Sex Differences In Cortisol Response Research Articles

Sex differences in cortisol response to corticotropin releasing hormone challenge over puberty: Pittsburgh Pediatric Neurobehavioral Studies

Consistent sex differences in regulation of the hypothalamic pituitary adrenocortical (HPA) axis have been shown in animal models and emerge over puberty. However, parallel work in humans is lacking despite implications for elucidating the emergence of sex differences in depression over puberty. We investigated sex differences in HPA response to corticotropin releasing hormone (CRH) challenge over puberty in a carefully screened normative sample. Participants were 68 healthy children (41% girls), ages 6-16, with no personal or family history of psychiatric disorder. Pubertal maturation was determined by Tanner staging. Following 24h of adaptation, 9-10 plasma cortisol samples were collected over 30-40 min pre-infusion baseline, 1 μg/kg CRH infusion, and 90-180 min post-infusion recovery. Thirty-seven participants completed 2+ CRH challenges allowing inclusion of cross-sectional and longitudinal data in all analyses. The influence of gender and pubertal maturation on parameters of cortisol response to CRH challenge was investigated using nonlinear mixed model methodology. Girls showed increasing total cortisol output following CRH challenge over puberty, while boys showed little change in total cortisol output over puberty. Increased cortisol output in girls was explained by slower reactivity and recovery rates leading to prolonged time to reach peak cortisol and delayed return to baseline over puberty. Girls also showed increasing baseline cortisol over puberty, while boys showed declining baseline over puberty. Results reveal subtle normative sex differences in the influence of pubertal maturation on HPA regulation at the pituitary level. This normative shift may tip the balance towards stress response dysregulation in girls at high risk for depression, and may represent one potential mechanism underlying elevated rates of depression among pubescent girls.

Sex differences in cortisol response to reboxetine

This study examined the cortisol response to reboxetine in a sample of healthy men and women. Forty healthy volunteers were randomly allocated to one of two treatment groups: placebo or 4 mg reboxetine under double-blind conditions. Saliva cortisol was measured pre, 1 and 1.5 h post-treatment. Mood and side-effects were also measured. A single oral dose of 4 mg reboxetine did not affect positive or negative mood but did produce some side-effects. It was also sufficient to increase cortisol release 1.5 h post-treatment compared to placebo. In addition, reboxetine lead to a significantly increased cortisol release in male compared to female volunteers. The results suggest that healthy male volunteers are more responsive to challenge with a noradrenergic compound than females.

Sex differences in cortisol response to noxious stress

Objectives Evidence has accumulated that men and women show different responses to noxious stimuli, with women exhibiting greater sensitivity to pain than men. Data concerning sex differences in cortisol response patterns have revealed inconsistent results so far. The purpose of the present study was to examine sex differences in subjective pain and cortisol response to a noxious stressor. Methods Seventy-six subjects (39 male and 37 female) were investigated by a modification of the cold pressor test that consisted of intermittent immersion of the hand into ice water (plunge test, PT). The PT was conducted twice, in consecutive trials, to guarantee a sufficient exposure to the noxious stressor for eliciting cortisol responses. In each trial, tolerance time and pain ratings visual analog scale (VAS) were assessed. Seven saliva samples (c1-c7) were collected to determine cortisol levels at baseline (c1-c2), directly before (c3) and 20 minutes after noxious stress (c4), and during recovery period (c5-c7). Results We found no significant sex differences in tolerance time in trial 1, but highly significant differences in tolerance time in trial 2, with higher tolerance times in men. No significant sex differences were found for the VAS ratings of pain intensity and unpleasantness in the 2 trials. In contrast, a significantly larger cortisol increase in men was observed compared with women. Analysis of covariance revealed that this result could not be attributed to sex differences in cortisol level at baseline and in tolerance time. Discussion The present study demonstrates that men show a larger cortisol response to a noxious stressor than women that is not attributable to sex differences in subjective pain. The conclusion of a causal relation between larger cortisol responses and higher pain tolerance thresholds in men is tempting but yet speculative.

Consistent sex differences in cortisol responses to psychological stress.

In four independent studies, sex differences in cortisol responses to psychological stress were investigated in healthy adolescents and adults (total n = 153). Public speaking and mental arithmetic in front of an audience (Studies 1-3) reliably induced increases in free cortisol levels in both sexes with 2- to 4-fold increases above baseline levels. Mean cortisol responses were 1.5- to 2-fold higher in men compared with women. In Study 3, cortisol profiles were additionally investigated after human corticotropin-releasing hormone (h-CRH) and bicycle ergometry until exhaustion. Here, both sexes showed very similar adrenocortical responses. Furthermore, men showed elevated cortisol levels in anticipation of the psychological stress situation without actually having to perform the tasks (Study 4). Under this condition cortisol concentration was unchanged or decreased in women. From these data we conclude that the observed sex difference does not reflect an overall lower responsiveness of the female adrenal cortex. Although these studies do not provide conclusive data, we suggest sex differences in cognitive and/or emotional responses to distressing psychosocial situations which in turn may influence cortisol secretion.