Decade of the Brain
Unlike the conceptualization of addiction as a malady of spirit promoted within 12-Step organizations, the brain disease model of addiction (BDMA) formed around the premise that neurobiological changes occur from drug-taking and, as a result, residence of this chronic disease and object of its study is the brain. This framing has been subtly refined, but emphasis on chronicity and the brain’s eminence remains undimmed (Heilig et al., 2016, 2021). The centrality of the brain cannot be overstated. However, the simplicity of the BDMA framing and the brain’s actual complexity makes the addiction-disease reduction satisfyingly useless. It is epistemically weak since conceptualizing addiction as disease does not help elucidate underlying mechanisms. Those exist objectively. It is clinically fraught in that the BDMA is not usable “off-the-shelf”: it’s framework cannot help addicted patients understand what occurred in their brains and how to learn new behaviors.
At the right level of analysis all maladaptive brain-mediated behaviors shaped by genes+environment could be labeled “disease.” There is argument in favor of this nosological hellscape, should we want it (Strickland & Smith, 2021). Conversely, we might (over)correct and refer to addiction as a primarily social disease. Aiming to fall in the explanatory middle, we might devote more to understanding the conditions in which people make drug-related decisions, including “decision” in our addiction definition. We can quibble about whether decisions reflect disease, but we cannot quibble about whether decisions occur within influential contexts when a person uses or stops using, or whether behavior is constrained and reinforced by endogenous and exogenous conditions (Acuff et al., 2022; Bickel et al., 2011, 2014).
Getting back to first principles
Possibly what is most neglected when studying and treating addiction are the desires and intentions preceding decisions and behaviors. The BDMA makes vague mention of the decoupling of desires and intentions from decisions and behaviors. This decoupling or discordance are how I described my heroin addiction in Journal of Substance Abuse Treatment. There, I questioned the value and stigmatizing power of the disease label and emphasized that the desires of drug-using people matter. They matter for making sense of behaviors, for planning treatment, and for measuring treatment “success.” A person wanting to use cocaine and using it should not be regarded similarly to a person not wanting to use cocaine and using it is. Yet, we seldom ask drug-using people what they want or take this into account when attempting to understand their behaviors. Perhaps a person would like to use less cocaine or use only after testing for fentanyl. Continued cocaine use despite a desire to stop is a problem in part because they believe it is. I am not arguing that cocaine addiction is healthy. There should be goals around decreasing harmful use; but we need not label addiction “disease” full stop to have these (Lie et al., 2022; Pickard, 2021).
The congruence between what a person wants, intends, decides, and does is a reflection of psychological health and greater volition. As a society, we can decide if an outcome’s moral valance or public health burden is one we want to embrace or stigmatize. Conversely, the breakdown of volition, wherein one chooses and does what they wish not to, reflects psychological dysfunction, defined in part by the person. As a society, we have a duty to aid people in such states and improve the contexts which foster them (Hammersley, 2022).
What is lost when we publicly promote oversimplified frameworks of addiction?
If decision precedes use, which my experience suggests it does, then insofar as addiction is pathology, perhaps the pathology is the degradation of one’s ability to harmonize competing distal and proximal desires and then choose and act as they wish? This degradation can be applied to many things besides drugs. Although BDMA suggests loss of “free will” as a hallmark of addiction, the decision-making component of addiction, the role of available choices, and the contexts in which decision-making occurs, are not highlighted in BDMA definitions promoted to lay people and patients.
Worth underscoring to these groups is that desires, intentions, decisions, and behaviors are dynamic and shaped by context. Cognitive capacities (and choices) shift during and after addiction. This should be said explicitly to addicted people and to the society that levels judgment about them. Without adequate explanation of the dynamic and complex nature of brains, patients may feel “stuck” or “damaged” and may be stigmatized.
One example of the impact of a disease framework came from a client who said he was told to conceptualize his addiction thusly: (Paraphrasing) “Before you start using, you’re a cucumber, but after you use awhile and you cross this line to where you’re an addict, well, then you’re a pickle. Once you’re a pickle, you can’t ever be a cucumber again.” The problem is that people are not cucumbers, nor are they pickles; they are complex human beings. Helping patients unlearn oversimplifications that indicate addiction is their fate signifies the low point we have unintentionally reached. Helping patients understand that they have a higher probability of using, compared to someone without SUD, is a practice clinicians should refine. Patients want to hear change is possible.
