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Home » What Exactly Is the Biopsychosocial Model of Addiction? – Psychology Today

What Exactly Is the Biopsychosocial Model of Addiction? – Psychology Today

Overnight, a young woman’s personality shifts, plunging her into a months-long medical mystery.
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Posted July 10, 2021 | Reviewed by Vanessa Lancaster
In light of the toll addiction takes on individuals, their families, communities, and society at large, it is understandable that many people want to know the answer to the question: What causes addiction? Why does one person end up using substances compulsively despite highly negative consequences, while another person can use substances occasionally without a loss of control?
Addiction can occur regardless of a person’s character, virtue, or moral fiber. The prominent belief several decades ago was that addiction resulted from bad choices stemming from a morally weak person. However, that view has long been discredited by scientific research. It is now known that biology plays an essential role in the disorder. In fact, in 1956, the American Medical Association declared alcoholism a disease that should be addressed with medical and psychological approaches (Mann et al., 2000).
However, considering one’s biological makeup only has its drawbacks, and research efforts have found that addiction is not that simple. There is no “addiction gene” or genetic sequence that accounts for all the variance in the experience of addiction. Instead, it is now known that many factors contribute to the development of addiction. Grisel (2019) noted, “the bottom line is that there are likely as many pathways to becoming an addict as there are addicts.”
So how are we conceptualizing the cause of addiction? The multifaceted disorder needs a multifaceted conceptualization, and we find that in the biopsychosocial model of addiction (Marlatt & Baer, 1988). Rather than pinpoint the one thing that causes addiction, we now understand that a constellation of factors contributes to a person being more or less at risk for addiction.
Some aspects are universal (e.g., the activation of the reward system by drugs of abuse). Yet many other elements are idiosyncratic, such as the intensity of the experience of reward and the functioning of the individual’s mesolimbic dopaminergic pathway in the brain. The biopsychosocial model provides a means of considering the myriad of factors that can contribute to the risk of addiction. Let’s take a look at each dimension of the model.
Genetics and biology are a part of the picture—albeit not the entire picture. Although there is no “addiction gene” to definitively identify a person as being at risk for addiction, it is evident through twin studies, adoption studies, family studies, and more recently, epigenetic studies that addiction has a genetic component. Individuals who are genetically predisposed for addiction enter the world with a greater risk of becoming addicted at some point in their lives.
There are many hypotheses to explain this genetic predisposition, such as the Reward Deficiency Syndrome (Blum et al., 1996; Blum et al., 2014), which posits that some individuals are born with underactive reward circuitry (referred to as hypodopaminergic functioning) that subsequently primes them to be more susceptible to the rewarding effects of drugs of abuse (Febo et al., 2017).
Additionally, many neurotransmitters are involved in the experience of reward (dopamine, opioids, GABA, serotonin, endocannabinoids, and glutamate; Blum et al., 2020). Thus deficiencies in any combination of these neurochemicals may contribute to a predisposition to addiction. It is important to note that one person’s reaction to the reward experience may be quite different from another’s. This realization should help us cultivate empathy for those with addiction—it is very likely that others truly do not know how drugs make them feel.
Along with genetics, another contributing factor to the risk of addiction is one’s psychological composition. This factor is as broad as it sounds and includes personality traits (like sensation-seeking and impulsivity), mental health concerns (like anxiety and depression), psychological constructs (like self-esteem and self-worth), and the psychological impact of an individual’s life experiences (such as trauma). Some individuals may be more affected by the rewarding effects of drugs of abuse because they are trying their best to regulate painful emotions.
For example, researchers have found a robust association between trauma and addiction (Dube et al., 2002, 2003; Giordano et al., 2016). Indeed, in the original Adverse Childhood Experiences (ACEs) study, Felitti et al. (1998) found that more ACEs increased the odds of subsequent drug and alcohol use. One explanation for this trend is that the toxic stress from trauma leads to a dysregulated stress response. An individual’s stress hormones (cortisol and adrenaline) are chronically elevated (Burke Harris, 2018; van der Kolk, 2014).
