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After finishing my doctorate in chemical pathology at the Royal Post-Graduate Medical School, London in 1960, I worked five years at Makerere Medical School in Uganda, and I became mainly interested in the pathogenesis of the problems of Ugandans. Possibly, their propensity to eating huge quantities of green bananas might have had something to do with their intestinal disorders which resulted in volvulus and double volvulus being the #1 reason for surgery: The green banana is rich in serotonin which stimulates intestinal motility. The other unique problem was endomyocardial fibrosis (EMF) a fibrotic condition which affects the endo- and myo-cardium, leading to heart failure and death. But the idea that diet was a factor in EMF did turn out to be right. Africa had taught me that nutrition was important. {}

A subsequent research fellowship with Professor Ernst Baranay at the University of Uppsala, Sweden taught me that the #1 killer in the Western World was coronary heart disease, unheard of in Africans in Uganda. The Swedes suggested it had something to do with the food. I heard in Uppsala a brilliant lecture by Dr. Bang from Denmark on blood cholesterol, arteries and saturated fat. So that narrowed the responsible food down to dietary lipids as a cause of atherosclerosis.

The Different Diseases of Africa and London: no CHD in Africans.

Whilst interested in EMF and other fascinating differences in the diseases of Africa and Europe, I felt that it would be a good idea to show my new bosses in London that I was also interested in what Londoners died from. The National Institutes of Health and the Albany Medical Center in Albany, New York in particular, had a major research program running in Uganda, comparing blood cholesterols in Ugandans with Americans (1). The bottom line was that Americans had loads of cholesterol circulating in their blood whereas the Ugandans had half the amount. We had added our little bit by showing that Ugandan, European and North American infants were no different at birth. However, the Europeans could be separated based on a rising blood cholesterol level at six years of age. At that age, the African children's blood cholesterols were little different from those in their first year of life, whereas the European children's levels were substantially higher. African blood pressure also remained singularly stable from childhood to the mid 20s.

Finding the Road to the Home of Poly.

It was a cold wintry night back home in London in 1967. We had just installed a machine called an S6 Research Gas Liquid Chromatograph (GLC), and my love affair with POLY was about to begin. She had a black funnel on her roof, a row of red, yellow, green and blue lights above lots of knobs for controlling gas flows, temperature of oven, detector, signal amplification, time of day, and a large but efficient pen recorder. She looked like a mock up of Dr. Who's Time Warp Drive for the Tardis! Inside, there was a coil of metal or glass tubing. The idea was that the operator straightened out the metal coil, dangled it in the stair well whilst he tapped in a sandy substance which had previously been laced with polyethylene glycol adipate, Apiezon or something that would grab the methyl esters of fatty acids. The column was re-coiled, replaced, the flow of inert gas adroitly turned on, the temperature raised and methyl esters injected all of which brought fatty acids out the other end, neatly separated in a nice marching order, like soldiers sorted by rank. The glass columns were more difficult. They had to be filled in the coiled state and people regularly broke them. The operator then spent a lot of time fitting the coil into the S6 oven. Between an injection port and an outlet to a flame ionization detector. You then injected onto the column standard mixtures of the methyl esters of palmitic, stearic, linoleic and linolenic acids, and reading everything and anything Bob Ackman had written on the subject (2).

African Buffalo and why Saturated fats are dangerous:

At that time, Ancel Keys' Seven Countries study was also pointing the finger of accusation at dietary saturated fats which were closely associated with coronary mortality (3). As these fats mostly came from animal sources our first analytical foray was to compare the fat from African and European meats. The European beef sounded like a good start. It gave us lots of peaks of 16 and 18 carbon chain lengths which were readily identified as mainly palmitic, stearic and oleic acids and not much else apart from some odd chain length and shorter chain length saturated fatty acids.

African Buffalo, Syncerus caffer, known to the locals with the much more sonorous, threatening and descriptive name of ‘Mbogo’ (pronounced Mmmm-bo-go) was our starting comparison. After all humans were supposed to have lived on the meat of these animals during the millions of years when the genome was finally shaped. We found the expected palmitic, stearic and oleic acids but to our astonishment, these were followed by a substantial peak for linoleic (20%) and a smaller but significant peak for linolenic acid (5%). Many more peaks followed. What were they? We asked the nice people at EMI for help. Our samples were shoved down a mass spectrometer and soon we had the empirical formula. Silver nitrate chromatography separates fatty acids based on the number of double bonds and that combined with hydrogenation to remove the double bonds gave us even more information.

