The relation of social to biological processes in disease.

A common language is developing which describes how social interaction can lead to disease. There is a consensus based on forty years of psychophysiological research that emotion is the crucial driving force in a chain of events leading from psychosocial interaction to neuroendocrine changes. These changes, in turn, can induce physiological abnormalities eventually leading to pathologic changes. The emotions involved have been presented in a model in which a sympathetic adrenal-medullary effort-relaxation axis is contrasted with a pituitary adrenal-cortical elation-dejection axis. A further pituitary-gonadotropic axis for social success as opposed to low social assets is described. Although overlapping, each system can be shown to be related to a separate neuroendocrine mechanism whose activity pattern may be either exaggerated or suppressed. Social scientists like Kemper and gender psychologists like Bakan speak of separate power (agentic) and status (communion) axes. They appear to correspond broadly to the neuroendocrine mechanisms mentioned earlier. The changes induced by emotions are sufficiently powerful to regularly override the neuroendocrine feedback controls that should restore homeostasis. These overrides will either gradually or sometimes abruptly--as in cardiac arrhythmia--lead to pathophysiological changes and so to disease states, which are eventually fatal. Although social supports and social assets are successful in keeping neuroendocrine disturbances to a minimum in a healthy society, if the milieu is disordered, one's vulnerability is increased.