Logo of worldpsychLink to Publisher's site
World Psychiatry. 2011 Jun; 10(2): 138–151.
PMCID: PMC3104888

Physical illness in patients with severe mental disorders. II. Barriers to care, monitoring and treatment guidelines, plus recommendations at the system and individual level


Physical disorders are, compared to the general population, more prevalent in people with severe mental illness (SMI). Although this excess morbidity and mortality is largely due to modifiable lifestyle risk factors, the screening and assessment of physical health aspects remains poor, even in developed countries. Moreover, specific patient, provider, treatment and system factors act as barriers to the recognition and to the management of physical diseases in people with SMI. Psychiatrists can play a pivotal role in the improvement of the physical health of these patients by expanding their task from clinical psychiatric care to the monitoring and treatment of crucial physical parameters. At a system level, actions are not easy to realize, especially for developing countries. However, at an individual level, even simple and very basic monitoring and treatment actions, undertaken by the treating clinician, can already improve the problem of suboptimal medical care in this population. Adhering to monitoring and treatment guidelines will result in a substantial enhancement of physical health outcomes. Furthermore, psychiatrists can help educate and motivate people with SMI to address their suboptimal lifestyle, including smoking, unhealthy diet and lack of exercise. The adoption of the recommendations presented in this paper across health care systems throughout the world will contribute to a significant improvement in the medical and related psychiatric health outcomes of patients with SMI.

Keywords: Physical illness, severe mental illness, physical health, health care, barriers, health disparities, monitoring and treatment guidelines

As outlined in the first part of this bi-partite publication 1, individuals with severe mental illness (SMI) are at an increased risk for a large number of physical disorders that require clinical attention. People with SMI are entitled to the same standards of care as the rest of the population. However, rates of undiagnosed and untreated medical illnesses are higher in SMI individuals, compared to the general population. Despite the fact that the higher morbidity and mortality of physical illnesses in SMI patients are largely due to modifiable lifestyle risk factors 1, there is sufficient evidence that disparities not only in health care access and utilization, but also in health care provision, contribute to these poor physical health outcomes 2,3. According to one recent study, people with psychotic disorders, bipolar disorder, or major depressive disorder have greatly increased odds of reporting difficulties in accessing care (odds ratios, OR=2.5-7.0) 4.

Although parity in access to and provision of health care should be conceived as a basic human right, a confluence of patient, provider, treatment and system factors has created a situation in which access to and quality of health care is problematic for individuals with SMI 5. Table Table11 summarizes the barriers to the recognition and management of somatic illnesses in SMI patients.

Table 1
Table 1 Barriers to the recognition and management of physical diseases in patients with severe mental illness (SMI)

In many cases, the SMI patients’ only contact with the health service is through the mental health care team. Moreover, because of their SMI, these patients are less capable than other patients of interpreting physical signs, as well as solving their problems and caring for themselves, which places an increased responsibility on the part of mental care workers to be in the fore front for the physical health care of these patients 6. Two consensus conferences have called on mental health care providers to take responsibility for the physical health of their patients 7,8. However, despite data suggesting that the sensitization of psychiatrists to expand their tasks to include assessments of both mental and physical health in SMI patients can be improved by consensus guidelines 9, many psychiatrists still consider their primary or, even, sole function to provide clinical care in terms of psychiatric symptom control and are reluctant to monitor physical health 6.

Although many barriers can be related to the patient and his/her illness, and/or to the clinician and his/her medical treatment, the reintegration of psychiatric care and general somatic services, with an ultimate goal of providing optimal services to this vulnerable patient population, seems to represent one of the most important challenges for psychiatric care today 7,10. However, this is only one part of the broader picture: 37% of 195 countries in the world do not even have a specified budget for mental health, and 25% of the countries (of the 101 countries that reported their mental health budget) spend less than 1% of their total health care budget on mental health 11. In some parts of the world, mental health resources are even poorer. In Africa and in the Western Pacific Regions, a mental health policy was found to be present in only half of the countries 12. Moreover, in developing as well as in developed countries, stigmatization, discrimination, erroneous beliefs and negative attitudes associated with SMI will have to be eliminated to achieve parity in health care access and provision. Due to differences between regions and countries (e.g., level of economic development, budgeting of health care, availability of mental health care personnel, etc.), the majority of actions should be adapted to the local needs and circumstances 7.


The excess mortality rates in persons with SMI are largely due to modifiable health risk factors 1. Therefore, the monitoring and treatment of these factors should be a part of clinical routine care of the psychiatrist. Furthermore, to address the problem of suboptimal medical treatment for patients with SMI, changes need to be made in the health care system and delivery 48, wherein the psychiatrist, once again, can and should play a pivotal role.


Physical health checks should focus on monitoring 49,50,51:

- weight gain and obesity (body mass index, BMI; waist circumference, WC);

- blood pressure;

- dietary intake;

- activity level and exercise;

- use of tobacco and alcohol or other substances;

- fasting blood levels of glucose;

- fasting blood levels of lipids, especially triglycerides and high-density lipoprotein (HDL)-cholesterol;

- prolactin levels (if indicated by reproductive system and/or sexual symptoms);

- cardiovascular disease (CVD) risk and electrocardiograph- ic (ECG) parameters;

- dental health;

- liver function tests, blood count, thyroid hormone, electrolytes (periodically, as indicated).

Many of these physical health monitoring tests are simple, easy to perform and inexpensive 6,52,53,54, and therefore can/should be implemented in the health care systems of developed as well as developing countries. Moreover, even in developing countries, several of these simple and inexpensive measurements (e.g., body weight and blood pressure) can be routinely done by health workers other than doctors.

Screening and assessment of physical health should begin with the patient’s personal and family history, covering 40: diabetes mellitus (DM), hypertension, CVD (myocardial infarction or cerebrovascular accident, including age at onset), smoking, diet, physical activity. Secondly, as the individual components of the metabolic syndrome (MetS) (see 1) are critical in predicting the morbidity and mortality of CVD, DM, cancer and other related diseases, these, as well as some other non-metabolic parameters, should be checked at baseline and measured regularly thereafter 46,51. Concerning metabolic parameters, one should remember that drug-naïve, first-episode patients, as well as children and adolescents with psychotic disorders, are at higher risk for metabolic side effects of medications 55,56. Higher baseline values of weight and visceral fat distribution, as well as laboratory evidence of impaired glucose and lipid metabolism, have been, although not consistently, reported for these patients 57. Likewise, young drug-naïve patients of non-Caucasian ethnicity with a personal or family history of metabolic risk factors are more likely to develop metabolic side effects 57.

Abdominal obesity

Psychiatrists should, regardless of the medication prescribed, monitor and chart BMI and WC of every patient with SMI at every visit, and should encourage patients to monitor and chart their own weight 58. WC seems to be a more useful measurement than BMI. Prospective data in patients with impaired glucose tolerance revealed that central adiposity, having a strong correlation with insulin resistance 59, better predicted future type 2 DM than BMI 60. WC is also a stronger indicator than BMI for systolic blood pressure, HDL-cholesterol, or triglycerides 61, and has been proposed as the best single measure to identify individuals at high risk for CVD and the MetS 52. It is also a simple tool to assess the likelihood of insulin resistance: in one study, a WC <100 cm excluded insulin resistance in 98% of males and 94% of females 61. This assessment can easily be done with a simple and inexpensive waist tape measure. The International Diabetes Federation (IDF) definition (see 1) provides sex- and race-specific criteria for defining elevated WC to identify people with central obesity, thus adapting this criterion to make it also applicable to non-Caucasian populations. However, multiple studies found that WC is rarely measured 62,63,64.

The other MetS criteria of blood pressure, fasting plasma glucose and fasting lipid profile should also be assessed, even if WC is normal. As the MetS components seem to cluster, the presence of one component often suggests the presence of the others.

