The majority of research indicating that environmental factors are prevalent in incidences of alcohol use disorder does not appear to consider genetic factors during the course of the experimentation. Ahern, Balzer, and Galea (2015) presented research that indicates that social factors are the primary cause for increases in alcohol use disorder while acknowledging that genetic factors were not considered (pp. 144-150). Palm (2014) presented a study that utilized lab rats to attempt to determine environmental causes that may lead to alcohol use disorder in humans. These increased vulnerabilities include the physical and social environments in which one was reared, the age at which an individual is first exposed to alcohol consumption, and an elevated risk-taking profile. This study provided insight into the chemicals in the brain that are affected by the use of various substances (pp. 69-70).

Olsson et al. (2011) presented research that establishes a connection to a specific genotype called 7R+ alleles to an increase in the use of tobacco, cannabis, and AUD. This genotype is not indicative of a family history of alcohol or drug abuse. Individuals with 7R+ alleles report increased use of tobacco, cannabis, and alcohol. However, other factors, such as insecure attachments caused by environmental factors, affect use as well. Those with insecure attachments reported a decrease in alcohol consumption while reporting an increase in tobacco and cannabis use (p. 724). King, McNamara, Hasin, and Cao (2015) indicate that the manner in which an individual’s response to alcohol is the determining factor for alcohol use disorder. AUD increases in individuals who exhibit more resistance to the sedative effects of alcohol while demonstrating higher levels of alcohol simulation and reward sensitivity. This can occur as a result of frequently consuming alcohol as the body has the ability to develop a resistance to alcohol which results in an increase in the amount consumed to attain the same effect.

Numerous studies have been conducted in attempts to determine if alcohol use disorder (AUD) is caused by genetics, environmental factors, or a combination of the two. The types of studies vary to provide insight into a variety of potential causes, including the effects of being introduced to alcohol at an early age and gene-environment interactions. Young-Wolff, Enoch, and Prescott (2011) presented a review of sixteen empirical studies to determine commonalities between the test subjects, the methods implemented for the research, and genotypic moderation of environmental risk. The specific criteria required the test subjects consist of twins who were adopted at young ages and molecular genetics articles published in English prior to June 2010. The research reviewed indicates that the age of introduction to alcohol is younger due to genetics associated with a family history of alcoholism and may lead to AUD in adulthood while placing an emphasis of socioeconomic factors that exist outside the confines of genetics.

The authors also claim that a definitive conclusion is not possible as the result of limitations within the methodology applied in each of the studies as well as the ability to apply variations within the results. Ystrom, Kendler, and Reighborn-Kjennerud (2013) performed a study consisting of 1,336 Norwegian twins. The basis for this study was to determine if there is a link between an early age of alcohol initiation (AAI) and AUD in adulthood. The results of this study indicate that there is a direct correlation between AAI and AUD in adulthood due to genetics (pp. 1830-1831). Lee et al. (2013) presents a study conducted on individuals between the ages of 10 and 33 to determine if consuming alcohol at a young age is a predictor for alcohol issues in adulthood. This study determines that there is a correlation between AAI and AUD while indicating that while genetics is a primary indicator for the development of these issues, environmental factors are also responsible for the prevalence of the development of AAI and AUD (p. 692).