Akinkuolie A.O.,Boston University |
Ngwa J.S.,Boston University |
Meigs J.B.,Massachusetts General Hospital |
Meigs J.B.,Harvard University |
And 3 more authors.
Clinical Nutrition | Year: 2011
Background &aim: n-3 PUFA has been shown to decrease the risk of several components of the metabolic syndrome; however, the role of n-3 PUFA on glucose metabolism is not clear. Our aim was to systematically review the effect of n-3 PUFA on IS by conducting a meta-analysis of available RCTs. Methods: We followed the guidelines of Cochrane's review of systematic interventions. We searched MEDLINE, EMBASE, CENTRAL and clinicaltrials.gov from the beginning of each database until October 2010. Meta-analysis was performed using a random effects model to estimate a pooled SMD and the corresponding 95% CI. Results: From 303 screened citations, 11 RCTs (n = 618) were eligible for inclusion in the analysis. In a pooled estimate, n-3 PUFA intervention had no effects on IS compared to placebo (SMD 0.08, 95% CI -0.11-0.28). Similarly, n-3 PUFA had no effects on IS in sub-group analyses (Type 2 diabetes vs. other population; QUICKI and other test subgroups). In the HOMA subgroup, n-3 PUFA was associated with a statistically significant increase in IS (SMD 0.30, CI 0.03-0.58) when compared to placebo. Conclusion: This meta-analysis is consistent with a lack of n-3 PUFA effects on IS. © 2011 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. Source
Rahilly-Tierney C.R.,Massachusetts Veterans Epidemiology and Information Research Center |
Rahilly-Tierney C.R.,Brigham and Womens Hospital |
Rahilly-Tierney C.R.,Harvard University |
Arnett D.K.,University of Alabama at Birmingham |
And 12 more authors.
Lipids in Health and Disease | Year: 2011
Background: We sought to examine whether 4 carrier status modifies the relation between body mass index (BMI) and HDL. The National Heart, Lung, and Blood Institute Family Heart Study included 657 families with high family risk scores for coronary heart disease and 588 randomly selected families of probands in the Framingham, Atherosclerosis Risk in Communities, and Utah Family Health Tree studies. We selected 1402 subjects who had 4 carrier status available. We used generalized estimating equations to examine the interaction between BMI and 4 allele carrier status on HDL after adjusting for age, gender, smoking, alcohol intake, mono- and poly-unsaturated fat intake, exercise, comorbidities, LDL, and family cluster. Results: The mean (standard deviation) age of included subjects was 56.4(11.0) years and 47% were male. Adjusted means of HDL for normal, overweight, and obese BMI categories were 51.2( 0.97), 45.0( 0.75), and 41.6( 0.93), respectively, among 397 4 carriers (p for trend < 0.0001) and 53.6( 0.62), 51.3( 0.49), and 45.0( 0.62), respectively, among 1005 non-carriers of the 4 allele (p-value for trend < 0.0001). There was no evidence for an interaction between BMI and 4 status on HDL(p-value 0.39). Conclusion: Our findings do not support an interaction between 4 allele status and BMI on HDL. © 2011 Rahilly-Tierney et al; licensee BioMed Central Ltd. Source
Rahilly-Tierney C.,Massachusetts Veterans Epidemiology and Information Research Center |
Rahilly-Tierney C.,Brigham and Womens Hospital |
Sesso H.D.,Brigham and Womens Hospital |
Djousse L.,Massachusetts Veterans Epidemiology and Information Research Center |
And 3 more authors.
American Heart Journal | Year: 2011
Background: Although cross-sectional studies have identified lifestyle factors associated with high-density lipoprotein cholesterol (HDL-C), no studies have examined the association between changes in lifestyle factors and long-term changes in HDL-C. Methods: We examined the association between changes in lifestyle factors and changes in HDL-C over a 14-year period in a cohort of 4,168 US male physicians, followed up between 1982 and 1997 and with HDL-C measured at both time points. Using linear regression, we examined the association between HDL-C change and categorized changes in alcohol consumption, physical activity, body mass index (BMI), and smoking, adjusting for age, baseline HDL-C, and other covariates. Results: Stable BMI of <25 kg/m 2 or BMI reduction from ≥25 to <25 kg/m2 were associated with increases in HDL-C of 3.1 to 4.7 mg/dL over 14 years. Alcohol consumption of ≥1 drink daily or increase in alcohol consumption from <1 to ≥1 drink daily was associated with increases in HDL-C of 2.4 to 3.3 mg/dL over 14 years. Adopting a sedentary lifestyle was associated with decreases in 14-year decreases in HDL-C. Conclusion: These findings suggest that reductions in BMI and increases in alcohol consumption are associated with 14-year increases in HDL-C, whereas decreases in physical activity are associated with 14-year decreases in HDL-C. © 2011, Mosby, Inc. All rights reserved. Source