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      HPA axis function and diurnal cortisol in post-traumatic stress disorder: A systematic review

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          Abstract

          Background

          There is inconsistency in the literature regarding the nature of hypothalamic-pituitary-adrenal (HPA) axis functionality in post-traumatic stress disorder (PTSD).

          Purpose

          The review aimed to investigate HPA axis functionality via the diurnal profile of cortisol as it relates to PTSD.

          Methods

          The authors conducted a systematic review of the literature from June 2017 – March 2019 in accordance with The PRISMA Statement in the following four databases: PubMed, MEDLINE, ScienceDirect and PsycINFO with Full Text. The search strategy was limited to articles in English language, published in peer-reviewed journals within the last decade and human studies. Search terms included “post-traumatic stress disorder” OR “PTSD”, AND “hypothalamic pituitary adrenal axis” OR “HPA axis” AND “diurnal cortisol” OR “cortisol”. PTSD sufferers of all trauma types, genders and socioeconomic statuses were included provided there was a “healthy” control group and an inclusion of reporting on inter-group measurements of diurnal cortisol profiles as a portrayal of HPA axis functionality.

          Results

          A total of 10 studies met the criteria for inclusion in this review. The association between HPA axis functionality and PTSD was evaluated by the measurement of salivary and/or plasma cortisol concentrations. Only two studies demonstrated an association between PTSD and diurnal cortisol when compared with respective control groups while three studies found no associations. The remaining five studies found partial, mostly negative associations between PTSD and diurnal cortisol.

          Conclusion

          Despite some indications of an association between PTSD and dysregulated HPA axis functionality as demonstrated by diurnal cortisol output, the current review has revealed mixed findings. As such, a complete understanding of HPA axis dysregulation as it relates to PTSD remains unestablished. Given the findings, further investigation into the relationship between PTSD trauma-exposed and non-PTSD trauma-exposed individuals and diurnal cortisol is warranted.

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          Most cited references27

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          Cortisol and post-traumatic stress disorder in adults: systematic review and meta-analysis.

          Marie-Louise Meewisse, Johannes Reitsma, Giel-Jan de Vries … (2007)
          Post-traumatic stress disorder (PTSD) has inconsistently been associated with lower levels of cortisol. To compare basal cortisol levels in adults with current PTSD and in people without psychiatric disorder. Systematic review and meta-analysis. Standardised mean differences (SMD) in basal cortisol levels were calculated and random-effects models using inverse variance weighting were applied. Across 37 studies, 828 people with PTSD and 800 controls did not differ in cortisol levels (pooled SMD=-0.12, 95% CI=-0.32 to 0.080). Subgroup analyses revealed that studies assessing plasma or serum showed significantly lower levels in people with PTSD than in controls not exposed to trauma. Lower levels were also found in people with PTSD when females were included, in studies on physical or sexual abuse, and in afternoon samples. Low cortisol levels in PTSD are only found under certain conditions. Future research should elucidate whether low cortisol is related to gender or abuse and depends on the measurement methods used.
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            The cortisol awakening response: more than a measure of HPA axis function.

            Angela Clow, Frank Hucklebridge, Tobias Stalder … (2010)
            In most healthy people morning awakening is associated with a burst of cortisol secretion: the cortisol awakening response (CAR). It is argued that the CAR is subject to a range physiological regulatory influences that facilitate this rapid increase in cortisol secretion. Evidence is presented for reduced adrenal sensitivity to rising levels of ACTH in the pre-awakening period, mediated by an extra-pituitary pathway to the adrenal from the suprachiasmatic nucleus (SCN). A role for the hippocampus in this pre-awakening regulation of cortisol secretion is considered. Attainment of consciousness is associated with 'flip-flop' switching of regional brain activation, which, it is argued, initiates a combination of processes: (1) activation of the hypothalamic pituitary adrenal (HPA) axis; (2) release of pre-awakening reduced adrenal sensitivity to ACTH; (3) increased post-awakening adrenal sensitivity to ACTH in response to light, mediated by a SCN extra-pituitary pathway. An association between the CAR and the ending of sleep inertia is discussed.
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              Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and meta-analysis.

