That diet might play a part as a cause of CHD was hypothesised by another American doctor, Ancel Keys, in 1953. Using data from seven countries in his ‘Seven Countries Study’, Keys compared the death rates from CHD and the amounts of fats eaten in those countries to demonstrate that heart disease mortality was higher in the countries that consumed more fat than it was in those countries that consumed less. (At that time, data from many more countries were available. It seems that Keys ignored the data from those that did not support his hypothesis.) And so the ‘diet/heart’ hypothesis was born.

But how do we know it is true? It is all very well having a theory, what you have to do then is prove it. In medicine, the usual way is to select two groups of people, as identical for sex, age, and lifestyle as possible. One group called the control group, carries on as normal while the other, called the intervention group, tries the new diet, drug or whatever. After a suitable time, the two groups are compared and differences noted.

Keys’ fat-diet/heart disease hypothesis was persuasive so, to test it, several large-scale, long-term, human intervention studies were set up in many parts of the world. These involved hundreds of thousands of subjects and hundreds of doctors and scientists and cost billions of dollars in an attempt to prove that a fatty diet caused heart disease.

Framingham Heart Study

The most influential and respected investigation of the causes of heart disease is the Framingham Heart Study. This study was set up in the town of Framingham, Massachusetts, by Harvard University Medical School in 1948 and is still going on today. It was this study that gave rise to the dietary ‘risk factors’ with which we all are so familiar today. The Framingham researchers thought that they knew exactly why some people had more cholesterol than others – they ate more in their diet. To prove the link, they measured cholesterol intake and compared it with blood cholesterol. Although subjects consumed cholesterol over a wide range, there was little or no difference in the levels of cholesterol in their blood and, thus, no relationship between the amount of cholesterol eaten and levels of blood cholesterol was found. (Although it is interesting that women who had the highest levels of cholesterol in their blood were ones who had eaten the least cholesterol.)

Next, the scientists studied intakes of saturated fats but again they could find no relation. There was still no relation when they studied total calorie intake. They then considered the possibility that something was masking the effects of diet, but no other factor made the slightest difference.

After twenty-two years of research, the researchers concluded:

“There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group.”

On Christmas Eve, 1997, after a further twenty-seven years, the Journal of the American Medical Association (JAMA) carried a follow-up report that showed that dietary saturated fat reduced strokes. As these tend to affect older men than CHD, they wondered if a fatty diet was causing those in the trial to die of CHD before they had a stroke. But the researchers discount this, saying:

“This hypothesis, however, depends on the presence of a strong direct association of fat intake with coronary heart disease. Since we found no such association, competing mortality from coronary heart disease is very unlikely to explain our results.”

In other words, after forty-nine years of research, they are still saying that they can find no relation between a fatty diet and heart disease.

Multiple Risk Factor Intervention Trial

One of the largest and most demanding medical studies ever performed on humans, The Multiple Risk Factor Intervention Trial (known in the medical world, by its initials, as MR. FIT) involved 28 medical centers and 250 researchers and cost $115,000,000. The researchers screened 361,662 men and deliberately chose subjects who were at very high risk to ensure that they achieved a statistically significant result. They cut cholesterol consumption by forty-two percent, saturated fat consumption by twenty-eight percent and total calories by twenty-one percent. Yet even then they didn’t succeed. Blood cholesterol levels did fall, but by only a modest amount and, more importantly, coronary heart disease was unaffected. Its originators refer to the results as “disappointing” and say in their conclusions:

“The overall results do not show a beneficial effect on Coronary Heart Disease or total mortality from this multifactor intervention.”

The Tecumseh Study

The Tecumseh Study attempted to correlate blood cholesterol levels measured one day with the amounts of fats eaten the previous day – but found none. Interestingly, It was demonstrated that people who ate the least cholesterol had the highest levels of blood cholesterol. Although not looking for it, this study also found that blood cholesterol levels were quite independent of whether the dietary fats were saturated or unsaturated. Thus another ‘diet-heart’ hypothesis, that only saturated fats are to blame, was invalidated.

WHO European Coronary Prevention Study

The results of the World Health Organisation’s European Coronary Prevention Study were called “depressing” because once again no correlation between fats and heart disease was found. They had cut saturated fats down to only eight percent of calorie intake daily, yet in the UK section there were more deaths in the intervention group than in the control group.

The North Karelia Project

North Karelia, which had Finland’s highest rates of heart disease, was compared with neighbouring Kuopio in The North Karelia Project. In North Karelia, risk factors were cut by seventeen percent over the period of the study. In North Karelia there was a reduction in both CHD mortality and total mortality. Also this study shows, however, that in Kuopio, the control group, where there were no restrictions, there was an even bigger decline in both CHD and total mortality.

These studies suggest that adopting a ‘healthy’ lifestyle may actually have inhibited the decline in heart disease. They certainly give it no support.

This paper does not allow me to go through the more minor studies but they all show little convincing correlation between either the amount of fat eaten and heart disease or the type of fat eaten and heart disease. A review of twenty-six studies published in 1992 concluded that:

“Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease. Claims of the opposite are based on preferential citation of supportive trials.”

