Associations between symptoms of depression and anxiety and cortisol responses to and recovery from acute stress

Abstract

Background: Anxiety disorders and major depressive disorder (MDD) have been associated with increased and blunted HPA axis reactivity to social stress. However, research focusing on associations between HPA axis responses to stress and symptoms of anxiety and depression among individuals without a diagnosis remains an understudied area of research. Methods: One hundred forty-three adults (52% female) completed the Trier Social Stress est (TSST). Symptoms of depression and anxiety were assessed prior to the TSST using the anxiety and depression subscales of the Hospital Anxiety and Depression Scale (HADS). HPA axis responses were assessed by measuring salivary cortisol at baseline and following the TSST. Reactivity to and recovery from stress were assessed using multilevel growth modeling controlling for age, BMI, and sex among the full sample and a subset of cortisol responders (n=72). Results: Anxiety symptoms were positively associated with flatter recovery slopes among the full sample (t(122.3)=2.082, p=.039). Among cortisol responders, depression symptoms were associated with steeper reactivity (t(63.32)=2.53, p=.026) and recovery (t(58.75)=−2.20, p=.03). Anxiety symptoms were associated with marginally flatter reactivity (t(64.00)=−1.97, p=.053) and significantly flatter recovery (t(59.22)=2.29, p=.025). Conclusion: Symptoms of anxiety and depression among individuals without a psychiatric diagnosis are associated with blunted and exaggerated cortisol responses to and recovery from

Sex Differences in Stress Reactivity to the Trier Social Stress Test in Virtual Reality

“…The common physical indices are cortisol and heart rate (Hellhammer and Schubert, 2012). In addition to physiological reactivity, the TSST will also induce psychological reactivity such as stress perception (Childs et al, 2006), anxiety and the insecurity affect (Fiksdal et al, 2019;Firk and Markus, 2009;Yim et al, 2010 ). According to neuroendocrine theory, when exposed to stressors, at rst the prefrontal cortex integrates the sensory input and evaluates the signi cance of information and then produces available coping strategies; second, the limbic system forms emotional responses; and in the end, physical systems such as the HPA system is aroused (Campbell and Ehlert, 2012).…”

Analyze of Saliva Cortisol as Biomarker in Healthy Distressed Subjects

“…Keywords: saliva, cortisol, stress, anxiety Vulnerability to stress, expressed by emotional distress (symptoms of anxiety and depression), has also as endocrine expression, through the modification of hypothalamo-pituitary-adrenal axis (HPA) parameters, most commonly studied being cortisol secretion [1]. Chronic stress may lead to both increase and decrease in cortisol levels in general population [2,3]. Even though cortisol and its derivatives are beneficial as antiinflammatory drugs, and can be used in a variety of medical conditions [4,5], chronic emotional distress in young healthy adults persistently activates the HPA, this being translated into an exaggerated sympathetic response and cortisol increase at subjects exposed to general stressors [6,7].…”

Cortisol reactivity in patients with anorexia nervosa after stress induction

“…Alterations in P AN manifest in hypercortisolemia (e.g., 10,11 ) disturbed physiological and behavioral processes 25 related to appetite 26 and energy expenditure 27 and a diminished sensitivity of the hypothalamic and pituitary centers to negative feedback, as evinced in reduced suppression of cortisol after a dexamethasone-suppression test (DST [28][29][30] ) and a blunted response to acute stress exposure 29,[31][32][33][34][35] . HPAA dysregulation in P AN has been also associated with childhood adversities 23,24,36 and psychological variables, such as pronounced ED-symptomatology, body-image concerns, and psychopathology (e.g., depression, distress [37][38][39][40][41][42] ). It is thought that these variables induce constant alertness and stress influencing HPAA functioning 36,43 .…”

“…This hypothesis is based on past studies related to the HPAA functionality in P AN suggesting abnormal functionality of the HPAA in P AN , as evinced by blunted reactivity to the TSST 29 , 33 – 35 and also reflected in a diminished sensitivity to negative feedback to the DST 28 , 29 and hypercortisolemia (e.g., 10 , 11 ). HPAA dysfunctions in P AN has been often associated with chronic stress 8 , 17 – 19 , pronounced ED-symptoms 36 , 43 , and psychopathology (e.g., 37 – 39 ). Since P AN in our study exhibit elevated basal cortisol levels, chronic stress, and psychological burden (compared with HC), a decreased sensitivity of the HPAA to negative feedback can be assumed.…”