Stress reactions have been shown to be influenced by a number of individual difference variables over which one has very little control. For example, our age, genetic constellation, developmental and medical history, and in most cases gender are variables we have no direct control over. By this time next year, we will all be one year older and still composed of the same constellation of genes that we possess today.

Although we may not be able to influence these variables, many of these factors have been shown to influence the magnitude and patterning of physiological stress responses observed under conditions in which we are exposed to standard environmental stressors.

For example, it has been shown that neuroendocrine and blood pressure responses to stress increase with age (Palmer, Ziegler, and Lake, 1978), males typically exhibit greater blood pressure reactions to standardized stressors than females (Allen et al., 1993; Saab, 1989), and black participants exhibit greater blood pressure responses to stress presentations than white counterparts (Anderson, McNeilly, and Myers, 1992).

In addition to genetic factors contributing to susceptibility to disease through behavioral responses and risk factors like alcoholism and smoking, the magnitude of physiological responses to standardized stressors administered in laboratory settings has been shown to possess a heritable component (Hewitt and Turner, 1995). Accordingly, patterns of physiological responsivity to stress among first-degree relatives tend to be more alike than among unrelated persons.

Finally, both significant developmental (McEwen, 1998) and medical events (Corse et al., 1982) have been shown to affect physiological response patterns to behaviorally elicited stress.