Reasons of Alcohol Addiction in Teenagers

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Table of Contents

Introduction
Discussion
Conclusion
Works Cited

Introduction

Background

Substance use disorder is a severe chronic disease that adversely affects the lives, health, and well-being of individuals when neglected or unaddressed in a proper and timely manner. Alcohol use disorder is one of the most prevalent conditions affecting people of various ages and resulting in severe comorbidities related to physical and mental health. Indeed, multiple research studies recognize liver cirrhosis, hepatocarcinoma, depression, and other mental and physical impairments, as well as negative social consequences, are correlated and dependent on alcoholism (Jain et al.; Jones et al. 721-722).

Alcohol intake in excessive amounts or for continuous periods of time increases the “risk of high blood pressure, high triglycerides, increased abdominal girth, and elevated blood glucose” (Jain et al. par. 8). Moreover, excessive alcohol consumption is a frequent cause of death.

The statistics on alcohol use consequences in relation to health and mortality demonstrate that it is a significant issue both nationally and globally. Indeed, according to the data provided by the Centers for Disease Control and Prevention (CDC), “alcohol use contributes to approximately 88,000 deaths annually in the United States” (Tawa et al. 507). Furthermore, on an annual global scale, more than one million individuals aged 15 and older have been diagnosed with alcohol addiction (Zaso et al. 216).

Such a high level of identified cases of alcohol use disorders is reflected by the statistical data on worldwide mortality rates induced by uncontrolled drinking. Indeed, as stated by Zaso et al., “139 million disability-adjusted life years and 3.3 million global deaths were attributed to alcohol in 2012” (2016). Such a high level of severe consequences of this disorder encourages scholars, health care professionals, and counselors work collaboratively to find answers to the questions and solutions to the problems of alcoholism.

As a clinical diagnosis, alcohol addiction is a well-documented condition that is characterized by particular characteristics. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition contains “11 criteria pertaining to excessive alcohol use, alcohol abuse, and alcohol dependence” (Tawa et al. 507). These criteria include but are not limited to continuous drinking and inability to stop in spite of health complications or mental health impairments. Given the clinical diagnoses, the wide-spread nature of the problem, and the severe consequences impacting the life and health of millions of people, the in-depth investigation of the causes of the disorder is of critical importance.

The topic of the hereditary nature of alcohol abuse has long been at the center of scholarly debate in biology. Much has been investigated in terms of the inherited likelihood of the consecutive generations to develop a dependence on alcohol if their family members have been impacted by the issue. The extensive research findings in this field indicate that there are multiple genes in a human organism that contribute to the likelihood of developing alcohol use disorder (Edenberg and McClintick 2281; Jain et al.; Tawa et al. 507-508; Wall et al. 59). However, there is a specific group of genes that have been identified to account for alcohol intake in particular.

Moreover, specific combinations of such genes are most contributive within the context of alcohol use disorder. As a result, studies demonstrate that “approximately 50% of the risk for developing alcohol use disorder is due to genetics, while the remaining percent may be due to either environmental factors, or gene-environment interactions” (Tawa et al. 507). The reverse mechanism is also observed; as discussed by Jain et al., alcoholism not only has a destructive effect on health but also causes genetic changes that provoke continuous biological processes harmful to the organism. Thus, the genetic factor is a particular cause in the development of alcohol use disorder.

In a similar manner, environmental drivers also significantly contribute to the etiology of alcoholism. They are related to lifestyle choices, behavior, and the variety of stressors a person is exposed to throughout life (Tawa et al. 507). Nonetheless, the addictive particularities of alcohol are perceived to be more influential at younger age. Indeed, as identified by scholars, early exposure to alcohol consumption, especially in adolescence, significantly increases the risks of mental, physical health, and social problems in adulthood (Byrnes et al. 152; Yuen et al. 1-2).

An individual’s pattern in alcohol drinking that might vary from regular to binge consumption “may be an important predictor of later alcohol problems, such as alcohol dependence symptoms and neglecting responsibilities because of drinking” (Yuen et al. 2). Moreover, alcohol intake is recognized to be “the leading global risk factor for burden of disease among people aged 10–24 years” (Yuen et al. 2). Thus, it is imperative to maximize efforts to study the biological underpinnings of the problem to enhance the options for finding more effective solutions.

