Drinking sweetened beverages does not increase risk of Crohn’s disease or ulcerative colitis

Wayne Kuznar, for MDLinx | June 27, 2018

The risks of developing Crohn’s disease (CD) or ulcerative colitis (UC) are not increased by consuming sweetened beverages, according to an examination of two large prospective cohorts by researchers from Boston, Sweden, and the United Kingdom. They found that the risk for CD associated with drinking one or more servings per day of a sweetened beverage was not significantly greater than the risk when drinking none.

Advertisement

Researchers found no significant associations between consumption of sweetened beverages and risk of either Crohn’s disease or ulcerative colitis.

As reported in Clinical Gastroenterology and Hepatology, they examined the association between consumption of sweetened-beverages and risk of CD and UC in two large prospective cohort studies in Sweden: the Swedish Mammography Study (SMC) and the Cohort of Swedish Men (CoSM).

In the SMC, 66,651 women completed questionnaires between 1987 and 1990 on diet, alcohol, weight, medication use, and reproductive and menopausal factors. For the CoSM, established in 1997, researchers included 45,906 middle aged and older men, and also provided information through questionnaire on lifestyle factors and medications, with follow-up questionnaires completed in 2008 and 2009. The current analysis included all subjects from the CoSM study and 38,984 from SMC who were still alive in 1997 and returned the dietary questionnaire. The median age of participants at baseline was 60 years.

For the purpose of the analysis, artificially sweetened drinks—which accounted for less than 10% of all soft drinks among men and less than 20% among women, were counted as sweetened beverages. Participants were asked to report their usual consumption of such beverages during the past year.

Through the end of December 2014, 349 incident cases of UC and 143 of CD were confirmed.

Higher consumption of sweetened beverages was not associated with an increased risk of UC (P=0.40) or CD (P=0.11).

Compared with participants who did not consume sweetened beverages, the age-adjusted hazard ratio (HR) of UC among participants with at least one serving per day of sweetened beverage was 1.26 (95% CI: 0.93-1.69). This estimate was not altered after adjusting for other covariates (P=0.40). Compared with non-consumers of sweetened beverages, the multivariate-adjusted HR of UC among participants with at least one serving per day of sweetened beverage was 1.14 (95% CI: 0.83-1.57).  

Compared with non-consumers, the age-adjusted HR of CD among participants with one or more servings per day of sweetened beverage was 1.18 (95% CI: 0.72-1.94), an estimate did not change after adjusting for other potential confounders (P=0.34). Compared with non-consumers, the multivariate-adjusted HR of CD among participants with at least one serving per day of sweetened beverage was 1.02 (95% CI: 0.60-1.73). The effect of the main finding was not modified by age, sex, smoking, or body mass index.

Results were similar when researchers compared risks of CD and UC among ever-users of sweetened beverages compared with non-users. When the models were adjusted for total sucrose intake independent of primary sugar content of the beverage, no significant association was seen, which was also true for when the analysis was restricted to elderly-onset inflammatory bowel disease.

“In two large prospective cohort studies, we observed no evidence for strong or clinically meaningful associations between sweetened beverage and risk of CD and UC.

Whether sweetened beverages play a role in development of earlier onset IBD (age < 40 years) is unknown and should be the focus of future investigation,” concluded the authors, led by Hamed Khalili, MD, MPH, Gastroenterology Unit, Massachusetts General Hospital. Boston, MA.

They also noted previous associations between sweetened beverage consumption and type 2 diabetes and cardiovascular disease, but results have been mixed with respect to levels of inflammatory markers.

 This work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, and a Crohn’s and Colitis Foundation Senior Research Award.

Advertisement