Research shows that genetics account for about 50-60% of the risk for developing alcohol use disorder (AUD), commonly referred to as alcoholism. This means if you have a family history of alcoholism, you may be more predisposed to it. However, genetics aren’t the whole story—environment, lifestyle, and personal choices also play significant roles.

• While genetics can account for up to 60% of AUD risk, not everyone with a family history of AUD will develop the condition.
• Genes make up about half of a person’s risk for developing alcohol use disorder (AUD).
• There is no one genetic test to look for whether someone is predisposed to AUD because there are hundreds of gene variations that could influence alcohol abuse.

Study of Twins

The sensitive mice tend to lose their inhibitions and pass out rather quickly, earning them the is alcoholism genetic 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. Having a close family relative, such as a parent, can account for up to 60% of your risk of developing 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) can have a hereditary component, but not everyone living with AUD has a family history of AUD.

Table 1. Criteria for alcohol use disorders.

Starting in the late 1940s, researchers in Chile bred rats that preferred to drink alcohol-containing solutions as well as rats that avoided alcohol (Mardones and Segovia-Riquelme 1983). Such selective breeding has been repeated numerous times with rats and mice, resulting in pairs of animal lines that differ with respect to a particular alcohol-related trait. Animals have been selected for many alcohol-related traits, including preference for alcohol, tolerance or sensitivity to alcohol’s effects, and withdrawal severity.

Are You Drinking Too Much?

• As gene-targeting technologies allow more specific experimental regulation of genes than simple deactivation or over-expression, these approaches will continue to provide important data.
• Oxidative stress occurs when harmful free radicals overwhelm the body’s antioxidant defenses, leading to damage to proteins, cell membranes, and DNA.
• With data like that, it’s clear to see why finding a gene responsible for alcohol abuse and dependence is so appealing.
• Your genetics don’t only increase your risk of AUD — they may have protective elements as well.

A hereditary condition is often used interchangeably with an inherited or genetic one, though it typically emphasizes the familial transmission of traits or conditions. Hereditary conditions are always inherited but may not account for non-familial genetic influences, meaning, you inherit a genetic factor that is not from your immediate family. However, when AUD is transmitted from generation to generation, it is hereditary.

• Future research should include a broader spectrum of drug addiction-related genes, neurodevelopment genes, and even tumor suppressor genes, as these biological processes have long been correlated with substance abuse as a post-effect.
• The table also exhibits the chromosomal positions of SNPs, minor alleles and their frequencies, and the P-value of HWE for drug addiction patients and healthy controls.
• Between the D2 dopamine receptor findings in the 1990s and 2020, researchers have identified more than a dozen variants for AUD.
• Variations in these genes influence how quickly alcohol breaks down, which, naturally, affects someone’s tolerance.

Support groups and aftercare programs can also play a helpful role in the long-term management of genetic alcoholism. Peer support groups and various types of aftercare provide ongoing support, guidance, and relapse prevention strategies to help individuals maintain sobriety and lead fulfilling lives. Treatment for genetic alcoholism typically involves a comprehensive approach that addresses both the physical and psychological aspects of the disorder.

Genetic disorders are diagnosable conditions directly caused by genetic mutations that are inherited or occur later in life from environmental exposure. The GI tract is exposed to very high levels of alcohol as it passes throughthe mouth, esophagus, stomach and intestinal tract, and most ethanol passes throughthe liver before entering the circulation. Alcohol levels in common drinks rangefrom approximately 5% (1.1 M) for beer, 11-15% for wine (∼3M) and 40% for spirits (∼9 M). The oral cavity and esophagus aredirectly exposed to those levels, and the liver is exposed to high levels from theportal circulation.

Beyond addressing the nature versus nurture debate, this research has a broader aim. According to Polimanti and Zhou, geneticists hope to be able to bring their findings to human healthcare in order to help predict and treat certain illnesses. This is called precision medicine, wherein a person’s treatment plan can be specially tailored based on their unique genetic makeup. Hugo Bellen, a geneticist at Baylor College of Medicine in Houston, Texas, said the study “lays the foundation for a genetic approach to dissecting the acute, and possibly the chronic, effects” of alcohol in people. That doesn’t mean you’ll absolutely develop AUD if you have a family member living with the condition. You may have a higher genetic predisposition, but the underlying causes of AUD are multifaceted and complex.

What does genetic risk mean?

As reviewed by Crabbe and colleagues (2006), most of the genes thus studied were found to influence some aspect of alcohol sensitivity. For example, of 84 different transgenic animals tested for effects on alcohol self-administration, one-quarter exhibited increased drinking, one-third exhibited decreased drinking, and 40 percent did not differ from control animals (Crabbe et al. 2006). This finding clearly demonstrates the multiplicity of genetic influences on alcohol responses. As gene-targeting technologies allow more specific experimental regulation of genes than simple deactivation or over-expression, these approaches will continue to provide important data.

Genes contributing to the risk of alcohol dependence

DSM-V14, 15 on the other hand consolidated Sobriety AD and abuse as a single disorder as AUD15,16. By considering AD and abuse under single umbrella increased the number of diagnosed subjects, but this number was still not large enough to design powerful GWAS studies. Therefore, many genetic studies of alcoholism also concentrated on nonclinical phenotypes, such as alcohol consumption and Alcohol Use Disorders Identification Test (AUDIT)17–19, from large population based cohorts. The AUDIT, a 10-item, self-reported test was developed by the World Health Organization as a screen for hazardous and harmful drinking and can be used as a total (AUDIT-T), AUDIT-Consumption (AUDIT-C) and AUDIT-Problems (AUDIT-P) sub-scores. To date, GWAS havefocused on common variants, with allele frequencies of 5% or higher.Most GWAS are case-control studies or studies of quantitative traits inunrelated subjects, but family-based GWAS provide another approach. GWAS arebeginning to yield robust findings, although the experience in many diseases isthat very large numbers of subjects will be needed.

While the genes offer a base for potential alcohol abuse, whether a person will develop a dependency is influenced by a combination of genetic and environmental factors. Remember that the research suggests that about half of a person’s risk for developing AUD comes from genetic factors? It is likely that, as for most complex diseases, alcohol dependence and AUDsare due to variations in hundreds of genes, interacting with different socialenvironments. An additional challenge in the search for genetic variants that affectthe risk for AUDs is that there is extensive clinical heterogeneity among thosemeeting criteria. Because the diagnosis of an AUD requires the presence of a set ofsymptoms from a checklist, there are many different ways one could meet thecriteria.