Exposure to stress activates both the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). A growing body of research points to the contribution of sex hormones (testosterone, estrogen, and progesterone), the end products of the hypothalamus-pituitary-gonadal (HPG) axis, in modulating stress reactivity. The present study aimed at investigating the potential modulating role of sex hormones on HPA and SNS reactivity to psychosocial stress. The reactivity, induced by the Trier Social Stress Test, was analyzed by measuring the levels of cortisol and alpha-amylase (markers for SNS activity) in four saliva samples each of 21 men and 37 women (17 not using oral contraceptives and in their luteal phase, and 20 women using oral contraceptives). In addition, basal sex hormones were sampled prior to the psychosocial stress exposure. Results revealed that controlling for testosterone, estrogen, and progesterone diminished the impact of stress on cortisol reactivity and on alpha-amylase reactivity. Moreover, controlling for sex hormones also diminished the differential pattern of cortisol reactivity in each experimental group among responders. Furthermore, correlation analyses revealed differences between groups in the association between sex hormones and alpha-amylase. The present findings indicate a modulatory role for sex hormones in HPA and SNS reactivity and emphasize the need for control of sex hormone fluctuations when examining cortisol and alpha-amylase reactivity to stress.

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The possible effects of stress and neurobiological stress mechanisms on visuospatial abilities remain largely unknown. In the current study, we examined the combined effect of sex hormones and both the hypothalamic–pituitary–adrenal axis (HPA-A) and the sympathetic nervous system (SNS) on stress-induced changes in visuospatial performance. A total of 107 participants completed a mental rotation task and were subsequently exposed to either to the Trier social stress test (TSST) or to a control condition before completing the mental rotation task again. HPA-A and SNS reactivity of the participants were evaluated by measuring salivary alpha amylase (sAA; an SNS activation marker) and cortisol in four saliva samples. Pre-stress levels of sex hormones (progesterone, estradiol, and testosterone) were also measured. The TSST enhanced mental rotation performance, and this enhancement was negatively correlated with baseline estradiol levels and positively correlated with the level of cortisol reactivity among men. In addition, controlling for baseline levels of testosterone, estradiol, and progesterone diminished this effect of stress. These results imply that the stress-induced facilitation of mental rotation performance is modulated by baseline sex hormones and provide preliminary support to the notion that a complex interaction between sex hormones and neuroendocrine stress mechanisms mediates the influence of stress on visuospatial performance.

Procrastination is prevalent among students, as well as the general population, and has negative impacts on various domains. Several models aimed to understand factors associated with procrastination, with some suggesting that anxiety plays a significant role. Biological factors have been shown to contribute to individual differences in procrastination; however, little attention has been paid to the role of neuroendocrine factors on procrastination. The primary question addressed in the present study is whether neuroendocrine factors (testosterone and cortisol) moderate the association between state anxiety and procrastination. Eighty-eight participants (29 men; 32 women using oral contraceptives; and 27 women not using oral contraceptives and in their luteal phase) were tested for biomarkers and completed questionnaires. Results show that state anxiety is positively correlated with procrastination. Furthermore, testosterone levels moderate the correlation between state anxiety and procrastination. As testosterone levels drop, the positive correlation between state anxiety and procrastination becomes stronger, but when testosterone levels are higher, no significant association between state anxiety and procrastination is found. Cortisol levels do not moderate the relationship between state anxiety and procrastination. The role of neuroendocrine factors for psychological outcomes is discussed.

The recommended fixed dosage of betamethasone for pregnancies at risk of preterm birth was determined in the 1970s, regardless of gestational age (GA), number of fetuses, and maternal weight. We aimed to examine the association between maternal and neonatal betamethasone serum levels and neonatal respiratory distress syndrome (RDS) and to examine whether levels correlate with maternal weight, GA, or number of fetuses. A prospective study was conducted at a single academic medical center between August 2016 and February 2019. Women received betamethasone and delivered between 28+0 and 34+6 weeks were included. Maternal serum levels (MSLs), and neonatal serum levels (NSLs) of betamethasone at delivery were analyzed using Corticosteroid enzyme‐linked immunosorbent assay kit. RDS was diagnosed according to clinical and radiographic findings. We assumed that the sensitivity of NSLs to detect RDS is 95%; hence, 150 neonates were needed (power 80%, alpha 0.05). Overall, 124 women were included; including 96 (77.4%) singletons, 26 (21.0%) twins, and 2 (1.6%) triplets, corresponding to 154 neonates. RDS was diagnosed in 35 neonates (22.7%). After adjusting for GA, time elapsed from the last dose, and number of doses, NSLs were associated with RDS (relative risk: 0.97, 95% confidence interval: 0.94–0.99, p = 0.011). A level of 6.00 ng/ml predicted RDS with a sensitivity of 80.0% and specificity of 64.7%. Adjusted MSLs were not associated with RDS. Both maternal and neonatal serum levels were not associated with the number of fetuses and maternal weight. In conclusion, NSLs are associated with RDS whereas MSLs are not.