Chaotic Environments and Adult Children of Alcoholics
The primary goal of this paper is two-fold: to challenge the belief that adult children of alcoholics tend to abuse alcohol as the result of genetic composition, and to show instead evidence that the unpredictable and chaotic home environment in which alcoholics grow up may be responsible. Adult children of alcoholics syndrome, mood alteration, and family history of alcoholism are explored. Addiction models and treatment plan implications are presented.
Keywords: abuse, addiction, chaos, home environments, alcoholics
According to the National Association for Children of Alcoholics (n.d.), out of the approximately 30 million children of alcoholics in the United States, 11 million are believed to be minors (younger than 18 years old) and the remainder (almost 20 million) are adult children. The term Adult Children of Alcoholics (ACoA) attempts to capture the shared characteristics typically found among those adults who grew up with either one or two alcoholic parents (Jones, Perera-Diltz, Sayers, Laux, & Cochrane, 2007). Alcoholic families are driven by a system of rigidity (arbitrary rules, lack of flexibility) where children develop a sense of chronic shock (Kritsberg, 1985). Kritsberg (1985) refers to chronic shock as an overwhelming fear that is never expressed or resolved, which commonly leads to shutting down. Prevented from expressing their emotions and from learning healthy coping skills in an alcoholic environment, coupled with poor family interaction patterns tend to place ACoAs at a higher risk for alcohol abuse (Woititz, 1984). In a move to augment Woititz’s (1984) findings, this essay reviews the risk for alcohol abuse among ACoAs from a complimentary paradigm: growing up in a chaotic family environment rather than having alcoholic parents may account for the tendency of alcohol abuse among ACoAs.
The ACoA Syndrome
A chaotic environment is fertile ground for the shared characteristics of ACoAs, known as the ACoA syndrome (Kritsberg, 1985). The ACoA syndrome is a developmental phenomenon shared by most if not all ACoAs, which describes “common symptoms and behaviors as the result of their common experience” (Kritsberg, 1985, p. 3). A kaleidoscope of characteristics engulf the syndrome, which is mostly grounded in fear: fear of abandonment, fear of intimacy, fear of change, chronic shock (a persistent state of apprehension), fear of making mistakes, feelings of inadequacy (fear of not being good enough) and poor coping skills (Kritsberg, 1985). Ratey and Johnson (1997) explain that syndromes are a constellation of traits that manifest themselves in a continuum depending on the individual’s psychological development. In other words, not all ACoAs may present all of the traits, but most ACoAs fall somewhere in the spectrum (Kritsberg, 1985; Woititz, 1984). Kritsberg (1985) insists the ACoA syndrome typically develops in response to a very rigid and chaotic family system that may be centered on the alcoholic.
Alcohol: A Mood-Altering Substance
An alcoholic is a person who abuses alcohol despite the consequences to self, finances, and interpersonal relationships. Alcohol is a depressant whose job is to suppress the central nervous system (CNS) while hijacking the brain’s mesolimbic reward system (Dodes, 2002). Encompassing a complex pleasure circuit, the mesolimbic reward system activates the limbic system (the seat of emotion), and at the same time deactivates the prefrontal cortex (the seat of reason) (Dodes, 2002). The dynamics involved in the nerve fibers of the reward pathway are believed to be responsible for the “sensation” or the feelings of euphoria sought by alcoholics (Heitzeg, Nigg, Yau, Zucker, & Zubieta, 2010, p. 287).
Although there may be different models to explain the etiology of substance abuse and addiction, there is a consensus among scholars that alcoholics attempt to alter their moods, such as depression, anxiety, anger, and feelings of inadequacy, through alcohol consumption (Dodes, 2002). Consequences of alcohol abuse are not only evident in the United States, but also are seen in families around the world. European studies focusing on adolescents from Austria, Germany, Czechoslovakia, Russia, Turkey, and Denmark show that “one family member’s substance abuse is often influenced by substance-using behaviors of others in the family” (Grüber, Celan, Golik-Grüber, Agius, & Murphy, 2007, p. 27). While ethnicity does not seem to play a significant role in the propensity toward alcohol abuse, other variables have been found to have an impact (Braitman et al., 2009). For instance, either having two alcoholic parents or having “an alcoholic father” increases the odds of alcohol abuse in both their male and female offspring (Braitman et al., 2009, p. 71).
