scholarly journals Racial (black-white) comparisons of the relationship of levels of endogenous sex hormones to serum lipoproteins during male adolescence: the Bogalusa Heart Study.

Circulation ◽  
1986 ◽  
Vol 74 (6) ◽  
pp. 1226-1234 ◽  
Author(s):  
S R Srinivasan ◽  
D S Freedman ◽  
G S Sundaram ◽  
L S Webber ◽  
G S Berenson
Metabolism ◽  
1994 ◽  
Vol 43 (4) ◽  
pp. 470-475 ◽  
Author(s):  
Sathanur R. Srinivasan ◽  
Christian Ehnholm ◽  
Wendy A. Wattigney ◽  
Gerald S. Berenson

2004 ◽  
Vol 89 (3) ◽  
pp. 1240-1245 ◽  
Author(s):  
Katharine H. Mikulec ◽  
Leah Holloway ◽  
Ruth E. Krasnow ◽  
Harold Javitz ◽  
Gary E. Swan ◽  
...  

1987 ◽  
Vol 40 (4) ◽  
pp. 309-318 ◽  
Author(s):  
David S. Freedman ◽  
Sathanur R. Srinivasan ◽  
Larry S. Webber ◽  
Gregory L. Burke ◽  
Gerald S. Berenson

2019 ◽  
Vol 48 (1) ◽  
pp. 79-89 ◽  
Author(s):  
Robert A Philibert ◽  
Meeshanthini V Dogan ◽  
James A Mills ◽  
Jeffrey D Long

Background.—The ability to predict mortality is useful to clinicians, policy makers and insurers. At the current time, prediction of future mortality is still an inexact process with some proposing that epigenetic assessments could play a role in improving prognostics. In past work, we and others have shown that DNA methylation status at cg05575921, a well-studied measure of smoking intensity, is also a predictor of mortality. However, the exact extent of that predictive capacity and its independence of other commonly measured mortality risk factors are unknown. Objective.—To determine the capacity of methylation to predict mortality. Method.—We analyzed the relationship of methylation at cg05575921 and cg04987734, a recently described quantitative marker of heavy alcohol consumption, to mortality in the Offspring Cohort of the Framingham Heart Study using proportional hazards survival analysis. Results.—In this group of participants (n = 2278) whose average age was 66 ± 9 years, we found that the inclusion of both cg05575921 and cg04987734 methylation to a base model consisting of age and sex only, or to a model containing 11 commonly used mortality risk factors, improved risk prediction. What is more, prediction accuracy for the base model plus methylation data was increased compared to the base model plus known predictors of mortality (CHD, COPD, or stroke). Conclusion.—Cg05575921, and to a smaller extent cg04987734, are strong predictors of mortality risk in older Americans and that incorporation of DNA methylation assessments to these and other loci may be useful to population scientists, actuaries and policymakers to better understand the relationship of environmental risk factors, such as smoking and drinking, to mortality.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Wei Chen ◽  
Sathanur R. Srinivasan ◽  
D. Michael Hallman ◽  
Gerald S. Berenson

This study examines the genetic influence ofβ-adrenergic receptor gene polymorphisms (β2-AR Arg16Gly andβ3-AR Trp64Arg) on the relationship of birthweight to longitudinal changes of blood pressure (BP) from childhood to adulthood in 224 black and 515 white adults, aged 21–47 years, enrolled in the Bogalusa Heart Study. Blacks showed significantly lower birthweight and frequencies ofβ2-AR Gly16 andβ3-AR Trp64 alleles and higher BP levels and age-related trends than whites. In multivariable regression analyses using race-adjusted BP and birthweight, low birthweight was associated with greater increase in age-related trend of systolic BP (standardized regression coefficientβ=−0.09,P=.002) and diastolic BP (β=−0.07,P=.037) in the combined sample of blacks and whites, adjusting for the first BP measurement in childhood, sex, age, and gestational age. Adjustment for the current body mass index strengthened the birthweight-BP association. Importantly, the strength of the association, measured as regression coefficients, was modulated by the combination ofβ2-AR andβ3-AR genotypes for systolic (P=.042for interaction) and diastolic BP age-related trend (P=.039for interaction), with blacks and whites showing a similar trend in the interaction. These findings indicate that the intrauterine programming of BP regulation later in life depends onβ-AR genotypes.


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