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Making a case for constructive reductionism
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Borsboom et al. argue that reductionism in psychopathology research has not yielded sufficient insights to understand the complexity of the systems that cause psychopathologies, nor has it provided effective treatments. This somewhat pessimistic verdict may apply when the philosophically driven and publicly nourished expectations are a full understanding and full cure of the known psychiatric disorders (Müller 2018). The leading framework for the last decades of neurobiological research in psychopathology was reductionism. Leading hypotheses were generated that suggested a single psychiatric disorder can be reduced, that is, causally explained and treated, to a dysfunction in a single target or single functional system of the brain. It can be argued that this may have been supported by the technical limitations of new empirical techniques. For instance, the view that a dysfunction in the dopaminergic (DA) system of the brain is the sole causal mediator for drug addiction development was massively driven by the advent of in vivo microdialysis (Westerink 1995). This technique proved that all drugs with addiction potential acutely enhance DA activity in the brain's reward circuitry, while non-addictive drugs do not (Di Chiara & Imperato 1988). Thereby, a single prominent and many-times-replicated finding was generalized to a functional theory (Koob 1992; McBride et al. 1999; Wise 2002) which did not pay tribute to the emerging complexity of the system (Salamone 1996). The therapeutic predictions based on this model, however, failed in practice (McCreary et al. 2015; Spanagel & Kiefer 2008), suggesting that the DA theory of addiction is at least incomplete (Nutt et al. 2015). One possible reason for that could have been the initial limitation of a key technique, in that only DA was measured and only dopaminergic innervated brain structures were considered. Empirical techniques advanced and showed that many more transmitter systems of the brain are dysregulated during...