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Genetics of depressive symptoms in adolescence.

ABSTRACT: 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.

SUBMITTER: Sallis H

PROVIDER: S-EPMC5580280 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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Genetics of depressive symptoms in adolescence.

Sallis Hannah H Evans Jonathan J Wootton Robyn R Krapohl Eva E Oldehinkel Albertine J AJ Davey Smith George G Paternoster Lavinia L

BMC psychiatry 20170831 1

<h4>Background</h4>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.<h4>Methods</h4>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. ...[more]

PMID: 28859627

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Project description:ImportanceDepressive symptoms have increased among US adolescents since 2010. It remains unclear as to what extent this increase will persist into young adulthood, potentially turning the youth mental health crisis into a young adult mental health crisis.ObjectiveTo test the association between birth cohort and adolescent depressive symptoms at ages 18, 19 to 20, and 21 to 22 years and changes in these symptoms by cohort.Design, setting, and participantsThis panel cohort study analyzed data from the Monitoring the Future longitudinal survey from 1990 to 2019, including birth cohorts from 1972 to 2001. Survey respondents were recruited from US high schools in 12th grade and were approximately aged 18 years (at baseline) through age 21 to 22 years (during mail and web follow-up). Data analysis was conducted from April to October 2023.ExposureDepressive symptoms score (>12 vs ≤12, with >12 representing top-decile scores) on a scale examining affective items (eg, "Life often seems meaningless").Main outcomes and measuresHigh (vs lower) depressive symptoms at ages 19 to 20 years and 21 to 22 years.ResultsThe 36 552 respondents included 18 597 females (50.5%), and most reported having a parent who graduated from college (44.8%). Among females, 19.1% (95% CI, 16.7%-21.4%) of the most recent birth cohort (born: 1997-2001) had high depressive symptoms at age 18 years, higher than any previous birth cohort. While prevalence declined by age 21 to 22 years, it remained higher than previous cohorts at that age. Among males, 13.4% (95% CI, 11.2%-15.6%) of the most recent birth cohort had high depressive symptoms at age 18 years, and prevalence increased through young adulthood. Males with high baseline depressive symptoms had 10.24 (95% CI, 7.01-14.97) times the odds of symptoms at age 19 to 20 years and 6.20 (95% CI, 3.93-9.78) times the odds of symptoms at age 21 to 22 years. Females with high baseline depressive symptoms had 9.16 (95% CI, 6.57-12.76) times the odds of symptoms at age 19 to 20 years and 7.28 (95% CI, 4.92-10.78) times the odds of symptoms at age 21 to 22 years. The magnitude of the associations did not vary over time. Population attributable fractions indicated that the total proportion of young adult symptoms associated with depressive symptoms at age 18 years among females has increased; in the most recent birth cohort, 55.25% (95% CI, 38.11%-65.13%) of depressive symptoms at age 21 to 22 years were associated with symptoms at age 18 years.Conclusions and relevanceThis panel cohort study found that increases in depressive symptoms in adolescence persisted into young adulthood, suggesting the need for primary prevention and mental health resources during the adolescent years.

Project description:Parental knowledge/monitoring is negatively associated with adolescents' depressive symptoms, suggesting monitoring could be a target for prevention and treatment. However, no study has rigorously addressed the possibility that this association is spurious, leaving the clinical and etiological implications unclear. The goal of this study was to conduct a more rigorous test of whether knowledge/monitoring is causally related to depressive symptoms. 7940 youth (ages 10.5-15.6 years, 49% female) at 21 sites across the U.S. completed measures of parental knowledge/monitoring and their own depressive symptoms at four waves 11-22 weeks apart during the COVID-19 pandemic. First, monitoring and depression were examined in standard, between-family regression models. Second, within-family changes in monitoring and depression between assessments were examined in first differenced regressions. Because the latter models control for stable, between-family differences, they comprise a stronger test of a causal relation. In standard, between-family models, parental monitoring and youths' depressive symptoms were negatively associated (standardized [Formula: see text]= -0.22, 95% CI = [-0.25, -0.20], p < 0.001). In first-differenced, within-family models, the association shrunk by about 55% (standardized [Formula: see text]= -0.10, 95% CI = [-0.12, -0.08], p < 0.001). The magnitude of within-family association remained similar when adjusting for potential time-varying confounders and did not vary significantly by youth sex, age, or history of depressive disorder. Thus, in this community-based sample, much of the prima facie association between parental knowledge/monitoring and youths' depressive symptoms was driven by confounding variables rather than a causal process. Given the evidence to date, a clinical focus on increasing parental knowledge/monitoring should not be expected to produce meaningfully large improvements in youths' depression.

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Genetics of depressive symptoms in adolescence.

Publications

Genetics of depressive symptoms in adolescence.

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