Blood pressure

High blood pressure in SMI patients is often missed 65. As the cost for measuring blood pressure is low, and hypertension is a relevant CVD risk factor, blood pressure can/ought to be assessed routinely, even at every visit. Hypertension can be defined as a systolic blood pressure $130 mm Hg or a diastolic blood pressure $85 mm Hg 66. This diagnosis requires at least two separate, independent measurements that fall both within the range of hypertension 65. Individuals with a systolic blood pressure of 120 to 130 mm Hg or a diastolic blood pressure of 80 to 85 mm Hg should be considered as pre-hypertensive and require lifestyle modifications to prevent heart disease 67.

Fasting blood glucose and lipid levels

A baseline measure of plasma glucose level should be collected for all patients before starting treatment 58. In patients starting antipsychotic (AP) treatment, finger prick tests should be carried out at baseline, 6 and 12 weeks to capture early cases of hyperglycemia and then, at minimum, yearly. Formal laboratory screening tests can then be carried out when necessary 68. Ideally, blood glucose measurement should be conducted in the fasting state, because this is the most sensitive measurement for the detection of developing glucose abnormalities. However, this can prove problematic to achieve. In cases where patients present non-fasting, it is preferable to conduct a random blood glucose test (and/or hemoglobin A1C test), rather than to miss the opportunity to screen 6. An abnormal test value (fasting plasma glucose ≥126 mg/dl or hemoglobin A1C value ≥6.5%) 69 suggests the possibility of DM. Fasting plasma glucose levels between 100 and 125 mg/dl (or hemoglobin A1C values of 5.7-6.4%) are indicative of pre-diabetes and should also prompt closer assessment and follow-up. However, the possibility of false positive results need to be excluded by at least one repeated measurement of fasting plasma glucose. If the abnormality is confirmed, the frequency of fasting plasma glucose measurements needs to be increased to 4 times a year to assess the speed of the rise. Likewise, if fasting plasma glucose levels are ≥126 mg/dl or hemoglobin A1C values are >6.4%, the possibility of false positive results needs to be excluded by at least one repeated measurement of fasting plasma glucose. If the second measurement confirms the abnormality, this should lead to a consultation with an internist or other primary health care provider for further assessment and, possibly, treatment. Importantly, hemoglobin A1C reflects the mean glucose levels during the past 3 months. This is excellent as a goal for treatment outcome, but probably not sensitive enough to detect hyperglycaemia in its early stages 70.

Patients who have significant risk factors for DM (family history, BMI ≥25, WC above critical values, gestational diabetes, minority ethnicity) should have their fasting plasma glucose level or hemoglobin A1C value monitored at the same time points as other patients starting medication (baseline, week 6 and 12), but thereafter they need to be checked more frequently (approximately every 3-6 months). Patients who are gaining 7% or more of their baseline weight should also have their fasting plasma glucose level or hemoglobin A1C value monitored more frequently, for example, every 4 months 58.

Because of its high mortality, special attention should be given to diabetic ketoacidosis (DKA). DKA signs and symptoms often develop quickly, sometimes within 24 hours. One may notice: polyuria and polydipsia, nausea and vomiting, abdominal pain, poor appetite, unintended weight loss, fatigue, Kussmaul respirations (a pattern of deep breathing and hyperventilation in response to metabolic acidosis), fruity-scented breath, somnolence and confusion. The presentation of a patient with DKA varies substantially depending on the severity of the episode (e.g., mild or moderately ill patients may only describe vague symptoms of fatigue, lethargy, poor appetite, or headache). In type 2 DM, polyuria and polydipsia may have been building for weeks to months. More specific signs of DKA, which can be detected through laboratory tests, include: blood glucose level >250 mg/dL, pH <7.3 and a moderate degree of ketonemia or ketonuria 71,72,73,74.

Lipid parameters (especially triglycerides and HDL-cholesterol) should also be assessed at baseline and at 3 months, with 12-monthly assessments thereafter. More frequent screening is unnecessary, unless in case of abnormal values. Abnormal values for total cholesterol are >190 mg/dl for patients without DM and >175 mg/dl for patients with DM. Abnormal low-density lipoprotein (LDL)-cholesterol values for patients without and with DM are >115 mg/dl and >100 mg/dl, respectively 65. However, the cost and lack of availability of this assessment may not make it feasible as a routine measure in all settings and patients.

CVD risk and ECG parameters

The patient’s individual CVD risk should be calculated from his/her age, sex, presence or absence of DM, smoking habit, systolic blood pressure and total cholesterol, or the ratio of total cholesterol to HDL-cholesterol with reference to published guidelines, local protocols or online risk calculators. These measurements are relatively simple and easily accessible 54.

In the psychiatric setting, it is often difficult to obtain an ECG as rapidly as in other acute medical settings. In less well economically developed countries, obtaining an ECG may be even more problematic. In these cases, whatever psychotropic a psychiatrist is intending to prescribe, patients should be asked about heart risks, such as family history of early cardiac death (i.e, <50 years in males and <55 years in females), personal history of a heart murmur, previous prescription of cardiac medications or anti-hypertensives, or if he/she has ever had an episode of simple syncope 51. Nevertheless, the measurement of ECG parameters as a baseline requirement deserves serious consideration. We propose that the ECG monitoring of patients with SMI has to be seen as a desired baseline parameter in order to assess the overall cardiac health status. As a general rule, we recommend that every patient should have an ECG measurement prior to the initiation of medication. Thereafter, depending on the advice given by a cardiologist, ECG monitoring can be repeated. A baseline ECG assessment is especially important in patients with clinical risk factors for arrhythmias, i.e., those with a family history of early cardiac death, personal history of a heart murmur, hypertension or diabetes, tachycardia at rest, irregular heart beats and fainting spells, particularly upon exertion.

Prolactin measurement

If possible, to have a reference value, prolactin levels should be measured in all patients at baseline. If too expensive, prolactin levels should only be measured in case sexual or reproductive system abnormalities are reported. Yet, these need to be asked about directly and monitored. Reproductive system abnormalities triggering prolactin level measurement include amenorrhea or oligomenorrhea (i.e, <9 periods per year), galactorrhea, gynecomastia in males, and/or breast tenderness and pain in females. Sexual dysfunction that should prompt prolactin measurement include new symptoms and/or those that coincided with antipsychotic treatment or dose change, including decreased libido, erectile or ejaculatory dysfunction, problems with arousal or orgasm. In these cases, prolactin should be measured every 3 months, especially when increasing the dose of known prolactin-elevating compounds. Although the clinician needs to be aware that laboratory ranges may differ between sites 75,76, in most laboratories normal prolactin values are set at 20 ng/ml (424 mIU/mL) for men and 25 ng/ml (530 mIU/L) for women 77. A complicating factor during measurement of prolactin levels is the presence of macroprolactin, which is essentially biologically inactive, but may lead to falsely high prolactin levels as measured by many assays 78. Conservative estimates suggest that the presence of macroprolactin leads to misdiagnosis in as many as 10% of all reported instances of biochemical hyperprolactinemia 79. In cases where measured prolactin is significantly raised, reporting of estimated monomeric prolactin instead of just “macroprolactin positive” can avoid unnecessary investigations.

With antipsychotic treatment, prolactin levels below 200 ng/ml and, mostly, below 100 ng/ml are most commonly observed. To date, the physiological relevance of these levels is unknown, unless hypogonadism (i.e., a state of markedly reduced sex hormone production) is the result, which has been associated with osteoporosis and fracture risk. The risk for breast cancer is much less clear. What seems to be certain is that any prolactin level that leads to hypogonadism should prompt a treatment change to a less prolactin elevating antipsychotic (e.g., quetiapine, aripiprazole or, in refractory patients, clozapine). Magnetic resonance imaging (MRI) of the sella turcica to rule out a prolactinoma should only be ordered after other reasons for prolactin elevation are excluded (e.g., chronic renal failure by assessing creatinine, hypothyroidism by assessing thyroid stimulating hormone, and pregnancy or oral contraception), if prolactin levels are above 200 ng/ml and do not decrease after a change to a lower risk agent, or if lateral visual deficits are observed, raising the suspicion of a prolactinoma 80.

Oral health

Although currently considered by many clinicians as not important, oral health needs to be scrutinized in the same way as other physical health problems 81,82. Risk factors for a poor oral health (e.g., smoking, medication side effects) and individual oral care needs should be assessed 83.

