Associations of adversity in childhood and risk factors for cardiovascular disease in mid-adulthood.
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ABSTRACT:
SUBMITTER: Anderson EL
PROVIDER: S-EPMC5915314 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectiveThe current study investigated mediators between childhood/adolescent adversities (e.g., dating violence, maltreatment, homelessness, and parental death), low socioeconomic status (SES) during adolescence, and cardiovascular disease (CVD) risk in young adulthood. The purpose of these analyses was to understand whether SES during adolescence and childhood/adolescent adversities affect CVD risk through similar pathways, including maternal relationship quality, health behaviors, financial stress, medical/dental care, educational attainment, sleep problems, and depressive symptoms.MethodsUsing the National Longitudinal Study of Adolescent to Adult Health (N = 14,493), which has followed US adolescents (Wave 1; M = 15.9 years) through early adulthood (Wave 4; M = 28.9 years), associations were examined between childhood/adolescent adversity and SES to 30-year CVD risk in young adulthood. The outcome was a Framingham-based prediction model of CVD risk that included age, sex, body mass index, smoking, systolic blood pressure, diabetes, and antihypertensive medication use at Wave 4. Path analysis was used to examine paths through the adolescent maternal relationship to young adult mediators of CVD risk.ResultsChildhood/adolescent adversity significantly predicted greater adult CVD risk through the following pathways: maternal relationship, health behaviors, financial stress, lack of medical/dental care, and educational attainment; but not through depressive symptoms or sleep problems. Lower SES during adolescence significantly predicted greater adult CVD risk through the following pathways: health behaviors, financial stress, lack of medical/dental care, and educational attainment, but not maternal relationship, depressive symptoms, or sleep problems.ConclusionsChildhood/adolescent adversities and SES affected CVD risk in young adulthood through both similar and unique pathways that may inform interventions.
| S-EPMC5558845 | biostudies-literature
Project description:IntroductionAssociations between childhood/adolescent adversity and poor adult physical health have been reported in past work. Much of this work has relied on either retrospective or prospective measures of childhood experiences. However, the effect of different assessment methods on potential stress buffering processes remains largely unknown.ObjectiveWe first examined the extent to which long-term cardiovascular disease risk (CVD) was predicted by reports obtained from 10-year old youth regarding adversity experienced in the prior year and those obtained from the same individuals as adults (age 29) regarding their experience of childhood adversity from ages 0-10, focusing in each case on similar types of adversity. To test stress buffering perspectives, we examined the effects of parental emotional support on the association between each measure of childhood adversities and cardiovascular health.MethodsWe used data from a longitudinal sample of 454 African Americans enrolled in the Family and Community Health Study. The outcome variable was a 30-year CVD risk score computed from the Framingham algorithm. The hypotheses were tested with beta regression models.ResultsThe findings revealed a link between childhood adversity and adult CVD risk at age 29, for both measures of adversity. Consistent with the stress-buffering hypothesis, prospectively assessed parental emotional support in adolescence, but not adulthood, buffered effects on cardiovascular risk for each type of assessment of childhood adversity.ConclusionsProspective and retrospective measures correlated in a manner similar to prior reports (i.e. significantly, but poorly). Further, in line with stress-buffering hypothesis, parental emotional support received at age 10 yielded different buffering effects than parental emotional support received at age 29. The study's findings suggest that theoretically consistent patterns of stress-buffering are detectable using either type of assessment of childhood adversity and provide useful information in the prediction of adult CVD risk.
| S-EPMC7042894 | biostudies-literature
Project description:Adverse childhood experiences (ACEs), defined as traumatic events in childhood that range from various forms of abuse to household challenges and dysfunction, have devastating consequences on adult health. Epidemiological studies in humans and animal models of early life stress (ELS) have revealed a strong association and insight into the mechanistic link between ACEs and increased risk of cardiovascular disease (CVD). This review focuses on the mechanistic links of ACEs in humans and ELS in mice and rats to vasoactive factors and immune mediators associated with CVD and hypertension risk, as well as sex differences in these phenomena. Major topics of discussion in this review are as follows: (a) epidemiological associations between ACEs and CVD risk focusing on hypertension, (b) evidence for association of ACE exposures to immune-mediated and/or vasoactive pathways, (c) rodent models of ELS-induced hypertension risk, (d) proinflammatory mediators and vasoactive factors as mechanisms of ELS-induced hypertension risk. We also provide some overall conclusions and directions of further research. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.
