ArticlePloS one2012
Longitudinal replication studies of GWAS risk SNPs influencing body mass index over the course of childhood and adulthood.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Genetic polymorphisms and their association with neurobiological and psychological factors in anorexia nervosa: a systematic review.Frontiers in psychology · 2024Pooled it
- Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial.Cardiovascular diabetology · 2014Trial
- Characterization of prevalent genetic variants in the Estonian Biobank body-mass index GWAS.Nature communications · 2025Article
- Variant-to-function analysis of the childhood obesity chr12q13 locus implicates rs7132908 as a causal variant within the 3' UTR of FAIM2.Cell genomics · 2024Article
- Maternal Age at Menarche Genes Determines Fetal Growth Restriction Risk.International journal of molecular sciences · 2024Article
- Variant-to-function analysis of the childhood obesity chr12q13 locus implicates rs7132908 as a causal variant within the 3' UTR ofbioRxiv : the preprint server for biology · 2023Article
- Maternal Age at Menarche Gene Polymorphisms Are Associated with Offspring Birth Weight.Life (Basel, Switzerland) · 2023Article
- Opposing effects of genetic variation in MTCH2 for obesity versus heart failure.Human molecular genetics · 2023Article
- Bayesian mixed models for longitudinal genetic data: theory, concepts, and simulation studies.Genomics & informatics · 2022Article
- "GENYAL" Study to Childhood Obesity Prevention: Methodology and Preliminary Results.Frontiers in nutrition · 2022Article
- Omics Approaches in Adipose Tissue and Skeletal Muscle Addressing the Role of Extracellular Matrix in Obesity and Metabolic Dysfunction.International journal of molecular sciences · 2021Review
- BDNF Gene as a Precision Skill of Obesity Management.Advances in experimental medicine and biology · 2021Article
- Dataset of allele and genotype frequencies of five polymorphisms candidate genes analyzed for association with body mass index in Russian women.Data in brief · 2020Article
- The Association Between Body Mass Index (BMI) and Sleep Duration: Where Are We after nearly Two Decades of Epidemiological Research?International journal of environmental research and public health · 2019Review
- Pathway analysis of rare variants for the clustered phenotypes by using hierarchical structured components analysis.BMC medical genomics · 2019Article
- Genetic risk score for adult body mass index associations with childhood and adolescent weight gain in an African population.Genes & nutrition · 2018Article
- Scientific Contributions of Population-Based Studies to Cardiovascular Epidemiology in the GWAS Era.Frontiers in cardiovascular medicine · 2018Article
- Genetic polymorphisms in genes related to risk-taking behaviours predicting body mass index trajectory among Mexican American adolescents.Pediatric obesity · 2017Article
- Influence ofBrain and behavior · 2017Article
- BMI loci and longitudinal BMI from adolescence to young adulthood in an ethnically diverse cohort.International journal of obesity (2005) · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Genome-wide association studies (GWAS) have identified multiple common variants associated with body mass index (BMI). In this study, we tested 23 genotyped GWAS-significant SNPs (p-value<5*10-8) for longitudinal associations with BMI during childhood (3-17 years) and adulthood (18-45 years) for 658 subjects. We also proposed a heuristic forward search for the best joint effect model to explain the longitudinal BMI variation. After using false discovery rate (FDR) to adjust for multiple tests, childhood and adulthood BMI were found to be significantly associated with six SNPs each (q-value<0.05), with one SNP associated with both BMI measurements: KCTD15 rs29941 (q-value<7.6*10-4). These 12 SNPs are located at or near genes either expressed in the brain (BDNF, KCTD15, TMEM18, MTCH2, and FTO) or implicated in cell apoptosis and proliferation (FAIM2, MAP2K5, and TFAP2B). The longitudinal effects of FAIM2 rs7138803 on childhood BMI and MAP2K5 rs2241423 on adulthood BMI decreased as age increased (q-value<0.05). The FTO candidate SNPs, rs6499640 at the 5 '-end and rs1121980 and rs8050136 downstream, were associated with childhood and adulthood BMI, respectively, and the risk effects of rs6499640 and rs1121980 increased as birth weight decreased. The best joint effect model for childhood and adulthood BMI contained 14 and 15 SNPs each, with 11 in common, and the percentage of explained variance increased from 0.17% and 9.0*10(-6)% to 2.22% and 2.71%, respectively. In summary, this study evidenced the presence of long-term major effects of genes on obesity development, implicated in pathways related to neural development and cell metabolism, and different sets of genes associated with childhood and adulthood BMI, respectively. The gene effects can vary with age and be modified by prenatal development. The best joint effect model indicated that multiple variants with effects that are weak or absent alone can nevertheless jointly exert a large longitudinal effect on BMI.
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Registered trials
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