Fatigue and Proinflammatory Cytokine Activity in Breast Cancer Survivors :

Despite a very large and growing literature demonstrating the significance of social support for health and well-being, surprisingly little is known about the social distribution of this crucial resource. This paper presents data on the distribution of social support and support resources across social class, marital status, age and gender, with the aims of contributing toward an understanding of the impact of social structures on processes of social support, and of assessing the hypothesis that epidemiological variations in mental health arise partially from social support differences. The epidemiology of perceived social support was found to correspond closely to the epidemiology of psychological distress and disorder. The single exception involved gender, where a positive rather than negative relationship was observed, with women demonstrating the highest levels of both social support and psychological distress. The observed patterns of variation in social support link this significant adaptive resource to one's locations in the social structure and reinforce the conclusion that it represents a promising intervention target. The practical importance of these results, however, are not matched by theoretical significance. Except in the case of marital status, our findings largely discount the hypothesis that the social distribution of mental health is partially attributable to social support differences.

A meta-analysis indicated that clinical depression was associated with several large alterations in cellular immunity. Analyzing only methodologically sound studies, reliable immune alterations included lowered proliferative response of lymphocytes to mitogens (effect size rs = .24-.45), lowered natural killer cell activity (r = .28), and alterations in numbers of several white blood cell populations (rs = .11-.77). Immune alterations were greater in both older and hospitalized samples. There was also evidence of a linear relation between intensity of depressive affect and indicators of cellular immunity. Estimates of sample sizes needed to detect reliable effects for each immune outcome are provided. How neuroendocrine mechanisms or health practices might link depression to immunity is discussed, and design features needed to better understand these pathways are specified.