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The real cause of GERD, and why we need stomach acid
Most people think that acid reflux is caused by an excess of stomach acid. This is a common medical myth, and one that has resulted in widespread misunderstanding of the condition and how to best treat it.
To properly understand what happens in acid reflux and the associated condition gastroesophageal reflux disease (GERD), let’s first consider normal digestion.
After you chew and swallow food, it travels down a tube known as the esophagus. At the end of the esophagus is a muscle known as the lower esophageal sphincter (LES), which is the “gatekeeper” between the end of the esophagus and the stomach. As the chewed-up food reaches the lower esophagus, the LES relaxes, opening the “door” to the stomach so that the food can undergo further degradation by hydrochloric acid (stomach acid) in the stomach. Normally, the LES constricts after food passes into the stomach, preventing the stomach acid from splashing up (or refluxing) into the esophagus.[1],[2]
In people affected by GERD, however, the LES has weaker tone and does not fully constrict after the food passes from the esophagus into the stomach. This essentially leaves the “door” between the esophagus and the stomach open, thus allowing stomach acid to backwash from the stomach up into the esophagus. This reflux of acid can irritate the cells lining the esophagus and cause symptoms like burning, pain, and even cough.[3],[4]
Aside from being unpleasant, heartburn left untreated in the long run can irritate the cells of the esophagus, leading to a condition known as Barrett’s esophagus and increasing the risk of esophageal cancer.[5]
The risks of conventional reflux treatments
Conventionally, reflux symptoms are treated with medications that either decrease the amount of acid produced in the stomach (proton pump inhibitors, or PPIs) or neutralize the acid after it’s produced in the stomach (calcium carbonate products like chewable or drinkable antacids).
When used in the short term during a “reflux crisis,” these medications put a bandage on the unpleasant symptoms, but do little if anything to address the cause of the reflux. These medications do nothing to address the weak tone of the LES – in fact they can even make it worse!
Furthermore, a long list of problems can develop as a result of long-term suppression of stomach acid. Most importantly, these problems include:
Infections and illnesses. You need stomach acid to kill the harmful bacteria, viruses, and fungi that you accidentally ingest. Without enough stomach acid, these bugs can wreak havoc, causing illness in the gut and beyond.[6]
Microbiome disturbances. Our bodies contain more microbial cells than human cells![7] The balance of good-and-bad bacteria, viruses, and fungi in our body affects more than just the gut. The microbiome (as this mix of microbes in the body is known) affects things like weight, mood, immune system function, diabetes risk, autoimmunity, and even COVID-19 outcomes. [8],[9],[10],[11],[12],[13] Acid-suppressing medications can disrupt the microbiome, leaving us susceptible to associated health problems.
Acid-suppressing medications can disrupt the microbiome, leaving us susceptible to associated health problems.
Nutritional deficiencies. Stomach acid is necessary to properly digest the food you eat and assimilate the nutrients found in both food and nutritional supplements. Low stomach acid – and drugs that reduce acid production – have therefore been associated with nutritional deficiencies, and can have devastating health effects in the long run. Examples include osteoporosis, skin problems, and anemia.[14],[15],[16],[17]
Dementia. Research has also shown a connection between low stomach acid and cognitive decline. A large population study showed that people who use PPI drugs for reflux have a higher risk of developing dementia.[18] Another study showed that taking PPIs for as little as ten days can negatively affect the memory of young, healthy individuals.[19] These findings are quite concerning, especially when we consider that the use of PPIs in the population has recently doubled.[20]
Other digestive complaints. Without proper hydrochloric acid to break down food, the intestines may become irritated while processing the under-digested food particles. This can cause gas, bloating, abdominal pain, and irregular bowel movements.[21] Long-term use of antacid medications have also been implicated in kidney disease.[22]
Aggravation of the root cause. While it initially seems intuitive to decrease hydrochloric acid levels in a condition associated with acid burning the cells of the esophagus, it’s important to recall that the cause of reflux isn’t too much stomach acid, but rather the leakage of that acid out of the stomach through the LES. Ironically, lower levels of stomach acid can cause poor LES tone. In turn, increasing stomach acidity can increase LES tone. This means that medications that neutralize stomach acid levels can actually worsen the root cause of GERD, thereby making those with reflux “hooked” on their conventional pharmaceutical remedies.
Medications that neutralize stomach acid levels can actually worsen the root cause of GERD.