Bob Ackman working in Halifax in Canadian Fisheries Research was, quite naturally, defining the fatty acid composition of fish and had worked out ways of identifying fatty acids based on relative retention times. Using all of these techniques we identified these later peaks as 1% dihomo-gammalinolenic acid (20:3ω6), 6% arachidonic acid (20:4ω6), 1% docosatetraenoic acid (22:4ω6), 3% eicosapentaenoic acid (20:5ω3) and 5% docosapentaenoic (22:5ω3). Unlike Bob's fish flesh, there was only a trace amount of docosahexaenoic acid (22:6ω3) in Mbogo meat. A total of 35% were polyunsaturated. After doing several Mbogos, we found the P/S ratio was about 0.7 compared to less than 0.1 for the beef.

Clearly, the difference between African wild and European captive, intensively reared beef was that the European meat was full of saturated fats whereas the African meat was full of polyunsaturated fatty acids. And it was not just a question of linoleic or ωω fatty acids: the whole gang was there with a full range of 3 and fatty acids. The ratio of the two families (ωωωω ωω) was about 3:1. There was a major difference with regard to the ω3 fatty acids when compared to Bob's data on fish. There was little detectable docosahexaenoic acid (DHA). The place we did find DHA was in the brain.

Andrew Sinclair, a young Australian, joined me from Canada. We bought a new GLC, and many traces later it was revealed that it was not just Mbogo that was different. The whole range of meats from wild species, pheasants, pigeons, partridge, monkeys, shrews, pigs, antelopes, deer, and elephants all had polyunsaturated-rich lipid in their meat. (4,5,6) The wild pig had 35% polys in their adipose tissue, 17.5% was linoleic and 17.5% linolenic! It was then that I fell in love with Poly.

The Rise of Poly's Enemies.

The next insight came while editing Sylvia Sikes paper on reproductive failure and aortic calcification found in elephants confined to the Murchison Falls National Park where they had eaten most of the trees and so had become confined to eating grass (7). A comparison of buffalo similarly confined to grassland with buffalo in their bush or woodland habitat revealed that the grassland animals had more saturated fatty acids in their tissue than did the woodland animals (8). The bush and woodland with their large oil-rich seeds and nuts and dark green leaves, provided more polys than grass.

Having reached this conclusion, it was not difficult to draw another, as to how our intensively-reared beef became so fatty in a saturated way. In the 17th century, the Acts of Enclosure not only deprived common people of land but also deprived the free-living animals of natural bush, herbs, sedges and woodland browse and confined them to `high energy' grass pastures. Both the ‘enclosures’ and the ‘finishing’ process in even more confined quarters restricted exercise. The farmer made more money the heavier the animal was at market, so there was a genetic selection for the heavier i.e. for the fatter animal. They were unconsciously selecting for obesity! As time went by, clever people developed high energy feeds to increase weight gain. In the early part of this century, pigs which had once been fed on linolenic- and linoleic-acid rich acorns in the winter, they were fed on high energy, carbohydrate-rich feeds all year round to harden their fat which otherwise would go rancid in the summer. Calves were removed from their mothers and fed artificial milk so more milk and butter could be sold. The beef industry was persuaded to use cereal and other feeds rich in protein and carbohydrates, made up from substances with little resemblance to the animals' natural diet in the belief that protein was good for beef.

The consequence was that weight gain was a wonder to behold! But we all know how to put on weight and what we put on when we do - fat! The health message to humans is plenty of exercise, reduced fat and calorie controlled diet. Our livestock were given precisely the opposite treatment: no exercise and high energy foods. That resulted in fat infiltrating pathologically between atrophying muscle fibres in a process called marbling. But the scientifically unfounded focus on protein rich, high energy foods did not stop there. In 1976 the Royal College of Physicians jointly with the British Cardiac Society, published its recommendations on the prevention of heart disease (9). Their report argued we should reduce the dietary saturated fat, reduce fatty, red meat consumption and increase the use of poultry which was lean. The demand for poultry rose sharply. Then some bright economist came along with a brilliant commercial solution. Cut off the surplus beef fat, which would make a great, high energy supplement for chickens. So they fed it to battery-reared chickens, which live only a short lifetime without ever seeing a blade of green grass or an insect. The weight gain efficiency of this tactic approaches unity. So the chicken, whose meat and fat is naturally polyunsaturated was over night transformed to a fatty bird with a carcass fat of over 20%. 1.2 Kg of chicken could contain 200g fat. If 600g of the remainder is meat, and if the water is removed, 120 g or 480 calories remain as protein. The 200 g fat translates to 1,800 calories so there is 3.75 times as much energy invested in the production of chicken fat compared to chicken protein. These figures are generous for carcass fats in battery chickens often exceed 20% and European beef is finished at over 25%, giving fat/protein ratios of up to 6 to 1!.

