Alcohol is a vehicle that depletes the body of vital nutrients and, most specifically, those in the B vitamin family. The nutrient deficiencies are most often rooted in malnutrition, malabsorption, and ethanol toxicity. Sudden or rapid alcohol exposure causes the cells of the liver to release their vitamin content, but even slow, continual exposure to alcohol disrupts many metabolic processes and gives rise to nutrient deficiencies.

Malnutrition

Nutrient depletion and alcoholism occur in a dose-dependent manner, and could be explained by the fact that those who drink the most alcohol generally consume the fewest nutrients through food, instead of relying on the caloric energy provided by ethanol. Malnutrition, therefore, is a great concern among chronic or excessive alcohol consumption. It is also found that those who rely on alcohol for calories tend to favor unhealthy food choices, explaining the nutrient deficiencies common in alcoholics and associated with numerous chronic diseases.

B vitamin depletion remains the foremost nutrient deficiency among those who consume alcohol. In an animal study where rats could freely partake of a 15% ethanol solution for 28 days, the content of vitamins B1, B2 (riboflavin), B6, and B5 (pantothenic acid) was lower in blood, urine or the liver when the diet was also low in these nutrients. Since many individuals who regularly drink alcohol also consume a standard diet deficient in many vital nutrients, it is critical that these individuals supplement with nutrients, adopt a nutrient-rich diet, and reduce alcohol consumption.

Malabsorption

Malabsorption often explains the nutrient deficiencies noted among moderate drinkers. Alcoholics malabsorb fat, nitrogen, sodium, thiamin, folic acid and vitamin B12. Pancreatic insufficiency, abnormal biliary secretion, and the direct effects of alcohol on the gastrointestinal tract are responsible for malabsorption. However, recent research shows that alcohol also alters the gut microbiota, which leads to hepatocyte damage, liver cirrhosis and liver failure. Both short term and long term alcohol use has been linked to changes in the gut microbiota, leading to a state of dysbiosis that favors proinflammatory bacteria and results in less short-chain fatty acid production. As the gut mucous barrier diminishes and the gut epithelium becomes permeable, endotoxins leak into the bloodstream, contributing to both liver damage and mental disturbance.

Interestingly, those who consumed excessive alcohol showed gastrointestinal alterations of the small intestine similar to those with untreated celiac disease, another condition for which malnourishment and malabsorption are classical markers and the resulting nutrient deficiencies have been responsible for comorbid conditions.

Neurological Effects

Chronic or continuous alcohol consumption is also associated with neurological damage, affecting the brain, periphery, mood, and cognition. Many of the resulting conditions are also linked with B vitamin deficiencies. For example, 25 to 66 percent of chronic alcoholics experience alcoholic neuropathy. Traditionally, this condition has been thought to develop as a result of the nutritional deficiencies (particularly, thiamin) common in those who consume alcohol. Alcohol reduces thiamin absorption, hepatic stores, and the ability to convert thiamin to its active form. The features of alcoholic neuropathy are identical to those of nonalcoholic thiamin deficiency neuropathy.

Chronic alcohol consumption is also associated with increased risk of traumatic brain injury, seizures, stroke, Wernicke’s encephalopathy, Korsakoff’s syndrome, hepatic encephalopathy, central pontine myelinolysis, alcoholic cerebellar degeneration, and alcohol-related dementia. Both Wernicke’s encephalopathy and its progressed form, Korsakoff’s syndrome, are direct results of a thiamin deficiency. Central pontine myelinolysis is an outcome of alcohol-induced electrolyte imbalances.

Finally, pellegra is frequently induced by alcohol and includes depression, dementia, anxiety, and other neurological manifestations. Pellegra is caused by a deficiency of niacin but is compounded by additional B vitamin deficiencies. Alcoholic pellagra encephalopathy is most commonly managed with niacin, other B vitamins and dietary protein.

Alcohol consumption greatly influences nutritional status and health, and should be evaluated in a complete health history. When either managing or preventing the potential health effects of alcohol consumption, it is vital to correct B vitamin deficiencies, address dysbiosis and gut damage with probiotics, support the liver, and support the brain and neurological system with neuroprotective nutraceuticals while giving nutritional guidance.

By Nicole Spear, MS, CNS