cation of cholesterol as a risk factor, various fractions of the lipid were examined
to determine which conferred the most risk. Similarly, there is mounting evi-
dence that the hostility component of the TABP confers risk for CHD. Scientific
search is currently underway to determine whether some facets of hostility con-
fer more risk than other components. This current state of scientific inquiry heavily
influenced our decision to select the present tide of this volume.

The lead chapter by Suls and Sanders begins with an assumption that there
are particular behaviors or patterns of behavior that are risk factors for CHD.
They address the important issue of the role of potential mechanisms or process-
es by which a behavioral risk factor may be translated into CHD. They devote
considerable attention to three processes that may be associated with a behavioral
risk factor: inborn structural weakness, proneness to physiologic hypeffespon-
sivity, and a tendency to be exposed to dangerous situations.

Dembroski and Czajkowski (Chapter 2) trace the historical development of
the TABP and describe the evolution of the component analyses of the TABP
in efforts to identify the "virulent" component that confers risk. The results ap-
pear to suggest that the hostility component probably is a risk factor for CHD.
Costa, McCrae, and Dembroski (Chapter 3) examine hostility in the broader
framework of theoretical and empirical advances associated with a comprehen-
sive five-factor model of personality in an attempt to show how a certain facet
of hostility can be integrated into one of the five major domains, namely, the
Agreeableness vs. Antagonism dimension. Integration of hostility with a broader
theory of personality should promote conceptual clarification of present notions
of hostility and other personality predictors of disease in psychosomatic research.

Siegman (Chapter 4) takes the position that hostility is no less multidimen-
sional than the TABP construct, with probably only some dimensions of hostility
being related to CHD. One distinction, suggested by earlier studies, is between
the experience of anger and hostility, or covert hostility, and the expression of
anger and hostility, or overt hostility and aggression (also see Costa et al., Chap-
ter 3). The evidence suggests a positive correlation between the expression of
hostility and the severity of coronary artery disease (CAD). Some evidence sug-
gests that expressed hostility also correlates positively with cardiovascular reac-
tivity and with the production of testosterone. On the other hand, the evidence
suggests a negative correlation between the experience of hostility, or covert hostil-
ity, and CAD, cardiovascular reactivity and testosterone production in challeng-
ing situations.

In discussing how overt anger and hostility become translated into CHD, Sieg-
man emphasizes the role of expressive manifestations of overt anger and hostili-
ty, especially that of loud (rapid) and interruptive speech. Of interest from a
prophylactic and rehabilitative perspective is the finding that by instructing peo-
ple to speak softly and slowly, one can significantly reduce their cardiovascular
reactivity. The chapter includes a biobehavioral model that proposes a synergis-
tic interaction between expressed anger and hostility, loud, rapid and interrup-

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