The consumer was fooled into paying 4 times as much for the increased chicken fat! But it was not even chicken fat; for a large part of it was coming from the beef tallow in the feed. To make matters worse, in the US it became fashionable to eat chicken fried in deep fat, which is very popular with restaurateurs because it can be kept hot around the clock. We know from the work of Holman (10) and of Brenner (11), that all fatty acids compete with each other in their metabolism. Thus these huge rises in consumption of saturated fats can be seen as the rise of the enemies of Poly.

The Bottom of the Saturated Animal Fat Pit

The final disaster came in 1983 when the protein/energy enthusiasts in our animal feed industry and in the Ministry decided they could substitute ground up offal from abattoirs for soya bean protein which had become pricey. The result was bovine spongiform encephalopahy (BSE) or mad cow disease. Their thought processes were by then so far removed from real animal science, and their perspective so out of focus from the normal, that they used waste products such as brain, spinal cords, and any other cheap waste to provide protein for animal feeds. They should have known about scrapie in sheep and Kuru in New Guinea people. These are spongiform disease(s) of the brain transmitted by prions which are brain proteins. The natives of New Guinea get the infection by eating other peoples’ brains without cooking them. It was a prion which they said caused BSE.

In the London Zoo Eland and other wild antelopes died from BSE! The one truth that our GLC had taught us was that wild animals were rich in polyunsaturated, essential fatty acids (EFAs). We had GLC data to show that when brought into captivity they lost substantial proportions of EFAs, linolenic acid in particular because they were fed on Zoo diets which used cattle feeding principles based on protein. The lucky ones not on concrete were on grass pasture.

A new explanation for BSE: Susceptibility through EFA deficiency

Clausen and Moller (12) had shown in 1967 that depleting rats of EFAs, depleted the blood brain barrier and made their brains susceptible to injection of brain protein and they died from an allergic encephalomyelitis. So Pierre Budowski and I postulated that replacing natural food and ultimately soya products with animal protein would have reduced their already reduced EFA status of our intensively reared beef animals. EFA deficiency would make their brains susceptible to attack from foreign protein (13).

Making rats deficient of EFAs to study encephalomyelitis is a long, tedious process so workers developed genetically susceptible models. Harbige (14) has now shown that one can reverse the genetic susceptibility by feeding gamma-linolenic acid which provided nearly 100% protection. So the experimental evidence has now gone the full cycle of creating susceptibility nutritionally, then genetically and finally reversing both with EFAs. However, our Ministry was not interested in following up this matter for reasons difficult to fathom. Proper feeding might well have reversed what was to become a major disaster (15).

We suspect, an acceptance of this new idea would have required recognition of a long track record of miss-shapen agricultural policy which emphasized protein and ignored polyunsaturates essential for life. A first step in reversal of BSE would be to allow calves to feed from their mothers instead of on synthetics. This farmers were forced to do so because of the collapse of the market! A second step would be to allow them access to their primary source of omega 3 fatty acids namely grass and green leaves. Scottish farmers who did this and had no BSE are rightly angry that they are suffering along with those who have it.

It is impossible to believe the story that underpinned the so called cause of BSE. It was claimed that a a rogue scrapie virus. Or prion, from a sheep’s brain entered the food chain causing the epidemic. No amount of mathematical modeling will provide a scenario of one sheep’s brain diluted across the millions of tons of animal feed causing an epidemic which affected the whole of the intensively reared herds within such a short space of time. Searches in the world of sheep revealed no such virus. You need hundreds and hundreds of sheep’s brains to get anywhere near a toxic oral dose and such a rate of infection in the sheep would have been obvious. On the other hand, depletion of brain specific fatty acids would do the trick on a massive scale because the feed had been made deficient on a massive scale. If chicken flocks are fed on an omega 3/anti-oxidant deficient diet, whole flocks will die within 30 days after hatching.

