# Atkins what a joke & con



## Cookie

So we all relate to high fat diets as were doing the ATKINS,what a load of codswollap,this type of diet has been around for over a century and millenia if you go by different diets from different cultures,*so over the next week I am going to post up all the different articles I have in this one thread(*so please have patience with me)and when you`ve read em post your questions and I`ll ty my hardest to answer them,*these articles I have got from all over the place so it will be nice to see them all in one place for all to read on this board.*

Enjoy

When one thinks of low-carbohydrate diets today, one tends to think that they are "new" or "revolutionary" in some way. Popular books certainly give that impression. But nothing could be further from the truth. I started eating a low-carbohydrate diet in 1962 when a doctor advised me that this was the best way to lose weight.

You may also think that these "new" low-carbohydrate regimes have been pioneered by far-seeing and learned medical men. Again, this is incorrect. The truth is that we would probably never have heard of diets where people could lose weight eating that most calorific of foods: fat, if it had not been for a 19th century English carpenter by the name of William Banting.

Only three men in history have been immortalized by having their names enter the English language as verbs. The first was an Irishman, Captain Boycott, whose name entered the language in the 1860s. Another was Louis Pasteur and the third was the subject of this article-William Banting, a man who came to have a great impact on many peoples' lives, one of whom is me.

Being overweight has affected a small proportion of the population for centuries but clinical obesity was relatively rare until the 20th century. Indeed obesity remained at a fairly stable low level until about 1980. Then its incidence began to increase dramatically. By 1992 one in every ten people in Britain was overweight; a mere five years later that figure had almost doubled. In the USA it is even worse: by 1991 one in three adults was overweight. That was an increase of eight percent of the population over just one decade despite the fact that Americans spend a massive $33 billion a year on "slimming."

It may be hard to believe, but this has occurred in the face of increasing knowledge, awareness and education about obesity, nutrition and exercise. It has happened despite the fact that calorie intake has gone down by twenty percent over the past ten years and exercise clubs have mushroomed. More people are cutting calories now than ever before in their history yet more of them are becoming overweight. There is now a pandemic of increasing weight across the industrialized world.

But it needn't be like that, for nearly 140 years ago one man changed the thinking on diet completely. It all started with a small booklet entitled Letter on Corpulence Addressed to the Public, not written by a dietician or a doctor, but by an undertaker named William Banting. It became one of the most famous books on obesity ever written. First published in 1863, it went into many editions and continued to be published long after the author's death. The book was revolutionary and it should have changed western medical thinking on diet for weight loss for ever.

William Banting was well-regarded in 19th century society. He was a fine carpenter and an undertaker to the rich and famous. But if he had remained only that, his name would probably be remembered today merely as the Duke of Wellington's coffin maker, if indeed it were remembered at all.

None of Banting's family on either parent's side had any tendency to obesity. However, when he was in his thirties, William started to become overweight and he consulted an eminent surgeon, a kind personal friend, who recommended increased "bodily exertion before any ordinary daily labours began." Banting had a heavy boat and lived near the river so he took up rowing the boat for two hours a day. All this did for him, however, was to give him a prodigious appetite. He put on weight and was advised to stop. So much for exercise!

He was then advised that he could remedy his obesity by "moderate and light food" but wasn't really told what was intended by this. He says he brought his system into a low, impoverished state without reducing his weight, which caused many obnoxious boils to appear and two rather formidable carbuncles. He went into hospital and was ably operated upon-but also fed into increased obesity.

Banting went into hospital twenty times in as many years for weight reduction. He tried swimming, walking, riding and taking the sea air. He drank "gallons of physic and liquor potassae," took the spa waters at Leamington, Cheltenham and Harrogate, and tried low-calorie, starvation diets; he took Turkish baths at a rate of up to three a week for a year but lost only six pounds in all that time, and had less and less energy.

He was assured by one physician, whom he calls "one of the ablest physicians in the land," that putting weight on was perfectly natural; that he, himself, had put on a pound for every year of manhood and he was not surprised by Banting's condition-he just advised "more exercise, vapour baths and shampooing and medicine."

Banting tried every form of slimming treatment the medical profession could devise but it was all in vain. Eventually, discouraged and disillusioned-and still very fat-he gave up. By 1862, at the age of 64, William Banting weighed 202 pounds and he was only 5 feet 5 inches tall. Banting says that although he was of no great weight or size, still, he says: "I could not stoop to tie my shoes, so to speak, nor to attend to the little offices humanity requires without considerable pain and difficulty which only the corpulent can understand. I have been compelled to go downstairs slowly backward to save the jar of increased weight on the knee and ankle joints and have been obliged to puff and blow over every slight exertion, particularly that of going upstairs."

He also had an umbilical rupture, and other bodily ailments. On top of this he found that his sight was failing and he was becoming increasingly deaf. Because of this last problem, he consulted an aural specialist who made light of his case, sponged his ears out and blistered the outer ear-without the slightest benefit and without enquiring into his other ailments. Banting was not satisfied: he left in a worse plight than when he went to the specialist.

Eventually, in August of 1862 Banting consulted a noted Fellow of the Royal College of Surgeons: an ear, nose and throat specialist. Dr. William Harvey. It was an historic meeting. Dr. Harvey had recently returned from a symposium in Paris where he had heard Dr. Claude Bernard, a renowned physiologist, talk of a new theory about the part the liver played in the disease of diabetes. Bernard believed that the liver, as well as secreting bile, also secreted a sugar-like substance that it made from elements of the blood passing through it. This started Harvey's thinking about the roles of the various food elements in diabetes and he began a major course of research into the whole question of the way in which fats, sugars and starches affected the body.

When Dr. Harvey met Banting, he was interested as much by Banting's obesity as by his deafness, for he recognised that the one was the cause of the other. So Harvey put Banting on a diet. By Christmas, Banting was down to 184 pounds and, by the following August, 156 pounds.

He had, he says, "little comfort and far less sound sleep."

Harvey's advice to him was to give up bread, butter, milk, sugar, beer and potatoes. These, he was told, contained starch and saccharine matter tending to create fat and were to be avoided altogether. When told what he could not eat Banting thought that he had very little left to live on. His kind friend soon showed him that really there was ample and Banting was only too happy to give the plan a fair trial. Within a very few days, he says, he derived immense benefit from it. The plan led to an excellent night's rest with 6 to 8 hours' sleep per night.

Fortunately for us today, Banting was quite a remarkable man. It is for this reason alone that we can know today what this miraculous diet was. In May 1863, at his own expense, Banting published the first edition of his now famous Letter on Corpulence in which he tells us of Harvey's diet plan (see below).

On this diet Banting lost nearly 1 pound per week from August 1862 to August 1863. In his own words he said: "I can confidently state that quantity of diet may safely be left to the natural appetite; and that it is quality only which is essential to abate and cure corpulence."

He went on: "These important desiderata have been attained by the most easy and comfortable means. . . by a system of diet, that formerly I should have thought dangerously generous."

After 38 weeks. Banting felt better than he had for the past 20 years. By the end of the year, not only had his hearing been restored, he had much more vitality and he had lost 46 pounds in weight and 12 1/4 inches off his waist. He suffered no inconvenience whatsoever from the new diet, was able to come downstairs forward naturally with perfect ease, go upstairs and take exercise freely without the slightest inconvenience, could perform every necessary office for himself, the umbilical rupture was greatly ameliorated and gave him no anxiety, his sight was restored, his other bodily ailments were ameliorated and passed into the matter of history.

*BANTING'S DIET PRIOR TO 1862 *

*BREAKFAST*: Bread and milk, or a pint of tea with plenty of milk and sugar, buttered toast.

*DINNER*: meat, beer, much bread (of which he had always been fond) and pastry.

*TEA*: a meal similar to breakfast.

*SUPPER*: generally a fruit tart or bread and milk.

*HARVEY'S DIET PLAN*

*BREAKFAST*: 4-5 ounces beef, mutton, kidneys, broiled fish, bacon or cold meat of any kind except pork,1 a large cup of tea (without milk or sugar), a little biscuit or one ounce of dry toast.

*DINNER*: 5-6 ounces of any fish except salmon, any meat except pork, any vegetable except potato, one ounce of dry toast, fruit of any pudding,2 any kind of poultry or game, and 2-3 glasses of good claret, sherry or Madeira (champagne, port, beer were forbidden).

*TEA*: 2-3 ounces fruit, a rusk or two and a cup of tea without milk or sugar.

*SUPPER*: 3-4 ounces of meat or fish, similar to dinner, with a glass or two of claret.

*NIGHTCAP*:Tumbler of grog: gin, whisky or brandy (without sugar) or a glass or two of claret or sherry.

1. Pork was not allowed as it was thought then that it contained starch.

2. Banting was not allowed the pastry. Banting was delighted. He would have gone through hell to achieve all this but it had not been necessary. Indeed the diet allowed so much food, and it was so easy to maintain, that Banting said of it: "I can conscientiously assert I never lived so well as under the new plan of dietary, which I should have formerly thought a dangerous, extravagant trespass upon health."

He says that this present dietary table is far superior to what he was eating before-"more luxurious and liberal, independent of its blessed effect, but when it is proved to be more healthful, the comparisons are simply ridiculous.

"I am very much better both bodily and mentally and pleased to believe that I hold the reins of health and comfort in my own hands.

"It is simply miraculous and I am thankful to Almighty Providence for directing me through an extraordinary chance to the care of a man who worked such a change in so short a time." It is quite obvious from these comments that Banting didn't need the strength of willpower that today's slimmer needs; that he found his weight-loss diet very easy to maintain.

He goes on to wish that the medical profession would acquaint themselves with the cure for obesity so that so many men would not descend into early graves, as he believed many did, from apoplexy, and would not endure on Earth so much bodily and mental infirmity.

Banting was so pleased with his progress that on top of Harvey's fees, he gave the doctor 350 pounds to be distributed amongst Harvey's favourite hospitals. Although despite this he still felt deeply obligated in a way that he could never hope to repay.

In fact, in 1868, Banting published a prospectus and started a fund to found and endow a new institution for the service of humanity- the Middlesex County Convalescent Hospital.

It was to be for those working-class people who could not afford to convalesce but had to return to work to make ends meet thus allowing no time to get over their hospital ordeal and so succumbed to relapses.

There was a small home at Walton-on-Thames which, although small, was, he thought, possibly sufficient for the purpose. Banting estimated that 312,000 pounds per year was needed to run it.

He put up 3,500 pounds, his son 3,100 and two other members of his family a further 350, With other patrons he raised a total of 35,000 pounds.

Banting charged nothing for the first two editions of his book-he didn't want to be accused of doing it merely for profit. He had printed 1,000 copies of the first edition and he gave them away.

The second edition numbered 1,500 which he also gave away although they cost him 6 pence each. Copies of the third edition, still in 1863, were sold at 1 pound each.

When Banting's booklet, in which he described the diet and its amazing results, was published, it was so contrary to the established doctrine that it set up a howl of protest among members of the medical profession. The "Banting Diet" became the center of a bitter controversy and Banting's papers and book were ridiculed and distorted. No one could deny that the diet worked, but as a layman had published it-and medical men were anxious that their position in society should not be undermined-they felt bound to attack it. Banting's paper was criticized solely on the grounds that it was "unscientific."

Later, Dr. Harvey had a problem too. He had an effective treatment for obesity but not a convincing theory to explain it. As he was a medical man, and so easier for the other members of his profession to attack, he came in for a great deal of ridicule until, in the end, his practice began to suffer.

However, the public was impressed. Many desperate overweight people tried the diet and found that it worked. Like it or not, the medical profession could not ignore it. Its obvious success meant that the Banting Diet had to be explained somehow.

To the rescue from Stuttgart came a Dr. Felix Niemeyer. He managed to make the new diet acceptable with a total shift in its philosophy. At that time, the theory was that carbohydrates and fat burned together in the lungs to produce heat. The two were called "respiratory foods." After examining Banting's paper, Niemeyer came up with an answer to the doctors' problem. All doctors knew that protein was not fattening, only the respiratory foods-fats and carbohydrates. He, therefore, interpreted "meat" to mean only lean meat with the fat trimmed off and this subtle change solved the problem. The Banting Diet became a high protein diet with both carbohydrate and fat restricted. This altered diet became enshrined in history and still forms the basis of slimming diets today.

Banting's descriptions of the diet are quite clear, however. Other than the prohibition against butter and pork, nowhere is there any instruction to remove the fat from meat and there is no restriction on the way food was cooked or on the total quantity of food which may be taken. Only carbohydrate-sugars and starches-are restricted. The reason that butter and pork were denied him was that it was thought at this time that they too contained starch.

Banting, who lived in physical comfort and remained at a normal weight until his death in 1878 at the age of 81, always maintained that Dr. Niemeyer's altered diet was far inferior to the one that had so changed his life. *THE BANTING DIET IS CONFIRMED*

Banting's Letter on Corpulence travelled widely. In the 1890s, an American doctor, Helen Densmore, modelled diets on Banting. She tells how she and her patients lost an average 10-15 pounds in the first month on the diet and then 6-8 pounds in subsequent months "by a diet from which bread, cereals and starchy food were excluded." Her advice to would-be slimmers was: "One pound of beef or mutton or fish per day with a moderate amount of the non-starchy vegetables will be found ample for any obese person of sedentary habits."

Dr. Densmore was scathing of those others of her profession who derided Banting's diet. She says of them: "Those very specialists who are at this time prospering greatly by the reduction of obesity and who are indebted to Mr. Banting for all their prosperity are loud, nevertheless, in their condemnation of the Banting method."

Over the following seventy years many epidemiological studies and clinical trials were conducted in several countries and the evidence mounted. There was by the mid-1950s no doubt that the low-carbohydrate diet worked and clinical trials at the Middlesex Hospital in London had demonstrated how it worked. Doctors could now put their overweight patients on a dietary regime which enjoyed overwhelming evidence of benefit and which was easy to follow and live on for life.

But it was not to be. Dieticians just couldn't seem to get their heads round the concept that eating what looked like a high-calorie diet could possibly be effective for weight loss. Or, perhaps they were afraid to lose face by admitting that they had been wrong. So they continued, myopically, to recommend that if you were overweight, it was your own fault -you were eating too much or not taking enough exercise, or both. That made life very easy for the dietician while it ruined the life of the patient. By the late 1970s fat was getting a bad name as a cause of heart disease (quite incorrectly as we now know). Now fat was banned for other health reasons and carbohydrates were advocated even more strongly.

Which is why, at the start of the 21st Century, at a time when most of us are dieting, are eating fewer calories and less fat, and taking more exercise than ever before in our history, we are getting fatter than ever before in our history.

It is no coincidence that obesity is sky-rocketing today-healthy eating advises a high-carbohydrate, lowfat diet. The exact opposite of Banting's diet.

Not long after Banting's Letter on Corpulence was published the verb "to Bant" entered the language and people losing weight said they were "Banting." It remained in common parlance well into this century and one still hears it occasionally today. Jan Freden, of Uppsala, Sweden, tells me that in Sweden, "Banting" is still the word most commonly used for dieting to achieve weight loss. So in Sweden they say: "Nej, tack, jag bantar" or "No thank you, I am banting."


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## Cookie

*Adventures in Diet*

*
**Part 1*
​


*By Vilhjalmur Stefansson*

*
*Harper's Monthly Magazine, November 1935.
​
In 1906 I went to the Arctic with the food tastes and beliefs of the average American. By 1918, after eleven years as an Eskimo among Eskimos, I had learned things which caused me to shed most of those beliefs. Ten years later I began to realize that what I had learned was going to influence materially the sciences of medicine and dietetics. However, what finally impressed the scientists and converted many during the last two or three years, was a series of confirmatory experiments upon myself and a colleague performed at Bellevue Hospital, New York City, under the supervision of a committee representing several universities and other organizations.

Not so long ago the following dietetic beliefs were common: To be healthy you need a varied diet, composed of elements from both the animal and vegetable kingdoms. You got tired of and eventually felt a revulsion against things if you had to eat them often. This latter belief was supported by stories of people who through force of circumstances had been compelled, for instance, to live for two weeks on sardines and crackers and who, according to the stories, had sworn that so long as they lived they never would touch sardines again. The Southerners had it that nobody can eat a quail a day for thirty days.

There were subsidiary dietetic views. It was desirable to eat fruits and vegetables, including nuts and co**** grains. The less meat you ate the better for you. If you ate a good deal of it, you would develop rheumatism, hardening of the arteries, and high blood pressure, with a tendency to breakdown of the kidneys - in short, premature old age. An extreme variant had it that you would live more healthy, happily, and longer if you became a vegetarian.

Specifically it was believed, when our field studies began, that without vegetables in your diet you would develop scurvy. It was a "known fact" that sailors, miners, and explorers frequently died of scurvy "because they did not have vegetables and fruits." This was long before Vitamin C was publicized.

The addition of salt to food was considered either to promote health or to be necessary for health. This is proved by various yarns, such as that African tribes make war on one another to get salt; that minor campaigns of the American Civil War were focused on salt mines; and that all herbivorous animals are ravenous for salt. I do not remember seeing a critical appendix to any of these views, suggesting for instance, that ***** tribes also make war about things which no one ever said were biological essentials of life; that tobacco was a factor in Civil War campaigns without being a dietetic essential; and that members of the deer family in Maine which never have salt or show desire for it, are as healthy as those in Montana which devour quantities of it and are forever seeking more.

A belief I was destined to find crucial in my Arctic work, making the difference between success and failure, life and death, was the view that man cannot live on meat alone. The few doctors and dietitians who thought you could were considered unorthodox if not charlatans. The arguments ranged from metaphysics to chemistry: Man was not intended to be carnivorous - you knew that from examining his teeth, his stomach, and the account of him in the Bible. As mentioned, he would get scurvy if he had no vegetables in meat. The kidneys would be ruined by overwork. There would be protein poisoning and, in general hell to pay.

With these views in my head and, deplorably, a number of others like them, I resigned my position as assistant instructor in anthropology at Harvard to become anthropologist of a polar expedition. Through circumstances and accidents which are not a part of the story, I found myself that autumn the guest of the Mackenzie River Eskimos.

The Hudson's Bay Company, whose most northerly post was at Fort McPherson two hundred miles to the south had had little influence on the Eskimos during more than half a century; for it was only some of them who made annual visits to the trading post; and then they purchased no food but only tea, tobacco, ammunition and things of that sort. But in 1889 the whaling fleet had begun to cultivate these waters and for fifteen years there had been close association with sometimes as many as a dozen ships and four to five hundred men wintering at Herschel Island, just to the west of the delta. During this time a few of the Eskimos had learned some English and perhaps one in ten of them had grown to a certain extent fond of white man's foods.

But now the whaling fleet was gone because the bottom had dropped out of the whalebone market, and the district faced an old-time winter of fish and water. The game, which might have supplemented the fish some years earlier, had been exterminated or driven away by the intensive hunting that supplied meat to the whaling fleet. There was a little tea, but not nearly enough to see the Eskimos through the winter - this was the only element of the white man's dietary of which they were really fond and the lack of which would worry them. So I was facing a winter of fish without tea. For the least I could do, an uninvited guest, was to pretend a dislike for it.

The issue of fish and water against fish and tea was, in any case, to me six against a half dozen. For I had had a prejudice against fish all my life. I had nibbled at it perhaps once or twice a year at course dinners, always deciding that it was as bad as I thought. This was pure psychology of course, but I did not realize it.

I was in a measure adopted into an Eskimo family the head of which knew English. He had grown up as a cabin boy on a whaling ship and was called Roxy, though his name was Memoranna. It was early September, we were living in tents, the days were hot but it had begun to freeze during the nights, which were now dark for six to eight hours.

The community of three or four families, fifteen or twenty individuals, was engaged in fishing. With long poles, three or four nets were shoved out from the beach about one hundred yards apart. When the last net was out the first would be pulled in, with anything from dozens to hundreds of fish, mostly ranging in weight from one to three pounds, and including some beautiful salmon trout. From knowledge of other white men the Eskimos consider these to be most suitable for me and would cook them specially, roasting them against the fire. They themselves ate boiled fish.

Trying to develop an appetite, my habit was to get up soon after daylight, say four o'clock, shoulder my rifle, and go off after breakfasts on a hunt south across the rolling prairie, though I scarcely expected to find any game. About the middle of the afternoon I would return to camp. Children at play usually saw me coming and reported to Roxy's wife, who would then put a fresh salmon trout to roast. When I got home I would nibble at it and write in my diary what a terrible time I was having.

Against my expectation, and almost against my will, I was beginning to like the baked salmon trout when one day of perhaps the second week I arrived home without the children having seen me coming. There was no baked fish ready but the camp was sitting round troughs of boiled fish. I joined them and, to my surprise, liked it better than the baked. There after the special cooking ceased, and I ate boiled fish with the Eskimos.