Healthy ways to soothe reflux
It is possible – and quite easy! – to treat GERD without having to rely on chalky drinks, chewable tablets, and other pharmaceutical medications. Check back next week to learn about natural strategies for improving digestive integrity and soothing an irritated esophagus.
References
Click here to see References[1] Gastroesophageal reflux disease (GERD). Mayo Clinic [Internet]. Accessed March 20, 2022. Available from: https://www.mayoclinic.org/diseases-conditions/gerd/symptoms-causes/syc-20361940
[2] Hershcovici T, et al. The lower esophageal sphincter. Neurogastroenterol Motil. 2011 Sep;23(9):819-30. doi: 10.1111/j.1365-2982.2011.01738.x.
[3] Richter JE, Rubenstein JH. Presentation and epidemiology of gastroesophageal reflux disease. Gastroenterol. 2018 Jan;154(2):267-76. doi: 10.1053/j.gastro.2017.07.045.
[4] Kellerman R, Kintanar T. Gastroesophageal reflux disease. Prim Care. 2017 Dec;44(4):561-73. doi: 10.1016/j.pop.2017.07.001.
[5] Maret-Ouda J, et al. Gastroesophageal reflux disease: a review. JAMA. 2020 Dec 22;324(24):2536-47. doi: 10.1001/jama.2020.21360.
[6] O’Connor A, O’Moráin C. Digestive function of the stomach. Dig Dis. 2014;32(3):186-91. doi: 10.1159/000357848.
[7] Sender R, et al. Revised estimates for the number of human and bacteria cells in the body. PLoS Biol. 2016 Aug 19;14(8):e1002533.
[8] Long J, et al. Association of oral microbiome with type 2 diabetes risk. J Periodontal Res. 2017 Jun;52(3):636-43.
[9] Foster JA, McVey Neufeld KA. Gut-brain axis: how the microbiome influences anxiety and depression. Trends Neurosci. 2013 May;36(5):305-12.
[10] Bouter KE, et al. Role of the gut microbiome in the pathogenesis of obesity and obesity-related metabolic dysfunction. Gastroenterol. 2017 May 1;152(7):1671-8.
[11] Chen B, et al. Integration of microbiome and epigenome to decipher the pathogenesis of autoimmune diseases. J Autoimmun. 2017 Sep 1;83:31-42.
[12] Patel P, Roper J. Gut microbiome composition is associated with COVID-19 disease severity. Gastroenterology. 2021 Aug;161(2):722-4.
[13] Gou W, et al. Gut microbiota may underlie the predisposition of healthy individuals to COVID-19. MedRxiv. 2020 Jan 1 [Preprint]. doi: 10.1101/2020.04.22.20076091.
[14] Sipponen P, Härkönen M. Hypochlorhydric stomach: a risk condition for calcium malabsorption and osteoporosis? Scand J Gastroenterol. 2010;45(2):133-8. doi: 10.3109/00365520903434117.
[15] Kitay AM, Geibel JP. Stomach and bone. Adv Exp Med Biol. 2017;1033:97-131.
doi: 10.1007/978-3-319-66653-2_6.
[16] Schulz U, Drunkenmölle R. Correlations between disorders of gastric secretion and skin diseases. Z Gesamte Inn Med. 1971 May 1;26(9):Suppl:112 c.
[17] Reutsch I, Sievers S. Relationship between hypochromic anemia and hydrochloric acid production in the stomach. Med Welt. 1971 Sep;22(36):1390-3. PMID: 5092914.
[18] Gomm W, et al. Association of proton pump inhibitors with risk of dementia: a pharmacoepidemiological claims data analysis. JAMA Neurol. 2016 Apr;73(4):410-6. doi: 10.1001/jamaneurol.2015.4791.
[19] Akter S, et al. Cognitive impact after short-term exposure to different proton pump inhibitors: assessment using CANTAB software. Alzheimers Res Ther. 2015 Dec 27;7:79. doi: 10.1186/s13195-015-0164-8.
[20] Rotman SR, Bishop TF. Proton pump inhibitor use in the U.S. ambulatory setting, 2002-2009. PLoS One. 2013;8(2):e56060. doi: 10.1371/journal.pone.0056060.
[21] Soybel DI. Anatomy and physiology of the stomach. Surg Clin North Am. 2005 Oct;85(5):875-94, v. doi: 10.1016/j.suc.2005.05.009.
[22] Maton PN, Burton ME. Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. Drugs. 1999 Jun;57(6):855-70. doi: 10.2165/00003495-199957060-00003.
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Dr. Erica Zelfand
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