In the end, the animal feed industry and the Ministry virtually destroyed the British beef industry. The effect in many European countries has been similarly serious. The Germans did not want to eat beef, and BSE has appeared in France. It is thought to be due to sly exporters of animal feeds including offal after it was banned in the UK. It has appeared in Japan even though the Japanese deny using imported or any other animal material in their feeds.

Thinking they knew better than Nature and evolution, leaders of the time led the farmers to this final disaster. The same arrogance has contributed a heavy toll in human health. The latest WHO statistics show how the UK and USA are world leaders in coronary mortality, obesity and diabetes, which are now being globalized to countries such as the Philippines, Malaysia, India and China. By 1992, heart disease, previously a rarity, had become the leading cause of death in Manila..

Homo Sapiens is Adapted to Poly foods, not to the Saturated Enemies

Being introduced to Poly by Mbogo has at least given me a new understanding of the meaning of nature, nutrition and health. It needs to be remembered that we emerged from the Stone Age only 150 generations ago. Our physiology is still adapted to eating wild foods, or if you like, Sir Robert McCarrison’s ”unsophisticated foods of Nature” . We are a wild strain in a modern nutritional environment. At the beginning of the 20th century, beef animals were already becoming obese. But then we used a lot of that beef tallow and sheep fat to make candles. With the advent of electric light bulbs, ways and means were found to put that fat into the food chain. We now eat the candles!

Today there are studies to show how the ω3 Poly fatty acids can reduce heart disease risk. The saturated fat of land animal fats increases it. There is current talk about nutritional treatment of adreno-leucodystrophies, treatment of cacexia, and the prevention of cancer. So Poly, given the right proportions, is protective.

The Mistake of Recommending Populations to Reduce Dietary Fat Intakes.

The astonishing fact is that from the Seven Countries Study in the1950s (3) it was clear that it was not the total amount of dietary fat that was related to death from heart disease, but the total amount of saturated fat. The Mediterranean people ate more or as much fat than we in England or North America, but had little heart disease. The fat was olive oil. It was the quality of fat that mattered.

Despite this knowledge and the consistent support from science, Health Ministries and their nutrition committees made recommendation after recommendation for their whole populations to reduce total fat intake. These recommendations put children and pregnant women at risk and have led to people producing and consuming synthetic dietary greases that are not fat. People can continue to eat pseudo-fat without digesting it or burning its calories, but with the risk of leaching fat-soluble vitamins out of our systems while becoming increasingly deficient in the essential fatty acids..

The excuse the Health Committees make is that by recommending people to reduce total fat they will reduce saturated fats because that is what accounts for most of the fat. There is however, no substitute in science for the truth. These recommendations were not based on the truth. They were grossly misleading. Had people been told the truth they would have needed to be given a modest amount of information and education about the different types of fat. Without that educational input, generations have grown up, and have been denied a proper understanding of the truth about fats. People do not understand the truth that there are essential fats needed for reproduction, intelligence and health. There are also non-essential fats. The saturated fats are in the non-essential group and too much of them interferes with the use of the essential fats, with a cost to our arteries. The FAO and WHO Expert Consultation in 1978 and again in 1995 (16) made the true point that in many parts of the world children should have more fat in their diet, but fat of the correct type. Maybe one day someone in a position of political and industrial influence will take the trouble to develop an understanding of the true nature of fat and begin to understand Poly and communicate her beauty to the public. Although she is complex lady with many characteristics, there is now very good evidence that she is naturally good for health.

The Future is at Stake

Understanding the true nature of fat is of paramount importance to the health and abilities of children born in the next generation. My learning the importance of nutrition to infant health was through the writings of many lipid scientists from many countries, writing in several lipid research journals, reporting basic biochemistry of EFA, and especially the inducing of EFA deficiency in infants by feeding milks without EFAs! The importance of this struck me forcibly when I learned simple facts about the chemistry of the brain (17) and linked this with another fact, namely that all land animals lost relative brain capacity in a logarithmic manner as body size increased (18).

Without doubt, the brain is the most important biological development which makes us humans different from other animals. Sixty percent of the structural material of the human brain is made up of lipids containing EFAs. This is where the shallowness of the thinking behind recommendations to reduce total fat intakes is highlighted.

During the development of the fetus and new born, the brain consumes more than 60% of the energy used by its whole body. To do this it requires a simultaneous development of the structure of blood vessels and heart to pump the blood to meet this prodigious demand. Again it is not just any old total fatty acid that is needed by the fetus, but it is the highly polyunsaturated fats that make up the linings of the blood vessels, heart cells immune system,, brain cells and their signaling devices. Reducing total fat content in the diet without making provision for those special requirements for polyunsaturated fatty acids could, at its simplest, jeopardize the health and intelligence of future generations.


