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  • Ovid Technologies (Wolters Kluwer Health)  (48)
  • 1
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    Soluble CD14 Levels in the Jackson Heart Study: Associations With Cardiovascular Disease Risk and Genetic Variants
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 41, No. 6 ( 2021-06)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 6 ( 2021-06)
    Abstract: sCD14 (soluble CD14) is a circulating pattern recognition receptor involved in inflammatory signaling. Although it is known that sCD14 levels vary by race, information on the genetic and cardiovascular disease (CVD) risk relationships of sCD14 in Black participants is limited. Approach and Results: We measured sCD14 in plasma at the baseline exam from n=3492 Black participants from the JHS (Jackson Heart Study). We evaluated associations between sCD14 and subclinical CVD measures, incident CVD events, and mortality under 3 levels of covariate adjustment. We used whole-genome sequence data from the Trans-Omics for Personalized Medicine program to identify genetic associations with sCD14. Adjusting for CVD risk factors and C-reactive protein, higher sCD14 was significantly associated with increased risk of mortality (hazard ratio, 1.25 [95% CI, 1.17–1.32]), incident coronary heart disease (hazard ratio, 1.28 [95% CI, 1.11–1.47] ), and incident heart failure (hazard ratio, 1.27 [95% CI, 1.15–1.41]), but not stroke (hazard ratio, 0.96 [95% CI, 0.84–1.09] ). Some of these relationships differed by age or sex: the association between sCD14 and heart failure was only observed in females; there was an association between sCD14 and stroke only at younger ages (in the lowest tertile of age, 〈 49.4 years). We replicated the association between sCD14 levels with African ancestry-specific allele (rs75652866) on the CD14 region of chromosome 5q31. We additionally identified 2 novel statistically distinct genetic associations with sCD14 represented by index variants rs770147646 and rs57599368, also in the chromosome 5q31 region. Conclusions: sCD14 independently predicts CVD-related outcomes and mortality in Black participants.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.121.316035
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 2
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    D-Dimer in African Americans : Whole Genome Sequence Analysis and Relationship to Cardiovascular Disease Risk in the Jackson Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 37, No. 11 ( 2017-11), p. 2220-2227
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 11 ( 2017-11), p. 2220-2227
    Abstract: Plasma levels of the fibrinogen degradation product D-dimer are higher among African Americans (AAs) compared with those of European ancestry and higher among women compared with men. Among AAs, little is known of the genetic architecture of D-dimer or the relationship of D-dimer to incident cardiovascular disease. Approach and Results— We measured baseline D-dimer in 4163 AAs aged 21 to 93 years from the prospective JHS (Jackson Heart Study) cohort and assessed association with incident cardiovascular disease events. In participants with whole genome sequencing data (n=2980), we evaluated common and rare genetic variants for association with D-dimer. Each standard deviation higher baseline D-dimer was associated with a 20% to 30% increased hazard for incident coronary heart disease, stroke, and all-cause mortality. Genetic variation near F3 was associated with higher D-dimer (rs2022030, β=0.284, P =3.24×10 –11 ). The rs2022030 effect size was nearly 3× larger among women (β=0.373, P =9.06×10 –13 ) than among men (β=0.135, P =0.06; P interaction =0.009). The sex by rs2022030 interaction was replicated in an independent sample of 10 808 multiethnic men and women ( P interaction =0.001). Finally, the African ancestral sickle cell variant ( HBB rs334) was significantly associated with higher D-dimer in JHS (β=0.507, P =1.41×10 –14 ), and this association was successfully replicated in 1933 AAs ( P =2.3×10 –5 ). Conclusions— These results highlight D-dimer as an important predictor of cardiovascular disease risk in AAs and suggest that sex-specific and African ancestral genetic effects of the F3 and HBB loci contribute to the higher levels of D-dimer among women and AAs.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.117.310073
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
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  • 3
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    Abstract 25: Epigenome-Wide DNA Methylation Analysis Reveals Novel Hematologic Trait Associations for African Americans in The Jackson Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Vol. 141, No. Suppl_1 ( 2020-03-03)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 141, No. Suppl_1 ( 2020-03-03)
