Depressive disorders are common mental health problems during adolescence. Many adolescents with depression describe difficulties with sleeping. Findings of previous studies regarding changes in objective sleep quality in adolescents with depressive disorders are heterogeneous.

This study aims to investigate differences in objective and subjective sleep quality between adolescents with depressive disorders and healthy peers, and to evaluate if potential changes in sleep occur concurrently with changes in the release of cortisol and alpha-amylase after awakening.

This non-interventional parallel study examines correlations between depressive disorders, sleep quality and release of stress hormones. Sleep quality in the past 2 weeks, severity of depressive symptoms, psychiatric comorbidities and stress response of 30 adolescents with depressive disorders and 30 healthy controls (N = 60) are assessed via questionnaires. In participants’ home environments, the objective sleep quality of seven consecutive nights is measured by sleep accelerometry. After awakening, participants answer sleep questionnaires to examine the subjective sleep quality of those nights. Furthermore, salivary cortisol and alpha-amylase are measured three times after awakening (+0 min, +30 min and +45 min after awakening).

Sleep is an important factor for prognosis and well-being in adolescents with depression. The results of this study can be highly valuable to integrate a more detailed examination of sleep quality and sleeping impairments in the treatment of adolescent depressive disorders.

Despite evidence of links between depression and violent outcomes, potential moderators of this association remain unknown. The current study tested whether a biological marker, cortisol, moderated this association in a longitudinal sample of adolescents.

Participants were 358 Dutch adolescents (205 boys) with a mean age of 15 years at the first measurement. Depressive symptoms, the cortisol awakening response (CAR) and violent outcomes were measured annually across 3 years. The CAR was assessed by two measures: waking cortisol activity (CAR area under the curve ground) and waking cortisol reactivity (CAR area under the curve increase). Within-individual regression models were adopted to test the interaction effects between depressive symptoms and CAR on violent outcomes, which accounted for all time-invariant factors such as genetic factors and early environments. We additionally adjusted for time-varying factors including alcohol drinking, substance use and stressful life events.

In this community sample, 24% of adolescents perpetrated violent behaviours over 3 years. We found that CAR moderated the effects of depressive symptoms on adolescent violent outcomes (βs ranged from −0.12 to −0.28). In particular, when the CAR was low, depressive symptoms were positively associated with violent outcomes in within-individual models, whereas the associations were reversed when the CAR was high.

Our findings suggest that the CAR should be investigated further as a potential biological marker for violence in adolescents with high levels of depressive symptoms.

Stress is an event that threatens homoeostasis and thus causes physiological and behavioural responses to reinstate equilibrium. Excessive and/or chronic stress can be psychologically and physiologically detrimental. Examinations can represent a significant source of stress for students. The hypothalamic–pituitary–adrenal axis (HPA) is the core endocrine stress system. Investigations into the HPA response to examinations have yielded inconsistent results. The aim of this study is to further explore the relationship between examination stress, HPA axis activity, mood, sleep and exercise in students undergoing a naturalistic examination period stressor.

In total, 16 medical students participated. Students completed self-reported stress, anxiety, mood, sleep and physical activity questionnaires, and provided saliva samples during an examination-free period and an examination period 1 month later. The cortisol awakening response, representative of HPA activity, was determined from saliva samples by enzyme-linked immunosorbent assay.

Anxiety levels increased (p=0.04) and mood decreased (p=0.05) during the examination period. There was concomitant decease in physical activity levels (p=0.02). There was no significant increase in HPA activity during the examination period (p=0.29). Sleep quality did not significantly worsen (p=0.55) during the examination period.

Examination periods are associated with increased anxiety levels, lower mood and decreased physical activity. Future studies incorporating examination results and cognitive function may help to identify potential protective interventional strategies, while optimising performance.

Animal studies suggest that maternal separation is associated with alterations in the hypothalamic–pituitary–adrenal (HPA) axis through effects that occur in a critical period following birth. Evidence for an association of the diurnal cortisol rhythm with maternal separation in humans is equivocal.

