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Introduction Inflammation is drawing attention as pathway between psychosocial stress and health, and basal HPA axis activity has been suggested to exert a consistent regulatory influence on peripheral inflammation. Here we studied the relationship between basal HPA axis activity and inflammatory and HPA axis acute stress reactivity. Methods We recruited 48 healthy individuals and collected saliva for diurnal cortisol sampling at 6 points. Participants were previously exposed to the Trier Social Stress Test (TSST) on two consecutive days. Plasma interleukin-6 (IL-6) and salivary cortisol reactivity to acute stress were measured, and their relationships with basal HPA axis activity were analyzed. Results Steeper cortisol awakening response (CAR) linear increase was related with stronger cortisol stress reactivity (γ = 0.015; p = 0.042) and marginally significantly with greater habituation (γ = 0.01; p = 0.066). Greater curvilinearity of CAR was related with stronger cortisol reactivity (γ = −0.014; p = 0.021) and greater cortisol habituation (γ = −0.011; p = 0.006). Steeper daily linear decline was related with significant or marginally significantly stronger cortisol and IL-6 reactivity (cortisol: γ = −0.0004; p = 0.06; IL-6: γ = −0.028; p = 0.031) and greater habituation (cortisol: γ = −0.002; p = 0.009, IL-6: γ = −0.015; p = 0.033). Greater curvilinearity of daily decline was related with stronger IL-6 reactivity (γ = 0.002; p = 0.024) and also greater cortisol and IL-6 habituation (cortisol: γ = 0.00009; p = 0.03, IL-6: γ = 0.001; p = 0.024). Conclusions Patterns of basal HPA axis activity that are related with healthier outcomes were found to be related with stronger initial cortisol and IL-6 reactivity and greater habituation. This is an important step in understanding the long-term health implications of acute stress responsiveness, and future studies should employ longitudinal designs to identify the direction of these relationships.

Effective adjustment of the stress systems to repeated stress is regarded as an adaptive response of the organism facing environmental threats. Given the intertwined relationship between the stress systems and the inflammatory system, it could be expected that inflammatory processes should adapt to repeated stress as well. However, only little is known about adaptational processes of the different components of the immune system in response to repeated stress, and how these might be related to adaptational processes of the hypothalamus-pituitary-adrenal (HPA) axis. We here examined N=22 healthy participants (mean age 23years, 50% female) and exposed them to a standardized laboratory stressor twice, 24h apart. Plasma interleukin 6 (IL-6), salivary cortisol and psychometric parameters were assessed repeatedly up to 120min post stress. Results revealed a significant day by time interaction for cortisol (F=5.06; p=0.013) and IL-6 (F=4.42; p=0.041), indicating habituation of HPA axis and sensitization of inflammatory stress responses. Cortisol habituation and inflammatory sensitization were inversely related when controlling for sex (r=-0.44; p=0.044). Explorative analyses revealed significant associations between the IL-6 response on the second exposure with perceived stress (r=0.58; p=0.004), vital exhaustion (r=0.57; p=0.009), depression (r=0.47; p=0.026) and purpose in life (r=-0.50; p=0.04). These findings may help to increase understanding of the still only rudimentary understood interplay of adaptational processes of endocrine and immune responses to repeated stress and might indicate a link between inflammatory disinhibition and psychological indicators of well-being.

People with type 1 diabetes are at risk for early- and late-onset hypoglycemia following exercise. Reducing this risk may be possible with strategic modifications in carbohydrate intake and insulin use. We examined the exercise preparations and management techniques used by individuals with type 1 diabetes before and after physical activity and sought to determine whether use of differing diabetes technologies affects these health-related behaviours.We studied 502 adults from the Type 1 Diabetes Exchange's online patient community, Glu, who had completed an online survey focused on diabetes self-management and exercise.Many respondents reported increasing carbohydrate intake before (79%) and after (66%) exercise as well as decreasing their meal boluses before (53%) and after (46%) exercise. Most reported adhering to a target glucose level before starting exercise (77%). Despite these accommodations, the majority reported low blood glucose (BG) levels after exercise (70%). The majority of users of both insulin pump therapy (CSII) and continuous glucose monitoring (CGM) (Combined) reported reducing basal insulin around exercise (55%), with fewer participants adjusting basal insulin when using other devices (SMBG only = 20%; CGM = 34%; CSII = 42%; p0.001). However, CSII and Combined users reported that exercise makes their BG levels harder to control (p0.05) and makes them feel less able to predict their BG levels while exercising (p0.001); they show agreement that fear of low BG levels keeps them from exercising (p0.01).These findings highlight the need for exercise-management strategies tailored to individuals' overall diabetes management, for despite making exercise-specific adjustments for care, many people with type 1 diabetes still report significant difficulties with BG control when it comes to exercise.

