Incidence of hypercortisolism and dexamethasone resistance increases with age among wild baboons.

While many features of the adrenocortical axis are unchanged with age in humans, there is a pattern of senescent hypercortisolism. This occurs basally, following threshold doses of dexamethasone, and in synergy with depression or Alzheimer's disease. An understanding of neuroendocrine aging is important, for both its gerontological implications, and determination of normative values for comparison with neuropsychiatric states. We have investigated whether aging is associated with hypercortisolism in a population of wild primates. The subjects were 108 yellow baboons (Papio cynocephalus) that have been under long-term study of Amboseli National Park in Kenya. Animals were anesthetized by blowgun under similar circumstances that allow for determination of basal cortisol concentrations. Sixty minutes later, 5.0 mg dexamethasone was administered to each animal, and cortisol determinations were made on serum collected immediately before administration and 6 hr later. Basal cortisol concentrations rose with age (p less than 0.028; r = 0.23). This occurred in a nonprogressive manner, in that there were no differences in concentrations among the youngest three quartiles of animals, whereas animals in the oldest quartile (older than approximately 16 years) had significantly higher values. In addition, there was a significant increase in postdexamethasone cortical concentrations with age (p less than 0.01; r = 0.31). This feature emerged progressively with age in both sexes. A number of possible artifactual causes of this senescent pattern could be eliminated, including medication confound, coincident disease, and body weight. These findings suggest that hypercortisolism and glucocorticoid feedback resistance might be general features of primate aging.