α-Linolenic Acid and Risk of Heart Failure: A Meta-Analysis.
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SUBMITTER: Wu J
PROVIDER: S-EPMC8764440 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPrior studies of α-linolenic acid (ALA), a plant-derived omega-3 (n-3) fatty acid, and cardiovascular disease (CVD) risk have generated inconsistent results.ObjectiveWe conducted a meta-analysis to summarize the evidence regarding the relation of ALA and CVD risk.DesignWe searched multiple electronic databases through January 2012 for studies that reported the association between ALA (assessed as dietary intake or as a biomarker in blood or adipose tissue) and CVD risk in prospective and retrospective studies. We pooled the multivariate-adjusted RRs comparing the top with the bottom tertile of ALA using random-effects meta-analysis, which allowed for between-study heterogeneity.ResultsTwenty-seven original studies were identified, including 251,049 individuals and 15,327 CVD events. The overall pooled RR was 0.86 (95% CI: 0.77, 0.97; I² = 71.3%). The association was significant in 13 comparisons that used dietary ALA as the exposure (pooled RR: 0.90; 95% CI: 0.81, 0.99; I² = 49.0%), with similar but nonsignificant trends in 17 comparisons in which ALA biomarkers were used as the exposure (pooled RR: 0.80; 95% CI: 0.63, 1.03; I² = 79.8%). An evaluation of mean participant age, study design (prospective compared with retrospective), exposure assessment (self-reported diet compared with biomarker), and outcome [fatal coronary heart disease (CHD), nonfatal CHD, total CHD, or stroke] showed that none were statistically significant sources of heterogeneity.ConclusionsIn observational studies, higher ALA exposure is associated with a moderately lower risk of CVD. The results were generally consistent for dietary and biomarker studies but were not statistically significant for biomarker studies. However, the high unexplained heterogeneity highlights the need for additional well-designed observational studies and large randomized clinical trials to evaluate the effects of ALA on CVD.
| S-EPMC3497923 | biostudies-literature
Project description:BackgroundFew studies have evaluated the association between the n-3 fatty acid α-linolenic acid (ALA) and the incidence of congestive heart failure (CHF).ObjectiveWe investigated whether plasma phospholipid concentrations and estimated dietary consumption of ALA are associated with incident CHF.DesignWe used data from the Cardiovascular Health Study, a prospective cohort study of cardiovascular diseases among adults aged ≥65 y, from 4 US communities. A total of 2957 participants free of prevalent heart disease and with available fatty acid measurements were included in biomarker analyses (30,722 person-years and 686 incident CHF events). A total of 4432 participants free of prevalent heart disease were included in dietary analyses (52,609 person-years and 1072 events). We investigated the association of ALA with incident CHF by using Cox regression.ResultsAfter adjustment for age, sex, race, education, smoking status, BMI, waist circumference, and alcohol consumption, plasma phospholipid ALA was not associated with incident CHF (HR for the highest compared with the lowest quartile: 0.97; 95% CI: 0.79, 1.21; P-trend = 0.85). Likewise, dietary ALA was not associated with incident CHF (adjusted HR for the highest compared with the lowest quartile: 0.96; 95% CI: 0.82, 1.20; P-trend = 0.97). We observed no association of biomarker or dietary ALA with nonvalvular CHF subtype. We also found little evidence of an association between ALA and CHF in subgroups based on age, sex, diabetes, fish consumption, BMI, or FADS2 genotype (rs1535).ConclusionALA intake is not associated with incident CHF in older adults. This trial was registered at clinicaltrials.gov as NCT00005133.
