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Colin MacKenzie M.D.
November 27, 2020

The Gastrointestinal System

The gastrointestinal (GI) system plays a major role in the absorption, production, and metabolism of alcohol, and alcohol can have a number of deleterious effects on this organ system. The gastrointestinal system can be thought of as a long tube that serves as the interface between the external environment and the internal organ systems and tissues of the body. The GI system is responsible for digestion, meaning it breaks the things you consume down into smaller components, such as amino acids, carbohydrate molecules, and fatty acids, that the body can then utilize as nourishment. Everything you eat and drink passes through your gastrointestinal system and has the potential to be absorbed into the bloodstream, whether it is helpful or harmful.  The gastrointestinal system can be “segmented” into the following parts:

  • Mouth
  • Throat
  • Esophagus
  • Stomach
  • Small and large intestines
  • Liver
  • Gallbladder
  • Pancreas

When consumed, alcohol (ethanol) makes contact with, and can have an effect on, the entire gastrointestinal system. The body absorbs alcohol throughout the entire gastrointestinal system, but 80% of the absorption happens in the stomach lining and small intestine. The liver is responsible for metabolizing most of the alcohol consumed, as it is the organ that contains most of the specialized enzymes responsible for converting alcohol into non-toxic components. 

Other organs also metabolize and/or excrete alcohol, but to a much smaller extent, such as the lungs, kidneys, and sweat glands. When the liver is not over-whelmed with alcohol, the amount excreted unchanged by these other organs is typically less than two percent.  However, their role in excretion can increase when intoxication is severe.   

But why has the body, especially the liver, developed these mechanisms to metabolize and excrete alcohol in the first place? Because our bodies produce alcohol naturally, and because it is a toxin, the body needs to eliminate it rapidly (more on this in future blogs). 

Alcohol’s Effects on the GI System

Alcohol can produce several functional and structural changes to the mucosal lining of the GI tract leading to various pathological outcomes when exposure is chronic.  These problems can alter the ability of the GI tract to breakdown and absorb essential nutrients such as vitamin B1 (or thiamine), or cause bleeding which can sometimes be fatal.  In addition, a damaged gastrointestinal lining can allow harmful substances and microbes into the blood stream and lymphatic systems causing systemic problems. Many organs in your body contribute to the digestive process including:

Inflammation and GI Bleeds

The mouth, pharynx, esophagus, and stomach are immediately exposed to undiluted alcohol immediately after ingestion.  Over time, this can lead to inflammation of the mucosal lining of these structures, including the tongue, mouth, and parotid glands. In the esophagus, this inflammation can lead to erosions of the mucosal layer producing chronic pain as well as motility issues. 

The sphincter at the base of the esophagus loses contractility after even one exposure to alcohol, which often leads to gastro-esophageal reflux, as stomach contents are no longer blocked by this barrier. When chronic, reflux can lead to a condition called Barrett’s Esophagus where the cells of the mucosa undergo structural changes predisposing the drinker to a higher risk of esophageal cancer.     

Most alcohol-related GI bleeds occur in the esophagus.  One cause of this bleeding is due to a combination of mucosal erosions and excessively high blood pressure in the veins of the esophagus due to liver disease. The mucosa will often erode into these highly pressurized veins (varicose veins) causing sudden bleeds that often need emergent care.  Another form of traumatic bleeding is seen with alcoholic binge drinking followed by frequent vomiting.  The high pressures caused by repeated retching can cause tears, called Mallory-Weiss tears, in an already stressed esophageal lining. A study that analyzed 220,000 “natural” deaths in Sweden revealed that 29% of those who died from varicose esophageal bleeds, and 47% of those who died from non-varicose upper GI bleeds, also had alcoholism.

One clinical pearl:  Sometimes it is possible to determine the general location of a GI blood from the presentation of the blood.  GI bleeds leading to hematemesis (vomiting blood) are almost always due to a bleeding lesion of esophageal or gastric origin.  If maroon or bright red blood is passed rectally, the origin is usually post-gastric (intestines or rectum), whereas melena (dark, sticky stool) is often of esophageal or gastric origin.   

Stomach

Alcohol increases gastric acid secretion.  It also causes inflammation and atrophy (shrinkage) of the gastric mucosa.  Alcohol also inhibits prostaglandins which are necessary to maintain the integrity of the gastric mucosa.  High concentrations of alcohol also decrease contractility of the stomach muscles decreasing the motility of the stomach and increasing the time it takes for gastric emptying.  Like seen in the venous system of the esophagus, the veins of the stomach also experience an increase in pressure in the presence of liver disease.  All these factors lead to an increased risk of gastric ulcer formation with subsequent GI bleeding. 

Small Intestine 

The small intestine is the site of the GI tract where most nutrients are absorbed.  Multiple studies have demonstrated altered absorption of nutrients in the small intestine when exposed to alcohol.  These studies have demonstrated changes in water, electrolyte, carbohydrate, fatty acid, protein, and vitamin absorption.  Vitamins related to critical physiological reactions in the body, such as cyanocobalamin (vitamin B12), thiamine (vitamin B1) and folate, have demonstrated a decrease in absorption in the presence of alcohol, though it is not clear if this malabsorption leads to the deficiency diseases seen in alcoholism.

Small Intestine Mucosal Villi Showing Arterial and Venous Capillaries

Direct alcohol contact also causes inflammation of the small intestine that can cause an increase in permeability of the mucosal lining leading to the passage of other toxins and microbes into the blood stream and lymph.  Alcohol in the small intestines also causes the release of damaging signaling molecules, such as cytokines and leukotrienes, that damage the capillaries of the mucosal lining causing blood clotting in these small vessels.  When extensive, this clotting impairs the passage of fluids and leads to swelling of the mucosal cells killing them.  Some research also demonstrates the production and passage into the blood stream of hepatotoxic cytokines and endotoxin from the overgrowth of certain bacterial species.   It is hypothesized that these harmful byproducts can penetrate the now hyper-permeable intestinal mucosa, and then go on to inflame liver tissue predisposing the alcoholic to cirrhosis.  

Large Intestine

Alcohol has been shown to increase the contractile motility of the large intestine and decrease the contractile strength of the rectal muscles. This may be the cause of the frequent diarrhea reported by individuals with alcoholism. 

Summary

This first of two part series on the impact of alcohol on the gastrointestinal system reviews the consequences of the abusive use of alcohol on the alimentary canal. Part two will review alcohol’s effects on the other organs of the gastrointestinal system. 

 

References:

Sjögren h, et al. Quantification of alcohol-related mortality in sweden. Alcohol alcohol. 2000 nov-dec;35(6):601-11. Doi: 10.1093/alcalc/35.6.601. Pmid: 11093968.

Bode, j.c. alcohol and the gastrointestinal tract. Advances in internal medicine and pediatrics 45:1–75, 1980. 

Bode, j.c., and bode, c. Alcohol malnutrition and the gastrointestinal tract. In: watson, r.r., and watzl, b., eds. Nutrition and alcohol. Boca raton, fl: crc press, 1992. Pp. 403–428.

Alcohol’s role in gastrointestinal tract disorders christiane bode, ph.d., and j. Christian bode, m.d. alcohol health & research world. Vol. 21, no. 1, 1997