How and when to screen

Physical screening and monitoring programs are well accepted by patients and can be implemented in a variety of settings. Contrary to general belief, it is not difficult to motivate most patients to take part in the fasting blood assessments, and most are keen to getting and discussing the results of the evaluations 53,54.

Screening patients using an algorithm 84, monitoring form 85 or risk chart 65,86 is a simpler option than using the more complex and detailed guidelines previously published. Although, over recent years, both national and international groups have developed screening and monitoring guidelines 58,84,87,88,89,90,91,92,93,94,95, these seem not to be routinely implemented in the clinical care of patients 62,64,96,97.

Follow-up monitoring should be done at appropriate intervals 98 (Table (Table2).2). Physical health assessments should be recorded on charts showing the times and results of the assessments compared with reference ranges 54. During initial phases of treatment, it is important to measure weight weekly to identify patients who gain weight rapidly. Waterreus and Laugharne 84 advocate screening of all patients on any medication at baseline (to identify high-risk individuals and to ensure early detection of changes in metabolic parameters), and, at the minimum, every 3 months. Other guidelines propose screening and monitoring at baseline, 3 months, 12 months and annually, unless patients gain at least 7% of baseline body weight or are at increased risk for adverse health outcomes (e.g., family history of DM or early cardiac death, personal history of overweight or obesity, gestational DM, minority ethnicity, etc.).

Table 2
Table 2 Routine measurements for use in monitoring and evaluation of physical health in SMI patients with normal baseline values (according to 64,65 and 88)

If the patient has central obesity, hypertensive blood pressure (≥130/85 mm Hg), pre-diabetes (fasting plasma glucose =100-125 mg/dL or hemoglobin A1C =5.7-6.4%) or DM (fasting plasma glucose ≥126 mg/dL or hemoglobin A1C >6.4%), or marked dyslipidemia (total cholesterol >350 mg/dL; LDL-cholesterol >160 mg/dL; triglycerides >300 mg/dL), he/she should be referred to primary care provider to treat these conditions, unless simple healthy lifestyle guidance or behavioural adjustment and/or switching to a lower cardiometabolic risk medication can address these medical conditions adequately 17,99.


Many, but not all, individuals with SMI either are unaware of the need to change or do not possess the knowledge and skills required to make lifestyle changes. Psychiatrists, physicians, nurses and other members of the multidisciplinary team can help educate and motivate people with SMI to address their lifestyle, including smoking, diet and exercise, through the use of effective behavioural interventions 57,100. Patients with SMI, as well as their family and caregivers, should be taught about healthy lifestyles and should receive psychoeducational packages to facilitate them. Psychoeducation does not need to be administered by a specialist (e.g., a nutritionist), nor does it require special training, but should be administered by staff at the mental health clinic. Lifestyle advice and interventions can be obtained using resources already available within the local mainstream service 6. Patients should be provided positive feedback and support 17 and treatment must be tailored to meet the individual needs of SMI patients 14. Non-pharmacological interventions, incorporating dietary and physical activity modifications, demonstrated promise in terms of preventing weight gain in schizophrenia 94,95,96,97,98,99,100,101,102,103. The impact on one’s overall health, even with simple life style changes, is considerable (Table (Table3).3). A healthy diet, regular physical activity and quitting smoking are the key components of lowering the prevalence and impact of modifiable risk factors. However, if lifestyle interventions do not succeed, medication, including statins, anti-hypertensive therapy or antidiabetic agents, may be indicated. These drugs should be prescribed and managed as for the general population and are generally well tolerated 109,110. Moreover, pharmacologic treatments added to reduce antipsychotic-related weight can be tried. To date, most evidence exists for metformin (500 to 1000 mg bid with meals) or topiramate (50-200 mg in divided doses) 111.

Table 3
Table 3 Impact of various interventions on overall health (see 103, 104, 105, 106, 107, 108-108)


Many patients with SMI do not know the components of a healthy diet 46. It is commonly known that patients with schizophrenia have a diet higher in fat 111, higher in refined sugar 112, lower in fiber 25, and poor in fruits and vegetables 113. Therefore, nutrition education may be beneficial 46. Patients should be advised to avoid juices and soft drinks containing sugar and, even, artificial sweeteners, as well as high calorie, high fat, and nutritionally poor food, such as fast food and unhealthy snacks. The importance of consuming healthy alternatives, such as fresh fruit and vegetables, fish, and lean meats in a balanced way, should be stressed by clinicians whenever possible. Although educating patients (as well as their family and caregivers) about healthy food is recommended, patients need to understand that lifestyle changes should be gradual. Most people who experience rapid weight loss without gradual behaviour modifications will return to their previous weight. Losing weight hastily increases the likelihood of developing cholesterol gallstones. Further, many toxins are stored in fat tissue and a rapid weight loss may release those toxins too quickly 46.

Changes in dietary composition can have substantial effects. Weight loss has many health-related benefits that are of particular importance to SMI patients, including a reduction in risk of DM and CVD, reduction of serum triglycerides and LDL-cholesterol concentrations, increase in HDL-cholesterol concentrations, and reduction in blood glucose concentrations and hemoglobin A1c among patients with type 2 DM. However, interventions that address nutrition, weight management and physical activity have not become a routine part of psychiatric care 98. The psychiatrist can involve the individual with SMI in educational and psychosocial programs that address the issues of health and wellness, which can reduce medical comorbidities in this population. These programs, such as “The Healthy Living” program, the “Small Changes” strategy and the “Solutions for Wellness” program have been shown to be effective in people with SMI 114,115,116,117,118,119. Table Table44 gives some examples of behavioural interventions to improve the health of patients with SMI.

Table 4
Table 4 Examples of behavioural interventions to improve the health of patients with severe mental illness (see 5, 44, 99)

Physical activity

Physical inactivity is one of the risk factors that theoretically can most easily be addressed and modified in individuals with SMI 100. People with schizophrenia are significantly more sedentary than the general population 120. Only 25.7% of these patients meet the minimum public health recommendation of 150 min a week of at least moderate-intensity physical activity 121,122. According to the guidelines of the American College of Sports Medicine and the American Heart Association, moderate-intensity physical activity between 150 and 250 min a week will provide modest weight loss and is effective in preventing weight gain. Greater amounts of physical activity (>250 min a week) can be associated with clinically significant weight loss 108. Physical activity can improve metabolic health status even in the absence of weight loss. There is evidence that physical activity with or without diet counselling is feasible and effective in reducing weight and improving cardiometabolic risk profile in people with schizophrenia 123. However, in patients who are obese, physical exercise should be accompanied by proper diet to achieve significant weight loss. For example, if a patient walks for 1 hour per day, about 200 calories are burned. While this is beneficial in terms of cardiovascular health, this energy expenditure will not result in substantial weight loss. More strenuous physical activities, such as jogging, may be necessary 46. Considering all these facts, patients should be advised to engage in at least 30 minutes of moderately vigorous activity (at least a brisk walk) on most days of the week 65.


A meta-analysis of worldwide studies demonstrated that schizophrenic patients, compared with the general population, have a higher prevalence of ever smoking, heavy smoking and high nicotine dependence, as well as of risk factors that make them more vulnerable to start smoking 124. Up to 85% of individuals with SMI will die and/or have a reduced quality of life because of a tobacco-related disease 48,125. Cessation of smoking is associated with approximately a 50% decrease in the risk of coronary heart disease 104, and a 75% decrease in the risk of high/very high 10-year cardiovascular events 126. Therefore, SMI patients should be strongly encouraged to stop smoking.

However, smoking cessation has important implications for the management of patients taking clozapine and olanzapine. Abrupt cessation of smoking is associated with a potentially serious risk of toxicity in patients taking clozapine, while olanzapine levels can also increase significantly. Cormac et al 127 found that the percentage of patients with a plasma clozapine level ≥1000 µg/l increased from 4.2% to 41.7% within the six month period following the smoking ban despite dose reductions. Therefore, plasma clozapine levels must be monitored closely and adjustments made in dosage, if necessary, for at least six months after cessation 127. Moreover, smoking cessation also increases the short-term risk for DM. In a prospective study, adults who quit smoking experienced an increased risk for incident DM that peaked within 3 years of quitting (hazard ratio, HR=1.91) but was still observable 6 years after quitting. The increased risk seems to be partially mediated by weight gain: withdrawal of nicotine may lead to increased appetite and excess caloric intake. Therefore, clinicians should consider countermeasures (e.g., use of nicotine replacement therapy), especially for heavy smokers 128.