| S-EPMC3396442 | biostudies-literature
Project description:Objectives: A systematic review and meta-analysis was performed to evaluate the potential prognostic role of serum uric acid (SUA) in patients with chronic heart failure (CHF). Methods: The Embase, PubMed, Web of Science and Cochrane Library databases were searched up to 5 April 2021 for relevant publications. Random effects model was used to pool data. STATA15.0 software was used to perform meta-analysis. Heterogeneity was assessed using the Cochran Q statistic (significance level of P < 0.10) and I 2 statistics (significance level of 50%). Results: Ultimately, 18 publications reporting adverse events in CHF patients were included. The results indicate reveal associations between a high level of SUA and the risk of all-cause mortality (HR 2.24, 95% CI 1.49-3.37), cardiovascular mortality (HR 1.14, 95% CI 1.06-1.23), and the composite of death or cardiac events (HR 1.26, 95% CI 1.01-1.56) in CHF patients. A 1 mg/dL increase in serum uric acid led to 4% (HR 1.04, 95% CI 1.02-1.05) and 9% (HR 1.09, 95% CI 1.03-1.17) increases in the risk of all-cause mortality and the composite endpoint of death or cardiac events in CHF patients, respectively. Conclusion: Serum uric acid is positively associated with the risk of adverse events in CHF patients. This study protocol has been registered at PROSPERO as CRD42021247084 (https://www.crd.york.ac.uk/PROSPERO). Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO.
| S-EPMC8715937 | biostudies-literature
Project description:Background: The association between α-linolenic acid (ALA) and mortality is inconsistent and has not been summarized systematically. Objective: The purpose was to conduct a meta-analysis that synthesized the results of prospective cohort studies to investigate associations between ALA intake and mortality. Methods: We conducted a comprehensive search on PubMed, Embase, and Web of Science databases on May 1, 2021, for relevant prospective cohort studies which reported associations of ALA (assessed by dietary surveys and/or ALA concentrations in body tissues) with mortality from all-cause, cardiovascular disease (CVD), and other diseases. Multivariable-adjusted relative risks (RRs) were pooled by a random or fixed-effects model. Results: A total of 34 prospective cohort studies, of which 17 reported dietary ALA intake, 14 for ALA biomarkers, and the remaining 3 reported both of intake and biomarkers. The studies included 6,58,634 participants, and deaths were classified into all-cause mortality (56,898), CVD mortality (19,123), and other diseases mortality (19,061). Pooled RRs of ALA intake were 0.93 (95% CI: 0.86, 1.01, I 2 = 71.2%) for all-cause mortality, 0.90 (95% CI: 0.83, 0.98, I 2 = 22.1%) for CVD mortality, and 0.94 (95% CI: 0.83, 1.06, I 2 = 73.3%) for other diseases mortality. The two-stage random-effects dose-response analysis showed a linear relationship between dietary ALA intake and CVD-mortality and each 0.5% energy increment of ALA intake was associated with a 5% lower risk of CVD-mortality (RR: 0.95; 95% CI: 0.90, 1.00). Pooled RRs per SD increment of ALA biomarkers were 0.99 (95% CI: 0.96, 1.01, I 2 = 27%) for all-cause mortality, 1.00 (95% CI: 0.98, 1.03, I 2 = 0%) for CVD mortality and 0.98 (95% CI: 0.95, 1.01, I 2 = 0%) for other diseases mortality. Conclusions: This meta-analysis summarizing the available prospective cohort studies indicated that ALA intake was associated with reduced risk of mortality, especially CVD mortality. Our findings suggest that ALA consumption may be beneficial for death prevention. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO; identifier: CRD42021264532.
| S-EPMC8595337 | biostudies-literature
Project description:The intake of the mainly plant-derived n-3 PUFA α-linolenic acid (ALA) has been reported to be associated with a lower risk of CHD. However, the results have been inconsistent. Therefore, the objective of the present study was to examine the association between the intake of ALA and the risk of CHD. Potential effect modification by the intake of long-chain n-3 PUFA (n-3 LCPUFA) was also investigated. Data from eight American and European prospective cohort studies including 148 675 women and 80 368 men were used. The outcome measure was incident CHD (CHD event and death). During 4-10 years of follow-up, 4493 CHD events and 1751 CHD deaths occurred. Among men, an inverse association (not significant) between the intake of ALA and the risk of CHD events and deaths was observed. For each additional gram of ALA consumed, a 15 % lower risk of CHD events (hazard ratios (HR) 0·85, 95 % CI 0·72, 1·01) and a 23 % lower risk of CHD deaths (HR 0·77, 95 % CI 0·58, 1·01) were observed. No consistent association was observed among women. No effect modification by the intake of n-3 LCPUFA was observed.
