ArticleLiterature Review

Parent-child separation and cardiometabolic outcomes and risk factors in adulthood: A systematic review

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Abstract

Background: Parent-child separation has been associated with negative mental health across childhood and adulthood, yet little is known about the long-term impacts for cardiovascular health. This systematic review synthesized and evaluated the quality of the literature examining the association between exposures to parent-child separation and cardiometabolic outcomes in adulthood. Methods: Following a registered protocol, online databases (Pubmed, PsycInfo, and Web of Science) were searched for relevant studies. Studies were included if they (a) defined the exposure before age 18 as institutionalization, foster care placement, parental incarceration, separation due to parents migrating for economic reasons, or asylum and war; and (b) quantified the association between parent-child separation and cardiometabolic events and diagnoses (e.g., coronary heart disease, diabetes) and risk factors (e.g., body mass index, fat distribution, serum-based metabolic markers, inflammatory markers in adulthood (≥ age 18). Studies lacking an unexposed comparison group were excluded. The risk for bias in each study was assessed with a modified Newcastle-Ottawa Scale. Results: Of the 1938 studies identified, 13 met our inclusion criteria. Two of the four studies examining associations between parent-child separation and cardiometabolic events and diagnoses found positive associations with coronary heart disease and diabetes. Amongst the 13 studies examining associations with any type of adult cardiometabolic risk factors, eight studies reported at least one positive association. Sub-analyses considering separate reasons for parent-child separation provided clearer insights: War evacuation was associated with hypertension and high blood pressure across four studies from the same cohort; out-of home care experiences largely evidenced null results across five different studies, and two studies on parental incarceration suggested positive associations with elevated inflammation, BMI and blood pressure. Conclusions: The connections between parent-child separation and adult cardiometabolic outcomes and risk factors are currently inconsistent. The results may depend on the reason for separation, age of assessment, analytic differences and other psychosocial variables that are often unmeasured in this literature.

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... Some studies show no significant differences between OHC and in-home care, and a few even indicate positive impacts. Additionally, certain studies focus on older children with longer placements, while others combine child welfare and juvenile justice placements, further complicating the overall assessment (Gypen et al., 2017;Kääriälä & Hiilamo, 2017;Maclean et al., 2016;Seker et al., 2022;Tang et al., 2023). ...
... Some studies show no significant differences between OHC and in-home care, and a few even indicate positive impacts. Additionally, certain studies focus on older children with longer placements, while others combine child welfare and juvenile justice placements, further complicating the overall assessment (Gypen et al., 2017;Kääriälä & Hiilamo, 2017;Maclean et al., 2016;Seker et al., 2022;Tang et al., 2023). ...
... For instance, emerging evidence examines long-term consequences of parent-child separation, a common type of ACE, on cardiovascular health in adults. 37 Fourth, because of the cross-sectional design, the study cannot support causality between ACEs and sleep duration. Finally, although not inherently a limitation of our study, it is important to note that the NSCH data we used did not have participants falling into all of the sleep duration categories (none aligned with scores of 70 or 90). ...
Article
Background Adverse childhood experiences (ACEs) and suboptimal sleep both negatively associate with cardiovascular health. Although an association between ACEs and suboptimal sleep in youth has been reported, there has been no investigation for differential effects among ACE subdomains. Objective We examined associations between total and subdomain ACEs and sleep duration, and age as a moderator. Methods Using the 2020–2021 National Survey of Children's Health and the American Heart Association Life's Essential 8 scoring algorithm, we created 3 sleep subgroups: (1) optimal, (2) suboptimal (≥1 to <2 hours below or ≥1 hour above optimal), and (3) very suboptimal (≥2 hours below optimal). We assessed association between ACEs (total and subdomains) and sleep duration using multinomial logistic regression, controlling for sex, age, race/ethnicity, caregiver's education, household income, habitual bedtime, and physical activity. We tested the interactions between ACEs and child's age. Results In children aged 6 to 17 years (N = 58 964), mean sleep duration score was 77.2 (95% confidence interval, 76.6–77.9). The mean number of ACEs was 0.89 (95% confidence interval, 0.87–0.91). Adjusting for covariates, each additional ACE increased the likelihood of falling into the suboptimal subgroup by 8% and the very suboptimal subgroup by 26%. There was an association between each subdomain of ACE and suboptimal sleep duration, with no significant interaction with age. Conclusions Our findings show a dose-response relationship between ACEs and suboptimal sleep duration—a new cardiovascular health indicator in Life's Essential 8. Healthcare providers should screen for ACEs and suboptimal sleep in children to reduce future cardiovascular disease risk.
... A search of electronic databases revealed 1 published study 19 matching our inclusion criteria, while another was published by collaborators during the preparation of this manuscript 20 (Fig. 1). Additionally, using citations in published systematic reviews, 18,33 we identified ten unpublished studies that had the potential to examine the relation between childhood care and adult cardiovascular disease. In combination, this resulted in 12 seemingly unique datasets. ...
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Background While individuals who were separated from their biological family and placed into the care of the state during childhood (out-of-home care) are more prone to developing selected adverse health problems in adulthood, their risk of cardiovascular disease is uncertain. Our aim was to explore this association by pooling published and unpublished results from prospective cohort studies. Methods We used two approaches to identifying relevant data on childhood care and adult cardiovascular disease (PROSPERO registration CRD42021254665). First, to locate published studies, we searched PubMed (Medline) until November 2023. Second, with the objective of identifying unpublished studies with the potential to address the present research question, we scrutinised retrieved reviews on childhood out-of-home care and other adult health outcomes. Included studies were required to satisfy three criteria: a cohort study in which the assessment of care was made prospectively pre-adulthood (in the avoidance of recall bias); data on an unexposed comparator group were available (for the computation of relative risk); and a diagnosis of adult cardiovascular disease events (coronary heart disease, stroke, or their combination) had been made (as opposed to risk factors only). Collaborating investigators provided study-specific estimates which were aggregated using random-effects meta-analysis. The Newcastle-Ottawa Scale was used to assess individual study quality. Findings Twelve studies (2 published, 10 unpublished) met the inclusion criteria, and investigators from nine provided viable results, including updated analyses of the published studies. Studies comprised 611,601 individuals (301,129 women) from the US, UK, Sweden, Finland, and Australia. Five of the nine studies were judged to be of higher methodological quality. Relative to the unexposed, individuals with a care placement during childhood had a 51% greater risk of cardiovascular disease in adulthood (summary rate ratio after age- and sex-adjustment [95% confidence interval]: 1.51 [1.22, 1.86]; range of study-specific estimates: 1.07 to 2.06; I² = 69%, p = 0.001). This association was attenuated but persisted after adjustment for socioeconomic status in childhood (8 studies; 1.41 [1.15, 1.72]) and adulthood (9 studies, 1.29 [1.11, 1.51]). Interpretation Our findings show that individuals with experience of out-of-home care in childhood have a moderately raised risk of cardiovascular disease in adulthood. Funding 10.13039/501100000265Medical Research Council; 10.13039/100000049National Institute on Aging; 10.13039/100010269Wellcome Trust.
