Genes Contributing to the Development of Alcoholism: An Overview Alcohol Research: Current Reviews

Researchers have used both case–control and family studies to identify genes related to alcoholism risk. In addition, different strategies such as candidate gene analyses and genome-wide association studies have been used. The strongest effects have been found for specific variants of genes that encode two enzymes involved in alcohol metabolism—alcohol dehydrogenase and aldehyde dehydrogenase. Accumulating evidence indicates that variations in numerous other genes have smaller but measurable effects. Several GWAS and meta-analyses studies have reported a vast number of risk alleles for alcohol dependence with little overlap among studies. This is attributable to different phenotypic assessments, use of different species and different preparations, including different tissues or brain regions analyzed, and genome-by-environment interactions.

Non-genetic factors like childhood trauma, poverty, early exposure to alcohol, or PTSD are all known to increase the likelihood of turning to substance abuse. Aside from risk factors, there are also positive “protective” factors that make a person less susceptible to alcohol addiction. These factors make people resilient even though they are in a high-risk environment. The home environment, particularly during formative years, can significantly influence one’s relationship with alcohol.

1. Although much work remains to be done, researchers already have made substantial progress.
2. The second step is metabolism of theacetaldehyde to acetate by ALDHs; again, there are many aldehyde dehydrogenases,among which ALDH2 has the largest impact on alcohol consumption20.
3. Because of this, people with the genes ADH1B and ALDH2 might be less likely to develop the condition than those without it.
4. Fruit flies encounter ethanol in their natural habitat, since larvae feed on fermented food sources, which provide substrates for lipid synthesis (Geer et al. 1985).

These factors further complicate the identification and confirmation of the role of any one gene. This overview briefly summarizes some of the strategies that can be used to identify specific gene variants that influence the risk of alcoholism and reviews some of the findings obtained to date, setting the stage for the following articles in this Special Section. Linkage studies are limited in terms of their spatial resolution, and thus, association studies that measure differences in allele frequencies between ‘case’ and ‘control’ populations were also pursued. Early association studies focused on a limited number of variants in or near genes selected a priori for their biological relevance to the trait of interest or physical location in the genome informed by prior linkage results. These inconsistent findings have tempered expectations and investment in both linkage and candidate gene studies.

It’s a chronic condition characterized by excessive and compulsive consumption of alcohol, despite harmful consequences. Our hereditary behaviors interact with our environment to form the basis of our decisions. Some people are more sensitive to stress, making it harder to cope with an unhealthy relationship or a fast-paced job.

Alcohol-induced epigenetic gene regulation: the next frontier

According to the DSM-5-TR, the more relatives you have living with AUD and the closer they are to you in relation, the higher your individual genetic risk becomes. 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.

Because of this, people with the genes ADH1B and ALDH2 might be less likely to develop the condition than those without it. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), 5.6% of adults in the United States were living with alcohol use disorder in 2019. The sensitive mice tend to lose their inhibitions and pass out rather quickly, earning them the nickname “long sleepers.” “Short sleepers” are mice that are genetically less sensitive to alcohol. They seem to lose fewer inhibitions and tolerate alcohol for longer before they pass out.

Is there an alcohol use disorder gene?

In genetics, the concordance rate signifies the likelihood of two individuals with similar genes manifesting the same condition. In collaboration with a co-author from the University of Texas, the researchers took brain samples of deceased people who suffered from alcohol use disorder. Thinking of addiction as genetic begins with understanding that addiction is a chronic relapsing brain disorder. “In many ways, it’s no different than having a family history with heart disease or diabetes,” says Dr. Anand.

It is expected that GWAS will continue to be the standard of investigation of current genetic efforts to understand AUD. As it has been done for other psychiatric phenotypes, GWAS in AUD will need a collaborative approach in the form of large meta-analyses (Cichon et al., 2009; Sklar et al., 2011). While efforts rehab for women are ongoing (Dick and Agrawal, 2008), no AUD GWAS meta-analysis currently exists. However, even those with a high genetic risk to substance abuse must first be driven by a nonhereditary factor to do it. The catalyst that leads to alcohol abuse is very often an environmental factor, such as work-related stress.

What are the protective factors for AUD?

There are hundreds of genes in a person’s DNA that may amplify the risk of developing an alcohol use disorder. Identifying these genes is difficult because each plays a small role in a much larger picture. Yet studies have shown that certain combinations of genes have a strong relationship to alcoholism.

Unlike GWAS, whole-genome sequencing is more likely to identify rare mutations, particularly recessive mutations, in exonic regions of the genome. 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). Alcohol Use Disorder teen drug abuse: signs risks and treatment (AUD) is a chronic psychiatric illness characterized by harmful drinking patterns leading to negative emotional, physical, and social ramifications. 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.

They show preference for ethanol containing food over non ethanol containing food in laboratory experiments because of the caloric value of ethanol (Pohl et al. 2012). Both Adh and Aldh contribute to ethanol resistance in Drosophila (Fry and Saweikis 2006). There are two Adh alleles, designated Slow (AdhS) and Fast (AdhF) based on their electrophoretic mobility, that differ by a single amino acid (McDonald et al. 1980). Fast homozygotes have a higher level of enzymatic activity than Slow homozygotes and higher tolerance to alcohol in laboratory toxicity tests (McKenzie and McKechnie 1978). The causes of AUD are complex and can involve a variety of factors, including early exposure to alcohol use, peer group pressure, and living with other mental health conditions. AUD isn’t directly caused by genetics, but genetics may predispose you to developing AUD later in life.

Drug use and addiction represent a public health crisis, characterized by high social, emotional, and financial costs to families, communities, and society. What this means for family members of alcoholics is that you are not necessarily going to misuse alcohol yourself. Factors like your environment and ability to handle situations triggering dependency are just as important as genetics.

AUD is a complex disorder, and likely hundreds if not thousands of genes contribute to its broad and varied phenotype. In addition, given the current chip-based methodology of GWAS, this technology by design misses rare de novo mutations or insertion/deletion variants (Stefansson et al., 2008; Walsh et al., 2008; Clarke and Cooper, 2010). Furthermore, several findings have been for intronic SNPs with no clear understanding of their underlying biological relevance.