Nut consumption in relation to all-cause and cause-specific mortality: a meta-analysis 18 prospective studies

2017 ◽  
Vol 8 (11) ◽  
pp. 3893-3905 ◽  
Author(s):  
Guo-Chong Chen ◽  
Ru Zhang ◽  
Miguel A. Martínez-González ◽  
Zeng-Li Zhang ◽  
Marialaura Bonaccio ◽  
...  

Nut consumption is associated with lower all-cause and cause-specific mortality risk and most of the survival benefits may be achieved at a relative low level of nut consumption (about 12 g d−1).

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2350
Author(s):  
Mohsen Mazidi ◽  
Niki Katsiki ◽  
Maciej Banach

Introduction: The links between flavonoid intake and mortality were previously evaluated in epidemiological studies. The aim of the present study was to perform a systematic review and meta-analysis of cohort studies evaluating the link of flavonoid consumption with total and cause-specific mortality. Methods: Prospective cohort studies reporting flavonoid intake and mortality data published up to 30th April 2019 (without language restriction) were searched using PubMed, Scopus and EMBASE database. Generic inverse variance methods and random effects models were used to synthesize pooled and quantitative data. Sensitivity analysis was also performed by a leave-one-out method. Results: Overall, 16 articles met the inclusion criteria (nine studies were performed in Europe, five in the USA, one in Asia and one in Oceania); a total of 462,194 participants (all adults aged >19 years) with 23,473 mortality cases were included in the final analysis. The duration of follow-up ranged from 4.8 to 28 years. Most of the studies assessed flavonoid intake using food frequency questionnaires, whereas four studies used interviews and 1 study used 4-day food records. The meta-analysis showed that flavonoid consumption was inversely and significantly associated with total (relative risk (RR): 0.87, 95% confidence interval (CI) = 0.77–0.99) and cardiovascular disease mortality risk (RR: 0.85, 95%CI = 0.75–0.97), but not cancer (0.86, 95%CI = 0.65–1.14) mortality risk. These findings remained robust in sensitivity analyses. Conclusions: The present findings highlight the potential protective role of flavonoids against total and cause-specific mortality. These results support the recommendations for flavonoid-rich foods intake to prevent chronic diseases.


2020 ◽  
Vol 6 (1) ◽  
pp. e000775
Author(s):  
Juan Pablo Rey Lopez ◽  
Angelo Sabag ◽  
Maria Martinez Juan ◽  
Leandro F M Rezende ◽  
Maria Pastor-Valero

ObjectiveTo examine whether vigorous-intensity physical activity confers additional reductions on all-cause and cause-specific mortality compared with moderate-intensity physical activity.DesignA systematic review (registered in PROSPERO CRD42019138995) and meta-analysis.Data sourcesThree electronic databases up to April 14 2020.Eligibility criteriaInclusion criteria were prospective studies that contained information about (1) moderate-intensity (3–5.9 metabolic equivalent tasks (METs)) and vigorous-intensity (≥6 METs) physical activities and (2) all-cause and/or cause-specific mortality. Exclusion criteria were prospective studies that (1) exclusively recruited diseased patients (eg, hypertensive patients and diabetics) or (2) did not account for total physical activity in their multivariable models (3) or did not adjust or exclude individuals with comorbidities at baseline or (4) used physically inactive participants as reference group.ResultsFive studies (seven cohorts using sex-specific results) were pooled into a meta-analysis. For all-cause mortality and controlling by total physical activity, vigorous-intensity physical activity (vs moderate) was not associated with a larger reduction in mortality (HR 0.95, 95% CI 0.83 to 1.09). After the exclusion of one study judged with critical risk of bias (Risk Of Bias in Non randomized Studies, ROBINS tool) from meta-analysis, results remained similar (HR 0.98, 95% CI 0.85 to 1.12). Due to the limited number of studies, meta-analyses for cancer and cardiovascular mortality were not performed.ConclusionsProspective studies suggest that, for the same total physical activity, both vigorous-intensity and moderate-intensity physical activities reduce all-cause mortality to the same extent. However, absence of evidence must not be interpreted as evidence of absence due to the existing methodological flaws in the literature.


