Skip to content

Sick at Heart: Understanding the Disease Model of Addiction

Substance use disorder (SUD) is an inherently opportunistic condition. It seizes every chance to ravage and destroy, to poison relationships and self-worth even as it poisons the body.

For far too long, one of the most diabolical weapons in addiction’s destruction has been stigmatization (1). Those experiencing addiction have historically been blamed and shamed for their condition, contributing to the silencing, the denial, and the lack of access to care that has ultimately decimated far too many families and claimed far, far too many lives (2).

In recent years, however, researchers, clinicians, and addiction specialists have increasingly come to recognize the very real physiological basis of addiction. This has, in turn, given rise to the disease model of addiction, a model which has helped to reduce stigmatization, increase access to care, and enhance the efficacy of addiction treatment. But what is the disease model of addiction, exactly, and why does it matter?

Simply put, the disease model of addiction explains that dependency is the result of complex, often interrelated, neurobiological and neurochemical processes that may be triggered by environmental, social, or personal factors. The disease model can help to explain, for example, why some people can live their entire lives using substances recreationally without ever becoming dependent, while others can become addicted with just one exposure. The disease model, in other words, recognizes addiction as a fundamentally physiological process just like any other disease, such as diabetes or cardiovascular disease.

Supplanting the Social Constructivist Model

Fundamentally, the disease model of addiction offers a new, more empowering, and more accurate understanding both of chemical dependency and of the often self-destructive and anti-social behaviors dependency instigates.

This more accurate view supplants older (mis)perceptions of addiction that viewed it as a matter of choice and as an index of moral virtue and strength of character (3, 4, 5). This so-called social constructivist model of addiction, as might be predicted, is often heavily laden with false assumptions and negative judgments, which frequently impact the overall quality of care while exacerbating disease progression.

The person who is experiencing a chemical dependency may find themselves bereft of their essential social and emotional support network, as friends and loved ones withdraw, wrongly believing that the addicted person could quit “if only they wanted to” or if they simply “had enough willpower.” Even more concerningly, the same stigmatization which all too often erodes the patient’s personal relationships may easily be found in clinical relationships. Studies have shown addiction stigmatization persists, even among healthcare providers (6, 7).

In addition, the external stigmatization of the social constructivist model often contributes to, galvanizes, or amplifies internalized stigmatization. The person experiencing addiction often blames him/herself for their inability to abstain (3, 4, 5, 8, 9). They may attribute it to a personal failure, weakness of character, or a lack of “real” commitment to being sober. They may repudiate themselves as “bad,” “defective,” “broken,” or simply “hopeless.”

The destructive power of stigmatization lies in the profound harm it does both to relationships and the addicted person’s sense of self-worth and self-efficacy. But the ravages of stigmatization extend far beyond this, perpetuating an antiquated and biased perspective on addiction that is patently and demonstrably false.

It presumes that dependency is a choice, and, through that presumption, it rationalizes and legitimizes “punishment” for the affected person. And such punishments often come in diverse and destructive forms, ranging from lost relationships and inadequate medical care to social repudiation and condemnation, as well as guilt and self-blame.

Understanding Addiction as a Disease

Though the stigmatizing of addiction is, unfortunately, a persistent reality today, the disease model has begun to supplant social constructivist models and, is greatly helping to destigmatize people who face addiction. This process by no means is intended to absolve the addicted individual of responsibility for their choices and behaviors.

What it is intended to do, however, is to cultivate and disseminate a more nuanced, more accurate, and more neutral understanding of addiction, its origins, and its trajectory. This is, in other words, an understanding of and response to chemical dependency that is rooted in empirical science, not in subjective moral judgments (9, 10, 11). This, in turn, reconfigures dependency-related behaviors as the often predictable manifestations of a disease process.