Childhood adversity is highly prevalent and linked to lasting psychological and physiological consequences. A potential mechanism for negative health outcomes is altered stress reactivity. While previous research has addressed associations of childhood adversity with stress system reactivity, sympathetic nervous system (SNS) stress reactivity is understudied. We therefore set out here to examining salivary alpha-amylase (sAA) reactivity in relation with childhood adversity. Forty-one healthy adult subjects (n = 24 male; n = 17 female) aged 18-34 years underwent the Trier Social Stress Test (TSST) and completed the Childhood Trauma Questionnaire (CTQ). Saliva for measurement of sAA was collected at three time points; before the TSST, immediately after, and 10 min post-TSST. We found that those with childhood trauma had a higher overall sAA response to the TSST, as seen in a repeated measures ANOVA (CTQ by time interaction: F(1.8,71.5) = 6.46, p = .01) and an independent samples t-test indicating higher sAA baseline to peak response (t = 3.22, p = .003). There was also a positive correlation between sAA reactivity and the CTQ subscales of childhood physical abuse (r = .46, p = .005) and emotional abuse (r = .37, p = .024). Healthy adults with low-to-moderate childhood adversity had a heightened sAA response immediately following the stressor. Higher SNS reactivity could be a link to negative health outcomes in adults with early adversity. Future research should address whether altered sAA reactivity is predictive of negative health outcomes in those with childhood adversity.

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 Test (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 stress. Such patterns could indicate increased risk for unhealthy HPA axis dysregulation, allostatic load, and disease.

Social self-preservation theory posits that stress is experienced when an aspect of an individual's identity has the potential to be negatively evaluated. Appearance is a central part of identity; however, little research has examined whether perceived appearance judgements are a source of social-evaluative stress. In addition, stress may be an explanatory link in the association between appearance perceptions and depressive symptoms. This study examined whether perceived appearance judgements were associated with increased stress and greater depressive symptoms among adults. Study 1 examined the associations between self-reported appearance judgements and cortisol stress responses in response to a laboratory stressor (Trier Social Stress Test) among 71 individuals aged 18-65. Study 2 assessed self-reported appearance judgements and depressive symptoms among 498 adults ages 18-65 via an online survey data collection. Appearance judgement was associated with a stronger cortisol response, higher self-reported stress, and greater depressive symptoms. Stress mediated all associations between appearance judgements and depressive symptoms and neither age nor gender moderated these associations. The findings suggest that appearance judgements contribute to psychological and biological stress processes and demonstrated that stress mediated the association between appearance judgements and depressive symptoms.

Acute stress induces increases in plasma inflammatory mediators, which do not habituate to repeated stress. Inflammation is a risk factor for age-related illnesses, highlighting the need to understand factors controlling inflammation. No studies have examined changes in pro- and anti-inflammatory gene expression in response to repeated acute stress in humans.RNA was isolated from peripheral blood before, 30 and 120min after exposure of n=32 healthy human participants to the Trier Social Stress Test (TSST) on two days. Gene expression of interleukin (IL)-6, IL-1β, nuclear factor (NF)-κB and IκB was measured repeatedly on both days. We further assessed leukocyte numbers, plasma IL-6, and salivary cortisol.Stress induced IL-6 (F=44.7; p0.001) and cortisol responses (F=18.6; p0.001). Cortisol responses habituated (F=5.1, p=0.003), but IL-6 responses did not (n.s.). All genes increased in response to initial stress (IL-6: F=3.8; p=0.029; IL-1β: F=7.1; p=0.008; NF-κB: F=5.1; p=0.009; IκB: F=4.7; p=0.013) and showed habituation to repeated stress (IL-6: t=2.3; p=0.03; IL-1β: t=3.9; p=0.001; NF-κB: t=2.1; p=0.041; IκB: t=3.1; p=0.005). Day 1 responses of IL-1β and IκB were not explained by changes in leukocyte populations, but IL-6 and NF-κB, as well as most day 2 changes were not independent of leukocyte populations.Stress response and habituation of pro- and anti-inflammatory gene expression as found here might indicate that even on an intracellular level, inflammatory responses to acute stress are adaptive in that they respond to initial, but habituate to repeated, similar stress. Future studies will need to test whether non-habituation is predictive of disease.

