Hickson D.A.,Jackson Heart Study |
Roux A.V.D.,University of Michigan |
Gebreab S.Y.,University of Michigan |
Wyatt S.B.,University of Mississippi Medical Center |
And 4 more authors.
American Journal of Public Health | Year: 2012
Objectives. We examined the social patterning of cumulative dysregulation of multiple systems, or allostatic load, among African Americans adults. Methods. We examined the cross-sectional associations of socioeconomic status (SES) with summary indices of allostatic load and neuroendocrine, metabolic, autonomic, and immune function components in 4048 Jackson Heart Study participants. Results. Lower education and income were associated with higher allostatic load scores in African American adults. Patterns were most consistent for the metabolic and immune dimensions, less consistent for the autonomic dimension, and absent for the neuroendocrine dimension among African American women. Associations of SES with the global allostatic load score and the metabolic and immune domains persisted after adjustment for behavioral factors and were stronger for income than for education. There was some evidence that the neuroendocrine dimension was inversely associated with SES after behavioral adjustment in men, but the immune and autonomic components did not show clear dose-response trends, and we observed no associations for the metabolic component. Conclusions. Findings support our hypothesis that allostatic load is socially patterned in African American women, but this pattern is less consistent in African American men. Source
Patel S.R.,Brigham and Womens Hospital |
Goodloe R.,Vanderbilt University |
De G.,Harvard University |
Kowgier M.,Samuel Lunenfeld Research Institute |
And 19 more authors.
PLoS ONE | Year: 2012
Although obstructive sleep apnea (OSA) is known to have a strong familial basis, no genetic polymorphisms influencing apnea risk have been identified in cross-cohort analyses. We utilized the National Heart, Lung, and Blood Institute (NHLBI) Candidate Gene Association Resource (CARe) to identify sleep apnea susceptibility loci. Using a panel of 46,449 polymorphisms from roughly 2,100 candidate genes on a customized Illumina iSelect chip, we tested for association with the apnea hypopnea index (AHI) as well as moderate to severe OSA (AHI≥15) in 3,551 participants of the Cleveland Family Study and two cohorts participating in the Sleep Heart Health Study. Among 647 African-Americans, rs11126184 in the pleckstrin (PLEK) gene was associated with OSA while rs7030789 in the lysophosphatidic acid receptor 1 (LPAR1) gene was associated with AHI using a chip-wide significance threshold of p-value<2×10-6. Among 2,904 individuals of European ancestry, rs1409986 in the prostaglandin E2 receptor (PTGER3) gene was significantly associated with OSA. Consistency of effects between rs7030789 and rs1409986 in LPAR1 and PTGER3 and apnea phenotypes were observed in independent clinic-based cohorts. Novel genetic loci for apnea phenotypes were identified through the use of customized gene chips and meta-analyses of cohort data with replication in clinic-based samples. The identified SNPs all lie in genes associated with inflammation suggesting inflammation may play a role in OSA pathogenesis. Source
Riestra P.,Human Genome Research Institutes |
Gebreab S.Y.,Human Genome Research Institutes |
Xu R.,Human Genome Research Institutes |
Khan R.J.,Human Genome Research Institutes |
And 4 more authors.
BMC Medical Genetics | Year: 2015
Background: Despite the important role of adiponectin in regulating general metabolic homeostasis, analysis of genetic determinants of adiponectin and the related cardio-metabolic traits in African American population has been limited and inconsistent. Considering the high genetic admixture of African Americans and thus the important population stratification that may confound the genetic-trait associations, the objective of this work was to perform a comprehensive analysis of the associations between ADIPOQ variants and adiponectin levels and obesity phenotypes in a large African American population from the Jackson Heart Study (JHS) cohort. Methods: Genotype data was available for 2968 JHS participants (1131men; 1837women). Single Nucleotide Polymorphisms (SNPs) were selected by a Tag-SNP Approach and literature review. The genotype imputation was performed using IMPUTE2 software and reference phased data from the 1000G project. PLINK software was used for the genetic analysis. Plasma specimens were analyzed by ELISA for adiponectin levels. All analyses were controlled for population stratification assessed by Individual Proportions of European Ancestry (PEA) estimates calculated in HAPMIX using ancestry informative markers (AIMs). Results: We found a gender-dependent association of some ADIPOQ variants and adiponectin levels. In women four of the studied polymorphisms (rs6444174, rs16861205, rs1403697, rs7641507) were associated with adiponectin levels after Bonferroni correction and controlling for the percentage of PEA, age, annual household income and smoking. These results were consistent with the haplotype analysis. The association between the rs12495941 variant and obesity is modulated by the PEA, so that the relationship between the G allele and a higher incidence of obesity was present in those individuals within the lower PEA group. In addition we found an effect modification of obesity on the association between the ADIPOQ rs6444174 SNP and BMI so that the presence of the T allele was negatively and significantly associated with BMI only in participants with a normal weight. Conclusions: In this large African American cohort, ADIPOQ variants were associated with adiponectin levels in a gender-dependent manner and the relationship of some of these variants with obesity and BMI was modulated by the PEA and obesity status respectively. This suggests that the effects of these polymorphisms on adiponectin and obesity phenotypes are subject to a strong interaction with genetic and environmental factors in African American population. © 2015 Riestra et al. Source
Campbell Jenkins B.W.,Jackson Heart Study |
Sarpong D.F.,Xavier University of Louisiana |
Addison C.,Jackson Heart Study |
White M.S.,Hinds Community College |
And 3 more authors.
International Journal of Environmental Research and Public Health | Year: 2014
This study examined: (a) differences in lung function between current and non current smokers who had sedentary lifestyles and non sedentary lifestyles and (b) the mediating effect of sedentary lifestyle on the association between smoking and lung function in African Americans. Sedentary lifestyle was defined as the lowest quartile of the total physical activity score. The results of linear and logistic regression analyses revealed that non smokers with non sedentary lifestyles had the highest level of lung function, and smokers with sedentary lifestyles had the lowest level. The female non-smokers with sedentary lifestyles had a significantly higher FEV1% predicted and FVC% predicted than smokers with non sedentary lifestyles (93.3% vs. 88.6%; p = 0.0102 and 92.1% vs. 86.9%; p = 0.0055 respectively). FEV1/FVC ratio for men was higher in non smokers with sedentary lifestyles than in smokers with non sedentary lifestyles (80.9 vs. 78.1; p = 0.0048). Though smoking is inversely associated with lung function, it seems to have a more deleterious effect than sedentary lifestyle on lung function. Physically active smokers had higher lung function than their non physically active counterparts. © 2014 by the authors; licensee MDPI, Basel, Switzerland. Source