Blunted Cortisol Response Research Articles

Expression of glucocorticoid inducible genes is associated with reductions in cornu ammonis and dentate gyrus volumes in patients with major depressive disorder.

Alterations of the glucocorticoid system and of hippocampal volumes have consistently been reported in patients with major depressive disorders (MDD). The aim of the present study was to investigate whether the messenger RNA (mRNA) expression of glucocorticoid inducible genes is associated with changes in the cornu ammonis (CA) and dentate gyrus subfields. Forty-three patients with MDD and 43 healthy controls were recruited and investigated with high resolution magnetic resonance imaging. Hippocampal subfields were measured using freesurfer. Measurement of whole blood mRNA expression of glucocorticoid inducible genes serum and glucocorticoid-regulated kinase 1 (SGK1), FK506 binding protein 5 (FKBP5), and glucocorticoid induced leucine zipper (GILZ) was performed. Patients with MDD had significantly smaller volumes of CA1, CA2/3, CA4/DG, and subiculum compared to healthy controls. In the regression analysis, the factor diagnosis had a significant moderating effect on the association of SGK1 and hippocampal volumes. Patients with low expression of SGK1 had significantly smaller CA2/3 and CA4/DG volumes compared to patients with high expression of SGK1 mRNA and to healthy controls with low/high expression of SGK1, respectively. Therefore, a lack of mRNA expression of glucocorticoid inducible genes in patients with MDD that seems to correspond to a blunted cortisol response is associated with smaller hippocampal CA and dentate gyrus volumes. SGK1 seems to be particularly relevant for stress-related mental disorders.

Lower morning to evening cortisol ratio is associated with cognitive impairment in men but not women: An analysis of 733 older subjects of the cross-sectional KORA-Age study

A dysregulated hypothalamic-pituitary-adrenocortical axis (HPA) is thought to play a role in the pathophysiology of cognitive impairment. Surprisingly, little agreement exists on the association of cortisol and cognitive impairment. Thus, we sought to examine the association between cognitive function and salivary cortisol levels in a representative sample of older men and women. A cross-sectional analysis was conducted among 733 study participants (65-90 years old, mean age=74.9) of the population-based KORA (Cooperative Health Research in the Region of Augsburg)-Age study. Associations were examined between cognitive function (determined by telephone interview for cognitive status-modified, TICS-m) and salivary cortisol measured upon waking (M1), 30min after awakening (M2), and in the late evening (E). In a dose response manner, lower morning (M1 and M2), and increased evening levels were observed in participants with probable dementia (4.5%, N=33) and slightly increased in those with mild cognitive impairment (MCI) (13.8%, N=101) compared to healthy individuals. Higher morning to evening ratios were associated with reduced odds of cognitive impairment, even after adjustments for important confounders (M1/E ratio: OR=1.50, 95% CI=1.08-2.07, M2/E ratio: 1.41, 1.01-1.95, per 1 standard deviation (SD) increase). However, the significant association of an increased risk for cognitive impairment was observed among men (M1/E: OR=1.94, 95% CI=1.24-3.02; M2/E=1.74, 1.12-2.71) but not women (M1/E: OR=1.11, 0.69-1.78; M2/E=1.09, 0.67-1.77). Our findings suggest that dysregulated HPA axis reactivity, evidenced by blunted diurnal cortisol responses, are associated with impaired cognitive function in an aged population.

In the Wake of the Great Recession: Economic Uncertainty, Communication, and Biological Stress Responses in Families

The impact of spouses' communication about economic uncertainty on biological stress responses was examined. The sample included 82 Latino and Caucasian couples and one of their adolescents. Wives with low economic uncertainty experienced the greatest cortisol increase to a stressful discussion with their spouse, while wives with high economic uncertainty experienced a blunted cortisol response. Husbands with high economic uncertainty exhibited a low, unresponsive cortisol pattern. Wives who experienced elevated cortisol used more corumination and had low community support. The amount parents talked about their financial worries to their adolescent was not associated with the adolescent's mental health or biosocial markers, but the parents' economic uncertainty and corumination with each other were negatively associated with their own mental health.

