scholarly journals Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents

2017 ◽  
Vol 29 (5) ◽  
pp. 1877-1893 ◽  
Author(s):  
Lisa R. Starr ◽  
Kimberly Dienes ◽  
Catherine B. Stroud ◽  
Zoey A. Shaw ◽  
Y. Irina Li ◽  
...  

AbstractChildhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus–pituitary–adrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14–17 years (cortisoln= 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk.

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Oh Jeong Kwon ◽  
Munsoo Kim ◽  
Ho Sub Lee ◽  
Kang-keyng Sung ◽  
Sangkwan Lee

It is important to reduce poststroke depression (PSD) to improve the stroke outcomes and quality of life in stroke patients, but the underlying mechanisms of PSD are not completely understood. As many studies implicate dysregulation of hypothalamic-pituitary-adrenal axis in the etiology of major depression and stroke, we compared the cortisol awakening response (CAR) of 28 admitted PSD patients with that of 23 age-matched caregiver controls. Saliva samples for cortisol measurement were collected immediately, 15, 30, and 45 min after awakening for two consecutive days. Depressive mood status in PSD patients was determined with Beck Depression Inventory and Hamilton Depression Rating Scale. Salivary cortisol levels of PSD patients did not rise significantly at any sampling time, showing a somewhat flat curve. Caregiver controls showed significantly higher CAR at 15 and 30 min after awakening compared to PSD patients even though the two groups did not differ at awakening or 45 min after awakening. Area-under-the-curve analysis revealed a significant negative correlation between the CAR and the degree of depression in PSD patients. Thus, our findings suggest that poststroke depression is closely related with dysfunctional HPA axis indicated by blunted CAR.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Adilson Marques ◽  
Duarte Henriques-Neto ◽  
Miguel Peralta ◽  
Priscila Marconcin ◽  
Élvio R. Gouveia ◽  
...  

AbstractGrip strength (GS) is an indicator of health and vulnerability and inversely associated with depressive symptoms. The aim of this study was to explore GS discrimination capacity for depression; and possible GS cut-off values for depression by sex and age group. Data from 2011 and 2015 on 20,598 (10,416 women) middle-aged and older adults from 14 European countries was analysed. GS was assessed by dynamometer, and depressive symptoms using the EURO-D scale. GS cut-off values for depression were calculated and logistic regression models were used to quantify the odds of having depression in 2011 and in 2015 according to being bellow or above the cut-off value. GS had a weak discriminant capacity for depression, with the area under the curve varying between 0.54 and 0.60 (p < 0.001). Sensitivity varied between 0.57 and 0.74; specificity varied between 0.46 and 0.66. GS cut-off values for discriminating depression were 43.5 kg for men and 29.5 kg for women aged 50–64 years, 39.5 kg for men and 22.5 kg for women aged ≥ 65 years. Having GS above the cut-off represents significant lower odds of depression in 2011 and 4 years later, in 2015. Healthcare practitioners and epidemiologic researchers may consider the low GS cut-off values to screen for potential depression risk. However, due to its weak discriminant values these cut-offs should not be used to identify depression.


2018 ◽  
Vol 49 (6) ◽  
pp. 997-1004 ◽  
Author(s):  
Rongqin Yu ◽  
Susan Branje ◽  
Wim Meeus ◽  
Philip Cowen ◽  
Seena Fazel

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


2017 ◽  
Vol 41 (S1) ◽  
pp. S142-S142
Author(s):  
V.M. Buonomenna ◽  
F. Marciello ◽  
V. Caivano ◽  
G. Cascino ◽  
G. D’Agostino ◽  
...  