... Research suggests a potential association between early childhood behaviors and psychiatric illness with adult obesity and BMI gain [38][39][40], while other research suggests that ACEs are associated with a range of childhood emotional and behavioral problems [41,42]. A recent literature review examining the associations between parental separation and cardiometabolic disease, noted that childhood psychosocial problems may act as a mediating or moderating mechanism [43]. This body of research is suggestive, in the light of the association between ACEs and cardiometabolic disease discussed above, that behavioral problems associated with parental imprisonment may moderate cardiometabolic disease risk in later life. ...
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Objectives Recent studies have demonstrated that parental imprisonment (PI) is associated with cardiometabolic risk later in life. However, underlying risk factors for these associations have not previously been explored. The present study examines how early childhood behaviors and parental imprisonment may be associated with cardiometabolic risk in adulthood. Methods The study follows a subset of 7,223 live, singleton births from 1981–1984 in Brisbane, Australia where data was collected on parental imprisonment at ages 5 & 14 and behaviors from the Child Behavioral Checklist (CBCL) at age 5. Our sample examines 1884 males and 1758 females whose mothers completed prenatal, age 5, and age 14 interviews and respondents completed one or more interviews at ages 14, 21, and 30. Multivariate regression was used to examine cross-sectional results, while individual growth models examined longitudinal patterns. Results Dividing analysis by sex, we examined how parental imprisonment was potentially mediated or moderated by CBCL subscale measures for aggression, social-attention-thought disorders and general internalizing. No associations were found among male respondents. Among female respondents, controlling for these behaviors, there was a significant association between parental imprisonment and higher systolic blood pressure at age 30, while all CBCL measures were found to moderate waist circumference at age 30 and BMI at ages 14, 21, and 30. Using individual growth curve modelling, we observed the increased CBCL aggression and SAT scores were more strongly associated with higher BMI in adulthood. Conclusions Using prospective cohort data, our results suggest that PI and high levels of behavioral problems are associated with significantly increased cardiometabolic risk in women, with potentially increasing risk in adulthood.
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Background: Individuals who were separated from their biological family and placed into the care of the state during childhood (out-of-home care) are more prone to developing selected physical and mental health problems in adulthood, however, their risk of cardiovascular disease (CVD) is uncertain. Accordingly, we pooled published and unpublished results from cohort studies of childhood care and adult CVD. Methods: We used two approaches to identifying relevant data on childhood care and adult CVD (PROSPERO registration CRD42021254665). First, to locate published studies, we searched PubMed (Medline) until November 2023. Second, with the aim of identifying unpublished studies with the potential to address the present research question, we scrutinised retrieved reviews of the impact of childhood state care on related adult health outcomes. All included studies were required to have prospective measurement of state care in childhood and a follow-up of CVD events in adulthood as the primary outcome (incident coronary heart disease and/or stroke). Collaborating investigators provided study-specific estimates which were aggregated using random-effects meta-analysis. The Newcastle-Ottawa Scale was used to assess individual study quality. Findings: Thirteen studies (2 published, 11 unpublished) met the inclusion criteria, and investigators from nine provided viable results, including updated analyses of the published studies. Studies comprised 611,601 individuals (301,129 women) from the US, UK, Sweden, Finland, and Australia. Relative to the unexposed, individuals with a care placement during childhood had a 50% greater risk of CVD in adulthood (summary rate ratio after basic adjustment [95% confidence interval]: 1.50 [1.22, 1.84]); range of study-specific estimates: 1.28 to 2.06; I2 = 69%, p = 0.001). This association was attenuated but persisted after multivariable adjustment for socioeconomic status in childhood (8 studies; 1.41 [1.15, 1.72]) and adulthood (9 studies, 1.28 [1.10, 1.50]). There was a suggestion of a stronger state care-CVD association in women. Interpretation: Our findings show that individuals with experience of state care in childhood have a moderately raised risk of CVD in adulthood. For timely prevention, clinicians and policy makers should be aware that people with a care history may need additional attention in risk factor management.
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Parent–child separation occurs for many reasons, both involuntary and voluntary. We review the effects on children and youth of parent–child separation due to several of the most common reasons that are responsible for the growth in this family circumstance worldwide. These include early institutionalization; war, persecution, and conflict; separation during asylum; trafficking; conscription into armed conflict; and being left behind when parents migrate for economic or other reasons. Overall, the effects of parent–child separation are consistently negative on children's social-emotional development, well-being, and mental health. They are more severe when the separation is prolonged or accompanied by other forms of deprivation or victimization. Mitigating and protective factors include earlier stable family placement in the case of early institutionalization, parent–child communication and parenting quality, and community support in the host community. We conclude with an evaluation of group, school-based, and community-based interventions for children and youth affected by parent–child separation.
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The negative health effects of early life adversity (ELA) continue long into adulthood. Changes in the physiological response to psychosocial stressors have been proposed to mediate this effect. However, many previous studies have come to contradicting conclusions as to whether ELA induces a long-term increase or decrease in stress reactivity. Therefore, we tested the association of ELA exposure and adult stress reactivity in a sample of early life adoptees and controls. Two previously validated stressful elements (bilateral feet CPT and the Paced Auditory Serial Addition Task (PASAT)) were combined in an extended Cold Pressor Test (CPT). This test was performed on 22 participants who had experienced severe ELA (separation from biological parents, institutionalization, and adoption in early childhood), and in 22 age-matched control participants. A prior history of ELA was associated with blunted reactivity of the hypothalamic-pituitary-adrenal (HPA) axis (Cohen´s d = 0.680). Cardiovascular reactivity remained unchanged, and affective reactivity (self-report ratings) were increased in participants exposed to ELA compared to the control group (range Cohen´s d: 0.642-0.879). Our results suggest that the activity of the HPA axis reactivity was inhibited in ELA participants. Importantly, cardiovascular stress responsiveness was not affected by ELA. This separation of the HPA axis and cardiovascular stress responses may best be explained by ELA selectively enhancing central feedback-sensitivity to glucocorticoids, but preserving cardiovascular/ autonomic stress reactivity.
