may increase the risk of inflammation of the pancreas (pancreatitis) and could also lead to cancerous changes in the tissue of the pancreas, triggering pancreatic cancer.

From the evidence discussed, it does appear that there may be an increased risk of these drugs having adverse effects, but further safety studies are needed to confirm this. People may be reassured that the bodies that regulate medication are aware of the potential risks and will be carefully reviewing the safety of these drugs.

For now, anyone with diabetes who has concerns about their treatment should speak with the healthcare professionals involved in their care. The risk to your health of suddenly stopping treatment for type 2 diabetes are likely to far outweigh any potential risk of harm to your pancreas.

Where did the story come from?

The news stems from an article published in the peer-reviewed British Medical Journal (BMJ) written by Deborah Cohen, the BMJ investigations editor. The article has been made available on an open access basis, so it is free to read or download.

No sources of funding or conflicts of interest are reported.

The article states that, "In the course of this investigation, the BMJ has reviewed thousands of pages of regulatory documents obtained under freedom of information and found unpublished data."

Specific methods for identifying and selecting these documents are not presented in the article, so it is not clear whether all the evidence related to this issue has been considered. The BMJ investigation also raised specific questions directly with drugs manufacturers.

What is the BMJ article about?

Cohen discusses two types of diabetes medication that both work in two main ways:

increasing the production of insulin, a hormone produced by the pancreas that helps the body's cells take up blood sugar (glucose) to use it for energy
suppressing glucagon secretion, another hormone released by the pancreas which has the opposite effect of insulin, causing the liver to release its glucose stores to increase blood sugar

The two types of medication under the spotlight are glucagon-like peptide-1 (GLP-1) agonists and dipeptidylpeptidase-4 (DPP-4) inhibitors. Neither of these drugs are first-line treatments for type 2 diabetes, but may be considered if first-line treatments are not working effectively on their own.

The GLP-1 agonist group includes two drugs called exenatide and liraglutide. In addition to increasing insulin release and suppressing glucagon, these drugs also slow stomach emptying. For this reason they can also help prevent weight gain.

Currently, GLP-1 agonists may be considered for people whose diabetes has not been controlled by standard first-line treatments, such as metformin and sulfonylurea, and who are obese (BMI above 35kg/m2).

The National Institute for Health and Care Excellence (NICE) currently recommends that treatment with these drugs should only be continued if the person demonstrates adequate blood sugar control and has lost at least 3% of their body weight within six months.

The DPP-4 inhibitor group includes the drugs linagliptin, saxagliptin, sitagliptin and vildagliptin. There are specific types of people who are considered suitable to take these drugs.

Broadly, they may also be prescribed when standard treatment with a combination of first-choice drugs for diabetes (metformin and sulfonylurea) has either failed to control blood sugar, is inappropriate, or alternative diabetes drugs are inappropriate. Again, these drugs should only be continued if there is adequate blood sugar control.

What does the BMJ article say about these diabetes drugs?

Because incretin mimetics stimulate the cells of the pancreas, there is the potential that they may also have adverse effects on the organ.

Recently, experts have had increasing concerns about the safety of incretin mimetics. In February 2013 an independent analysis of health insurance data found that people taking exenatide and sitagliptin were at twice the risk of being admitted to hospital with inflammation of the pancreas (acute pancreatitis) compared with people taking other diabetic drugs.

The actual size of the risk to the individual was low – only 0.6%, or six in every 1,000 people taking the drugs. But even if individual risk is low, health watchdogs have to consider the fact that these types of drugs are taken by hundreds of thousands of people.

In April 2013, analysis of data from the US Food and Drug Administration (FDA) also showed increases in cases of pancreatitis and pancreatic cancer among people taking incretin mimetics compared with those taking other diabetic drugs.

Both the FDA and the European Medicines Agency (EMA) are said to have confirmed to the BMJ that their own analyses also show increased reports of pancreatic cancer with these drugs.

However, the agencies have emphasised that this does not necessarily mean that the drugs directly cause these adverse effects. It could possibly be the case that it is type 2 diabetes itself, rather than the drugs, that is increasing the risk of pancreatic cancer.

In March 2013, both agencies said that they would review study data showing that some organ donors who had taken incretin mimetics have demonstrated pre-cancerous changes in the pancreas.

Despite these findings, the risks are said to be fiercely contested by manufacturers. The drug company Merck has presented data from a pooled review of almost 34,000 people who have taken DPP-4 inhibitors and found no connection with pancreatic cancer.

However, other manufacturers appear to have some concerns about inflammation of the pancreas (pancreatitis) related to the use of these drugs. Bristol-Myers Squibb and AstraZeneca have sent a letter to the UK Medicine and Healthcare products Regulatory Agency (MHRA) saying: "A review of reports of pancreatitis from post-marketing experience revealed that signs of pancreatitis occurred after the start of saxagliptin treatment and resolved after discontinuation, which is suggestive of a causal relationship. Moreover, pancreatitis has been recognised as an adverse event for other DPP-4 inhibitors."

The BMJ article goes on to further discuss the "increasingly fractious debate among scientists and doctors played out last month in the specialty journal Diabetes Care", before going on to discuss the problems that have been observed in animals given the drugs:

Diabetic rats were given sitagliptin, metformin, or a combination of both drugs. Rats given sitagliptin had problems in their pancreas – enlargement, pancreatitis, or changes in the cells that could indicate early cancerous changes. At an ensuing meeting between experts and manufacturers held at the American Diabetes Association, one expert stated that the results in rats could suggest an increase in the risk of pancreatic cancer and that if the results were true, the future of the drugs could be in doubt. However, he said that, "concern had to be balanced against the lack of data indicating similar effects in humans." Other experts suggested that the rat model used was not reliable.
A study in mice genetically predisposed to developing pancreatitis and pancreatic cancer found that they developed pancreatitis and pre-cancerous changes more quickly when given exenatide. Another study in non-diabetic rats also showed overgrowth in the cells of their pancreatic ducts when given exenatide. Supporters of the drugs question the methods used in these studies.
There is disputed evidence from monkeys that suggests that there may be an increase in pancreas weight among young healthy monkeys given liraglutide.

The BMJ article also discusses lawsuits in the USA related to the possible link between exenatide and acute pancreatitis. This led to a judge allowing an independent pathologist to review the manufacturer's slides of slices of pancreas from monkeys treated with exenatide – the manufacturer reportedly initially refused access to these slides. The pathologist found more chronic inflammation and pancreatic disease in the treated monkeys than untreated controls.

A team from the University of California, Los Angeles (UCLA) analysed data from 2004-09 recorded in the FDA adverse event database. It found that the odds of pancreatitis were increased about six- to tenfold with exenatide and sitagliptin, and the odds of pancreatic cancer increased just under threefold with both drugs. The team noted the limitations of their study and advised that it was interpreted with caution.

Industry representatives and medical societies were reported to have heavily criticised the methods of the original study – for example, saying that it did not include information about other factors that could affect the results (potential confounders)

A later analysis by the US Institute for Safe Medication Practices (ISMP) found that all five incretin mimetics were together associated with more than 25 times the rate of pancreatitis than that seen in people with diabetes taking other drugs. The DPP-4 inhibitors were associated with 13.5 times higher rates of pancreatic cancer, and the GLP-1 agonists had rates 23 times higher than other diabetic drugs.

For some of the drugs (linagliptin and saxagliptin) there was only a single case of pancreatic cancer, and changes in risk were not significant.

What did the BMJ article conclude?

The BMJ article raises concerns their investigation found that, despite misgivings about the safety of these drugs, "companies have not done critical safety studies; nor have regulators requested them", and that, "access to raw data that would have helped resolve doubts about the safety of these drugs has been denied".

It says that although the individual pieces of evidence may seem inconclusive, a "more coherent and worrying picture emerges" when they are "considered alongside other emerging and longstanding evidence".

Conclusion

This article presents important concerns that glucagon-like peptide-1 (GLP-1) agonists and dipeptidylpeptidase-4 (DPP-4) inhibitors could potentially increase the risk of inflammation and cancerous changes in the pancreas.

The agencies that regulate medicines in Europe and the USA are aware of these issues, and told the BMJ that their analyses show increased reporting of pancreatic cancer among people taking these types of drugs.

However, the agencies note that it has not been established whether these drugs directly cause the adverse effects seen in the pancreas. Both agencies are reviewing emerging evidence on safety in this area.

For now, anyone with diabetes who has been prescribed these drugs and has concerns should speak with the healthcare professionals involved in their care.

Do not stop taking any diabetes medication unless you are advised to do so by the doctor in charge of your care. If you stop taking this medication without medical advice, you are at a much higher risk of developing complications related to diabetes, such as heart disease, stroke, kidney damage and even blindness, than you are at risk of developing pancreatic cancer.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Diabetes drugs taken by thousands linked to cancer of the pancreas and other serious health problems. Daily Mail, June 10 2013

No evidence speed cameras raise crash risk

Mon, 10 Jun 2013 13:33:00 EST

'Speed cameras 'increase risk of serious or fatal crashes,'' the Daily Mail tells us, while The Guardian, covering the same report, says 'Speed cameras reduce serious road accidents'. So you could be forgiven for being more than a little confused.

So what is the picture – do they increase or decrease injuries and fatal crashes?

The main objective of the report published last month by the RAC Foundation was to provide guidance on how speed camera data (which has been publicly available since 2011) should be analysed and interpreted. And not, despite the media’s take on the report, to provide simple figures on the number of collisions and fatalities in the vicinity of each camera.

For this reason, the report mostly consists of detailed discussion into statistical analysis and not real-world outcomes. Though it did provide some data for nine local authorities and road safety partnerships.

The figures for the nine regions reviewed present somewhat mixed results.

Five of the regions showed significant decreases both in the number of fatal or serious collisions (FSCs – decreases ranging from 24–53%), and collisions resulting in personal injury of any severity (PICs – decreases ranging from 20-32%) following introduction of cameras.

However, four of the regions did not find the introduction of cameras to have had a significant effect on FSCs and PICs.

Based on the data provided for the regions studied, we can only conclude that speed cameras have helped to reduce the number of collisions resulting in fatality or injury in some areas. But that in other areas they have had no significant effect.

However, no evidence is presented here to suggest they increase the risk of fatality or injury as was reported in some sections of the UK media.

Who produced the report and what evidence did it look at?

The report, published last month, titled ‘Guidance on the use of speed camera transparency data’ was conducted by the Royal Automobile Club (RAC) Foundation and authored by Richard Allsop, Professor of Transport Studies, of University College London.

The RAC Foundation is a charity focusing on road safety and transport issues.

The report says that since Summer 2011, data relating to fixed speed cameras has been made available to the public and is presented on the websites of local authorities or road safety partnerships. A list of these websites can be found through on the Department for Transport.

Available data contains information for the period 1990 to 2010 on the number of collisions and casualties near each camera, typically on a 0.4 km to 1.5 km section of road. The RAC have used this information to find, for each camera, the year by year numbers of:

fatal or serious collisions (FSC)
number of people killed or seriously injured (KSI) in the FSCs
collisions resulting in personal injury of any severity (PIC)
number of casualties of all severity (CAS) in the PIC

Information is also available from websites regarding:

observations of the speed of traffic near the camera on certain dates
the numbers of offences detected by the cameras and actions taken in respect of the offenders

However, these things were not the focus of this report.

The RAC Foundation considered that the general public needed guidance on how to interpret this data, and this was the focus of the report. The Foundation downloaded data from nine local authorities and road safety partnerships and conducted statistical analysis before submitting their findings for independent peer review. The nine areas covered a mix of metropolitan and shire counties, including Warwickshire, Lincolnshire, Merseyside and Sussex.

The focus of this report was to ‘discuss a number of ways in which the data can be analysed, and provide users of the data [with] practical advice on the scope and nature of the available data and on their analysis and interpretation’. It was not, as the media implied, to produce simple figures on collision and fatality rates.

The hope is that once an agreed method of analysis is reached, simple figures on collision and fatality rates, will be made available.

What were the main findings of the report?

The report initially raises several practical difficulties of examining the data:

asking holders of data to make them available in a recommended form does not necessarily result in the data being made available in that form or at all
websites and their addresses often change, so any central source of such addresses needs to be robust with respect to such changes
users will want to work with data, not just read information on a screen or printout, so data should be mounted in a format that enables use with minimum transcription, that is in a spreadsheet or analogous format
while users should of course be free to make their own analyses and interpretations of data that is made available, this can be helped by objective and non-directive advice about the nature and characteristics of the data concerned and pointers towards available techniques that are appropriate for application to data of that kind

The focus of their report is a fairly complex discussion of how to statistically interpret the data and look at how number of collisions in the vicinity of one camera relates to those in the whole partnership areas, and how numbers of FSC, KSI, PIC and CAS relate to each other.

Since the media focus is on changes in the numbers of collisions and fatalities, below is some of the data presented in appendices.

The following regions demonstrate significant decreases in PICs and FSCs since camera establishment:

24 cameras in Warwickshire showed a 25% decrease in the number of PICs and 38% decrease in the numbers of FSC in the vicinity of cameras since their establishment. In the three years prior to cameras in this area, PICs had been rising by 14% and FSCs rising by 57%
15 cameras in Leicester, Leicestershire and Rutland showed a 28% decrease in the number of PICs and a 53% decrease in FSCs since camera establishment. In the three years prior to cameras in this area, PICs had been rising by 14% and FSCs decreasing by 1%
42 cameras in Staffordshire and Stoke on Trent (an area of fewer crashes) showed a 32% decrease in the number of PICs and 44% decrease in FSCs since camera establishment. In the three years prior to cameras in this area PICs had been decreasing by 3% and FSCs decreasing by 1%
26 cameras in Staffordshire and Stoke on Trent (an area of more crashes) showed a 23% decrease in the number of PICs and 29% decrease in FSCs since camera establishment. In the three years prior to cameras in this area PICs had been decreasing by 13% and FSCs decreasing by 29%
55 cameras in Sussex showed a 21% decrease in the number of PICs and 36% decrease in FSCs since camera establishment. In the three years prior to cameras in this area, PICs had been increasing by 11% and FSCs increasing by 30%
203 cameras in Thames Valley showed a 20% decrease in the number of PICs and 24% decrease in FSCs since camera establishment. In the three years prior to cameras in this area PICs had been increasing by 3% and FSCs decreasing by 2%

Three of the remaining regions showed non-significant changes:

47 cameras in Cambridgeshire and Peterborough showed a 1% increase in the number of PICs since camera establishment (though a 42% drop in FSCs)
50 cameras in Lincolnshire showed a 9% decrease in the number of PICs and 15% decrease in FSCs since camera establishment
33 cameras in Merseyside showed an 11% increase in the number of PICs and 5% increase in FSCs since camera establishment
56 cameras in South Yorkshire showed a 1% increase in the number of PICs and 16% decrease in FSCs since camera establishment

How accurate was the media coverage?

In general, the media's coverage of this report was rather confusing and contradictory.

It appears the media wanted to report on the extent to which speed cameras decrease – or increase – the number road collisions and fatalities.

However, this wasn’t the objective of this report, which was a lot more complex, and focused on guiding people in how to interpret available data on speed cameras.

The Daily Mail’s coverage of the report was particularly poor and arguably disingenuous. The claim that “Speed cameras increase the risk of serious or fatal accidents” is simply not backed up by the data.

The Mail seems to be resorting to what, in academic circles, is known as cherry picking – that is, focusing on the data that supports your argument while ignoring the data that doesn’t.

It was the case that at 21 camera sites the number of accidents went up – though whether this was due to speed cameras remains unproven. Leaving that issue aside, the Mail ignores any data from the remaining 530 camera sites where the number of accidents and fatalities went down.

Such a distortion of evidence is disturbing.

Based on the data provided for the regions studied here we can only conclude that speed cameras have helped to reduce the number of collisions resulting in fatality or injury – or that in some areas they have had no effect. However, no evidence is presented here to suggest that they increase them.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Speed cameras 'increase risk of serious or fatal crashes': New RAC investigation raises doubts over their usefulness. Daily Mail, June 7 2013

Reality check: do speed cameras reduce serious road accidents? The Guardian, June 7 2013

Speed cameras cut deaths and serious injuries "by more than a quarter". The Daily Telegraph, June 7 2013

Speed cameras cut car crashes by more than a quarter, research reveals. Daily Mirror, June 7 2013

Speed cameras ‘increase risk of serious car crashes’ in some areas, RAC claims. Metro, June 7 2013

New Down’s syndrome blood test 'more reliable'

Fri, 07 Jun 2013 14:33:00 EST

“A new test can reliably tell if an unborn baby has Down’s syndrome without putting it at risk,” Metro reports.

Screening for Down’s syndrome is currently offered to all pregnant women.

However, the current screening test has a false positive rate (that is, the results suggest a problem when the foetus is in fact healthy) of around 3-4%.
This means many women have needless invasive testing, using chorionic villus sampling (CVS) or amniocentesis. Both of these procedures carry around a one in 100 risk of causing a miscarriage.

If the false positive rate of the screening test could be reduced this would reduce the number of women who need invasive testing, resulting in fewer miscarriages.

This new screening technique involves analysing the small amounts of foetal DNA found in the mother’s blood stream.

After testing 1,005 women, researchers found the new technique had a much lower false positive rate (around 0.1%). This means many fewer normal pregnancies had an unnecessary invasive diagnostic test with the new test. However, in about 2% of women the new test did not produce a result, meaning that the conventional screening technique had to be used.

These results are promising, but until the findings are replicated in larger studies, it is unlikely the current national screening procedures will be changed.

Where did the story come from?

This research was carried out at King’s College Hospital and University College Hospital in London.

It was published in the peer-reviewed journal, Ultrasound in Obstetrics and Gynecology.

It was funded by The Fetal Medicine Foundation: a research, education and training charity. The Foundation is funded by an associated private clinic, which carries out ultrasound scans for pregnant women and donates all profits to the Foundation, and by private donations.

The research was covered by many news sources and generally, the findings were reported reasonably. However, there are a few inaccuracies.

Many of the news sources suggest the new test can pick up more foetuses with the conditions (is more sensitive) than the existing test. While previous studies have suggested that this might be the case, this was not the case in the current study. Both tests picked up the same number of cases where the screening tests were performed successfully.

However, the new test did not work on the blood sample for one pregnancy that turned out to be affected by Down’s syndrome, which was picked up by the existing screening test. Larger studies may provide a better estimate of how sensitive the new test is.

Some reports, including the BBC and Daily Mail correctly state that the current screening programme includes both an ultrasound scan and a blood test, but, The Daily Telegraph only states that ultrasound is used.

What kind of research was this?

This was a study looking at a new screening test for detecting three specific chromosomal abnormalities called ‘trisomies’ early in pregnancy. It compared this new test against an existing screening test. Both tests require women with at risk pregnancies to have an invasive diagnostic test to confirm the results.

Initial studies have suggested that the new screening test could reduce the number of women who needed to have the invasive diagnostic test, but still identify most of the affected foetuses.

In trisomies, foetuses carry all or part of an extra chromosome 21 (called trisomy 21 or Down’s syndrome), or chromosome 18 (called trisomy 18 or Edwards’ syndrome), or chromosome 13 (called trisomy 13 or Patau syndrome). These conditions are rare but Down's syndrome is the most common. All three conditions have a large impact on the health and development of the foetus, with the effects of Down’s syndrome generally less severe than the other two syndromes. Many babies with Edwards’ or Patau syndrome will miscarry or be still born, and those that survive to birth rarely live for longer than a year.

Currently, women are offered screening for Down’s syndrome in the first trimester of pregnancy. This screening involves what is called the “combined test” which includes an ultrasound scan to measure the thickness of the soft tissue at the back of the foetus’ neck and taking a blood sample to measure certain proteins in the mother’s blood. The results of this test and the mother’s age are used to calculate the risk of the foetus being affected by Down’s syndrome. The combined screening test picks up about 90% of foetuses with Down’s syndrome. This test also sometimes identifies foetuses with trisomy 13 or 18.

Women whose screening test results show that they are at higher risk of having an affected foetus are offered a diagnostic test to check whether the fetus does have Down’s syndrome. However, this confirmation involves an invasive procedure, either chorionic villus sampling or amniocentesis to collect cells from the foetus that are found in the placenta or in the fluid surrounding the foetus. The combined screening test picks up about 90% of foetuses with Down’s syndrome. This test also sometimes identifies foetuses with trisomy 13 or 18. The problem with both of these invasive procedures is that they is that they carry around a one in a 100 chance of causing a miscarriage.

Not all foetuses the combined test identifies as having an increased risk of Down’s syndrome have the condition. About 5% of pregnancies which are not affected by Down’s syndrome will have a combined test result suggesting they are at risk, they are called false positives.

Researchers would like to have a test returning fewer false positives, to reduce the number of women who have invasive testing unnecessarily.

The new screening test assessed in this study is based on testing the small amounts of foetal genetic material (DNA) found in the mother’s blood stream. This is now possible due to advances in DNA technology.

What did the research involve?

The researchers enrolled 1,005 pregnant women attending their clinic in London who were not having twins and were at the right time in their pregnancy to offer the screening tests.

Women in the study were between 20 and 49 years old. Most had conceived naturally (85.7%), with 11.6% having conceived by IVF and 2.7% having conceived after taking drugs to promote ovulation.

They took blood samples from the women at 10 weeks into their pregnancy to perform the new DNA-based screening test and part of the existing screening test (called the combined test), and at 12 weeks they performed the ultrasound needed as part of the combined test.

The analysis of the blood samples for the new DNA-based screening test was done in the US. The parents had counselling before the tests to explain what they were and what the implications of the findings might be. Both the existing and new screening tests evaluate how much risk a woman has of having a foetus affected by one of the three conditions.

For trisomy 18 and 21, the doctors relied on the results of the new DNA-based screening test to counsel the parents about their risk of having an affected baby and what their options were if they were at high risk. For example, if the DNA-based test suggested the women had low risk of these conditions, the women were reassured that their risk was low regardless of the result of the combined test.

For trisomy 13, because affected foetuses often have many abnormalities detected by ultrasound, which is part of the existing screening test but not the new screening test, the doctors used the results of both tests.

If the DNA-based screening test found that the foetus was at low risk, but the combined test suggested they were at very high risk, the parents were still advised to consider having invasive diagnostic testing. If the DNA-based test did not give a result then the result for the combined test was used.

Women who were not identified as being at high risk, or not found to have a trisomy on diagnostic testing, went on to have the usual second trimester ultrasound scan that looks for problems in the developing foetus.

What were the basic results?

The DNA-based test gave a result in about 95% of women (957 women), and failed on the first attempt in about 5%. The failed tests were repeated on a second blood sample for most of the women (40 out of 48 women) – they worked in this second sample for 27 of these 40 women.

The new screening test suggested that among the 984 women:

967 had very low risk (<0.01%) for all three trisomies
11 were at high risk (>99%) for trisomy 21 only
five were at high risk (>99%) for trisomy 18 only
one had an increased risk (34% risk) for trisomy 13 only

One woman whose pregnancy was at high risk for trisomy 21 had a miscarriage before her planned diagnostic test. The remaining 16 women whose pregnancies were identified as being at increased risk for trisomy all had CVS for diagnostic testing. Fifteen were confirmed as having the trisomy they had been predicted as being at high risk for.

One pregnancy predicted as being at high risk of trisomy 18 was not found to have a trisomy on diagnostic testing. This foetus was 20 weeks old at the time the paper was written and appeared to be normal in the second trimester ultrasound.

Assuming this foetus did not have trisomy 18, this would mean that the new test had a false positive rate of 0.1% – so one in 1,000 women without a trisomy pregnancy would be offered invasive testing.

One foetus did not have results for the DNA-based test but was found to be at high risk of trisomy 21 from the combined test and so had CVS and was found to have trisomy 21.

Overall, the combined screening test identified 5% of women (49 women) to be at increased risk of trisomy 21 (over 1% risk). Sixteen of these women were found to have a trisomy pregnancy on diagnostic testing.

This meant the test had a false positive rate of 3.4%, meaning that 34 in 1,000 women with a normal pregnancy would be offered invasive testing.

All of the cases of trisomy 13, 18, and 21 identified as being at increased risk by the DNA-based test were also identified as being at increased risk by the combined test.

The one pregnancy incorrectly identified as being at high risk of trisomy 18 by the new DNA-based test was not identified as being at increased risk on the combined test.

As well as the 16 women who had invasive diagnostic testing due to a high-risk result in the new screening test, invasive diagnostic testing was also carried out on four who had no result on the new test but were at high risk on the combined test, and 12 who had a low risk on both tests.

Most of the pregnancies without high risk on the screening tests or diagnostic testing (968 women) had not reached term at the time the paper was published. So it is not clear if any trisomies were missed in these pregnancies.

How did the researchers interpret the results?

The researchers concluded that routine use of the new screening test for trisomies 21, 18 and 13 at 10 weeks into pregnancy is feasible, and gives fewer false positive results than the existing screening test for trisomy 21. The results of the screening test still needed to be confirmed by invasive diagnostic testing.

Conclusion

The current study suggests that screening for trisomies 13, 18, and 21 using a DNA based maternal blood test may identify similar numbers of affected foetuses to the current screening test. However, the new screening test appears to be better at ruling out the condition in women with normal pregnancies, this means that fewer women would be offered unnecessary invasive diagnostic testing.

There are a few important points to note:

Not all women in this study had given birth when the study was published, and these babies will need to be assessed to make sure that no cases of trisomy were missed.
If this test does become more widely used, it is unlikely to be used on its own to screen for these trisomies. It is more likely to be used as part of an overall screening strategy for these conditions. For example, combined testing could be used in cases where the new test did not provide a result, and ultrasound is likely to continue to be used to identify those foetuses with abnormalities. It will be important to assess the overall potential effect of whatever screening strategy is proposed.
The current test only looked at women at 10 weeks into their pregnancy, other studies would be needed to determine whether the test performed similarly at other stages in pregnancy.
These three conditions are relatively rare, and therefore only a few women in this study had them. Larger studies are needed to confirm these findings, and the newspapers suggest that such studies are ongoing. These studies will also need to confirm what level of risk on this new test should be considered high, and prompt an offer of diagnostic testing.
Invasive diagnostic testing is still needed to confirm the results, as although the false positive rate is much lower with the new test, it does still have some false positives – where a foetus is predicted as being at high risk but found to be unaffected.

The cost of the test (currently not conducted by labs in the UK) is quoted at £400 in the papers. This is likely to be too high a cost for all 700,000 pregnancies per year in the UK.

The researchers mention the possibility of only using the test in women who tested positive on the current screening test but before the invasive diagnostic test. This could cut down on the number of the new tests needed, and also reduce the need for invasive testing for some of the women who test positive on the combined test.

Alternatively, the news reports suggest the researchers hope the cost of the new test may fall.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Blood test for Down's syndrome detection hailed. The Independent, June 7 2013

New Down’s syndrome test offers ‘major increase in detection rate’. Metro, June 7 2013

New Down's syndrome blood test which can reliably detect if an unborn baby has genetic condition is to go on trial at two hospitals. Daily Mail, June 7 2013

New Down's syndrome blood test more reliable, say researchers. The Guardian, June 7 2013

New Down’s Syndrome blood test to go on trial. The Daily Telegraph, June 7 2013

Early Down's test 'more sensitive'. BBC News, June 7 2013

Links To Science

Gil MM, Quezada MS, Bregant B, et al. Implementation of maternal blood cell-free DNA testing in early screening for aneuploidies. Ultrasound in Obstetrics & Gynecology. Published online June 7 2013

Scientists identify gene pattern linked to autism

Fri, 07 Jun 2013 12:33:00 EST

The Independent reports that "Scientists have identified a genetic pattern common to people with autism that is linked to the way messages are sent in the brain".

These findings come from a study that looked at genetic variations – alterations in the genetic code that can sometimes have serious effects on the body.

The researchers were looking at the genes affected by one specific group of rare genetic variations that had been found in 181 people with autistic spectrum disorder. Autistic spectrum disorders (ASDs) are a range of disorders that affect behaviour, social interaction and language and communication skills.

The researchers wanted to find out whether there was any relationship between the biological roles of the many different genes affected by these variations. They hoped that this might help to explain why changes to different genes could result in the same types of ASD symptoms.

The researchers found that in around half of the people the variations affected a genes or genes that could be shown to have interrelated biological roles. Many of these roles were linked to how nerve cells pass messages to each other. This suggests that some of the symptoms of ASD could be caused by abnormal signalling inside the brain.

The genetics of autistic spectrum disorders is complex, with many different genes seeming to play a role in different people. This study focused on one type of genetic variation, but other genetic variations as well as environmental factors could also contribute to ASD.

This type of study helps researchers to understand the biology and genetics of these disorders. For now, the findings do not have direct implications for the diagnosis or treatment of these conditions.

Where did the story come from?

The study was carried out by researchers from the University of Oxford, as well as other research centres in France, the US and Canada. It was funded by the Medical Research Council and a European Union grant.

The study was published in the peer-reviewed open-access journal PLoS Genetics.

It was covered in an appropriate way by The Independent, without any overstatement of the implications of these findings. For now, these findings largely help researchers to understand autistic spectrum disorders better. They do not currently have direct implications for the diagnosis or treatment of these conditions.

What kind of research was this?

This was a laboratory study looking at the genetics of autistic spectrum disorders (ASDs). ASDs are a group of disorders in which the individual’s social interaction and communication are affected.

Studies have suggested that genes play an important role in causing the conditions, but the researchers say that the genetic cause is only known in about 20% of cases.

The researchers who conducted this study hypothesised that different people with ASDs may have different rare genetic variations that contribute to their condition, but that the genes affected may all be involved in the same biological processes or pathways.

In this study they wanted to look at some of the genes that may be involved in causing ASDs to see if their biological roles are interrelated. They hoped that this would improve their understanding of the genetics and biology of ASDs.

What did the research involve?

The researchers were interested in a specific type of genetic variation where people have different numbers of copies of certain pieces of their DNA. These are called copy number variations or CNVs. CNVs are a type of genetic variation where people are either missing a piece or pieces of their DNA or have multiple copies of these pieces.

The researchers had information on CNVs that had been found in 181 people with ASDs in previous studies.

The researchers also used information on CNVs from a group of people without any psychiatric condition (a control group).

They did not look at CNVs that were found both in the control group and in the ASD group, as these would be less likely to be contributing to causing the ASDs.

They identified which genes were affected by these CNVs by locating them using maps of the human genome, which are long lists of the ‘letter’ sequence of the building blocks making up human DNA.

They then used a database that collects information on the effect of different mouse genetic mutations to identify what happens in mice that have disrupted versions of these genes. They did this to help them to identify what roles the genes play in the body.

They also looked at what proteins were encoded by the genes, and what other proteins these proteins interact with in the cells.

Using this information they identified what biological processes and pathways the different genes played a role in and how they were all interrelated.

They used computer programmes to come up with an interlinking map or network showing how these genes were related.

What were the basic results?

The researchers found that 187 genes affected by copy number variations (CNVs) could be shown to be connected in a single network of interrelated biological roles. CNVs affecting one or more of these 187 genes were found in 45% of the people with ASDs.

This network also contained 22 other genes that have previously been found to be associated with ASDs.

Many of the proteins being produced by these genes were playing roles in the transmission of electrical messages between nerve cells.

The people with ASDs who had these CNVs had an average of three CNVs within this network.

The people with ASDs who only had one CNV tended to have that CNV in a gene that was very central to the network. This was thought to indicate that the single affected gene in these cases was playing an important role.

How did the researchers interpret the results?

The researchers concluded that they had identified an extensive biological network of ASD-related genes. This network can show how different genes may cause ASD by affecting interlinked biological processes and pathways.

Conclusion

This study has identified a complex network of interrelated functions for some of the genes potentially associated with autistic spectrum disorders.

The genetics of these disorders is complex, with many different genes seeming to play a role in different people.

This study shows how these different genetic variations may result in the same group of conditions.

This study focused on one particular type of genetic variation, known as copy number variations. Other types of genetic variations may also be involved with ASD. There may also be environmental factors involved.

This type of study helps researchers to understand the biology and genetics of these disorders better.

The findings of this study do not currently have direct implications for the diagnosis or treatment of these conditions. They help to add another ‘piece to the puzzle’ of our understanding of ASDs, but the puzzle is still a long way from being fully solved.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Scientists find gene pattern in autism patients. The Independent, June 7 2013

Links To Science

Noh HJ, Ponting CP, Boulding HC, et al. Network Topologies and Convergent Aetiologies Arising from Deletions and Duplications Observed in Individuals with Autism. PLoS One. Published online June 6 2013

4-D scans may show babies cry in the womb

Thu, 06 Jun 2013 13:33:00 EST

"Babies practise frowning in the womb so they can show when they are unhappy after birth," reports the Daily Mirror.

The story comes from a small study that looked at '4-D' ultrasound scans of the facial movements of 15 unborn babies during the later stages of pregnancy. These 4-D scans combine detailed 3-D images over time. They can provide a real-time moving image of the baby while it’s still in the womb.

The researchers found that the babies, as they matured, showed more complex facial expressions including more complete signs of pain and distress. These signs included lowered brows, a wrinkled nose and parted lips. It is important to highlight that the study did not show that the babies were actually in pain.

The researchers’ theory is that the babies were just practising these expressions. As any sleep-deprived parent will tell you, crying is a newborn’s main method of communication. It may be the case that the babies were pulling faces to prepare for life after birth, which is an interesting, but still unproven, hypothesis.

Where did the story come from?

The study was carried out by researchers from the University of Durham and Lancaster University. There is no information about external funding. The study was published in the peer-reviewed open-access journal PLoS One.

The study was covered fairly in the media. Most papers pointed out the researchers’ conclusions that the unborn babies were not actually in pain – just practising “the faces they’ll need out in the big bad world” as the Daily Mail put it.

What kind of research was this?

This was a study of the facial movements of 15 foetuses during weeks 24 to 36 in the womb. Researchers aimed to show that foetal facial expression becomes increasingly complex from the second (around weeks 14 to 27) to third trimester (weeks 28 onwards) of pregnancy. In particular, they set out to test the theory that, as healthy foetuses mature, their facial movements can express recognisable signs of pain or distress.

They say that, with advances in treatments for babies still in the womb, the question of identifying foetal facial expressions, especially those of pain, is becoming increasingly important.

What did the research involve?

Researchers used 4-D ultrasound scans to observe the facial expressions of 15 healthy foetuses – eight girls and seven boys – during the second and third trimesters of pregnancy.

The faces and upper bodies of the unborn babies were scanned for 10 minutes at 24, 28, 32 and 36 weeks of pregnancy. The unborn babies were not stimulated during these observation periods.

Using an accepted system of coding, researchers had previously identified 19 facial movements that could be observed on foetuses and coded from the 4-D scans. In particular, they identified six facial movements shown to have a significant relationship to pain and distress and which have been used to identify pain in various populations. These were:

lowering the brows
nose wrinkling
raising of upper lip
deepening of nasolabial furrows (the furrows are the ‘smile lines’ running from the nostrils to each corner of the mouth)
lips parting
mouth stretch

They defined a combination of these expressions as the "pain/distress gestalt" (a "gestalt" is a combination where the whole is greater than the sum of its parts). In this case, researchers defined this as a pattern of co-ordinated movements that would be viewed by an observer as expressing pain or distress. This "gestalt", they say, is supported by previous research into facial expressions.

Using the coding system, the researchers analysed how often all 19 facial movements occurred simultaneously or within a second of each other. In particular, they wanted to know how often facial expressions included in the “pain/distress gestalt” occurred together.

They used standard statistical methods to analyse their results.

What were the basic results?

The researchers say the foetuses made “significant progress” towards more complex facial expressions, involving more co-occurring movements, as their gestational age increased. In particular, their analysis of facial movements thought to make up the “pain/distress gestalt” became more complete as the foetuses matured.

For example, at 24 weeks, three of the facial movements identified with pain expression co-occurred in only 5% of the “facial events” while, at 36 weeks, co-occurrence was observed in more than one-fifth (21.2%). However, the co-occurrence of five or more of these facial movements was rare at any age (0% at 24 weeks and 0.5% at 36 weeks).

How did the researchers interpret the results?

The researchers say the study shows it is possible for foetuses to show facial behaviours that can be determined as an expression of pain or distress. As the foetus matures, the combination of movements associated with pain or distress increases.

The researchers suggest that rather than indicating pain, the development of these expressions may have a role in preparing the foetus for life outside the womb and the need to alert carers to pain experiences. They theorise that the increasingly complex facial expressions, rather than a sign of distress, are actually a sign of healthy development. As such, the researchers suggest that they could be used to identify normal and abnormal development.

Conclusion

This study contributes to a fascinating field of research – the development of foetal facial expression. However, its conclusion that babies in the womb gradually develop complex facial expressions that indicate pain is based on observations of only a very small number of foetuses. Similarly, the researchers’ hypothesis that babies are “practising” pain/distress expressions for life once they are born remains a theory and one that would be extremely hard to prove.

It is also important to highlight that the study did not show that the unborn babies were actually feeling pain in the womb. The scanning was taking place when the mothers were at rest, in cases of healthy pregnancy, so there would be no particular reason for any of the babies to be in pain or distress.

It is far too soon to say whether, with future research, foetal facial expressions could one day be used to help doctors distinguish between normal and abnormal development.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

Babies practise crying in the womb, Durham researchers claim. BBC News, June 6 2013

Unborn babies practise the faces they'll need out in the big bad world! Scans show them grimacing and wrinkling their noses. Daily Mail, June 6 2013

Babies learn to grimace in the womb to prepare for pain after birth. Daily Mirror, June 6 2013

Unborn Babies Can Show Pain in The Womb. Sky News, June 6 2013

Links To Science

Reissland N, Francis B, Mason J. Can Healthy Fetuses Show Facial Expressions of “Pain” or “Distress”? PLoS One. Published online June 5 2013

Paper towels may be more hygienic than hand dryers

Thu, 06 Jun 2013 12:33:00 EST

The Mail Online has encouraged readers to "ditch the hand dryers", as "paper towels are more hygienic". The debate on the relative merits of paper towels versus hot air dryers may appear trivial, but the issue can be a matter of life and death.

Hand drying is an essential part of the hand washing process, as wet skin helps spread bacteria. In environments where people are vulnerable to the effects of infection, such as hospitals, thorough hand washing and drying could save lives.

The Mail reports on a review of 12 studies looking at how hygienic different hand drying techniques are. To borrow a pun from the Mail, it looks like paper towels win "hands down".

The review found the advantages of paper towels include that they dry the hands more quickly, remove more bacteria and are less likely to lead to cross-contamination. However, the review's authors did not include details of the methods used in the studies involved, so it is difficult to assess how valid their results are.

Unfortunately, we usually don't have much choice about the type of drying method we use in public or workplace bathrooms. The most important thing to remember is that whatever drying facilities are provided, it is just as important to dry your hands thoroughly as it is to wash them thoroughly with soap.

Where did the story come from?

The study was carried out by researchers from Queensland University of Technology and other organisations in Australia and China. No funding source was reported.

It was published in the peer-reviewed medical journal, Mayo Clinic Proceedings.

Mail Online covered this review reasonably well, although the limitations of the review were not mentioned.

As an aside, the study is actually from 2012, so it is a little puzzling why it is hitting the headlines now.

What kind of research was this?

This was a narrative review of the evidence on the effectiveness of hand drying techniques to prevent the spread of bacteria. The review included studies published since the 1970s.

Bacteria is more likely to be passed from wet skin than dry skin, making proper hand drying an essential component of the hand washing process in order to prevent the spread of infections.

This prevention of the spread of infection is especially important in settings such as hospitals and clinics. The authors sought to identify the most effective drying technique and make recommendations on its use for healthcare professionals.

What did the research involve?

The study authors searched several databases for studies that compared at least two hand drying methods and reported results on different aspects of hand drying effectiveness. The various factors considered were:

amount of water removed
effectiveness of removal of bacteria
prevention of cross-contamination

The authors compared several techniques, including paper towels, cloth towels, electric hot air dryers, jet air dryers and evaporation (air drying).

This was a narrative review, so the authors didn't statistically pool the study results as would be the case with a meta-analysis. Based on the analyses presented in each identified study, the researchers are able to suggest how the various techniques compare. However, they did not provide a pooled statistical estimate of effectiveness for each technique.

What were the basic results?

The researchers identified 12 articles that were included in the review.

Drying effectiveness

Two studies assessed how efficiently different methods removed water from the hands. The authors report that:

one study compared cloth towels with hot air dryers and found that 10 seconds of drying with a cloth towel was approximately equivalent to 45 seconds of using a hot air dryer
the other study found that 10 seconds of drying with either paper towels or jet air dryers was equally efficient at removing water, while hot air dryers took about 40 seconds to achieve the same level of dryness

Bacteria removal and drying method

Seven studies assessed the effectiveness of different techniques of removing bacteria from the hands and reported inconsistent results.

One study found that paper towels reduced the number of all types of bacteria, air dryers increased their number, while jet air dryers increased the number of some, but not all bacteria. The increases seen from jet air dryers were less than those seen with hot air dryers.

