Research Article: Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Date Published: March 23, 2010

Publisher: Public Library of Science

Author(s): Dariush Mozaffarian, Renata Micha, Sarah Wallace, Martijn B. Katan

Abstract: Dariush Mozaffarian and colleagues conduct a systematic review and meta-analysis to investigate the effect of consuming polyunsaturated fats in place of saturated fats for lowering the risk of coronary heart disease.

Partial Text: Reduction in saturated fatty acid (SFA) consumption is traditionally a major focus of dietary recommendations to reduce coronary heart disease (CHD) risk. However, effects of such a strategy on clinical CHD events are surprisingly poorly established in both randomized controlled trials (RCTs) [1]–[8] and prospective cohort studies [9]. Prior meta-analyses of RCTs have either studied the effects of very heterogeneous dietary fat interventions on very heterogeneous combinations of cardiovascular outcomes [10], or studied effects of dietary fat interventions on intermediate risk markers, such as blood lipids [11]. Furthermore, although dietary guidelines often recommend reduction in SFA consumption, such guidelines often do not highlight any specific nutrient as preferable for replacing SFA in the diet [12]–[14], implying that any macronutrient replacement (unsaturated fats, carbohydrate, or protein) will produce similar effects.

We followed the Quality of Reporting of Meta-analyses (QUOROM – now PRISMA (http://www.prisma-statement.org/)) [25] guidelines throughout the design, implementation, analysis, and reporting of this meta-analysis (see Text S1 for PRISMA Statement).

The identified RCTs included a total of 1,042 CHD events among 13,614 participants (Table 1) [1]–[8],[32]–[34]. Average PUFA consumption ranged from 4.0%E to 6.4%E (weighted mean 5.0%E) in the control groups and from 8.0%E to 20.7%E (weighted mean 14.9%E) in the intervention groups. Diet was assessed in the majority of trials by either direct analysis of provided foods or by multiple-day weighed diet records. Four trials evaluated secondary prevention populations, three trials evaluated primary prevention populations, and one trial evaluated a mixed population of individuals with and without established CHD. Many of the trials had design limitations, such as single-blinding, inclusion of electrocardiographically defined clinical endpoints, or open enrollment. All trials utilized blinded endpoint assessment. Quality scores were in the modest range and relatively homogeneous: all trials had quality scores of either 2 or 3. Combining all trials, the pooled risk reduction for CHD events was 19% (RR = 0.81, 95% CI 0.70–0.95, p = 0.008) (Figure 2). Statistical evidence for substantial between-study heterogeneity was not present (Q-statistic p = 0.13; I2 = 37%). In evaluating potential for publication bias, the trial by Watts et al. [8] was clearly a potential outlier both in terms of sample size and risk reduction. Excluding this trial, there was little change in the overall pooled result: RR = 0.82, 95% CI 0.70–0.95; p heterogeneity = 0.11, I2 = 42%. Visual inspection of the resulting funnel plot indicated some potential for publication bias (Figure S1), with a borderline Begg’s test (continuity corrected p = 0.07), although such determinations are limited when the number of studies is relatively small.

In this meta-analysis of RCTs, increasing PUFA consumption as a replacement for SFA reduced the occurrence of CHD events by 19%; each 5%E greater PUFA consumption reduced CHD risk by 10%. Whereas nearly all these trials were insufficiently powered to detect a significant effect individually, the pooled results demonstrate a significant benefit of replacing PUFA for SFA on clinical CHD events. Thus, this is only the second dietary intervention, together with consumption of long-chain omega-3 fatty acids (fish oil) [7],[35]–[37], that has now been clearly demonstrated to reduce cardiovascular events in RCTs.

Source:

http://doi.org/10.1371/journal.pmed.1000252

 

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