Overweight and obese individuals, who comprise approximately two-thirds of the U.S. population, are at increased risk for developing a range of diseases. This increased risk may be due in part to maladaptive stress responses within this group, including heightened low-grade inflammation and HPA axis non-habituation. In this study we tested the relationship between adiposity, plasma interleukin-6 (IL-6) and HPA axis responses to repeated stress.Sixty-seven healthy participants were exposed to the Trier Social Stress Test (TSST) on two consecutive days. We collected saliva for cortisol measurements at baseline and at 1, 10, 30, 60 and 120min post-TSST, and blood for plasma IL-6 measurements at baseline and 30 and 120min post-TSST.Stress exposure induced significant increases of cortisol and IL-6 on both days (cortisol: F=38, p0.001; IL-6: F=90.8; p0.001), and repeated exposure was related with cortisol habituation (F=8.2; p0.001) and IL-6 sensitization (F=5.2; p=0.022). BMI and body fat were related with higher cortisol responses to repeated stress (BMI: beta=0.34; p=0.014; body fat: beta=0.29; p=0.045), and with higher IL-6 responses to repeated stress (BMI: beta=0.27, p=0.044; body fat: beta=0.37; p=0.006).Taken together, individuals with higher measures of adiposity showed less efficient HPA axis habituation as well as sensitization of IL-6 responses to repeated acute stress. These findings point to maladaptive stress response patterns in overweight humans, which, through exposure to higher levels of inflammatory mediators, might partially explain diseases related with overweight and/or obesity.

Background: The aim was to explore the impact of diabetes-related technology to ensure that such devices are used in a way that returns maximum benefit from a medical and psychological perspective. Method: Spouses and caregivers of people with type 1 diabetes were invited to complete an online questionnaire about their experiences with diabetes technologies used by their family members. Participants were recruited via the Glu online community website. Questions explored impact on daily living, frequency and severity of hypoglycemia, and diabetes-related distress. Results: In all, 100 parents/caregivers and 74 partners participated in this survey. Average (mean) duration of living with a person with type 1 diabetes was 16 years (SD = 13) for partners, with duration of diabetes for children being 4.2 ± 3.2 years. Average duration of current therapy was 8.3 ± 7.3 years for adults and 3.4 ± 2.9 years for children. Of the participants, 86% partners and 82% parents/caregivers reported diabetes technology had made it easier for their family members to achieve blood glucose targets. Compared to partners, parents/caregivers reported more negative emotions ( P < .001) and decreased well-being ( P < .001) related to their family members type 1 diabetes. Diabetes-related distress was common, as was sleep disturbance associated with device alarms and fear of hypoglycemia. Reduced frequency and severity of hypoglycemia related to device use was reported by approximately half of participants. Conclusion: There is little doubt about the medical benefit of diabetes technologies and their uptake is increasing but some downsides were reported. Barriers to uptake of technologies lie beyond the mechanics of diabetes management. Supporting users in using diabetes technology to achieve the best possible glycemic control, in the context of their own life, is crucial. Furthermore, understanding these issues with input from the type 1 diabetes community including family members and caregivers will help innovation and design of new technology.

In this study we tested the hypothesis that participants higher in dispositional self-compassion would show lower stress-induced reactivity of salivary alpha-amylase (sAA), a marker of sympathetic nervous system activation. Thirty-three healthy participants (18–34 years old) were exposed to a standardized laboratory stressor on two consecutive days. Self-compassion, self-esteem, and demographic factors were assessed by questionnaire and sAA was assessed at baseline and at 1, 10, 30, and 60 minutes following each stressor. Self-compassion was a significant negative predictor of sAA responses on both days. This relationship remained significant when controlling for self-esteem, subjective distress, age, gender, ethnicity, and Body Mass Index (BMI). These results suggest that self-compassion may serve as a protective factor against stress-induced physiological changes that have implications for health.

