This genetic and environmental variability (i.e., heterogeneity) makes the task of identifying individual genes difficult. However, the COGA project was designed with these difficulties in mind and incorporated strategies to meet the challenges. This article briefly reviews these strategies and summarizes some of the results already obtained in the ongoing COGA study. A changing definition of the heterogeneous phenotype of AUD may also pose a challenge to identifying genetic variants through GWAS. The above studies used the DSM-IV-TR criteria for alcohol dependence in order to define the phenotype. As the field of psychiatry transitions to the DSM-5 criteria for AUD, there may also be changes in the functional variants identified by GWAS.

Factors like your environment and your ability to handle situations that may trigger dependency are just as important. These are things that we can remain mindful of as we continue to develop an understanding of alcoholism on a personal basis. «These genes are for risk, not for destiny,» stressed Dr. Enoch Gordis, director of the National Institute on Alcohol Abuse and Alcoholism. He added that the research could help in identifying youngsters at risk of becoming alcoholics and could lead to early prevention efforts.

Am I at Risk of Becoming Addicted to Alcohol?

On the other hand, not having genes linked to alcoholism doesn’t mean you won’t develop an addiction. The NIDA study found that the genes involved in alcohol abuse were concentrated in 51 chromosomal areas in the body. The genes involved are players in a variety of basic body function, such as cell-to-cell communications, the control of protein synthesis, cell-to-cell interactions, and regulation development. It may be that dysregulation in these areas makes a person vulnerable to alcohol or other drug abuse.

These coding regions may have a strong impact on disease etiology and shed new light into possible pathophysiological mechanisms (Cirulli and Goldstein, 2010; Ng and Kirkness, 2010; Kato, 2015). Research has suggested that it’s a combination of the above risk factors as well as genetics that could determine whether or not you develop alcohol use disorder. Some mental health conditions may be a risk factor for developing alcohol use disorder, including clinical depression and schizophrenia, which also have a genetic component. For example, it has already provided a test of new methods for genetic analysis, as presented at the Genetic Analysis Workshop 11 (Begleiter et al. 1999).

Does Everyone with Alcoholic Parents Develop AUD?

Various studies have examined how BDNF impacts the interaction between alcohol preference and anxiety. For example, Pandey and colleagues (2006) reduced BDNF levels in the extended amygdala by introducing small molecules that can inhibit BDNF expression https://ecosoberhouse.com/ (i.e., antisense oligodeoxynu­cleotides) into the CeA or MeA. The low BDNF levels resulted in reduced BDNF signaling, as evidenced by decreased levels of the phosphorylated forms of CREB and another regulatory molecule (Pandey et al. 2006).

• Awareness of the need for large sample sizes for GWAS has resulted in the formation of large scale collaborations for sharing data, such as the Psychiatric Genomics Consortium [82].
• Over the past two decades, several genes
  underlying susceptibility have been identified.
• The heavy drinking that often occurs in alcohol use disorder, and can also occur in short-term episodes called binge drinking, can lead to a life-threatening overdose known as alcohol poisoning.
• This paper identified risk loci (positions in the chromosome), in 2019, with shared effects on alcoholism, heroin, and methamphetamine dependence.
• That is, a predisposition to metabolize the substance in such a way that the pleasurable effects are more prominent than adverse effects such as nausea and headaches increases a person’s risk of developing an alcohol use disorder.
• While the underlying pathophysiology of AUD is poorly understood, there is substantial evidence for a genetic component; however, identification of universal genetic risk variants for AUD has been difficult.

This has resulted in a paradigm shift away from gene centric studies towards analyses of gene interactions and gene networks within biologically relevant pathways. Several study designs—including case–control studies, population studies, and family studies—have been used to test whether a specific gene or gene variant affects risk for a disease (for more information, see the article by Foroud and Phillips, pp. 266–272). For example, it is much easier to collect individual cases (i.e., people with alcoholism) and control subjects (i.e., nonalcoholic people) or samples of the general population than it is to recruit family samples. On the other hand, family studies avoid the problem of incomplete ethnic/population matching1 that can confound case–control studies. Furthermore, family studies can be more powerful than case–control studies if different variants (i.e., alleles) of the same gene affect a given trait in different families, because multiple families can show an effect of that gene despite not sharing the same alleles. In addition, broad regions of the genome generally are inherited within a family, increasing the sensitivity of the approach to detect an effect; however, the tradeoff is that for the same reason, family studies have less resolution to identify the specific allele(s) involved.

