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During
the past century, life expectancy at birth has increased substantially.
A cost of this
increase in longevity is a greater incidence of diseases of aging. It is possible that age-related increases in morbidity and mortality reflect the progression of disease processes that take decades to reach clinical manifestation. Alternatively chronic diseases may be consequences of biological aging, or the progressive decline in physiologic ability to meet environmental demands. Of recent interest is determining why some individuals appear to age more quickly, and thus succumb to chronic diseases of aging earlier than others. One factor that has been proposed to contribute to vulnerability to a range of age-related chronic diseases is psychosocial and/or environmental stress. Stress has been linked with increased all cause morbidity and morality and has been hypothesized to contribute to overall aging of the organism. Evidence from observational studies in humans supports a link between chronic psychosocial stress and decreased telomere length and telomerase activity, both molecular level markers of cellular aging. Chronic psychosocial stress also has been associated with increased oxidative stress, which may be an underlying cause of many aspects of aging. Findings from animal research suggest that stress is reliably associated with enhanced macrophage function, which may provide a pathway to increased oxidative stress and thus cellular aging. To date, no study has reported the effects of an acute laboratory stressor on telomerase activity, oxidative stress, or macrophage function in humans. The primary goal of the proposed study is to expand upon existing research on chronic stress and biological aging by examining whether exposure to |
| . | acute laboratory
stress is associated with changes in two markers of biological aging,
telomerase activity and oxidized lipids and a related immunological factor, macrophage function. We hypothesize that exposure to an acute laboratory stressor will be associated with decreased telomerase activity, increased oxidized lipid levels and increased macrophage function.
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| Revised 9/30/2007 la/tc |
