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Introduction
Addictions represent a complex phenomenon characterized by the presence of behavioral, physiological, and psychological changes, the diversity of which makes the establishment of the core cause of addiction disorders and their etiology a challenging task. As opposed to more recent multi-causal approaches to comprehending addictions, single-cause models offer partially relevant explanations of processes involved in dependencies. By discussing and illustrating four approaches to addictions, including the personality theory, the neurobiological, the family disease, and the genetic models of addiction, this essay demonstrates non-multi-cause models’ ability to reveal particular contributors to addictions.
The Personality Theory Model (Psychological Models)
Overview
This model suggests that certain personality traits predispose a person to develop harmful addictions. Particularly, the so-called “alcoholic personality” is described as a combination of immaturity, the inability to be alone, excessive impulsivity, a low frustration threshold, and other traits (Capuzzi et al., 2020, p. 9). The high amount of negative affect is hypothesized to contribute to the search for ways to distract from negative emotions, including psychoactive substances (Capuzzi et al., 2020; Dash et al., 2019). The model implies that certain traits act as additional predisposing factors rather than the direct causes of addiction.
Example
One example of this model is the alcoholic personality theory; this approach relates features that imply dependency and persistent negative emotionality to the risks of alcoholism. Having no access to non-destructive ways of battling emotions and overcoming one’s impulsivity, such as seeking professional psychological help, an individual with this personality type may engage in alcohol use and gradually become addicted when trying to stay in an elevated mood. In this case, personality traits and no access to relevant services encourage an individual to develop a destructive way of coping with negativity.
Explanatory Power
The personality model is viable as there are strong correlations between Big Five personality traits and addictions, and the trend remains strong even in siblings raised in the same conditions. Having studied 3.700 siblings and twins, Dash et al. (2019) demonstrated a strong link between the combination of low agreeableness and conscientiousness with high neuroticism and a high prevalence of addictive disorders, including alcoholism and gambling. The use of blood relatives minimizes the impact of environmental differences, providing support for the model.
The Neurobiological Model (Biological Models)
Overview
This model posits that addictions stem from processes affecting neurotransmitters. Starting to use addictive drugs regularly results in changes to the chemistry of the brain that take place as a multi-stage process, the reversibility of which is still open for discussion (Capuzzi et al., 2020; Zehra et al., 2018). Since this approach is extremely complex, different hypotheses have been proposed depending on the type of addictive substance.
Example
One example of this model is the three-stage neurobiological framework of addiction proposed by Volkow and Koob. According to it, repeated exposure to addictive substances promotes motivational neural circuits’ dysregulation in three stages, including “binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation” (Zehra et al., 2018, p. 439). Each stage is associated with behavioral changes, ranging from short-term memory issues to withdrawal syndrome, peculiar neurophysiological adaptations, and neuroimaging findings.
Explanatory Power
The model offers a strong explanation since the neurophysiological and behavioral changes that it predicts are observable. For instance, Zehra et al. (2018) list a variety of imaging findings peculiar to each stage of addiction, making the process observable rather than hypothetical. Also, the existing pharmacological treatments for cannabis addiction are believed to target the three stages of addiction specified in the Volkow and Koob model (Zehra et al., 2018). The model’s intersections with the realities of addiction and treatment lend credibility to this approach.
The Family Disease Model (Family Models)
Overview
The family disease model seeks to place an individual’s addiction into a family-related context. According to it, one person’s addiction implies the presence of “a disorder or disease” affecting the entire family, requiring engaging all family members in therapy sessions to help the addicted member effectively (Capuzzi et al., 2020, p. 9). Therefore, this perspective prioritizes the assumption that addiction heavily influences the entire family, requiring the need for family recovery.
Example
An example of this model is a situation in which an addicted individual exhibits certain behaviors that influence the entire family’s mental well-being. For instance, an alcoholic father can become violent and abusive, creating severe psychological distress for his spouse and children. Such stressful experiences’ effects can be long-lasting, causing mental health issues or even the risk of following in the addicted person’s footsteps, making therapy for the entire family an optimal choice.
Explanatory Power
The model explains addiction successfully since relatives’ emotional distress and “contagious” addictions are common phenomena. According to Markova and Yariy (2018), the wives of men addicted to alcohol develop behavioral and combined maladjustment, which creates the desire for addictive behaviors involving caffeine-containing beverages and nicotine, in over 70% of cases, thus proving the need for counseling and rehabilitation measures aimed at family members. Therefore, in line with the model, one person’s addiction is unlikely to leave the family unaffected.
The Genetic Model (Biological Models)
Overview
The model explains vulnerability to substance use disorders with reference to a genetic predisposition for developing addictions later in life. Based on the evidence of alcoholism running in families and adopted children’s similarity to their biological parents in terms of alcohol use patterns, this model’s proponents suggest that inherited metabolic defects might cause alcoholism as they interact with environmental factors (Capuzzi et al., 2020; Edenberg et al., 2019). Therefore, the genetic model posits that some individuals are genetically predisposed to alcoholism and are more likely to develop it compared to other people when experiencing the same challenges and environmental contributors to alcohol use disorders.
Example
One example is a child of parents with a severe addiction disorder taken from this dysfunctional family and adopted by a non-alcoholic couple at a very young age. Suppose that the adoptive parents have biological offspring and avoid revealing the truth about adoption to anyone, including the child. Their children grow up and experience their first encounter with alcohol under peer pressure, but only the adopted child fails to control his/her alcohol consumption and gradually develops an addiction.
Explanatory Power
The model offers a valid explanation since there is generalizable evidence to demonstrate correlations between genetic variants and the risks of problematic alcohol intake. Specifically, as per a genome-wide association study in over 50.000 individuals, different variants of the ADH1B gene are associated with protective effects against alcoholism or an increased propensity to drinking (Edenberg et al., 2019). Relevant variations have also been found in the ALDH2 gene (Edenberg et al., 2019). Although the model remains imperfect due to a multitude of genes that could be potentially involved in addictions, these clear links add to its credibility.
Conclusion
In summary, the four models’ explanatory value can be supported with reference to different sources, including correlational studies, neuroimaging research, and statistics pertaining to addictions’ influences on patients’ families. However, it is crucial to note that the theories offer some hypothetically relevant factors that should be implemented with attention to the patient’s personal history and individual challenges. The motivations for engaging in risky behaviors require substantial analysis in each clinical case to offer meaningful plans of action.
References
Capuzzi, D., Stauffer, M. D., & Sharpe, C. (2020). History and etiological models of addiction. In D. Capuzzi & M. D. Stauffer (Eds.), Foundations of addictions counseling (4th ed., pp. 1-23). Pearson.
Dash, G. F., Slutske, W. S., Martin, N. G., Statham, D. J., Agrawal, A., & Lynskey, M. T. (2019). Big Five personality traits and alcohol, nicotine, cannabis, and gambling disorder comorbidity. Psychology of Addictive Behaviors, 33(4), 420-429. Web.
Edenberg, H. J., Gelernter, J., & Agrawal, A. (2019). Genetics of alcoholism. Current Psychiatry Reports, 21(4), 1-7. Web.
Markova, M., & Yariy, V. (2018). Codependence in wives of husbands with alcohol dependence. Fundamental and Applied Researches in Practice of Leading Scientific Schools, 30(6), 14-22. Web.
Zehra, A., Burns, J., Liu, C. K., Manza, P., Wiers, C. E., Volkow, N. D., & Wang, G. J. (2018). Cannabis addiction and the brain: A review. Journal of Neuroimmune Pharmacology, 13(4), 438-452. Web.
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