A blunted diurnal cortisol response in the lower educated does not explain educational differences in coronary heart disease: Findings from the AGES-Reykjavik Study

Lower educational attainment generally is a strong predictor of coronary heart disease (CHD). The underlying mechanisms of this effect are, however, less clear. One hypothesis is that stress related to limitations imposed by lower socioeconomic status elicits changes in hypothalamic-pituitary-adrenal axis functioning, which, in turn, increases risk of CHD. In a large cohort study, we examined whether educational attainment was related to risk of fatal and non-fatal CHD and the extent to which salivary cortisol mediated this relation independent of potential confounders, including lifestyles. Data came from 3723 participants aged 66 through 96 from the Age, Gene/Environment Susceptibility (AGES) – Reykjavik Study. Between 2002 and 2006, data were collected using questionnaires and examinations including morning and evening salivary samples. Hospital admission records and cause of death registries (ICD-9 and ICD-10 codes) were available until December 2009. Linear regression and Cox proportional hazards analyses were performed. Even after adjustment for potential confounders, including lifestyle, persons with lower educational attainment showed a blunted cortisol response and also greater risk of incident CHD. However, our data did not support the role of cortisol as a mediator in the association between education and CHD in an older sample (192).

Long term effects of childhood trauma on cortisol stress reactivity in adulthood and relationship to the occurrence of depression.

Childhood trauma may have longstanding effects on individuals' propensity to react adversely to stress, and also predisposes individuals to suffer from depression. The current study aimed to examine stress reactivity in individuals with and without a history of childhood trauma by measuring cortisol responses to the passive viewing of stressful images, specifically including images relevant to childhood trauma. In addition, participants with and without a diagnosis of current depression were studied to investigate whether cortisol stress reactivity may underlie resilience or vulnerability to depression. The study involved 17 healthy participants with and 24 without a history of childhood trauma; and 21 depressed patients with and 18 without a history of childhood trauma. Salivary cortisol was measured before, during and after participants were shown affectively laden images, including standardised scenes from the International Affective Picture System and also images suggestive of childhood abuse. Cortisol stress reactivity to the passive image viewing was compared between groups. In those who had experienced childhood trauma, cortisol stress responses were overall low and the same in those who were depressed and those who were not (mean stress reactivity variable - depressed: 0.8 nmol/l; non-depressed: 0.72 nmol/l). In contrast, cortisol stress reactivity was raised in depressed subjects relative to those who were not depressed in those without a history of childhood trauma (mean stress reactivity variable - depressed: 3.75 nmol/l; non-depressed: 0.1 nmol/l). A history of childhood trauma has longstanding effects on adulthood cortisol responses to stress, particularly in that depressed individuals with a history of childhood trauma show blunted cortisol responses. However, there were no differences between abused depressed and abused non-depressed subjects on cortisol stress responses, suggesting that such a finding does not explain subsequent susceptibility to depression. On the other hand, patients who experience depression without a history of childhood trauma show enhanced cortisol stress reactivity, which could help explain the aetiology of their depressive illnesses. Differences between the current findings and those using other pharmacological and stress challenge paradigms may relate to the type of stimuli used and to dysfunction at different levels of the hypothalamic-pituitary-adrenal (HPA) axis.

A single nucleotide polymorphism in the corticotropin receptor gene is associated with a blunted cortisol response during pediatric critical illness.

The cortisol response during critical illness varies widely among patients. Our objective was to examine single nucleotide polymorphisms in candidate genes regulating cortisol synthesis, metabolism, and activity to determine if genetic differences were associated with variability in the cortisol response among critically ill children. This was a prospective observational study employing tag single nucleotide polymorphism methodology to examine genetic contributions to the variability of the cortisol response in critical illness. Thirty-one candidate genes and 31 ancestry markers were examined. Patients were enrolled from seven pediatric critical care units that constitute the Eunice Kennedy Shriver Collaborative Pediatric Critical Care Research Network. Critically ill children (n = 92), age 40 weeks gestation to 18 years old, were enrolled. Blood samples were obtained from all patients for serum cortisol measurements and DNA isolation. Demographic and illness severity data were collected. Single nucleotide polymorphisms were tested for association with serum free cortisol concentrations in context of higher illness severity as quantified by Pediatric Risk of Mortality III score greater than 7. A single nucleotide polymorphism (rs1941088) in the MC2R gene was strongly associated (p = 0.0005) with a low free cortisol response to critical illness. Patients with the AA genotype were over seven times more likely to have a low free cortisol response to critical illness than those with a GG genotype. Patients with the GA genotype exhibited an intermediate free cortisol response to critical illness. The A allele at rs1941088 in the MC2R gene, which encodes the adrenocorticotropic hormone (corticotropin, ACTH) receptor, is associated with a low cortisol response in critically ill children. These data provide evidence for a genetic basis for a portion of the variability in cortisol production during critical illness. Independent replication of these findings will be important and could facilitate development of personalized treatment for patients with a low cortisol response to severe illness.