*II*
​
By midwinter I had left my cabin-boy host and, for the purposes of anthropological study, was living with a less sophisticated family at the eastern edge of the Mackenzie delta. Our dwelling was a house of wood and earth, heated and lighted with Eskimo-style lamps. They burned seal or whale oil, mostly white whale from a hunt of the previous spring when the fat had been stored in bags and preserved, although the lean meat had been eaten. Our winter cooking however, was not done over the lamps but on a sheet-iron stove which had been obtained from whalers. There were twenty-three of us living in one room, and there were sometimes as many as ten visitors. The floor was then so completely covered with sleepers that the stove had to be suspended from the ceiling. The temperature at night was round 60*F. The ventilation was excellent through cold air coming up slowly from below by way of a trap door that was never closed and the heated air going out by a ventilator in the roof.

Everyone slept completely naked - no pajama or night shirts. We used cotton or woolen blankets which had been obtained from the whalers and from the Hudson's Bay Company.

In the morning, about seven o'clock, winter-caught fish, frozen so hard that they would break like glass, were brought in to lie on the floor till they began to soften a little. One of the women would pinch them every now and then until, when she found her finger indented them slightly, she would begin preparations for breakfast. First she cut off the head and put them aside to be boiled for the children in the afternoon (Eskimos are fond of children, and heads are considered the best part of the fish). Next best are the tails, which are cut off and saved for the children also. The woman would then slit the skin along the back and also along the belly and getting hold with her teeth, would strip the fish somewhat as we peel a banana, only sideways where we peel bananas, endways.

Thus prepared, the fish were put on dishes and passed around. Each of us took one and gnawed it about as an American does corn on the cob. An American leaves the cob; similarly we ate the flesh from the outside of the fish, not touching the entrails. When we had eaten as much as we chose, we put the rest on a tray for dog feed.

After breakfast all the men and about half the women would go fishing, the rest of the women staying at home to keep house. About eleven o'clock we came back for a second meal of frozen fish just like the breakfast. At about four in the afternoon the working day was over and we came home to a meal of hot boiled fish.

Also we came home to a dwelling so heated by the cooking that the temperature would range from 85* to 100*F. or perhaps even higher - more like our idea of a Turkish bath than a warm room. Streams of perspiration would run down our bodies, and the children were kept busy going back and forth with dippers of cold water of which we naturally drank great quantities.

Just before going to sleep we would have a cold snack of fish that had been left over from dinner. Then we slept seven or eight hours and the routine of the day began once more.

After some three months as a guest of the Eskimos I had acquired most of their food tastes. I had to agree that fish is better boiled than cooked any other way, and that the heads (which we occasionally shared with the children) were the best part of the fish. I no longer desired variety in the cooking, such as occasional baking - I preferred it always boils if it was cooked. I had become as fond of raw fish as if I had been a Japanese. I like fermented (therefore slightly acid) whale oil with my fish as well as ever I liked mixed vinegar and olive oil with a salad. But I still had two reservations against Eskimo practice; I did not eat rotten fish and I longed for salt with my meals.

There were several grades of decayed fish. The August catch had been protected by longs from animals but not from heat and was outright rotten. The September catch was mildly decayed. The October and later catches had been frozen immediately and were fresh. There was less of the August fish than of any other and, for that reason among the rest, it was a delicacy - eaten sometimes as a snack between meals, sometimes as a kind of dessert and always frozen, raw.

In midwinter it occurred to me to philosophize that in our own and foreign lands taste for a mild cheese is somewhat plebeian; it is at least a semi-truth that connoisseurs like their cheeses progressively stronger. The grading applies to meats, as in England where it is common among nobility and gentry to like game and pheasant so high that the average Midwestern American or even Englishman of a lower class, would call them rotten.

I knew of course that, while it is good form to eat decayed milk products and decayed game, it is very bad form to eat decayed fish. I knew also that the view of our populace that there are likely to be "ptomaines" in decaying fish and in the plebeian meats; but it struck me as an improbable extension of the class-consciousness that ptomaines would avoid the gentleman's food and attack that of a commoner.

These thoughts led to a summarizing query; If it is almost a mark of social distinction to be able to eat strong cheeses with a straight face and smelly birds with relish, why is it necessarily a low taste to be fond of decaying fish? On that basis of philosophy, though with several qualms, I tried the rotten fish one day, and if memory servers, like it better than my first taste of Camembert. During the next weeks I became fond of rotten fish.

About the fourth month of my first Eskimo winter I was looking forward to every meal (rotten or fresh), enjoying them, and feeling comfortable when they were over. Still I kept thinking the boiled fish would taste better if only I had salt. From the beginning of my Eskimo residence I had suffered from this lack. On one of the first few days, with the resourcefulness of a Boy Scout, I had decided to make myself some salt, and had boiled sea water till there was left only a scum of brown powder. If I had remembered as vividly my freshman chemistry as I did the books about shipwrecked adventurers, I should have know in advance that the sea contains a great many chemicals besides sodium chloride, among them iodine. The brown scum tasted bitter rather than salty. A better chemist could no doubt have refined the product. I gave it up, partly through the persuasion of my host, the English speaking Roxy.

The Mackenzie Eskimos, Roxy told me, believe that what is good for grown people is good for children and enjoyed by them as soon as they get used to it. Accordingly they teach the use of tobacco when a child is very young. It then grows to maturity with the idea that you can't get along without tobacco. But, said Roxy, the whalers have told that many whites get along without it, and he had himself seen white men who never use it, while the few white women, wives of captains, none used tobacco. (This, remember, was in 1906.)

Now Roxy had heard that white people believe that salt is good for, and even necessary for children, so they begin early to add salt to the child's food. That child then would grow up with the same attitude toward salt as an Eskimo has toward tobacco. However, said Roxy, since we Eskimos were mistaken in thinking tobacco so necessary, may it be that the white men are mistaken about salt? Pursuing the argument, he concluded that the reason why all Eskimos dislike salted food and all white men like it was not racial but due to custom. You could then, break the salt habit as easily as the tobacco habit and you would suffer no ill result beyond the mental discomfort of the first few days or weeks.

Roxy did not know, but I did as an anthropologist, that in pre-Columbian times salt was unknown or the taste of it disliked and the use of it avoided through much of North and South America. It may possibly be true that the carnivorous Eskimos in whose language the word salty, mamaitok, is synonymous with with evil-tasting, disliked salt more intensely than those Indians who were partly herbivorous. Nevertheless, it is clear that the salt habit spread more slowly through the New World from the Europeans than the tobacco habit through Europe from the Indians. Even today there are considerable areas, for instance in the Amazon basin, where the natives still abhor salt. Not believing that the races differ in their basic natures, I felt inclined to agree with Roxy that the practice of slating food is with us a social inheritance and the belief in its merits a part of our folklore.

Through this philosophizing I was somewhat reconciled to going without salt, but I was nevertheless, overjoyed when one day Ovayuak, my new host in the eastern delta, came indoors to say that a dog team was approaching which he believed to be that of Ilavinirk, a man who had worked with whalers and who possessed a can of salt. Sure enough, it was Ilavinirk, and he was delighted to give me the salt, a half-pound baking-powder can about half full, which he said he had been carrying around for two or three years, hoping sometime to meet someone who would like it for a present. He seemed almost as pleased to find that I wanted the salt as I was to get it. I sprinkled some on my boiled fish, enjoyed it tremendously, and wrote in my diary that it was the best meal I had had all winter. Then I put the can under my pillow, in the Eskimo way of keeping small and treasured things. But at the next meal I had almost finished eating before I remembered the salt. Apparently then my longing for it had been what you might call imaginary. I finished without salt, tried it at one or two meals during the next few days and thereafter left it untouched. When we moved camp the salt remained behind.

After the return of the sun I made a journey of several hundred miles to the ship Narwhal which, contrary to our expectations of the late summer, had really come in and wintered at Herschel Island. The captain was George P. Leavitt, of Portland, Maine. For the few days of my visit I enjoyed the excellent New England cooking, but when I left Herschel Island I returned without reluctance to the Eskimo meals of fish and cold water. It seemed to me that, mentally and physically, I had never been in better health in my life.



*III*
​
During the first few months of my first year in the Arctic, I acquired, though I did not at the time fully realize it, the munitions of fact and experience which have within my own mind defeated those views of dietetics reviewed at the beginning of this article. I could be healthy on a diet of fish and water. The longer I followed it the better I liked it, which meant, at least inferentially and provisionally, that you never become tired of your food if you have only one thing to eat. I did not get scurvy on the fish diet nor learn that any of my fish-eating friends ever had it. Nor was the freedom from scurvy due to the fish being eaten raw - we proved that later. (What it was due to we shall deal with in the second article of this series.) There were certainly no signs of hardening of the arteries and high blood pressure, of breakdown of the kidneys or of rheumatism.

These months on fish were the beginning of several years during which I lived on an exclusive meat diet. For I count in fish when I speak of living on meat, using "meat" and "meat diet" more as a professor of anthropology than as the editor of a housekeeping magazine. The term in this article and in like scientific discussions refers to a diet from which all things of the vegetable kingdom are absent.

To the best of my estimate then, I have lived in the Arctic for more than five years exclusively on meat and water. (This was not, of course, one five-year stretch, but an aggregate of that much time during ten years.) One member of my expeditions, Storker Storkersen, lived on an exclusive meat diet for about the same length of time while there are several who have lived on it from one to three years. These have been of many nationalities and of three races - ordinary European whites; natives of the Cape Verde Islands, who had a large percentage of ***** blood; and natives of the South Sea Islands. Neither from experience with my own men nor from what I have heard of similar cases do I find any racial difference. There are marked individual differences.

The typical method of breaking a party into a meat diet is that three of five of us leave in midwinter a base camp which has nearly or quite the best type of European mixed diet that money and forethought can provide. The novices have been told that it is possible to live on meat alone. We warn them that it is hard to get used to for the first few weeks, but assure them that eventually they will grow to like it and that any difficulties in changing diets will be due to their imagination.

These assertions the men will believe to a varying degree. I have a feeling that in the course of breaking in something like twenty individuals; two or three young men believed me completely, and that this belief collaborated strongly with their youth and adaptability in making them take readily to the meat.

Usually I think, the men believe that what I tell of myself is true for me personally, but that I am peculiar, a freak - that a normal person will not react similarly, and that they are going to be normal and have an awful time. Their past experience seems to tell them that if you eat one thing every day you are bound to tire of it. In the back of their minds there is also what they have read and heard about the necessity for a varied diet. They have specific fears of developing the ailments which they have heard of as caused by meat or prevented by vegetables.

We secure our food in the Arctic by hunting and in midwinter there is not enough good hunting light. Accordingly we carry with us from the base camp provisions for several weeks, enough to take us into the long days. During this time, as we travel away from shore, we occasionally kill a seal or a polar bear and eat their meat along with our groceries. Our men like these as an element of a mixed diet as well as you do beef or mutton.

We are not on rations. We eat all we want, and we feed the dogs what we think is good for them. When the traveling conditions are right we usually have two big meals a day, morning and evening, but when we are storm bound or delayed by open water we eat several meals to pass the time away. At the end of four, six or eight weeks at sea, we have used up all our food. We do not try to save a few delicacies to eat with the seal and bear, for experience has proved that such things are only tantalizing.

Suddenly, then we are on nothing but seal. For while our food at sea averages ten percent polar bear there may be months in which we don't see a bear. The men go at the seal loyally; they are volunteers and whatever the suffering, they have bargained for it and intend to grin and bear it. For a day or two they eat square meals. Then the appetite begins to flag and they discover as they had more than half expected, that for them personally it is going to be a hard pull or a failure. Some own up that they can't eat, while others pretend to have good appetites, enlisting the surreptitious help of a dog to dispose of their share. In extreme cases, which are usually those of the middle-aged and conservative they go two or three days practically or entirely without eating. We had no weighing apparatus; but I take it that some have lost anything from ten to twenty pounds, what with the hard work on empty stomachs. They become gloomy and grouchy and, as I once wrote, "They begin to say to each other, and sometimes to me, things about their judgment in joining a polar expedition that I cannot quote."

But after a few days even the conservatives begin to nibble at the seal meat, after a few more they are eating a good deal of it, rather under protest and at the end of three or four weeks they are eating square meals, though still talking about their willingness to give a soul or right arm for this or that. Amusingly, or perhaps instructively, they often long for ham and eggs or corned beef when, according to theory, they ought to be longing for vegetables and fruits. Some of them do hanker particularly for things like sauerkraut or orange juice; but more usually it is for hot cakes and syrup or bread and butter.

There are two ways in which to look at an abrupt change of diet - how difficult it is to get used to what you have to eat and how hard it is to be deprived of things you are used to and like. From the second angle, I take it to be physiologically significant that we have found our people, when deprived, to long equally for things which have been considered necessities of health, such as salt; for things where a drug addiction is considered to be involved, such as tobacco; and for items of that class of so-called staple foods, such as bread.

It has happened on several trips, and with an aggregate of perhaps twenty men, that they have had to break at one time their salt, tobacco, and bread habits. I have frequently tried the experiment of asking which they would prefer; salt for their meal, bread with it, or tobacco for an after-dinner smoke. In nearly every case the men have stopped to consider, nor do I recall that they were ever unanimous.

When we are returning to the ship after several months on meat and water, I usually say that the steward will have orders to cook separately for each member of the party all he wants of whatever he wants. Especially during the last two or three days, there is a great deal of talk among the novices in the part about what the choices are to be. One man wants a big dish of mashed potatoes and gravy; another a gallon of coffee and bread and butter; a third perhaps wants a stack of hot cakes with syrup and butter.

On reaching the ship each does get all he wants of what he wants. The food tastes good, although not quite so superlative as they had imagined. They have said they are going to eat a lot and they do. Then they get indigestion, headache, feel miserable, and within a week, in nine cases out of ten of those who have been on meat six months or over, they are willing to go back to meat again. If a man does not want to take part in a second sledge journey it is usually for a reason other than the dislike of meat.

Still, as just implied, the verdict depends on how long you have been on the diet. If at the end of the first ten days our men could have been miraculously rescued from the seal and brought back to their varied foods, most of them would have sworn forever after that they were about to die when rescued, and they would have vowed never to taste seal again - vows which would have been easy to keep for no doubt in such cases the thought of seal, even years later, would have been accompanied by a feeling of revulsion. If a man has been on meat exclusively for only three or four months he may or may not be reluctant to go back to it again. But if the period has been six months or over, I remember no one who was unwilling to go back to meat. Moreover, those who have gone without vegetables for an aggregate of several years usually thereafter eat a larger percentage of meat than your average citizen, if they can afford it.


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## Cookie

*Adventures in Diet*

*
**Part 2*

*
*
​


*By Vilhjalmur Stefansson*

*
*Harper's Monthly Magazine, December 1935.
​
Now that the experiments in diet which K****n Anderson and I undertook at Bellevue Hospital have been accepted by the medical world, it is difficult to realize that there could have been such a storm of excitement about the announcement of the plan, such a violent clash of opinions, such near unanimity to the prediction of dire results.

The feeling that decisive controlled test were needed began to spread after I told one of the scientific heads of the Food Administration in 1918 that I had lived for an aggregate of more than five years with enjoyment on just meat and water. A turning point came in 1920 when I had an hour for explaining a meat regimen to the physicians and staff at the Mayo Clinic. The concluding phase began in 1928 when Mr. Anderson and myself entered Bellevue Hospital to give science the first chance in its history to observe human subjects while they lived through the chill of winter and the heat of summer, for twelve months, on an exclusive meat diet. We were to do it under conditions of ordinary city life.

At the beginning of our northern work in 1906 it was the accepted view among doctors and dietitians that man cannot live on meat alone. They believed specifically that a group of serious diseases were either caused directly by meat or preventable only by vegetables. Those views were still being held when the autumn of 1918, an old friend, Frederic C. Walcott (later Senator from Connecticut), decided that my experiences and the resulting opinions were revolutionary in certain fields, and introduced me to Professor Raymond Pearl of John Hopkins, who was then with the U.S. Food Administration in Washington. Pearl considered several of the things I told him upsetting to views then held; he questioned me before a stenographer, and sent the mimeographed results to a number of dietitians. Their replies varied from concurrence with him (and me) to agreement with David Hume that you are likelier to meet a thousand liars than one miracle.

Pearl was convinced that neither fibs nor miracles were involved and proposed that we write a book on dietetics. I agreed. But cares intervened and things dragged.

In 1920 I had the above-mentioned chance to speak at the Mayo Clinic, Rochester, Minnesota. One of the Mayo brothers suggested that I spend two or three weeks there to have a check-over and see whether they could not find evidences of the supposed bad effects of meat. I wanted to do this but commitments in New York prevented.

Then one day while talking with the gastro-enterologist Dr. Clarence W. Lieb, I told him of my regret that I had not been able to take advantage of the Mayo check-over. Lieb said there were good doctors in New York, too, and volunteered to gather a committee of specialists who would put me through and examination as rigid as anything I could get from the Mayos.

The committee was organized, I went through the mill, and Dr. Lieb reported the findings in the Journal of the American Medical Association for July 3, 1926, "The Effects of an Exclusive Long-Continued Meat Diet." The committee had failed to discover any trace of even one of the supposed harmful effects.

With this publication the Lieb and Pearl events merge. For when the Institute of American Meat Packers wrote asking permission to reprint a large number of copies for distribution to the medical profession and to dietitians, Lieb, Pearl and I went into a huddle. The result was a letter to the Institute saying that we refused permission to reprint, but suggesting that they might get something much better worth publishing, and with right to publish it, if they gave a fund to a research institution for a series of experiments designed to check, under conditions of average city life, the problems which had arisen out of my experiences and views. For it was contended by many that an all-meat diet might work in a cold climate though not in a warm, and under the strenuous conditions of the frontier though not in common American (sedentary) business life.

We gave the meat packers warning that, if anything, the institution chosen would lean backward to make sure that nothing in the results could even be suspected of having been influenced by the source of the money.

After much negotiating, the Institute agreed to furnish the money. The organization selected was the Russell Sage Institute of Pathology. The committee in charge was to consist of leaders in the most important sciences that appeared related to the problem, and represented seven institutions:

American Museum of Natural History: Dr. Clark Wissler.

Cornell University Medical College: Dr. Walter L. Niles.

Harvard University: Drs. Lawrence J. Henderson, Earnest A. Hooton, and Percy Howe.

Institute of American Meat Packers: Dr. C. Robert Moulton.

John Hopkins University: Drs. William G. McCallum and Raymond Pearl.

Russell Sage Institute of Pathology: Drs. Eugene F. DuBois and Graham Lusk.

University of Chicago: Dr. Edwin O. Jordan.

Unattached: Dr. Clarence W. Lieb, private practice, and Vilhjalmur Stefansson.

The Chairman of the committee was Dr. Pearl. The main research work of the experiment was headed by Dr. DuBois, who is now Physician-in-Chief of the New York Hospital and was then as he still is, Medical Director of the Russell Sage Institute of Pathology. Among his collaborators were Dr. Walter S. McClellan, Dr. Henry B. Richardson, Mr. V. R. Rupp, Mr. G. F. Soderstrom, Dr. Henry J. Spencer, Dr. Edward Tolstoi, Dr. John C. Torrey and Mr. Vincent Toscani. The clinical supervision was in charge of Dr. Lieb.

After meetings of the supervising committee, the election of a smaller executive committee and much discussion, it was decided that, while the experiment would be directed at strictly scientific problems, there might be side glances now and then toward common folk beliefs and the propaganda of certain groups. For instance, our definition of a meat diet as "a diet from which all vegetable elements are excluded" would permit us to use milk and eggs, for they are not vegetables. But some vegetarians are illogical enough to allow milk and eggs; we agreed to be correspondingly illogical and exclude them. This forestalled the possible cry that we were saved from the ill effects of a vegetable-less diet by the eggs and the milk.

The aim of the project was not, as the press claimed at the time, to "prove" something or other. We were not trying to prove or disprove anything; we merely wanted to get at the facts. Every aspect of the results would be studied, but special attention would be paid to certain common views, such as that scurvy will result from the absence of vegetable elements, that other deficiency diseases may be produced, that the effect will be bad on the circulatory system and on the kidneys, that certain harmful micro-organisms will flourish in the intestinal tract, and that there will be insufficient calcium. The broad question was, of the supervising doctors and by the testimony of the subjects themselves.

The test was originally planned on me alone, but I might be struck by lightening before conclusions were reached, or I might get run over by a truck, and that would be construed, by mixed-dieters and vegetarians, as showing impairment of mental alertness and bodily vigor through the monotony and poison of meat. It was difficult to find a colleague, for you cannot make this sort of experiment on just anybody that appears if you consider two elementary cases.

