Dataset Information

Youth Adversities Amplify the Association between Adult Stressors and Chronic Inflammation in a Domain Specific Manner: Nuancing the Early Life Sensitivity Model.

ABSTRACT: There is strong evidence that chronic, systemic inflammation hastens onset of the diseases of old age that ultimately lead to death. Importantly, several studies suggest that childhood adversity predicts chronic inflammation. Unfortunately, this research has been plagued by retrospective reports of childhood adversity, an absence of controls for adult stressors, and a failure to investigate various competing models of the link between childhood adversity and chronic inflammation. The present study was designed to address these limitations. Using 18 years of data collected from 413 African Americans (58% female) included in the Family and Community Health Study, hierarchical regression analyses provided support for a nuanced early life sensitivity explanation for the link between early adversity and adult chronic inflammation. Controlling for health risk behaviors and adult SES, late childhood (ages 10-12) adversity amplified the association between adult adversity (age 29) and chronic inflammation. This interaction operated in a domain-specific fashion. Harsh parenting amplified the relation between intimate partner hostility and inflammation, whereas early discrimination amplified the relation between adult discrimination and inflammation. These findings suggest that individuals may be primed to respond physiologically to adverse adult circumstances that resemble those experienced earlier in life.

SUBMITTER: Simons RL

PROVIDER: S-EPMC7685217 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Youth Adversities Amplify the Association between Adult Stressors and Chronic Inflammation in a Domain Specific Manner: Nuancing the Early Life Sensitivity Model.

Simons Ronald L RL Woodring David D Simons Leslie Gordon LG Sutton Tara E TE Lei Man-Kit MK Beach Steven R H SRH Barr Ashley B AB Gibbons Frederick X FX

Journal of youth and adolescence 20190102 1

There is strong evidence that chronic, systemic inflammation hastens onset of the diseases of old age that ultimately lead to death. Importantly, several studies suggest that childhood adversity predicts chronic inflammation. Unfortunately, this research has been plagued by retrospective reports of childhood adversity, an absence of controls for adult stressors, and a failure to investigate various competing models of the link between childhood adversity and chronic inflammation. The present stu ...[more]

PMID: 30603835

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Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by severe fear in social situations and avoidance of these. Multiple genetic as well as environmental factors contribute to the etiopathology of SAD. One of the main risk factors for SAD is stress, especially during early periods of life (early life adversity; ELA). ELA leads to structural and regulatory alterations contributing to disease vulnerability. This includes the dysregulation of the immune response. However, the molecular link between ELA and the risk for SAD in adulthood remain largely unclear. Evidence is emerging that long-lasting changes of gene expression patterns play an important role in the biological mechanisms linking ELA and SAD. Therefore, we conducted a transcriptome study of SAD and ELA performing RNA sequencing in peripheral blood samples. Analyzing differential gene expression between individuals suffering from SAD with high or low levels of ELA and healthy individuals with high or low levels of ELA, 13 significantly differentially expressed genes (DEGs) were identified with respect to SAD whilst no significant differences in expression were identified with respect to ELA. The most significantly expressed gene was MAPK3 (p=0.003) being upregulated in the SAD group compared to control individuals. In contrary, weighted gene co-expression network analyses (WGCNA) identified only modules significantly associated with ELA (p≤0.05), not with SAD. Furthermore, analyzing interaction networks of the genes from the ELA-associated modules and the SAD-related MAPK3) revealed complex interactions of those genes. Gene functional enrichment analyses indicate a role of signal transduction pathways as well as inflammatory responses supporting an involvement of the immune system in the association of ELA and SAD. In conclusion, we did not identify a direct molecular link between ELA and adult SAD by transcriptional changes. However, our data indicate an indirect association of ELA and SAD mediated by the interaction of genes involved in immune-related signal transduction.

Dataset Information

Youth Adversities Amplify the Association between Adult Stressors and Chronic Inflammation in a Domain Specific Manner: Nuancing the Early Life Sensitivity Model.

Publications

Youth Adversities Amplify the Association between Adult Stressors and Chronic Inflammation in a Domain Specific Manner: Nuancing the Early Life Sensitivity Model.

Similar Datasets

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