Minority Health and Health Equity Archive

Permanent URI for this collectionhttp://hdl.handle.net/1903/21769

Welcome to the Minority Health and Health Equity Archive (MHHEA), an electronic archive for digital resource materials in the fields of minority health and health disparities research and policy. It is offered as a no-charge resource to the public, academic scholars and health science researchers interested in the elimination of racial and ethnic health disparities.

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Author: search.filters.author.Levy, Daniel

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    Genetic variability of smoking persistence in African Americans.
    (2011) Hamidovic, Ajna; Kasberger, John L; Young, Taylor R; Goodloe, Robert J; Redline, Susan; Buxbaum, Sarah G; Benowitz, Neal L; Bergen, Andrew W; Butler, Kenneth R; Franceschini, Nora; Gharib, Sina A; Hitsman, Brian; Levy, Daniel; Meng, Yan; Papanicolaou, George J; Preis, Sarah R; Spring, Bonnie; Styn, Mindi A; Tong, Elisa K; White, Wendy B; Wiggins, Kerri L; Jorgenson, Eric
    To date, most genetic association analyses of smoking behaviors have been conducted in populations of European ancestry and many of these studies focused on the phenotype that measures smoking quantity, that is, cigarettes per day. Additional association studies in diverse populations with different linkage disequilibrium patterns and an alternate phenotype, such as total tobacco exposure which accounts for intermittent periods of smoking cessation within a larger smoking period as measured in large cardiovascular risk studies, can aid the search for variants relevant to smoking behavior. For these reasons, we undertook an association analysis by using a genotyping array that includes 2,100 genes to analyze smoking persistence in unrelated African American participants from the Atherosclerosis Risk in Communities study. A locus located approximately 4 kb downstream from the 3'-UTR of the brain-derived neurotrophic factor (BDNF) significantly influenced smoking persistence. In addition, independent variants rs12915366 and rs12914385 in the cluster of genes encoding nicotinic acetylcholine receptor subunits (CHRNA5-CHRNA3-CHRNB4) on 15q25.1 were also associated with the phenotype in this sample of African American subjects. To our knowledge, this is the first study to more extensively evaluate the genome in the African American population, as a limited number of previous studies of smoking behavior in this population included evaluations of only single genomic regions.
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    Association of Parental Heart Failure with Risk of Heart Failure in Offspring
    (2006) Lee, Douglas S.; Pencina, Michael J.; Benjamin, Emelia J.; Wang, Thomas J.; Levy, Daniel; O’Donnell, Christopher J.; Nam, Byung-Ho; Larson, Martin G.; D’Agostino, Ralph B.; Vasan, Ramachandran S.
    Background The association between heart failure in parents and the prevalence of left ventricular systolic dysfunction and the risk of heart failure in their offspring has not been investigated in a community-based setting. Methods We examined the cross-sectional association of heart failure in parents with the prevalence of left ventricular systolic dysfunction, as well as left ventricular mass, internal dimensions, and wall thickness, in 1497 participants of the Framingham Offspring Study (mean age, 57 years; 819 women) who underwent routine echocardiography. We also investigated prospectively whether heart failure in parents increased the risk of heart failure in 2214 offspring (mean age, 44 years; 1150 women). Results As compared with the 1039 participants whose parents did not have heart failure, the 458 participants in the cross-sectional cohort who had at least one parent with heart failure were more likely to have increased left ventricular mass (17.0 percent vs. 26.9 percent), left ventricular internal dimensions (18.6 percent vs. 23.4 percent), and left ventricular systolic dysfunction (3.1 percent vs. 5.7 percent); the multivariable- adjusted odds ratios were 1.35 (95 percent confidence interval, 0.99 to 1.84), 1.29 (95 percent confidence interval, 0.96 to 1.72), and 2.37 (95 percent confidence interval, 1.22 to 4.61), respectively. In the longitudinal cohort, heart failure developed in 90 offspring during follow-up (mean length of follow-up, 20 years). The age- and sex adjusted 10-year incidence rates of heart failure were 2.72 percent among offspring with a parent with heart failure, as compared with 1.62 percent among those without a parent with heart failure. This increase in risk persisted after multivariable adjustment (hazard ratio, 1.70; 95 percent confidence interval, 1.11 to 2.60). Conclusions Heart failure in parents is associated with an increased prevalence of left ventricular systolic dysfunction cross-sectionally and an elevated risk of heart failure longitudinally. Our data emphasize the contribution of familial factors to the heart failure burden in the community.