According to the National Association for Children of Alcoholics, there are 18 million children of alcoholics (COA) in the United States, and 11 million of those children are under the age of 18 (NACOA). The heritability of developing an Alcohol Use Disorder (AUD), or how much genetics effect the likelihood of developing an AUD in COAs is estimated to be between 50% and 60% (McGue et al., 1999, p. 109). There are neurological and genetic predispositions that can put COAs in a vulnerable position to develop an AUD, but these predispositions are not completely understood as of yet. It is essential to understand the biological reasons behind this risk so interventions can be put in place to stop COAs from developing an AUD as their parent did. Without interventions, the cycle of passing an AUD from parent to child can continue.

Adolescents are the most critical age group to target, as many studies have found early alcohol intake to be associated with higher risk of developing an AUD later in life, specifically ages 14-19 are the most critical years for alcohol addiction intervention (Nees et al., 2016, p. 5). Neurological Predispositions: The two areas of the brain that are most clearly affected by a family history of AUD are the amygdala and the Mesolimbic Dopamine Pathway (MDP: including the Ventral Tegmental Area and Nucleus Accumbens which is the reward pathway of the brain). These regions (amygdala and MDP) are most well-known for emotion and reward processing, respectively. Those with an AUD tend to have smaller amygdala volumes, which is also seen in individuals with a family history of AUD (Dager et al., 2015, p. 413). Those without a family history, however, do not tend to have smaller amygdala volumes (Dager et al., 2015, p.413). This is important to understand for COAs because this may contribute to an increased risk of alcoholism by creating a faster link to alcohol-related cue-response learning, which is dependent on amygdala volume (Hill et al. in Dager et al., 2015, p. 413). Another brain region commonly associated with AUD is the Mesolimbic Dopamine Pathway: AUD can affect a variety of genes that influence this pathway in different manners, although no conclusive story has yet been found (Morozova et al., 2012, p. 2). It should be noted that there is hypersensitivity of this pathway during adolescence. This could lead to conflicting results because, if the pathway is already activated during adolescence, it could conflate the results. There is also a genetic basis to what can affect this pathway in COAs leading to an increased risk of an AUD (Nees et al., 2012, p. 993).

Genetic Predispositions: As previously stated, a large percentage of AUD is heritable. Many genes have been studied that have a basis in alcohol addiction, such as critical signaling molecules including ANKK1 and a protein-coding gene, HOMER1. Variations in these genes seem to be as important as personality in later adolescent years in terms of the likelihood of developing an AUD (Nees et al., 2012, p. 991). Animal models of addiction have also been useful for identifying genetic predispositions: another gene, AUTS2, has also been identified in humans, mice, and Drosophila as associated with alcohol sensitivity (Nees et al., 2016, p. 5). Variations in these genes allow for the more likely development of an AUD among COAs.

On a different note, an intriguing genetic model of relapsing and pursuing alcohol involves the epigenetics of how anxiety can impact alcohol abuse. Epigenetics is how gene expression can be modified in a manner other than the alteration of genetic code. As seen in the figure below, adopted from Pandey et al., the acute use of alcohol relaxes chromatin (the proteins around which DNA is bound), leading to a change of which genes are expressed, resulting in a decrease in anxiety. This process changes, however as one progresses from acute to chronic use and again once withdrawal occurs. In withdrawal, chromatin is condensed leading to more expression in genes and increased anxiety. This adds to the addiction cycle by causing those with alcohol use disorders to go back to the drug to relieve their anxiety (Pandey et al., 2017, p. 78). Adolescent exposure to alcohol causes higher expression of HDAC2, an enzyme that further condenses chromatin, which maintains this cycle through high stress and drinking behaviors in adulthood (Pandey et al., 2017, p. 78). This is an explanation for how alcohol use at a young age can quickly change into an AUD. This, on top of other risk factors for COAs, puts adolescent COAs at high risk of developing an addiction if they experiment with alcohol. While there are many findings of genetic and neurological predispositions for AUD, there is no cohesive theory of all risk factors for COAs.

Role of Personality: Early adolescent alcohol use is associated with an increased risk of developing an AUD (Nees et al., 2016, p. 5). Additionally, there is a relationship between the age of first use of alcohol and the rate of transition to alcohol abuse. Personality traits (such as sensation seeking, impulsivity, extraversion, etc.) are the most crucial factors in explaining early adolescent drinking (with a mean age of 14.37). Variations in the genes mentioned above (ANKK1 and HOMER1) seem to be equally as important as these personality traits in later adolescent drinking developing into an AUD (with a mean age of 16.45) (Nees et al. 2016 p. 4,Ayer et al., 2011, p. 1302). A later age of onset is associated with a faster transition to an AUD. However, those with an early onset also had an overall higher risk of AUD, but this transition happened slower than those with a later age of onset. This difference between early adolescence and late adolescence is partially due to genetics, but might also be due to different drinking patterns, less parental control, and increased peer influence.