Another study found that hot air dryers were the least effective method of removing bacteria.

Two studies that looked at various drying methods reported no difference in the amount of bacteria left on the hands.

Another study reported that using a hot air dryer with ultraviolet light for 30 seconds was more effective than paper towels, but that rubbing the hands together under a hot air dryer was less effective.

However, a final study reported that 10 seconds of holding the hands still under a hot air dryer was better at removing rotaviruses and E. coli than 10 seconds using either paper or cloth towels.

Bacteria removal and drying technique

One study found that 10 seconds of using a hot air dryer was associated with more bacteria on the hands than not using a dryer at all. It found that rubbing the hands together under a hot air dryer prevented bacteria removal. Using a jet air dryer for 10 seconds was found to be more effective at removing bacteria than using a hot air dryer for 30-35 seconds. This study also reported that using a paper towel was the best method of removing bacteria, especially from the fingertips.

One of the studies found that rubbing the hands together under a hot air dryer for 15 seconds significantly increased the amount of bacteria on the hands, while holding the hands still under the dryer for the same amount of time decreased the amount of bacteria, although it's not clear whether this was significant. This study also found that paper towels were more effective at removing bacteria from the fingertips than from the palm of the hand and fingers.

Preventing cross-contamination

When examining the effect of the methods on bacterial transmission or cross-contamination, the researchers found one study that investigated the risk of cross-contamination in a hospital setting. It compared the spread of bacteria using a hot air dryer versus using paper towels and found that the electric dryers spread the bacteria up to three feet (about a metre) from the unit, while no dispersal was found when using paper towels.

A second study reported that hot air dyers led to a large number of airborne bacteria near the dryer, but no such spread was seen with either paper or cloth towels.

A third study found that jet air dryers in a washroom were found to spread bacteria up to two metres (around six feet), while paper towels and hand dryers were better at not contaminating the washroom.

How did the researchers interpret the results?

The authors concluded that, "From a hygiene viewpoint, paper towels are superior to electric air dryers" and that, "drying hands thoroughly with a single-use, disposable paper towels is the preferred method of hand drying in healthcare".

Conclusion

This review suggests that using paper towels to dry the hands is more effective than other methods at actually getting the hands dry, reducing the amount of bacteria on them, and preventing contamination of the washroom environment.

There are, however, limitations to this review that should be considered before concluding that hot air dryers or jet dryers are ineffective:

The review did not report the quality of the various studies included. When determining whether the results of a study are valid, it is important to establish whether the research methods were sufficient to minimise bias and confounding. As the review did not report this, it is unclear how valid the studies' results are.
The studies' methods varied and this could influence the consistency of results across the experiments. The amount of time spent drying, the method of measuring bacteria levels and other differences may account for the variation in results.

Identifying hygiene behaviours to help minimise the risk of cross-infection has become increasingly important. Much research has gone into the most effective hand washing techniques. The good news is that, whatever the limitations of the review, its findings support current hand washing recommendations.

This review suggests that paper towels are the best option for settings where containing infections is critical, and may be more effective than hot air dryers.

However, if you have no choice – as is the case in most public toilets and workplace washrooms – and only hot air dryers are provided, take extra time to dry your hands thoroughly. There is little evidence that they are any worse than hand towels, other than the extra time spent drying your hands.

There is some sensible advice for doctors on how they should wash their hands contained in NICE guidelines on infection control. You may want to make sure that your doctor or nurse knows about, and follows, this advice.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Ditch the hand dryer: Paper towels are more hygienic because they remove more germs. Mail Online, June 4 2013

Links To Science

Huang C, Ma W, Stack S. The Hygienic Efficacy of Different Hand-Drying Methods: A Review of the Evidence. Mayo Clinic Proceedings. Published online June 1 2012

NICE publishes guidance on cutting down smoking

Wed, 05 Jun 2013 13:33:00 EST

"Smokers urged to 'cut down' rather than quit," The Daily Telegraph reports. The story comes from landmark national guidance on how healthcare professionals should help smokers who find it difficult to give up. The guidance, produced by the National Institute for Health and Care Excellence (NICE), is the first in the world to say that nicotine replacement therapy such as patches and nasal sprays can be used to help hardened smokers reduce the amount they smoke.

Quitting smoking altogether is the healthiest thing you can do if you smoke, but this new guidance addresses the fact that many smokers may not be ready or able to quit in one go, while others want to stop smoking without giving up nicotine. For these people, NICE recommends a pragmatic "harm reduction" approach that includes the use of nicotine replacement therapy.

Professor Mike Kelly, director of the NICE Public Health Centre, said: "Over 79,000 deaths in England each year are due to smoking tobacco. Put simply, people smoke for the nicotine, but die because of the tar in tobacco. However, nicotine inhaled from smoking tobacco is highly addictive, which is why people find it so difficult to stop smoking.

"If you are a smoker, quitting smoking is the best way to improve health, and stopping in one step is most likely to be successful. This guidance recommends harm reduction as an additional new option, particularly for those who are highly dependent on smoking who want to quit but can't just stop in one go."

Why is NICE producing this guidance?

NICE points out that although the best way to reduce the harm from smoking is to stop completely, many people are unable to do this in one step. For example, only 4% who try to give up without help are successful for a year or longer, and only 15% of those who quit using the NHS Stop Smoking Service.

NICE says that although existing evidence is not clear about the health benefits of reducing smoking, people who cut down on how much they smoke are more likely to stop smoking eventually, particularly if they are using licensed nicotine-containing products.

The guidance recommends a "harm reduction" approach, with or without the temporary or long-term use of licensed nicotine-containing products.

The options it addresses are:

stopping smoking, but using licensed nicotine-containing products as long as necessary to prevent relapse
cutting down before stopping smoking (cutting down to quit)
smoking reduction
temporary abstinence from smoking, such as stopping smoking during your working day

NICE says the advice is particularly relevant to people who are highly dependent on nicotine and groups of people whose smoking prevalence is higher than average. It says this includes people with mental illness, those from lower socioeconomic groups, and lesbian, gay, bisexual and transgender people.

It also says evidence shows that reductions in smoking without the support of a nicotine replacement product are unlikely to yield any health benefits. This is due to what is known as compensatory smoking, where you "make up" for missed cigarettes by smoking more at home or inhaling more deeply.

What are NICE's main recommendations on smoking?

NICE's guidance is mainly aimed at healthcare professionals and organisations. For this reason, its recommendations relate to what these professionals and organisations should do to help people who smoke quit or cut down.

Raising awareness of licensed nicotine replacement therapy

NICE wants organisations responsible for tackling tobacco use, such as local authorities, to promote licensed nicotine-containing products as safer to use than tobacco. They should also provide information on how to get them.

Self-help materials

Stop smoking services, manufacturers of nicotine-containing products and retailers should provide self-help advice on how to cut down gradually, as well as provide information about the benefits of doing so using nicotine-containing products for people who smoke a lot.

Choosing a 'harm reduction' approach

Anyone involved in stop smoking programmes and support should explain harm reduction for anyone who does not want, or is not ready, to stop smoking completely. Nicotine-containing products make it easier to cut down, increase the chances of stopping in the long term, and should be recommended or supplied.

Behavioural support

Stop smoking services should help smokers set goals on cutting down, such as increasing intervals between cigarettes and delaying the first cigarette of the day.

Advising on licensed nicotine-containing products

Stop smoking services should reassure people that nicotine-containing products are a safe and effective way of reducing the amount they smoke. They can be used as a complete or partial substitute for tobacco in the short or long term, and NICE advises that it is better to use these products and reduce the amount people smoke than allow them to continue smoking at their current levels.

Services should also explain how to use these products correctly and in a sufficiently high dose to control cravings. For example, people should replace each cigarette with a nicotine-containing product, such as a lozenge or gum – ideally before the usual time they would have had the cigarette – to allow for slower nicotine release.

NICE points out that some nicotine-containing products are not licensed (for example, electronic cigarettes and topical gels) and, "their effectiveness, safety and quality cannot be assured", but also says they are likely to be less harmful than cigarettes.

Supplying nicotine-containing products

Stop smoking services, GPs and other healthcare professionals, prison health service staff, custody officers and police medical examiners should offer all types of nicotine-containing products to people who smoke as part of a harm reduction strategy, either singly or in combination.

These products can also be used to help prevent a relapse in people who have stopped or reduced the amount they smoke. For example, patches could be offered with gum or lozenges. Smokers should be advised that using more than one product is more likely to be successful, particularly with heavier smokers.

Supporting temporary abstinence

Stop smoking services should offer advice and support to people who want to abstain from smoking temporarily.

Conclusion

If you are worried about your smoking – and you should be worried if you smoke – your GP will be able to advise you on the best ways to quit or cut down. GPs provide a useful first point of contact for a range of stop smoking services that should be able to help you cut down and eventually quit.

Don't be discouraged if you have tried to quit before and failed. Like a driving test, many people don't make it first time around, but most will get there in the end.

Finally, don't make it needlessly hard for yourself. Going "cold turkey" (trying to quit without the help of nicotine replacement therapy) has a very low success rate. You are much more likely to cut down or quit for good if you use a nicotine replacement therapy product, such as gum, patches, lozenges or a spray.

Read more about established, evidence-based methods you can use to break the habit.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Smokers urged to 'cut down' rather than quit. The Daily Telegraph, June 5 2013

Cut down if you can't quit: Doctors concede that some smokers just can't stop - and that gum and patches are safe alternative. Mail Online, June 5 2013

E-cigarettes: health revolution or fresh pack of trouble? The Guardian, June 4 2013

Nice Guidelines Advise Smokers To Cut Down On Habit. Huffington Post, June 5 2013

Controversial advice on chemicals in pregnancy

Wed, 05 Jun 2013 12:33:00 EST

The Daily Mail reports on the warning for pregnant women that household chemicals could pose a threat to their babies. ‘Don’t paint the nursery and avoid non-stick frying pans’ the Mail continues.

The news is based on advice to pregnant or breastfeeding women in a report from the Royal College of Obstetricians and Gynaecologists (RCOG).

The report, titled ‘Chemical exposure during pregnancy: dealing with potential, but unproven, risks to child health’ warns that pregnant and breastfeeding women could be exposed to harmful chemicals through:

food packaging
ordinary household products
medicines
personal care items such as moisturisers

It is important to stress that the advice is framed in a safety-first approach. There is no credible evidence that any of the items listed above pose a threat to birth outcomes.

A large amount of uncertainty exists because carrying out studies to assess these risks is difficult. This is because virtually all pregnant women are exposed to certain chemicals as they are found in everyday products.

The report provides a list of recommendations and examples of how women can avoid these potentially harmful chemicals (such as to minimise purchasing household furniture, frying pans or cars – see below for more details).

However, these recommendations are based on little evidence of any risk to the child. It recommends women put ‘safety first’ and assume a risk is present even when it may be small or proven not to be harmful.

Reassuringly, the report does say that one option is for mothers to do nothing and acknowledges that it may be difficult to avoid certain exposures.

The advice has prompted criticism by some, arguing that causing stress during pregnancy could do more damage than a theoretical, and as yet unproven, risk of chemical exposure.

Who are RCOG?

The Royal College of Obstetricians and Gynaecologists (RCOG) is a professional membership organisation based in the UK. According to their website, they encourage the study and advancement of the science and practice of obstetrics and gynaecology (women’s reproductive health). They do this through education and training for their members as well as publication of clinical guidelines and reports for patients and practitioners working in this area.

According to the RCOG press release, the report has been produced by an RCOG Scientific Advisory Committee. It says these papers are up to date reviews of emerging or controversial scientific issues of relevance to obstetrics and gynaecology and that the papers are intended to raise awareness of such issues.

Why has this report been produced?

According to the report, no official advice or guidelines exist that inform women who are pregnant or breastfeeding of the potential risks that some chemical exposures could pose for their babies.

Co-author of the paper, Dr Michelle Bellingham from the University of Glasgow, says, ‘there is much conflicting anecdotal [single observations] evidence about environmental chemicals and their potentially adverse effects on developing babies.’

She adds, ‘The information in this report is aimed at addressing this problem and should be conveyed routinely in infertility and antenatal clinics so women are made aware of key facts that will allow them to make informed choices regarding lifestyle changes.’

What evidence did the report look at?

The report states there is some evidence linking exposure to some chemicals during pregnancy with negative birth outcomes. Encouragingly, it emphasizes that this evidence is only of an association and there is no evidence that one causes the other (causality). It also says that some studies show no association between chemical exposure and disease. This evidence is not provided in detail but links to the primary research are included in the report.

The report mentions that other studies looking at this issue have investigated the effects of chemicals on pregnant animals. However, as the report points out, it is often difficult to interpret animal research and caution should be exercised when trying to generalise these findings to humans. In part, because in some of these studies the animals are exposed to levels of chemicals that would never occur in a real world human setting.

The focus of the report, it says, was to provide examples of where chemical exposures can be avoided.

What recommendations did the report make?

The report recommends the best approach for pregnant women is ‘safety-first’. It says this is ‘to assume there is a risk present even when it may be minimal or eventually unfounded.’

Other recommendations provided in the report include:

use fresh food rather than processed food wherever possible
reduce use of food and drink in cans or plastic containers
minimise the use of personal care products such as moisturisers, cosmetics, shower gels and fragrances
minimise the purchase of newly produced household furniture such as fabrics, non-stick frying pans, and cars while pregnant or breastfeeding
avoid paint fumes and all pesticides, such as fly spray
only take over-the-counter medicines when necessary
do not assume safety of all ‘natural’ named products

Despite this list of recommendations, the report acknowledges that it may be difficult for mothers to deal with the uncertainty of chemical exposure risks and that one option is do nothing.

How has the report been received?

It is fair to say that the report has not been universally well received. Many commentators have criticised the findings as being needlessly alarmist without providing any credible evidence of a threat posed by everyday chemical exposure. Ultimately the report, in the words of the critics, provides little in the way of useful advice.

Tracey Brown, of the Sense About Science charitable trust was quoted by BBC News as saying “Pregnancy is a time when people spend a lot of time and money trying to work out which advice to follow, and which products to buy or avoid. The simple question parents want answered during pregnancy is: 'Should we be worried?'

"What we need is help in navigating these debates about chemicals and pregnancy. Disappointingly, the RCOG report has ducked this."

Conclusion

Nervous mothers-to-be may want to take on board RCOG’s recommendations, though as previously mentioned, the evidence to back up these recommendations is lacking. It is important not to lose sight of established harms that are known to cause damage to a pregnancy:

smoking
drinking alcohol
using drugs
certain types of medication, such as medications used to treat epilepsy
eating certain foods, such as pate or liver

Read more about health and wellbeing in pregnancy in the NHS Choices Pregnancy and baby guide.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Food packaging and furniture: What to avoid when you're pregnant. The Independent, June 5 2013

A mum-to-be? Don't paint the nursery and avoid non-stick frying pans: Pregnant women warned over risk to baby from exposure to chemicals. Daily Mail, June 5 2013

Expectant mothers told not to paint the nursery or use non-stick frying pans in case of chemical exposure. The Daily Telegraph, June 5 2013

Chemicals: a worry for pregnant women? BBC News, June 5 2013

Pregnancy safety advice prompts criticism. BBC News, June 5 2013

Pregnant Women Warned Of Chemical Exposure. Sky News, June 5 2013

Pregnant women warned over household products. ITV News, June 5 2013

Claim that statins damage muscles 'overblown'

Tue, 04 Jun 2013 13:33:00 EST

"Statins could lead to muscular injuries, scientists warn,” reports The Daily Telegraph.

The headline is based on a new study looking at whether statins – drugs used to reduce blood cholesterol levels – increased the risk of damage and pain to muscles and bones.

The study involved US soldiers, veterans and their families, comparing the likelihood of musculoskeletal conditions among statin users with non-users. The study found that musculoskeletal conditions, injuries and pain are more common among statin users than non-users. However, the actual increase was very small; varying between 1% and 3%. On average, 85% of non-users reported having a musculoskeletal condition compared to 87% of statin users.

While any noticeable adverse effects are obvious and make for a simple news story, the benefits (such as reducing risk of heart attacks, heart disease, and stroke) can be more difficult to see.

For the vast majority of people prescribed a statin, these benefits are likely to outweigh any small increase in risk of musculoskeletal problems.

Where did the story come from?

The study was carried out by researchers from Brooke Army Medical Centre, the Uniformed Service University of Health Sciences, the University of Texas, and the South Texas and North Texas Veterans Affairs Health Care Systems. It was funded by the US National Institutes of Health.

The study was published in the peer-reviewed journal JAMA Internal Medicine.

This research was widely reported in the media and the reporting was mixed. However, the Mail's headline may have given the impression that the risk of muscle damage to statin users was very high.

The coverage of the study itself was accurate. The Daily Mail’s coverage was particularly good, placing the increase in risk in an appropriate context as well as providing expert opinion on the benefits of statins.

What kind of research was this?

This was a retrospective cohort study which aimed to determine whether statin use is associated with musculoskeletal conditions, including joint disease (such as osteoarthritis) and injury, in a military healthcare system.

In this study, statin users were matched with non-users so their baseline characteristics were similar.

A cohort study is the ideal study design to address this question. However, despite the fact that the researchers tried to ensure there were as few differences as possible between statin users and statin non-users at baseline, it is possible that other factors (confounders) are responsible for the associations seen. A randomised controlled trial would be required to show a cause and effect relationship.

Links To The Headlines

Statins could lead to muscular injuries, scientists warn. The Daily Telegraph, June 4 2013

Statins can weaken muscles and joints: Cholesterol drug raises risk of problems by up to 20 per cent. Daily Mail, June 4 2013

Statins linked to pain in joints. Daily Express, June 4 2013

Links To Science

Mansi I, Frei CR, Pugh MJ, et al. Statins and Musculoskeletal Conditions, Arthropathies, and Injuries. JAMA Internal Medicine. Published online June 3 2013

Vegetarian diet linked to longer lifespan

Tue, 04 Jun 2013 12:33:00 EST

“Veg diet key to living longer,” reports today’s Daily Express front page headline.

Its story is prompted by a large, well-designed, long-term study into vegetarian dietary patterns and their effects on reported mortality (death). The main finding was that vegetarians had a 12% reduction in the risk of death from any cause compared with non-vegetarians.

However, the researchers’ definition of ‘vegetarian’ was quite broad and may horrify some vegetarians as it included people who ate meat and fish once a week or less. Dietary patterns were only measured at the start of the study, and these can change over time. The study also had a relatively short follow-up to determine whether dietary patterns might affect the risk of death.

It’s also worth noting that vegetarians tended to live healthy lifestyles, and this could have influenced the results.

While this study cannot show direct cause and effect between diet and death risk, it highlights an important point. Even if you do not want to stop eating meat there is plenty you can ‘borrow’ from the ‘vegetarian lifestyle’ to improve your health, such as eating plenty of fresh fruit and vegetables.

Where did the story come from?

The study was carried out by researchers from Loma Linda University, California and was funded by the US National Cancer Institute and National Institute of Food and Agriculture. It was published in the peer-reviewed journal, JAMA Internal Medicine.

The results of the research were generally well covered in the media. However, the Mail Online website presented speculation as fact in its headline: it states that people who avoid meat have better health due to low blood pressure. Although this is a possible and plausible explanatory factor, the current study did not investigate the blood pressure of vegetarians.

What kind of research was this?

This was a prospective cohort study set in the US that aimed to evaluate the association between vegetarian dietary patterns and mortality (death).

A cohort study is the ideal study design to address this question. However, cohort studies cannot show cause and effect, as it is possible that other factors (confounders) are responsible for the associations seen. Ideally, the effects of a particular diet on a clinical outcome would be assessed through a randomised controlled trial. However, this is unlikely to be feasible when investigating an outcome such as mortality, which would need a long duration of follow-up; and also it would be difficult to randomise people to eating meat, or not eating meat, which comes down to personal choice.

What did the research involve?

The diet of 73,308 men and women participating in the Adventist Health Study 2 was assessed. The Adventist Health Study 2 is an ongoing cohort study involving members of the Seventh Day Adventist church (a Christian denomination) where the promotion of a healthy diet and lifestyle is a tenet of Adventist teaching.

The people’s diets were assessed when they entered the study (between 2002 and 2007) using a food frequency questionnaire. Based on the results of the questionnaire, the participant’s diet was classified into one of five dietary patterns:

non-vegetarian (ate fish and meat more than once per week)
semi-vegetarian (ate fish and meat but not more than once per week)
pesco-vegetarian (ate seafood at least once per month but all other meats less than once per month)
lacto-ovo-vegetarian (consumed dairy and egg products but fish and all other meats less than once per month)
vegan (consumed eggs, dairy, fish and all other meats less than once per month)

For some analysis, vegan, lacto-ovo-vegetarian, pesco-vegetarian and semi-vegetarian were combined as “vegetarian”.

Deaths that occurred up until the end of 2009 were identified from the US National Death Index.

The researchers analysed the relationship between vegetarian dietary patterns and all-cause and cause-specific mortality.

What were the basic results?

During a mean (average) follow-up of 5.79 years there were 2,570 deaths.

The results were adjusted for the following confounders:

age
gender
race
smoking status
exercise
income
education
marital status
alcohol intake
geographical region
amount of sleep per night

After adjustments, vegetarians (all vegetarians combined) had a 12% reduction in the risk of death from any cause compared with non-vegetarians (hazard ratio (HR) 0.88, 95% confidence interval (CI) 0.80 to 0.97).

Vegetarians also had a reduced risk of death from causes other than cardiovascular disease or cancer (HR 0.85, 95% CI 0.73 to 0.99). More specifically, vegetarians had a reduced risk of death from kidney problems and deaths from hormonal (endocrine) problems. Male vegetarians only also had a significantly reduced risk of death from ischaemic (coronary) heart disease and from cardiovascular disease overall.

The different classes of vegetarians were then considered separately. The researchers found that compared to non-vegetarians:

Pesco-vegetarians had a significantly reduced risk, in both sexes combined, of death from any cause (HR 0.81, 95% CI 0.69 to 0.94), death from ischaemic heart disease (HR 0.65, 95% CI 0.43 to 0.97) and non-cardiovascular, non-cancer death (0.71, 95% CI 0.54 to 0.94).
Lacto-ovo-vegetarians had a significantly reduced risk in both sexes combined for all-cause mortality (HR 0.91, 95% CI 0.82 to 1.00).
Vegans had a significantly reduced risk, in both sexes combined, of deaths from non-cancer, non-cardiovascular causes (HR 0.74, 95% CI 0.56 to 0.99).

When men and women were examined separately, reductions in risk were larger and more often significant for men than for women.

How did the researchers interpret the results?

“Vegetarian diets are association with lower all-cause mortality and with some reductions in cause-specific mortality. Results appeared to be more robust in males. These favourable associations should be considered carefully by those offering dietary guidance.”

Conclusion

This large, well-designed cohort study has found an association between vegetarian dietary patterns and reduced risk of death.

This study has the advantage that it included a large number of participants consuming various diets.

However, as this study is a cohort study, it cannot show cause and effect, as it is possible that other factors are responsible for the associations seen. Although the researchers adjusted for many of these factors, it was found that the vegetarian groups tended to be older, more highly educated and more likely to be married, to drink less alcohol, to smoke less, to exercise more and to be thinner. The reduced risk of death may be due to other lifestyle factors of vegetarians rather than diet.

In addition, the study has some other limitations, which were pointed out by the researchers:

The study had a relatively short follow-up. Although the average follow-up was almost six years, this is quite short to address how dietary patterns might affect the risk of death.
Dietary patterns were only measured at baseline, and it is possible that dietary patterns change over time.
The researchers included in the ‘vegetarian’ category people who eat fish and meats, but not more than once per week. This is not what a vegetarian diet is traditionally taken to mean.

This study was also conducted in a select population sample of Seventh Day Adventists, who have particular health and lifestyle characteristics. They tend to be much healthier than the population at large (for example, smoking and alcohol are discouraged among Adventists), and enjoy a greater average life expectancy.

This may mean that the differences observed between vegetarians and non-vegetarians in this study may differ from what would be observed in study of other population samples.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Vegetarian diet could cut early death risk. Daily Express, June 4 2013

Are vegetarian diets secret to long life? Mail Online, June 4 2013

Links To Science

Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian Dietary Patterns and Mortality in Adventist Health Study 2. JAMA Internal Medicine. Published online June 3 2013

Michael Douglas: 'oral sex caused my throat cancer'

Mon, 03 Jun 2013 14:33:00 EST

The actor Michael Douglas discussed his recent throat cancer treatment in an interview with The Guardian this weekend, and revealed that he blamed oral sex for his condition.

When asked by the newspaper if his throat cancer was caused by his many years of heavy drinking and smoking he replied: "No, because without wanting to get too specific this particular cancer is caused by HPV, which actually comes about from cunnilingus." Could he be right? Here are some facts about HPV, oral sex and cancer risk.

What is HPV?

The Human papilloma virus (HPV) is the name for a group of viruses that affect your skin and the moist membranes lining your body, for example, in your cervix, anus, mouth and throat.

There are more than 100 types of HPV – 40 of which can affect the genital area.

The HPV virus is very common and is easily spread by sexual activity. As many as half the population will be infected at some time in their life. In most cases, the virus doesn't do any harm because your immune system gets rid of the infection. But in some cases, the infection persists and can lead to health problems.

Can HPV really cause cancer?

Yes. While many types of HPV are harmless, other high-risk types can cause abnormal tissue growth and trigger the onset of cancer.

Cancers linked to HPV infection include:

Some types of HPV can also cause verrucas, skin warts and genital warts.

How can HPV infection be prevented?

Using a condom during sex, including oral and anal sex, can help to prevent HPV infection. However, as condoms do not cover the entire genital area and are often put on after sexual contact has begun, a condom is not always a guarantee against the spread of HPV.

Is there a HPV vaccine?

There are actually two vaccines against HPV: Cervarix and Gardasil. Cervarix protects against two very high-risk types (HPV-16 and HPV-18).

Gardasil also protects against these types, as well as two types that cause genital warts.

The Gardasil vaccine is now part of the NHS childhood vaccination programme and is routinely offered to secondary school girls aged 12 and 13. Giving the vaccine several years before a person is likely to become sexually active increases its effectiveness.

The HPV vaccination programme is intended mainly to reduce the number of cervical cancer cases in the future.

Can boys have the vaccine?

There is no clinical reasons why boys cannot have the vaccine, but it is not currently recommended as part of the NHS vaccination schedule.

If you want your son to be vaccinated then you will have to pay for the vaccine. The course of vaccination consists of three doses with each dose costing around £150.

So did oral sex cause Michael Douglas's cancer?

Based on the available evidence it is impossible to say.

But given what we know about risk factors for these types of cancer, his years of smoking and drinking could well have played a significant part.

The two biggest risk factors for these types of cancer are drinking alcohol and smoking. The risk is even higher if you are both a heavy drinker and a heavy smoker.

What can I do to reduce my cancer risk?

The four most effective methods you can do to reduce your risks are:

And while wearing a condom may only provide limited protection against HPV it does offer more effective protection against other nasty STIs (as well as being a good method of contraception to prevent unplanned pregnancies).

Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Michael Douglas on Liberace, Cannes, cancer and cunnilingus. The Guardian, June 2 2013

It's oral sex, not smoking: Michael Douglas says his throat cancer was caused by stress and the human papillomavirus (HPV) – and also says 'cunnilingus is the best cure'. The Independent, June 3 2013

Doctors question Michael Douglas' 'dubious' claim that he contracted throat cancer from 'oral sex'. Mail Online, June 3 2013

Did oral sex cause Michael Douglas's cancer? Channel 4 News, June 3 2013

Oral sex gave me cancer. The Sun, June 3 2013

Cocktail of skin cancer drugs 'shrinks melanomas'

Mon, 03 Jun 2013 14:33:00 EST

“A cocktail of drugs can reduce advanced skin cancer tumours by more than 80 per cent,” reports the Mail Online.

The news is based on a small early stage trial of a combination of two drugs, nivolumab and ipilimumab, in people with advanced melanoma (an often fatal form of skin cancer). Both of these ‘monoclonal antibody’ drugs work by encouraging the immune system to attack cancerous cells.

Nivolumab and ipilimumab work in slightly different ways, so the researchers hoped that combining the two would lead to a more effective treatment.

The study found that just over half (535) of the people treated with the highest dose of the drugs (and who had acceptable side effects) showed a measurable response to the drugs. All of these people showed at least an 80% reduction in the size of their tumour.

Advanced melanoma is difficult to treat so the results are encouraging. Unfortunately shrinkage of the tumours does not necessarily mean that the cancer has been cured. Longer-term studies are needed to assess what effect the combination has on life expectancy and overall survival.

The results of the current trial mean it is likely that this will be tested in further trials.

Read more about clinical trials into melanoma in the UK, many of which are recruiting participants.

Where did the story come from?

The study was carried out by researchers from the Memorial Sloan-Kettering Cancer Center and other research centres in the US, as well as researchers from Bristol-Myers Squibb and Dako North America. It was funded by Bristol-Myers Squibb and Ono Pharmaceutical, the manufacturers of the drugs being tested. The study was published in the peer-reviewed New England Journal of Medicine.

A conflict of interest, made clear in the research paper, is that many of the researchers are employees or hold stock in the pharmaceutical company that makes both drugs (Bristol-Myers Squibb).

The Mail Online’s report of the study was of a good quality.

What kind of research was this?

This was a paper reporting an ongoing phase I trial of a new combination of drugs in people with advanced melanoma. The drugs used were nivolumab and ipilimumab: both are antibodies that block different proteins which normally help the cancer to evade the immune system.

Ipilimumab has already been granted a license in the UK for use in adults with advanced melanoma who have been previously treated, but whose treatment has not worked or has stopped working. The National Institute for Health and Care Excellence (NICE) has more information on the use of ipilimumab in the NHS.

Nivolumab is a newer drug, has not yet been granted a license for use in the UK, and is currently only available for people who are taking part in clinical trials.

Ipilimumab alone has previously been shown to improve survival in people with advanced melanoma. Different types of cancer, including melanoma, have also been shown to respond to treatment with nivolumab alone. This study wanted to test what happened if both drugs were used together.

A phase I study is the first stage of testing a new drug or combination of drugs in a small number of people to see if their disease shows a response and what the side effects are. If the results are favourable, the drugs would go on to phase II testing of dosing and safety issues in more people and then finally phase III trials to compare it to other accepted treatments.

What did the research involve?

The researchers recruited 86 adults with advanced melanoma skin cancer that had spread to the lymph nodes or spread further in the body (stage III or IV), which could be measured and could not be surgically removed.

To be eligible, people had to be relatively well, with no symptoms or symptoms that only restricted strenuous activity, and have a life expectancy of at least four months.

People who had been treated with these types of drugs before, whose cancer had spread to their nervous system and had not been treated, or who had autoimmune disease, HIV, or hepatitis B or C were excluded.

The researchers were testing two different approaches:

a concurrent regimen: giving nivolumab and ipilimumab together every three weeks for a total of four doses, followed by nivolumab alone every three weeks for a total of four doses, and then both nivolumab and ipilimumab together every 12 weeks for up to eight doses
a sequenced regimen: giving nivolumab every two weeks for up to 48 doses in people who had already had at least three doses of ipilimumab. People who had complete response to ipilimumab, or progression of their cancer with evidence of clinical deterioration, or a history of serious adverse effects with ipilimumab were excluded

The two drugs were injected into a vein, and the researchers tested increasing doses of the drugs in successive groups of patients. The participants had their responses monitored using a modified version of standard World Health Organization criteria. These criteria rate response to treatment as complete or partial. Complete response means disappearance of all measurable tumours for at least four weeks, partial response was a reduction by in the size of the measurable tumours by 50% for at least four weeks and no new lesions.

Participants were followed for up to 2.5 years after the start of their treatment. If they initially had a complete response, a partial response, or stable disease for at least 24 weeks but then progressed, they could have the treatment they originally received, again.

What were the basic results?

The researchers treated 53 people with the drugs at the same time, and 33 with the drugs in sequence.

Overall, 40% of people treated concurrently showed an objective response – responded to the treatment – (either complete or partial). Most people who responded had a partial response (16 people), with a few having a complete response (5 people). Of these people, 31% showed a reduction in tumour size of at least 80%. Among the 17 people who received the highest dose of the concurrent regimen that had an acceptable level of side effects, just over half (nine people, 53%) showed an objective response (three complete and six partial). These people all showed a reduction in tumour size of at least 80%.

Almost all participants given the drugs at the same time (93%) had some side effects, mainly rash (55%), itchy skin (47%), fatigue (38%), and diarrhoea (34%). Just over half (53%) had more serious side effects (called grade 3 and 4 events), and in 21% these events meant the dose had to be adjusted.

Fewer people receiving the drugs in sequence showed an objective response (20%), with 73% having side effects, and 18% having the more serious grade 3 or 4 side effects.

With both treatment methods, the side effects were manageable and could be reversed with appropriate treatment. There were no treatment-related deaths.

How did the researchers interpret the results?

The researchers concluded that nivolumab and ipilimumab given together had a “manageable safety profile” and gave rapid responses which appeared to be larger than that previously seen with either of the drugs alone.

Conclusion

This phase I study has suggested that combining two drugs – nivolumab and ipilimumab – can produce a response in people with advanced melanoma with an acceptable safety profile. This type of study is a first step in human studies of new drugs or combinations of drugs.

The authors themselves note that some caution is required due to the small size of the study and the potential for the participants not to be representative of the wider patient population. The results in this study mean the researchers are likely to carry out larger studies comparing this combination of drugs against the combined drugs alone and possibly against other treatments.

The National Institute for Health and Care Excellence (NICE) has recommended ipilimumab given alone as an option for treating advanced melanoma (that has spread (metastatic) or cannot be surgically removed) in people who have received previous treatment.

Nivolumab is a new drug which has not yet gone through the procedure to be granted a license for general use in Europe. Given the generally positive results of this study, it is likely the manufacturer will seek a licence at some point in the future. This usually requires the results of phase III trials to be available.

If this does happen, it is likely that NICE will review the evidence on the drug either alone or in combination with ipilimumab to make a decision on whether it should be made available on the NHS for people with advanced melanoma.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Taking certain cocktail of skin cancer drugs 'can reduce growth of tumours by 80%'. Mail Online, June 2 2013

Links To Science

Wolchok JD, Kluger H, Callahan MK, et al. Nivolumab plus Ipilimumab in Advanced Melanoma. The New England Journal of Medicine. Published online June 2 2013

Are short, intense exercise bursts enough to stay fit?

Mon, 03 Jun 2013 14:33:00 EST

'Just 12 minutes of intensive exercise per week is enough to improve your health if you are overweight,' according to The Daily Telegraph. The paper reports on the findings of a study into the phenomenon of high-intensity interval training (HIIT). It's claimed that HIIT can deliver many of the benefits of conventional exercise in a much shorter time.

Two groups of overweight and inactive, but otherwise healthy, middle-aged men either followed a programme of:

four bursts of intense exercise for four minutes, each separated by three minutes of lower intensity exercise, three times a week (plus a 10-minute warm-up and a five-minute cool-down), or
a single burst of intense exercise for four minutes, three times a week (plus the warm-up and cool-down)

After 10 weeks, both groups had improved their bodies' maximal oxygen uptake (a measure of fitness) and lost weight.

This suggests that in healthy overweight men, a regular programme based on a single burst of intense exercise may bring similar fitness benefits to a programme involving repeated bursts of intense exercise.

However, this was a very small and relatively short-term study. Ideally, larger studies are needed to explore the longer term effects of this type of exercise programme in more diverse groups of people.

HIIT may not be safe for everyone, especially if you have health problems or are not currently doing any exercise. Check with your GP first.

Where did the story come from?

The study was carried out by researchers from the K.G. Jebsen Center for Exercise in Medicine in Norway, and other research centres in Norway, Canada and the USA. It was funded by the K.G. Jebsen Foundation, the Norwegian Council of Cardiovascular Disease, the Norwegian Research Council, St Olav's University Hospital, Norway, and the Eckbos Foundation.

It was published in the peer-reviewed open access medical journal PLoS ONE.

The Telegraph and Mail Online website reported this study quite accurately, but both suggested that the single burst of exercise group did just 12 minutes of exercise per week. In fact, including the warm-up and cool-down sessions, they actually did 57 minutes of exercise per week.

What kind of research was this?

This was a randomised controlled trial (RCT) looking at the effects of regular short bursts of intensive endurance training on fitness.

Current official guidelines in the UK recommend that healthy adults should do:

at least 150 minutes per week of moderate intensity aerobic exercise a week, or
75 minutes of vigorous exercise a week, with an equivalent mix of moderate- and vigorous-intensity aerobic activity every week (for example, two 30-minute runs plus 30 minutes of fast walking)

Doing muscle-strengthening activities on two or more days is also recommended. Read more about the physical activity guidelines for adults.

Many people find that even though they want to get fitter through exercise, it can be difficult to find the time. In the current study, researchers wanted to assess the effects of two shorter, high-intensity exercise programmes on fitness levels.

This type of study is the best way of comparing two different treatments or interventions, as the groups should be well balanced at the start of the trial. This means any differences at the end of the trial can be attributed to the intervention received.

What did the research involve?

The researchers enrolled 26 overweight men (BMI between 25 and 30) who were healthy but inactive. They were aged 35-45 and had not exercised regularly for at least two years prior to the study. Men with heart problems, lung disease, high blood pressure, kidney failure, or orthopaedic or neurological problems were not eligible to participate.

The men were randomly assigned to do one of two exercise programmes on an inclined treadmill three times a week for 10 weeks. One programme involved a single four-minute intense period of exercise (single burst group), and the other consisted of four bouts of four minutes' intense exercise separated by three minutes of "active recovery" (multiple burst group). The researchers say that each burst was the equivalent of a four-minute quick walk uphill at an 8-10% gradient, or rapidly walking up six to 10 flights of stairs.

Before both types of sessions, the men warmed up for 10 minutes by walking, jogging and running on an inclined treadmill with the aim of reaching 70% of their maximum heart rate. During the four-minute intense parts of their exercise, they aimed to reach 90% of their maximum heart rate.

The men whose programme included active recovery periods aimed to reach 70% of their maximum heart rate in these periods. Both groups of men also had a five-minute cool-down session at the end of their workout. Overall, the groups did 19 minutes (single burst group) and 40 minutes (multiple burst group) of exercise in total.

The researchers took various measures of fitness and cardiovascular risk. The main outcome they were interested in was the men's maximal oxygen uptake (VO2max), which is the maximum amount of oxygen they could consume each minute per kg of bodyweight while doing exercise. A higher VO2max indicates a higher level of fitness, and previous research has linked a higher VO2max measurement with a reduced risk of death. They also measured:

blood pressure
levels of fats, sugars and other substances in the blood
body composition
BMI

What were the basic results?

The group doing the single burst of intense exercise had slightly higher BMIs at the start of the study (average BMI 27.8 compared with 27.0 in the multiple burst group). Two men in this group dropped out of the study – one because of back pain and one because he moved out of the area – and were not included in the analysis.

After the 10-week study period, the groups did not show statistically significant differences in change in any outcome. Both groups showed an increase in maximal oxygen consumption.

The single burst exercise group showed a 10% improvement, and the multiple burst group showed a 13% improvement. The difference between groups in this outcome did not quite reach statistical significance.

Both groups showed a reduction in weight: 1.8kg in the single burst group and 2.1kg in the multiple burst group. However, the researchers point out that short bursts of intense exercise are unlikely to achieve the kind of sustained weight loss needed to tackle obesity.

Fasting blood sugar level was also reduced in both groups. Blood pressure showed a statistically significant reduction in the single bout group, but not in the repeated bout group. Levels of one form of cholesterol (oxidised LDL cholesterol) showed a statistically significant reduction in the repeated bout group, but not in the single bout group.

How did the researchers interpret the results?

The researchers concluded that a single short bout of intense exercise performed three times a week "may be a time-efficient strategy to improve VO2max and reduce blood pressure and fasting glucose in previously inactive but otherwise healthy middle-aged individuals".

Conclusion

This small study has suggested that short periods of intense exercise can increase fitness to a similar level as sustained exercise, and show similar effects on outcomes such as weight. But this study has some limitations, including:

The study was very small, involving just 26 men. This may mean that the results may not be as representative of the general population of similar men as a larger sample would be. It also means that it is less able to detect differences between the groups in their statistical tests, even if they exist.
The study only included overweight but healthy men. The results may not apply to other groups of people.
There was no group that didn't exercise at all or do less intensive exercise, so we can't tell what would have happened with these types of programmes.
The study was only relatively short term and therefore could not look at long-term outcomes, such as whether weight loss was maintained or if there was an increased risk of heart attack.

Overall, the study suggests that fitness may be improved by regular exercise sessions that include a short, intensive bout of exercise. This may be encouraging for people who feel they don't have enough time to exercise. And for most people, some exercise is better than none.

