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.
It is apparent that when one is speaking about stress and its effect on the body, processes seem to proceed in circular fashion. For example, the nervous system regulates the physiological and behavioral responses to stresses, and yet the brain is a "target of the mediators of those responses through circulating hormones" (McEwen 2004, 4). Body fat again comes into play because one of the coping methods the brain uses is 'comfort foods' which temporarily reduce the stress. On the other hand, while comfort foods appear to reduce anxiety, "inactivity that may accompany the stressors or depression that caused the reach for comfort foods may result in chronically elevate glucocorticoids, which in turn may have resulted from the intake of the comfort food or poor sleep from inactivity or ongoing stress. In any case, insulin levels increase. Along with the glucocorticoids, the promote the deposition of body fat....which promotes the deposition of plaque in the arteries and, putatively, in the brain as well. This leads to more psychological 'events' that may lead to more behaviors that lead to higher insulin levels...and so on. 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 allostatic state, on the other hand, "results form an imbalance of the primary mediators" of the metabolism. These mediators include hormones of the hypothalamo-pituitary-adrenal (HPA) axis, catecholmines and cytokines. All these 'mediators' react with each other to create a "network of reciprocal effects" (McEwen 2004, 3). lso 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
Some common words found in the essay are:
Baum Stein, Chronic Stress, ScienceDaily November, Daily October, blood pressure, chronic stress, immune function, , mcewen 2004, comfort foods, Disease AD, shapiro 1996 18, behavioral responses, stress hormones, memory learning, 2004 3, shapiro 1996, acute chronic stress,
Approximate Word count = 1451
Approximate Pages = 6 (250 words per page double spaced)
|