Assume the news of a stock market crash that ruins them is conveyed to a number of people after they have eaten a good meal. Digestion may stop almost at the point of the mental shock. Obviously the sickness which follows that meal is not caused by the food, as such.

Or ask some impressionable friend to lunch. Serve them veal, of good quality and well cooked. When dinner is over you inquire about the veal; they will answer with the usual compliments. Then you say that your case has been proved. Rover died and they have eaten him. If your stage setting and acting have been at all adequate, a few at least of your company will make a dive from the room. What sickens them is not the meat of a dog but the idea that they have eaten dog.

The Russell Sage experiment then could not be made upon anybody controlled by any strong dietetic belief, such as that meat is harmful, that abstinence from vegetables brings trouble, that you tire of a food if you have to eat the same thing often. But almost everyone holds these or similar beliefs. So we were practically compelled to secure subjects from members of one of my expeditions; they were the only living Europeans we knew who had used meat long enough to eliminate completely the mental hazards.

One man fortunately was available. He was Karsten Anderson, a young Dane who had been a member of my third expedition. During that time he had lived an aggregate of more than a year on strictly meat and water, suffering no ill result and, in fact being on one occasion cured by meat from scurvy which he had contracted on a mixed diet. Moreover, he knew from experience of a dozen members of the expedition that his healthful enjoyment of the diet was not peculiar to himself but common to all those who had tried it, including members of three races - ordinary whites, Cape Verde Islanders with a strain of ***** blood, and South Sea Islanders.

But there were other things which made Anderson almost incredibility suitable for our test. For several years he had been working on his own in Florida spending most of practically every day outdoors, lightly clad and enjoying the benefits (such as they are) of a sub-tropical sunlight. In that mental and physical environment he had naturally been on a diet heavy in vegetable elements, and had suffered constantly from head colds, his hair was thinning steadily; and he had developed a condition involving intestinal toxemia such as would ordinarily cause a doctor to look serious and pronounce: "You must go light on meat." or "I am afraid you'll have to cut out meat entirely."

We could find no one but Anderson whose mind would leave his body unhandicapped. So, in January 1928, the test began with the two of us. It was under the direct charge of Dr. DuBois and his staff in the dietetic ward of Bellevue Hospital, New York City.

A storm of protests from friends broke upon us when the press announced that we were entering Bellevue. These were based mainly upon the report that we were going to eat our meat raw and the belief that we were using lean meat exclusively. The first was just a false rumor; the trouble under the second head was linguistic.

Eating meat raw, our friends chorused, would make us social outcasts. It is proper to serve oysters raw, and clams, in the United States; herring raw in Norway; several kinds of fish raw in Japan; and beef raw almost anywhere in the world if only you change the name and call it rare. The fashion of giving raw meat to infants was spreading, but we were babes neither in years nor in stature and could not take advantage of that dispensation.

The answer to the raw meat scare was to explain a basic procedure of our experiments - Anderson and I were to select our food by palate (so long as it was meat). It proved that in most of our meals for a year he leaned to medium cooking and I to well done.

The linguistic trouble came from a recent change of American usage. In Elizabethan English meat was any kind of food, as in the expression "meat and drink." In modern England this has narrowed down to what is implied by the rhyme about Jack Sprat eating no fat and his wife no lean, although they both ate meat. In the United States meat, in the last few years has become a synonym for lean. The meaning can become even narrower, as when somebody, usually a woman, tells you that she is strictly forbidden by her physician to touch meat, but that she is permitted all the chicken she wants, with an occasional lamb chop. To that woman meat signifies lean beef.

In the linguistic sense, then we pacified our friends by reference to Mr. and Mrs. Sprat. Our diet would be of meat in the English sense. We were just going to live under modern conditions on the food of our more or less remote ancestors; the food, too, of certain contemporary "primitive hunters."


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## Cookie

II

During our first three weeks in Bellevue Hospital we were fed measured quantities of what might be called a standard mixed diet; fruits, cereals, bacon and eggs, that sort of thing for breakfast; meats, vegetables including fruits for lunch and dinner. During this time various specialists examined us from practically every angle that seemed pertinent.

Most tedious, and let us hope correspondingly valuable, were the calorimeter studies. With no food since the evening before, we would go in the late morning to the calorimeter room and sit quite for an hour to get over the physiological effect of having perhaps walked up a single flight of stairs. Then as effortlessly as we could, we slid into calorimeters which were like big coffins with glass sides, and everybody waited about an hour or so until we had got over the disturbance of having slid in. The box was now closed up, and for three hours we lay there as nearly motionless as we could well be while a corps of scientists visible through the glass puttered about and studied our chemical and other physiological processes. We were not permitted to read and cautioned even against thinking about anything particularly pleasant or particularly disagreeable, for thoughts and feelings heat or cool you, speed things up or slow them down, play hob generally with "normal" processes.

(Dr. DuBois told of a calorimeter test ruined by mental disturbance. A nervous Romanian had developed an intense dislike for a fellow-patient named Kelly. During the second hour of an experiment that had been going very well, Max caught a glimpse of the hated Kelly through the window. This raised his metabolism ten percent during that whole hour.)

With the air we breathed and the rest of our intakes and excretions carefully analyzed, with our blood chemistry determined and a check on such things as the billions of living organisms which inhabit the human intestinal tract, we were ready for the meat.

During the three weeks of mixed diet and preliminary check-up, we had been free to come and go. Now we were placed under lock and key. Neither of us was permitted at any time, day or night to be out of sight of a doctor or nurse. This was in part the ordinary rigidity of a controlled scientific experiment, but it was in some part a bow to the skepticism of the mixed diet advocates and to the emotional storms which were sweeping the vegetarian realms.

Not was the skepticism and excitement all newspaper talk. One of the leading European authorities, most orthodox and belonging to no particular school, was touring the United States. He called on us during the preliminary three weeks and assured the presiding physicians most solemnly that we should be unable to go more than four or five days on meat. He had tried it out himself on experimental human subjects who usually broke down in about three days. These breakdowns, I thought, were of psychological antecedents; but our European authority instituted they were strictly psychological - quite independent of emotions.

The experiment started smoothly with Andersen, who was permitted to eat in such quantity as he liked such things as he liked, provided only that they came under our definition of meat - steaks, chops, brains fried in bacon fat, boiled short-ribs, chicken, fish, liver and bacon. In my case there was a hitch, in a way foreseen.

For I had published in 1913, on pages 140-142 of My Life with the Eskimo, an account of how some natives and I became ill when we had to go two or three weeks on lean meat, caribou so skinny that there was no appreciable fat behind the eyes or in the marrow. So when Dr. DuBois suggest that I start the meat period by eating as large quantities as I possibly could of chopped fatless muscle, I predicted trouble. But he countered by citing my own experience where illness had not come until after two or three weeks, and he now proposed lean for only two or three days. So I gave in.

The chief purpose of placing me abruptly on exclusively lean was that there would be a sharp contrast with Andersen who was going to be on a normal meat diet, consisting of such proportions of lean and fat as his own taste determined.

As said, in the Arctic we had become ill during the second or third fatless week. I now became ill on the second fatless day. The time difference between Bellevue and the Arctic was due no doubt mainly to the existence of a little fat, here and there in our northern caribou - we had eaten the tissue from behind the eyes, we had broken the bones for marrow, and in doing everything we could to get fat we had evidently secured more than we realized. At Bellevue the meat, carefully scrutinized, had been as lean as such muscle tissue can be. Then, in the Arctic we had eaten tendons and other indigestible matter, we had chewed the soft ends of bones, getting a deal of bulk that way when we were trying to secure fat. What we ate at Bellevue contained no bulk material, so that my stomach could be compelled to hold a much larger amount of lean.

The symptoms brought on at Bellevue by an incomplete meat diet (lean without fat) were exactly the same as in the Arctic, except that they came on faster - diarrhea and a feeling of general baffling discomfort.

Up north the Eskimos and I had been cured immediately when we got some fat. Dr. DuBois now cured me the same way, by giving me fat sirloin steaks, brains fried in bacon fat, and things of that sort. In two or three days I was all right, but I had lost considerable weight.

III

For the first three weeks I was watched day and night by the Institute staff. My exercise was supposed to be about that of an average business man. I went out for walks, but always under guard. If I telephoned, the attendant stood at the door of the booth; if I went into a shop, he was never more than a few feet away; and he was always vigilant. As Dr. DuBois explained, and as I well knew in advance, this was not because the supervising staff were suspicious of me but rather because they wanted to be able to say that they knew of their own knowledge my complete abstinence from all solids and liquids, except those which I received in Bellevue and which I ate and drank under the watch of attendants.

But my affairs unfortunately demanded that I travel widely through the United States and Canada. This was an added reason why Andersen had been secured for the experiment. When after three weeks, they had to put me on parole, so to speak, they retained him under lock and key for a total of something over 90 days.

Those who believed that a meat diet would lead to death had set at anything from four to fifteen days the point where Dr. Lieb, as clinical supervisor, would have to call a halt in view of danger to the subjects. Those who expected a slower breakdown had placed the appearance of the dread symptoms long before 90 days. In any case, Anderen reported back to the hospital constantly after he left it and I whenever I was in town.

After my three weeks and Andersen's thirteen, and with the constant analyses of excretions and blood when we came back to the hospital for check-ups, the doctors felt certain they would catch us if we broke diet. Moreover, long before the thirteen weeks ended they had satisfied themselves that Andersen had no longing for fruits or other vegetable materials and therefore, no motive for breach of contract.

Toward the end of the covenanted year Andersen and I returned to Bellevue for final intensive studies of some weeks on the meat diet, and then our first three weeks on a mixed diet. At this end of the experiment all went smoothly with me, but not so with Andersen.

My trouble, it will be remembered, had been that at the outset they stuffed me with lean, permitting no fat. His difficulty , or at least annoyance, began on the second day after he completed a year on the meat (January 25, 1929) when they asked him to eat all the fat he could, to the nausea limit, permitting only a tiny bit of lean, about 45 grams per day. There they kept him on the verge of nausea for a week. The second week they added his first taste of vegetables in a year, thrice-cooked cabbage netting about 35 grams of carbohydrate per day. The third week they omitted the cabbage but retained the high proportion of fat to lean.

These three weeks, Andersen says, were the only difficult part of the experiment. Looking back at it now, he thinks if it were possible to separate the nausea from the other unpleasantness there would have been a good deal left over - that he wasn't, properly speaking, well at the end of the third week. However, that is speculation if not imagination.

Returning to facts, we have the ominous one that pneumonia epidemic was sweeping New York. The hospital was crowded with patients; some of the staff got the disease, and with them Andersen. It was Type II pneumonia in his case, and the physicians were gravely worried, for this type was proving deadly in that epidemic, carrying off fifty percent of its Bellevue victims. Andersen, however, reacted quickly to treatment, ran an unusually short course, and convalesced rapidly.

IV

The broad results of the experiment were, so far as Andersen and I could tell, and so far as the supervising physicians could tell, that we were in at least as good average health during the year as we had been during the three mixed-diet weeks at the start. We thought our health had been a little better than average. We enjoyed and prospered as well on the meat in midsummer as in midwinter, and felt no more discomfort from the heat than our fellow New Yorkers did.

In view of beliefs that are strangely current it is worth emphasizing that we liked our meat as fat in July as in January. This ought not to surprise Americans (though it usually does) for they know or have heard that fat pork is a staple and relished food of the ***** in Mississippi. Our ***** literature is rich with the praise of opossum fat, nor did ******* develop the taste for fats in our Southern States for Carl Akerly relates from tropical Africa such yarns of fat gorging as have not yet been surpassed from the Arctic. A frequent complaint of travelers in Spain is against foods that swim in oil and there are similar complaints when we visit Latin America. We find, when we stop to think that many if not most tropical people love greasy food.

Then there is the parallel belief that the largest meat consumption is in cold countries. True, the hundred-percent centers are way up north, the Eskimos, Samoyeds, Chukchis. But the heaviest meat eaters who speak English are the Australians, tropical and sub-tropical., while the nearest you come to an exclusive meat among people of European stock is in tropical Argentina where the cowboys live on beef and maté. They like their meat fat and (so an Argentinian New Yorker tells me) will threaten to quit work, or at least did twenty years ago, if you attempt to feed them in any considerable part on cereal, greens, and fruits.

It appears that, excepting as tastes are controlled by propaganda and fashion, the longing for fat, summer or winter, depends on what else you eat. If yours is a meat diet then you simply must have fat with your lean; other wise you would sicken and die. But since fats, sugars, and starches are in most practical respects dietetically equivalent, you eat more of any one of them on a mixed diet if you decrease the combined amount of the other two.

Sir Hubert Wilkins, when we were living in the Arctic together, both living exclusively on meats, told me what remains my best single instance of how fats are crowded out by commerce, fashion and expense. The expense is frequently not the least fat, which is only about twice as nourishing as sugar, costs, as I write at my neighborhood grocery 50 cents per pound (bacon) or 35 cents a pound (butter) while sugar is only 5 1/2.

Sir Hubert's father, the first white child born in South Australia, told that when he was young the herdsman, who were the majority of the population, lived practically exclusively on mutton (sometimes on beef) and tea. At all times of year they killed the fattest sheep for their own use and when in the open, which was frequently, they roasted the fattest parts against a fire with a dripping pan underneath, later dipping the meat into the drippings as they ate. But then gradually commerce developed, breads and pastries began to be used, jams and jellies were imported or manufactured, and with the advance of starches and sugars, the use of fat decreased. Now, except that the Australians eat rather more meat per year than people do in the British Isles, the proportion of fat to the rest of the diet is probably about the same in Australia as elsewhere within the Empire.

A conclusion of our experiment which the medical profession seemingly find difficult to assimilate, but which at the same time is one of our clearest results, is that a normal meat diet is not a high protein diet. We averaged about a pound and a third of lean per day and half a pound of fat (this is about like eating a two pound broiled sirloin with the fat such a steak usually has on it). That seems like eating mostly lean; but grow technical and you find, in energy units, that we were really getting three-quarters of our calories from the fat. That is what the scientists meant when they said at the end of our diet had proved to be not so very high in protein.

That meat, as some have contended is a particularly stimulating food I verified during our New York experiment to the extent that it seems to me I was more optimistic and energetic than ordinarily. I looked forward with more anticipation to the next day or the next job and was more likely to expect pleasure or success. This may have a bearing on the common report that the uncivilized Eskimos are the happiest people in the world. There have been many explanations - that a hunter's life is pleasant, and that the poor wretches just don't know how badly off they are. We now add the suggestion that the optimism may be directly caused by what they eat.

Some additional fairly precise things can be said of how we fared during the year on meat. For instance, with Dr. DuBois as a pacemaker, we used every few weeks to run around the reservoir in Central Park and thence to his house, going up the stairs two or three at a time, plumping down on cots and having scientific attendants register our breathing, pulse rate, and other crude reactions. These tests appear to show that our stamina increased with the lengthening of the meat period.

Andersen, who had had one head cold after another when working nearly stripped outdoors in his Florida orange grow, suffered only two or three attacks during the meat year in New York, and those light. He did not regain his hair but he reported that there had been a marked decrease in the shedding. As said, according to the reports of the doctors, Andersen was troubled when he came from Florida with certain toxin-producing intestinal micro-organisms in relation to which physicians at that time ordinarily prescribed elimination of meat from the diet. This condition did not make trouble for him while on the meat.

A phase of our experiment has a relation to slimming, slenderizing, reducing, the treatment of obesity. I was "about ten pounds overweight" at the beginning of the meat diet and lost all of it. This reminds me to say that Eskimos, when still on their native meats, are never corpulent - at least I have seen none. They may be well fleshed. Some especially women, are notably heavier in middle age than when young. But they are not corpulent in our sense.

When you see Eskimos in their native garments you do get the impression of fat round faces on fat round bodies, but the roundness of face is a racial peculiarity and the rest of the effect is produced by loose and puffy garments. See them striped and you do not find the abdominal protuberances and folds which are numerous at Coney Island beaches and so persuasive in arguments against nudism.

There is no racial immunity among Eskimos to corpulence. You prove that by how quickly they get fat and how fat they grow on European diets.

Only one serious fear of the experiments was realized - our diet for the year turned out low in calcium. This was not demonstrated by any tests upon Andersen or me, and certainly you could not have proved it by asking us or looking at us, for we felt better and looked healthier than our average for the years immediately previous. The calcium deficiency appeared solely through the food analysis of the chemists.

Part of our routine was to give the chemists for analysis pieces of meat as nearly as possible identical with those we ate. For instance, lamb would be split down through the middle of the spine and we had the chops from one side cooked for us, while they got the chops from the other side to analyze. When the diet was sirloin steaks, they received ones matching ours. The only way in which the diet was not identical with the food analyzed was that Andersen and I followed the Eskimo custom of eating fish bones and chewing the rib ends; from these sources we no doubt obtained a certain amount of calcium.

Toward the latter part of the test it became startlingly clear, on paper that we were not getting enough calcium for health. But we were healthy. The escape from that dilemma was assume that a calcium deficiency which did not hurt us in our one year might destroy us in ten or twenty.

You study bones when you look for a calcium deficiency. The thing to do then, was to examine the skeletons of people who had died at a reasonably high age after living from infancy upon an exclusive meat diet. Such skeletons are those of Eskimos who are known to have died before the European influences came in. The Institute of American Meat Packers were induced to make a subsidiary appropriation to the Peabody Museum of Harvard University where Dr. Earnest A. Hooton, Professor of Physical Anthropology, under took a through going study with regard to the calcium problem in the relation to the Museum's collection of the skeletons of meat eaters. Dr. Hooton reported no signs of calcium deficiency. On the contrary, there was every indication that the meat eaters had been liberally, or at least adequately, supplied. The had suffered no more in a lifetime from calcium deficiency than we had in our short year (really short, by the way for we enjoyed it).


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Adventures in Diet

Part 3

By Vilhjalmur Stefansson

Harper's Monthly Magazine, January 1936.

Scurvy has been the great enemy of explorers. When Magellan sailed around the world four hundred years ago many of his crew died from it and most of the others were at times so weakened that they could barely handle the ships. When Scott's party of four went to the South Pole twenty three years ago their strength was sapped by scurvy; they were unable to maintain their travel schedule and died. Nor has scurvy been the nemesis of explorers only. Twenty years ago the British Army in the Near East was seriously handicapped, and last October an American doctor reported a hundred Ethiopian soldiers per day dying of scurvy. The disease worked havoc during the Alaska and Yukon gold rushes following 1896. Scores of miners died and hundred suffered.

Medical profession and laity equally believed for more than a hundred years that they knew exactly how to prevent and cure the disease, yet the method always failed on severe test.

The premise from which the doctors started was that vegetables, particularly fruits, prevent and cure scurvy. Since diet consists of animals and plants, the statement came to take the form that scurvy is cause by meat and cured by vegetables. Finally the doctors standardized on lime juice as the best of preventatives and cures. They name it a sure cure, a specific. Lawmakers followed the doctors. It is on the statute books of many countries that on long voyages the crews are to be supplied with lime juice and induced or compelled to take it.

Obtained from officers of the Royal Canadian Mounted Police, and from sourdoughs, I have in my diaries and notes many a case of suffering and death caused by scurvy in the Alaska and Yukon gold rushes. The miner generally began to sicken toward the end of winter. He had been living on beans and bacon, on biscuits, rice, oatmeal, sugar, dried fruits and dried vegetables. When he recognized his trouble as scurvy he made such efforts as were possible to get the things which he believed would cure him. Apparently the miners had the strongest faith in raw potatoes. These had to be brought from afar, and there are heroic tales of men who struggled through the wilderness to succor a comrade with a few pounds of them. There were similar beliefs in the virtues of onions and some other vegetables. Curiously, there was either no belief in those vegetables which were obtainable, or else there was a belief that they should be treated in a way which. we now understand, destroys their value. For instance a man might have been cured or at least helped with a salad of leaves or even bark of trees. What the miners did with the pine needles and willow drink the tea. If they had fresh meat they boiled it to shreds and drank the broth. Death frequently occurred in two to four months from recognized onset of the disease.

Ignoring the decimation of armies, and the burden of this disease in many walks of civil life through past ages, we turn to the explorers, the class most widely publicized as suffering from and dying of scurvy.

It is unusual to rank James Cook of a hundred and fifty years ago with the foremost explorers of all time. Part of his fame may be attributed to his having discovered how to prevent and cure scurvy. Medical books name him as pioneer in the field, saying that we owe to him the conquest of a dread disease. For he demonstrated that with vegetables (again particularly fruits) scurvy could be prevented on the longest voyages. By statement or inference these books assert that from this developed the knowledge according to which we extract and bottle the juice of the lime, stock ships with it, prevent and cure scurvy.

