Integrated models in psychiatry: the state of the art

Abstract

Social psychiatry has now been a part of psychiatry as a scientific discipline for a century, since Ilberg [1] and Southard [2] first used the term. The remit of social psychiatry is broad, ranging from investigations of social factors in the aetiology of mental disorders, to community psychiatry and health services research, to global and public mental health. However, given psychiatry’s primary orientation to the medical and biological, social psychiatry has held a rather tenuous position, perhaps even more so now, since rapid advances in genetics and neuroscience promise to unearth the basic biological underpinnings of mental disorders. However, intriguingly these advances have demonstrated social psychiatry is central to understanding mental disorders more fully, in all its facets [3]. Indeed, through recent research on genetics and neurobiology, it has become increasingly clear that the social combines with, and impacts on, the biological and the psychological, in a multitude of ways, to increase risk for mental disorders. The idea of such integrated models of mental disorder is not new. For instance, more than 30 years ago, George Engel [4] discussed the clinical application of a biopsychosocial model and, more recently, Kenneth Kendler [5, 6] put forward strong philosophical arguments for what he coined ‘pluralistic explanatory models’. Recently, research on integrated models of mental disorder has gained momentum and, while still limited in extent, we have never been as close to generating robust evidence on the interplay of the social, psychological, and biological. One prominent example of this is research on gene–environment interactions in common mental disorders and (to a lesser degree) in schizophrenia and other psychoses [7–10]. Recent advances in epigenetic profiling, for example, allow us now to investigate the impact of environmental exposures on gene expression to increase the risk of mental disorder [11]. Further, the current upsurge in social neuroscience has generated (initial) insights into neural mechanisms through which environmental exposures may impact on the development of mental disorders [12]. There is also an emerging evidence on neuroendocrine and inflammatory mechanisms that may link childhood adversity and risk of mental disorders, including psychoses [13]. Finally, recent advances in clinical psychology further suggest that repeated exposure to social adversity can link to mental disorder (including more severe forms such as psychosis) through specific cognitive and affective mechanisms (e.g. social cognitive biases, stress sensitivity, disturbances in affect, etc.). This is not to imply that the social does not warrant investigation in its own right. Mental disorders are intrinsically social. They are shaped by, and in turn shape, social contexts and experiences. However, in abandoning the (presumed) polarities between the social, psychological and biological, and embracing an evidence-based approach for identifying biological and psychological mechanisms, integrated investigations of mental disorders add (even) more weight to the social as a (potential) contributory cause of the onset and outcomes of mental disorders. This, in turn, poses methodological challenges both in terms of optimising measurement of the social and in applying (and developing) novel epidemiological methods that allow us to test how specific social contexts and experiences combine, in multiple ways, with specific psychological and biological mechanisms in the origins of mental disorders. U. Reininghaus (&) C. Morgan Section of Social Psychiatry, Health Service and Population Research Department, NIHR Biomedical Research Centre, Centre for Epidemiology and Public Health, Institute of Psychiatry, King’s College London, London, UK e-mail: ulrich.reininghaus@kcl.ac.uk