Effects of Psychosocial Treatment in Prolonging Cancer Survival May Be Mediated by Neuroimmune Pathways

Authors

  • DAVID SPIEGEL,

    1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 300 Pasteur Road, Stanford, California 94305-5544 USA
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  • SANDRA E. SEPHTON,

    1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 300 Pasteur Road, Stanford, California 94305-5544 USA
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  • ABBA I. TERR,

    1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 300 Pasteur Road, Stanford, California 94305-5544 USA
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  • DANIEL P. STITES

    1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 300 Pasteur Road, Stanford, California 94305-5544 USA
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Abstract

Abstract: Research has provided growing evidence of links between the social environment and cancer progression. Indeed, social support in the form of marriage, frequent daily contact with others, and the presence of a confidant may all have protective value against cancer progression. Furthermore, retrospective data suggest that major stressful life events are more prevalent in patients with relapse or malignancy, and thus may contribute to cancer morbidity. Initial studies of the effects of psychosocial intervention with cancer patients have provided some promising results. In three randomized prospective trials, protective effects of psychosocial interventions on cancer progression have been confirmed, while one matching and one randomized study showed no survivial effect after psychosocial treatment. Though more research is clearly needed in this area, this body of evidence suggests that psychosocial factors have potentially powerful modulating effects on the course of disease. Here we review evidence of one possible mechanism whereby psychosocial factors may influence disease-resistance capabilities: the neuro-immune connection. Suppressive effects of stress on immune function are well documented, and these effects have been shown to be modulated by social support. Thus, it is reasonable to hypothesize that supportive social relationships may buffer the effects of cancer-related stress on immunity, and thereby facilitate the recovery of immune mechanisms that may be important for cancer resistance. Data addressing this hypothesis are reviewed.

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