Obesity and Sugared Drinks: Studies Spotlight Genetics, Weight Loss

September 25, 2012

September 21, 2012 (San Antonio, Texas) — A trio of studies released today bring light as well as new twists to ongoing controversies about the impact of sugar-sweetened vs nonsugared drinks on obesity and even whether a person's genetics can influence how sugary beverages affect weight gain [1,2,3].

One randomized trial saw less fat-related weight gain in kids who substituted artificially sweetened beverages for sugar-sweetened ones. Another, with mixed results, explored whether regular home delivery of noncaloric drinks to overweight or obese adolescents would replace sugared drinks in their diet and reduce weight gain.

And increasing consumption of sugar-sweetened beverages seemed to potentiate the obesity-promoting effects of genes known to be associated with body-mass index (BMI) in an analysis of >30 000 people enrolled in three prospective cohort studies.

All three studies were published online today by the New England Journal of Medicine to coincide with their presentation here at Obesity 2012, the annual scientific meeting of the Obesity Society.

Double-Blinded Trial

An 18-month randomized trial of schoolchildren aged four to 11 years in the Netherlands lends support to the common real-world weight-control strategy of substituting noncaloric beverages, including those that are artificially sweetened, for conventional sugar-sweetened drinks.

Of the study's 641 participating children--who were eligible because they regularly consumed sugar-sweetened drinks--about 80% were considered normal weight at baseline and only a few were obese, reported the authors, led by Janne C de Ruyter (EMGO Institute for Health and Care Research, VU University Amsterdam, the Netherlands). They were assigned to receive one daily 250-mL serving of a noncarbonated beverage that was either artificially sweetened or had 104 kcal of sucrose. The two types of beverage were matched in appearance and taste and were custom-made for the study by a soft-drinks company.

Mean weight gain by the end of the study was 6.35 kg and 7.37 kg in the "sugar-free" and "sugar" groups, respectively. Measurements of skinfold thickness and body electrical impedance showed that reduced accumulation of fat mass accounted for a major part of the weight-gain difference.

Encouragement to Drink Sugar-Free

When 224 students in grade 9 or 10 in the US were randomized to a yearlong, home-based strategy aimed at replacing sugared drinks in their diet with noncaloric drinks or to a no-intervention control group, there was no significant effect on the primary end point of BMI measured at two years or in percentage of body fat. The intervention significantly improved both BMI and weight, however, at one year.

The two-year outcome was in spite of the strategy's success in getting the 110 adolescents who received the sugar-free drinks to largely give up sugared ones, during both the year of intervention and observational second year, according to Dr Cara B Ebbeling (Boston Children's Hospital, MA) and colleagues.

The intervention included every-other-week home delivery of noncaloric beverages (including bottled water and noncaloric sweetened drinks), "check-in" visits at the home, and regular encouragement by mail and phone to consume the delivered drinks and avoid sugar-sweetened ones.

A prespecified analysis identified an interaction between ethnicity and BMI and weight changes at both one and two years that was apparently associated with significant intervention effects in the study's small group of Hispanics, according to the authors.

Evidence for Genetic Predisposition

The greater intake of sugar-sweetened drinks, the more pronounced effect obesity-related genes can have on weight gain, suggests a combined analysis of a cohort of women (n=6934) from the Nurses' Health Study (NHS) and men (n=4423) from the Health Professionals Follow-up Study (HPFS).

The observation was separately explored and replicated in a cohort (n=21 740) from the Women's Genome Health Study (WGHS), according a report with first author Dr Qibin Qi (Harvard School of Public Health, Boston, MA).

The group used a scoring system based on 32 single-nucleotide polymorphisms related to BMI to reflect burden of genetic predisposition to adiposity. After adjustment for behavioral risk factors for weight gain, the BMI increase associated with every 10 high-risk alleles became progressively more pronounced with rising intake of sugar-sweetened beverages in the combined NHS/HPFS cohort (p<0.001). The jump in BMI for every 10 alleles at each intake level went from 12% at intake of one to four servings/month, to 38% at two to six servings/week, to 78% at one or more servings/day.

No such relationship was seen for intake of artificially sweetened beverages.

Although not conclusive, the current findings, along with a large observational evidence base, "support a causal relationship" between consumption of sugar-sweetened drinks and weight gain and obesity risk, according to Qi et al. Their own data, they write, "suggest that persons with greater consumption of sugar-sweetened beverages may be more susceptible to genetic effects on adiposity. Viewed differently, persons with a greater genetic predisposition to obesity appeared to be more susceptible to the deleterious effects of sugar-sweetened beverages on BMI."

Supports Recommendations, Policy Decisions

"This is a clear example of gene–environment interaction," observes Dr Sonia Caprio (Yale University, New Haven, CT) in an editorial accompanying all three studies [4]. The observations of Qi et al, she writes, support an exploration of whether reduced intake of sugar-sweetened beverages might more effectively cut the risk of obesity in people with higher genetic-predisposition scores.

The two randomized trials, especially the one by de Ruyter et al, Caprio writes, should encourage development of "recommendations and policy decisions to limit consumption of sugar-sweetened beverages, especially those served at low cost and in excessive portions, to attempt to reverse the increase in childhood obesity."

de Ruyter had no commercial relationships; disclosures for the coauthors are listed in the paper. Ebbeling had no commercial relationships; disclosures for the coauthors are listed in the paper. Qi had no disclosures; support for genotyping was provided by Merck Research Laboratories; Amgen provided support for genotyping in the WGHS study; and disclosures for coauthors are listed in paper. Caprio had no relevant disclosures.