Key clinical point: In a large observational study, switching from a high-inflammatory diet to a lower-inflammatory diet was associated with a significant decrease in risk for Crohn’s disease, even after accounting for potential confounders.
Major finding: Adults who initially consumed a proinflammatory diet and then switched to a low-inflammatory diet had a statistically similar risk for Crohn’s disease as adults who consumed a low-inflammatory diet at both time points. The 95% confidence interval for the hazard ratio crossed 1.0 (HR, 1.51; 95% CI, 0.76-3.00).
Study details: Food questionnaire and medical data from 166,903 women and 41,931 men in the Nurses’ Health Study (1984-2014), Nurses’ Health Study II (1991-2015), and Health Professionals Follow-up Study (1986-2012).
Disclosures: The National Institutes of Health, the Beker Foundation, the Chleck Family Foundation, and the Crohn’s & Colitis Foundation provided funding. Three coinvestigators disclosed ties to AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Gilead, Janssen, Kyn Therapeutics, and Merck, Pfizer, Policy Analysis Inc., and Takeda.
Lo C-H et al. Gastroenterology. 2020 May 1. doi: 10.1053/j.gastro.2020.05.011.
Diet is the single most modifiable risk factor influencing inflammatory bowel disease (IBD) development. Accordingly, animal studies show that specific nutrients and food additives impact gut barrier function and/or microbiota, thereby influencing disease development. However, using these studies to provide humans practical dietary advice has been difficult, in part because effects of isolated food components can be quite different from those of complex foods. The complex nature of human foods has also stymied epidemiologic approaches to determine how diet influences IBD risk. This difficulty is exacerbated by the potential of IBD itself to influence diet, likely beginning long before disease diagnosis.
Lo and colleagues surmount these problems by developing the “empirical dietary inflammatory pattern” (EDIP), which is a metric that quantifies the proinflammatory potential of one’s overall diet based on the extent to which its components associate with proinflammatory cytokine levels in a large healthy human cohort. Retrospective application of this metric to three large human cohorts found that consumption of proinflammatory diets increased risk of developing Crohn’s disease but not ulcerative colitis. This indicates, perhaps not surprisingly, that a central means by which diet influences risk of Crohn’s is by promoting inflammation in susceptible hosts. Furthermore, while this approach implicated the usual suspects, such as low-fiber processed foods, in promoting Crohn’s, it also found a protective role for pizza, perhaps reflecting the anti-inflammatory action of its tomato-based components. It should soon be possible for persons with high genetic risk for Crohn’s to use the EDIP to discern how their diet is influencing that risk and, moreover, designing practical strategies to mitigate it.
Andrew T. Gewirtz, PhD, is a professor at Georgia State University’s Institute for Biomedical Sciences, Atlanta. He has no conflicts.