Pathways to inflammation in adolescence through early adversity, childhood depressive symptoms, and body mass index: A prospective longitudinal study of Chilean infants.
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SUBMITTER: Reid BM
PROVIDER: S-EPMC6899213 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVE:Childhood social adversity has been associated with an increased risk of depression and other psychiatric disorders in adolescence and early adulthood. However, the role of timing and accumulation of adversities has not yet been established in longitudinal studies. We examined the association between childhood adversities and adolescent depressive symptoms, and the impact of timing and accumulation of adversity. METHOD:Longitudinal data were obtained from the Child Development Supplement to the Panel Study of Income Dynamics (n=2223), a nationally representative survey of US families that incorporates data from parents and their children. Negative binomial regression analysis was used to estimate effects of childhood social adversity on adolescent depressive symptoms, presented as Incidence Rate Ratios with 95% confidence intervals. RESULTS:Children exposed to social adversity reported higher levels of adolescent depressive symptoms captured by two depression scales. Single-parent household and residential instability were particularly associated with depressive symptoms. A positive relationship was found between cumulative adversity and the risk of adolescent depression. The timing of exposure appeared to have little effect on the risk of adolescent depressive symptoms. LIMITATIONS:The structure of the data implies that alternative causal pathways cannot be fully discounted. The self- or parent-reported data is subject to recall bias. CONCLUSION:Our findings support the long-term negative impact of childhood adversity on adolescent depressive symptoms, regardless of when in childhood the adversity occurs. Policies and interventions to reduce adolescent depressive symptoms need to consider the social background of the family as an important risk or protective factor.
| S-EPMC5671805 | biostudies-literature
Project description:ObjectiveThe 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).MethodsOur 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.ResultsAlmost 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.ConclusionsExposure 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.
| S-EPMC4964593 | biostudies-literature
Project description:We use longitudinal data across a key developmental period, spanning much of childhood and adolescence (age 5 to 17, years 2006-2018) from the UK Millennium Cohort Study, a nationally representative study with an initial sample of just over 19,000. We first examine the extent to which inequalities in overweight, obesity, BMI and body fat over this period are consistent with the evolution of inequalities in health behaviours, including exercise and healthy diet markers (i.e., skipping breakfast) (n = 7,220). We next study the links between SES, health behaviours and adiposity (BMI, body fat), using rich models that account for the influence of a range of unobserved factors that are fixed over time. In this way, we improve on existing estimates measuring the relationship between SES and health behaviours on the one hand and adiposity on the other. The advantage of the individual fixed effects models is that they exploit within-individual changes over time to help mitigate biases due to unobserved fixed characteristics (n = 6,883). We observe stark income inequalities in BMI and body fat in childhood (age 5), which have further widened by age 17. Inequalities in obesity, physical activity, and skipping breakfast are observed to widen from age 7 onwards. Ordinary Least Square estimates reveal the previously documented SES gradient in adiposity, which is reduced slightly once health behaviours including breakfast consumption and physical activity are accounted for. The main substantive change in estimates comes from the fixed effects specification. Here we observe mixed findings on the SES associations, with a positive association between income and adiposity and a negative association with wealth. The role of health behaviours is attenuated but they remain important, particularly for body fat.
| S-EPMC8671115 | biostudies-literature
Project description:Low birth-weight has been associated with depression and related outcomes in adults, and with problem behaviours in children. This study aimed to examine the association between low birth-weight for gestation and depressive symptoms in children and adolescents and to examine whether the relationship is moderated by genetic risk for depression. An epidemiological, genetically sensitive design was used including 2,046 twins aged 8-17 years (1,023 families). Data were obtained by parental report and analysed using regression analysis. A small but significant association between birth-weight for gestation and early depressive symptoms was observed. The unit increase in depressive symptoms per unit decrease in birth-weight for gestation was greater for individuals at genetic or familial risk for depression. For low birth-weight children, genetic risk for depression moderated the influence of birth-weight for gestation in predicting early depressive symptoms. Birth-weight for gestation is moderated by genetic and familial risk for depression in influencing early depression symptoms. These observations have clinical implications in that the impact of being small for gestational age on depressive symptoms is greater in children at familial/genetic risk although the association between birth weight and depression does not imply causality.