| S-EPMC6534788 | biostudies-literature
Project description:Early life stunting may have long-term effects on body composition, resulting in obesity-related comorbidities. We tested the hypothesis that individuals stunted in early childhood may be at higher cardiometabolic risk later in adulthood. 1753 men and 1781 women participating in the 1982 Pelotas (Brazil) birth cohort study had measurements of anthropometry, body composition, lipids, glucose, blood pressure, and other cardiometabolic traits at age 30 years. Early stunting was defined as height-for-age Z-score at age 2 years below -2 against the World Health Organization growth standards. Linear regression models were performed controlling for sex, maternal race/ethnicity, family income at birth, and birthweight. Analyses were stratified by sex when p-interaction<0.05. Stunted individuals were shorter (β = -0.71 s.d.; 95% CI: -0.78 to -0.64), had lower BMI (β = -0.14 s.d.; 95%CI: -0.25 to -0.03), fat mass (β = -0.28 s.d.; 95%CI: -0.38 to -0.17), SAFT (β = -0.16 s.d.; 95%CI: -0.26 to -0.06), systolic (β = -0.12 s.d.; 95%CI: -0.21 to -0.02) and diastolic blood pressure (β = -0.11 s.d.; 95%CI: -0.22 to -0.01), and higher VFT/SAFT ratio (β = 0.15 s.d.; 95%CI: 0.06 to 0.24), in comparison with non-stunted individuals. In addition, early stunting was associated with lower fat free mass in both men (β = -0.39 s.d.; 95%CI: -0.47 to -0.31) and women (β = -0.37 s.d.; 95%CI: -0.46 to -0.29) after adjustment for potential confounders. Our results suggest that early stunting has implications on attained height, body composition and blood pressure. The apparent tendency of stunted individuals to accumulate less fat-free mass and subcutaneous fat might predispose them towards increased metabolic risks in later life.
| S-EPMC5894958 | biostudies-literature
Project description:BackgroundPathogen-specific and overall infection burden may contribute to atherosclerosis and cardiovascular disease (CVD), but the effect of infection severity and timing is unknown. We investigated whether childhood infection-related hospitalisation (IRH, a marker of severity) was associated with subsequent adult CVD hospitalisation.MethodsUsing longitudinal population-based statutorily-collected administrative health data from Western Australia (1970-2009), we identified adults hospitalised with CVD (ischaemic heart disease, ischaemic stroke, and peripheral vascular disease) and matched them (10:1) to population controls. We used Cox regression to assess relationships between number and type of childhood IRH and adulthood CVD hospitalisation, adjusting for sex, age, Indigenous status, socioeconomic status, and birth weight.Results631 subjects with CVD-related hospitalisation in adulthood (≥ 18 years) were matched with 6310 controls. One or more childhood (< 18 years) IRH was predictive of adult CVD-related hospitalisation (adjusted hazard ratio, 1.3; 95% CI 1.1-1.6; P < 0.001). The association showed a dose-response; ≥ 3 childhood IRH was associated with a 2.2 times increased risk of CVD-related hospitalisation in adulthood (adjusted hazard ratio, 2.2; 95% CI 1.7-2.9; P < 0.001). The association was observed across all clinical diagnostic groups of infection (upper respiratory tract infection, lower respiratory tract infection, infectious gastroenteritis, urinary tract infection, skin and soft tissue infection, and other viral infection), and individually with CVD diagnostic categories (ischaemic heart disease, ischaemic stroke and peripheral vascular disease).ConclusionsSevere childhood infection is associated with CVD hospitalisations in adulthood in a dose-dependent manner, independent of population-level risk factors.
| S-EPMC4418819 | biostudies-literature
Project description:Although it is assumed that epigenetic mechanisms, such as changes in DNA methylation (DNAm), underlie the relationship between adverse intrauterine conditions and adult metabolic health, evidence from human studies remains scarce. Therefore, we evaluated whether DNAm in whole blood mediated the association between prenatal famine exposure and metabolic health in 422 individuals exposed to famine in utero and 463 (sibling) controls. We implemented a two-step analysis, namely, a genome-wide exploration across 342,596 cytosine-phosphate-guanine dinucleotides (CpGs) for potential mediators of the association between prenatal famine exposure and adult body mass index (BMI), serum triglycerides (TG), or glucose concentrations, which was followed by formal mediation analysis. DNAm mediated the association of prenatal famine exposure with adult BMI and TG but not with glucose. DNAm at PIM3 (cg09349128), a gene involved in energy metabolism, mediated 13.4% [95% confidence interval (CI), 5 to 28%] of the association between famine exposure and BMI. DNAm at six CpGs, including TXNIP (cg19693031), influencing β cell function, and ABCG1 (cg07397296), affecting lipid metabolism, together mediated 80% (95% CI, 38.5 to 100%) of the association between famine exposure and TG. Analyses restricted to those exposed to famine during early gestation identified additional CpGs mediating the relationship with TG near PFKFB3 (glycolysis) and METTL8 (adipogenesis). DNAm at the CpGs involved was associated with gene expression in an external data set and correlated with DNAm levels in fat depots in additional postmortem data. Our data are consistent with the hypothesis that epigenetic mechanisms mediate the influence of transient adverse environmental factors in early life on long-term metabolic health. The specific mechanism awaits elucidation.
