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The genes with the clearest contribution to the risk for alcoholism andalcohol consumption are alcohol dehydrogenase 1B (ADH1B) andaldehyde dehydrogenase 2 (ALDH2; mitochondrial aldehydedehydrogenase), two genes central to the metabolism of alcohol (Figure 1)20. Alcohol is metabolized primarily in the liver, although thereis some metabolism in the upper GI tract and stomach. The first step in ethanolmetabolism is oxidation to acetaldehyde, catalyzed primarily by ADHs; there are 7closely related ADHs clustered on chromosome 4 (reviewed in20).
Genes can play an important role, however, by affecting processes in the body and brain that interact with one another and with an individual’s life experiences to produce protection or susceptibility. Teasing these effects apart is challenging, and to date fewer than https://ecosoberhouse.com/ a dozen genes that influence one’s risk for alcoholism have been identified, although more surely exist. Recent estimates indicate that 5.6% of individuals meet criteria for a past year AUD [2], resulting in significant social, economic and public health costs [3,4].
According to information published by the National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, research shows that your genetic makeup accounts for approximately 50% of the likelihood that you will develop an AUD. If an adolescent’s friends drink heavily, they are more likely to drink to conform. In addition, religious background and culture may also play a role in a person’s decision-making. Genetic diseases, on the other hand, are illnesses that are caused by mutations in the person’s DNA.
While heredity and genetics are closely linked, they can mean different things from a medical perspective. There are also countless environmental factors (work, stress, relationships) that may lead to alcoholism. Environmental factors, as well as gene and environment interactions, account for the remainder of the risk. Among the behavioral traits is alcoholism inherited parents can pass on to their children is a predisposition toward alcohol abuse and addiction. Janowsky’s group proposed that muscarinic supersensitivity–that is, an enhanced effect of acetylcholine on the muscarinic cholinergic receptors–in persons prone to depression and related conditions was an underlying source of imbalance in the brain.
Sanchez-Roige explained that variants, or alleles, of these particular SNPs are “protective” against a variety of alcohol behaviors, from excessive alcohol drinking to alcohol use disorder. Sanchez-Roige explained that variants, or alleles, of these particular SNPs are “protective” against a variety of alcohol behaviors, from excessive alcohol drinking to alcohol use disorder. As we have learned more about the role genes play in our health, researchers have discovered that different factors can alter the expression of our genes. Scientists are learning more and more about how epigenetics can affect our risk for developing AUD.
Critics have argued that genetic research into alcohol dependence and other forms of addiction, including smoking, is not cost-effective from a public health perspective. For instance, some claim that it would make more sense to direct resources toward reducing the use of potentially addictive substances across the board than to identify–and potentially stigmatize–the individuals who would be most affected by such reductions. Undoubtedly, there is value in limiting the use of alcohol, nicotine and other mood-altering drugs in general. There is also value, however, in supporting individual self-knowledge as it pertains to susceptibility so that people can make informed choices for themselves and in shaping a culture that regards this as a positive goal.