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Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.

ABSTRACT: Previous studies on intake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective cohort studies to summarize the evidence regarding the relation of dietary LA intake and CHD risk.We searched MEDLINE and EMBASE databases through June 2013 for prospective cohort studies that reported the association between dietary LA and CHD events. In addition, we used unpublished data from cohort studies in a previous pooling project. We pooled the multivariate-adjusted relative risk (RR) to compare the highest with the lowest categories of LA intake using fixed-effect meta-analysis. We identified 13 published and unpublished cohort studies with a total of 310?602 individuals and 12?479 total CHD events, including 5882 CHD deaths. When the highest category was compared with the lowest category, dietary LA was associated with a 15% lower risk of CHD events (pooled RR, 0.85; 95% confidence intervals, 0.78-0.92; I(2)=35.5%) and a 21% lower risk of CHD deaths (pooled RR, 0.79; 95% confidence intervals, 0.71-0.89; I(2)=0.0%). A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events (RR, 0.91; 95% confidence intervals, 0.87-0.96) and a 13% lower risk of CHD deaths (RR, 0.87; 95% confidence intervals, 0.82-0.94).In prospective observational studies, dietary LA intake is inversely associated with CHD risk in a dose-response manner. These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD.

SUBMITTER: Farvid MS

PROVIDER: S-EPMC4334131 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature

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Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.

Farvid Maryam S MS Ding Ming M Pan An A Sun Qi Q Chiuve Stephanie E SE Steffen Lyn M LM Willett Walter C WC Hu Frank B FB

Circulation 20140826 18

<h4>Background</h4>Previous studies on intake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective cohort studies to summarize the evidence regarding the relation of dietary LA intake and CHD risk.<h4>Methods and results</h4>We searched MEDLINE and EMBASE databases through June 2013 for prospective cohort studies that reported the association between diet ...[more]

PMID: 25161045

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Project description:BackgroundCurrent evidence on associations between intakes of linoleic acid (LA), the predominant n-6 (ω-6) fatty acid, and mortality is inconsistent and has not been summarized by a systematic review and meta-analysis.ObjectiveThe aim was to perform a systematic review and meta-analysis of prospective cohort studies to examine associations between LA intake and mortality.MethodsWe conducted a comprehensive search of MEDLINE and EMBASE databases through 31 July 2019 for prospective cohort studies reporting associations of LA (assessed by dietary surveys and/or LA concentrations in adipose tissue or blood compartments) with mortality from all causes, cardiovascular disease (CVD), and cancer. Multivariable-adjusted RRs were pooled using random-effects meta-analysis.ResultsThirty-eight studies reporting 44 prospective cohorts were identified; these included 811,069 participants with dietary intake assessment (170,076 all-cause, 50,786 CVD, and 59,684 cancer deaths) and 65,411 participants with biomarker measurements (9758 all-cause, 6492 CVD, and 1719 cancer deaths). Pooled RRs comparing extreme categories of dietary LA intake (high vs low) were 0.87 (95% CI: 0.81, 0.94; I2 = 67.9%) for total mortality, 0.87 (95% CI: 0.82, 0.92; I2 = 3.7%) for CVD mortality, and 0.89 (95% CI: 0.85, 0.93; I2 = 0%) for cancer mortality. Pooled RRs for each SD increment in LA concentrations in adipose tissue/blood compartments were 0.91 (95% CI: 0.87, 0.95; I2 = 64.1%) for total mortality, 0.89 (95% CI: 0.85, 0.94; I2 = 28.9%) for CVD mortality, and 0.91 (95% CI: 0.84, 0.98; I2 = 26.3%) for cancer mortality. Meta-regressions suggested baseline age and dietary assessment methods as potential sources of heterogeneity for the association between LA and total mortality.ConclusionsIn prospective cohort studies, higher LA intake, assessed by dietary surveys or biomarkers, was associated with a modestly lower risk of mortality from all causes, CVD, and cancer. These data support the potential long-term benefits of PUFA intake in lowering the risk of CVD and premature death.

Project description:ObjectiveTo clarify the role of dietary carbohydrate, glycemic index (GI), and glycemic load (GL) in progression from health to coronary heart disease (CHD) by determining disease-nutrient risk relation (RR) values needed for intake ranges within jurisdictions and across the globe.MethodsWe performed a literature search of MEDLINE and EMBASE for prospective cohort studies that used truly valid dietary instruments in heathy adults published from January 1, 2000, to June 5, 2018. Relevant observations were extracted by 2 reviewers independently. We used dose-response meta-analysis accounting for nonindependence of results within studies. Bradford-Hill criteria were used to assess causality.ResultsEligible studies had a mean follow-up of 11 years (range, 5-19 years), were conducted in North America, Europe, and East Asia, and yielded combined RRs of 1.44 (95% CI, 1.25-1.65) per 65 g/d GL (11 studies) and 1.24 (95% CI, 1.12-1.38) per 10 U GI (10 studies) (glucose scale). The CHD-carbohydrate RR on GI was 1.66 (95% CI, 1.23-2.25) per 98 g/d of carbohydrates per 10 units GI. The 65 g/d GL, 10 U GI, and 98 g/d carbohydrate values corresponded to oral intakes from the 10th to the 90th percentiles within sampled populations. Inconsistencies were minor (I 2 ≤20%), as were small-study effects (P=.61 for GL and P=.26 for GI). Funnel plots were symmetric. Cubic spline dose-response meta-analysis yielded RRs as follows: across the global range for GL (55-290 g/d), 5.5 (95% CI, 3.1-9.8) (I 2 =0); for GI (47-82 U), 2.71 (95% CI, 1.47-4.40) (I 2 =0); and for the CHD-carbohydrate dependence on GI (50-80 U), 4.57 (95% CI, 1.86-11.4) (I 2 =16%). Bradford-Hill criteria indicated that these relations were probably causal.ConclusionStrong and probably causal CHD-GL and GI RRs exist within populations. The RRs were remarkably higher across global exposures. The results support the consideration of these markers of carbohydrate food quality in dietary guidelines for general populations.Trial registrationPROSPERO Identifier: CRD42013004504.

