Alcohol: Reducing the Risks
When alcohol (ethanol) is ingested, some is absorbed through the stomach lining and some is broken down by enzymes in the stomach, but most (about 80%) passes into the small intestine and is absorbed rapidly into the blood. The presence of food in the stomach slows transit to the small intestine, delaying absorption. On the other hand, when the stomach is empty, alcohol moves quickly to the intestines and is absorbed into the blood (Cederbaum 2012; Paton 2005; Manzo-Avalos 2010).
Absorbed alcohol travels to organs and tissues via the blood, and most is converted into acetaldehyde, primarily in the liver, by a family of enzymes called alcohol dehydrogenases. Acetaldehyde is a toxin and carcinogen that can cause nausea, vomiting, headache, and fatigue (Wang, Li 2016). Most acetaldehyde produced from alcohol is converted by the enzyme aldehyde dehydrogenase into acetate, which can be used for cellular energy production in tissues throughout the body (Cederbaum 2012), making alcohol a rich source of empty calories—about 7 kilocalories per gram (Tayie 2016). Individuals with a genetic variation that limits their production of aldehyde dehydrogenase have been found to be more susceptible to hangover, suggesting a possible role for acetaldehyde as a contributor to hangover symptoms (Wall 2000; Yokoyama 2005).
Nutrients Influence Alcohol Metabolism
Certain nutrients are essential for the metabolism of alcohol. For example, zinc and vitamin B3 are necessary for the proper function of alcohol dehydrogenase enzymes (Cederbaum 2012).
An important form of vitamin B3 called nicotinamide adenine dinucleotide (NAD+) is reduced to NADH during alcohol metabolism (Cederbaum 2012). NAD+ is required for many fundamental biological processes, including the metabolism of glucose, fats, and proteins. When depleted during alcohol metabolism, NAD+ may be unavailable for other important biological processes such as DNA repair, which could contribute to some of alcohol’s toxic effects. As demonstrated in animal and clinical studies, NAD+ levels can be boosted by the nutrient nicotinamide riboside (Trammell 2016).
The microsomal ethanol oxidizing system is another pathway—an alternative to the alcohol dehydrogenase enzyme pathway—for metabolizing alcohol (Han 2016; Cederbaum 2012; Kawaratani 2013). However, alcohol metabolism through the microsomal ethanol oxidizing system produces a damaging free radical called 1-hydroxyethyl radical (Cederbaum 2012; Stoyanovsky 1998). Nutrients including vitamins C and E, glutathione, as well as the glutathione cofactors N-acetylcysteine and selenium, participate in neutralizing the 1-hydroxyethyl radical (Stoyanovsky 1998; Ronis 2005; Clausen 1988; Roes 2002), while alcohol consumption can deplete these nutrients (Puntarulo 1999). Obtaining optimal amounts of these nutrients through diet and supplementation may help attenuate alcohol toxicity.