Explanatory Models for Psychiatric Illness

Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University Medical School, Richmond, VA 23298-0126, USA.
American Journal of Psychiatry (Impact Factor: 12.3). 07/2008; 165(6):695-702. DOI: 10.1176/appi.ajp.2008.07071061
Source: PubMed


How can we best develop explanatory models for psychiatric disorders? Because causal factors have an impact on psychiatric illness both at micro levels and macro levels, both within and outside of the individual, and involving processes best understood from biological, psychological, and sociocultural perspectives, traditional models of science that strive for single broadly applicable explanatory laws are ill suited for our field. Such models are based on the incorrect assumption that psychiatric illnesses can be understood from a single perspective. A more appropriate scientific model for psychiatry emphasizes the understanding of mechanisms, an approach that fits naturally with a multicausal framework and provides a realistic paradigm for scientific progress, that is, understanding mechanisms through decomposition and reassembly. Simple subunits of complicated mechanisms can be usefully studied in isolation. Reassembling these constituent parts into a functioning whole, which is straightforward for simple additive mechanisms, will be far more challenging in psychiatry where causal networks contain multiple nonlinear interactions and causal loops. Our field has long struggled with the interrelationship between biological and psychological explanatory perspectives. Building from the seminal work of the neuronal modeler and philosopher David Marr, the author suggests that biology will implement but not replace psychology within our explanatory systems. The iterative process of interactions between biology and psychology needed to achieve this implementation will deepen our understanding of both classes of processes.

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    • "To address this issue, some investigators have recently broadened the scope of research on vulnerability for affective lability to account for the fact that cognitive factors interact with biological processes and socialenvironmental exposures to shape risk for affective disorders . Indeed, several multi-factorial models of psychopathology have now been proposed (e.g., Gibb et al. 2013; Kendler 2008; Slavich and Irwin 2014; Slavich et al 2010). The most rapidly growing body of research in this context focuses on how genetic factors interact with environmental exposures to shape risk for affective disorders (e.g., Caspi et al. 2010; Munafó et al. 2009). "
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    • "I remarked above that combining the perspectives of different levels into coherent explanations of mental illness is a difficult task. Whilst impressive work has been done—particularly by Kenneth Kendler (e.g. 2008, 2012) and by Kendler and John Campbell (e.g. 2009, 2014)—to demonstrate the need for multi-level explanations in psychiatry and to consider how they are best formulated, the question of what makes a good explanation for a given purpose has been ignored. We know, for example, that some cases of depression are best explained primarily in"
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