The official dietary recommendations continue to advise a reduction in saturated fat (SFA) and an increase in the polyunsaturated fat (PUFA). The justification is that the SFA will reduce the Blood cholesterol (TC) and therefore lower the risk of developing heart disease. The same rationale is used to justify the advice to increase the intake of PUFA, which should also reduce the TC. It is therefore relevant to consider the results of some studies which investigate the effects of changes in the dietary fat on the TC.
Way back in the 1960s members of the Anti-Coronary Club in New York volunteered to participate in a trial (1). A total of 814 men aged between 40 and 59 years old were placed on the “Prudent Diet” which involved a very substantial reduction in their intake of animal fat, which is rich in SFA, and a corresponding increase in that of PUFA. A separate group of 463 men which carried on as normal was used as the control for comparison.
In this investigation there is no question that the TC was lowered. However there were 9 deaths due to heart disease in those on the Prudent Diet but not a single death in the control group. Even more worrying was the fact that the total mortality was about 2.5 times greater in those consuming the “healthier” diet!
A trial conducted in London under the auspices of the MRC investigated the effect of a cholesterol-lowering diet diet in the prevention of relapse in men aged under 60 years recently recovered from their first myocardial infarction. 199 men recently discharged from hospital were randomly allocated to the experimental group were given a diet low in saturated fats and containing 85 gm of soya-bean oil daily. There was a control group of 194 men who consumed their usual diet. All of them participated for at least 2 years but some continued for over 6 years. Those in the experimental group lowered the TC from a mean initial figure of 272 to 213 mg. per 100 ml. at six months (22% fall). The level in the controls fell from 273 to 259 mg. per 100 ml. (6% fall). Suspected relapses were assessed at regular intervals by a review committee unaware of the patient’s diet group.
Although there were 45 major relapses in the test group and 51 in the controls, those which resulted in death were 25 in each. It was concluded that relapses were not related to initial TC level, to change in cholesterol level during the trial, nor, in any consistent way, to observance of the dietary regimen (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 SFA with safflower oil. It is an excellent opportunity to study the impact of increasing the PUFA. In the original report, deaths due to cardiovascular disease and coronary heart disease were not shown. In an analysis of the data conducted recently by Chris Ramsden and colleagues it has been possible to gain insight into the effects of the different types of fats (3).
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. The control group received no specific dietary instruction. However, some participants began replacing butter with margarine if they had suffered a coronary event.
The results 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. 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 PUFA resulted in an increase in 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. This investigation must be regarded as highly relevant because the changes are precisely those which are being recommended by the authorities in the UK and in most of the world. It is obvious that the favourable results confidently predicted have not materialized.
It is also important to note that although there was a decline in the TC levels of both groups it was much greater in the intervention group. This provides further confirmation that lowering TC does not result in a corresponding reduction in the coronary death rate.

Although the TC levels in both groups fell but the decline was much greater in the intervention group than it was in the control group. The cholesterol theory predicts that the death rate attributed to heart disease would be therefore be less than in the control group. In reality it was 70% GREATER than in the control group and only slightly less for all-cause mortality. This is further evidence that the benefits which have been claimed for lowering cholesterol simply do not materialize in the real world.
The case for reducing SFA and increasing PUFA is full of holes as far as the impact on the blood cholesterol levels are concerned. When researchers have attempted to confirm it, they have failed totally. Although the TC has been lowered successfully there certainly has not been the improvement in health so confidently predicted by those who formulate and implement the current policies. Despite this the advice from the NHS and health professionals here in the UK and in most other countries continues to emphasise the importance of limiting the intake of SFA. Furthermore there are many products on the market which are actively promoted on the grounds that that they are high in PUFAs and will therefore “lower cholesterol”!


1. G Christakis et al (1966) Journal of the American Medical Association 198 (6) pp 597-604
3. C E Ramsden et al (2013) British Medical Journal 346:e8707