As show above intimated, however, the good physicians, with their faith in lime juice as a specific, overlooked its constant failure upon severe test.

How stoutly the faith was kept is shown by the British polar expedition of Sir George Nares. When he returned to England in 1876 after a year and a half, he reported much illness from scurvy, some deaths, and a partial failure of his program as a result. In his view fresh meat could have saved his men. But the doctors, as we shall see when we consider how they later advised Scott, soon forgot whatever impression was made by Nares. They seem to have scared themselves with the old doctrines by a series of assumptions: that the lime juice on the Nares expedition might have been deficient in acid content; that some of the victims did not takes as much of it as needed; and that perhaps it was too much to expect of even the marvelous juice to cope with all the things which tended to bring on scurvy - absence of sunlight, bad ventilation, lack of amusement and exercise, insufficient cleanliness.

Particularly because Nares medical court of inquiry had closed on a note of cleanliness and "modern sanitation," you would think the medical world might have felt a severe jolt when they read how Nansen and Johansen had wintered in the Franz Josef Islands, (now Nansen Land) in 1895-96. They had lived in a hut of stones and walrus leather. The ventilation was bad, to conserve fuel; the fire smoked, so that the air was additionally bad; there was not a ray of daylight for months; during this time they practically hibernated, seldom going outdoors at all and taking as little exercise as appears humanly possible. Yet their health was perfect all winter and they came out of their hibernation in as good physical condition as any men ever did out of any kind of Arctic wintering. Their food had been lean and the fat of walrus.

Tens, if not hundreds of thousand of scientists in medicine and the related branches must have seen this account, for Nansen's books were bestsellers in practically every language and newspapers were full of the story. Yet the effect was negligible. The doctors and dietitians still continued to pontificate on meat producing scurvy and on the contributory bad effects of what they called insufficience of ventilation, cleanliness, sunlight and exercise. They still prescribed lime juice and put their whole dependence on it and other vegetable products.

Excuses for lime juice have persisted to our day. It was for instance, demonstrated with triumph recently that the meaning of "lime" had changed during the last hundred years, explaining the claim that it worked better in the eighteenth than in the nineteenth century - then the juice was made from lemons called limes; now it is made from limes called limes.

The antiscorbutic value of lemons may be far greater than that of limes per ounce, but that does not go to the root of the matter. For proof of this consider how Nansen's experience was re-enforced and interpreted by four expeditions during two decades, two of them commanded by Robert Falcon Scott, one by Ernest Henry Shackleton, one by me.

II

Scott, in 1900, sought the most orthodox scientific counsel when outfitting his first expedition. He followed advice by carrying lime juice and by picking up quantities of fruits and vegetable things as he passed New Zealand on his way to the Antarctic. He saw to it that the diet was "wholesome," that the men took exercise, that they bathed and had plenty of fresh air. Yet scurvy broke out and the subsequently famous Shackleton was crippled by it on a journey. They were pulling their own sledges at the time so they must of had enough exercise. There was plenty of light with the sun beating on them, and there was plenty of fresh air. To believers in the catch words and slogans of their day, to believers in the virtues of lime juice, the onset of the scurvy was a baffling mystery.

That is was Shackleton's scurvy which most interfered with the success of the first Scott expedition was particularly unfortunate, if you think of the jealousies it aroused, the enmities it caused. Scurvy, as disease go, is really one of the cleanest and least obnoxious; but in English the name of it is a term of opprobrium - "a scurvy fellow," "a scurvy trick." Shackleton may have smarted as much under that word-association as he did under the charge that his weakness had been Scott's main handicap. The passion to clear his name, in every sense, drove him to the organization of an expedition, which many in Britain considered unethical - a subordinate, with indecent haste and insistence, crowding forward to eclipse his commander.

The crucial element in the first Shackleton expedition, to the students of scurvy, is the fact that Shackelton was an Elizabethan throwback in the time of Edward VII. He was a Hawkins or a Drake, a buccaneer in spirit and method. He talked louder and more than is good form in modern England. He approached near to brag and swagger. He caused frictions, aroused and fanned jealousies, and won the breathless admiration of youngsters who would have followed Dampier and Frobisher with equal enthusiasm in their piracies and in their explorations.

The organization, and the rest of the first Shackleton expedition, went with a hurrah. They were as careless as Scott had been careful; they did not have Scott's type of backing, scientific or financial. They arrived helter skelter on the shores of the Antarctic Continent, pitched camp, and discovered that they did not have enough food for the winter, nor had they taken such painstaking care as Scott to provide themselves with fruits or other antiscorbutics in New Zealand. Compared with Scott's, their routine was slipshod as to cleanliness, exercise, and several of the ordinary hygienic prescriptions.

What signifies is that Scott's men, with unlimited quantities of jams and marmalades, cereals and fruits, grains, curries, and potted meats, had been little inclined to add seals and penguins to their dietary. With Shackleton it was neither wisdom or acceptance of good advise but dire necessity which drove to such use of penguin and seal that Dr. Alister Forbes Mackay, physician from Edinburgh, who was a member of that Shackleton expedition and later physician of my ship the Karluk, told me he estimated half the food during their stay in the Antarctic was fresh meat.

In spite of the lack of care, (indeed, as we now see it, because of their lack), Shackleton had better average health than Scott. There was never a sign of scurvy; every man retained his full strength; and they accomplished that spring what most authorities still consider the greatest physical achievement ever made in the southern polar regions. With men dragging the sledge a considerable part of the way, they got to latitude 88° 23 S., practically within sight of the Pole.

Scott began his second venture as he had begun the first, by asking the medical profession of Britain for protection from scurvy and by receiving from them once more the good old advice about lime juice, fruits, and the rest. In winter quarters he again placed reliance on that advice and on constant medical supervision, on a planned and carefully varied diet, on numerous scientific tests to determine the condition of the men, on exercise, fresh air, sanitation in all its standard forms. The men lived on the foods of the United Kingdom, supplemented by the fruit and garden produce of New Zealand. Because they had so much which they were used to, they ate little of what they had never learned to like, the penguins and seals.

Once more they started their sledge travel after a winter of sanitation. The results had previously be disappointing; now they were tragic. While scurvy did not prevent them from reaching the South Pole, it began to weaken them on the return and progressed so rapidly that the growing weakness prevented them, if only by ten miles, from being able to get back to the final provision depot.

Those who have ignored the scurvy have sometimes claimed that if Scott had reached the depot he would have been able to reach the base camp eventually. This becomes more than doubtful when you realize that the progressive decrease of vigor, both mental and bodily, was not going to be helped by even the largest meals, if those meals were of food lacking antiscorbutic value.

The story of Scott and his companions, especially through the last few weeks, is among the boldest in any language; through it they became national heroes and world heroes. But in the speech of their countrymen (though not in many another European tongue), scurvy sounds unclean. It appeared necessary to Scott's surviving comrades, and to those in Britain who knew the truth, to take care that the tabooed word should not sully a glorious deed.

To suppress the association of a disease with the beauty and heroism of Scott's death may have been worth while at the time; but it can scarcely be deplored by anyone - and must be praised by scientists - that Commander Edward G. R. Evans, now Admiral, Scott's second-in-command, after a time gave out the scurvy information, including the statement that he himself had been ill.

It is irrational, at least now that emotions have calmed, to blame Scott. No one was to blame, for they all acted according to the light of their day. If anybody was to blame it was primarily those who gave medical advice to the expedition before it sailed; secondarily, it was the chief medical officer, rather than the commanding officer, of the expedition.

It seems strange, now, that a comparison of the Scott and Shackleton experiences did not fully enlighten the doctors on the true inwardness of scurvy; but of course part of the explanation is that the Scott medical information was suppressed. Therefore, it remained for my own expedition to demonstrate, so far as polar expeditions are concerned, and for the Russell Sage experiments to call to the attention of the medical profession, the most practical and only simple way of curing scurvy. For no matter how good the juice of limes (or lemons), it is difficult to carry, it deteriorates, and you may lose it, as by a shipwreck. The thing to do is to find you antiscorbutics where you are, pick them up as you go.

On my third expedition it happened as circumstantially related in a book called "The Friendly Arctic", that three men came down with scurvy though disobeying the instructions of the commander and living without his knowledge for two or three months chiefly on European foods when they were supposed to be living chiefly on meat.

It seems to take from one to three months for even a bad diet to produce recognizable scurvy, but there after developments are rapid through the next few weeks. In the case of my men it was about three weeks ( as they later thought) after they noticed the trouble and about ten days after they complained of it to me, when one of them was so weak we had to carry him on a sledge, while the other was barely able to stagger along, holding on behind. By then every joint pained, their gums were as soft as "American" cheese, their teeth so loose that they came out with almost the gentlest of pulls.

We were 60 or 80 miles from land on drifting sea ice when the trouble stared, and we hastened ashore to get a stable camp for the invalids. It would have been no fun, with sick men on your hands, if the site of your camp started disintegrating under pressure and tumbling about.

We reached an island (about 900 miles north of the Arctic Circle) the coast of which was known although the interior had never been explored. We traveled a few miles inland, established a camp, hunted caribou (there were two of us well, out of four) and began the all-meat cure. Fuel was pretty scarce, so we cooked only one meal a day; besides, I thought raw food might work better. We cooked the breakfast in a lot of water. The patients finished the boiled meat while it was hot and kept the broth to drink during the rest of the day. For their other meals they ate slightly frozen raw meat, with normal digestion and good appetite. We divided up the caribou Eskimo style, so the dogs got organs and entrails, hams, shoulders, and tenderloin, while the invalids, and we hunters got heads, briskets, ribs, pelvis and the marrow from the bones.

On this diet all pain disappeared from every joint within four days and the gloom was replaced by optimism. Inside a week both men said that they had no realization of being ill as long as they lay still in bed. In two weeks they were able to begin traveling, at first riding on the sledges and walking alternately. At the end of a month they felt as if they had never been ill. No signs of the scurvy remained except that the gums, which had receded from the teeth, only partly regained their position.

By comparing notes later with Dr. Alfred Hess, the leading New York authority on scurvy, I found that when I was getting these results with a diet from which all vegetable elements were absent, he was getting the same results in the same length of time through a diet where the main reliance was upon grated raw vegetables and fruits and upon fresh fruit juices.

There is no doubt, as the quantitative studies have shown, that the percentage of Vitamin C, the scurvy preventing factor, is higher in certain vegetable elements than in any meats. But it is equally true that the human body needs only such a tiny bit of Vitamin C that if you have some fresh meat in your diet every day, and don't over cook it, there will be enough C from that source alone to prevent scurvy. If you live exclusively on meat you get from it enough vitamins not only to prevent scurvy but as said in a previous article, to prevent all other deficiency diseases.

Closing the subject of vitamins in relation to long expeditions, we had better emphasize that there has recently been such progress in the extraction, concentration and storage of Vitamin C that it is now possible to carry with you enough to last several years and of such quality that it will not deteriorate to the point of uselessness. But why carry coals to Newcastle? if you are in the tropics, pick a fruit, or eat a green; if you are at sea, throw a line outboard and catch a fish; if you are in the Antarctic, use seals and penguins; if in the Arctic, hunt polar bears, and seals, caribou and the rest of the numerous game. True enough, if you make a journey inland into the Antarctic Continent or toward the center of Greenland, where there is no game because the land is permanently snow-covered, you have to carry food with you. In that case you might as well take lemon juice. It is one of the most portable sources and they know now how to make and pack it so that its qualities as well as quantities will last you.


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III

A bulletin conspicuous in the subways co-operated some time ago with the New York Commissioner of Health by displaying this notice:

FOR SOUND TEETH

BALANCED DIET with

VEGETABLES : FRUIT : MILK

BRUSH TEETH

VISIT DENTIST REGULARLY

Shirley W. Wynne, M.D.

Commissioner of Health

During the same time the ether was full and the magazine pages were crowded with advertising which told you that mouth chemistry is altered by a paste, a powder, or a gargle so as to prevent decay, that a clean tooth never decays, that a special kind of toothbrush reaches all the crevices, that a particular brand of fruit, milk or bread is rich in elements for tooth health. There were toothbrush drills in the schools. Mothers throughout the land were scolding, coaxing, and bribing to get children to use the preparations, eat the foods, and follow the rules that insured perfect oral hygiene.

Meantime there appeared a statement from Dr. Adelbert Fernald, Curator of the Museum of Dental School, Harvard University, that he had been collecting mouth casts of living Americans, from the most northerly Eskimos south to the Yucatan. The best teeth and the healthiest mouths were found among people who never drank milk since they had ceased to be suckling babes and who never in their lives tasted any of the other things recommended for sound teeth by the New York Commissioner of Health. These people, Eskimos, never use tooth paste, tooth powder, tooth brushes, mouth wash, or gargle. They never take any pains to cleanse their teeth or mouths. They do not visit their dentist twice a year or even once in a lifetime. Their food is exclusively meat. Meat, be it noted, was not mentioned in the advertisement issued by Dr. Wayne.

Teeth superior on the average to those of the presidents of our largest tooth-paste companies are found in the world to-day, and have existed during past ages, among people who violate every precept of current dentifrice advertising. Not all of them have lived exclusively on meat; but so far as an extensive correspondence with authorities has yet been able to show me, a complete absence of tooth decay from entire communities has never existed in the past, and does not exist now, except among people in whose diet meat is either exclusive or heavily predominant.

Our Bellevue experiments threw a light on tooth decay, but the key to the situation lies more in the broad science of anthropology. I now give, by sample and by summary, things personally known to me from anthropological field work.

My first anthropological commission was from the Peabody Museum of Harvard University when they sent John W. Hasting and me to Iceland in 1905. We found in one place a medieval graveyard that was being cut away by the sea. Skulls were rolling about in the water at high tide, at low tide we gathered them and picked up scattered teeth here and there. As wind and water shifted the sands we found more and more teeth until there was a handful. Later we got permission to excavate the cemetery, and eventually we brought with us to Harvard a miscellaneous lot of bone which included 80 skull, and as said, a great many loose teeth.

The collection has been studied by dentists and physical anthropologists without the discovery of a single cavity in even one tooth.

The skulls in the Hastings-Stefansson collection represent persons of ordinary Icelandic blood. There were no aborigines in that island when the Irish discovered it some time before 700 A. D. When the Norsemen got there in 860 they found no people except the Irish. It is now variously estimated that in origin the Icelanders are from 10 percent to 30 percent Irish, 40 percent to 50 percent Norwegian, the remainder, perhaps 10 percent, from Scotland, England, Sweden, and Denmark.

None of the people whose blood went into the Icelandic stock are racially immune to tooth decay, nor are the modern Icelanders. Then why were the Icelanders of the Middle Ages immune?

An analysis of the various factors make it pretty clear that their food protected the teeth of the medieval Icelanders. The chief elements were fish, mutton, milk and milk products. There was a certain amount of beef and there may have been a little horse flesh, particularly in the earliest period of the graveyard. Cereals were little important and might be used for beer rather than porridge. Bread was negligible and so were all other elements from the vegetable kingdom, native or imported.

My mother, who as born on the north coast of Iceland, remembered from the middle of the nineteenth century a period when bread still was as rare as caviar is in New York to-day - she tasted bread only three or four times a year and then only small pieces when she went with her mother visiting. So far as bread existed at her own house, it was used as a treat for visiting children. The diet was still substantially that of the Middle Ages, though the use of porridge was increasing. She did not remember hearing of toothache in her early youth but did remember accounts of it as a painful rarity about the time when she left for America in 1876. Soon after arrival in the United States (Wisconsin, Minnesota, Dakota,) and in Canada (Nova Scotia, Manitoba) the Icelandic colonists became thoroughly familiar with the ravages of caries. They probably had teeth as bad as those of the average American long before 1900.

There is then at least one case of a north-European people whose immunity from caries (to judge from the Hastings-Stefansson collection and common report) approached 100 percent for a thousand years, down to approximately the time of the American Civil War. The diet was mainly from the animal kingdom. Now that it has become, both in America and Iceland approximately the same as the average for the United States or Europe, Icelandic teeth show a high percentage of decay.

I began to learn about another formerly toothacheless people when I joined the Mackenzie River Eskimos in 1906. Some of them had been eating European foods in considerable amount since 1889, and toothache and tooth decay were appearing, but only in the mouths of those who affected the new foods secured from the Yankee whalers. The Mackenzie people agreed that toothache and cavities had been unknown in the childhood of those then approaching middle age while there were many of all ages still untouched, the ones who kept mainly or wholly to the Eskimo diet. Here and in many other places, this is somewhere between 98 and 100 percent from animal sources. There are districts, like parts of Labrador and of western and southwestern Alaska, where even before the coming of Europeans there was considerable use of native vegetable elements nowhere furnished as much as 5 percent of the average yearly caloric intake of the primitive Eskimos, even in south-western Alaska.

Dr. Alex Hirdlicka, Curator of Anthropology in the National Museum, Washington, writes me that he knows of no case of tooth decay among Eskimos of the present or past who were uninfluenced by European habits. Dr. S. G. Ritchie, of Dalhousie University, wrote after studying the skeletal collection gathered by Mr. Diamond Jenness on my third expedition: " In all the teeth examined there is not the slightest trace of caries."

I brought about 100 skulls of Eskimos, who had died before Europeans came in, to the American Museum of Natural History, New York. These have been examined by many students, but no sign of tooth decay has yet been discovered.

Dr. M. A. Pleasure examined at the American Museum of Natural History 283 skulls said to be Eskimo of pre-European date. He found a small cavity in one tooth; but when the records where check it turned out that the collector, Rev. J. W. Chapman of the Episcopal Board of Missions, who now lives in New York City, had sent that skull to the Museum as one of an Athabasca Indian, not of an Eskimo.

The slate is, therefore, clean to date. Not a sign of tooth decay has yet been discovered among that one of all peoples which most completely avoids the foods, the precepts, and the practices favored for dental health by the New York Commissioner of Health, the average dentist, the toothbrush drillmasters of the schools, and the dentifrice publicists.

IV

When addressing conventions and societies of medical men, I usually state the oral hygiene case somewhat as above but in more detail. If there is rebuttal from the floor, it invariably takes the form of contending that the tooth health of primitive people is due to their chewing a lot and eating co**** food. The advantage of that argument to the dentist, whose best efforts have failed to save your teeth is obvious. It gives him an excuse. He can from the doctrine make a case that not all your care, even when support by his skill and science, can preserve teeth in a generation of soft foods, that give no exercise to the teeth and no friction to the gums.

But it is deplorably hard to square anthropology with this comfortable excuse of the dentist. Among the best teeth of a mixed-diet world are those of a few South Sea Islanders who as yet largely keep to their native diets. Similar or better tooth condition is described, for instance, from the Hawaiian Islands by the earliest visitors. But can you think of a case less fortunate for the chewing-and-co****-food advocates? The animal food of these people was chiefly fish, and fish is soft to the teeth, whether boiled or raw. Among the chief vegetable elements was poi, a kind of soup or paste. Then they used sweet potatoes.

It would be difficult to find a New Yorker or Parisian who does not chew more, and use co****r food, than the South Sea Islanders did on the native diets which gave them in at least some cases 97 percent freedom from caries, a record no block on Park Avenue can approach.

Nor do Eskimos chew much, as compared with us. So far as their meat is raw it can be chewed like a raw oyster - slips down similarly. When perfectly fresh meat is cooked, two main causes determine toughness: the age of the beast and the manner of cooking. The chief food animal of inland Eskimos is the caribou. A young caribou is as fleet as a heifer; an old one is as slow as a cow. Therefore the wolves get the clumsy old which drop behind when the band flees, and the Eskimos seldom have a chance to secure an animal that is more than three or four. Such young caribou are not tough, no matter how cooked.

I do not know a corresponding logical demonstration for seals, but I can testify from helping to eat thousands that their meat is never tough - at least not in comparison with the beefsteaks you sometimes get in New York chophouses.

Then there are Eskimos who live practically exclusively on fish. As said, you can't chew them when they are raw; there is not much chewing when they are eaten boiled. the only condition under which fish become tough, or rather hard, is when they are dried. Some Eskimos use dried fish; others do not.

There is for separated districts a wide difference in the amount of Eskimo chewing, but no one has reported that health of the teeth is better among heavy chewers. How could it be when as yet no caries has been found either among the lightest or heaviest masticators?

It is used as a second line of defense by the mastication advocates that even if Eskimos perhaps don't chew their food so very much they do chew skins a great deal. Their chewing of leather is far less than you might believe from what has been said by a particular kind of writer and pictured in certain movies. In any case, skin chewing is mainly by the women, and it is not easy to bring under the conditions of modern scientific thought the idea that the wife's chewing preserves her husband's teeth.

