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Drink, Binge and the Genetic Link

ponsible for alcohol metabolism was Aldehyde Dehydrogenase and ALDH1 was discovered to be the underlying gene. A slow metabolizing gene variant of ALDH1, which was common in South East Asian populations, caused the aldehyde build up in these individuals, ensuring a 6-fold decreased risk for alcoholism.

Alcohol dehydrogenase is another enzyme that takes an active part in alcohol metabolism. The variants of the ADH genes enhance the risk of alcoholism. It is also associated with early and heavy drinking, and alcohol-related problems.

Various research groups have documented links between the different chromosomal regions and risk for alcohol dependence. For instance, variants of the gene that codes for GABA receptors on the cell surface increases risk to alcoholism. GABA is a common inhibitory neurotransmitter in the mammalian nervous system. Research is underway to find out the underlying mechanism. It has been observed that there is a loss of inhibition in those with the variant genes, and this has lead to some of them externalizing their behavioral problem. Individuals with variants of this gene have demonstrated conduct problems and usually get into trouble with the law. Another neurotransmitter that is evaluated is acetylcholine. The variants of the genes that encode acetylcholine receptors, such as CHRM2 are known to play a role in influencing alcoholism and depression, thereby prompting individuals with these variants to internalize their problem.

Examining certain endophenotypes has helped to establish familial alcohol-dependence. Although a physical trait, endophenotypes are not visible but can be measured and they help to reveal the biological basis of a disorder. The electrical activity of the brain is one such endophenotype, which can be evaluated using electroenc
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