These individuals may experience constant hyperarousal, hypervigilance, anxiety, and abuse drugs may be an effective way to regulate these emotional experiences (Felitti et al., 1998). Thus, numerous psychological factors and experiences can increase the risk of changing how one feels (or regulating emotions) via drugs of abuse.
The third factor in the biopsychosocial model is the social environment. Social norms, availability, accessibility, legality, modeling, expectancies, societal approval, visibility, targeting practices, and cultural beliefs all influence the experience of addiction. An individual exposed to drug use at an early age can be influenced by social modeling (or learning via observation). Additionally, certain environments have specific social norms related to drug use (e.g., “Everyone experiments a little with drugs in college”).
Furthermore, some communities are targeted more heavily with alcohol and tobacco advertisements and have more availability of drugs of abuse than others, particularly impoverished communities (Primack et al., 2007; Rose et al., 2019). Therefore, the social environment in which one exists contributes to their risk of addiction.
The factors that increase an individual’s risk for addiction are numerous, yet they all find their place in the biopsychosocial model of addiction (Marlatt & Baer, 1988). Taken together, this model provides a holistic conceptualization of addiction that acknowledges the complexity of the disorder and provides guidance toward a solution, which must necessarily be multifaceted and holistic as well. The more we know about the biopsychosocial model, the more we can foster accurate empathy for those with addiction and work toward effective treatment and prevention efforts.
Blum, K., Baron, D., McLaughlin, T., & Gold, M. S. (2020). Molecular neurological correlates of endorphinergic/dopaminergic mechanisms in reward circuitry linked to endorphinergic deficiency syndrome (EDS). Journal of Neurological Sciences, 411, Article 116733.
Blum, K., Cull, J. G., Braverman, E. R., & Comings, D. E. (1996). Reward deficiency syndrome. American Scientist, 84, 132-146
Blum, K., Oscar-Berman, M., Demetrovics, Z., Barh, D., & Gold, M. S. (2014). Genetic addiction risk score (GARS): Molecular neurogenetic evidence for predisposition to reward deficiency syndrome (RDS). Molecular Neurobiology, 50, 765-796.
Burke Harris, N. (2018). The deepest well: Healing the long-term effects of childhood adversity. Bluebird.
Dube, S. R., Anda, R. F., Felitti, V. J., Edwards, V. J., & Croft, J. B. (2002). Adverse childhood experiences and personal alcohol abuse as an adult. Addictive Behaviors, 27, 713-725.
Dube, S. R., Dong, M., Chapman, D. P., Giles, W. H., Anda, R. F., & Felitti, V. J. (2003). Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: The adverse childhood experiences study. Pediatrics, 111, 564-572.
Febo, M., Blum, K., Badgaiyan, R. D., Baron, D., Thanos, P. K., Colon-Perez, L. M., Demotrovics, Z., & Gold, M. S. (2017). Dopamine homeostasis: Brain functional connectivity in reward deficiency syndrome. Frontiers in Bioscience, 22, 669-691.
Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., Koss, M. P., & Marks, J. S. (1998). Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The adverse childhood experiences (ACE) study. American Journal of Preventive Medicine, 14, 245-258
Giordano, A. L., Prosek, E. A., Stamman, J., Callahan, M. M., Loseu, S., Bevly, C. M., Cross, K., Woehler, E. S., Calzada, R.-M. R., & Chadwell, K. (2016). Addressing trauma in substance abuse treatment. Journal of Alcohol and Drug Education, 60(2), 55–71.
Grisel, J. (2019). Never enough: The neuroscience and experience of addiction. Scribe.
Mann, K., Hermann, D., & Heinz, A. (2000). One hundred years of alcoholism: The twentieth century. Alcohol and Alcoholism, 35, 10-15.
Marlatt, G. A., & Baer, J. S. (1988). Addictive behaviors: Etiology and treatment. Annual Review of Psychology, 39, 223-252
Primack, B. A., Bost, J. E., Land, S. R., & Fine, M. J. (2007). Volume of tobacco advertising in African American markets: Systemic review and meta-analysis. Public Health Reports, 122, 607-615.
Rose, S. W., Mayo, A., Ganz, O., Perreras, L., D’Silva, J., & Cohn, A. (2019). Perceived racial/ethnic discrimination, marketing, and substance use among young adults. Journal of Ethnicity in Substance Abuse, 18, 558-577.
van der Kolk, B. A. (2014). The body keeps the score: Brain, mind, and body in the healing of trauma. Penguin Books.
Amanda Giordano, Ph.D., LPC, is an associate professor at the University of Georgia and the author of A Clinical Guide to Treating Behavioral Addictions.
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Overnight, a young woman’s personality shifts, plunging her into a months-long medical mystery.


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