New book in Dutch

Eet vet word slank

Eet vet word slank gepubliceerd januari 2013

In dit boek lees je o.a.: * heel veel informatie ter bevordering van je gezondheid; * hoe je door de juiste vetten te eten en te drinken kan afvallen; * hoe de overheid en de voedingsindustrie ons, uit financieel belang, verkeerd voorlichten; * dat je van bewerkte vetten ziek kan worden.

Trick and Treat:
How 'healthy eating' is making us ill
Trick and Treat cover

"A great book that shatters so many of the nutritional fantasies and fads of the last twenty years. Read it and prolong your life."
Clarissa Dickson Wright

Natural Health & Weight Loss cover

"NH&WL may be the best non-technical book on diet ever written"
Joel Kauffman, PhD, Professor Emeritus, University of the Sciences, Philadelphia, PA

Reducing Deaths from Heart Attacks and Cancer

by Wayne Martin

This is to suggest that deaths from heart attacks and cancer can be reduced by half without changing our lifestyles all that much.

First I will address the subject of deaths from the kind of heart attack now called myocardial infarction (MI) but which seventy years ago was called coronary thrombosis. There are in the USA now about 500,000 such deaths a year, but this is a new disease that has come about in this century. Prior to 1925, there was almost no knowledge of this disease.1

I have had a long exchange with Dr. Rodney Finlayson, who is now in retirement in North Devon in England. Beginning in 1975, he did a study of the records of several London hospitals back to 1869 looking for case histories that were obvious cases of death from MI. Here is what he found. His figures are a ratio of deaths from MI per unit of population.

From 1869 until 1900, there was one MI death per unit. By 1910, there were 10 MI deaths per unit. This was the time when machine-made cigarettes were on the market, and Dr. Finlayson suggested that cigarette smoking had caused deaths from MI to increase by a factor of ten. By 1980, MI deaths per unit of population had increased to 80.2

Dr. Finlayson did not know it, but at the same time Dr. Alaster Mackinnon had been doing a similar study in Yorkshire. This study was of a constant population of about 22,000. The Mackinnon results were the same as in the Finlayson study; that is, MI deaths increased in a ratio of one in 1900, to 10 in 1910, to 80 in 1980.3

There were in the late 1960s reports of two populations in the world who were as free from MI deaths as was the English population in 1900. One such population was the black population in Uganda and the other was the North Indians living near Udiapur.4,5

This suggests that we could again be as free from MI deaths as was the population of England in 1900.

We will now go back to 1882 when Bizzozero discovered blood platelets and suggested that they start all blood clots. He had it all figured out right then that the beginning of all blood clots is a white or platelet thrombus. He said that in a blood clot, there is first the platelet thrombus followed by the more massive fibrin thrombus.6 The only problem was that he was about the only doctor in the world who thought that way, although the editor of The Lancet in 1883 made favorable comment about Bizzozero's discovery. Nearly all doctors then were certain that there were no such things as blood platelets. In 1926, Tait and Burk of the University of Montreal redid the work of Bizzozero and said that 'yes,' that was the nature of a blood clot.7 They had no better luck in convincing doctors than did Bizzozero, however. At this time, a blood clot was made of fibrin, and while at long last it was agreed that there were such things as blood platelets, they had nothing to do with disease or blood clots.

In 1930, Professor Karl Link of the University of Wisconsin discovered warfarin and said that it would tend to prevent the formation of the fibrin portion of a blood clot. Thereafter, his university made millions of dollars on the sale of warfarin to kill rats. A big dose of warfarin will cause rats to die of internal bleeding.

In 1945, doctors began to treat heart attack patients with a low dose of warfarin to prevent the formation of fibrin in coronary artery blood clots. Thereafter, heart attack patients by the millions were maintained on a low dose of warfarin for year upon year.