However, it's important to note that the men in this study were healthy, with no heart disease, high blood pressure, or orthopaedic or lung problems. Short bouts of very intensive exercise may not be suitable for people who have these conditions.

It is always good to check with your GP if you are committed to getting fit but have been inactive for some time. Read more advice about starting a new exercise plan.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Twelve minutes' exercise per week 'enough to stay fit'. The Daily Telegraph, May 30 2013

Forget lengthy gym workouts: Just 12 minute of exercise a week can get couch potatoes fit. Mail Online, May 30 2013

Links To Science

Tjønna AE, Leinan IM, Bartnes AT. Low- and High-Volume of Intensive Endurance Training Significantly Improves Maximal Oxygen Uptake after 10-Weeks of Training in Healthy Men. PLos One. Published online May 29 2013

Fans of bondage and S&M report better mental health

Fri, 31 May 2013 14:33:00 EST

“Could bondage be good for you?”, is the somewhat surprising question asked on the Mail Online website.

This article is prompted by a Dutch study assessing the mental health of people into bondage-discipline, domination-submission and sado-masochism (BDSM) compared to those with more ‘vanilla’ sexual tastes.

The researchers make the case that there is an (in their view, mistaken) assumption that people who engage in BDSM practices have some sort of mental health disorder or mental distress.

They decided to test this assumption by analysing responses of nearly 1,000 Dutch BDSM ‘practitioners’ to a series of personality and wellbeing questionnaires and comparing them to a control group.

People who engaged in BDSM appeared to have a good mental health profile, and compared to control participants were:

less neurotic
more extraverted
more open to new experiences
more conscientious
less sensitive to rejection
had a higher sense of wellbeing

However, we don’t know how other Dutch BDSM participants (or the rest of the world) are faring. It could be that the people who chose to take part in this survey represent those with the best sense of health and wellbeing.

Where did the story come from?

The study was carried out by researchers from Tilburg University in the Netherlands and was published in the peer-reviewed Journal of Sexual Medicine. No sources of funding are reported and the authors report no conflicts of interest.

The Mail Online’s headline that ‘bondage could be good for you’ and that ‘S&M enthusiasts are healthier’, are not supported by this survey. A more accurate, if slightly less arresting, headline would be ‘People who choose to take part in an S&M survey claim to enjoy better psychological health’.

What kind of research was this?

This was a cross-sectional study into the sexual practices of bondage-discipline, dominance-submission and sadism-masochism (BDSM). BDSM is typified by sexual role-play involving suppression, physical restriction, games playing, ‘power exchange’, and sometimes pain.

There have been suggestions that people choose to take part in BDSM due to mental illness (psychopathology). For example, people who engage in such practices may have vulnerable mental health and could be susceptible to abuse. However, contrary previous research has shown that people who take part in BDSM have good psychological health.

The current study aimed to see how people who practice BDSM differed psychologically from a control group who did not practice BDSM. The researchers aimed to answer this through self-reported assessments of:

the ‘big five’ dimensions of personality: neuroticism, extraversion, openness to experience, agreeableness and conscientiousness
rejection sensitivity (based on whether a person overestimates the possibility of being rejected by others, as well as the emotional impact following rejection)
attachment style (the persistent and emotionally significant bond that individuals form with others)
subjective wellbeing

They were particularly interested in whether there were differences within people who engage in BDSM, depending on whether they generally took a dominant or submissive role (or switched).

What did the research involve?

This study included those who responded to an advert posted on the largest BDSM web forum in The Netherlands. The recruitment advert explained that it was a study mapping the psychology of the practice of BDSM and responses were anonymous.

Of the 1,571 who started the questionnaire, just over 902 (51% male) completed it and were included in this study. The 434 control participants were recruited via an advert in a popular Dutch women’s magazine (Viva) asking people to participate in confidential online research labelled simply ‘a study about human behaviour’. The majority of these control participants (70%) were women.

Personality was assessed using the 60-item short version of a questionnaire called the Five Factor Personality Inventory where responses were on a five-point scale from one (“not at all applicable to me”) to five (“very applicable to me”). For example, it includes an item assessing neuroticism by asking people to rate on this five-point scale the statement: “I rarely feel lonely or sad.”

Participants also completed a 40-item Attachment Styles Questionnaire. This used a five-point scale as well, and had sections on:

confidence in relationships
discomfort with closeness
relationships as secondary dimensions (for example, whether their relationships are superficial)
need for approval
preoccupation

They completed a Rejection Sensitivity Questionnaire that included 16 scenarios where the participant indicated their degree of concern or anxiety about an outcome, as well as the perceived likelihood of that outcome. For example, “How worried or anxious will you be if your classmate won’t lend you his notes?” and then, “Do you expect that this person will lend you his notes?”

The World Health Organization-Five Well-being Index (WHO-5) was also used to assess subjective wellbeing by five items asking about feelings in the last two weeks.

The researchers carried out statistical analyses looking at the relationship between responses across the different assessment tools, and how this varied between BDSM and non-BDSM control participants.

What were the basic results?

Among the people who took part in BDSM there was a clear difference in the role adopted by men and women. Among men:

a third (33.4%) were submissive
almost half dominant (48.3%)
the remainder switched roles (18.3%).

Contrary to the picture of a woman with a whip accompanying the Mail article:

the majority of women took submissive roles (75.6%)
only a small minority were dominant (8%)
with the remainder switching roles (16.4%)

After controlling for age, sex and gender, the researchers found that compared with control participants, people who took part in BDSM were generally:

less neurotic
more extraverted
more open to new experiences
more conscientious
less sensitive to rejection
had higher subjective well-being

However, BDSM practitioners were ‘less agreeable’ than control participants. In psychological terms, this means that they were less likely to get along with friends, family members and co-workers.

When the researchers looked at the effect of the role played within BDSM, if differences were observed, scores were generally more favourable for those with a dominant than a submissive role.

How did the researchers interpret the results?

The researchers conclude that, ‘BDSM may be thought of as a recreational leisure, rather than the expression of psychopathological processes’.

Conclusion

This cross-sectional research provides only a single snapshot of how the Dutch people who took part in this online survey are feeling at a single point in time. There are many components to health, and the questionnaires used by the researchers did not assess whether the participants have any diagnosed physical or mental health conditions.

These self-reported questionnaires do not give us a clear picture of the participants’ overall health, how they are functioning in everyday life, or of their longer term health outlook. Consequently, media headlines implying BDSM is good for you or has health benefits (mental or physical), while potentially true, are not actually backed up by the research in question.

Also, the responses only represent those who chose to take part in the questionnaires. For the survey respondents who took part in BDSM and knew the nature of the research, it could be that those who chose to take part in this survey represent those with the best sense of health and wellbeing.

We can’t assume that the psychological health of these people reflects those of the wider world of BDSM – who do not use this Dutch website, or who do and chose not to take part. Similarly, the control participants reflect only a very small sample of people. Also, largely by the nature of their recruitment method by a woman’s magazine, they were predominantly women. The psychological health of these 434 – mainly female – adults cannot be assumed to reflect that of the general non-BDSM population.

Overall, this research does not find that BDSM is associated with adverse psychological health or wellbeing, but this cannot be concluded with much certainty due to the way in which the study was carried out.

There is evidence that regular sex in the context of a romantic realtionship can lead to health benefits.

But should you invest in a pair of handcuffs for your health and wellbeing? Well, that would appear to be more an issue of personal preference rather than evidence-based science.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Could bondage be good for you? S&M enthusiasts are 'healthier and less neurotic' than those with a tamer sex life. Mail Online, May 30 2013

Links To Science

Wismeijer AAJ, van Assen ALM. Psychological Characteristics of BDSM Practitioners. The Journal of Sexual Medicine. Published online May 16 2013

No evidence Nordic diet prevents heart disease

Fri, 31 May 2013 14:33:00 EST

"Roll out the reindeer and berries for Nordic health fix," The Daily Telegraph tells us, reporting that a Scandinavian diet can lower cholesterol and may reduce the risk of heart disease. Meanwhile, the Mail Online website tells us to "forget the Mediterranean diet" in favour of Nordic foods.

There is a wide range of evidence that the Mediterranean diet, with plenty of fresh fruit and vegetables as well as beans, wholegrains, olive oil and fish, can be good for the heart. But is the same true for the staples of Nordic diets? The current study is not able to answer this question for us.

The study in question involved 200 white Nordic people with metabolic syndrome who had either a ‘healthy’ or ‘average’ Nordic diet for up to six months.

Researchers found that the ‘healthy’ diet had no effect on glucose tolerance and insulin sensitivity, nor did it improve weight or blood pressure. They did find small decreases in ‘bad’ cholesterol levels and fat-binding proteins in the ‘healthy’ group, but these were not the main outcomes investigated and are of limited importance for our health. Because this study of the Nordic diet was quite short, it is not clear whether these changes would have any lasting benefits.

If you are worried about your cholesterol levels you are advised to follow a healthy diet with plenty of fresh fruit and vegetables and low amounts of saturated fat and sugar.

Where did the story come from?

The study was carried out by researchers from the University of Eastern Finland and other academic institutions in Scandinavia. Funding was provided by various sources including NordForsk, the Academy of Finland, the Finnish Diabetes Research Foundation and the Finnish Foundation for Cardiovascular Research.

The study was published in the peer-reviewed Journal of Internal Medicine.

The Daily Telegraph and the Mail Online have both exaggerated the findings of this study. The researchers did not find any significant difference in the outcomes it had set out to examine – insulin sensitivity and glucose tolerance. These are two biological markers used to assess the risk of developing diabetes.

The only significant changes seen were a small increase in non-HDL cholesterol and a change in one inflammatory marker. These slight changes cannot be interpreted to mean that a person is at lower risk of cardiovascular disease as a result of eating a healthy Nordic diet.

What kind of research was this?

This was a randomised controlled trial (the SYSDIET trial) investigating the effect that a Nordic diet might have on levels of cholesterol and other fats in the blood, blood pressure, insulin sensitivity and inflammatory markers. These are all components of what is medically known as ‘metabolic syndrome’ – a collection of risk factors associated with increased risk of cardiovascular disease.

Insulin is the hormone that controls blood glucose levels. It is produced by our bodies when blood glucose levels are high and it causes the body’s cells to take up glucose and use it for energy. Measuring insulin sensitivity means looking at how sensitive the body’s cells are to the action of insulin. People with reduced insulin sensitivity (also called insulin resistance or glucose intolerance) can’t regulate their blood sugar very well, which means they are at risk of developing – or may already have – type 2 diabetes.

A randomised controlled trial such as this is the best way of looking at the short-term effects of the diet (the trial was up to six months long). However, it cannot reliably show what the longer term effects of the diet are, or its effect on disease outcomes such as heart attack or stroke.

What did the research involve?

The SYSDIET trial recruited people by advertisement at six centres – two in Finland, two in Sweden, one in Iceland and one in Denmark.

Eligible participants were required to have features of metabolic syndrome:

a body mass index categorising them as overweight or obese (BMI 27-38), and
glucose intolerance (defined by set criteria)

The researchers did not include people with major chronic diseases, excluding metabolic syndrome.

Two hundred people took part in the study. The average age was 55, the average BMI 31.6, 67% were women and all were of white ethnicity. They were randomly allocated to follow either the ‘healthy Nordic diet’ or a control diet for 18-24 weeks (the shorter duration was used in four of the six centres).

The control group was described as following the ‘average Nordic diet’. The control diet was based on the same number of calories as the ‘healthy’ diet, but included higher salt and saturated fat, and lower fibre, fish, fruit and vegetables. The researchers gave the participants the key food items for the diet they were following (for example, the Nordic diet group were given wholegrain cereals, while the control group got low fibre cereals).

At the start of the study, the researchers measured the participants’ height, weight and blood pressure, and did various tests on their blood. The participants also underwent an oral glucose tolerance test. At 12 weeks and at their final visit (18 or 24 weeks) these measurements were repeated. At the time of starting the study, and at weeks two, 12, 18 and 24 participants completed a four-day food diary to check their compliance with their assigned diets. Participants were advised to keep weight and physical activity constant and not to change their smoking and drinking habits or drug treatment throughout the study.

The researchers were mainly interested in insulin sensitivity and glucose tolerance. However, their secondary outcomes of interest were other components of metabolic syndrome including blood fats, blood pressure and inflammatory markers.

What were the basic results?

The study was completed by 92% of those assigned to the ‘healthy’ Nordic diet, but only 73% of those assigned to the control diet.

Over the course of the trial there were no significant changes in body weight within either group, and no differences in weight between groups at the end of 18-24 weeks. There were also no significant differences between groups in glucose tolerance or insulin sensitivity (the main outcomes the trial set out to examine), and neither were there any differences in blood pressure.

There was no significant difference in the actual levels of LDL (often described as ‘bad cholesterol’) and HDL (so-called ‘good cholesterol’) levels.

A significant difference was found in non-HDL cholesterol levels between the healthy and control groups, with non-HDL levels in the healthy Nordic diet group being much lower. Non-HDL cholesterol is a measurement of total cholesterol level minus HDL. While the lower levels of non-HDL cholesterol levels found in the healthy Nordic diet are encouraging in terms of health outcomes, they do not represent the sort of important improvement that would be signified by a drop in LDL levels.

There was a borderline significant decrease in the ratio of LDL to HDL cholesterol in the ‘healthy’ diet group. There was also a significant decrease in the ratio of two fat-binding proteins in the ‘healthy’ diet group, and a significant increase in the level of one inflammatory marker in the control group.

How did the researchers interpret the results?

The researchers conclude that the ‘healthy Nordic diet’ improves blood fat profile and has a beneficial effect on low-grade inflammation.

Conclusion

This was a well-designed randomised controlled trial that took place across several Nordic locations. The study took careful clinical measures of elements of metabolic syndrome at several points during the trial, and used food diaries at regular intervals to check compliance to the assigned diet.

However, it provides no reliable proof that the ‘healthy’ Nordic diet is any better than the ‘average’ Nordic diet at improving components of metabolic syndrome and, in turn, no proof that it reduces the risk of cardiovascular disease.

Importantly, this study found no significant results for its main aim (which was to see if the healthy ‘Nordic’ diet affected glucose tolerance and insulin sensitivity of people with metabolic syndrome). The study also found that the Nordic diet had no effect on weight or blood pressure. The only statistically significant differences were small borderline significant decreases in non-HDL cholesterol levels and fat-binding proteins among people following the healthy Nordic diet. People following the normal Nordic diet were found to have increases in one inflammatory marker.

However, the effects of these two diets on the cardiovascular system have only been assessed in the short-term. It is not clear whether these small changes would have had any real life significance to people (for example, whether they would stop people dying of heart disease) if they were continued for longer.

It is worth noting that the study involved people of Nordic, white ethnicity and those with metabolic syndrome so its results may not be applicable to other groups. The higher dropout rate in the control group also reduces the reliability of the results.

Finally, it is also worth noting that, despite the media hype, this study was not directly comparing a ‘healthy’ Nordic diet with a ‘healthy’ Mediterranean diet. Until there is reliable evidence comparing the two dietary patterns, this research cannot tell us which is the best way to keep the heart healthy.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Eat the 'Noma diet' to cut cholesterol, study finds. The Daily Telegraph, May 30 2013

Forget the Mediterranean diet, Nordic foods could be the key to avoiding heart disease, say scientists. Mail Online, May 31 2013

Links To Science

Uusitupa M, Hermansen K, Savolainen MJ, et al. Effects of an isocaloric healthy Nordic diet on insulin sensitivity, lipid profile and inflammation markers in metabolic syndrome – a randomized study (SYSDIET). Journal of Internal Medicine. Published online March 2 2013

Avatars may help control 'voices' in schizophrenia

Thu, 30 May 2013 13:33:00 EST

"Scientists are examining whether computer-generated avatars can help patients with schizophrenia," The Guardian explains. The headlines report on a small study of a novel therapy technique that attempts to tackle auditory hallucinations, where people hear voices in their head.

Hearing voices is a common symptom in people with schizophrenia. In most cases, the voices are hostile, rude and often frightening, making statements like "you are worthless" or "if you don't do what I say, you are going to die".

The study involved schizophrenia patients who had not responded to medication. The patients created a computer-generated face with a voice (avatar) that they thought was similar to the hallucinated voice. They were then encouraged to confront and challenge the avatar, which was "controlled" by a therapist.

Compared with a group of patients who continued to receive standard treatment for schizophrenia (antipsychotic medication), people who had "avatar therapy" showed greater improvements. These improvements were in the frequency and intensity of their hallucinations and their beliefs about how evil and controlling the hallucinations were.

This was a very small study, but the results are encouraging and, in a few cases, striking. One man, who reported hearing the voice of the devil for more than 15 years, found the voice disappeared after just two sessions, saying the treatment had "given him his life back".

Of course, anecdotes such as this do not provide a sufficient evidence base we can use to evaluate a treatment, so a larger trial is being conducted to evaluate this approach.

Where did the story come from?

The study was carried out by researchers from University College London and the Royal Free and University College Medical School, and was funded by the National Institute of Health Research and Bridging Funding from the Camden and Islington NHS Foundation Trust.

It was published in the peer-reviewed British Journal of Psychiatry.

The research was covered appropriately by both BBC News and The Guardian.

What kind of research was this?

This was a randomised controlled trial (RCT) that tested a new therapeutic technique intended to give schizophrenia patients who experience auditory hallucinations (hear voices) control over their hallucinations. A randomised controlled trial is considered the gold standard in determining the effectiveness of a therapy.

Auditory hallucinations (voices) are often abusive, critical or commanding. When asked, people with schizophrenia consistently report that feeling helpless is the worst aspect of these hallucinations.

Standard therapy often includes advice to ignore the voices and not engage with them. However, some studies have shown that patients who talk to their "voices" tend to feel more in control.

The researchers report that it is difficult to talk to an invisible entity (voice or auditory hallucination) that is continuously abusive. This means that therapists have difficulties "steering" a conversation between the patient and the voice in a way that helps the patient.

The researchers wanted to test if putting a face to the voice may make it easier for patients to communicate with their hallucination and gain control.

This was a small proof-of-concept study, and larger trials are needed in order to validate the findings and assess the effectiveness of the intervention more precisely.

What did the research involve?

The researchers recruited 26 patients who had heard "persecutory" (abusive) voices for at least six months and continued to experience these hallucinations even after treatment with antipsychotic medication. The researchers say that around one in four people with schizophrenia fail to respond to antipsychotic drugs.

Patients were randomly assigned to two groups:

14 patients created a computer-based face and voice to communicate with (an avatar)
12 patients were treated as usual, which consisted of ongoing antipsychotic medication for seven weeks

The patients in the intervention group created an avatar similar to the entity they believed was talking to them, essentially giving a human face to the voice they were hearing. Custom-made voice software was used to create a voice that matched the hallucination.

The therapist was then able to use this real-time voice software to speak through the avatar, with the voice heard by the patient. This was designed to let the patient and the hallucination have a conversation. During the sessions, the therapist and patient were in separate rooms and the therapist was able to talk to the patient directly, as well as through the avatar.

Talking directly to the patient in a traditional way, the therapist encouraged the patient to stand up to their hallucination. During the course of the conversation, the therapist allowed the avatar to increasingly come under the patient's control, and shifted the character of the avatar from abusive to helpful and encouraging.

Patients were then given a recording of these sessions to listen to in order to reinforce their sense of control. Patients could complete up to six 30-minute sessions.

The researchers analysed three main outcomes, which were:

Frequency and disturbing qualities of hallucinations – this was measured using the hallucinations section of the Psychotic Symptom Rating Scale.
Patient experience related to the voices – this was measured using two subscales of the Beliefs About Voices Questionnaire: the omnipotence scale (which assesses the power that the patient perceives the voice has) and the malevolence scale (which assesses the patient's belief about the evil intentions of the voice). This questionnaire assesses the delusions that patients hold about their hallucinations.
Depression (common among people with schizophrenia) – this was measured using the Calgary Depression Scale.

Within each group, researchers calculated the difference in scores from the beginning of the trial to seven weeks after treatment began, and statistically compared these differences between the avatar treatment and usual care groups.

This was a small trial. However, it was reportedly powered to detect a clinically meaningful reduction in the omnipotence score. This calculation assumed a 25% dropout rate among the participants. The researchers didn't report whether the trial was powered to detect differences in the other outcome measures.

What were the basic results?

Most of the participants in the trial were unemployed (54%), had heard voices for more than 10 years (58%), and were fully compliant with their planned drug treatment (85%). There were no significant differences between the groups in the three outcome measures at the beginning of the trial.

Five patients from the avatar group dropped out of the study and were excluded from the analysis.

Compared with the usual care group, the avatar therapy group showed significantly greater improvement at the end of treatment in:

the frequency of their hallucinations
the disturbing qualities of their hallucinations
delusions about their hallucinations

There was no significant difference in depression scores between the groups.

The effect size of the therapy was quoted as 0.8. Effect size is a standardised way of measuring the average difference between two groups. A result of 0.8 is usually interpreted as a large effect.

How did the researchers interpret the results?

The researchers concluded that the reductions seen in the frequency and intensity of the hallucinations, and the patients' beliefs about the omnipotence and malevolence of the voices, "are clinically important considering that the patients' hallucinations had failed to respond to many years of the most effective antipsychotic drugs available".

Conclusion

This study suggests that avatars may have a therapeutic role in the treatment of auditory hallucinations. As the patients enrolled in the trial continued to hear voices despite medication, this new therapy could be an exciting option for a number of patients and their families.

It is important to remember, however, that this was a small proof-of-concept trial, and that the results will need to be replicated in larger – and preferably longer term – trials.

There were several limitations of the study, many of which were discussed by the authors in their published article.

Effects of therapists' intervention

Comparing the avatar therapy with treatment as usual did not allow the researchers to control for the time and attention the patient received during the sessions. It could be the case that it was the experience of being treated – in the sense of regular interaction with the therapist, rather than the treatment itself – that improved symptoms. This may be a type of placebo effect that improved patients' self-esteem, making them better equipped to deal with their voices. The researchers suggest that further studies should include an active control in order to consider this potential confounder.

Could other therapists replicate these results?

The therapy was delivered by a single therapist with an intimate knowledge of the concepts underpinning the study. This raises the question of whether it would be possible to teach the skills required to achieve similar positive results and, if so, how long the training would take.

Patients who dropped out were excluded from the results

The analyses only included those patients who completed the therapy as well as the questionnaires. This could potentially bias the results if the patients who dropped out were less likely to improve. Future trials would ideally undertake an intention-to-treat analysis (where all results of all participants, whether or not they dropped out, are considered) and attempt to account for any missing data. This is particularly relevant, as there was a high drop-out rate of just over a third in the avatar group. As the researchers discuss, it would seem that avatar therapy is not suited to all patients.

Some patients were unable to focus on the single avatar and voice due to simultaneously hearing multiple voices, while other patients were unable to complete the therapy due to the fear instilled by their voices. Part of the benefits of a pilot study is that the selection of suitable patients can be refined for a larger trial, also ensuring that all aspects of the intervention are ideal. Knowing why five people did not complete the study will be important information for future research.

The researchers also discussed an unexpected positive result – three patients stopped hearing the hallucinations altogether. One patient had heard a voice for more than 16 years, and another, who had heard a voice for more than three years, reported that, "It was as if she left the room".

Whether this amounts to a permanent recovery from auditory hallucinations in the long term is not clear. And it is also not clear how common recovery from auditory hallucinations is with other forms of therapy. It will be interesting to see if future studies are able to assess this.

A further phase III trial is being developed in an effort to independently further test the effects of the avatar system on auditory hallucinations, measuring outcomes in more detail and refining exactly what parts of the treatment work best. The results of this trial, whether positive or negative, should make for interesting reading.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New hope to treat schizophrenia with therapist-controlled avatars. The Guardian, May 29 2013

Avatars ease voices for schizophrenia patients. BBC News, May 29 2013

Links To Science

Leff J, Williams G, Huckvale MA, et al. Computer-assisted therapy for medication-resistant auditory hallucinations: proof-of-concept study. British Journal of Psychiatry. Published online February 21 2013

High-dose painkiller heart risk: small but significant

Thu, 30 May 2013 13:33:00 EST

"Study links painkillers to increased risk of heart attack," The Independent reports. This major study found that high doses of the non-steroidal anti-inflammatory drugs (NSAIDs) type of painkiller increased the risk of serious conditions such as heart attacks.

NSAIDs, such as ibuprofen, diclofenac, naproxen and coxibs, are widely used to relieve pain and inflammation.

Many people with painful long-term conditions, such as rheumatoid arthritis, are prescribed high doses of NSAIDs on a long-term basis. It is thought that these people have an increased risk of serious heart conditions compared with those who just take an occasional low-dose ibuprofen pill for a headache.

This new review of hundreds of studies found that coxibs and diclofenac increased the risk of major vascular events – mainly heart attacks – by a third, while ibuprofen was also associated with a greater risk of heart attack. High-dose naproxen did not affect the risk of heart attack.

The actual risk to individuals is small. For example, this study found that for every 1,000 patients taking a high dose of coxib or diclofenac for a year, three more had a major vascular event, one of which was fatal, compared with placebo.

Every treatment comes with both benefits and risks. Your doctor can provide you with information to allow you to make an informed choice and can help you to weigh the benefits of these painkillers against this small risk of a serious side effect.

Where did the story come from?

The study was carried out by researchers from the University of Oxford and was funded by the UK Medical Research Council and the British Heart Foundation. It was published in the peer-reviewed medical journal The Lancet.

It was widely reported in the UK media, and the quality of the reporting was generally of a high standard. Unlike in previous ‘drug-scare’ stories most media sources put the individual risk in its proper context, explaining that it is very small. They also reported the comments made by the researchers that people taking the occasional low dose of an NSAID are unlikely to be at risk.

What kind of research was this?

This research involved meta-analyses of randomised controlled trials (RCTs), including nearly 354,000 participants. The study looked at the risks of NSAIDs compared with placebo treatment and the comparable risks of different NSAIDs. Popular NSAIDs include the older types – ibuprofen, diclofenac, naproxen – and newer cox-II inhibitors (coxibs). Coxibs include celecoxib, etoricoxib and rofecoxib (rofecoxib was withdrawn from the market in 2004 because of concerns over an increased risk of heart attack and stroke).

The researchers were particularly interested in the risk of major cardiovascular events and gastrointestinal complications. They point out that previous research has found that both older and newer types of NSAIDs have a risk of vascular events, while the newer coxib-type NSAIDs are thought to have fewer gastrointestinal effects than older NSAIDs.

This review aimed to provide more accurate estimates of the size, timing and severity of the risk, among different types of patients.

What did the research involve?

The researchers carried out searches of randomised controlled trials that either compared the risks of NSAIDs with placebo treatment or compared the risk of one NSAID with another. The main risks they looked at were of major vascular and coronary events (heart attack, coronary death, stroke, death from any of these and heart failure) and of gastrointestinal complications (perforation of the stomach lining, obstruction or bleeding).

They searched various electronic databases, clinical trial registers, reference lists of relevant papers and also made contact with pharmaceutical companies. Trials (up to 2011) were eligible if they were properly randomised, lasted at least four weeks and compared an NSAID with either a placebo (or open control) or another NSAID.

All trials were reviewed for their eligibility by two researchers, who recorded the key characteristics of the trials that might affect the risk of bias (such as method of randomisation). Where possible, the researchers used data on individual participants or aggregate data (a standard format of results provided by the original researchers). They used standard meta-analytical techniques to give estimates of the risks.

What were the basic results?

The researchers included 639 trials in their analysis. Almost all trials involved a coxib or a high-dose NSAID (diclofenac 150mg daily, ibuprofen 2,400mg daily, naproxen 1,000mg daily).

Coxibs and diclofenac increased the risk of a major vascular event by about a third (coxibs rate ratio (RR) 1.37, 95% confidence interval (CI) 1.14–1.66; diclofenac RR 1.41, CI 1.12–1.78). Most of this increased risk was due to an increase in major coronary events such as heart attack.
Ibuprofen also significantly increased major coronary events (RR 2.22, CI 1.10–4.48), but not major vascular events, such as stroke.
Of 1,000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events (one of which was fatal) compared with placebo.
Naproxen did not significantly increase major vascular events (RR 0.93, CI 0.69–1.27).
The risk of death from a vascular event was increased significantly by coxibs (RR 1.58, 99% CI 1.00–2.49) and diclofenac (RR 1.65, CI 0.95–2.85), but the increase seen with ibuprofen (RR 1.90, CI 0.56–6.41) and naproxen (RR 1.08, 0.48–2.47, p=0.80) was not significant.
Heart failure risk was roughly doubled by all NSAIDs.

All NSAIDs increased upper gastrointestinal complications:

naproxen RR 4.22, CI 2.71–6.56
ibuprofen RR 3.97, CI 2.22–7.10
diclofenac RR 1.89, CI 1.16–3.09
coxibs RR 1.81, CI 1.17–2.81

A further hypothetical analysis by the researchers indicated that the increased risk of heart attacks is highest in those with a previous history of heart disease or risk factors such as high cholesterol.

How did the researchers interpret the results?

The researchers say that the vascular risks of high-dose diclofenac, and possibly ibuprofen, are comparable to coxibs, whereas high-dose naproxen is associated with less vascular risk than other NSAIDs.

Although NSAIDs increase vascular and gastrointestinal risks, they say that the size of these risks can be predicted, which could help guide doctors making decisions on medications for their patients.

Conclusion

This large review adds to, and expands on, the current evidence on the risks of vascular disease and gastrointestinal complications for different NSAIDs. It largely concentrates on trials of high doses of NSAIDs that can only be prescribed by a doctor. It is unclear from this study whether there is any risk from taking lower doses available over the counter. While most experts advise that low-dose NSAIDs, taken occasionally, are safe for most people, an accompanying editorial points out that there are still “large gaps” in evidence on the risks with lower doses of NSAIDs.

While the risk to individuals is small, it is important to remember that high doses of NSAIDs are used by millions of people worldwide to manage chronic pain, for example from arthritis. Even a one in 1,000 risk of NSAID-associated death would amount to 1,000 deaths in a population of 1 million. Such risks are worth bearing in mind when deciding on treatment with your doctor.

This means that any evidence that improves the safety of prescribing of this kind of medication is vital. The evidence presented in this study is likely to be of particular interest to organisations that advise doctors on which drugs to prescribe, such as NICE (the National Institute for Health and Care Excellence).

As an accompanying editorial argues, “identification of safe and effective strategies for chronic pain is sorely needed. In the meantime, long-term use of high dose NSAIDs should be reserved for those who receive considerable symptomatic benefit from the treatment and understand the risks”.

Anyone concerned about using NSAIDs on a long-term basis should seek the advice of their GP or the doctor in charge of their care.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Study links painkillers to increased risk of heart attack. The Independent, May 30 2013

Painkiller taken for arthritis is heart risk. The Daily Telegraph, May 30 2013

Painkillers taken by millions could increase heart risk: Prolonged use 'leads to significant danger'. Daily Mail, May 30 2013

Common painkillers 'pose heart risk'. BBC News, May 30 2013

Painkillers may increase risk of heart attacks, strokes and death. Metro, May 30 2013

Painkillers 'could increase risk' of heart problems. ITV News, May 30 2013

Links To Science

Coxib and traditional NSAID Trialists' (CNT) Collaboration. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. The Lancet. Published online May 30 2013

No proof coffee causes obesity and diabetes

Wed, 29 May 2013 13:33:00 EST

'Is your caffeine fix making you fat?' is the compelling question posed by the Mail Online website, which goes on to report that a study 'shows five cups of coffee a day could cause obesity.' But the study in question involved mice, not people, and a chemical found in coffee, not coffee itself.

The research explored the effects of a substance called chlorogenic acid (CGA), a component of coffee. The rodents were given CGA to see how it affected their fatness and glucose regulation, which is related to the risk of developing type 2 diabetes.

Mice given a high-fat diet supplemented with CGA appeared to display signs of worse glucose regulation than those given the high-fat diet only, which suggests that consuming high levels of CGA may not be good for you.

Despite this finding, the headline 'five cups of coffee a day could cause obesity' was way off the mark. The study only demonstrated that a high-fat diet made the mice fatter, but did not prove that CGA – and by association coffee – makes you fatter, as the headline implies.

This study alone does not support the notion that coffee causes obesity. Still, drinking five or more cups of caffeinated coffee a day can lead to symptoms such as irritability and insomnia.

Where did the story come from?

The study was carried out by researchers from universities in Australia and Malaysia and was funded by the Australian Research Council.

It was published in the peer-reviewed Journal of Agricultural and Food Chemistry.

Both the Mail Online and The Daily Telegraph's reporting of the study seems pretty wide of the mark. The Telegraph's headline, 'Regular coffee drinkers 'at increased risk of weight gain',' is a major extrapolation of the actual study results.

In mitigation, it appears that their reporting was influenced by an overenthusiastic discussion of the potential implications of the research by the researchers themselves.

What kind of research was this?

This was a laboratory-based animal study using male mice. The researchers suggest that the increasing prevalence of what is known in the medical profession as "metabolic syndrome" demands new treatments and prevention strategies.

Metabolic syndrome is the medical term for a combination of diabetes, high blood pressure and obesity. It puts you at greater risk of heart disease, stroke and other conditions affecting blood vessels (cardiovascular diseases)

The researchers point out that human observational studies have consistently linked higher coffee consumption with a lower risk of type 2 diabetes. It is thought that certain dietary polyphenols (organic chemical molecules found in food and drink) can have beneficial effects on several features of metabolic syndrome, such as reducing blood pressure.

Chlorogenic acid (CGA) is one of the most commonly consumed polyphenols in our diet and is a major component of coffee. CGA is also found in fruit such as plums, apples and berries. The researchers wanted to better understand how diet and CGA intake might interact to reduce the risk of certain components of metabolic syndrome, namely obesity, glucose intolerance and insulin resistance.

Insulin is the hormone that controls blood glucose. It is produced when blood glucose levels are high, causing the body's cells to take up glucose and use it for energy. When a person is described as having "glucose intolerance" and "insulin resistance" it means their body's cells are less sensitive to the action of insulin, so they can't regulate their blood sugar as well. This means they are at risk of developing – or may already have – type 2 diabetes.

Animal studies are a useful place to begin to develop a better understanding of the biological underpinnings of diseases. However, mice and men are not identical, so we can't assume positive findings in mice will lead to positive findings in people – this needs to be tested directly in studies involving humans.

What did the research involve?

The researchers designed a study that involved giving male mice a controlled diet over a 12-week period. Mice were either given:

a normal diet
a high-fat diet, or
a high-fat diet and CGA

The researchers say that they used CGA at a dose that would be realistically attainable through the diet (1g per kg of food), rather than an exceptionally high experimental amount. In their article, they describe how people can obtain up to 1g of CGA from the daily consumption of coffee, but do not specify how many cups or the strength of the coffee.

The researchers tested the effects of the three diets on the following measures of metabolic syndrome:

high-fat diet-induced obesity – how fat the mice got due to their high-fat diet
glucose intolerance – an umbrella term for blood glucose levels that are higher than normal
insulin resistance – when the body fails to respond to the normal actions of the hormone insulin, which is essential for maintaining blood glucose levels within a normal range
fatty acid oxidation – the process where fats are broken down for energy in a cell
insulin signalling – essential for maintaining blood glucose levels within a normal range

Their analysis was appropriate and looked at whether the above measures of metabolic syndrome were influenced by the three different diets.

What were the basic results?

The study found that all the mice gained weight in the 12 weeks, with those on the normal diet gaining the least. Compared with mice on the normal diet, both groups on the high-fat diet gained significantly more weight, both with and without CGA.

However, mice given the high-fat diet plus CGA were no slimmer than mice fed a high-fat diet only. This is interesting, as you can buy CGA extracts as a slimming aid, suggesting that it may potentially be less effective than advertised.

Mice given a high-fat diet plus CGA had increased insulin resistance (a bad sign) compared with mice fed a high-fat diet only, which theoretically suggests a higher risk of type 2 diabetes. Likewise, the livers of mice fed a high-fat diet supplemented with CGA appeared to have a poorer fatty acid oxidation process than those given just the high-fat diet.

How did the researchers interpret the results?

Recognising their research was different to what had been found in some previous studies, the researchers concluded that, "Our results do not support the hypothesis that CGA can prevent development of features of the metabolic syndrome."

Conclusion

This rodent research suggests that mice given a high-fat diet supplemented with the polyphenol chlorogenic acid (CGA) fared worse than those given a high-fat diet. But this was only in terms of measures of glucose regulation that are related to the risk of developing type 2 diabetes.

The researchers point out that other studies have found that giving CGA to mice improved measures of their glucose regulation. When there are contradictory results from different studies like this, it can indicate that the biological processes involved are not fully understood. Because of this, these results are not likely to be reliable on their own. A better consensus of what is going on may come through further research into the area.

There are further limitations with this research to consider when thinking about the impact of this study:

The equation of the amount of CGA given to the mice to five cups of coffee in humans was relatively crude and may not be accurate. However, the researchers did make an effort to give the mice a dose of CGA that they thought might be roughly equivalent to the amount a person could get through drinking coffee, although it wasn't clear what type or strength of coffee this would be.
The researchers suggest that the results could have been influenced by the bacteria present in the guts of the mice. They suggest the gut bacteria can degrade CGA, which would alter its biological effect in the body. The precise combination of gut bacteria varies from mouse to mouse and person to person. This may account for some of the different results seen in this area of research, and would need to be measured in further studies.

This study represents preliminary research in mice and is a long way from being directly applicable to humans, as some of the media coverage implies. Further research is required to work out if coffee polyphenols are able to protect against metabolic syndrome and type 2 diabetes in humans or, alternatively, if they make people more vulnerable to these conditions.

Established ways of protecting against the harmful effects of metabolic syndrome include:

losing weight
getting active
eating healthily to keep blood pressure, cholesterol and blood sugar levels under control
stopping smoking
cutting down on alcohol

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Is your caffeine fix making you fat? Study shows five cups of coffee a day could cause obesity. Mail Online, May 28 2013

Regular coffee drinkers 'at increased risk of weight gain'. The Daily Telegraph, May 28 2013

Links To Science

Mubarak A, Hodgson JM, Considine MJ, et al. Supplementation of a High-Fat Diet with Chlorogenic Acid Is Associated with Insulin Resistance and Hepatic Lipid Accumulation in Mice. Journal of Agricultural and Food Chemistry. Published online April 15 2013

End of week surgery 'has higher death risk'

Wed, 29 May 2013 13:33:00 EST

The Daily Mail's front page warns that there's “82% more chance of dying in surgery at weekend”, after a major study examined whether death rates following planned surgery changed depending on what day of the week the patient had their operation.

The risk of dying after planned (elective) surgery is very small. The researchers looked at more than 4 million elective procedures conducted in NHS hospitals in England between 2008-2011 and there were 27,582 recorded deaths – an overall mortality risk of around 0.67%.

However, the researchers found a statistically significant increase in the death risk as the week progressed. Patients who had their operation on a Friday or Saturday were respectively 44% and 82% more likely to die within the next 30 days, than those having surgery on a Monday.

This is an important study which suggests evidence of a “weekday effect”, in which patients having operations closer to the end of the week, or at the weekend itself, have poorer outcomes. The causes of this weekend effect remain unclear, although the authors suggest it could be due to reduced staffing levels or less experienced staff working at the weekend.

It is possible that patients having elective procedures scheduled at the weekend have a different “risk profile” to others, but despite this potential limitation, the findings from this research raise important concerns for policymakers.

You can use NHS Choices to compare local hospitals’ surgical mortality rates.

Where did the story come from?

The study was carried out by researchers from the Dr Foster unit and St Mary’s Hospital, at Imperial College, London. The study was funded by Dr Foster Intelligence, an independent healthcare information company, and the National Institute of Health Research.

The study was published in the peer-reviewed British Medical Journal and has been published on an open-access basis so it is free to download and read.

Not surprisingly, given the implications of the study, it was widely covered in the UK media. The reporting on the study was broadly accurate, though one fact not widely mentioned was that only about 4.5% of elective procedures are carried out at weekends. It is also worth noting that while the Mail’s headline may have suggested these were deaths on the operating table, the death rates were actually calculated to include the 30 days after the operation.

What kind of research was this?

This was a retrospective analysis of national hospital data, taken from all acute and specialist hospitals in England carrying out elective (planned) surgery from the years 2008-9 to 2010-11. Its aim was to examine the association between mortality and the day surgery was carried out.

The researchers point out that previous research has suggested a “weekend effect” – that is, worse outcomes for patients admitted at weekends rather than weekdays.

However, studies in other countries have found no such effect, suggesting that the “weekend effect” may only occur in certain national healthcare systems and is not universal.

The researchers also say that while some research has suggested a higher risk of death for patients admitted for emergencies at the weekends, this could be because those admitted at weekends are more severely ill. They therefore decided to concentrate on mortality rates for planned surgery only.

What did the research involve?

