Introduction

Researchers in the health field are increasingly inclined to attribute the development of chronic disease in part to prolonged exposure to aspects of the environment that we find stressful or challenging. Epidemiological data unequivocally show that psychosocial factors have a substantial influence on the development of chronic illness, often as great or greater than traditional biological risk factors. However, the mediators of the stress-disease relationship remain poorly specified, though a clearer picture has emerged over the past few decades.

In the broadest sense, the perturbations in various biological measures, occasioned by chronic exposure to stressful situations, will ultimately lead to a dysregulation of those biological systems, and these, over time, may be implicated in the development of heart disease or cancer or rheumatoid arthritis, or any number of chronic illnesses. Given the need to cope with stress and to strive to overcome the barrage of obstacles and frustrations most of us encounter in the 21st century, the relevant biological systems may have little chance to shut off and give the vegetative systems a chance to perform their housekeeping chores.

Department of Biobehavioral Health, The Pennsylvania State University, 315 Health and Human Development East, University Park, PA 16802, USA e-mail: [email protected]

One means of studying the mechanisms that underlie the stress-disease relationship is by examining the attributes of a particular stressor on the biological measures of interest. For example, were one interested in the acute effects of negative marital interactions on heart rate, he or she might compare dyads based on their levels of social support (a self-selected grouping) or couples exposed or not exposed to an anger management intervention (an experimental strategy). In this particular study one would measure heart rate - a continuous measure - throughout the baseline and stressor phases.

Most studies of the evaluation of the effects of stress on physiological responses are similar in structure. First, the biological parameter of interest - blood pressure, perhaps, or cortisol, or markers of inflammatory responses - is assessed while the subject is resting, to establish a baseline, or comparison, level. Next, the subject is exposed to a presumed stressor ("stressor" is an ambiguous and broad term that might include a challenging task, an arousal of anger, a foot placed in an ice-water bath, and many others) and the physiological parameter(s) of interest are assessed during the exposure. The difference between the baseline and stressor levels has been labeled the "reactivity" to the stimulus. Often, a third phase will be employed in which the subject is allowed to rest following the stressor to provide a measure of "recovery" of the parameter to pre-stress levels (Fig. 41.1).

The structure of the typical study is simple and straightforward. However, as is often the case, the devil is in the details. How should baseline best be measured? Should the subject be

A. Steptoe (ed.), Handbook of Behavioral Medicine, DOI 10.1007/978-0-387-09488-5_41, © Springer Science+Business Media, LLC 2010

Phase In Study

Baseline

Stress

Recovery

" " " JMeaS^ements

Time

Fig. 41.1 Schematic representation of a typical psychophysiological stress study protocol

Time

Fig. 41.1 Schematic representation of a typical psychophysiological stress study protocol sitting up or prone? Allowed to read magazines, or even to fall asleep? Which stressor is going to be administered: Does it matter? If one is going to have the subject count backwards by 13s - a common laboratory task - should the experimenter harass the subject during the task? Should the task be made easier for subjects who cannot perform the arithmetic at all? Why mental arithmetic rather than a Stroop color-naming task, or an interpersonal stressor, or any number of other stimuli that can be used to provoke a physiological response?

For the most part, the stress-reactivity model was limited in earlier years to blood pressure, heart rate, and serum catecholamines. However, it is clear that several biological systems, including but not limited to the cardiovascular system, the hypothalamic-pituitary-adrenal axis, and the immune system, are implicated as mediators of stressor effects on chronic illness. An important advance over the past two or so decades has been the expansion of the stress-reactivity model to include a broader array of outcomes than heretofore tended to be assessed, illustrating the interdisciplinary nature of this research.

The aim of this chapter is to provide an introduction to the methodology by which the effects of stress on physiological outcomes are assessed. This chapter focuses on the independent variables rather than the outcomes; other chapters will go into detail concerning the specifics of various dependent measures.

However, the specifics of measurement of particular outcomes do not, as a rule, change the essential model. Rather, they call for adjustments in subtle aspects of the procedures. Reference to cardiovascular outcomes will be common in this chapter, as much of what we know in the laboratory was learned in studies of stressor effects on heart rate and blood pressure.

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