- Email: [email protected]
Burnout, hair cortisol, and timing: Hyper- or hypocortisolism?
Psychoneuroendocrinology xxx (xxxx) xxx–xxx
Contents lists available at ScienceDirect
Psychoneuroendocrinology journal homepage: www.elsevier.com/locate/psyneuen
Short Communication Burnout, hair cortisol, and timing: Hyper- or hypercortisolism? Modern human life is characterized by a specific set of challenges that spread across our private and professional lives. In particular in our professional lives, many of us are motivated to strive for ever greater successes, and are willing to invest more and more of our time to achieve work goals. In addition to those motivated by personal or their company’s successes, many humans are altruistically motivated to give more and more of their time and energy to care for others, most prominently in health care or teaching professions. While dedication to work, and the feeling of meaning and purpose one might derive from this, can be extremely fulfilling and a source of life satisfaction, negative consequences frequently occur, one of which being burnout. In contrast to the concept of chronic stress, which describes ongoing strains and stresses of life per se, and that is reasonably well studied both in terms of psychological and biological consequences (Juster et al., 2011; Kudielka and Wüst, 2010; Lupien et al., 2009; Rohleder, 2012), burnout is better described as a consequence of exposure to chronic work, but also certain non-work stressors in combination with intra-personal and situational conditions (Maslach et al., 2001; Melamed et al., 1999). The syndrome of burnout has been defined as a combination of emotional exhaustion, physical fatigue, and cognitive weariness (Melamed et al., 2006), and/or as severe energy depletion, dysfunctional attitudes towards work, in particular cynicism, and a lack of professional efficacy (Maslach et al., 2001). It has further been described as the result of inefficient coping with stress, and consequently, the depletion of an individual’s coping resources (Melamed et al., 1999). Consequently, burnout leads to increased frequency of sick leaves, to early retirements, and has been associated with significant health issues including cardiovascular disease and type 2 diabetes (Melamed et al., 2006), leading to significant costs, both for societies and human well-being. Given these consequences, it is important to improve our understanding of both, the factors leading to burnout, as well as pathways from burnout to health issues. As with most research addressing psychological constructs related to stress, or stress-related diseases, research has first concentrated on the hypothalamus-pituitary-adrenal (HPA) axis, with limited success and mixed results, with reports of higher HPA axis activity in burned out individuals (e.g. Melamed et al., 1999), systematic reviews and meta-analyses finding no relationships (e.g. Danhof-Pont et al., 2011), and another meta-analytic study reporting that a lower cortisol awakening response (CAR) seems to be characteristic for burnout (Chida and Steptoe, 2009). 1. What kind of biological alterations can we expect in burnout? In the related field of chronic stress research, findings on HPA axis alterations were similarly difficult to reconcile, with a similarly confusing mix of studies showing higher, lower, or unchanged HPA axis parameters. This was of course not made easier by different expectations. Due to the fact that acute stress activates the HPA axis, it was expected by some that chronic stress should be associated with hypercortisolism, and there were data supporting this. Others were expecting an exhaustion of HPA axis resources as being proposed very early by Selye (Selye, 1936), and there were also data supporting this assumption. Progress was further complicated by the fact that basal HPA axis activity has so many different parameters, which seem to be reflecting different aspects of activity. Only those that take into account the system’s diurnal rhythm have proven to be interpretable, and only taking into account type and timing of chronic stress permitted Miller et al. in a seminal meta-analytic study to reconcile previously conflicting findings (Miller et al., 2007). In a simplified way, their findings were that in early stages of chronic stress, HPA axis activity tends to be higher, while it will decrease with longer duration of chronic stress to ultimately reach a state of hypocortisolism and a loss of circadian rhythm. This is in line with other authors linking chronic stress to hypocortisolism, and proposing hypocortisolism as key factor in the development of stress-related disease (e.g. Fries et al., 2005). However, another key issue emerging from chronic stress research is that it is by no means sufficient to only investigate HPA axis changes, in order to understand health consequences. First of all, the HPA axis is not the only stress