It is well known that severe mental disorders are increasingly portrayed by various mental health organizations and advocacy groups, including NIMH and NARSAD, as neurobiological brain diseases analogous to chronic medical diseases such as diabetes and epilepsy. Research on the social or psychobiological origins of these disorders has progressively decreased as neurogenetic and neurobiological research, of a radical reductionistic form, has become the leading paradigm. I have previously posted research summaries (primarily conducted in Europe ) demonstrating that both the schizophrenias and bipolar disorders can be initiated and significantly affected by sociocultural and psychological processes. Social psychiatric research has been seriously undermined by the hegemony of reductionistic biological theories. We are at a point in our zeitgeist in which psychiatric residents, social work and psychology interns are primarily exposed to these scientifically limited models of etiology and treatment despite lip service being given to a biopsychosocial perspective.
Periodically, politically incorrect publications will emerge challenging these series of pronouncements about mental disorders being only or primarily neurobiological brain disorders (for a recent example see Dan Blazer's The Age of Melancholy: Major Depression and its Social Origins published in 2005 by the Taylor & Francis Group -- Blazer is a Professor of Psychiatry and former Chair of the Department of Medical Education at Duke University School of Medicine). In addition to the scientific challenges to reductionism issuing from replicated epidemiological and outcome studies, there are replicated and robust research studies emerging from within molecular biology itself demonstrating the limited nature of neurobiological reductionism. These are far too numerous to mention here in this listserve format. However, to give one excellent example of what I am referring to, I will review some recent research on the effects of prenatal stress on the developing fetal neuroaxis and adult psychopathology.
It is well known that the roots of severe mental illnesses are often observed in early development -- these models are referred to as neurodevelopmental theories of schizophrenia. They encompass such wide ranging research as neuronal migration patterns, early observational studies examining neuromotor, hedonic, social isolation, learning difficulties etc. The point is that this research is used as evidence that these disorders are primarily neurogenetic and neurobiological in origin. Personally, I would have no problem with this perspective, but only if the terms genetics and biology were expanded to include the significant effects of experience (e.g., epigenetics and human relationships) on CNS structure and function. Unless we do this we are at risk for confusing correlation with causation and on an a priori basis eliminating significant sources of etiological import. These neuroreductionistic trends are seriously challenged by examining the research on prenatal stress. Unfortunately, neurodevelopmental, genetic and epidemiological (e.g., twin studies) studies do not consider this as a potential source of error variance, even though consistently replicated research findings point to it as a key variable in both physical and mental disorders.
Several retrospective studies have confirmed that chronic mental stress during pregnancy significantly increases the likelihood of disturbed physical and psychological development (Jones & Tauscher 1978; Meijer 1985; Lou et al 1994; Fuchs & Czeh 2005). An association has been demonstrated between maternal stress and later development of schizophrenia in the developing child (Huttunen & Niskanen 1978; Myhrman et al 1996; van Os & Selten 1998), as well as depressive symptomatology (Watson et al 1999; Brown et al 2000). Lemaire et al (2000) examined the effects of prenatal stress in rats. These investigators found that prenatal stress induced a life span reduction of hippocampal neurogenesis (birth of new neurons) and decline in total granule cell numbers which were accompanied by learning impairment in hippocampally mediated tasks, e.g., spatial learning. A recent study investigating whether prenatal stress can alter neural, hormonal, and behavioral status in nonhuman primates demonstrated that prenatal stress, both early and late in pregnancy, resulted in reduced hippocampal volume and an inhibition of dentate gyrus neurogenesis. Hippocampal volume reduction is one of the more robust findings in schizophrenia research (as well as observed in major depressive disorder, PTSD, etc.). These changes in hippocampal volume were associated with elevated cortisol levels (upregulation of the limbic-hypothalmic-pituitary-adrenal axis-LHPA), as well as lower levels of exploration (separation anxiety? negative symptomatology?) and restlessness (higher motor levels). These and many other research studies (which I have previously posted -- particularly, links between prenatal stress and later development of schizophrenia) demonstrate that the prenatal environment can alter behavior, deregulate neuroendocrine and neurobiological systems, and affect hippocampal plasticity and structure in a persistent manner.
This research on the effects of prenatal stress is another link in the chain of research evidence demonstrating the need to move beyond neuroreductionism to the inclusion of sociocultural and psychological factors, not only in the course and outcome of the severe mental disorders, but in their initiation and onset as well.
Brian Koehler PhD
New York University
80 East 11th Street #339
New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net