Hypothesis

While both environment and genes play a role in predetermining the likelihood of a person’s alcohol addiction, the spectrum of the determinants that trigger the abusive behavior is wide. Different combinations of genes have been found to induce excessive and uncontrolled alcoholic beverage consumption. Environmental factors include the social surroundings influencing an individual, behavioral patterns in family and peers, employment characteristics, stress, educational, and other determinants.

From a logical perspective, one might assume that the environment representative of the combination of changeable factors is possible to be adjusted or altered in order to minimize the potential of the disease development (Enoch and Albaugh 461-462). Therefore, it is important to clarify whether this assumption means that the environmental factors dominate the genetic predisposition toward alcohol addiction. Since the manipulations with the environment are capable (in theory) of reducing the likelihood of the development of alcohol dependence, then genetics might not necessarily dominate.

However, the failure of some individuals to respond adequately to environment alterations or treatment indicates that genetic inclination and the supposed hereditary alcohol dependence becomes a driving force in the occurrence of the disorder (Enoch and Albaugh 461). Many currently available research studies indicate that alcohol use disorder is a moderately heritable condition, implying that both environmental and genetic indicators play a partial role in the development of the disease (Zaso et al. 216). Nonetheless, most research studies involve participants of all ages concentrating more on the socioeconomic or ethnic characteristics of individuals with alcohol use disorder (Chartier et al., Environmental Influences on Alcohol Use 446; Chartier et al., Interactions between Alcohol Metabolism Genes and Religious Involvement 393; Enoch and Albaugh 461; Zaso et al. 216; Zheng et al. 79).

Such a vulnerable age population as adolescents have not been adequately investigated from the perspective of the interplay of environmental and genetic factors in alcohol consumption patterns. Therefore, it is vital to conduct research and identify whether the genetic predisposition to alcoholism prevails over environmental characteristics in teenage alcohol abuse behavior.

In essence, the present research paper is aimed at testing the validity of the hypothesis addressing the correlation between environment and genetics. It is assumed that if teenagers with alcohol metabolism genes are not exposed to environmental factors that reinforcing continuous alcohol intake, they will not develop alcohol use disorder. Therefore, the variables that are of critical importance to the study are alcohol metabolism genes (independent variable), environmental factors (independent variable), and alcohol use disorder occurrence (dependent variable).

Hypothesis: The presence of genes of alcohol metabolism outweigh the influence of environmental factors in the development of alcohol dependence in teenagers.

The developed hypothesis will be tested upon the addressing of four specifically designed objectives for the present research study.

Objectives

Taking into consideration the multifaceted and complicated nature of the research topic and the compound hypothesis that involves two independent variables, the objectives are aimed at collecting separate sets of data. Findings contributing to the theoretical investigation of both genetic processes and environmental contributors and their impact on the development of addiction to alcohol will be included. The four objectives are as follows.

Objective 1: To identify the epigenetics of alcohol metabolism, as presented in the current scholarly literature.
Objective 2: To identify the influence of alcohol metabolism genes on alcohol use disorder in teenagers.
Objective 3: To identify the environmental factors that influence more frequent and continuous alcohol consumption leading to dependence on a general scale.
Objective 4: To identify the influence of environmental factors on adolescent alcohol use disorder development.

Methods

The choice of methodology predetermines the outcomes of research and outlines the scope of possible findings in accordance with the objectives. The present research study design is a qualitative integrative literature review. Given the interdisciplinary nature of the research problem that incorporates the field of biology, genetics, and sociology, the literature review is a design that allows for fulfilling the requirements of collecting interdisciplinary qualitative data. The method of a literature review is “an excellent way of synthesizing research findings to show evidence on a meta-level and to uncover areas in which more research is needed” (Snyder 334). In particular, an integrative or critical literature review is aimed at assessing the content of studies in order to synthesize findings.

Since the ultimate goal of the present research study is to test the hypothesis, the choice of the integrative literature review method will allow for providing an adequate set of data accordingly. The data analysis method that is used is content analysis. According to Snyder, the purpose of an integrative literature review is “to critically analyze and examine the literature and the main ideas and relationships of an issue” (334-335). Therefore, the selection of methods is validated by the nature of the research, intended goals, and the particularities of the topic.

