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Medscape J Med. 2008; 10(8): 189.
Published online Aug 12, 2008.
PMCID: PMC2562148

Soft Drinks and Weight Gain: How Strong Is the Link?

Abstract

Context

Soft drink consumption in the United States has tripled in recent decades, paralleling the dramatic increases in obesity prevalence. The purpose of this clinical review is to evaluate the extent to which current scientific evidence supports a causal link between sugar-sweetened soft drink consumption and weight gain.

Evidence acquisition

MEDLINE search of articles published in all languages between 1966 and December 2006 containing key words or medical subheadings, such as “soft drinks” and “weight.” Additional articles were obtained by reviewing references of retrieved articles, including a recent systematic review. All reports with cross-sectional, prospective cohort, or clinical trial data in humans were considered.

Evidence synthesis

Six of 15 cross-sectional and 6 of 10 prospective cohort studies identified statistically significant associations between soft drink consumption and increased body weight. There were 5 clinical trials; the two that involved adolescents indicated that efforts to reduce sugar-sweetened soft drinks slowed weight gain. In adults, 3 small experimental studies suggested that consumption of sugar-sweetened soft drinks caused weight gain; however, no trial in adults was longer than 10 weeks or included more than 41 participants. No trial reported the effects on lipids.

Conclusions

Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.

Introduction

It is well known that obesity has become a national epidemic in the United States, and it is now estimated that more than 65% of US adults are either overweight or obese.[1] Obesity has been linked to numerous serious health problems, including cardiovascular disease, type 2 diabetes, and some types of cancers.[2]

Over the past several decades, an increase in the consumption of sugar-sweetened soft drinks has paralleled this increase in obesity.[3] Mean per capita sugar-sweetened soft drink consumption now averages approximately 12 oz per day – a 3-fold increase over the past 3 decades. Approximately 73% of adolescent boys and 62% of adolescent girls consume carbonated soft drinks (mostly sugar-sweetened) on any given day.[4]

The majority of the 15 relevant cross-sectional studies and 10 relevant prospective cohort studies have found an adverse association between sugar-sweetened soft drink consumption and body weight.[5] However, the specific effects of sugar-sweetened soft drinks on body weight and cardiovascular risk factors have not been sufficiently documented due to a paucity of clinical trial evidence. In adults, only 3 small trials are relevant.[68] In adolescents, 2 clinical trials indicated that efforts to replace sugar-sweetened soft drinks with noncaloric beverages slow weight gain.[9,10]

The purpose of this article is to review data on soft drink consumption and marketing trends and to summarize the results of observational and intervention studies that evaluated the relationship between soft drink consumption and body weight.

Soft Drink Consumption and Marketing Trends

The United States has experienced dramatic increases in soft drink consumption over the past few decades, largely due to economic and societal forces encouraging this behavior. In 2004, Americans spent $66 billion on carbonated drinks, and the soft drink industry produced approximately 52 gallons per year of sugar-sweetened and “diet” soda – or 18 oz per day – for every man, woman, and child in the United States.[11] In 1942, the US annual production of carbonated drinks was approximately 2 oz per person per day,[11] such that in the last 6 decades, per capita soda production has increased nearly 10-fold. The proportion of persons of every age consuming soft drinks has increased over the past 20 years, as have portion sizes of soft drinks and the number of servings consumed.[12] Between 1977 and 2001, Americans increased total energy from soft drinks from 2.8% of energy to 7.0% of energy, which translates into almost tripling of calories per day (from 50 kcal to 144 kcal).[12] During this time period, soft drink intake also increased from 4.1% to 9.8% of energy for 19- to 39-year olds, the group that consumed the highest levels of caloric beverages and soft drinks.[12]