The researchers collected hospital administrative data on patient “episodes of care”, from acute admission to final discharge, for all English NHS hospitals for the three most recent financial years. The records included information on age, sex, source of admission, the patient’s diagnosis, length of stay, date of procedure and date of death. They also had information on any other illnesses (called comorbidity) and their social and economic deprivation scores.

The researchers extracted records of all the planned patient procedures over the three years. As few elective procedures are carried out at weekends (only 4.5% of the total in the UK), they analysed Saturday and Sunday together in one category. They excluded from their analysis any admissions with missing information on age, length of stay or surgery date.

Mortality was defined as any death occurring within 30 days of the procedure (whether in hospital or after discharge). Researchers also looked at deaths within two days of the procedure, to examine shorter-term outcomes.

As well as looking at all elective surgery, they focussed on patients undergoing five higher risk major surgical procedures:

removal of oesophagus and/or stomach
removal of colon and/or rectum,
coronary artery bypass graft
repair of abdominal aortic aneurysm
removal of lung

They included hip replacement, knee replacement, hernia repair, varicose vein surgery and tonsillectomy in one analysis, as these are low risk procedures where few surgical related deaths occurred.

The researchers analysed patient deaths within 30 days, by day of the week, both overall and for the selected procedures defined above. They adjusted the results for:

age
sex
ethnic group
socioeconomic group
comorbidities
number of emergency admissions in the past 12 months and year

They carried out further statistical tests to ensure the results were valid.

What were the basic results?

The researchers found that during this period:

there were 4,133,346 inpatient admissions for elective surgery
there were 27,582 deaths within 30 days of the date of the procedure (overall crude mortality rate 6.7 per 1,000)
4.5% of elective surgery was carried out at the weekend
the risk of death within 30 days increased with each day of the week on which the procedure was performed (starting with Monday)
the risk of death was 44% and 82% higher respectively, if the procedures were carried out on Friday (odds ratio (OR) 1.44, 95% confidence interval (CI) 1.39 to 1.50) or a weekend (OR 1.82, 95% CI 1.71 to 1.94) compared with Monday
mortality within two days of the procedure was also 42% and 167% higher if it was carried out on Friday or the weekend respectively compared with Monday
for four of the five high risk procedures, mortality was higher at the end of the working week and at weekends compared with Mondays
the low risk procedures had higher mortality rates when carried out on Friday compared to Monday, although there was no difference in risk between the weekend and Mondays

How did the researchers interpret the results?

The researchers say their study suggests there is a higher risk of death for patients who have elective surgical procedures carried out later in the working week, as well as at the weekend. The reasons behind this remain unknown, they say, but point out that serious complications are likely to occur within the first 48 hours after an operation.

Failure to “rescue” a patient with complications after surgery could be due to reduced staffing over a weekend as well as a lack of more experienced staff working during that time.

Conclusion

This study suggests there is a higher death rate among patients undergoing planned surgery, both before and during weekends. As the authors say, the reason for this is unknown but it could be due to reduced staffing levels or other resources.

The study’s key strengths were its use of a large national database and its inclusion of all deaths within 30 days of an elective procedure, eliminating the potential bias of only counting deaths that occurred in hospital.

However, it is possible that other factors, called confounders might have affected the results of this study, although the researchers adjusted their results for several of these.

For example, the researchers found those who had planned surgery over the weekend had slightly longer waiting times than those having surgery in the week, which might indicate that their condition was more (or less) severe. However, as the researchers point out, this would not explain the increase in mortality rates from Monday to Friday.

Even though the overall risk of death from elective surgery was small, such a significant variation will be of concern to patients and policymakers alike.

The results of the study are likely to lead to further calls for changes to the patterns of working for healthcare teams in order to improve patient outcomes.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

If you’re going to get sick, make sure it’s on a Monday: Research reveals death rates are higher for operations performed on Thursdays and Fridays. The Independent, May 29 2013

Surgery 'has growing death risk through the week'. BBC News, May 29 2013

You have 82% more chance of dying after surgery at the weekend: Shocking death toll following routine NHS operations. Daily Mail, May 29 2013

NHS risk of death from elective surgery far greater at end of week, study finds. The Guardian, May 28 2013

'Higher death rates' for end of week operations. ITV News, May 29 2013

Patients 44% more likely to die in Friday surgery rather than Monday - and weekends are even worse. Daily Mirror, May 29 2013

NHS surgery: death risk rises through the week. Channel 4 News, May 29 2013

Links To Science

Aylin P, Alexandrescu R, Jen MH, et al. Day of week of procedure and 30 day mortality for elective surgery: retrospective analysis of hospital episode statistics. BMJ. Published online May 28 2013

Molecule limits heart attack damage in mice

Tue, 28 May 2013 14:33:00 EST

"Heart attack drug may reduce tissue damage," says the BBC.

This headline was based on new research in mice. The research showed that a molecule called MitoSNO may be able to reduce the tissue damage that can occur after a heart attack.

The heart pumps oxygen-rich blood around the body, but it also needs its own oxygen supply to function properly. When a person has a heart attack, the blood supply to the heart becomes blocked, starving areas of heart tissue of oxygen.

This can cause damage to the heart muscles and, in many cases, can result in heart failure (where the heart struggles to meet the body’s demand for oxygen). Previous research has found that some of the damage to the heart is caused by chemicals called reactive oxygen species (ROSs). ROSs damage the heart and also inhibit the body’s ability to repair damaged heart tissue.

In this new study, researchers injected MitoSNO into mice after an induced heart attack. The MitoSNO was injected as the blood was returning to the heart. Doing this stopped such high levels of ROSs being produced and protected a greater proportion of the heart tissue from damage than a control treatment.

While this research is still in its early stages, understanding and harnessing the protective effect of MitoSNO appears to provide an avenue for future research to investigate new ways to protect the heart from damage after a heart attack.

Where did the story come from?

The study was carried out by a collaboration of researchers from institutions in the UK, New Zealand and the US. It was funded by organisations from these three countries.

The research publication states a conflict of financial interest as two of the study authors hold an EU patent on the technology described in this publication.

It was published in the peer-reviewed journal Nature Medicine.

The BBC coverage of the research was accurate and well-balanced.

What kind of research was this?

This was laboratory-based research using mice to investigate new ways to help repair heart tissue after it has been starved of oxygen.

When a person has coronary (ischaemic) heart disease some of the blood vessels are clogged up by fatty deposits. If the supply of blood is restricted it can cause a type of chest pain, known as angina, which is often triggered by physical activity.

If the supply of blood to the heart becomes completely blocked it starves the muscles and tissues of the heart of oxygen, which results in a heart attack. Without oxygen, areas of heart tissue start to die, leading to potentially life-threatening damage.

To treat coronary heart disease, doctors attempt to unblock the blood vessels and restart the blood supply to the heart as soon as possible. However, even if this is successful, as the blood re-enters the damaged heart muscle, the oxygen-starved cells start to release high levels of chemicals called reactive oxygen species (ROSs). This causes damage to the heart cells themselves and surrounding heart tissue. This means that although the blood supply has been restored to the heart, damage still occurs and the heart tissue may not recover fully.

ROSs are thought to be produced by a cell structure called the mitochondria. Cells in the mitochondria act like tiny batteries, producing the energy cells need to function.

This new research investigated ways to target the mitochondria during the initial stages of restarting the blood flow to the heart, to stop the high levels of ROSs being produced, so the heart could repair itself more fully.

What did the research involve?

The research investigated the effects of a molecule called mitochondria-selective S-nitrosating agent, MitoSNO, in reducing the production of ROSs in the mitochondria of recovering mouse heart tissue.

The researchers created an artificial model of a heart attack using mice. They blocked one of the mice’s main blood vessels to the heart for 30 minutes, starving the heart tissue of oxygen. This was followed by 120 minutes of ‘reperfusion’ (where blood flow to the heart was re-established).

The researchers injected some mice with MitoSNO just before reperfusion started. In one experiment, they tracked the location of the injected MitoSNO molecules to see if they targeted the mitochondria. In a second experiment, the researchers measured the protective effect of MitoSNO on tissue damage caused by the heart attack. In a third experiment, they injected MitoSNO 10 minutes after reperfusion had started to see if it had any protective effect, and to see how important the timing of the injection was.

A further series of experiments was undertaken to attempt to uncover the exact mechanism by which MitoSNO was having its protective effect on the recovering heart tissue.

What were the basic results?

As the researchers expected, the study found that the MitoSNO travelled to the mitochondria when injected. Their main finding, however, was that injecting MitoSNO at the start of reperfusion helped protect against damage associated with reperfusion. They measured this protection as the percentage of damaged tissue in a specific zone of the heart. Around 30% of the target heart tissue was damaged in mice not receiving MitoSNO, but only 10% in mice that did receive MitoSNO.

The researchers were able to establish that the protective effect was due to MitoSNO interacting with a molecule called mitochondrial complex I. This interaction slowed the reactivation of the mitochondria during the first few minutes of the reperfusion, thereby decreasing the harmful ROS production.

Interestingly, it appeared that MitoSNO would only work if injected at the start of reperfusion, later injection of the molecule did not protect the heart, so timing appeared to be very important.

How did the researchers interpret the results?

The researchers concluded that their results, “identify rapid complex I reactivation as a central pathological feature of ischemia-reperfusion injury and show that preventing this reactivation by modification of a cysteine switch is a robust cardioprotective mechanism and hence a rational therapeutic strategy”.

In lay terms, they say that MitoSNO may offer the potential to be a useful treatment if given in the immediate aftermath of a heart attack.

Conclusion

This laboratory-based research in mice, which used a simulation designed to mimic the effects of a heart attack, appears to show that the molecule MitoSNO can prevent some of the heart tissue damage of a heart attack and the consequences of the return of blood to the heart (reperfusion).

It is important to remember this was a small, early study in mice. Further studies in rodents would be needed to confirm these initial findings as true and accurate.

Furthermore, this study was carried out in mice and the results may not be the same for people. Research in humans would be needed to understand fully the human biological processes involved and to establish whether MitoSNO is effective or safe when used in a similar way for real people. These experiments would need to include a rigorous assessment of the safety of the molecule.

Despite the limitations, this intriguing research does highlight a potential biological target for further research. Ultimately, researchers hope to harness the protective effects of MitoSNO to reduce the damage in, and therefore aid the recovery of, people who have recently suffered heart failure due to lack of oxygen.

Heart failure can have a significant adverse impact on quality of life so any treatment that can prevent or repair damage to the heart would be very valuable.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Heart attack drug may reduce tissue damage. BBC News, May 27 2013

Links To Science

Chouchani ET, Methner C, Nadtochiy SM, et al. Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I. Nature Medicine. Published online May 26 2013

Stem cell stroke treatment trial results 'show promise'

Tue, 28 May 2013 13:33:00 EST

'Stroke patients see signs of recovery in stem cell trial,' BBC News reports. The news, which has saturated the media, is based on a press release from the University of Glasgow. This press release reports further positive early findings of the world's first clinical trial of the use of brain stem cells to treat stroke.

This research – known as the PISCES trial – is a phase I trial. Such trials typically involve giving a small number of people a new treatment to see if it is safe. They are not designed to test if the treatment is effective, so any results that suggest this should be treated with caution.

This study looked at the safety and tolerability of a stem cell therapy called ReN001 in the treatment of ischaemic stroke, where the blood supply to the brain is blocked by a blood clot.

The findings, which were reported in a press release, suggest that the nine people included in the study experienced no adverse effects and showed a modest improvement in stroke-related symptoms.

However, the full findings from the PISCES trial are yet to be published in a peer-reviewed journal. Until this happens, it is worth exercising a little healthy scepticism about the claims being made. This research is still at a very early stage, and, as the professor in charge of the trial points out, the improvement in symptoms could be down to the placebo effect.

It is likely that the encouraging results seen in this trial will lead to a phase II trial involving larger groups of stroke patients. This type of trial may give a better picture about whether ReN001 stem cell therapy is truly effective in the treatment of stroke.

What is a stroke?

A stroke is a serious medical condition that occurs when blood supply to the brain is disrupted, leading to a loss of, or reduction in, brain function. There are two types of stroke:

Ischaemic stroke accounts for about 80% of strokes. In ischaemic strokes, the blood supply to an area of the brain is cut off due to a blood clot.
Haemorrhagic stroke is where there is a leakage of blood in the brain due to a blood vessel bursting. This blood causes pressure on the brain, eventually leading to damage.

This new stem cell treatment development only relates to ischaemic stroke. With ischaemic stroke, the disruption of the blood supply to the brain can starve brain cells of oxygen, causing them to die. It is not uncommon to see large areas of damaged tissue on the brain scans of people who have had an ischaemic stroke.

Depending on the part of the brain affected, people who have had a stroke may experience difficulties with speech and language, orientation and movement, or memory. These problems can be permanent or temporary.

Any advances in the treatment of stroke are particularly important – about 150,000 people in the UK have a stroke each year, with potentially devastating consequences. The only current treatment for ischaemic stroke occurs in the acute phase of the condition (within several hours of the stroke), when anti-clotting agents are administered to dissolve the clot that has blocked the blood flow to the brain. Unfortunately, only a small proportion of patients get to hospital in time to be treated in this way.

There are no existing treatments for an ischaemic stroke beyond the initial acute phase. However, rehabilitation can alleviate the disabilities caused by a stroke.

What are stem cells?

Stem cells are the very early (precursor) cells that can develop into almost all other types of cell in the body, such as skin, muscle or blood cells. They are the building blocks of the body and are unique because they can renew themselves. They also have the ability to form different specialised cell types.

Broadly, there are two types of stem cell: embryonic stem cells, found in early embryos and in significant numbers in the foetus and cord blood at birth, and adult stem cells, which are found in small numbers in bone marrow and blood.

There is currently a great deal of medical research looking at the potential for harnessing the regenerating power of stem cells to repair damaged tissue and fight disease. This is based on the idea that stem cells could be used to produce appropriate cells to repair or replace damaged tissue.

What are the implications of this stem cell research?

The PISCES study is the world's first clinical trial of a neural stem cell therapy for stroke patients. The phase I trial was designed to look at whether the use of the experimental treatment (ReN001 therapy) was safe and tolerable. This type of safety trial precedes tests of effectiveness. As such, treatments in phase I trials are usually applied at low dosages and in small numbers of people.

In this trial, the stem cell therapy was initially tested at lower doses in three people. After this was found to be safe and tolerable, it was tested on a further six people at higher doses. The researcher leading the PISCES study, Professor Keith Muir of the University of Glasgow, said: "Data from the first nine patients treated has shown no cell-related or immunological adverse effects."

This early stage of testing has shown positive findings, but the effectiveness of the therapy, and further information on possible adverse effects, needs to be tested in larger phase II and phase III trials before any conclusions can be drawn about how well it works and how safe it is for treating people who have had an ischaemic stroke.

What could happen next?

The University of Glasgow press release reports that the phase I trial is drawing to a close and its results will be published in 2014. It also states that an application for a phase II trial is expected to be submitted to the UK regulators in July 2013.

If the application is approved, the trial is likely to start later this year. The proposals for this phase II trial mean that it will be carried out across several research centres, and will look at how well the stem cell treatment works for an initial group of 20 stroke patients.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Stroke patients see signs of recovery in stem-cell trial. BBC News, May 27 2013

Stroke patients show signs of recovery in stem cell treatment trial. The Daily Telegraph, May 27 2013

Five stroke victims showing improvement following pioneering stem cell therapy. Daily Mirror, May 27 2013

Stroke victims 'recovering' after pioneering stem cell therapy. Metro, May 27 2013

Patients left paralysed after a stroke can now move again thanks to injections of stem cells into their brains. Mail Online, May 27 2013

New hope for stroke patients. Daily Express, May 28 2013

Stroke Victims Improve After Stem Cell Trial. Sky News, May 27 2013

Could open plan offices be bad for your health?

Fri, 24 May 2013 13:33:00 EST

Open plan offices make employees “less productive, less happy, and more likely to get sick” reports the Mail Online website.

The article is actually based on a number of studies, but the one we found most interesting was a national survey from 2011, conducted in Denmark, looking at self-reported sick days of open plan workers compared to individual office workers.

The study found that people working in an enclosed office space reported lower levels of sickness compared to those working in an open office.

Theories offered by the researchers as to why this may be the case, include:

open plan offices expose people to more noise which could increase their stress levels, making them more vulnerable to illness
the open plan design makes it easier for viruses to spread from one worker to another

Still, as the researchers themselves point out, this type of study cannot prove either theory.

A limitation of the study is that it relied on self-reporting. People were asked to remember and estimate the number of sick days they had over the past year. So participants could have consistently over or underestimated the time off they’d taken, depending on their circumstances.

If you do think that your place of work may be impacting on your health, visit the NHS Choices Workplace health section for advice on useful steps you can take.

Where did the story come from?

The study was carried out by researchers from Denmark and was funded by the Danish Ministry of Employment and the Danish Working Environment Research Fund.

The study was published in the peer-reviewed Scandinavian Journal of Work, Environment and Health.

The Mail Online’s reporting was generally accurate on the study in question. The website also discussed evidence from other studies looking at the impact of open plan offices on stress levels, productivity and health.

We cannot comment on the accuracy of the reporting of these others studies as we have not looked at them.

What kind of research was this?

This was a cross-sectional study aiming to find out whether shared and open plan offices are associated with more days off sick than cellular offices comprising one occupant.

A cross-sectional study is a good way of assessing a situation at one point in time, or asking people to recall their recent experiences. The main weakness of this study type is that it cannot establish cause and effect, for example, whether open plan offices cause people to be off sick more often or whether people who are generally of sick more often tend to work in open plan offices. The method also struggles when it involves asking people to recall events of interest from the past, which can be prone to error or bias – specifically recall bias.

It could be the case that people are more likely to recall being genuinely sick with the flu than when they decided to “pull a sickie” because they fancied a lie-in in bed.

What did the research involve?

The research involved a subset of the results from a national survey of Danish inhabitants between 18 and 59 years of age, consisting of 2,403 employees that reported working in offices.

Based on the survey results, office workers were divided into four categories according to type of office:

cellular offices comprising one occupant
shared offices comprising two occupants
shared offices comprising three to six occupants
open plan offices comprising more than six occupants

The different types of offices were characterised according to self-reported number of occupants in the space.

Sickness absence was assessed with the question “In total, how many sick days have you taken in the last year?”

The main comparison was self-reported sickness absence days depending on the type of office.

The analysis was adjusted for factors that could influence the rate of days off sick (confounders), which included:

age
gender
socioeconomic status
body mass index (BMI)
alcohol consumption
smoking habits
physical activity during leisure time

What were the basic results?

The average (mean) number of self-reported sick days in the last year by number of people in the office was as follows:

one occupant: 4.9 days
two occupants: 8.0 days
three to six occupants: 7.1 days
more than six occupants: 8.1 days

Compared to cellular offices containing one person, this meant:

occupants in two person offices had 50% more days of sickness absence, (rate ratio (RR) 1.50, 95% confidence interval (95% CI) 1.13 to 1.98)
occupants in three to six person offices had 36% more days of sickness absence, (RR 1.36, 95% CI 1.08 to 1.73)
occupants in open plan offices (more than six people) had 62% more days of sickness absence (RR 1.62, 95% CI 1.30 to 2.02)

How did the researchers interpret the results?

The researchers’ concluding remarks are included below in full:

“Open plan offices have become popular because they are designed to facilitate communication and accommodate knowledge sharing. However, our study showed that occupants sharing an office had a significantly higher number of days of sickness absence than those in cellular offices. Consequently, employees, employers, and society in general pay a high price for the benefits of open plan offices in terms of sickness absence and loss of productivity.”

Conclusion

This survey-based research suggested people in open plan offices may experience more days of sickness than people who have their own office and don’t share. The results only show an association and do not prove cause and effect. Neither did the research investigate what might be causing this relationship, although it did speculate about this in its discussion of the results.

The study had some strengths, including that it managed to recruit a reasonable number of people, but it also had many drawbacks that limit the conclusions that can be drawn from it.

The main weaknesses of the study were picked up and acknowledged by the study authors themselves, but were not discussed in the media reporting. They include how both the type of office classification and sickness absence were based on self-reports. Self-reporting sickness absence during the last 12 months may be prone to error in recalling the detail accurately. It may also be a source of recall bias if one group systematically under or overestimate the number of sick leave days they had taken. This could lead to misleading results. However, the reporting of the number of occupants in the office space is not likely to be affected by memory or a source of bias.

The research only looked at sick days. The Mail Online’s reporting about people in open plan offices being “less productive and less happy” was drawn from other research. This could well be accurate, but was not reviewed here.

Nonetheless, in the discussion, the researchers of the Danish study pointed to five possible explanations for how open plan offices might lead to more sickness leave:

higher noise exposure in the open plan office
differences in the type of ventilation used
people in shared and open plan offices are more likely to be exposed to viruses than occupants in cellular offices
difference in psychosocial work environment, for example, lack of privacy in the open plan office causing problems and sickness
open plan offices may reduce employees’ autonomy (discretion and freedom to work), leading to higher stress levels

Another possible explanation, not discussed by the researchers, could be cultural. If you work in a large office where your co-workers are frequently taking days off sick, then you may be more tempted to take time off yourself.

None of the above explanations were explored in the Danish study and all remain speculative.

A common reason that the open-plan office environment is popular with employers is they tend to be cheaper in terms of operating costs such as heating and lighting.

An arguably interesting avenue of research would be to see if the perceived economic benefits of an open-plan office were actually outweighed by the alleged disadvantages, such as increased levels of sickness and reduced productivity.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Open-plan offices make employees 'less productive, less happy, and more likely to get sick'. Mail Online, May 23 2013

Links To Science

Pejtersen JH, Feveile H, Christensen KB, Burr H. Sickness absence associated with shared and open-plan offices – a national cross sectional questionnaire survey. Scandinavian Journal of Work, Environment and Health. Published online May 2011

Breast cancer enzyme may slow tumour growth

Fri, 24 May 2013 12:33:00 EST

"Cancer cell enzymes shown to act as 'good cops'," is the headline on the BBC News website.

The BBC reports on laboratory research into an enzyme called MMP-8 and its effects on breast cancer. The research reveals that while MMP-8 appears to stimulate the growth of breast cancer cells in the short-term, it may slow tumour growth in the long-term.

Scientists are likely to want to explore new treatments that use MMP-8’s ability to slow tumour growth in this way. However, this study used laboratory-grown cells, which don’t behave in the same way as tumour cells within the body. It could be the case that the effect of MMP-8 is different when studied in people.

Nonetheless, this research provides new understanding about how the MMP-8 enzyme influences the growth and development of laboratory-grown breast cancer cells. And while this research has limited immediate implications for people with breast cancer it does contribute new understanding that may help to treat the disease in the future.

Where did the story come from?

The study was carried out by researchers from the University of East Anglia (UK) and the University of Vermont College of Medicine (USA) and was funded by Breast Cancer Campaign, Cancer Research UK, the European Union Framework Programmes 6 and local Norfolk fundraisers.

The study was published in the Journal of Biological Chemistry, a peer-reviewed science journal. It was published as an open-access article so it is free to download.

The reporting of the research was mixed. While the Mail Online exaggerated the results of the study by describing a “breakthrough” that “turns previous thinking on its head”, the BBC coverage was more restrained, including comment from Cancer Research UK on how the research provides "very early clues" about how the enzyme might recruit cells to fight breast cancer.

What kind of research was this?

This was a laboratory study exploring the role of an enzyme called matrix metalloproteinase-8 (MMP-8) in the growth of breast cancer tumour cells.

MMP-8 performs many essential jobs in a normal cell. The researchers say it is known to activate certain immune system signals (called interleukin-6 and interleukin-8), which are types of molecules that regulate and orchestrate the actions of the immune system.

The researchers comment that, traditionally, scientists thought MMP-8 helped cancer cells grow and spread, but more recent research has suggested it may also prevent cancer cell growth.

This research sought to find out if, and how, MMP-8 inhibited tumour cell growth in laboratory-grown breast cancer cells.

Understanding the biology and chemistry of processes involved in diseases such as cancer through laboratory studies is essential if we want to discover new ways to prevent and treat them.

What did the research involve?

The researchers grew human breast cancer tumour cells in a laboratory. Some cancer cells were deliberately engineered to lack a properly functioning MMP-8 enzyme (called “mutant MMP-8”), whereas others had a fully functional version (known as the “wild-type” version). The intention was to see what effect this had on the ability of the cancer cells to grow and develop.

The researchers paid particular attention to the effect of this manipulation on the immune system signalling molecules interleukin-6 (IL-6) and IL-8, which are known to be involved in the growth and development of cancer cells. Genetic changes within the cells were also measured.

All the research was carried out in artificially grown laboratory cells and no tests were done in people with cancer.

What were the basic results?

The research found tumour cells containing the wild-type MMP-8 had elevated levels of IL-6 and IL-8 and that, in the short-term, this was associated with higher levels of tumour cell growth. Cells lacking a working MMP-8 enzyme had lower levels of IL-6 and IL-8 and did not grow as well.

However, in the longer term, activity of the MMP-8 enzyme was found to inhibit the growth of the tumour cells and it was found that the IL-6 and IL-8 levels were no longer elevated.

Interestingly, the small number of cells with a working MMP-8 enzyme that did keep on growing in the long-term had somehow maintained their elevated levels of IL-6 and IL-8 but these were no longer dependent on MMP-8 activity. The relationship had changed from the short- to the long-term.

This showed that in the early stages of tumour growth MMP-8 activity stimulated IL-6 and IL-8, which helped the tumour grow, but, later on, MMP-8 activity limited tumour growth and the IL-6 and IL-8 levels returned to normal.

Only cancer cells where MMP-8 activity had become disconnected from IL-6 and IL-8 levels were able to keep growing in the longer term.

How did the researchers interpret the results?

The researchers concluded that their research showed a “causal connection” between “MMP-8 activity and the IL-6/IL-8 network”, which showed MMP-8 influences the signalling of pro-inflammatory factors (IL-6 and IL-8) that “conventionally promote tumour cells’ growth and development”.

Conclusion

This laboratory study provides new understanding about how the MMP-8 enzyme interacts with inflammatory signals (IL-6 and IL-8). MMP-8 might be something of a double-edged sword. While it stimulates the growth of cancerous cells in the short-term, it may also suppress growth in the long-term.

As with all laboratory studies, new or different discoveries need to be replicated by other research groups to ensure they are accurate and the results weren’t due to chance.

Assuming the research results are valid they could provide an opportunity for cancer researchers to investigate and possibly devise new methods of using MMP-8 activity to supress breast tumour cell growth. However, the research found that some tumour cells kept growing despite the presence of MMP-8. This highlights that cancer cells differ, and that, often, what works in one place and setting may not work in others.

It is important to remember that the researchers investigated breast cancer cells only, so this study alone does not tell us anything about the role of MMP-8 in other cancer types. Similarly, the research used artificially grown breast cancer cells, which may not behave in exactly the same way as tumour cells within a human body.

This research into a new target for drug development provides new and interesting understanding that other researchers can build on. An improved understanding of the biology underpinning breast cancer may lead to the development of new treatments.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Cancer cell enzymes shown to act as 'good cops'. BBC News, May 24 2013

Breast cancer cells can suppress tumour growth 'by releasing protective proteins'. Mail Online, May 24 2013

Links To Science

Thirkettle S, Decock J, Arnold H, et al. Matrix metalloproteinase-8 (collagenase-2) induces the expression of interleukins-6 and -8 in breast cancer cells. The Journal of Biological Chemistry. Published online May 30 2013

Do iPads and electric lights disturb sleep?

Thu, 23 May 2013 13:33:00 EST

"Terrible night's sleep? Blame your mobile phone" is the advice on the Mail Online website, as "exposure to artificial light 'fools' the brain into staying awake."

This – and similar headlines in the Daily Express, The Guardian and Metro newspapers – is based on a recent opinion piece in the journal Nature, which has published a dedicated supplement on the science of sleep.

The opinion piece suggests that the invention of electric light has altered our sleep patterns over the last century. In particular, the widespread use of LED lights, which we rely on to view smartphones, tablets, televisions and laptops screens, is disrupting our sleep.

This, the author suggests, could have potentially serious health consequences, as poorly controlled insomnia can cause both physical and mental health problems.

As an opinion piece, this should not be taken as evidence that light exposure hampers our ability to sleep. However, it does suggest several ways the two may be linked. The piece offers the theory that one causes the other, but these associations have not been directly tested. But given that the author is a specialist in sleep medicine, his opinion cannot simply be dismissed out of hand.

Who wrote the opinion piece?

The editorial was written by Charles Czeisler, a professor of sleep medicine at Harvard Medical School and chief of the division of sleep medicine at Brigham and Women's Hospital in Boston, US.

Over the past 35 years Dr Czeisler has published widely on sleep, the impact of light on sleep, and the effect of restricted sleep on human behaviour and performance.

What arguments are made?

Dr Czeisler suggests that since the invention of electric light, there has been a fundamental shift in our sleep patterns. He argues that light has enabled us to evolve into a "24/7 society", and that many of the features of this transformation – early starting times at work and school, long commutes, high doses of caffeine – lead to us getting insufficient amounts of sleep.

Dr Czeisler's arguments for the link between the increasing use of electric light and disrupted sleep have highlighted several issues.

The biological effect of artificial light

Dr Czeisler argues that exposure to artificial light during the evening and at night could block the effects of brain cells that help promote feelings of sleepiness, as well the "sleep hormone" melatonin.

At the same time, artificial light could also stimulate brain cells associated with alertness.

The combination of these effects could result in many of us feeling much less sleepy in the evening than we would normally.

Time-trends in light use, cost and sleep

Dr Czeisler reports that the cost of generating light dropped dramatically over the last 50 years, which was associated with an increase in the use of artificial light.

At the same time that the use of artificial light increased, reported levels of sleep deficiency also went up. A recent study looking at data in England from 1993 to 2007 found a continual increase in people seeking treatment for sleep disorders.

However, it is important to note that, as with any observational time-trend data, this argument only outlines associations between light consumption and sleep deficiency, and should not be interpreted as there being a causal relationship based on this editorial alone.

Increased use of LEDs

Dr Czeisler suggests that the recent move from traditional incandescent light bulbs to more energy efficient solid-state light-emitting diodes (LEDs) could further disrupt our sleep.

LEDs are commonly used in TVs, computer screens and handheld electronic devices such as tablets. These LEDs are typically rich in shortwave length (blue and blue-green) light, which the cells in our retina are more sensitive to.

He offers the theory that time in front of these blue light-rich screens at night will be more disruptive to our sleep than incandescent lighting.

Interestingly, one of the final discussion points in the editorial is about our ability to control the wavelengths emitted by LEDs. Dr Czeisler suggests that any adverse effect of exposure to these lights at night could be mitigated by replacing blue heavy light with red or orange heavy light in the evenings.

This editorial offers interesting discussion points surrounding the relationship between light – especially evening or nighttime exposure to light – and difficulty sleeping.

What evidence is cited?

Dr Czeisler's article makes reference to several publications, mainly centred around trends in the average number of hours adults and children sleep each night, and the prevalence of the adverse effects of sleep deprivation. As an opinion piece, the overall discussion points are narrative in nature and are not based on any individual piece of research or evidence.

This specific article on its own cannot provide evidence of a direct link between light exposure and sleep deprivation. However, it is not intended to do so. It offers a broad introduction to a series of articles on the topic, and suggests we consider the ways in which technological changes may impact our ability to get a good night's sleep.

Conclusion

It is certainly possible to reduce your exposure to artificial lights. For example, you could dump your smartphone, give away your iPad, banish television from your home, and refuse to work in any job that involves using a computer. But adopting this kind of luddite lifestyle is probably not to most people's tastes.

One proven method of improving your sleep is what is known as "sleep hygiene". This is where you control both physical and environmental factors in order to promote sleep.

Examples of good sleep hygiene include:

not drinking tea and coffee four hours before bedtime
avoiding drinking alcohol or smoking before bed
using thick blinds or curtains, or wearing an eye mask if the early morning sunlight or bright streetlamps affect your sleep
wearing ear plugs if noise is a problem

Links To The Headlines

Peering at bright screens after dark could harm health, doctor claims. The Guardian, May 22 2013

Terrible night's sleep? Blame your mobile phone: How exposure to artificial light 'fools' the brain into staying awake. Mail Online, May 22 2013

How your iPad tablet could mess with a good night's sleep. Metro, May 23 2013

Links To Science

Czeisler C. Perspective: Casting light on sleep deficiency. Nature. Published online May 23 2013

Research could lead to 'universal' flu vaccine

Thu, 23 May 2013 12:33:00 EST

“Scientists create new flu vaccine that works against many different strains of the virus,” The Independent reports.

This headline, and several others like it, is based on early stage research into the development of alternative flu vaccine technologies. While the results of this research are promising, they do not mean that a universal flu jab has been developed.

The study used a new technique where two proteins are bound together to form a nanoparticle. These nanoparticles stimulated an immune response to a greater variety of flu strains than the currently available flu jab.

It is important to stress that this work was carried out in ferrets not humans. Ferrets do have biological similarities to humans, at least in the way they respond to flu and the flu vaccine, so this is a genuinely intriguing development.

But it will take several years of further clinical trials to assess whether this technique can lead to a safe and effective ‘universal flu’ vaccine for humans.

Currently, the best bet is to take measures to protect yourself during peak flu season. This includes regularly washing your hands, staying home from work or school if you have the flu and getting a yearly flu jab if you’re at risk of serious complications.

Where did the story come from?

The study was carried out by researchers from the Vaccine Research Center, part of the US National Institutes of Health (NIH) and was supported by the NIH. The lead researcher is now based at Sanofi, a pharmaceutical company that manufactures vaccines.

The study was published in the peer-reviewed journal Nature.

BBC News reports the findings of the study in an appropriate manner. The headline “Universal flu jab 'edges closer'” and the warning that “a vaccine which could defeat all flu was a long way off” properly convey the stage this research is at.

But most other reporting on this study failed to do this. For example, The Independent’s headline “Scientists create new flu vaccine that works against many different strains of the virus” is premature and does not reflect the early stage of technology development that this research is at.

While the work is a step towards a universal vaccine, the technology has not yet been developed and tested to a point at which it could replace the annual flu jab.

What kind of research was this?

This was a laboratory and animal study that investigated a new approach to generating flu vaccines.

Current vaccines are designed to protect against three strains of the flu virus that health experts expect to be widely circulating in the population during any given year.

This current approach is limited by the fact that the annual vaccine may not match the most common strains circulating that year. This approach also means seasonal flu vaccinations must be carried out annually to ‘catch-up’ with any changes in flu strains.

The aim of this study was to develop a technique targeting a protein that is common to a wide variety of flu viruses, thus priming the body to mount an immune response to a broader range of flu strains.

This research is at a fairly early stage, but it does suggest that it may be possible to develop a universal flu vaccine. The technology will need to be tested further in animals. It will then need to be proven to be safe and effective for people during clinical trials before a ‘universal jab’ could be made available.

What did the research involve?

Researchers fused together two proteins – one, called ferritin, which stores iron and occurs naturally in our blood; the other, called haemagglutinin (HA), which is a viral protein responsible for the initial stages of flu infection. It works by attaching the flu virus to the cell it is going to infect.

Individual ferritin proteins naturally come together and form a smooth hollow ball. Researchers thought that fusing ferritin and haemagglutinin would result in a similar sphere with HA spikes, and that the resulting nanoparticle would be recognised by antibodies.

They further thought that when the spheres were injected into animals they would trigger the body to mount an immune response against a range of flu strains.

To test the ability of this ferritin-haemagglutinin nanoparticle to initiate an immune response, researchers first immunised ferrets with either a traditional flu vaccine or the new complex. They measured the HA titres (titres indicate the number of antibodies the body has produced that recognise the HA spike) three weeks later, and compared the titre levels between the two groups.

Researchers then tested the ability of the ferritin-haemagglutinin complex to protect against a range of flu strains. Three groups of ferrets (one immunised with the new complex, one immunised with a traditional flu vaccine and one non-immunised control group) were exposed to a variety of flu strains. The immune response across the groups was then compared.

What were the basic results?

The researchers found that when the ferritin and haemagglutinin proteins were fused together, the proteins self-assembled into a nanoparticle with haemagglutinin spikes sticking out from the core.

When the nanoparticle was exposed to an antibody known to target HA, the researchers found that it bound to the antibody in a similar manner as traditional flu vaccines.

They say this indicates that the newly developed ferritin-haemagglutinin particles resembled the HA spike of the flu virus, which, in theory, could stimulate an immune response against a flu infection.

Three weeks after immunisation, the researchers found that ferrets injected with the ferritin-haemagglutinin nanoparticle had levels of antibodies (antibody titres) that were approximately ten times higher than those seen in the ferrets injected with the traditional flu vaccine.

They also found that a single injection of these nanoparticles produced an immune response similar to two immunisations with a traditional vaccine.

When challenged with different flu strains, the ferritin-haemagglutinin immunised group of ferrets demonstrated an earlier immune response than the control group, and suffered less weight loss than both the traditionally immunised and non-immunised ferrets, which researchers say further demonstrates the protective effect of the new ferritin-haemagglutinin particles.

How did the researchers interpret the results?

The researchers conclude that this new HA-nanoparticle technology “represents a foundation for a new generation of influenza vaccines and could be adapted to create vaccines for a wide variety of pathogens”.

Conclusion

This is promising research that takes us a step closer to developing a universal flu vaccine. Despite headlines suggesting otherwise, no universal jab has yet been developed.

The researchers say that this new particle is capable of enhancing the body’s immune response compared with the currently used flu vaccine, and that the new complex offers protection against a wider variety of flu strains.

It is important to remember that this research is still in its early stages. This technology development may well lead to the generation of a new type of vaccine. However, significant research is still required to move from the current stage to an available universal flu jab.

Until then, the advice for protecting yourself during flu season remains the same:

Practise good hygiene – wash your hands regularly, clean commonly used surfaces and use tissues when you cough or sneeze.
Consider getting an annual flu jab if you are at risk of severe flu complications. Groups at high risk for complications include those over the age of 65, pregnant women and people who have a weak immune system or underlying health condition such as a chronic heart or respiratory disease.

Read more about preventing the spread of flu.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Universal flu jab 'edges closer'. BBC News, May 23 2013

An end to annual flu injections? Scientists develop new 'universal' jab against all strains of influenza which could last a lifetime. Mail Online, May 23 2013

Scientists create new flu vaccine that works against many different strains of the virus. The Independent, May 22 2013

Concept flu vaccine may be breakthrough. Sky News, May 23 2013

Links To Science

Kanekiyo M, Wei C, Yassine HM, et al. Self-assembling influenza nanoparticle vaccines elicit broadly neutralizing H1N1 antibodies. Nature. Published online May 22 2013

Could a mother's lack of iodine harm her child's IQ?

Wed, 22 May 2013 14:33:00 EST

“Mothers’ diets may harm IQs of two babies in three,” warns The Independent. The newspaper reports on its front page that iodine deficiency is widespread among pregnant women.

Iodine is recognised to play a role in the healthy development of the baby’s brain and nervous system while in the womb and the World Health Organization recommends that pregnant women eat iodine-rich foods.

Severe lack of iodine is one of the leading causes of brain damage in the developing world. But a new study, reported in most of the media today, suggests that even mild-to-moderate iodine deficiency during pregnancy may be associated with poorer cognitive function in the child.

In this large study, the iodine levels of pregnant women were measured, and their child’s IQ at age eight and reading ability at age nine were tested.

The researchers found that children of women who didn’t get enough iodine were more likely to be in the lowest quartile for verbal IQ, reading accuracy and reading comprehension. However, there was no significant difference in overall IQ.

A study of this kind has limitations, for example the fact that it relies on measurements being taken at a single point in time. Also, although the researchers adjusted for many factors that may have influenced the relationship (for example, parental lifestyle and socioeconomic factors), the study cannot prove a direct cause and effect relationship between a mother’s iodine consumption during pregnancy and her child’s cognitive ability. It is also not clear whether the differences seen in the children’s verbal and reading skills would translate into ‘real-world’ problems for these children.

Nevertheless, the study does highlight the need for pregnant women to get enough iodine during pregnancy.

Where did the story come from?

The study was carried out by researchers from the University of Surrey and the University of Bristol. No specific funding was reported for the current study, but researchers were supported by the Waterloo Foundation, the Commission of the European Communities, the US National Oceanographic and Atmospheric Administration and Wassen International. The latter is a company that makes and sells iodine supplements. However, none of these organisations had any role in how the study was conducted or how the collected data was interpreted.

This study used information taken from a much larger ongoing cohort study known as the Avon Longitudinal Study of Parents and Children (ALSPAC), which is looking at the health outcomes of children born during the 1990s. The ALSPAC study is supported by the Medical Research Council, the Wellcome Trust and the University of Bristol.

The study was published in the peer-reviewed medical journal The Lancet.

The media reporting is generally representative of the study, although the Mail Online headline writers got into a serious muddle. When they first published the story they used the headline “Drinking organic milk in pregnancy is 'vital for the baby's future brain power'". This was then changed later in the day – "Drinking organic milk in pregnancy could be harming baby’s IQ".