By 1955, it was decided that treatment with warfarin was not doing much to prevent a second heart attack,8 so cholesterol was discovered as being the cause of heart attacks. Cholesterol in foods such as eggs would settle out of blood like mud out of water, clogging the arteries and causing a heart attack. As blood clots seemed to no longer be the problem, the name of the disease was changed to myocardial infarction.

The Prudent Diet

It was then found that the polyunsaturated liquid vegetable fats, such as corn oil, in the diet would reduce cholesterol in blood a little, which led to the birth of the Prudent Diet. In the Prudent Diet, the amount of polyunsaturated vegetable fatty acids in the diet should be double the saturated animal fat.

It is difficult to believe, but almost overnight cardiologists had unlimited faith in the Prudent Diet as being the ultimate answer to the pandemic of heart attacks. Having said that everyone should live on the Prudent Diet to keep from having a heart attack, cardiologists then set about to prove this to be true.

The first study was the Joliffe Anti-Coronary Club in New York City. Joliffe was a doctor working for the city. He was a diabetic and a vascular wreck. He was in a wheelchair and had gone blind in one eye. He looked to the Prudent Diet for his salvation.

The control group in this trial was men of wealth on Wall Street who could afford good food. They had a diet that included lots of eggs, butter, cheese, and beef. The Prudent Diet group was mostly teaching staff at city universities. A drug firm made a special margarine rich in polyunsaturated fats to be part of the Prudent Diet. The Prudent Diet was very strict in having almost no butterfat and very little red meat.

The trial ran for four years and was hailed as a great success for the Prudent Diet, as total serum cholesterol was reduced by 25 percentage points. One had to read the fine print, however, to discover that eight men on the Prudent Diet died of MI, whereas none of the controls eating eggs, butter, and beef died of a heart attack.9 Then Dr. Joliffe died, it was said of complications of his diabetic condition. He may have had a heart attack.

Cardiologists then decided that to prove the need for the Prudent Diet, there would have to be an anti-coronary club formed, with over a million men enrolled. This was the National Diet Heart Study, and it was formed by Dr. Irwine Page of the Cleveland Clinic, who had survived a heart attack. This trial had millions of dollars of US government funds to support it. There were food warehouses set up in seven cities, where men on the Prudent Diet could get (free) the proper food, which included polyunsaturated donuts.

Before they would get one million men involved, there would first be a pretrial of two thousand men. This pretrial ran for three years, and the results were an utter failure. There were exactly the same number of heart attacks, both fatal and non-fatal, in both groups, the ones on the Prudent Diet and the controls.10 This trial had been started with the maximum of PR and fanfare. It was terminated with no public announcement for "reasons of cost." I saw Dr. Page at the beginning of this trial, and he was absolutely confident that the Prudent Diet was going to keep him from having another heart attack. He then died of a second heart attack.

Here is a thought. In the Joliffe trial there were no MI deaths among the controls, who were living on a diet very much like the diet of 1900 in the USA. In the National Diet Heart Study, there were the same number of fatal heart attacks in both the Prudent Diet group and the control group. By this time, the entire nation was living on something very close to the Prudent Diet. The men in the Prudent Diet group were living on a diet that was just a little more Prudent.

In England, during the same time, there was a trial that had patients who had survived a heart attack. Here again, the Prudent Diet was an utter failure, with the same number of heart attack deaths in both the Prudent Diet group and the controls.11

Then there was an 8-year trial of the Prudent Diet at a VA hospital in California, in which cancer deaths increased among the patients on the Prudent Diet by 15%.11a Not long after that, there was an editorial in the British Medical Journal asking if polyunsaturated fats were causing cancer, with a strong suggestion that they were.12

By now we were up to 1970 and, notwithstanding the failures of the Prudent Diet trials, the Prudent Diet had become engraved in stone as the way to not have a heart attack. Most of the population of our Western World was living on something very close to the Prudent Diet by then.