Soft drinks are aggressively marketed, and 2 companies – Coca-Cola and PepsiCo – dominate sales in the United States. In 1999, Coca-Cola held a 44% market share worth $7.5 billion in sales, whereas PepsiCo held a roughly 30% share of the US market.[11] In 2004, Coca-Cola spent $2.2 billion on global promotions and sold $22 billion worth of beverages in the same year.[11] Coca-Cola sells its soft drinks in the United States at 2 million stores, at more than 450,000 restaurants, and from 1.4 million vending machines and coolers. Industry-wide, in 2000, 3 million soft drink vending machines dispensed about one seventh of all soft drinks sold.[11]

High-fructose corn syrup is the principal sweetener for regular soft drinks. In 1970, high-fructose corn syrup represented < 1% of all caloric sweeteners available for consumption in the United States, but in the 1980s, the high-fructose corn syrup market jumped rapidly as the soft drink industry began to use this inexpensive, sweet corn-based syrup instead of sucrose. Due to the low cost of the sweetener, which consists of 55% fructose, 42% glucose, and 3% other sweeteners, it made it profitable to replace sucrose with high-fructose corn syrup, and by 2000 it represented 42.0% of all added caloric sweeteners in the American diet.[13,14] Today, sugar-sweetened beverages consist of 7% to 14% added sweeteners, which are most often high-fructose corn syrup, and soft drinks are the largest source of added sweeteners, accounting for one third of the added sugar intake in the American diet.[14] Total consumption of fructose has increased by 30% in the United States over the past 30 years.[13] From 1970 to 1997, annual per capita intake of high-fructose corn syrup increased from 0.5 lb to 62.4 lb.[3] The increase in high-fructose corn syrup consumption over the past several decades exceeds the increase in intake of any other food or food group during that time. High-fructose corn syrup is now used not only in sweetening carbonated beverages, but also baked goods, candies, salad dressings, and other processed foods.[3]

Observational Studies

As reported in a recent systematic review, 15 cross-sectional studies are relevant in the evaluation of the relationship between soft drink consumption and body weight.[5] Of the 15 cross-sectional studies, 13 were in children or adolescents, of which 9 found positive associations (6 significant,[1520] 3 not statistically significant[2123]); 3 found no association[2426]; and 1 found mixed results.[27] In adults, both cross-sectional studies found positive associations.[28,29] A major limitation of such cross-sectional studies is the uncertainty of temporal relationships. For example, body weight may affect beverage selection, and vice versa. If a substantial proportion of obese adults chose diet drinks as a weight loss strategy, it could mask a true causal relationship. Also, a cross-sectional design cannot be used to carefully link changes in soft drink to changes in body weight.

Ten prospective cohort studies are relevant. Of these, 6 were in children or adolescents; 4 of those found significant positive associations,[17, 3032] and 2 studies with limited statistical power found nonsignificant associations.[33,34] In adults, all 4 found positive associations,[28, 3537] but only 2 were statistically significant.[35,37] Examples are summarized below.

Ludwig and colleagues,[30] in a 19-month prospective longitudinal study of 548 school-aged children, examined the relationship between sweetened beverage consumption and body mass index (BMI) at baseline and then 19 months later. They found that for each additional 12-oz serving of sugar-sweetened beverage consumed, the BMI increased (mean 0.24 kg/m2; 95% CI 0.10-0.39; p=0.03) and the odds of obesity increased (odds ratio [OR] 1.60; 95% confidence interval [CI], 1.14-2.2.4; P = .02). Although this study did find a significant positive relationship between consumption of sugar-sweetened beverages and BMI changes, many of the outcomes of the study were based on self-reports, such as height, weight, physical activity, dietary intake, and sweetened beverage consumption.

