A study conducted in mice by researchers at the University of Michigan Medical School and the Howard Hughes Medical Institute suggests that acid-suppressing medications—specifically proton pump inhibitors (PPIs) such as Prilosec® and Prevacid®—may aggravate some of the conditions they are intended to treat.
In the study, mice treated with the proton pump inhibitor omeprazole for two months developed increased stomach inflammation and greater bacterial overgrowth compared to untreated mice. Even healthy mice, when exposed to long-term acid suppression, developed inflammatory changes related to bacterial colonization.
Bacterial overgrowth in the stomach triggers an inflammatory response, leading to the production of cytokines—chemical messengers involved in immune signaling. These cytokines stimulate the release of gastrin, a hormone that signals the stomach’s acid-producing cells (parietal cells) to increase hydrochloric acid production. From a physiological standpoint, stomach acid serves as a defense mechanism designed to suppress or eliminate invading microorganisms. Suppressing acid production with drugs such as omeprazole interferes with this natural defense.
The researchers compared normal mice with mice genetically unable to produce gastrin. When treated with acid-suppressing drugs, both groups developed increased gastric inflammation and bacterial overgrowth. Antibiotic treatment resolved the gastritis in mice receiving acid-suppressing medication, suggesting that bacterial overgrowth—rather than excess acid—was driving the inflammation.
Interestingly, low stomach acid combined with inflammation led to an increase in both G-cells (which produce gastrin) and parietal cells (which produce hydrochloric acid). These cellular changes correlated with inflammation rather than with actual acid levels.
Juanita L. Merchant, one of the study’s authors, commented:
“In treating patients with gastrointestinal disorders, physicians usually aim to increase the pH of the stomach, particularly in patients in intensive care, to protect the stomach lining from ulceration—historically believed to be caused solely by stomach acid. There is also the prevailing belief that most ulcers are due to Helicobacter pylori. One important point from our research is that blocking acid secretion long-term to treat bacterial overgrowth or Helicobacter infection may actually create additional problems.”
The researchers also noted that increased stomach acid does not necessarily inhibit Helicobacter pylori. In fact, H. pylori is better adapted to low-acid environments. While suppressing acid has been viewed as a strategy to control Helicobacter, the study emphasizes that other bacteria can also contribute to chronic gastritis and may increase cancer risk.
Merchant added:
“The medical community needs to think more broadly about chronic infections in organs such as the stomach, colon, bladder, and liver, because persistent inflammation in these tissues can ultimately lead to cancer. While Helicobacter pylori is rightly considered a significant carcinogen, other organisms may also drive chronic inflammation with serious long-term consequences.”
This research appeared in the January 2002 issues of Gastroenterology and American Journal of Physiology – Gastrointestinal and Liver Physiology.
