In BLOG 15, I explained that there are serious doubts about the rationale which underpins the recommendation to increase the intake of polyunsaturates (PUFAs) which are the omega-6 fatty acids(omega 6s).

Nevertheless foods which are high in PUFAs continue to be promoted as healthy. As recently as 2009 the American Heart Association (AHA) reviewed its position. It was concluded that the combined results of a range of studies provided:

“ evidence that replacing saturated fat or refined carbohydrates….with omega-6 PUFAs reduces        CHD risk

It went on to recommend that consumption of at least 5% to 10% of energy from omega 6s would reduce the risk of heart disease relative to lower intakes. Furthermore higher levels appear to be safe and would probably be beneficial(1).

However the quality of much of the research used to justify this recommendation has been seriously questioned. In a thorough examination of the relevant critical investigations, Chris Ramsden and colleagues discovered that in a number of these trials mixtures of omega-3s and omega-6s were actually used but it had been assumed that only omega 6s were present. When the investigations were separated into those which contained mixtures and those which consisted of omega-6s only a very different picture emerges. Those with mixed omega-3/omega-6s did actually result in a significant reduction in the risks of non-fatal heart attacks of 27%. For non-fatal heart attacks plus CHD death the reduction in risk was 22 %. By contrast, omega-6 specific PUFA diets increased risk of all CHD endpoints, with the increased risk of death from all causes approaching statistical significance.

This excellent analysis makes it abundantly clear that the benefits which were being attributed to omega-6s were actually being achieved by the presence of omega-3s which had not been recognised by the researchers who had actually done the work. As a consequence the conclusions presented were wrong(2).

The Sydney Diet Heart Study (SDHS), conducted between 1966 and 1973 was a randomized control trial in which the intervention group was advised to replace the saturated fatty acids(SFA) with safflower oil. This is a concentrated source of the omega 6 PUFA Linoleic Acid (LA) and does not contain any omega-3. Hence it is an excellent opportunity to study the impact of increasing the omega-6. In the original report, deaths due to cardiovascular disease and coronary heart disease were not shown. This latest paper which was published recently in the BMJ (5 February 2013)(3) is based on the complete data which have been obtained by Christopher Ramsden and his colleagues. This has enabled them to undertake a more detailed and complete analysis than appeared in the original report.

The participants were 458 men aged 30-59 years at the outset who had experienced a coronary event shortly before the commencement of the trial.

The intervention group received instructions to increase their PUFA intake to about 15% of food energy, and to reduce their intake of SFA to less than 10% of food energy. To achieve this target, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine. Liquid safflower oil was substituted for animal fats, common margarines and shortenings in cooking oils, salad dressings, baked goods, and other products, and was also taken as a supplement. Safflower oil polyunsaturated margarine was used in place of butter and common margarines. Safflower oil is a concentrated source of omega-6 LA and contains no other reported PUFAs. The control group received no specific dietary instruction. However, some participants began substituting polyunsaturated margarine for butter if they suffered a coronary event.

All participants were monitored for just over 3 years on average. Diets were assessed regularly by means of a 7-day log. The results in Table 1 show that the PUFA content of the diet in the intervention group more than doubled and the SFA content was reduced to below 10% of total energy. There were also changes in the diet of the control group but these were very much smaller. Compared with the control group, the intervention group had an increased risk of all cause mortality (17.6% v 11.8%; hazard ratio 1.62). The corresponding values for cardiovascular mortality (17.2% v 11.0%; 1.70) and for coronary heart disease), and mortality from coronary heart disease (16.3% v10.1%; 1.74) were similar. This study demonstrates that selectively increasing omega-6 PUFA LA from safflower oil and safflower polyunsaturated margarine increased rates of death from cardiovascular disease, coronary heart disease, and all cause mortality compared with a control diet rich in SFA from animal fats and common margarines. When this result is taken in conjunction with other investigations it is highly probable the raised level of LA is the critical factor responsible for the increased mortality rates which have been observed. The authors concluded that:

These findings could have important implications for worldwide dietary advice to substitute n-6 LA, or PUFAs in general, for SFA”

 It also important to note that although there was a decline in the blood cholesterol levels of both groups it was much greater in the intervention group. According to the conventional “diet/cholesterol/heart disease theory” this should have been accompanied by a reduction in deaths from heart disease. The fact that this did not happen is further evidence that this theory just does not stand up to rigorous examination.




                         BASELINE                          FOLLOW-UP
PUFA,%E 6.2 6.1 8.4 15.4
SFA,%E 15.6 16.2 13.5 9.3
PUFA:SFA 0.41 0.38 0.63 1.72



This work totally vindicates those who have reached the conclusion that ratios of omega-6: omega-3 which are higher than about 4 are damaging to health. Where this applies then the emphasis should be to increase consumption of omega-3 and reduce that of omega-6. There can be no possible justification for recommending increased consumption of omega-6 PUFAs in countries such as the UK and the USA which have a relatively high incidence of heart disease and obesity. There is no question that those who do so will be increasing their requirement for omega-3s and this may well be damaging to their health. In fact there are strong indications that it would be beneficial to reduce the intake on omega-6s. eg by replacing margarines and spreads which are high in omega-6s with butter.



  1. W S Harris et al (2009) Circulation 119 (6) pp 902-907
  2. C E Ramsden et al(2010) British Journal of Nutrition 104 (11)pp1586-1600
  3. C E Ramsden et al(2013) British Medical Journal 346:e8707