Once at a talk to a medical group I encountered a further argument. Is it not true that Eskimo men use the teeth a great deal in their crafts? Do they not bite wood, ivory, or metal to hold, pull out, twist, and so one? The best I could think of was to agree that Eskimos pull nails with their teeth because they have good teeth than that they have good teeth because they pull nails.

There are several reasons why the teeth of many Eskimos wear down rapidly. They usually meet edge to edge, where ours frequently overlap, and that tends to cause wear. Some Eskimos wind-dry fish or meat, sand gets in, and to an extent makes them like sandpaper. Both sexes, but especially men, use their teeth for biting on hard materials. Both sexes, but especially the women, use their teeth for softening skins. A wearing toward the pulp may, therefore, take place in early middle-life. What then happens is stated by Dr. Richie (whom we have already quoted) with relation to the Coronation Gulf Eskimos:

"Coincident with this extreme wear of the teeth the dental pulps have taken on their original function with conspicuous success. Sufficient new dentine of fine quality has been formed to obliterate the pulp chambers and in some cases even the root canals of the teeth. This new growth of tissue is found in every case where access to the pulp chambers has been threatened. There has therefore been no destruction of the pulps through infection and consequently alveolar abscesses are apparently unknown."

Total absence of caries from those who live wholly on meat is then definite. Cessation of decay when you transfer from a mixed to a meat diet happens usually, perhaps always. The rest of the picture is not so clear.

Caries has been found in the teeth of mummies in Egypt, Peru, and in our own Southwest. These ancient people were mixed-diet eaters, depending in considerable part on cereals. Their teeth were better than ours, though not so good as the Eskimos. If you want a dental law, you can approximate it by saying that the most primitive people usually have the best teeth. You can add that in some cases a highly vegetarian people while not attaining the 100 percent perfection of meat eaters, do nevertheless, have very good teeth as compared with ours.

It is contended by the Hawaiian Sugar Planters Association Health Research Project that the shift from good to execrable teeth among the mixed diet Polynesians there has been due to years of cereals. I have seen no comment of theirs upon the (I should think) great increase of sugar consumption that has been synchronic with the deterioration of Hawaiian teeth.

On the view that diet is the greatest factor in saving teeth, the anthropologists have been getting support from experiments conducted by institutions and by scattered students. Some dentists are here contributing nobly to a research, and to a campaign of education, that seems bound to deplete their income. My probing has not revealed thus far corresponding unselfishness among the dentifrice manufacturers.

A serious mouth disease, next after caries, is pyorrhea. He who runs cannot read the marks so readily on human skeletons; but it seems at least probable that the medieval Icelanders, the Eskimos, and others who have left teeth free from cavities, were also free from, or at least not severely afflicted by, pyorrhea. Similarly, the modern investigators have found Eskimos who are still living on their native foods to have an unusually good average condition of general oral health, therewith absence of pyorrhea.

One of the things we noticed in the general well-being of our New York year on meat and similar years in the Arctic was the absence of headaches. I used to have them frequently before going north and have them occasionally whenever I am on a mixed diet. The whys and wherefores are not clear and what we say on this point is more tentative than any other part of this statement.

It was noticed in the X-ray pictures during our New York meat year that we had far less gas in the intestinal tract when on meat than when on a mixed diet - practically no gas. The work of Dr. John C. Torrey showed that neither did digestion and elimination produce those offensive smells which are found in vegetarianism and on a mixed diet But whether the freedom from a certain kind of intestinal food decomposition was what led to the freedom from headache is no more than a working hypothesis.

The prevention of headache by abstaining from vegetables has been recorded in books. An outstanding case is that of Francis Parkman, the historian, who suffered with headaches all his life except, as he states, during one period when he was living with an Indian tribe chiefly or exclusively on meat. This testimony, though by an eminent man widely read, and though a fair sample of the testimony of meat eaters, commanded little attention for the physicians. It should be said in their defense, however, that Parkman himself does not proclaim the experience as a triumphant discovery. He rather puts it the other way about, that in spite of being compelled to live on meat, he was free from the headaches that plagued him the rest of his days.

Professor Raymond Pearl, nearly twenty years ago, while he was at the Maine Agricultural Experiment Station, proved that chickens know more than professors about what is good for chickens to eat. Now several experiments appear in a good way to establish that children, if given complete freedom to choose among foods undisguised by sauces and artificial flavors will select better for their own health and strength than the mother or child specialist. One of the things frequently noticed about these children is that they eat large quantities of a single item which they happen to like. Our living for years on a single item which we liked was from the point of view no more than carrying forward a childhood tendency.


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## Cookie

V

More than twenty-five years have passed since the completion of my first twelve months on meat and more than six years since the completion in New York of my sixth full meat year. All the rest of my life I have been a heavy meat eater, and I am now fifty-six. That should be long enough to bring out the effects. Dr. Clarence W. Lieb will report in the American Journal of Gastroenterology that I still run well above my age average on those points where meat has been supposed to cause deterioration. The same is the verdict of my own feelings. Rheumatism, for instance, has yet to give me its first twinge.

The broadest conclusion to be drawn from our comfort, enjoyment, and long-range well-being on meat is that the human body is a sounder and more competent job than we give it credit for. Apparently you can eat healthy on meat without vegetables, on vegetables without meat, or on a mixed diet.

Two stories summarize one of the most interesting sides of the case, the dental. In 1903 I heard the Dean of the dental school of the University of Pennsylvania say in a lecture that he thought dentists to that year had done more harm than good, but would thereafter be doing more good than harm. In 1928 when I told this to Dr. Percy Howe, Director of the Forsyth Dental Infirmary for Children, he said he thought the good Dean had been premature by at least twenty years. As I understand Dr. Howe, much good was done in particular cases by dentists long ago, but it is only within the past ten years or so that the average for good has overbalanced the harm by any very heavy proportion.

While meat eaters seem to average well in heath, we must in our conclusion draw a caution from the most complete modern example of them the Eskimos of Coronation Gulf, when he was anthropologist on my third expedition, that the two chief causes of death were accidents and old age. This puts in a different form my saying that these survivors of the stone age were the healthiest people I have ever lived among. I would say the community, from infancy to old age, may have had on the average the health of an equal number of men about twenty, say college students.

The danger is that you may reason from this good health to a great longevity. But meat eaters do not appear to live long. So far as we can tell, the Eskimos, before the white men upset their physiological as well as their economic balance, lived on the average at least ten years less than we. Now their lives average still shorter; but that is partly from communicated diseases.

It has been said in a previous article that I found the exclusive meat diet in New York to be stimulating - I felt energetic and optimistic both winter and summer. Perhaps it may be considered that meat is, overall, a stimulating diet, in the sense that metabolic processes are speeded up. You are then living at a faster rate, which means you would grow up rapidly and get old soon. This is perhaps confirmed by that early maturing of Eskimo women which I have heretofore supposed to be mainly due to their almost complete protection from chill - they live in warm dwellings and dress warmly so that the body is seldom under stress to maintain by physiological processes a temperature balance. It may be that meat as a speeder-up of metabolism explains in part both that Eskimo women are sometimes grandmothers before the age of twenty-three, and that they usually seem as old at sixty as our women do at eighty.

So you could live on meat if you wanted to; but there is no driving reason why you should. Moreover vegetables are fundamentally economical. You can get several times more food value from an acre of corn than from the pigs that ate the corn.

The thing to do then, probably, is to go on as you have been doing, but adding to your mental equipment, if it be a novelty, the idea that several at least of the disadvantages of a meat diet are compensated for by advantages


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## Cookie

Comments About Stefansson's Conclusions

Some people who disagree with a low-carbohydrate lifestyle are quick to grasp at some of Stefansson's conclusions as evidence the Eskimos' all fish diet was unhealthy. The Eskimos probably did not have an optimal diet, but their diet cannot be blamed for all of Stefansson's concluding remarks. The Eskimos proved that our current Recommended Daily Allowance (RDA) for vitamins and minerals must be wrong. Their diet would appear to be low in vitamin C and vitamin K, but they did not develop scurvy or develop illnesses as the result of a vitamin K deficiency. The Eskimos proved the current nutritional theory of a "balanced diet" is nonsense. The most healthy diet has the majority of calories coming from meat and natural animal fats while avoiding carbohydrates.

Humans would quickly die on a diet of all fruit. Humans would suffer multiple nutritional deficiencies and diseases on a diet of all grains, legumes or rice. Humans live wonderfully healthy on a diet of all meat and natural animal fats which includes the organ meats.

Stefansson's opinion that people would be better off by raising grains instead of animals for food was wrong at the time and continues to be wrong today. There are no scientific facts to prove this statement. Primitive societies that switched from being primarily meat eaters to becoming primarily grain eaters suffered a sharp decline in health as proven by multiple studies.

The Eskimos may have appeared to age more quickly than white Europeans for several reasons:

They were exposed to extreme temperature ranges their entire life.

They may have been exposed to excessive smoke from fires in their huts.

They may have been effected by the reduced amount of sun light.

The life span of the Eskimos would naturally be shorter than that of other societies for several reasons which have nothing to do with nutrition:

The extreme temperature exposure is expected to cause some percentage of deaths.

The hunting and fishing practices are high risk endeavors that cause deaths by accident.

Fluctuations in food supply are known to have caused starvation among the Eskimos.

Infection was a major cause of death for which the people had little understanding.

The Eskimos had many health advantages compared to white Europeans of their day. These health benefits can be clearly credited to their all meat diet of salmon, such as:

Perfect dental health. They had no dental caries within the entire community.

Excellent skeletal health without any signs of osteoporosis.

They had no cancer of any kind.

They had no heart disease or cardiovascular disease of any kind.

They had no intestinal diseases that have been reported by Stefansson or others.

They had no Type 2 diabetes because it is caused by eating carbohydrates.

They had no obesity because obesity is caused by eating carbohydrates.

Stefansson continued to live on the Eskimo diet for many decades, in very good health, until his death at the age of 83.


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## Jock

Superb read and very interesting info, you really must be one smart cookie!


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## SA12

Can someone post a 3 line summary? 

Nice post! lol


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## Biker

br3ach said:


> Can someone post a 3 line summary?
> 
> Nice post! lol


The atkins diet shouldn't even be called the atkins diet, it's been about for many years and long before he was even born.

That do mate?


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## Cookie

*Part 1: Introduction *
​


The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact. T H Huxley
​
Over the past couple of decades there has been a growing concern about fats and cholesterol. Dieticians, nutritionists and doctors have been telling us that fat is a killer. Governments have introduced national policies based around its reduction. Eat less cholesterol, saturated fat and salt, eat more fibre-rich foods we are all told. The evidence is incontrovertible that if we do not, we are doomed to the West's greatest killer - heart disease.

But is the evidence so clear? Despite the certainty implied by the propaganda, the debate continues in the medical journals, behind the scenes. Is diet a killer? Apart from those with a very rare disease, has cholesterol got anything to do with heart disease - or any other disease? And even if it has, will a change of diet be beneficial?

Like all debates, this one about cholesterol has two sides. The Cholesterol Myth explores the evidence on which present healthy eating' dietary recommendations are based.

Much of the evidence used in the cholesterol debate is complex. Nevertheless, with so much of only one side of the debate having been published and your having been subjected to so much that is misleading, I will try to explain the other side in as much detail as this paper allows.

*THE B. M. A. AND THE GOVERNMENT RECOMMEND THAT THE BRITISH PEOPLE SHOULD DRINK EIGHTY PERCENT MORE MILK, EAT FIFTY-FIVE PERCENT MORE EGGS, FORTY PERCENT MORE BUTTER AND THIRTY PERCENT MORE MEAT. *

On the basis of research in the 1920s and 1930s by Sir John Boyd Orr and others, that was the advice given to the British people in 1938. The Government introduced free school milk - full cream, that is - and later we 'went to work on an egg'. As a consequence, child deaths from diphtheria, measles, scarlet fever and whooping cough fell dramatically - well before the introduction of antibiotics and widespread immunisation. Rickets, called 'the English Disease' because it was so wide-spread, and other deficiency diseases were relegated to the past. Other factors helped, but most important of all was the better nutrition that gave children a higher resistance. The recommendations above shaped our diet for nearly fifty years and helped to give us a mean life expectancy that is now among the highest in the world. Sixty years in 1930, our mean life expectancy had climbed to seventy years by 1960 and to seventy-five years by 1990. Now we are told they are shortening our lives - killing us with coronary heart disease. Why the sudden change? To discover that, we need to know something of the history of coronary heart disease and how the strategy to combat it evolved.

*Coronary heart disease *

There are many diseases that affect the heart but the one that the 'healthy eating' strategies seek to prevent is Coronary Heart Disease (CHD), more correctly called ischaemic heart disease (IHD). CHD is a condition where the coronary arteries that supply blood to nourish the heart muscle are narrowed by a build-up of material on their walls (an atheroma) to such an extent that they become blocked. This cuts off the blood supply to part of the heart muscle, and we have a heart attack. The narrowing also encourages the clotting of blood and, in consequence, it is possible for a clot to cause a heart attack long before the atheroma is large enough to do so. The material generally blamed for the build-up is cholesterol and the 'healthy eating' advice given to the public to reduce the incidence of CHD is aimed simply at reducing the levels of cholesterol in the blood.

*Cholesterol *

Because of the propaganda, you can be forgiven for thinking that cholesterol is a harmful alien substance that should be avoided at all costs. In fact, nothing could be further from the truth. Cholesterol is an essential component in the body. It is found in all the cells of the body, particularly in the brain and nerve cells. Body cells are continually dying and new ones being made. Cholesterol is a major building block from which cell walls are made. Cholesterol is also used to make a number of other important substances: hormones (including the sex hormones), bile acids and, in conjunction with sunlight on the skin, vitamin D 3 . The body uses large quantities of cholesterol every day and the substance is so important that, with the exception of brain cells, every body cell has the ability to make it.

Cholesterol may be ingested in animal products, but less than twenty percent of your body's cholesterol needs will be supplied in this way. Your body then makes up the difference. If you eat less cholesterol, your body merely compensates by making more. Although the media and food companies still warn against cholesterol in diet, it has been repeatedly demonstrated that the level of cholesterol in your blood is affected very little by the amount of cholesterol you eat.

*Cholesterol and CHD *

For reasons still unknown, coronary heart disease suddenly took off during the 1920s throughout the industrialised world. By the 1940s it was becoming the major cause of premature death. And nobody knew why.

In 1950 an American doctor, John Gofman, hypothesised that blood cholesterol was to blame. This was supported in 1951 when pathologists were sent to Korea to learn about war wounds by dissecting the bodies of dead soldiers. To their surprise they discovered unexpected evidence of coronary heart disease: unexpected for they knew that death from heart disease was extremely rare under middle age and these men averaged only twenty-two years of age. So the pathologists performed detailed dissections on the hearts of the next 300 corpses. In thirty-five percent they found deposits of fibrous, fatty material sticking to the artery walls. A further forty-one percent had fully formed lesions, and in three percent of the soldiers these lesions were sufficiently large that they blocked at least one coronary artery. Thus, over three-quarters of all the men examined showed evidence of serious coronary heart disease - and they were barely out of their teens.

Doctors now had a problem. As there are no symptoms with the partial blockage of the coronary arteries, how could they tell, without resorting to surgery, who was in danger? They had to find what was different in those with the disease and those free of it.

To cut a long story short, they found cholesterol in the material that builds up on artery walls and causes them to become blocked; people who died of heart disease often had high levels of cholesterol in their blood; and those who suffered the rare hereditary disease, familial hypercholesterolaemia (hereditary high blood cholesterol), also suffered a higher incidence of CHD. And so, not unnaturally perhaps, cholesterol and heart disease became linked.

But there are a number of significant points that the cholesterol theory overlooks. For example, there is a marked difference between the build-up found in those with familial hypercholesterolaemia and those with coronary heart disease: hypercholesterolaemia causes large deposits at the mouths of the coronary arteries, often leaving the arteries themselves unblocked, and so does not reproduce the type of obstruction found in coronary heart disease. People with myxoedema or nephrosis also have high blood cholesterol levels - yet in them, there is no increase in the incidence of CHD. Neither is raised blood cholesterol a predictor of CHD in people over sixty. It has also long been known that simple events, such as putting a cuff around the arm prior to taking a blood sample, or fear of the needle, can result in raised cholesterol values. And, even where these are avoided, large fluctuations are known with peak to nadir variations of as much as twenty-three percent. Lastly, cholesterol is only one of the constituents of an atheroma and, if you think about it, cholesterol is so necessary and so widespread in the body, it would have been surprising if it had not been found. Nevertheless the lowering of blood cholesterol became the sole objective in the fight against CHD; and the two principal methods used to achieve this are with diet and drugs.


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## Cookie

*Part 2: Dietary Fats and Heart Disease *
​
*
*

For what a man would like to be true, that he more readily believes. Francis Bacon

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. As Table I shows, 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.)


*Table I: *Cholesterol intake - The Framingham Heart Study  *Blood Cholesterol in Those * *Cholesterol *

*Intake *

*Below Median *

*Intake *

*Above Median *

*Intake *





*mg/day *
​




*mmol/l *
​




*mmol/l *
​
*Men *



704 ± 220.9
​




6.16
​




6.16
​
*Women *



492 ± 170.0
​




6.37
​




6.26
​


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 centres 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, Table II demonstrates that the 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.


*Table II *: Fat intake and blood lipids - The Tecumseh Study  *Blood Cholesterol in Thirds * *Daily Intake: *



*Lower *
​




*Middle *
​




*Upper *
​
Fat - total (g) 



128
​




134
​




133
​
Fat Saturated (g) 



52
​




54
​




54
​
Polyunsat/Sat ratio 



0.51
​




0.51
​




0.51
​
Cholesterol (mg) 



554
​




566
​




533
​


*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. As Table III shows, in North Karelia there was a reduction in both CHD mortality and total mortality. Table III also 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.


*Table III: *Age Adjusted Rates/1,000. Age Group 30-64 years - The North Karelia Project.  



*1970/1 *
​
*
*





*1976/7 *
​
*
*





*Decline *
​
 *Total Mortality * *Men *N Karelia 



13.8
​




11.6
​




16%
​
Kuopio 



13.6
​




11.4
​




16%
​
*Women *N Karelia 



4.8
​




3.9
​




19%
​
Kuopio 



5.0
​




3.8
​




24%
​
*CHD Mortality * *Men *N Karelia 



7.7
​




6.3
​




18%
​
Kuopio 



7.7
​




5.8
​




25%
​
*Women *N Karelia 



2.5
​




1.7
​




32%
​
Kuopio 



2.5
​




1.6
​




36%
​


These figures 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.
​
I find difficulty understanding 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 let me do a similar comparison.



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.


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


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.


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.


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.


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.


Lastly, the World Health Organisation 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.

*Margarine - a natural food? *

The polyunsaturated fats used to make margarine are generally obtained from vegetable sources such as sunflower seed, cottonseed, and soybean. As such they might be thought of as natural foods. Usually, however, they are pressed on the public in the form of highly processed margarines, spreads and oils and, as such, they are anything but natural.

In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion. This was enough to cause Perrier to be removed from supermarket shelves. The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents. Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product. That is 700 times as much as fourteen parts per billion.

The oils then go through more than ten other processes: degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, . . . that include heat treatment at 140 o -160 o with a solution of caustic soda; the use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product; the addition of antioxidants such as butylated hydroxyanisol (E320). These antioxidants are again usually petroleum based and are widely believed to cause cancer.

The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.

The heat treatment alone is enough to render these margarines nutritionally inadequate. When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.

Recent United States studies showed that heart disease worsened in those who switched from butter to polyunsaturate-rich margarine. Research published in March 1993, confirmed this. In a study that involved 85,000 nurses, women who ate just four teaspoons of polyunsaturated margarine a day had a sixty-six percent increased risk of CHD compared to those who ate none. A review of men's experience in the Framingham Study published in 1995 also found that 6 teaspoons a day (mean of lowest intake vs mean of highest), increased risk by nearly a third. The authors conclude:



*"Intake of margarine may predispose to development of CHD in men". *


You may be interested in a list of the ingredients that may be present in butter and margarine:




*Butter: *

milk fat (cream),

a little salt

*Margarine: *

Edible oils,

edible fats,

salt or potassium chloride,

ascorbyl palmitate,

butylated hydroxyanisole,

phospholipids,

tert-butylhydroquinone,

mono- and di-glycerides of fat-forming fatty acids,

disodium guanylate,

diacetyltartaric and fatty acid esters of glycerol,

Propyl, octyl or dodecyl gallate (or mixtures thereof),

tocopherols,

propylene glycol mono- and di-esters,

sucrose esters of fatty acids,

curcumin,

annatto extracts,

tartaric acid,

3,5,trimethylhexanal,

ß-apo-carotenoic acid methyl or ethyl ester,

skim milk powder,

xanthophylls,

canthaxanthin,

vitamins A and D.