Treating tobacco dependence is effective in patients with SMI. There is emerging evidence that people with SMI can stop smoking 129,130,131,132. Moreover, treatments that work in the general population appear to be approximately equally effective in SMI patients. The evidence also suggests that treating tobacco dependence in SMI patients with stable psychiatric conditions does not worsen mental state 133. Finally, although staff from psychiatric hospitals often express concerns that adopting a smoke-free policy would have a negative impact on the hospital’s treatment milieu, this is not necessarily the case 134. Therefore, at a minimum, psychiatric professionals should assess tobacco use in all patients, advise all tobacco users to quit, assist patients in developing a quit plan, and arrange follow-up 100. If necessary and possible, patients can be referred to a smoking cessation service, which can offer behavioural counselling, nicotine replacement therapy or other pharmacological interventions 65.

Blood pressure

Target blood pressure levels of less than 130/85 mmHg are recommended. Lifestyle changes, such as stopping smoking, reducing salt intake, weight reduction and increased exercise, may be sufficient to reduce mildly elevated blood pressure, although some patients are likely to require pharmacological therapy 65. Recently updated European guidelines stress the importance of choosing anti-hypertensive agents best suited to the individual patient’s needs 86,135.

Oral health

Oral health advice, support and education should be provided to SMI patients, appropriate to their needs. Preventive and treatment programmes need to be tailored to meet the individual needs of patients with different diagnoses, severity and stages of mental illness. These should include dietary issues, smoking, and oral side effects of medication, namely dry mouth and carbohydrate craving. Advice on the dietary control of sugars and the importance of sugar free lubrication to relieve the symptoms of a dry mouth are essential to reduce the adverse oral side effects of some psychotropic drugs.

Psychiatrists should be made more aware of the importance of oral health habits. Therefore, training for clinicians in the identification of oral health risk factors such as smoking and of oral side effects of medication, and on proper oral hygiene techniques, is necessary 83. Above all, patients with SMI need encouragement and support to make regular use of dental services. Another option are regular visits by dental care personnel 136. The psychiatrist should search for dentists who do not stigmatize patients and who are willing to take care of this vulnerable population. On discharge from the hospital, procedures for ensuring continuity of dental care should be established. Formal training for the dental team regarding social and behavioural aspects of mental illness and oral medication side effects can be provided 79.

QTc prolongation and sudden cardiac death

AP or antidepressants (AD) known to be associated with QTc prolongation should not be prescribed for SMI patients with known heart disease, a personal history of syncope, a family history of sudden cardiac death at an early age (especially if both parents had sudden cardiac death), or congenital long QT syndrome (see 58). Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended in patients presenting with torsade de pointes 137.

Sexual health and pregnancy

Before beginning treatment, the SMI patient should be asked about symptoms possibly related to elevated prolactin, such as loss of libido, erectile and ejaculatory (dys)function or menstrual irregularities 54,58. If patients are receiving medications known to be associated with prolactin elevation, these baseline questions should be asked at every visit after starting the medication or until the dose is stable. When sexual dysfunction is identified, potential management strategies include decreasing the dose, switching to a prolactin-sparing medication, or specifically targeting sexual function by prescribing drugs such as dopamine agonists 138,139 or a partial agonist 140. Switching should be considered when prolactin elevation is persistently >50 ng/mL (>1000 mIU/L). When even a mildly elevated level persists for more than 3 months, dose reduction or switching to a prolactin-sparing medication should be considered. If a psychiatrist has any doubt regarding the cause of the raised prolactin, and levels are above 200 ng/ml, or the patient has symptoms suggestive of a cause other than medication-related hyperprolactinemia, then referral to an endocrinologist is recommended 141. Nevertheless, psychiatrists should also be aware that even minimal to moderate hyperprolactinemia can be the precursor of a serious underlying problem, such as a pituitary tumor 58.

Until there are more controlled prospective data on the impact of drugs on foetal and later development, the clinician will continue to work in a state of uncertainty, weighing partially estimated risks against managing individual clinical problems. On the basis of the available data, generalization is impossible and recommendations should be made on a drug-by-drug basis. The risks and benefits must always be carefully weighed for each patient on an individual basis. In general, the use of psychotropic medication during pregnancy is indicated when risk to the foetus from exposure to this medication is outweighed by the risks of untreated or exacerbated psychiatric illness in the mother 142. Women who require treatment should always discuss the risks and benefits of pharmacotherapy with their physician and, if it is felt that treatment should be continued during pregnancy, the available evidenced-based information will be of help in this important decision 143.

Importantly, advice on contraception and sexually transmitted infection prevention should also be given as part of routine mental health care 54.

Specific treatment advice on medication

Many psychiatrists are reluctant to switch medication, despite the presence of physical health issues 6. Nevertheless, consideration should be given to switching AP, AD and/or mood stabilizer medication when a SMI patient gains significant amount of weight (>5% of initial weight), or shows hyperglycemia, hyperlipidemia, or other significant adverse effects (e.g., clinically significant cardiometabolic side effects) during therapy. The switching protocol should, however, consider the entire psychiatric and physical condition of the patient and the pharmacological profiles of both agents 54. Another option is to add a pharmacological agent to reverse or prevent the medication-induced adverse event (e.g., metformin or topiramate to attenuate weight gain in patients taking AP) 111,144.

If DM or another severe physical illness has been diagnosed, the SMI patient should be referred to specialist services, including diabetology, endocrinology and cardiology, to receive the appropriate health care.


Our recommendations are organized at two levels of action: system level (state and health care institutions) and individual level (clinicians, patients, family) (Table (Table55).

Table 5
Table 5 Recommended system and individual level actions to address identified gaps in the assessment and treatment of physical health in patients with severe mental illness (SMI)

System level

• Designate the population with SMI as a health disparity population. There is still a significant lack of awareness of the physical health and health care access problems for people with SMI. Therefore, state and health care institutions first have to identify and designate people with SMI as a health disparity population before the problem can be handled appropriately. Psychiatrists can play an important role in this process of raised awareness by addressing the current disparity with policy makers and budget decision makers.

• Educate the health care community. National and local education initiatives should be implemented to disseminate information widely about physical health risks in persons with SMI and to encourage awareness of the current disparity.

• Train the health care community. In addition to educational initiatives, mental health care personnel also need to be trained in adequately assessing and measuring CVD health and other (e.g., oral) health risks. Training in SMI issues should be offered to primary care clinicians.

• Improve access to and care of physical health of the SMI population. State and health care institutions should improve access to and care of physical health of the SMI population to ensure prevention, screening, and treatment of general health care issues. They have to build adequate capacity to serve the physical health care needs of the SMI population.

• Reduce stigma and discrimination. Stigma is a widespread and well-documented major access barrier for people with SMI. It lessens the responsiveness of the health services and may cause people with SMI to delay or to avoid seeking treatment altogether 145. Education interventions and personal contact with persons with SMI can be used to reduce public stigma and discrimination 22. If necessary, anti-discrimination legislation should be enforced and initiatives be implemented to ensure equal access to health care.

• Bridge the collaboration gap between physical and mental health care and promote a policy of coordinated and integrated mental and physical health care for persons with SMI. The reintegration of psychiatric care and general somatic services, with an ultimate goal of providing optimal services to this vulnerable patient population, seems to represent the most important challenge for psychiatric care today 146,147.

• Address funding for these necessary service improvements. Raise and provide adequate funding for the educational campaigns, health assessment tools, and service integration. In developing countries this funding tends to be very low or nonexistent.

Individual level

• Take responsibility for the physical health of the SMI patient. Unless there is a clear provision of specific general somatic health care services for SMI patients, the psychiatrist should assume responsibility for the somatic health of his/her patients. He/she has to keep a check on the situation, as SMI patients may not seek help themselves until the problem is severe, or may not be aware of potentially harmful physical conditions until monitoring and education have been done.

