Microscopic colitis is a common cause of chronic watery diarrhea among the elderly. Although the prevalence of celiac disease appears to be higher in patients with microscopic colitis, the relationship between dietary gluten intake and risk of microscopic colitis among individuals without celiac disease has not been explored.
We conducted a prospective study of 160,744 US women without celiac disease enrolled in the Nurses’ Health Study (NHS) and the NHSII. Dietary gluten intake was estimated using validated food frequency questionnaires every 4 years. Microscopic colitis was confirmed through medical records review. We used Cox proportional hazard modeling to estimate the multivariable-adjusted hazard ratio (HR) and 95% confidence interval (CI).
We documented 219 incident cases of microscopic colitis over more than 20 years of follow-up encompassing 3,716,718 person-years (crude incidence rate: 5.9/100,000 person-years) in NHS and NHSII. Dietary gluten intake was not associated with risk of microscopic colitis (P trend = 0.88). Compared to individuals in the lowest quintile of energy-adjusted gluten intake, the adjusted HR of microscopic colitis was 1.18 (95% CI: 0.77–1.78) for the middle quintile and 1.03 (95% CI: 0.67–1.58) for the highest quintile. Additional adjustment for primary dietary sources of gluten including refined and whole grains did not materially alter the effect estimates (All P trend ≥ 0.69). The null association did not differ according to lymphocytic or collagenous subtypes (P heterogeneity = 0.72) and was not modified by age, smoking status, or body mass index (All P interaction ≥ 0.17).
Dietary gluten intake during adulthood was not associated with risk of microscopic colitis among women without celiac disease.
1Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA;
2Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA;
3Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA;
4Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA;
5Harvard Medical School, Boston, MA, USA;
6Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA;
7Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA;
8South Australian Health and Medical Research Institute, Infection and Immunity Theme, School of Medicine, Flinders University, Adelaide, SA, Australia;
9Department of Medicine, Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden;
10Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden;
11Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden;
12Broad Institute of MIT and Harvard, Cambridge, MA, USA;
13Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA;
14Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
Correspondence: Hamed Khalili, MD, MPH. E-mail: email@example.com
Received March 29, 2018
Accepted July 31, 2018