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Background: A growing body of research identifies the harmful effects that adverse childhood experiences (ACEs; occurring during childhood or adolescence; eg, child maltreatment or exposure to domestic violence) have on health throughout life. Studies have quantified such effects for individual ACEs. However, ACEs frequently co-occur and no synthesis of findings from studies measuring the effect of multiple ACE types has been done. Methods: In this systematic review and meta-analysis, we searched five electronic databases for cross-sectional, case-control, or cohort studies published up to May 6, 2016, reporting risks of health outcomes, consisting of substance use, sexual health, mental health, weight and physical exercise, violence, and physical health status and conditions, associated with multiple ACEs. We selected articles that presented risk estimates for individuals with at least four ACEs compared with those with none for outcomes with sufficient data for meta-analysis (at least four populations). Included studies also focused on adults aged at least 18 years with a sample size of at least 100. We excluded studies based on high-risk or clinical populations. We extracted data from published reports. We calculated pooled odds ratios (ORs) using a random-effects model. Findings: Of 11 621 references identified by the search, 37 included studies provided risk estimates for 23 outcomes, with a total of 253 719 participants. Individuals with at least four ACEs were at increased risk of all health outcomes compared with individuals with no ACEs. Associations were weak or modest for physical inactivity, overweight or obesity, and diabetes (ORs of less than two); moderate for smoking, heavy alcohol use, poor self-rated health, cancer, heart disease, and respiratory disease (ORs of two to three), strong for sexual risk taking, mental ill health, and problematic alcohol use (ORs of more than three to six), and strongest for problematic drug use and interpersonal and self-directed violence (ORs of more than seven). We identified considerable heterogeneity (I2 of >75%) between estimates for almost half of the outcomes. Interpretation: To have multiple ACEs is a major risk factor for many health conditions. The outcomes most strongly associated with multiple ACEs represent ACE risks for the next generation (eg, violence, mental illness, and substance use). To sustain improvements in public health requires a shift in focus to include prevention of ACEs, resilience building, and ACE-informed service provision. The Sustainable Development Goals provide a global platform to reduce ACEs and their life-course effect on health. Funding: Public Health Wales.
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Background: Early life adversity that increases the risk of growth stunting is hypothesized to increase the risk of obesity and, in girls, early onset puberty. This hypothesis was tested in children adopted from orphanages. Methods: Post-institutionalized (PI) youth were compared with youth reared in comparable families (non-adopted; NA) on height, weight, pubertal stage, and fat mass (127 PI, 80 female; 156 NA, 85 female, aged 7-14 years). Anthropometrics at adoption were obtained from first US clinic visits. Results: 25% of PIs were height stunted (<3rd percentile) at adoption. Years post adoption, PIs had lower BMI-for-age (p = .004); height-for-age (p < .001); and less body fat (p < .001) than NAs, but did not differ by sex. Pubertal status did not differ by group or sex. The anthropometric findings held when the stunted-at-adoption subset was examined; they were also less likely to be in central puberty than other PI youth. Conclusion: Early deprived orphanage care increases the risk of growth stunting but not obesity in children adopted into US families and does not independently contribute to early onset puberty for PI girls. The role of the environment following early adversity may modify the impact of early adverse care.Pediatric Research (2017); doi:10.1038/pr.2017.35.
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Objective: The study aims to evaluate the association between exposure to childhood adversity and insomnia, with an emphasis on the role of adversity type, timing, and accumulation (i.e., the number of specific types of adversities the child reported being exposed to). Methods: Our analytic sample comprised 9582 adolescents from the National Comorbidity Survey Replication Adolescent Supplement (NCS-A), a nationally representative population-based sample. We examined the association between 18 different types of retrospectively reported adversities (capturing interpersonal violence, accidents and injuries, social network or witnessing events, and other adverse events) and risk of self-reported past-year insomnia. We also examined whether the age at first exposure to adversity was associated with the risk of insomnia, and whether exposure to a greater number of different types of adversities (ie, accumulation) conferred an elevated risk of insomnia. In addition, we performed a sensitivity analysis excluding adolescents with a past-year diagnosis of major depression, dysthymia, post-traumatic stress disorder (PTSD), or generalized anxiety disorder. Results: Almost one-third of adolescents reported insomnia, with a higher prevalence among girls and those from racial/ethnic minority groups. Adolescents exposed to at least one childhood adversity of any type (59.41%) were more likely than their nonexposed peers to experience insomnia (across adversities, prevalence ratios (PRs) ranged from 1.31 to 1.89). Risk of insomnia differed based on the age at first exposure to adversity as well as the type of adversity. Adolescents exposed to a greater number of different types of adversities had a higher risk of insomnia compared to those experiencing fewer adversities. These results were similar, by and large, to those obtained after excluding adolescents with at least one of the four past-year psychiatric disorders. Conclusions: Exposure to adversity confers an elevated risk of insomnia. This association varied by type, timing, and accumulation of exposure and did not appear to be driven by psychiatric disorders. Given the well-documented physical and mental health consequences of insomnia, such findings further support the need for practitioners to screen children for exposure to childhood adversity and insomnia symptoms.
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Objectives To examine the relative contribution of childhood experience, measured by childhood violence and childhood happiness, and adult well-being on adult eating preferences and behaviours, independent of proximal factors such as current deprivation. Design A cross-sectional, stratified, randomised sample survey using retrospective measures of childhood violence and happiness and self-reported measures of current well-being. Setting The North West Region of England between September 2012 and March 2013. Participants Individuals aged 18–95-year-olds from randomly selected households (participation was successful for 90% of eligible households and 78% of the total visited addresses; n=11 243). Outcomes Dichotomised measures for preference of healthy foods or ‘feel good’ foods and low or high daily fruit and vegetable consumption. Results After correcting for demographics, combined categories for childhood experience and dichotomised measures of adult well-being were found to be significantly related to adult food preferences and eating behaviours. Participants with unhappy and violent childhoods compared to those with happy and non-violent childhoods had adjusted ORs (95% CI, significance) of 2.67 (2.15 to 3.06, p<0.001) of having low daily fruit and vegetable intake (two or less portions) and 1.53 (1.29 to 1.81, p<0.001) of choosing ‘feel good’ foods over foods which were good for their long term health. Conclusions Daily intake of fruit and vegetables, linked to non-communicable diseases, and preference for ‘feel good’ foods, linked to obesity, are affected by childhood experience and adult well-being independent of demographic factors. Preventative interventions which support parent–child relationships and improve childhood experience are likely to reduce the development of poor dietary and other health-risk behaviours.
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Previous studies have linked childhood adversity to low-grade inflammation via C-reactive protein (CRP) levels. This study analyzed the association between low-grade inflammation and prior biological parental incarceration. Data from the National Longitudinal Study of Adolescent to Adult Health (1994–2008) were analyzed using multinomial logistic regression models. Measures included high-sensitivity (hs)-CRP (<3 mg/L = reference, 3–10 mg/L = low-grade inflammation, and >10 mg/L = acute inflammation), parent incarceration occurring in the child’s lifetime, and frequency and timing of incarceration with respect to child’s age (0–18 years or >18 years vs. never) of incarceration. Analyses were stratified by child’s gender. Final sample sizes were n = 5,396 males and n = 6,447 females for maternal incarceration and n = 4,956 males and n = 5,860 females for paternal incarceration. In models with and without potential mediators, females whose fathers were ever incarcerated were more likely to have hs-CRP levels of 3–10 mg/L than females whose fathers were never incarcerated (adjusted odds ratio [AOR]: 1.44, 95% confidence interval [CI]: [1.09, 1.91]). Additionally, daughter’s age (<18 years; AOR: 1.48, 95% CI: [1.11, 1.97]) and frequency of father’s incarceration were significant (AOR: 1.24, 95% CI: [1.04, 1.49]). No mediating effects were observed. Males whose fathers were incarcerated when they were ≥18 years were less likely to have hs-CRP levels of 3–10 mg/L than those whose father was never incarcerated; the association was nonsignificant in the mediated model. Further investigation is needed on the physiological effects of exposure to parental incarceration and interventions to support children.
