A recent study published by the American Journal of Epidemiology by several scientists including Dr. Peter H. R. Green, the founder of the Columbia University Celiac Disease Center and a Medical Advisory Board member for the Celiac Disease Foundation, has found a link between a particular bacterial strain typically found in the human gut and a lower risk for developing celiac disease. Celiac Disease Foundation strongly encourages our community to support  celiac disease research and the nation’s research centers.

 Celiac disease (CD) has become more common in the United States over the past several decades for reasons not yet established; in the last 50 years alone, the disease has had up to a four-fold increase in prevalence.  Recent studies of stored blood serum have confirmed that this increase is due to a rise in the disease incidence rate, not just an increase in the disease detection rate.

It is likely that environmental factors that can affect CD are responsible for this rise in prevalence. There are many proposed environmental factors such as infant feeding practices and time of dietary gluten introduction. Another potential factor is microbial exposure, as was the focus for a recent paper distributed by the American Journal of Epidemiology. The study, titled “Decreased Risk of Celiac Disease in Patients with Helicobacter pylori Colonization” was published in issue 12 of the 178th volume, in December of 2013. As the title suggests, it looked to find a relationship between the bacterium Helicobacter pylori and CD.

The authors, led by first author Dr. Benjamin Lebwohl, the Assistant Professor of Clinical Medicine and Epidemiology at Columbia University, had multiple reasons to investigate H. pylori’s association with CD. It has previously been established that H. pylori present in the stomach can help protect against asthma and other atopic diseases, CD is triggered by gluten digestion which might be affected by pH and the gastric mucosa, something H. pylori could modulate, and lastly, the increased CD prevalence in the U.S. coincides with declining rates of H. pylori.

In order to determine the relationship between H. pylori and CD, Lebwohl and his colleagues looked at a large database of pathological data and primarily looked at those patients who had gastric and duodenal biopsies at the same time. The gastric biopsy tested for the presence of H. pylori and the duodenal biopsy looked for villous atrophy, signifying CD. The authors also looked at medical insurance and zip code data to account for race, gender, and socioeconomic status.

In total, 136,179 patients who had duodenal and gastric biopsies at the same time were identified, including 2,689 patients with CD. Lebwohl and his colleagues found a strong, inverse association between H. pylori presence and CD. In patients without CD, H. pylori prevalence was found to be 8.8% while it was only 4.4% in patients with CD. The inverse relationship remained strong for all age groups, for both males and females, and when accounting for socioeconomic status.

The bacteria H. pylori is typically acquired as an infant while CD can develop at any time, typically much later than infancy. This means that having H. pylori in your gut somehow decreases your chances of developing CD is more likely than the alternative explanation that having CD somehow causes lower rates of H. pylori presence.

There have been previous studies investigating the relationship between H. pylori and CD that have had conflicting results. Some studies have found no correlation between the two while one study even found increased rates of H. pylori presence in patients with CD. However, these were all much smaller studies that were not able to adjust for socioeconomic factors.

The authors admit there are some limitations to this study despite its large size. It only incorporated patients who had duodenal and gastric biopsies at the same time. The population of people who undergo both those biopsies at the same time could have different characteristics than the general public, or patients who only underwent one biopsy at a time which could affect the results. The authors tried to account for the latter by also examining patients who had a duodenal biopsy and then a prior gastric biopsy on record. The inverse relationship between H. pylori and CD still remained strong in that repeated analysis.

The authors conclude that there is a strong and robust, inverse relationship between H. pylori and CD. Patients with CD had lower rates of H. pylori presence when compared to patients without CD and that relationship remained after accounting for age, gender, and socioeconomic status. This conclusion suggests that H. pylori might be able to protect against CD. Future studies should investigate the bacterium’s effect on gluten in the gastrointestinal tract and also its effect on the immune system as possible methods of protection against CD.


The article “Decreased Risk of Celiac Disease in Patients with Helicobacter pylori Colonization” can be found in volume 178, issue 12 of the American Journal of Epidemiology.