The empirical and theoretical work presented in this chapter demonstrates that a number of stages are needed in creating a comprehensive model of stress that can be used to address the primary questions posed in the Introduction to this book. Certainly, the important distinction between stressors and stress responses needs to be incorporated into such a model, as does acknowledgment that individual factors influence the magnitude and patterning of stress responses.

Further, in order to integrate the important facets from the literature on the stress??“health relation, it is clear that an interactive or transactional model would be necessary.

Diathesis??“stress models have been useful in discussing the interaction of environmental and genetic factors in several forms of psychiatric disorders (for example, Zubin and Ludwig, 1983). In this terminology, an individual possesses a vulnerability or diathesis that places him or her at increased risk for developing a specific psychiatric disorder.

This vulnerability could be either genetic or environmental; regardless of origin, it places an individual at increased risk for the disorder. Not all persons with the vulnerability, however, develop the psychiatric diagnosis. Only those exposed to specific environmental conditions or stressors experience the full range of symptoms required to make the clinical diagnosis.

The vulnerability model serves as the foundation for the comprehensive model of stress outlined in Figure 3.3. In this model, individual difference factors serve as the vulnerability factor that interacts with environmental stressors to direct the magnitude and type of acute stress response observed. To return momentarily to the two men whose homes were lost in Hurricane Andrew, this model can be used to explain their differential stress responses.

Although the environmental stressor was identical for both of them, one man was clearly better equipped to handle the nature of the stressor than the other. While we may not be able to determine, from the brief news report seen on television, what specific individual difference factor was responsible for the difference in observed responses, it is clear that these two men were different regarding their vulnerability to stress.

Figure 3.3. A comprehensive model of stress.

The fundamental progression from stressor to acute stress response to chronic stress response depicted in this comprehensive model of stress is consistent with all existing models of stress. Obviously, some previous models go into much more detail regarding specific components of this one (McEwen, 1998; Selye, 1956) and, as such, these previous models can usefully be integrated into this broader model of stress.

The comprehensive model clearly recognizes the transactional nature of both the acute and chronic stress responses as evidenced by the inclusion of bidirectional arrows. Although specific stress responses may not have caused the initial environmental stressor, they can become additional stressors themselves.

For example, Franklin’s father, who suffered a heart attack three years ago, now exhibits health-related worries and concerns (acute cognitive stress reactions) that were not evident prior to the heart attack and his diagnosis of cardiovascular disease.

As such, the experience of having a heart attack adds one more stressor to his life. In this regard, chronic stress conditions serve as the foundation for subsequent acute stress responses, and consequently, the magnitude of acute stress reactions is influenced by these chronic stress conditions.

A central role is assigned in this model of stress to individual difference variables, both inherited and acquired, that influence the nature of the acute stress response to specific environmental stressors. It is generally believed that as the magnitude of the environmental stressor and the vulnerability to stress increase, the more complicated and in tense acute stress response is observed.

Figure 3.4. Relation between environmental stress and vulnerability factors in predicting the magnitude of acute physiological responses to stress.

Imagine that we could systematically rank environmental stressors as well as overall individual vulnerability to stress quantitatively. In this regard, our rankings of environmental stressors would probably rate having an argument with an employer higher than being five minutes late to a nonessential meeting, but considerably lower than experiencing a concentration camp confinement.

Likewise, our measure of vulnerability factors would probably rate a person with newly learned coping skills higher in vulnerability to stress than a person equipped with a vast array of stress coping skills. An individual with no coping skills at all would likely be rated higher than both others on our global measure of vulnerability to stress. Assuming some amount of linearity of these conceptually derived variables, they would be expected to interact with one another to determine the intensity of the observed acute stress response.

As seen in Figure 3.3, highly vulnerable individuals under extreme environmental stress would exhibit the most intense stress reactions. Individuals high in vulnerability but under minimal environmental stress and individuals low in vulnerability but under heightened environmental stress would exhibit moderate stress reactions. Finally, individuals with low vulnerability to stress who are under conditions of minimal environmental stress would demonstrate minor acute stress reactions, if any at all.