Anger responses to psychosocial stress predict heart rate and cortisol stress responses in men but not women.

While previous research has suggested that anger and fear responses to stress are linked to distinct sympathetic nervous system (SNS) stress responses, little is known about how these emotions predict hypothalamus-pituitary-adrenal (HPA) axis reactivity. Further, earlier research primarily relied on retrospective self-report of emotion. The current study aimed at addressing both issues in male and female individuals by assessing the role of anger and fear in predicting heart rate and cortisol stress responses using both self-report and facial coding analysis to assess emotion responses. We exposed 32 healthy students (18 female; 19.6±1.7 yr) to an acute psychosocial stress paradigm (TSST) and measured heart rate and salivary cortisol levels throughout the protocol. Anger and fear before and after stress exposure was assessed by self-report, and video recordings of the TSST were assessed by a certified facial coder to determine emotion expression (FACS). Self-reported emotions and emotion expressions did not correlate (all p>.23). Increases in self-reported fear predicted blunted cortisol responses in men (β=0.41, p=.04). Also for men, longer durations of anger expression predicted exaggerated cortisol responses (β=0.67 p=.004), and more anger incidences predicted exaggerated cortisol and heart rate responses (β=0.51, p=.033; β=0.46, p=.066, resp.). Anger and fear did not predict SNS or HPA activity for females (all p>.23). The current differential self-report and facial coding findings support the use of multiple modes of emotion assessment. Particularly, FACS but not self-report revealed a robust anger-stress association that could have important downstream health effects for men. For women, future research may clarify the role of other emotions, such as self-conscious expressions of shame, for physiological stress responses. A better understanding of the emotion-stress link may contribute to behavioral interventions targeting health-promoting ways of responding emotionally to stress.

Cortisol response to an experimental stress paradigm prospectively predicts long-term distress and resilience trajectories in response to active police service

Heterogeneity in glucocorticoid response to experimental stress conditions has shown to differentiate individuals with healthy from maladaptive real-life stress responses in a number of distinct domains. However, it is not known if this heterogeneity influences the risk for developing stress related disorders or if it is a biological consequence of the stress response itself. Determining if glucocorticoid response to stress induction prospectively predicts psychological vulnerability to significant real life stressors can adjudicate this issue. To test this relationship, salivary cortisol as well as catecholamine responses to a laboratory stressor during academy training were examined as predictors of empirically identified distress trajectories through the subsequent 4 years of active duty among urban police officers routinely exposed to potentially traumatic events and routine life stressors (N = 234). During training, officers were exposed to a video vignette of police officers exposed to real-life trauma. Changes in salivary 3-methoxy-4-hydroxyphenylglycol (MHPG) and cortisol in response to this video challenge were examined as predictors of trajectory membership while controlling for age, gender, and baseline neuroendocrine levels. Officers who followed trajectories of resilience and recovery over 4 years mounted significant increases in cortisol in response to the experimental stressor, while those following a trajectory of chronic increasing distress had no significant cortisol change in response to the challenge. MHPG responses were not associated with distress trajectories. Cortisol response prospectively differentiated trajectories of distress response suggesting that a blunted cortisol response to a laboratory stressor is a risk factor for later vulnerability to distress following significant life stressors.

The role of stress in absenteeism: cortisol responsiveness among patients on long-term sick leave.

