Alcohol use disorder Symptoms and causes

People who meet criteria for dependence often have multiple cases of alcoholism in their families. ADH1B and ALDH2 may also protect against both alcohol consumption and alcohol use disorder. One size does not fit all and a treatment approach that may work for one person may not work for another. Treatment can be outpatient and/or inpatient and be provided by specialty programs, therapists, and health care providers. Health care professionals use criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), to assess whether a person has AUD and to determine the severity, if the disorder is present.

is alcoholism inherited

Regional websites

A changing definition of the heterogeneous phenotype of AUD may also pose a challenge to identifying genetic variants through GWAS. The above studies used the DSM-IV-TR criteria for alcohol dependence in order to define the phenotype. As the field of psychiatry transitions to the DSM-5 criteria for AUD, there may also be changes in the functional variants identified by GWAS. Future GWAS should focus on the endophenotypes of AUD in order to better understand the genetic connections to specific behavioral symptoms. Likewise, it will be important to separate the role of genetic variants due other substance use disorders and to comorbid psychiatric disorders.

Characteristics of the studied population

  • The first step in ethanolmetabolism is oxidation to acetaldehyde, catalyzed primarily by ADHs; there are 7closely related ADHs clustered on chromosome 4 (reviewed in20).
  • Without enough folate, vitamin B6, and vitamin B12, this conversion process becomes inefficient and homocysteine levels increase.
  • Both folate and B12 are involved in making red blood cells, and a shortage of either can result in anemia.
  • Genome-wide data on 14,904 DSM-IV diagnosed AD individuals and 37,944 controls from 28 case/control and family-based studies were meta-analyzed for PGC’s AD GWAS.
  • Overall, the evidence suggests that the amount of folic acid in a typical multivitamin does not cause any harm—and may help prevent some diseases, especially among people who do not get enough folate in their diets, and among individuals who drink alcohol.

Based on previous linkage studies, the strongest associations have been identified in the alcohol metabolism genes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Alcohol metabolism is a two-step process where ethanol is first oxidized to acetaldehyde by ADH and then further oxidized to acetate by ALDH. Accumulation of the toxic intermediate acetaldehyde can cause adverse physiological symptoms, including flushing syndrome, tachycardia, and nausea. The rate at which acetaldehyde is produced and converted to the waste product acetate is influenced by genetic variations encoding the isoenzymes of ADH and ALDH. Individuals with isoforms of ADH that oxidize ethanol at a faster rate and/or isoforms of ALDH that oxidize acetaldehyde at a slower rate are protected against AUD due to the unpleasant effects that result from acetaldehyde accumulation.

Genetic Testing Information

It’s difficult to determine the precise contribution of gene and environmental interactions in alcohol use disorders. However, the environment tends to have a stronger influence on the development of alcohol and drug abuse than genetics. Those with a history of alcoholism in their family have the highest risk of becoming alcoholics. If you have multiple relatives with alcohol addictions or other substance use disorders, you may have inherited the genes that put you at risk. The more family members (related by birth) you have with an alcohol problem, the higher your risk.

is alcoholism inherited

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. Sober House The investigators chose a family study design to allow the use of multiple methods of genetic analysis. Systematic recruitment from outpatient and inpatient alcoholism treatment facilities and assessment of families initially was carried out at six sites across the United States, with a seventh site more recently. The study also included a large sample of control families that were randomly selected from the community.

  • Researchers have used both case–control and family studies to identify genes related to alcoholism risk.
  • Majority of genomic data for large alcohol consumption and AUD meta-analysis was either from UKBiobank or from Million Veterans Project.
  • These findings reinforce the notion that there are different paths to alcohol dependence and different physiological pathways underlying them.
  • Theories suggest that for certain people drinking has a different and stronger impact that can lead to alcohol use disorder.
  • Variations in genes that affect the metabolism (breakdown) of alcohol in the body have been studied as factors that can increase or decrease the risk of alcohol use disorder.
  • Your genetics don’t only increase your risk of AUD — they may have protective elements as well.

For the analyses, the researchers chose a split-sample design—two groups of subjects (i.e., an initial sample and a replication sample) were analyzed independently; this approach allows investigators to examine the reproducibility of the initial study findings. Despite the evidence supporting the prominence of genetic factors in AUD’s etiology, the identification of genetic risk variants has been difficult and labor intensive. With recent advances in technology, the most promising results stem from recent GWAS, which have helped to identify new variants in the genetics of AUD.

Although studies spanning multiple approaches have suggested a genetic basis for AUD, identification of the genetic risk variants has been challenging. Some promising results are emerging from GWAS studies; however, larger sample sizes are needed to improve GWAS results and resolution. As the field of genetics is rapidly developing, whole genome sequencing could soon become the new standard of interrogation of the genes and neurobiological pathways which contribute to the complex phenotype of AUD. In our previous study [17], we screened 2186 patients with suspicion of hereditary optic neuropathy, analyzing them using our sequencing panel of 87 nuclear genes.

Interestingly, these variations in GABRA2 do not change the protein structure of the GABAA receptor; instead they seem to modify production of the affected protein subunit, perhaps reducing the total number of functioning receptors. Clues in Human VariationsGenes powerfully influence a person’s physiology by giving rise to some 100,000 different types of protein, each of which has a direct role in the daily functioning of the body and brain or in regulating the activity of other genes. The strong connection between variations in basic physiology and an individual’s susceptibility to alcohol problems is well illustrated by the very first gene to be identified as affecting the risk of developing alcohol dependence. Alcohol use disorder does not have a clear pattern of inheritance, although many affected individuals have a family history of problems with alcohol or other substances. Children of people with alcohol use disorder are two to six times more likely than the general public to develop alcohol problems. This increased risk is likely due in part to shared genetic factors, but it may also be related to environment, lifestyle, and other nongenetic influences that are shared by members of a family.

We understand the importance of approaching each work integrally and believe in the power of simple.