Handbook of Health Psychology

By Andrew Baum; Tracey A. Revenson et al. | Go to book overview

39
Hostility (and Other Psychosocial Risk Factors): Effects on Health and the Potential for Successful Behavioral Approaches to Prevention and Treatment
Redford B. Williams
Duke University Medical Center

There was a time, not very long ago, when behavioral medicine researchers studying the effects of psychosocial factors on health and disease gathered themselves into guilds-not unlike those medieval guilds of armorers, goldsmiths, cobblers, and the like-each specializing in a rather narrow area of inquiry. In the early 1970s, for example, the Type A Behavior Pattern (TABP) guild was powerful and prominent at national meetings and in the research literature. By the early 1980s, however, the TABP guild was in decline, with negative studies leading to the formation of the hostility guild, the membership of which was drawn largely from the old TABP guild.

The hostility guild extended its hegemony in the 1980s (easily documented by a Medline search for papers with “hostility” in the keyword list), but it was soon under challenge from other guilds (i.e., the depression guild, the social support guild, the job strain guild), all with members who seemed to be engaged in a zero-sum game: There's only a limited amount of psychosocial risk factor “capital” available, and to the extent your risk factor is up, mine is down. This competition among psychosocial risk factor guilds led to a kind of internecine warfare, with engagements taking the form of statements like, “It's not hostility that's responsible for increased coronary risk; it's the low social support among hostile people that's really doing the damage.”

I participated in this warfare, often with gusto, on both the giving and receiving ends of the zero-sum debate-often defending my favorite risk factor, hostility, against the encroachments of those carrying the banner of depression, social support, or job strain. It was not a very satisfying endeavor, however, when I so often found myself at odds with other investigators who were not only good friends but also respected colleagues. By nature a lumper rather than a splitter, I began in the early 1990s to search for some means of reconciling, in my own mind if nowhere else, the competing factions. The initial phase of this search culminated in my 1993 presidential address to the American Psychosomatic Society (R. B. Williams, 1994), in which I hypothesized that the clustering of health damaging behavioral (smoking, high alcohol consumption, and dysregulated eating) and biological (increased sympathetic and HPA axis function, decreased parasympathetic function, and dysregulated immune system function) characteristics in persons with high hostility levels is mediated by reduced serotonergic function in the central nervous system.

The major advance here was to move away from the spurious notion that risk characteristics act independently of each other-“Is it hostility or the increased smoking (or sympathetic excess, higher cholesterol, etc.)?” Instead, I was beginning to realize, researchers need to look at the joint effects of clusters

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