and physiological features of a heart attack, including chest pain, abnormalities on the electrocardiogram, and elevated cardiac enzymes (reflecting damaged heart muscle) (2). The condition has variously been termed takotsubo cardiomyopathy, left- ventricular apical ballooning, myocardial stunning, stress cardiomyopathy, or in the more vernacular parlance of the New York Times, broken heart syndrome (prompted by a medical review that was published just before Valentine’s Day). In general accord with the speculation of Cannon, broken heart syndrome appears to be triggered by an exaggerated autonomic nervous system response, characterized by sympathetic activation and high levels of the stress hormone epinephrine (adrenalin) (3). It is important to note in these cases that psychological states, as mild as they may be, are able to induce a clear and demonstrable organ pathology.
Physiological abnormalities or dysfunctions underlie medical conditions, and indeed, constitute the defining features of disease states. An important question, however, is how those dysfunctions come to be. There are many ways in which disease develops — traumatic injuries, biotic infections, degenerative conditions — and the list goes on. The fields of psychophysiology, psychosomatic or behavioral medicine, and health psychology are particularly concerned with how psychological and behavioral factors impact physiological systems and thus health. Of particular interest are those psychological dimensions that uniquely impact
physiology. An example comes from the
study of Herpes Simplex viral infections. Herpes Simplex viruses are responsible
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for cold sores (HSV type I) and genital herpes (HSV type IT). Once contracted, herpes virus infections generally remain for life, although they are characterized by periodic eruptions and remissions. During the latter, the immune system effectively dampens viral activity and the virus retreat to a more or less dormant state. Although multiple factors likely contribute to the reactivation of HSV, one trigger appears to be stress— the defacing cold sore that erupts, for example, just before the prom or an important date. Ohio State researchers sought an animal model of this reactivation, so the underlying links and mediators could be studied. Try as they might, however, the research group was unable to reactivate HSV infections in mice with standard laboratory stressors, such as restraint-stress or shock. In a collaborative effort, we pointed out that the stressors that lead to HSV reactivation in humans were often of a social nature. Indeed, for both humans and mice, social relations are central to happiness, adaptation and even survival. In light of this, a social stressor was introduced into the project (changing the housing groupings and thus disrupting established social relations). The social stress, but again not physical stressors, resulted in significant HSV reactivation (4). Psychological factors, and in this case a specific social psychological variable, uniquely impacted an important aspect of viral immunity. This early finding led to a series of studies that have elucidated physiological pathways that mediate the relationship between social stress, immune function and HSV reactivation. But, what is it that makes social stress unique and distinct from physical stressors?
We have identified a probable general contributor to the differences
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