Rates of IBD have been increasing worldwide. According to the Centers for Disease Control and Prevention (CDC), approximately three million Americans are diagnosed with IBD each year, up one million from incidence in the late 1990s. Consumption of a western diet, including fructose, is associated with increasing rates of obesity and diabetes, and IBD may be an additional disease that fructose intake exacerbates.
“The increasing incidence of IBD parallels higher levels of fructose consumption in the United States and other countries,” says study leader David Montrose, assistant professor in the pathology department and faculty researcher in the Stony Brook University Cancer Center.
“Our findings provide evidence of a direct link between dietary fructose and IBD and support the concept that high consumption of fructose could worsen disease in people with IBD. This is important because it has the potential to provide guidance on diet choices for IBD patients, something that is currently lacking.”
Montrose, along with colleagues at Weill Cornell Medicine, tested three mouse models of IBD. They fed the mice high amounts of fructose, which worsened colonic inflammation along with notable effects in their gut bacteria including changes in their type, metabolism, and localization within the colon. Complementary mechanistic work demonstrated that the microbiota is causally linked to the detrimental effects of the high fructose diet.
The paper concludes that the “excess dietary fructose consumption had a pro-colitic effect that can be explained by changes in the composition, distribution, and metabolic function of resident enteric microbiota.”
Montrose says several next steps are planned to expand on these findings. These include the development of interventions to prevent the pro-inflammatory effects of dietary fructose as well as evaluating whether this diet increases colitis-associated development of cancer. This second point is particularly important because people with IBD are at increased risk of developing colon cancer due to a lifetime of chronic inflammation of the gut.
The findings appear in the journal Cellular and Molecular Gastroenterology and Hepatology.