Early life stressors are associated with elevated inflammation, a key physiological risk factor for disease. However, the mechanisms by which early stress leads to inflammation remain largely unknown. Using a longitudinal data set, we examined smoking, alcohol consumption, and body mass index (BMI) as health-behavior pathways by which early adversity might lead to inflammation during young adulthood. Contemporaneously measured early adversity predicted increased BMI and smoking but not alcohol consumption, and these effects were partially accounted for by chronic stress in young adulthood. Higher BMI in turn predicted higher levels of soluble tumor necrosis factor receptor type II (sTNF-RII) and C-reactive protein (CRP), and smoking predicted elevated sTNF-RII. These findings establish that early adversity contributes to inflammation in part through ongoing stress and maladaptive health behavior. Given that maladaptive health behaviors portend inflammation in young adulthood, they serve as promising targets for interventions designed to prevent the negative consequences of early adversity.

Objective

The current study examined the prospective effects of exposure to stressful conditions in early childhood on physical health in young adulthood, and explored continuing exposure to stressors, as well as depression, in adolescence as possible mechanisms of this relationship.

Method

A prospective longitudinal design was used to examine 705 mother-child pairs from a community-based sample, followed from offspring birth through age 20 years. Mothers provided contemporaneous assessments of early adverse conditions from offspring birth through age 5. Offspring responses to the UCLA Life Stress Interview, Structured Clinical Interview for DSM Disorders, Physical Functioning subscale of the SF-36 Health Survey, and questions about the presence of chronic disease were used to assess youth stress at age 15, depression from ages 15-20, and physical health at age 20.

Results

Early adversity conferred risk for elevated levels of social and nonsocial stress at youth age 15, as well as depression between ages 15 and 20. Social and nonsocial stress, in turn, had effects on physical health at age 20, directly and indirectly via depression.

Conclusion

Findings suggest that early adverse conditions have lasting implications for physical health, and that continued exposure to increased levels of both social and nonsocial stress in adolescence, as well as the presence of depression, might be important mechanisms by which early adversity impacts later physical health.

Objective

Poor physical health in childhood is associated with a variety of negative health-related outcomes in adulthood. Psychosocial pathways contributing to the maintenance of physical health problems from childhood to young adulthood remain largely unexamined, despite evidence that factors such as negative mood and stress impact physical health.

Design

The current study tested the direct and indirect effects of ongoing health, chronic stress, health-related chronic stress, and depressive symptoms at age 20 on the link between health problems in childhood and young adulthood (age 21) in a longitudinal sample (n = 384).

Main outcome measures

The hypotheses were tested using a multiple mediation path analysis framework; the primary outcome measure was a composite index of health status markers in young adulthood.

Results

The proposed model provided an adequate fit for the data, with significant total indirect effects of the four mediators and significant specific indirect effects of health-related chronic stress and depressive symptoms in maintaining health problems from childhood into young adulthood.

Conclusions

Health problems are maintained from early childhood into young adulthood in part through psychosocial mechanisms. Depressive symptoms and health-related chronic stress have significant, unique effects on the relationship between health problems in early childhood and young adulthood.

Early life stressors are associated with elevated inflammation, a key physiological risk factor for disease. However, the mechanisms by which early stress leads to inflammation remain largely unknown. Using a longitudinal data set, we examined smoking, alcohol consumption, and body mass index (BMI) as health-behavior pathways by which early adversity might lead to inflammation during young adulthood. Contemporaneously measured early adversity predicted increased BMI and smoking but not alcohol consumption, and these effects were partially accounted for by chronic stress in young adulthood. Higher BMI in turn predicted higher levels of soluble tumor necrosis factor receptor type II (sTNF-RII) and C-reactive protein (CRP), and smoking predicted elevated sTNF-RII. These findings establish that early adversity contributes to inflammation in part through ongoing stress and maladaptive health behavior. Given that maladaptive health behaviors portend inflammation in young adulthood, they serve as promising targets for interventions designed to prevent the negative consequences of early adversity.

Objective

Poor physical health in childhood is associated with a variety of negative health-related outcomes in adulthood. Psychosocial pathways contributing to the maintenance of physical health problems from childhood to young adulthood remain largely unexamined, despite evidence that factors such as negative mood and stress impact physical health.

Design

The current study tested the direct and indirect effects of ongoing health, chronic stress, health-related chronic stress, and depressive symptoms at age 20 on the link between health problems in childhood and young adulthood (age 21) in a longitudinal sample (n = 384).

Main outcome measures

The hypotheses were tested using a multiple mediation path analysis framework; the primary outcome measure was a composite index of health status markers in young adulthood.

Results

The proposed model provided an adequate fit for the data, with significant total indirect effects of the four mediators and significant specific indirect effects of health-related chronic stress and depressive symptoms in maintaining health problems from childhood into young adulthood.

Conclusions

Health problems are maintained from early childhood into young adulthood in part through psychosocial mechanisms. Depressive symptoms and health-related chronic stress have significant, unique effects on the relationship between health problems in early childhood and young adulthood.