system, and not the only one altered with chronic stress exposure, and in particular the sympathetic nervous system (SNS), or its sub component, the sympathetic adrenal medullary (SAM) system, needs to be taken into account. We have shown, for example, that experiencing a family member going through brain cancer treatment for almost a year does not affect basal HPA axis activity, but was related with alterations in SNS activity (Rohleder et al., 2009). Secondly, changes in either of these stress systems are seldom sufficient to understand downstream health consequences of chronic stress exposure. In the same cancer caregiver study, we also found that in the absence of HPA axis changes, chronic stress had severe consequences on downstream mechanisms, in particular inflammation (Rohleder et al., 2009). In related studies, Miller and Cole for example have repeatedly confirmed and expanded on such findings, showing that transcriptional activity in pathways responsive to cortisol is markedly decreased in various conditions of chronic life stress, while the HPA axis per se was unchanged (e.g. Miller et al., 2008, 2009). This is not meant to question the validity of studying the HPA axis in burnout, as done by Penz et al. here (Penz et al., 2017). On the contrary – Since the study of burnout appears to be in its infancy compared to the study of chronic stress in general, above considerations were meant to set the stage of what to reasonably expect when assessing HPA axis activity in burnout. Learning from what we know about chronic stress and its biological consequences, and considering that burnout could be regarded as a consequence of long-term exposure to chronic stress, with inefficient coping (Melamed et al., 1999), the following would be expected: (1) lower overall cortisol and relatively flatter diurnal profiles; (2) higher SNS activity with http://dx.doi.org/10.1016/j.psyneuen.2017.10.008
0306-4530/ © 2017 Elsevier Ltd. All rights reserved.
Psychoneuroendocrinology xxx (xxxx) xxx–xxx
Short Communication
altered diurnal profiles; (3) upregulation of transcripts responsive to inflammatory stimuli and down-regulation of glucocorticoid responsive transcripts; (4) higher inflammatory markers in plasma. 2. Where does the paper by Penz et al. fit in here? in their study of more than three-hundred working adults found a positive relationship of burnout with cortisol measured in hair (HCC), reflecting cortisol concentrations over three months prior to data collection (Penz et al., 2017). In other words – they found the contrary of what we would expect based on the literature, and based on conceptually comparing burnout with chronic stress: Hypercortisolism. In more detail, they found that those with a total burnout score above a threshold characterizing “severe burnout symptoms” was the most consistent predictor of higher hair cortisol, along with the subscale reduced efficiency, while continuous scores as well as subscales for emotional exhaustion and cynicism were less reliably associated with high cortisol. Notably, relationships held after controlling for depression. 3. What do these unexpected findings of hypercortisolism in burnout mean? Several explanations are conceivable to explain the finding of hypercortisolism in those with high burnout in this sample. One explanation might simply be that this is just another study the big data pool of mixed data. This is of course not a satisfying explanation and none that moves the field forward. It is also unlikely that the study differs too much from other studies in terms of participants or burnout assessment, as the sample is of reasonable size, assessment of burnout uses similar tools than the majority of other studies, and participants are normal working adults recruited from the general population. More promising explanations might be found in the issue of timing, and in the fact that hair cortisol was used here for the first time in the study of burnout. 4. Is hair cortisol so different from other measures of HPA axis activity that it explains the unexpected finding of hypercortisolism? There are data supporting the notion that hair cortisol does not differ so much from other measures to explain an unexpected finding. Short et al. (2016) for example reported that hair cortisol concentrations from a strand of hair reflecting a one-month period of time was significantly associated with integrated salivary cortisol assessed diurnally over the same month (Short et al., 2016). Stalder et al. (2017) in their meta-analysis of chronic stress and hair cortisol report that hair cortisol is only positively associated with chronic stress if the stress is still ongoing, and negatively related when stress is absent (Stalder et al., 2017). While this does not perfectly line up with findings summarized by Miller et al. (Miller et al., 2007), it does point in the right direction, and as Stalder et al. note, they only