Decline In Cortisol Levels Research Articles

Response of the pituitary-adrenal axis to hypoglycemic stress in women with the polycystic ovary syndrome.

The role of the adrenals in the polycystic ovary syndrome (PCOS) is debated. Both single steroid-converting enzyme abnormalities and increased adrenal activity have received support. The conventional Synacthen test using pharmacological doses of ACTH results in unphysiological levels of ACTH. Therefore, we used insulin-induced hypoglycemia (0.15 IU/kg BW) to asses the responses of ACTH, cortisol, pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and androstenedione in 18 women with PCOS and in 17 normal women of similar age and body mass index. The blood glucose concentration at 30 min was 2 mmol/L or less in all women, i.e. well below the threshold of the hormonal counterregulatory response. The women with PCOS showed a lower ACTH response, expressed as the maximum increment above basal [mean (95% confidence interval): PCOS, 11.1 (6.9-15.3); controls, 19.9 (13.8-26) pmol/L; P < 0.05], but a quantitatively comparable [PCOS, 207.2 (148.5-266.5); controls, 167.1 (100.6-233.2) nmol/L; P = NS] and more prompt cortisol response than the controls (by chi2 test, P < 0.05), resulting in a higher molar ratio between the maximum increments of cortisol and ACTH [PCOS, 13.9 (8.7-19); controls, 8.8 (5.7-12); P < 0.05]. The women with PCOS did, however, show a more rapid decline in cortisol levels than the controls (P < 0.05 at 120 and 180 min). The responses of the androgens and intermediate adrenal steroids were similar in women with PCOS and controls. The findings suggest an adaptation to increased adrenal reactivity to endogenous ACTH in women with PCOS. Exposure to hypoglycemia as a model of stress was not followed by hypersecretion of adrenal androgens and revealed no signs of steroid enzyme disturbances in women with PCOS.

Age-dependent decline in cortisol levels and clinical manifestations in patients with ACTH-independent Cushing's syndrome.

Adrenocortical cells change with age in both subcellular morphology and level of steroidogenesis. This study evaluates the influence of aging on hypercortisolism and clinical manifestations in patients with ACTH-independent Cushing's syndrome due to a cortisol-secreting adrenal adenoma (CS). Restrospective study. Thirty-six (33 females and 3 males) with CS. 31 healthy controls were age- and sex-matched to CS patients. Patient age at diagnosis was compared to the degree of hypercortisolism and clinical manifestations. The degree of hypercortisolism was estimated using serum cortisol levels and urinary free cortisol excretion. Positive clinical manifestations were quantified using 12 symptoms and signs which resulted in a clinical score for each patient. Endogenous creatinine clearance, estimated disease duration and gender were analysed as possible factors affecting adenoma-secreated cortisol. Patient age correlated negatively with serum cortisol level (r = -0.417, P = 0.0107, n = 36) and urinary excretion of free cortisol (r = -0.613, P = 0.0002, n = 31). Analysis of Spearman's rank correlation showed that the clinical score decreased with age (rho = -0.631, P = 0.0004, n = 33). Oedema, weakness/myopathy, hirsutism, striae and psychological changes were infrequent symptoms in the elderly. Using stepwise multiple regression analysis, we estimated the clinical score (Y) by factors of serum cortisol levels (X1:nmol/l), age (X2: years of age) and gender (X3: gender; female = 1, male = 0), i.e. Y = 4.771 + 0.004 X1 - 0.064 X2 + 2.548 X3 (r = 0.743, P < 0.0001, n = 33). Results suggested that aging both suppressed cortisol secretion and repressed manifestations directly as an independent factor, although its direct effect may be weak. Our findings indicated the importance of age as a factor modulating hormonal levels and possible clinical manifestations in patients with cortisol-secreting adenomas.

Neuroticism, locus of control, type A behaviour pattern and occupational stress

The aim of this study was to investigate the relationship between individual differences in personality and susceptibility to stress in the workplace. Stress in lecturers employed by a computer training organization was assessed by means of self-report and measurement of salivary cortisol output during lecturing and non-lecturing weeks. Neuroticism, Type A behaviour pattern and locus of control were measured. Self-reported stress was found to be much greater during lecturing weeks, but cortisol levels were unaffected by working conditions. There was a significant positive correlation between neuroticism and locus of control and a negative correlation between locus of control and Type A behaviour pattern that approached significance. Multiple regression was employed to explore relations between personality and stress. Subjects with lower neuroticism scores yielded a bigger increase in reported stress, in the lecturing compared with the non-lecturing week, than subjects with high neuroticism scores. Type B subjects showed a progressive decrease in cortisol over the working week while Type A counterparts showed a resurgence of cortisol towards the end of the week. Finally, Type B subjects having an internal locus of control showed a faster decline in cortisol level during the lecturing week than the other subjects. Implications of these results are discussed in terms of the importance simultaneously incorporating a variety of individual differences in personality dimensions and stress indices in research designs.

Lymphocyte glucocorticoid receptor number in posttraumatic stress disorder

The authors' objective was to investigate the possibility that glucocorticoid receptor changes may be involved in the dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in posttraumatic stress disorder (PTSD). They measured the number of lymphocyte cytosolic glucocorticoid receptors and plasma cortisol concentrations in 15 consecutively admitted male combat Vietnam veterans with PTSD and in a normal comparison group of 11 subjects. Both the patients and the normal comparison subjects showed a morning-to-afternoon decline in glucocorticoid receptor concentrations, paralleling the normal diurnal decline in cortisol levels. The number of glucocorticoid receptors was 63% greater in the morning and 26% greater in the afternoon in the patients with PTSD than in the normal subjects. No group differences in cortisol levels were observed, nor were glucocorticoid receptor number and cortisol levels correlated. The number of morning glucocorticoid receptors was positively correlated with symptoms of PTSD and anxiety. These results provide further evidence for a dysregulation of the HPA axis in PTSD. The finding that patients with PTSD had a substantially greater number of lymphocyte glucocorticoid receptors than normal comparison subjects is consistent with the authors' previous observations of low 24-hour urinary cortisol excretion in subjects with PTSD. Furthermore, the receptor changes observed are opposite of those reported in major depressive disorder. The present data, along with other findings of HPA abnormalities in PTSD, support the possibility of a greater negative feedback sensitivity at one or more levels of the HPA axis.

Feedback from meal-related peaks determines diurnal changes in cortisol response to exercise.

Diurnal variations in cortisol response to exercise and their relation to the events of the day were assessed by comparing daily cortisol patterns on the control day and on days when exercise was performed at different times. A remarkable midday cortisol peak coincided with the noon meal, but cortisol levels were irregularly affected by an identical meal in the evening. However, the exercise produced equal increases when performed during quiescent periods (i.e. without any secretory peaks at 1000, 1430, 1700, and 2130 h), but peak levels for exercise at 2130 h were significantly lower because of the lower basal levels in the evening. When the same exercise was performed at 1300 h (i.e. coinciding with the postprandial peak), only a brief leveling-off interrupted the decline in cortisol levels. The meal-related evening peak, if any, provoked a similar decrease in response to exercise performed at 2000 h. Similarly, the midday peak itself was reduced by a prior exercise-induced cortisol rise. These results show that the daily cortisol pattern results from the interactions between the meal-related peaks, especially the major midday cortisol peak, and the exercise-induced increases, both of which inhibit the response to subsequent stimulation. The identical responses to exercise at the different quiescent periods tested, despite a general downward trend in basal cortisol levels, establish the primacy of such feedback mechanisms over those responsible for the circadian rhythm.