| S-EPMC4301411 | biostudies-literature
Project description:BACKGROUND: Early treatment may alter progression to overt heart failure (HF) in asymptomatic individuals with stage B HF (SBHF). However, the identification of patients with SBHF is difficult. This systematic review sought to examine the strength of association of clinical factors with incident HF, with the intention of facilitating selection for HF screening. METHODS: Electronic databases were systematically searched for studies reporting risk factors for incident HF. Effect sizes, typically HRs, of each risk variable were extracted. Pooled crude and adjusted HRs with 95% CIs were computed for each risk variable using a random-effects model weighted by inverse variance. RESULTS: Twenty-seven clinical factors were identified to be associated with risk of incident HF in 15 observational studies in unselected community populations which followed 456 850 participants over 4-29 years. The strongest independent associations for incident HF were coronary artery disease (HR=2.94; 95% CI 1.36 to 6.33), diabetes mellitus (HR=2.00; 95% CI 1.68 to 2.38), age (HR (per 10 years)=1.80; 95% CI 1.13 to 2.87) followed by hypertension (HR=1.61; 95% CI 1.33 to 1.96), smoking (HR=1.60; 95% CI 1.45 to 1.77), male gender (HR=1.52; 95% CI 1.24 to 1.87) and body mass index (HR (per 5 kg/m(2))=1.15; 95% CI 1.06 to 1.25). Atrial fibrillation (HR=1.88; 95% CI 1.60 to 2.21), left ventricular hypertrophy (HR=2.46; 95% CI 1.71 to 3.53) and valvular heart disease (HR=1.74; 95% CI 1.07 to 2.84) were also strongly associated with incident HF but were not examined in sufficient papers to provide pooled hazard estimates. CONCLUSIONS: Prediction of incident HF can be calculated from seven common clinical variables. The risk associated with these may guide strategies for the identification of high-risk people who may benefit from further evaluation and intervention.
| S-EPMC4395833 | biostudies-other
Project description:Objective?-Linolenic acid (ALA) is considered to be a cardioprotective nutrient; however, some epidemiological studies have suggested that dietary ALA intake increases the risk of prostate cancer. The main objective was to conduct a systematic review and meta-analysis of case-control and prospective studies investigating the association between dietary ALA intake and prostate cancer risk.DesignA systematic review and meta-analysis were conducted by searching MEDLINE and EMBASE for relevant prospective and case-control studies.Included studiesWe included all prospective cohort, case-control, nested case-cohort and nested case-control studies that investigated the effect of dietary ALA intake on the incidence (or diagnosis) of prostate cancer and provided relative risk (RR), HR or OR estimates.Primary outcome measureData were pooled using the generic inverse variance method with a random effects model from studies that compared the highest ALA quantile with the lowest ALA quantile. Risk estimates were expressed as RR with 95% CIs. Heterogeneity was assessed by ?(2) and quantified by I(2).ResultsData from five prospective and seven case-control studies were pooled. The overall RR estimate showed ALA intake to be positively but non-significantly associated with prostate cancer risk (1.08 (0.90 to 1.29), p=0.40; I(2)=85%), but the interpretation was complicated by evidence of heterogeneity not explained by study design. A weak, non-significant protective effect of ALA intake on prostate cancer risk in the prospective studies became significant (0.91 (0.83 to 0.99), p=0.02) without evidence of heterogeneity (I(2)=8%, p=0.35) on removal of one study during sensitivity analyses.ConclusionsThis analysis failed to confirm an association between dietary ALA intake and prostate cancer risk. Larger and longer observational and interventional studies are needed to define the role of ALA and prostate cancer.