The disease model of addiction, more specifically, holds that dependency is driven by physiological processes. Cravings and compulsions are the results of a combination of genetic, physiological, and biochemical processes, just as chronic conditions such as diabetes or heart disease are. And much like heart disease and diabetes, the condition may be triggered or worsened by environment, lifestyle, and personal choice, but that does not eradicate the underlying physical basis of the condition. Similar to other chronic diseases, it is one that is to be managed, if not cured.

The disease model of addiction not only eliminates the stigmatization, blaming, and shaming that have for too long been associated with dependency, but it also greatly enhances the efficacy of addiction recovery protocols. These protocols combine evidence-based approaches that address the physiological components of dependency with lifestyle changes to promote long-term sobriety

The Science Is In

The disease model did not emerge in a vacuum. Rather, it is the product of nearly half a century of addiction research, which includes the in-depth study of the neurobiological, neurochemical, and epigenetic origins of SUD (10, 11, 12).

For example, researchers have found functional and structural differences in the brains of those experiencing addiction. The brain’s reward centers, and particularly its ability to release and absorb dopamine, have been found to be significantly compromised in many who have experienced addiction (11). Similarly, advanced neuro-imaging studies have been used to identify the unique chemical and morphological characteristics of the brains of those who experience addiction in contradistinction to those who never progress from casual, recreational substance use into full-blown substance abuse (10).

Likewise, a vast and growing body of literature has explored the genetic basis of addiction, including the dynamic and complex interplay between genetics and environment (12). These studies have gone far in explaining the heritability of addiction, including the role of substance exposure in altering gene expression and, as a result, both perpetuating addictive tendencies long after the substance has been withdrawn as well as introducing a genetic predisposition to addiction into the family line (12).

This speaks to the physiological, rather than wholly social, environmental, and individual basis of addiction, helping to explain why biological relatives who may have vastly different personality types and who may live in radically distinct social environments may both still experience, or be predisposed to, SUD.

Talk to the Animals

The neurobiological, neurochemical, and epigenetic studies of addiction in humans are far from the only evidence supporting the disease model. Indeed, the origins of the disease model lie in animal studies, which have demonstrated that addictive behaviors in both animals and humans share similar genetic, functional, and physiological attributes (13, 14, 15). This includes similarities in anatomical structures in the brains of humans and laboratory rodents (13).

Similarly, in a study of the therapeutic potential of oxytocin to reduce drug-seeking in “addicted” rodents, Leong et al. (2018) found that the effects of neurochemical mechanisms of dependency in the brain’s reward centers were similar in humans and non-human animals (14).

In another study using animal models to explore the neurobiological basis of food addiction and binge eating disorders, Novelle and Diéguez (2018) found that the same neural pathways evinced in compulsive/addictive behaviors in animals are also activated in humans experiencing addiction.

What these animal studies show, ultimately, is that addiction is a physiological process that may be aggravated or mitigated, but not wholly determined by, social, environmental, and personal factors.

How Bayshore Can Help

At Bayshore, our multidisciplinary team of recovery experts understands the multifaceted nature of addiction, including its physiological attributes. We specialize in providing individualized and whole-person care, including the use of evidence-based therapies to treat addiction and any co-occurring disorders, or mental illnesses. We are certified to offer pharmaceutical therapies as needed, in conjunction with mental health and lifestyle support. Our mission is to equip our clients with an innovative, integrated, and individualized approach to recovery to help them build the happy, healthy future they deserve. Contact us today to discuss how Bayshore can help you or someone you love!

At Bayshore Retreat we have extensive knowledge in treating substance abuse and co-occurring mental health issues. We understand that Mental Health Disorders can be the root cause of substance abuse. We use the latest scientific research and holistic approach for drug and alcohol addiction treatment.

