Time filter

Source Type

Li Y.-H.,Key Laboratory for Clinical Cardiovascular Genetics | Li Y.-H.,Peking Union Medical College | Zhou C.-H.,Peking Union Medical College | Pei H.-J.,Peking Union Medical College | And 5 more authors.
Chinese Medical Journal | Year: 2013

Background The association between fish consumption and heart failure (HF) incidence is inconsistent. Methods We performed a systematic search of Pubmed and Embase (from 1953 to June 2012) using key words related to fish and HF. Studies with at least three categories of fish consumption reporting both relative risk (RR) and corresponding 95% confidence interval (CI) for HF incidence were included. The pooled RR and 95%CI were calculated using a fixed or random-effects model. The generalized least squares regression model was used to quantify the dose-response relationship between fish consumption and HF incidence. Results Five prospective cohort studies including 4750 HF events of 170 231 participants with an average of 9.7-year follow-up were selected and identified. Compared with those who never ate fish, individuals with higher fish consumption had a lower HF incidence. The pooled RRs for HF incidence was 0.99 (95%CI, 0.91 to 1.08) for fish consumption 1 to 3 times per month, 0.91 (95%CI, 0.84 to 0.99) for once a week, 0.87 (95%CI, 0.81 to 0.95) for 2 to 4 times per week, and 0.86 (95%CI, 0.84 to 0.99) for 5 or more times per week. An increment of 20 g of daily fish intake was related to a 6% lower risk of HF (RR: 0.94, 95% CI, 0.90 to 0.97; P for trend = 0.001). Conclusions This meta-analysis suggests that there is a dose-dependent inverse relationship between fish consumption and HF incidence. Fish intake once or more times a week could reduce HF incidence.

Jia L.,Key Laboratory for Clinical Cardiovascular Genetics | Jia L.,Peking Union Medical College | Liu X.,Key Laboratory for Clinical Cardiovascular Genetics | Liu X.,Peking Union Medical College | And 9 more authors.
American Journal of Clinical Nutrition | Year: 2010

Background: The effect of cocoa products on lipid changes is controversial. Objectives: We aimed to identify and quantify the effect of cocoa on total cholesterol, LDL cholesterol, and HDL cholesterol. Design: A comprehensive literature search was conducted for relevant trials of cocoa on lipid profile.Weighted mean differences were calculated for net changes in lipid concentrations by using fixed-effects or random-effects models. Previously defined subgroup analyses were performed to identify the source of heterogeneity. Results: Eight trials (involving 215 participants) were included and evaluated. Because there was only one relatively longer-term study, we focused on the short-term data to evaluate the effects of cocoa on plasma lipid. Cocoa consumption significantly lowered LDL cholesterol by 5.87 mg/dL (95% CI: -11.13, -0.61; P< 0.05) and marginally lowered total cholesterol by 5.82 mg/dL (95% CI: -12.39, 0.76; P = 0.08). However, no significant change was seen in LDL cholesterol in high-quality studies (3 studies included; -4.98 mg/dL; 95% CI: -13.18, 3.21; P = 0.23). Subgroup analyses suggested a cholesterol-lowering effect only in those subjects who consumed a low dose of cocoa and with cardiovascular disease risks. There was no evidence of a dose-effect relation, of any effect in healthy subjects, or of any change in HDL cholesterol. Conclusions: Short-term cocoa consumption significantly reduced blood cholesterol, but the changes were dependent on the dose of cocoa consumption and the healthy status of participants. There was no dose response and no effect in healthy participants. Future high-quality studies are needed to determine the efficiency of moderate cocoa consumption on lipid profile in long-term intervention and in subjects with other cardiometabolic risk factors © 2010 American Society for Nutrition.

Li W.,Key Laboratory for Clinical Cardiovascular Genetics | Xu J.,Key Laboratory for Clinical Cardiovascular Genetics | Wang X.,Key Laboratory for Clinical Cardiovascular Genetics | Chen J.,Key Laboratory for Clinical Cardiovascular Genetics | And 3 more authors.
Atherosclerosis | Year: 2010

Objective: Previous case-control studies suggested the single nucleotide polymorphisms of lymphotoxin-α (LTA) gene and galectin-2 (LGASL2) gene are associated with coronary artery disease and myocardial infarction. However, other studies did not confirm this relationship. The objective was to assess the relationship of LTA gene, LGALS2 gene and coronary artery disease, using a meta-analysis. Methods: Databases, including PubMed, EMbase, CBM and CNKI, were searched to get the genetic association studies. Data were extracted by two authors and pooled odds ratio (OR) and 95% confidence interval (CI) were calculated. Result: The meta-analysis included 20640 (LTA-A252G) and 10552 (LGALS2-C3279T) cases, 15388 (A252G) and 10545 (C3279T) controls. The pooled OR of 252G was 1.02 (95%CI: 0.97-1.07) compared to wild type allele in dominant model, and was 1.00 (95%CI: 0.94-1.07) in recessive model. The pooled OR of 3279T was 0.95 (95%CI: 0.89-1.01) compared to wild type allele in dominant model, and was 0.89 (95%CI: 0.78-1.00) in recessive model. None of the polymorphisms was found to associate with coronary artery disease. Conclusion: In present study, the LTA gene and LGALS2-C3279T are not associated with coronary artery disease. © 2009 Elsevier Ireland Ltd. All rights reserved.

Loading Key Laboratory for Clinical Cardiovascular Genetics collaborators
Loading Key Laboratory for Clinical Cardiovascular Genetics collaborators