Family History as a Variable
A longitudinal study that followed participants from 12 years of age to 31 by Warner, White, and Johnson (2007) showed that a combination of both early experimentation with alcohol and a family history of alcoholism are predictors of a “problem-drinking trajectory” (p. 56). Warner et al. reached their arguments based on a number of analyses including the application of Rutgers Alcohol Problem Index (RAPI). The RAPI is a psychometric instrument used to discern how problematic alcohol consumption may be perceived by a population and has received support among scholars. Neal, Fromme, and Corbin (2006) found RAPI to have acceptable validity and reliability and “test-retest correlations between 89 and 92” (p. 402). Warner et al. concluded that age at drinking onset alone is not sufficient to predict a problematic drinking trajectory. Instead, Warner et al. predict those who start drinking at an early age (adolescence) who also have a family history of alcoholism (ACoAs) are at higher risk to abuse alcohol as adults than those who do not have an alcoholic family history (non-ACoAs).
ACoAs vs. Non-ACoAs
Intrigued by the presence of alcohol in the family as a probable variable in the offspring’s alcohol abuse, Jones et al. (2007) led a research study to investigate the differences in alcohol consumption between ACoAs and non-ACoAs. With that in mind, the researchers divided the participants in two groups: those who identified themselves as having grown up with a substance-abuse parent and those who did not. Jones et al. applied the Self-Administered, Stand-Alone Screening Instrument (SASSI-3) to the participants. The SASSI-3 is a questionnaire unrelated to substance abuse. The rationale for asking substance-unrelated questions is an attempt to bypass the tendency of denial often found among those abusing a substance. After analyzing the results, Jones et al. noted no difference in the consumption of alcohol between the ACoA and non-ACoA groups. Jones et al. concluded that the culprit in an alcoholic home may not be so much the substance per se, but “the chaos associated with the substance use that may lead to the ACoA traits” (p. 24). In other words, the chaos and unpredictability experienced in alcoholic families may explain the ACoA syndrome, and the high risk of alcohol abuse among ACoAs (Kritsberg, 1985; Woititz, 1984).
Chaos and Unpredictability
In concert with Jones et al.’s (2007) theory of unpredictability, Ross and Hill (2001) conducted a study where participants from different ethnic and socioeconomic backgrounds were recruited from ongoing studies at the University of Michigan Alcohol Research Center. One group of adult children of alcoholics and one group of adults who had parents who drank moderately during social events were investigated. The researchers’ mission was to isolate unpredictability (lack of consistency) and chaos in the family as variables in developing alcohol abuse in adulthood. In agreement with Jones et al. (2007), Ross and Hill (2001) propose that “the chaotic nature” and the “unpredictability” in the home may be the precursors to alcohol abuse in adulthood (p. 610). Factors such as parental rejection or uninvolvement, abusive discipline and punishment, and systematic broken promises were the underpinnings measured in the unpredictability index (Ross & Hill, 2001).
Ross and Hill (2001) argued that their study revealed “parental unpredictability, rather than parental alcoholism per se, was associated with alcohol misuse . . . and [shows] why all children from alcoholic homes do not have problems with alcohol themselves” (p. 630). These researchers point out that the significance of unpredictability, which they found in homes of adult children of divorce, adult children of economic adversity, and among ACoAs is the factor linking these adult children, which cannot be over-emphasized (Ross & Hill, 2001).
Basing their premise on Bowlby’s (1969) theory of attachment and loss, Ross and McDuff (2008) contend that unpredictability is a derivative of insecure attachment between caregivers and their children. Attachment describes the bond children form with their caregivers. Attachments range in a continuum from secure to insecure (avoidant) depending on the caregiver’s availability and willingness to meet children’s needs (Bowlby, 1969). Insecure attachments are damaging to children because they tend to send implicit and explicit messages that they are not important enough to receive care (Bowlby, 1969). This mindset is unconsciously carried into adulthood, becoming the underpinning of the ACoA syndrome (Kritsberg, 1985).
In an effort to support their argument on unpredictability, Ross and McDuff (2008) administered both Ross and Hill’s (2001) Family Unpredictability Scale (FUS) and Ross and McDuff’s (2008) Retrospective Family Unpredictability Scale (Retro-FUS) to the participants in their study. Retro-FUS is specifically designed for ACoAs, and both FUS and Retro-FUS evaluate the degree of inconsistencies in discipline, nurturance, meals, and general family dysfunction. As a corollary, Hodgins, Maticka-Tyndale, El-Guebaly, and West’s (1993) Children of Alcoholics Screening Test (CAST) also was used to specifically distinguish ACoAs from non-ACoAs in the study. It is worth mentioning that the CAST has received support among the academic community for its accuracy in measuring specific family dynamics in the alcoholic home (Lease & Yanico, 1995). Ross and McDuff (2008) conclude that growing up in an unpredictable environment is an important factor placing the ACoAs at higher risk for abusing alcohol compared with non-ACoAs.