  1. Lanzillotta-Rangeley, J., Zeller, T. A., Beachler, T., Litwin, A. H., Clark, A., & Stem, J. (2021). The Impact of the Disease Model of Substance Use Disorder on Evidence Based Practice Adoption and Stigmatizing Attitudes: A Comparative Analysis. Pain management nursing : official journal of the American Society of Pain Management Nurses, 22(5), 616–622. https://doi.org/10.1016/j.pmn.2021.03.004
  2. Wilson H. (2020). How stigmatizing language affects people in Australia who use tobacco, alcohol and other drugs. Australian journal of general practice, 49(3), 155–158. https://doi.org/10.31128/AJGP-07-19-4998
  3. Matthews, S., Dwyer, R., & Snoek, A. (2017). Stigma and Self-Stigma in Addiction. Journal of bioethical inquiry, 14(2), 275–286. https://doi.org/10.1007/s11673-017-9784-y
  4. Goodyear, K., Haass-Koffler, C. L., & Chavanne, D. (2018). Opioid use and stigma: The role of gender, language and precipitating events. Drug and alcohol dependence, 185, 339–346. https://doi.org/10.1016/j.drugalcdep.2017.12.037
  5. Kaggwa M. M. (2021). Simplifying Addiction. Substance abuse and rehabilitation, 12, 23–26. https://doi.org/10.2147/SAR.S307387
  6. Brondani, M. A., Alan, R., & Donnelly, L. (2017). Stigma of addiction and mental illness in healthcare: The case of patients’ experiences in dental settings. PloS one, 12(5), e0177388. https://doi.org/10.1371/journal.pone.0177388
  7. Biancarelli, D. L., Biello, K. B., Childs, E., Drainoni, M., Salhaney, P., Edeza, A., Mimiaga, M. J., Saitz, R., & Bazzi, A. R. (2019). Strategies used by people who inject drugs to avoid stigma in healthcare settings. Drug and alcohol dependence, 198, 80–86. https://doi.org/10.1016/j.drugalcdep.2019.01.037
  8. Moore, K. E., Stein, M. D., Kurth, M. E., Stevens, L., Hailemariam, M., Schonbrun, Y. C., & Johnson, J. E. (2020). Risk Factors for Self-stigma among Incarcerated Women with Alcohol Use Disorder. Stigma and health, 5(2), 158–167. https://doi.org/10.1037/sah0000182
  9. Bozinoff, N., Anderson, B. J., Bailey, G. L., & Stein, M. D. (2018). Correlates of Stigma Severity Among Persons Seeking Opioid Detoxification. Journal of addiction medicine, 12(1), 19–23. https://doi.org/10.1097/ADM.0000000000000355
  10. Uhl, G. R., Koob, G. F., & Cable, J. (2019). The neurobiology of addiction. Annals of the New York Academy of Sciences, 1451(1), 5–28. https://doi.org/10.1111/nyas.13989
  11. Solinas, M., Belujon, P., Fernagut, P. O., Jaber, M., & Thiriet, N. (2019). Dopamine and addiction: what have we learned from 40 years of research. Journal of neural transmission (Vienna, Austria : 1996), 126(4), 481–516. https://doi.org/10.1007/s00702-018-1957-2
  12. Stewart, A. F., Fulton, S. L., & Maze, I. (2021). Epigenetics of Drug Addiction. Cold Spring Harbor perspectives in medicine, 11(7), a040253. https://doi.org/10.1101/cshperspect.a040253
  13. Spanagel R. (2017). Animal models of addiction. Dialogues in clinical neuroscience, 19(3), 247–258. https://doi.org/10.31887/DCNS.2017.19.3/rspanagel
  14. Leong, K. C., Cox, S., King, C., Becker, H., & Reichel, C. M. (2018). Oxytocin and Rodent Models of Addiction. International review of neurobiology, 140, 201–247. https://doi.org/10.1016/bs.irn.2018.07.007
  15. Novelle, M. G., & Diéguez, C. (2018). Food Addiction and Binge Eating: Lessons Learned from Animal Models. Nutrients, 10(1), 71. https://doi.org/10.3390/nu10010071,

 

Call Now Button