Genetic factors influencing alcohol dependence

Genetic factors influencing alcohol dependence

These strategies depend on the premise that for a particular position in the DNA of these genes, more than one possible form exists. The study methods used to identify genes that affect the risk for alcohol dependence assume that the presence of certain alleles increases the risk of alcoholism. These variants that affect risk can be located either directly within a gene or near a gene. Epigenetics, the study of changes in gene expression without alterations to the underlying DNA sequence, plays a significant role in alcoholism.

Alcohol Addiction Hereditary: Understanding the Genetic Link

This review summarizes insights from model organisms as well as human populations that represent our current understanding of the genetic and genomic underpinnings that govern alcohol alcohol rehab metabolism and the sedative and addictive effects of alcohol on the nervous system. These longitudinal data have been instrumental in COGA’s ability to chart the etiology and course of alcohol use and AUD across the lifecourse. We have since conducted several studies that have disentangled family history into elements of genetic liability, nurture and density of risk (e.g., References 23, 24, 25). We were also able to examine the risk posed by early initiation of alcohol use on later drinking milestones using several analytic paradigms (e.g., References 29, 30). More recently, our longitudinal design has facilitated characterizations of remission and recovery in AUD (e.g., References 31, 32, 33).

Treatment Process

But when it comes to more complex human features, the connection to our genes is less clear. The impact of is alcoholism genetic or environmental genes on behavior like alcohol use or even sexual orientation has long been the subject of scientific debate. In 1959, inbred mouse strains first were shown to differ in their tendency to drink alcohol (McClearn and Rodgers 1959), and studies with inbred strains continue to this day. Each inbred strain possesses a random collection of genes (i.e., genotype), but all the animals within a strain are genetically identical. This reduction in the genetic variation among the animals studied could increase the power to identify genes contributing to alcohol-related traits.

Can alcohol use disorder be genetic?

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. The greatest success story for alcohol-related QTL mapping in rodents has been the discovery of a quantitative trait gene (QTG)9 that affects acute withdrawal severity from both alcohol and pentobarbital in mice. Originally, investigators mapped several QTLs contributing to this trait to locations on various mouse chromosomes (Buck et al. 1997). Subsequent studies with a variety of specifically created genetic animal models gradually narrowed down the size of the DNA region (i.e., reduced the confidence interval) around one of these QTLs until only a few genes remained within the confidence interval. Functional studies then demonstrated that the most likely gene contributing to the trait was Mpdz, which encodes a protein containing multiple structural components known as PDZ-domains (Shirley et al. 2004). Studies of this gene’s pattern of expression in the brain and of the functions of the MPDZ protein continue, as do studies to identify the receptor molecules with which MPDZ interacts (e.g., the serotonin 2C receptor) (Chen et al. 2008a; Reilly et al. 2008).

• If alcoholism runs in your family, that doesn’t mean you are fated to become an alcoholic.
• This has led to groundbreaking insights into why some individuals might experience adverse reactions to alcohol, offering a protective factor against excessive consumption.
• Alcoholism is influenced by both genetic and environmental factors, with genetics playing a significant role.
• By the same measure, those who choose not to drink alcohol at all during their lives will not develop AUD, even if they are unknowingly at high risk, genetically speaking.

However, environmental factors, such as drinking behavior modeled by parents or peers, can also influence alcohol tolerance and drinking behavior. Within both the U.S. and Scandinavian studies, no significant gender differences were found in the genetic contribution to alcoholism risk. In the Scandinavian data, genetic factors appear to be more important in women than in men (a pattern that is seen in both the Swedish adoption and Swedish twin studies), but no statistically significant difference exists. Based on the U.S. data, genetic effects account for approximately 60 percent of the variance in alcoholism risk in both men and women, and the twin data suggest that there is no significant effect of family environment.

• One trait that has been found to be genetically determined is alcohol preference of inbred mouse strains.
• These groups typically have a lower risk of developing alcohol use disorder compared to other populations.
• Social and environmental factors like peer influence, family dynamics, availability of alcohol, and cultural norms surrounding alcohol use also significantly contribute to the risk of developing alcoholism.
• Second, two studies appear to be outliers, producing results at variance with the general trend.
• Hereditary predisposition to AUD is one of the risk factors identified by these results.

Dr. Wakim is a board-certified psychiatrist with a passion for and expertise in addiction, mood disorders, trauma-related disorders and the subspecialty of interventional psychiatry. He obtained his medical degree from West Virginia University where he also completed his residency training, finishing as chief resident. Dr. Wakim co-founded and served as the CEO of Transformations leading to a successful merger with Shore Capital in May 2021. He is purpose driven towards improving the standard of and removing stigma related to behavioral healthcare.

Mental Illness and Alcohol Addiction

• These microRNAs also offer a new experimental method for silencing the expression of specifically targeted genes.
• The first approach—the one that this article will focus on—is a statistical perspective.
• Variants of the alcohol-metabolizing enzymes ADH and ALDH genes significantly impact the risk of developing the alcohol addiction gene and alcohol dependence.
• Each of these endophenotypes is likely to reflect the actions of multiple genes and to relate to both genetic and environmental influences (Schuckit et al., 2004b; Crabbe et al., 2006).
• These vulnerabilities can impact factors such as alcohol metabolism, tolerance, and the brain’s reward pathways.
• For example, the social environment plays such a crucial role in shaping drinking behaviors in humans, but it is difficult to identify corresponding rat and mouse behaviors and environmental factors.

Conversely, families that foster open communication and support can mitigate these risks and encourage healthier coping strategies. In households where excessive drinking is normalized, children may view alcohol use as a standard coping mechanism. These dynamics can increase the likelihood of developing unhealthy https://ecosoberhouse.com/ drinking habits. While genetics may set the stage, it’s the combination of environment, mental health, and personal choices that determines the outcome.

These factors encompass genetics, family history, one’s current environment, gender, and mental health conditions. Stress in both work and home life can trigger alcohol addiction, with alcohol often providing a temporary sense of relief and happiness amidst stress. 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.