We examined whether maternal separation in childhood is associated with diurnal cortisol pattern in 3712 middle-aged men and women. Two aspects of cortisol release were examined: the cortisol awakening response (CAR) and the diurnal slope in cortisol throughout the day.

Maternal separation in childhood was reported by 12% of participants. Those participants who reported maternal separation had a larger CAR and flatter slopes in cortisol levels compared to those who did not report maternal separation [adjusted mean CAR in those reporting no separation versus separation: 7.1, 95% confidence interval (CI) 6.7–7.5 v. 8.4, 95% CI 7.3–9.5, p = 0.02, corresponding to adjusted mean diurnal slope: −0.129 (95% CI −0.130 to −0.128) v. −0.126 (95% CI −0.128 to −0.124), p = 0.01]. In participants who reported maternal separation, the age of separation was not associated with either cortisol measure (p = 0.11). The association between maternal separation and slope in cortisol secretion was largely explained by smoking behaviour and marital status at the time of sample collection whereas that of the CAR was explained by childhood psychosocial, material factors and adult health behaviours.

Our findings suggest that maternal separation in childhood is associated with alterations in the diurnal cortisol pattern in middle age. These associations are predominantly accounted for by adult circumstances and behaviours.

The cortisol awakening response (CAR) has been shown to predict major depressive episodes (MDEs) over a 1-year period. It is unknown whether this effect: (a) is stable over longer periods of time; (b) is independent of prospective stressful life events; and (c) differentially predicts first onsets or recurrences of MDEs.

A total of 270 older adolescents (mean age 17.06 years at cortisol measurement) from the larger prospective Northwestern-UCLA Youth Emotion Project completed baseline diagnostic and life stress interviews, questionnaires, and a 3-day cortisol sampling protocol measuring the CAR and diurnal rhythm, as well as up to four annual follow-up interviews of diagnoses and life stress.

Non-proportional person-month survival analyses revealed that higher levels of the baseline CAR significantly predict MDEs for 2.5 years following cortisol measurement. However, the strength of prediction of depressive episodes significantly decays over time, with the CAR no longer significantly predicting MDEs after 2.5 years. Elevations in the CAR did not significantly increase vulnerability to prospective major stressful life events. They did, however, predict MDE recurrences more strongly than first onsets.

These results suggest that a high CAR represents a time-limited risk factor for onsets of MDEs, which increases risk for depression independently of future major stressful life events. Possible explanations for the stronger effect of the CAR for predicting MDE recurrences than first onsets are discussed.

It is well known that the hypothalamic–pituitary–adrenal (HPA) axis is compromised in major depression and bipolar disorder. There is increasing evidence that subtle HPA abnormalities, such as elevated cortisol levels, precede the development of an affective disorder. Interpersonal stress is also associated with the development of affective disorders. The present study sought to determine whether interpersonal chronic and episodic stress moderated the relationship between cortisol levels in the natural environment and risk status, defined as having a parent with bipolar disorder.

Sixty-two offspring of parents with bipolar disorder (OBD) and 60 offspring with no family history of affective disorders (OFH−), aged 19.48 years (s.d.=3.38, range 14–28), completed interviews assessing mental disorders and chronic and episodic stress, and provided saliva samples over 3 days.

Regression analyses revealed that the OBD who experienced high interpersonal chronic stress displayed a larger cortisol rise following awakening than the OBD reporting low interpersonal chronic stress. The same relationship was also found for levels of non-interpersonal chronic stress. The OBD who reported experiencing severe interpersonal episodic stress exhibited higher levels of daytime cortisol than the OBD reporting interpersonal episodic stress of mild severity. Importantly, none of the above relationships were detected in the OFH−. Each of the interactions between family history of affective disorders and stress remained after controlling for age, gender and offspring lifetime affective disorders and current non-affective disorders.

A biological sensitivity to stress may underlie the susceptibility to affective disorders among the OBD.