Depression in patients with rheumatoid arthritis: description, causes and mechanisms

Eliminating health disparities is a fundamental, though not always explicit, goal of public health research and practice. There is a burgeoning literature in this area, but a number of unresolved issues remain. These include the definition of what constitutes a disparity, the relationship of different bases of disadvantage, the ability to attribute cause from association, and the establishment of the mechanisms by which social disadvantage affects biological processes that get into the body, resulting in disease. We examine current definitions and empirical research on health disparities, particularly disparities associated with race/ethnicity and socioeconomic status, and discuss data structures and analytic strategies that allow causal inference about the health impacts of these and associated factors. We show that although health is consistently worse for individuals with few resources and for blacks as compared with whites, the extent of health disparities varies by outcome, time, and geographic location within the United States. Empirical work also demonstrates the importance of a joint consideration of race/ethnicity and social class. Finally, we discuss potential pathways, including exposure to chronic stress and resulting psychosocial and physiological responses to stress, that serve as mechanisms by which social disadvantage results in health disparities.

The purpose of this review is to assess the relationship between mood disorders and development, course, and associated morbidity and mortality of selected medical illnesses, review evidence for treatment, and determine needs in clinical practice and research. Data were culled from the 2002 Depression and Bipolar Support Alliance Conference proceedings and a literature review addressing prevalence, risk factors, diagnosis, and treatment. This review also considered the experience of primary and specialty care providers, policy analysts, and patient advocates. The review and recommendations reflect the expert opinion of the authors. Reviews of epidemiology and mechanistic studies were included, as were open-label and randomized, controlled trials on treatment of depression in patients with medical comorbidities. Data on study design, population, and results were extracted for review of evidence that includes tables of prevalence and pharmacological treatment. The effect of depression and bipolar disorder on selected medical comorbidities was assessed, and recommendations for practice, research, and policy were developed. A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between mood disorders and many medical illnesses. In addition, there is evidence to suggest that mood disorders affect the course of medical illnesses. Further prospective studies are warranted.

Sickness behaviour represents the expression of the adaptive reorganization of the priorities of the host during an infectious episode. This process is triggered by pro-inflammatory cytokines produced by peripheral phagocytic cells in contact with invading micro-organisms. The peripheral immune message is relayed to the brain via a fast neural pathway and a slower humoral pathway, resulting in the expression of pro-inflammatory cytokines in macrophage-like cells and microglia in the brain. The cellular and molecular components of this previously unsuspected system are being progressively identified. These advances are opening new avenues for understanding brain disorders, including depression.