by Vignesh Subramanian, October 18, 2021
Today, nearly every major medical organization in the United States defines drug addiction as a primary brain disease – a progressive, relapsing disorder driven not by choice, but rather by neural dysfunction. From patient advocacy organizations like the American Medical Association and the American Society of Addiction Medicine to top research organizations like the National Institutes of Health and the National Institute on Drug Abuse, this characterization of compulsive substance misuse is believed to effectively counter stigmatization of treatment while still accounting for biological and psychological realities. Yet if one is to evaluate other possible classifications and the present state of diagnostic protocols in fair measure, it could be reasonably asserted that a discussion is still to be had about the addict’s role in their own entrapment. The degree to which addiction may be considered a chronic illness is therefore contingent on not just the relativity of its prognosis, but also on what physicians believe to be appropriate recourse.
The scientific tenets of addiction agreed on by psychologists, neurobiologists, and practitioners alike are key to judging the applicability of the brain disease model. Unwarranted assumptions about either the appositeness of a standard of comparison or a propensity for self-domestication can derail precedents set and determinations previously made by the discipline in question. It is fair to accept the medical discipline’s rhetoric on the need for restrictiveness in exposition, defining “chronic illness” as controllable but hitherto incurable conditions often identifiable by long periods of latency and protracted clinical course .
Proponents and opponents of the brain disease model also concur on the neurochemistry behind addiction. It starts with unregulated surges of the neurotransmitter dopamine in response to drug consumption occurring in the basal ganglia, the area of the brain tasked with executive functions that, among other behavior, enable learning from the ‘reward’ of brief ecstasy . An affinity for a substance leading to increased use will cause neural circuits to adapt by restructuring receptors, by scaling back sensitivity to the drug’s effects – requiring more consumption to attain the same euphoric “high” – and by increasing tolerance of the substance as this subconscious demand is satisfied, completing the cycle . The patient eventually develops dependence (inability to function without the substance) and dysphoria (a state of unease in the drug’s absence), fomenting cravings that prioritize reducing pain over experiencing pleasure . The cycle is ultimately difficult to break, for reasons that demonstrate the true interplay of biology and behaviorism: parallel remodeling of the extended amygdala – tasked with controlling responses to stress – and the prefrontal cortex, which manages decision making, drives the user to form associations between increased consumption and decreased stress, causing inhibitory pathways to shut down as short-term reward is favored and sought after .
At no point in this slippery slope beyond the first ‘gateway’ use is the chemical compulsion of a drug resistible or reversible; indeed, the same reward circuits that drive addiction account for most human physiological needs, including reproductive activities . In that regard, addiction is not just subconscious, but natural, solely dangerous in excess; patients of more socially sanctioned chronic illnesses – diabetes, heart disease, skin cancer – are victims of similar bet-hedging, whether it be by consumption of processed carbohydrates and meats, lack of exercise, or even sun exposure. Opponents of the brain disease model argue that the problem is initial awareness of risk: addicts must understand that intoxication is a precursor of worse to come, and addiction has a spectrum of severity, making accurate diagnosis difficult if not impossible . With no physical measures of identifying mental health disorders (such as objective lab tests using biomarkers) yet deployed in medical practice, physicians must rely on neuropsychological assessments and dissociated imaging scans to compare a patient’s cognitive impairment with normal executive function and processing abilities. Such measures have found that neural changes associated with addiction matched those of “deep habits, Pavlovian learning, and prefrontal disengagement”, but did not match the “development-learning orientations” of various mental illnesses . In other words, addiction stimulates synaptic pruning and neuroplasticity (the ability of neurons in the brain to change connections and reorganize) just as a conventionally developed brain does, but in atypical patterns poorly reflecting normal maturation and psychological tendencies. This information only sharpens the question of whether addiction is truly an aberration of the mind’s development or simply a collection of varying and even rectifiable effects elicited by the drug itself; to put it metaphorically, would a stabbing through the heart be considered cardiovascular illness? The concept of placing addiction on par with the likes of Alzheimer’s and Parkinson’s disease – surrounded by questions of whether all manipulated neuroplasticity is pathogenic, whether addicts can be responsible for consciously committed actions, and what even constitutes a problem with the brain – is thus far from conclusive.
Acceptance – or lack thereof – of substance addiction as a brain disease has had and will continue to have wide-ranging implications for patient protections under law and avenues of treatment. Distinguishing between the public perceptions of users’ behavior and the intimate worldviews of addicts as shaped by their battles for recovery help sustain the idea that addiction medicine can be entirely recontextualized into being a centerpiece of public health. For example, even if addiction is not to be considered a disease of the brain, its contribution to the later development of chronic illnesses such as lung disease, stroke and HIV/AIDS makes addiction treatment itself a form of preventative medicine rather than rehabilitation alone . Conversely, if classification of addiction as a brain disease remains the status quo, it might justify dependence as a ‘side effect’ of self-medication started because of lack of access to care, much the way it is for some substances with addictive potential – like selective serotonin reuptake inhibitors (SSRIs) and opiates – that are used and abused as antidepressants and for pain management, respectively . As is clearly evident, proponents and opponents of the brain disease model ultimately do not disagree on the facts of addiction, but simply emphasize different contexts that, when taken to their conclusions, have different implications for diagnosis and stigmatization; both camps have proven willing, however, to oversee an explosion of medicalization that address those biological and psychological realities . Today, trained physicians can administer pharmaceutical agonists and antagonists in clinics and other outpatient settings; the importance of psychosocial therapy, monitoring and follow-up in addiction treatment has been amplified; and the establishment of drug courts and diversion and harm reduction programs attests to the idea that drug consumption is not inherently a moral failing and that natural reactions to its effects can be less painfully anticipated and controlled .
Addiction is a convoluted condition: it has an onset influenced by environmental conditions but no infection agent, has little known pathological prognosis but a tendency to run in families, and displays outward behavioral changes but is not anatomically degenerative. A disease model that assumes partial responsibility on the part of the addict but recognizes the extent to which addiction rewires the brain is perhaps the best road on which to pursue a patient freedom-centric means of battling dependency and decay.
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