Our results show that a relatively limited and well-defined panel of SNPs identified based on our CFG analysis could differentiate between alcoholism subjects and controls in three independent cohorts. The fact that our genetic testing worked for both alcohol dependence and alcohol abuse suggests that these two diagnostic categories are actually is alcoholism inherited overlapping, supporting the DSM-V reclassification of a single category of alcohol use disorders. GFAP (glial fibrillary acidic protein), a top candidate gene with a CFG score of 9.5, is an astrocyte intermediate filament-type protein involved in neuron–astrocyte interactions, cell adhesion, process formation and cell–cell communication.
However, the specific causes are still unknown, and identifying the biological basis for this risk is a vital step in controlling the disease.1 Explore whether alcoholism is passed down through biological families and how you can avoid an AUD if alcohol misuse runs in your family. In more anecdotal cases where, for example, celebrity offspring of infamous drug and alcohol abusers, whether they’ve always been sober or whether they’re on a program, it’s hard to say if genetics or environment played a part. We examined the available scientific literature to provide an overview of different approaches that are being integrated increasingly to advance our knowledge of the genetic bases of alcoholism. Examples of genes that have been shown to influence vulnerability to alcoholism and related phenotypes are also discussed.
In the study of complex disorders, it has become apparent that quite
large sample sizes are critical if robust association results are to be
identified which replicate across studies. Unfortunately, studies of alcohol
dependence have not yet attained these sample sizes. Meta-analyses, which
combine results across a number of studies in order to attain the critical
sample sizes needed, are being developed. Thus far, two genes that regulate how alcohol is metabolized seem to be the strongest indicators for alcohol dependence and addiction. Researchers are discovering other gene variants that also point toward a greater likelihood of alcohol abuse or alcoholism. One goal of QTL mapping is to determine the gene or genes responsible for the QTL, that is, the quantitative trait gene.
- Ethanol treatment was shown to alter the levels of several genes in SH-SY5Y neuroblastoma cells that are involved in the synthesis and metabolism of norepinephrine (Thibault et al., 2000).
- SNP–SNP allelic epistasis was tested for each distinct pair of SNPs between genes, using the PLINK software package (Supplementary Table S5).
- The alcohol use severity phenotype mapped to chromosomes 4 and 12, whereas the withdrawal phenotype mapped to 6, 15 and 16.
- First, there may be something about identical twin males, genetically speaking, that makes them more likely to express an alcohol use disorder if one twin has one as compared to females (50 percent versus 30 percent).
This information allows a correlation analysis that defines chromosomal regions linked with the behavioural differences. For alcohol behaviours, there are always multiple regions, so this is a ‘quantitative’ trait and the regions linked with the trait are quantitative trait loci (QTLs). Besides other addictions, alcoholism also coexists frequently with other psychiatric diseases, including both internalizing disorders (e.g. depression and anxiety) as well as externalizing disorders [e.g. Antisocial personality disorder (ASPD), conduct disorder (CD) and attention deficit hyperactivity disorder (ADHD)] [1,7,16]. Twin studies reveal consistently the existence of shared genetic influences between alcoholism and externalizing disorders [17-20].
The Genetics of Alcohol Use Disorder
They don’t identify as having alcohol use disorder, so they wouldn’t be comfortable in an Alcoholics Anonymous meeting, and they can stop anytime they want to. Alcohol intolerance occurs when your body doesn’t have the proper enzymes to break down (metabolize) the toxins in alcohol. Other ingredients commonly found in alcoholic beverages, https://ecosoberhouse.com/ especially in beer or wine, can cause intolerance reactions. ADHD tends to run in families and, in most cases, it’s thought the genes you inherit from your parents are a significant factor in developing the condition. Research shows that parents and siblings of someone with ADHD are more likely to have ADHD themselves.
