Association of dietary, circulating, and supplement fatty acids with coronary risk.

Abstract

TO THE EDITOR: We appreciate that Chowdhury and colleagues (1) have corrected some of the gross errors in their original paper. Of note, the inverse association of intake of long-chain -3 polyunsaturated fatty acids (PUFAs) with cardiovascular disease (CVD) risk is now significant. We also appreciate the sensitivity analysis showing that with exclusion of the outlying SDHS (Sydney Diet Heart Study), the included randomized, controlled trials (RCTs) show benefit of replacing saturated fatty acids (SFAs) with PUFAs. The extreme diet used in that study was never recommended or consumed in the United States. It included a trans fat‐based margarine and probably very little -3 PUFAs, because sunflower oil was used to replace other fats as much as possible. However, other serious problems with Chowdhury and colleagues’ analysis remain. They report that the nonsignificant findings for biomarkers of long-chain -3 fatty acid intake are based on total long-chain -3 PUFAs in only 4 studies. However, in the Supplement Tables, long-chain -3 PUFAs were actually examined in 13 studies, and findings for the specific long-chain PUFAs (eicosapentaenoic and docosahexaenoic acids) were robustly and significantly inverse. Thus, the results for both intake and biomarkers for long-chain -3 fatty acids support benefit. Although the findings for RCTs vary, these results would be expected because many of the populations studied had relatively high intake of -3 fatty acids and most individuals would likely experience little benefit. The analysis for -6 PUFAs still includes only 8 studies and omits others included in Jakobsen and coauthors’ (2) pooled analysis of original data and other published papers. The data on intake of -6 PUFAs from the Kuopio Heart Study (3), the study with the most positive association, are erroneous because the denominator is almost double the number of healthy participants. Contrary to what Chowdhury and colleagues state, they apparently included persons with prevalent CVD at baseline instead of limiting the analysis to healthy persons. The original study reported a relative risk (RR) of 0.38 (95% CI, 0.20 to 0.70) for fatal CVD among those with higher intake of PUFAs. Chowdhury and colleagues still do not acknowledge the earlier pooled analysis of primary data based on a larger number of studies, which allowed direct comparisons among different types of fats. In that analysis, substitution of SFAs with PUFAs was associated with lower risks for coronary heart disease (CHD) (2). The large body of data showing that replacing SFAs with monosaturated fatty acids (MUFAs) or PUFAs reduces low-density lipoprotein (LDL) cholesterol is still not recognized. Although Chowdhury and colleagues say that their conclusions did not change, a more inclusive and correct review of available evidence would support the replacement of SFAs with PUFAs.