Studies of populations at high risk for alcoholism.
The evidence supporting genetic factors in alcoholism comes from family studies (an alcoholic biological parent is seen in 31 per cent of alcoholics), twin studies (MZ concordance 55 per cent and 28 per cent for DZ twins), and adoption studies (alcoholism 44 per cent higher in adopted out offspring of alcoholics than controls). Once the presence or absence of a biological alcoholic parent is controlled for, rearing experiences and parental loss do not increase the risk for alcoholism. This conclusion justifies the search for genetic factors which might mediate the increased risk, particularly in groups identified as being at high risk for the development of alcoholism. The methodological assets and liabilities of the 'high risk' approach are reviewed, with reference to a detailed discussion of existing longitudinal and cross-sectional studies of high-risk populations. There is little convincing evidence that measurable personality attributes or differences in rate of ethanol breakdown contribute to alcoholism vulnerability, although high risk groups may have a unique EEG pattern in childhood, and in early adulthood decreased intensity of ethanol response, and increased acetaldehyde may be important.
D000079:Acetaldehyde / Q000097:blood; D000300:Adoption; D000437:Alcoholism / Q000097:blood / Q000150:complications / Q000235:genetics*; D001289:Attention Deficit Disorder with Hyperactivity / Q000235:genetics; D003071:Cognition; D004200:Diseases in Twins; D004299:Dopamine beta-Hydroxylase / Q000097:blood; D004361:Drug Tolerance; D004569:Electroencephalography; D004777:Environment; D000431:Ethanol / Q000378:metabolism; D006801:Humans; D008995:Monoamine Oxidase / Q000097:blood; D019964:Mood Disorders / Q000150:complications; D010551:Personality; D012107:Research Design; D012306:Risk
D000431:Ethanol; D004299:Dopamine beta-Hydroxylase; D008995:Monoamine Oxidase; D000079:Acetaldehyde