Schulze and colleagues,[35] using longitudinal data from the Nurses Health Study II (1991-1999 data), showed that a higher consumption of sugar-sweetened beverages was associated with an increase in weight and an increased risk of developing type 2 diabetes among women. Over a 4-year period, weight gain was highest among women who increased their sugar-sweetened soft drink consumption from 1 or less drinks per week to 1 or more drinks per day (multivariate-adjusted means, +4.69 kg for 1991 and +4.20 kg for 1995 through 1999). After adjusting for potential confounders, women who consumed 1 or more sugar-sweetened soft drinks per day also had a relative risk for type 2 diabetes of 1.83 (95% CI, 1.42-2.36; P < .001) compared with those who consumed less than 1 sugar-sweetened soft drink per month.

Berkey and coworkers[17] conducted a prospective cohort study that included 11,654 9- to 14-year-old boys and girls participating in the US Growing Up Today Study. After adjustment for potential confounders, the study found that each additional 12-oz serving of sugar-sweetened beverage intake predicted a 4% increase in BMI for boys and a 3% increase in girls over 3 years. Boys gained 0.10 kg/m2 for 1 sweetened beverage serving and 0.14 kg/m2 for 2 or more servings, whereas girls gained 0.07 kg/m2 for each sweetened beverage serving added and 0.10 kg/m2 for 2 or more servings.

Welsh and colleagues,[32] in a cohort study spanning 2 years, examined the association between soft drink consumption and overweight at follow-up among 10,904 children aged 2 and 3 years. They found that in children who were overweight or at risk for overweight at baseline, those in the upper 3 quartiles of soft drink consumption were approximately twice as likely to be overweight at follow-up, compared with those in the lower quartile of soft drink consumption.

Newby and colleagues[33] studied dietary data of 1345 2- to 5-year-old children in a prospective, longitudinal study over 8 months and found that weight change was not significantly related to intakes (per ounce) of sweetened beverage consumption (Beta = -0.01, SE = 0.02; P = .50). Additionally, they found no association between BMI and drinks, such as milk or fruit juice, that were consumed in larger quantities. Possible underreporting of “unhealthy” beverage consumption by parent reporters is a potential limitation of this and other similar studies.

Blum and coworkers,[34] in a study of 166 third- through fifth-grade children over 2 years, examined changes in sweetened beverage consumption and changes in BMI z scores. They observed that children who were overweight actually increased their consumption of diet soft drinks, not sugar-sweetened soft drinks. Study limitations included a very small sample size, lack of nonwhites, and self-reported intake data.

Intervention Studies

Five published clinical trials examined the relationship between soft drink consumption and body weight: 2 in children or adolescents[9,10] and 3 in adults.[68] Designs differ markedly.

James and colleagues,[10] in a cluster-randomized controlled trial (n = 644; 29 clusters), found that a school-based educational program achieved a modest reduction in soft drink consumption. At 12 months the incidence of overweight and obese children increased 7.5% in the control group, and decreased 0.2% in the intervention group (mean difference, 7.7%; 95% CI, 2.2% to 13.1%).[10]

Ebbeling and coworkers[9] randomized 103 adolescents – who regularly consumed sugary soft drinks – to receive home delivery of noncaloric beverages or not. At 25 weeks, the control group had no change in beverage consumption habits, and the intervention group had an 82% decrease in sweetened beverage consumption. BMI increased 0.21 units in the control group and 0.07 in the treatment group (overall treatment effect, -0.14 BMI units; -0.75 + 0.34 units in highest tertile baseline BMI).[9]

Raben and coworkers[8] randomized 41 overweight adults to receive 10 weeks of soda and solid foods sweetened with either aspartame or 150 g sucrose. The aspartame group lost 1.0 kg, and the sucrose group gained 1.6 kg (treatment effect, 2.6 kg; 95% CI, 1.3-3.8). Sixty percent of the treatment effect was due to body fat changes.[8]

Tordoff and Alleva,[7] in a crossover trial with 30 normal-weight adults, provided 1.15 L/day soda sweetened with either high-fructose corn syrup or aspartame, or no soda, for 3 weeks each in random order. Relative to no soda, in women (n = 9) regular soda was significantly (P < .01) associated with 0.97 + 0.25 kg weight gain, and no weight change with aspartame soda. In men (n = 21) regular soda was not associated with weight change, whereas a 0.25 + 0.29 kg weight loss was significantly associated (P < .05) with aspartame soda.[7]

