The effect of birth-weight with genetic susceptibility on depressive symptoms in childhood and adolescence.
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ABSTRACT:
SUBMITTER: Rice F
PROVIDER: S-EPMC1705530 | biostudies-other | 2006 Oct
REPOSITORIES: biostudies-other
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Project description:BackgroundEarly-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence.MethodsData came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures.ResultsYouth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level.ConclusionsThis study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns.
| S-EPMC9886425 | biostudies-literature
Project description:Childhood obesity is a global public health problem. Understanding the molecular mechanisms that underlie early origins of childhood obesity can facilitate interventions. Consistent phenotypic and genetic correlations have been found between childhood obesity traits and birth weight (a proxy for in-utero growth), suggesting shared genetic influences (pleiotropy). We aimed to (1) investigate whether there is significant shared genetic influence between birth weight and childhood obesity traits, and (2) to identify genetic loci with shared effects. Using a statistical approach that integrates summary statistics and functional annotations for paired traits, we found strong evidence of pleiotropy (P < 3.53 × 10-127) and enrichment of functional annotations (P < 1.62 × 10-39) between birth weight and childhood body mass index (BMI)/obesity. The pleiotropic loci were enriched for regulatory features in skeletal muscle, adipose and brain tissues and in cell lines derived from blood lymphocytes. At 5% false discovery rate, 6 loci were associated with birth weight and childhood BMI and 13 loci were associated with birth weight and childhood obesity. Out of these 19 loci, one locus (EBF1) was novel to childhood obesity and one locus (LMBR1L) was novel to both birth weight and childhood BMI/obesity. These findings give evidence of substantial shared genetic effects in the regulation of both fetal growth and childhood obesity.
| S-EPMC7794220 | 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: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: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.
| S-EPMC11325205 | biostudies-literature
Project description:Different pathways likely underlie the association between early weight gain and cardiovascular disease risk. We examined whether birth weight for length relationship and weight gain up to 2 years of age are associated with lipid profiles and blood pressure (BP) in early adolescence and determined whether childhood adiposity mediates these associations. Data from QUALITY (Quebec Adipose and Lifestyle Investigation in Youth), a cohort of white children with parental history of obesity, were analyzed (n=395). Sex-specific weight for length z scores from birth to 2 years were computed. Rate of postnatal weight gain was estimated using individual slopes of weight for length z-score measurements. Percentage of body fat was measured at 8 to 10 years. Fasting lipids and BP were measured at 10 to 12 years. Using path analysis, we found indirect effects of postnatal weight gain, through childhood adiposity, on all outcomes: Rate of postnatal weight for length gain was positively associated with childhood adiposity, which in turn was associated with unfavorable lipid and BP levels in early adolescence. In contrast, small beneficial direct effects on diastolic BP z scores, independent of weight at other time points, were found for birth weight for length (β=-0.05, 95% CI, -0.09 to -0.002) and for postnatal weight gain (β=-0.02, 95% CI, -0.03 to -0.002). Among children with at least 1 obese parent, faster postnatal weight gain leads to cardiovascular risk factors in early adolescence through its effect on childhood adiposity. Although heavier newborns may have lower BP in early adolescence, this protective direct effect could be offset by a deleterious indirect effect linking birth weight to later adiposity.
| S-EPMC5586463 | biostudies-literature
Project description:IntroductionDepressive symptoms are highly prevalent in adolescence, highlighting the need for early identification of precursors. Research into psychopathological symptoms predicting depressive psychopathology in adolescents is therefore of great relevance. Moreover, given that the prevalence of depressive symptomatology in adolescence shows marked differences between girls and boys, insight into potential sex-specific differences in precursors is important.MethodsThis study examined the relationships between emotional problems, conduct problems, hyperactivity/inattention, peer problems, and difficulties in prosocial behaviour at age 10 (Strengths and Difficulties Questionnaire), and the presence of depressive symptoms at age 15 (Depression Screener for Teenagers). Using data from 2824 participants of the GINIplus and LISA birth cohorts, the association of each SDQ subscale at age 10 years with the presence of depressive symptoms at age 15 years was analyzed using sex-specific logistic regression, adjusting for potential confounders.ResultsEmotional problems [odds ratio (OR) 1.99, p = 0.002 for boys and OR 1.77, p < 0.001 for girls] and peer problems (OR 2.62, p < 0.001 for boys, OR 1.91, p = 0.001 for girls) at age 10 showed an increased risk for the presence of depressive symptoms at age 15. Additionally, boys with conduct problems at age 10 were at greater risk of showing depressive symptoms in adolescence (OR 2.50, p < 0.001).DiscussionBased on the identified prospective relationships in our study, it might be of particular importance to tailor prevention approaches during childhood to peer and emotional problems to reduce the risk of depressive psychopathology in adolescence. Moreover, particularly in boys, it seems important to also target conduct problems in childhood as a precursor of depressive symptoms in the adolescent period.
