Certain genetic variations, such as cytochrome enzymes in the liver, can also influence how quickly a person metabolizes drugs. According to a review from 2016, genes that promote alcohol metabolism and the production of enzymes, such as alcohol dehydrogenase and aldehyde dehydrogenase, can be protective against AUD. The more genetic factors you have, the higher your risk may be of having AUD. Your genetics can influence how likely you are to develop AUD, but there’s currently no evidence of a specific gene that directly causes AUD once you start drinking. With current review, we aim to present the recent advances in genetic and molecular studies of AUDs. Recent successes in genetic studies of AUDs will definetely motivate researchers and lead to better therapeutic interventions for this complex disorder.
- Thus it is not surprising that diseases of the GI system,including cirrhosis, pancreatitis, and cancers of the upper GI tract are affected byalcohol consumption80-86.
- According to the 2021 National Survey on Drug Use and Health, AUD affects approximately 29.5 million people in the United States.
- Research shows that genetic and environmental factors play a role in its development.
- It is likely that, as for most complex diseases, alcohol dependence and AUDsare due to variations in hundreds of genes, interacting with different socialenvironments.
It’s a chronic condition characterized by excessive and compulsive consumption of alcohol, despite harmful consequences. Research shows that genes are responsible for about half of the risk for AUD. Environmental factors, as well as gene and environment interactions account for the remainder of the risk. While genetics can account for up to 60% of AUD risk, not everyone with a family history of AUD will develop the condition. Your genetics don’t only increase your risk of AUD — they may have protective elements as well. The sensitive mice tend to lose their inhibitions and pass out rather quickly, earning them the nickname “long sleepers.” “Short sleepers” are mice that are genetically less sensitive to alcohol.
What gene is responsible for increased AUD risk?
Majority of genomic data for large alcohol consumption and AUD meta-analysis was either from UKBiobank or from Million Veterans Project. Several other cohorts from dbGAP also contributed to large sample size of alcohol consumption GWAS by Liu et al, 2019. Genome-wide data on 14,904 DSM-IV diagnosed AD individuals and 37,944 controls from 28 case/control and family-based studies were meta-analyzed for PGC’s AD GWAS. Some genes may contribute to an increased susceptibility to addictionsin general. It is now appreciated that a whole spectrum of allele frequencies andeffect sizes may play roles, from common variations with small effects throughrare variants of large effect.
Information about the underlying genetic factors that influence risk to AUD can be derived from multiple levels of AUD including amounts of drinks (Alcohol consumption), severity and symptoms of alcohol abuse and dependence. Commonly, genome wide association studies (GWAS) of alcoholism have focused on phenotypes based on the Diagnostic & Statistical Manual of Mental Disorders (DSM)[14]. In the 4th edition of the DSM (DSM-IV), alcohol dependence (AD) and abuse were considered as mutually exclusive diagnoses that together made up AUDs. DSM-V[14, 15] on the other hand consolidated AD and abuse as a single disorder as AUD[15],[16]. By considering AD and abuse under single umbrella increased the number of diagnosed subjects, but this number was still not large enough to design powerful GWAS studies.
Alcohol Misuse Is Influenced by Environmental and Genetic Factors
†Note that the official names of several ADH genes have been changed, and theliterature has been confused by some groups using non-standard names for some ofthe genes29. By Buddy TBuddy T is a writer and founding member of the Online Al-Anon Outreach Committee with decades of experience writing about alcoholism. Because he is a member of a support group that stresses the importance of anonymity at the public level, he does not use his photograph or his real name on this website. Your socioeconomic status can directly affect your mental and physical well-being.
If you live in a situation of poverty, for example, or in an area with limited resources, you may be less likely to have access to quality foods, community services, or adequate healthcare. Your socioeconomic status is made up of economic and societal factors such as your income, level of education, 11 famous heavy drinkers in history and their favorite drinks employment, location of residence, and available resources. Alcohol use disorder (AUD) can have a hereditary component, but not everyone living with AUD has a family history of AUD. This article does not contain any studies with human or animal subjects performed by any of the authors.
Research shows that genetic and environmental factors play a role in its development. Alcohol use disorder (AUD) often seems to run in families, and we may hear about scientific studies of an “alcoholism gene.” Genetics certainly influence our likelihood of developing AUD, but the story isn’t so simple. Is there any scientific evidence that your genes may predispose you to have an alcohol dependency if your parents or grandparents did?
While genetics can play a significant role in your overall AUD risk assessment, it isn’t the only factor that can elevate your chances of developing AUD. Researchers at the University of California at San Francisco (UCSF) are using fruit flies to find the genetic causes of alcoholism. According to scientists, drunken drosophila fruit drug addiction blog flies behave the same way humans do when they are drunk. In addition, a fruit fly’s resistance to alcohol appears to be controlled by the same molecular mechanism as humans. Recognizing alcoholism as a disease promotes early intervention, access to appropriate healthcare services, and ongoing support for people struggling with AUD.
As whole exome and whole genome sequencingtechnologies come down in cost, they are being applied to identifying rarevariants. For studies of rare variants, families are quite valuable for sortingout true positives from the background of individual variations that we allharbor. There is evidence that heavy episodic (binge) drinking, which results inexposure of tissues to high levels of alcohol, alcohol withdrawal timeline is particularly harmful81, 87, 88. Binge drinkingis generally defined as a man consuming 5 standard drinks within 2 hours; women are typically smaller and have a lower percentage of body water, so 4 standarddrinks can reach similar alcohol levels. A standard drink is defined in the US as 12ounces of beer, 5 ounces of wine or 1.5 ounces of spirits, all of which approximate14 g of pure ethanol).
Alcoholism’s Genetic Component
NIAAA is committed to learning more about how genes affect AUD so that treatment—and prevention efforts—can continue to be developed and improved. There is a growing body of scientific evidence that shows alcoholism has a genetic component. According to the American Academy of Child & Adolescent Psychiatry, children of alcoholics are four times more likely than other children to become alcoholics.
Phenotypes/ traits to study AUD
PECRis located within broad linkage peaks for several alcohol-related traits,including alcoholism66,comorbid alcoholism and depression67, level of response to alcohol68, and amplitude of the P3(00)response69, 70. 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.
First and perhaps foremost, most studies ofalcohol-related phenotypes have been small – hundreds or a few thousandsamples. Most robust associations that have been reported in common disease haveemployed tens of thousands of samples and are now beginning to combine severalstudies of these magnitude into even larger meta analyses. The alcohol researchcommunity has begun to form larger consortia for meta-analyses and it is anticipatedthat with the resulting increase in sample size the number of robust associationswill increase. A second approach that will likely benefit the alcohol researchcommunity will be greater examination of pathways or gene sets.
Thus, thegenes and SNPs found through GWAS have had little overlap with previous findingsbased on candidate genes/pathways and linkage analyses. Like many other complex traits, alcoholism appears to be clinically and etiologicaly hetrogenous[13]. This implies that there might be several steps and intermediate conditions in the development of AUD.