Neither claim is supported by this study. The study did not assess women’s dietary iodine intake from different sources. So it is not possible to say how many women drank organic milk and whether those who did were more likely to be in the iodine deficient group.

What kind of research was this?

The researchers say that the World Health Organization considers iodine deficiency to be “the single most important preventable cause of brain damage” worldwide. Iodine has a role in regulating the thyroid gland, and thyroid hormones have a role in brain and nervous system development.

The researchers say that changes to dairy farming after the 1930s increased the amount of iodine in milk in the UK. After this and due to the reduction in cases of goitre associated with thyroid problems in the UK it was considered that iodine intake in the UK was sufficient.

However, some more recent UK studies have suggested that mild iodine deficiency may be quite common among adolescent schoolgirls and pregnant women.

The current study used data collected from participants in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort study to see whether there was an association between pregnancy iodine levels and child cognitive performance. The researchers speculated that women with lower iodine levels during pregnancy would have children with poorer cognitive outcomes.

What did the research involve?

The ALSPAC cohort was eligible to all pregnant women in southwest England with a due date between April 1991 and December 1992.

A total of 14,541 pregnant women were enrolled and 13,988 of their children survived for at least 12 months.

The researchers selected 1,040 women for whom they could measure iodine in the first trimester of pregnancy (up to 12 weeks) and their child’s IQ when they were eight years old.

Iodine was measured in a single urine sample. Urinary iodine levels are said to be a good indicator of iodine levels in the body as 90% of ingested iodine is excreted into the urine. However, the results would have been more accurate if the researchers had been able to measure iodine based on 24-hour urine collection.

To try to reduce the impact of this issue, the researchers looked at the iodine-to-creatinine ratio, which is said to be a good way to get a more accurate iodine measurement. The researchers defined adequate iodine as an iodine-creatinine ratio of 150 micrograms or more per litre. Iodine deficiency was sub-categorised as mild-to-moderate (50 to 150) or severe (less than 50).

Child IQ at the age of eight was assessed using a validated scale (the Wechsler Intelligence Scale for Children). At the age of nine psychologists also assessed children’s reading speed, accuracy and comprehension.

The researchers looked at the association between pregnancy iodine status and IQ at the age of eight and reading at the age of nine. They adjusted analyses for a wide range of confounders including:

mother’s age
mother’s ‘parenting score’ (assessed by looking at cognitive stimulation of the baby, parental education and socioeconomic status)
home environment, including baby’s emotional and cognitive environment
family adversity
stressful events during pregnancy
infant birth weight and prematureness
breastfeeding history
maternal smoking and alcohol intake
other dietary factors during pregnancy, including intakes of omega-3 fatty acids and iron

What were the basic results?

The researchers found that, overall, the women in the study had an average (median) urinary iodine concentration of 91 micrograms per litre, and average iodine-to-creatinine ratio of 110 micrograms per litre. About two-thirds of women in the study (67%) were iodine deficient in pregnancy. None of the women was using an iodine supplement.

Compared with mothers with adequate pregnancy iodine, those with iodine deficiency were significantly younger and less educated, but had less exposure to stressful life events in pregnancy.

Compared with children of women with adequate pregnancy iodine levels and after adjustment for confounders, children of women with iodine deficiency were at significantly higher risk of:

having a verbal IQ score in the lowest quartile (odds ratio 1.58, 95% confidence interval (CI) 1.09 to 2.30)
having a reading accuracy score in the lowest quartile (odds ratio 1.69, 95% CI 1.15 to 2.49)
having a reading comprehension in the lowest quartile (odds ratio 1.54, 95% CI 1.06 to 2.23)

However, there was no significant association between pregnancy iodine deficiency and performance IQ or overall IQ score – only verbal IQ. There was also no significant association between iodine deficiency and reading score or number of words read per minute – only reading accuracy and comprehension.

How did the researchers interpret the results?

The researchers say that their results demonstrate the importance of having adequate iodine intake during early pregnancy. They say that the results “emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient”. The researchers consider iodine deficiency during pregnancy to be an important public health issue that needs attention.

Conclusion

This is a valuable study that demonstrates that in this subsample of a large cohort of pregnant women in the UK, the majority had inadequate iodine levels during pregnancy.

They also found that this deficiency was associated with poorer verbal IQ in their children at the age of eight, and reading accuracy and comprehension at the age of nine.

The study benefits from its relatively large sample size, from the fact that it followed participants up over time and from the fact that it adjusted for extensive confounding factors.

However, there are some limitations to this study:

As the researchers say, several 24-hour urine collections would have been the ideal way to measure iodine levels, rather than a single measure, but this would be impractical in a large-scale study.
It would also be useful to continue to reassess the children’s IQ and reading performance at different time points, particularly as the associations were only found for certain measures of IQ and reading ability. Related to this, it is also unclear what impact these differences in verbal IQ and reading accuracy and comprehension would have had on the children’s learning and school performance. Children’s IQs are not thought to be fixed for life but can change over time.
Studies in other population samples from other countries would be valuable.

The researchers note that a randomised controlled trial assessing the effect of iodine supplementation in pregnant women on child cognitive ability in areas with mild-to-moderate iodine deficiency would be valuable. They say that they hope to run such a trial in the UK, as current evidence from trials in this area is weak.

Overall, the study highlights the need for pregnant women to obtain sufficient iodine during pregnancy. The World Health Organization recommends that pregnant and breastfeeding women consume 250 micrograms of iodine a day.

Dietary sources of iodine include dairy products and fish. Pregnant or breastfeeding women who are unable or unwilling to eat these types of iodine-rich dietary sources may need supplements.

If you are pregnant or breastfeeding and are concerned about your iodine levels, speak to your GP or midwife before taking supplements. Supplements will not be suitable for every woman.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Mothers' diets may harm IQs in two-thirds of babies. The Independent, May 22 2013

Iodine deficiency 'may lower UK children's IQ'. BBC News, May 22 2013

Women who drink organic milk in pregnancy could be harming their baby's IQ. Mail Online, May 22 2013

Enough iodine vital in pregnancy – study. The Guardian, May 22 2013

Links To Science

Bath SC, Steer CD, Golding J, et al. Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC) . The Lancet. Published online May 22 2013

Cold weather may increase blood pressure

Wed, 22 May 2013 12:33:00 EST

'Bad weather could raise your blood pressure and even kill you,' is the unnecessarily alarmist headline in the Daily Mail. It reports on a large, complex study that looked for any association between changes in weather and blood pressure rates.

The research focused on patients at a blood pressure clinic in Glasgow and looked at two consecutive visits the patients made within a 12-month period. The researchers combined these findings with Met Office weather data from the time of these visits to assess whether changes in patients' blood pressure were related to changes in the weather.

They found that decreases in temperature and sunshine, or increases in rainfall and frost, were associated with a slight increase in blood pressure.

In the longer term, individuals whose blood pressure seemed sensitive to decreases in temperature and sunshine had slight increases in blood pressure. They also seemed to have overall shorter survival than people insensitive to weather changes.

We know that our bodies respond to temperature changes, so it is plausible that temperature could influence blood pressure. But factors other than the weather may have had a role to play in the blood pressure results seen.

It is also important to point out that the minor increases in blood pressure detected by the study could in many cases be compensated for by taking more exercise or improving your diet.

Where did the story come from?

The study was carried out by researchers from the University of Glasgow. One of the study authors was supported by a Wellcome Trust Capacity Strengthening Strategic Award to the Public Health Foundation of India and a consortium of UK universities.

It was published in the peer-reviewed Journal of the American Heart Association.

The quality of the Daily Mail's reporting of this study is mixed. On the negative side, it presents an over-simplistic conclusion that cannot be drawn from the complex analysis used in this study. The claim made in the headline that 'bad weather...can kill you' is needlessly sensationalised.

On the plus side, its story does contain useful advice from a spokesperson from Blood Pressure UK: "Until we can control the weather, we can still rely on more traditional ways of controlling our blood pressure, such as eating more fruit and vegetables, less salt and alcohol, and taking more exercise."

What kind of research was this?

The researchers say that there is growing evidence that outdoor temperature has an influence on blood pressure, with blood pressure being higher in winter and lower in summer.

This is believed to be because the constriction of blood vessels at colder temperatures increases blood pressure. However, it is unclear whether the temperature-related response differs among individuals.

The current study aimed to examine people's individual changes in blood pressure in response to a range of weather patterns. The researchers also wanted to see whether this was predictive of longer term blood pressure control and mortality.

What did the research involve?

The study included 16,010 people from the Glasgow Blood Pressure Clinic (47% male) who had been referred by their GP in order to control their high blood pressure.

Information on the monthly average weather for the west of Scotland was obtained from the UK Met Office. The Met Office has used a consistent method to analyse climate patterns since 1961, and can provide weather for square kilometre grid points across the UK. Information on four aspects of weather was used in the study:

air frost
air temperature
rainfall
sunshine

Each visit every person made to the Blood Pressure Clinic was mapped to the mean monthly weather of the west of Scotland. Mean monthly measurements for each of the four aspects of weather were ranked from the lowest to the highest measurement, and then split into four equal groups called quartiles. The lowest quartile (Q1) contained the lowest 25% of measurements and the highest quartile (Q4) contained the highest 25% of measurements.

For each person, the researchers looked at pairs of consecutive clinic visits that were at least one month apart but within the same 12-month period. They were interested in pairs of visits where weather either remained constant (both visits in the same weather quartile) or where weather was very different (one visit in the lowest quartile and one visit in the highest quartile). They categorised the weather for these clinic visits as:

Q1 to Q4, where weather for the first clinic visit was in the lowest quartile and the subsequent visit was in the highest quartile
Q4 to Q1, where weather for the first clinic visit was in the highest quartile and the subsequent visit was in the lowest quartile
Qn to Qn, where both the first and the second clinic visits were in the same weather quartile – there was no change in weather patterns

For each individual, the researchers examined changes in their blood pressure and heart rate between the two visits, and looked at how the size and direction of this change (up or down) related to the change in weather.

The researchers used the General Register Office for Scotland to obtain information on deaths among the participants and causes of death. Mortality information was available up to 2011, allowing up to 35 years of follow-up.

Analyses were adjusted for factors known to influence blood pressure (confounders), including:

age
smoking
alcohol
high body mass index (BMI)
kidney disease

What were the basic results?

The average age of individuals at their first clinic visit was 51 years, and most were overweight (mean BMI was 28). The average length of follow-up for each person was 6.5 years.

The researchers found that when there was consistent weather between the two clinic visits (Qn to Qn), there was:

an average 2.1% decrease in systolic blood pressure (the upper figure of a blood pressure measurement) with consistent air frost
a 2.2% decrease with consistent temperature
a 1.7% decrease with consistent rainfall
a 2.2% decrease with consistent sunshine

For change from high to low weather extremes, there was:

about a 2% increase in systolic blood pressure with a decrease in temperature and sunshine
no significant change in systolic blood pressure with a decrease in air frost and rainfall

For change from low to high weather extremes, there was:

a 1.4% increase in systolic blood pressure with an increase in air frost
a 0.8% increase in blood pressure for an increase in rainfall
there was no consistent pattern in blood pressure with a change in temperature from low to high

When the researchers compared the blood pressure changes seen with consistent weather patterns, a change in the weather from the highest to lowest quartile was associated with about a 6% increase in systolic blood pressure when there was a decline in temperature and sunshine, and about a 4% increase in systolic blood pressure when there was a decline in air frost.

Compared with consistent weather, a change from the lowest to highest quartile was associated with 2-6.6% increases in systolic blood pressure for all four weather characteristics assessed.

Looking at longer term changes over five or more years, people whose blood pressure changed when there was a decline in temperature experienced a 2.68mmHg increase in their systolic blood pressure, and a 1.84mmHg increase in their diastolic blood pressure (the lower figure in a blood pressure measurement), compared with people whose blood pressure seemed insensitive to temperature change.

A similar 1.31mmHg increase in systolic blood pressure and a 1.22mmHg increase in diastolic blood pressure was seen for people who were sensitive to a decline in sunshine.

Looking at survival data, people who were insensitive to temperature or sunlight change seemed to have longer survival than people who were sensitive to a decline in temperature or sunlight.

There were no significant longer term differences in blood pressure or survival between people insensitive to temperature or sunlight change, or in people sensitive to an increase in weather extremes.

How did the researchers interpret the results?

The researchers have concluded that for the first time they have demonstrated the extent of alterations in blood pressure between consecutive clinic visits associated with changes in weather in people with high blood pressure.

They have extrapolated that knowing a person's blood pressure response to weather could help prevent doctors making unnecessary changes to blood pressure medication.

Conclusion

This study has used a complex method of analysis in order to look at how individuals' blood pressure at consecutive visits within a one-year period varied according to changes in the weather.

The study benefits from its large population sample and long follow-up. The blood pressure measurements taken at this specialist clinic are also likely to be reliable.

Our bodies do respond to changes in temperature and it is biologically plausible that temperature can affect our blood pressure. The researchers have adjusted for many factors known to influence blood pressure, such as age, high BMI and kidney disease.

However, it is still difficult to say with certainty that all blood pressure changes seen in people between clinic visits were solely down to changes in the weather. For example, the researchers did not have complete information about the blood pressure medications being used by the patients, or their levels of physical activity. These factors could also be influencing the findings.

Another limitation is that blood pressure would have been recorded inside the clinics and may not be representative of what blood pressure would have been if it had been taken outside, with full exposure to the weather.

The research was conducted in individuals from the Glasgow area and it is difficult to say whether similar responses would be seen in people in other locations, particularly people living in vastly different climates.

Similarly, the study only looked at people with high blood pressure. It is not clear whether people with normal blood pressure also experience similar changes in their blood pressure in response to weather changes.

The individuals in the study seem to have been variably sensitive to different changes in the weather. It is not yet clear exactly how a person's blood pressure treatment could be individualised according to their sensitivity to weather change, and whether this would successfully reduce blood pressure variability.

One final important point to make is that although we have no control over the weather, we can control a wide range of factors that contribute towards high blood pressure, such as:

the amount of exercise you take
diet – if your blood pressure is high, you should cut down on salt, saturated fat and sugar, and eat plenty of fruit and vegetables
quitting smoking, if you smoke
the amount of alcohol you drink

Read more about proven lifestyle changes you can make to reduce your blood pressure risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Bad weather could raise your blood pressure and even kill you. Daily Mail, May 21 2013

Chilly days can kill by raising blood pressure. Daily Express, May 22 2013

Links To Science

Aubinière-Robb L, Jeemon P, Hastie CE, et al. Blood Pressure Response to Patterns of Weather Fluctuations and Effect on Mortality. Hypertension. Published online May 6 2013

Sharing a bed with your baby ups risk of cot death

Tue, 21 May 2013 13:36:00 EST

"Bed-sharing 'raises cot death risk fivefold'," BBC News reports. The news has featured in much of the media, with headlines based on a large analysis of previous studies into the risk of cot death, or sudden infant death syndrome (SIDS), associated with bed-sharing.

Bed-sharing is where babies sleep in the same bed as their parents. It has long been known that bed-sharing with a parent who smokes or has consumed drugs or alcohol increases the risk of SIDS.

This new study aimed to see if bed-sharing still increased the risk of SIDS in the absence of these risk factors.

The researchers found a fivefold increase in the risk of SIDS associated with bed-sharing in breastfed babies who were under three months old, had parents who did not smoke, and when the mother had not had any alcohol or drugs.

The risk of SIDS was even higher when the parents smoked, drank or used drugs.

It is important to note that the researchers did not conclude that babies should not be brought into their parents' bed for comfort and feeding, only that they should not sleep in the same bed as their parents.

It is also important to be aware that the overall risk of SIDS is very small and it is a rare condition. However, there are simple steps parents can take to reduce the risk of SIDS (see box), and it is well worth following this potentially life-saving advice.

Where did the story come from?

The study was carried out by an international team of researchers from the London School of Hygiene and Tropical Medicine, the University of Glasgow and the Medical Research Council, UK; the Children's University Hospital, Ireland; the University of Auckland, New Zealand; and the University of Muenster, Germany.

No external sources of funding were reported, although the original research this report is based on was funded by a number of governmental bodies, charities and trusts.

The study was published in the peer-reviewed open access medical journal, BMJ Open.

The story was well reported by the media.

What kind of research was this?

This study combined information from individuals in five large case-control studies. These studies had collected data on babies who died from SIDS (cases) and babies of a similar age who were still alive (controls).

The researchers were interested in bed-sharing specifically. The research aimed to resolve the uncertainty over whether there is a risk of SIDS associated with bed-sharing in breastfed babies where neither parent smoked.

What did the research involve?

The researchers combined individual data from studies in the UK, Europe and Australasia. In total, information was collected for 1,472 babies who died from SIDS and 4,679 control infants, all under one year of age. Control infants were randomly selected normal infants of a similar age, from a similar location and born at a similar time.

The researchers estimated the risk associated with bed-sharing in relation to breastfeeding, smoking, and the mother's recent alcohol consumption or illegal drug use. This was after they had controlled for other important risk predictors, including:

whether the baby slept in the parents' room or elsewhere
the position in which the baby was put to sleep
mother's age
mother's relationship status
the number of children the mother had had previously
the baby's birth weight

What were the basic results?

The researchers found that 22.2% of cases and 9.6% of controls reported a history of bed-sharing. Bed-sharing increased the risk of SIDS fivefold (adjusted odds ratio [OR] 5.1, 95% confidence interval [CI] 2.3 to 11.4) compared with room-sharing (assuming the baby was placed on his or her back in a cot in the parents' room) when:

neither parent smoked
the mother did not drink
the baby was less than three months old
the baby was breastfed, and
there were no other risk factors

The researchers estimate that the absolute risk of SIDS for room-sharing infants was 0.00008 (eight per 100,000) when neither parent smoked and the baby was less than three months old, breastfed, and had no other risk factors.

Bed-sharing increased the absolute risk of SIDS by 0.15 per 1,000. This means the absolute risk from bed-sharing was 0.00023 (0.23 per 1,000).

Bed-sharing, smoking and alcohol use all increased the risk of SIDS. However, the risks associated with bed-sharing decreased as the baby got older.

How did the researchers interpret the results?

The researchers concluded that, "Bed-sharing for sleep when the parents do not smoke or take alcohol or drugs increases the risk of SIDS. Risks associated with bed-sharing are greatly increased when combined with parental smoking, maternal alcohol consumption and/or drug use. A substantial reduction of SIDS rates could be achieved if parents avoided bed-sharing."

Conclusion

This large case-control study combined information from five studies to investigate the risk of sudden infant death syndrome (SIDS) associated with bed-sharing.

It found that bed-sharing is associated with a fivefold increase in the risk of SIDS compared with room-sharing for babies who were less than three months old, breastfed, sharing with non-smoking parents, and the mother had not had alcohol or drugs.

Smoking, alcohol and drug use are already recognised risk factors for SIDS and greatly increase the risk associated with bed-sharing.

The researchers have not concluded that babies should not be brought into the parents' bed for comfort and feeding. Rather, they advise that babies should not sleep in their parents' bed. It is also worth highlighting the very small actual risk of SIDS, both for non-sharing and bed-sharing babies.

Although this study was appropriately designed and controlled for, a number of potential factors that could affect the risk of SIDS and the causes of SIDS are not firmly established. This means that there may be other factors responsible for the observed increase in risk associated with bed-sharing.

To decrease the risk of SIDS, current advice recommends:

putting your baby to sleep on their back – the safest place for them to sleep is in a cot in a room with you for the first six months
do not smoke
do not share a bed with your baby, particularly if you have been drinking or have taken drugs
never sleep with your baby on a sofa
do not let your baby get too hot and keep your baby's head uncovered
if possible, breastfeed your baby

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Bed-sharing 'raises cot death risk fivefold'. BBC News, May 21 2013

Sudden infant death risk 'is five times higher if the baby sleeps in its parents' bed'. Daily Mail, May 20 2013

Sudden infant death risk greater when parents share bed with babies. The Guardian, May 20 2013

Parents warned sharing bed with babies increases risk of cot death. The Independent, May 21 2013

Sharing bed with babies raises cot death risk. The Daily Telegraph, May 20 2013

Cot Death Risks Of Babies Bed Sharing. Sky News, May 21 2013

Links To Science

Carpenter R, McGarvey C, Mitchell EA, et al. Bed sharing when parents do not smoke: is there a risk of SIDS? An individual level analysis of five major case–control studies. BMJ Open. Published online May 20 2013

Claims vitamin B prevents Alzheimer's are unproven

Tue, 21 May 2013 13:35:00 EST

'Should you be taking vitamin B to protect against Alzheimer's?,' asks the Daily Mail.

Its question is prompted by new research into whether a daily dose of vitamin B could reduce the loss of brain tissue in people with mild cognitive impairment. Mild cognitive impairment is thought to be a risk factor for developing Alzheimer’s disease.

The researchers were particularly interested in the effects of B vitamins on ‘grey matter’ – brain tissue. Grey matter consists of a complex mixture of nerve cells and is found in regions of the brain associated with higher cognitive functions, such as memory and reasoning. Previous studies have found that in people with Alzheimer’s disease, certain regions of grey matter begin to shrink, and this may contribute towards the symptoms of the disease.

This research clearly shows that grey-matter loss in certain regions of the brain was reduced with B vitamin treatment – and the results were particularly striking in patients with high levels of an amino acid called homocysteine.

However, whether the reduction in grey matter shrinkage caused by the vitamin B treatment reduced the likelihood of participants developing Alzheimer’s disease, is unknown.

Until further trials have confirmed the benefits of B vitamin supplements and found that they outweigh any potential harms, the best way to keep healthy in mind and body is to eat a balanced diet, control your weight and blood pressure, and to take some exercise.

Where did the story come from?

The study was carried out by researchers from the University of Oxford, the University of Warwick, and the University of Oslo, Norway. It was funded by a wide range of charitable organisations and research institutes.

The study was published in the peer-reviewed Proceedings of the National Academy of Sciences of the United States of America (PNAS).

The researchers hold patents on the use of B vitamins to treat Alzheimer’s disease or mild cognitive impairment, meaning they could benefit financially if vitamin B treatments were licensed for this use.

This story was widely reported in the media. The Daily Express went with the headline “The daily vitamin B pill that halts the ravages of dementia” and The Daily Telegraph with “Vitamin B could stave off Alzheimer’s”. Unfortunately, these headlines are a little optimistic, as although the study found that vitamin B reduced loss of grey matter in certain parts of the brain, especially in older people with high levels of the amino acid homocysteine, the effects this reduction had on an individual’s risk of developing Alzheimer’s disease were not assessed.

What kind of research was this?

This was a randomised controlled trial that aimed to determine whether B vitamins are effective in preventing the shrinkage of grey matter in areas of the brain known to be vulnerable to Alzheimer’s disease, especially those regions linked to mental processes.

This was a secondary analysis of data collected in a previous study which found that B vitamins reduce whole volume brain shrinkage.

A randomised controlled trial is the best type of study design to address this question.

What did the research involve?

The researchers randomised 156 elderly volunteers with memory complaints who fulfilled criteria for mild cognitive impairment to receive B vitamin treatment (folic acid 0.8mg/day, vitamin B12 0.5mg/day, vitamin B6 20mg/day) or placebo for 24 months.

Images of the participants’ brains were taken at the start and end of the study using magnetic resonance imaging (MRI). The researchers compared the images to see whether B vitamins prevented shrinkage of grey matter in areas of the brain affected by the Alzheimer’s disease, especially those regions linked to mental processes.

What were the basic results?

Grey matter volumes were similar at the start of the study in both groups. Over the course of the study, areas of grey matter shrunk in both the placebo and B vitamin groups. However, participants who received B vitamins had less shrinkage of certain areas of grey matter than participants who received placebo.

The researchers report that significant reductions in grey matter loss were seen in some of the regions most affected in Alzheimer’s disease.

The researchers drew on the results of previous research, which has found that levels of an amino acid called homocysteine may play a role in cognitive impairment, Alzheimer’s disease and vascular dementia.

They found that participants with higher homocysteine levels had smaller brain volume, and a faster reduction in brain size.

B vitamin treatment had no effect in participants who had homocysteine levels below the median (average), but significantly reduced grey matter loss in participants with homocysteine levels above the median.

The researchers also monitored changes in participants’ scores on a variety of neuropsychological scales. They found that scores were correlated with grey matter loss in certain regions, some of which shrunk less with vitamin-B treatment than placebo in participants with high homocysteine levels.

Based on these findings, the researchers suggest that changes in vitamin B12 levels that occur with B vitamin treatment leads to a reduction in homocysteine levels. This decreases the rate of grey matter loss. This in turn affects neuropsychological functioning.

How did the researchers interpret the results?

The researchers conclude that, “our results show that B-vitamin supplementation can slow the atrophy [shrinkage] of specific brain regions that are a key component of the Alzheimer’s disease process and that are associated with cognitive decline.”

They go on to suggest that “further B vitamin supplementation trials focusing on elderly subjects with high homocysteine levels are warranted to see if progression to dementia can be prevented.”

Conclusion

This two-year long randomised controlled trial found that B vitamin treatment significantly reduces loss of grey matter in certain regions of the brain in elderly volunteers with mild cognitive impairment. The researchers report that these regions are specifically vulnerable to Alzheimer’s disease. B vitamin treatment was beneficial for the subgroup of participants who had higher than average levels of an amino acid called homocysteine.

This research clearly shows that grey matter loss in certain regions of the brain was reduced with B vitamin treatment. This follows on from the researchers’ previous findings that B vitamin treatment slows brain shrinkage.

However, it is less clear whether the reduction in grey matter actually had any real health impact on individual people. Although the researchers report that loss of grey matter was linked to declining neuropsychological scores, they do not specifically report that participants who received the B vitamins improved their brain function scores. Whether the B vitamin treatment actually prevented Alzheimer’s disease is also unknown.

B vitamins are a recurring focus of Alzheimer’s disease research, and they have been studied in both the prevention and treatment of the disease. This may partly be because vitamin B deficiency can have an effect on brain function.

For more background information about vitamin B, Alzheimer’s, and how it has been reported in the news, read the Behind the Headlines special report on ‘Alzheimer's in the news’

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Should you be taking vitamin B to protect against Alzheimer's? Daily Mail, May 21 2013

Vitamin B could stave off Alzheimer's. The Daily Telegraph, May 20 2013

The daily vitamin B pill that fights dementia. Daily Express, May 21 2013

Links To Science

Douaud G, Refsum H, de Jager CA, et al. Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment. PNAS. Published online May 20 2013

Job stress may raise our 'bad cholesterol' levels

Mon, 20 May 2013 13:33:00 EST

'A stressful job really can kill you – by raising your cholesterol,' reports the Mail Online website. This headline is based on Spanish research that looked at the relationship between job stress and lipid (fat) levels in the blood of more than 90,000 people.

The research found that people who reported difficulties coping with their job had higher levels of what has been dubbed "bad cholesterol" (LDL cholesterol) and lower levels of "good cholesterol" (HDL cholesterol). High levels of LDL cholesterol can clog up the arteries, increasing an individual's risk of developing cardiovascular diseases such as coronary heart disease.

A significant strength of this study is its size – an impressive 90,000 people participated. But the study did not look at diet, which can also affect cholesterol levels. It could well be the case that people in stressful jobs tend to have unhealthy diets and it is this, rather than stress itself, that is to blame for their higher "bad" cholesterol rates.

While increased LDL levels are a risk factor for cardiovascular diseases, this study did not explore the effect this would have on people's long-term health. The Mail Online's claim that a stressful job will kill you is therefore not supported by this study.

Where did the story come from?

The study was carried out by researchers from Ibermutuamur – a mutual insurance company dealing with work-related accidents and occupational illnesses – and two universities in Spain. There were no external sources of funding for the study.

It was published in the peer-reviewed Scandinavian Journal of Public Health.

The Mail Online's headline over-interprets the research, as the study did not assess whether people in stressful jobs were more likely to die. The body of the story was reasonably accurate, but it did not highlight that this type of study cannot prove that one factor is definitely causing another.

What kind of research was this?

This was a cross-sectional study that explored whether there is a link between job stress and abnormal levels of fats (lipids) in the blood.

Some studies have found a link between job stress and an increased risk of coronary disease. There are various theories about how this link might come about – for example, by stress increasing the likelihood of unhealthy habits such as smoking.

Some studies have also suggested that stress could directly influence levels of lipids in the blood by possibly adversely affecting the body's metabolism. However, these studies have been small and in selected populations, and have had mixed results.

In the current study, researchers wanted to assess stress and lipid levels in a large representative sample of workers. As this study is cross-sectional, both stress and lipid levels were assessed at the same time. This means the study cannot establish whether participants' lipid levels were directly influenced by their stress levels.

What did the research involve?

The study involved workers covered by the Ibermutuamur insurance company who had yearly medical check-ups. More than 430,000 participants were recruited between 2005 and 2007, and a study questionnaire was sent out to more than 100,000 randomly selected individuals. Completed questionnaires were returned by 91,593 of these people.

The questionnaire included the question, "During the last year, have you frequently felt that you cannot cope with your usual job?". Participants who answered "yes" were considered to have job stress.

The questionnaire also included 11 questions relating to anxiety and depression symptoms, such as "Have you felt keyed up, on edge?" and "Have you had difficulty relaxing?".

The researchers took fasting blood samples from participants and measured levels of total cholesterol, HDL cholesterol (so-called "good" cholesterol), and levels of a type of lipid called triglycerides. The levels of so-called "bad" cholesterol were calculated based on these measurements.

Participants were classed as having abnormal lipid levels based on pre-specified levels if they reported taking lipid-lowering medication or had been diagnosed as having abnormal lipid levels.

The researchers then looked at whether abnormal lipid levels are linked to job stress. They took into account the following confounders:

age
gender
smoking
basic measures of alcohol consumption and physical leisure activity
obesity
type of job ("blue collar" or "white collar")

What were the basic results?

Job stress was reported by 8.7% of participants. Participants reporting job stress also had higher levels of anxiety and depression symptoms.

After the researchers took into account factors that could affect the results and adjusted them accordingly, people who reported job stress were found to have 10% higher odds of having abnormal lipid levels (odds ratio [OR] 1.1, 95% confidence interval [CI] 1.04 to 1.17).

They also had increased odds of:

high levels of "bad" cholesterol (LDL)
low levels of "good" cholesterol (HDL)
a high total cholesterol to "good" cholesterol ratio
a high "bad" cholesterol to "good" cholesterol ratio

How did the researchers interpret the results?

The researchers concluded that their results support an association between job stress and abnormal lipid levels in the blood.

Conclusion

This study has found an association between job stress and abnormal lipid levels in the blood. Its strengths include the large number of workers assessed (more than 40,000) and the use of the same methods to assess all of the participants.

However, the fact that both job stress and lipid levels were assessed at the same time means it is not possible to say for certain whether job stress might have directly caused changes in blood lipid levels.

There are also other limitations and points to note:

The study did not assess diet. People with job stress may have less healthy diets, which could account for the differences seen in the blood lipid levels, rather than these differences being a direct impact of job stress.
Job stress was assessed by a single question, which may not fully capture all aspects of job stress. Also, different people may consider different things stressful, and the question did not disentangle the exact stressful workplace situations and an individual's ability to cope with them.
Workers who were off sick would not have had the routine medical check-up. This means the sample may have missed some people with more serious health problems with stress.
The authors acknowledge that the effect of job stress seen is relatively small – a 10% increase in the odds of having abnormal lipid levels.

Overall, it is not clear from this study whether stress is a direct cause of the increased lipid levels seen. Studies looking at whether interventions to reduce work stress can reduce lipid levels in the blood would provide an indication if this is in fact the case.

Despite these limitations, there is a wide range of good quality evidence that workplace stress can have a harmful effect on your physical and mental health.

While some people may thrive on pressure, persistent high levels of stress are likely to be harmful.

Read more about what you can do to reduce your levels of workplace stress.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A stressful job really CAN kill you - by raising your cholesterol. Mail Online, May 17 2013

Links To Science

Catalina-Romero C, Calvo E, Sánchez-Chaparro MA, et al. The relationship between job stress and dyslipidemia. The Scandinavian Journal of Public Health. Published online January 2 2013

Vitamin D may help treat severe asthma

Mon, 20 May 2013 12:33:00 EST

”Sunshine vitamin 'may treat asthma'”, BBC News informs us, as a new lab-based study suggests vitamin D could help control symptoms of severe asthma.

Asthma is caused by inflammation of the airways, related to malfunctioning of the body’s immune system. In theory, the immune system mistakes harmless substances, such as dust mites, as a threat and triggers inflammation of the lungs and airways (which causes the symptoms of asthma).

The study in question looked at IL-17A, which is one of the molecules thought to be associated with the malfunctioning immune response seen in asthma. Researchers examined whether vitamin D had an effect on the levels of the molecule produced by white blood cells in a laboratory experiment.

Researchers found that vitamin D reduced the levels of IL-17A produced by cells from people with asthma. This included cells from people who had previously failed to respond to the treatment of choice for severe asthma – oral corticosteroids – often referred to as steroids.

While this study suggests that vitamin D can have an effect on IL-17A levels in the laboratory, it is certainly too early to hail vitamin D as a potential “cure” for asthma. A positive effect on cells in the lab does not guarantee vitamin D supplements will improve symptoms for people with asthma. Clinical trials in people with asthma are ongoing to test whether this will be the case.

Where did the story come from?

The study was carried out by researchers from King’s College London; Queen Mary, University of London, and the Homerton University NHS Foundation Trust. It was funded by Asthma UK and the National Institute for Health Research, and some researchers received Medical Research Council Funding. The study was published in the peer-reviewed Journal of Allergy and Clinical Immunology.

This study was reported by the BBC, Daily Mail, and the Daily Express. The BBC correctly points out that treating asthma patients with vitamin D “has not yet been tested”. The main text of the Mail’s coverage is generally accurate, although their headline suggests that “Vitamin D ‘helps beat the symptoms of asthma’”, when this was not assessed by the study. The Express’s coverage over-interprets the results by suggesting that “Soaking up sun could be a cure for asthma” or could be “the best way of treating asthma”.

What kind of research was this?

This was a laboratory study looking at the effect of vitamin D on one type of white blood cell (T helper cells called TH17 cells) from people with asthma.

One type of T helper cell called TH2 is known to be involved in inflammation of the airways in asthma. However, some evidence suggests that other T cells may also play a role.

TH17 cells are involved in defending the body against bacterial and fungal infections. There is some evidence that these cells may be involved in severe asthma. Also, one of the inflammatory substances produced by these cells, called IL-17A, may exacerbate asthma and reduce patients’ ability to respond to standard treatment for severe asthma – oral corticosteroids (steroids).

Previously, studies had shown that vitamin D could influence the T cells from patients with severe asthma, and also affect TH17 cells. The researchers in the current study wanted to see if vitamin D affected IL-17A production by TH17 cells collected from asthma patients. They also wanted to see whether this effect was different in people who were resistant to steroid treatments.

What did the research involve?

The researchers took blood from 10 healthy adults and 28 patients with moderate to severe asthma and extracted white blood cells, including T cells. The patients had to have had diagnosed asthma for at least six months. Of the patients, 18 had asthma that did not respond as well to oral steroid treatment (steroid resistant asthma), and 10 had asthma that responded to steroids.

The researchers grew the white blood cells in the laboratory, either with or without vitamin D and the steroid dexamethasone, and looked at how much IL-17A was being produced. They assessed whether this varied between people with and without asthma, or in people with steroid resistant asthma.

What were the basic results?

White blood cells from people with asthma produced higher levels of IL-17A than those from non-asthmatic patients. Furthermore, white blood cells from people with steroid resistant asthma produced the highest levels of IL-17A.

Treating the white blood cells with vitamin D reduced the production of IL-17A. This reduction occurred in cells from people with steroid-resistant asthma and steroid-sensitive asthma, and was not affected by adding the steroid dexamethasone.

How did the researchers interpret the results?

The researchers concluded that their results support the hypothesis that vitamin D could improve disease control in people with asthma by reducing IL-17A levels, regardless of whether the person’s asthma is steroid-resistant.

Conclusion

The current laboratory study suggests that vitamin D can reduce white blood cell production of an inflammatory molecule implicated in asthma.

These results were obtained from cells in the laboratory, and further research will be needed to determine whether this effect will also be seen if people with asthma are given vitamin D.

While the results perhaps give a reason to investigate vitamin D further, not all treatments showing initially positive results in laboratory studies go on to have a positive effect on real-world clinical outcomes.

The good news is, as the Daily Mail reports, the results of this study are being followed up with a randomised controlled trial in participants with steroid resistant asthma.

Randomised controlled trials are the best way of testing if treatments are effective. This trial, and others, will tell us if vitamin D works as a treatment for asthma and if so, who it might be effective at treating.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Sunshine vitamin 'may treat asthma'. BBC News, May 20 2013

Vitamin D 'helps beat symptoms of asthma’. Daily Mail, May 20 2013

Soaking up sun could be a cure for asthma. Daily Express, May 20 2013

Links To Science

Nanzer AM, Chambers ES, Ryanna K, et al. Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion. The Journal of Allergy and Clinical Immunology.

Rise in number of unpaid carers and young carers

Fri, 17 May 2013 14:33:00 EST

"Children are picking up the caring roles the state has abandoned," The Guardian says, while The Independent says that 180,000 children work as unpaid carers.

These new figures come from the Office for National Statistics, which has pulled together data on unpaid care in England and Wales from the 2011 census.

The census (which has been carried out every 10 years since the middle of the nineteenth century) reveals an increase in the proportion of the population who are providing unpaid care.

This has risen from 11.5% in 2001 to 11.9% in 2011 in women, and from 8.8% to 9% in men. There tend to be more female carers than male, with the highest burden of care falling on the 50-64 age group for both sexes.

A related report produced by the charity The Children’s Society – based on the same data – has highlighted the issue of children acting as unpaid carers.

The charity's report describes how the census data estimated that there are around 160,000 unpaid young carers in England. It goes on to explain that this is likely to be an underestimate.

What does the ONS find about the gender of carers?

Just over half (58%) of the 5.41 million people providing some level of unpaid care in England are female and 42% are male. This higher proportion of female carers is consistent across all regions. Female carers are representative of 11.9% of the total female population of England and Wales, and male carers are representative of 9% of the male population. Ten years ago these figures were 11.5% and 8.8%.

The level of care provided was most often between one and 19 hours a week. However, 2.9% of the female population and 2% of the male population provided 50 or more hours of care a week. In 2011 in England, 9.5% of the male working population and 13.3% of the female working population were also providing some level of unpaid care. In England, 1.2% of the female population and 1% of the male population were in full-time employment at the same time as providing 50 or more hours of unpaid care. If you are a working carer, read the NHS Choices advice on combining caring with working or studying.

Links To The Headlines

180,000 children work as unpaid carers for relatives. The Independent, May 16 2013

Carers putting their own health at risk, census shows. The Daily Telegraph, May 16 2013

Children are picking up the caring roles the state has abandoned. The Guardian, May 16 2013

Young carers: Quarter of a million children provide care for others. BBC News, May 16 2013

Time-lapse technique may boost success rate of IVF

Fri, 17 May 2013 14:33:00 EST

“IVF advance triples couples' chances of having a baby”, The Daily Telegraph reports.

The innovation in question is actually based on an old imaging technique called time-lapse photography, where a camera is set to record a series of images at regular intervals. This technology is now available for monitoring the development of IVF embryos before they are transferred into the womb.

The researchers in this study developed a way of using the information collected to identify which embryos had a low or high chance of having an abnormal number of chromosomes (called aneuploidy). Aneuploidy can reduce the chances of embryos successfully implanting and resulting in a healthy live birth.

In this study, the researchers looked back at time-lapse imaging for embryos from 69 couples who had IVF. They wanted to know if their technique correctly identified embryos which were more likely to result in a pregnancy or live birth.

The time-lapse cameras allowed the researchers to potentially ‘screen’ embryos for risk of aneuploidy. From this, they would then be able to choose the low risk embryos for implantation.

The researchers found that 73% of the embryos their assessment would have classed as low risk resulted in a pregnancy at five to six weeks, and 61% resulted in a live birth. These rates were higher compared to the overall rate for all embryos (at any risk level), where the pregnancy rate was 42% and the live birth rate was 39%. However, it is important to restate that the new system was not used to intervene, so the results are based purely on observation.

While the results are promising, the technique is still in its early stages. Further research is needed to more widely test the technique and directly compare its results to standard methods.

Where did the story come from?

The study was carried out by researchers from CARE Fertility, an independent provider of fertility treatment and related services in the UK and Ireland. No sources of financial support were reported and the authors reported that they had no financial or commercial conflicts of interest.

The study was published in the peer-reviewed medical journal, Reproductive Biomedicine Online.

The study was well reported in the media, with BBC News coverage including an informative video to explain the technique.

However, potentially confusing figures are reported in other parts of the media.