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Background and objectives: Foster youth have high rates of health problems in childhood. Little work has been done to determine whether they are similarly vulnerable to increased health problems once they transition to adulthood. We sought to prospectively evaluate the risk of cardiovascular risk factors and other chronic conditions among young adults formerly in foster care (FC) and young adults from economically insecure (EI) and economically secure (ES) backgrounds in the general population. Methods: We used data from the Midwest Evaluation of the Adult Functioning of Former Foster Youth (FC group; N = 596) and an age-matched sample from the National Longitudinal Study of Adolescent Health (EI and ES groups; N = 456 and 1461, respectively). After controlling for covariates, we performed multivariate regressions to evaluate health outcomes and care access by group at 2 time points (baseline at late adolescence, follow-up at 25-26 years). Results: Data revealed a consistent pattern of graduated increase in odds of most health outcomes, progressing from ES to EI to FC groups. Health care access indicators were more variable; the FC group was most likely to report having Medicaid or no insurance but was least likely to report not getting needed care in the past year. Conclusions: Former foster youth appear to have a higher risk of multiple chronic health conditions, beyond that which is associated with economic insecurity. Findings may be relevant to policymakers and practitioners considering the implementation of extended insurance and foster care programs and interventions to reduce health disparities in young adulthood.
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Research demonstrating that socioeconomic status (SES) differentials in health are smaller at older ages often considers only individual SES measures (e.g., income, education) but not community SES measures (e.g., community poverty rate), although the gerontological literature suggests that community context may be particularly salient in the lives of older adults. This study uses two national surveys of adults, each matched with census data about respondents' communities, to examine whether the association between community SES and individual health is stronger at consecutively older age groups. The association between community SES and health is nonexistent or weak during younger adulthood, stronger through middle ages, strongest at ages 60 to 69, and weak again at ages 70 and older. At ages 60 to 69, community SES effects are stronger than or comparable to individual SES effects. Community SES should be considered an important dimension of SES when exploring the impact of SES on health over the life course.
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Although recent studies suggest that 13% of young adults, including at least one-fourth of African Americans, experience parental incarceration, little research has examined links between parental incarceration and physical health. Using data from the National Longitudinal Study of Adolescent Health (1994–2008) and gender-based theories of stress, the authors examined whether parental incarceration is associated with increased body mass index among women but not men. Panel analysis spanning adolescence and adulthood, controlling for stressful life events, internalizing behaviors, and a range of individual, familial, and neighborhood characteristics, reveals that body mass index for women who have experienced parental incarceration is 0.49 units (P < 0.004) higher than that for women whose parents have never been incarcerated. This association is not evident among men. Similarly, in change score models between waves II and IV, women experiencing parental incarceration have a 0.92-unit increase in body mass index (P < 0.026) relative to women who did not have a parent undergo incarceration. In supplemental analysis examining if gender differences in incarceration stress response (externalizing vs. internalizing) explain these findings, the authors found that obesity status moderates the relation between depression and parental incarceration. Results suggest a stress internalization process that, for the first time, links parental incarceration with obesity among women.
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Among people exposed to major psychological stressors in early life, there are elevated rates of morbidity and mortality from chronic diseases of aging. The most compelling data come from studies of children raised in poverty or maltreated by their parents, who show heightened vulnerability to vascular disease, autoimmune disorders, and premature mortality. These findings raise challenging theoretical questions. How does childhood stress get under the skin, at the molecular level, to affect risk for later diseases? And how does it incubate there, giving rise to diseases several decades later? Here we present a biological embedding model, which attempts to address these questions by synthesizing knowledge across several behavioral and biomedical literatures. This model maintains that childhood stress gets "programmed" into macrophages through epigenetic markings, posttranslational modifications, and tissue remodeling. As a consequence these cells are endowed with proinflammatory tendencies, manifest in exaggerated cytokine responses to challenge and decreased sensitivity to inhibitory hormonal signals. The model goes on to propose that over the life course, these proinflammatory tendencies are exacerbated by behavioral proclivities and hormonal dysregulation, themselves the products of exposure to early stress. Behaviorally, the model posits that childhood stress gives rise to excessive threat vigilance, mistrust of others, poor social relationships, impaired self-regulation, and unhealthy lifestyle choices. Hormonally, early stress confers altered patterns of endocrine and autonomic discharge. This milieu amplifies the proinflammatory environment already instantiated by macrophages. Acting in concert with other exposures and genetic liabilities, the resulting inflammation drives forward pathogenic mechanisms that ultimately foster chronic disease.
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Strong, graded relationships between exposure to childhood traumatic stressors and numerous negative health behaviors and outcomes, healthcare utilization, and overall health status inspired the question of whether these adverse childhood experiences (ACEs) are associated with premature death during adulthood. This study aims to determine whether ACEs are associated with an increased risk of premature death during adulthood. Baseline survey data on health behaviors, health status, and exposure to ACEs were collected from 17,337 adults aged >18 years during 1995-1997. The ACEs included abuse (emotional, physical, sexual); witnessing domestic violence; parental separation or divorce; and growing up in a household where members were mentally ill, substance abusers, or sent to prison. The ACE score (an integer count of the eight categories of ACEs) was used as a measure of cumulative exposure to traumatic stress during childhood. Deaths were identified during follow-up assessments (between baseline appointment date and December 31, 2006) using mortality records obtained from a search of the National Death Index. Expected years of life lost (YLL) and years of potential life lost (YPLL) were computed using standard methods. The relative risk of death from all causes at age < or =65 years and at age < or =75 years was estimated across the number of categories of ACEs using multivariable-adjusted Cox proportional hazards regression. Analysis was conducted during January-February 2009. Overall, 1539 people died during follow-up; the crude death rate was 91.0 per 1000; the age-adjusted rate was 54.7 per 1000. People with six or more ACEs died nearly 20 years earlier on average than those without ACEs (60.6 years, 95% CI=56.2, 65.1, vs 79.1 years, 95% CI=78.4, 79.9). Average YLL per death was nearly three times greater among people with six or more ACEs (25.2 years) than those without ACEs (9.2 years). Roughly one third (n=526) of those who died during follow-up were aged < or =75 years at the time of death, accounting for 4792 YPLL. After multivariable adjustment, adults with six or more ACEs were 1.7 (95% CI=1.06, 2.83) times more likely to die when aged < or =75 years and 2.4 (95% CI=1.30, 4.39) times more likely to die when aged < or =65 years. ACEs are associated with an increased risk of premature death, although a graded increase in the risk of premature death was not observed across the number of categories of ACEs. The increase in risk was only partly explained by documented ACE-related health and social problems, suggesting other possible mechanisms by which ACEs may contribute to premature death.
