Effect of childhood trauma on adult depression and neuroendocrine function: sex-specific moderation by CRH receptor 1 gene
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Variations of the corticotropin-releasing hormone receptor 1 (CRHR1) gene appear to moderate the development of depression after childhood trauma. Depression more frequently affects women than men. We examined sex differences in the effects of the CRHR1 gene on the relationship between childhood trauma and adult depression. We recruited 1,063 subjects from the waiting rooms of a public urban hospital. Childhood trauma exposure and symptoms of depression were assessed using dimensional rating scales. Subjects were genotyped for rs110402 within the CRHR1 gene. An independent sample of 78 subjects underwent clinical assessment, genotyping, and a dexamethasone/CRH test. The age range at recruitment was 18-77 years and 18-45, for the two studies respectively. In the hospital sample, the protective effect of the rs110402 A-allele against developing depression after childhood trauma was observed in men (N = 424), but not in women (N = 635). In the second sample, the rs110402 A-allele was associated with decreased cortisol response in the dexamethasone/CRH test only in men. In A-allele carriers with childhood trauma exposure women exhibited increased cortisol response compared men; there were no sex differences in A-allele carriers without trauma exposure. This effect may, however, not be related to gender differences per se, but to differences in the type of experienced abuse between men and women. CRHR x environment interactions in the hospital sample were observed with exposure to physical, but not sexual or emotional abuse. Physical abuse was the most common type of abuse in men in this cohort, while sexual abuse was most commonly suffered by women. Our results suggest that the CRHR1 gene may only moderate the effects of specific types of childhood trauma on depression. Gender differences in environmental exposures could thus be reflected in sex-specific CRHR1 x child abuse interactions.
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Specific CRHR1 polymorphisms interact with ELS/CT to increase the risk of adult depression.
“Bradley et al. reported in two separate cohorts, independently, that specific CRHR1 polymorphisms interact with ELS/CT to increase the risk of adult depression (390), similar to Heim et al. (391), while Ben-Efraim et al. (392) reported comparable findings with respect to suicide attempts.”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [391]
The Results (Study 1; page unavailable) report an interaction between CRHR1 rs110402 and childhood abuse on adult depressive symptoms, but it was significant in men, not women. The significant interaction by abuse type was limited to physical abuse, and the A allele was described as protective rather than as increasing risk. The claim omits these qualifications. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn psychiatry, depression is conceptualized as heterogeneous, multifactorial in causation, and believed to arise from cumulative effects of genetics, adverse events in childhood, and ongoing life stressors.
“Moreover, in psychiatry depression is conceptualized as heterogeneous, multifactorial in causation, and it is believed to arise from the cumulative effects [56–58] of genetics [59–62], adverse events in childhood [63–66], and ongoing life stressors [67–70].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [65]
In an independent sample, Heim et al. found an interaction of early life stress, particularly physical abuse, and CRHR1 rs110402 in predicting depression in men only.
“Using an independent sample, these authors also examined the interaction between CRHR1 rs110402 and ELS in predicting depression, again finding an interaction of ELS (particularly physical abuse) and CRHR1 in men only.”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Heim et al. (2009)
Heim et al. found a gene-environment interaction such that men reporting early life stress with an A allele had decreased cortisol responses compared with women reporting early life stress, but responses of men and women without early life stress did not differ.
“In addition, there was a GxE interaction such that men reporting ELS with an A allele had decreased cortisol responses compared with women reporting ELS, but responses of men and women without ELS did not differ.”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Heim et al. (2009)
Heim et al. (2009) partially replicated Tyrka et al.'s findings in a Dex/CRH study, finding that men but not women who were carriers of the A allele had decreased cortisol responses compared with men with the G/G genotype.
“Men, but not women, who were carriers of the A allele had decreased cortisol responses compared with men with the G/G genotype.”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Heim et al. (2009)
Evidence from studies reviewed here supports the existence of differences in the impact of type of early life stress, and these effects may be gender-specific.
“Evidence from studies reviewed here supports the existence of differences in the impact of type of ELS, and these effects may be gender-specific (Cicchetti et al. 2007; Heim et al. 2009; Sjoberg et al. 2006).”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Heim et al. 2009
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- Authors
- Heim, C.
- Affiliations
- Emory University (US)
- Corresponding author
- Heim, Christine
- ORCID
- Heim, Christine
- Venue
- Frontiers in Behavioral Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2009
- Volume
- 3
- Pages
- 41-41
- ISSN
- 1662-5153 (ISSN-L)
- PMC
- PMC2821197
- OpenAlex
- W2015231166
- Cited by
- 245
- References
- 37
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 8 · 2023: 3 · 2022: 8 · 2021: 6 · 2020: 14 · 2019: 19 · 2018: 24 · 2017: 19 · 2016: 31 · 2015: 20 · 2014: 17 · 2013: 9 · 2012: 22
- FWCI
- 7.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Behavioral Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Abbott Laboratories
- American Foundation for Suicide Prevention
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- American Psychiatric Institute for Research and Education
- CeNeRx
- National Alliance for Research on Schizophrenia and Depression
- ACADIA Pharmaceuticals
- H. Lundbeck A/S
- National Institutes of Health (UL1TR000454)
- National Heart, Lung, and Blood Institute
- National Institute of Mental Health
- National Institute on Drug Abuse
- National Center for Advancing Translational Sciences
- UCB Pharma
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Keywords
- childhood trauma, adult depression, CRH receptor 1, sex differences, gene-environment interaction, cortisol response, neuroendocrine function, physical abuse, sexual abuse, emotional abuse, genetic moderation
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