Article courtesy of Daniel Weber. Daniel comments:
For many years Proton Pump Inhibitors (PPIs) were claimed to be without side-effects, although many of us in the CAM profession found that unlikely. This latest study shows how right we were and how wrong the biomedical industry was. Hydrochloric acid is absolutely necessary for functioning digesting and immune systems. Masking a problem only creates further problems as we know. There are better ways of managing reflux.
Proton Pump Inhibitors: Risks of Long-term use
PPIs are among the most commonly prescribed classes of drugs and their use is increasing, in particular for long term treatment, often being over-prescribed and used for inappropriate conditions. In recent years, considerable attention has been directed towards a wide range of adverse side effects, and even when a potential underlying biological mechanism is plausible, the clinical evidence of the adverse effect is often weak. Several long term side effects have been investigated ranging from interaction with other drugs, increased risk of infection, reduced intestinal absorption of vitamins and minerals, and more recently, kidney damage and dementia.
The gastric acid environment plays a major role in the physiologic pathways through which most micronutrients and drugs are digested and absorbed. Changes related to long-term gastric acid inhibition may interfere in particular with the absorption of several vitamins and minerals. This includes iron, magnesium, calcium and Vitamin B12.
PPI treatments enhance the production of amyloid-b leading to elevated levels in brains of mice. This is similar to the deposition of amyloid-b peptides seen in the pathogenesis of Alzheimer’s disease. Moreover, low Vitamin B12 status has been associated with cognitive deficit highlighting a possible role of vitamin malabsorption due to long term PPI treatment. PPIs have been increasingly suspected of causing renal damage, particularly among older patients. Indeed, acute interstitial nephritis is the most frequently observed acute kidney damage in PPI users.
Gastric acid secretion plays a pivotal role in the digestive process also as a part of the local defensive system against orally ingested pathogens. In this context, the reduced acid secretion induced by PPIs could alter the composition of the gastrointestinal (GI) flora and may facilitate bacterial ascending colonisation from the lower to upper intestinal tracts. Thus, the changes in the intestinal microflora represent a plausible biological explanation for increased susceptibility to GI infections during PPI therapy.
Several studies examined the potential risk of community-acquired pneumonia among subjects treated with PPIs. Upper GI bacterial overgrowth, a possible consequence of long term PPI treatment, may lead to an increased susceptibility to respiratory infections by potential micro-aspiration or translocation into the lungs. Several recent studies tried to define a correlation between chronic PPI use and the development of gastric cancer. Gastrin has been found to be involved in tumorigenesis in the GI tract and it has been demonstrated that high gastrin levels have a trophic effect also on colon cancer cells in vitro, thus, theoretically hypergastrinaemia could lead to development of colonic adenoma and colorectal cancer.
Ref: 2016 DOI:10.1111/jgh.13737