had very few studies in that section of their analysis. Similarly, summarizing data on Posttraumatic Stress Disorder (PTSD) and hair cortisol, Steudte-Schmiedgen et al. (2016) found support for a conclusion in line with Miller et al.’s results, i.e. that longer duration or time since trauma was related with lower hair cortisol (Steudte-Schmiedgen et al., 2016). While there are also findings of hair cortisol being positively related with conditions that could be considered similar to chronic stress, such as discrimination (Jackson et al., 2016; O’Brien et al., 2017), low social status (Ursache et al., 2017; Zilioli et al., 2017), and with trauma (Mewes et al., 2017), all these findings, taken together, do not support an explanation of hair cortisol simply “measuring the opposite” as other traditional ways of assessing HPA axis activity. These findings tell us that this finding of hypercortisolism in burnout needs to be taken seriously, which leads to the next question or potential explanation: 5. What role does timing play with regard to hypercortisolism in burnout? As summarized above, a generally accepted notion in chronic stress research is the occurrence of hypocortisolism after longer exposure to a chronically stressful condition, such as chronic life or work stress, or a longer time living with the memory of an experienced trauma (Miller et al., 2007). With regard to burnout, and based on the assumption that burnout in a way follows chronic work stress, or develops in later stages of prolonged work stress, one would expect HPA axis activity to be diminished, and diurnal profiles to be relatively flat. Given that diurnal cortisol production appears to be related with cortisol measured in hair (Short et al., 2016), one would expect to see this hypocortisolism in hair cortisol as well. Unfortunately, timing hair sample relative to onset and duration of burnout is not reported in this study, and consequently was not tested for its association with cortisol concentrations in hair. That leaves this important question up for speculation. The authors do speculate along these lines. They argue that their finding of a stronger association of reduced efficacy with cortisol, in comparison to a weak or non-existent association of emotional exhaustion with cortisol could indicate that participants here were indeed in an earlier stage of burnout, assuming that reduced efficacy develops before emotional exhaustion (Penz et al., 2017). Of course, ultimate answers can only result from future studies, or future reports resulting from the Dresden Burnout Study. 6. Conclusions present data here showing that burnout, and in particular, severe burnout and reduced work efficacy are related with increased HPA axis activity, i.e. hypercortisolism, measured in hair reflecting a three-month time period. These findings are stimulating and exciting, as they incorporate a relatively novel technique, and apply it – for the first time – to a stress-related syndrome, burnout, that is in need of being better understood. Findings of hypercortisolism are not in line with expectations, which is unlikely to be explained by methodological weaknesses or recruitment of an atypical sample. It is much more likely that the findings here are indeed reflective of HPA axis (over-)activity. This finding underscores the importance of hair cortisol as an addition to our psychoneuroendocrinology toolbox, and at the same time raises important and stimulating questions for further research, for example: What is the timeline of HPA axis alterations in burnout, or during chronic work stress leading to burnout? How does hair cortisol develop in participants over time? Is hair cortisol in burnout a better predictor of health development than other HPA axis markers? Is hair cortisol sufficient to predict development of symptoms or do we need to assess additional mediators such as SNS activity, glucocorticoid signaling, or inflammation? Answers to these questions will require studies that dare to go deeper into the cell, and at the same time permit longer observation periods. Such answers will be exciting and will hopefully help us to better understand burnout, and to better protect humans from its consequences. 2
Psychoneuroendocrinology xxx (xxxx) xxx–xxx
Short Communication
