Glycemic control among U.S. Hispanics/Latinos with diabetes from the HCHS/SOL Sociocultural Ancillary Study: Do structural and functional social support play a role?

BACKGROUND: Social support is one potential source of health-related resiliency in Hispanics with diabetes. PURPOSE: This study examined relationships of structural (i.e., social integration) and functional (i.e., perceived) social support with glycemic control (glycosylated hemoglobin; HbA1c) in the Hispanic Community Health Study/Study of Hispanics (HCHS/SOL) Sociocultural Ancillary Study. METHODS: This study included 766 men and women representing multiple Hispanic ethnic backgrounds, aged 18-74 years, with diagnosed diabetes who completed fasting blood draw, medication review, and measures of sociodemographic factors, medical history, structural support (Cohen Social Network Index), and functional support (Interpersonal Support Evaluation List-12). RESULTS: After adjusting for sociodemographic covariates and medication, a one standard deviation increase in functional support was related to an 0.18 % higher HbA1c (p = 0.04). A similar trend was observed for structural support; however, this effect was non-significant in adjusted models. CONCLUSION: Greater functional support was associated with poorer glycemic control in Hispanics

Associations of structural and functional social support with diabetes prevalence in U.S. Hispanics/Latinos: Results from the HCHS/SOL Sociocultural Ancillary Study

BACKGROUND: Little research has examined associations of social support with diabetes (or other physical health outcomes) in Hispanics, who are at elevated risk. PURPOSE: We examined associations between social support and diabetes prevalence in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) Sociocultural Ancillary Study. METHODS: Participants were 5181 adults, 18–74 years old, representing diverse Hispanic backgrounds, who underwent baseline exam with fasting blood draw, oral glucose tolerance test, medication review, sociodemographic assessment, and sociocultural exam with functional and structural social support measures. RESULTS: In adjusted analyses, one standard deviation higher structural and functional social support related to 16% and 15% lower odds, respectively, of having diabetes. Structural and functional support were related to both previously diagnosed diabetes (OR = .84 and .88, respectively) and newly recognized diabetes prevalence (OR = .84 and .83, respectively). CONCLUSIONS: Higher functional and structural social support are associated with lower diabetes prevalence in Hispanics/Latinos

Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: Two genome-wide association studies

We tested whether genetic factors distinctly contribute to either development of coronary atherosclerosis or, specifically, to myocardial infarction in existing coronary atherosclerosis. We did two genome-wide association studies (GWAS) with coronary angiographic phenotyping in participants of European ancestry. To identify loci that predispose to angiographic coronary artery disease (CAD), we compared individuals who had this disorder (n=12 393) with those who did not (controls, n=7383). To identify loci that predispose to myocardial infarction, we compared patients who had angiographic CAD and myocardial infarction (n=5783) with those who had angiographic CAD but no myocardial infarction (n=3644). In the comparison of patients with angiographic CAD versus controls, we identified a novel locus, ADAMTS7 (p=4.98×10-13). In the comparison of patients with angiographic CAD who had myocardial infarction versus those with angiographic CAD but no myocardial infarction, we identified a novel association at the ABO locus (p=7.62×10-9). The ABO association was attributable to the glycotransferase-deficient enzyme that encodes the ABO blood group O phenotype previously proposed to protect against myocardial infarction. Our findings indicate that specific genetic predispositions promote the development of coronary atherosclerosis whereas others lead to myocardial infarction in the presence of coronary atherosclerosis. The relation to specific CAD phenotypes might modify how novel loci are applied in personalised risk assessment and used in the development of novel therapies for CAD. The PennCath and MedStar studies were supported by the Cardiovascular Institute of the University of Pennsylvania, by the MedStar Health Research Institute at Washington Hospital Center and by a research grant from GlaxoSmithKline. The funding and support for the other cohorts contributing to the paper are described in the webappendix. © 2011 Elsevier Ltd

Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies

BACKGROUND: We tested whether genetic factors distinctly contribute to either development of coronary atherosclerosis or, specifically, to myocardial infarction in existing coronary atherosclerosis. METHODS: We did two genome-wide association studies (GWAS) with coronary angiographic phenotyping in participants of European ancestry. To identify loci that predispose to angiographic coronary artery disease (CAD), we compared individuals who had this disorder (n=12,393) with those who did not (controls, n=7383). To identify loci that predispose to myocardial infarction, we compared patients who had angiographic CAD and myocardial infarction (n=5783) with those who had angiographic CAD but no myocardial infarction (n=3644). FINDINGS: In the comparison of patients with angiographic CAD versus controls, we identified a novel locus, ADAMTS7 (p=4\ub798 710(-13)). In the comparison of patients with angiographic CAD who had myocardial infarction versus those with angiographic CAD but no myocardial infarction, we identified a novel association at the ABO locus (p=7\ub762 710(-9)). The ABO association was attributable to the glycotransferase-deficient enzyme that encodes the ABO blood group O phenotype previously proposed to protect against myocardial infarction. INTERPRETATION: Our findings indicate that specific genetic predispositions promote the development of coronary atherosclerosis whereas others lead to myocardial infarction in the presence of coronary atherosclerosis. The relation to specific CAD phenotypes might modify how novel loci are applied in personalised risk assessment and used in the development of novel therapies for CAD. FUNDING: The PennCath and MedStar studies were supported by the Cardiovascular Institute of the University of Pennsylvania, by the MedStar Health Research Institute at Washington Hospital Center and by a research grant from GlaxoSmithKline. The funding and support for the other cohorts contributing to the paper are described in the webappendix