​
*Dietary fat patterns *

The total amount of fats in our diet today, according to the MAFF National Food Survey, is almost the same as it was at the beginning of this century. What has changed, to some extent, is the types of fats eaten. At the turn of the century we ate mainly animal fats that are largely saturated and monounsaturated. Now we are tending to eat more polyunsaturated fats - it's what we are advised to do.

It is interesting to compare the growth of heart disease in this country with intakes of different fats. The next graph illustrates the birth of CHD in Britain together with the intake of animal fat since the beginning of the century. When compared with the CHD curve, it is clear that there is no obvious relationship

If we plot CHD together with intakes of margarines and vegetable shortenings, however, we find a different curve.



Margarine use began around the turn of the century. Butter was expensive. The poor bought margarine as a substitute for butter and sales were brisk. The rapid rise in margarine consumption was followed a couple of decades later by that dramatic rise in heart disease deaths.
​
If there is a causal relationship between fat intake and heart disease, these two graphs suggest to me that it is the margarines that are the more likely candidates for suspicion.

*Polyunsaturated fats and Cancer *

Body cell walls are made of cholesterol. The graph below demonstrates that the human body's fat make-up is largely of saturated and monounsaturated fatty acids. We contain very little polyunsaturated fat. Cell walls have to allow the various nutrients that body cells need from the blood, but stop harmful pathogens. They must be stable. An intake of large quantities of polyunsaturated fatty acids changes the constituency of cholesterol and body fat. Cell walls become softer and more unstable.


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Many laboratories have shown that diets high in polyunsaturates promote tumours. It has been known since the early 1970s that it is linoleic acid that is the major culprit. As Professor Raymond Kearney of Sydney University put it in 1987:

*

"Vegetable oils (eg Corn oil and sunflower oil) which are rich in linoleic acid are potent promoters of tumour growth."

*Carcinogens - background radiation, ultraviolet radiation from the sun, particles in the air we breathe and the food we eat - continually attack us all. Normally, the immune system deals with any small focus of cancer cells so formed and that is the end of it. But linoleic acid suppresses the immune system. Indeed it is so good at this that in the 1970s sunflower oil was given to kidney transplant patients to prevent kidneys being rejected - until an excess of cancer deaths was reported. With a high intake of margarine, therefore, a tumour may grow too rapidly for the weakened immune system to cope thus increasing our risk of a cancer.

Since 1974, the increase of polyunsaturated fats has been blamed for the alarming increase in malignant melanoma (skin cancer) in Australia. We are all told that the sun causes it. Are Australians going out in the sun any more now than they were fifty years ago? They are certainly eating more polyunsaturated oils: even milk has its cream removed and replaced with vegetable oil. Victims of the disease have been found to have polyunsaturated oils in their skin cells. Polyunsaturated oils are oxidised readily by ultra-violet radiation from the sun and form harmful 'free radicals'. These are known to damage the cell's DNA and this can lead to the deregulation we call cancer. Saturated fats are stable. They do not oxidise and form free radicals.

Malignant melanoma is also said to be increasing in this country. Does the sun cause this? In Britain the number of sufferers is so small as to be relatively insignificant. Even so, it is not likely that the sun is to blame since all the significant increase is in the over-seventy-five-year-olds. People in this age group tend to get very little sun.

Melanoma occurs ten times as often in Orkney and Shetland than it does on Mediterranean islands. It also occurs more frequently on areas that are not exposed to the sun. In Scotland, for example, there are five times as many melanomas on the feet as on the hands; and in Japan, forty per cent of pedal melanomas are on the soles of the feet.

In 1991, two studies, from USA and Canada, found that linoleic acid, the major polyunsaturated fatty acid found in vegetable oils, increased the risk of breast tumours. This, it seems, was responsible for the rise in the cancers noted in previous studies. Experiments with a variety of fats showed that saturated fats did not cause tumours but, when small amounts of polyunsaturated vegetable oil or linoleic acid itself was added, this greatly increased the promotion of breast cancer.

A study of 61,471 women aged forty to seventy-six, conducted in Sweden, looked into the relation of different fats and breast cancer. The results were published in January 1998. This study found an inverse association with monounsaturated fat and a positive association with polyunsaturated fat. In other words, monounsaturated fats protected against breast cancer and polyunsaturated fats increased the risk. Saturated fats were neutral.

All polyunsaturated margarines, from the brand leader to shops' 'own brands' are around thirty-nine percent linoleic acid. Of cooking oils, sunflower oil is fifty percent and safflower oil seventy-two percent linoleic acid. Butter, on the other hand, has only a mere two percent and lard is just nine percent linoleic acid. Linoleic acid is one of the essential fatty acids. We must eat some to live, but we do not need much. The amount found in animal fats is quite sufficient.

Because of the heart disease risk, in 1994 the manufacturers of Flora changed its formula to cut out the trans fats and other manufacturers have since followed. But that still leaves the linoleic acid.

*The anti-cancer fat *

Linoleic acid is one of the essential fatty acids that our bodies need but cannot synthesise. We must eat some to survive. Fortunately there is one form of linoleic acid that is beneficial. Conjugated linoleic acid (CLA) differs from the normal form of linoleic acid only in the position of two of the bonds that join its atoms. But this small difference has been shown to give it powerful anti-cancer properties. Scientists at the Department of Surgical Oncology, Roswell Park Cancer Institute, New York and the Department of Biochemistry and Molecular Biology, New Jersey Medical School, showed that even at concentrations of less than one percent, CLA in the diet is protective against several cancers including breast cancer, colorectal cancer and malignant melanoma.

Conjugated linoleic acid has one other difference from the usual form - it is not found in vegetables but in the fat of ruminant animals. The best sources are dairy products and the fat on red meat, principally beef. It is another good reason not to give up eating red meat or to cut the fat off.

Scientists at the University of Wisconsin also believe that CLA has a slimming action. They put the dramatic increase in obesity in the USA down to Americans not eating beef fat.

*Monounsaturated fats *

Several populations in the world, Eskimos and those in the Mediterranean countries for example, eat high-fat diets yet have very low incidences of heart disease. This realisation has led to research scientists switching their attentions to monounsaturated fats found in fish oils and olive oil.

Although the supposed virtues of monounsaturated fats are being talked of in the press as possible saviours of Western man, the monounsaturated theory is not new. It was first demonstrated over thirty years ago that giving people more unsaturated fats could lower blood cholesterol. However, surveys of countries with different tastes in fats and oils have failed to show that this protects against heart disease. For example, Norwegians, who eat a lot of saturated fats, have lower rates of the disease than New Zealanders who eat a similar amount. But if, as has been suggested, the Norwegians are protected by the monounsaturated oils in the fish that they eat, then why is it that in Aberdeen, where a lot of fish is also consumed, the heart disease rate is double that of Oslo? Proponents also forget that many other people, such as the Maasai tribes of Africa, who don't eat either fish or olive oil, also have a low incidence of heart disease.

There is also no evidence that either mono- or polyunsaturated oils are of benefit to those who have already suffered a heart attack. As long ago as 1965 survival rates were studied in patients eating different oils. Splitting patients into three groups, who were given polyunsaturated corn oil, monounsaturated olive oil and saturated animal fats respectively, it was found that only the corn oil lowered blood cholesterol levels. At first sight, therefore, it seemed that men in the polyunsaturated group had the best chance of survival. However, at the end of the two-year trial only fifty-two percent of the polyunsaturated corn oil group were still alive and free of a fresh heart attack. Those on the monounsaturated olive oil fared little better: fifty-seven percent survived and had no further attack. Those eating the saturated animal fats, however, fared much better with seventy-five percent surviving and without a further attack.

*Breast Cancer. *The Swedish study by Alicia Wolk and colleagues mentioned above did find, however, that monounsaturated fats were protective against breast cancer.

Animal fats such as lard are around 43% Saturated, 47% Mono-unsaturated and 10% Polyunsaturated - which the evidence suggests is just about ideal.


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*Part 3: The Bran Wagon *
​
*
*



The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact. T H Huxley
​
The belief that regular bowel movement is important for health is very ancient. But the present theory is based on Dr. Dennis Burkitt's discovery that relatively few rural black Africans suffer from cancer of the colon. He attributed this to their relatively crude diet.

The theory was that, as fibre made food travel through the gut faster, it allowed less time for cancer-inducing agents to form. This, of course, presupposed that food became carcinogenic in the gut and there was no evidence that it did. Neither was there any evidence that moving food through the intestine at a faster rate decreased the risk of colon cancer. Moreover, the rural Africans' lifestyle was far from that of the Western city dweller: their diet is different, but also they were not exposed to so many pollutants, toxins or mental stresses. Indeed, there were many factors that could have been responsible for a difference in disease patterns. Other communities - the Mormons of Utah, for example - also enjoyed a low incidence of colon cancer yet they ate a low-fibre diet.

So the theory was unsubstantiated at the time and it was to be disproved in practice later as the rural Africans moved into towns and adopted a Western style low fibre diet. Their incidence of colon cancer has remained low and this has continued with the second generation. Nevertheless, these later findings were not publicised. Burkitt's theories caught the attention of the media. Always ready to exploit a good story, they expanded what was at best a very weak hypothesis into a treatment dogma that teaches that fibre is a panacea for all manner of illnesses.

Commercial interests were quick to see the potential in the recommendation and jump on the bran wagon. Burkitt's recommendation was based on vegetable fibre, but bran (cereal fibre) has a far higher fibre content and bran was a practically worthless by-product of the milling process that, until then, had been thrown away. Almost overnight, it became a highly priced profit maker. Although totally inedible, backed by Burkitt's fibre hypothesis, bran could now be promoted as a valuable food. But Dr. Hugh Trowell, Burkitt's partner and another strong advocate of dietary fibre, stated in 1974 that: *

"A serious confusion of thought is produced by referring to the dietary fibre hypothesis as the bran hypothesis, for many Africans do not consume cereal or bran"

**Fibre and coronary heart disease *

The idea that fibre could protect against heart attacks was hypothesised by Trowell in 1972, again based on research on rural Africans. The dietary intervention trials mentioned earlier, however, concluded that increasing dietary fibre had no beneficial effect on heart disease.

*Fibre and other diseases. *

It may be useful at this stage to consider the claims for fibre in curing or preventing other diseases. For example, bran has been a popular way to manage irritable bowel syndrome (IBS) for about thirty years, despite the fact that no placebo-controlled study of bran in IBS has yet shown any convincing beneficial effect. A study, published in 1994, found that while fruit fibre was effective, bran only made the situation worse. Far from being a cure for IBS, they found that it was the bran that was causing it! Bran also caused bowel disturbances, abdominal distension and pain.

Moreover, there is no direct evidence that an increase of fibre by itself will prevent or cure the other diseases. With respect to colon cancer, Burkitt's theory was questioned with the suggestion that the low cancer rates in rural Africans may be due to their high early death rates from other causes, so that they do not reach the age at which cancer peaks in Europeans. As the Africans' life expectancy was only forty years at the time Burkitt did his research and Western cancers don't peak until the age of sixty-five, one wonders why this wasn't noticed before.

There is also a growing scepticism in the USA that lack of fibre causes cancer; some studies even suggesting that a fibre-enhanced diet increases the risk of colon cancer.

*Other adverse effects *

Tests into the supposed benefits of dietary fibre soon showed that there could be other harmful side effects. All the nutrients in food are absorbed through the gut wall and this takes time. Fibre, by speeding food through the gut faster so that less nutrients are absorbed, inhibits the absorption of iron, calcium, phosphorus, magnesium, energy, proteins, fats and vitamins A, D, E and K. This happens with all types of fibre although with a normal Western-style, nutrient-rich diet, the loss caused by vegetable fibre intake is unimportant. More importantly, phytate found in cereal fibre (bran) also binds with calcium, iron and zinc making them indigestible, which in turn causes malabsorption. One study, for example, showed that subjects absorbed more iron from white bread than from wholemeal bread even though their intakes of iron were fifty percent higher with the wholemeal bread. Bran has also been shown to cause faecal losses of calcium, iron, zinc, phosphorus, nitrogen, fats, fatty acids and sterols, thus depleting the body of these materials.

These findings are a cause for concern in several sections of the population who are at considerable risk from eating too much fibre - and bran fibre in particular:



The incidence of *osteoporosis *(brittle bone disease) is increasing and now affects one in two post-menopausal women, one in five of whom will die as a direct result. Osteoporosis is also increasingly affecting men. Osteoporosis is caused by several factors, but lack of calcium is the basic problem. Bran both inhibits the absorption of calcium from food and depletes the body of the calcium it has. Moreover, zinc, which bones need to heal, is another mineral whose absorption is adversely affected by bran.


Sufferers from *Alzheimer's Disease *(senile dementia) are found to have abnormal amounts of aluminium in their brains. Tests on the people of Guam and parts of New Guinea and Japan, who get Alzheimer's disease at a much younger age, suggest that it is lack of calcium, causing a hormonal imbalance that permits the aluminium to penetrate the brain.


Infants may suffer similar *brain damage *if fed soy-based baby milk as this too has a high phytate content, inhibiting the absorption of zinc, which is essential for proper brain development.


Vitamin deficiency diseases such as *rickets *that were common in Britain until a diet high in dairy products and meat was advocated are on the increase again. The situation is getting so bad here that doctors suggest that vegetarian-based fad diets should be classified a form of child abuse.


In the UK, USA, Canada and South Africa the intake of 'anti-nutrients' such as dietary fibre that impair the absorption of iron, accompanied by a low intake of meat (another result of the diet-heart recommendations), is producing a real risk of *iron deficiency anaemia. *


*Depression, anorexia, low birth weight, slow growth, mental retardation *, and *amenorrhoea *are associated with deficiencies of zinc and the first five of these are also associated with a deficiency of iron.


Lastly, excess fibre affects the *onset of menstruation, retards uterine growth *and, later, is associated with *menstrual dysfunction *.

Because of the phytate, Professor David Southgate, arguably the world's leading authority on the effects of fibre, concludes that infants, children, young adolescents and pregnant women whose mineral needs are greater should be protected from excessive consumption of fibre.

Writing of the *colon cancer *risk, Drs. H. S. Wasan and R. A. Goodlad of the Imperial Cancer Research Fund stated in 1996:

*

"Until individual constituents of fibre have been shown to have, at the very least, a non-detrimental effect in prospective human trials, we urge that restraint should be shown in adding fibre supplements to foods, and that unsubstantiated health claims be restricted." . . . "Specific dietary fibre supplements, embraced as nutriceuticals or functional foods, are an unknown and potentially damaging way to influence modern dietary habits of the general population."

*Until fibre can be shown not to be detrimental they suggest that

*

"restraint should be shown in adding fibre supplements to foods, and that unsubstantiated health claims should be restricted".

*January 1999 saw the publication of the largest trial into the effects on fibre on colon cancer ever conducted. After studying 88,757 women for sixteen years, doctors at the Brigham and Women's Hospital and Harvard Medical School say that

*

"No significant association between fiber intake and the risk of colorectal adenoma was found." . . . "Our data do not support the existence of an important protective effect of dietary fiber against colorectal cancer or adenoma."

**Summary *

Bran is bad news. While there is not too much harm from fruit fibre, the usual bran that is pushed at us - wheat bran- should be avoided like the plague it is.


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Part 4: The Dangers of Low Blood Cholesterol

Nature has taken good care that theory should have little effect on practice. Samuel Johnson

Low blood cholesterol and cancer

So far advertisers and news media have concentrated on the supposed danger from high levels of blood cholesterol. The dangers of low blood cholesterol levels have largely been ignored.

Countries with diets high in saturated fats also tend to have high levels of colon cancer. In 1974 a review of the Framingham data and those from Keys' 'Seven Countries' study was carried out. It was expected to show that the cancer could also be blamed on high blood cholesterol. However, the baffled researchers found the opposite: those with the cancer had cholesterol levels that were lower than average.

Reports of more than twenty studies into the relation between blood cholesterol and cancer have been published since 1972. Most have reported an association between low blood cholesterol and cancer. The authors of the Renfrew and Paisley Study conclude:

"it may be a mistake to assume that dietary advice given to the general population to reduce the intake of saturated fat will necessarily reduce overall mortality."

In a study from the USA published in 1990, changes in blood cholesterol over time were studied in patients with colon cancer. The doctors found that there had been an average thirteen percent decline in blood cholesterol levels in the ten years prior to diagnosis of the cancer compared with an average increase of two percent in the control group. Both those with the cancer and those free from it had similar blood cholesterol levels initially. It is possible that the decline in blood cholesterol levels was a result of the cancer, not the cause of it, but this is ruled out by the investigators. They compare cholesterol studies with apparently contrary findings and show that in reality they are consistent. Comparing those that reported normal or high cholesterol readings several years prior to diagnosis with others where, at the time of diagnosis, levels were low, they conclude that it was a long term lowering of blood cholesterol levels that gave rise to the cancers. Interestingly, the average blood cholesterol level of those who developed the cancers declined to an average 5.56 mmol/l and yet the British government's Health of the Nation strategy still aims to reduce everyone's levels to below 5.2 mmol/l.

Low cholesterol means more strokes

Published at about the same time was a very large study in Japan, covering two decades, which concluded that low levels of blood cholesterol also increase the incidence of stroke.

Over the past few decades, Japan has experienced a rapid change in its living and eating patterns. The Japanese are eating more total fat, saturated fatty acids and cholesterol, animal fats and protein, and less rice and vegetables. This has provided a unique opportunity for a large-scale, natural experiment into the effects of those changes.

Investigators have shown that this change to Western and urban eating patterns, departing as it does from centuries old traditions, has been accompanied by a general lowering of blood pressure and a large decline in the incidence of stroke deaths and cerebral haemorrhage between the 1960s and the 1980s. They attribute this decline to an increase in blood cholesterol levels over the period. Supporting their findings were the results of a follow-up of 350,000 men screened for the MRFIT in the United States that showed that the risk of death from cerebral haemorrhage in middle-aged men was six times greater if they had low blood cholesterol levels.

On Christmas Eve, 1997, yet one more study's results were headlined in the press. The Framingham researchers said that "Serum cholesterol level is not related to incidence of stroke . . ." and showed that for every three percent more energy from fat eaten, strokes would be cut by fifteen percent. They conclude:

"Intakes of fat and type of fat were not related to the incidence of the combined outcome of all cardiovascular diseases or to total or cardiovascular mortality."

So, after forty-nine years of research, they are still saying that there is no relation between a fatty diet and heart disease. The evidence now is clear and unequivocal: animal fats are not harmful.

Two more studies, which considered total blood cholesterol levels and mortality in the elderly, were published in the Lancet almost simultaneously in 1997. In the first, scientists working at the Leiden University Medical Centre found that

"each 1 mmol/l increase in total cholesterol corresponded to a 15% decrease in mortality".

Similarly, doctors at Reykjavik Hospital and Heart Preventive Clinic in Iceland noted that the major epidemiological studies had not included the elderly. They too studied total mortality and blood cholesterol in the over 80s to show that men with blood cholesterol levels over 6.5 had less than half the mortality of those whose cholesterol level was around the 5.2 we are told is "healthy".

Low cholesterol and Alzheimer's Disease

Approximately half of the brain is made up of fats. Dr. F. M.Corrigan and colleagues, writing in 1991 about the relief of Alzheimer's Disease, ask that "strategies for increasing the delivery of cholesterol to the brain should be identified". In the fight against Alzheimer's disease, they recommend increasing fat intake.

And at the other end of life

In 1991 the US National Cholesterol Education Programme recommended that children over two years old should adopt a low-fat, low-cholesterol diet to prevent CHD in later life. A table showing a good correlation between fat and cholesterol intakes and blood cholesterol in seven to nine-year-old boys from six countries supported this advice. What it did not show, however, was the strong correlation between blood cholesterol and childhood deaths in those countries. These are at Table V. As is clearly demonstrated, the death rate rises dramatically as blood cholesterol levels fall. So for children too, low blood cholesterol is unhealthy.

Table V: Blood cholesterol and mortality in under-5s in six countries

Blood

cholesterol Childhood

deaths

Finland 4.9 7

Netherlands 4.5 9

USA 4.3 12

Italy 4.1 12

Philippines 3.8 72

Ghana 3.3 145

Low blood cholesterol, aggressive behaviour and suicide

Lastly, since 1992, several observers have noted increases in suicides among those undertaking cholesterol-lowering dietary regimes. Decreases in blood cholesterol cause decreases in serotonin receptors leading to increased microviscosity and affecting the balance of cerebral lipid metabolism which could have profound effects on brain function.

In institutions, aggressive people and those with antisocial personality have been found to have lower blood cholesterol levels than normal: Typically 5.04mmol/l vs 6.02mmol/l. Mental patients with high blood cholesterol (7.55mmol/l) were less regressed and withdrawn than those with lower (4.80mmol/l).