ObjectiveThis study aimed to (1) See whether increased or decreased variation relate to subjective reports of common somatic and psychological symptoms for a population on long-term sick leave; and (2) See if this pattern in variation is correlated with autonomic activation and psychological appraisal.MethodsOur participants (n = 87) were referred to a 3.5-week return-to-work rehabilitation program, and had been on paid sick leave >8 weeks due to musculoskeletal pain, fatigue and/or common mental disorders. An extensive survey was completed, addressing socio-demographics, somatic and psychological complaints. In addition, a physician and a psychologist examined the participants, determining baseline heart rate, medication use and SCID-I diagnoses. During the 3.5-week program, the participants completed the Trier Social Stress Test for Groups. Participants wore heart rate monitors and filled out Visual Analogue Scales during the TSST-G.ResultsOur participants presented a low cortisol variation, with mixed model analyses showing a maximal increase in free saliva cortisol of 26% (95% CI, 0.21–0.32). Simultaneously, the increase in heart rate and Visual Analogue Scales was substantial, indicating autonomic and psychological activation consistent with intense stress from the Trier Social Stress Test for Groups.ConclusionsThe current findings are the first description of a blunted cortisol response in a heterogeneous group of patients on long-term sick leave. The results suggest lack of cortisol reactivity as a possible biological link involved in the pathway between stress, sustained activation and long-term sick leave.

Differences in HPA-axis and heart rate responsiveness to psychosocial stress in children with autism spectrum disorders with and without co-morbid anxiety.

Children and adolescents with autism spectrum disorder (ASD) have much higher rates of anxiety disorders relative to their typically developing peers. However, there have been few attempts to investigate what physiological parameters may be associated with this elevated rate of anxiety. Therefore, this study investigated the physiological correlates of anxiety in ASD, with a focus on whether measures of heart rate and cortisol responsiveness to psychosocial stress differentiate those participants with ASD with and without a co-occurring anxiety disorder. A total of 75 male participants aged 10-16 years with normal intellectual ability underwent a psychosocial stress test. The participants included healthy controls (n=23), ASD only (ASD; n=20) and ASD with a comorbid anxiety disorder (ASDanx; n=32). Heart rate, heart rate variability and salivary cortisol were compared by fitting a piecewise regression model to examine baseline levels and change over time within and between the rest, stress and recovery phases of the stress test. The ASDanx group had different response patterns from both the ASD and control groups. The ASDanx group was characterized by a blunted cortisol and heart rate response to psychosocial stress. Furthermore, in the ASDanx group, reduced heart rate and cortisol responsiveness were significantly related to increased anxiety symptoms. This is the first study to report a possible physiological basis for co-occurring anxiety disorders in children and adolescents with ASD. It is possible that a non-adaptive physiological response to psychosocial stress may be related to the high prevalence of co-occurring anxiety disorders in people with ASD.

Brief, pre-retrieval stress differentially influences long-term memory depending on sex and corticosteroid response

Previous work has indicated that stress generally impairs memory retrieval. However, little research has addressed discrepancies that exist in this line of work and the factors that could explain why stress can exert differential effects on retrieval processes. Therefore, we examined the influence of brief, pre-retrieval stress that was administered immediately before testing on long-term memory in males and females. Participants learned a list of 42 words varying in emotional valence and arousal. Following the learning phase, participants were given an immediate free recall test. Twenty-four hours later, participants submerged their non-dominant hand in a bath of ice cold (Stress) or warm (No Stress) water for 3min. Immediately following this manipulation, participants’ memory for the word list was assessed via free recall and recognition tests. We observed no group differences on short-term memory. However, male participants who showed a robust cortisol response to the stress exhibited enhanced long-term recognition memory, while male participants who demonstrated a blunted cortisol response to the stress exhibited impaired long-term recall and recognition memory. These findings suggest that the effects of brief, pre-retrieval stress on long-term memory are sex-specific and mediated by corticosteroid mechanisms.