1. Shaper A.G. and Jones, K.W. (1962) Serum cholesterol in camel herding nomads. Lancet, ii, 1305.

2. Ackman, R.G. (1969) Gas-liquid chromatography of fatty acids and esters. In “Methods in Enzymology” (J.M. Lowenstein ed.) Vol. XIV, pp. 329-381.

3. Keys, A. (1970) Coronary Heart Disease in Seven Countries. Circulation, 42. (Suppl. 1)

4. Crawford, M.A. (1968) Fatty acid ratios in free living and domestic animals. Lancet (i): 1329 1333.

5. Crawford, M.A. (1968) Fatty acid ratios in free living and domestic animals. Lancet (i): 1329 - 1333.

6. Crawford, M.A., Gale, M.M. and Woodford, M.H. (1969) Linoleic acid and linolenic acid elongation products in muscle tissue of Syncerus caffer and other ruminant species. Biochem. J. 115: 25 27.

7. Sikes, S. K. (1968) Observations on the ecology of arterial disease in the African Elephant (Loxodonia Africana) in Kenya and Uganda. In Comparative Nutrition of Wild Animals, Symp. Zool. Soc. London, 21: 251-273.

8. Crawford, M.A., Gale, M.M., Woodford, M.H. and Casperd, N.M. (1970) Comparative studies on fatty acid composition of wild and domestic meats. Int. J. Biochem. 1: 295 305.

9. Royal College of Physicians of London and British Cardiac Society (1976) Prevention of Coronary Heart Disease: Chairman A.G.Shaper, Journal of the Royal College of Physicians of London. Vol. 10.

10. Holman, R.T. (1970) Biological activities of and requirements for polyunsaturated fatty acids. In ‘Progress in the Chemistry if Fats and Other Lipids’ (R.T.Holman, ed), Vol. 9, Part 5, 611-682., Pergamon Press, Oxford.

11. Brenner, R.R. and Peluffo, R.O. (1966) Effect of saturated and unsaturated fatty acids on the desaturation in vitro, of palmitic, stearic, oleic, linoleic and linolenic acids. J. Biol. Chem. 241:, 5213 - 5219.

12. Clausen J and Moller D (1967) Allergic encephalomyelitis induced by brain antigen after deficiency polyunsaturated fatty acids during myelination. Acta Neurol Scand 43: 375-388.

13. Crawford, M.A., Budowski, P., Drury, P., Ghebremeskel, K., Harbige, M., Leighfield, M., Phylactos, A. and Williams, G. (1991) The nutritional contribution to Bovine Spongiform Encephalopathy. Nutr. and Health 7: 61 68.

14. Harbige, L.S., Yeatman, N., Amor, S. and Crawford, M.A. (1995) Prevention of experimental autoimmune encephalomyelitis in Lewis rats by a novel fungal source of gamma-linolenic acid. Br. J. Nut., 74: 701-715.

15. Crawford, M.A. and Ghebremeskel, K. (1996) The equation between food production, nutrition and health. In “Food Ethics”, ed Ben Mepham, Routeledge, London. pp64-100.

16a. Food and Agricultural Organization and World Health Organizations of the United Nations (1977), Nutrition Report no 3. ‘The Role of Dietary Fats and Oils in Human Nutrition’, FAO, Rome.

16b. Food and Agricultural Organization and World Health Organizations of the United Nations (1995), ‘The Role of Dietary Fats and Oils in Human Nutrition’, FAO, Rome.

17. Crawford, M.A. and Sinclair, A.J. (1972) Nutritional influences in the evolution of the mammalian brain. In Lipids, malnutrition and the developing brain: 267 292. Elliot, K. and Knight, J. (Eds.). A Ciba Foundation Symposium (19 21 October, 1971). Amsterdam, Elsevier.

18. Crawford, M.A., Cunnane, S.C. and Harbige, L.S. (1993) A new theory of evolution: quantum theory. IIIrd International Congress on essential fatty acids and eicosanoids, Am. Oil Chem. Soc. ed A.J. Sinclair, R. Gibson, Adelaide, 87 95.

Michael A. Crawford, PhD., FIBiol., FRCPath.,

Institute of Brain Chemistry and Human Nutrition,

London Metropolitan University,

166-222 Holloway Road, London N7 8DB, UK.


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