Discussion

Data for Objective 1: The Epigenetics of Alcohol Metabolism as Presented in the Current Scholarly Literature

The genetic predisposition of individuals to alcohol addiction is derived from the alterations in genes. Multiple research studies have been designed to identify particular alcohol-related risk alleles. The genetic influence of ethanol metabolism is proven to be consistent over time. A study conducted by Vadigepalli and Hoek was devoted to investigating the persistence of genetic memory of alcohol intake across time (845-848). The findings demonstrated that “ethanol-induced epigenetic changes account for altered regulation of cell function that persists well after ethanol or its metabolites have disappeared” (Vadigepalli and Hoek 848).

The effect of the substance on the genes, regardless of the enzyme particularities, is preserved for minutes or even decades and leads to the intergenerational transmission of the memory. As the authors state, such a mechanism on a genetic level has a “potential to drive persistent gene regulatory changes underlying fetal alcohol syndrome, cancer, and metabolic disorders” (Vadigepalli and Hoek 848). Therefore, it is evident that alcohol has a direct influence on the genetic codes of individuals inducing predictable responses in consecutive generations. However, it is important to understand how alcohol addiction correlates with particular genetic composition.

The process of alcohol metabolism is commonly considered as a primary framework for understanding the molecular and neurobiological processes that take place following alcohol consumption. In particular, two enzymes play a key role in alcohol metabolism in the human liver, representing two stages of ethanol metabolism. They include alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) (Chartier et al., Interactions between Alcohol Metabolism Genes and Religious Involvement 395; Tawa et al. 508; Wall et al. 61). The first enzyme, ADH, catalyzes ethanol contained in alcoholic drinks by breaking it into acetaldehyde, which is then transferred to the second stage of alcohol metabolism. This second stage involves the second enzyme, ALDH, which produces acetate out of acetaldehyde.

The particularities of these two processes predetermine how a person’s body will respond to alcohol. According to Wall et al., the importance of the quality of these stages of alcohol metabolism is explained by the fact that “accumulation of acetaldehyde can lead to heightened responses as well as unpleasant reactions” (61). Importantly, each individuals’ alcohol metabolism enzymes have variants or alleles depending on the genetic code inherited from parents. As a result, the individuals who have genetically designed isoenzymes of ADH that catalyze ethanol faster and isoenzymes of ALDH that catalyze acetaldehyde more slowly are characterized by reduced risk of alcohol use disorder (Tawa et al. 508).

Indeed, the examples of such isomorphs are ADH1B*2 single-nucleotide polymorphism (SNP) rs1229984 (Arg48His), ADH1C*2 SNP rs698 (Ile350Val), and ALDH2*2 SNP rs671, which trigger particular ethanol oxidation, thus performing a protective role in alcohol use disorder development (Tawa et al. 508; Wall et al. 61). Moreover, additional neurobiological processes of a genetic level are associated with alcohol addiction. They include D2 dopamine receptor (DRD2), dopamine transporter (SLC6A3), serotonin transporter (SLC6A4), tryptophan hydroxylase 1 (TPH1), and others (Tawa et al. 509).

As a demonstration of hereditary implications of an alcohol use disorder, the similarities in isomorphs responsible for ethanol metabolism have been found. For example, studies with multiethnic participants found that “the ADH1C*2 allele … was associated with an increased risk for alcohol dependence compared with the ADH1C*1 or A allele (Chartier et al., Interactions between Alcohol Metabolism Genes and Religious Involvement 395). Overall, the extensive investigation of the patterns in isomorphs of enzymes across different populations demonstrates a particular rate of consistency, implying genetic predisposition to alcoholism in individuals with particular enzyme variants.

Data for Objective 2: The Influence of Alcohol Metabolism Genes on Alcohol Use Disorder in Teenagers

Given the age-specific and developmental particularities of adolescents, their predisposition to alcohol intake is increased. The differences in teenagers’ responses to alcohol addiction treatment have been studied by several scholars to identify the particularities of individual perception of alcohol-related behaviors. While the influence of peers and the environment is more researched, the occurrence of gene variations in teenagers is particularly important to discuss.

The combinations of ADH and ALDH isomorphs are consistently observed across different age groups, implying their relevance to teenage individuals (Chartier et al., Interactions between Alcohol Metabolism Genes and Religious Involvement 395; Wall et al. 61). Nonetheless, the particularities of alcohol use disorder manifestations and underlying processes related to adolescents, in particular, have not been sufficiently addressed in scientific literature.

