Our members and visitors send us excellent questions that can help others suffering from GERD. Today’s question helps us to shed a little more light on damage done to the esophagus by acid reflux. Proton pump inhibitors (PPIs) reduce acid, so it stands to reason that they are beneficial long-term to avoid Barrett’s esophagus and cancer. However, sometimes what seems reasonable in not necessarily true.
One thing I do not understand. My reflux-induced esophagitis (diagnosed by endoscopy) seems to have healed with proton pump inhibitors (PPIs). Since Barrett’s is a complication of esophagitis, why do you say that PPIs, or any other acid reflux medication, cannot prevent Barrett’s?
The role of PPIs in the treatment of GERD
This is an excellent question and logic suggests that acid reflux medication, including powerful PPIs, should stop GERD from progressing to Barrett’s esophagus. There are many good uses for PPIs, including healing complications like esophagitis diagnosed during an endoscopy. Esophagitis results from the acid in your stomach contacting the lining of your esophagus, and the best way to promote healing is to reduce acidity in the stomach.
GERD results when the lower esophageal sphincter (LES) doesn’t work properly to keep the contents of the stomach. So while PPIs reduce stomach acidity and help things like esophagitis heal, they do not stop reflux from occurring and they cannot stop GERD from progressing to more serious complications such as Barrett’s esophagus and esophageal cancer. This has been proven by many research studies and written about extensively on our website. In an article written by Dr. Tom DeMeester, he discusses this issue with great clarity:
“According to a study by Dr. Blair Jobe at the University of Pittsburg, PPI-treated GERD patients, who have mild or absent symptoms while on the medication, were 60 percent more likely to have Barrett’s esophagus, a precancerous condition, than those with more severe symptoms while on the medication. Disappointedly, a good response to the medication does not eliminate the risk of cancer. In another ongoing long-term study conducted in Europe, researchers determined that today’s treatment model, which is predominantly focused on drug therapy, does not stop the progression of the disease. More importantly, of all the risk factors studied, which included diet, obesity, smoking, alcohol use and family history, the one factor with the highest odds ratio associated with progression from mild to severe disease and leading to Barrett’s Esophagus was daily PPI use.”
Why does GERD lead to Barrett’s esophagus and esophageal cancer?
There is ongoing research to better understand the connection of two elements that could be the culprits: pepsin and bile. Both are important elements for digestion and both can be refluxed into the esophagus for those with GERD. Pepsin is a digestive enzyme that is inactive in an alkaline environment, but become very active when the stomach creates hydrochloric acid during and after a meal. Unfortunately, research has proven that pepsin is deposited in the esophagus during reflux. That pepsin, inactive in an alkaline environment due to PPI use, can be reactivated in the esophagus if acid is present, as would be the case with a cola drink for example. According to Dr. Jamie Koufman in an article on DoctorOZ.com, “Outside the protected stomach, pepsin, bathed in acid, digests you! And when pepsin attacks your sensitive airway and esophageal tissues, you can suffer all kinds of problems.“
Bile has been proven to be extremely carcinogenetic and Dr. Chandrasoma discussed a clinical research article in his post: Examining the role of Bile in Barrett’s Esophagus. Research at the University of Rochester was summarized by Dr. Chandrasoma as follows: “The importance of this finding is that it provides further evidence that treating GERD with acid suppressive drugs, while controlling symptoms, does not prevent conversion of the squamous lining of the esophagus to the columnar (intestinal type) lining that signifies Barrett’s esophagus. The epithelial change that is associated with cancer is not prevented by PPI therapy. This would explain why treatment of GERD with PPIs and other acid suppressive agents has been associated with an increasing incidence of both Barrett’s esophagus and reflux-induced adenocarcinoma in the past five decades. If bile and not acid is the culprit for generating Barrett esophagus and cancer, treating GERD with PPIs is not addressing the cause of these conditions.”
I hope this helps explain the role of PPIs and GERD progression.
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