Association of Childhood Trauma Exposure with Inflammatory Biomarkers Among Midlife Women.
Ontology highlight
ABSTRACT:
SUBMITTER: Nguyen JK
PROVIDER: S-EPMC7757571 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
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.
| S-EPMC7672511 | biostudies-literature
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.
| S-EPMC6324370 | biostudies-literature
Project description:Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain.We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models.For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 ?g/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5).Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.
| S-EPMC4841679 | biostudies-literature
Project description:BackgroundConnectedness and attachment are vital parts of humanity. Loneliness, a state of distress in reaction to perceived detachment and isolation, is reported by over one-third of U.S. adults and is associated with numerous physical and mental health consequences. What contributes to loneliness, especially in women and minority populations, is poorly understood, but this population is also at greater risk for abuse and trauma. Our study aimed to further understand loneliness in urban midlife women and to explore the relationship that may exist with trauma(s).MethodsTo identify primacies for mental health care, female midlife participants (N=50) of a long-standing urban community-based cohort focused on health improvement completed a one-time audiotaped interview with both quantitative assessments and a qualitative interview. Loneliness was assessed by the UCLA 3-item Loneliness Scale. Using semi-structured interviews, open-ended questions facilitated a discussion regarding mental health needs and experiences. Interview transcripts were coded and analyzed following a grounded theory methodology. Themes around loneliness and trauma emerged. The transcripts were coded using the same methodology and coders as the individual interviews. Twenty women participated in two optional focus groups.ResultsParticipants had a mean age of 50, with the majority identifying as Black/African American (N=37) and unemployed (N=33). Three themes emerged regarding perceived causes of loneliness: trauma, the burden of responsibilities for others, and secondary to unhealthy relationships. Loneliness associated with trauma will be explored here; other themes are beyond the scope of this paper and will be discussed in subsequent analyses. Quantitative results suggest that physical abuse (loneliness scores 5.4 vs. 4.0, p=0.003), as well as emotional abuse and neglect (loneliness scores 5.6 vs. 4.4, p=0.01), were associated with greater loneliness.ConclusionIn urban midlife low-income women, lifetime physical abuse and emotional abuse/neglect are associated with increased feelings of loneliness. Qualitative data provide insight into how participants viewed their traumatic histories, ways in which the trauma has ongoing influence, and how they experience loneliness. Though further investigation is needed, trauma-informed approaches should be considered in both primary care and mental health settings with a focus on mitigating loneliness and providing appropriate support and trauma treatment.
| S-EPMC9608918 | biostudies-literature
Project description:The dysregulation of the inflammatory and neuroendocrine systems seen in major depressive disorder (MDD) may persist after remission and this is associated with a higher risk of relapse. This vulnerable subgroup may be characterized by a history of childhood trauma. In a single-blind randomized placebo-controlled crossover study, 21 women with remitted recurrent MDD and 18 healthy controls were exposed to psychosocial stress (Trier social stress test) or inflammatory stress (typhoid vaccine), or both, to investigate the effects of childhood trauma on the neuroendocrine and inflammatory responses. Childhood trauma was assessed using the Childhood Trauma Questionnaire and participants were dichotomized into a traumatized and non-traumatized group. Serum adrenocorticotropic hormone (ACTH), cortisol, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and interleukin (IL)-6 were measured at regular intervals after each intervention. The effects of trauma, time, and intervention on these parameters were modeled by fitting linear mixed models. Childhood trauma in itself did not have a main effect on the outcome measurements. However, an interactional effect of trauma with stressor type was found in the remitted MDD group: trauma was associated with higher cortisol levels only after adding immunological to psychosocial stress, and with lower TNF-α levels in response to vaccination. This suggests the existence of a vulnerable trauma-associated MDD endophenotype.
| S-EPMC6956125 | biostudies-literature
Project description:BackgroundExposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM2.5) exposure and CVD. Coarse particulate matter (PM10-2.5) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain.MethodsWe examined the association between ambient concentrations of PM10-2.5 and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM10-2.5, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM10-2.5 exposure and markers, including demographic, health and other covariates.ResultsEach interquartile (4 μg/m3) increase in one-year PM10-2.5 exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: - 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM10-2.5 and PAI-1 remained unchanged with adjustment for PM2.5, ozone, nitrogen dioxide, and carbon monoxide.ConclusionsLong-term PM10-2.5 exposure may be associated with changes in coagulation independently from PM2.5, and thus, contribute to CVD risk in midlife women.
| S-EPMC7643259 | biostudies-literature
Project description:BackgroundExposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain.ObjectivesThis study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women.MethodsAnnual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors.ResultsShort-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment.ConclusionsExposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.
| S-EPMC5584622 | biostudies-literature
Project description: Not available
| S-EPMC3291097 | biostudies-literature
Project description:Psychosis-like experiences (PLEs), or attenuated positive symptoms of psychosis, present along a severity continuum and have been associated with distressing thoughts and impairments in functioning. Although knowledge of the clinical importance of PLEs is expanding, risk factors for their expression are still poorly understood. Sleep disturbances are one known factor that exacerbate PLEs expression and distress, and trauma exposure is associated with occurrence of PLEs, as well as increased risk of later sleep difficulties. This study examined the joint influences of sleep and trauma on PLEs in an undergraduate sample. Self-report questionnaires on presence and distress of PLEs, sleep problems, and occurrence of previous traumatic experiences were completed by participants (N=409). In order to determine the unique impact of sleep on PLEs, three sets of predictors: sociodemographic, psychosocial (including trauma), and sleep were entered in steps into a hierarchical multiple regression model. In the final model, specific sleep domains uniquely predicted PLEs, while previous trauma exposure, which was a significant predictor when entered in step two with other psychosocial variables, was no longer a significant predictor. Results suggest the possibility that disruptions in sleep following or occurring alongside a traumatic experience may somehow contribute to, or exacerbate the presence of PLEs.
| S-EPMC6129231 | biostudies-other
Project description:BackgroundChildhood trauma (CT) is associated with altered brain anatomy. These neuroanatomical changes might be more pronounced in individuals with a psychiatric disorder. Post-traumatic stress disorder (PTSD) and borderline personality disorder (BPD) are more prevalent in individuals with a history of CT.ObjectiveIn this study, we examined limbic and total brain volumes in healthy women with and without a history of CT and in females with PTSD or BPD and a history of CT to see whether neuroanatomical changes are a function of psychopathology or CT.MethodIn total, 128 women (N = 70 healthy controls without CT, N = 25 healthy controls with CT, N = 14 individuals with PTSD, and N = 19 individuals with BPD) were recruited. A T1-weighted anatomical MRI was acquired from all participants for Freesurfer-based assessment of total brain, hippocampus, and amygdala volumes. Severity of CT was assessed with a clinical interview and the Childhood Trauma Questionnaire. Group differences in hippocampal and amygdala volumes (adjusted for total brain volume) and total brain volume (adjusted for height) were characterized by analysis of covariance.ResultsVolume of the total brain, hippocampus, and amygdala did not differ between the four groups (p > .05). CT severity correlated negatively with total brain volume across groups (r = -0.20; p = .029).ConclusionsCT was associated with reduced brain volume but PTSD or BPD was not. The association between CT and reduced brain volume as a global measure of brain integrity suggests a common origin for vulnerability to psychiatric disorders later in life.
| S-EPMC8462923 | biostudies-literature