[dropcap]L[/dropcap]ow stomach acid production is a common disorder in celiac disease and dermatitis herpetiformis that is characterized by lack of sufficient hydrochloric acid needed 1) to properly digest food, which results in malnutrition and subsequent nutritional deficiencies, and 2) to destroy swallowed bacteria and other microbes, which may allow infections to develop.
It is also common in the general population, as well, affecting 50% of people age 60 years and about 80% by age 85 years. Nevertheless, low stomach acid is not generally looked for as a cause of acute and chronic disorders that rob health with far-reaching effects.
[box type=”shadow” ]Understanding Stomach Acid Production and Function
The stomach digests incoming food into a liquid state, thereby releasing nutrients so they can be absorbed by the small intestine. Powerful stomach muscles churn food and mix it with gastric juice, dissolving and breaking it down.
Gastric juice is produced by gastric glands located in the stomach lining. These numerous, microscopic glands produce about 3 liters of juice a day. Gastric juice is composed of a high concentration of
Arrows Show Abnormal Movement of Gastric Acid in Gastroesophageal Reflux Disease.
What Is Gastroesophageal Reflux Disease (GERD)?
[dropcap]G[/dropcap]ERD is an upper digestive disorder that is characterized by a decrease in lower esophageal sphincter pressure (LES,) which allows the abnormal reflux or backflow of stomach contents into the esophagus. It is also called erosive esophagitis or reflux esophagitis and is the most common disorder of the esophagus.
The esophagus is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).
The lower esophageal sphincter is located at the junction of the esophagus and the stomach. It functions like a circular band to tighten after food is ingested in order to prevent its going back up the esophagus.
Q: How does reflux damage the esophagus?
A: Damage to the lining of the esophagus is induced by the caustic, chemical action of acid and pepsin in gastric juice and, in severe cases, also bile salts, that back upwards from the stomach through an impaired LES. Gastric acid combined with pepsin or bile salts seems to be more harmful to the esophageal epithelial layers than gastric acid alone.1
Pepsin is normally produced by the stomach to dissolve protein in swallowed food. Unfortunately, when the esophagus is inflamed, pepsin will act on it to break down the protein in its sore wall. These sores are called erosions.
Importantly, refluxate to the esophagus in patients with acid suppression therapy is different from those in patients without. Higher levels of secondary bile acids are detected in patients with acid suppression therapy. Even if acid suppression is successful, weakly acidic reflux with bile acids can damage the esophagus.1
Damage starts at the luminal surface (inside where food passes through) of the squamous epithelium (tough surface cells) and progresses through the underlying layers into the submucosa.
One of the primary functions of the esophageal epithelium is to protect the underlying tissue from mechanical and chemical damage by acting as a barrier. The epithelial layers of the distal esophagus need to withstand reflux from the stomach and its contents. When the epithelium fails to protect the underlying tissue from this damage, it leads to erosions, esophagitis, and may lead to Barrett’s esophagus.1
Barrett’s esophagus and esophageal small cell cancer are severe complications of GERD that can be fatal.
GERD can result from too much, or more commonly, too little stomach acid.
What Is Gastroesophageal Reflux Disease (GERD) In Celiac Disease and/or Gluten Sensitivity?
Sources:
Chen X, Oshima T, Tomita T, Fukui H, Watari J, Matsumoto T, Miwa H. Acidic bile salts modulate the squamous epithelial barrier function by modulating tight junction proteins. Am J Physiol Gastrointest Liver Physiol. 2011 Aug;301(2):G203-9. doi: 10.1152/ajpgi.00096.2011. Epub 2011 May 26. [↩] [↩] [↩]
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