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Association of <emph type="ital">FKBP5</emph> Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults
Open accessAbstract
CONTEXT: In addition to trauma exposure, other factors contribute to risk for development of posttraumatic stress disorder (PTSD) in adulthood. Both genetic and environmental factors are contributory, with child abuse providing significant risk liability. OBJECTIVE: To increase understanding of genetic and environmental risk factors as well as their interaction in the development of PTSD by gene x environment interactions of child abuse, level of non-child abuse trauma exposure, and genetic polymorphisms at the stress-related gene FKBP5. DESIGN, SETTING, AND PARTICIPANTS: A cross-sectional study examining genetic and psychological risk factors in 900 nonpsychiatric clinic patients (762 included for all genotype studies) with significant levels of childhood abuse as well as non-child abuse trauma using a verbally presented survey combined with single-nucleotide polymorphism (SNP) genotyping. Participants were primarily urban, low-income, black (>95%) men and women seeking care in the general medical care and obstetrics-gynecology clinics of an urban public hospital in Atlanta, Georgia, between 2005 and 2007. MAIN OUTCOME MEASURES: Severity of adult PTSD symptomatology, measured with the modified PTSD Symptom Scale, non-child abuse (primarily adult) trauma exposure and child abuse measured using the traumatic events inventory and 8 SNPs spanning the FKBP5 locus. RESULTS: Level of child abuse and non-child abuse trauma each separately predicted level of adult PTSD symptomatology (mean [SD], PTSD Symptom Scale for no child abuse, 8.03 [10.48] vs > or =2 types of abuse, 20.93 [14.32]; and for no non-child abuse trauma, 3.58 [6.27] vs > or =4 types, 16.74 [12.90]; P < .001). Although FKBP5 SNPs did not directly predict PTSD symptom outcome or interact with level of non-child abuse trauma to predict PTSD symptom severity, 4 SNPs in the FKBP5 locus significantly interacted (rs9296158, rs3800373, rs1360780, and rs9470080; minimum P = .0004) with the severity of child abuse to predict level of adult PTSD symptoms after correcting for multiple testing. This gene x environment interaction remained significant when controlling for depression severity scores, age, sex, levels of non-child abuse trauma exposure, and genetic ancestry. This genetic interaction was also paralleled by FKBP5 genotype-dependent and PTSD-dependent effects on glucocorticoid receptor sensitivity, measured by the dexamethasone suppression test. CONCLUSIONS: Four SNPs of the FKBP5 gene interacted with severity of child abuse as a predictor of adult PTSD symptoms. There were no main effects of the SNPs on PTSD symptoms and no significant genetic interactions with level of non-child abuse trauma as predictor of adult PTSD symptoms, suggesting a potential gene-childhood environment interaction for adult PTSD.
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“Importantly, SNPs in the FKBP5 gene that are associated with higher FKBP5-mRNA induction upon cortisol release (rs1360780, rs9296158, rs3800373, and rs9470080) are also associated with increased PTSD symptom severity in those with high levels of child abuse (Binder et al, 2008).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Binder et al, 2008
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“FKBP5 single nucleotide polymorphisms have additionally been shown to interact with early trauma to predict both PTSD and major depression (36,37), possibly through involvement of allelespecific, environmentally dependent changes in methylation of specific cytosine-phosphate-guanine (CpG) sites (38).”
From Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation (2016) · cites this paper as [36]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“As first shown by Binder et al. (385), specific single-nucleotide poly-morphisms (SNPs) of the FKBP5 gene interacting with ELS/CT predict the level of adult PTSD symptoms.”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [385]
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In the citing paper
“Interestingly, some alleles of these FKBP5-SNPs are associated with enhanced glucocorticoid sensitivity, whereas other alleles of these SNPs are associated with GR resistance in individuals with PTSD (Binder et al, 2008).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Binder et al, 2008
In the citing paper
“Moreover, these interaction effects remained significant even after controlling for potential confounds (i.e., depressive symptoms, age, sex, non-child abuse trauma, genetic ancestry).”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Binder et al. 2008
In the citing paper
“FKBP5 interacted with reported childhood maltreatment to predict PTSD symptoms.”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Binder et al. 2008
In the citing paper
“polymorphisms in both the GR and the GR-associated heat-shock protein FKBP5 have been shown to predict clinical response.48”
From Early life adversity and the epigenetic programming of hypothalamic-pituitary-adrenal function (2014) · cites this paper as [48]
In the citing paper
“Also, recently several single nucleotide polymorphisms of the FK506 binding protein 5 (FKBP5) were found to interact with childhood trauma in order to create PTSD susceptibility [195].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [195]
In the citing paper
“This study was the first to identify a correlation of FKBP51 gene variants with response to antidepressant treatment, and also with the reactivity of the HPA axis in the dexamethasone (DEX)-CRH test.”
From FKBP51 and FKBP52 in signaling and disease (2011) · cites this paper as [73]
In the citing paper
“Further, PTSD has long been associated with intrinsic [e.g., age and gender (48, 49)], environmental (e.g., exposure to trauma, rearing environment, degree of social support), and genetic factors (50–52).”
From Conditioned fear associated phenotypes as robust, translational indices of trauma-, stressor-, and anxiety-related behaviors (2014) · cites this paper as [51]
In the citing paper
“a functional variant in FKBP5, a gene encoding a co-chaperone of the glucocorticoid receptor, increases risk for PTSD following trauma 96 .”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [96]
In the citing paper
“with evidence that childhood trauma modifies the genetic risk for PTSD 96 .”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [96]
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Metadata
- Authors
- Binder, E. B.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Binder, Elisabeth B.
- ORCID
- Binder, Elisabeth B.
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2008-03-19
- Volume
- 299
- Issue
- 11
- Pages
- 1291
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC2441757
- OpenAlex
- W2166401337
- Semantic Scholar
- ad909ca1aa67b7fa8a5e7cc745e773d2e0fba820
- Cited by
- 1,362
- References
- 95
- Citations by year
- 2026: 37 · 2025: 30 · 2024: 49 · 2023: 42 · 2022: 50 · 2021: 50 · 2020: 82 · 2019: 65 · 2018: 90 · 2017: 84 · 2016: 113 · 2015: 113 · 2014: 109 · 2013: 106 · 2012: 81
- FWCI
- 96.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000454)
- National Institute of Mental Health (R01MH042088, P50MH058922, MH58922, MH 071537, MH069884, R01MH071537, MH42088, R56MH071537, K01MH069884)
- National Institute on Drug Abuse (DA015766, K02DA015766)
- National Center for Research Resources (M01RR000039)
- National Center for Advancing Translational Sciences
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- post-traumatic stress disorder, childhood abuse, FKBP5, gene-environment interaction, single nucleotide polymorphisms, trauma exposure, PTSD symptom severity, genetic risk factors, stress-related genes, rs1360780
- MeSH terms
- Tacrolimus Binding Protein 5, Adolescent, Adult, Aged, Aged, 80 and over, Child, Child Abuse, Cross-Sectional Studies, Dexamethasone, Female, Humans, Hydrocortisone, Male, Middle Aged, Poverty, Receptors, Glucocorticoid, Regression Analysis, Risk Factors, Severity of Illness Index, Stress Disorders, Post-Traumatic, Urban Population, Polymorphism, Single Nucleotide, Tacrolimus Binding Proteins
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