Among some clinicians the genetic model has gained clamor because of the frequency of alcoholism observed in certain families (Wang et al., 2011). To identify the contributing gene or genes to alcohol dependence, Wang et al. (2011) conducted a study of a small sample of Australian twins and concluded there is no gene or group of genes responsible for the main effect of alcohol dependence, but rather the possibility that an individual with a certain genotype such as monamine oxidase A (MAOA) may have an increased risk for alcohol dependence. However, this increased risk would most likely only occur when those “subjects are exposed to environmental stressors” (Wang et al., 2011, p.1295). Examples of environmental factors may include the individual’s personality, coping strategies, or family system. These researchers conclude by stating that it is unclear how the genetic influence may or may not interfere in alcohol dependence and to what degree.
Also interested in exploring the genetic influence in alcohol abuse, Clarke et al. (2010) analyzed twin studies while conducting their own study. These researchers argue that stress activates certain responses in the brain, such as the locus coeruleus (LC), a structure located in one of the ventricles and sensitive to the activation (by a gene) to produce cortisol during times of stress. Clarke et al.’s argument is based on the notion that this dynamic between the stress and the production of cortisol may drive an individual to alcohol abuse to decrease the activity in LC, supposedly bringing a sense of calm during stressful situations. In other words, the gene activating the LC may be responsible for mediating the effect of alcohol which has been detected in twin studies.
As expected, the genetic model has its critics because they argue it has not yet established a definite or persuasive relationship between genes and alcoholism (Dodes, 2002). In his 1986 article, Peele unveils his concern for the popularity of the genetic model to explain the etiology of alcohol abuse. Peele (1986) argues the data obtained to form the basis of the genetic model for alcoholism do not take into account important variables. These variables may include the unique differences among alcoholics as well as within ACoAs; how the alcohol abuse may unfold in many individuals and how any of these variables may be affected by a family environment that may or may not include a history of alcoholism (Peele, 1986).
Peele (1986) insists there is no evidence that ACoAs inherit a “genetic liability for alcoholism” (p. 63). Peele explains the phenomenon observed in twins from biological alcoholic parents only shows a correlation between having alcoholic parents and abusing alcohol. Additional information about family dynamics where twins grew up, such as divorce, financial instability, or chaos in the family was not included in the research with twins (Clarke et al., 2010; Wang et al., 2011). Peele (1986) emphasized that the genetic model has “dangerous consequences” because it appears to deny the human complexity involved in substance abuse, and because it may prevent counselors from digging deep into the core issues of addiction with their clients (p. 63). Peele is supported by other scholars who believe ACoAs are modeling substance abuse behavior rather than having a genetic composition for alcoholism (Braitman, 2009).
Moreover, Dodes (2002) concedes that although some genes may “influence the susceptibility to developing alcoholism” (p. 81), it is not realistic to believe that one single gene or even a group of genes would have the power to produce one single specific behavior such as alcohol addiction or dependence. Dodes explains that genes are a sequence of DNA (molecules), but DNA not only contains additional information that is non-genetic, but DNA also controls whether genes are activated or not. The non-genetic factors in the DNA may include variables such as individual experiences, coping strategies, family environment and emotions. Even if a genetic predisposition is in place, that predisposition is not likely to materialize without the significant influence of the environment (Dodes, 2002).
In agreement with Peele (1986), Ross and Hill (2001, 2004) and Ross and McDuff (2008) divert from the genetic model, and instead lean toward the psychological models which focus on the learned maladaptive patterns of behavior. Other approaches include neurobiological models which attribute alcohol abuse as the result of the person’s brain functions (Heitzeg et al., 2010). Once the memory circuit makes an association between a substance and pleasure, addicts quickly learn to repeat the process to obtain a relief from their negative feelings such as loss, depression, anxiety and anger (Heitzeg et al., 2010). Some models overlap with each other, but all of them attempt to explain the substance abuse phenomenon.
