作者: Howard J. Edenberg , Jeanette N. McClintick
DOI: 10.1111/ACER.13904
关键词: Acetaldehyde 、 Biology 、 Genetics 、 Linkage disequilibrium 、 Alcohol 、 ALDH2 、 Ethanol metabolism 、 ADH1B 、 Aldehyde dehydrogenase 、 Alcohol dependence
摘要: Alcohol use disorders (AUDs) are complex traits, meaning that variations in many genes contribute to the risk, as does environment. Although total genetic contribution risk is substantial, most individual make only very small contributions. By far strongest contributors functional 2 involved alcohol (ethanol [EtOH]) metabolism. A variant dehydrogenase 1B (ADH1B) protective people of European and Asian descent, a different same gene those African descent. strongly aldehyde (ALDH2) essentially found Asians. This highlights need study wide range populations. The likely mechanism protection against heavy drinking AUDs both cases alteration rate metabolism EtOH at least transiently elevates acetaldehyde. Other ADH ALDH variants, including ADH1C, have also been implicated affecting behavior for alcoholism. pattern linkage disequilibrium region differences among populations complicate analyses, particularly regulatory variants. critical review focuses upon they affect AUDs.