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.-Ramsden(2013)

Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR. (2013)

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 Feb 4;346:e8707.
DOI: 10.1136/bmj.e8707.
pubmed

Summary: 458 Australian men (aged 39-59) with a recent coronary event – so high likelihood of a recurrence – were randomly split into two groups and fed for 6 years 2 different diets in a blinded study (so the men didn’t know which group they were in).  The controls were given no specific dietary advice.  The intervention were given a diet with saturated fats (from animal fats, common margarines, and shortenings) replaced with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine).

Results: The 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).


We reckon: This data was buried from the conclusion of the trial in 1973 until the release of this re-evaluation of the data in 2012 because the results disproved the diet-heart hypothesis – namely that replacing saturated fat with polyunsaturated fats would lower Cholesterol and that would lower heart disease.  This study shows that it lowered LDL (-13.3%) AND YET increased the risks of cardiovascular disease (by 70%).  The mechanism proposed is that polyunsaturated fatty acids are more prone to oxidation, more likely to appear in the small dense atherogenic LDL and more likely to appear in atherosclerotic plaques – so the reduction of the amount of LDL has no apparent direct effect on CVD but the oxidation the lipids that it carries does.

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