    Abstract: Cardiovascular disease (CVD) is the leading cause of death in the U.S. and disproportionately affects African Americans (AAs). Routinely measured circulating red blood cell traits, which are highly heritable and differ by ethnicity, are independent predictors for CVD-related traits including hypertension, stroke, coronary heart disease, and CVD mortality. Many genetic loci associated with red blood cell count (RBC), hemoglobin (HGB), hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), and red cell distribution width (RDW) have been identified. However, identified genetic variants do not fully explain the heritability of these traits. Epigenetic alterations in DNA methylation likely also explain a portion of red cell trait variance, and detecting methylation quantitative trait loci (meQTLs) can provide critical insight into the development of CVD and CVD health disparities. We performed an epigenome-wide association analysis to identify CpG sites at which DNA methylation levels are associated with red blood cell traits in 1753 participants from the Jackson Heart Study, a population-based cohort of AAs. DNA methylation was measured by the Illumina MethylationEPIC array, interrogating approximately 850,000 CpG sites in peripheral blood mononuclear cells at the baseline exam. Associations were assessed using linear mixed models adjusted for age, sex, cell proportions, genetic ancestry, and experimental batch effects. A Bonferroni-corrected p-value of 9x10 -8 was used to assess statistical significance. We identified many significant differentially methylated CpG sites associated with red blood cell traits. Analysis of RBC, HGB, MCV, MCH, and MCHC revealed a novel highly significant association with a CpG annotated to a non-coding RNA (cg11703701; RBC P = 5.19x10 -22 , HGB P = 1.19x10 -11 , MCV P = 4.69x10 -59 , MCH P = 2.68x10 -67 , MCHC P = 2.32x10 -31 ), as well as a strong signal for a reprogramming-specific differentially methylated region (cg04321267; RBC P = 1.67x10 -16 , HGB P = 3.58x10 -12 , MCV P = 2.12x10 -49 , MCH P = 1.74x10 -57 , MCHC P = 5.91x10 -30 ). Multiple CpGs annotated to genes HBA1 and HBA2 were associated with RBC, MCV, MCH, and MCHC, while ITPKB (cg23740281; HGB P = 4.88x10 -10 , HCT P = 6.20x10 -11 ) and ALDH2 (cg17969951; HGB P = 3.03x10 -11 , HCT P = 8.31x10 -9 ) were significantly associated with both HGB and HCT. Additional CpG sites were significantly associated with HCT ( PLXND1 cg22902177; P = 7.54x10 -11 and ARL1 cg23903357; P = 9.86x10 -11 ) and RDW ( CPNE2 cg09018739; P = 3.03x10 -22 ). These findings shed light on potential hematologic and CVD mechanisms in understudied populations. Future work will explore the role of neighboring SNPs in mediating observed methylation-trait associations, and replicate results in an additional multi-ethnic cohort.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.141.suppl_1.25
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 4
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    Abstract P223: Larger Effect Sizes of Established BMI Genetic Variants During Adolescence, a Vulnerable Period of Weight Gain
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. suppl_10 ( 2012-03-13)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. suppl_10 ( 2012-03-13)
    Abstract: In the past five years genome-wide association studies (GWAS) have identified common genetic loci associated with body mass index (BMI) mainly in European middle-aged adult populations. The influence of these loci in adolescence, a period of risk for weight gain, and whether there are different associations across adolescent groups at highest risk (e.g., ethnic minority populations), remains largely unknown. We examined whether obesity susceptibility loci identified from previous GWAS in adults were associated with BMI in an ethnically diverse adolescent cohort. Using 8918 participants from the National Longitudinal Study of Adolescent Health, or Add Health (aged 12-21 years in 1996, 52.6 % female), we assessed the association of 43 SNPs, selected based on statistical significance in previous GWAS, with BMI across four ethnic US subpopulations (5,296 European Americans, EA, 1,815 African Americans, AfA, 1,356 Hispanic Americans, HA, and 451 Asian Americans, AsA). Buccal cells from participants were extracted and genotyped using TaqMan (sample call rate: 97.5%, SNP call rate: 100%). Inverse normal transformed BMI residuals, adjusted for gender and age, were used in ethnicity-stratified models with SNPs in PLINK, assuming an additive model. An inverse-variance-weighted meta-analysis was used to combine results across the 4 ethnic groups. Average BMI across all ethnic groups was 23.6±5.2 kg/m2, ranging from 22.6±5.2 kg/m2 in AsA to 24.3±5.8 kg/m2 in AfA. The effect estimates for all 43 SNPs were directionally consistent across ethnicity with previously published results. Of the 43 SNPs, 20 were associated with BMI at p 〈 0.05 in the meta-analysis (17 in EA, 7 in AfA, 4 in HA, and 5 in AsA). Based on t-test comparisons, 16 of the 20 SNPs had larger and 2 loci had smaller effect sizes (p 〈 0.05) in the Add Health adolescent sample than published effect sizes for BMI in adults. Only FTO (rs9939609) showed significant heterogeneity across ethnicity (p=0.01 for I2=73.5). TMEM18 (rs6548238, meta-analysis p-value p=1.32E-10), had one of the largest differences in effect size compared to middle-aged European adults (Willer et al 2009) with a per allele increase of 0.70±0.11 kg/m2 in this sample versus 0.26±0.07 kg/m2 in adults (beta[SE] difference = 0.44[0.08] ; p=1.4E-08). Variants associated with BMI in adults were also associated with BMI in adolescents, with some comparatively larger effects during this vulnerable period. R01HD057194