Varieties of drug-using experiences
After years of intravenous heroin addiction, I am in sustained remission. I drink alcohol socially and have infrequently used drugs since I was addicted. Accordingly, I have a greater likelihood of injecting heroin today compared to someone without my past. The probability of my doing this is low, partially because of my environment and the non-drug choices I have. I am fortunate that my desire to use heroin is mostly absent. I could go buy heroin today, but I don’t want to. If heroin fell onto my desk, however, I am unsure what I would do.
That I would even deliberate using heroin is what some might characterize as a symptom of my brain disease.
That I would even deliberate using heroin is what I posit is an indicator that my brain is not particularly diseased.
If I choose to use heroin, after having not used in years, I am unsure if that decision would reflect disease. If so, what framework explains my initial desire, intention, and decision to try heroin? We know traits and states presumed to increase the probability of use initiation, but we don’t (yet) call those diseases. If the outcome (injecting heroin) is the same, but one occurs when I am a cucumber and the other when I am a pickle, then perhaps I was never not diseased. Perhaps I was always a pickle. Or, perhaps, the drug-related decisions people make are more complicated and heterogenous than the BDMA suggests. People are not pickles.
Do no harm
Today, I do not know nor care if my brain is “diseased.” However, there are many contemplating change or in early recovery being told they are pickles, that there is treatment but no remedy for what they suffer from. This handicaps their ability to view themselves as capable of change. It also hinders other’s ability to see them as capable of change. The consequences of perceived permanence are not abstractions: Children are never returned to parents; people are not hired; trust remains broken between partners.
The assumption “once an addict, always an addict” is one that the BDMA reinforces, meaning that even if it was not epistemically unnecessary for doing science, we might pragmatically refrain from espousing its bedrock notions: we need addicted people to believe that addiction is not a treatable chronic disease, but rather an addressable condition that leaves them changed but poised for further change.
Original article: Smith, K. E. (2022). Disease and decision. Journal of Substance Abuse Treatment, 108874. https://doi.org/10.1016/j.jsat.2022.108874
Acuff, S. F., Tucker, J. A., Vuchinich, R. E., & Murphy, J. G. (2022). Addiction is not (only) in the Brain: Molar behavioral economic models of etiology and cessation of harmful substance use. In Evaluating the brain disease model of addiction (pp. 459-474). Routledge.
Bickel, W. K., Jarmolowicz, D. P., Mueller, E. T., & Gatchalian, K. M. (2011). The behavioral economics and neuroeconomics of reinforcer pathologies: implications for etiology and treatment of addiction. Current Psychiatry Reports, 13(5), 406-415.
Bickel, W. K., Johnson, M. W., Koffarnus, M. N., MacKillop, J., & Murphy, J. G. (2014). The behavioral economics of substance use disorders: reinforcement pathologies and their repair. Annual Review of Clinical Psychology, 10, 641.
Hammersley, R. (2022). Addiction is a Human Problem, but Brain Disease Models Divert Attention and Resources away from Human-Level Solutions. In Evaluating the Brain Disease Model of Addiction (pp. 176-186). Routledge.
Heilig, M., Epstein, D. H., Nader, M. A., & Shaham, Y. (2016). Time to connect: bringing social context into addiction neuroscience. Nature Reviews Neuroscience, 17(9), 592-599.
Heilig, M., MacKillop, J., Martinez, D., Rehm, J., Leggio, L., & Vanderschuren, L. J. (2021). Addiction as a brain disease revised: why it still matters, and the need for consilience. Neuropsychopharmacology, 46(10), 1715-1723.
Lie, A. K., Hansen, H., Herzberg, D., Mold, A., Jauffret-Roustide, M., Dussauge, I., ... & Campbell, N. (2022). The Harms of Constructing Addiction as a Chronic, Relapsing Brain Disease. American Journal of Public Health, 112(S2), S104-S108.
Pickard, H. (2021). Is addiction a brain disease? A plea for agnosticism and heterogeneity. Psychopharmacology, 1-15.
Strickland, J. C., & Smith, K. E. (2021). Comment on Heilig et al.: The centrality of the brain and the fuzzy line of addiction. Neuropsychopharmacology, 46(10), 1703-1704.