Abstract
Recent advances in brain imaging methods as well as increased sophistication in neuroscientific modeling of the brain’s reward systems have facilitated the study of neural mechanisms associated with addiction such as processes associated with motivation, decision-making, pleasure seeking, and inhibitory control. These scientific activities have increased optimism that the neurological underpinnings of addiction will be delineated, and that pharmaceuticals that target and change these mechanisms will by themselves facilitate early intervention and even full recovery. In this paper, we argue that it is misguided to construe addiction as just or primarily a brain chemistry problem, which can be adequately treated by pharmaceutical interventions alone.
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Notes
- 1.
A sound theory of pharmaceuticals for addiction’s substrates must resist falling prey to what may be called the pharmaceutical temptation of the one over the many, which is a variety of monocausal thinking. The neural-causal etiology of addiction is not some one single personal subsystem; for example, it is not a dictatorship of the neural reward system. The best hope for an addict may sometimes be to combine psychotherapies with complements of drugs. But treatment, drugs used or not used, is enfeebled without appreciating that addicts are persons and addiction is a way of being in the world.
- 2.
It is worth noting the distinction between multiplex self and multitudinous self. The multiplex self, a concept introduced by Flanagan, explains what the personal identity of those with typical cognition consists in. It refers to persons playing multiple roles simultaneously; i.e., the self is multiplex because the person represents and exhibits different parts of themselves to different audiences in different environments. For instance, “my philosopher self, my baseball-coach self, my religious self, my parental self—are played for different audiences. Different audiences see who we are differently” (Flanagan 1996: 71). Suggesting that the self is multiplex means that identity exists despite chronic transformations and synchronic conflicts between these different facets of a person, since there is a narrative connectedness between them. This narrative connectedness is due to the authorial work of the agent, who tells the story of her life and thus holds different strains together. If this unifying authorship falls apart, we end up with atypical cognition: we no longer deal with a multiplex self, but rather with multiple selves. The concept of multitudinous self, introduced by Tekin, on the other hand, considers the self to be complex matrix, individuated and constituted by five dimensions: ecological, interpersonal, temporal, private, and conceptual (following the Neisserian selves). Unlike the multiplex self, multitudinous self considers psychopathology or atypical cognition to be a possible feature of the self. Multiplex self, in so far as it is a conceptual representation of the self to the self, and others, can be situated within the conceptual dimension of the multitudinous self. The model of multitudinous self aims to (i) get at the complexity of “real people,” (ii) provide opportunities for scientists to use abstractions and idealizations and study it scientifically, and (iii) encourage a wholesome approach to psychopathology without sidestepping the complexity of persons. The inspiration for the name of this model is the poem “Song of Myself” by Walt Whitman, in which he proclaims, “Do I contradict myself? Very well, then, I contradict myself; (I am large—I contain multitudes).” Special thanks to Flanagan, who steered Tekin in the direction of these lines, hence the word “multitudinous.”
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Tekin, Ş., Flanagan, O., Graham, G. (2017). Against the Drug Cure Model: Addiction, Identity, and Pharmaceuticals. In: Ho, D. (eds) Philosophical Issues in Pharmaceutics. Philosophy and Medicine, vol 122. Springer, Dordrecht. https://doi.org/10.1007/978-94-024-0979-6_13
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