References Chida, Y., Steptoe, A., 2009. Cortisol awakening response and psychosocial factors: a systematic review and meta-analysis. Biol. Psychol. 80 (3), 265–278. http://dx.doi.org/10.1016/j. biopsycho.2008.10.004. Danhof-Pont, M.B., van Veen, T., Zitman, F.G., 2011. Biomarkers in burnout: a systematic review. J. Psychosom. Res. 70 (6), 505–524. http://dx.doi.org/10.1016/j.jpsychores.2010.10. 012. Fries, E., Hesse, J., Hellhammer, J., Hellhammer, D.H., 2005. A new view on hypocortisolism. Psychoneuroendocrinology 30 (10), 1010–1016. http://dx.doi.org/10.1016/j.psyneuen. 2005.04.006. Jackson, S.E., Kirschbaum, C., Steptoe, A., 2016. Perceived weight discrimination and chronic biochemical stress: A population-based study using cortisol in scalp hair. Obesity 24 (12), 2515–2521. http://dx.doi.org/10.1002/oby.21657. Juster, R.-P., Sindi, S., Marin, M.-F., Perna, A., Hashemi, A., Pruessner, J.C., Lupien, S.J., 2011. A clinical allostatic load index is associated with burnout symptoms and hypocortisolemic profiles in healthy workers. Psychoneuroendocrinology 36 (6), 797–805. http://dx.doi.org/10.1016/j.psyneuen.2010.11.001. Kudielka, B.M., Wüst, S., 2010. Human models in acute and chronic stress: assessing determinants of individual hypothalamus-pituitary-adrenal axis activity and reactivity. Stress 13 (1), 1–14. http://dx.doi.org/10.3109/10253890902874913. Lupien, S.J., McEwen, B.S., Gunnar, M.R., Heim, C., 2009. Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nat. Rev. Neurosci. 10 (6), 434–445. http://dx. doi.org/10.1038/nrn2639. Maslach, C., Schaufeli, W.B., Leiter, M.P., 2001. Job burnout. Annu. Rev. Psychol. 52, 397–422. http://dx.doi.org/10.1146/annurev.psych.52.1.397. Melamed, S., Ugarten, U., Shirom, A., Kahana, L., Lerman, Y., Froom, P., 1999. Chronic burnout, somatic arousal and elevated salivary cortisol levels. J. Psychosom. Res. 46 (6), 591–598. Retrieved from. http://www.ncbi.nlm.nih.gov/pubmed/10454175. Melamed, S., Shirom, A., Toker, S., Berliner, S., Shapira, I., 2006. Burnout and risk of cardiovascular disease: evidence, possible causal paths, and promising research directions. Psychol. Bull. 132 (3), 327–353. http://dx.doi.org/10.1037/0033-2909.132.3.327. Mewes, R., Reich, H., Skoluda, N., Seele, F., Nater, U.M., 2017. Elevated hair cortisol concentrations in recently fled asylum seekers in comparison to permanently settled immigrants and non-immigrants. Transl. Psychiatry 7 (3), e1051. http://dx.doi.org/10.1038/tp.2017.14. Miller, G.E., Chen, E., Zhou, E.S., 2007. If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. Psychol. Bull. 133 (1), 25–45. http://dx.doi.org/10.1037/0033-2909.133.1.25. Miller, G.E., Chen, E., Sze, J., Marin, T., Arevalo, J.M.G., Doll, R., et al., 2008. A functional genomic fingerprint of chronic stress in humans: blunted glucocorticoid and increased NFkappaB signaling. Biol. Psychiatry 64 (4), 266–272. http://dx.doi.org/10.1016/j.biopsych.2008.03.017. Miller, G.E., Chen, E., Fok, A.K., Walker, H., Lim, A., Nicholls, E.F., et al., 2009. Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling. Proc. Natl. Acad. Sci. U. S. A. 106 (34), 14716–14721. http://dx.doi.org/10.1073/pnas.0902971106. O’Brien, K.M., Meyer, J., Tronick, E., Moore, C.L., 2017. Hair cortisol and lifetime discrimination: moderation by subjective social status. Health Psychol. Open 4 (1). http://dx.doi.org/ 10.1177/2055102917695176. 2055102917695176. Penz, M., Stalder, T., Miller, R., Ludwig, V.M., Kanthak, M.K., Kirschbaum, C., 2017. Hair cortisol as a biological marker for burnout symptomatology. Psychoneuroendocrinology. http:// dx.doi.org/10.1016/j.psyneuen.2017.07.485. Rohleder, N., Marin, T.J., Ma, R., Miller, G.E., 2009. Biologic cost of caring for a cancer patient: dysregulation of pro- and anti-inflammatory signaling pathways. J. Clin. Oncol. 27 (18), 2909–2915. http://dx.doi.org/10.1200/JCO.2008.18.7435. Rohleder, N., 2012. Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems – 2011 Curt Richter Award Winner. Psychoneuroendocrinology 37 (3), 307–316. http://dx.doi.org/10.1016/j.psyneuen.2011.12.015. Selye, H., 1936. A syndrome produced by diverse noxious agents. Nature 138, 32–36. Short, S.J., Stalder, T., Marceau, K., Entringer, S., Moog, N.K., Shirtcliff, E.A., et al., 2016. Correspondence between hair cortisol concentrations and 30-day integrated daily salivary and weekly urinary cortisol measures. Psychoneuroendocrinology 71, 12–18. http://dx.doi.org/10.1016/j.psyneuen.2016.05.007. Stalder, T., Steudte-Schmiedgen, S., Alexander, N., Klucken, T., Vater, A., Wichmann, S., et al., 2017. Stress-related and basic determinants of hair cortisol in humans: a meta-analysis. Psychoneuroendocrinology 77, 261–274. http://dx.doi.org/10.1016/j.psyneuen.2016.12.017. Steudte-Schmiedgen, S., Kirschbaum, C., Alexander, N., Stalder, T., 2016. An integrative model linking traumatization, cortisol dysregulation and posttraumatic stress disorder: insight from recent hair cortisol findings. Neurosci. Biobehav. Rev. 69, 124–135. http://dx.doi.org/10.1016/j.neubiorev.2016.07.015. Ursache, A., Merz, E.C., Melvin, S., Meyer, J., Noble, K.G., 2017. Socioeconomic status, hair cortisol and internalizing symptoms in parents and children. Psychoneuroendocrinology 78, 142–150. http://dx.doi.org/10.1016/j.psyneuen.2017.01.020. Zilioli, S., Slatcher, R.B., Fritz, H., Booza, J.C., Cutchin, M.P., 2017. Brief report: neighborhood disadvantage and hair cortisol among older urban African Americans. Psychoneuroendocrinology 80, 36–38. http://dx.doi.org/10.1016/j.psyneuen.2017.02.026.