BDNF and Epigenetic Mechanisms in Stress and Alcoholism

Moreover, histone modifications and DNA methylation are involved in the dysphoric states induced by acute and chronic stress (Elliott et al. 2010; Fuchikami et al. 2009; Hunter et al. 2009; Tsankova et al. 2006). Specifically, various studies have demonstrated that epigenetic mechanisms are involved in the regulation of BDNF gene transcription, which in turn plays a role in the modulation of synaptic structure and function (He et al. 2010; Lubin et al. 2008; Tsankova et al. 2006). However, multiple studies have shown that some of these genes have been identified, including two genes of alcohol metabolism, ADH1B and ALDH2, that have the strongest known effects on risk for alcoholism. Studies are revealing other genes in which variants impact risk for alcoholism or related traits, including GABRA2, CHRM2, KCNJ6, and AUTS2. This question stumped many until a 2008 study by the National Institution on Alcohol Abuse and Alcoholism proved that genetic factors play a huge role in those that struggle with alcohol abuse. Since then, specific genes that play a direct role in the development in the reward center of the brain have been located.

As researchers have noted, other genes (beyond the cluster that NIDA found) can play a role in the development of an alcohol use disorder. Second, if an identical twin has a sister or brother who has an alcohol use disorder, the odds are not that they will also develop one. Among males, it’s 50 percent, not 51 percent, which would mean that the development of an alcohol use disorder was more likely than not. As yet, no GABRA2 functional variant has been detected is alcoholism inherited to explain the yin yang haplotype (or tag SNP) associations with alcoholism-related phenotypes. HapMap data and other studies [52] reveal moderate long distance linkage disequilibrium across GABRA2 and the closely adjacent gene GABRG1 raising the possibility that the functional locus is in GABRG1. The results of several studies suggest that there are likely to be independent, complex contributions to alcoholism vulnerability from both linked genes [52–54].

This finding led to the discovery of the association of GABRA2 with AUD, a robust, widely replicated finding that will be discussed below. For the study, the researchers used genetic data from the multi-ethnic Million Veteran Program (MVP), a national, voluntary research program sponsored by the Department of Veterans Affairs, which includes white, African-American, Latino, and Asian participants. The diverse study sample is notable, in that it included more than 50,000 African-Americans, one of the largest genome-wide studies of this population. Scores from the Alcohol Use Disorder Identification Test-Consumption (AUDIT-C) screenings and AUD diagnoses were obtained from the same population (a total of 274,424 people) to conduct the GWAS for the two traits. The researchers also analyzed other data from health records to look for correlations between genes and diseases, as well as other non-alcohol related traits. Based on previous linkage studies, the strongest associations have been identified in the alcohol metabolism genes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).

A study in Sweden followed alcohol use in twins who were adopted as children and reared apart. The incidence of alcoholism was slightly higher among people who were exposed to alcoholism only through their adoptive families. However, it was dramatically higher among the twins whose biological fathers were alcoholics, regardless of the presence of alcoholism in their adoptive families. You might also find it helpful to confide in a trusted loved one whose support can be instrumental in your recovery. You could also look for support groups online or in your area for people with substance use disorders. There isn’t one single “alcohol use disorder gene.” Rather, there are many different genes that may influence whether someone develops an alcohol use disorder.

Genetics and Alcoholism: Is Alcoholism Genetic or Hereditary?

This condition has been present in human history since men learned to ferment fruit – which is about 10 million years ago. Learn more about hereditary alcoholism, including the latest research on genetic variants, from the Delphi Behavioral Health Group. Alcohol use disorder is a diagnosis made when an individual has severe problems related to drinking alcohol. Alcohol use disorder can cause major health, social, and economic problems, and can endanger affected individuals and others through behaviors prompted by impaired decision-making and lowered inhibitions, such as aggression, unprotected sex, or driving while intoxicated.