Structural Stigma and Hypothalamic–Pituitary–Adrenocortical Axis Reactivity in Lesbian, Gay, and Bisexual Young Adults

Youth exposed to extreme adverse life conditions have blunted cortisol responses to stress. This study aims to examine whether growing up in highly stigmatizing environments similarly shapes stigmatized individuals' physiological responses to identity-related stress. We recruited 74 lesbian, gay, and bisexual young adults (mean age = 23.68) from 24 states with varying levels of structural stigma surrounding homosexuality. State-level structural stigma was coded based on several dimensions, including policies that exclude sexual minorities from social institutions (e.g., same-sex marriage). Participants were exposed to a laboratory stressor, the Trier Social Stress Test (TSST), and neuroendocrine measures were collected. Lesbian, gay, and bisexual young adults who were raised in highly stigmatizing environments as adolescents evidenced a blunted cortisol response following the TSST compared to those from low-stigma environments. The stress of growing up in environments that target gays and lesbians for social exclusion may exert biological effects that are similar to traumatic life experiences.

Evidence for a normal HPA axis response to psychosocial stress in patients remitted from depression

The purpose of this study was to investigate subjective mood and the effect of a psychosocial stress challenge on cortisol response in patients remitted from depression in comparison to healthy controls. Only few studies on small samples have been conducted on the influence of psychosocial stress on HPA system responsivity in this group. Results regarding patients who have achieved clinical remission from depression remain inconclusive so far. In comparison to healthy controls, some studies found blunted cortisol responses to a psychological stressor in patients with remitted depression. However, others found no differences. This discrepancy may be due to use of heterogeneous stress measures or dissimilar sample sizes and characteristics, e.g. including patients with comorbid generalized anxiety or patients with an unknown duration of remission. The present study included 77 healthy controls and 70 unipolar depressed patients who had achieved stable, full remission for at least 6 months (average 31 months) with no further Axis I disorder. Participants underwent the Trier Social Stress Test and salivary cortisol levels and mood were assessed repeatedly during the experimental procedure. For both groups, we observed a marked cortisol response and worsening of mood after the stress challenge. However, no differences between formerly depressed patients and healthy participants were observed. Assuming a disturbed HPA system regulation in acute depression, we interpret these findings as evidence for a restored HPA axis function in fully remitted patients.

Blunted cortisol response to stress is associated with higher body mass index in low-income preschool-aged children.

No known studies have tested the hypothesis that a blunted pattern of cortisol reactivity to stress, which is often found following exposure to chronic life stressors, is associated with a higher body mass index (BMI) in very young children. Low-income children (n=218, mean age 56.6 (range: 38.1-78.5; SD 7.0) months, 49.1% male, 56.4% white, 16.1% black, 11.5% Hispanic/Latino) participated in a series of behavioral tasks designed to elicit stress. Cortisol was sampled in saliva 5 times during the protocol, and area under the curve (AUC), representing total cortisol output during stress elicitation, was calculated. Children were weighed and height measured and body mass index (BMI) z-score was calculated. Linear regression was used to evaluate the association between cortisol AUC and BMI z-score, controlling for child age, sex, and race/ethnicity (non-Hispanic white vs. not); primary caregiver weight status (overweight, defined as BMI ≥ 25 vs. not); and family income-to-needs ratio. Mean child BMI z-score was 0.88 (SD=1.03). Mean cortisol AUC was 6.11 μg/dL/min (SD=10.44). In the fully adjusted model, for each 1-standard deviation unit decrease in cortisol AUC, the child's BMI z-score increased by 0.17 (SE 0.07) standard deviation units (p<0.02). A blunted cortisol response to stress, as is often seen following chronic stress exposure, is associated with increased BMI z-score in very young children. Further work is needed to understand how associations between stress, cortisol, and elevated body mass index may develop very early in the lifespan.

Blunted HPA axis response to stress is related to a persistent Dysregulation Profile in youth

The Child Behavior Checklist Dysregulation Profile (DP) in youth has been shown to be a predictor of psychopathology later in life. We examined the activity of the hypothalamic pituitary adrenal (HPA) axis in youth with remitted, new, persistent, and no DP. Data from 489 youth (47% boys) participating in a Dutch longitudinal general population study were included (Wave 1 mean age=11.5, Wave 2=14.2). Wave 2 diurnal cortisol patterns and levels in response to a laboratory stress paradigm were compared in youth with DP at Wave 1 only, Wave 2 only, both Waves, and neither Wave. Youth with the DP at Wave 2 only or at both time points showed blunted cortisol responses to stress relative to the other two groups. There were no group or sex differences in diurnal cortisol activity. More research is needed to determine how the association between DP symptoms and HPA axis functioning changes over time.

