Theo Nash
Alcohol use disorders (AUDs) are characterized by harmful drinking patterns that lead to negative emotional, physical, and social ramifications. There is substantial evidence that AUDs have a genetic component, with variations in a large number of genes affecting risk. A meta-analysis of twin and adoption studies estimated the heritability of AUDs to be around 40-50%, with similar magnitudes of genetic influence in men and women. However, the identification of universal genetic risk variants for AUDs has been challenging due to the complex and heterogeneous nature of the disorder.
| Characteristics | Values |
|---|---|
| Alcohol Use Disorder (AUD) | 0.49 [95% confidence interval (CI) 0.43–0.53] |
| AUD in males | 40.0% (95% CI 0.23–0.56) |
| AUD in females | 0.241 (95% CI 0.00–0.52) |
| AUD in both sexes | 0.36 (95% CI 0.22–0.50) |
| Genetic influences on AUD | Similar in magnitude in men and women |
| Genes associated with AUD | ADH1B, ALDH2, GABRA2, CHRM2, KCNJ6, AUTS2 |
| Heritable trait variable | EEG-β |
| Heritable neuroelectric correlates of cognitive processes | Theta ERO |
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What You'll Learn
Alcohol metabolism genes
The primary enzymes involved in alcohol metabolism are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). These enzymes occur in several forms, which are encoded by different genes. There are variants (alleles) of these genes that encode enzymes with different characteristics and which have different ethnic distributions.
The ADH1B, ADH1C, and ALDH2 genes have been studied for their association with altered kinetic properties of the resulting enzymes. For example, certain ADH1B and ADH1C alleles encode particularly active ADH enzymes, resulting in a more rapid conversion of alcohol to acetaldehyde. These alleles have a protective effect against alcoholism. Noncoding variants in both ADH and ALDH genes may also influence alcohol metabolism and, consequently, the risk of alcoholism.
The ALDH2 gene, for instance, encodes an inactive ALDH enzyme, resulting in acetaldehyde accumulation and a protective effect. Similarly, the ADH1B*2, ADH1B*3, ADH1C*1, and ALDH2*2 alleles have been associated with lower rates of alcohol dependence. These alleles may lead to an accumulation of acetaldehyde during alcohol metabolism, resulting in heightened subjective and objective effects. The prevalence of these alleles differs among ethnic groups, with ADH1B*2 found frequently in Northeast Asians and occasionally in Caucasians, and ADH1B*3 found predominantly in people of African ancestry.
The ADH4 gene has also been implicated in alcohol metabolism, with studies confirming the presence of variations across the entire gene. Non-coding variants in the ADH1A and ADH1B genes have been associated with alcoholism risk in European-Americans, while variants in ADH1C have been linked to risk in Native Americans. Additionally, a study indicated that there is an important site in the region containing the ADH genes that affects alcohol metabolism but is unrelated to the coding variations in ADH1B or ADH1C.
Furthermore, the ALDH1A1 gene, found on chromosome 9, and the ALDH2 gene, found on chromosome 12, play a role in metabolizing acetaldehyde produced during ethanol oxidation. These genes have similar structures, and the proteins they encode share a high level of sequence identity.
Mammals, including humans, have a long evolutionary relationship with ethanol, which may be linked to the consumption of fermenting fruits and nectars. Genetic variations in ADH IV enzymes suggest that ethanol metabolism is variable and evolutionarily plastic. Comparative genetic analyses of ADH7 across mammals have identified loss-of-function mutations that impact enzymatic function.
In summary, numerous coding and non-coding variations in the ADH genes can affect the risk for alcoholism. These genetic variants interact with individual characteristics, such as ethnicity, and environmental factors to influence alcohol involvement and drinking patterns. Further studies are needed to fully understand the specific effects of these gene variations and their impact on alcohol-related problems.
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Genetic susceptibility factors
Alcohol use disorders (AUDs) are characterised by harmful drinking patterns that lead to negative emotional, physical, and social ramifications. AUDs have been found to have a strong genetic component, with a heritability estimate of 0.49 (95% confidence interval of 0.43-0.53). This estimate is supported by twin and adoption studies, which indicate similar magnitudes of genetic influence in both males and females.
GWAS studies have identified a heterogeneous list of SNPs associated with AUDs and alcohol-related phenotypes, indicating the complex and heterogeneous nature of the disorder. SNPs in GABRA2 have been linked to excess EEG fast activity in alcohol-dependent individuals, and analyses of 117 families affected by alcohol dependence found a significant association between theta ERO and several SNPs in KCNJ6.
Additionally, EEG-β, which is associated with alcohol dependence, is a heritable trait variable. Offspring of alcoholics exhibit increased EEG-β power, even without exposure to alcohol, suggesting a genetic link.
While the identification of universal genetic risk variants for AUDs remains challenging, ongoing genetic studies, including GWAS, continue to contribute to our understanding of the genetic underpinnings of AUDs and their susceptibility factors.
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Environmental risk factors
While there are no singular causes of serious alcohol-related problems, there are dozens of risk factors that interact differently in each individual. Here are some environmental risk factors that can contribute to the development of alcohol use disorders (AUDs):
Family and Early Life Experiences
Growing up with an alcoholic parent or in a family where heavy drinking is practised or encouraged increases the risk of developing an alcohol problem. In such families, heavy drinking is often normalised, glamorised, socially acceptable, and even expected or desirable. Additionally, childhood trauma or neglect can also increase the risk of AUDs.
