Short of drinking to the point of intoxication, alcohol is probably good for us in some ways; it’s what happens to it during metabolism that is responsible for most of the toxic effects. From hangovers to cancer, the danger is due to a toxic metabolite called acetaldehyde, a class 1 carcinogen. Alcohol, which is non-carcinogenic by itself, is converted into acetaldehyde by enzymes called alcohol dehydrogenases (ADH), and there is considerable variation in ADH from person to person. Also variable is individual levels of the enzyme aldehyde dehydrogenase (ALDH) that disposes of acetaldehyde by converting it into innocuous acetic acid (vinegar.) Because ALDH plays such a critical role in detoxification, it is a key to understanding how the risks of drinking might be tempered. Research is revealing ways that we may be able to boost our ALDH levels and thereby tilt the risk/benefit ratio of moderate drinking in our favor.
This is mostly preclinical evidence, though the premise appears to be legit. The first approach uses supplements that enhance the body’s natural production of ALDH. One molecule being tested is hederagenin, derived from the common ivy plant and present in quinoa. A study from the National University of Science and Technology in Seoul, Korea, found that the pro-inflammatory effects of alcohol could be alleviated in rats, by stimulating increased production of ALDH from hederagenin added to their chow. This was a well-designed study, and the authors extrapolated that hederagenin could be used to prevent alcoholic liver injury in humans. But outside of politics, most people aren’t rats, and clinical studies on the use of hederagenin are lacking (most therapies that appear promising in lab animals fail in human clinical trials.) Also, there are potentially serious side-effects of hederagenin that may explain toxic effects of eating ivy observed in dogs, cats, and cattle. So I’m not ready to stock up on this one just yet, but it’s worth keeping an eye on.
Another research group from Korea tested a mulberry extract, based on the idea that mulberry fruit is high in anthocyanins (polyphenols which also give red wine its color). Their rats were given either a mulberry extract or placebo, followed by a standardized dose of alcohol. Peak serum alcohol and acetaldehyde levels were lower in the supplement group.
Yet another Korean lab* may have found a different approach. A team from the Chung-Ang University College of Medicine in Seoul noted that a significant proportion of acetaldehyde metabolism in some people comes from colonic bacteria, our gut microbiome, and they speculated on whether this could be enhanced. Certain fermented dairy products are made with bacteria known to contain naturally high levels of ALDH, so they investigated whether this could be used as a probiotic. They identified 5 species, (3 of dairy origin and 2 of nondairy origin) which showed ALDH activity, and used the one with the highest ALDH production (L. chungangensis) to make cream cheese. This was then fed to rats before giving them alcohol. The ones given the cream cheese canapés before the drinking party had lower serum levels of acetaldehyde.
A handful of clinical trials have been reported, but most are of low quality. One exception is a randomized double blind crossover study from India that found faster elimination of blood acetaldehyde along with significant decreases in oxidative stress and C-reactive protein (a marker of inflammation) using a standardized polyphenolic extract of clove buds (Clovinol).
Other than augmenting our colonic flora with ALDH-producing cream cheese bacteria, most of what’s been tried is based on plant extracts containing polyphenol antioxidants. It’s tempting to conclude that wine should be the favored drink because it is naturally high in polyphenols, but that hasn’t been specifically looked at with respect to acetaldehyde metabolism. There is one very intriguing study from Japan that may shed some light on this, by looking at oral cavity bacteria. Cancers of the oral cavity have long been known to have an association with alcohol consumption, and the connection may be the major influence of the oral microbiome on acetaldehyde levels in saliva. Comparing salivary acetaldehyde concentration after consuming beer, wine, or shochu (similar to sake but with 25-30% alcohol), the lowest levels were found with red wine, despite its higher alcohol content relative to beer. Clearly there’s a lot more to learn about this subject, and it is of vital importance to anyone interested in healthy drinking.
*Most of the research in this field is from Asia, where up to 40% of people have a variant of ALDH resulting in slower metabolism of alcohol. This causes a characteristic facial flushing and buildup of acetaldehyde, and increased risk of oral and upper airway cancer in those who drink despite these unpleasant side-effects.
Eriksson CJ. Genetic-epidemiological evidence for the role of acetaldehyde in cancers related to alcohol drinking. Adv Exp Med Biol. 2015;815:41-58.
 Kim GJ, Song DH, Yoo HS, Chung KH, Lee KJ, An JH. Hederagenin Supplementation Alleviates the Pro-Inflammatory and Apoptotic Response to Alcohol in Rats. Nutrients. 2017 Jan 6;9(1).
 Zeng J, Huang T, Xue M, Chen J, Feng L, Du R, Feng Y. Current knowledge and development of hederagenin as a promising medicinal agent: a comprehensive review. RSCAdv., 2018,8,24188–24202.
 Yang HJ, Kim MJ, Kang ES, Kim DS, Park S. Red mulberry fruit aqueous extract and silk proteins accelerate acute ethanol metabolism and promote the anti oxidant enzyme systems in rats. Mol Med Rep. 2018 Jul;18(1):1197-1205.
 Konkit M, Kim K, Kim JH, Kim W. Protective effects of Lactococcus chungangensis CAU 28 on alcohol-metabolizing enzyme activity in rats. J Dairy Sci. 2018 Jul;101(7):5713-5723.
 Mammen RR, Natinga Mulakal J, Mohanan R, Maliakel B, Illathu Madhavamenon K. Clove Bud Polyphenols Alleviate Alterations in Inflammation and Oxidative Stress Markers Associated with Binge Drinking: A Randomized Double-Blinded Placebo-Controlled Crossover Study. J Med Food. 2018 Nov;21(11):1188-1196.
 Yokoyama A, Tsutsumi E, Imazeki H, Suwa Y, Nakamura C, Mizukami T, Yokoyama T. Salivary acetaldehyde concentration according to alcoholic beverage consumed and aldehyde dehydrogenase-2 genotype. Alcohol Clin Exp Res. 2008 Sep;32(9):1607-14.