The so-called “cholesterol/diet/heart disease” theory is based on the belief that the risks of death due to heart disease are associated with the concentration of cholesterol in the blood (TC). In other words if you have a high TC you can lower your chances of developing heart disease by reducing the TC level. It is claimed that the saturated fat (SFA) in the diet will raise the TC and that the polyunsaturated fat (PUFA) will lower it. Hence it follows that consumers are advised to reduce their intake of SFA and increase that of the PUFA.

Therefore it is highly relevant to examine the results of investigations where these changes have been made to see what actually happens.

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 carried on as normal was used as the control for comparison.

The results are shown in Table 1’

Table 1 Death rates and Total Cholesterol (TC) levels in the Anti-Coronary Club Study

Prudent Diet Control
TC level mmol/L 5.8 6.7
Coronary death rate /100 1.1 0
All-cause death rate /100 3.4 1.3

 

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!

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. 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. 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 (2).

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 in Table 2 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 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.

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.

Table 2 Changes in the Composition of Dietary Fatty Acids

BASELINE FOLLOW-UP
CONTROL INTERVENTION CONTROL INTERVENTION
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

The Lyon Heart Study is one of the most successful investigations which demonstrate that a change in diet results in a significant improvement in the survival rates of men and women aged <70 years old who have experienced a heart attack (3).

Volunteers who had survived a heart attack were allocated to either a control group (n=303) or an experimental group(n=302). Those in the experimental group were advised to consume a Mediterranean type diet which involved a reduction in the consumption of total fat, saturated fat and linoleic acid (omega-6s) and an increase in the consumption of oleic acid (mainly olive oil) and alpha-linolenic acid (omega-3s). The participants were seen 8 weeks after the beginning of the trial and then again every year for up to 5 years.

At the first follow-up (minimum period 1 year) it was found that those on the Mediterranean diet had a much better chance of survival than those in the control group. As a consequence the decision was taken to stop the trial so that those in the control group were free to make changes to their diet and follow the advice given to the experimental group if they so wished. Nevertheless the research team continued with the original plan and a final assessment of all existing participants was done after about 4 years.

It was found that the death rate attributed to heart disease has been reduced by 65% in those consuming the Mediterranean diet while the all-cause death rate has been reduced by over a half. Because of the decision to effectively halt the trial after the first year this means that almost certainly these values are an under estimate. It cannot be over-emphasised that this is an enormous reduction which is even more impressive when the short time frame is recognised. It is also very much greater than anything that has been achieved using drugs.

It is highly significant that the values for TC were virtually the same for both groups demonstrating the futility of the current focus on reducing TC as a means of controlling heart disease. The values for the “bad” LDL cholesterol were also the same for the controls and experimental groups.

It is absolutely essential that anyone who is being advised to reduce their TC should be made aware of this information.

  • On the one hand, it is obvious that those who successfully reduced their TC by altering the fat content of their diet INCREASED their risk of heart disease, despite the fact that the justification for making change would decrease the risk.
  • On the other hand, an unprecedented reduction in deaths due to heart disease and to all causes was achieved even though the cholesterol in the blood remained unchanged.

So if you think increasing your consumption of PUFA will be beneficial because it will lower you cholesterol, then you should think again. In reality it may be damaging to your health. Similarly the case for not eating butter is demolished by these results. There is plenty of evidence to show that many of the individual fatty acids are important nutrients, not to mention the presence of key fat-soluble vitamins including vitamins A,D and K2.

REFERENCES

  1. G Christakis et al (1966) Journal of the American Medical Association 198 (6) pp 597-604
  1. C E Ramsden et      al(2013) British Medical Journal 346:e8707
  2. M de Lorgeril et al(1996) Journal of the American College of Cardiology 28 (5) pp 1103-1108