One that seemed to support the ‘healthy’ recommendations was a Finnish trial published in 1975. In the five years that the trial ran, cholesterol levels were lowered significantly, and the study was hailed as a success. But in December 1991 the results of a 10-year follow-up to that trial found that those people who continued to follow the carefully controlled, cholesterol-lowering diet were twice as likely to die of heart disease as those who didn’t – some success! Professor Michael Oliver, writing in the British Medical Journal commenting on the results, writes

“As multiple intervention against risk factors for coronary heart disease in middle aged men at only moderate risk seem to have failed to reduce both morbidity and mortality such interventions become increasingly difficult to justify. This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration. Not to do so may be ethically unacceptable.”

Despite this wealth of evidence, nutritionists and the media continue to mislead us. They tell us, for example, that the recent fall in the numbers of heart deaths in the USA is because Americans are eating less fat. The graph below, however, shows clearly that while CHD in the USA peaked in the 1950s and has fallen consistently since, this is against a background of rising fat intake.

It is difficult to understand how the fat hypothesis gained such credibility in the USA as its history more than most does not support it. The North American continent had been opened up by explorers and trappers who lived, very healthily, as did the Amerindians, almost entirely on fresh meat and pemmican. As real pemmican is half dried lean meat and half rendered animal fat, and as fat has over twice the calorific value of protein, more than seventy percent of the energy in their diet came from fat.

Dieticians also say that the British had less CHD in the 1940s when fat was rationed. However, the decade of rationing went on into the early 1950s with fat being the last food to come off ration in 1954. Again the graph shows clearly that the most rapid rise in CHD occurred during that period.

Also, during the period of rationing, British farmers had a very low incidence of heart disease when one would have expected their intake of fats, particularly animal fats, to have been higher than most.

Experience in other countries

Keys based his fat-causes-heart disease hypothesis on a comparison between countries. When we are told that we are ‘the sick man of Europe’, we are also compared to other countries. So lets do a similar comparison.

1. In Japan, intakes of animal fat have more than doubled since the end of the Second World War. Over the same period their incidence of coronary heart disease has fallen consistently. In Israel too an increased consumption of saturated fats was followed by a fall in coronary deaths.

2. The dietary changes in Sweden parallel those in the USA, yet heart disease mortality in Sweden was rising while American rates were falling.

3. There is also a threefold variation in rates of heart disease between France and Finland even though fat intake in those two countries is very similar.

4. Among south Asians in Britain there is an unusually high incidence of heart disease, yet living on largely vegetarian diets, they have low levels of blood cholesterol and eat diets that are low in saturated fat.

5. Indians in South Africa have probably the highest rates of coronary disease in the world yet there is no apparent reason why they should based on the current dietary hypotheses.

6. Until recently, Indians in India had a very low incidence of heart disease while using ghee (clarified butter), coconut oil and mustard seed oil – all of which are highly saturated. The epidemic of heart disease in India began only after these were replaced with peanut, safflower, sunflower, sesame and soybean oils, all of which are high in polyunsaturated oils.

7. Lastly, the World Health Organization is apparently in ignorance of epidemiological data that do not support its recommendation to reduce dietary saturated fat. While it talks of coronary heart disease being responsible for most deaths in Caribbean countries, fat intake there is remarkably low.

Polyunsaturated fats

The arguments for the polyunsaturated fat hypothesis are no more convincing than those for the cholesterol theory. The claim is that unsaturated fats have a protective or preventative effect on CHD. But in Israel, when consumption of polyunsaturated fats was about twice that of most Western countries, there was a very high incidence of CHD. Those given high polyunsaturated diets in a trial in New South Wales fared significantly worse than those on a free diet. And this is the finding in most trials that have increased the ratio of polyunsaturated fats.

From as early as 1971, an excess of cancer deaths has been reported in trials using diets that were high in polyunsaturated fats. Polyunsaturated fats are also blamed for a doubling in the incidence of gallstones in the general public.

One of the pioneers of the polyunsaturated-fat-prevents-CHD hypothesis was the American cardiologist E. H. Ahrens Jr.. After twenty-five years of further research, however, he concluded that it was “irresponsible” to continue to press the polyunsaturated fat recommendations on the general public. He went on:

“If the public’s diet is going to be decided by popularity polls and with diminishing regard for the scientific evidence, I fear that future generations will be left in ignorance of the real merits, as well as the possible faults in any dietary regimen aimed at prevention of coronary heart disease.”

Another of the original proponents of the low-fat, low-cholesterol hypothesis, and a member of the Norwegian Council for Diseases of the Heart and Arteries, Professor Jens Dedichen of Oslo, also changed his mind. In the 1950s Norway launched a cholesterol-lowering regimen in which soy margarine, that is high in polyunsaturated fatty acids, replaced butter, and soy oil was used extensively. During the subsequent 20 years the increase in the use of soy-based products was accompanied by a steep and continuing rise in deaths from coronary thrombosis. Professor Dedichen drew attention to the failure of the programme – and received a very hostile reaction from his colleagues.

Also castigated were members of the National Academy of Sciences and the National Research Council of America when in a report of May 1980, they stated that prevention of heart disease could not be achieved by reducing blood cholesterol using either diet or drugs, and said that such measures should be abandoned.