2019 ◽  
Vol 122 (11) ◽  
pp. 1262-1270
Author(s):  
Mohsen Mazidi ◽  
Niki Katsiki ◽  
Dimitri P. Mikhailidis ◽  
Maciej Banach

AbstractLittle is known about the association between dietary choline intake and mortality. We evaluated the link between choline consumption and overall as well as cause-specific mortality by using both individual data and pooling prospective studies by meta-analysis and systematic review. Furthermore, adjusted means of cardiometabolic risk factors across choline intake quartiles were calculated. Data from the National Health and Nutrition Examination Survey (1999–2010) were collected. Adjusted Cox regression was performed to determine the risk ratio (RR) and 95 % CI, as well as random-effects models and generic inverse variance methods to synthesise quantitative and pooling data, followed by a leave-one-out method for sensitivity analysis. After adjustments, we found that individuals consuming more choline had worse lipid profile and glucose homeostasis, but lower C-reactive protein levels (P < 0·001 for all comparisons) with no significant differences in anthropometric parameters and blood pressure. Multivariable Cox regression models revealed that individuals in the highest quartile (Q4) of choline consumption had a greater risk of total (23 %), CVD (33 %) and stroke (30 %) mortality compared with the first quartile (Q1) (P < 0·001 for all comparison). These results were confirmed in a meta-analysis, showing that choline intake was positively and significantly associated with overall (RR 1·12, 95 % CI 1·08, 1·17, I2 = 2·9) and CVD (RR 1·28, 95 % CI 1·17, 1·39, I2 = 9·6) mortality risk. In contrast, the positive association between choline consumption and stroke mortality became non-significant (RR 1·18, 95 % CI 0·97, 1·43, P = 0·092, I2 = 1·1). Our findings shed light on the potential adverse effects of choline intake on selected cardiometabolic risk factors and mortality risk.


BMJ Open ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. e032742 ◽  
Author(s):  
Simiao Tian ◽  
Yazhuo Liu ◽  
Ao Feng ◽  
Keli Lou ◽  
Huimin Dong

IntroductionMetabolically healthy obese phenotype (MHO) refers to obese individuals with an adequate metabolic profile and absence of metabolic syndrome. Many prospective studies have reported the benign condition relating the MHO phenotype and its potential role in reducing risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality. However, inconsistent results were found and the question remains controversial. We aim to conduct a systematic review and meta-analysis to clarify the associations these associations from relevant prospective studies.Methods and analysisThe Preferred Reporting Items for Systematic Reviews and Meta-Analyses for Protocols 2015 statement was used to prepare this protocol. MEDLINE, Web of Science databases, EMBASE and Cochrane Database will be used for literature search from their inception up to December 2019 with restriction of published studies in English. Published prospective studies reporting adjusted relative risk (RR) estimates for the association between MHO phenotype and cardiovascular disease, total cancer, all-cause or cause-specific mortality will be included. The process of study screening, selection and data extraction will be performed independently by two reviewers, and the risk of bias for the studies included will be assessed using the Newcastle-Ottawa Quality Assessment Scale. HRs or RRs for disease events and mortality with 95% CIs will be considered as primary outcomes, and summary HRs/RRs will be pooled using random-effects models. The Cochrane’s Q and the I2statistics will be used to assess and quantify heterogeneity, respectively. Subgroup analysis will also be carried out according to study characteristics to investigate potential sources of heterogeneity.Ethics and disseminationAs this meta-analysis is performed based on the published studies, no ethical approval and patient safety considerations are required. The findings of the study will be reported and submitted to a peer-reviewed journals for publication.PROSPERO registration numberCRD42019121766.


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