Childhood adversity is associated with a host of mental and physical health problems across the lifespan. Individuals who have experienced childhood adversity (e.g., child abuse and neglect, family conflict, poor parent/child relationships, low socioeconomic status or extreme poverty) are at a greater risk for morbidity and premature mortality than those not exposed to childhood adversity. Several mechanisms likely contribute to the relationship between childhood adversity and health across the lifespan (e.g., health behaviors, cardiovascular reactivity). In this paper, we review a large body of research within the field of psychoneuroimmunology, demonstrating the relationship between early life stress and alterations of the immune system. We first review the literature demonstrating that childhood adversity is associated with immune dysregulation across different indices, including proinflammatory cytokine production (and its impact on telomere length), illness and infection susceptibility, latent herpesvirus reactivation, and immune response to a tumor. We then summarize the growing literature on how childhood adversity may alter epigenetic processes. Finally, we propose future directions related to this work that have basic and applied implications.
Childhood trauma is associated with negative perinatal health outcomes including mood disorders and shorter gestation. However, effects of early life exposures on maternal biology are poorly delineated. This study examined associations between childhood trauma and inflammation, as well as the mediating role of obesity in this relationship.This study examined a racially diverse sample of 77 pregnant women assessed in early, mid, and late pregnancy. Assessments included the Childhood Trauma Questionnaire, Center for Epidemiologic Studies-Depression Scale, serum CRP, IL-6, and TNF-α, and prepregnancy BMI.Per linear mixed models, while no direct relationships were observed between childhood trauma with IL-6 or TNF-α, physical (95% CI: 0.007, 0.080) and emotional (95% CI: 0.005, 0.046) abuse as well as emotional neglect (95% CI: 0.010, 0.051) predicted elevated CRP. Effects remained after adjustment for race, income, education, smoking status, medical conditions, and depressive symptoms. PROCESS analyses showed BMI mediated the relationship between physical abuse and both serum CRP (95% CI: 0.014, 0.062) and IL-6 (95% CI: 0.009, 0.034).Exposure to childhood trauma, particularly emotional abuse, physical abuse, and emotional neglect, is associated with inflammation in pregnant women. Obesity served as 1 pathway by which physical abuse contributed to elevations in serum CRP and IL-6. Interventions targeting maternal obesity prior to pregnancy may help mitigate the effects of childhood trauma on perinatal health. These findings have relevance for understanding biological and behavioral pathways by which early life exposures contribute to maternal health. (PsycINFO Database Record
Abstract Purpose Older adults with hematologic malignancies (HM) have unique challenges due to age and fitness. The primary aim of this pilot study was to benchmark the ability of multiple biomarkers of aging (p16, epigenetic clocks, T cell gene expression profiles, and T cell receptor excision circles (TREC) to identify frailty as measured by a clinical impairment index (I 2 ) in patients with HM. Methods 70 patients newly diagnosed with HM had peripheral blood T lymphocytes (PBTL) analyzed for p16 INK4a expression using the OSU_Senescence Nanostring CodeSet. PBTL epigenetic age was measured using 7 epigenetic clocks, and TREC were quantified by qRT-PCR. A composite clinical impairment index (I 2 ) was generated by combining values from 11 geriatric metrics (Independent Activities of Daily Living (iADL), physical health score, Short Physical Performance Battery (SPPB), Body Mass Index (BMI), Eastern Cooperative Oncology Group (ECOG) performance status, self-reported KPS, Blessed Orientation Memory Concentration (BOMC), polypharmacy, Mental Health Inventory (MHI)-17, Medical Outcomes Study (MOS) subscales). Clinical frailty was defined as a score of 7 or greater on the I 2 . Results Age-adjusted p16 INK4a was similar in newly diagnosed patients and healthy controls ( p > 0.1). PBTL p16 INK4a levels correlated positively with the Hannum [r = 0.35, 95% CI (0.09–0.75); p adj. = 0.04] and PhenoAge [r = 0.37, 95% CI (0.11–0.59); p adj. = 0.04] epigenetic clocks. The discrimination ability of the I 2 model was calculated using the area under the receiver operating characteristic curve (AUC). After adjusting for chronologic age and disease group, baseline p16 INK4a [AUC = 0.76, 95% CI (0.56–0.98); p = 0.01], Hannum [AUC = 0.70, 95% CI (0.54–0.85); p = 0.01], PhenoAge [AUC = 0.71, 95% CI (0.55–0.86); p = 0.01], and DunedinPACE [AUC = 0.73, 95% CI (0.57–0.88); p = < 0.01] measures showed the greatest potential to identify clinical frailty using the I 2 . Conclusions Our pilot data suggest that multiple blood-based aging biomarkers have potential to identify frailty in older adults with HM. Implications for Cancer Survivors We developed the I 2 index to quantify impairments across geriatric domains and discovered that PBTL p16, Hannum, PhenoAge, and DunedinPACE are promising indicators of frailty in HM.