| S-EPMC1705530 | biostudies-other
Project description:Body dissatisfaction and depressive symptoms are commonly experienced during adolescence and increase the risk of adverse health outcomes, especially eating disorders. However, the dominant temporal associations between these two experiences (i.e., whether one is a risk factor for the other or the two are mutually reinforcing) has yet to be fully explored. We examined the associations between body dissatisfaction and depressive symptoms assessed at baseline and 5- and 10-year follow-up in younger (M age = 12.9 years at baseline, 56% female, n = 577) and older (M age = 15.9 years at baseline, 57% female, n = 1,325) adolescent cohorts assessed as part of Project Eating Among Teens and Young Adults. Associations between body dissatisfaction and depressive symptoms were examined using cross-lagged models. For females, the dominant directionality was for body dissatisfaction predicting later depressive symptoms. For males, the picture was more complex, with developmentally sensitive associations in which depressive symptoms predicted later body dissatisfaction in early adolescence and early adulthood, but the reverse association was dominant during middle adolescence. These findings suggest that interventions should be tailored to dynamic risk profiles that shift over adolescence and early adulthood, and that targeting body dissatisfaction at key periods during development may have downstream impacts on depressive symptoms.
| S-EPMC6343674 | biostudies-literature
Project description:BACKGROUND:Despite many attempts to understand the genetic architecture of depression, little progress has been made. The majority of these studies, however, have been carried out in adults and do not account for the potential influence of development. METHODS:The Avon Longitudinal Study of Parents and Children (ALSPAC) is a longitudinal pregnancy cohort which recruited participants between April 1991 and December 1992. Analyses were replicated in two independent European cohorts. Genome-wide complex trait analysis (GCTA) software was used to investigate SNP-heritability (h2SNP) of depression across adolescence, the role of puberty was investigated by stratifying these estimates according to pubertal onset. Genome-wide association studies were performed to identify genetic variants associated with depression at different stages of development. RESULTS:Heritability was estimated between the ages of 11 and 18 with sample sizes ranging from 3289 to 5480. Heritability was low with an apparent peak was found at age 13 (h2 = 0.17, p = 0.006). Confidence intervals around these estimates suggest an upper-bound to h2SNP of around 30%. A variant located on chromosome 7 was found to be associated with depressive symptoms at age 13 in ALSPAC (rs138191010: ? = 0.142, p = 2.51 × 10-8), although this was not replicated. CONCLUSIONS:Although power is a potential limitation, the observed patterns provide interesting hypotheses surrounding the heritability of depression at different developmental stages. We found substantially lower estimates for depressive symptoms at age 11 (0.07) compared to those previously estimated in adults (0.21). We also found a peak in heritability at age 13. These findings suggest environmental factors are likely to be more important in the aetiology of depressive symptoms in early adolescence than in adulthood.
| S-EPMC5580280 | biostudies-literature
Project description:An increasing number of studies have addressed how adolescents' social media use is associated with depressive symptoms. However, few studies have examined whether these links occur longitudinally across adolescence when examined at the individual level of development. This study investigated the within-person effects between active social media use and depressive symptoms using a five-wave longitudinal dataset gathered from 2891 Finnish adolescents (42.7% male, age range 13-19 years). Sensitivity analysis was conducted, adjusting for gender and family financial status. The results indicate that depressive symptoms predicted small increases in active social media use during both early and late adolescence, whereas no evidence of the reverse relationship was found. Yet, the associations were very small, statistically weak, and somewhat inconsistent over time. The results provide support for the growing notion that the previously reported direct links between social media use and depressive symptoms might be exaggerated. Based on these findings, we suggest that the impact of social media on adolescents' well-being should be approached through methodological assumptions that focus on individual-level development.