Project description:ObjectiveTo evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death.DesignEvaluation of recovered data from the Sydney Diet Heart Study, a single blinded, parallel group, randomized controlled trial conducted in 1966-73; and an updated meta-analysis including these previously missing data.SettingAmbulatory, coronary care clinic in Sydney, Australia.Participants458 men aged 30-59 years with a recent coronary event.InterventionsReplacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). Controls received no specific dietary instruction or study foods. All non-dietary aspects were designed to be equivalent in both groups.Outcome measuresAll cause mortality (primary outcome), cardiovascular mortality, and mortality from coronary heart disease (secondary outcomes). We used an intention to treat, survival analysis approach to compare mortality outcomes by group.ResultsThe intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).ConclusionsAdvice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.Trial registrationClinical trials NCT01621087.

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.

Project description:ObjectiveTo investigate and quantify the potential dose-response association between egg consumption and risk of coronary heart disease and stroke.DesignDose-response meta-analysis of prospective cohort studies.Data sourcesPubMed and Embase prior to June 2012 and references of relevant original papers and review articles.Eligibility criteria for selecting studiesProspective cohort studies with relative risks and 95% confidence intervals of coronary heart disease or stroke for three or more categories of egg consumption.ResultsEight articles with 17 reports (nine for coronary heart disease, eight for stroke) were eligible for inclusion in the meta-analysis (3,081,269 person years and 5847 incident cases for coronary heart disease, and 4,148,095 person years and 7579 incident cases for stroke). No evidence of a curve linear association was seen between egg consumption and risk of coronary heart disease or stroke (P=0.67 and P=0.27 for non-linearity, respectively). The summary relative risk of coronary heart disease for an increase of one egg consumed per day was 0.99 (95% confidence interval 0.85 to 1.15; P=0.88 for linear trend) without heterogeneity among studies (P=0.97, I(2)=0%). For stroke, the combined relative risk for an increase of one egg consumed per day was 0.91 (0.81 to 1.02; P=0.10 for linear trend) without heterogeneity among studies (P=0.46, I(2)=0%). In a subgroup analysis of diabetic populations, the relative risk of coronary heart disease comparing the highest with the lowest egg consumption was 1.54 (1.14 to 2.09; P=0.01). In addition, people with higher egg consumption had a 25% (0.57 to 0.99; P=0.04) lower risk of developing hemorrhagic stroke.ConclusionsHigher consumption of eggs (up to one egg per day) is not associated with increased risk of coronary heart disease or stroke. The increased risk of coronary heart disease among diabetic patients and reduced risk of hemorrhagic stroke associated with higher egg consumption in subgroup analyses warrant further studies.

Project description:BackgroundInsulin resistance is a precursor of numerous chronic diseases, including cardiovascular disease (CVD). The fasting insulin concentration is considered a reasonable surrogate of insulin resistance, especially among nondiabetic individuals.ObjectiveWe aimed to quantitatively summarize the literature on the association of fasting insulin concentrations with risk of hypertension, stroke, and coronary heart disease (CHD) by conducting a meta-analysis of prospective cohort studies.DesignEligible studies were identified by searching PubMed and EMBASE through January 2013. Additional information was retrieved through Google Scholar or a hand review of the reference lists from relevant articles. Prospective cohort studies that reported RRs and corresponding 95% CIs for the association of interest were identified. Data were extracted independently by 2 investigators, and the weighted RRs and 95% CIs for the associations were obtained by using a random-effects model.ResultsOf the 22 identified studies, 10 reported results on hypertension (36,617 individuals and 4491 cases), 7 on stroke (27,887 individuals and 1550 cases), and 9 on CHD (22,379 individuals and 1986 cases). Comparison of the highest with the lowest quantile of fasting insulin concentrations showed a pooled RR (95% CI) of 1.63 (1.35, 1.97) for hypertension, 1.18 (0.87, 1.60) for stroke, and 1.50 (1.28, 1.77) for CHD. Each 50-pmol/L increment in fasting insulin was associated with a 25% increase in risk of hypertension [RR: 1.25 (1.14, 1.36)] and a 16% increase in risk of CHD [RR: 1.16 (1.10, 1.22)] but was not associated with risk of stroke [RR: 0.999 (0.99, 1.01)].ConclusionsA higher fasting insulin concentration or hyperinsulinemia was significantly associated with an increased risk of hypertension and CHD but not stroke. This meta-analysis suggests that early fasting insulin ascertainment in the general population may help clinicians identify those who are potentially at high risk of CVD.

Dataset Information

Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.

Publications

Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.

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