New research in the emergent fields of behavioral perinatology has confirmed in my mind the intersubjective nature of the person. The mother-fetal unit is a closely interconnected dynamic process, with each impacting on the other in ways that are recently coming to greater light. Nature is profound in her wisdom, which is conserved across the generations. The mother’s brain-mind is intimately impacting on the fetal developing CNS, as the fetus is literally on the mother’s mind/brain-fetal cells which can transform into oligodentrocytes, neurons, and immune cells cross the mother’s blood brain barrier in order to serve neuroprotective functions for the mother (since motherhood is a very stressful time in many ways). The placenta serves transitional functions between the maternal and fetal brains. Wadhwa (2005) noted:
“the maternal-placental-fetal neuroendocrine system is the primary physiological mediator of the effects of prenatal stress on adverse fetal outcomes because it constitutes the fundamental substrate for fetal growth, development and parturition, and because pathways through which alterations in other systems (e.g., immune, vascular) produce pathophysiological consequences are mediated, in part, by maternal-placental-fetal neuroendocrine processes” (p. 53).
(This is taken from Perinatal Stress, Mood and Anxiety Disorders: From Bench to Bedside edited by A. Riecher-Rössler & M. Steiner for Karger-Bibliotheca Psychiatrica No. 173)
Unfortunately, neuroscience research in schizophrenia fails to control for this important source of variance, particularly when comparing MZ & DZ twin pairs for concordance for schizophrenia. MZ twins often share a common chorion (blood supply), whereas DZ twins never do. The point is that prenatal stress, mediated by neuroendocrine processes (my doctoral research in the 1970’s involved the impact of neuroendocrine processes on a chronic metabolic illness. i.e., Type I diabetes) can result in reduced morphological changes in the hippocampus (among other changes)-a key structure in schizophrenia research. This change has been known for many years and schizophrenia researchers continue to ignore this important source of variance.
As Matthews and Meaney (2005), in their Maternal adversity, vulnerability and disease, pointed out:
“The probability of chronic illness is strongly influenced by environmental conditions prevailing during development...Studies with primate and rodent models show that the development of the hippocampus is impaired by fetal glucocorticoid [cortisol] exposure or by prenatal stress...Evidence from clinical intervention studies with high-risk infants and developmental neurobiology suggests that neurocognitive development is influenced by the quality of the postnatal environment” (pp. 28-29).
Gene expression is subject to early life programming to a degree never suspected before (Freud was correct in his speculation that early childhood experience plays a significant role in adult reaction patterns). Recent neurobiological research documents that events in early life exert an apparently permanent effect on gene expression and therefore the phenotype of the organism.
Matthews and Meaney (2005) noted:
“Elevated exposure to biologically active glucocorticoids in fetal life can permanently alter the expression of hepatic [liver] genes (i.e., PEPCK, glucose kinases) that are key regulators of glucose and fat metabolism. Collectively, these effects increase the capacity for lipid metabolism, decrease glucose clearance and render the organism vulnerable to hyperlipidaemia, glucose intolerance and hyperglycaemia” (p. 30).
Recent research has extended the scope of the fetal programming hypothesis beyond that of the liver.
Postnatal experience can override these environmentally induced predispositions (in which earlier research appeared to be ‘genetic,’ i.e., an issue of sequencing not epigenetic regulation of gene expression) to a significant degree as documented in the primate and rat research of Suomi and Meaney, respectively (as well as many other researchers). I do hope that one day contemporary psychiatry and clinical psychology will catch up to current research in epigenetics and the significant impact of the social environment on developmental neurobiology-and,importantly, to apply this research to actual clinical disorders. So far, this has been limited to selective disorders, e.g., PTSD and anxiety/mood disorders. The psychotic disorders have been exported to outdated reductionistic genetic and neurobiological research (with the exception of some European psychiatric research centers, e.g., in the research of Jim van Os and colleagues at Maastricht University, the Netherlands) which may be partly entrenched because of powerful sociocultural and economic biases.
(This is the first part in a series of research findings which will document the significant impact of the social environment on the developing fetal neuroaxis)
Brian Koehler PhD
New York University
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New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net