Functional genetic polymorphisms associated with Brain-Derived Neurotrophic Factor (BDNF) and serotonin (5-HTTLPR) have demonstrated associations with depression in interaction with environmental stressors. In light of evidence for biological connections between BDNF and serotonin, it is prudent to consider genetic epistasis between variants in these genes in the development of depressive symptoms. The current study examined the effects of val66met, 5-HTTLPR, and family environment quality on youth depressive symptoms in adolescence and young adulthood in a longitudinal sample oversampled for maternal depression history. A differential susceptibility model was tested, comparing the effects of family environment on depression scores across different levels of a cumulative plasticity genotype, defined as presence of both, either, or neither plasticity alleles (defined here as val66met Met and 5-HTTLPR 'S'). Cumulative plasticity genotype interacted with family environment quality to predict depression among males and females at age 15. After age 15, however, the interaction of cumulative plasticity genotype and early family environment quality was only predictive of depression among females. Results supported a differential susceptibility model at age 15, such that plasticity allele presence was associated with more or less depressive symptoms depending on valence of the family environment, and a diathesis-stress model of gene-environment interaction after age 15. These findings, although preliminary because of the small sample size, support prior results indicating interactive effects of 5-HTTLPR, val66met, and environmental stress, and suggest that family environment may have a stronger influence on genetically susceptible women than men.

Objective

The current study examined the prospective effects of exposure to stressful conditions in early childhood on physical health in young adulthood, and explored continuing exposure to stressors, as well as depression, in adolescence as possible mechanisms of this relationship.

Method

A prospective longitudinal design was used to examine 705 mother-child pairs from a community-based sample, followed from offspring birth through age 20 years. Mothers provided contemporaneous assessments of early adverse conditions from offspring birth through age 5. Offspring responses to the UCLA Life Stress Interview, Structured Clinical Interview for DSM Disorders, Physical Functioning subscale of the SF-36 Health Survey, and questions about the presence of chronic disease were used to assess youth stress at age 15, depression from ages 15-20, and physical health at age 20.

Results

Early adversity conferred risk for elevated levels of social and nonsocial stress at youth age 15, as well as depression between ages 15 and 20. Social and nonsocial stress, in turn, had effects on physical health at age 20, directly and indirectly via depression.

Conclusion

Findings suggest that early adverse conditions have lasting implications for physical health, and that continued exposure to increased levels of both social and nonsocial stress in adolescence, as well as the presence of depression, might be important mechanisms by which early adversity impacts later physical health.

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for the development of depression, with evidence that peer and academic difficulties mediate predictions of later depression from ADHD. In the present study, we hypothesized that parent-child relationship difficulties may be an additional potential mediator of this association. Academic, peer, and parent-child functioning were tested as mediators of the association of attention problems and depression in two distinctly different yet complementary samples. Study 1 was a cross-sectional sample of 5- to 10-year-old children (N = 230) with and without ADHD. Study 2 was a prospective longitudinal sample of 472 youth, followed prospectively from birth to age 20 years, at risk for depression. Despite differences in age, measures, and designs, both studies implicated peer and parent-child problems as unique mediators of depressive symptoms, whereas academic difficulties did not uniquely mediate the ADHD-depression association. Furthermore, inattention symptoms, but not hyperactivity, predicted depressive symptoms via the disruption of interpersonal functioning. The inclusion of oppositional defiant disorder into models impacted results and supported its independent role in parent-child problems. Implications include support for interventions that target interpersonal competence, which may effectively reduce the risk of depression among children with ADHD.

Objectives

The current study investigated prospective associations between youth sleep problems across childhood and adolescence, as well as the relationship between chronic youth sleep problems and young adult health. Exploratory analyses investigated this sleep-health relationship in the context of several established risk factors, including youth depression and environmental stress.

Design

This project is an extension of the Mater-University Study of Pregnancy, a longitudinal study that followed more than 7000 children across early development.

Setting

Brisbane, Australia.

Participants

Seven hundred ten mother-child dyads assessed from birth to age 20.

Measurements

We used maternal report measures to assess the persistence of youth sleep problems. We used structural equation modeling to explore the relationship between chronic maternal-reported youth sleep problems and subjective reports of young adult health quality and to assess whether associations remained when other potential health risks were included in the model.

Results

Path analyses revealed that sleep problems in early childhood predicted sleep problems in middle adolescence, which predicted sleep problems at age 20. Structural equation models showed that chronic youth sleep problems predicted youth health quality at age 20 (β = .263, P < .001) over and above the effects of early adversity, chronic childhood illness, maternal depression, lifetime youth depression, and chronic youth stress.

Conclusions

Chronic sleep problems can emerge in childhood and may contribute to negative health outcomes in young adulthood. Chronic youth sleep problems remain a significant predictor of poor health when tested against other known health risk factors, suggesting that sleep may be an important health intervention target.

Objective

To investigate the genetic architecture of internalizing symptoms in childhood and adolescence.

Method

In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.

Results

The meta-analysis of overall internalizing symptoms (INT_overall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, n_effective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|r_g| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |r_g| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.

Conclusion

Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.