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.125.suppl_10.AP223
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 5
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    Plasma Levels of Soluble Interleukin-2 Receptor α : Associations With Clinical Cardiovascular Events and Genome-Wide Association Scan
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 35, No. 10 ( 2015-10), p. 2246-2253
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 10 ( 2015-10), p. 2246-2253
    Abstract: Interleukin (IL) -2 receptor subunit α regulates lymphocyte activation, which plays an important role in atherosclerosis. Associations between soluble IL-2Rα (sIL-2Rα) and cardiovascular disease (CVD) have not been widely studied and little is known about the genetic determinants of sIL-2Rα levels. Approach and Results— We measured baseline levels of sIL-2Rα in 4408 European American (EA) and 766 African American (AA) adults from the Cardiovascular Health Study (CHS) and examined associations with baseline CVD risk factors, subclinical CVD, and incident CVD events. We also performed a genome-wide association study for sIL-2Rα in CHS (2964 EAs and 683 AAs) and further combined CHS EA results with those from two other EA cohorts in a meta-analysis (n=4464 EAs). In age, sex- and race- adjusted models, sIL-2Rα was positively associated with current smoking, type 2 diabetes mellitus, hypertension, insulin, waist circumference, C-reactive protein, IL-6, fibrinogen, internal carotid wall thickness, all-cause mortality, CVD mortality, and incident CVD, stroke, and heart failure. When adjusted for baseline CVD risk factors and subclinical CVD, associations with all-cause mortality, CVD mortality, and heart failure remained significant in both EAs and AAs. In the EA genome-wide association study analysis, we observed 52 single-nucleotide polymorphisms in the chromosome 10p15-14 region, which contains IL2RA , IL15RA , and RMB17 , that reached genome-wide significance ( P 〈 5×10 −8 ). The most significant single-nucleotide polymorphism was rs7911500 ( P =1.31×10 −75 ). The EA meta-analysis results were highly consistent with CHS-only results. No single-nucleotide polymorphisms reached statistical significance in the AAs. Conclusions— These results support a role for sIL-2Rα in atherosclerosis and provide evidence for multiple-associated single-nucleotide polymorphisms at chromosome 10p15-14.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.115.305289
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 6
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    Autosomal Genome-Wide Scan for Coronary Artery Calcification Loci in Sibships at High Risk for Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 22, No. 3 ( 2002-03), p. 418-423
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 3 ( 2002-03), p. 418-423
    Abstract: Abstract— Coronary artery disease (CAD) is the leading cause of mortality in the developed world. Although several CAD risk factors, including measures of lipid metabolism, obesity, and blood pressure, have a genetic basis, many genes for CAD susceptibility have yet to be identified. Coronary atherosclerosis is the major cause of CAD, but many with coronary atherosclerosis lack symptoms. Thus, a major limitation of using symptomatic CAD endpoints (eg, sudden coronary death, myocardial infarction) as a study outcome is substantial disease misclassification. Coronary artery calcification (CAC) is part of the atherosclerotic process and is an independent predictor of CAD endpoints. In the present study, CAC was noninvasively quantified by electron beam computed tomography. We performed genome-wide multipoint mode-of-inheritance-free linkage analysis on affected sib pairs, defined as being ≥ the 70th sex- and age-specific percentile for CAC quantity, in a sample of 29 families enriched for hypertension. Almost 95% of participants were asymptomatic for CAD. Our LOD score (log 10 odds in favor of linkage) results provide evidence that chromosomal regions 6p21.3 (maximum LOD score=2.22, P =0.00070) and 10q21.3 (maximum LOD score=3.24, P =0.000057) may harbor genes associated with subclinical coronary atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/hq0302.105721
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
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  • 7
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    Autosomal genomewide linkage scan for coronary artery calcification loci.