Nicolas Rohleder Chair of Health Psychology, Institute of Psychology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany E-mail address: [email protected]
3
Contents lists available at ScienceDirect
Psychoneuroendocrinology journal homepage: www.elsevier.com/locate/psyneuen
Short Communication Burnout, hair cortisol, and timing: Hyper- or hypercortisolism? Modern human life is characterized by a specific set of challenges that spread across our private and professional lives. In particular in our professional lives, many of us are motivated to strive for ever greater successes, and are willing to invest more and more of our time to achieve work goals. In addition to those motivated by personal or their company’s successes, many humans are altruistically motivated to give more and more of their time and energy to care for others, most prominently in health care or teaching professions. While dedication to work, and the feeling of meaning and purpose one might derive from this, can be extremely fulfilling and a source of life satisfaction, negative consequences frequently occur, one of which being burnout. In contrast to the concept of chronic stress, which describes ongoing strains and stresses of life per se, and that is reasonably well studied both in terms of psychological and biological consequences (Juster et al., 2011; Kudielka and Wüst, 2010; Lupien et al., 2009; Rohleder, 2012), burnout is better described as a consequence of exposure to chronic work, but also certain non-work stressors in combination with intra-personal and situational conditions (Maslach et al., 2001; Melamed et al., 1999). The syndrome of burnout has been defined as a combination of emotional exhaustion, physical fatigue, and cognitive weariness (Melamed et al., 2006), and/or as severe energy depletion, dysfunctional attitudes towards work, in particular cynicism, and a lack of professional efficacy (Maslach et al., 2001). It has further been described as the result of inefficient coping with stress, and consequently, the depletion of an individual’s coping resources (Melamed et al., 1999). Consequently, burnout leads to increased frequency of sick leaves, to early retirements, and has been associated with significant health issues including cardiovascular disease and type 2 diabetes (Melamed et al., 2006), leading to significant costs, both for societies and human well-being. Given these consequences, it is important to improve our understanding of both, the factors leading to burnout, as well as pathways from burnout to health issues. As with most research addressing psychological constructs related to stress, or stress-related diseases, research has first concentrated on the hypothalamus-pituitary-adrenal (HPA) axis, with limited success and mixed results, with reports of higher HPA axis activity in burned out individuals (e.g. Melamed et al., 1999), systematic reviews and meta-analyses finding no relationships (e.g. Danhof-Pont et al., 2011), and another meta-analytic study reporting that a lower cortisol awakening response (CAR) seems to be characteristic for burnout (Chida and Steptoe, 2009). 1. What kind of biological alterations can we expect in burnout? In the related field of chronic stress research, findings on HPA axis alterations were similarly difficult to reconcile, with a similarly confusing mix of studies showing higher, lower, or unchanged HPA axis parameters. This was of course not made easier by different expectations. Due to the fact that acute stress activates the HPA axis, it was expected by some that chronic stress should be associated with hypercortisolism, and there were data supporting this. Others were expecting an exhaustion of HPA axis resources as being proposed very early by Selye (Selye, 1936), and there were also data supporting this assumption. Progress was further complicated by the fact that basal HPA axis activity has so many different parameters, which seem to be reflecting different aspects of activity. Only those that take into account the system’s diurnal rhythm have proven to be interpretable, and only taking into account type and timing of chronic stress permitted Miller et al. in a seminal meta-analytic study to reconcile previously conflicting findings (Miller et al., 2007). In a simplified way, their findings were that in early stages of chronic stress, HPA axis activity tends to be higher, while it will decrease with longer duration of chronic stress to ultimately reach a state of hypocortisolism and a loss of circadian rhythm. This is in line with other authors linking chronic stress to hypocortisolism, and proposing hypocortisolism as key factor in the development of stress-related disease (e.g. Fries et al., 2005). However, another key issue emerging from chronic stress research is that it is by no means