We had a visit from the Honorable Jason Luan, Associate Minister of Health, Mental Health and Addiction on Tuesday, September 17, 2019. It was our pleasure to host him, his Chief of Staff Marshall K. Smith and Ministerial Assistant Eric Engler. They spent a couple hours on site, touring our facility, listening the problems we face and about the work we do, but most importantly taking the time to talk with Our House clients. It was a wonderful visit and all three of these men were kind and truly engaged in the work we do.
“Normative thinking about addiction has traditionally been divided between, on the one hand, a medical model which sees addiction as a disease characterized by compulsive and relapsing drug use over which the addict has little or no control and, on the other, a moral model which sees addiction as a choice characterized by voluntary behaviour under the control of the addict. Proponents of the former appeal to evidence showing that regular consumption of drugs causes persistent changes in the brain structures and functions known to be involved in the motivation of [behaviour]. On this evidence, it is often concluded that becoming addicted involves a transition from voluntary, chosen drug use to non-voluntary compulsive drug use. Against this view, proponents of the moral model provide ample evidence that addictive drug use involves [voluntarily] chosen behaviour. In this paper, we argue that although they are right about something, both views are mistaken. We present a third model that neither rules out the view of addictive drug use as compulsive…nor that it involves [voluntarily] chosen [behaviour].”
“Drug use and drug addiction are severely [stigmatized] around the world. Marc Lewis does not frame his learning model of addiction as a choice model out of concern that to do so further encourages stigma and blame. Yet the evidence in support of a choice model is increasingly strong as well as consonant with core elements of his learning model. I offer a responsibility without blame framework that derives from reflection on forms of clinical practice that support change and recovery in patients who cause harm to themselves and others. This framework can be used to interrogate our own attitudes and responses…so that we can better see how to acknowledge the truth about choice and agency in addiction…while avoiding stigma and blame, and instead [maintain] care and compassion alongside a commitment to working for social justice and good. “
“I show that Pickard’s argument against the irresistibility of addiction fails because her proposed dilemma, according to which either drug-seeking does not count as action or addiction is resistible, is flawed; and that is the case whether or not one endorses Pickard’s controversial definition of action. Briefly, we can easily imagine cases in which drug-seeking meets Pickard’s conditions for agency without thereby implying that the addiction was not irresistible, as when the drug addict may take more than one route to go meet her dealer.”
“The psychiatric category of addiction has recently been broadened to include new [behaviours]. This has prompted critical discussion about the value of a concept that covers so many different substances and activities. Many of the debates surrounding the notion of addiction stem from different views concerning what kind of a thing addiction fundamentally is. In this essay, we put forward an account that conceptualizes different addictions as sharing a cluster of relevant properties (the syndrome) that is supported by a matrix of causal mechanisms. According to this “addiction-as-a-kind” hypothesis, several different kinds of substance and [behavioural] addictions can be thought of as instantiations of the same thing – addiction. We show how a clearly articulated account of addiction can facilitate empirical research and the theoretical integration of different perspectives on addiction. The causal matrix approach provides a promising alternative to existing accounts of the nature of psychiatric disorders, the traditional disease model, and its competitors. It is a positive addition to discussions about diagnostic criteria…and sheds light on how psychiatric classification may be integrated with research done in other scientific fields. We argue that it also provides a plausible approach to understanding comorbidity. “
“If one believes that the brain is, in some as yet unspecified way, the organ of mind and behaviour, then all human behaviour has a neurobiological basis. Neuroscience research over the past several decades has provided more specific reasons for believing that many addictive phenomena have a neurobiological basis. The major psychoactive drugs of dependence have been shown to act on neurotransmitter systems in the brain (Nutt 1997; Koob 2000); common neurochemical mechanisms underlie many of the rewarding effects of these drugs and the phenomena of tolerance and withdrawal symptoms (Hyman & Malenka 2001; Koob 2000), and there is evidence for a genetic vulnerability to addiction (Nestler 2001; Uhl 1999) that is mediated by genes that regulate the metabolism of psychoactive drugs and the brain neurotransmitter systems on which they act (Uhl 1999). “
“Biomedical science has been remarkably successful in explaining illness by categorizing diseases and then by identifying localizable lesions such as a virus and neoplasm in the body that cause those diseases. Not surprisingly, researchers have aspired to apply this powerful paradigm to addiction. So, for example, in a review of the neuroscience of addiction literature, Hyman and Malenka (2001, p. 695) acknowledge a general consensus among addiction researchers that ‘[a]ddiction can appropriately be considered as a chronic medical illness.’ Like other diseases, ‘Once addiction has taken hold, it tends to follow a chronic course.’ (Koob and La Moal 2006, p. ?). Working from this perspective, much effort has gone into characterizing the symptomology of addiction and the brain changes that underlie them. Evidence for [the] involvement of dopamine transmission changes in the ventral tegmental area (VTA) and nucleus accumbens (NAc) have received the greatest attention. Kauer and Malenka (2007, p. 844) put it well: ‘drugs of abuse can co-opt synaptic plasticity mechanisms in brain circuits involved in reinforcement and reward processing’. Our goal in this chapter to provide an explicit description of the assumptions of medical models, the different forms they may take, and the challenges they face in providing explanations with solid evidence of addiction.”