IntroductionAlthough the available evidence strongly supports an association between depression and coronary heart disease (CHD), the possible biological link between these two conditions still remains to be clarified. The hypothalamus-pituitary-adrenal (HPA) axis is the main endogenous system mediating the stress response and changes in cortisol secretion have been associated with depressed mood in patients with CHD. Therefore, the study of the correlation between cortisol levels and depressed mood in acute coronary syndrome (ACS) patients could help to clarify the nature of the relationship between ACS and the risk to develop a depressive syndrome.ObjectiveWe aimed to explore the relationships between HPA axis activity and depressed mood in ACS patients.AimsThe purpose of this study was to determine whether the cortisol awakening response (CAR) is associated and/or predict depressive symptoms in patients with an ACS.MethodPatients admitted to an ACS ward were asked to fill in the Beck Depression Inventory (BDI) and to collect saliva samples in the morning to measure their CAR. All the procedures were carried out within 1 week after an ACS. Patients were asked again to fill in the BDI six months after their ACS.ResultsA lower CAR was associated with higher BDI scores after 6 months from an ACS.ConclusionsOur preliminary results suggest that hypoactivity of the HPA axis in the first week of an ACS may predict more severe depressive symptoms after 6 months from the ACS.


Author(s):  
Rebecka Keijser ◽  
Susanne Olofsdotter ◽  
Kent W. Nilsson ◽  
Cecilia Åslund

AbstractFKBP5 gene–environment interaction (cG × E) studies have shown diverse results, some indicating significant interaction effects between the gene and environmental stressors on depression, while others lack such results. Moreover, FKBP5 has a potential role in the diathesis stress and differential susceptibility theorem. The aim of the present study was to evaluate whether a cG × E interaction effect of FKBP5 single-nucleotide polymorphisms (SNPs) or haplotype and early life stress (ELS) on depressive symptoms among young adults was moderated by a positive parenting style (PASCQpos), through the frameworks of the diathesis stress and differential susceptibility theorem. Data were obtained from the Survey of Adolescent Life in Västmanland Cohort Study, including 1006 participants and their guardians. Data were collected during 2012, when the participants were 13 and 15 years old (Wave I: DNA), 2015, when participants were 16 and 18 years old (Wave II: PASCQpos, depressive symptomology and ELS) and 2018, when participants were 19 and 21 years old (Wave III: depressive symptomology). Significant three-way interactions were found for the FKBP5 SNPs rs1360780, rs4713916, rs7748266 and rs9394309, moderated by ELS and PASCQpos, on depressive symptoms among young adults. Diathesis stress patterns of interaction were observed for the FKBP5 SNPs rs1360780, rs4713916 and rs9394309, and differential susceptibility patterns of interaction were observed for the FKBP5 SNP rs7748266. Findings emphasize the possible role of FKBP5 in the development of depressive symptoms among young adults and contribute to the understanding of possible differential susceptibility effects of FKBP5.


2021 ◽  
Vol 11 (6) ◽  
pp. 723
Author(s):  
Evangelos Karanikas ◽  
Nikolaos P. Daskalakis ◽  
Agorastos Agorastos

Traumatic stress may chronically affect master homeostatic systems at the crossroads of peripheral and central susceptibility pathways and lead to the biological embedment of trauma-related allostatic trajectories through neurobiological alterations even decades later. Lately, there has been an exponential knowledge growth concerning the effect of traumatic stress on oxidative components and redox-state homeostasis. This extensive review encompasses a detailed description of the oxidative cascade components along with their physiological and pathophysiological functions and a systematic presentation of both preclinical and clinical, genetic and epigenetic human findings on trauma-related oxidative stress (OXS), followed by a substantial synthesis of the involved oxidative cascades into specific and functional, trauma-related pathways. The bulk of the evidence suggests an imbalance of pro-/anti-oxidative mechanisms under conditions of traumatic stress, respectively leading to a systemic oxidative dysregulation accompanied by toxic oxidation byproducts. Yet, there is substantial heterogeneity in findings probably relative to confounding, trauma-related parameters, as well as to the equivocal directionality of not only the involved oxidative mechanisms but other homeostatic ones. Accordingly, we also discuss the trauma-related OXS findings within the broader spectrum of systemic interactions with other major influencing systems, such as inflammation, the hypothalamic-pituitary-adrenal axis, and the circadian system. We intend to demonstrate the inherent complexity of all the systems involved, but also put forth associated caveats in the implementation and interpretation of OXS findings in trauma-related research and promote their comprehension within a broader context.


2016 ◽  
Vol 74 ◽  
pp. 203-211 ◽  
Author(s):  
Corinna Reichl ◽  
Anne Heyer ◽  
Romuald Brunner ◽  
Peter Parzer ◽  
Julia Madeleine Völker ◽  
...  

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