Trauma Matters: Integrating Genetic and Environmental Components of PTSD

Marchese, Shelby; Huckins, Laura

doi:10.1002/ggn2.202200017

Cited by 6 publications

(7 citation statements)

References 196 publications

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“…In the future, weighting and partitioning traumas based on type and severity, coupled with differentiating between childhood and adulthood exposures, may elucidate unique encoding mechanisms for specific types of traumas. Our analyses assumed that multiple traumas linearly impact molecular response, but trauma burden may in fact confer a nonlinear effect 7,100 . Studies examining the subjective experience of trauma are necessary to discern these biological consequences.…”

Section: Discussionmentioning

confidence: 99%

“…Traumatic stress is associated with significant physical and psychological comorbidities [1][2][3][4] , and increases the risk for and severity of many psychiatric and non-psychiatric medical disorders [5][6][7][8][9][10] . Given that only some individuals who experience trauma will ultimately develop psychiatric disorders 11 , a long-standing hypothesis is that stress susceptibility may be genetically encoded 12 .…”

Section: Introductionmentioning

confidence: 99%

“…7,100 . Studies examining the subjective experience of trauma are necessary to discern these biological Second, interventions aimed at reducing neuropsychiatric risk should consider mitigating the exposure to and impact of traumatic experiences on particularly vulnerable individuals.…”

mentioning

confidence: 99%

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Common genetic variation impacts stress response in the brain

Seah,

Signer,

Deans

et al. 2023

Preprint

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To explain why individuals exposed to identical stressors experience divergent clinical outcomes, we determine how molecular encoding of stress modifies genetic risk for brain disorders. Analysis of post-mortem brain (n=304) revealed 8557 stress-interactive expression quantitative trait loci (eQTLs) that dysregulate expression of 915 eGenes in response to stress, and lie in stress-related transcription factor binding sites. Response to stress is robust across experimental paradigms: up to 50% of stress-interactive eGenes validate in glucocorticoid treated hiPSC-derived neurons (n=39 donors). Stress-interactive eGenes show brain region- and cell type-specificity, and, in post-mortem brain, implicate glial and endothelial mechanisms. Stress dysregulates long-term expression of disorder risk genes in a genotype-dependent manner; stress-interactive transcriptomic imputation uncovered 139 novel genes conferring brain disorder risk only in the context of traumatic stress. Molecular stress-encoding explains individualized responses to traumatic stress; incorporating trauma into genomic studies of brain disorders is likely to improve diagnosis, prognosis, and drug discovery.Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Common genetic variation impacts stress response in the brain

Seah,

Signer,

Deans

et al. 2023

Preprint

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“…There is still no conclusion on the causes of chronic posttraumatic stress disorder in the academic community [2]. This paper lists the theoretical models proposed by four schools with significant influence in the past and the current popular conceptual models based on stress theory.…”

Section: Etiologymentioning

confidence: 99%

Chronic Posttraumatic Stress Disorder: A Prolonged Nightmare of Aftershocks

Chu

2023

LNEP

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This article is an overview of chronic posttraumatic stress disorder incorporating its etiology, treatments, certain controversies, and recommendations for future development. Based on the diagnostic criteria of DSM-5 and ICD-10 and the research and summary of previous literature. This paper summarizes the etiology of chronic posttraumatic stress disorder under the theoretical models of five schools (including the biological, psychodynamic, cognitive/information processing model, behavioral model, and current etiological conceptualization based on anxiety disorders). Their influence and application, the current commonly used treatment methods and their effectiveness, the current controversies regarding the definition and treatment of chronic PTSD, and recommendations for future research. Overall, based on previous theoretical research and practical treatment, this paper discusses chronic posttraumatic stress disorder from different perspectives and puts forward the existing problems in current research, thus not only offering readers a relatively comprehensive understanding of chronic traumatic stress disorder but also having multiple orientations of summarizing historical research and facing the future.

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“…The burden of PTSD varies by sex 3,13 , with rates of lifetime PTSD about twice as high in females compared to males 14 . Understanding why PTSD prevalence differs by sex is complex; rather than simply capturing intrinsic biological sex differences in risk, differences may reflect gendered environments including trauma exposure (e.g., interpersonal violence) [15][16][17][18][19] or available supports. Male, female, and intersex patients may also have different experiences within healthcare systems, including where and how care is received, access to care, and their diagnostic journey for PTSD.…”

Section: Introductionmentioning

confidence: 99%

Comorbidity Profiles of Posttraumatic Stress Disorder Across the Medical Phenome

Hicks,

Niarchou,

Goleva

et al. 2023

Preprint

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BackgroundPrior epidemiological research has linked PTSD with specific physical health problems, but the comprehensive landscape of medical conditions associated with PTSD remains uncharacterized. Electronic health records (EHR) provide an opportunity to overcome prior clinical knowledge gaps and uncover associations with biological relevance that potentially vary by sex.MethodsPTSD was defined among biobank participants (total N=123,365) in a major healthcare system using two ICD code-based definitions: broad (1+ PTSD or acute stress codes versus 0; NCase=14,899) and narrow (2+ PTSD codes versus 0; NCase=3,026). Using a phenome-wide association (PheWAS) design, we tested associations between each PTSD definition and all prevalent disease umbrella categories, i.e., phecodes. We also conducted sex-stratified PheWAS analyses including a sex-by-diagnosis interaction term in each logistic regression.ResultsA substantial number of phecodes were significantly associated with PTSDNarrow(61%) and PTSDBroad(83%). While top associations were shared between the two definitions, PTSDBroadcaptured 334 additional phecodes not significantly associated with PTSDNarrowand exhibited a wider range of significantly associated phecodes across various categories, including respiratory, genitourinary, and circulatory conditions. Sex differences were observed, in that PTSDBroadwas more strongly associated with osteoporosis, respiratory failure, hemorrhage, and pulmonary heart disease among male patients, and with urinary tract infection, acute pharyngitis, respiratory infections, and overweight among female patients.ConclusionsThis study provides valuable insights into a diverse range of comorbidities associated with PTSD, including both known and novel associations, while highlighting the influence of sex differences and the impact of defining PTSD using EHR.

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Trauma Matters: Integrating Genetic and Environmental Components of PTSD

Cited by 6 publications

References 196 publications

Common genetic variation impacts stress response in the brain

Common genetic variation impacts stress response in the brain

Chronic Posttraumatic Stress Disorder: A Prolonged Nightmare of Aftershocks

Comorbidity Profiles of Posttraumatic Stress Disorder Across the Medical Phenome

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