The heritability of alcohol use disorders: a meta-analysis of twin and adoption studies PMC

Progress in the molecular genetic study of AUD and related phenotypes is being made. Nonetheless, significant efforts are needed to conduct GWAS of more specific AUD risk factors, such as alcohol sensitivity, to more fully understand how individual genetic loci contribute to AUD risk. In doing so, we will be better positioned to understand the etiologic relations between these AUD https://ecosoberhouse.com/ risk factors and how their confluence ultimately increases risk for AUD. Populations in 1000 Genomes were used as reference for their corresponding population.

Alcoholism and Genetics

As it relates to alcoholism, genes, environment and social interaction can all affect a person’s risk level for alcohol addiction. Research is proving that alcoholism is a complex genetic disease, and there are many genes that affect its risks. For example, the ADH1B and ALDH2 genes have been shown to have strong effects on alcoholism risks. Other genes, including GABRA2, CHRM2, KCNJ6, and AUTS2, may also significantly affect risks.

Data availability

A lack of naturally occurring endorphins is hereditary and can contribute to alcoholism. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) publishes that about 16 million Americans struggle with an alcohol use disorder (AUD). Alcohol is one of the most commonly consumed psychoactive substances in the world. It is, however, an addictive substance, and problematic use can lead to both alcohol dependence and the onset of alcoholism. Young adult twins and their non-twin siblings were participants in the Nineteen and Up study24. A total of 2,772 cases and 5,630 is alcoholism inherited controls were defined using DSM-III-R and DSM-IV criteria.

Tables

Jellinek was instrumental in establishing alcoholism as a disease with scientific considerations, per the Journal of Studies on Alcohol and Drugs. Both ALDH2 and ADH1B are genes that are involved in how alcohol is metabolized in the body. The journal Alcohol Research and Health publishes that the presence of these genes can actually act as a protector against alcoholism. This is because that if you have one of these genes, you will struggle to metabolize alcohol safely, leading to nausea, rapid heart rate, and flushing when alcohol is consumed. Environmental factors, as well as gene and environment interactions, account for the remainder of the risk. Too much alcohol affects your speech, muscle coordination and vital centers of your brain.

The Genetic Link: Hereditary Factors in Alcoholism and How it Affects You

• This compounds the risk of problematic drinking, alcohol dependence, and addiction.
• Heterogeneity was tested with likelihood ratio tests by equating the parameters across studies.
• Majority of genomic data for large alcohol consumption and AUD meta-analysis was either from UKBiobank or from Million Veterans Project.
• It is still held that genetics accounts for about half of the risk of alcoholism.

Genetics, as well as social and environmental factors, strongly influence alcohol dependency. Environmental factors also account for the risk of alcohol and drug abuse.2 Scientists are learning more about how epigenetics affect our risk of developing AUD. A review of studies from 2020, which looked at a genome-wide analysis of more than 435,000 people, found 29 different genetic variants that increased the risk of problematic drinking.

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The test is free, confidential, and no personal information is needed to receive the result. They are essential in influencing the brain’s function and response to addictive substances like alcohol. Certain genetic variations, such as cytochrome enzymes in the liver, can also influence how quickly a person metabolizes drugs. But while genetics influence our likelihood of developing alcoholism, it’s more complex. What this means for family members of alcoholics is that you are not necessarily going to misuse alcohol yourself.

Overview of the Genetics of Alcohol Use Disorder

• Note that the official names of several ADH genes have been changed, and theliterature has been confused by some groups using non-standard names for some ofthe genes29.
• The National Institute on Alcohol Abuse and Alcoholism (NIAAA), a subset of the government’s health-focused .gov entities, has been at the forefront of alcohol research.
• There is evidence that heavy episodic (binge) drinking, which results inexposure of tissues to high levels of alcohol, is particularly harmful81, 87, 88.
• If you produce fewer endorphins naturally, it can make it harder for you to feel happy without alcohol and, therefore, increases the desire to drink bigger quantities more often.
• Approximately 75% of the families were ascertained via a proband in treatment for alcohol dependence.

It’s essential to note that while fraternal twins have distinct genetic profiles, identical twins share the exact genome. Given this genetic similarity, if heredity plays a significant role in alcoholism, identical twins should exhibit a pronounced concordance rate. In genetics, the concordance rate signifies the likelihood of two individuals with similar genes manifesting the same condition. A comprehensive association study conducted jointly by the University of Washington and the University of Queensland meticulously tracked the lives of 5,889 male and female twins, delving deep into the genetics of alcohol use disorder. Researchers from the IU Alcohol Research Center used animal models to explore the genetics of alcohol use disorder.

What does genetic risk mean?

In healthcare, such findings can guide interventions, from outpatient treatments to more intensive care, based on an individual’s genetic risk. The transparency of research, ensured by accessible journal papers, is vital in addressing the societal impacts of heavy drinking. Recent research from Indiana University has shed light on the significant role genes play in the development of alcohol use disorders (AUDs).

What are the risk factors for AUD?

Similarly, our ability to measure the brain’s activity during resting state and during various cognitive tasks with exquisite temporal accuracy, allows us to develop and implement EEG protocols that uniquely address questions regarding the course of AUD. The accompanying review (3. Brain Function) covers the available brain function data and resulting findings in detail. Second, estimates of shared environmental effects can be biased upward by assortative mating for AUDs. This is because when spouses have correlated liabilities for AUD, the correlation between the genetic factors of DZ twins and siblings would be higher than 0.5, which is assumed in the model. The spousal correlation for AUD was estimated at equal to +0.12 as found in one prior large-scale general population study (Maes et al. 1998). Accordingly, some proportion of our estimate of shared environmental effects for AUD may be a result of assortative mating.