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Background Prolonged parent–child separation is associated with a broad array of poor developmental outcomes. A potential pathway may be through changes in inflammatory processes. However, relatively little is known about the relationship between parent–child separation pattern (timing and duration) and inflammatory burden. The aim of this study was to investigate whether parent–child separation since birth is associated with inflammatory burden in adolescents. Methods A total of 574 adolescents (mean age 12.07 years, SD: 0.62) were enrolled from rural areas of Chizhou, Anhui Province, China. Parent-child separation was reported mainly by primary caregivers, and other adverse childhood adversities (ACEs) were derived from adolescents semi-structured interview or questionnaire. Blood samples were collected from venepuncture for C-reactive protein (CRP) as well as soluble urokinase plasminogen activator receptor (suPAR). Results Nearly 40% (232/574) participants experienced parent–child separation, among which more than 1 of 4 persistently separated from both parents since birth. Both CRP and suPAR levels were significantly higher among adolescents persistently separated from both parents, compared with those who did not separate from both parents (CRP: 1.75 vs. 1.36 mg/L, P < 0.001; suPAR: 2.85 ng/mL vs. 2.55 ng/mL, P < 0.001). After adjusted for demographic covariates, body mass index, ACEs as well as parental characteristics, persistent parent–child separation was associated with elevated suPAR (B = 0.30; 95% CI, 0.12–0.48) and CRP (B = 1.34; 95% CI, 1.02–1.75). No similar associations were observed between inflammatory burden with current or early childhood parent–child separation groups. Adolescents who exposed to persistent parent–child separation were more likely to have elevated suPAR levels even if they did not have elevated CRP levels (aOR, 4.26, 95% CI, 1.23–14.80; P = 0.022). Conclusion Elevated inflammatory burden observed in persistent parent–child separation adolescents highlights the need to support children and adolescents undergoing separation from both parents in order to minimize the long-term impact on disease vulnerability.
Article
Background Parent-child separation has been shown to increase the risk of a range of mental and physical health conditions later in life. Hypothalamic-pituitary-adrenal axis (HPA) dysregulation may help to explain this association. However, few studies have examined the effect of maternal separation on cortisol in late adulthood. Methods We examined the relationship between maternal separation in childhood and hair cortisol concentrations in late adulthood, using data from the Whitehall II study (n=3969, mean age: 70 y, range: 60-83 y). Additionally, the role of childhood (adverse childhood experiences (ACEs), material disadvantage, and parenting), adult (marital status and social position), and health measures (health behaviors, cardiovascular health and medication, and depression) in this association were examined. Finally, we examined age of separation and reason for separation. Analysis was carried out using linear regression. Results Hair cortisol concentrations (pg/mg) among participants who reported maternal separation during childhood were higher (B=0.179, 95% CI 0.041-0.317, p=0.01) compared to those who did not report separation. This effect was robust to adjustment by childhood, adult, and health measures. Among participants who reported separation, age at onset and reason for separation were not significantly associated with hair cortisol concentrations. Conclusion In older age individuals, hair cortisol concentrations were higher in those who reported maternal separation during childhood. This effect was independent of a wide variety of factors suggesting that there are lifelong pathways between early life separation and HPA functioning in old age.
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As clinicians delivering health care, we are very good at treating disease but often not as good at treating the person. The focus of our attention has been on the specific physical condition rather than the patient as a whole. Less attention has been given to psychological health and how that can contribute to physical health and disease. However, there is now an increasing appreciation of how psychological health can contribute not only in a negative way to cardiovascular disease (CVD) but also in a positive way to better cardiovascular health and reduced cardiovascular risk. This American Heart Association scientific statement was commissioned to evaluate, synthesize, and summarize for the health care community knowledge to date on the relationship between psychological health and cardiovascular health and disease and to suggest simple steps to screen for, and ultimately improve, the psychological health of patients with and at risk for CVD. Based on current study data, the following statements can be made: There are good data showing clear associations between psychological health and CVD and risk; there is increasing evidence that psychological health may be causally linked to biological processes and behaviors that contribute to and cause CVD; the preponderance of data suggest that interventions to improve psychological health can have a beneficial impact on cardiovascular health; simple screening measures can be used by health care providers for patients with or at risk for CVD to assess psychological health status; and consideration of psychological health is advisable in the evaluation and management of patients with or at risk for CVD.
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Early adversity has been shown to sensitize individuals to the effects of later stress and enhance risk of psychopathology. Using a longitudinal randomized trial of foster care as an alternative to institutional care, we extend the stress sensitization hypothesis to examine whether early institutional rearing sensitizes individuals to stressful events in adolescence engendering chronic low-grade inflammation. At baseline, institutionalized children in Romania (ages 6–31 months) were randomly assigned to foster care or to remain in usual care within institutions. A group of never-institutionalized children was recruited as an in-country comparison sample. At ages 12 and 16, participants reported stressful events. At age 16, Interleukin-6 (IL-6) and C-reactive protein (CRP) were derived from blood spots. Among children assigned to care as usual, more stressful events at age 12, but not age 16, were associated with higher IL-6. In the same group, stressful events at age 16 were associated with higher CRP, though these effects attenuated after adjusting for covariates. These associations were not observed in the foster care or never-institutionalized groups. The findings suggest that heightened inflammation following stress exposure is one pathway through which early neglect could compromise physical health. In contrast, early family care might buffer against these risks.
Article
Background Children who have been exposed to public (out-of-home) care experience a range of negative outcomes by late adolescence and early adulthood. The longer-term impact of childhood care is, however, uncertain. Aim To examine if there is a prospective association between childhood public care and adverse life outcomes in middle-age. Methods We used data from the UK 1958 birth cohort study of 18 558 individuals. Parents reported offspring care status at age 7, 11 and 16. An array of social, criminal, cognitive, and health outcomes was self-reported by cohort members at age 42 (71% response proportion in eligible sample) and a cognitive test battery was administered at age 50 (62% response). Results A total of 420 (3.8%) of 11 160 people in the analytical sample experienced childhood public care by age 16. Net of confounding factors, experience of public care (vs none) was linked to 11 of the 28 non-mutually exclusive endpoints captured in middle-age, with the most consistent effects apparent for psychosocial characteristics: 4/7 sociodemographic (eg, odds ratio; 95% confidence interval for homelessness: 2.1; 1.4 to 3.1); 2/2 antisocial (eg, use of illicit drug: 2.0; 1.2 to 3.5); 2/3 psychological (eg, mental distress: 1.6; 1.2 to 2.1); 1/3 health behaviours (eg, current cigarette smoker: 1.7; 1.3 to 2.2); 2/8 somatic health (physical disability: 2.7; 1.9 to 3.8); and 0/5 cognitive function (eg, beta coefficient; 95% confidence interval for immediate word recall: −0.1; −0.3 to 0.1) endpoints. Conclusions The present study suggests that selected associations apparent between childhood care and outcomes in adolescence and early adulthood are also evident in middle-age.
