cloaking hidden backlink mu-plugins {"id":5280,"date":"2020-12-09T16:25:44","date_gmt":"2020-12-09T16:25:44","guid":{"rendered":"https:\/\/www.mmu.ac.ke\/photojournalism\/?p=5280"},"modified":"2026-02-24T08:02:58","modified_gmt":"2026-02-24T08:02:58","slug":"health-topics-genetics-and-alcohol-use-disorder","status":"publish","type":"post","link":"https:\/\/www.mmu.ac.ke\/photojournalism\/2020\/12\/09\/health-topics-genetics-and-alcohol-use-disorder\/","title":{"rendered":"Health Topics: Genetics and Alcohol Use Disorder National Institute on Alcohol Abuse and Alcoholism NIAAA"},"content":{"rendered":"
The rate at which alcohol is metabolized and the nature and fate of its degradation products are important factors that determine its physiological effects. The human genome contains five ADH classes with a total of seven closely related genes located on chromosome 4q. While there are 18 genes encoding members of the ALDH enzyme family, only ALDH2 plays a major role in oxidizing acetaldehyde in the liver (Edenberg 2013). This review describes the genetic approaches and results from the family-based Collaborative Study on the Genetics of Alcoholism (COGA). COGA was designed during the linkage era to identify genes affecting the risk for alcohol use disorder (AUD) and related problems, and was among the first AUD-focused studies to subsequently adopt a genome-wide association (GWAS) approach.<\/p>\n
Recent genome-wide studies (GWAS) have pinpointed specific genetic variants linked to this predisposition. Alcohol intolerance is mostly genetic and especially common among people of East Asian descent. It is caused by a variation in the ALDH2 gene, which leads to a buildup of acetaldehyde, a toxic byproduct of alcohol. This results in symptoms such as facial flushing, rapid heartbeat, nausea, and headaches even after small amounts of alcohol, often discouraging drinking and lowering the risk of developing alcohol use disorder. Other relevant cell types for AUDIT-C, but not for AUD, included cardiovascular, adrenal or pancreas, liver, and musculoskeletal. Thus, although heavy drinking is prerequisite to the development of AUD, the latter is a polygenic disorder and variation in Alcoholics Anonymous<\/a> genes expressed in the CNS (e.g., DRD2) may be necessary for individuals who drink heavily to develop AUD.<\/p>\nFindings of the 2023 multiancestry GWAS of PAU<\/h2>\n