Given the well-documented deleterious health effects, poor sleep has become a serious public health concern and increasing efforts are directed toward understanding underlying pathways. One potential mechanism may be stress and its biological correlates; however, studies investigating the effects of poor sleep on a body's capacity to deal with challenges are lacking. The current study thus aimed at testing the effects of sleep quality and quantity on cortisol responses to acute psychosocial stress. A total of 73 college-aged adults (44 females) were investigated. Self-reported sleep behavior was assessed via the Pittsburgh Sleep Quality Index and salivary cortisol responses to the Trier Social Stress Test were measured. In terms of sleep quality, we found a significant three-way interaction, such that relative to bad sleep quality, men who reported fairly good or very good sleep quality showed blunted or exaggerated cortisol responses, respectively, while women's stress responses were less dependent on their self-reported sleep quality. Contrarily, average sleep duration did not appear to impact cortisol stress responses. Lastly, participants who reported daytime dysfunctions (i.e. having trouble staying awake or keeping up enthusiasm) also showed a trend to blunted cortisol stress responses compared to participants who did not experience these types of daytime dysfunctions. Overall, the current study suggests gender-specific stress reactivity dysfunctions as one mechanism linking poor sleep with detrimental physical health outcomes. Furthermore, the observed differential sleep effects may indicate that while the body may be unable to maintain normal hypothalamic-pituitary-adrenal functioning in an acute psychosocial stress situation after falling prey to low sleep quality, it may retain capacities to deal with challenges during extended times of sleep deprivation.

Failure of the hypothalamus-pituitary-adrenal (HPA) axis to habituate to repeated stress exposure is related with adverse health outcomes, but our knowledge of predictors of non-habituation is limited. Rumination, defined as repetitive and unwanted past-centered negative thinking, is related with exaggerated HPA axis stress responses and poor health outcomes. The aim of this study was to test whether post-stress rumination was related with non-habituation of cortisol to repeated stress exposure. Twenty-seven participants (n=13 females) were exposed to the Trier Social Stress Test (TSST) twice on consecutive afternoons. Post-stress rumination was measured after the first TSST, and HPA axis responses were assessed by measuring salivary cortisol 1 minute before, and 1, 10, 20, 60, and 120 minutes after both TSSTs. Stress exposure induced HPA axis activation on both days, and this activation showed habituation indicated by lower responses to the second TSST (F= 3.7, p=.015). Post-stress rumination after the first TSST was associated with greater cortisol reactivity after the initial stress test (r = 0.45, p < 0.05) and with increased cortisol responses to the second TSST (r = 0.51, p < 0.01), indicating non-habituation, independently of age, sex, depressive symptoms, perceived life stress, and trait rumination. In summary, results showed that rumination after stress predicted non-habituation of HPA axis responses. This finding implicates rumination as one possible mechanism mediating maladaptive stress response patterns, and it might also offer a pathway through which rumination might lead to negative health outcomes.

We examined the hypothesis that self-compassion is associated with lower levels of stress-induced inflammation. On two consecutive days, plasma concentrations of interleukin-6 (IL-6) were assessed at baseline and at 30 and 120 minutes following exposure to a standardized laboratory stressor in a sample of 41 healthy young adults. Participants who were higher in self-compassion exhibited significantly lower day 1 IL-6 responses, even when controlling for self-esteem, depressive symptoms, demographic factors, and distress. Self-compassion was not related to day 2 IL-6 response but was inversely related to day 2 baseline IL-6 levels, and to increase in baseline IL-6 from day 1 to day 2. These findings suggest that self-compassion may serve as a protective factor against stress-induced inflammation and inflammation-related disease.