Article
Background: The hypothalamic-pituitary-adrenocortical (HPA) axis had been proved to calibrate to early-life adversity and puberty may reverse the calibration. This study examines the consequences of prolonged parent-child separation on HPA axis reactivity and the pubertal recalibration hypothesis. Methods: Totally of 144 participants aged 8.75 to 15.25 (mean age 12.50 years, SD: 1.32) were enrolled from rural areas of Chizhou city, Anhui Province of China in 2019. Data on parent-child separation was collected from parents. Self-reported Peterson Pubertal Development Scale was used to assess pubertal maturation and HPA axis stress reactivity was measured using the Trier Social Stress Test for Children. Results: For children at early stage of puberty, childhood parent-child separation experiences were associated with blunted HPA axis reactivity (B = -1.888, p = 0.034); while for those at later stage of puberty, HPA axis reactivity was similar between children experienced early childhood separation and those without separation (AUCi: B = -0.426, p = 0.878). In contrast, for children experienced persistent parent-child separation, blunted HPA axis reactivity was observed (all p < 0.05). Limitations: Due to the cross-sectional nature of this study, conclusions about causality remain speculative. Conclusions: The effect of parent-child separation on dysregulation of HPA axis acts in a time-dependent manner. This finding provides support for the pubertal recalibration hypothesis suggesting that a focus of improving environment in adolescence would help those individuals reared initially in non-supportive conditions.
Book
Cardiovascular Implications of Stress and Depression provides an in-depth examination into how exposure to stress influences risk for cardiovascular disease and how depression is associated with this relation. This authoritative volume examines causal pathways linking stress, depression, and cardiovascular disease as well as providing mechanistic insights into how environmental stress could possibly lead to cardiovascular diseases. This work also considers how therapeutic approaches to prevent or ameliorate depression inform our understanding of whether stress causes cardiovascular disease. Current information about mechanistic factors, clinical and epidemiological aspects, and management issues associated with stress/depression are presented. Insight into the mechanisms behind how chronic stress and depression leads to cardiovascular diseases and its role in existing diseases (such as obesity, hypertension, and diabetes) is also explored.
Article
Objectives: To determine the effects of foster care vs institutional care, as well as disruptions in the caregiving environment on physical development through early adolescence. Study design: This was a randomized controlled trial of 114 institutionalized, though otherwise healthy, children from 6 orphanages and 51 never institutionalized control children living in birth families (family care group) in Bucharest, Romania. Children were followed from baseline (21 months, range 5-31) through age 12 years for caregiving disruptions and growth trajectories and through age 14 years for pubertal development. Results: Children randomized to the foster care group showed greater rates of growth in height, weight, and body mass index (BMI) through age 12 years than institutionalized group. Tanner development was delayed in institutionalized group boys compared with foster care group and family care group boys at 12 but not 14 years. There were no differences in Tanner development and age of menarche among foster care group, institutionalized group, and family care group girls at ages 12 and 14 years. More disruptions in caregiving between 30 months and 12 years moderated decreases in growth rates of height in foster care group and weight in foster care group and institutionalized group across age. institutionalized group boys with ≥2 disruptions showed lower Tanner scores at age 12 vs institutionalized group and foster care group boys with <2 disruptions. foster care group girls with ≥2 disruptions had higher Tanner scores at age 14 vs foster care group girls with <2 disruptions. Age of menarche was not affected by caregiving disruptions. Conclusions: For children who experienced early institutionalization, stable placement within family care is essential to ensuring the best outcomes for physical developmental. Trial registration: clinicaltrials.gov: NCT00747396.
Article
Medically and economically vulnerable adults experience various challenges that can impact their health. Within this vulnerable population, there may be individuals who are even more vulnerable, those who have a history of involvement with the foster care system. The purpose of this study was to evaluate the difference of reported health-related problems between adults with previous foster care experience and other vulnerable adults. Physical, mental, and relational health was evaluated in this study. Practice and policy implications for mental health and medical professionals are discussed.
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Cardiovascular disease remains the leading cause of disease burden globally, which underlies the continuing need to identify new complementary targets for prevention. Over the past 5-10 years, the pooling of multiple data sets into 'mega-studies' has accelerated progress in research on stress as a risk and prognostic factor for cardiovascular disease. Severe stressful experiences in childhood, such as physical abuse and household substance abuse, can damage health and increase the risk of multiple chronic conditions in adulthood. Compared with childhood stress and adulthood classic risk factors, such as smoking, high blood pressure, and high serum cholesterol levels, the harmful effects of stress in adulthood are generally less marked. However, adulthood stress has an important role as a disease trigger in individuals who already have a high atherosclerotic plaque burden, and as a determinant of prognosis and outcome in those with pre-existing cardiovascular or cerebrovascular disease. In real-life settings, mechanistic studies have corroborated earlier laboratory-based observations on stress-related pathophysiological changes that underlie triggering, such as lowered arrhythmic threshold and increased sympathetic activation with related increases in blood pressure, as well as pro-inflammatory and procoagulant responses. In some clinical guidelines, stress is already acknowledged as a target for prevention for people at high overall risk of cardiovascular disease or with established cardiovascular disease. However, few scalable, evidence-based interventions are currently available.
Article
Objective: Early life stress (ELS) has been shown to influence health later in life. Functioning of the hypothalamic-pituitary-adrenal (HPA) axis, regulated partly by FKBP5 gene, may moderate these effects. We examined whether FKBP5 single nucleotide polymorphisms (SNPs) interact with ELS on type 2 diabetes, cardiovascular disease, and quantitative glycemic traits. Methods: 1,728 Helsinki Birth Cohort Study participants born 1934-44 were genotyped for FKBP5 SNPs (rs1360780, rs9394309, rs9470080), administered a 2-h (75 g) oral glucose tolerance test and a questionnaire on physician-diagnosed and medication use for chronic diseases at a mean age of 61.5 years. Of the participants, 273 had been exposed to ELS, operationalized as separation from their parents, at a mean age of 4.7 years due to evacuations during WWII. Results: ELS interacted with FKBP5 SNPs in the analyses of fasting (rs1360780, p=.015), 30-min (rs1360780, p=.031; rs9394309, p=.041) and incremental insulin (rs1360780, p=.032; rs9394309, p=.028; rs9470080, p=.043), insulin area under the curve (rs1360780, p=.044), and impaired fasting glucose (IFG) (rs9470080, p=.049); among carriers of at least one copy of minor allele, but not among major allele homozygotes, insulin values were higher as were the odds for IFG if they had been separated compared to if they had not. Corresponding associations were found with a haplotype formed by minor alleles in all three SNPs for fasting, 30-min, and incremental insulin (p<.05). Conclusions: FKBP5 polymorphisms in combination with ELS exposure predict higher insulin and glucose values in midlife. Our findings support the role for HPA axis dysregulation in health-related metabolic outcomes.