The evidence presented herewith may carry some important implications for how addiction counselors may want to approach their treatment plan with those suffering from alcohol addiction or dependence. This paper argues that many addiction programs have failed to meet the needs of those suffering from substance abuse because the problem may not be the substance per se, but the consequences of growing up with maladaptive coping strategies that might have served to survive in a chaotic environment, but are no longer efficient. This paper claims that those suffering from addiction are able to continue their addiction likely because they have enablers in their household who are either consciously or unconsciously supporting the addiction. Addiction counselors may wish to consider involving those in the family who may be deriving a secondary gain from the addict’s addictive behavior. Both the person with addictions and the person supporting the addictions may be getting a payoff—a possible distraction to a traumatic childhood experience based on a chaotic environment.
Bowlby, J. (1969). Attachment and loss: Vol.1, Attachment. New York, NY: Basic Books.
Braitman, A., Kelley, M., Ladage, J., Schroeder, V., Gumienny, L., Morrow, J., & Klostermann, K. (2009). Alcohol and drug use among college student adult children of alcoholics. Journal of Alcohol and Drug Education, 53(10),
Clarke, T., Dempster, E., Docherty, S., Desrivieres, S., Lourdsamy, A., Wodarz, N., Ridinger, M., Maier, W., Rietschel, M., & Schumann, G. (2010). Multiple polymorphisms in genes of the adrenergic stress system confer vulnerability to alcohol abuse. Addiction Biology, 17, 202–208.
Dodes, L. (2002). The heart of addiction. New York, NY: Harper-Collins.
Grüber, E., Celan, J., Golik- Grüber, V., Agius, M., & Murphy, S. (2007). The relationship between having smoking or drinking parents and the occurrence of smoking or drinking in their adolescent children. Alcoholism, 43(1),
Heitzeg, M., Nigg, J., Yau, W., Zucker, R., & Zubieta, J. (2010). Striatal dysfunction marks preexisting risk and medial prefrontal dysfunction is related to problem drinking in children of alcoholics. Biological Psychiatry, 68(3),
Hodgins, D., Maticka-Tyndale, E., El-Guebaly, N., & West, M. (1993). The CAST-6: Development of a short-form of the Children of Alcoholics Screening Test. Addictive Behaviors, 18, 337–345.
Jones, A., Perera-Diltz, D., Salyers, M., Laux, J., & Cochrane, W. (2007). Testing hypothesized differences between adult children of alcoholics (ACOAs) and non-ACOAs in a college student sample. Journal of College Counseling, 10, 19–26.
Kritsberg, W. (1985). The adult children of alcoholics syndrome. Pompano Beach, FL: Bantam Books.
Lease, S., & Yanico, B. (1995). Evidence of validity for the children of alcoholics screening test. Measurement and Evaluation in Counseling and Development, 27(4), 200–210.
National Association for Children of Alcoholics. (n.d.). Children of addicted parents: Important facts. Retrieved from http://www.nacoa.net/pdfs/addicted.pdf., pp. 1–4.
Neal, D., Corbin, W., & Fromme, K. (2006). Measurement of alcohol-related consequences among high school and college students: Application of item response models to the Rutgers alcohol problem index. Psychological Assessment, 18(4), 402–414.
Peele, S. (1986). The implications and limitations of genetic models of alcoholism and other addictions. Journal of Studies on Alcohol, 47(1), 63–73.
Ratey, J., & Johnson, C. (1997). Shadow syndromes. New York, NY: Pantheon Books.
Ross, L. T., & Hill, E. M. (2001). Drinking and parental unpredictability among adult children of alcoholics: A pilot study. Substance Use & Misuse, 36(5), 609–638.
Ross, L. T., & Hill, E. M. (2004). Comparing alcoholic and nonalcoholic parents on the family unpredictability scale. Psychological Reports, 94(3), 1385–1391.
Ross, L. T., & McDuff, J. (2008). The retrospective family unpredictability scale: Reliability and validity. Journal of Child and Family Studies, 17, 13–27.
Wang, K., Liu, X., Aragam, N., Jian, X., Mullersman, J., Liu, Y., & Pan, Y. (2011). Family-Based association analysis of alcohol dependence in the COGA sample and replication in the Australian twin-family study. Journal of Neural Transmission, 118(9), 1293–1299.
Warner, L., White, H., & Johnson, V. (2007). Alcohol initiation experiences and family history of alcoholism as predictors of problem-drinking trajectories. Journal of Studies on Alcohol and Drugs, 68(1), 56–65.
Woititz, J. (1984). Adult children of alcoholics. Alcoholism Treatment Quarterly, 1, 71–99.
Martha Nodar is a graduate counseling student at Mercer University in Atlanta, Georgia. Correspondence can be addressed to Martha Nodar, Mercer University, 3056 Anderson Place, Decatur, GA 30033, firstname.lastname@example.org.