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The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis AS RECENTLY as 1900, tuberculosis, influenza, and pneumonia were the leading causes of death in our country (1). For the most part, however, these infectious diseases, as well as those of poor hygiene or undernutrition, no longer plague us. Instead, we succumb most frequently to heart disease and cancer, diseases of slow degeneration (1). Most of all, unlike so many in the generations before us, we are in a position to age. Regardless of what else occurs, we age, we become more constrained by the discrepancy between what we were and what we have become, and each step becomes harder. The goal in the study of aging is not to halt the process, because we can no more be cured of aging than of birth. The goal, instead, is to slow and soften the sharpest edges of the biological unraveling that constitutes aging. Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stress to cumulatively damage aging tissue. This content is only available as a PDF. Author notes * The studies described were made possible by a predoctoral grant from the National Institute on Aging (to R.M.S.). † Mathers Fellow of the Life Sciences Research Foundation. Copyright © 1986 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Endocrine Reviews Oxford University Press

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

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Publisher
Oxford University Press
Copyright
Copyright © 1986 by The Endocrine Society
ISSN
0163-769X
eISSN
1945-7189
DOI
10.1210/edrv-7-3-284
Publisher site
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Abstract

AS RECENTLY as 1900, tuberculosis, influenza, and pneumonia were the leading causes of death in our country (1). For the most part, however, these infectious diseases, as well as those of poor hygiene or undernutrition, no longer plague us. Instead, we succumb most frequently to heart disease and cancer, diseases of slow degeneration (1). Most of all, unlike so many in the generations before us, we are in a position to age. Regardless of what else occurs, we age, we become more constrained by the discrepancy between what we were and what we have become, and each step becomes harder. The goal in the study of aging is not to halt the process, because we can no more be cured of aging than of birth. The goal, instead, is to slow and soften the sharpest edges of the biological unraveling that constitutes aging. Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stress to cumulatively damage aging tissue. This content is only available as a PDF. Author notes * The studies described were made possible by a predoctoral grant from the National Institute on Aging (to R.M.S.). † Mathers Fellow of the Life Sciences Research Foundation. Copyright © 1986 by The Endocrine Society

Journal

Endocrine Reviews – Oxford University Press

Published: Aug 1, 1986

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