DiMeglio and Mattes,[6] in a crossover trial with 15 normal-weight adults, provided 450 calories of regular soda (1 L) or jelly beans in random order for 4 weeks each (with 4-week washout between). During the jelly bean phase, total caloric intake was unchanged from baseline, but during the soda phase, total caloric intake was increased by the amount of soda, plus a little more. BMI increased during the liquid phase only (P < .05). These results provide evidence that caloric intake from sugar-sweetened soda is not compensated for by a reduction in usual caloric intake.[6]

Mechanisms by Which Soft Drinks May Promote Obesity and Related Diseases

There are 4 main mechanisms by which soft drinks may promote obesity and cardiovascular risk factors: direct caloric increases, appetite stimulation, adverse metabolic effects of high-fructose corn syrup consumption, and replacement of milk and other beneficial dietary intake.

Sugar-sweetened soft drinks typically contain 140-150 calories per 12-oz serving. If normal dietary intake decreased by an equivalent amount of calories per serving, then weight change would not be expected. However, as noted above, DiMeglio and Mattes[6] found that there was no decrease in usual dietary intake in response to 450 calories per day from sucrose-sweetened soda. (The daily caloric intake was equal to baseline intake plus the caloric intake attributed to the soda.) In the same study subjects, a solid sucrose supplement in the form of jelly beans was associated with a caloric reduction from baseline dietary intake that perfectly compensated for the caloric load provided by the jelly beans, such that the daily caloric intake remained unchanged. Others have reported similar findings.[38,39] Hypothetically, sugar solutions may fail to trigger satiety in the same way that solid preparations do; however, the physiologic mechanisms have not been fully determined.

Appetite stimulation associated with rapidly changing glucose and/or insulin levels may be caused by rapidly absorbed, high glycemic carbohydrates, including those found in sugar-sweetened soft drinks. A rapidly falling serum glucose level is a well-known appetite stimulant, and carefully conducted human studies have attributed increased hunger and caloric intake to differences in glycemic index or glycemic load intake, and associated differences in glucose and insulin levels.[40,41] The DiMeglio data described above may not support this hypothesis because the glycemic load of the jelly beans vs the soda was probably similar.[6]

Fructose, found in similar amounts in both sucrose and high-fructose corn syrup, may hypothetically promote obesity more than an equivalent amount of glucose. A study by Elliott and coworkers[42] examined the relationship between fructose, weight gain, and the insulin resistance syndrome and found that fructose, compared with glucose, is preferentially metabolized to lipid in the liver. In animal studies, fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension, although data in humans are less clear.[42] Because fructose has limited insulin-stimulating effects, the consumption of foods and beverages that contain fructose produce smaller amounts of insulin than glucose-containing carbohydrates. In addition, because leptin production is regulated by insulin responses to meals, circulating leptin concentrations are reduced by the consumption of fructose. Bray and coworkers[13] have also found that the digestion, absorption, and metabolism of fructose differ from those of glucose, noting that when large amounts of fructose are ingested, the fructose provides a relatively unregulated source of carbon precursors for hepatic lipogenesis. Furthermore, a recent study conducted in mice suggested that the consumption of fructose-sweetened beverages increases adiposity more than the consumption of either sucrose-sweetened or artificially sweetened beverages.[43]