| S-EPMC7459880 | biostudies-literature
Project description:Psychotic disorders and major depression, both typically adult-onset conditions, often co-occur. At younger ages psychotic experiences and depressive symptoms are often reported in the community. We used a genetically sensitive longitudinal design to investigate the relationship between psychotic experiences and depressive symptoms in adolescence. A representative community sample of twins from England and Wales was employed. Self-rated depressive symptoms, paranoia, hallucinations, cognitive disorganization, grandiosity, anhedonia, and parent-rated negative symptoms were collected when the twins were age 16 (N = 9618) and again on a representative subsample 9 months later (N = 2873). Direction and aetiology of associations were assessed using genetically informative cross-lagged models. Depressive symptoms were moderately correlated with paranoia, hallucinations, and cognitive disorganization. Lower correlations were observed between depression and anhedonia, and depression and parent-rated negative symptoms. Nonsignificant correlations were observed between depression and grandiosity. Largely the same genetic effects influenced depression and paranoia, depression and hallucinations, and depression and cognitive disorganization. Modest overlap in environmental influences also played a role in the associations. Significant bi-directional longitudinal associations were observed between depression and paranoia. Hallucinations and cognitive disorganization during adolescence were found to impact later depression, even after controlling for earlier levels of depression. Our study shows that psychotic experiences and depression, as traits in the community, have a high genetic overlap in mid-adolescence. Future research should test the prediction stemming from our longitudinal results, namely that reducing or ameliorating positive and cognitive psychotic experiences in adolescence would decrease later depressive symptoms.
| S-EPMC4988737 | biostudies-literature
Project description:Childhood adversity may lead to depressive relapse through its long-lasting influence on stress sensitivity. In line with the stress sensitization hypothesis, minor (daily) stress is associated with depressive relapse. Therefore, we examine the impact of childhood adversity on daily stress and its predictive value on prospectively assessed depressive symptoms in recurrently depressed patients.Daily stress was assessed in recurrently depressed adult patients, enrolled into two randomized trials while remitted. The reported intensity and frequency of dependent and independent daily stress was assessed at baseline. Independent stress is externally generated, for example an accident happening to a friend, while dependent stress is internally generated, for example getting into a fight with a neighbor. Hierarchical regression analyses were performed with childhood adversity, independent and dependent daily stress as predictor variables of prospectively measured depressive symptoms after three months of follow-up (n = 138).We found that childhood adversity was not significantly associated with a higher frequency and intensity of daily stress. The intensity of both independent and dependent daily stress was predictive of depressive symptom levels at follow-up (unadjusted models respectively: B = 0.47, t = 2.05, p = 0.041, 95% CI = 0.02-0.92; B = 0.29, t = 2.20, p = 0.028, 95% CI = 0.03-0.55). No associations were found between childhood adversity and depressive symptoms at follow-up.No evidence was found supporting stress sensitization due to the experience of childhood adversity in this recurrently depressed but remitted patient group. Nevertheless, our research indicates that daily stress might be a target for preventive treatment.Trial A: Nederlands Trial Register NTR1907 Trial B: Nederlands Trial Register NTR2503.
| S-EPMC4230942 | biostudies-literature
Project description:BACKGROUND:Polyunsaturated fatty acids (PUFA) status in childhood may be associated with adiposity development. OBJECTIVE:To assess associations of serum PUFA biomarkers in childhood with change in body mass index (BMI)-for-age Z scores (BMIZ) through adolescence. METHODS:We quantified serum PUFA at ages 5 and 10 years among 418 children from Santiago, Chile. BMI was measured at 5, 10, and 16 years. We compared BMIZ change through age 16 years between quartiles of PUFA at 5 and 10 years and PUFA change 5-10 years by fitting growth curves from mixed effects models. RESULTS:At age 5 years, serum docosahexaenoic acid was inversely associated with BMIZ change from ages 5 to 16 years. At age 10 years, arachidonic acid (AA) was nonlinearly positively related to BMIZ change from ages 10 to 16 years. Change in AA and the ?5-desaturase (D5D) activity index between 5 and 10 years were each positively associated with BMIZ change from ages 10 to 16 years. Change in eicosapentaenoic acid was inversely associated with change in BMIZ. CONCLUSIONS:Serum long-chain n-3 PUFA in middle childhood were associated with less BMI gain through adolescence, whereas AA and D5D activity was related to greater BMI gain.
| S-EPMC6827434 | biostudies-literature