The Prudent Diet Causes Heart Attacks

Then there were five population studies all of which suggested that the Prudent Diet was causing heart attacks. First there was the Roseto, Pennsylvania, study. This small city is 100% Italian? prosperous Italians. If the Prudent Diet was right, then what these Italians were doing was wrong. They had in their diet lots of cheese and meatballs, and the main fat in their diet was olive oil, which is not very polyunsaturated. In 1955, among this Italian population, there were only one-third the MI deaths as compared to other cities in eastern Pennsylvania and the nation as a whole. Here it was suggested that living in big families reduced the stresses of life, thus preventing heart attacks. In no way could it be suggested that the Prudent Diet was causing deaths from MI.

By 1970, the population of Roseto was having the same number of MI deaths as the nation, doctors having persuaded them to live on the Prudent Diet.13

Next there was the Boston Irish Brothers Study. Here brothers were found where one brother remained in Ireland and one went to Boston. In 1965, the population of Ireland had in their diet large amounts of saturated animal fat in milk, butter, and meat, and very little of the "good polyunsaturated fats." Again, if the Prudent Diet was right, then the diet in Ireland was wrong. It was fully expected that the brothers in Boston who were living on a diet near to the Prudent Diet would be having fewer MI deaths than the brothers in Ireland. What was found was just the opposite, with the butter-eating brothers in Ireland having far fewer MI deaths.14

Cardiologists said that men in Ireland did more walking around, which kept them from having MI deaths. Again there could be no suggestion that the Prudent Diet was causing MI deaths.

Then there was a study in India. The North Indians were found to be nearly free from MI deaths. These Indians in 1970 were the world's biggest eaters of butter fat as ghee. By religion, they could eat some meat. They were also the world's biggest eaters of onions and garlic.

At this time, there was a strict vegetarian population in the South of India who lived on the Prudent Diet more closely than anyone in the USA. They had a high fat diet in which all the fat was polyunsaturated vegetable oil or margarine made from it. They were having 15 times the MI deaths as compared to the butterfat-eating North Indians.15

By 1988, things had changed in the North of India. Low-cost liquid polyunsaturated vegetable oil had priced ghee out of the market. Also, doctors were teaching the Prudent Diet. By then the death rate from MI in North India had increased to match that in the USA.16

Then there is the South of France-Scotland study. The population of the South of France was eating much more butter and cheese than the population of Scotland. Both populations had elevated serum cholesterol; however, the population in Scotland was having five times the death rate from MI among men and 11 times greater among women. The difference was that the French were drinking about 400 cc. a day of wine. One of the good things in wine is bioflavonoid antioxidants.17 There will be more on this later. [See Part II, in the September/October issue of Well Being Journal .]

Then there is the population on Okinawa. This population again was compared to Scotland. Here again both populations had elevated serum cholesterol, the same in both nations; however, there was only about 10% the MI death rate among the population of Okinawa as compared to Scotland. There was almost none of the polyunsaturated fats in the diet in Okinawa. These people raise a lot of swine, and the main fat in their diet is lard. They also eat a lot of fish.

Polyunsaturated Fatty Acids Increase MI Deaths

So, in the population studies that have been done to date, adding polyunsaturated fatty acids to the diet seems to have been increasing MI deaths.

I have had a long friendship with Professor Terrence Anderson who last was Head of the School of Public Health at the University of British Columbia. He maintains that the pandemic of MI death that has happened since 1900 has been caused by adding to the diet large amounts of polyunsaturated vegetable fats from which the antioxidants have been removed.18 It is a fact that as MI deaths have increased 80-fold since 1900, polyunsaturated fats have increased in the diet by a factor of three. He cited references that corn oil from which the antioxidants have been removed is cardiotoxic.

It is a fact that MI deaths have increased in direct proportion to the increase in polyunsaturated fats in our diet.

Just look at the fats in the diet in 1900, when MI was unknown and most rare. They were butter and lard. The only polyunsaturated vegetable oil to be had then was cottonseed oil, and the use of it was minuscule.