sufficient to only investigate HPA axis changes, in order to understand health consequences. First of all, the HPA axis is not the only stress system, and not the only one altered with chronic stress exposure, and in particular the sympathetic nervous system (SNS), or its sub component, the sympathetic adrenal medullary (SAM) system, needs to be taken into account. We have shown, for example, that experiencing a family member going through brain cancer treatment for almost a year does not affect basal HPA axis activity, but was related with alterations in SNS activity (Rohleder et al., 2009). Secondly, changes in either of these stress systems are seldom sufficient to understand downstream health consequences of chronic stress exposure. In the same cancer caregiver study, we also found that in the absence of HPA axis changes, chronic stress had severe consequences on downstream mechanisms, in particular inflammation (Rohleder et al., 2009). In related studies, Miller and Cole for example have repeatedly confirmed and expanded on such findings, showing that transcriptional activity in pathways responsive to cortisol is markedly decreased in various conditions of chronic life stress, while the HPA axis per se was unchanged (e.g. Miller et al., 2008, 2009). This is not meant to question the validity of studying the HPA axis in burnout, as done by Penz et al. here (Penz et al., 2017). On the contrary – Since the study of burnout appears to be in its infancy compared to the study of chronic stress in general, above considerations were meant to set the stage of what to reasonably expect when assessing HPA axis activity in burnout. Learning from what we know about chronic stress and its biological consequences, and considering that burnout could be regarded as a consequence of long-term exposure to chronic stress, with inefficient coping (Melamed et al., 1999), the following would be expected: (1) lower overall cortisol and relatively flatter diurnal profiles; (2) higher SNS activity with http://dx.doi.org/10.1016/j.psyneuen.2017.10.008
0306-4530/ © 2017 Elsevier Ltd. All rights reserved.
Psychoneuroendocrinology xxx (xxxx) xxx–xxx
Short Communication
altered diurnal profiles; (3) upregulation of transcripts responsive to inflammatory stimuli and down-regulation of glucocorticoid responsive transcripts; (4) higher inflammatory markers in plasma. 2. Where does the paper by Penz et al. fit in here? in their study of more than three-hundred working adults found a positive relationship of burnout with cortisol measured in hair (HCC), reflecting cortisol concentrations over three months prior to data collection (Penz et al., 2017). In other words – they found the contrary of what we would expect based on the literature, and based on conceptually comparing burnout with chronic stress: Hypercortisolism. In more detail, they found that those with a total burnout score above a threshold characterizing “severe burnout symptoms” was the most consistent predictor of higher hair cortisol, along with the subscale reduced efficiency, while continuous scores as well as subscales for emotional exhaustion and cynicism were less reliably associated with high cortisol. Notably, relationships held after controlling for depression. 3. What do these unexpected findings of hypercortisolism in burnout mean? Several explanations are conceivable to explain the finding of hypercortisolism in those with high burnout in this sample. One explanation might simply be that this is just another study the big data pool of mixed data. This is of course not a satisfying explanation and none that moves the field forward. It is also unlikely that the study differs too much from other studies in terms of participants or burnout assessment, as the sample is of reasonable size, assessment of burnout uses similar tools than the majority of other studies, and participants are normal working adults recruited from the general population. More promising explanations might be found in the issue of timing, and in the fact that hair cortisol was used here for the first time in the study of burnout. 