• Screen the patient’s personal and family history at baseline to identify high-risk patients and to ensure early detection of changes in critical parameters. For patients with a personal or family history of obesity, high blood pressure, DM, heart disease or cerebrovascular accident, or with high or borderline values on metabolic criteria, drugs with lower risk of adverse effects should be chosen.

• Adopt ongoing surveillance methods. Surveillance of the overall health status of SMI patients should include continued monitoring of weight, BMI, WC, blood pressure, fasting plasma glucose, fasting lipids, smoking, physical inactivity, diet, oral and sexual health, as well as adverse effects of the used psychotropic medications.

• Use an algorithm, monitoring form, or risk chart during the patient’s screening. This is a simpler and better option than using the more complex and detailed published guidelines to monitor the physical health of the SMI patient.

• If weight gain (>5% of initial weight), glucose abnormalities, hyperlipidemia, or other adverse effects during therapy occur, consider switching to medications with lower risk profiles. Switching from higher to lower risk medications has been shown to reduce cardiovascular and endocrine risk factors 65, but needs to be done in a careful and informed way 148.

• Communicate monitoring findings to the primary care teams and specialist services, including diabetology, endocrinology and cardiology. Ensure that people with SMI who have been identified to be at risk of developing CVD and/or DM be appropriately managed. People with SMI who have established CVD and/or DM should be treated in primary care.

• Forge stronger collaborations with these medical specialists and other health care professionals. Coordinated and integrated physical care of patients with SMI has the greatest chance of improving their physical health care outcomes 53. These collaborations should seek to develop comprehensive educational efforts, aimed at improving the knowledge of primary care physicians about SMI patients, to reduce stigmatization and erroneous beliefs, as well as the knowledge of the psychiatrist, to better monitor and manage physical illness in SMI patients. Integrated care models should be developed. These include co-location of services (locating a primary health care team close to mental health services, with good links between primary care staff and mental health staff, is highly effective in improving the physical health of those with SMI), having staff from one service visit another on a regular basis, or appointing case managers to liaise between services and coordinate the overall care for the patient. Another option involves a multidisciplinary team of health workers including medical specialists, as well as psychiatrists 149.

• Include lifestyle modifications into education and treatment programs for SMI patients. Nutrition, exercise and behavioural strategies should be incorporated and tailored to the SMI population.

• Strive to encourage and improve the patient’s adherence to psychiatric, medical and behavioural interventions.

• Support wellness, personal empowerment and individual responsibility in patients with SMI, enabling them to make healthy choices for recovery, and promote their individual efforts. Specific programs (e.g., the Health and Recovery Peer Program) exist to help people with SMI to become more effective managers of their chronic illnesses, improving a range of self-management and health outcome measures, including patient activation and greater likelihood of using primary care medical services 150.

The adoption of these recommendations, summarized in Table Table5,5, across health care systems throughout the world (with adaptations based on specific local situations), will contribute to a significant improvement in the medical and related psychiatric health of patients with SMI. The improved physical health outcomes in SMI patients will benefit both patients and societies. This benefit will come from improving functioning, and reducing suffering and physical health care costs that arise from poorly screened and managed patients with advanced physical illnesses compounded on the presence and effects of psychiatric conditions. Even small changes in the monitoring and management of physical disorders that do not have to be costly can make a positive change in this generally underserved and disadvantaged patient group.


The production of this educational module is part of the WPA Action Plan 2008-2011 and has been supported by the Lugli Foundation, the Italian Society of Biological Psychiatry, Pfizer and Bristol Myers Squibb.