A physician can tell you if you need assistance, work with you to put together a plan of treatment for alcohol abuse, possibly including medication, and/or refer you to a support group, counseling, or treatment center. The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) provides eleven criteria, of which at least two must be present over twelve months for an alcoholism diagnosis. Most clinicians use the term “alcohol use disorder” to help emphasize the disease value of the disorder and reduce inhibitions to seek medical help. In the United States, the prevalence of any drinking in 12 months in 2012 rose from approximately 65% to just over 72%. Scientists most highly observe this increase in women, rural citizens, those with lower socioeconomic status, and minorities.
Environment Vs. DNA
The disease often progresses relatively inconspicuously and slowly, usually over several years. Sufferers can be unaware of the severity of their illness and may deny it altogether. The number of people suffering from alcoholism and the resulting social and economic consequential damage is often higher in absolute figures in Europe and the USA than for other drugs. No, you are not destined to become an alcoholic just because your parents were an alcoholic.
- Fraternal twins do not have identical chromosome pairs; hence, they look different from each other.
- Nevertheless, we think this simple scoring system provides a good separation of genes, with specificity provided by human data and sensitivity provided by animal model data.
- There is a growing body of scientific evidence that alcoholism has a genetic component.
- Another of our recent papers found that resident children of parents who have substance use disorders and related behavioral challenges will engage in similar behaviors more than the genetics of the child would predict.
- Over time, heavy drinking makes the organ fatty and lets thicker, fibrous tissue build up.
Rodent studies show that differences in alcohol sensitivity among strains have a genetic component, and for most behaviours, the heritability is in the range of 0.2–0.5 (Crabbe et al., 1990). Crosses between inbred strains are valuable tools for determining which chromosomal regions determine these genetic differences. This requires a number (for example, 20–80) of different recombinant inbred strains or individual F2 generation animals. These genetic tools are readily available for mice and have more limited availability for rats. The behavioural sensitivity of these strains or individuals as well as differences in DNA sequence (SNPs) among these strains or individuals are determined.
From 2001 – 2012, the condition increased by 50%, and this increase was more pronounced in women, rising 80% over the time frame. In 2020, one estimate suggested that as many as 18 million adults in the country struggle with alcohol addiction. Studies about the relationship between alcoholism and genetics go back over 80 years. Today, we have made tremendous progress learning that there is no “alcoholism gene” but genetic markers that accentuate dependence. In 1849, the Swedish physician Magnus Huss was the first to define excessive drinking as a disease.
Such isolated populations, and large families within them, are likely to confer the advantage of reduced genetic heterogeneity. A non-exhaustive list of convergent findings across studies includes a region on chromosome 4q, that contains the alcohol dehydrogenase (ADH) gene cluster [96,97,99,100], and a chromosome 4p region near the centromere containing a γ-aminobutyric acid receptor (GABAA) gene cluster [96,99]. In the COGA sample there was also evidence for linkage to chromosomes 1 and 7, and to chromosome 2 at the location of an opioid receptor gene . A region on chromosome 1 was linked to alcoholism and affective disorder in the COGA data set , supporting further the existence of a genetic overlap between alcoholism and internalizing disorders.
Alcohol Use Disorder Should Be Treated Now
Multiple expression data sets and informatic approaches were used to identify candidate genes for alcoholism in rats (Rodd et al., 2007). Ethanol was administered using chronic free-choice consumption and intracranial self-administration (into ventral tegmental area) models. Overlapping expression data were then filtered using human genetic linkage data, human tissue data (post-mortem brain, lymphocytes and fibroblasts) and biological roles data. Analysis of gene expression data identified ∼3000 significantly changed genes across brain regions and experimental paradigms. The list of candidate genes was further reduced by identifying those changed in all three experiments and those that were changed in at least two out of three experiments.
He added that the research could help in identifying youngsters at risk of becoming alcoholics and could lead to early prevention efforts. 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. A study in Sweden followed alcohol use in twins who were adopted as children and reared apart.