The Times reported that the new technique “could give a 78% chance of success” while the Daily Mail reports that “Early trials show 78% of women having the test will have a healthy baby”.

The Guardian’s reporting suggests that “Doctors in Nottingham who devised the procedure say it could raise live birthrates at their clinic to 78%...” and this may be where this figure has come from.

However, this 78% figure does not come from the research paper itself, which reports that 61% of the low risk embryos successfully resulted in a live birth – not 78%.

What kind of research was this?

This study looked at whether the novel technique based on time-lapse images of IVF embryos might help select the embryos most likely to successfully produce a baby.

Until now, the researchers say that the vital decision about which IVF embryo should be selected and transferred into the mother’s womb is mainly based on between two and six observations of the developing embryo under the microscope.

To observe the embryo’s development, doctors have had to remove the culture dish containing the embryos from the very controlled environment of the incubator and place them under a microscope in the ambient air of the laboratory. This is usually only performed once a day to minimise disturbance to the embryo.

The authors of the study report that a major reason for IVF failure and miscarriage is that the implanted embryo has an abnormal number of chromosomes (aneuploidy). To accurately detect any chromosomal abnormality requires an invasive biopsy of the developing embryo, followed by genetic testing.

Currently it is not possible to reliably identify those embryos with an increased chance of aneuploidy with the normal microscopic observations of the embryo.

The current study tested a way of identifying the embryos at low risk of having abnormal numbers of chromosomal, using time-lapse imaging of the embryo. A relatively new system now allows doctors to obtain a stream of thousands of microscopic images of developing embryos (time-lapse images), without having to remove embryos from the incubator.

Using this system, the researchers previously found that embryos with an abnormal number of chromosomes take a different length of time to reach certain developmental stages than normal embryos. Based on this, they developed a method to identify those embryos at low, medium, and high risk of having an abnormal number of chromosomes.

In their current study, the researchers looked back at the results of IVF procedures where the embryos had been assessed using time-lapse imaging. They wanted to see if their method could identify those embryos which were more likely to go on to successfully implant, develop and be born.

It is important to note that the study did not actually use the method to select embryos for implantation – it only looked at what might have happened if the method had been used.

This is an appropriate first step for this type of research and, if the results are promising, the method would need to go on to be tested “for real” to select embryos, to see if it performed better than standard methods.

What did the research involve?

This study looked at the treatment outcomes for 88 embryos from 69 couples who attended the CARE Fertility clinic in Manchester between April 2011 and December 2012, and who had a known outcome from their IVF.

This meant that they knew if transfer of the embryo(s) had resulted in:

failed implantation – where the woman had a negative pregnancy test
clinical pregnancy – defined as the presence of a developing embryo with a heart beat at between six and eight weeks of pregnancy
a live birth – identified through the mother completing a clinic delivery outcome form, which according to regulations is reported to the UK Human Fertilisation and Embryology Authority

The researchers excluded cases where two embryos were implanted but did not both have the same outcome, as they would not be able to tell which embryo had which outcome.

The egg cells collected from the women had been fertilised using intra-cytoplasmic sperm injection (ICSI), where a single sperm is injected directly into the egg. The fertilised eggs were then placed into the time-lapse incubator for culturing and imaging for five to six days.

The inbuilt microscope took images of the fertilised egg cell every 20 minutes. The image-analysis software recorded the precise timing of developmental events as they occurred. The embryos had been selected using standard existing methods before being transferred into the womb (that is, not using the new risk assessment method).

The researchers used this previously collected data model to assess the embryos, and grade whether the embryos were at low, medium or high risk of having an abnormal number of chromosomes. They then looked at what proportion of each of these three groups of embryos had achieved clinical pregnancy and live birth, and if this differed between the groups.

What were the basic results?

The researchers found that of the 88 embryos they assessed, 33 were at low risk for having an abnormal number of chromosomes, 51 at medium risk, and four at high risk.

Overall, 42% of the embryos successfully implanted and had a fetal heart beat at five to six weeks.

Among the low risk embryos, almost three-quarters (73%) successfully implanted and had a fetal heart beat at five to six weeks, compared to a quarter (25.5%) of medium risk embryos and no high risk embryos.

This meant that the 73% figure for low risk embryos is a relative increase of 74% compared with the rate for all embryos (42%) – what the media has translated as a ‘74% chance of successful pregnancy’.

The researchers had data on whether or not women had a live birth for 46 of the embryos (18 low risk, 26 medium risk, two high risk). The rest of the pregnancies had not reached term during the study period.

Overall, 39% of the embryo transfers resulted in a live birth. Among the low risk embryos, 61% resulted in a live birth. Among medium risk embryos, 19% resulted in live birth. None of the high risk embryos resulted in a live birth.

Therefore, the 61% figure for low risk embryos is a relative risk increase of 56% compared with the rate for all embryos (39%) – this is where media reports of the ‘increasing live birth rates to above 50%’ come from.

How did the researchers interpret the results?

The researchers say that their risk classification model using time-lapse imaging introduces a non-invasive way of selecting the embryos that are at a low risk of having an abnormal number of chromosomes. They say that this can result in higher likelihood of successful pregnancy and live birth.

Conclusion

This study reports on a new technique using ‘time-lapse imaging’ to non-invasively identify the IVF embryos least likely to have abnormal numbers of chromosomes.

An embryo having an abnormal number of chromosomes is one of the reasons IVF can be unsuccessful.

By looking back at the results of previous IVF procedures, the study showed that embryos identified as being low risk using the new method were the most likely to result in a live birth.

To date, IVF techniques rely on removing the embryo from the incubator about once daily over the course of five to six days to view its development under the microscope. As such, current methods only allow for a few static images which cannot give a reliable indication of whether an embryo has chromosome abnormalities, and also disturb the developing embryo. To select the best embryo for implantation, biopsies of the embryo have to be taken to examine the genes. The new technique potentially offers a non-invasive way to assess the risk of chromosome abnormality using detailed time-lapse images.

The results of this study are promising, but there are some limitations:

It only assessed the outcomes for only 69 couples who received care at one fertility service. Larger numbers of embryos would ideally need to be assessed to confirm the results. Ideally, prospective studies comparing this new technique with standard techniques would also be carried out.
The researchers note that their methods and results may not be directly transferable to other laboratories or other types of patient populations.

The technique, while potentially promising, is still in an early stage of development.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

IVF could be revolutionised by new technique, says clinic. The Guardian, May 17 2013

'Most exciting breakthrough in IVF treatment in 30 years' could triple number of births. The Independent, May 17 2013

IVF advance triples couples' chances of having a baby. The Daily Telegraph, May 17 2013

IVF test that 'trebles the chance of a baby': Photo method helps doctors implant best embryo. Daily Mail, May 17 2013

IVF 'may be boosted by time-lapse embryo imaging'. BBC News, May 17 2013

New IVF Technique Could Triple Number Of Births. Sky News, May 17 2013

IVF time lapse photographing technique breakthrough could help avoid miscarriages and triple number of births. Daily Mirror, May 17 2013

New IVF technique using time-lapse photos to increase number of healthy births. Metro, May 17 2013

Links To Science

Campbell A, Fishel S, Bowman N, et al. Retrospective analysis of outcomes after IVF using an aneuploidy risk model derived from time-lapse imaging without PGS. Reproductive BioMedicine Online. Published online May 13 2013

Absent fathers linked to depression risk in girls

Thu, 16 May 2013 14:33:00 EST

“Study shows girls with absent fathers more likely to develop depression," the Mail Online has revealed.

It reports on a large UK study that found that girls whose biological fathers were absent during the first five years of their childhood had an increased risk of symptoms of depression. No increase in risk was found for girls whose fathers were absent later in childhood, and no increase in risk was found for boys with absent fathers.

Researchers collected information regarding the physical absence of the biological father during childhood, as well as information on depression symptoms when the child was 14. They assessed whether there was any association between these factors.

During their analysis, the researchers took into account several factors that may influence the link, such as family characteristics. However, despite the researchers' efforts to take these variables into account, the reasons why a father may be absent from the family home can be incredibly complicated. This means we can’t be sure whether other factors have produced the association between absent fathers and depression in girls.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and was funded by the UK Medical Research Council, the Wellcome Trust and the University of Bristol.

The study was published in the peer-reviewed journal Psychological Medicine.

Media coverage of this research was broadly accurate, though neither ITV nor Mail Online outlined any of the study’s limitations.

What kind of research was this?

This was an analysis of data from a prospective cohort study called the Avon Longitudinal Study of Parents and Children. This is a study that has been ongoing since the 1990s that assesses influences on the health and development of children.

The researchers were interested in the potential link between the absence of the biological father in early childhood and the risk of mental health problems. They were specifically interested in symptoms of depression that were not necessarily severe enough to be considered clinical depression.

As a prospective cohort study, this research is less likely to be affected by certain types of bias, especially recall bias. It was important that the researchers collected data on the effect of family factors on the children’s mental health at the time, rather than at a later date, to help ensure the information was accurate. Prospective studies allow for this.

What did the research involve?

The researchers measured two main factors:

absence of the biological father during childhood
experience of depressive symptoms during the teenage years

To measure parental absence, the researchers used questionnaires, filled out by the children’s mothers regularly throughout the children’s lives. These questionnaires asked whether the ‘present live-in father-figure is the natural father of the child and, if not, how old the child was when the natural father stopped living with the family’. This information was used to divide the children into three groups:

biological father present
biological father not present during the first five years of life (during early childhood)
biological father not present from age 5 to 10 (during middle childhood)

To assess the teenagers’ experiences of depressive symptoms, the researchers asked the study participants to complete a 13-item questionnaire when they were approximately 14 years old. This asked about the presence of certain symptoms over the previous two weeks. The questionnaire is reported to be a reliable and valid measure of depression in children. Children scoring 11 or higher on this questionnaire were considered to have high levels of depressive symptoms. This is not the same as being diagnosed with depression, however.

The researchers then analysed the data, comparing the risk of having high levels of depressive symptoms among children whose biological father left during early or middle childhood to the risk in children whose fathers were still living with them. These analyses were adjusted for several factors (confounders) that could be linked to both the absence of the father and depressive symptoms, including:

socioeconomic status (including home or car ownership, major financial problems, family size and parents’ jobs)
mother’s characteristics (including having a child before the age of 20, experiencing depression during pregnancy), and
any parental conflict between the mother and her current partner

Separate analyses were carried out for boys and girls, to determine whether the child’s gender had any impact on the relationship between father’s absence and depressive risk.

What were the basic results?

There were approximately 14,500 children in the original cohort study, approximately 11,000 of whom had data available on the presence or absence of their biological father. Among these children, approximately 6,000 had available data regarding depressive symptoms at age 14.

Overall, girls reported higher levels of depressive symptoms than boys, regardless of whether their father lived with them or not – a trend that has also been found in previous studies.

Girls

The study included:

374 girls whose father left during early childhood, 87 (23.3%) of whom had high depressive symptoms at age 14
193 girls whose father left during middle childhood, 27 (14.0%) of whom had high depressive symptoms at age 14
2,295 girls whose father was present throughout childhood, 332 (14.5%) of whom had high depressive symptoms at age 14

Boys

The study included:

357 boys whose father left during early childhood, 30 (8.4%) of whom had high depressive symptoms at age 14
185 boys whose father left during middle childhood, 17 (9.2%) of whom had high depressive symptoms at age 14
2,227 boys whose father was present throughout childhood, 166 (7.4%) of whom had high depressive symptoms at age 14

When assessing the association between the absence of the father in early childhood and teenage depressive symptoms, researchers found that:

Girls with absent fathers during early childhood had a 53% greater chance of experiencing high levels of depressive symptoms compared with girls with fathers present during this time (odds ratio [OR] 1.53, 95% confidence interval [CI] 1.07 to 2.21).
Boys with absent fathers were no more likely to report high levels of depressive symptoms at age 14 than boys whose fathers were present during early childhood (OR 1.08, 95% CI 0.65 to 1.79).

There was no significant association between middle childhood father absence and teenage depressive symptoms.

How did the researchers interpret the results?

The researchers concluded that “father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls”.

Conclusion

This large prospective cohort study suggests that there is a link between a father’s absence during the first few years of life and a girl’s risk of experiencing depressive symptoms.

This study has several strengths, including its large sample size, its long-term follow-up and prospective collection of data for the analyses. It also attempted to consider confounding variables during the analysis and was based in the UK, which helps to ensure that the results are applicable here.

There are some limitations, however, that should be taken into account, including the following.

Only a third of the original cohort was analysed due to missing data on key factors. It is unclear to what extent those included differed from the entire population-based cohort. The researchers report that drop-outs were more likely among participants in lower socioeconomic groups. This factor is linked to both parental absence and depressive symptoms, so it could reduce the validity of the results and how much we can infer from them.
The adjusted analyses further reduced the available sample size due to missing data on confounding factors, and the researchers suggest that this may have resulted in loss of statistical power to detect an effect.
Several potential confounders were not included in the analysis, and could have influenced the results. The study authors report some of these potential confounders (quality of parent-child relationship, the father’s involvement in the child’s life regardless of whether he lived in the same house).
The questionnaire used to assess depressive symptoms is not a measure of clinical depression. A high score on this questionnaire does not indicate that the child has or will develop a diagnosable depressive disorder.

Overall, this study suggests that early childhood family environments may play an important role in the mental health of children. At this stage we don’t know what accounts for the study’s results, and the researchers say that this should inspire future research into the possible biological and psychological mechanisms underpinning this relationship.

Depression is one of the most common mental health conditions, yet there is very little good quality evidence about how to prevent people developing depression. Research that gives us insight into the factors that increase children’s likelihood of developing depression would be invaluable.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A quarter of young girls with absent fathers 'grow into depressed teenagers': Researchers say boys cope better with parental separation. Mail Online, May 15 2013

Study shows girls with absent fathers more likely to develop depression. ITV News, May 15 2013

Links To Science

Culpin I, Heron J, Araya R, et al. Father absence and depressive symptoms in adolescence: findings from a UK cohort. Psychological Medicine. Published online May 14 2013

Human embryo stem cells cloning breakthrough

Thu, 16 May 2013 12:33:00 EST

"Human embryonic stem cells created from adult tissue for first time," The Guardian reports, while the Daily Mail's front page leads with the somewhat fanciful warning that new research raises the "spectre of cloned babies".

These headlines are based on newly published research into the use of a technique known as somatic cell nuclear transfer (SCNT) as part of embryonic stem cell research. It should be noted that no babies were born as a result of this research, and the researchers had no intention of producing a live cloned human being.

SCNT involves taking donated egg cells from women and removing their genetic material. These are then fused with human cells – in this case skin cells – and the fused cell begins behaving in a similar way to an embryo by producing human stem cells.

This research is the first time the technique has been successful using human cells.

When these stem cells were tested, researchers found that the cells were able to develop into other types of cells in a manner similar to that seen in stem cells derived directly from embryos.

The researchers say that this could have exciting implications. The technique could potentially be used to take skin cells from a patient to create "personalised" stem cells. The resulting stem cells could then possibly be used to repair damaged tissue, or even treat genetic conditions.

However, there remain ethical concerns over the implications of using SCNT to develop stem cells. These concerns, as well as scientific and financial considerations, will need to be taken into account as this field continues to develop.

Where did the story come from?

The study was carried out by researchers from Oregon Health and Science University (OHSU) and Boston University School of Medicine in the US, as well as Mahidol University in Thailand. It was funded by OHSU, the Leducq Foundation and the US National Institutes of Health, and was published in the peer-reviewed journal, Cell.

Media coverage of this study was as varied as people's feelings are about stem cell research. It ran from the medically hopeful headline of The Independent ("Human cloning breakthrough raises hopes for treatment of Parkinson's and heart disease"), to a straight-to-the-facts headline from The Guardian ("Human embryonic stem cell created from adult tissue for first time"), to fear and controversy from the Daily Mail ("New spectre of cloned babies: Scientists create embryos in lab that 'could grow to full term'").

Despite its headline and further warnings of "designer babies", the Daily Mail does provide a quite useful figure outlining the process the scientists used in the research.

What kind of research was this?

This was a laboratory study that aimed to produce embryonic stem cells from adult skin cells. Embryonic stem cells are unique in that they are able to develop (or differentiate) into other types of cells. Because of this, it is thought that they could play a critical role in the treatment of a wide variety of diseases.

Researchers have been looking into ways of using a patient's own cells to create embryonic stem cells, as this would ensure that the genetic material in any cells used therapeutically would match the patient's DNA. In theory, this should prevent the body from rejecting the cell.

The researchers report that previous attempts to produce embryonic stem cells using this technique have failed, as the cells stopped dividing before they reached an advanced enough stage. During their experiments, researchers identified two reasons for this inability to sufficiently grow the cells and developed techniques to overcome these limiting factors.

Laboratory studies are necessary for developing techniques and procedures that may one day lead to new medical therapies.

This study will no doubt be very exciting for researchers working with stem cells, but we're still a long way from the findings of this study being translated into new treatments for conditions such as Parkinson's disease or heart disease.

What did the research involve?

The researchers used a technique called somatic cell nuclear transfer (SCNT) to transfer genetic material from adult human skin cells into a human egg cell in order to produce embryonic stem cells. SCNT has been used to clone animals before, and is thought to have potential applications in the study and treatment of human diseases.

SCNT involved taking the nucleus (the part of a cell containing most of the genetic information) from a person's skin cells, inserting its cells into a donor's unfertilised egg cell that had its nucleus removed. The skin cell nucleus was then fused with the donor egg cell. Once this happened, the person's genetic material was in a vehicle that was theoretically able to divide.

Researchers then optimised methods to prompt the egg cell to start and continue to divide using electricity and chemical compounds, including caffeine.

Once this cell division yielded approximately 150 cells – a stage called a blastocyst – researchers were able to isolate the embryonic stem cells. The researchers then tested these stem cells to see if their genetic material retained any traces of the genetic material from donor egg cell's nucleus. They also tested whether or not the embryonic stem cells were able to develop into other types of cells.

What were the basic results?

The researchers were able to use SCNT to generate human embryonic stem cells. These cells were found to match the nuclear genetic material of the person's skin cells, and did not contain any trace of the donor egg's nuclear genetic material.

The embryonic stem cells were able to develop into several different types of cells, including heart cells. They were also found to express genes similar to those expressed by embryonic stem cell lines derived following IVF procedures, which the researchers referred to as "genuine" embryonic stem cells.

How did the researchers interpret the results?

The researchers say that this study represents the first successful attempt at generating human embryonic stem cells following somatic cell nuclear transfer.

They say that the observed ability for these embryonic stem cells to develop into heart cells demonstrates their potential use in regenerative medicine.

Conclusion

This research represents the first time that human embryonic stem cells have been developed using the "cloning technique" known as somatic cell nuclear transfer (SCNT).

It is important to note that this study did not attempt to clone a human being by creating a baby in a lab. It is unclear at this point whether the cells in this study would continue to stably divide in a manner sufficient for an embryo to develop to full-term.

While this study is certainly a breakthrough for researchers in the field, its findings are unlikely to translate quickly into regenerative medicine or other medical therapies.

There are some scientific limitations to the approach, including the fact that only a fraction of the fused cells were able to divide sufficiently to reach the blastocyst stage and, of those that did, not all were able to generate stable embryonic stem cell lines.

It is also worth considering that donated egg cells from women are required before SCNT can be carried out, potentially limiting the ability of scientists to generate stem cells on an "industrial" basis.

SCNT does not represent the only approach to embryonic stem cell development. Researchers around the world continue to investigate several methods for developing and using stem cells. It is not immediately clear how the current research will fit into this field, or whether it will trigger a major shift in stem cell research.

In addition to these scientific hurdles, there are ethical and financial considerations that will likely need to be addressed.

Despite these issues, this research does represent a breakthrough in the use of SCNT in the stem cell research field and has implications for disease research.

What the study emphatically does not represent is an impending expansion into cloning babies.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Human embryonic stem cells created from adult tissue for first time. The Guardian, May 15 2013

Embryonic stem cells: Advance in medical human cloning. BBC News, May 15 2013

New spectre of cloned babies: Scientists create embryos in lab that 'could grow to full term'. Daily Mail, May 15 2013

Cloning breakthrough by US scientists. The Daily Telegraph, May 15 2013

Stem Cells Made From Cloned Human Embryos. Sky News, May 15 2013

Cloned babies fear as stem cells are created from skin. Daily Express, May 16 2013

Links To Science

Tachibana M, Amato P, Sparman M, et al. Human Embryonic Stem Cells Derived by Somatic Cell Nuclear Transfer. Cell. Published online May 15 2013

Drug combination offers hope for osteoporosis

Wed, 15 May 2013 13:33:00 EST

“Double drug hope for brittle bone sufferers”, reports the Daily Mail.

This headline follows a small but well-designed trial of treatments for postmenopausal osteoporosis. As women go through the menopause, levels of the hormone oestrogen begin to fall. This drop in oestrogen can lead to a thinning and weakening of the bones, increasing the risk of broken bones (fractures).

While current treatments can help prevent further weakening of the bones, they are not particularly effective at restoring bone strength – known as bone mineral density (BMD). In this study, researchers found that using a combination of teriparatide (Forsteo) and denosumab (Prolia) led to a significant improvement in BMD, when compared to using either medicine on its own.

While this research is encouraging, there are still questions that need answering. For instance, it isn’t clear whether this combination treatment is effective at preventing fractures (more participants would be required) or safe past 12 months (the length of this study).

Similarly, the research was mainly in white, city-dwelling postmenopausal women, so the effectiveness may differ in women from different places and ethnic backgrounds. Similarly, it is not clear whether it would benefit men with osteoporosis (which is less common, but still accounts for roughly 20% of cases).

Aside from these limitations, this research is a positive step forward in the search for new treatment options for osteoporosis. The encouraging results are likely to lead to further, larger studies.

Where did the story come from?

The study was carried out by researchers from at the Massachusetts General Hospital, Boston (US) and was funded by the National Center for Research Resources as well as the pharmaceutical manufactures Amgen and Eli Lilly.

Amgen manufactures denosumab and Eli Lilly manufactures teriparatide.

However, the publication states that the funders of the study had no role in study design, data collection, data analysis, data interpretation, or the writing of the report.

The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.

The study was published in the peer-reviewed medical journal The Lancet.

The media reporting generally described the research findings accurately although discussion about the limitations of the research was minimal.

What kind of research was this?

This research used a randomised control trial (RCT) to test whether combining two approved osteoporosis medicines (teriparatide and denosumab) would improve bone mineral density in postmenopausal women.

Osteoporosis is a condition that affects the bones, causing them to become weak and fragile and more likely to break (fracture). These fractures most commonly occur in the spine, wrist and hips, but can affect other bones such as the arm or pelvis. Approximately 3 million people in the UK are thought to have osteoporosis. Although commonly associated with postmenopausal women, osteoporosis can also affect men, younger women and children.

The two drugs, teriparatide and denosumab, are already used individually to treat osteoporosis but they work in slightly different ways. So the researchers wanted to test whether there was any added benefit of using the two drugs together.

Despite drugs being available for osteoporosis, the researchers’ say no currently approved treatment actually restores normal bone density in most patients with osteoporosis – they merely halt the decline. And options for those with severe osteoporosis are limited; the resulting risk of fracture, aside from affecting people’s quality of life, puts a considerable strain on the NHS. It is estimated that there are around a quarter of a million fractures each year in the UK. This means there is a continual need for new or improved treatments.

An RCT is one of the most reliable ways of testing whether a new drug, or in this case combination of drugs, is effective.

What did the research involve?

Between September 2009 and January 2011 the researchers enrolled 100 postmenopausal women (aged 45 years or older, with at least 36 months since last period) with osteoporosis who were at high risk of bone fracture. Women were enrolled through a mailing advertisement and on referral to Massachusetts General Hospital in Boston (US).

Bone mineral density is measured by ‘T-score’ and is simply the number of units, known as standard deviations, above or below the expected average for a healthy 30-year-old adult of the same sex and ethnicity as the patient. Only about 2.5% of women would have a T-score less than -2.0, for example.

The researchers defined high fracture risk as either:

T-score –2.5 or less at the spine, hip, or femoral neck
T-score –2.0 or less with at least one risk factor; fracture after age 50 years, parental hip fracture after age 50 years, previous overactive thyroid, inability to get up from a chair with arms raised, or current smoking
T-score –1.0 or less already with history of a fracture from osteoporosis

Women were split into three equal groups to receive 20 microgram teriparatide daily, or 60 milligram denosumab every six months, or both.

Bone mineral density was measured at 0, 3, 6, and 12 months. This included measuring bone density at the lumbar spine, hip bone and neck of the femur using low-dose x-rays and bone biomarkers. Calcium intake (which can influence bone strength) was also recorded at the start of the study through a food frequency questionnaire.

Women who completed at least one study visit after baseline were assessed in a modified intention-to-treat analysis. Physicians interpreting bone mineral density assessments and the laboratory staff doing bone-marker assays were unaware of patients’ treatment groups.

The analysis compared changes in bone density from baseline (the start of the study) to the different time points (3, 6, and 12 months) for each of the different locations (spine, hip bone, and neck of femur).

What were the basic results?

Of the 100 eligible women, 94 completed the 12 month study. At 12 months, the main findings were that:

Lumbar spine bone density had increased significantly more in the combination group (9.1%, standard deviation (SD) 3.9) than in the teriparatide (6.2%, SD 4.6) or denosumab (5.5%, SD 3.3) groups.
Femoral-neck bone density also increased more in the combination group (4.2%, SD 3.0) than in the teriparatide (0.8%, SD 4.1) and denosumab (2.1%, SD 3.8) groups.
Total hip bone density also increased more in the combination group (4.9%, SD 2.9; teriparatide, 0.7% SD 2.7; denosumab 2.5%, SD 2.6).

All these results were statistically significant.

How did the researchers interpret the results?

The researchers concluded that, “combined teriparatide and denosumab increased bone mineral density more than either agent alone and more than has been reported with approved therapies.” Furthermore, “combination treatment might, therefore, be useful to treat patients at high risk of fracture.”

Conclusion

This small but well-conducted RCT showed that combining licensed osteoporosis medicines teriparatide and denosumab may increase bone density more than either medicine used on their own, in postmenopausal women at high risk of bone fracture.

The researchers highlighted that their results were not consistent with previous trials looking at combination therapies for osteoporosis, which found no benefit of combining them.

However, previous research did not use the same combination of medicines in the same dose as the present trial. It could be the case that the dosages used in previous research were not given at the optimal level.

And while the study showed statistically significant differences in bone density at 12 months, this does not necessarily mean the treatment lead to a reduced rate of fractures – which is the ultimate aim of treating osteoporosis. Larger, longer-term studies are required to see what impact this combination treatment has on fracture risk, as well as assessing how safe and effective both drugs are in the longer-term.

This is particularly relevant because teriparatide is only licensed to be used for a maximum of 24 months (a point the Daily Mail usefully highlighted). It remains to be seen what would happen when this combination of therapies were stopped – would the benefits be reversed, and would it be safe to continue using the medicine longer than recommended?

These issues would need to be thoroughly addressed before this potentially useful combination could feasibly be routinely used in the NHS.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

The double drug hope for brittle bone sufferers. Daily Mail, May 15 2013

Links To Science

Tsai JN, Uihlein AV, Lee H, et al. Teriparatide and denosumab, alone or combined, in women with postmenopausal osteoporosis: the DATA study randomised trial. The Lancet. Published online May 15 2013

'Broken' body clock may be linked to depression

Wed, 15 May 2013 13:33:00 EST

"Depressed people are out of sync with the rest of the world because their body clocks are broken," reports the Mail Online website, while The Independent claims that depressed people live in a "different time zone".

The story comes from a study that looked at the activity of genes thought to be involved in regulating the body's internal clock – the innate sense that most people have of the changes over a 24-hour day to night cycle (circadian rhythms).

Researchers did a detailed study of gene expression, the effect that certain proteins contained inside individual genes have on genetic activities inside the body.

The study involved examining brain tissue taken from people who donated their brains to science after their deaths. Of the sample, 55 people had no history of psychiatric illness, while 34 patients had a history of severe depression (major depressive disorder, or MDD).

Researchers found that the gene activity associated with regulating circadian rhythms was much weaker, and often disrupted, in the brains of patients who had MDD.

These results possibly present, as philosophers put it, a "causality dilemma" (a chicken and egg problem) – does depression lead to a disrupted body clock, or does a disrupted body clock make people vulnerable to depression?

It is too early to say what help these findings may be in the understanding and treatment of MDD.

Where did the story come from?

The study was carried out by researchers from the University of Michigan, the University of California, Weill Cornell Medical College, Stanford University and the HudsonAlpha Institute for Biotechnology, and was supported by the Pritzker Neuropsychiatric Disorders Research Fund.

It was published in the peer-reviewed Proceedings of the National Academy of Sciences.

Both the Mail Online and The Independent covered the research uncritically. Given the specialised nature of this research, it's not surprising that both of the news stories appeared to be strongly based on an accompanying press release and were not a critical appraisal of the study itself.

What kind of research was this?

This was laboratory research using donated post-mortem brains. In it, researchers analysed in detail the gene expression of certain genes thought to be associated with circadian rhythm regulation at the time of death.

The authors point out that a common symptom of major depressive disorder is the disruption of circadian patterns, which can trigger symptoms of insomnia as well as excessive daytime sleepiness and fatigue (feeling tired all the time). However, to date there is no direct evidence of "circadian clock dysregulation" in the brains of patients with major depressive disorder.

What did the research involve?

Researchers used human brain tissue taken from a US donor programme with the consent of next of kin. They also took information from medical records, medical examiners and interviews with relatives to record the donors' previous physical health, medication use, psychiatric problems, substance use and details of death.

This was done in order to assess whether donors had a major depressive disorder, a severe form of depression that has a significant impact on day-to-day living.

They also assessed whether physiological stress at the time of death would have had an effect on gene expression, and took account of this potential confounding factor.

Researchers analysed the brain tissue of 55 donors with no history of psychiatric or neurological illness and 34 patients with major depressive disorder. Using specialist techniques called DNA microarray, they measured the expression of genes thought to be associated with regulating circadian rhythms in different areas of the brain.

They used the control group to build a detailed picture of circadian gene expression in brain tissue and compared the results with those found in the brains of people with MDD. They also used the rise and fall of the top 100 "cyclic" genes in 60 of the donors to predict the time of death in all the others, both cases and controls.

What were the basic results?

In the brain tissue from donors without major depressive disorder, they found that the activity of "circadian" genes at certain times of the day and night was consistent with data derived from other diurnal (day-active) mammals. More than 100 genes showed "consistent cyclic patterns" over six brain regions.

However, in the brains of patients with MDD gene expression of cyclic patterns was far weaker and more disrupted, with the patients' day pattern of gene activity often resembling a night pattern.

They found that predictions of time of death were more accurate among controls than for those with MDD.

How did the researchers interpret the results?

The researchers say the results provide convincing evidence that there is a "rhythmic rise and fall" in the activity of hundreds of genes in the human brain associated with regulating the day/night cycle. There is also evidence that the activity of genes associated with circadian rhythms is abnormal in people with MDD.

The study identifies hundreds of genes in the human brain that are likely to be involved in the sleep/wake cycle. The researchers conclude that daily rhythms in these genes are "profoundly dysregulated" in MDD. They say the results pave the way for the identification of new biomarkers and treatments for mood disorders.

Conclusion

This study is of interest, but at the moment it has little bearing on our understanding and treatment of depression. It could lead to new insights and treatments in the future, but there is no guarantee that this will be the case.

Also, as the authors point out, gene activity can result from many factors, including disease and drug history. In particular, it should be pointed out that:

the researchers relied on only 55 patients to build a "normal" picture of genetic expression associated with the sleep/wake cycle
it is not clear whether those in the MDD group had all been formally diagnosed with MDD or how long they had had depression, and it is possible there were errors in the classification of patients either with or without MDD

In conclusion, it is too early to say whether this study's findings might help in the understanding and treatment of major depressive disorders.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New forensic technique for estimating time of death by checking internal clock of the human brain. The Independent, May 13 2013

Out of sync with the world: Depressed people suffer with 'broken body clocks'. Mail Online, May 14 2013

Links To Science

Zi JZ, Bunney BG, Meng F, et al. Circadian patterns of gene expression in the human brain and disruption in major depressive disorder. PNAS. Published online May 13 2013

Is the rise in neurological deaths due to modern life?

Tue, 14 May 2013 13:33:00 EST

'Technology, food additives and air pollution are causing people to develop dementia earlier than ever,' reports the Mail Online website. But this is a claim with little to no evidence to support it.

The study the Mail reports on looked at death rates in 10 developed countries, including the UK and the US. The researchers specifically focused on what they termed "neurological deaths". These are deaths arising from conditions that affect the brain and nervous system, such as motor neurone disease and dementia.

This study found that the overall death rate has fallen over the past 30 years. But levels of neurological deaths have risen significantly when comparing data from 2008-10 to comparative data from 1979-81.

It is not clear why there has been such a rise in the number of deaths from neurological disorders. The researchers speculate that the fact that people are living longer, there have been major improvements in diagnostic techniques, and significant changes in lifestyle and the environment – such as the increased use of food additives, more pollution, and new technologies such as wi-fi and mobile phones – could all contribute to the rising numbers.

It is the claim about modern technology that captured the Mail's imagination the most. But the key word here is "speculate": more research is needed to see whether factors such as "technology, food additives and air pollution" could be held responsible for the rise in neurological deaths.

Where did the story come from?

The study was carried out by researchers from Bournemouth University and Southampton University. There was no funding to declare. It was published in the peer-reviewed journal, Public Health.

This story was covered poorly by the Mail Online website. Speculation about the possible causes of the increase in deaths from neurological diseases was reported as fact.

What kind of research was this?

This was an observational study that aimed to see how total deaths (mortality) and deaths specifically from neurological causes in older adults (aged 55 to 74 years) varied between the periods 1979-81 and 2008-10 in 10 major developed countries (Australia, Canada, France, Germany, Italy, Japan, Netherlands, Spain, the UK and the US).

This type of study can tell us how death rates and deaths from neurological causes vary over time, but it cannot tell us why these rates vary.

In order to investigate whether any of the factors suggested by the Mail Online – such as electronic devices, food additives and air pollution – play a role, ideally a randomised controlled trial, or more likely a cohort study, would have to be performed.

Even these types of studies could be difficult to carry out. Given that certain technologies such as mobile phones are now a global phenomena, it would be hard to isolate a mobile-free control group.

What did the research involve?

The researchers compared World Health Organization (WHO) data on total mortality and deaths due to neurological causes in people aged between 55 and 74 years old for the period 1979-81 with data from 2008-10 (or for the latest years available) in 10 major developed countries.

Neurological deaths were analysed as a whole, or divided into "nervous disease deaths" and "Alzheimer's and other dementia deaths". Nervous disease deaths included deaths from various conditions where there was inflammation or degeneration of the nervous system, including multiple sclerosis, motor neurone disease and Parkinson's disease.

What were the basic results?

The researchers found that total mortality for people aged between 55 and 74 years old fell substantially in every country over the 30-year period. On average, there was a fall of 45% from 25,620 deaths per million men in 1979-81, to 14,158 deaths per million men in 2008-10. For women, there was a decrease of 54% from 13,591 deaths per million in 1971-81 compared with 6,195 deaths per million in 2008-10.

In contrast, in people aged between 55 and 74 years old deaths from neurological causes rose by at least 10% in men in seven countries, and in women in eight countries. Total neurological deaths for both women and men rose significantly in Australia, Canada, Germany, Italy, Spain, the UK and the US.

Total neurological deaths increased significantly only in women in the Netherlands. On average, there were 275 deaths per million due to neurological causes in men in 1979-81. This rose to 332 deaths per million in 2008-10, an increase of 21%. In women, there were 101 deaths per million due to neurological causes on average in 1971-81, rising to 260 deaths per million in 2008-10, an increase of 29%.

When deaths from nervous diseases and Alzheimer's and other dementias were considered separately:

In men, deaths from nervous diseases rose from 144 deaths per million in 1979-81 to 203 deaths per million in 2008-10 on average across the 10 countries surveyed.
Seven countries had at least 10% increases in death rates from nervous diseases in men. Rates fell by at least 10% in the other three countries.
In women, deaths from nervous diseases rose from 104 deaths per million to 137 deaths per million on average. Six countries had at least 10% increases in the rate of death from nervous diseases in women. Rates fell by at least 10% in two other countries.
In men, deaths from Alzheimer's and other dementias rose slightly from 128 deaths per million in 1979-81 to 130 deaths per million in 2008-10 on average. Death rates from Alzheimer's and other dementias rose by at least 10% in men in five countries, and fell by at least 10% in three countries.
In women, deaths from Alzheimer's and other dementias rose from 86 deaths per million to 123 deaths per million on average.
Death rates from Alzheimer's and other dementias rose by at least 10% in women in seven countries, and fell by at least 10% in two countries.

How did the researchers interpret the results?

The researchers conclude that in contrast to major reductions in general mortality, mortality due to neurological deaths has increased in the majority of the countries analysed. They state that, "These results pose a major public health problem".

The researchers go on to discuss potential explanations for the increase in neurological deaths seen, including:

the fact that people are living longer, making it more likely that they will develop and possibly die from some of the diseases considered to be diseases of older people
improved diagnostic techniques, allowing more diagnoses of neurological diseases to be made
lifestyle or environmental factors, which may increase the risk of developing some of these diseases

Conclusion

This research has found that the death rate in people aged between 55 and 74 years old has fallen over the past 30 years in 10 developed countries (Australia, Canada, France, Germany, Italy, Japan, Netherlands, Spain, the UK and the USA). However, during this period deaths from neurological disorders such as Alzheimer's and other dementias (such as vascular dementia), Parkinson's disease and multiple sclerosis have increased on average.

The reasons for this increase in neurological deaths can only be speculated about. The researchers suggest that the fact that people are living longer, improvements in diagnostic techniques, and changes in lifestyle and the environment could contribute to the increase.

However, although this type of study can tell us how death rates and deaths from neurological causes are varying over time, it cannot tell us why these rates might be varying. More research is required to see whether factors such as "technology, food additives and air pollution" really are responsible for the increase in death rates due to neurological disorders.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Technology, food additives and air pollution are causing people to develop dementia earlier than ever, says leading scientist. Mail Online, May 13 2013

Links To Science

Pritchard C, Mayers A, Baldwin D. Changing patterns of neurological mortality in the 10 major developed countries – 1979-2010. Public Health. Published online April 19 2013

Angelina Jolie’s breast surgery announcement

Tue, 14 May 2013 13:33:00 EST

Writing in the New York Times, actress Angelina Jolie has announced that she has recently undergone a double mastectomy (where both breasts are surgically removed) followed by breast reconstruction surgery.

She writes that this is because genetic testing revealed she had a 87% chance of developing breast cancer in later life, as well as a 50% risk of ovarian cancer. This means she took a decision to have ‘preventative surgery’.

Jolie explained: "I decided to be proactive and to minimise the risk as much I could. I made a decision to have a preventive double mastectomy.

"Cancer is still a word that strikes fear into people’s hearts, producing a deep sense of powerlessness. But today it is possible to find out through a blood test whether you are highly susceptible to breast and ovarian cancer, and then take action."

What genes contribute to breast cancer risk?

A number of genes, associated with breast cancer, have been identified. These include BRCA1, BRCA2, TP53 or PTEN. Every women has these genes, but if a fault (mutation) develops in one of the genes then it can increase the risk of a women developing breast cancer.

It is estimated that around 1 in 500 women have a high-risk mutation in one of the genes associated with breast cancer.

What is the risk if you have a faulty breast cancer gene?

If you have a faulty gene, it doesn't mean you'll definitely develop breast cancer, but you are at a higher risk.

Having a fault in one of the breast cancer genes raises the risk of developing breast cancer to between 50% and 85%. In other words, out of every 100 women with a faulty gene, between 50 and 85 of them will develop breast cancer in their lifetime.

Are all women routinely tested for faulty genes?

No. Testing, provided by the NHS, is usually only offered to women thought to be at high risk of having a faulty gene. These include:

women with a strong family history of breast cancer where a living family member with breast or ovarian cancer is available for testing
women with a family history of several relatives developing early-onset breast cancer (cancer that develops before the age of 50), as this is often associated with having a faulty gene

Gene testing is also available from private clinics. The tests can be expensive, with prices ranging from around £2,000 to £3,000. The Pink Lotus Breast Center, where Angelina Jolie had her treatment, states that it screens for BRCA gene mutations in women without cancer who:

have two or more family members with breast cancer, one under the age of 50
have a previously identified BRCA mutation in the family at any age
are of Ashkenazi Jewish descent with a family history of breast or ovarian cancer

Will I need a mastectomy if I am found to have a faulty gene?

No. There are a range of treatment options available to you.

Firstly, there is the option of what is known as active monitoring. This is where you receive annual screening in the form of mammograms or MRI scans (or sometimes both) to monitor the state of your breast tissue.

Changes in your lifestyle can also reduce your individual breast cancer risk. These include eating a healthy diet, taking plenty of exercise and maintaining a healthy diet.