4. Is hair cortisol so different from other measures of HPA axis activity that it explains the unexpected finding of hypercortisolism? There are data supporting the notion that hair cortisol does not differ so much from other measures to explain an unexpected finding. Short et al. (2016) for example reported that hair cortisol concentrations from a strand of hair reflecting a one-month period of time was significantly associated with integrated salivary cortisol assessed diurnally over the same month (Short et al., 2016). Stalder et al. (2017) in their meta-analysis of chronic stress and hair cortisol report that hair cortisol is only positively associated with chronic stress if the stress is still ongoing, and negatively related when stress is absent (Stalder et al., 2017). While this does not perfectly line up with findings summarized by Miller et al. (Miller et al., 2007), it does point in the right direction, and as Stalder et al. note, they only had very few studies in that section of their analysis. Similarly, summarizing data on Posttraumatic Stress Disorder (PTSD) and hair cortisol, Steudte-Schmiedgen et al. (2016) found support for a conclusion in line with Miller et al.’s results, i.e. that longer duration or time since trauma was related with lower hair cortisol (Steudte-Schmiedgen et al., 2016). While there are also findings of hair cortisol being positively related with conditions that could be considered similar to chronic stress, such as discrimination (Jackson et al., 2016; O’Brien et al., 2017), low social status (Ursache et al., 2017; Zilioli et al., 2017), and with trauma (Mewes et al., 2017), all these findings, taken together, do not support an explanation of hair cortisol simply “measuring the opposite” as other traditional ways of assessing HPA axis activity. These findings tell us that this finding of hypercortisolism in burnout needs to be taken seriously, which leads to the next question or potential explanation: 5. What role does timing play with regard to hypercortisolism in burnout? As summarized above, a generally accepted notion in chronic stress research is the occurrence of hypocortisolism after longer exposure to a chronically stressful condition, such as chronic life or work stress, or a longer time living with the memory of an experienced trauma (Miller et al., 2007). With regard to burnout, and based on the assumption that burnout in a way follows chronic work stress, or develops in later stages of prolonged work stress, one would expect HPA axis activity to be diminished, and diurnal profiles to be relatively flat. Given that diurnal cortisol production appears to be related with cortisol measured in hair (Short et al., 2016), one would expect to see this hypocortisolism in hair cortisol as well. Unfortunately, timing hair sample relative to onset and duration of burnout is not reported in this study, and consequently was not tested for its association with cortisol concentrations in hair. That leaves this important question up for speculation. The authors do speculate along these lines. They argue that their finding of a stronger association of reduced efficacy with cortisol, in comparison to a weak or non-existent association of emotional exhaustion with cortisol could indicate that participants here were indeed in an earlier stage of burnout, assuming that reduced efficacy develops before emotional exhaustion (Penz et al., 2017). Of course, ultimate answers can only result from future studies, or future reports resulting from the Dresden Burnout Study. 6. Conclusions present data here showing that burnout, and in particular, severe burnout and reduced work efficacy are related with increased HPA axis activity, i.e. hypercortisolism, measured in hair reflecting a three-month time period. These findings are stimulating and exciting, as they incorporate a relatively novel technique, and apply it – for the first time – to a stress-related syndrome, burnout, that is in need of being better understood. Findings of hypercortisolism are not in line with expectations, which is unlikely to be explained by methodological weaknesses or recruitment of an atypical sample. It is much more likely that the findings here are indeed reflective of HPA axis (over-)activity. This finding underscores the importance of hair cortisol as an addition to our psychoneuroendocrinology toolbox, and at the same time raises important and stimulating questions for further research, for example: What is the timeline of HPA axis alterations in burnout, or during chronic work stress leading to burnout? How does hair cortisol develop in participants over time? Is hair cortisol in burnout a better predictor of health development than other HPA axis markers? Is hair cortisol sufficient to predict development of symptoms or do we need to assess additional mediators such as SNS activity, glucocorticoid signaling, or inflammation? Answers to these questions will require studies that dare to go deeper into the cell, and at the same time permit longer observation periods. Such answers will be exciting and will hopefully help us to better understand burnout, and to better protect humans from its consequences. 2
Psychoneuroendocrinology xxx (xxxx) xxx–xxx
Short Communication
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Nicolas Rohleder Chair of Health Psychology, Institute of Psychology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany E-mail address: [email protected]
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