Inflammation and stress
Most of us have learned by now that stress is not good for your health. One of the reasons is that stress can aggravate the immune system causing inflammation. Long term inflammation has been shown to cause or play a role in many diseases such as heart disease, arthritis, cancer and many other chronic diseases. Stress causes the release of chemicals in our body that can lead to inflammation. Below are summaries of research articles that show the relation between stress and inflammation.
UCLA research into stress and inflammation
Researchers from UCLA found that stress reactions can increase inflammation
in the body. For those who experience chronic stress problems, this can lead to
serious complications like heart disease, depression and asthma.
Inflammation and stress article from American Journal of Psychiatry
A recent study has shown that there is a link between stress and an overactive inflammatory response. In a study that was published in the Sep. 1, 2006 issue of the American Journal of Psychiatry, individuals with major depression were shown to have an exaggerated inflammatory response to psychological stress in comparison to those who do not have depression. These findings suggest that increased inflammatory response to stress in depressed patients may be a link between depression and other diseases, brought on by an overactive inflammatory system. Stress and the inflammatory response: a review of neurogenic inflammation.
Stress and the inflammatory response:
In response to psychological or certain physiological stressors, an
inflammatory process may occur through release of neuropeptides (especially
substance P or other inflammatory mediators) from sensory nerves and the
activation of mast cells or other inflammatory cells. Central neuropeptides,
including corticotropin releasing factor and perhaps substance P as well,
initiate a systemic stress mobilization response by activating the sympathetic
nervous system, hypothalamic pituitary axis, and the renin angiotensin system,
thus releasing stress hormones (catecholamines, corticosteroids, growth hormone,
glucagon, and renin) which, together with cytokines induced by stress, initiate
the acute phase response and the induction of acute phase proteins, essential
mediators of inflammation. CNS norepinephrine may also induce the acute phase
response by macrophage activation and cytokine release. Increase in lipids with
stress may also be a factor in macrophage activation and lipopolysaccharide
release which may induce cytokines from hepatic Kupffer cells, subsequent to an
enhanced absorption from the gastrointestinal tract during psychological stress.
The brain is capable of initiating or inhibiting the inflammatory process. The
inflammatory response is contained within the psychological stress response
which was a later development in human evolution. Moreover, the same
neuropeptides (i.e., CRF and possibly substance P) mediate both stress and
inflammation. Cytokines evoked by either a stress or inflammatory response may
utilize similar somatosensory pathways to signal the brain. Repeated episodes of
acute or chronic psychogenic stress may produce chronic inflammatory changes
which may result in atherosclerosis in the arteries or chronic inflammatory
changes in other organs as well.
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Arthritis can develop as a result of an infection. For example, bacteria that cause gonorrhea or Lyme disease can. Infectious arthritis can cause serious damage, but usually clears up completely with antibiotics. Scleroderma is a systemic disease that involves the skin, but may include problems with blood vessels, joints, and internal organs. Fibromyalgia syndrome is soft-tissue rheumatism that doesn't lead to joint deformity, but affects an estimated 5 million Americans, mostly women. The approximate number of cases in the United States of some common forms of arthritis.
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Most of the information in the site is compiled by editors from information provided by the National Institutes of Health. We are in the process of updating our pages. In the past we have not made reference to the source for information provide by our editors. In the next few weeks we hope to have all our pages marked as to the source.
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