In 1980, cardiologists resurrected platelets and blood clots as a cause of MI deaths?and told everyone over 40 to take aspirin to prevent having a heart attack. One factor in the prevention of MI is the adhesiveness of platelets, as the greater the adhesion of platelets, the greater the chance of having a coronary blood clot.

Then came a series of trials on aspirin in the prevention of MI. The results were about the same as with the Prudent Diet trials. There were, in the 1970s, two trials in England that were failures. No benefit or very slight benefit was found for aspirin in the prevention of MI.19,20 This was followed by a much larger government-financed trial in the USA, reported in 1980. This trial was an abject failure, with much bleeding of the stomach due to aspirin and no benefit at all in the prevention of MI.21

Doctors felt that the case could be made for aspirin if only doctors were the subjects. A trial in England among doctors was again a failure;22 however, a larger trial among doctors in the USA was hailed as a great success. In this American trial, non -fatal heart attacks were reduced by 40%. The bad news, however, was that fatal heart attacks were not reduced and moreover overall survival was not increased.23 Nonetheless, as the result of this trial, it was suggested or even demanded that all men over 40 should be taking aspirin.

There was something a bit different about this trial among doctors in the USA. Bufferin was used, and Bufferin contains both aspirin and some magnesium. Magnesium is greatly beneficial to the heart. It reduces platelet adhesion, is a vasodilator, and is a potent antiarrhythmic agent.24

Platelet Adhesiveness

At the National Heart Hospital in London circa 1970, they were using a test for platelet adhesion and the results were stated as PAI, platelet adhesiveness index. In this test, a blood sample was taken and a platelet count was made. Then a second blood sample was taken, and this time the blood was passed over glass beads. If half the platelets stuck to the beads, PAI was 50. Patients who had survived a heart attack would have PAI of 50 and hence were considered to be at risk of death from a second heart attack. Young women who never suffer from MI have PAI of 20, yet they will have proper blood clots in wounds.

At the National Heart Hospital, in the years 1960 to 1965, they did a PAI test on every MI patient to come to this hospital, and they never found a single patient with PAI less than 40. They felt anyone with a PAI of less than 40 was not going to have a heart attack. Put another way, they felt that the great problem about MI was one of blood clots in coronary arteries.

The idea of testing for PAI never came to the USA.

There are all kinds of things other than aspirin that reduce PAI, one of which is the drug dipyridamole. Here mention will be made of the European Stroke Prevention Study.25 About 90% of strokes are thrombotic strokes, blood clots in blood vessels in the brain. This trial had as subjects patients who had had an indication of a stroke. First, aspirin alone was used with little or no benefit. Then dipyridamole was added to treatment, 300 mg a day, and the results were outstanding. Stroke deaths were reduced by 50%, heart attack deaths by 35%, and cancer deaths by 25%.

There are so many things that reduce PAI better than aspirin. Vitamin E at 400 IU a day will.26 So will vitamin B6 at over 40 mg a day. There was an editorial in The Lancet a few years ago on how anti-thrombic vitamin B6 is at over 40 mg.27 So is fish oil.28 This is the omega-3 fatty acid that we have been hearing so much about of late. Then from the University of Wisconsin of late has been a report that purple grape juice at 10 oz. a day will reduce PAI better than aspirin. It has been suggested that gamma linolenic acid in evening primrose oil will reduce PAI better than anything else. Also the oils of onion and garlic will reduce PAI. Ground ginger also is greatly effective in reducing PAI and, like aspirin, it will reduce pain. It is highly anti-inflammatory.29

It is a sad state of affairs that doctors in the USA have gotten most men over 40 taking aspirin, while not setting up a test to see if it is, in fact, reducing PAI.