Considering the scope of problematic consequences associated with teenage alcoholism, including antisocial behavior, mental and physical health impairments, and alcoholism risks in adulthood, teenage alcohol dependence is approached from the perspective of treatment effectiveness. Since genetically designed particularities of ethanol oxidation are reliant on the enzyme combinations that have demonstrated reduced risks in alcohol use disorder development, the scientists expect that individuals with such phenotypes would respond to treatment better.

Indeed, as demonstrated by the study conducted by Zheng et al., the qualities of the glucocorticoid receptor (NR3C1) gene predetermine the perceptivity of alcoholism treatment interventions in teenagers (79). The individual differences between participants’ genotypes indicate adolescents’ different rates of predisposition to alcohol intake initiation and continuous binge drinking. The findings of the study strengthen the implications of biological data for the development of effective treatment approaches and interventions aimed at reducing the risks or consequences of alcohol addiction in adolescents.

Data for Objective 3: The Environmental Factors that Influence more Frequent and Continuous Alcohol Consumption Leading to Dependence on a General Scale

Unlike genetic predisposition, environmental factors’ contribution to the development of various substance use disorders, including alcohol abuse, has been broadly investigated. However, the heterogeneity of influencing factors triggering addictive behaviors implies the complexity of study findings and probable inconsistency of results across different populations. Indeed, since environments vary depending on social, economic, and cultural particularities, it is difficult to estimate the definite way in which an individual is impacted by the environment. Nonetheless, the studies that have investigated this issue have provided an extensive domain of data illustrating the dependence of alcohol use disorder development on external determinants.

There are several spheres that constitute an environment for an individual. The spectrum of influences these environmental factors may have on an individual varies from enforcing to reducing risks. Indeed, they have been categorized into the social trigger and social control mechanisms (Chartier et al., Environmental Influences on Alcohol Use 448). Social control mechanisms, such as alcohol laws, policies, cohort effects; community work including advertising, religious affiliation; and social networks, such as marriage, family, and friends, might become either constraints or opportunities for excessive alcohol consumption.

Similarly, such social trigger mechanisms as economic opportunities or poverty; neighborhood safety, discrimination; childhood maltreatment or family drinking history might become either nurturing or adverse contributors to alcohol addiction (Chartier et al., Environmental Influences on Alcohol Use 448). Therefore, the exposure to a combination of such factors is found to be most influential in triggering positive alcohol response on a genetic level.

The variety of environmental factors embodies the different spheres of life a person encounters throughout the lifespan. They include culture, religion, society, family, the level of neighborhood advantages, access to alcohol, economic status, and childhood adversity or trauma (Enoch and Albaugh 462; Mennis et al. 6; Wall et al. 66-67). All of these factors might have positive (constraining) or negative (reinforcing) effects. Indeed, cultural traditions related to drinking are inherently philosophical and socially accepted. As the findings of a study conducted by Wall et al. demonstrate, cultural differences imply various alcohol consumption patterns (67).

For example, Confucian culture cultivates moderate drinking as a norm, thus obstructing excessive alcohol consumption, which might become a constraint for people (even those genetically predisposed to alcohol addiction). In comparison, Korean culture pays much attention to alcohol use, which is thought to be important “to socialize and drink heavily, which may result in greater acceptance of heavy drinking and alcohol problems or religious” (Wall et al. 67). Given such a significant difference in cultural factors, it is expected that people’s drinking patterns in behavior will be different depending on the cultural domains they live in.

In a similar manner, the neighborhood to which a person belongs also plays a pivotal role in determining the likelihood of excessive drinking. Indeed, it is found that disadvantaged neighborhoods are commonly impacted by high poverty levels, high crime prevalence rate, diminished health quality, and other adverse characteristics of life. Therefore, people who live in such neighborhoods are continuously exposed to negative influences and stress. Therefore, “residing in neighborhoods characterized by disadvantage and disorder can produce chronic stress due to the trauma of continuous economic struggle and exposure to this disorder,” resulting in substance abuse as a coping mechanism (Mennis et al. 4). Thus, an individual with a genetic predisposition to alcohol dependence is much more likely to develop alcohol use disorder in a disadvantaged neighborhood.

Another important issue that should be discussed within the context of environmental factors is access to substances. As defined by Mennis et al., “ready access to substances lowers the barriers to acquiring, using, and abusing substances, thus facilitating substance use initiation and potential abuse” (3). On the contrary, the lack of access to alcohol, which might be manifested through policy constraints regulating the selling or serving of alcoholic beverages, economic inability to buy a drink, or other determinants, become barriers. Thus, even an individual with a genetic predisposition caused by the presence of gene variations contributing to addiction will not be able to develop alcohol use disorder without having the ability to obtain a beverage.

