1496 Epigenetic perspective of burnout

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IntroductionDespite burnout received an increasing attention in occupational health, there are no binding diagnostic criteria to identify burnout ‘cases’. The main aggravating factor is the overlap between burnout and depression. The lack of diagnostic consensus resulted in several attempts to identify biomarkers of burnout, but the results were inconsistent. However, epigenetic biomarkers of burnout have not been investigated so far even though DNA methylation is implicated as a mediator between environmental stress and psychopatology. Therefore, our aim is to investigate epigenetic (DNA methylation) correlates of burnout, compare them to those present in depression and explore their biomarker potential.MethodsWe conducted a systematic literature review to gain an insight into DNA methylation mechanisms related to chronic stress, burnout and depression. The biomarker potential of genes derived from the literature review will be tested in a cross-sectional and a cohort study.ResultsWe identified four genes as potential burnout biomarkers: glucocorticoid receptor gene (NR3C1), brain derived neurotrophic factor gene (BDNF), serotonin transporter gene (SLC6A4) and tyrosine hydroxylase (TH) gene. Methylation of NR3C1 displayed differed patterns in chronic stress and depression. SLC6A4 was hypermethylated in chronic stress, depression and burnout. Methylation levels of BDNF displayed different patterns associated with work-related stress compared to those correlated with depressive symptoms in the same human sample. Work-related stress affected methylation of TH gene in a single study.ConclusionAdditional research exploring DNA methylation patterns in burnout and comparing them to those in depression could offer a better understanding of epigenetic dimensions beyond these constructs and their overlap. Moreover, carefully designed longitudinal studies are necessary for revealing the cause-effect relationship of epigenetic changes and their clinical correlates.

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