The relationship between serum cortisol,adrenaline, blood glucose and lipid profile of undergraduate students under examination stress

BackgroundStress is an extremely adaptive phenomenon in human beings and cortisol is a known stress hormone. Examination has been described as a naturalistic stressor capable of affecting human health.ObjectivesTo estimate the relationship between serum cortisol, adrenaline, fasting blood glucose (FBG) and lipid profile during examination stress.MethodsTwo hundred and eight (208) apparently-healthy undergraduate students (aged, 24 ± 6 years) were involved in the study. Exactly 5 mls of venous blood was collected from each subject 1–3 hours before a major examination. A second assessment was done on the same students 3–4 weeks before any examination (control samples). Cortisol and adrenaline were assayed using ELISA techniques, FBG was assayed using enzymatic method while lipid parameters were assayed using standard enzymatic-spectrophotometric methods.ResultsThere was statistically significant increase in serum cortisol, adrenaline, Total cholesterol, HDL-cholesterol and LDL-cholesterol levels in students under examination stress compared to the non examination period (p=0.001, 0.013, 0.0001, 0.0001 and 0.0001, respectively). FBG showed no significant increase. There was also significant positive correlation (r=0.297, p=0.032) between serum cortisol and TC/HDL ratio (cardiac risk factor) before examination stress but not during the stress period.ConclusionsSignificant positive correlation was observed between cortisol and TC/HDL ratio before examination stress.     

Temporal features of elevated hair cortisol among earthquake survivors

This study aimed to determine the effect on hair cortisol level of a chronic stress response from the Wenchuan earthquake, and to explore the temporal features of elevated hair cortisol. We recruited two cohorts of earthquake survivors: cohort A consisted of 12 male adults and 8 females and cohort B of 20 male adolescents, with 23 and 29 participants as controls, respectively. Their hair samples closest to the scalp were assayed with mass spectrometry to determine cortisol content. Results revealed that hair cortisol content in survivors of cohort A was significantly higher than in the control. For survivors of cohort B, hair cortisol levels increased 6 and 22 weeks after the earthquake and decreased 43 weeks after the outburst. In conclusion, the chronic stress response elicited by the earthquake resulted in elevated hair cortisol. Timing since the earthquake outburst played an important role in the long‐term response of the HPA axis to a major acute stressor.     

急性冠状动脉综合征患者头发皮质醇水平与倦怠的相关性及其对生活质量的影响研究

背景　头发皮质醇水平是一个反映慢性压力的指标,课题组前期研究结果提示倦怠可能是急性冠状动脉综合征（ACS）的独立危险因素,但目前国内尚缺乏关于头发皮质醇水平与倦怠和ACS的研究。目的　探讨ACS患者头发皮质醇水平与倦怠的相关性,以及头发皮质醇水平对患者出院1个月后生活质量的影响。方法　以2015年3月-2018年2月因首次发生ACS收住昆明医科大学第一附属医院心内科的89例患者为试验组,以同期在本院进行年度体检的42例健康者为对照组。取两组受试者少量头发进行皮质醇水平检测,采用哥本哈根倦怠量表（CBI）的一般倦怠子量表评估ACS患者的倦怠水平,采用生活质量8条简明量表（SF-8）和西雅图心绞痛量表（SAQ）评估ACS患者出院１个月后的生活质量。对头发皮质醇数据进行自然对数转换,两组头发皮质醇水平比较采用成组t检验,并采用多重线性回归排除混杂因素对结果的影响;ACS患者头发皮质醇水平和倦怠的相关性采用偏相关分析;构建多重线性回归模型分析ACS患者头发皮质醇水平与出院1个月后生活质量的关系。结果　75例ACS患者和38例健康者提供了头发样本进行皮质醇水平检测。ACS患者的头发皮质醇水平高于健康者〔（2.00±1.82）ln ng/g比（1.59±1.48）ln ng/g,t=2.42,P=0.017〕,构建多重线性回归模型排除性别、年龄、体质指数、工作状况、受教育程度、吸烟、饮酒的影响后,组别是头发皮质醇水平的影响因素〔b（95%CI）=2.038（0.198,3.878）,P=0.037〕。偏相关分析结果显示,排除性别、年龄、体质指数、工作状况、受教育程度、婚姻状况、吸烟、饮酒、Killip心功能分级、既往史、心血管病家族史的影响后,ACS患者的头发皮质醇水平与倦怠评分呈正相关（偏相关系数为0.303,P=0.011）。ACS患者头发皮质醇水平是出院1个月后SF-8生理健康评分、SAQ心绞痛稳定状态和心绞痛发作频率评分的影响因素〔b（95%CI）分别为-1.459（-1.984,-0.934）、-8.821（-15.629,-2.013）、-6.342（-12.653,-0.031）,P均<0.05〕。结论　ACS患者的头发皮质醇水平高于健康者;在ACS患者中,倦怠与头发皮质醇水平呈正相关关系;基线头发皮质醇水平高的ACS患者出院1个月后的生活质量较差。     

