Johannes D. Veldhuis, MD


March 15, 2000

In This Article


Aging can be viewed as a stochastic process resulting from a greater disorderliness of regulatory mechanisms that results in reduced robustness of the organism to intercurrent stress and disease. The notion of greater disorderliness in aging is illustrated by the erosion of the orderly neuroendocrine feedback regulation of the secretion of LH, FSH, ACTH, and GH. These changes are manifested as menopause, andropause, adrenopause, and somatopause. Aging-related disruption of metabolic processes is associated with a higher prevalence of diseases such as type 2 diabetes and cancer in older individuals.

Although the dysregulation of neurohormone outflow from the CNS constitutes one of the earliest measurable facets of endocrine aging, many questions remain to be answered by aging research. What is the exact mechanism of CNS integrative failure? To what degree does peripheral endocrine gland insufficiency (eg, testis, ovary) contribute to disruption in the aging feedback-axis (eg, GnRH-LH)? What gender differences underlie the neuroendocrine changes that occur with aging? What is the contribution of the neuroregulatory alterations to the risk of frailty and/or eventual disability?