1. A.G. Gibbon, Ischemic necrosis of the heart. Lancet, 1925, i, pp. 1270-9.

2. Rodney Finlayson, Ischaemic Heart Disease, aortic aneurysms and atherosclerosis in the city of London 1868-1982. Medical History Supplement 5, 1995, pp. 151-69.

3. Alastair Mackinnon, The origin of the modern epidemic of coronary heart disease in England, Journal of the Royal College of General Practitioners, April 1987, pp. 174-6.

4. Wilber Thomas et al., Incidence of myocardial infarction with venous and pulmonary thrombosis and embolism. The American Heart Journal, Jan. 1960, pp. 41-47.

5. S.L. Malhotra, The American Journal of Clinical Nutrition, Vol. 20, May 1997, pp. 462-74.

6. G. Bizzozero, Virchows Archiv fur Pathologische Anatomie und Physiologie und fur Klinische Medizin 1882, Vol. 90, p. 261.

7. H.E. Burk and John Tait, Blood coagulation as by intravenous injection of tissue extract. Quarterly Journal of Experimental Physiology, 16, 1925, pp. 111-27.

8. Irving Wright et al., Report of the committee for the evaluation of anticoagulant in treatment of coronary thrombosis with myocardial infarction. American Heart Journal, Vol. 36, 1948, pp. 801-15.

9. JAMA, Nov. 7, 1966, pp 129-35.

10. Circulation, March 1968. The entire issue devoted to this trial.

11. Lancet, 1968, ii, pp. 693-6.

11a. American Heart Association Monograph No. 25, 1969. This entire monograph was devoted to this trial.

12. British Medical Journal Editorial, August 11, 1973.

13. Stewart Wolf et al., The Roseto Study, Transactions of the American Climatological Association, Vol. 85, 1973, pp. 100-112.

14. Fredrick Stare et al., Nutritional and epidemiologic factors related to heart attacks, World Review of Nutrition and Dietetics, Vol. 12, 1970, pp 1-42.

15. S.L. Malhotra, American Journal of Clinical Nutrition , Vol. 20, May 1967, pp. 462-74.

16. Bihari Raheja, Ghee, cholesterol and heart disease. Lancet, Nov. 14, 1987, p. 114.

17. S. Renaud and M. deLorgeril Whine, Alcohol, platelets and the French Paradox for coronary heart disease, Lancet, June 20, 1992, pp. 1523-6.

18. Terence Anderson, Nutritional Muscular Dystrophy and human myocardial infarction, Lancet, August 11, 1973, pp. 298-302.

19. C.H. Hammond and L. Garfinkel, Aspirin and coronary heart disease findings of a prospective study. British Medical Journal, 2: 1984, pp. 269-71.

20. Lancet, 1979, ii, pp. 1313-16.

21. Aspirin myocardial infarction study group. JAMA, Feb. 15, 1980, Vol. 243, pp. 661-9.

22. R. Peto et al., Randomized trial of prophylactic daily aspirin among British male doctors, British Medical Journal, 1988, Vol. 296, pp. 313-6.

23. Final report on the aspirin component of the ongoing physicians' health study, NEJM, July 20, 1989, pp. 129-35.

24. James Landauer, Reply to physicians' health study, NEJM, April 7, 1988, p. 925.

25. European Stroke Prevention Study, Lancet, Dec. 12, 1987, pp. 1351-3.

26. W.D. McDonald, Inhibition of human platelet cyclo-oxygenase by alpha tocopherol, Prostaglandins and Medicine, Vol. 4, 1980, pp. 79-85.

27. Editorial. Is vitamin B6 an antithrombic agent?, Lancet, June 13, 1981, p. 1299.

28. S. Moncada et al., Eicosapentaenoic acid and the prevention of thrombosis and atherosclerosis. Lancet 1978, i, pp. 18-20.

29. K.C. Srivastava and T. Mustafa, Ginger in rheumatoid and musculoskeletal disorders, Medical Hypotheses, 1992, Vol. 39, pp. 342-8.


Last updated: 20 July 2002

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