Data for Objective 4: The Influence of Environmental Factors on Adolescent Alcohol Use Disorder Development.

While environmental factors are observed to be highly influential across the lifespan, they play a particular role in the development of alcohol addiction in minors due to their developmentally conditioned vulnerability to outside influences. Teenagers come through a developmental phase when socialization is pivotal. Peer pressure, social roles, and the opinion of others are the leading triggers of an adolescent lifestyle choice and behavioral patterns. Therefore, adolescents’ susceptibility to environmental influences is more vividly manifested than in any other age.

The family environment is highly demonstrative of the acceptable behaviors for teenagers. If parents are drinkers, a child is more likely to initiate alcohol consumption at an earlier age regardless of genetic predisposition to dependence on substances. The studies that have investigated the drinking patterns in families with adopted children vividly demonstrate this pattern. Indeed, as Wall et al. state, in families with adopted adolescents, “the effect of ALDH2*2 was moderated by environmental influences of parental alcohol use and misuse as well as sibling alcohol use” (67). This goes in accord with the findings concerning the effects of the factor of access to substances. The presence of alcoholic drinks at home increases the likelihood of a teenager initiating consumption that might trigger abuse (Mennis et al. 3). Therefore, family and access to alcohol play a decisive role in teenagers’ excessive drinking.

Hypothesis Testing Results

The presented data related to each of the four objectives allows for synthesizing the findings and stating whether the hypothesis can be proven true or false. The hypothesis that was tested in the present study was as follows. The presence of genes of alcohol metabolism outweighs the influence of environmental factors in the development of alcohol dependence in teenagers.

The collected data indicating the particularities of gene variants associated with adolescent alcohol use disorder and the environmental factors contributing to the development of alcohol dependence allows for proving the hypothesis false. The findings retrieved in the result of the integrative literature review do not allow for accepting the hypothesis. There have been insufficient data collected to establish that the presence of alcohol metabolism genes prevails in alcohol addiction in comparison to environmental factors.

The diversity of opinions related to the dominant role of either genetics or environment in alcohol addiction appears to obtain a more prominent direction toward the environment as a driving force for adolescent alcoholism. Indeed, several studies have shown that despite evident genetic correlations between alcohol metabolism genes and consecutive alcohol use disorder development, much contribution is reliant on environment (Chartier et al., Interactions between Alcohol Metabolism Genes and Religious Involvement 395; Tawa et al. 508; Vadigepalli and Hoek 845; Wall et al. 61).

It was directly stated that “many of these genetic risk variants are dependent on gene-environment interactions and replication of findings has been difficult due to the generally small expected effect size … and genetic heterogeneity” (Tawa et al. 509). Moreover, Edenberg and McClintick identified that apart from the identified types of enzymes responsible for the quality of alcohol metabolism in the liver, there multiple other genes that regulate the interaction with the environment (2297). Thus, the strengths of genetic predispositions are significantly adjusted to the quality of environmental influences.

Since teenagers are particularly susceptible to external influencers, their environment becomes a driving determinant of alcohol-related behavior. Such gene-environment correlation predetermines two options. The first one entails a scenario according to which a teenager genetically predisposed to alcohol use disorder encounters negative environmental influences. In such a case, alcoholism is practically impossible to avoid. However,

“in positive conditions with ample resources and support such as intervention, … genetic susceptible individuals achieve better outcomes” (Zheng et al. 80). Without exposure to the triggers of alcohol consumption and only living among the barriers to alcohol intake, a person with a genetic predisposition will be able to neither initiate nor abuse alcohol. This conclusion provides a solid basis for rejecting the hypothesis.

Conclusion

In summation, alcohol use disorder is a severe psychiatric condition that affects millions of people around the world on an annual basis. The adverse consequences of binge drinking and addiction to alcohol include physical health imperilments, mental disorders, diminished overall quality of life, and high mortality rates. Teenagers, as a vulnerable population, from a developmental point of view, are particularly susceptible to alcoholism. Since the recent scientific findings indicate that alcohol addiction is genetically predisposed, it is important to investigate how this genetic predisposition correlates with environmental influences to which individuals are continuously exposed.

