Over the years, an increasing body of research has emerged looking at the genetic risk factors for alcoholism. Although some associations are inconclusive, research so far demonstrates that genetic factors may have a significant influence on one’s likelihood to develop harmful drinking habits.
Within this research, replicated genetic risk factors for alcoholism involve genes linked to metabolism. A good example of this is a variant of ALDH2. For alcohol to be consumed, certain genes typically encode proteins that convert it into acetaldehyde, and then into acetate. Should certain genes prevent its conversion to acetate however, such as a certain variant of ALDH2, it builds up in the body. As acetaldehyde is a toxin, this build-up then typically leaves drinkers feeling hot and nauseous, discouraging them from further drinking (Szalavitz: 2015).
This particular version of ALDH2 is known to be common in Asian populations. A meta-analysis of 15 studies looking at the drinking habits of 4,500 Chinese, Japanese, Korean and Thai participants found that those who had this ALDH2 variant were nine times less likely to develop alcoholism than others with different versions of the gene (Luczak: 2006). However, despite the gene’s presence, it’s activation is still highly dependent on environmental factors. For example, between 1979 and 1992, the percentage of Japanese people who developed alcoholism while having this gene variant jumped from 2.5% to 13% thanks to the development of a heavy drinking culture among businessmen and the declining economic climate (Ray: 2016).
Meanwhile, a variant of a gene known as GABRB1, has been associated with increased alcohol consumption. In a study looking at mice, researchers found that mice with certain mutations of the gene preferred drinking alcohol (10% ethanal) over water, unlike regular mice. In fact, they enjoyed alcohol so much that they were willing to work to obtain alcoholic drinks by pushing a lever for long periods of time to the point of intoxication (Newcastle University: 2013).
But how does it work? The gene GABRB1 codes for the beta 1 subunit, an important component of the GABAa receptor in the brain that responds to GABA, an inhibitory chemical messenger that regulates brain activity. The researchers found that this specific mutation in the gene caused the receptor to activate spontaneously, without a normal GABA trigger. Such changes were particularly present in areas of the brain responsible for emotions and reward. As the electrical signals in these regions increased, so did the mice’s desire to drink (ibid.). Although similar observations in alcohol consumption have been made in middle-aged people, adolescents with the same mutation did not necessarily have the same response, meaning further research is necessary to confirm, and understand, any association in humans.
To conclude, although genes seem to play a major role in how we metabolise and respond to alcohol consumption neurologically, it appears that they leave one more predisposed to a certain relationship with alcohol, rather than guarantee one. Thus, to properly understand the causes of alcoholism. more research looking at how these genetic factors interact with and are triggered by environmental factors is needed.
Szalavitz, Maia: Nature
Luczak SE. et al: Pub Med
Ray, Lara A.: US National Library of Medicine
Fowler, CD: Pub Med
Newcastle University, Science Daily