1. De Hert M, Correll CU, Cohen D. Physical illness in patients with severe mental disorders. I. Prevalence, impact of medications and disparities in health care. World Psychiatry. 2011;10:52–77. [PMC free article] [PubMed]
2. Lawrence D, Stephen K. Inequalities in health care provision for people with severe mental illness. J Psychopharmacol. in press.
3. De Hert M, Schreurs V, Vancampfort D. Metabolic syndrome in people with schizophrenia: a review. World Psychiatry. 2009;8:15–22. [PMC free article] [PubMed]
4. Bradford DW, Kim MM, Braxton LE. Access to medical care among persons with psychotic and major affective dis-orders. Psychiatr Serv. 2008;59:847–852. [PubMed]
5. Parks J, Svendsen D, Singer P, editors. Morbidity and mortality in people with serious mental illness. Alexandria: National Association of State Mental Health Program Directors (NASMHPD) Medical Directors Council; 2006.
6. Millar H. Management of physical health in schizophrenia: a stepping stone to treatment success. Eur Neuropsychopharmacol. 2008;18:S121–S128. [PubMed]
7. Fleischhacker WW, Cetkovich-Bakmas M, De Hert M. Comorbid somatic illnesses in patients with severe mental disorders: clinical, pol-icy, and research challenges. J Clin Psychiatry. 2008;69:514–519. [PubMed]
8. Essock SM, Miller AL, Buchanan RW. Physical health monitoring of patients with schizophrenia. Am J Psychiatry. 2004;161:1334–1349. [PubMed]
9. Bobes J, Alegría AA, Saiz-Gonzalez MD. Change in psychiatrists’ attitudes towards the physical health care of patients with schizophrenia coinciding with the dissemination of the Consensus on Physical Health in Patients with Schizophrenia. Eur Psychiatry. in press. [PubMed]
10. Maj M. Physical health in persons with severe mental illness: a public health and ethical priority. World Psychiatry. 2009;8:1–2. [PMC free article] [PubMed]
11. Saxena S, Sharan P, Garrido M. World Health Organization’s Mental Health Atlas 2005: implications for policy development. World Psychiatry. 2006;5:179–184. [PMC free article] [PubMed]
12. World Health Organization. Mental Health Atlas, revised version. Geneva: World Health Organization; 2005.
13. Phelan M, Stradins L, Morrison S. Physical health of people with severe mental illness. BMJ. 2001;322:443–444. [PMC free article] [PubMed]
14. Robson D, Gray R. Serious mental illness and physical health problems: a discussion pa-per. Int J Nurs Stud. 2007;44:457–466. [PubMed]
15. Colton CW, Manderscheid RW. Congruencies in increased mortality rates, years of potential life lost, and causes of death among public mental health clients in eight states. Prev Chronic Dis. 2006;3:A42–A42. [PMC free article] [PubMed]
16. Saraceno B, van Ommeren M, Batniji R. Barriers to improvement of mental health services in low-income and middle-income countries. Lancet. 2007;370:1164–1174. [PubMed]
17. Kane JM. Creating a health care team to manage chronic medical illnesses in patients with severe mental illness: the public policy perspective. J Clin Psychiatry. 2009;70:37–42. [PubMed]
18. Lambert TJ, Velakoulis D, Pantelis C. Medical comorbidity in schizophrenia. Med J Aust. 2003;178:S67–S70. [PubMed]
19. Zeber JE, McCarthy JF, Bauer MS. Datapoints: self-reported access to general medical and psychiatric care among veterans with bipolar disorder. Psychiatr Serv. 2007;58:740–740. [PubMed]
20. Cradock-O’Leary J, Young AS, Yano EM. Use of general medical services by VA patients with psychiatric disor-ders. Psychiatr Serv. 2002;53:874–878. [PubMed]
21. World Health Organization. Mental health and physical health: a call to action. The Mental and Physical Health Platform. Geneva: World Health Organization; 2003.
22. Thornicroft G, Alem A, Dos Santos RA. WPA guidance on steps, obstacles and mistakes to avoid in the implementation of community mental health care. World Psychiatry. 2010;9:67–77. [PMC free article] [PubMed]
23. Maj M. Mistakes to avoid in the implementation of community mental health care. World Psychiatry. 2010;9:65–66. [PMC free article] [PubMed]
24. Kendrick T. Cardiovascular and respiratory risk factors and symptoms among general prac-tice patients with long-term mental illness. Br J Psychiatry. 1996;169:733–739. [PubMed]
25. Brown S, Birtwistle J, Roe L. The unhealthy lifestyle of people with schizophrenia. Psychol Med. 1999;29:697–701. [PubMed]
26. Brown S, Inskip H, Barraclough B. Causes of the excess mortality of schizophrenia. Br J Psychiatry. 2000;177:212–217. [PubMed]
27. Hennekens CH. Increasing global burden of cardiovascular disease in general populations and patients with schizophrenia. J Clin Psychiatry. 2007;68:4–7. [PubMed]
28. Brugha TS, Wing JK, Smith BL. Physical health of the long-term mentally ill in the community. Is there unmet need? Br J Psychiatry. 1989;155:777–781. [PubMed]
29. Horvitz-Lennon M, Kilbourne AM, Pincus HA. From silos to bridges: meeting the general health care needs of adults with se-vere mental illnesses. Health Aff. 2006;25:659–669. [PubMed]
30. Jeste DV, Gladsjo JA, Lindamer LA. Medical comorbidity in schizophrenia. Schizophr Bull. 1996;22:413–430. [PubMed]
31. Goldman LS. Medical illness in patients with schizophrenia. J Clin Psychiatry. 1999;60:10–15. [PubMed]
32. Ananth J. Physical illness and psychiatric disorders. Compr Psychiatry. 1984;25:586–593. [PubMed]
33. Hennekens CH, Hennekens AR, Hollar D. Schizophrenia and increased risks of cardiovascular disease. Am Heart J. 2005;150:1115–1121. [PubMed]
34. Nasrallah HA, Meyer JM, Goff DC. Low rates of treatment for hypertension, dyslipidemia and diabetes in schizo-phrenia: data from the CATIE schizophrenia trial sample at baseline. Schizophr Res. 2006;86:15–22. [PubMed]
35. Goff DC, Sullivan LM, McEvoy JP. A comparison of ten-year cardiac risk estimates in schizophrenia patients from the CATIE study and matched controls. Schizophr Res. 2005;80:45–53. [PubMed]
36. Frayne SM, Halanych JH, Miller DR. Disparities in diabetes care: impact of mental illness. Arch Intern Med. 2005;165:2631–2638. [PubMed]
37. Druss BG, Bradford WD, Rosenheck RA. Quality of medical care and excess mortality in older patients with mental disor-ders. Arch Gen Psychiatry. 2001;58:565–572. [PubMed]
38. Druss BG, Rosenheck RA, Desai MM. Quality of preventive medical care for patients with mental disorders. Med Care. 2002;40:129–136. [PubMed]
39. Burns T, Cohen A. Item-of-service payments for general practitioner care of severely mentally ill persons: does the money matter? Br J Gen Pract. 1998;48:1415–1416. [PMC free article] [PubMed]
40. Paton C, Esop R, Young C. Obesity, dyslipidaemias and smoking in an inpatient population treated with an-tipsychotic drugs. Acta Psychiatr Scand. 2004;110:299–305. [PubMed]
41. Greening J. Physical health of patients in rehabilitation and recovery: a survey of case note records. Psychiatr Bull. 2005;29:210–212.
42. Lai DW, Chau SB. Effects of service barriers on health status of older Chinese immigrants in Can-ada. Soc Work. 2007;52:261–269. [PubMed]
43. Sernyak MJ. Implementation of monitoring and management guidelines for second-generation antipsychotics. J Clin Psychiatry. 2007;68:14–18. [PubMed]
44. Sokal J, Messias E, Dickerson FB. Comorbidity of medical illnesses among adults with serious mental illness who are receiving community psychiatric services. J Nerv Ment Dis. 2004;192:421–427. [PubMed]
45. Parks J, Radke AQ, editors. Obesity reduction and prevention strategies for individuals with serious mental ill-ness. Alexandria: National Association of State Mental Health Program Directors (NASMHPD) Medical Directors Council; 2008.
46. Fagiolini A, Goracci A. The effects of undertreated chronic medical illnesses in patients with severe mental disorders. J Clin Psychiatry. 2009;70:22–29. [PubMed]
47. Druss BG, von Esenwein SA, Compton MT. A randomized trial of medical care management for community mental health settings: the Primary Care Access, Referral, and Evaluation (PCARE) study. Am J Psychiatry. 2010;167:151–159. [PMC free article] [PubMed]
48. Vreeland B. Bridging the gap between mental and physical health: a multidisciplinary ap-proach. J Clin Psychiatry. 2007;68:26–33. [PubMed]
49. National Collaborating Centre for Mental Health Commissioned by the National Insti-tute for Health and Clinical Excellence. Schizophrenia. Core interventions in the treatment and management of schizophrenia in adults in primary and secondary care (update) www.guidance.nice.org.uk. [PubMed]
50. Saravane D, Feve B, Frances Y. Drawing up guidelines for the attendance of physical health of patients with se-vere mental illness. Encephale. 2009;35:330–339. [PubMed]
51. Kerwin R. Connecting patient needs with treatment management. Acta Psychiatr Scand. 2009;438:33–39. [PubMed]
