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Association of Childhood Trauma Exposure with Inflammatory Biomarkers Among Midlife Women.

ABSTRACT: Background: Childhood abuse has been associated with poor health outcomes in adulthood. However, the physiologic pathways by which abuse is linked to health are not fully elucidated. Inflammation plays a significant role in the pathophysiology of multiple chronic diseases. We tested whether childhood trauma exposure was related to increased systemic inflammation in midlife women. Materials and Methods: Participants were 304 nonsmoking perimenopausal and postmenopausal women aged 40 to 60 years and free of cardiovascular disease. They completed questionnaires assessing psychosocial and behavioral factors, including childhood trauma, anthropometric measures, wrist actigraphy sleep measurements, and a fasting blood draw for inflammatory markers high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6). Associations between childhood trauma and inflammatory markers were tested in linear regression models controlling for age, race/ethnicity, education, body mass index, anti-inflammatory medication use, and alcohol consumption. Other covariates considered included sleep continuity and depressive symptoms. Results: A total of 44.8% of the sample experienced at least one type of childhood abuse/neglect. Women with a history of emotional abuse had higher IL-6 levels than women without this history in multivariate models (β = 0.077, standard error = 0.032, p = 0.017). Results were not accounted for by covariates and persisted additionally controlling for depressive symptoms and sleep. Childhood abuse/neglect was not related to hsCRP. Conclusions: Childhood emotional abuse was associated with higher levels of IL-6 in midlife women. Assessing childhood trauma exposure along with inflammatory markers may be important for the development of prevention strategies at midlife to prevent chronic diseases later in life.

SUBMITTER: Nguyen JK

PROVIDER: S-EPMC7757571 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ImportanceChildhood lead exposure has been linked to disrupted brain development, but long-term consequences for structural brain integrity are unknown.ObjectiveTo test the hypothesis that childhood lead exposure is associated with magnetic resonance imaging (MRI) measurements of lower structural integrity of the brain in midlife.Design, setting, and participantsThe Dunedin Study followed a population-representative 1972-1973 birth cohort in New Zealand (N = 564 analytic sample) to age 45 years (until April 2019).ExposuresChildhood blood lead levels measured at age 11 years.Main outcomes and measuresStructural brain integrity at age 45 years assessed via MRI (primary outcomes): gray matter (cortical thickness, surface area, hippocampal volume), white matter (white matter hyperintensities, fractional anisotropy [theoretical range, 0 {diffusion is perfectly isotropic} to 100 {diffusion is perfectly anisotropic}]), and the Brain Age Gap Estimation (BrainAGE), a composite index of the gap between chronological age and a machine learning algorithm-estimated brain age (0 indicates a brain age equivalent to chronological age; positive and negative values represent an older and younger brain age, respectively). Cognitive function at age 45 years was assessed objectively via the Wechsler Adult Intelligence Scale IV (IQ range, 40-160, standardized to a mean of 100 [SD, 15]) and subjectively via informant and self-reports (z-score units; scale mean, 0 [SD, 1]).ResultsOf 1037 original participants, 997 were alive at age 45 years, of whom 564 (57%) had received lead testing at age 11 years (302 [54%] male) (median follow-up, 34 [interquartile range, 33.7-34.7] years). Mean blood lead level at age 11 years was 10.99 (SD, 4.63) μg/dL. After adjusting for covariates, each 5-μg/dL higher childhood blood lead level was significantly associated with 1.19-cm2 smaller cortical surface area (95% CI, -2.35 to -0.02 cm2; P = .05), 0.10-cm3 smaller hippocampal volume (95% CI, -0.17 to -0.03 cm3; P = .006), lower global fractional anisotropy (b = -0.12; 95% CI, -0.24 to -0.01; P = .04), and a BrainAGE index 0.77 years older (95% CI, 0.02-1.51 years; P = .05) at age 45 years. There were no statistically significant associations between blood lead level and log-transformed white matter hyperintensity volume (b = 0.05 log mm3; 95% CI, -0.02 to 0.13 log mm3; P = .17) or mean cortical thickness (b = -0.004 mm; 95% CI, -0.012 to 0.004 mm; P = .39). Each 5-μg/dL higher childhood blood lead level was significantly associated with a 2.07-point lower IQ score at age 45 years (95% CI, -3.39 to -0.74; P = .002) and a 0.12-point higher score on informant-rated cognitive problems (95% CI, 0.01-0.23; P = .03). There was no statistically significant association between childhood blood lead levels and self-reported cognitive problems (b = -0.02 points; 95% CI, -0.10 to 0.07; P = .68).Conclusions and relevanceIn this longitudinal cohort study with a median 34-year follow-up, higher childhood blood lead level was associated with differences in some MRI measures of brain structure that suggested lower structural brain integrity in midlife. Because of the large number of statistical comparisons, some findings may represent type I error.

Project description:ImportanceBeing exposed to trauma is a common childhood experience associated with symptoms and impairments in childhood.ObjectiveTo assess the association between cumulative childhood trauma exposure and adult psychiatric and functional outcomes.Design, setting, and participantsProspective, population-based cohort study of 1420 participants. A community representative sample of participants was assessed with structured Child and Adolescent Psychiatric Assessment interviews up to 8 times in childhood (ages 9-16 years; 6674 observations; 1993-2000) for lifetime trauma exposure as defined by the Diagnostic and Statistical Manual of Mental Disorders. Participants were followed up 4 times in adulthood (ages 19, 21, 25, and 30 years; 4556 observations of 1336 participants; 1999-2015) with the structured Young Adult Psychiatric Assessment Interview for psychiatric outcomes, functional outcomes, and evidence of a disrupted transition to adulthood. Analysis was completed in 2018.ExposureParticipants were assessed with the structured Child and Adolescent Psychiatric Assessment interview (parent and self-report) up to 8 times in childhood for lifetime trauma exposure (ages 9-16 years; 6674 observations; 1993-2000).Main outcomes and measuresParticipants were assessed up to 4 times with the structured Young Adult Psychiatric Assessment interview (self-report) in adulthood (ages 19, 21, 25, and 30 years; 4556 observations of 1336 participants; 1999-2015) for psychiatric outcomes, functional outcomes, and evidence of a disrupted transition to adulthood.ResultsAmong the 1420 study participants, 630 (49.0%) were female and 983 (89.4%) were white. By age 16 years, 30.9% of children (n = 451) were exposed to 1 traumatic event, 22.5% (n = 289) were exposed to 2 such events, and 14.8% (n = 267) were exposed to 3 or more. Cumulative childhood trauma exposure to age 16 years was associated with higher rates of adult psychiatric disorders (odds ratio for any disorder, 1.2; 95% CI, 1.0-1.4) and poorer functional outcomes, including key outcomes that indicate a significantly disrupted transition to adulthood (eg, failure to hold a job and social isolation). Childhood trauma exposure continued to be associated with higher rates of adult psychiatric and functional outcomes after adjusting for a broad range of childhood risk factors, including psychiatric functioning and family adversities and hardships (adjusted odds ratio for any disorder, 1.3; 95% CI, 1.0-1.5).Conclusions and relevanceCumulative childhood trauma exposure was associated with poor adult outcomes even after accounting for many of the childhood and family factors associated with both trauma exposure and poor adult outcomes. Childhood trauma exposures are common, but often preventable, thus providing a clear target for child-focused public health efforts to ameliorate long-term morbidity.

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Association of Childhood Trauma Exposure with Inflammatory Biomarkers Among Midlife Women.

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