The two most common causes for low stomach acid, hypochlorhydria, are H. pylori infection of the stomach and autoimmune gastritis.
While H. pylori can cause hyperchlorhydria (increased stomach acid) early in the infectious process, hypochlorhydria (low stomach acid later) is a common late manifestation. Because the symptoms of hyperchlorhydria, hypochlorhydria, and esophageal acid reflux are similar, it is not uncommon to see people taking stomach acid-suppressing medications for years for the wrong reasons.
For instance, if H. pylori leads to hypochlorhydria, taking a proton pump inhibiting drug like Prilosec or Aciphex provides no benefit and may add to complications such as cultivating small intestinal bacterial overgrowth, SIBO. Likewise, if esophageal acid reflux was really SIBO all along—as it often is—it will not respond to acid-suppressing drug, or respond only partially, while SIBO (and all its long-term consequences) goes unaddressed.
It is, no doubt, a tangle, but a tangle that is most commonly not disentangled by the cursory approach that dominates in most healthcare settings, from the primary care doctor’s office who reflexively prescribes stomach acid-suppressing drugs to the gastroenterologist most interested in scheduling more endoscopies.
While the prevalence of H. pylori in the U.S. has been decreasing (though still quite prevalent), the incidence of autoimmune gastritis is increasing.
Autoimmune gastritis involves an autoimmune attack against the stomach lining’s parietal cell antibodies. As a result, parietal cells become casualties, resulting in the long-term consequences of autoimmune gastritis: hypochlorhydria, iron deficiency, and vitamin B12 deficiency. Iron deficiency results because stomach acid is required to extract iron from food, while B12 deficiency develops because the parietal cells no longer produce the so-called “intrinsic factor” necessary for B12 absorption when it reaches the ileum further down the intestinal tract. If uncorrected, iron deficiency can lead to a form of anemia, microcytic (meaning small red blood cells), while B12 deficiency can lead to a macrocytic (large red blood cells) anemia. In advanced stages, the stomach lining becomes atrophied (“atrophic gastritis”) and stops producing stomach acid altogether.
Atrophy of the stomach lining, whether triggered by H. pylori or autoimmune gastritis, can both result in reduction in stomach acid that, in turn, causes levels of the hormone gastrin to rise in the bloodstream. An abnormally high gastrin blood level is therefore a reliable sign that there is insufficient stomach acid present. The high gastrin level also stimulates abnormal growth of the stomach lining, a process that can lead to stomach cancer.
Autoimmune gastritis is closely associated with Hashimoto’s thyroiditis, with over 50% of people carrying anti-thyroperoxidase antibodies. It is also commonly associated with vitiligo, alopecia, myasthenia gravis, autoimmune hepatitis, and celiac disease–conditions associated with wheat/grain consumption. Autoimmune gastritis can also occur in tandem with H. pylori infection.
The conventional medical solutions are—no surprise—generally unsatisfactory, solutions such as removal of the stomach or blocking the action of the hormone gastrin with the drug, netazepide. For this reason, we shall be exploring alternative methods to deal with this tricky problem in our Undoctored Inner Circle, as well as ways to identify hypochlorhydria on your own and how to identify H. pylori and eradicate it without the doctor or prescription medications.