52. Straker D, Correll CU, Kramer-Ginsberg E. Cost-effective screening for the metabolic syndrome in patients treated with second-generation antipsychotic medications. Am J Psychiatry. 2005;162:1217–1221. [PubMed]
53. De Hert M, van Winkel R, Silic A. Physical health management in psychiatric settings. Eur Psychiatry. 2010;25:S22–S28. [PubMed]
54. Heald A, Montejo AL, Millar H. Management of physical health in patients with schizophrenia: practical recom-mendations. Eur Psychiatry. 2010;25:S41–S45. [PubMed]
55. Correll CU, Manu P, Olshanskiy V. Cardiometabolic risk of second-generation antipsychotic medications during first-time use in children and adolescents. JAMA. 2009;302:1765–1773. [PMC free article] [PubMed]
56. De Hert M, Dobbelaere M, Sheridan EM. Metabolic and endocrine adverse effects of second-generation antipsychotics in children and adolescents: a systematic review of randomized, placebo controlled trials and guidelines for clinical practice. Eur Psychiatry. in press. [PubMed]
57. Hasnain M, Fredrickson SK, Vieweg WV. Metabolic syndrome associated with schizophrenia and atypical antipsychot-ics. Curr Diab Rep. 2010;10:209–216. [PubMed]
58. Marder SR, Essock SM, Miller AL. Physical health monitoring of patients with schizophrenia. Am J Psychiatry. 2004;161:1334–1349. [PubMed]
59. Wagenknecht LE, Langefeld CD, Scherzinger AL. Insulin sensitivity, insulin secretion, and abdominal fat: the Insulin Resistance Atherosclerosis Study (IRAS) Family Study. Diabetes. 2003;52:2490–2496. [PubMed]
60. de Vegt F, Dekker JM, Jager A. Relation of impaired fasting and postload glucose with incident type 2 diabetes in a Dutch population: the Hoorn Study. JAMA. 2001;285:2109–2113. [PubMed]
61. Wahrenberg H, Hertel K, Leijonhufvud BM. Use of waist circumference to predict insulin resistance: retrospective study. BMJ. 2005;330:1363–1364. [PMC free article] [PubMed]
62. Newcomer JW, Nasrallah HA, Loebel AD. The Atypical Antipsychotic Therapy and Metabolic Issues National Survey: prac-tice patterns and knowledge of psychiatrists. J Clin Psychopharmacol. 2004;24:S1–S6. [PubMed]
63. Barnes TR, Paton C, Cavanagh MR. A UK audit of screening for the metabolic side effects of antipsychotics in com-munity patients. Schizophr Bull. 2007;33:1397–1403. [PMC free article] [PubMed]
64. Mackin P, Bishop DR, Watkinson HM. A prospective study of monitoring practices for metabolic disease in antipsy-chotic-treated community psychiatric patients. BMC Psychiatry. 2007;7:28–28. [PMC free article] [PubMed]
65. De Hert M, Dekker JM, Wood D. Cardiovascular disease and diabetes in people with severe mental illness. Posi-tion statement from the European Psychiatric Association (EPA), supported by the European Association for the Study of Diabetes (EASD) and the European Society of Cardiology (ESC) Eur Psychiatry. 2009;24:412–424. [PubMed]
66. Alberti KG, Eckel RH, Grundy SM. Harmonizing the metabolic syndrome: a joint interim statement of the Interna-tional Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–1645. [PubMed]
67. Chobanian AV, Bakris GL, Black HR. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560–2572. [PubMed]
68. Mackin P. Cardiac side effects of psychiatric drugs. Hum Psychopharmacol. 2008;23:3–14. [PubMed]
69. International Expert Committee. International Expert Committee report on the role of the A1C assay in the diag-nosis of diabetes. Diabetes Care. 2009;32:1327–1334. [PMC free article] [PubMed]
70. Hanssens L, De Hert M, Van Eyck D. Usefulness of glycosylated haemoglobin (HbA1c) to screen for diabetes in pa-tients with schizophrenia. Schizophr Res. 2006;85:296–297. [PubMed]
71. De Beer K, Michael S, Thacker M. Diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome – clinical guidelines. Nurs Crit Care. 2008;13:5–11. [PubMed]
72. Silversides JA, Farling PA. Diabetic ketoacidosis guidelines and protection from aspiration pneumoni-tis. Diabet Med. 2009;26:829–829. [PubMed]
73. Charles RA, Bee YM, Eng PH. Point-of-care blood ketone testing: screening for diabetic ketoacidosis at the emergency department. Singapore Med J. 2007;48:986–989. [PubMed]
74. Wilson JF. In clinic. Diabetic ketoacidosis. Ann Intern Med. 2010;152:ITC1/1-15. [PubMed]
75. Peuskens J, Pani L, De Hert M. Antipsychotics and hyperprolactinemia. Unpublished paper
76. Peveler RC, Branford D, Citrome L. Antipsychotics and hyperprolactinaemia: clinical recommendations. J Psychopharmacol. 2008;22:98–103. [PubMed]
77. Emiliano AB, Fudge JL. From galactorrhea to osteopenia: rethinking serotonin-prolactin interac-tions. Neuropsychopharmacology. 2004;29:833–846. [PubMed]
78. Bushe C, Yeomans D, Floyd T. Categorical prevalence and severity of hyperprolactinaemia in two UK cohorts of patients with severe mental illness during treatment with antipsychotics. J Psychopharmacol. 2008;22:56–62. [PubMed]
79. Tschoner A, Engl J, Rettenbacher MA. Is second-generation antipsychotic-induced hyperprolactinemia due to biologi-cally active prolactin or to biologically inactive macroprolactin? Results from a prospective study. J Clin Psychiatry. 2009;70:293–294. [PubMed]
80. Correll CU, Carlson HE. Endocrine and metabolic adverse effects of psychotropic medications in children and adolescents. J Am Acad Child Adolesc Psychiatry. 2006;45:771–791. [PubMed]
81. Persson K, Axtelius B, Söderfeldt B. Oral health-related quality of life and dental status in an outpatient psychiatric population: a multivariate approach. Int J Ment Health Nurs. 2010;19:62–70. [PubMed]
82. Nielsen J, Munk-Jørgensen P, Skadhede S. Determinants of poor dental care in patients with schizophrenia: a historical, pro-spective database study. J Clin Psychiatry. in press. [PubMed]
83. British Society for Disability and Oral Health. Oral health care for people with mental health problems – guidelines and recom-mendations. www.bsdh.org.uk.
84. Waterreus AJ, Laugharne JD. Screening for the metabolic syndrome in patients receiving antipsychotic treat-ment: a proposed algorithm. Med J Aust. 2009;190:185–189. [PubMed]
85. Castle D, Lambert T, Melbourne S. A clinical monitoring system for clozapine. Australas Psychiatry. 2006;14:156–168. [PubMed]
86. Graham I, Atar D, Borch-Johnsen K. European guidelines on cardiovascular disease prevention in clinical practice: full text. Eur J Cardiovasc Prev Rehabil. 2007;14:S1–S113. [PubMed]
87. Allison DB, Newcomer JW, Dunn AL. Obesity among those with mental disorders: a National Institute of Mental Health meeting report. Am J Prev Med. 2009;36:341–350. [PubMed]
88. van Winkel R, De Hert M, Van Eyck D. Screening for diabetes and other metabolic abnormalities in patients with schizophrenia and schizoaffective disorder: evaluation of incidence and screening meth-ods. J Clin Psychiatry. 2006;67:1493–1500. [PubMed]
89. Barnett AH, Mackin P, Chaudhry I. Minimising metabolic and cardiovascular risk in schizophrenia: diabetes, obesity and dyslipidaemia. J Psychopharmacol. 2007;21:357–373. [PubMed]
90. Cahn W, Ramlal D, Bruggeman R. Prevention and treatment of somatic complications arising from the use of antip-sychotics. Tijdschr Psychiatr. 2008;50:579–591. [PubMed]
91. Citrome L, Yeomans D. Do guidelines for severe mental illness promote physical health and well-being? J Psychopharmacol. 2005;19:102–109. [PubMed]
92. Cohn TA, Sernyak MJ. Metabolic monitoring for patients treated with antipsychotic medications. Can J Psychiatry. 2006;51:492–501. [PubMed]
93. De Hert M, van Eyck D, De Nayer A. Metabolic abnormalities associated with second generation antipsychotics: fact or fiction? Development of guidelines for screening and monitoring. Int Clin Psychopharmacol. 2006;21:11–15. [PubMed]
94. De Nayer A, De Hert M, Scheen A. Belgian consensus on metabolic problems associated with atypical antipsychot-ics. Int J Clin Pract. 2005;9:130–137.
95. Sáiz Ruiz J, Bobes García J, Vallejo Ruiloba J. Consensus on physical health of patients with schizophrenia from the Spanish Societies of Psychiatry and Biological Psychiatry. Actas Esp Psiquiatr. 2008;36:251–264. [PubMed]
96. Buckley PF, Miller DD, Singer B. Clinicians’ recognition of the metabolic adverse effects of antipsychotic medica-tions. Schizo-phr Res. 2005;79:281–288. [PubMed]
97. Haupt DW, Rosenblatt LC, Kim E. Prevalence and predictors of lipid and glucose monitoring in commercially in-sured patients treated with second-generation antipsychotic agents. Am J Psychiatry. 2009;166:345–353. [PubMed]
98. American Diabetes Association. American Psychiatric Association; American Association of Clinical Endocri-nologists; North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27:596–601. [PubMed]
99. International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. www.idf.org.
100. Vreeland B. Treatment decisions in major mental illness: weighing the outcomes. J Clin Psychiatry. 2007;68:5–11. [PubMed]
