The term "alcohol use disorder" (AUD) is a recently recommended term that encompasses two categorizations, alcohol abuse and alcohol dependence. The Disease Ontology distinguishes between substance abuse and substance dependence, and thus uses two separate terms: alcohol use disorder, DOID:1574, and alcohol dependence, DOID:0050741. Individuals at risk for AUDs are sensitive to alcohol's rewarding effects and/or resistant to its aversive and sedating effects. AUD has multiple genetic risk factors, most as yet undefined, as well as environmental/social risk factors.
Fruit flies are exposed to ethanol in their natural habitat, since larvae feed on fermented food sources. Ethanol provides a chemical signal for flies to locate food and oviposition sites. Flies are attracted to low concentrations of ethanol, but are repelled by high concentrations; olfactory and gustatory responses differ. Over time, flies will increasingly overcome an aversive stimulus in order to consume ethanol. Intake of low concentrations of ethanol stimulates locomotor activity, whereas high concentrations induce phenotypes similar to human alcohol intoxication, including locomotor impairments, loss of postural control, sedation, and immobility (Morozova et al., 2014; FBrf0237874).
Experimental techniques and assays used to study alcohol response, sensitivity, and tolerance in flies are described in Rodan and Rothenfluh, 2010 (FBrf0211728) and in Engel et al., 2019 (FBrf0241958).
In addition to characterization of individual candidate genes, systems genetics approaches have been used in flies to identify genetic networks associated with alcohol sensitivity. Park et al., 2017 (FBrf0235911) provide an extensive review of work done in flies, including recent genomic-level studies. Lowenstein and Velazquez-Ulloa, 2018 (FBrf0238815) review work done in flies relevant to several different addictive drugs, including alcohol, and highlight commonalities.
For candidate susceptibility loci studied using Drosophila models see the "Related Diseases" section, below, or go to the FlyBase Human Disease Model Report Index (http://flybase.org/lists/FBhh/). See also the FlyBase chemical report for ethanol (FBch0000064).
[updated Mar. 2024 by FlyBase; FBrf0222196]
[ALCOHOL DEPENDENCE](https://omim.org/entry/103780)
The 2013 Diagnostic and Statistical Manual of Mental Disorders (DSM) combined the two former categorizations of abnormal alcohol use (alcohol abuse and alcohol dependence) into one diagnosis: alcohol use disorder. The severity of an individual's AUD is broken into classifications: mild, moderate, or severe. "Alcoholism" is a non-medical term often used to describe a severe form of alcohol use disorder. (https://www.therecoveryvillage.com/recovery-blog/alcoholism-alcohol-use-disorder-whats-difference/)
Excessive alcohol consumption is associated with increased risk of different types of cancer, higher cardiovascular disease mortality, birth defects, liver diseases, and neuropsychiatric disorders (Morozova et al., 2014; pubmed:24395673).
Alcoholism can be defined as persistence of excessive drinking over a long period of time despite adverse health effects and disruption of social relations (Morozova et al., 2014; pubmed:24395673).
Alcoholism is a multifactorial, genetically influenced disorder. [from MIM:103780; 2017.12.19]
Twin studies show that monozygotic twins are more alike in risk for alcoholism than fraternal twins; twin and family studies suggest that approximately 45-65% of the liability is genetic (Edenberg and Foroud, 2014; pubmed:25307596).
Susceptibility to the inebriating effects of alcohol and alcohol addiction can be viewed as quantitative traits that result from the cumulative effects of multiple segregating genes and their interactions with the environment (Morozova et al., 2014; pubmed:24395673).
Alcohol resistance and acquired tolerance have distinct genetic origins (reviewed in FBrf0235911).