The consumption of milk has greatly decreased over the past few decades, whereas sugar-sweetened soft drink consumption has greatly increased. Energy intake from milk decreased by 38% between 1977 and 2001.[12] It has been shown that this trade-off between sweetened drinks and milk has led to a lower daily intake of protein, calcium, phosphorous, magnesium, zinc, and vitamin A at the highest level of sweetened drink consumption (> 2 glasses or 12 oz/day).[44] Harnack and colleagues[45] found similar results in children and adolescents, particularly at high levels of soft drink consumption. French and coworkers[4] also noted that soft drinks may affect the dietary quality of youth by displacing milk consumption, which can reduce calcium intake among children and increase their risk for osteoporosis and bone fracture. Nielsen and Popkin[12] have hypothesized that because dairy products may have a favorable effect on weight, reducing milk intake may be associated with increased weight gain, especially if the milk is being replaced with drinks of a higher caloric value. Popkin and colleagues,[46] however, citing the 2005 Dietary Guidelines for Americans, noted that there was no sufficient evidence that milk consumption reduced, or prevented, weight gain.

Closing the Data Gap

Clinical trials would be necessary to conclusively demonstrate a causal link between sugar-sweetened soft drink consumption and weight gain. In principle, the most conclusive evidence would come from serial measurements of body weight and various other measures of adiposity in the context of large, multicenter, long-term, randomized trials, in which nationally representative groups of participants consumed controlled amounts of regular soft drinks vs a calorie-free control beverage. In practice, limited resources and logistical barriers would be expected to confine the design and implementation of clinical trials aiming to answer questions of causality. Two examples are noted below.

A major consideration in the design of a randomized trial is the choice of control group (or groups). For example, as a comparison to regular cola, one could arguably use artificially sweetened cola, unsweetened carbonated water with caramel coloring, or plain bottled water – or all of these. Artificially sweetened cola would be most similar to regular cola in taste, but the sweetener may not be inert. Unsweetened alternatives are likely to be less palatable than the regular soft drink, resulting in differential fluid volume intakes during outpatient testing. Selecting a single control group leaves the study open to criticism, whereas selecting multiple control groups implies statistical power to differentiate weight effects between control groups, which would likely require impractical numbers of participants.

Use of a randomized crossover design rather than a single-beverage assignment for each participant is a consideration. The crossover design increases statistical power to find differences between beverage types, and may help reduce the possibility of differential participant withdrawal rates that might occur with a design that uses a single-beverage assignment for each participant. However, care must be taken to ensure an adequate “washout” between beverage phases, such that body weight returns to baseline. This design would potentially increase study duration for each participant in exchange for decreased numbers of participants required.

Summary and Conclusion

Sugar-sweetened soft drink intake has increased dramatically during the past few decades, yet the magnitude of the weight gain and adverse health effects caused by soft drinks are poorly understood due to a paucity of clinical trial data. Despite preliminary data from observational studies that support an association between soft drink consumption and weight gain, the weaknesses of this type of study design raise uncertainty in regard to the magnitude of weight change, and other clinical effects expected as a result of drinking more or less of these beverages. Three small intervention trials in adults, with treatment periods of 10 weeks or less, have observed weight gain associated with sugar-sweetened beverages. These studies have not reported the effects on lipid levels and other cardiovascular risk factors. More comprehensive intervention trials designed to evaluate the effects of soft drink consumption on body weight and cardiovascular risk factors could potentially fill the data gaps to better inform patients, clinicians, and policy makers.

Footnotes

Reader Comments on: Soft Drinks and Weight Gain: How Strong Is the Link? See reader comments on this article and provide your own.

Readers are encouraged to respond to the author at gro.dcm@fflowe or to George Lundberg, MD, Editor in Chief of The Medscape Journal of Medicine, for the editor's eyes only or for possible publication as an actual Letter in the Medscape Journal via email: ten.epacsdem@grebdnulg

Contributor Information

Emily Wolff, Boston University School of Medicine, Boston, Massachusetts Author's email: gro.dcm@fflowe.

Michael L. Dansinger, Lipid Metabolism Laboratory, Jean Mayer Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts; Division of Endocrinology, Diabetes, and Metabolism, Tufts Medical Center, Boston, Massachusetts; Editor, Clinical Nutrition and Obesity section, The Medscape Journal of Medicine.

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