The initial scholarly sources overview was used to construct a hypothesis that claimed that the presence of genes of alcohol metabolism outweighs the influence of environmental factors in the development of alcohol dependence in teenagers.

In the course of integrative literature review, data contributing to the understanding of the genetic mechanisms and environmental factor interaction in relation to alcohol use disorder development in teenagers was collected. As a result, the hypothesis was rejected due to the lack of direct claims that the availability of enzyme isomorphs responsible for favorable alcohol metabolism dominates over environmental factors. The implications of diverse and multifaceted interaction between genotype and environment have been found. The limitations of the present research study are related to the sporadic choice of research articles.

Also, since there are constraints in terms of the opportunities to conduct a quantitative study with participants due to the global epidemic, the study was conducted as a literature review concentrating on qualitative content analysis. Despite minor limitations, the study results allow for obtaining evidence-based insights into the dependence of alcohol use disorder on environmental and genetic factors. Further research is encouraged to enhance the findings and articulate functional and effective treatment interventions for adolescent alcohol abusers.

Works Cited

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Chartier, Karen G., et al. “Environmental Influences on Alcohol Use: Informing Research on the Joint Effects of Genes and the Environment in Diverse US Populations.” The American Journal on Addictions, vol. 26, no. 5, 2017, pp. 446-460.

Chartier, Karen G., et al. “Interactions between Alcohol Metabolism Genes and Religious Involvement in Association with Maximum Drinks and Alcohol Dependence Symptoms.” Journal of Studies on Alcohol and Drugs, vol. 77, no. 3, 2016, pp. 393-404.

Edenberg, Howard J., and Jeanette N. McClintick. “Alcohol Dehydrogenases, Aldehyde Dehydrogenases, and Alcohol Use Disorders: A Critical Review.” Alcoholism: Clinical and Experimental Research, vol. 42, no. 12, 2018, pp. 2281-2297.

Enoch, Mary‐Anne, and Bernard J. Albaugh. “Genetic and Environmental Risk Factors for Alcohol Use Disorders in American Indians and Alaskan Natives.” The American Journal on Addictions, vol. 26, no. 5, 2017, pp. 461-468.

Jain, Subodh Kumar, Sapna Sedha, and Meeta Mishra. “Genetic Polymorphism and Alcohol Metabolism.” Genetic Polymorphisms. IntechOpen, 2019. Web.

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Mennis, Jeremy, Gerald J. Stahler, and Michael J. Mason. “Risky Substance Use Environments and Addiction: A New Frontier for Environmental Justice Research.” International Journal of Environmental Research and Public Health, vol. 13, no. 6, 2016, pp. 1-15.

Snyder, Hannah. “Literature Review as a Research Methodology: An Overview and Guidelines.” Journal of Business Research, vol. 104, 2019, pp. 333-339.

Tawa, Elisabeth A., Samuel D. Hall, and Falk W. Lohoff. “Overview of the Genetics of Alcohol Use Disorder.” Alcohol and Alcoholism, vol. 51, no. 5, 2016, pp. 507-514.

Vadigepalli, Rajanikanth, and Jan B. Hoek. “Alcohol and Epigenetic Regulation: Do the Products of Alcohol Metabolism Drive Epigenetic Control of Gene Expression in Alcohol-Related Disorders?” Alcoholism, Clinical and Experimental Research, vol. 42, no. 5, 2018, pp. 845-848.

Wall, Tamara L., Susan E. Luczak, and Susanne Hiller-Sturmhöfel. “Biology, Genetics, and Environment: Underlying Factors Influencing Alcohol Metabolism.” Alcohol Research: Current Reviews, vol. 38, no. 1, 2016, pp. 59-68.

Yuen, Wing See, et al. “Adolescent Alcohol Use Trajectories: Risk Factors and Adult Outcomes.” Pediatrics, vol. 146, no. 4, 2020, pp. 1-11.

Zaso, Michelle J., et al. “Meta-Analysis on Associations of Alcohol Metabolism Genes with Alcohol Use Disorder in East Asians.” Alcohol and Alcoholism, vol. 54, no. 3, 2019, pp. 216-224.

Zheng, Yao, et al. “Glucocorticoid Receptor (NR3C1) Gene Polymorphism Moderate Intervention Effects on the Developmental Trajectory of African-American Adolescent Alcohol Abuse.” Prevention Science, vol. 19, no. 1, 2018, pp. 79-89.

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