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 103, No. suppl_1 ( 2001-03), p. 1352-1352
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 103, No. suppl_1 ( 2001-03), p. 1352-1352
    Abstract: P10 Coronary artery calcification (CAC), quantified by electron beam computed tomography, provides a measure of extent of coronary atherosclerosis in asymptomatic and symptomatic individuals. It is well recognized that coronary artery disease and CAC are complex processes that are influenced by many genetic and environmental factors. Several aspects of CAC quantity make genetic studies of it particularly challenging. These include the non-normality of CAC frequency distributions and the strong age- and sex-dependence of CAC levels. To search for regions that may contain genes influencing CAC quantity, a genome-wide scan was conducted on a sample enriched for hypertension from the Epidemiology of Coronary Artery Calcification Study. The genome-wide linkage scan was based on 370 anonymous markers spanning the 22 autosomal chromosomes in 29 families. The analysis sample consisted of 20 affected sib-pairs, 8 affected sib-trios and 1 family with 6 affected siblings. Here, affection status was defined as being above the 70th sex- and age-specific percentile based on a reference population. Mode-of-inheritance-free qualitative linkage analysis was used to analyze sib-pair data. Maximum multipoint lod scores were calculated using the computer software Genehunter-2. Weighted analyses were conducted using Holmans “possible triangle” constraint. The overall maximum lod scores were observed on chromosomes 6 (lod=2.22) and 10 (lod=3.24). Additional lod scores greater than 1.0 were observed on chromosomes 2, 14, 15 and 17. These results identify regions that may harbor genes involved in high sex- and age-specific levels of CAC (supported by HL46292).
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.103.suppl_1.9998-10
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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  • 8
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    Abstract P254: Genome-wide Association and Admixture Study of Iron-related Phenotypes in African Americans
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 129, No. suppl_1 ( 2014-03-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. suppl_1 ( 2014-03-25)
    Abstract: Introduction: Iron deficiency is a heritable risk factor for various serious diseases, including cardiovascular disease (CVD). Genome-wide association studies (GWAS) have identified several variants associated with iron-related phenotypes in individuals of primarily European descent. African Americans (AA) have, on average, greater levels of iron deficiency compared to European Americans, but no large-scale genetic studies for iron-related phenotypes have been performed in individuals of African ancestry to date. Methods: We conducted genome-wide admixture mapping studies and GWASs for serum iron, serum ferritin, transferrin saturation (SAT), and total binding iron capacity (TIBC) in 2347 AA participating in the Jackson Heart Study (JHS). Results: Higher proportions of estimated global African ancestry were significantly associated with lower levels of iron (p=2.4x10 -5 ), SAT (p=0.0019) and TIBC (p=0.042) and a number of chromosomal regions were observed to have local ancestry estimates nominally associated with these measures. We observed significant associations (P 〈 5x10 -8 ) between serum TIBC levels and multiple independent single nucleotide polymorphisms (SNPs) around TF, a well-established region for iron and transferrin levels in Caucasians, and SNPs near two novel genes: HDGFL1 and MAF. In addition, we replicated four other established loci in our AA samples including SLC17A1 , HFE , HIST1H2BJ and TMPRSS6 . Conclusions: 1) We observed SNPs in or near three genes, TF , HDGFL1 and MAF that were significantly associated with TIBC in AA. 2) We observed that both global and local genetic admixture are important predictors of iron measures in AA, further implicating the importance of certain genetic risk factors in the AA population. 3) We have also replicated four other established loci in our AA samples demonstrating the importance of some genetic risk factors for iron related measure across multiple populations. Future fine-mapping studies, incorporating less common variants, and functional studies should be undertaken to better characterize these loci and to ultimately identify the functional variants directly influencing TIBC levels in AA.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.129.suppl_1.p254
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 9
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    Abstract P262: Evidence for association between SH2B1 gene variants and glycated hemoglobin in non-diabetic European American young adults: The Add Health study
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 129, No. suppl_1 ( 2014-03-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. suppl_1 ( 2014-03-25)