Dr Matthew G Dunnigan of Stobhill General Hospital, Glasgow, concludes that:

"Without definite data on all-cause mortality and with current unresolved concerns about excess deaths from non-cardiac causes in RCTs, decisions to embark on lifelong lipid lowering drug treatment in most patients with primary hypercholesterolaemia depend on the doctor's interpretation of available evidence. As in other situations in which certainty is illusory, this varies from evangelical enthusiasm for lowering lipid concentrations to therapeutic nihilism


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Part 5: Cholesterol-Lowering Drugs

For every problem there is a solution, neat, plausible and wrong. H L Mencken

Although it became clear that a change in diet had little effect on CHD, that did not end the scientists' efforts to demonstrate that CHD could be prevented. If diet couldn't do it, then intervention with drugs would provide the evidence. And since drugs could be controlled much more strictly, and used in conjunction with placebos, the findings would be more demonstrable. But the drugs used to reduce blood cholesterol have all proved to be something of a disaster.

Launched on the public in 1961, Triparanol causes the levels of blood cholesterol to fall by inhibiting the liver's ability to make cholesterol. Two years later it was with- drawn because of serious side effects. Luckily for triparanol's manufacturers, a public scandal was avoided as the media's attentions were focussed on another drug marketed at the same time and by the same company - thalidomide.

More recently, a number of other drugs have been the subject of extensive and expensive trials. First was Cholestyramine (Questran) which reduces cholesterol by interfering with digestion. The gall bladder manufactures bile acid from cholesterol, and the bile acid is used in the intestine to digest fats. But when the drug is present in the gut, it binds with the bile acid, removing it from its normal function. Because the drug is indigestible, it, together with the bile acid, is excreted and the gall bladder has to make more by drawing cholesterol from the bloodstream.

As the trial would be very expensive, the scientists examined 480,000 men over a period of three years to find suitable subjects. They had to be men in the coronary age group and with extremely high blood cholesterol levels. As such men are in the most vulnerable group, their chances of success were greatly increased.

The investigators confidently announced in advance that blood cholesterol levels would be lowered by an average of 28% and, after seven years, coronary heart disease would be reduced by 50% in the treatment group.

At the end of the trial, however, cholesterol levels had fallen by less than a quarter of that called for at the start and heart disease rates were hardly affected. The $142 million trial was a total flop. Even if it had proved a success, however, those participating were so unrepresentative of the population that the question of its efficacy for the typical adult would still have remained. Another flaw that became apparent was an increase in the incidence of oral-gastro-intestinal cancers which could not be dismissed as a random chance. In the Lipid Research Clinics trial there were 21 cases and 8 deaths from gastrointestinal cancer in those taking the drug, compared to 11 cases and just 1 death in the control group.

Other organisations tested other drugs. The World Health Organisation sponsored its own trial with Clofibrate (Atromid). This too was targeted against cholesterol and was confidently expected to lower blood cholesterol levels by 30%.

As with cholestyramine, the levels were lowered by much less than the expected amount and at the end of the trial it became clear that there had been many more deaths in the group taking clofibrate than in the control group - notably from gallstones, and cancer of the liver and digestive system. In the WHO clofibrate trial, as Table IV demonstrates, the drug killed more than it saved.

Table IV: WHO European Primary Prevention Trial with Clofibrate. 9.6-year follow up

Clofibrate Placebo

Cause of death 5,331 men 5,296 men

CHD 157 138

Stroke 30 19

Other cardiovascular diseases 21 16

Cancers 125 99

Other medical 30 13

Accidents 31 30

Unknown 2 2

All causes (Total) 396 317

Among other drugs to be tested were:

a. The female hormone Oestrogen on the theory that if premenopausal women did not get heart disease, perhaps oestrogen would protect men. But the hormone caused heart attacks rather than preventing them.

b. The hormone Dextrothyroxine , which lowers cholesterol levels, abandoned quickly when an increase in mortality was noticed in the treatment group.

c. The vitamin Niacin, which looked promising, but although there appeared to be a reduction in non-fatal heart attacks, there were marked side effects: skin disorders such as darkening, itches and rashes, as well as digestive problems and gout.

d. Gemfibrozil (Lopid) was tested and again an increase in deaths was noticed in the treatment group although this time the numbers did not reach statistical significance.

e. Compactin which worked in a similar way to triparanol was withdrawn hurriedly and in some secrecy. The reason this time appears to be connected with cancer in dogs.

f. Lastly, despite the previous experiences with triparanol and compactin, yet another inhibitor, Lovastatin, has been approved for lifetime use on the general public after tests of very short duration only. (Derivatives pravastatin and simvastatin are marketed as Lipostat and Zocor.)

A study of all trials into cholesterol lowering by drugs up to 1987 showed an increase in mortality in those treated with drugs of 13.6%.

In 1993 a meta-analysis of all randomised controlled trials of cholesterol-lowering treatments showed that only those with very high risk showed any evidence of benefit. In all others mortality was increased. Its authors conclude that:

"Currently evaluated cholesterol-lowering drugs seem to produce mortality benefits in only a small proportion of patients at very high risk of death from coronary heart disease . . . a cautious approach to the use of cholesterol lowering drugs should be advocated".

Despite this, nearly eight times as many prescriptions for cholesterol-lowering drugs were being issued just 6 years later!


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Part 6: Has Anyone Gained?

So far we have been looking at cholesterol lowering in terms of numbers of deaths, but the trials have shown impressive results in the reduction of non-fatal heart attacks and a consequent improvement in the quality of life. In the case of drugs, the reduction was in the order of twenty-three percent. Many see this as proof that lowering cholesterol in the total population, by whatever means, is worth fighting for.

But those trials were conducted on men rather than women. They were also conducted on those who had hypercholesterolaemia or, at least, very high blood cholesterol levels - not people with normal levels. They totally overlook the now well-established, non-linear relation between blood cholesterol and heart disease that indicates that lowering blood cholesterol in the general population is not economically worthwhile. The widespread agreement that the mainstay of the campaign should be a change in diet and lifestyle for all also overlooks the complete lack of evidence that such a course would have any significant beneficial effect. It even overlooks the fact that the trials involving cholesterol lowering by dietary means did not show any significant reductions in blood cholesterol.

In 1992 a report of 19 major studies published over the past twenty years suggested that public policy for reducing blood cholesterol should be reviewed. The graph below plots the relative mortality risk from all causes associated with levels of blood cholesterol in men and women. In the case of women, you can see clearly that risk rises as blood cholesterol falls. The report's author, Dr. Hulley, states:

"We are coming to realise that the resulting cardiovascular research, which represents the great majority of the effort so far, may not apply to women".

With men, the situation is more complicated as the curve is U-shaped. However, it is still noticeable that the risk with low cholesterol is similar to the risk with high cholesterol. Dr. Hulley concludes:

"the findings call into question policies built over several decades on evidence that focussed only on CHD as an outcome . . . it may be time to review national policies aimed at shifting the entire population distribution of blood cholesterol to the left."

Another analysis based on a number of American studies estimated that on a lifelong programme of cholesterol reduction by diet, the gain in life expectancy for those at very high risk (that is the 1 in 500 with hypercholesterolaemia) would be between eighteen days and twelve months, and for those at low risk (that is the other 499) between three days and three months. That is not very much with which to tempt people to endure a lifetime of unpalatable diets. And these figures assumed that cholesterol lowering was both effective and safe: they didn't take into account the increased risk of other debilitating and fatal diseases. Once these are added to the equation, it becomes quite evident that the current campaign is certain to do more harm than good. A study of Maori in New Zealand showed that those with the lowest levels of blood cholesterol had the highest mortality. Findings also borne out by the Framingham Study.

What we have then is a number of very large-scale, long-term human intervention studies showing that lowering blood cholesterol is possible but that it has no beneficial effect on coronary heart disease in the general population, and other studies showing that a low blood cholesterol level, or the methods used to attain it, are increasing the incidence of other serious killer diseases.

Thirty years ago it was said that

"current medical thinking . . . is that while cholesterol may be involved in some way with arteriosclerosis and heart disease, it is no longer held to be the main factor." . . . "A recent survey of cholesterol findings in geriatric cases involving arteriosclerosis showed a significant number of patients to have normal or low cholesterol."

Those remarks have been confirmed by all the major studies published to date. Forty years after the Framingham Heart Study began, its researchers looked at total mortality and cholesterol. The evidence was that for those with low cholesterol levels, deaths from non-cardiac causes offset any reduced incidence of heart disease. There was "no increased overall mortality with either high or low serum cholesterol levels" among men over forty-seven years of age. There was no relationship with women older than forty-seven or younger than forty. The researchers also concluded that people whose cholesterol levels are falling may be at increased risk.

And ten years later the Framingham researchers say: "Intakes of fat and type of fat were not related to the incidence of the combined outcome of all cardiovascular diseases or to total or cardiovascular mortality." Thus we now have fifty years of studies all demonstrating that animal fat is harmless.


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Part 7: So Where Does That Leave Heart Disease?

All published efforts to help by drug or dietary reduction of blood cholesterol have uniformly failed. Sir John McMichael, Professor Emeritus of Medicine, University of London

Is coronary heart disease really the major killer it's made out to be? It is true that a large percentage of deaths in Britain are attributed to CHD. The question is: Is this a cause for concern? As you can see in Table VI, CHD deaths have increased in people over seventy-five years of age. But does this illustrate a problem?

Table VI: - CHD Mortality in UK Over Age 70 by Sex and Age

Ages

70-74

75-79

80-84

Over 85

Men

1975 16297

12561

8666

6270

1995 13379

12975

12223

10254

Women

1975 10598

12868

12589

14617

1995 7695

9915

13717

21263

ICD 410-414

It is a fallacy to believe that if these people had modified their diet or lifestyle, they would still be alive. Despite what the health industry tells us, we are not an immortal species and cannot expect to live forever. I suggest that these figures merely show that people tended to live longer in 1995 than in 1975. This is true of both sexes and that, surely, is a good thing.

Premature death from CHD is a legitimate concern. If dietary change can reduce premature deaths it is arguably to their advantage that people be urged to change their ways. However, Table VII illustrates clearly that CHD deaths have fallen considerably in all under-seventy age groups and both sexes over the past two decades.

Table VII: - CHD Mortality in UK Under Age 70 by Sex and Age

Ages

40-44

45-49

50-54

55-59

60-64

65-69

Men

1975 1290

2914

5783

7214

11678

15448

1995 643

1473

2261

3766

6170

9591

Women

1975 202

473

1072

1902

3950

7104

1995 124

262

480

979

2028

4188

ICD 410-414

Some say that this is evidence that 'healthy eating' is working. Do not be misled. This reduction cannot be the result of the 'healthy diet' recommendations - they only began with the COMA report of 1984, but premature CHD deaths had started to decline nearly twenty years before in 1965, as is graphically illustrated below in men aged 40-44.

This was a time when people were brought up or spent the greater part of their lives with the recommendations with which this paper began. They had free, full-cream milk at school, ate bread and dripping and fried breakfasts. During the period after World War II when deaths from CHD peaked and started to fall, rationing had ended and a diet that was relatively high in fat was the vogue.

Not that this will come as any surprise to the Medical Research Council. In its report on the Caerphilly Study published in 1993, the MRC's Epidemiology Unit at Cardiff showed that men who drank more than a pint of full-cream milk a day had only one tenth the incidence of heart disease as those who drank none. They also demonstrated that those who ate a high-energy diet lived longer than those who cut dietary fats. Their findings indicate that far from being a killer, the diet we are told to avoid by the nutritionists may actually protect us against heart disease!

These findings confirmed a Japanese study of 1992. Japan has low levels of death from coronary heart disease but Okinawa has the lowest of all. While blood cholesterol levels are generally low in Japan, Okinawa's levels are much higher: similar to those in Scotland. In 1994 a paper examined the relationship of nutritional status to further life expectancy and health in the Japanese elderly based on three epidemiological studies. It found that Japanese who lived to the age of one hundred were those who got their protein from meat rather than from rice and pulses. The centenarians also had higher intakes of animal foods such as eggs, milk, meat and fish. Significantly, their carbohydrate intake was lower than that of their fellow countrymen who died younger.

An example of increasing risk

I have noticed, as I preach my gospel, that many women say "I'd rather drink skimmed milk. I don't like the taste of full-cream milk now, it's too rich". This is a trend that worries me.

We all need calcium but women need a good supply to prevent osteoporosis in later life. Milk is the best dietary source of calcium. As all the calcium in milk is in the milk, not in the cream, skimmed milk contains slightly more calcium than full-cream milk. On the face of it, therefore, it looks like a good idea to drink skimmed milk. BUT for calcium to be absorbed from the gut, it has to be there in the presence of fat and vitamin D - and skimmed milk contains neither. As a result, while just over fifty percent of the calcium in full-cream milk is absorbed, only about five percent is absorbed from skimmed milk. AND if you drink your skimmed milk with bran muesli for breakfast, you probably won't absorb even that five percent.

In 1979 the late Professor Sir John McMichael performed an inquest on the diet/heart hypothesis. Pointing out that

"All published efforts to help by drug or dietary reduction of blood cholesterol have uniformly and convincingly failed" . . . "we need a fresh approach to the problem at scientific level and should avoid further public speculation and confusion by repeated propaganda through the media until we have clarified our own professional minds and shaken off what most critical doctors are likely to regard as an untenable hypothesis of causation."

It is a pity that no-one seems to have taken any notice of him.

Fat has over twice the energy value of either carbohydrates or proteins, and other essential nutrients: lipids used in the brain and central nervous system without which we become irritable and aggressive; sterols, precursors of the bile acids and a number of hormones (including the sex hormones); and the fat-soluble vitamins A, D, E and K. The late Dr. John Yudkin, when Professor of Nutrition and Dietetics at London University, called fat the most valuable food known to man. It is both stupid and wasteful to throw it away.


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Part 8: A Question of Ethics

Is it ethical to impose a regime on people in the hope that heart disease will be reduced? Surely prevention is better than cure, you may say. But is it? Such an attitude ignores the real possibility that such intervention may do more harm than good. 'Preventative' medicine as practised in the case of heart disease, takes two forms. Firstly we are to change our lifestyles, and secondly we are screened by our doctors on an opportunity basis.

But this screening is not prevention of the disease, it is merely the early detection of it. For such procedures to be of use a number of criteria are well established. One important one is that the disease should be both common and serious, as screening for an uncommon disease will throw up many false results. These will inevitably incur the cost of further testing, and cause unnecessary anxiety which itself is harmful.

The first problem with screening in CHD, is deciding what to test for. As a predictor of coronary risk, total blood cholesterol turns out to be irrelevant, and merely testing for that is regarded by many experts as misguided. Far more reliable, they claim, is measurement of HDL (the 'good' cholesterol). However, in a test of the accuracy of checking for HDL at various laboratories, values differed by as much as 40% in 95% of the samples tested. In another study, 16 instruments manufactured by nine companies were tested in 44 laboratories. In this test, although the inaccuracies of the machines were lower at 3.6-4.4%, biases attributed to the methods used ranged from -6.8% to +25%. The accuracy of desktop machines is even more suspect.

A third study to evaluate the ability of cholesterol screening to detect individuals with blood cholesterol abnormalities concluded that 41% of those with abnormal levels would not be detected using present guidelines.

Another criterion is that an effective treatment for the disease is available, as there is little point in early diagnosis or detection of a disease for which there is no effective remedy.

Some will say that we do know the cause of coronary heart disease; it is high cholesterol, or too much fat in our diets, or not enough exercise. Or it could be something else. In 1981, two hundred and forty six 'risk factors' for heart disease were listed. That number is now well over three hundred. These so called risk factors include having English as a mother tongue, having a diagonal crease in the left earlobe, not taking siestas, not eating mackerel, snoring and wearing tight underpants. What a list of this size really tells us is that we have little idea what causes coronary heart disease. And it is certain that if all the 300 plus do play a part, we have no chance of defeating the disease.

A director of the Health Education Programme of the American Medical Association denounced the lifestyle changes with their false promise of benefit as a quasi- religious crusade when in 1984 he wrote: " Constant lifestyle self-scrutiny in search of risk factors, denial of pleasure, rejection of the old evil lifestyle and embracing a rigorous new one are followed by periodical affirmations of faith at revival meetings. . . the self-righteous intolerance of some wellness zealots borders on health fascism. Historically, humans have been at greatest risk while being improved in the best image of their possibilities as seen by somebody else."

Telling people who feel fit and well that they are not and, that if they do not make major changes to their lives, they could drop dead at any moment, not only worries them unnecessarily, it can have a profound effect on their attitudes to life. The benefits of mass screening are doubtful and the risk of harm is high. Such intervention, therefore, can only be justified ethically when either the patient has requested it or symptoms are such as to make it desirable.

If we go to our doctor with a complaint and he treats us with the best medical knowledge, he should not be held responsible for defects in that knowledge. If, however, the doctor initiates treatment without being consulted by the patient, then he is in a very different situation. Cochrane and Holland write that before advocating a course of action in such circumstances, " He should, in our view, have conclusive evidence that screening can alter the natural history of disease in a significant proportion of those screened." If he does not, he may be held responsible for any harm done.

But in the case of heart disease, recognised medical standard tests and ethics have been thrown out the window. The recommendations were forced on the public even before they had been tested, and now the perpetrators are afraid to admit that they could have been wrong. But until they do, whole populations are suffering unnecessarily.

In the United States blood cholesterol level testing for all is routine and that nation is becoming a nation of 'cholesterophobics'. More concerned with death than with life, many interviewed said that their lives were ruined as, if they had a treat, it was accompanied by feelings of guilt. One of COMA's principles is that the measures should " afford a reasonable prospect of improvement in life expectancy overall, and in the quality of life for the population as a whole." Experience around the world, and particularly from the United States, makes it certain that neither of those principles will be met.

In Britain, general practitioners, practice nurses and health visitors are starting to use desk-top cholesterol testing machines, the majority of which have been loaned by drug companies. A suggestion in the Lancet is that this is designed merely to enhance the drug companies' profits by increasing sales of cholesterol-lowering drugs, and questions their ethics. There is also the question of the psychological harm that could be done to people in view of the United States experience of the inaccuracy of such machines.

Medical bias towards illness

There is evidence that the medical profession is biassed in favour of diagnosing illness rather than health. A classic example was a test run in New York on 1,000 11-year-old children and their tonsils. On first examination 61% were found to have had their tonsils already removed. The other 39% were re-examined by a group of doctors who recommended tonsillectomy operations for 46% of them. The rest were again examined by yet another team and, again, nearly half were recommended for operations to remove their tonsils. After three examinations, only 65 of the original 1,000 had not been recommended for the operation. The test ended there as they ran out of physicians to perform the examinations. However, if the physicians had had their way, it is obvious that a great many unnecessary operations would have been performed.

High error rate in diagnoses

The bias towards illness may also combine with a high diagnostic error rate. Post- mortem examinations in a British university hospital showed that of the patients who had died of a diagnosed specific heart disease, over half had actually died of something else. And when the same sample was tested in different laboratories, different results were given in 25% of cases. Diagnostic machines, it seems, are no better. In a competition between doctors and computers in 83 cases recommended for pelvic surgery, pathology showed that both the doctors and computers were right in only 22 cases. In 37 the computers proved the doctors' diagnoses wrong, in 11 the doctors showed the machines to be in error and in 10 cases they were both wrong.

Variations between countries

There also exists a large variation between diagnostic and prescribing practices between countries which makes comparisons between them of little use. For example, in Britain, a patient is 7 times more likely to be prescribed a course of vitamins than in Sweden, and in Sweden, 8 times more likely to get gamma globulin medication than in Britain. United States surgeons perform operations twice as readily as in Britain and the French will amputate almost anything. Appendicitis and deaths attributed to it is diagnosed in Germany 3 times more frequently than in any other country.

And so to the cost

In the late 1980s, intervention alone in the United States was estimated at $14 billion a year. The cost of cholestyramine for an estimated five million people at 1990's prices was $10 billion to which up to another $10 billion must be added for laboratory tests and doctors' services. In Britain, if we also undertook a mass screening and cholesterol reducing programme, it has been suggested that drug treatment would be recommended for 10% of men aged 40-69 and, as a result, the NHS drug bill in England and Wales, £2.3 billion in 1992, would be increased by 20%. To put it in terms more familiar to the average person, the cost of the drugs alone would be between £80 and £120 per person per month. The evidence suggests that for that money we might be able to delay a fatal heart attack in the average person by between 3 days and 3 months - but shorten that person's life by a larger amount as he or she died of cancer, osteoporosis or stroke.