Background Previous research indicates that ethnic differences in subjective social status (SSS), inflammatory markers, and stress reactivity may exist. However, no studies have examined the relationship between SSS and ethnicity in the context of IL-6 responses to repeated stress. Methods Eighty-five adults (51% female, mean age = 37.9 years) completed the Trier Social Stress Test (TSST) on two consecutive days. Blood samples were collected at 1 minute prior and 30 minutes and 2 hours post-TSST for measurement of plasma IL-6. Community and United States SSS were assessed using MacArthur ladders. Results The sample consisted of n = 80 participants (n = 51 white, n = 29 non-white). Both TSSTs induced increases in plasma IL-6 (F = 65.1, p 0.001 ), with higher responses to the second exposure (F = 7.85, p = 0.006). Community SSS was positively associated with IL-6 responses to the first TSST (r = 0.24, p = 0.03) but not the second (r = −0.01, p = 0.9). Whites rated themselves higher than nonwhites in SSS (Community, trend, p = 0.053; US, p = 0.009). Regression analyses revealed a significant SSS by NW interaction predicting IL-6 responses to the first TSST (beta = 0.82, p = 0.046), with higher SSS predicting elevated IL-6 responses only in non-whites. Conclusions Subjective Social Status ratings were sensitive to race and predicted IL-6 responses to the TSST in only non-white individuals. Ethnicity and SSS may play a role in social evaluation, a key component of social stress. More research is needed to determine the nature these associations.

Rationale Depressive symptoms are associated with exaggerated inflammatory and altered cortisol stress responses. Cortisol has been shown to stimulate IkB gene expression, which counteracts pro-inflammatory cytokine production. Increased inflammation is a risk factor for disease, highlighting the need to understand factors controlling inflammation. No studies have examined IkB expression in response to acute stress in relation with depressive symptoms. Methods We recruited n = 48 healthy individuals and exposed them to the Trier Social Stress Test (TSST). Stress responses of plasma Interleukin-6, salivary cortisol, as well as inhibitory kappa-B (IkB) gene expression in peripheral blood, were measured before, as well as 30, and 120 min after stress. We also assessed self-reported depressive symptoms, post-stress mood, and stress appraisals. Results Stress exposure induced increases in IL-6 and cortisol (IL-6: F = 42.41, p 0.001 ; cortisol: F = 15.98, p 0.001 ). IkB expression increased after stress with a peak at 30 min and recovery at 120 min (F = 13.11, p 0.001 ). Depressive symptoms were positively related with IkB expression 30 min after stress (beta = 0.30, p = 0.05), and this relationship was mediated by decreases in positive affect. Conclusions: These show that in individuals with more depressive symptoms, acute stress translates into upregulated gene expression of inhibitory kappaB, which might be mediated through stronger decreases in mood. Higher IkB might allow better down regulation of inflammation, but could also be a response to stronger inflammatory reactivity in general.

Rationale: Acute stress is accompanied by an inflammatory response and some individuals show sensitization to repeated stress. Increased peripheral inflammation is a risk factor for many age-related illnesses, highlighting the need to understand factors controlling inflammation. No studies have examined changes in pro- and anti-inflammatory gene expression in response to repeated acute stress in humans. Methods: We recruited n = 31 healthy individuals and examined gene expression of IL-6, IL-1beta, RelA and IkappaB before, 30 and 120 min after exposure to the Trier Social Stress Test (TSST) on two days. We assessed the inflammatory response by measuring plasma IL-6, and cortisol as the major anti-inflammatory stress hormone. Results: Stress exposure induced inflammatory and cortisol responses (IL-6: F = 49.3, p F = 13.7, p ∗ time interaction F = 4.2, p = 0.011) but IL-6 responses did not (n.s.). IL-6 and IL-1beta gene expression increased on Day 1, but not on Day 2 (day ∗ time interaction: IL-6: F = 106, p = 0.001; IL-1beta: F = 7.9, p = 0.006). RelA expression increased on both days (time effect F = 5.0, p = 0.013). IkB expression increased then decreased below baseline on Day 1, and decreased post-TSST on Day 2 (day ∗ time interaction: F (2,54) = 5.4, p = 0.08). There was no relationship between IL-1Beta, IkB, and RelA with plasma IL-6 or cortisol, or between cortisol and plasma IL-6. Conclusions: Taken together, results show a response pattern of pro- and anti-inflammatory gene expression characterized by differential stress responses and habituation patterns that are in disjunction with patterns of cortisol and plasma IL-6 responses to repeated stress. This indicates that increases in plasma concentrations of inflammatory cytokines are unlikely to originate solely from de novo transcription within PBMCs, but that alternative or additional sources of plasma inflammatory cytokines need to be explored.