Genetic Influences on Alcoholism Risk: A Review of Adoption and Twin Studies

Subsequent analysis showed that AUTS2 was implicated in alcohol consumption in mice and alcohol sensitivity in drosophila 69. We employed gSEM to examine multivariate associations between alcohol use, AUD, and life satisfaction. This study builds upon our previous work demonstrating both improved model fit after partitioning genetic variance into separate alcohol use and AUD factors26 and differential genetic associations across these factors and PTSD22.

What are the protective factors for AUD?

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition, text revision (DSM-5-TR), a clinical diagnostic guidebook, indicates that AUD often runs in families at a rate of 3–4 times higher compared with the general population. Alcohol use disorder (AUD) is a diagnosis once referred to as “alcoholism.” It’s a condition characterized by patterns of excessive alcohol misuse despite negative consequences and major distress in important areas of daily function. Every person carries two copies of every gene, one inherited from the mother and one inherited from the father. Policies regulating the sale and use of alcohol can serve as important tools in preventing alcohol problems and merit increased attention among tribes. However, although such policies may succeed to some extent in community settings such as reservations, they may be more difficult to implement in urban or rural settings in which American Indians are only a small portion of the total population.

Candidate gene studies of AUD and related traits

A summary of the studies examined in this article, organized by the trend between alcohol and weight gain/obesity can be found in Table 1. May (1992) listed 107 policy options that could be considered by tribes to control levels of use within communities. The options were divided into the categories of controlling supply, shaping drinking practices, and reducing social and physical harm. All options are not feasible everywhere, but a core set could be implemented in most communities. A strong research initiative to evaluate the what percentage of alcoholism is genetic effects of policy implementation and changes also seems warranted.

Alcohol Intake and Obesity: Experimental Evidence

The distribution of ADH1B and ALDH2 coding variants differs greatly among different populations; for both genes, the protective alleles most commonly are found in people of East Asian origin (for more information, see the article by Eng et al. in this issue). For example, ADH4 variants strongly affect alcoholism risk in populations of European descent (Edenberg et al. 2006). Furthermore, noncoding variations in various alcohol-metabolizing enzymes likely also affect risk for alcoholism (Edenberg et al. 2006). Although not necessarily a cause or consequence of alcohol abuse or alcoholism, other mental disorders often co-occur with alcohol disorders. No studies have compared the prevalence of co-occurring psychiatric disorders between Indians and non-Indians, but clearly such disorders are common among Indian populations. Robin and colleagues (1998) found that among a large group of adults from a Southwestern tribe, binge drinkers were 5.5 times more likely to have had a psychiatric problem than nondrinkers.

Alcohol Intake and Obesity: Observational Evidence

Gene names in humans are written in all caps and are italicized, whereas the acronyms for the encoded proteins are all caps but not italicized. 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.

• To our knowledge, there does not appear to be any experimental evidence specifically testing the effects of heavy/binge drinking, or of drinking spirits or a combination of alcohol sources on weight gain/obesity.
• The class I ADH enzymes encoded by the ADH1A, ADH1B and ADH1C genes contribute about 70% of the total ethanol oxidizing capacity, and the class II enzyme encoded by ADH4 contributes about 30% 19.
• This style of drinking is only one of a wide range of styles practiced within Indian communities; aside from the research conducted by May (1995), however, little has been done to characterize the various patterns.
• Indeed, work by our group using gSEM found that the best fitting model was one that differentiated genetic factors for alcohol use and AUD relative to models with all alcohol-related indicators loading onto a single factor26.
• The strongest and most consistent findings for GWAS for AUD are for alcohol metabolizing genes, as in a recent study in an East Asian (Korean) sample of alcoholics in which ALDH2 and ADH1B showed up as GWAS signals with genome-wide significance 68.
• While cross-sectional and longitudinal studies have controlled for a number of important lifestyle factors, there are many to consider when examining body weight regulation.