| S-EPMC9288954 | biostudies-literature
Project description:BackgroundMaternal smoking (MS) is associated with low birthweight (BW) but adult obesity in offspring, however, it remains unknown whether it modifies offspring's genetic susceptibility to obesity on BW, adult body weight, and birth-to-adulthood body weight tracking pattern.MethodsThis study included 246,759 UK Biobank participants with information on MS, BW (kg), adult body weight and BMI (kg/m2). Individual polygenetic score (PGS) was created on the basis of 97 BMI-associated genetic loci. We calculated individual birth-to-adulthood percentile change, and body weight tracking patterns that combined BW levels (<2.5, 2.5-4.0, and ≥4.0 as low, normal and high BW [LBW, NBW, and HBW]) and adulthood obesity status (≥30 as obesity [OB] and <30 as non-obesity [NOB]), including LBW-to-OB, LBW-to-NOB, NBW-to-OB, NBW-to-NOB, HBW-to-OB, and HBW-to-NOB.ResultsParticipants exposed to MS had a 0.108 kg lower BW (95% CI, -0.114 to -0.102), a 1.418 kg higher adult body weight (95% CI, 1.291-1.545), and a 6.91 greater percentile increase of body weight from birth to adulthood (95% CI, 6.62-7.21), compared with those nonexposed (all P < 0.001). In comparison to participants of NBW-to-NOB, MS was associated with an approximately twofold higher risk of LBW-to-OB (odds ratio [OR] 1.98, 95% CI 1.87-2.10), and a reduced likelihood of HBW-to-NOB (0.85, 95% CI 0.82-0.88). The increases in BW, adult body weight, and birth-to-adulthood percentile change per increment of 10 BMI-PGS were 0.021 vs. 0.012, 2.50 vs. 2.11, and 4.03 vs. 3.55, respectively, for participants exposed vs. nonexposed to MS (all Pinteraction < 0.05).ConclusionOur results indicate that exposure to MS is associated with an increased risk of transition from low BW-to-adulthood obesity, and reduced likelihood of change from high BW-to-normal adult body weight. MS may modify the relation of genetic susceptibility to obesity and body weight in offspring.
| S-EPMC10243517 | biostudies-literature
Project description:ObjectiveBoth stressful intrauterine milieus and genetic susceptibility have been linked to later-life diabetes risk. The current study aims to examine the interaction between low birth weight, a surrogate measure of stressful intrauterine milieus, and genetic susceptibility in relation to risk of type 2 diabetes in adulthood.Research design and methodsThe analysis included two independent, nested case-control studies of 2,591 type 2 diabetic case subjects and 3,052 healthy control subjects. We developed two genotype scores: an obesity genotype score based on 32 BMI-predisposing variants and a diabetes genotype score based on 35 diabetes-predisposing variants.ResultsObesity genotype scores showed a stronger association with type 2 diabetes risk in individuals with low birth weight. In low-birth weight individuals, the multivariable-adjusted odds ratio (OR) was 2.55 (95% CI 1.34-4.84) by comparing extreme quartiles of the obesity genotype score, while the OR was 1.27 (1.04-1.55) among individuals with birth weight >2.5 kg (P for interaction = 0.017). We did not observe significant interaction between diabetes genotype scores and birth weight with regard to risk of type 2 diabetes. In a comparison of extreme quartiles of the diabetes gene score, the multivariable-adjusted OR was 3.80 (1.76-8.24) among individuals with low birth weight and 2.27 (1.82-2.83) among those with high birth weight (P for interaction = 0.16).ConclusionsOur data suggest that low birth weight and genetic susceptibility to obesity may synergistically affect adulthood risk of type 2 diabetes.
| S-EPMC3507591 | biostudies-literature
Project description:BackgroundThere are both genetic and environmental factors which contribute to a child's chances of being obese. When low birth weight (LBW) has been specifically evaluated relative to its association with childhood obesity, the results have produced conflicting findings. This study aims to describe the relationship between birth weight and childhood obesity and investigate the influence that residence and household wealth has on this relationship.MethodsI performed a secondary analysis on the 2013 Riskesdas (or Basic Health Research), a cross-sectional, nationally representative survey of the Indonesian population. Height, weight, information regarding child's birth weight, and basic characteristics of the study population were collected from parents with children aged 0 to 5 years (n = 63,237) in 2013. The exposure was child's birth weight and the outcomes were child's current weight, BMI z-score, and obesity. Data were analyzed by using multiple linear regression and multiple logistic regression.ResultsI found a significant increase in the weight, BMI z-score, and risk of childhood obesity to be associated with LBW. LBW children in rural area were associated with higher BMI z-score (mean ± standard error: 1.44 ± 0.02) and higher odds (odds ratio (95% confidence interval): 7.46 (6.77-8.23)) of obesity than those in urban area. LBW children from low class families were associated with higher BMI z-score (1.79 ± 0.04) and had higher odds (14.79 (12.47-17.54)) of obesity than those from middle class and wealthy families.ConclusionsEffective prevention and intervention to childhood obesity as early as possible are imperative. As far as this study was concerned, efforts, policies, and targets are required to reduce the prevalence of LBW. Children born of LBW, who live in a rural area and from low income families, should be emphatically intervened as early as possible.
| S-EPMC8111737 | biostudies-literature