The FHE Health team is committed to providing accurate information that adheres to the highest standards of writing. If one of our articles is marked with a ‘reviewed for accuracy and expertise’ badge, it indicates that one or more members of our team of doctors and clinicians have reviewed the article further to ensure accuracy. This is part of our ongoing commitment to ensure FHE Health is trusted as a leader in mental health and addiction care. “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.
Resurgence Behavioral Health acknowledges that genetic factors can influence an individual’s susceptibility to alcohol addiction. Some genes may contribute to an increased susceptibility to addictions
in general. Analyses of RNA expression in lymphoblastoid cell lines suggested that SNPs
within this region on chromosome 5 had cis-acting regulatory
effects on the expression of HTR1A or
IPO11. 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. Prevention and education programs can address this risk as part of regular medical checkups.
The primary analyses were based upon determining the extent of allele sharing among siblings who meet diagnostic criteria for alcoholism. The primary COGA definition of being affected with alcoholism requires a person to meet both DSM–III–R criteria for alcohol dependence and the Feighner criteria (Feighner et al. 1972) for definite alcoholism. If siblings who are alcoholic share more alleles at a marker than would be expected based on chance, this suggests that genes within the chromosomal region containing the marker contribute to the risk of alcoholism. Recent estimates indicate that 5.6% of individuals meet criteria for a past year AUD [2], resulting in significant social, economic and public health costs [3,4].
This could be because not everyone inherits their parent’s genes linked to AUD. Alcohol is metabolized primarily in the liver, although there
is some metabolism in the upper GI tract and stomach. The first step in ethanol
metabolism is oxidation to acetaldehyde, catalyzed primarily by ADHs; there are 7
closely related ADHs clustered on chromosome 4 (reviewed in20). The second step is metabolism of the
acetaldehyde to acetate by ALDHs; again, there are many aldehyde dehydrogenases,
among which ALDH2 has the largest impact on alcohol consumption20. Moving forward, continued efforts to integrate large GWAS datasets examining alcohol use remain critical to the detection and replication of genome-wide significant associations. It is hoped that such information will ultimately lead to improved prevention and treatment efforts.
That is why understanding how the disorder originates is important, but addressing the disease in a clinically appropriate treatment environment is necessary to successfully overcoming the disorder and achieving sustained sobriety. Anybody can develop an SUD, and they can do it for any number of reasons in their life. The genetic connection to addiction comes through inherited levels of dopamine, a neurotransmitter made in your brain. Disease can be woven into your DNA — and that includes the disease of drug addiction.
The role of a person’s environment in AUD shows differences when comparing people with parents addicted to alcohol versus other family members. Majority of genomic data for large alcohol consumption and AUD meta-analysis was either from UKBiobank or from Million Veterans Project. Several other cohorts from dbGAP also contributed to large sample size of alcohol consumption GWAS by Liu et al, 2019.
Perhaps the largest challenge is the way in which the AUD diagnosis is operationalized. The DSM-5 [1] currently requires the endorsement of any 2 of 11 criteria to reach the diagnostic threshold for AUD at the mild severity level. 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. Recognizing alcoholism as a disease promotes early intervention, access to appropriate healthcare services, and ongoing support for people struggling with AUD. While alcohol addiction isn’t entirely preventable, specific measures can reduce its risk. Just as risk factors increase your chance of experiencing a condition, protective factors lower your risk.
However, this is not to diminish the impact that an environment can have on an individual’s personality development and tendency toward addictive patterns and habits. If you need help treating your alcoholism, you can look for various treatment plans and programs to cater to your needs. Someone without can you inherit alcoholism this gene is less likely to control their urge to keep drinking alcohol. If someone has a mutation in this area and does not produce enough GABA while sober, they are likelier to abuse alcohol to feel better. This discomfort often acts as a natural deterrent, limiting their alcohol intake.
