Diathesis

Abstract: About one million suicides and ten million suicide attempts occur worldwide each year. Suicide is not simply a response to stress, but generally a complication of a psychiatric disorder. A proposed stress–diathesis model is described in clinical and neurobiological terms. Neurobiological correlates of the diathesis for suicidal acts point to the involvement of the serotonergic and noradrenergic systems, and the ventromedial prefrontal cortex. Some treatments seem to reduce suicide risk independently of an effect on the primary psychiatric disorder, perhaps by reducing the diathesis.

Abstract: There is a substantive literature on the behavioral effects of psychosocial stressors on schizophrenia. More recently, research has been conducted on neurohormonal indicators of stress responsivity, particularly cortisol release resulting from activation of the hypothalamic-pituitary-adrenal (HPA) axis. This article integrates the psychosocial and biological literatures on stress in schizophrenia, and it offers specific hypotheses about the neural mechanisms involved in the effects of stressors on the diathesis. Both the behavioral and biological data indicate that stress worsens symptoms and that the diathesis is associated with a heightened response to stressors. A neural mechanism for these phenomena is suggested by the augmenting effect of the HPA axis on dopamine (DA) synthesis and receptors. Assuming the diathesis for schizophrenia involves an abnormality in DA receptors, it is proposed that the HPA axis acts as a potentiating system by means of its effects on DA. At the same time, DA receptor abnormality and hippocampal damage render the patient hypersensitive to stress. This neural diathesis-stress model is consistent with findings on prenatal factors and brain abnormalities in schizophrenia, and it provides a framework for explaining some key features of the developmental course and clinical presentation.

Abstract: Vulnerability to Psychopathology: A Biosocial Model Marvin Zuckerman. Washington, DC: American Psychological Association. 1999, 535 pp., (hardcover). A great deal has been learned about psychopathology, but still many questions remain. One of the most important questions remaining to be answered is why people are vulnerable to the different variants of psychopathology ? Zuckerman has made this broad question the focus of his new book. It is a book that is remarkable by its scholarship. It provides a compendium of information on the history of mental disorders, and research findings on their course, diagnosis and prevalence, comorbidity, demographic features, genetic and biological characteristics, and social factors, and is punctuated by a strong biological orientation. Zuckerman indicates that his new book was written as a "logical sequel" to his previous book on the Psychobiology of Personality (Zuckerman, 1991). His book, which is divided into eight chapters, provides a review of the wealth of findings on psychopathology. The first cluster of chapters of the book deals with general considerations including diathesis-stress models (chapter 1), and diagnosis (chapter 2); the second cluster, and main body of the book (chapters 3 to 7), describes theory and research on a selected number of specific disorders, and the final concluding chapter is concerned with the prognosis of the future science of psychopathology. In the first chapter we learn that diathesis-stress theories are not monolithic but exhibit great variety. His model extends Paul Meehl's orientation to schizoprhenia to other disorders, and thus focuses on a biological diathesis and social stress (e.g., parenting) that increases risk of disorders. Zuckerman's book largely restricts the term diathesis to genetic and biological factors. As it happens, then, he questions the basis for the notion of cognitive vulnerability. His grounds for this are that the concept of a cognitive predisposition to psychopathology is not empirically well supported, and that it could simply be a "typical expression of a biological disposition" (p. 7), or other "interpersonal" and "developmental" factors (p. 197). For example, he suggests that research has not adequately demonstrated that cognitive factors predict subsequent levels of depression or other disorders, and are not simply state-manifestations of the disorders. These views are challenged by recent research of the Temple-Wisconsin depression project (e.g., Alloy, Abramson, Hogan et al., 2000). Although Zuckerman's book clearly reflects a monumental undertaking of scholarship, its review of the rapidly advancing cognitive literature on psychopathology is dated. Readers who are interested in a cognitively oriented approach to vulnerability to psychopathology will thus need to look for other references (e.g., Alloy & Riskind, in press). Along with his restriction of the concept of vulnerability to biological diathesis, Zuckerman's book pays little attention to methodological issues, and particularly to issues important for cognitively oriented researchers. Readers who are interested in such issues will have to turn to other sources, such as the excellent chapter by Alloy, Abramson, Raniere, & Dyller, (1999). …