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Interventionist causal models in psychiatry: repositioning the mind–body problem

Published online by Cambridge University Press:  10 October 2008

K. S. Kendler  and
J. Campbell
K. S. Kendler*
Affiliation:
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, and Human and Molecular Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA
J. Campbell
Affiliation:
Department of Philosophy, University of California, Berkeley, CA, USA
*
*Address for correspondence: K. Kendler, M.D., Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University Medical School, Box 980126, 800 E. Leigh Street, Room 1-123, Richmond, VA 23298-0126, USA. (Email: [email protected])
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Abstract

Background

The diversity of research methods applied to psychiatric disorders results in a confusing plethora of causal claims. To help make sense of these claims, the interventionist model (IM) of causality has several attractive features. First, it connects causation with the practical interests of psychiatry, defining causation in terms of ‘what would happen under interventions’, a question of key interest to those of us whose interest is ultimately in intervening to prevent and treat illness. Second, it distinguishes between predictive-correlative and true causal relationships, an essential issue cutting across many areas in psychiatric research. Third, the IM is non-reductive and agnostic to issues of mind–body problem. Fourth, the IM model cleanly separates issues of causation from questions about the underlying mechanism. Clarifying causal influences can usefully structure the search for underlying mechanisms. Fifth, it provides a sorely needed conceptual rigor to multi-level modeling, thereby avoiding a return to uncritical holistic approaches that ‘everything is relevant’ to psychiatric illness. Sixth, the IM provides a clear way to judge both the generality and depth of explanations. In conclusion, the IM can provide a single, clear empirical framework for the evaluation of all causal claims of relevance to psychiatry and presents psychiatry with a method of avoiding the sterile metaphysical arguments about mind and brain which have preoccupied our field but yielded little of practical benefit.

Keywords

Causalityinterventionist modelmind–bodypsychiatry
Type
Editorial Review
Information
Psychological Medicine , Volume 39 , Issue 6 , June 2009 , pp. 881 - 887
Copyright
Copyright © Cambridge University Press 2008

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References

Briggman, KL, Abarbanel, HD, Kristan, WB Jr. (2005). Optical imaging of neuronal populations during decision-making. Science 307, 896–901.CrossRefGoogle ScholarPubMed
Craver, CF (2007). Explaining the Brain. Clarendon Press.CrossRefGoogle Scholar
Durkheim, E (1897). Le Suicide 1897 [English translation, 1951]. Glencoe, IL: Free Press.Google Scholar
Ebrahim, S, Davey, SG (2008). Mendelian randomization: can genetic epidemiology help redress the failures of observational epidemiology? Human Genetics 123, 15–33.CrossRefGoogle ScholarPubMed
Gold, I, Stoljar, D (1999). A neuron doctrine in the philosophy of neuroscience. Behavioral and Brain Sciences 22, 809–869.CrossRefGoogle ScholarPubMed
Irons, DE, McGue, M, Iacono, WG, Oetting, WS (2007). Mendelian randomization: a novel test of the gateway hypothesis and models of gene-environment interplay. Developmental Psychopathology 19, 1181–1195.CrossRefGoogle ScholarPubMed
Kendler, KS, Gardner, CO, Prescott, CA (2003). Personality and the experience of environmental adversity. Psychological Medicine 33, 1193–1202.CrossRefGoogle ScholarPubMed
Kendler, KS, Karkowski, LM, Prescott, CA (1999). Causal relationship between stressful life events and the onset of major depression. American Journal of Psychiatry 156, 837–841.CrossRefGoogle ScholarPubMed
Kendler, KS, Neale, MC, Kessler, RC, Heath, AC, Eaves, LJ (1993). A longitudinal twin study of personality and major depression in women. Archives of General Psychiatry 50, 853–862.CrossRefGoogle ScholarPubMed
Loehlin, JC (1992). Genes and Environment in Personality Development. Sage Publications: Newbury Park, CA.Google Scholar
Pearl, J (2000). Causality Models, Reasoning, and Inference. Cambridge University Press: Cambridge.Google Scholar
Rutter, M (2007). Prodeeding from observed correlation to causal inference: the use of natural experiments. Perspectives on Psychological Science 2, 377–395.CrossRefGoogle ScholarPubMed
Salib, E (2003). Effect of 11 September 2001 on suicide and homicide in England and Wales. British Journal of Psychiatry 183, 207–212.CrossRefGoogle ScholarPubMed
Schaffner, KF (1994). Psychiatry and Molecular Biology: Reductionistic Approaches to Schizophrenia in Philosophical Perspectives on Psychiatric Diagnostic Classification. Johns Hopkins University Press: Baltimore.Google Scholar
Spirtes, P, Glymour, C, Scheines, R (1993). Causation, Prediction and Search. Springer-Verlag: New York.CrossRefGoogle Scholar
Woodward, J (2003). Making Things Happen. Oxford University Press: New York.Google Scholar
Woodward, J, Hitchcock, C (2003). Explanatory generalizations, Part I: a counterfactual account. Nous 37, 1–24.CrossRefGoogle Scholar