Re-socializing the Vulnerable Brain: Building an Ethically Sustainable Brain Disease Model of Addiction

Abstract

According to the brain disease model of addiction (BDMA), substance addiction is a chronic, relapsing brain disease. The BDMA is currently influential in informing addiction policy and the development of new treatments, but remains highly controversial across the addiction research community. We draw on resources from philosophy of science and applied ethics to reexamine the methodological and ethical implications of the BDMA and offer a new forward-looking and constructive conceptualization of the BDMA as a heuristic reductionist research hypothesis. We argue that this not only allows a sharper delineation of the empirical shortcomings of the BDMA, but also helps skeptical social scientists appreciate and incorporate the empirical successes of the BDMA to a broader, social understanding of addictions. We apply this view to the ethical implications of the BDMA, especially to the key concept of vulnerability. The BDMA states that it is the brain that has been hijacked by the drug and the brain thus compels the individual to act in ways that are often disastrous for the individual. The proponents of the BDMA ascribe "vulnerability" to multiple levels of organization, such as genes, specific neural systems, the brain, and the person, thus resulting in confusion and highly problematic ethical, social and even legal implications. The BDMA locates the vulnerability firmly within the individual and treats it as a matter of susceptibility to changes in brain chemistry. This may well be a part of the phenomenon, but the kind of vulnerability relevant for understanding and treating addiction is, however, embedded in normativity, as it concerns the agency of individuals with addiction. Agency is not simplistically reducible to the competencies of the individual, but rather it is also constituted in the interactions with their environment.

Automaticity: schema modes in addiction

“…However, we have not discussed what happens at a brain level. It is important to note that a critique on automaticity theories or habit theories on addiction, is inherently also a critique on the brain disease model of addiction [BDMA; e.g., ( 75 )] that poses that drug use causes long-term changes in specific brain regions, resulting in pathological (and automatic) drug-seeking behavior. Whereas automaticity theories draw direct links between automatic, stimulus-driven behaviors and the brain [e.g., ( 34 , 35 )] we do not make assumptions about how the development of psychopathology in general and specifically substance abuse is related to changes in specific brain regions.…”

The labels and models used to describe problematic substance use impact discrete elements of stigma: A registered report.

“…Providing an explicit explanation for the etiology of problematic substance misuse may therefore directly influence stigmatizing perceptions, and this may particularly be the case when participants believe that this messaging is relayed by a trusted professional (e.g., health care practitioner or scientist; Wiens & Walker, 2015; see also Bogren, 2019). Despite the brain disease model of addiction being contested and vehemently debated (see Hall et al, 2015; Hart, 2017; Heather et al, 2018; Heilig et al, 2021; Heim, 2014; Kuorikoski & Uusitalo, 2018; Leshner, 1997; Volkow et al, 2016), it has gained prominence in public understanding (Vederhus et al, 2016), likely because it is commonly defined in such a way by national organizations (National Institute on Alcohol Abuse & Alcoholism, 2021; National Institute on Drug Abuse, 2021) and endorsed by health care professionals (Lawrence et al, 2013; see also Hickman, 2014; Russell et al, 2011). We therefore assess whether the explicit etiological label of “chronically relapsing brain disease” elicits public stigma relative to the “problem” label.…”

The labels and models used to describe problematic substance use impact discrete elements of stigma: A Registered Report

“…Providing an explicit explanation for the aetiology of problematic substance misuse may therefore directly influence stigmatising perceptions, and this may particularly be the case when participants believe that this messaging is relayed by a trusted professional (e.g., healthcare practitioner or scientist; Wiens & Walker, 2015; see also Bogren, 2019). Despite the brain disease model of addiction being contested and vehemently debated (see Hall et al, 2015;Hart, 2017;Heather et al, 2019;Heim et al, 2014;Heilig et al, 2021;Leshner, 1997;Kuorikoski & Uusitalo, 2018;Volkow et al, 2016), it has gained prominence in public understanding (Vederhus et al, 2016), likely because it is commonly defined in such a way by national organisations (NIAAA, 2021;NIDA, 2021) and endorsed by healthcare professionals (Lawrence et al, 2013; see also Hickman, 2014;Russell et al, 2011). We therefore assess whether the explicit aetiological label of 'chronically relapsing brain disease' elicits public stigma relative to the 'problem' label.…”