11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess

The adverse metabolic effects of prescribed and endogenous glucocorticoid (GC) excess, Cushing syndrome, create a significant health burden. We found that tissue regeneration of GCs by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), rather than circulating delivery, is critical to developing the phenotype of GC excess; 11β-HSD1 KO mice with circulating GC excess are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis, adiposity, hypertension, myopathy, and dermal atrophy of Cushing syndrome. Whereas liver-specific 11β-HSD1 KO mice developed a full Cushingoid phenotype, adipose-specific 11β-HSD1 KO mice were protected from hepatic steatosis and circulating fatty acid excess. These data challenge our current view of GC action, demonstrating 11β-HSD1, particularly in adipose tissue, is key to the development of the adverse metabolic profile associated with circulating GC excess, offering 11β-HSD1 inhibition as a previously unidentified approach to treat Cushing syndrome.Estimates suggest that 1–2% of the population of the United States and United Kingdom take prescribed glucocorticoids (GCs) for the treatment of a broad spectrum of inflammatory and autoimmune diseases (1, 2). Despite the efficacy of GCs, 70% of patients experience an adverse systemic side-effect profile. The resultant Cushingoid features include central obesity, proximal myoatrophy, hypertension, skin thinning, osteoporosis, hepatic steatosis, insulin resistance, and type 2 diabetes (3, 4). Collectively, this contributes to increased risk of cardiovascular morbidity and mortality (5, 6). These features are replicated in patients with much rarer endogenous GC excess (Cushing syndrome), as first described by Harvey Cushing in 1932 (7). Current medical therapeutic options that reverse the tissue-specific consequences of hypercortisolism are limited.GC availability and action depend not only upon circulating levels but also on tissue-specific intracellular metabolism by 11β-hydroxysteroid dehydrogenases (11β-HSDs). Key metabolic tissues including liver, adipose tissue, and skeletal muscle express 11β-HSD type 1 (11β-HSD1), which coverts inactive cortisone to active cortisol [11-dehydrocorticosterone (11DHC) and corticosterone (CORT) in rodents, respectively] (8). In the setting of GC excess, the relative contribution to the metabolic effects induced by GCs of simple delivery of active GCs (cortisol or CORT) to a target tissue, compared with the regeneration of active GCs by 11β-HSD1 within the tissue, has not been determined.Type 2 11β-HSD (11β-HSD2) is predominately expressed in the kidney, colon, and salivary gland and catalyzes the inactivation of cortisol to cortisone (CORT to 11DHC in rodents). This not only protects the mineralocorticoid receptor from occupancy by cortisol but also crucially provides substrate for 11β-HSD1 in peripheral tissues.Transgenic animal models have highlighted the critical role of 11β-HSD1 in the regulation of metabolic phenotype in individual tissues. Mice overexpressing 11β-HSD1, specifically in adipose tissue, develop visceral obesity, insulin resistance, dyslipidemia, and hypertension (9, 10). Similarly, liver-specific 11β-HSD1 overexpression results in insulin resistance and hypertension, but not obesity (11). Importantly, circulating CORT levels were not elevated in either model, suggesting increased intracellular GC availability underpins the observed phenotypes. Indeed, this was confirmed in the adipose-specific 11β-HSD1–overexpressing mice, where twofold higher intraadipose CORT levels were recorded in comparison with WT controls (9). Ultimately, this has led to the development of selective 11β-HSD1 inhibitors as a potential treatment for patients with diabetes, obesity, and hypertension (12, 13).Although it is clear that 11β-HSD1 has a critical role to play in governing GC availability, its potential dynamic role in the setting of GC excess has not been fully explored (14–16). We have previously reported a patient with Cushing disease who was protected from the classic Cushing phenotype, owing to a functional defect in 11β-HSD1 activity, as evidenced by serum and urinary biomarkers (17). Based on this observation, we have hypothesized that tissue intrinsic 11β-HSD1 activity is the major determinant of the manifestations of GC excess and that 11β-HSD1 deletion will ameliorate the associated metabolic abnormalities. To determine the relative tissue-specific contribution to this effect, we have generated tissue-specific 11β-HSD1 deletions in liver and adipose tissue.     

Body mass index,waist circumference and body fat are positively correlated with hair cortisol in children: A systematic review and meta‐analysis

The current body of research lacks a meta‐analysis of the relationship between hair cortisol concentration (HCC) and anthropometry in children. Therefore, this systematic review and meta‐analysis was conducted to examine this relationship and explore possible moderators between HCC and body mass index (BMI/BMI z‐score). Eleven databases were searched: CINAHL, Cochrane, Embase, PsycEXTRA, Psychology and Behavioral Sciences, PsycINFO, PubMed, Scopus, Social Sciences Full Text, Sociological Abstracts and Web of Sciences. Random‐effects models and exploratory moderator analyses with mixed‐effects models were performed using the Comprehensive Meta‐Analysis software. The meta‐analysis showed small positive correlations between HCC and BMI (r = 0.08, 95% confidence interval [CI]: 0.02, 0.14, n = 18, p = .009), BMI z‐score (r = 0.10, 95% CI: 0.03, 0.16, n = 12, p = .003), waist circumference (r = 0.10, 95% CI: 0.04, 0.17, n = 10, p = .001) and body fat including fat mass index (r = 0.06, 95% CI: 0.02, 0.11, n = 3, p = .005). The relationship between HCC and BMI/BMI z‐score was significantly moderated by children's sex. Results from this meta‐analysis provide initial objective support for a small positive relationship between HCC and anthropometric factors.     

Relationship between effort–reward imbalance and hair cortisol concentration in female kindergarten teachers

Objective

The present study aims to investigate the relationship between effort–reward imbalance and hair cortisol concentration among teachers to examine whether hair cortisol can be a biomarker of chronic work stress.

Methods

Hair samples were collected from 39 female teachers from three kindergartens. Cortisol was extracted from the hair samples with methanol, and cortisol concentrations were measured with high performance liquid chromatography–tandem mass spectrometry. Work stress was measured using the effort–reward imbalance scale.

Results

The ratio of effort to reward showed significantly positive association with hair cortisol concentration.

Conclusion

The cortisol concentration in the system increases with the effort–reward imbalance. Measurement of hair cortisol can become a useful biomarker of chronic work stress.