“Protection and Damage from Acute and Chronic Stress”

If there is a failing in the article, “Protection and Damage from Acute and Chronic Stress,” it lies in the fact that the author failed to pay much attention to life stages of the stressed organism. One of the more interesting findings reported recently on the Web site ScienceDaily.com was that early life stresses, at least in mice, can lead to later cognitive impairment, while giving a selective serotonin reuptake inhibitor such as Prozac can dramatically improve adult animals’ adaptability to new stimuli. The report concluded that the two studies “point to exciting new approaches for potentially lessening or preventing these long-term changes that can lead to disease or psychopathologies” (ScienceDaily November 3, 2004).

Another mouse study also looked at the later effects of early stressors, in this case, prolonged separation of mother and offspring during the first two weeks of life. The researchers found that such an event “altered immune, endocrine and behavioral responses to acute ‘Theiler’s virus’ infection in mice” (Science Daily October 1, 2004).

This study is notable in that it traces the development of later chronic disease that mimics human multiple sclerosis to this early stress event.

The end of life is also ignored by McEwen. There, too, studies have found that there is an association between stress, in this case, particularly oxidative stress in the pathogenesis of Alzheimer’s Disease (AD) lesions (Baum and Stein 1995, 11). The same metabolic byproduct, the free radicals-a product of metabolic dysfunction-are present in the AD and in atherosclerosis. On this point, McEwen does offer some solid information: Atherosclerosis is also a result of metabolic dysfunction caused by stress (2004, 4).

However, McEwen is much more well-rounded in terms of assessing the protection and damage caused by stress. For example, McEwen has “shown that stress hormones produced by the adrenal gland can enhance immune function in rats. These findings further show that hormones released during an acute stress response may help prepare the immune system for a potential challenge, such as wounding or infection, with stress perception by the brain serving as an early warning signal” (Bonner 1999).

Effects of acute and chronic stress.

It is possible that stress can be relatively neutral. In experiments with exposing dogs to stressful conditions, including administration of saline infusions, researchers discovered in the 1980s that when stress and saline were discontinued, the blood pressure that had risen receded, and no pathological change in hypertension was recorded in the test animals. “Although one may speculate that longer exposure might lead to a permanent state of hypertension, the fact remains that we still do not have a clear-cut demonstration of chronic hypertension produced by a stress paradigm” (Shapiro 1996, 18).

That may have been true in 1996, but in 2004, McEwen reported a connection- a connection, moreover, that is attended by a constellation of other factors that seem to be the result of excessive stress. McEwen noted that acute stress may promote immune function “by enhancing movement of immune cells to places in the body where they are needed to defend against a pathogen; yet, chronic stress suppresses the immune function and uses the same hormonal mediators to suppress immune function” (2004, 3).

Abdominal obesity is a central concept regarding the transition of useful stress, the sort that helps protect against disease pathogens, to damaging stress, or the sort of stress that enhances the ability of the body to create disorders such as, notably, high blood pressure (hypertension), and other cardiovascular damage. McEwen explains it all in terms of states called allostatic and homeostatic states. The homeostatic state is concerned with those systems essential to life. And the allostatic state, on the other hand, “results from an imbalance of the primary mediators” of the metabolism.


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