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Diagnosing the BDMA Arguments from Philosophy of Science & ethics
Jaakko Kuorikoski (University of Tampere, New Social research) Susanne Uusitalo (University of Helsinki)
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We declare no conflicts of interest
We declare no conflicts of interest. Jaakko Kuorikoski & Susanne Uusitalo
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BDMA Addiction is a pathology of an organ (i.e., the brain)
Explanatory factor within the individual, yet outside her agency Emphasizes the pathological changes in the brain Changes in D2 receptors, connectivity, grey matter loss… The promise of pharmacological treatments Behavior compulsive/habitual vs. choice The habit model (stimulus-response) Pleasure account Learning accounts Incentive salience account Hall et al. 2017: “According to NIDA, addiction is: “a chronic relapsing brain disease” characterised by compulsive drug seeking and use, despite harmful consequences. The key evidence presented for this assertion is that chronic drug use produces changes in dopamine (DA) activity and transmission over time, affecting motivation, goal-directed behaviour, attention and memory. It is also claimed that DA rewires the brain in the striatum, amygdala, hippocampus and prefrontal cortex (PFC), “hijacking” the brain.” Hall et al. “According to the BDMA, these structural cortical changes comprise the anatomical basis for the brain disease model, especially the reduced connections between the prefrontal cortex and striatum that are reflected in a loss of grey matter in persons with long term addiction. The BDMA implies that these changes are either irreversible or, at least, very hard to reverse.” JAAKKO; tässä sanotaan grey matter! Lewisin replyssä: “Hall et al. make mention of many junctures where my interpretations clearly differ, such as posing neuroplasticity (e.g., pruning) rather than pathology to make sense of the loss of grey matter volume in the prefrontal cortex (PFC) and the loss of functional connectivity between the PFC and striatum.”
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Wanted: mechanisms of addiction
Addiction research should aim at causal knowledge Treatment and prevention Not only how subjects experience their situation, nor only ”variable sociology” Limitations and costs of RCTs Need for integrating knowledge of social, psychological, and (neuro)physiological mechanisms Mechanistic explanation: explaining properties of the whole with the properties of the parts and their mutual organization It is completely uninformative to start by noting that ”it is complex” or ”everything is connected”!
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Diagnosing the BDMA: Reductionist heuristics
Reductionist research heuristics: Start with simplifying assumptions and learn about the importance of organization by learning how and why they fail! Localization hypotheses (this part does this) Reductionist hypothesis: the whole is merely a sum of its parts (organization does not matter) Sensible reductionism
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Diagnosing the BDMA: Reductionist heuristics
BDMA as a consequence of applying reductionist heuristics to the role of the brain within the individual... and also to the role of the individual within the social Differences in behavior across subjects are mostly due to differences in their brains Problems in social interaction are mostly due to problems in individual behavior (decision making/self-control etc.) Reductionism also within the brain: addiction as the hysteresis of the dopamine system, insula as ”the island of addiction”
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Biases of reductionist research heuristics
Localization of relational/systemic properties: Addiction as a malfunction/maladaptation of the dopamine system Addiction as a (stable) property of an individual Look for intra-systemic explanations and regard them as ”more fundamental” Search for causes of problematic behavior within the agent and regard these causes as "the essence" of the problem Search for causes of social dysfunction in properties of agents In theorizing, simplify environment before simplifying the system e.g. ignore social constituents and distributed strategies of self-control W. Wimsatt
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Biases of reductionist research heuristics
Ignore observations of interactional/historical patterns e.g. Ignore the history of the problem behavior in the ”diagnosis” Prefer experimental designs with constant environmental variables e.g., manipulate/compare intrinsic states of the subject… … by using standardized tests in controlled environments Key difficulty in the integration of neuroscience with the social: neuroscientific accounts do not map neatly to our folk- psychological accounts of agency and social interaction Dichotomy of choice vs disease as a symptom of this mismatch
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What does NOT follow… If a part is causally relevant to the problematic behaviour of the whole, then intervening on the part is the most effective strategy for improving the behavior of the whole Cf. NIDA funding of neuroscience Localizing functional properties to parts is always explanatorily relevant for the behaviour of the whole Conceptualizing social behaviour and interaction is difficult (perhaps impossible) without agentive concepts Neuroscientific findings are explanatory relevant only if they discriminate between psychological (cognitive and affective) mechanisms Reductionist research strategies vs reductionist conclusions! It is sensible to investigate addiction as-if it were a brain disease, but it may not be effective (or right!) to treat addicts as-if they had a brain disease ”(risk-taking, novelty-seeking, and high sensitivtity to peer pressure)… might reflect the incomplete development of brain regions (eg, myelination of frontal lobe regions)” ”mechanisms that are responsible for the stress-induced increase in the vulnerability to drug use are not yet well understood, but evidence suggests that the stress-responsive neuropeptide CRF is involved through its effect in the amygdala and hypothalamitic-pituitary-adrenal axis”
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Why this matters In terms of prevention and treatment
Identification with BDMA For individual: Challenges to beliefs of efficacy (agency) Fairness: Ignoring other kind of vulnerabilities For the society: (Too?) narrow a target population Non-identification with BDMA Treshold of seeking help rises Not seeking help
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