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.

Dysfunction in major stress response systems during the acute aftermath of trauma may contribute to risk for developing posttraumatic stress disorder (PTSD). The current study investigated how PTSD diagnosis and symptom severity, depressive symptoms, and childhood trauma uniquely relate to diurnal neuroendocrine secretion (cortisol and alpha-amylase rhythms) in women who recently experienced interpersonal trauma compared to non-traumatized controls (NTCs).

Using a longitudinal design, we examined diurnal cortisol and alpha-amylase rhythms in 98 young women (n = 57 exposed to recent interpersonal trauma, n = 41 NTCs). Participants provided saliva samples and completed symptom measures at baseline and 1-, 3-, and 6-month follow-up.

Multilevel models (MLMs) revealed lower waking cortisol predicted the development of PTSD in trauma survivors and distinguished at-risk women from NTCs. Women with greater childhood trauma exposure exhibited flatter diurnal cortisol slopes. Among trauma-exposed individuals, lower waking cortisol levels were associated with higher concurrent PTSD symptom severity. Regarding alpha-amylase, MLMs revealed women with greater childhood trauma exposure exhibited higher waking alpha-amylase and slower diurnal alpha-amylase increase.

Results suggest lower waking cortisol in the acute aftermath of trauma may be implicated in PTSD onset and maintenance. Findings also suggest childhood trauma may predict a different pattern of dysfunction in stress response systems following subsequent trauma exposure than the stress system dynamics associated with PTSD risk; childhood trauma appears to be associated with flattened diurnal cortisol and alpha-amylase slopes, as well as higher waking alpha-amylase.

A large body of literature suggests that childhood trauma exposure is a non-specific risk factor for development of eating disorders (EDs) later in life. One potential mechanism through which early traumatic experiences may increase the risk for EDs is represented by long-lasting changes in the body stress response system.

We investigated the activity of the hypothalamus-pituitary-adrenal axis and of the sympathetic nervous system in adult ED patients with or without a history of childhood trauma exposure.

We recruited 35 women with EDs, admitted to the Eating Disorders Center of the Department of Psychiatry of the University of Naples “Luigi Vanvitelli”. Participants filled in the Childhood Trauma Questionnaire (CTQ), to assess exposure to childhood trauma. They were instructed to collect saliva samples at awakening and after 15, 30 and 60 minutes, in order to measure cortisol levels and salivary alpha-amylase (sAA), a marker of the sympathetic nervous system activity.

According to the CTQ cut-off scores, 21 ED women were classified as maltreated (Mal) participants and 14 women as no-maltreated (noMal) ED participants. Compared to noMal ED women, Mal ED participants showed significantly decreased cortisol awakening response (CAR) and sAA morning secretion.

Present findings confirm that childhood trauma exposure impairs the CAR of adult patients with EDs and show that also the morning secretion of sAA is decreased in childhood maltreated adult ED patients. Therefore, our study shows for the first time a dampening in the basal activity of both components of the endogenous stress response system in childhood maltreated adult ED women.

The stress response involves the activation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). As a role for stress in determining of the onset and the natural course of eating disorders (EDs) has been proposed, the study of the psychobiology of the stress response in patients with anorexia nervosa (AN) and bulimia nervosa (BN) should be helpful in understanding the pathophysiology of these disorders. The two neurobiological components of the stress response can be easily explored in humans by the measurement of salivary cortisol and α-amylase response to a stressor. Therefore, we assessed salivary cortisol and α-amylase responses to the Trier Social Stress Test (TSST) in symptomatic patients with AN and BN compared to healthy controls.

Seven AN women, eight BN women and eight age-matched healthy females underwent the TSST between 1530 and 1700 h. Salivary cortisol and α-amylase levels were measured by an enzyme-linked immunosorbent assay (ELISA).

Compared to healthy women, AN patients showed a normal cortisol response to the TSST, although this occurred at significantly increased hormone levels, and an almost complete absence of response of α-amylase. BN women, however, exhibited enhanced pre-stress levels of salivary α-amylase but a normal response of the enzyme and cortisol to the TSST.

These findings demonstrate, for the first time, the occurrence of an asymmetry between the HPA axis and SNS components of the stress response in the acute phase of AN but not in BN. The pathophysiological significance of this asymmetry remains to be determined.