There is also the option of waiting to see if breast cancer develops, and if it does it can be treated using conventional methods as with other breast cancers. Breast cancer cure rates are good and continue to improve. The chance of making a full recovery, especially if the cancer is detected early, are relatively high.

Ultimately, there is no right or wrong answer about what you should do. Your care team can provide advice that will allow you to make an informed decision about your treatment. But the decision is only one you can make.

What happens if I decide to have a preventative mastectomy?

As much breast tissue as possible is removed through a single cut horizontally or diagonally across the chest under general anaesthetic. It’s a physically and emotionally draining operation. Expect some pain and fatigue afterwards and to spend one or two nights in hospital. It generally takes three to six weeks to recover fully.

What is breast reconstruction?

Basically, new breasts are formed from skin and muscle from your back, stomach or buttocks, or by using implants. It’s often possible to have reconstruction straight away – in the same operation as the mastectomy – though you can have it done later. Angelina Jolie had her breasts reconstructed with implants nine weeks after her double mastectomy. If your nipples have to be removed during the mastectomy, then they can be reconstructed with skin from another part of your body, and the areola created by tattooing.

Will the new breasts look and feel the same as before?

Reconstructed breasts won’t feel the same to you as your real ones did – the nerves have been cut, so they’ll always be numb, and there will be noticeable scars, but women generally report being happy with the cosmetic outcome.

Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

My Medical Choice. New York Times, May 14 2013

Could a good mood make you eat more food?

Tue, 14 May 2013 13:33:00 EST

‘Research has found emotional eaters tend to eat more when happy’, reports the Mail Online website.

The news is based on a small study looking at whether experimentally altering mood has an effect on the amount of calories a person eats.

The researchers examined the effects on what they describe as ‘emotional eaters’ – people who reported using food as a coping mechanism for emotions.

A group of 86 students, who said they were either emotional or non-emotional eaters, were shown TV and movie clips to evoke either a positive, negative or neutral mood. The researchers then assessed how much the students ate when provided with bowls of crisps and chocolate, as well as assessing their change in mood.

Emotional eaters who were shown the positive mood-inducing scenes significantly increased their food intake compared to emotional eaters shown the neutral mood-inducing scenes. However, the negative mood-inducing scenes had no effect on food intake of emotional or non-emotional students.

The common assumption is that emotional eaters eat more when in a negative mood, but this study provides very limited evidence to suggest that this may not always be the case.

However, because this experiment was based in a laboratory and researchers did not measure how hungry people were, even this finding should be viewed with caution. As ever, more and better research is needed if people with eating disorders or weight problems are to be helped effectively.

Where did the story come from?

The study was carried out by researchers from Maastricht University in The Netherlands and was funded by the Netherlands Organisation for Scientific Research. It was published in the peer-reviewed journal, Appetite.

The story was picked up by the Mail Online website and it was covered appropriately, although the limitations of the study could have been described in more detail.

What kind of research was this?

This was a laboratory study looking at the effect of experimentally influencing mood changes in a group of students reported to be emotional or non-emotional eaters, and then looking at the effect on their food and calorie intake.

The researchers say emotional eaters are thought to increase their food intake in response to negative emotions, but little is known about the effect of positive emotions on their food intake. Meanwhile, non-emotional eaters are not believed to change their intake levels in response to emotions, and they might even restrict food intake in response.

The main limitation of this research is that a study of a small, select population sample under experimental conditions can only provide very limited indications about the possible influence emotions may have upon the eating patterns of different people in daily life.

For example, if you thought that researchers could be measuring how much you were eating it could make you, perhaps unconsciously, reluctant to eat as much as you normally would. Alternatively, being in this type of study could make you nervous, leading you to eat more than you normally would.

What did the research involve?

The researchers recruited 86 psychology students in their second year at Maastricht University in the Netherlands who received credit points for their participation. The students were predominantly female (75%) and had an average age of 21.6 years (range 19 to 43).

The students answered a series of questionnaires to assess their mental health and eating behaviours. Emotional eating was assessed using a questionnaire called the Dutch Eating Behaviour Questionnaire (DEBQ). Students were asked, ‘Do you have a desire to eat when you’re feeling lonely?’ and provided answers on a five-point Likert scale that ranged from ‘never’ to ‘very often’.

The researchers then carried out a series of experiments in a laboratory setting that aimed to change the student’s mood. Students were randomly allocated to view clips from television or films that aimed to evoke either a positive, negative or neutral mood:

28 students were shown two clips to evoke a positive mood. Firstly, they were shown a scene from the television series Mr Bean (which showed Mr Bean struggling to copy answers from his neighbour during an exam). The second clip was taken from the movie ‘When Harry Met Sally’ which showed the famous scene where Meg Ryan’s character simulates an orgasm in front of other diners in a restaurant.
28 students were shown one negative clip from the film ‘The Green Mile’, which showed an innocent man being executed.
30 students were shown part of a documentary about fishing to evoke a neutral mood.

The students were told to give in to the emotions the clips evoked, and were presented with bowls containing 191g of chocolate (white, milk and dark, equivalent to 1,000 kcal), 225g of salted crisps (1,229 kcal) and 225g of ketchup crisps (1,217 kcal). The bowls were weighed before and after the experiment to determine the amount of food eaten and calorie intake.

The students were asked to assess their mood using a visual analogue scale (this is essentially a straight line – where the far left of the line represents poor mood and the far right represents very good mood) at five points during the experiment:

before the experiment began
immediately after watching the television or movie scenes
5 minutes after the experiment
10 minutes after the experiment
15 minutes after the experiment

The students were told when entering the laboratory that they were taking part in an experiment on the effect of movie clips on taste perception.

The researchers analysed their results using validated methods and adjusted the results for gender, body mass index (BMI), external eating and dietary restraint as assessed by the DEBQ, and negative mood as assessed by the Positive and Negative Affect Schedule (PANAS).

What were the basic results?

Overall, there was no significant difference between emotional eaters eating more than non-emotional eaters who were shown positive, negative or neutral clips.

When looking specifically at only the emotional eaters:

those shown the positive mood-inducing scenes significantly increased their intake of food compared to those shown the neutral mood-inducing scenes
there was no difference in food intake between students shown negative mood-inducing scenes and those shown neutral or positive mood-inducing scenes

How did the researchers interpret the results?

The researchers concluded that self-reported emotional eaters respond in a different way to emotions than non-emotional eaters. They say that emotional eaters ate more in a positive mood compared to a neutral mood, whereas non-emotional eaters ate about the same amount in both conditions.

In discussing the results, the researchers say the findings could be of value for the treatment of obesity.

Conclusion

Overall, this small study provides very limited evidence to suggest emotional eaters eat more when feeling in a positive mood. There are several limitations to this study, some of which are noted by the researchers. These include the facts that:

the laboratory setting may not be an appropriate setting to test emotional eating with different mood feelings. It is possible that students felt uncomfortable in this setting and limited their food intake as they were being watched
the students were told they were partaking in an experiment of taste perceptions, so may have been inclined to eat more than they normally would have because of what they were told the study was looking at
no hunger measurements were taken during the study and how hungry each student was could have greatly affected the results
there was no group included in the study that did not eat, so it is not possible to say from the findings that the changes in mood were due to food intake
all of the participants were students, so findings may not be the same as if the same experiments were carried out in different groups who report being emotional eaters

To draw firmer conclusions about the effects of mood on emotional eating, larger studies of different groups are required that carry out experiments in more natural environments.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Forget comfort eating - could happiness be the reason you're piling on the pounds? Mail Online, May 13 2013

Links To Science

Bongers P, Jansen A, Havvermans R, et al. Happy eating: The underestimated role of overeating in a positive mood. Appetite. Published online April 10 2013

No proof that red hair raises skin cancer risk

Mon, 13 May 2013 13:33:00 EST

'Redheads are at increased risk of skin cancer even if they don't spend time in the sun,' is the headline on the Mail Online website.

The story refers to a discussion piece in a journal that outlines theories about the results of some animal experiments. This research involved mice genetically engineered to have red fur and predisposed to develop melanoma.

Although exposure to ultraviolet (UV) light is known to be a major risk factor for melanomas, the researchers found that genetically engineered mice with red fur still had a high risk of developing melanomas even without UV exposure.

The article discusses potential explanations for why this could be the case, and these theories now need to be tested to see if they are correct.

It is not yet clear how well these animal studies represent what happens in people with red hair. It would be very difficult to test this directly, as keeping people completely away from sunlight would be impractical and potentially unethical.

UV light exposure is known to increase the risk of melanoma in redheads and non-redheads alike. It is important that people with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn, despite this news.

Where did the story come from?

The article was written by researchers from the Cutaneous Biology Research Center at Massachusetts General Hospital in the US.

No sources of funding for the article were reported. It was published as an "Ideas and Speculations" article in the journal BioEssays. These pieces are described as "creative thinking and predictions on open questions and recent developments in biology".

It is not clear whether the article is peer-reviewed.

The news is based on an article by researchers that presents possible explanations for their previous finding that genetically engineered mice with red fur and a predisposition to melanoma develop this cancer even without UV exposure.

Some of the Mail Online reporting suggests that the findings of this research are more conclusive than is possible to say at this stage: "Scientists have discovered that the production of red hair pigment causes an increased risk of melanoma".

However, the BioEssays article was only presenting possible explanations for observations from animal experiments. It was not claiming to have definitive proof that these findings apply to humans.

What kind of article was this?

This was an article discussing the potential link between the red pigment in red hair and skin cancer.

People with red hair and fair skin are known to be at greater risk of getting melanoma, the least common but most serious form of skin cancer, which is responsible for around two thousand deaths a year in the UK.

In general, it is thought that redheads' pale skin makes them more susceptible to UV damage from the sun's rays.

However, the authors of the article say that a recent study from their lab suggests that the pigment that causes hair to turn red (pheomelanin) could itself be linked to the increased risk of cancer, even without UV exposure.

In their article, the authors discuss two possible ways in which the red pigment in red hair might increase the risk of cancer. These preliminary ideas – or hypotheses – are based on previous research and a general understanding of human and cancer biology.

A hypothesis is a possible explanation of why something that researchers have observed might happen. Researchers design experiments to test whether their hypothesis is correct. This process is fundamental to the scientific method.

What did the article say?

The researchers first describe how the red colour in red hair is made, and discuss the results of their recent study before going on to present their hypotheses.

Specific cells in the skin called melanocytes make two kinds of pigment – a brown pigment called eumelanin and a red-orange pigment called pheomelanin. A biochemical process within cells determines how much of each pigment is made.

This process involves a protein called MC1R, which influences the switch between the production of these pigments based on the strength of the signal it sends to the cell and whether the cell has enough of the amino acid cysteine.

In redheads, variations in the gene for the MC1R protein means that it sends weak signals. This means that the cells' stores of cysteine are usually enough for it to favour producing the red/orange pigment pheomelanin.

The researchers recently carried out a study where they introduced a genetic mutation commonly found in melanoma cells into the melanocytes of mice. When they also introduced a genetic mutation into these mice that inactivated the MC1R protein, the mice had red fur and developed melanoma, even without UV exposure. If they introduced another genetic mutation that stopped pigment being made altogether, the mice were albino but they did not develop melanoma.

This led the researchers to suspect that the red pigment pheomelanin could be itself increasing the risk of melanoma. Their research also found that the mice with red fur had more damage to their skin cell DNA caused by very reactive chemicals called free radicals. Free radicals can cause damage to cells at a molecular level.

The researchers do not yet know how the red pigment might be linked with the free radical DNA damage that can increase the risk of melanoma. However, they have presented two hypotheses:

The first hypothesis

The researchers' first hypothesis was that the red pigment itself might generate more free radicals, and that these cause DNA damage that could lead to melanoma. They say that the red pigment is already known to make free radicals when it is exposed to UVA light, but it may be able to do this without UVA light. These free radicals could potentially:

damage DNA directly
damage its building blocks, or
use up the cell's stores of antioxidants, making it more vulnerable to damage by other free radicals

The researchers also discuss in detail the biochemical ways in which the red pigment might generate free radicals.

The second hypothesis

The second hypothesis was that the process of making the red pigment might use up the cell's stores of antioxidants, rather than the red pigment itself. This might make the cells more vulnerable to damage by other free radicals.

They say that the amino acid cysteine used in making the red pigment is also found in the most important antioxidant in the cell, glutathione. If cysteine is used to make the red pigment, this might reduce the cell's ability to make this antioxidant.

The researchers report that red-haired wild boars have been found to have less glutathione in their muscles. However, they acknowledge that it is not possible to say from this whether there is less glutathione due to free radicals from the red pigment itself or the making of the red pigment.

What were the researchers' conclusions?

The researchers presented two hypotheses that could explain how the red skin and hair pigment pheomelanin could increase the risk of the skin cancer melanoma.

They say that their two proposed methods could both be occurring, and that more research could help identify how redheads can reduce their risk of melanoma.

Conclusion

The researchers' article discusses potential ways in which the red pigment found in the cells of people with red hair might increase the risk of melanoma, the most serious form of skin cancer. It is not a standard report of a research study, but the authors put forward potential explanations for their previous research findings. These now need to be tested to see if they are correct.

The researchers' previous research found that mice genetically engineered to be predisposed to melanoma and red fur developed melanomas even without UV exposure. It is not clear to what extent these genetically engineered mice represent what happens in humans.

It would be very challenging to test this – keeping people completely away from UV light would not be feasible or ethical, as we need some sun exposure to make vitamin D, which is needed to make and maintain strong bones. For this reason, research in mice can be very helpful.

It is important that redheads do not take this news as a reason not to protect themselves from the effects of the sun. We already know that UV light exposure increases the risk of melanoma in people regardless of hair colour. People with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn.

Read more about reducing your melanoma risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Redheads are at increased risk of skin cancer even if they don't spend time in the sun. Mail Online, May 10 2013

Links To Science

Morgan AM, Lo J, Fisher DE. How does pheomelanin synthesis contribute to melanomagenesis? BioEssays. Published online May 7 2013

New coronavirus 'likely' to spread person to person

Mon, 13 May 2013 12:33:00 EST

‘WHO warns that a deadly novel coronavirus could be passed from person to person’, The Independent reports.

The news – featured in much of the media – is based on the latest ‘state of play’ advice from the World Health Organization (WHO) on the novel coronavirus (nCV).

nCV, which is genetically similar to the SARS virus, was first reported in the autumn of 2012 and appears to have originated in the Middle East.

Initial symptoms of nCV are similar to a severe case of the flu and include:

fever
cough
shortness of breath
breathing difficulties

Unlike flu, nCV is thought to have a high risk of causing serious, life-threatening, complications such as pneumonia and kidney failure.

What have the WHO said about nCV?

The WHO has confirmed that as of May 12 2013 there have been 34 confirmed cases – the majority of which occurred in Saudi Arabia.

The current thinking is that the virus mainly affects people who are already ill and have a weakened immune system.

How does nCV compare to SARS?

Despite nCV being similar to SARS (both come from the coronavirus ‘family’ of viruses) there are important differences between the two.

The bad news is that nCV appears to be much more deadly than SARS. Of the 34 people who have contracted it, 18 have died. Resulting in a death rate (or in medical terms, a case fatality rate) of around 52%.

The good news is that nCV seems to be far less contagious than SARS.

From the available evidence, it seems that nCV can only spread from person to person if prolonged close physical contact takes place. In other words, you may catch it if you share a home with an infected person, but not if you share a bus or an airplane.

While remaining vigilant to any potential threat, the WHO does not consider nCV to pose the same kind of potential threat as SARS or swine flu.

What is being done to counter the threat of nCV?

Global research efforts into nCV are being lead by the Kingdom of Saudi Arabia. It is currently in the process of establishing surveillance systems to track any further spread of infection.

Saudi health officials are also trying to establish the source of the virus and how it spreads.

Is there any treatment for nCV?

A recent study found that two anti-viral drugs, ribavirin and interferon-alpha 2b, can help slow the replication of the virus in human cells. This may potentially help reduce the risk of complications such as kidney failure.

However, there is currently no effective vaccine for nCV.

Is there any threat to people in the UK?

Based on the current evidence, the threat to people living in the UK is thought to be minimal.

One issue of concern is that visitors to Saudi Arabia during the Hajj in October could contract the infection.

This risk should be reduced if you take some common-sense precautions, such as:

washing your hands frequently
cover your mouth and nose when you sneeze or cough
avoid sharing food, drink and utensils
regularly clean surfaces with disinfectant

Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

New coronavirus can spread between humans, says WHO official. The Guardian, May 13 2013

WHO says new coronavirus may be passed person to person. BBC News. May 12 2013

WHO warns that deadly novel coronavirus could be passed from person to person. The Independent, May 13 2013

Coronavirus: Infection 'Spreads Between People'. Sky News, May 13 2013

Second French coronavirus case. ITV News, May 13 2013

Young blood may help rejuvenate old hearts

Sun, 12 May 2013 00:33:00 EST

The Daily Mail claims a study has found a ‘Vampire treatment that rejuvenates ageing hearts’.

But before you go to grab your cloak and false pointy teeth, the research it reports on was actually in mice.

The study looked at possible ways to treat age-related cardiac hypertrophy – when the muscles of the heart become thickened, leading to a corresponding decrease in functioning ability.

Researchers joined the blood circulation of pairs of young and old mice. And one month later they looked at the resulting effects on the animal’s heart muscle.

They found that old mice who shared blood with young mice had reduced levels of cardiac hypertrophy compared to similar mice not treated with ‘young blood’.

The researchers suggest that this could be due to a chemical called growth differentiation factor 11 (GDF-11), which is high in the blood of young mice, and could help repair tissue damage.

An obvious limitation of the study is that results in mice do not always apply to humans. In humans, heart failure is where the heart cannot pump enough blood to meet the body’s needs, and this can have many different causes.

Thickening of the heart muscle is just one type of heart failure, which can be caused by high blood pressure, but can also be an inherited condition.

It is difficult to know to what extent the same growth factor could be responsible for heart muscle thickening in people with this type of heart failure. Also, its relevance – if any – to other types of heart failure (for example due to muscle damage following heart attack, due to an abnormal heart rhythm, or due to heart valve disease) is even less clear.

The findings are of scientific interest but are not going to miraculously reverse the entire disease process of heart failure in humans.

Where did the story come from?

The study was carried out by researchers from the Harvard Stem Institute and other research institutes in the US, and was funded by the American Heart Association, Glenn Foundation and National Institute of Health.

The study was published in the peer-reviewed scientific journal: Cell.

The Mail over-interprets the findings from this animal research. It is also unclear where the sub-headline ‘could be ready for use in clinical trials within 4 years’ has come from.

What kind of research was this?

The researchers say that loss of normal heart function leading to heart failure is one of the most debilitating diseases of ageing.

In particular, they discuss the type of heart failure that is often caused by high blood pressure, where the heart muscle becomes thickened and stiff (cardiac hypertrophy) so the heart chambers cannot dilate so well and fill with blood. This is known as ‘diastolic’ heart failure, as it relates to a problem when the heart is trying to refill with blood (diastolic), rather than contract (systolic).

The researchers suggest that animal studies have previously shown that chemicals circulating in the body of a young animal have been shown to restore function to the skeletal muscle of an old animal.

This process was done by what is called ‘parabiosis’ where two animals are surgically joined and so share their blood circulation.

The current animal study aimed to use a parabiosis model to try and reverse the thickening of heart muscle.

What did the research involve?

For their experiments the researchers used old mice (aged about two years) and young mice (aged two months). They used parabiosis to surgically join the blood circulation of pairs of old and young mice.

After they had been joined for one month, the researchers analysed samples from the heart muscle of the mouse pairs.

For comparison they also looked at the effect of shared blood circulation between young-young and old-old mice pairs.

They also compared with a ‘sham’ parabiosis where they surgically joined the tissue of pairs of young and old mice (at the knee joint), but without sharing their circulation.

To look into what could be the cause of any observed effects upon heart muscle, they also intensively monitored the blood pressure of mice while they were joined, and looking at levels of different chemicals in the blood of young and old mice.

What were the basic results?

The researchers found that the effect of surgically combining the circulation of the young and old mice pairs was clearly visible. The hearts of old mice that had their circulation joined to a young mouse looked much smaller and were less heavy than those of old mice who had been joined to old mice.

When they looked at the heart muscle cells under the microscope they found that the cells of old mice joined to young mice had a significantly smaller cross-sectional area than those of old mice joined to old mice, or those in the ‘sham’ parabiosis condition where their circulation hadn’t been joined to the young mice.

The effect of parabiosis on heart muscle cells was similar in both male and female old mice.

Meanwhile, the heart muscle cells of the young mice were no different in any of their three combinations (young-young, young-old or sham parabiosis).

They also carried out a number of experiments into what could be having the observed effects.

They ruled out that the smaller heart muscle cells of the old mice could have been caused by a reduction in their blood pressure. This was because all of the joined mice actually showed increases in their blood pressure compared to before they were joined.

They also considered the possibility that the changes could be due to behavioural change from the physical constraint of being joined to another mouse, rather than any effect of the shared blood.

However, if this was the case then it would be expected the heart muscles of old mice in the sham parabiosis would also have decreased in size, and they had not.

Overall, the researchers considered the effects could be due to some chemical in the shared circulation. Separately analysing the blood from young and old mice they found that several components of their blood are different. In particular, levels of a molecule called growth differentiation factor 11 (GDF-11) are found to be lower in the blood of older mice.

When they went on to treat the heart muscle cells from rats with GDF-11 in the laboratory, they found that GDF-11 prevents the thickening of the heart cells. In a further experiment involving older female mice, the hearts of a group injected with GDF-11 were significantly lighter and the cells were significantly smaller than those of a group injected with a placebo.

How did the researchers interpret the results?

The researchers’ animal experiments suggest that the thickening of heart muscle can be influenced at least in part by certain chemicals circulating in the blood. They suggest that GDF-11 could reverse thickening of heart muscle, and so conclude that ‘at least one component of age-related diastolic heart failure is hormonal in nature and reversible’.

Conclusion

This study finds that sharing the circulation of young and old mice appears to reverse the age-related thickening of heart muscle cells in the older animal, and it seems this could be due to a certain growth factor in the blood of the young animal. The findings will be of scientific interest, and further our understanding of the processes of heart ageing in animals.

However, the findings have very limited direct relevance to humans, and do not suggest a new treatment for heart failure.

It is also certainly unknown at this point whether increasing levels of this factor in the blood of people with this type of heart failure would somehow reverse the entire disease process. Its relevance to other types of heart failure not associated with thickened heart muscle is even less clear.

Even if further research were to demonstrate that this growth factor could have a potential role in heart failure treatments in humans; joining the circulation of young people with those with heart failure in the manner used in this study is clearly not a possibility.

If the chemical were to be extracted from donor blood, or synthetically produced, there would still be many safety issues to considered, even if the treatment were found to have an effect.

Overall the research does not suggest a new treatment for heart failure in humans, though it may represent the first step towards a possible treatment at some point at the future.

However, due to the uncertainties discussed above it is impossible to estimate the likelihood of this prediction becoming fact.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

The vampire treatment that 'rejuvenates' ageing hearts: Dose of young blood can reverse life-threatening thickening of organ. Daily Mail, May 10 2013

Links To Science

Loffredo FS, Steinhauser ML, Jay SM, et al. Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell. Published online May 9 2013

Pollution may increase diabetes risk

Sun, 12 May 2013 00:33:00 EST

‘Children's exposure to traffic pollution could…lead to diabetes' BBC News explains, reporting on a German study.

The study included around 400 children aged 10. Researchers looked at measures of air pollution and proximity to the nearest road at the address each child had lived as a baby.

They also measured each child’s blood sugar and insulin levels.

The second measurement allowed them to calculate each child’s level of insulin resistance – to what extent the cells of the body fail to respond to the hormone insulin (which the body uses to convert blood sugar into energy).

Once insulin resistance reaches a certain level, the symptoms of type 2 diabetes can develop.

The researchers found an association between exposure to air pollution and increased levels of insulin resistance.

However, an association is not the same as proof of a direct causal effect. Living near a busy road would usually imply that a child lives in an urban environment. So there could be a range of environmental factors, other than air pollution, affecting levels of insulin resistance (as well as a wide-range of other possible individual genetic and health-related factors).

The study also does not tell us whether any insulin resistance measured in the child actually had any clinical significance and would lead to a child developing diabetes in later life.

Due to these limitations, further studies in other population samples would be useful.

Where did the story come from?

The study was carried out by researchers from German Center for Diabetes Research and other institutions in Germany, and was funded by German Federal Ministry of Education and Research, and The European Community’s Seventh Framework Programme.

The study was published in the peer-reviewed medical journal Diabetologia.

The quality of the reporting on the study in the UK media is mixed. The BBC News headline gives an accurate representation of the current study as it includes the all-important word ‘may’. However, the Mail Online’s headline linking air pollution to a child’s risk of developing diabetes may be misleading.

This study has many limitations, not least, that increased levels of insulin resistance in childhood, while a risk factor, is not a guarantee that a child will grow up to develop type 2 diabetes.

Also, the association between childhood and diabetes may confuse some readers into thinking that the study was looking at type 1 diabetes – the form of the condition that normally begins in childhood and where the body’s own immune system destroys the insulin-producing cells, so the person is not able to produce any insulin at all.

What kind of research was this?

This was a cohort study looking at whether there was an association between air pollution and insulin resistance.

The researchers say that previous research has shown that traffic and air pollution may increase the risk of diseases affecting the lungs and cardiovascular system.

This is speculated to be due to exposure to pollution that may trigger oxidative stress (a disruption in the body’s ability to repair cellular damage). Pollution could also lead to low levels of inflammation in certain cells of the immune system and those lining the blood vessels.

Animal studies have also suggested that pollution may make cells of the body more resistant to the action of insulin – the hormone released from the pancreas that helps the body to make use of the glucose in the blood.

The researchers say that no study has yet looked at whether traffic-related air pollution can lead to insulin resistance in school-aged children. This German cohort study aimed to look at the relationship between particulate matter in the air and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they reached the age of 10.

The limitations of such a study include it being difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10.

There may be many other genetic, environmental and health-related factors involved.

The study also does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it is related to later development of type 2 diabetes in adult life.

What did the research involve?

The researchers included sub-groups of 10-year-old children taking part in two separate birth cohorts in Munich, South Germany and Wesel, West Germany:

The German Infant Study enrolled almost 6,000 healthy newborns and was a trial looking at the effect of a hypoallergenic infant formulae on a child’s risk of allergy (in addition to looking at other environmental and genetic influences).
The Lifestyle-Related Factors study included just over 3,000 healthy newborns and was an observational study looking at the effect of lifestyle factors on the child’s immune system and risk of allergies.

The present study included 397 children randomly sampled from these two cohorts (though 82% came from the Munich cohort) who had blood samples taken for insulin and glucose measurement at age 10, and who had information available for air pollution exposure at the time they were born.

To measure pollution exposure at the birth address, the researchers used models to estimate levels of:

nitrogen dioxide (N02)
particulate matter of less than 2.5 micrometres in diameter
particulate matter of less than 10 micrometres in diameter

Particulate matter is the term for a mixture of solid particles and liquid droplets found in the air.

Measurements were taken at selected monitoring sites on three occasions over 14 consecutive days, and in different seasons.

When conducting their analyses, factors taken into account at each monitoring site were location, surrounding land use, population density and traffic patterns.

Other factors taken into account that could have an influence on the results (confounders) related to the individual child included:

parental education (used as an indicator of socioeconomic status)
exposure to second-hand smoke
height and weight at age 10
whether they had started to go through puberty

What were the basic results?

There were no differences between children in the two cohorts, except that those from Wesel were more likely to have been exposed to second-hand smoke and to be of lower socioeconomic status. Pollutant levels were also higher in Wesel than Munich.

After adjustment for all potential study-centre and child-related confounding factors, each two-point standard deviation increase in nitrogen dioxide levels was associated with a 15.8% increase in insulin resistance (95% confidence interval (CI) 3.8 to 29.1).

Each two-point standard deviation increase in particulate matter of less than 10 micrometres in diameter, was associated with a 17.5% increase in insulin resistance (95% CI 1.9 to 35.6). There was no significant association with particulate matter of less than 2.5 micrometres in diameter.

Distance to the nearest road, as would be expected, was significantly associated with pollutant levels (shorter distance equalled higher levels of nitrogen dioxide and particulate matter). Shorter distance to the road was also associated with increased insulin resistance (each 500 metre decrease in distance to road increased insulin resistance by 6.7%, 95% CI 0.3 to 13.5).

The researchers found that the link between pollution levels and insulin resistance was stronger in children who had not moved from their birth address by age 10.

How did the researchers interpret the results?

The researchers conclude that traffic-related air pollution may increase the risk of insulin resistance in children. They say that the associations observed may have important public health implications despite the small effect seen.

Conclusion

This German study looked at the relationship between air pollution and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they were aged 10. Though links were found between increasing levels of nitrogen dioxide and levels of particles less than 10 micrometres in diameter and increasing insulin levels at age 10, there are important limitations to bear in mind:

Though the researchers have attempted to adjust for many potential confounders, it is difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10, when there may be many other genetic, environmental and health-related factors involved.
The confidence intervals around the increase in insulin resistance with each incremental increase in pollutant levels are very wide. For example, each increase in particles of less than 10 micrometres was associated with a 17.5% increase in insulin resistance, but the actual increase could lie anywhere between 1.9% and 35.6%. This means we can have less confidence in the reliability of these estimates.
The study does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it will be related to higher risk of developing type 2 diabetes in adult life.
Also, as mentioned above, the news headlines should not be wrongly interpreted to mean that a child has increased risk of developing type 1 diabetes – the type that readers may associate with start in childhood.
Lastly, the results are based on only a relatively small sample of children from two regions in Germany. Studies of much larger samples from different countries would give more weight to any observations.

Overall, this study cannot prove that air pollution increases a child’s risk of developing diabetes, only that there may be an association with insulin resistance.

As it is unlikely that we are going to live in a world free from air pollution anytime soon, the most effective way of reducing your child’s diabetes risk is to encourage them to take plenty of exercise and eat a healthy diet. These types of good habits in childhood often carry on into adulthood meaning that your child is more likely to maintain a healthy weight – a proven method of reducing type 2 diabetes risk.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Diabetes: dirty air 'may raise' insulin resistance risk. BBC News, May 10 2013

Why living near a busy road could be dangerous for your child's health: Traffic pollution linked to diabetes risk in children. Mail Online, May 10 2013

Air pollution could raise diabetes risk. The Daily Telegraph, May 10 2013

Links To Science

Thiering E, Cyrys J, Kratzsch J, et al. Long-term exposure to traffic-related air pollution and insulin resistance in children: results from the GINIplus and LISAplus birth cohorts (PDF, 278KB). Published online May 9 2013

US guidelines recommend CT scans for smokers

Sun, 12 May 2013 00:33:00 EST

Older people with a history of smoking heavily should be offered annual low-dose CT scans to screen for lung cancer according to new US guidelines reported by the Reuters news agency.

These guidelines recommend that annual CT (computerised tomography) scans should be offered to current or former smokers aged 55-74 who have smoked 20 cigarettes a day for 30 years or more. However, screening should only be offered in facilities that can provide high standards of clinical care, the guidelines say.

Screening means testing everyone in a particular population for early stages of a disease before they have any symptoms. In the UK, screening is already in place for some cancers, such as bowel and breast cancer, but lung cancer is not currently screened for.

Mass-population screening, such as that carried out for bowel and breast cancer, is unfeasible for lung cancer because of the cost. One study has estimated that to save one lung cancer death would cost around $250,000. However, focusing resources on high-risk groups, as recommended in the US guidelines, is a more cost-efficient approach.

Heavy smokers are particularly at risk of developing lung cancer because cigarettes contain a number of cancer-causing substances (carcinogens).

Screening could be of particular use in heavy smokers because the symptoms of lung cancer often do not develop until the cancer is at an advanced stage. This makes treatment of the condition challenging.

The US guidelines point to research that suggests that these recommendations could cut rates of lung cancer deaths in smokers or ex-smokers by around 20%.

Who produced the guidelines?

The guidelines on screening have been produced by the American College of Chest Physicians.

They form part of comprehensive guidance for US doctors on the diagnosis and management of lung cancer.

What are the pros and cons of CT screening for lung cancer?

An obvious pro of CT screening for lung cancer is that it could cut lung cancer deaths. Lung cancer is one of the leading preventable causes of death in the UK and around the world.

However, no screening technique is without risk.

One risk, often overlooked, is the danger of false positives. This is where the screening test detects a sign that turns out to be harmless. In cases of lung cancer this would usually be when a lesion (abnormality in tissue) is detected, but the lesion turns out to be non-cancerous (benign).

In the general population, the rates of false positives for screening could be unacceptably high. For example, the authors say that more than 90% of nodules found by CT in the studies they looked at turned out to be benign.

This figure drops dramatically for high-risk groups, such as smokers, but one study quoted in the guidelines estimated that the false positive rate in high-risk groups could still be around one in four.

While CT scans themselves have a very low risk of causing complications, other more invasive procedures used to confirm or discount a diagnosis of lung cancer do not.

Screening could subject people to unnecessary tests that turn out to cause them harm, and there is still the possibility of false negatives. No matter how good a test is, it is likely that some cancers will be missed, leading to false reassurance.

There is also risk from radiation exposure. Although one low-dose CT scan involves only a small amount of radiation, if further imaging is required it can rapidly drive up the radiation dose patients receive.

What evidence did the guidelines look at?

The guidelines looked at evidence on the effectiveness of different methods of screening for lung cancer. These were:

chest X-ray
examining mucus from the airways for abnormal cells (sputum cytology)
low-dose CT screening

The guidelines’ authors conducted a systematic review of randomised controlled trials (RCTs) and observational studies looking at the effectiveness of the different methods of screening. Most of the studies focused on middle-aged or older people with a history of smoking and, therefore, at high risk of lung cancer. In particular, they examined the death rates from lung cancer among people at high risk who were screened by low-dose CT, X-ray or sputum analysis.

The review also looked at the potential downsides of screening, including:

the death rates, or complications resulting from further investigations of any suspected cancers, in people who had been screened
the death rates from radiation exposure of people who had low-dose CT screening
the rate of surgery for benign disease

What were the results?

The main finding came from one large RCT (the National Lung Screening Trial), involving more than 53,000 participants who had three annual rounds of screening. This trial showed a 20% reduction in the rate of death from lung cancer in people who were screened with low-dose CT, compared with those screened using a chest X-ray (relative risk 0.80, 95% confidence interval 0.73 to 0.93).

This trial also found that low-dose CT posed “few harms” when carried out in the context of a structured programme of care. The risk of death or major complications from further investigations into harmless conditions was between 4.1 and 4.5 per 10,000.

Other research found that using chest X-rays or sputum analysis did not reduce lung cancer deaths.

What recommendations on screening did the guidelines make?

The guidelines recommend that:

Smokers and former smokers aged 55-74 who have smoked for 30 pack-years or more and who either continue to smoke or have quit within the past 15 years should be offered annual screening with low-dose CT.
This should only be done in settings that can deliver the same standard of care provided to participants in the big lung cancer screening trial.
CT screening should not be offered to people who do not meet the above criteria, say the guidelines. For example, if they are younger or older or have smoked less, since benefits outside the high-risk group are uncertain.
Screening for lung cancer using X-rays or sputum analysis is not recommended.

Links To The Headlines

Older, heavy smokers should get CT scan for lung cancer, doctors group advises. Reuters, May 2013

Links To Science

Detterbeck FC, Mazzone PJ, Naidich DP, et al. Screening for Lung Cancer: Diagnosis and Management of Lung Cancer, 3rd ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. Published online May 2013

Are the middle classes in denial about alcohol use?

Sun, 12 May 2013 00:33:00 EST

"Middle class professionals… are the country’s biggest problem drinkers," is the stark and somewhat misleading claim in The Daily Telegraph, with similar claims appearing across the UK media.

The story is based on a study looking at just 49 ‘white collar’ people’s attitudes towards alcohol consumption. The study involved interviewing five small groups in a ‘focus group’ setting.

Researchers found that among these small groups:

problem drinking was something that was seen to happen to other people – such as teenagers in city centres or binge drinkers in pubs
if regular alcohol consumption did not significantly disrupt day-to-day functioning (such as in work or parenting skills) or lower social standards, then it was acceptable and harm-free
regular ‘controlled’ drinking at home (for example as a way to relax), was also acceptable and harm-free

It is important to note the study was very small and these findings may not be applicable to other countries or cultures. However, the attitudes reported suggest that key messages of some public health campaigns about reducing harm from alcohol are going unheard or being ignored.

It is not just binge drinking that can damage your body; regularly drinking above the recommended limits – whatever the social context – can also be harmful.

Where did the story come from?

The study was carried out by researchers from Newcastle University and the University of Sunderland, UK and was funded by the Public Health NHS Directorate Stockton-on-Tees.

It was published in the peer-reviewed journal, BMC Public Health and made freely available to read on an open-access basis.

The story was picked up widely in the media. While the findings of the study were reported accurately, the tone of some of the reporting was slightly confusing.

It appears that some of the media fail to understand the nature and implication of this method of qualitative research. Such studies can provide useful insights into people’s attitudes and behaviours; however, they cannot provide hard statistical evidence. So headlines such as the Daily Express’s “Middle class ‘drink more than teens’” are misleading, as are sweeping statements like the Telegraph’s “Middle class professionals who drink at home are the country’s biggest problem drinkers”.

What kind of research was this?

This was a qualitative study looking at the drinking habits of a small number of adult ‘white collar workers’ in the UK. The study explored their views on alcohol use, how public health messages about alcohol are perceived, and the role alcohol plays in the workers' personal and professional lives.

The researchers say that little is known about white collar workers’ views on drinking alcohol.

Qualitative research uses individual in-depth interviews, focus groups or questionnaires to collect, analyse and interpret data on people’s behaviours and the reasons behind them. Typically, the number of participants is relatively small, but the transcripts from interviews and focus groups provide a large amount of data. Such studies report on meanings, concepts, definitions, metaphors, characteristics, symbols, and descriptions. As such, their conclusions can be more subjective than quantitative research, as questions are often exploratory and open-ended.

What did the research involve?

The researchers carried out interviews with 49 volunteers (17 male, 32 female) from five workplaces in the UK. The participants were aged between 21 and 55 years and were all working full time (at least 35 hours per week). To be included, participants had to be working in managerial, supervisory, clerical or other professional roles, referred to by the researchers as ‘white collar workers’.

Group interviews (focus groups) were carried out by the researchers at each of the five workplaces during lunch breaks. The five focus groups were made up of workers from:

local government offices (focus groups one and two)
a private sector chemical storage company (focus group three)
a prison (focus group four)
a tax office (focus group five)

The group interviews lasted between 45 and 75 minutes and were led by two researchers. The researchers used open-ended questions loosely based around four main themes related to drinking alcohol:

lifestyle behaviours
drinking at home
variations in drinking during the week
the effect of drinking on work

The researchers say areas of agreement and disagreement were explored with the participants, and that questions were continually adapted depending on the flow of conversation. The participants were informed that the purpose of the research was not to find out the quantity or frequency of alcohol consumption of the volunteers. The volunteers were given a £5 voucher and lunch for their time.

The researchers then used a particular technique called ‘constant comparison’ to analyse their results and grouped findings into themes relating to views of alcohol.

What were the basic results?

After analysing the focus group findings, the researchers reported three main themes.

Unacceptable or problem drinking

Unacceptable or problem drinking was perceived by the volunteers as being associated with long-term, heavy or binge drinking of ‘others’. The researchers reported that the participants highlighted ‘others’ as including young people, people with complex needs, and other stereotypes. The perception of excessive drinking was associated with looks and behaviour, rather than how much they have drunk. Personal drinking was viewed as a controlled choice rather than something they ‘need to do’.

Drinking at home

Drinking at home was considered normal, convenient and a socially acceptable form of relaxation from the responsibilities of work or parenting. Volunteers reported less drinking at ‘leisure premises’ such as a bar or pub, and driving was identified as the greatest factor influencing drinking behaviours. Drinking alcohol was considered part of everyday life and not something that interferes with other parts of life or causes harm.

Effect of drinking on functioning

Ability to function at work and act responsibly were key indicators of whether drinking was within acceptable limits. So, if a person was able to maintain employment in skilled jobs, they were therefore perceived to be drinking in a way that was not considered harmful. Despite awareness of guidelines for drinking, little notice was taken by participants and there was confusion about what a ‘unit’ was, the researchers report. Public health messages were also considered to have little or no personal relevance.

The researchers say that discussions indicated that the volunteers' reported alcohol use exceeded recommended guidelines for both the amount and how often drinking occurred. Interestingly, when the ill effects of alcohol were discussed, they were reported as only in relation to coping with a hangover and the loss of valuable time while feeling unwell. More subtle, insidious adverse effects such as gradual loss of liver function did not appear to occur to the volunteers.

