scholarly journals Fish Consumption and Coronary Heart Disease: A Meta-Analysis

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2278
Author(s):  
Bo Zhang ◽  
Ke Xiong ◽  
Jing Cai ◽  
Aiguo Ma

Epidemiological studies on the impact of fish consumption on coronary heart disease (CHD) incidence have shown inconsistent results. In addition, in terms of CHD mortality, although previous meta-analyses showed that fish consumption reduces the risk of CHD, six newly incorporated studies show that fish consumption has no impact on CHD. Therefore, the results still need to be verified. The purpose of this study is to quantitatively evaluate the impact of fish consumption on CHD incidence and mortality. Relevant studies were identified from PubMed, Web of Science, and Embase databases up to October 2019. The multivariate-adjusted relative risks (RRs) for the highest versus the lowest fish consumption categories and the 95% confidence intervals were computed with a random-effect model. A restricted cubic spline regression model was used to assess the dose–response relationship between fish consumption and CHD incidence and mortality. Forty prospective cohort studies were incorporated into research. Among them, 22 studies investigated the association between fish consumption and CHD incidence (28,261 cases and 918,783 participants), and the summary estimate showed that higher fish consumption was significantly associated with a lower CHD incidence [RR: 0.91, 95% CI: (0.84, 0.97); I2 = 47.4%]. Twenty-seven studies investigated the association between fish consumption and CHD mortality (10,568 events and 1,139,553 participants), and the summary estimate showed that higher fish intake was significantly associated with a lower CHD mortality [RR: 0.85, 95% CI: (0.77, 0.94); I2 = 51.3%]. The dose–response analysis showed that the CHD incidence and mortality were reduced by 4%, respectively, with a 20 g/day increment in fish consumption. This meta-analysis indicates that fish consumption is associated with a lower CHD incidence and mortality.

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Miao-En Yao ◽  
Peng-Da Liao ◽  
Xu-Jie Zhao ◽  
Lei Wang

Abstract Background Previous clinical studies have suggested that trimethylamine-N-oxide (TMAO) could contribute to the development of atherosclerosis cardiovascular disease. However, the synthetic analysis in coronary heart disease (CHD) was not yet performed. We aimed to clarify the relationship between elevated plasma concentrations of TMAO and the incidence of major adverse cardiovascular events (MACE) in CHD patients. Methods Meta-analysis and dose-response analysis of hazard ratio data from prospective observational studies reporting on the association between TMAO plasma concentrations and the incidence of MACE in patients with CHD were conducted. Results Of the 2369 published articles identified in the search, seven papers, with data from nine cohort studies (10,301 patients), were included in the meta-analysis. Combined data showed that elevated plasma TMAO concentrations could increase 58% higher risk of MACE in patients with CHD (hazard ratios [HR]: 1.58; 95% confidence interval [CI] = 1.35–1.84, P = 0.000). For follow-up ≥ 1 year, it was associated with 62% higher risk of MACE in patients with longer-term than shorter-term (HR for follow-up ≥ 4 years: 1.96; 95% CI = 1.52–2.52 vs one to 3 years: 1.34; 95% CI = 1.26–1.43, P = 0.004). The dose-response analysis revealed a ‘J’ shaped association between TMAO concentration and the incidence of MACE (P = 0.033), with the concentration above 5.1 μmol/L being associated with HR of > 1. Conclusions Elevated levels of TMAO are associated with an increased incidence of MACE in patients with CHD. TMAO concentration of 5.1 μmol/L may be a cut-off value for prognosis.


2020 ◽  
Vol 78 (4) ◽  
pp. 1775-1782
Author(s):  
Nanyang Liu ◽  
Jiahui Sun ◽  
Xiyuan Wang ◽  
Ming Zhao ◽  
Qianqian Huang ◽  
...  