Article
Controversy exists over the role of stress and depression in the pathophysiology of type 2 diabetes mellitus. Depression has been shown to increase the risk for progressive insulin resistance and incident type 2 diabetes mellitus in multiple studies, whereas the association of stress with diabetes is less clear, owing to differences in study designs and in forms and ascertainment of stress. The biological systems involved in adaptation that mediate the link between stress and physiological functions include the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous and immune systems. The HPA axis is a tightly regulated system that represents one of the body's mechanisms for responding to acute and chronic stress. Depression is associated with cross-sectional and longitudinal alterations in the diurnal cortisol curve, including a blunted cortisol awakening response and flattening of the diurnal cortisol curve. Flattening of the diurnal cortisol curve is also associated with insulin resistance and type 2 diabetes mellitus. In this article, we review and summarize the evidence supporting HPA axis dysregulation as an important biological link between stress, depression, and type 2 diabetes mellitus.
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Type 2 diabetes mellitus (DM) is a disease characterized by dysfunction of various organs. Recent studies have shown a close relationship between DM and telomere attrition in leukocytes. In patients with DM or impaired glucose tolerance, excessive oxidative stress induces damage to telomeres and shortens their length. Furthermore, it is suggested that telomere length is a good surrogate marker for mortality and diabetic complications in DM patients. We recently found that telomere length in pancreatic β-cells is also shortened in DM patients, potentially leading to an impaired capacity for proliferation and insulin secretion, and accelerated cell death. In contrast, leukocyte telomere length has also been reported in patients with obesity or insulin resistance, both of which are frequently associated with type 2 DM. In an animal model, it has been shown that telomere attrition in adipose tissue induces insulin resistance. Taken together, the available data suggest that hyperglycemia, oxidative stress, and telomere attrition in pancreatic β-cells and adipocytes create a vicious cycle that underlies the pathophysiology of type 2 DM. Inhibition of telomere attrition in various organs, including pancreatic β-cells, could be a new approach for preventing the progression of DM and its complications. Geriatr Gerontol Int 2016; 16 (Suppl. 1): 66-74.
Article
Significance Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although rodent models support this possibility, results from human studies have been decidedly mixed. Using data from an experimental study examining whether random assignment to a caregiving environment alters development of the autonomic nervous system and hypothalamic–pituitary–adrenal axis in humans, we provide causal evidence for persistent effects of the early caregiving environment on stress response system functioning in humans with effects that differ markedly from those observed in rodent models. We also provide evidence of a sensitive period in human development during which the environment is particularly likely to alter stress response system development.
Article
Adverse childhood experiences (ACEs) represent substantial threats to public health and affect about 58% of youth in the US. In addition to their acute effects such as injury and physical trauma, ACEs are associated with an increased risk of several negative health outcomes throughout the life course. Emerging evidence suggests that sleep disorders may be one such outcome, but existing studies have not been systematically reviewed and summarized. We conducted a systematic review to summarize the evidence concerning the relationship between ACEs and sleep disorders and disturbances, with a focus on adult women. Original publications were identified through searches of the electronic databases MEDLINE, Embase, and Web of Science using the keywords "childhood," "adversity," "abuse," and "sleep" as well as searches of the reference lists of eligible studies. Studies evaluating ACEs that occurred before 18 years of age and sleep outcomes that were assessed at 18 years or older were adjudicated and included. A total of 30 publications were identified. Of the 30 studies, 28 were retrospective analyses and there was vast heterogeneity in the types of ACEs and sleep outcomes measured. The majority of retrospective studies (N = 25 of 28) documented statistically significant associations between sleep disorders including sleep apnea, narcolepsy, nightmare distress, sleep paralysis, and psychiatric sleep disorders with a history of childhood adversity. In many studies, the strengths of associations increased with the number and severity of adverse experiences. These associations were corroborated by the two prospective studies published to date. Notably, investigators have documented statistically significant associations between family conflict at 7-15 years of age and insomnia at 18 years of age (odds ratio, OR = 1.4; 95% confidence interval, CI = 1.2-1.7) and between childhood sexual abuse and sleep disturbances 10 years later in adult women (β = 0.24, p <0.05). There is a growing scientific body of knowledge suggesting an association between ACEs and multiple sleep disorders in adulthood. The available evidence indicates the need to develop treatment strategies such as trauma-informed care for survivors of abuse who suffer from sleep disorders and disturbances. Further, longitudinal studies among diverse populations are needed to improve the overall understanding of this association and to investigate potential gender and racial/ethnic disparities in the strength of the association. Copyright © 2014 Elsevier B.V. All rights reserved.
Article
Early life stress (ELS) poses a risk for mental disorders and aging-related diseases. Accelerated biological aging, reflected in shorter leukocyte telomere length (LTL), may underlie these risks. We examined whether objectively recorded ELS and retrospectively self-reported traumatic experiences across the lifespan are associated with LTL in later adulthood. Of 1486 participants, 215 had been exposed to ELS, namely to temporary separation from both parents in childhood. Participants self-reported emotionally or physically traumatic experiences across the lifespan at a mean age of 63.2 years. LTL was measured using a quantitative PCR method at a mean age of 61.5 years. Separation or self-reported traumatic experiences were not associated with LTL. However, separated participants who self-reported traumatic experiences had shorter LTL. Our results suggest that while ELS or self-reported traumatic experiences are not per se associated with LTL measured decades later, ELS may in combination with self-reported traumatic events be associated with accelerated biological aging.
Article
Approximately one out of every five patients with cardiovascular disease (CVD) suffers from major depressive disorder (MDD). Both MDD and depressive symptoms are risk factors for CVD incidence, severity and outcomes. Great progress has been made in understanding potential mediators between MDD and CVD, particularly focusing on health behaviors. Investigators have also made considerable strides in the diagnosis and treatment of depression among patients with CVD. At the same time, many research questions remain. In what settings is depression screening most effective for patients with CVD? What is the optimal screening frequency? Which therapies are safe and effective? How can we better integrate the care of mental health conditions with that of CVD? How do we motivate depressed patients to change health behaviors? What technological tools can we use to improve care for depression? Gaining a more thorough understanding of the links between MDD and heart disease, and how best to diagnose and treat depression among these patients, has the potential to substantially reduce morbidity and mortality from CVD.
Article
Early-life stress may influence health later in life. We examined morbidity and mortality from cardiovascular disease over 60 years in individuals separated temporarily from their parents in childhood due to World War II. We studied 12,915 members of the Helsinki Birth Cohort Study born from 1934 to 1944, of whom 1726 (13.4%) had been evacuated aboard without their parents to temporary foster families for an average of 1.8 (standard deviation = 1.1) years at an average age of 4.6 (standard deviation = 2.4) years. Data on parental separations were extracted from the Finnish National Archives. Information on use of medication for coronary heart disease and hypertension was derived from the National Register of Medication Reimbursement, and information on coronary events, stroke, and cardiovascular deaths was derived from Finnish Hospital Discharge Register and Causes of Death Register between Years 1971 and 2003. Participants who were separated in childhood used medications for coronary heart disease more frequently than those who were not separated (7.2% versus 4.5%, respectively; hazard ratio [HR] = 1.29, 95% confidence interval [CI] = 1.04-1.59; p = .02). No associations between separation and all-cause mortality (HR = 1.04, 95% CI = 0.90-1.20) or cardiovascular mortality (HR = 0.94, 95% CI = 0.72-1.21) or hospitalizations for cardiovascular disease or stroke were observed. Early-life stress may possibly be a factor predisposing to coronary heart disease decades later, but no evidence was found for increased risk of hospitalizations or mortality.