101. Faulkner G, Cohn T, Remington G. Interventions to reduce weight gain in schizophrenia. Schizophr Bull. 2007;33:654–656. [PMC free article] [PubMed]
102. Faulkner G, Cohn T, Remington G. Interventions to reduce weight gain in schizophrenia. Cochrane Database Syst Rev. 2007;1:CD005148. [PMC free article] [PubMed]
103. Alvarez-Jiménez M, Hetrick SE, González-Blanch C. Non-pharmacological management of antipsychotic-induced weight gain: sys-tematic review and meta-analysis of randomised controlled trials. Br J Psychiatry. 2008;193:101–107. [PubMed]
104. Hennekens CH. Increasing burden of cardiovascular disease: current knowledge and future di-rections for research on risk factors. Circulation. 1998;97:1095–1102. [PubMed]
105. Rich-Edwards JW, Manson JE, Hennekens CH. The primary prevention of coronary heart disease in women. N Engl J Med. 1995;332:1758–1766. [PubMed]
106. Bassuk SS, Manson JE. Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. J Appl Physiol. 2005;99:1193–1204. [PubMed]
107. Brock CM, King DS, Wofford MR. Exercise, insulin resistance, and hypertension: a complex relationship. Metab Syndr Relat Disord. 2005;3:60–65. [PubMed]
108. Donnelly JE, Blair SN, Jakicic JM. American College of Sports Medicine Position Stand. Appropriate physical activ-ity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc. 2009;41:459–471. [PubMed]
109. Cormac I. Promoting healthy lifestyles in psychiatric services. In: Physical heath in mental health. Final report of a scoping group. Royal College of Psychiatrists. 2009:62–70.
110. Laurent SM, Simons AD. Sexual dysfunction in depression and anxiety: conceptualizing sexual dysfunc-tion as part of an internalizing dimension. Clin Psychol Rev. 2009;29:573–585. [PubMed]
111. Maayan L, Correll CU. Management of antipsychotic-related weight gain. Expert Rev Neurother. 2010;10:1175–1200. [PMC free article] [PubMed]
112. Ryan MC, Collins P, Thakore JH. Impaired fasting glucose tolerance in first-episode, drug-naive patients with schizophrenia. Am J Psychiatry. 2003;160:284–289. [PubMed]
113. Stokes C, Peet M. Dietary sugar and polyunsaturated fatty acid consumption as predictors of se-verity of schizophrenia symptoms. Nutr Neurosci. 2004;7:247–249. [PubMed]
114. McCreadie RG. Scottish Schizophrenia Lifestyle Group. Diet, smoking and cardiovascular risk in people with schizophrenia: descriptive study. Br J Psychiatry. 2003;183:534–539. [PubMed]
115. Menza M, Vreeland B, Minsky S. Managing atypical antipsychotic-associated weight gain: 12-month data on a multimodal weight control program. J Clin Psychiatry. 2004;65:471–477. [PubMed]
116. Vreeland B, Minsky S, Menza M. A program for managing weight gain associated with atypical antipsychot-ics. Psychiatr Serv. 2003;54:1155–1157. [PubMed]
117. Gabriele JM, Dubbert PM, Reeves RR. Efficacy of behavioral interventions in managing atypical antipsychotic weight gain. Obes Rev. 2009;10:442–455. [PubMed]
118. Hill JO, Peters JC, Catenacci VA. International strategies to address obesity. Obes Rev. 2008;9:41–47. [PubMed]
119. Hill JO, Wyatt HR. Small changes: a big idea for addressing obesity. Obes Manage. 2006;2:227–331.
120. Roick C, Fritz-Wieacker A, Matschinger H. Health habits of patients with schizophrenia. Soc Psychiatry Psychiatr Epidemiol. 2007;42:268–276. [PubMed]
121. Faulkner G, Cohn T, Remington G. Validation of a physical activity assessment tool for individuals with schizophre-nia. Schizophr Res. 2006;82:225–231. [PubMed]
122. US Department of Health and Human Services. Physical activity guidelines for Americans. Washington: US Department of Health and Human Services; 2008.
123. Vancampfort D, Knapen J, De Hert M. Cardiometabolic effects of physical activity interventions for people with schizo-phrenia. Phys Ther Rev. 2009;14:388–398.
124. De Leon J, Diaz FJ. A meta-analysis of worldwide studies demonstrates an association between schizophrenia and tobacco smoking behaviors. Schizophr Res. 2005;76:135–157. [PubMed]
125. Garcia-Portilla MP, Saiz PA, Benabarre A. Impact of substance use on the physical health of patients with bipolar disor-der. Acta Psychiatr Scand. 2010;121:437–445. [PubMed]
126. Bobes J, Arango C, Garcia-Garcia M. Healthy lifestyle habits and 10-year cardiovascular risk in schizophrenia spec-trum disorders: an analysis of the impact of smoking tobacco in the CLAMORS schizophrenia cohort. Schizophr Res. 2010;119:101–109. [PubMed]
127. Cormac I, Brown A, Creasey S. A retrospective evaluation of the impact of total smoking cessation on psychiat-ric inpatients taking clozapine. Acta Psychiatr Scand. 2010;121:393–397. [PubMed]
128. Yeh HC, Duncan BB, Schmidt MI. Smoking, smoking cessation, and risk for type 2 diabetes mellitus: a cohort study. Ann Intern Med. 2010;152:10–17. [PubMed]
129. Addington J, el-Guebaly N, Campbell W. Smoking cessation treatment for patients with schizophrenia. Am J Psychiatry. 1998;155:974–976. [PubMed]
130. George TP, Ziedonis DM, Feingold A. Nicotine transdermal patch and atypical antipsychotic medications for smoking cessation in schizophrenia. Am J Psychiatry. 2000;157:1835–1842. [PubMed]
131. Weiner E, Ball MP, Summerfelt A. Effects of sustained-release bupropion and supportive group therapy on ciga-rette consumption in patients with schizophrenia. Am J Psychiatry. 2001;158:635–637. [PubMed]
132. George TP, Vessicchio JC, Termine A. A placebo controlled trial of bupropion for smoking cessation in schizophre-nia. Biol Psychiatry. 2002;52:53–61. [PubMed]
133. Banham L, Gilbody S. Smoking cessation in severe mental illness: what works? Addiction. 2010;105:1176–1189. [PubMed]
134. Hollen V, Ortiz G, Schacht L. Effects of adopting a smoke-free policy in state psychiatric hospitals. Psychiatr Serv. 2010;61:899–904. [PubMed]
135. Mansia G, De Backer G, Dominiczak A. 2007 ESH-ESC Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hyperten-sion (ESH) and of the European Society of Cardiology (ESC) Blood Press. 2007;16:135–232. [PubMed]
136. Shaw MJ, Shaw L. The effectiveness of differing dental health education programmes in improving the oral health of adults with mental handicaps attending Birmingham adult training cen-tres. Commun Dent Health. 1991;8:139–145. [PubMed]
137. European Heart Rhythm Association. Heart Rhythm Society, Zipes DP et al. ACC/AHA/ESC 2006 guidelines for man-agement of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol. 2006;48 [PubMed]
138. Baggaley M. Sexual dysfunction in schizophrenia: focus on recent evidence. Hum Psychopharmacol. 2008;23:201–209. [PubMed]
139. Molitch ME. Medication-induced hyperprolactinemia. Mayo Clin Proc. 2005;80:1050–1057. [PubMed]
140. Shim JC, Shin JG, Kelly DL. Adjunctive treatment with a dopamine partial agonist, aripiprazole, for antipsy-chotic-induced hyperprolactinemia: a placebo-controlled trial. Am J Psychiatry. 2007;164:1404–1410. [PubMed]
141. Walters J, Jones I. Clinical questions and uncertainty – prolactin measurement in patients with schizophrenia and bipolar disorder. J Psychopharmacol. 2008;22:82–89. [PubMed]
142. Trixler M, Gáti A, Fekete S. Use of antipsychotics in the management of schizophrenia during preg-nancy. Drugs. 2005;65:1193–1206. [PubMed]
143. Einarson A, Boskovic R. Use and safety of antipsychotic drugs during pregnancy. J Psychiatr Pract. 2009;15:183–192. [PubMed]
144. Miller LJ. Management of atypical antipsychotic drug-induced weight gain: focus on met-formin. Pharmacotherapy. 2009;29:725–735. [PubMed]
145. Corrigan PW, Larson JE, Rüsch N. Self-stigma and the “why try” effect: impact on life goals and evidence-based practices. World Psychiatry. 2009;8:75–81. [PMC free article] [PubMed]
146. Craddock N, Craddock B. Patients must be able to derive maximum benefit from a psychiatrist’s medical skills and broad training. World Psychiatry. 2010;9:30–31. [PMC free article] [PubMed]
147. Hollins S. Bridging a cultural divide within medicine: a role for psychiatrists? World Psychiatry. 2010;9:32–33. [PMC free article] [PubMed]
148. Correll CU. From receptor pharmacology to improved outcomes: individualizing the selec-tion, dosing, and switching of antipsychotics. Eur Psychiatry. 2010;25:S12–S21. [PubMed]
149. Millar H. Development of a health screening clinic. Eur Psychiatry. 2010;25:S29–S33. [PubMed]
150. Druss BG, Zhao L, von Esenwein SA. The Health and Recovery Peer (HARP) Program: a peer-led intervention to im-prove medical self-management for persons with serious mental illness. Schizophr Res. 2010;118:264–270. [PMC free article] [PubMed]

Articles from World Psychiatry are provided here courtesy of The World Psychiatric Association
PubReader format: click here to try


Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...


  • MedGen
    Related information in MedGen
  • PubMed
    PubMed citations for these articles

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...