This article reviews the burgeoning literature on the relationship of mood disorders and heart disease. Major depression and depressive symptoms, although commonly encountered in medical populations, are frequently underdiagnosed and undertreated in patients with cardiovascular disease (CVD). This is of particular importance because several studies have shown depression and its associated symptoms to be a major risk factor for both the development of CVD and death after an index myocardial infarction. This review of the extant literature is derived from MEDLINE searches (1966-1997) using the search terms "major depression," "psychiatry," "cardiovascular disease," and "pathophysiology." Studies investigating pathophysiological alterations related to CVD in depressed patients are reviewed. The few studies on treatment of depression in patients with CVD are also described. Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity. Recommendations for future research are proposed.

The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment.

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.

Schizophrenia: A neural diathesis-stress model.

Context Although differences in clinical characteristics exist between major depressive disorder (MDD) and bipolar disorder (BD), consistent structural brain abnormalities that distinguish the disorders have not been identified. Objectives To investigate structural brain changes in MDD using meta-analysis of primary studies; assess the effects of medication, demographic, and clinical variables; and compare the findings with those of a meta-analysis of studies on BD. Data Sources The MEDLINE, EMBASE, and PsycINFO databases were searched for studies from January 1, 1980, to February 2, 2010. Study Selection Two hundred twenty-five studies that used magnetic resonance imaging or x-ray computed tomography to compare brain structure in patients with MDD with that of controls were included in an online database, and 143 that measured common brain structures were selected for meta-analysis. Data Extraction Twenty-five variables, including demographic and clinical data, were extracted from each study, when available. For the meta-analysis, mean structure size and standard deviation were extracted for continuous variables, and the proportion of patients and controls with an abnormality in brain structure was extracted for categorical variables. Data Synthesis Compared with the structure of a healthy brain, MDD was associated with lateral ventricle enlargement; larger cerebrospinal fluid volume; and smaller volumes of the basal ganglia, thalamus, hippocampus, frontal lobe, orbitofrontal cortex, and gyrus rectus. Patients during depressive episodes had significantly smaller hippocampal volume than patients during remission. Compared with BD patients, those with MDD had reduced rates of deep white matter hyperintensities, increased corpus callosum cross-sectional area, and smaller hippocampus and basal ganglia. Both disorders were associated with increased lateral ventricle volume and increased rates of subcortical gray matter hyperintensities compared with healthy controls. Conclusions The meta-analyses revealed structural brain abnormalities in MDD that are distinct from those observed in BD. These findings may aid investigators attempting to discriminate mood disorders using structural magnetic resonance imaging data.

Structural neuroimaging studies in major depressive disorder. Meta-analysis and comparison with bipolar disorder

The anatomy of mood disorders-review of structural neuroimaging studies

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). …

Vulnerability to Psychopathology: A Biosocial Model

Limbic-hypothalamic-pituitary-adrenal axis activity and ventricular-to-brain ratio studies in affective illness and schizophrenia.

Objective: Lateral ventricle enlargement in schizophrenia has been positively correlated with poor premorbid competence, negative symptoms, and poor treatment response and negatively correlated with concentrations of homovanillic acid (HVA), a dopaminergic metabolite. The authors provide further evidence of a reciprocal relationship between lateral ventricle size and dopaminergic activity in schizophrenia

Lateral Ventricle-Brain Ratio and Balance Between CSF HVA and 5-HIAA in Schizophrenia

Natural killer cell activity in schizophrenia and schizoaffective disorder: a pilot study

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Limbic-hypothalamic-pituitary-adrenal axis activity and ventricular-to-brain ratio studies in affective illness and schizophrenia.

Lateral Ventricle-Brain Ratio and Balance Between CSF HVA and 5-HIAA in Schizophrenia

Natural killer cell activity in schizophrenia and schizoaffective disorder: a pilot study