Background: The emergence of the coronavirus disease 2019 (COVID-19) has brought large challenges to dementia patients. We reviewed the existing literature on COVID-19 to assess the incidence and mortality of dementia comorbidities in COVID-19 patients. Objective: To investigate the impact of pre-existing dementia comorbidities on COVID-19. Methods: We searched the PubMed, Embase, and Web of Science databases for patients with preexisting dementia who were diagnosed with COVID-19. The statistical data on the prevalence and mortality of dementia comorbidities were examined. A fixed-or random-effect model was used to calculate the overall pooled risk estimates. Forest plots were generated to show the summarized results. Results: A total of 265 articles were retrieved from the three databases. After removing duplicates and performing two screenings, 10 articles were selected for meta-analysis, including 119,218 participants. Overall, the meta-analysis of the 10 studies showed that the incidence of dementia in COVID-19 patients was (R: 9%, [95% CI: 6% to 13%]). Moreover, the meta-analysis of 9 studies showed that the mortality rate of individuals with dementia after being infected with COVID-19 was higher than that of individuals with no dementia (OR: 5.17 [95% CI: 2.31 to 11.59]). Substantial heterogeneity was observed in this meta-analysis. Significant publication bias was also found. Conclusion: Emerging literature shows that dementia comorbidities are a high risk factor for the prevalence and mortality of COVID-19. Our results should have an impact on preventive interventions and encourage more targeted approaches to prioritize older people with specific risk factors, such as dementia.


2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Mohadeseh Ahmadi ◽  
Bruce Lanphear

Abstract Background Coronary heart disease (CHD), the leading cause of death worldwide, has declined in many affluent countries but it continues to rise in industrializing countries. Objective To quantify the relative contribution of the clinical and population strategies to the decline in CHD mortality in affluent countries. Design Meta-analysis of cross-sectional and prospective studies. Data sources PubMed and Web of Science from January 1, 1970 to December 31, 2019. Method We combined and analyzed data from 22 cross-sectional and prospective studies, representing 500 million people, to quantify the relative decline in CHD mortality attributable to the clinical strategy and population strategy. Result The population strategy accounted for 48% (range = 19 to 73%) of the decline in CHD deaths and the clinical strategy accounted for 42% (range = 25 to 56%), with moderate inconsistency of results across studies. Conclusion Since 1970, a larger fraction of the decline in CHD deaths in industrialized countries was attributable to reduction in CHD risk factors than medical care. Population strategies, which are more cost-effective than clinical strategies, are under-utilized.


2022 ◽  
Vol 8 ◽  
Author(s):  
Chaoxiu Li ◽  
Wenying Wu ◽  
Yumeng Song ◽  
Shuang Xu ◽  
Xiaomei Wu

Background: Evidence suggests that the total bilirubin has a protective effect on coronary heart disease (CHD), but the dose-response relationship remains controversial, and there is no meta-analysis to assess the relationship.Methods: As of October 1, 2021, relevant literature was selected from four databases (PubMed, Web of Science, Cochrane Library, and Embase) by using a retrieval strategy. The dose-response curve between the total bilirubin and CHD was fitted by a restricted cubic spline. Stata 12.0 was used for statistical analysis.Results: A total of 170,209 (6,342 cases) participants from 7 prospective studies were analyzed in our meta-analysis. We calculated the pooled relative risks (RRs) and 95% CIs for the association between serum bilirubin level and risk of CHD using random-effects models. Compared with the first quantile, the bilirubin level in the third quantile had a protective effect on the risk of CHD (RR, 0.90; 95% CI, 0.82–0.99). The restricted cubic spline functions depicted a U-type curve relationship between bilirubin (3.42–49 μmol/L) and CHD (Plinear < 0.001). When the bilirubin level was in the range of 3.42–13μmol/L, the protective effect of bilirubin on CHD was enhanced with increasing bilirubin levels. When the bilirubin level exceeded 13μmol/L, the protective effect of bilirubin weakened, and a dangerous effect gradually appeared with further increases in bilirubin levels.Conclusions: Compared with a low bilirubin level, a high bilirubin level has a protective effect on the risk of CHD, and there was a U-shaped dose-response relationship between them.


2014 ◽  
Vol 76 (1) ◽  
pp. 44-57 ◽  
Author(s):  
Frank Doyle ◽  
Daniela Rohde ◽  
Aleksandra Rutkowska ◽  
Karen Morgan ◽  
Grainne Cousins ◽  
...  

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