Psychological Response and Cortisol Reactivity to In Vitro Fertilization Treatment in Women With a Lifetime Anxiety or Unipolar Mood Disorder Diagnosis

Knowledge regarding the emotional and physiologic response of women with psychiatric disorders undergoing in vitro fertilization (IVF) treatments is rather limited. We evaluated psychological adjustment and cortisol reactivity to IVF treatment in women with a lifetime diagnosis of a unipolar mood or anxiety disorder compared to those without such a diagnosis. Women undergoing IVF treatments (N = 121) were interviewed from January 2006 to December 2007 to assess for the presence of a history of a lifetime DSM-IV-TR unipolar mood or anxiety disorder. They were evaluated prospectively at baseline, at ovulation, and before the pregnancy test. Primary outcome measures included assessments of depressive and anxiety symptoms (Center for Epidemiologic Studies Depression Scale and State-Trait Anxiety Inventory, respectively) and plasma cortisol levels. Of 108 participants included in the study, 19.4% (n = 21) were determined to have a lifetime Axis I unipolar mood or anxiety diagnosis. Women with lifetime Axis I psychopathology showed significantly greater symptom elevation for depression (F2,194 = 10.97, P < .001) and for anxiety (F2,194 = 3.4813, P = .033) compared to the group without psychopathology. A different physiologic pattern was observed for cortisol response: whereas the group without psychopathology responded physiologically to the stressful treatment with continuously elevated cortisol levels, a blunted cortisol response was observed for the group with lifetime psychopathology (F2,200 = 2.9, P = .05). Women diagnosed with a lifetime unipolar mood or anxiety disorder developed robust symptom exacerbation during IVF treatment compared to women without an Axis I diagnosis. Conversely, the women with a lifetime diagnosis are characterized by a blunted cortisol response, indicating a pattern of dissociation between the robust increase in anxiety and depression and cortisol response to the acute psychological stress. This study emphasizes the need for a psychiatric screening prior to IVF treatment and for the utilization of preventive psychiatric and psychological interventions.

Stress and immune function of social drinking college students before and after spring break

Numerous studies have focused on the social aspects of collegiate holiday drinking; however, physiological measures are frequently overlooked. This project examined stress and immune function among collegiate social drinkers before and after spring break (SB). Saliva and questionnaires were collected from 29 students (9 males) at baseline and post‐SB. Participants were categorized as cortisol non‐responders (CNR; n=14) or cortisol increasers (CI; n=13) depending on their change in cortisol over SB (&lt; 0.03 μg/dL change = CNR; ≥ 0.03 μg/dL change = CI). CNRs and CIs were matched on gender, age, baseline alcohol use and family history of alcoholism. Repeated measures ANOVAs examined differences over time and between groups on quantity/frequency of alcohol use (QFI), IgA and DHEAS. Time x group interactions were noted for QFI (F(1,22)=4.96; p=.04) and IgA (F(1,19)=5.27; p=.03). CNRs doubled their alcohol use over SB (p=.02) and CIs decreased in IgA over SB (p&lt;.05). Changes in QFI and IgA were positively correlated among CIs (r=.63; p=.04) but were unrelated among CNRs. Compared to CNRs, CIs exhibited higher DHEAS levels overall. Blunted cortisol responses have been previously associated with risk for addictive disorders. The current results highlight the importance of physiological variables to the study of collegiate holiday drinking.

