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: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: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: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: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: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
Project description:BackgroundDifferences between verbal and non-verbal cognitive development from childhood to adulthood may differentiate between those with and without psychotic symptoms and affective symptoms in later life. However, there has been no study exploring this in a population-based cohort.MethodThe sample was drawn from the MRC National Survey of Health and Development, and consisted of 2384 study members with self-reported psychotic experiences and affective symptoms at the age of 53 years, and with complete cognitive data at the ages of 8 and 15 years. The association between verbal and non-verbal cognition at age 8 years and relative developmental lag from age 8 to 15 years, and both adult outcomes were tested with the covariates adjusted, and mutually adjusted for verbal and non-verbal cognition.ResultsThose with psychotic experiences [thought interference (n = 433), strange experience (n = 296), hallucination (n = 88)] had lower cognition at both the ages of 8 and 15 years in both verbal and non-verbal domains. After mutual adjustment, lower verbal cognition at age 8 years and greater verbal developmental lag were associated with higher likelihood of psychotic experiences within individuals, whereas there was no association between non-verbal cognition and any psychotic experience. In contrast, those with case-level affective symptoms (n = 453) had lower non-verbal cognition at age 15 years, and greater developmental lag in the non-verbal domain. After adjustment, lower non-verbal cognition at age 8 years and greater non-verbal developmental lag were associated with higher risk of case-level affective symptoms within individuals.ConclusionsThese results suggest that cognitive profiles in childhood and adolescence differentiate psychiatric disease spectra.
| S-EPMC5729848 | biostudies-literature
Project description:BackgroundDepression is a common and disabling condition with a high relapse frequency. Maternal mental health problems and experience of traumatic life events are known to increase the risk of behavior problems in children. Recently, genetic factors, in particular gene-by-environment interaction models, have been implicated to explain depressive etiology. However, results are inconclusive.MethodsStudy participants were members of the SESBiC-study. A total of 889 mothers and their children were followed during the child's age of 3 months to 12 years. Information on maternal depressive symptoms was gathered postpartum and at a 12 year follow-up. Mothers reported on child behavior and traumatic life events experienced by the child at age 12. Saliva samples were obtained from children for analysis of 5-HTTLPR and BDNF Val66Met polymorphisms.ResultsMultivariate analysis showed a significant association between maternal symptoms of depression and anxiety, and internalizing problems in 12-year-old children (OR 5.72, 95% CI 3.30-9.91). Furthermore, carriers of two short alleles (s/s) of the 5-HTTLPR showed a more than 4-fold increased risk of internalizing problems at age 12 compared to l/l carriers (OR 4.73, 95% CI 2.14-10.48). No gene-by-environment interaction was found and neither depressive symptoms postpartum or traumatic experiences during childhood stayed significant in the final model.ConclusionsConcurrent maternal symptoms of depression and anxiety are significant risk factors for behavior problems in children, which need to be taken into account in clinical practice. Furthermore, we found a main effect of 5-HTTLPR on internalizing symptoms in 12-year-old children, a finding that needs to be confirmed in future studies.
| S-EPMC3615948 | biostudies-literature
Project description: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.
| S-EPMC5510745 | biostudies-literature
Project description:Depression is a debilitating mental illness with clear developmental patterns from childhood through late adolescence. Here, we present data from the Gene Environment Mood (GEM) study, which used an accelerated longitudinal cohort design with youth (N = 665) starting in 3rd, 6th, and 9th grades, and a caretaker, who were recruited from the general community, and were then assessed repeatedly through semistructured diagnostic interviews every 6 months over 3 years (7 waves of data) to establish and then predict trajectories of depression from age 8 to 18. First, we demonstrated that overall prevalence rates of depression over time, by age, gender, and pubertal status, in the GEM study closely match those trajectories previously obtained in past developmental epidemiological research. Second, we tested whether a genetic vulnerability-stress model involving 5-HTTLPR and chronic peer stress was moderated by developmental factors. Results showed that older aged adolescents with SS/SL genotype, who experienced higher peer chronic stress over 3 years, were the most likely to be diagnosed with a depressive episode over time. Girls experiencing greater peer chronic stress were the most likely to develop depression. This study used repeated assessments of diagnostic interviewing in a moderately large sample of youth over 3 years to show that depression rates increase in middle to late adolescence, or postpubertally, and that the gender difference in depression emerges earlier in adolescence (age 12.5), or postpubertally. Additionally, genetically susceptible older adolescents who experience chronic peer stress were the most likely to become depressed over time.
| S-EPMC4662048 | biostudies-literature