              Matthew Morris, Bruce Compas, Judy Garber (2012)
              Exposure to traumatic stress is associated with increased risk for posttraumatic stress disorder (PTSD) and alterations of hypothalamic-pituitary-adrenocortical (HPA) function. Research linking traumatic stress with HPA function in PTSD has been inconsistent, however, in part due to (a) the inclusion of trauma-exposed individuals without PTSD (TE) in control groups and (b) a failure to consider comorbid major depressive disorder (MDD) and moderating variables. This meta-analysis of 47 studies (123 effect sizes, N=6008 individuals) revealed that daily cortisol output was lower for PTSD (d=-.36, SE=.15, p=.008) and PTSD+MDD (d=-.65, SE=.25, p=.008) groups relative to no trauma controls (NTC); TE and NTC groups did not differ significantly from each other. Afternoon/evening cortisol was lower in TE (d=-.25, SE=.09, p=.007) and PTSD (d=-.27, SE=.12, p=.021) groups and higher in PTSD+MDD groups (d=.49, SE=.24, p=.041) relative to NTC. Post-DST cortisol levels were lower in PTSD (d=-.40, SE=.12, p<.001), PTSD+MDD (d=-.65, SE=.14, p<.001), and TE groups (d=-.53, SE=.14, p<.001) relative to NTC. HPA effect sizes were moderated by age, sex, time since index event, and developmental timing of trauma exposure. These findings suggest that enhanced HPA feedback function may be a marker of trauma-exposure rather than a specific mechanism of vulnerability for PTSD, whereas lower daily cortisol output may be associated with PTSD in particular. Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Kathryn E. Speer
                Stuart Semple
                Nenad Naumovski
                Nathan M. D'Cunha
                Andrew J. McKune
                Journal
                Journal ID (nlm-ta): Neurobiol Stress
                Journal ID (iso-abbrev): Neurobiol Stress
                Title: Neurobiology of Stress
                Publisher: Elsevier
                ISSN (Electronic): 2352-2895
                Publication date PMC-release: 04 June 2019
                Publication date Collection: November 2019
                Publication date (Electronic): 04 June 2019
                Volume: 11
                Electronic Location Identifier: 100180
                Affiliations
                [a ]Discipline of Sport and Exercise Science, Faculty of Health, University of Canberra, Canberra, ACT, 2601, Australia
                [b ]Research Institute for Sport and Exercise, University of Canberra, Canberra, ACT, 2601, Australia
                [c ]Faculty of Health, University of Canberra, Canberra, ACT, 2601, Australia
                [d ]Discipline of Biokinetics, Exercise and Leisure Sciences, School of Health Sciences, University of KwaZulu-Natal, Durban, KwaZulu-Natal, 4000, South Africa
                [e ]Collaborative Research in Bioactives and Biomarkers (CRIBB) Group, University of Canberra, Bruce, ACT, 2617, Australia
                [f ]University of Canberra Health Research Institute (UC-HRI), Canberra, ACT, 2617, Australia
                Author notes
                [∗ ]Corresponding author. University of Canberra Research Institute for Sport and Exercise (UCRISE), Canberra, ACT, 2601, Australia. katie.speer@ 123456canberra.edu.au
                Article
                Publisher ID: S2352-2895(18)30108-5 Publisher ID: 100180
                DOI: 10.1016/j.ynstr.2019.100180
                PMC ID: 6582238
                PubMed ID: 31236437
                SO-VID: 09f7d93d-dd89-4d90-aa08-a05ec50bee69
                Copyright © © 2019 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 19 December 2018
                Date revision received : 17 April 2019
                Date accepted : 3 June 2019
                Categories
                Subject: Review article

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