Re: Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis
7 February 2013
To the Editors,
The study entitled “Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis” has a serious flaw. The PUFA-supplemented (intervention) group may have been provided with atherogenic trans fat, and the investigators cannot prove otherwise. In this report Ramsden et al. used updated statistical techniques and new clinical end points endpoints to reanalyze data from a study conducted from 1966-1973 where young and mid-aged male participants with a history of CVD were instructed to reduce dietary saturated fat and replace calories with about 15% of dietary energy coming from PUFA (1,2). Participants in the intervention group were offered both safflower-based margarine and safflower oil because the investigators presumed these two fat sources are nutritional equivalents. They were probably not the same.
Participants in the intervention group consumed “Miracle” Margarine, a product based on safflower oil. Hydrogenation of safflower oil itself creates a grainy product low in linoleic acid, so high-linoleic safflower oil margarine products were created by blending liquid safflower oil with another hydrogenated oil stock (3). Miracle Margarine used in the original study was either low in linoleic acid (due to hydrogenation of the safflower oil itself) or the oil was blended with another commercially hydrogenated fat to create a plastic margarine product. An investigation by Bernfeld, Homburger, & Kelley, published in 1962, indicated that the fatty acid composition of most margarines of the time were about 50-60% 18:1 monounsaturated fats (including oleic and trans isomers) and about 20-30% 18:2 linoleic acid, even in those products having high-PUFA claims on the label (4). None of the 22 margarines studied had a majority of fatty acids coming from PUFA. Another report from the same time period indicates that commercially produced hydrogenated fats, like those added to safflower oil to make margarine, were generally composed of about 25-40% trans fats (5). Fatty acid composition of margarines in the 1960s investigation were not comparable to liquid vegetable oil, despite package claims. The only reference supporting the healthful content of Miracle Margarine is a very general press release from the company who made the product (6). It is probable that Miracle Margarine had significant trans fatty acid content. An independent chemical analysis would have confirmed whether the composition of Miracle Margarine differed from other commercially available margarines or safflower oil. Though trans fats were not yet conclusively implicated in CVD risk at the time of the original study, scientists in the mid 20th century suspected hydrogenated fats were not healthful (5).
The authors noted that the lack of trans fat quantification was a limitation of the study (1). Ramsden et al., used an analysis of MUFA as a surrogate for trans fats, but MUFA cannot stand-in for trans fats because there are too many healthful sources of dietary MUFA. Atherogenic trans fats may have been provided to the participants as a part of the intervention, and such an addition of trans fats could have been responsible for an increase in all-cause mortality. As an editorial piece related to this study points out, interpretation of dietary studies where multiple fatty acid components are changed must be interpreted with caution (7). In the case of this reanalysis, readers should exercise caution in attributing the results to dietary PUFA when the intervention group received PUFA sources that were likely laced with trans fats.
In addition to increasing PUFA intake, participants in the intervention group reported reduced dietary saturated fat, cholesterol, and calorie intake from baseline. A negative energy balance was verified with a slight mean drop in BMI. As expected, circulating total cholesterol and triglycerides were reduced in the intervention group, but mortality outcomes were not improved consequent to these circulating lipid and anthropometric changes, which is unexpected and interesting. The more important question arising from this study may be why a dietary intervention that improved all of these commonly used surrogate end points did not reduce all-cause mortality?
Jean Gutierrez, PhD, RD
Assistant Professor of Exercise Science
The George Washington University
1. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: Evaluation of recovered data from the Sydney diet heart study and updated meta-analysis. BMJ. 2013;346:e8707.
2. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Adv Exp Med Biol1978;109:317-30.
3. Blum JE. The role of safflower oil in edible oil applications. J Am Oil Chem Soc. 1966 Jun;43(6):416-7.
4. Bernfeld P, Homburger F, Kelley TF. Fatty acid contents of margarines and other table fats. Am J Clin Nutr. 1962 Dec;11:554-8.
5. Brown JB. Changes in nutritive value of food fats during processing and cooking. Nutr Rev. 1959 Nov;17:321-5.
6. Significant points from the annual report of Marrickville Holdings. Sydney Morning Herald1965 Nov 19.
7. Calder P. Old study sheds new light on the fatty acids and cardiovascular health debate. BMJ. 2013:346:f493.
Competing interests: None declared
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