Article
Severe stress experienced in early life may have long-term consequences on adult physiological functions. We studied the long-term effects of separation on blood pressure levels in non-obese subjects who were separated temporarily in childhood from their parents during World War II (WWII). The original clinical study cohort consists of people born during 1934-1944 in Helsinki, Finland. This substudy includes 1361 non-obese subjects (body mass index <30 kg m(-2)). Of these, 192 (14.1%) had been evacuated abroad during WWII. The remaining subjects served as controls. Blood pressure levels and use of blood pressure medication were studied. The separated subjects had significantly higher systolic blood pressure values than the non-separated (148.6+21.5 vs 142.2+19.6 mm Hg, P<0.0001) in adult life. Those subjects separated in early childhood had markedly higher systolic and diastolic blood pressure values in adult life compared with the non-separated (154.6 vs 142.5 mm Hg; 95% confidence interval (CI) 2.6-14.7; P<0.005 and 90.8 vs 87.7 mm Hg; 95% CI 1.0-7.3; P<0.02, respectively). Systolic blood pressure was also higher in the group separated for a duration of <1 year (151.7 vs 142.2 mm Hg; 95% CI 0.0-12.4; P<0.05) compared with the non-separated. Besides being separated, age at separation and duration of separation also influenced blood pressure levels in adult life. This could be due to early hormonal and metabolic programming, during plastic periods in early life, influencing blood pressure levels in adult life.Journal of Human Hypertension advance online publication, 16 February 2012; doi:10.1038/jhh.2012.6.
Article
Little is known about whether the childhood family psychosocial environment affects coronary heart disease (CHD). Study objectives were to evaluate associations of childhood family psychosocial environment (termed "risky families"; characterized by cold, unaffectionate interactions, conflict, aggression, neglect, and/or low nurturance) with calculated risk for CHD. Study participants included 3554 participants of the Coronary Artery Risk Development in Young Adults Study, aged 33 to 45 years. Childhood family psychosocial environment was measured using a risky family questionnaire via self-report. Ten-year CHD risk was calculated using the validated Framingham risk algorithm. In a multivariable-adjusted regression analysis adjusted for age, race/ethnicity, and childhood socioeconomic position, a 1-unit (range, 0-21) increase in risky family score was associated with 1.0% (95% confidence interval = 0.4%-1.7%) and 1.0% (95% confidence interval = 0.2%-1.8%) higher CHD risk in women and men, respectively. Multiple mediation analyses suggested significant indirect effects of education, income, depressive symptomatology, and anger-out expression in women and education in men, indicating that these may be mediating mechanisms between childhood psychosocial environment and CHD risk. Of the modifiable Framingham algorithm components, smoking (in women and men) and high-density lipoprotein (in women) were the factors most strongly associated with risky family score. Childhood family psychosocial environment was positively associated with the calculated 10-year CHD risk. Mechanisms may include the potential negative impact of childhood family psychosocial environment on later-life socioeconomic position (e.g., education in men and women) and/or psychosocial functioning (e.g., depression and anger-out expression in women), which may in turn lead to higher CHD risk, particularly through smoking (in men and women) and low level of high-density lipoprotein cholesterol (in women).
Article
Although the link between out-of-home placement and mental health problems in youth has been well-documented, few studies have examined the long-term functioning of adults with a history of out-of-home placement. In the present study, data from the California Women's Health Survey were used to examine the odds of recent mental and physical health problems, low educational attainment, and economic adversity for women, ages 18 and older, with (n=368) or without (n=9240) a history of out-of-home placement. Results revealed that history of out-of-home placement was associated with mental health problems, poor subjective health, smoking, obesity, low educational attainment, living in poverty, and use of public assistance in adulthood. Routine screening for mental health problems, as well as early intervention and prevention efforts, should be targeted to youth in or transitioning to out-of-home placement in an effort to prevent long-term mental health problems. Educational interventions that facilitate collaboration between foster care agencies and the schools should be tested to learn whether they are associated with greater employment opportunities and better economic functioning in adulthood.
Article
To evaluate associations between perceived quality of parental emotional care and calculated 10-year risk for coronary heart disease (CHD). Little is understood about the role of parental emotional care in contributing to the risk for CHD. The study sample was composed of 267 participants from the New England Family Study. Quality of parental emotional care was measured, using a validated short version of the Parental Bonding Instrument (PBI) as the average care scores for both parents (range = 0-12), with higher scores indicating greater care. Ten-year CHD risk was calculated, using the validated Framingham Risk Algorithm that incorporates the following prevalent CHD risk factors: age, sex, diabetes, smoking, total cholesterol, high-density lipoprotein cholesterol, and blood pressure. Multiple linear regression assessed associations of PBI with calculated CHD risk after adjusting for childhood socioeconomic status, depressive symptomatology, educational attainment, and body mass index. Among females, a 1-unit increase in the parental emotional care score resulted in a 4.6% (p = .004) decrease in the 10-year CHD risk score, after adjusting for covariates. There was no association between parental emotional care score and calculated CHD risk score in males (p = .22). Quality of parental emotional care was inversely associated with calculated 10-year CHD risk in females, and not males. Although the gender differences need further investigation and these findings require replication, these results suggest that the early childhood psychosocial environment may confer risk for CHD in adulthood.
Article
Animal models have linked early maternal separation with lifelong changes in hypothalamic-pituitary-adrenocortical (HPA) axis activity. Although this is paralleled in human studies, this is often in the context of other life adversities, for example, divorce or adoption, and it is not known whether early separation in the absence of these factors has long term effects on the HPA axis. The Finnish experience in World War II created a natural experiment to test whether separation from a father serving in the armed forces or from both parents due to war evacuation are associated with alterations in HPA axis response to psychosocial stress in late adulthood. 282 subjects (M=63.5 years, SD=2.5), of whom 85 were non-separated, 129 were separated from their father, and 68 were separated from both their caregivers during WWII, were enlisted to participate in a Trier Social Stress Test (TSST), during which we measured salivary cortisol and, for 215 individuals, plasma cortisol and ACTH concentrations. We used mixed models to study whether parental separation is associated with salivary and plasma cortisol or plasma ACTH reactivity, and linear regressions to analyse differences in the baseline, or incremental area under the cortisol or ACTH curves. Participants separated from their father did not differ significantly from non-separated participants. However, those separated from both parents had higher average salivary cortisol and plasma ACTH concentrations across all time points compared to the non-separated group. They also had higher salivary cortisol reactivity to the TSST. Separated women had higher baselines in plasma cortisol and ACTH, whereas men had higher reactivity in response to stress during the TSST. Participants who had experienced the separation in early childhood were more affected than children separated during infancy or school age. Separation from parents during childhood may alter an individual's stress physiology much later in adult life.