Burnout among high school students is linked to their telomere length and relatedness with peers.

School burnout is a serious concern, as it impairs students' health and academic success. According to the Conservation of Resources Theory, burnout results from the depletion of personal coping resources and can be counteracted by supportive social relationships. However, it is not yet clear how students' relatedness with their peers is linked to their burnout. Next to students' self-reported fatigue, biomarkers such as telomere length (TL), which presents an indicator of aging, complement stress research. To identify school-related factors that may prevent students from experiencing burnout and to link TL to students' self-reported burnout, the current study investigated how relatedness with peers as well as TL at the beginning of the school year explained students' burnout at the end of the school year. The sample included 78 students (Mage = 13.7 ± 0.7 years; 48% girls). Results of multilevel analysis in Mplus indicate that, over the school year, students with higher TL and those who experienced relatedness with their peers reported lower levels of burnout. Moreover, students who felt related to their peers exhibited a longer TL. The study implies that students' relatedness with their peers may be a promising setscrew to prevent students' burnout and support their physical health. This is one of the first studies to link TL with school-related variables such as burnout and relatedness to peers in a non-clinical student sample, providing a baseline for interventions and future interdisciplinary studies in the field of education and stress.

Moderator Effects of Life Stress on the Association between MAOA-uVNTR, Depression, and Burnout.

BACKGROUND: The serotonergic and noradrenergic systems have a strong impact on several affective disorders and are key targets for psychopharmacological therapy. With respect to pathogenesis, there is a growing body of evidence showing an influence of a promoter repeat polymorphism (MAOA-uVNTR) altering the expression rate of monoamine oxidase A. However, only a few studies investigate its influence on depression with only 2 of them considering the moderating effects of life stress. For burnout, there are no studies so far investigating the genetic basis. OBJECTIVES: The aim of the present study was to replicate an interaction effect of MAOA-uVNTR and life stress on depression, and extend these possible findings to the burnout syndrome. Especially, the latter one might help in understanding the underlying mechanisms of burnout and its association to depression. METHOD: A total of n = 1,541 participants (n = 1,099 healthy controls, n = 442 inpatients with affective disorders) provided genetic samples and filled in self-report questionnaires measuring depression, burnout, and the extent of experienced stressful life events (SLEs). RESULTS: A life stress x MAOA-uVNTR interaction on depression and burnout was observed in women suggesting that carriers of the high expressing allele (MAO-H) with many SLEs had the highest scores in both burnout and depression. In men, there was only a weak effect of MAOA-uVNTR on depression. CONCLUSIONS: The results suggest a more pronounced reactivity to adverse environmental factors in carriers of the MAO-H allele. Especially the effect of life stress and MAOA-uVNTR on burnout should be independently replicated in the future as this is the first study showing this association.

Role of NR3C1 and SLC6A4 methylation in the HPA axis regulation in burnout.

BACKGROUND: Work-related stress and burnout have become major occupational health concerns. Dysregulation of HPA axis is considered one of the central mechanisms and is potentially moderated through epigenetics. In the present study, we aim to investigate epigenetic regulation of the HPA axis in burnout, by focusing on salivary cortisol and cortisone and DNA methylation of the glucocorticoid receptor gene (NR3C1) and the serotonin transporter gene (SLC6A4). METHODS: We conducted a cross-sectional study with 59 subjects with burnout and 70 healthy controls recruited from the general population. All participants underwent a clinical interview and psychological assessment. Saliva samples were collected at 0, 30 and 60 min after awakening and were used to quantify cortisol and cortisone. Pyrosequencing was performed on whole blood-derived DNA to assess DNA methylation. RESULTS: There were no between-group differences in cortisol levels, whereas burnout participants had higher levels of cortisone. Job stress was associated with increased cortisol and cortisone. We observed both increased and decreased NR3C1 and SLC6A4 methylation in the burnout group compared to the control group. Some of these methylation changes correlated with burnout symptoms dimensionally. Increased methylation in a specific CpG in the SLC6A4 promoter region moderated the association between job stress and burnout. DNA methylation in this CpG was also associated with increased cortisol. In addition, average methylation of NR3C1 was negatively associated with cortisone levels. LIMITATIONS: This is a cross-sectional study and therefore no conclusions on causality could be made. CONCLUSIONS: We provide first evidence of changes in DNA methylation of NR3C1 and SLC6A4 in burnout, which were further associated with cortisol and cortisone. Further, increased cortisol and cortisone seemed to reflect job stress rather than burnout itself.

Chronic stress exposure, diurnal cortisol slope, and implications for mood and fatigue: Moderation by multilocus HPA-Axis genetic variation.

Chronic stress exposure has been shown to alter hypothalamic-pituitary-adrenal (HPA) axis functioning, which may mediate its effects on psychopathology and negative health outcomes. The nature of the chronic stress-HPA axis dysregulation is unclear and individuals likely vary in the extent to and manner in which indices of HPA axis regulation, such as diurnal cortisol slope, are influenced by chronic stress. We examined whether HPA-axis-linked genetic variation moderates the association between chronic stress and diurnal cortisol slope, and potential implications for mood and fatigue (possible manifestations of negative clinical outcomes). 211 adolescents (M age 15.89, 54.5% female) completed chronic stress interviews and provided DNA samples. Participants then provided saliva samples at waking and 12 h post-waking for two consecutive weekdays. HPA-axis genetic variation was calculated using a multilocus genetic profile score (MGPS) approach, using ten SNPs from CRHR1, NR3C1, NR3C2, and FKBP5 to generate an additive score of HPA-axis-linked genetic risk. Neither chronic stress nor MGPS directly predicted diurnal slope, but MGPS moderated the association between chronic stress and diurnal slope, with stress predicting a high waking cortisol followed by steep slope among youth with low but not high MGPS scores. MGPS also interacted with chronic stress to predict both negative affect and fatigue, and moderated the indirect effect of chronic stress on mood and fatigue via diurnal slope. Results suggest that diurnal cortisol regulation may be one mechanism by which genetic risk intensifies the association between chronic stress and negative outcomes.