content-documents/house-oversight-nov/07/HOUSE_OVERSIGHT_021298.md

---
title: "House Oversight: Estate Documents (Nov 12) (HOUSE_OVERSIGHT_021298)"
source: "House Oversight: Estate Documents (Nov 12)"
sourceUrl: "https://www.justice.gov/epstein"
date: "2026-01-01"
category: "House Oversight"
eftaNumber: "HOUSE_OVERSIGHT_021298"
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externalUrl: "https://ep-nov-12.greg.technology"
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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 II). 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
HOUSE_OVERSIGHT_021298