Academic journal article Alcohol Research: Current Reviews

Alcohol and Gut-Derived Inflammation

Academic journal article Alcohol Research: Current Reviews

Alcohol and Gut-Derived Inflammation

Article excerpt

In large amounts, alcohol and its metabolites can overwhelm the gastrointestinal tract (GI) and liver and lead to damage both within the GI and in other organs. Specifically, alcohol and its metabolites promote intestinal inflammation through multiple pathways. That inflammatory response, in turn, exacerbates alcohol-induced organ damage, creating a vicious cycle and leading to additional deleterious effects of alcohol both locally and systemically. This review summarizes the mechanisms by which chronic alcohol intake leads to intestinal inflammation, including altering intestinal microbiota composition and function, increasing the permeability of the intestinal lining, and affecting the intestinal immune homeostasis. Understanding the mechanisms of alcohol-induced intestinal inflammation can aid in the discovery of therapeutic approaches to mitigate alcohol-induced organ dysfunctions.

Key words: Alcohol consumption; alcohol use, abuse, and dependence; chronic alcohol use; organ damage; gastrointestinal (GI) tract; liver; metabolites; gut-derived inflammation; intestinal inflammation; intestinal microbiota

The gastrointestinal (GI) tract, as the first line of contact with anything ingested into the body, is at particular risk for damage by toxins. And mounting research suggests that poor gastrointestinal health plays a significant role in the body's overall health. Connecting the dots, anything that may cause GI damage, may have consequences far beyond the intestines. In fact, researchers have begun to discover that alcohol, particularly if consumed chronically and in larger amounts, induces a process initiated in the gut that promotes inflammation throughout the body (Patel et al. 2015). This alcohol-induced intestinal inflammation may be at the root of multiple organ dysfunctions and chronic disorders associated with alcohol consumption, including chronic liver disease, neurological disease, GI cancers, and inflammatory bowel syndrome. This review summarizes the mechanisms by which chronic alcohol intake leads to intestinal inflammation. These mechanisms include alcohol's influences on intestinal microbiota, on the integrity of the barrier between the intestine and the rest of the body, and on immune function within and outside the GI tract. The factors that can modify alcohol-induced gut inflammation and organ damage and the resulting pathologies that are a consequence of gut-derived inflammation are described. Although there may be large gender, racial, and interindividual variations in alcohol's effect on the GI tract, depending on differences in alcohol absorption, distribution, and elimination, they are not the focus of the current review.

Alcohol Metabolism and the Gut

Once consumed, alcohol is absorbed mainly in the upper intestinal tract by diffusion and then enters the liver via the portal vein. Therefore, the effect of alcohol on the distal small intestine and colon should largely come from its circulatory levels. That said, the luminal concentration of alcohol in the latter parts of the small intestine, close to the colon, reaches up to 200 mg/100 ml within an hour of drinking 2 to 2 1/2 standard alcoholic drinks (0.8 g/kg) (Halsted et al. 1973).

The majority of alcohol metabolism in humans occurs in the liver, in cells called hepatocytes. During social drinking, defined here as an average of two standard drinks, the body typically processes the ingested alcohol with no deleterious effects through a process called oxidative conversion, during which the enzyme alcohol dehydrogenase (ADH) converts alcohol into the toxin acetaldehyde. Acetaldehyde dehydrogenase (ALDH) then converts acetaldehyde into acetate. Another alcohol metabolism pathway, the microsomal ethanol-oxidizing system (MEOS), handles a small portion of alcohol metabolism in social drinkers but a significant portion of alcohol metabolism when the body needs to process larger amounts of alcohol. MEOS leads to the production of oxygen free radicals, which can cause cellular damage. …

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