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Theoretical Perspectives on Mental Health and Illness: Introduction to Part I
Sharon Schwartz, Professor of Epidemiology, Columbia University, Mailman School of Public Health,
Cheryl Corcoran, Assistant Professor of Psychiatry, Columbia University; Research Scientist, New York State Psychiatric Institute
The biological understanding of mental illness views it as a disease of the brain. The biological revolution in psychiatry was sparked by evidence for a genetic component to psychiatric disorders and pharmaceutical advances in drug therapies, which added to understanding of the chemistry of the brain and neuronal communication (neurochemistry). Furthermore, advances in neuroscience or neuroanatomy (which combines the findings from several scientific disciplines) have furthered our understanding of the relationship between the structure of the brain and human behavior. Schwartz and Corcoran provide an overview of what biological psychiatrists know about the brain and its function and dysfunction (neuroanatomy), neurochemistry, and genetics. Psychiatric medications affect the level of neurotransmitters, and hence correct dysfunctions in the neuronal communications systems. Schizophrenia has been hypothesized to result from an excess of dopamine, and the symptoms of schizophrenia are often reduced with the administration of medications which block specific dopamine receptors. Yet this evidence does not demonstrate that the cause of schizophrenia is a chemical imbalance as not all people respond to medications. The medications only affect some of the symptoms of schizophrenia, and studies report inconsistent responses. Contradictory findings and gaps also exist in knowledge of the role played by neurotransmitter dysfunctions in depression. While the evidence for a genetic link to schizophrenia and depression is compelling, Schwartz and Corcoran describe a variety of methodological problems which make heritability estimates questionable.
Furthermore, the specific mode of transmission and interactions among genetic and environmental factors need further examination. The biological revolution has pointed to the complexity of understanding mental illness. Schwartz and Corcoran conclude by outlining what role sociologists can play in researching the factors which affect the etiology and course of mental disorder, and in using the information gained by biological psychiatrists to further understanding of the relationship between social and biological factors. The student will want to read this chapter carefully and identify what information they thought was incontrovertible (i.e., schizophrenia is caused by a particular gene) has in fact not been verified.
That recent decades have witnessed a biological revolution in psychiatry is undeniable. A presidential proclamation branded the 1990s “The Decade of the Brain.” President Obama announced the BRAIN (Brain Research through Advancing Innovative Neurotechnologies) initiative in 2013 to promote an understanding of the brain functions underlying health and disease (http://braininitiative.nih.gov/about.htm).
This chapter focuses on three areas: brain structure and function (neuroanatomy), brain activity (functional brain imaging), and gene effects (genetics). Information from each area is beginning to be integrated, with the goal of understanding biological disease processes. The chapter focuses on the neurons because it is their functioning that is largely the basis of theories of psychiatric disorders at the level of analysis, with the recognition that the glial cells that support the neurons may also be relevant. Researchers have used several methods to test the hypothesis that psychiatric disorders reflect dysfunctions in neuronal communication systems. Researchers have also examined postmortem brain tissue to see changes in the shapes of neurons and their connections. Sociological analyses of the social construction of psychiatric disorders are also important; particularly at this juncture when the number of disorders officially recognized in psychiatry is growing at an unprecedented rate.
The purpose of this study was to investigate patterns of mental disorders comorbid with PTSD symptoms in young Israeli men exposed to combat.
Six hundred and seventeen subjects were selected via a general population sample and evaluated in a two-phase case-identification procedure, culminating in a modified SADS–L interview, administered by psychiatrists.
Major depressive disorder (OR=3.2), substance use disorders (OR=1.9) and personality disorders (OR=3.0) occurred more frequently in men reporting symptoms of PTSD than in men who had been under fire who did not report symptoms. With the possible exception of personality disorders, comorbid disorders did not constitute risk factors for PTSD. Comorbid PTSD and RDC disorders were associated with increased help-seeking.
The results suggest similar rates and types of PTSD comorbidity in Israeli war veterans as in veterans in the US assessed in general population studies, and are consistent with shared risk factors for PTSD and comorbid disorders.
An appropriate choice of controls in case/control studies of specific psychiatric disorders is crucial for valid risk-factor assessment. One suggested approach to control-group selection, the use of a well control group, is the focus of this paper. While using well controls has intuitive appeal, this paper shows that such a procedure can lead to ambiguous and biased results.
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