    Abstract: Introduction: Glycated hemoglobin (HbA1c) is a marker of long-term glycemic control, and elevated HbA1c is a risk factor for type 2 diabetes and cardiovascular disease. Few genome-wide association studies(GWAS) have been performed for HbA1c, although very large scale GWAS for obesity, a related trait, have identified multiple loci that have been widely replicated. We tested 43 single nucleotide polymorphisms (SNPs) from 41 well-established obesity susceptibility gene regions for association with HbA1c in a nationally representative sample of European American (EA), African American (AA) and Hispanic American (HA) young adults. Methods: We performed association analysis in race-stratified models using data from participants (age 24-34 years, median age=28 years) from the National Longitudinal Study of Adolescent Health (Add Health) Study (n = 5641 EA; n = 1740 AA; n = 1444 HA) without type 2 diabetes. We tested for additive genotype effects at each locus using linear mixed models, including a random intercept for school and family clusters, and two levels of covariate adjustment (model 1: age, sex, smoking, and geographic region; model 2: model 1 covariates plus BMI). We used Bonferroni adjustment for 43 SNPs and considered P 〈 0.0011 to be statistically significant. Results: Means (SD) for HbA1c % across the sample were 5.4(0.3) in EA, 5.7(0.4) in AA, and 5.5(0.3) in HA. We observed significant evidence for association with HbA1c for two SNPs near SH2B1 in EAs (rs4788102, P = 2.2x10-4; rs7359397, P = 9.8x10-4) for the model 1 adjustment, although both results were slightly attenuated after additional adjustment for BMI (rs4788102, P = 1.7x10-3; rs7359397, P = 4.6x10-3). No SNPs reached statistical significance after multiple test correction in either AAs or HAs. SH2B1 rs4788102 was nominally significant in AAs for the BMI-adjusted model (P = 0.02), although the estimated direction of effect was in the opposite direction as that observed in EAs. Conclusions: These results suggest that polymorphisms in the obesity gene SH2B1 , for which rare deletions and mutations have been observed in obese individuals with extremely high insulin resistance, are associated with HbA1c in EA young adults. Our findings further suggest these associations are largely independent of BMI.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.129.suppl_1.p262
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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    Abstract P152: Obesity Susceptibility Loci and Longitudinal BMI from Adolescence to Young Adulthood in an Ethnically Diverse Cohort
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation Vol. 127, No. suppl_12 ( 2013-03-26)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 127, No. suppl_12 ( 2013-03-26)
    Abstract: Genome-wide association (GWA) studies have identi[[Unable to Display Character: & #64257;]]ed nearly 50 common variants for obesity, many of which influence body mass index (BMI), a common proxy for obesity assessed in large epidemiological studies. The associations of these variants with change in BMI across the life course are not well understood, but are of particular interest during the transition from adolescence to young adulthood, a high risk period for weight gain. The current study assessed the association of 41 established obesity SNPs with change in BMI during the period between adolescence and young adulthood in an ethnically diverse, nationally representative cohort, the National Longitudinal Study of Adolescent Health, followed for 13 years. Race/ethnicity-stratified linear mixed models accounted for sampling design, family relatedness, and repeated measures of BMI. Models included a SNP-by-year interaction term and adjusted for sex, age at baseline, current smoking, and geographic region. Analyses included 6383 European American (EA), 2252 African American (AA) and 1700 Hispanic American (HA) participants with measurements from 1996 (ages 12-21 y) to 2008 (ages 24-34 y), with an average of 2.6 observations per individual. For analyses in AA we excluded SNPs (n=14) that failed to capture signal of functional variant in a recent African American population genome-wide association study (Monda et al 2012). Average BMI gain over the 13-year period was 4.9 (SD=5.0) kg/m 2 , with higher increases in AA 5.8 (SD=5.7) kg/m 2 and HA 5.5 (SD=5.6) kg/m 2 . Model results for the 41 SNPs in EA and HA and 27 SNPs in AA suggest that SNP by year interactions show nominal significance (p 〈 0.05) for 12 SNPs in EA, 2 SNPs in HA and 1 SNP in AA. After correction for multiple testing (n=41 tests, p 〈 0.0012), 1 SNP remained significant for EA (rs2287019, near QPCTL ) and none in AA or HA. Each effect allele for rs2287019 contributed an increase of 0.030(SE=0.009) kg/m 2 per year to BMI in EA. These findings suggest that the locus near QPCTL and possibly other obesity loci play a role in the trajectory of BMI across the period from adolescence to young adulthood, a period with high risk for subsequent adult obesity. These findings may help inform the biological processes that influence weight gain at this vulnerable period of the life cycle and may provide information that is useful for the design of effective interventions to prevent weight gain.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.127.suppl_12.AP152
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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