The Effects of Soy and Whey Protein Supplementation on Acute Hormonal Responses to Resistance Exercise in Men

Objective: For many resistance-trained men concerns exist regarding the production of estrogen with the consumption of soy protein when training for muscle strength and size. Thus, the purpose of this investigation was to examine the effects of soy and whey protein supplementation on sex hormones following an acute bout of heavy resistance exercise in resistance trained men. Methods: Ten resistance-trained men (age 21.7 ± 2.8 [SD] years; height 175.0 ± 5.4 cm; weight 84.2 ± 9.1 kg) volunteered to participate in an investigation. Utilizing a within subject randomized crossover balanced placebo design, all subjects completed 3 experimental treatment conditions supplementing with whey protein isolate (WPI), soy protein isolate (SPI), and maltodextrin placebo control for 14 days with participants ingesting 20 g of their assigned supplement each morning at approximately the same time each day. Following supplementation, subjects performed an acute heavy resistance exercise test consisting of 6 sets of 10 repetitions in the squat exercise at 80% of the subject's one repetition maximum. Results: This investigation observed lower testosterone responses following supplementation with soy protein in addition to a positive blunted cortisol response with the use of whey protein at some recovery time points. Although sex hormone binding globulin (SHBG) was proposed as a possible mechanism for understanding changes in androgen content, SHBG did not differ between experimental treatments. Importantly, there were no significant differences between groups in changes in estradiol concentrations. Conclusion: Our main findings demonstrate that 14 days of supplementation with soy protein does appear to partially blunt serum testosterone. In addition, whey influences the response of cortisol following an acute bout of resistance exercise by blunting its increase during recovery. Protein supplementation alters the physiological responses to a commonly used exercise modality with some differences due to the type of protein utilized.

Gender Specific Effect of Psychological Stress and Cortisol Reactivity on Adolescent Risk Taking

The purpose of this study was to evaluate how psychological stress, gender and cortisol response to stress relate to risk behavior among 132 14-18year old adolescents. Participants completed a laboratory based risk task prior to and immediately after a computerized psychological stress task, and salivary cortisol was collected from pre-stress to 60min following initial stress exposure. Results indicate that adolescent boys (n = 59) and girls (n = 73) demonstrate different patterns of risk taking (RT) in response to stress, such that boys evidenced an increase in RT following stress exposure, whereas girls evidenced a decrease in RT. In addition, a gender by cortisol interaction demonstrated that for boys, both a smaller total cortisol output (AUCg) and peak cortisol response to stress (PC) was associated with greater stress-induced RT. Both cortisol measures were unrelated to stress-induced RT among girls. Taken together, data suggest that among boys, a blunted cortisol response to stress underlies an increase in risk taking in the context of psychological stress. Further research with an additional behavioral stress task is needed prior to drawing conclusions regarding the relation between female gender, cortisol response to stress, and risk taking in the context of psychological stress.

Relation between corticosterone and fear‐related behavior in mice selectively bred for high or low alcohol preference

Blunted cortisol responses to stress or trauma have been linked with genetic (familial) risk for both alcoholism and post-traumatic stress disorder (PTSD). Mouse lines selectively bred for high (HAP) or low (LAP) alcohol preference may be a relevant model of genetic risk for co-morbid alcoholism and PTSD in humans. HAP mice show greater fear-potentiated startle (FPS), a model used to study PTSD, than LAP mice. The relation between corticosterone (CORT) and FPS behavior was explored in four experiments. Naïve male and female HAP2 and LAP2 mice received fear-conditioning or control treatments, and CORT levels were measured before and immediately after fear-conditioning or FPS testing. In two other experiments, HAP2 mice received CORT (1.0, 5.0 or 10.0 mg/kg) or a glucocorticoid receptor antagonist (mifepristone; 25.0 and 50.0 mg/kg) 30 minutes before fear conditioning. HAP2 mice exposed to fear conditioning and to control foot shock exposures showed lower CORT after the fear-conditioning and FPS testing sessions than LAP2 mice. A trend toward higher FPS was seen in HAP2 mice pretreated with 10.0 mg/kg CORT, and CORT levels were the lowest in this group, suggesting negative feedback inhibition of CORT release. Mifepristone did not alter FPS. Overall, these results are consistent with data in humans and rodents indicating that lower cortisol/CORT levels after stress are associated with PTSD/PTSD-like behavior. These findings in HAP2 and LAP2 mice suggest that a blunted CORT response to stress may be a biological marker for greater susceptibility to develop PTSD in individuals with increased genetic risk for alcoholism.