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, free radicals-a product of metabolic dysfunction-are present in 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.