2018-01-31 | GSE78743 | GEO
Project description:ImportanceSevere forms of common chronic oral infections or inflammations are associated with increased cardiovascular risk in adults. To date, the role of childhood oral infections in cardiovascular risk is not known because no long-term studies have been conducted.ObjectiveTo investigate whether signs of oral infections in childhood are associated with cardiovascular risk factors and subclinical atherosclerosis in adulthood.Design, setting, and participantsThe cohort study (n = 755) was derived from the Cardiovascular Risk in Young Finns Study, an ongoing prospective cohort study in Finland initiated in 1980. Participants underwent clinical oral examinations during childhood, when they were aged 6, 9, or 12 years and a clinical cardiovascular follow-up in adulthood in 2001 at age 27, 30, or 33 years and/or in 2007 at age 33, 36, or 39 years. Cardiovascular risk factors were measured at baseline and during the follow-up until the end of 2007. Final statistical analyses were completed on February 19, 2019.Main outcomes and measuresFour signs of oral infections (bleeding on probing, periodontal probing pocket depth, caries, and dental fillings) were documented. Cumulative lifetime exposure to 6 cardiovascular risk factors was calculated from dichotomized variables obtained by using the area-under-the-curve method. Subclinical atherosclerosis (ie, carotid artery intima-media thickness [IMT]) was quantified in 2001 (n = 468) and 2007 (n = 489).ResultsThis study included 755 participants, of whom 371 (49.1%) were male; the mean (SD) age at baseline examination was 8.07 (2.00) years. In this cohort, 33 children (4.5%) had no sign of oral infections, whereas 41 (5.6%) had 1 sign, 127 (17.4%) had 2 signs, 278 (38.3%) had 3 signs, and 248 (34.1%) had 4 signs. The cumulative exposure to risk factors increased with the increasing number of oral infections both in childhood and adulthood. In multiple linear regression models, childhood oral infections, including signs of either periodontal disease (R2 = 0.018; P = .01), caries (R2 = 0.022; P = .008), or both (R2 = 0.024; P = .004), were associated with adulthood IMT. The presence of any sign of oral infection in childhood was associated with increased IMT (third tertile vs tertiles 1 and 2) with a relative risk of 1.87 (95% CI, 1.25-2.79), whereas the presence of all 4 signs produced a relative risk of 1.95 (95% CI, 1.28-3.00). The associations were more obvious in boys: if periodontal disease were present, the corresponding estimate was 1.69 (95% CI, 1.21-2.36); if caries, 1.46 (95% CI, 1.04-2.05); and if all 4 signs of oral infections, 2.25 (95% CI, 1.30-3.89). The associations were independent of cardiovascular risk factors.Conclusions and relevanceOral infections in childhood appear to be associated with the subclinical carotid atherosclerosis seen in adulthood.
| S-EPMC6487573 | biostudies-literature
Project description:ObjectiveTo investigate the relation between preterm birth (gestational age <37 weeks) and risk of CKD from childhood into mid-adulthood.DesignNational cohort study.SettingSweden.Participants4 186 615 singleton live births in Sweden during 1973-2014.ExposuresGestational age at birth, identified from nationwide birth records in the Swedish birth registry.Main outcome measuresCKD, identified from nationwide inpatient and outpatient diagnoses through 2015 (maximum age 43 years). Cox regression was used to examine gestational age at birth and risk of CKD while adjusting for potential confounders, and co-sibling analyses assessed the influence of unmeasured shared familial (genetic or environmental) factors.Results4305 (0.1%) participants had a diagnosis of CKD during 87.0 million person years of follow-up. Preterm birth and extremely preterm birth (<28 weeks) were associated with nearly twofold and threefold risks of CKD, respectively, from birth into mid-adulthood (adjusted hazard ratio 1.94, 95% confidence interval 1.74 to 2.16; P<0.001; 3.01, 1.67 to 5.45; P<0.001). An increased risk was observed even among those born at early term (37-38 weeks) (1.30, 1.20 to 1.40; P<0.001). The association between preterm birth and CKD was strongest at ages 0-9 years (5.09, 4.11 to 6.31; P<0.001), then weakened but remained increased at ages 10-19 years (1.97, 1.57 to 2.49; P<0.001) and 20-43 years (1.34, 1.15 to 1.57; P<0.001). These associations affected both males and females and did not seem to be related to shared genetic or environmental factors in families.ConclusionsPreterm and early term birth are strong risk factors for the development of CKD from childhood into mid-adulthood. People born prematurely need long term follow-up for monitoring and preventive actions to preserve renal function across the life course.
