Endocrine Abstracts

Aging in both men and women is linked with a decline in diurnal variations in cortisol secretion. Cortisol secretion is increased during circadian nadir and possibly in total through the day. Reduced suppressibility of cortisol after dexamethasone (DEX) administration and increased ACTH secretion with aging are well documented. It appears that aging associates with the decrease in cortisol negative feedback efficacy on HPA axis due to underexpression of mineralocorticoid receptors (MRs) and imbalance of MRs to glucocorticoid receptors (GRs) in hippocampus (HC). Chronically elevated glucocorticoids (GCs) in mice, but not in the other species, lead to neuronal cell loss in the HC. In contrast to these results, an age-related decline in peripheral cortisol values from 30 to 60 years of age within the obese subjects has been observed. This may be explained by emotional eating which reduce HPA axis activity by CRF suppression. No such correlation was found in healthy individuals with normal body-mass-index (BMI). It seems that ‘healthy’ aging does not lead to enhanced HPA axis activity and peripheral cortisol levels rather decline with aging. Parental regulation of hippocampal GR expression as well as the priming effect of high GC concentrations on the future responses to stressors imprint life history through epigenetic changes within HC. Additionally, men and women tend to react differently with stress–both psychologically and biologically. Clinical significance of reduced adrenal androgen production (DHEA and DHEAS) with aging is not well established. Aldosterone secretion appears to be slightly reduced in elderly whereas sympathetic tone vary from organ to organ. Altogether aging associated changes in HPA activity only in a part depends on genetic background. Individual differences in stress reactivity might be important risk factor for gender-specific health problems in men and women.