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ScienceDaily (Aug. 27, 2008) Most people
would agree that stress increases your risk for
illness and this is particularly true for severe
long-term stresses, such as caring for a family
member with a chronic medical illness.
However, we still have a relatively
limited understanding of exactly how
stress contributes to the risk for
illness. In the August 15th issue of
Biological Psychiatry, researchers
shed new light on one link between
stress and illness by describing a
mechanism through which stress
alters immune function.
In a very promising preliminary study,
Miller and colleagues found that the
pattern of gene expression differed
between caregivers of family
members with cancer relative to a
matched group of individuals who did
not have this type of life stress. They
found that among the caregivers,
even though they had normal cortisol
levels in their blood, the pattern of
gene expression in the monocytes, a
type of white blood cell involved in
the body's immune response, was
altered so that they were relatively less responsive to the
anti-inflammatory actions of cortisol, but relatively more
responsive to pro-inflammatory actions of a transcription factor
called nuclear factor-kappa B, or NF-!B.
Gregory Miller, Ph.D., corresponding author, explains more
simply that, although "caregivers have similar cortisol levels as
controls, their cells seem to be 'hearing' less of this signal. In
other words, something goes awry in caregivers' white blood
cells so they are not able to 'receive' the signal from cortisol
that tells them to shut down inflammation."
Thus, the current findings might help to explain why the
caregivers would seem to be in a chronic pro-inflammatory
state, a condition of immunologic activation. This activated
state could contribute to the risk for a number of medical
illnesses, such as depression, heart disease, and diabetes. Dr.
Miller remarks that part of the importance of these findings is
"because people have traditionally thought that higher cortisol
is the reason that stress contributes to disease, but this work
shows that, at least in caregivers, it's actually the opposite -
there's too little cortisol signal being heard by the cells, rather
than too much."
However, many important related questions still remain
unanswered, as noted by John H. Krystal, M.D., Editor of
Biological Psychiatry and affiliated with both Yale University
School of Medicine and the VA Connecticut Healthcare
System. He comments that in addition to not knowing how
stress produces these altered patterns of gene expression in
the immune system, "we don't know how to account for the
resilience of some stressed people exposed to severe
sustained stress or the vulnerability of some people to
relatively mild stress." He adds that "the better that we
understand the underlying molecular mechanisms that link
stress to illness, the more likely we are to make progress in
answering these important questions," and this article is
certainly a vital step in that direction.
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Chronic Stress Alters Our Genetic Immune Response
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Chronic Stress Alters Our Genetic Immune Response http://www.sciencedaily.com/releases/2008/08/080827100816.htm
1 of 2 2012-01-06 2:23 PM
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Story Source:
The above story is reprinted from materials provided by
Elsevier, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For
further information, please contact the source cited above.
Journal Reference:
Miller et al. A Functional Genomic Fingerprint of Chronic
Stress in Humans: Blunted Glucocorticoid and
Increased NF-!B Signaling. Biological Psychiatry, 2008;
64 (4): 266 DOI: 10.1016/j.biopsych.2008.03.017
1.
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/080827100816.htm
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Chronic Stress Alters Our Genetic Immune Response http://www.sciencedaily.com/releases/2008/08/080827100816.htm
2 of 2 2012-01-06 2:23 PM

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