| S-EPMC6490674 | biostudies-literature
Project description:Previous studies have shown that socio-demographic factors, childhood socioeconomic status (CSES), childhood traumatic experiences (CTEs), social support and behavioral factors are associated with health and well-being in adulthood. However, the relative importance of these factors for mental health, health, and well-being has not been studied. Moreover, the mechanisms by which CTEs affect mental health, health, and well-being in adulthood are not clear. Using data from a representative sample (n = 12,981) of the adult population in Tromsø, Norway, this study examines (i) the relative contribution of structural conditions (gender, age, CSES, psychological abuse, physical abuse, and substance abuse distress) to social support and behavioral factors in adulthood; (ii) the relative contribution of socio-demographic factors, CSES, CTEs, social support, and behavioral factors to three multi-item instruments of mental health (SCL-10), health (EQ-5D), and subjective well-being (SWLS) in adulthood; (iii) the impact of CTEs on mental health, health, and well-being in adulthood, and; (iv) the mediating role of adult social support and behavioral factors in these associations. Instrumental support (24.16%, p < 0.001) explained most of the variation in mental health, while gender (21.32%, p < 0.001) explained most of the variation in health, and emotional support (23.34%, p < 0.001) explained most of the variation in well-being. Psychological abuse was relatively more important for mental health (12.13%), health (7.01%), and well-being (9.09%), as compared to physical abuse, and substance abuse distress. The subjective assessment of childhood financial conditions was relatively more important for mental health (6.02%), health (10.60%), and well-being (20.60%), as compared to mother's and father's education. CTEs were relatively more important for mental health, while, CSES was relatively more important for health and well-being. Respondents exposed to all three types of CTEs had a more than two-fold increased risk of being mentally unhealthy (RR Total Effect = 2.75, 95% CI: 2.19-3.10), an 89% increased risk of being unhealthy (RR Total Effect = 1.89, 95% CI: 1.47-1.99), and a 42% increased risk of having a low level of well-being in adulthood (RR Total Effect = 1.42, 95% CI: 1.29-1.52). Social support and behavioral factors mediate 11-18% (p < 0.01) of these effects. The study advances the theoretical understanding of how CTEs influence adult mental health, health, and well-being.
| S-EPMC4879780 | biostudies-literature
Project description:ObjectiveAlthough emerging evidence indicates that increased variability in cardiovascular risk factors (CVRFs) among populations at midlife or later is a reliable predictor of adverse health outcomes, it is unknown whether intraindividual CVRF variability during childhood or adolescence is an independent predictor of later-life diabetes. We aimed to examine the association of CVRF variability during childhood with diabetes in later life.Research design and methodsWe included 1,718 participants who participated in the Bogalusa Heart Study and had measures at least four times during childhood (aged 4-19 years). The mean follow-up period was 20.5 years. Intraindividual CVRF variabilities during childhood were calculated using SD, coefficient of variation, deviation from age-predicted values, and residual SD based upon four to eight serial measurements in childhood.ResultsIncreased variability in BMI or HDL cholesterol (HDL-C) during childhood, irrespective of the indices used, was significantly positively associated with later-life diabetes risk independent of their respective mean levels in childhood and other possible confounding factors. In combined analysis, the magnitude of the association with diabetes risk was similar for high childhood BMI variability and high childhood HDL-C variability. After adjustments for potential confounding variables, other CVRF variabilities including systolic/diastolic blood pressure, total cholesterol, triglycerides, and LDL cholesterol were not significantly associated with diabetes.ConclusionsIncreased BMI and HDL-C variabilities during childhood were significant risk factors for the development of diabetes independently of diverse risk factors, which may offer new insights into the childhood origin of adult-onset diabetes.
| S-EPMC6702606 | biostudies-literature