Stress and Mental Health
External stress is one of the most potent environmental risk factors for AUDs. Individuals who have experienced trauma, especially in childhood, or accumulated significant stressors throughout their lives, may be prone to heavy drinking patterns. A person's stress response is influenced by the type of stressor, its intensity, timing, duration, genetic makeup, and drinking history. The interplay of these genetic and environmental factors can also lead to or worsen mental health conditions such as anxiety and depression, which further raise the risk of AUDs.
Social and Cultural Norms
The social and cultural environment plays a significant role in alcohol consumption patterns. People who live closer to alcohol retail stores or bars are said to have a more positive outlook on drinking and are more likely to participate. Additionally, alcohol advertising can influence societal norms by portraying drinking as an acceptable, fun, and relaxing pastime. Heavy drinking may be normalised in certain social circles, increasing the risk for individuals within those groups.
Economic Factors
Income and economic development can also influence alcohol consumption patterns. For example, individuals of higher socioeconomic status may have greater access to alcohol and be exposed to social circles where drinking is more prevalent. Conversely, individuals of lower socioeconomic status may be more susceptible to stress and trauma, which are risk factors for AUDs.
Education
Level of education has a complex relationship with alcohol-related problems. Higher education may provide individuals with the knowledge and resources to make informed choices about alcohol consumption and protect themselves from harmful effects. However, it can also expose individuals to social drinking norms, especially in certain cultural or societal contexts.
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Age-related changes
While the heritability of serious alcohol-related problems was not found, it is known that genetic factors play a role in the vulnerability to alcohol-related harm. Early studies have found evidence of moderate to strong genetic influences on alcoholism, with heritability estimates ranging from 40% to 60%. These estimates vary between men and women, with some studies suggesting that alcoholism is more heritable in men, while others indicate comparable heritability in both sexes.
Physiological changes related to aging can also increase the risks of alcohol consumption. For example, older adults may experience a decline in eyesight and hearing, as well as slower reflexes. These changes can lead to an increased risk of falls, automobile collisions, and other accidents, even after consuming a small amount of alcohol. The sensation of dizziness, feeling high, or intoxication may occur more easily in older adults due to these physiological changes.
Age-related medical conditions, such as high blood pressure and ulcers, can be exacerbated by alcohol consumption. Additionally, older individuals tend to take more medications, and mixing alcohol with prescription or over-the-counter drugs can lead to serious interactions and adverse effects. The management of alcohol withdrawal in elderly persons should be closely supervised by healthcare professionals, and elder-specific alcohol treatment programs are often recommended to improve outcomes.
The challenges and life changes that can occur with aging may also contribute to alcohol-related problems. For example, reduced income, failing health, loneliness, and the loss of loved ones can lead some older adults to turn to alcohol as a coping mechanism. While overall alcohol consumption tends to decrease with age, heavy drinking patterns may persist or develop for the first time during later years.
Young adults, particularly those aged 18 to their late 20s, are at the greatest risk for alcohol use disorder (AUD). Brain development is still ongoing during this stage of life, and the transitions and stressors associated with emerging adulthood can increase the vulnerability to developing problematic drinking patterns.
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Learned behaviour
Drinking behaviours are learned behaviours. Rituals like buying rounds of drinks, discussing wine types, and even how we behave when drunk are all learned behaviours. Young people have to learn to drink, and alcohol is an acquired taste and intoxication an acquired 'pleasure'. This is why alcohol marketing often targets younger drinkers, reinforcing the idea that not enjoying alcohol is odd. Drinking behaviours are subject to a multitude of influences, and people's relationships with alcohol change throughout their lives.
Imprinting is another form of learned behaviour, where individuals imitate their parents or other influential figures in the early stages of their life. This can be observed in the drinking habits of adolescents, who may mirror the drinking behaviours of their parents or peers.
Habituation is a process where an individual fails to respond to a stimulus after repeated exposure. In the context of alcohol, an individual may initially dread drinking during social events like Freshers' Week due to the potential negative consequences. However, through repeated exposure, they may become habituated to drinking in such settings, potentially leading to a change in their drinking patterns.
While learned behaviours play a significant role in drinking habits, it is important to acknowledge that genetics and environmental factors also contribute to an individual's relationship with alcohol. For example, certain genetic variations influence liver enzymes responsible for ethanol metabolism, leading to a higher risk of health issues among individuals of East Asian descent who consume alcohol. Additionally, age-related changes in alcohol processing increase the sensitivity of older adults to alcohol, raising their risk for health problems.
Understanding the interplay between learned behaviour, genetics, and environmental factors is crucial in addressing alcohol-related problems and promoting positive changes in drinking behaviours.
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Frequently asked questions
There is strong evidence that alcohol use disorders (AUD) have a genetic component, with a heritability estimate of 0.49 (95% confidence interval of 0.43-0.53).
Genetic risk factors for AUD include variations in genes related to alcohol metabolism, such as ADH1B and ALDH2, which increase the risk for alcoholism. Other genes with variants that impact risk include GABRA2, CHRM2, KCNJ6, and AUTS2.
Yes, both genetic and environmental factors contribute to AUD. The proportion of shared environmental variance in the development of AUD is estimated to be 0.10 (95% CI 0.03-0.16).
While there are differences in the prevalence of AUD between males and females, the estimated heritability of AUD is similar in both sexes when data is aggregated across studies.
Specific examples include increased power in the β frequency of the electroencephalogram (EEG-β), which is a heritable trait found in alcoholics and their offspring, as well as frontal theta band event-related oscillations (theta ERO), which are highly heritable neuroelectric correlates of cognitive processes that are impaired in individuals with AUD and their offspring at high risk.