| S-EPMC3657642 | biostudies-literature
Project description:Although dietary α-linolenic acid (ALA) or linolenic acid (LA) intake was reported to be epidemiologically associated with a lower prevalence of hypertension, recent clinical trials have yielded conflicting results. Comparable experimental evidence for the roles of these two different fatty acids is still lacking and the underlying mechanisms need to be further elucidated. Our data showed that ALA but not LA supplementation alleviated systolic blood pressure elevation and improved ACh-induced, endothelium-dependent vasodilation in both spontaneously hypertensive rats (SHRs) and AngII-induced hypertensive mice. In addition, SHRs displayed reduced vascular Sirtuin 3 (SIRT3) expression, subsequent superoxide dismutase 2 (SOD2) hyperacetylation and mitochondrial ROS overproduction, all of which were ameliorated by ALA but not LA supplementation. In primary cultured endothelial cells, ALA treatment directly inhibited SIRT3 reduction, SOD2 hyperacetylation, mitochondrial ROS overproduction and alleviated autophagic flux impairment induced by AngII plus TNFα treatment. However, these beneficial effects of ALA were completely blocked by silencing SIRT3. Restoration of autophagic flux by rapamycin also inhibited mitochondrial ROS overproduction in endothelial cells exposed to AngII plus TNFα. More interestingly, SIRT3 KO mice developed severe hypertension in response to a low dose of AngII infusion, while ALA supplementation lost its anti-hypertensive and endothelium-protective effects on these mice. Our findings suggest that ALA but not LA supplementation improves endothelial dysfunction and diminishes experimental hypertension by rescuing SIRT3 impairment to restore autophagic flux and mitochondrial redox balance in endothelial cells.
| S-EPMC6997421 | biostudies-literature
Project description:Overweight and obesity are highly prevalent worldwide and are associated with cardiovascular disease (CVD) risk factors, including systematic inflammation, dyslipidemia, and hypertension. Alpha-linolenic acid (ALA) is a plant-based essential polyunsaturated fatty acid associated with reduced CVD risks. This systematic review and meta-analysis aimed to investigate the effects of supplementation with ALA compared with the placebo on CVD risk factors in people with obesity or overweight (International Prospective Register of Systematic Reviews Registration No. CRD42023429563). This review included studies with adults using oral supplementation or food or combined interventions containing vegetable sources of ALA. All studies were randomly assigned trials with parallel or crossover designs. The Cochrane Collaboration tool was used for assessing the risk of bias (Version 1). PubMed, Web of Science, Embase, and Cochrane library databases were searched from inception to April 2023. Nineteen eligible randomized controlled trials, including 1183 participants, were included in the meta-analysis. Compared with placebo, dietary ALA supplementation significantly reduced C-reactive protein concentration (standardized mean difference [SMD] = -0.38 mg/L; 95% confidence interval [CI]: -0.72, -0.04), tumor necrosis factor-α concentration (SMD = -0.45 pg/mL; 95% CI: -0.73, -0.17), triglyceride in serum (SMD = -4.41 mg/dL; 95% CI: -5.99, -2.82), and systolic blood pressure (SMD = -0.37 mm Hg; 95% CI: -0.66, -0.08); but led to a significant increase in low-density lipoprotein cholesterol concentrations (SMD = 1.32 mg/dL; 95% CI: 0.05, 2.59). ALA supplementation had no significant effect on interleukin-6, diastolic blood pressure, total cholesterol, or high-density lipoprotein cholesterol (all P ≥ 0.05). Subgroup analysis revealed that ALA supplementation at a dose of ≥3 g/d from flaxseed and flaxseed oil had a more prominent effect on improving CVD risk profiles, particularly where the intervention duration was ≥12 wk and where the baseline CVD profile was poor.
| S-EPMC10721518 | biostudies-literature
Project description:BACKGROUND:There are differences among the outcomes regarding cognitive impairment in heart failure (HF) because the evidence is fragmented and sample size is small. Therefore we aimed to systematically review and analyze the available evidence about the association between HF and dementia. METHODS:In the present study, we searched for articles published until August 2019 in the following databases: PubMed, Web of Science, EMBASE, Medline and Google Scholar. The pooled multivariate odds ratio (OR) or relative risk (RR) and 95% confidence intervals (CI) were obtained by the use of STATA 12.0 software. RESULTS:The meta-analysis showed a positive association between HF and risk of all-cause dementia (OR/RR?=?1.28, 95% CI 1.15 to 1.43, I?=?70.0%, P?<?0.001). Additionally, the study showed no significant association between HF and risk of Alzheimer's disease (AD) (OR/RR?=?1.38, 95% CI 0.90 to 2.13, I?=?74.8%, P?=?0.008). CONCLUSION:In conclusion, HF was associated with an increased risk of developing dementia. In addition, large scale prospective studies are essential to explore the associations between HF and risk of AD.
| S-EPMC7004760 | biostudies-literature