Finally, lunchtime drinking at work was considered a 'thing of the past' and very much taboo.

How did the researchers interpret the results?

The researchers say that this study helps reveal the meanings attached to alcohol use by white collar workers and identifies resistance to public health messages. They say, "these findings suggest that current public health interventions have not been effective in engaging this group who are likely to drink at unhealthy levels but be highly resistant to reducing their alcohol consumption – especially as they do not consider their use to be problematic unless it impairs their capacity to fulfil responsibilities or function at work".

They conclude by saying, "future public health messages around alcohol should be less focused upon the crime and personal safety implications of irresponsible drinking and be more sensitive to the lifestyles and long-term health of the populations they target".

They add that further research is needed to identify which factors (other than driving) would engage white collar workers to change their views and drinking behaviours.

Conclusion

Overall, this research provides some early findings of so-called ‘white collar’ workers' views of drinking behaviours in the UK.

Although the study was very small, with only 49 volunteers' views analysed, it is useful in determining emerging themes, and the researchers do state that there was relative consistency across the five groups. The researchers also note that ‘strong personalities’ within the group may have influenced how the other participants responded.

Research among larger groups of white collar workers is needed to draw firmer conclusions about the drinking culture in the UK. It is worth noting that these findings may not be applicable to other countries or cultures. Ethnicity, cultural identity and religious beliefs of the participants were not reported, which may have influenced how participants responded to the questions.

One important final message to stress – and one that seems to have not been grasped by the volunteers in the study – is that it is not where you drink, why you drink, or who you drink with that matters. It is how much you drink.

Regularly exceeding the recommended daily amounts for alcohol can harm your health, regardless of whether it is with three litres of strong white cider on a park bench, or a bottle of Californian merlot in front of a DVD box set.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Middle class wine drinkers 'think they know better than health experts'. The Daily Telegraph, May 8 2013

Middle classes are 'ignoring the dangers of using casual drinking to combat stress'. Daily Mail, May 9 2013

Alcohol abuse: Concern over middle-aged middle classes using booze to relieve stress. Daily Mirror, May 8 2013

Middle class ‘drink more than teens’. Daily Express, May 9 2013

Links To Science

Ling J, Smith KE, Wilson GB, et al. The ‘other’ in patterns of drinking: A qualitative study of attitudes towards alcohol use among professional, managerial and clerical workers. BMC Public Health. Published online October 23 2012

Call for improved safety data on medical implants

Sun, 12 May 2013 00:33:00 EST

The need to improve the safety of medical devices such as hip and breast implants made the headlines today. The Daily Telegraph reports that experts are calling for an end to the "secrecy" surrounding how they are regulated.

The story is based on an opinion piece published in the British Medical Journal, which calls for European data on medical devices, including their safety and any adverse effects, to be made available to the public.

A second, related, article makes the point that the regulation of medical implants, and the collection and publication of related data on patient safety, fails to match that of medications.

Collecting and publishing high quality data could help prevent widespread problems with medical implants, such as those seen with Poly Implant Prothèse (PIP) breast implants.

The PIP scandal caused global concern after it was discovered that French-made breast implants contained industrial rather than medical grade silicone.

Concerns have also been raised about metal-on-metal hip replacements wearing down sooner than had been expected, potentially causing damage to surrounding tissue.

The authors argue that EU proposals for new legislation to regulate medical devices, which are currently being debated, should include their proposals to develop systems for collecting evidence.

What is the problem?

The article has been written by experts from the interventional procedures advisory committee of the National Institute for Health and Care Excellence (NICE). This body looks at the evidence on medical implants and devices, as well as surgical procedures, to see if they are safe, clinically effective and provide good value for money.

The experts point out that some medical devices and surgical procedures are introduced and used by health professionals with little evidence about their safety from clinical trials or observational data.

The term “medical devices” covers a huge range of materials, from very basic supplies, such as bandages, to extremely complex equipment, such as life-support machines.

The report says that the regulations concerning the evidence required on both efficacy and safety of new devices are less stringent than those for medicines. In many cases, data on safety and the possibility of adverse events is not routinely collected.

In addition, many medical devices are produced by small specialist firms that lack the funding and experience to conduct adequate research.

Within Europe, regulations require manufacturers to obtain a CE mark of quality for a new device. However, for the CE mark to be given, the amount of evidence needed on safety is usually small.

In contrast, the amount of evidence on patient safety needed before a new drug can legally be brought to market is huge.

The report also says that there are no legal frameworks governing the introduction of new medical or surgical procedures – whether or not they involve a new device – and the evidence on safety and effectiveness is usually poor. The reasons why the evidence is poor include lack of commercial sponsorship and the difficulties of setting up research trials.

All these factors mean that when a device or procedure starts to be used on patients, there is limited data on both its efficacy and short-term safety. “Adoption of the new procedure or device is typically driven by marketing and the enthusiasm of clinicians, rather than by evidence,” say the authors.

There is also no organised system of collecting data on devices and procedures once they are in use.

What recommendations does the analysis make?

The report proposes several solutions to the problem of inadequate data collection on the safety and efficacy of medical devices and procedures. These include:

Device tracking. An efficient device-tracking mechanism (like a barcode) would make it easier to inform patients and recall devices where necessary and improve monitoring and data collection.
Use of registers. Countries and health systems should be encouraged to use existing procedure registers (such as NICE guidance in the UK) and set up new ones where needed. The UK’s National Joint Registry is one example.
Data linkage. New registers should be linked to routinely collected health services data, national mortality statistics and other sources of relevant information.
Bypassing patient consent. Getting patients’ consent to use their data in registers has failed in the past. The authors suggest that where data collection is in the public interest, patient consent should not be required.
International collaboration. Sharing data between countries may help.
Post-market surveillance. Data collected by device manufacturers could provide useful information about the use of products worldwide.
Adopting a framework for collecting evidence on new procedures. The authors say there is now a well recognised framework for generating evidence on any new procedure, from its first use into the long-term.

What happens next?

Some headway has recently been made into improving the safety of devices, says the report. It points out that the European Commission has adopted proposals for two new regulations on medical and surgical devices to improve patients’ safety. If they are agreed these regulations will apply from 2017.

However, the authors point out that proposed changes to legislation, both in Europe and elsewhere, do not include suggestions to improve the collection of data.

An accompanying commentary by a research group at Herdecke University in Germany argues that Europe needs “a central, transparent and evidence-based regulation process for devices”.

They have submitted a petition to the European Commission, European Parliament and European Council arguing for the regulation process to be centralised with independent assessment “by a new public body similar to the European Medicines Agency”.

They also recommend that post-marketing surveillance should be legally compulsory “to ensure that benefits and harms of the device in real world settings are similar to those shown in clinical trials”.

Finally, the German researchers call for transparency of the assessment process and results.

They believe that all available data on medical devices “should be publicly accessible and should include all relevant information concerning assessment, including data on safety, performance, and incidents”.

However, as the authors of this report point out, the outcome of discussion with the relevant authorities is “difficult to predict”.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Experts call for transparency over medical devices. The Daily Telegraph, May 8 2013

Links To Science

Campbell C, Stainthorpe AC, Longson CM. How can we get high quality routine data to monitor the safety of devices and procedures? BMJ. Published online May 7 2013

Antibiotics may help ease chronic back pain

Sun, 12 May 2013 00:33:00 EST

News that back pain could be "cured" by antibiotics has prompted wide media coverage, with The Independent reporting that "Half a million sufferers of back pain 'could be cured with antibiotics'."

The headlines are based on research into chronic lower back pain that showed some cases may be caused by a bacterial infection. Researchers found evidence that antibiotic treatment of a specific type of chronic lower back pain was more effective than placebo pills at reducing back pain and disability one year after treatment began.

Although antibiotics may also be effective for other types of back pain, this was not established by this study. While the results appear genuinely encouraging, this study involved patients with a very specific type of lower back pain. This means the results may be different in other people with different types of back pain.

There is also the potential risk this research could lead to the indiscriminate use of antibiotics in the hope of curing all back pain. This has negative consequences for both the individual and the community, as bacteria become resistant to antibiotics over time.

The study authors themselves say they do not support the idea that all patients with lower back pain should have a trial course of antibiotics, and state that excessive use of antibiotics should be avoided.

The findings of this research are positive but, as the study authors acknowledge, they will need to be confirmed in bigger studies in more diverse populations.

Where did the story come from?

The study was carried out by researchers from university hospitals in Denmark and was funded by the Danish Rheumatism Association and other foundations.

It was published in the peer-reviewed European Spine Journal.

A related study in the same journal and by the same researchers, also discussed in the media, provided good quality evidence that some types of lower back pain are associated with bacterial infection.

The media coverage was overexcited and may have generally overstated the significance of this research, implying that most people with lower back pain may benefit from antibiotics. The research was in a subgroup of lower back pain sufferers, so any treatment developed further down the line would not be suitable for all.

While the researchers had no conflicts of interest, much of the UK media's reporting of the study included quotes from neurosurgeon Peter Hamlyn, who claimed the research was "the stuff of Nobel Prizes…[and] is going to require us to rewrite the textbooks".

Hamlyn was not involved in the research, but he was reported to have funded a website that promotes the type of treatment used in the study, Modic Antibiotic Spinal Treatment. Only The Independent highlighted this potential conflict of interest.

What kind of research was this?

The research was a double-blind randomised control trial (RCT) looking at how well an antibiotic worked at treating long-term back pain in a subgroup of lower back pain sufferers.

The specific subgroup of lower back pain sufferers being studied had signs of bone swelling in their lower back that can only be detected through an MRI scan. The exact medical term for these changes is Modic type 1 changes, or bone oedema.

The theory was that, in some cases, this bone swelling might be caused by a bacterial infection. This meant that treatment with antibiotics represented a new avenue for the researchers to explore in an effort to treat this type of lower back pain.

A randomised control trial is an appropriate study design to test this hypothesis.

What did the research involve?

The researchers recruited 162 adult patients who had lower back pain for more than six months following a spinal disc herniation, commonly known as a slipped disc. To take part in the study they also had to have disease-related changes in the vertebrae next to the previous slipped disc site, so-called Modic type 1 changes, or bone oedema. These were confirmed through multiple MRI scans.

This select group of patients was randomised to receive either 100 days of antibiotic treatment with amoxicillin clavulanate tablets three times a day, or 100 days of an identical placebo.

Their health was evaluated at the start of the study, with participants unaware of which group they would be randomised to. Further evaluation of their health was also done without them knowing whether they had received placebo or antibiotics. Evaluation took place at the end of the 100-day treatment and again one year from the start of the study.

The researchers focused on changes in disease-specific disability and back pain. Disease-specific disability was measured using the Roland Morris Disability questionnaire (RMDQ). This is a 23-item questionnaire where the patient answers 23 yes or no questions related to the impact back pain has on their daily activities and quality of life. The questionnaire results in a scale score from zero to 23, with higher scores being worse.

Back pain was also measured using a patient-completed rating scale. Clinically relevant improvements in both measures were defined in advance of the results of the study – for instance, a 30% reduction for the RMDQ.

They also recorded changes in leg pain, number of hours with pain in the last four weeks, perceived health, days with sick leave, "bothersomeness", constant pain and disease-related changes observed under MRI.

The statistical analysis of the results was appropriate, and compared pain and disease changes in the group given antibiotics with those given placebo.

What were the basic results?

Of the 162 patients enrolled at the start, 147 (90.7%) completed the end-of-treatment questionnaires after 100 days, and 144 (88.9%) completed the one-year follow-up MRI scans, questionnaires and physical health checks.

Patients assigned to the placebo and antibiotic groups generally had similar characteristics at the start of the study.

The key results were:

The group given antibiotics improved their disease-specific disability and back pain scores after treatment (100 days) and showed even larger improvements at the one-year time point.
Back pain assessed by the RMDQ improved from 15 in the antibiotic group to 11.5 at 100 days and seven at one year, compared with a fall from 15 in the placebo group to 14 at 100 days remaining unchanged at 14 after one year.
In comparison with the placebo group, the improvements observed using antibiotics were statistically significantly better.
The magnitude of the improvement in disease-specific disability and back pain scores after treatment with antibiotics was also deemed clinically important using criteria defined before the start of the study.
Patients reported that pain relief and improvement in disability started gradually – for most patients, six to eight weeks after starting antibiotic tablets, and for some at the end of the treatment period (100 days).
Improvements reportedly continued long after the end of the treatment period – at least for another six months – and some patients reported continuing improvement at one-year follow-up.
Less disease-related changes were detected in the vertebrae of the spine in patients given antibiotics than those given placebo. Changes were assessed from the start of the study to the one-year time point, with statistically significant differences seen.
Overall, side effects were more common in the antibiotic group (65%) compared with the placebo group (23%). However, these side effects were described by the researchers as generally minor and were related to stomach upsets such as loose bowel movements, flatulence (farting) and burping.

How did the researchers interpret the results?

The researchers concluded that, "The antibiotic protocol [treatment] in this study was significantly more effective for this group of patients than placebo in all the primary and secondary outcomes."

They highlighted how "for the primary outcome measures, disease-specific disability and lumbar pain, the effect magnitude was also clinically significant."

Conclusion

This well-designed double-blind RCT shows that the antibiotic treatment of chronic lower back pain caused by swelling of the spinal vertebrae is more effective than placebo at reducing back pain and disease-related disability

The study had many strengths, including its randomised double-blind design, adequate sample size and one-year follow-up point.

However, it did have some limitations, including the fact that:

Patients varied at the start of the study. More people in the placebo group had lower grades of vertebrae change. This is hard to explain if allocation to the two groups had been completely concealed and fair, although it may have favoured improvements in the placebo group and therefore may not have influenced the results.
Blinding of the participants may have been broken unintentionally. As this antibiotic caused such predictable bowel side effects in 65% of people taking the active treatment, it is possible that the participants knew they were taking an active treatment and therefore may have reported the subjective scores differently form the placebo group. The researchers did not report any testing for fidelity of the blinding, such as asking participants if they could guess which group they were in.

As strong as this research it is, it is not definitive. Further research, most likely with larger numbers of people in the study, will be needed to confirm these findings before any treatment is likely to be approved and licensed for routine use in UK. There will also need to be extensive safety investigations.

Crucially, the study recruited a very select group of lower back pain sufferers who showed small changes in their vertebrae next to the site of a previous slipped disc. This select group therefore is not representative of all lower back pain sufferers.

This research certainly does not advocate giving antibiotics to all lower back pain sufferers. However, if the results are confirmed in subsequent studies and this form of treatment is deemed safe, it may provide a new treatment option for this type of lower back pain in the future. This is cause for much optimism.

The researchers' estimate that approximately 35-40% of long-term back pain sufferers experience excess fluid in the spinal vertebrae and could potentially benefit from this type of treatment in the future. However, it is unclear how accurate this estimate is, and may indeed be an overestimate.

Even if all these hurdles are overcome, media talk of a "back pain cure" could still be premature. Antibiotics may help relieve symptoms, but there is currently no conclusive evidence that they can correct the underlying causes of chronic back pain.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

How back pain can be beaten with antibiotics: Breakthrough could cure 40% of sufferers. Daily Mail, May 7 2013

Back pain breakthrough could eliminate need for major operations. The Guardian, May 7 2013

Antibiotics could cure 40pc of chronic back pain patients. The Daily Telegraph, May 7 2013

Back pain 'can be cured with a £114 dose of antibiotics'. Metro, May 7 2013

'The stuff of Nobel prizes': The backache breakthrough? Half a million sufferers 'could be cured with antibiotics'. The Independent, May 7 2013

Antibiotics could relieve back pain for 40% of sufferers. ITV News, May 7 2013

Miracle cure for back pain: Agony ended by everyday antibiotics. Daily Express, May 8 2013

Links To Science

Albert HB, Sorensen JS, Christensen BS, Manniche C. Antibiotic treatment in patients with chronic low back pain and vertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled trial of efficacy. European Spine Journal. Published online April 2013

Hungry shoppers may choose unhealthier foods

Sun, 12 May 2013 00:33:00 EST

"Hungry shoppers 'buy more calories'," BBC News reports in a story based on a very small short-term study. The somewhat artificial study examined the effects of people skipping meals due to everything from busy lifestyles to intermittent diets such as the 5:2 diet.

These intentional or unintentional fasts may lead to unhealthy food choices being made at the shops. This research looked at whether being deprived of food for just a few hours has an effect on the types of food people opt for.

During a simulated shopping experience, the researchers found that people who were hungry selected more high-calorie foods than people who had just eaten a snack.

Similarly, people who went food shopping during times of the day when the researchers expected them to be hungry (late afternoon) purchased more high-calorie foods than people who shopped when the researchers thought they were less likely to be hungry (early afternoon).

However, no definitive conclusions can be drawn from these findings. The research had many limitations, including the fact that the first study was laboratory-based and laboratory findings may not reflect the real world.

But it is common sense to grab a bite to eat before heading to the shops, and might be worth a try if you do find that shopping when hungry means you make less healthy food choices.

Where did the story come from?

The study was carried out by researchers from Cornell University in the US and was funded by the university. It was published in the peer-reviewed Journal of the American Medical Association (JAMA) Internal Medicine.

The BBC covered the study well, if slightly uncritically, as the study's limitations were not discussed.

What kind of research was this?

This research included two components (a laboratory study and a field study) designed to determine whether short-term food deprivation changes affect food shopping habits.

The researchers say that food deprivation has been shown to change how much food people buy, and fasting is known to alter how the brain reacts to certain foods. They were interested to know whether shopping while hungry also effects the types of food people purchase.

Laboratory and field studies can provide interesting information about how people may react in given situations, but they are prone to bias and confounding. These potential limitations should be kept in mind when considering the results of the study.

What did the research involve?

In the first part of the study, the researchers recruited 68 paid participants with ages ranging from 18 to 62 years. They were asked to avoid eating for five hours prior to the start of the experiment.

The participants were grouped together in sessions of six to 12 people. In half of these sessions, a plate of crackers was offered at the beginning of the experiment and participants were asked to eat enough of the crackers so that they were not hungry. The participants were not offered any food in the remaining sessions.

The groups then completed an experiment meant to simulate buying groceries online. The online store offered a mix of lower calorie foods (including fruits, vegetables and chicken breasts) and higher calorie foods (including sweets, salty snacks and red meat). The products were displayed without prices. The researchers recorded and compared the food choices of individuals who did not eat prior to the study with those who had been offered a snack.

The second study involved the observation of individuals in a more natural setting. The researchers tracked the food purchases of 82 people.

The first group were tracked during the early afternoon, or "low hunger hours" (between 13:00 and 16:00), when the researchers expected them to have had lunch and therefore not be hungry.

The second group was tracked during the early evening, or "high hunger hours" (16:00 to 19:00), when researchers thought they would have gone several hours without a meal.

The researchers characterised the food purchases as either high-calorie or low-calorie, and compared the number of foods that fell into each category between the two participant groups.

They statistically compared the number of low-calorie items, the number of high-calorie items, and the ratio of low- to high-calorie purchases between the groups.

What were the basic results?

The researchers found that participants in the hungry and not-hungry groups of the laboratory study chose a similar number of total items (approximately 14 in the hungry group versus 12 in the not-hungry group).

The two groups also chose similar numbers of low-calorie foods (approximately eight in both groups), but the hungry group selected significantly more high-calorie items (an average of nearly six, compared with four in the not-hungry group).

During the field study, the researchers found that participants in the evening group purchased fewer low-calorie items (approximately eight items) than the afternoon group (approximate average of 11 items). There was no statistical difference in the number of high-calorie foods purchased (approximately four in both groups).

The ratio of low- to high-calorie items (with a higher ratio indicating better food choices overall) was significantly higher in the early afternoon group (approximately four low-calorie items per each high calorie item) compared with the evening group (approximately 2.5 low-calorie items per each high-calorie choice).

How did the researchers interpret the results?

The researchers concluded that, "even short-term fasts can lead people to make more unhealthy food choices" by picking fewer low-calorie foods.

Conclusion

This study suggests that how hungry you are when you shop for food can have an impact on the food you choose.

This may not be too surprising for anyone who has made a quick trip to the shops while hungry and found themselves at the till with a basket full of crisps and biscuits, but no fruit or vegetables.

While interesting, the study has some limitations that should be noted:

Both experiments were fairly small, with less than 100 people in each.
A laboratory-based study such as the first experiment tends to be stronger the more it mimics the real world. A simulated online grocery shopping experience that removes item price as a contributing factor is less likely to mirror real-life decision making.
The field study makes assumptions about hunger levels based on the time of day. This may not be a reliable manner in which to assess hunger – for instance, individuals shopping during the "low hunger hours" of 13:00 to 16:00 may have skipped lunch, while individuals in the "high hunger hours" may have had a late lunch, a snack, or an early dinner.
Field studies are prone to confounding due to difficulties measuring and controlling for different factors that may also have an influence. It is not reported how the afternoon and evening shoppers differed, and it is possible that the relationship between the time of day and shopping choices was influenced by different participant characteristics, such as age, employment, education, or socioeconomic status, and not by hunger.

The researchers say that short-term fasting is fairly common and can arise from skipping a meal, either intentionally as part of a religious fast or in an effort to lose weight, or unintentionally due to chaotic work schedules.

However, given that it is pretty easy and low-risk to grab a snack before heading out to the supermarket, this may seem like a sensible thing to do – it may have the benefit of subtly changing the foods you buy and consume throughout the week.

If you are trying to lose weight or eat a healthier diet, it may be a good idea to plan your shopping in advance. Options include using an online grocery site or, for a more low-tech equivalent, a good old-fashioned shopping list.

The NHS Choices 5 A DAY meal planner can also help you plan your weekly shop.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Hungry shoppers 'buy more calories'. BBC News, May 6 2013

Links To Science

Tal A, Wansink B. Fattening Fasting: Hungry Grocery Shoppers Buy More Calories, Not More Food. JAMA Internal Medicine. Published online May 6 2013

No evidence of cure to prevent hair going grey

Sun, 12 May 2013 00:33:00 EST

“Cure for grey hair is on its way say scientists,” the Daily Mirror reports, with The Daily Telegraph adding that grey hair will become ‘a thing of the past’.

You may be surprised to learn that the study the media reports on had absolutely nothing to do with grey hair. In fact, the stories were loosely based on a tiny study into what happens in a common skin condition called vitiligo. Vitiligo causes depigmentation (loss of colour) of the skin, leading to white patches on the skin and hair.

The current study included 10 people with what is called ‘segmental’ vitiligo, where the condition affects the area of skin supplied by a particular nerve. They found that changes in skin colour were accompanied by the accumulation of two chemicals in the skin: hydrogen peroxide and peroxynitrite.

The researchers then demonstrated that using a compound that when exposed to ultraviolet light was known to reduce hydrogen peroxide levels led to white patches on skin and eyelashes becoming repigmented.

While the results of the study could theoretically be extrapolated as providing a potential treatment for grey hair, much more research is required to see if such a treatment would be both safe and effective.

This study does offers possible hope of a treatment for segmental vitiligo though, again, further research is required.

Where did the story come from?

The study was carried out by researchers from E. M. Arndt University, Germany and the University of Bradford, UK. It was funded by the American Vitiligo Research Foundation and by private donations.

The study was published in the peer-reviewed Federation of American Societies for Experimental Biology (FASEB) journal.

This story was poorly reported in the media, with all headlines speculating that the findings could lead to a cure for grey hair. The current study did not investigate the causes of, or possible treatments of, grey hair. However, the research focused on vitiligo, specifically looking at segmental vitiligo.

Though the blame for the poor reporting of the study can be put at the door of the press office of the FASEB, which issued a press release almost entirely focused on the grey hair angle. This is a textbook example of public relations officers ‘sexing up’ a dry but worthy piece of research in order to gain maximum media coverage. And – credit where credit is due – they did an excellent job of that. Unfortunately, in doing so they obscured the truth.

Whether peer-reviewed journals should be engaging in these types of disingenuous practises, which arguably damage the public understanding of science, is a matter of debate. However, FASEB are not alone in this, as recent research found that academics, journals and news reporters all share the blame for the spin found in around half of all medical reporting.

What kind of research was this?

This was a laboratory study and case series report into the mechanics of the skin condition vitiligo and whether learning more about it could lead to new treatments.

Vitiligo can be divided into two forms: segmental and nonsegmental vitiligo. Nonsegmental vitiligo is the more common, in which the white patches that appear are symmetrical (the same places on both sides of the body, for example both hands could be affected). In nonsegmental vitiligo, two chemicals – hydrogen peroxide and peroxynitrite – accumulate in the skin.

Nonsegmental vitiligo can be treated with a pseudocatalase, which is activated by narrow-band UVB light. This reduces the concentrations of hydrogen peroxide, allowing the lost skin colour to return.

In the less common segmental form of vitiligo, the affected skin lies in a dermatome, which is a particular area of skin supplied by a single nerve, so it usually affects only one side of the body.

Segmental and non-segmental vitiligo can also co-exist, giving rise to ‘mixed’ vitiligo.

This study aimed to see whether the accumulation of hydrogen peroxide and peroxynitrite which occurs in nonsegmental vitiligo also occurs in segmental vitiligo, and if so, if the light activated pseudocatalase could also be of use in segmental vitiligo.

The laboratory study is the ideal study design to investigate the mechanism behind segmental vitiligo. However, the treatment was only tested in a very small number of people with vitiligo. Well-conducted trials involving much larger numbers of people are needed before it can be determined how effective it is.

What did the research involve?

The researchers looked to see whether hydrogen peroxide and peroxynitrite (and the oxidation products produced when these chemicals react with other molecules in the cell) are present in the skin of people with segmental vitiligo. To do this they examined four people with segmental vitiligo and six people with mixed vitiligo (where the person has both segmental vitiligo and nonsegmental vitiligo). For comparison, they selected five healthy controls matched for age and skin type.

The researchers then determined whether treatment with narrow-band UVB activated pseudocatalase, which reduces the levels of hydrogen peroxide, could allow repigmentation.

What were the basic results?

The researchers found that hydrogen peroxide and peroxynitrite (and substances that are formed by reactions of these chemicals with molecules in the cell), are present in the skin of people with segmental vitiligo.

The researchers report that treatment with narrow-band UVB activated pseudocatalase, which reduces the levels of hydrogen peroxide, allowed repigmentation of the skin and eyelashes of five people with vitiligo regardless of whether they had segmental vitiligo only, or in association with nonsegmental vitiligo.

How did the researchers interpret the results?

The researchers conclude that their findings, “offer new treatment intervention for lost skin and hair colour”.

Conclusion

This study aimed to investigate whether two chemicals – hydrogen peroxide and peroxynitrite – accumulate in the skin of people with segmental vitiligo, which affects up to a quarter of people with vitiligo.

They then looked at whether treatment with a light-activated pseudocatalase, that reduces the concentration of hydrogen peroxide, would allow the lost skin colour to return.

They found that the treatment was successful in five people with segmental vitiligo (either isolated or in combination with nonsegmental). The study offers hope of a possible treatment for segmental vitiligo, although so far it has been tested in only very few patients.

Well-conducted trials in much larger numbers of people will be needed before it can be determined how effective it is.

Although previous research has demonstrated that hydrogen peroxidase also accumulates in grey hair follicles, this study did not look at whether treatment with pseudocatalases or other substances could be used to treat grey hair.

For this rather fundamental reason, it is not possible to say from this study whether or not there could be a cure for grey hair.

However, the potential market for an effective hair colouring treatment is huge: recent figures show that the hair dye market is essentially recession-proof. It would be surprising if this study did not lead to further research into the applications of the techniques used in the study.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Cure for grey hair is on its way say scientists. Daily Mirror, May 7 2013

Grey hair 'a thing of the past' after scientists discover why follicles become discoloured. The Daily Telegraph, May 6 2013

Is this the end of costly dyes? Scientists working on cure for grey hair. The Independent, May 6 2013

Grey Hair Treatment Discovered By Scientists. Sky News, May 6 2013

Links To Science

Schallreuter KU, Salem MAEL, Holtz S, Panske A. Basic evidence for epidermal H2O2/ONOO−-mediated oxidation/nitration in segmental vitiligo is supported by repigmentation of skin and eyelashes after reduction of epidermal H2O2 with topical NB-UVB-activated pseudocatalase PC-KUS. The FASEB Journal. Published online April 29 2013

Breast cancer rates in under-50s at record high

Sun, 12 May 2013 00:33:00 EST

Much of the UK media are covering the release of data that indicates breast cancer rates in the under-50s are now at a record high. Changes in childbirth patterns and alcohol consumption could be to blame, according to a leading charity.

The news follows new data released by Cancer Research UK. Its data shows that breast cancer diagnoses among women aged under 50 have now reached an all-time high, breaking the 10,000 mark for the first time in 2010. One in five diagnosed breast cancer cases are now in women under the age of 50.

Possible explanations for the increases are speculated to be due to known hormonal risk factors for cancer – such as having children later in life. Increased alcohol intake, another risk factor for breast cancer, could also be involved.

The rise in the number of new cases is not restricted to the under-50s: there has been a steady increase in the number of cases diagnosed for women of all ages since the 1970s.

But the rise isn’t necessarily as bad as it sounds. For example it could reflect better breast awareness and improved diagnosis and screening, which in turn might lead to early treatment and improved chances of survival.

The good news is that – despite the increase in breast cancer diagnoses – breast cancer deaths are actually falling. An increasing number of women are now survivors of breast cancer.

What does the data show?

Breast cancer is the most common cancer among women, accounting for almost a third of all new cancer cases in women. Cancer Research UK reports how their latest statistics revealed that in 2010, there were 10,000 new cases diagnosed among women aged under 50. This is an 11% increase from 15 years previously in 1995 when there were 7,700 cases of breast cancer diagnosed among women in this age group.

One in five breast cancers (20%) are now diagnosed in women aged under 50. Nearly half of breast cancers (48%) are diagnosed in women aged between 50 and 69 – the age group currently invited for breast cancer screening.

However, the rise in the number of breast cancer cases is not restricted to the under-50s. Since the 1970s there has been a gradual and steady increase in the number of breast cancer cases. Overall there was an 18% increase in rates between 1995 and 2010.

What are the possible reasons behind the increased rates among younger women?

Cancer Research UK says that, though it is not clear why cases of breast cancer are increasing among younger women, alcohol intake and hormonal factors may play a role.

Alcohol

Alcohol is an established risk factor for breast cancer. Cancer Research UK reports that the combined results of two large systematic reviews of the published evidence, in addition to findings from the UK Million Women Study, suggest that each additional unit of alcohol per day can increase a woman’s risk of the disease by between 7% and 12%. The research suggests that by the age of 80, roughly the following number of women will have developed breast cancer:

9 out of 100 if they don't drink at all
10 out of 100 if they have two drinks a day
13 out of 100 if they have six drinks a day

However, as Cancer Research UK does say, the possible risk increase from alcohol is less compared to the greater influence of other factors – particularly hormonal factors.

Hormonal factors

Very generally, increased exposure to the hormone oestrogen is associated with increased risk of breast cancer because it can stimulate breast cancer cells to grow. Higher lifetime oestrogen exposure is associated with:

starting periods at a younger age
going through the menopause at a later age
use of the combined oral contraceptive pill (which contains oestrogen)
fewer (or no) pregnancies
shorter duration of (or no) breastfeeding
use of HRT (which contains oestrogen)

Both having children and breastfeeding are known to be protective against breast cancer. In theory the younger a woman is when she has her first pregnancy, and the more pregnancies she has in her lifetime, further decreases her risk. Similarly, the more a woman breastfeeds will decrease her risk. Therefore, modern western lifestyles (that include women generally starting families later and having smaller families) may give some possible explanation to the increase in breast cancer rates among younger women.

Are there any positive signs?

Despite the increased rates among women overall and specifically among women aged under 50, Cancer Research UK does report some good news: that fewer women than ever before are now dying from breast cancer. This due to better treatment, the charity says.

The rate of women aged under 50 who are dying from breast cancer has fallen by 40% since the early 1990s. Twenty years ago, the death rate from breast cancer in the under-50s was 9 per 100,000 women in the UK. By late 2000, this had fallen to 5 per 100,000 women. More than 8 in 10 women diagnosed with breast cancer before the age of 50 are now reported to survive the disease for at least five years.

Although not discussed by the Cancer Research UK report, the rise in cases could be a reflection of increased awareness of breast cancer and increased rates of diagnosis and improvement in screening techniques.

As a concluding message, Sara Hiom, Cancer Research UK’s director of health information, says: “Breast cancer is more common in older women, but these figures show that younger women are also at risk of developing the disease. Women of all ages who notice anything different about their breasts, including changes in size, shape or feel; a lump or thickening; nipple discharge or rash; dimpling, puckering or redness of the skin, should see their GP straight away, even if they have attended breast cancer screening.

“It’s more likely not to be cancer, but if it is, detecting it early gives the best chance of successful treatment,” she added.

What can I do to reduce my risk of breast cancer?

Unlike some other cancers, the body of evidence about proven methods of reducing risk is relatively small. Though most experts would recommend that:

you stick to the recommended alcohol consumption rates for women
you take plenty of exercise
you maintain a healthy weight
avoid smoking

It is also important that you attend breast cancer screening appointments when invited. Women aged 50 to 70, who are registered with a GP, are automatically invited for screening every three years.

Read more about the NHS Breast Screening Programme.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Breast cancer cases in UK under-50s top 10,000 a year. BBC News. May 3 2013

Breast cancer rates increase among younger women. The Guardian, May 3 2013

Breast cancer cases soar to 27 a day among the under-50s... and experts fear modern lifestyles are to blame. Daily Mail, May 3 2013

Under-50s with breast cancer at record high. The Daily Telegraph, May 3 2013

Breast cancer on the rise in under 50s who now account for 1 in 5 cases. Daily Mirror, May 3 2013

Links To Science

Cancer Research UK. Breast cancer in women under 50 tops 10,000 cases for first time. May 3 2013

No proof kids of lone parents are less intelligent

Sun, 12 May 2013 00:33:00 EST

"Children brought up by two parents are more intelligent," is the baseless claim on the Mail Online website.

The headline fails to mention that the research the story is based on involved only mice. Not until eight paragraphs into the news story does the Mail reveal this crucial point.

The scientific study involved housing baby mice with either their mother only, with both 'parents' or with their mother and a matched female 'parent'. These baby mice were then subjected to a series of tests designed to assess their development. After the testing, researchers took tissue samples from the brains of the mice.

The researchers found that:

male mice housed with two parents seemed to have better threat-recognition abilities than those who were raised by a single mouse mum
female mice housed with two parents seemed to have better motor co-ordination
being housed with two parents did seem to affect brain development, although the pattern of development differed between male and female mice

Interesting as this is, it is hard to see how it applies to human families. This study cannot be used to conclude that children raised by one parent will have behavioural differences from, or will be less intelligent than, those raised by two parents.

Where did the story come from?

The study was carried out by researchers from the University of Calgary in Canada and was funded by the Canadian Institutes of Health Research and awards from Alberta Innovates Health Solutions.

The study was published in the peer-reviewed scientific journal PLOS one, which is free to read for all on an open-access basis.

The Mail’s story exaggerates the findings of this unusual animal study. Most of the article reads as if the research were directly relevant to humans or carried out in humans. The Mail encourages this idea by illustrating the story with a picture of a couple with their toddler. It is only in the eighth paragraph of the Mail’s report that the fact that the study was in mice is revealed. The paper offers no thoughts about how relevant research on mice is to humans.

However, much of the exaggeration in the Mail’s reporting can be traced back to a press release about the research issued by the University of Calgary.

What kind of research was this?

This was animal research aiming to investigate the effect that early life experiences can have on brain development, emotions and social behaviour.

In particular, the researchers were interested in the theory that low maternal care leads to changes in the area of the brain involved with memory and emotions (the hippocampus). This may then lead to increased stress and increased sensitivity to changes in emotion and mood (emotional reactivity).

They say that previous studies have shown that when pregnant rodents have been exposed to stress the female offspring developed a smaller hippocampus. As the effect was not seen in male offspring this suggested there may be some gender difference.

This study aimed to see whether parental care offered by two rodent parents rather than one had an effect on brain cell development. Further, the researchers wanted to see whether any changes in development had an effect on the behaviour of the offspring, and whether the effect was different in male and in female offspring.

This study may be of interest to scientists and psychologists, and offers a possible insight into the factors that may influence animal brain development and behaviour. But it is hard to determine if, or how, the results can ever be applied directly to humans.

What did the research involve?

This research involved eight-week-old female and male mice, who were fed a normal diet and housed under 12-hour light/dark conditions. They were allowed to mate freely. Pregnant females were removed and placed in different parental conditions for the duration of pregnancy, through birth and until weaning at 21 days. In total, 269 animals were involved.

The three conditions were:

maternal-only condition – the offspring were housed with their mother only
maternal-virgin condition – the offspring were housed with their mother and an age-matched virgin female mouse
maternal-paternal condition – the offspring were housed with the mated male-female pair

When housed under the three conditions the researchers observed the time that the parent mice spent in parenting behaviours, such as nursing, licking and grooming, and nest building.

When the offspring were weaned at 21 days they were housed with their littermates. They then completed a series of behavioural tasks ranging from least to most stressful. The tasks included:

different maze tasks, including water mazes
light-dark tasks (seeing how long mice spent in light and dark compartments when allowed to navigate freely)
horizontal ladder tests (looking at how well they walked across the differently-spaced rungs of a ladder)
tests of social preference (looking at interest in exploring different objects that stimulated the senses)
tests of passive avoidance (of an electric shock)
tests of fear conditioning (observing their time spent frozen and motionless when they were exposed to different shocks and sounds)

The researchers also examined tissue samples from the brains of the offspring mice to investigate any biological differences in their brain development.

What were the basic results?

Before weaning, the researchers observed that the parenting behaviour of the mother mouse was no different in the three conditions. Nor did the displays of parenting behaviour from the virgin-female and father-mouse differ from each other in those two respective conditions.

When the researchers worked out the average time spent licking and grooming the offspring (a marker of parental attention), the offspring in the two-parent conditions (either maternal-virgin or maternal-parent) received more attention than those in the maternal-only condition.

Overall, they found effects of parenting upon offspring behaviour and brain cell development differed between male and female offspring. In the various tasks, males raised in the two-parent conditions showed more fear conditioning, by displaying more freezing behaviour than males raised in the maternal-only condition. Meanwhile, females raised in the two-parent conditions showed better co-ordination when walking across the ladder than females in the maternal-only condition. The two-parent females also displayed more interest in exploring different objects.

This suggests that being raised in an environment with the biological mother and another adult mouse (male or female), may improve or accelerate some, but not all, developmental skills.

Two-parent care also had more effect on the male mouse brain. Male offspring in both the two-parent conditions had more growth of cells in a certain part of the hippocampus (the dentate gyrus). Parenting experience didn’t seem to have an effect on the hippocampus of the female offspring. However, females raised under the two-parent conditions did show greater proliferation of the white matter (the nerve fibres) of the brain.

How did the researchers interpret the results?

The researchers say that early life experiences can have an effect on brain development and behaviour, and that this persists through life. Male and female offspring appear to be affected in different ways.

They note in the abstract of their published research article (but do not describe in detail in the main research methods or results) that some of the brain development and behavioural advantages due to two-parent upbringing can stay with the mice throughout life and can be transmitted to the next generation.

Conclusion

This animal study suggests that male and female mice raised in two-parent conditions display differences in their brain cell development and behaviour compared with mice raised with only their mother.

While there are similarities between mice and men, it would be a mistake to assume that the findings in this mice study can be applied to humans. There are many important differences between the parenting of mice and people, and many differences in biology and social development that make it impossible to translate these findings to people.

Nonetheless, this study will be of interest to scientists and psychologists and offers a possible insight into the factors that may influence animal brain development and behaviour. Future research can build on these findings.

It should not be assumed from this study that children raised by one parent will have behavioural differences from those raised by two parents. The Mail Online also mistakenly suggests that this study supports the idea that children brought up by two parents are more intelligent. Apart from the fact that it was a rodent study, the study did not examine the ‘intelligence’ of the mice, so this assumption is groundless.

The main differences observed were that male mice from two-parent families seemed to freeze more when exposed to a perceived threat, and that female mice from two-parent families were more interested in exploring objects and better at walking over a ladder. It is a distortion of the evidence to conclude from this that children from two-parent families are more intelligent.

If you are shocked by the reporting of this study, first by the University of Calgary’s press office (or to be specific, its Hotchkiss Brain Institute) and then by the Mail Online, you may want to read about a study published in 2012. It found that half of all health reporting is subject to some sort of ‘spin’ with researchers and academic press offices shouldering a large proportion of the blame.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Children brought up by two parents are more intelligent - because they develop more brain cells. Mail Online, May 2 2013

Links To Science

Mak GK, Antle MC, Dyck RH, Weiss S. Bi-Parental Care Contributes to Sexually Dimorphic Neural Cell Genesis in the Adult Mammalian Brain. PLoS One. Published online May 1 2013

Young blood may help rejuvenate old hearts

Fri, 10 May 2013 13:33:00 EST