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Cited by 466Posttraumatic Stress Disorder ResearchStress Responses and CortisolChild Abuse and Trauma

Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: A systematic review and meta-analysis

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Morris, Matthew C., Compas, Bruce E., Garber, Judy·2012·Clinical Psychology Review
DOI 10.1016/j.cpr.2012.02.002PMC PMC3340453
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Abstract

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.

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  • Dysfunction of the HPA axis and blunted cortisol response has been found in adults with PTSD.

    “Dysfunction of the HPA axis and blunted cortisol response has been found in adults with PTSD [11,12].”

    From Biological Embedding of Early-Life Adversity and a Scoping Review of the Evidence for Intergenerational Epigenetic Transmission of Stress and Trauma in Humans (2023) · cites this paper as [11]

    The Discussion (HPA markers of vulnerability to PTSD; page unavailable) reports lower daily cortisol output in PTSD groups, supporting altered HPA function and reduced cortisol secretion. It does not establish a blunted cortisol response to a stressor: the measured reduction concerns basal output, and the authors suggest that lower basal activity may allow a rapid response to trauma-related cues. (LLM, conf=0.82)

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  • The compounded effect of concerns regarding contracting the virus, the psychological impact of being locked down, combined with worries about employment may lead to anxiety, depression and/or post-traumatic stress symptomology.

    “The compounded effect of concerns regarding contracting the virus, the psychological impact of being ‘locked down’, combined with worries about employment may lead to anxiety, depression and/or post‐traumatic stress symptomology (Morris et al., 2012).”

    From Living through lockdown: A qualitative exploration of individuals' experiences in the UK. (2022) · cites this paper as Morris et al., 2012

    The paper’s opening section states that trauma exposure increases vulnerability to PTSD and major depressive disorder. It does not address the claimed combination of infection concerns, lockdown and employment worries, or establish that those circumstances lead to anxiety symptoms. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Abnormally low baseline levels of plasma cortisol are typically observed in PTSD.

    “abnormally low baseline levels of plasma cortisol are typically observed in this disorder [173]”

    From Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory (2015) · cites this paper as [173]

  • PTSD also shows neuroendocrine abnormalities, neurocognitive changes, emergent psychosocial stressors, and genetic predispositions.

    “a disorder that also shows the above neuroendocrine abnormalities [161, 172, 173] as well as neurocognitive changes [249, 250], emergent psychosocial stressors [251], and genetic predispositions [252].”

    From Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory (2015) · cites this paper as [173]

  • Trauma survivors in the current study had abnormally low cortisol levels.

    “We also found abnormally low cortisol levels in trauma survivors, corroborating prior work47.”

    From Elevated brain cannabinoid CB1 receptor availability in post-traumatic stress disorder: A positron emission tomography study (2013) · cites this paper as [47]

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Research works printed but not linked: 2

  1. *Lemieux AM 1998 Abuse-related posttraumatic stress disorder: Challenge to the norepinephrine-to-cortisol hypothesis (Doctoral dissertation, University of Wisconsin, Madison) Dissertation Abstracts International 59 2B 0908
  2. Yehuda R Harvey H 1997 Relevance of neuroendocrine alterations in PTSD to cognitive impairments of trauma survivors Read D Lindsay S Recollections of Trauma: Scientific Research and Clinical Practice 221 252 New York Plenum Press

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Authors
Morris, M. C., Compas, B. E., & Garber, J.
Affiliations
  • Meharry Medical College (US)
  • Vanderbilt University (US)
Corresponding author
Morris, Matthew C.
ORCID
Venue
Clinical Psychology Review
Publisher
Elsevier BV
Published
2012-06
Volume
32
Issue
4
Pages
301-315
ISSN
0272-7358 (ISSN-L)
DOI
10.1016/j.cpr.2012.02.002
PMC
PMC3340453
OpenAlex
W2158809703
Cited by
466
References
173
Citations by year
2026: 20 · 2025: 21 · 2024: 21 · 2023: 26 · 2022: 30 · 2021: 39 · 2020: 47 · 2019: 42 · 2018: 49 · 2017: 36 · 2016: 40 · 2015: 28 · 2014: 33 · 2013: 30 · 2012: 4
FWCI
4.39
Type
journal article
Language
en
Open access
Licence
Locations
  • Clinical Psychology Review (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Vanderbilt Institute for Clinical and Translational Research
  • Georgia Clinical and Translational Science Alliance
  • Department of Science and Technology, Ministry of Science and Technology, India
  • Commercializations Promotion Agency for R and D Outcomes
  • National Institutes of Health
  • Centers for Disease Control and Prevention (R01HM069940)
  • Institute for Clinical and Translational Research, University of Wisconsin, Madison
  • National Institute of Mental Health (T32 MH 18921, RC1MH088329, R01MH068391, T32MH018921, R01MH069940, R01MH64735, F31MH084425, R01MH064735)
  • National Institute on Drug Abuse (R01DA017805)
  • National Center for Research Resources (G12RR003032, KL2RR024977, TL1RR024978, UL1RR024975)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
Keywords
post-traumatic stress disorder, major depressive disorder, comorbidities, hypothalamic-pituitary-adrenal axis, cortisol, trauma exposure, diurnal cortisol rhythm, sex differences, age differences, time since trauma
MeSH terms
Circadian Rhythm, Depressive Disorder, Major, Major Depressive Disorder, Dexamethasone, Female, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Male, Pituitary-Adrenal System, Stress Disorders, Post-Traumatic

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