The effect on the NHS

Sir William Beveridge set up the National Health Service on the assumption that "there exists in any population a strictly limited amount of illness which, if treated under conditions of equity, will eventually decline." It was calculated that the cost of the service would fall as the rates of illness went down. No-one considered that the NHS would redefine and broaden its service to such an extent that only budgetary restrictions would keep it from expanding indefinitely.

The increasing sophistication of treatments available and demanded of the National Health Service are putting it under a tremendous strain. To spend scarce money and resources on any unnecessary treatment is waste, but to waste billions of pounds on such unproven and dubious hypotheses as the present, so-called 'healthy eating' recommendations is quite irresponsible and, in the long term, can only be harmful.

Dr Halfdan Mahler, Director General, the World Health Organisation recognised such waste when he said in 1984:

"The major - and most expensive - part of medical technology as applied today appears to be far more for the satisfaction of the health professions than for the benefit of the consumers of health care."

Side effects

The current 'diet-heart' strictures and media pressure aimed at ever lower blood cholesterol levels, have driven more people towards unnatural and unhealthy cult diets. Consequently, there has been a rapid rise in the incidence of infant malnutrition, deficiency diseases and other killer or debilitating diseases. Without sufficient dietary fat, the body is unable to use the fat soluble vitamins. Without vitamin D the body cannot utilise calcium. In conjunction with an increase of bran in the diet, this is another possible factor in the growing incidences of diseases such as osteoporosis and rickets.

Vegetarian traits are increasing. As animal products are the only natural source of vitamin B-12, Vegans, who eat no such animal products, run a real risk of pernicious anaemia. Bottles of pills are not a good substitute as they are generally poorly absorbed. Fermented soy products, such as tempeh, and spirulinas found in health-food shops, which are supposed to contain vitamin B-12, for the most part contain only analogues of the vitamin which are not active for humans and which, in some cases, actually block vitamin B-12 metabolism. Children of Vegans also usually have a lower body weight and height and suffer other health problems.

Doctors in Britain are reporting cases in 'the muesli belt' of severe nutritional disorders which include kwashiorkor, marasmus and rickets which are due solely to their parents' food faddism. Until recently, these diseases were only found among severely malnourished children in Africa. In Britain it is becoming so serious that they suggest that such cases should be regarded as forms of child abuse. But are the parents to blame? Could not some of the blame for this deplorable situation be fairly laid at the doors of the nutritionists?

Doctors in the USA also are reporting ever increasing numbers of children suffering from nutritional dwarfing and other deficiency problems attributable entirely to pressures to eat nutrient-poor, low-calorie foods because they are 'healthy'. These children are destined to have far-reaching problems beyond just being smaller than their peers. It has been shown that adults whose birth-weights early rates of growth were low have a much higher incidence of CHD. Brain growth and intelligence are also found to be much lower in such undernourished children.

We really seem incapable of learning from previous experiences. During World War II, when we are supposed to have been so healthy, protein-calorie deficiency was so pronounced that in many people pathology showed there was as much as 25% loss of muscle from their hearts - and similar patterns of protein deficiency are found today.

And it is not just humans who suffer side effects. In the constant quest for ever leaner meat, food animals are being engineered which could not survive naturally. Belgian Blue cattle, for example, bred to provide lean meat, have double muscles. This makes the calves too large to pass along the birth canal and they have to be delivered by Caesarean section. Other cattle and pigs are fed hormones to make them grow with less fat. As yet it is anyone's guess what the long-term consequences of this will be on both the animals and humans.

The strictures against red meat also mean that fewer cattle and sheep are being reared and more fields are used to grow cereals, rape and other vegetable crops. Unlike the animals, which on the whole produce natural fertiliser for the pastures, the vegetable and cereal crops require large amounts of manufactured nitrogen fertilisers to be spread. As we know, these leach in ever-increasing quantities out of the soil to pollute our water supplies. Grass, the food of the cattle and sheep, on the other hand, locks the nitrates in the soil, thus preventing pollution.

The Mediterranean diet

The 'Mediterranean' diet is healthier than ours, we are told. We should eat what the French, Italians and Spanish eat. That could be right - but not for the reasons usually given.

The Mediterranean diet is what the health fanatics advocate because, they say, it is low in fat. This is nonsense! Obviously, they have never been there. They don't seem to know that northern Italians love butter, that bowls of pork dripping are sold on Spanish markets or that the Spanish spread it thickly on their toast for breakfast. They don't know that goose fat is used to make cassoulet in the south of France, or that throughout the Mediterranean the sausages, salamis and pâtés all contain up to fifty percent fat.

The Mediterranean diet may be healthier than the British but, contrary to popular belief, it is very far from being a low-fat diet!

However, there are a number of major differences between the Mediterranean countries and Britain that may play a significant part in their effects on health. Not only is the food eaten by the average working family in southern Europe very different from that eaten by a typical family in Britain, more importantly, the way it is bought, presented and eaten is also different. A brief list of the principal differences is tabled below.

Mediterranean Eating Pattern

British Eating Pattern

The average Mediterranean diet comprises natural, unprocessed meat, vegetables and fruit that are usually bought fresh daily. The average British diet is composed of packaged, highly processed foods with chemical additives.

Meat plays an important part in the diet We are told to eat less meat

Fats eaten are butter, olive oil and unprocessed animal fats Fats eaten are highly processed margarines, low-fat fat substitutes, and vegetable oils.

Meals are taken slowly, without hurrying. Lunch usually takes up to two hours - and is followed by a siesta . Food is rushed. Lunches are eaten on the run or combined with work. Often, they are junk-food snacks.

Over sixty percent of energy intake is before 2.00 pm. The largest meal is eaten in the evening

Wine (believed to be protective against heart disease), is drunk during meals as part of that meal. Beer, wines and spirits are drunk in the evening after the evening meal.

Cholesterol testing

Imagine it is 2.00 a.m., you are lying in bed when you hear a noise downstairs that you know is caused by a burglar. You know how quickly your heart starts to race. Well, that is how quickly your cholesterol level can rise - and for the same reason. One of the effects of the 'fight or flight' reflex is to raise blood cholesterol. Any form of physical or mental stress has this effect. So if you run to your doctor's, your cholesterol level will be higher than if you walked; if you have been standing it will be higher than if you sat. If you are anxious, or your doctor looks worried, it will be higher. If your blood cholesterol were tested hourly throughout a day, or daily over a month, it would not be unusual to find a wide variation in values.

Blood cholesterol levels also rise naturally as you get older so that while a reading of 9 mmol/l is high at the age of twenty, it is perfectly normal if you are fifty.

Cholesterol measurements are not very accurate - less than eighty percent - even when conducted in a laboratory. A survey showed that on the same sample, laboratories could differ by as much as 1.3 mmol/l. When it is tested with a doctor's desktop machine the accuracy will inevitably be lower.

To put it in perspective, let us assume that you are around thirty years old and your cholesterol level is a perfectly respectable 6.0 mmol/l. You hurry to the surgery and are anxious about the result. This could raise it by twenty-five percent to 7.5. If it is sent to a laboratory giving the high readings it could be raised by a further 1.3. Your perfectly normal 6.0 is now a high 8.8!

In fact, so many variables affect cholesterol levels that a one-off test is a waste of time, and an unnecessary worry for the patient that can do more harm than good. Bear that in mind if you are subjected to a cholesterol test.


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Part 9: The Dangers of a "Healthy" Diet

'Healthy eating' tells us to eat low-fat, high-carbohydrate diets but in the last few years of the Twentieth Century several papers demonstrated the harm this could do.

Obesity

Back in 1932 obese patients on different diets lost weight thus:

Average daily losses on high carbohydrate/low fat diet - 49g

Average daily losses on low carbohydrate/high fat diet - 205g

Drs Lyon and Dunlop say:

"The most striking feature of the table is that the losses appear to be inversely proportionate to the carbohydrate content of the food. Where the carbohydrate intake is low the rate of loss in weight is greater and conversely."

It's no coincidence that the numbers of people getting fat has risen dramatically since 'healthy eating' was advocated. As long ago as 1863 it was shown that low-fat, high-carbohydrate diets make people fat. The medical world is at last waking up to this fact. In 1994 Professor Susan Wooley of the University of Cincinnati's College of Medicine and David M Garner, Director of Research at the Beck Institute for Cognitive Therapy and Research wrote that:

"The failure of fat people to achieve a goal they seem to want and to want almost above all else must now be admitted for what it is: a failure not of those people but of the methods of treatment that are used."

In other words, blaming the overweight for their problem and telling them they are eating too much and must cut down, is simply not good enough. It is the dieticians' advice and the treatment offered that are wrong. Wooley and Garner conclude:

"We should stop offering ineffective treatments aimed at weight loss. Researchers who think they have invented a better mousetrap should test it in controlled research before setting out their bait for the entire population. Only by admitting that our treatments do not work and showing that we mean it by refraining from offering them can we undo a century of recruiting fat people for failure."

In 1997 two more Americans, Drs AF Heini and RL Weinsier noticed the trend and blamed it on low-fat diets saying:

"Reduced fat and calorie intake and frequent use of low-calorie food products have been associated with a paradoxical increase in the prevalence of obesity".

Heart disease and diabetics

Obese people tend to go on to suffer type II diabetes (NIDDM) and diabetics are more prone to heart disease. For this reason patients with NIDDM are counselled to eat a 'healthy' low-fat, high-carb diet. But as a paper in the medical journal, Diabetes Care , pointed out

"Low-fat, high-carbohydrate diets eaten by patients with diabetes (NIDDM) have been shown to lead to higher day-long plasma glucose, insulin, triglycerides, and VLDL-TG, among other negative effects. In general, study has demonstrated that multiple risk factors for coronary heart disease are worsened for diabetics who consume the low-fat, high-carbohydrate diet so often recommended to reduce these risks."

In June 1999 the 81st Annual Meeting of The Endocrine Society was told:

" A very high-fat, low-carbohydrate diet has been shown to have astounding effects in helping type 2 diabetics lose weight and improve their blood lipid profiles. The thing many diabetics coming into the office don't realize is that other forms of carbohydrates will increase their sugar, too. Dieticians will point toward complex carbohydrates . . . oatmeal and whole wheat bread, but we have to deliver the message that these are carbohydrates that increase blood sugars, too ."

. . .and postmenopausal women

In 1997 it was discovered that

"Low-fat, high-carbohydrate diets [15% protein, 60% carbohydrate, 25% fat] increase the risk of heart disease in post-menopausal women."

. . . in fact everyone

Dr. Gerald M. Reaven, of Stanford University School of Medicine in California, and colleagues compared the effects of a low-fat, high-carbohydrate diet [25% fat, 60% carb, 15% protein] with a high-fat, low-carbohydrate diet [45% fat, 40% carb, 15% protein], on blood fats and cholesterol. They found their subjects had significantly higher fasting plasma triglyceride concentrations, remnant lipoprotein cholesterol concentrations, and remnant triglyceride concentrations when they were on the high-carbohydrate, low-fat diet, both after fasting and after breakfast and lunch. The study participants also had significantly lower HDL (the 'good' cholesterol) concentrations on this diet. The authors conclude:

"Given the atherogenic potential of these changes in lipoprotein metabolism, it seems appropriate to question the wisdom of recommending that all Americans should replace dietary saturated fat with [carbohydrate]."

But then, in 1992, from the Framingham study again came:

"In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol" . . . "we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."

Low-fat, high-carb diet and breast cancer

And that's not all:

The largest and most comprehensive study on diet and breast cancer to date found that:

women with the lowest intake of fat had a significantly higher incidence of breast cancer and

women with the highest intake of starch also had a significantly higher incidence of breast cancer.

Saturated fats were not implicated in breast cancer.

The biggest study so far into the relation between breast cancer and fat intake is the Nurses' Health Study, conducted by Harvard University Medical School. A total of 88,795 women free of cancer in 1980 were followed up for 14 years. Comparing breast cancer rates in women who derived more than thirty percent of their calorie intake from fat with women who derived less than twenty percent of calories from fat, they show that those on low-fat diets had a higher rate of breast cancer than those who ate more. They went on to look at the various different types of fats and found that breast cancer rates were lower for all types except one: omega-3 fish oils, which are touted as 'healthy', were the only ones that increased cancer rates. However, the increase was small. Dr Michelle Holmes and colleagues conclude:

"We found no evidence that lower intake of total fat or specific major types of fat was associated with a decreased risk of breast cancer" .

Carbohydrates are not healthy

As we have seen so far, the emphasis on increasing carbohydrates at the expense of fats has not been an unqualified success. And there are good reasons for this.

We have known since 1863 that carbohydrates cause obesity; since 1935 that they cause diabetes; since 1941 that they increase aggressiveness and criminality in children; for almost 30 years promote coronary heart disease; and more recently that they increase the risk of cancers. So is it merely coincidence that diseases in whose aetiology carbohydrates are implicated have risen so dramatically since we have eaten more carbohydrates?

No. Healthy eating is becoming something of a disaster. The best advice appears to be that we should:

reduce carbohydrate intake and

increase our intake of animal fats.

To sum up, what emerges from this discussion is:

Fats

The totality of evidence suggests that we should eat animal fats in preference to vegetable oils because:

Polyunsaturated fats found in margarines and cooking oils may lower cholesterol levels but they increase cancer risk.

Trans-fats found in highly processed margarines and oils also increase CHD risk.

'Healthy' omega-3 oils may increase cancer risk.

Monounsaturated fats are no better as far as heart disease is concerned but they may reduce cancer risk.

Saturated fats are healthier in CHD, particularly if you have already had a heart attack. They are not implicated as a cause of cancer.

Conjugated linoleic acid found only in animal fats is a powerful anti-cancer agent.

Animal fats are just under half saturated and just under half monounsaturated, with a small, but sufficient proportion of polyunsaturated fats.

Carbohydrates

Carbohydrate intake from sugars and starches in breakfast cereals, bread, pasta, rice, et cetera, should be reduced because they increase diseases including obesity, cancer, diabetes and CHD.

Bran

Bran (cereal fibre) should be avoided like the plague.

Conclusion

An assessment of all the cholesterol-lowering dietary trials published in 1987 showed an aggregate six percent more deaths in those who adopted a cholesterol-lowering diet over those on a free diet. A similar review of drug trials showed an aggregate of over thirteen percent more deaths in those taking cholesterol-lowering drugs.

More resources, time and money have been spent over the last fifty years on coronary heart disease than any other disease in medical history and all it has proved is that doctors don't know as much as they thought they did. If half a century of serious research has failed to find a causal link between a fatty diet and heart disease, it can only be because there is no link.

To make intelligent decisions you must be given advice that is based on proven facts rather than unfounded assumptions. And the facts at present seem to be that milk, cream, butter, meat and fresh fruit and vegetables are the healthy foods whilst high-in-polyunsaturates spreads and oils, bran flakes and packaged foods are not.

Seventy years after it began we still do not know what caused the dramatic rise in coronary heart disease deaths in the 1920s or why coronary mortality is now falling. But one thing that the last fifty years of studies has demonstrated is that cholesterol has had very little to do with it.

The research has also demonstrated no evidence of a need to endure an unpalatable, fatless, bran-laden diet. Apart from being less pleasurable to eat, it is now clear that 'healthy eating' is not so healthy after all.


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## turbo

Interesting!


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## hackskii

Ahhh!!!!Haaaa!!!!

Read most already from biohazard. 

Loved every minute of it.

Thanks for posting Cookie, I massivly appreciate it.

This is my favorite read in a long time.

I will add some to this shortly

Cheers!


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## Cookie

THE TRUTH ABOUT SATURATED FATS

By Mary Enig,phd & Sally Fallon

Fats from animal and vegetable sources provide a concentrated source of energy in the diet; they also provide the building blocks for cell membranes and a variety of hormones and hormonelike substances. Fats as part of a meal slow down absorption so that we can go longer without feeling hungry. In addition, they act as carriers for important fat-soluble vitamins A, D, E and K. Dietary fats are needed for the conversion of carotene to vitamin A, for mineral absorption and for a host of other processes.

Politically Correct Nutrition is based on the assumption that we should reduce our intake of fats, particularly saturated fats from animal sources. Fats from animal sources also contain cholesterol, presented as the twin villain of the civilized diet.

The Lipid Hypothesis

The theory-called the lipid hypothesis-that there is a direct relationship between the amount of saturated fat and cholesterol in the diet and the incidence of coronary heart disease was proposed by a researcher named Ancel Keys in the late 1950's. Numerous subsequent studies have questioned his data and conclusions. Nevertheless, Keys' articles received far more publicity than those presenting alternate views.

The vegetable oil and food processing industries, the main beneficiaries of any research that found fault with competing traditional foods, began promoting and funding further research designed to support the lipid hypothesis.

The most well-known advocate of the lowfat diet was Nathan Pritikin. Actually, Pritikin advocated elimination of sugar, white flour and all processed foods from the diet and recommended the use of fresh raw foods, whole grains and a strenuous exercise program; but it was the lowfat aspects of his regime that received the most attention in the media. Adherents found that they lost weight and that their blood cholesterol levels and blood pressure declined.

The success of the Pritikin diet was probably due to a number of factors having nothing to do with reduction in dietary fat-weight loss alone, for example, will precipitate a reduction in blood cholesterol levels-but Pritikin soon found that the fat-free diet presented many problems, not the least of which was the fact that people just could not stay on it. Those who possessed enough will power to remain fat-free for any length of time developed a variety of health problems including low energy, difficulty in concentration, depression, weight gain and mineral deficiencies.1

Pritikin may have saved himself from heart disease but his lowfat diet did not spare him from cancer. He died, in the prime of life, of suicide when he realized that his Spartan regime was not curing his leukemia. We shouldn't have to die of either heart disease or cancer-or consume a diet that makes us depressed.

When problems with the no-fat regime became apparent, Pritikin introduced a small amount of fat from vegetable sources into his diet-something like 10% of the total caloric intake. Today the Diet Dictocrats advise us to limit fats to 25-30% of the caloric intake, which is about 2 1/2 ounces or 5 tablespoons per day for a diet of 2400 calories. A careful reckoning of fat intake and avoidance of animal fats, they say, is the key to perfect health.

The "Evidence" Supporting The Lipid Hypothesis

These "experts" assure us that the lipid hypothesis is backed by incontrovertible scientific proof. Most people would be surprised to learn that there is, in fact, very little evidence to support the contention that a diet low in cholesterol and saturated fat actually reduces death from heart disease or in any way increases one's life span. Consider the following:

Before 1920 coronary heart disease was rare in America; so rare that when a young internist named Paul Dudley White introduced the German electrocardiograph to his colleagues at Harvard University, they advised him to concentrate on a more profitable branch of medicine.

The new machine revealed the presence of arterial blockages, thus permitting early diagnosis of coronary heart disease. But in those days clogged arteries were a medical rarity, and White had to search for patients who could benefit from his new technology. During the next forty years, however, the incidence of coronary heart disease rose dramatically, so much so that by the mid fifties heart disease was the leading cause of death among Americans.

Today heart disease causes at least 40% of all US deaths. If, as we have been told, heart disease results from the consumption of saturated fats, one would expect to find a corresponding increase in animal fat in the American diet. Actually, the reverse is true. During the sixty-year period from 1910 to 1970, the proportion of traditional animal fat in the American diet declined from 83% to 62%, and butter consumption plummeted from eighteen pounds per person per year to four.

During the past eighty years, dietary cholesterol intake has increased only 1%. During the same period the percentage of dietary vegetable oils in the form of margarine, shortening and refined oils increased about 400% while the consumption of sugar and processed foods increased about 60%.2

The Framingham Heart Study is often cited as proof of the lipid hypothesis. This study began in 1948 and involved some 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals-those who consumed little cholesterol and saturated fat and those who consumed large amounts. After 40 years, the director of this study had to admit:

"In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . .

We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."3 The study did show that those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease; but weight gain and cholesterol levels had an inverse correlation with fat and cholesterol intake in the diet.4

In a multi-year British study involving several thousand men, half were asked to reduce saturated fat and cholesterol in their diets, to stop smoking and to increase the amounts of unsaturated oils such as margarine and vegetable oils.

After one year, those on the "good" diet had 100% more deaths than those on the "bad" diet, in spite of the fact that those men on the "bad" diet continued to smoke! But in describing the study, the author ignored these results in favor of the politically correct conclusion: "The implication for public health policy in the U.K. is that a preventive program such as we evaluated in this trial is probably effective. . . ."5

The U.S. Multiple Risk Factor Intervention Trial, (MRFIT) sponsored by the National Heart, Lung and Blood Institute, compared mortality rates and eating habits of over 12,000 men. Those with "good" dietary habits (reduced saturated fat and cholesterol, reduced smoking, etc.) showed a marginal reduction in total coronary heart disease, but their overall mortality from all causes was higher.

Similar results have been obtained in several other studies. The few studies that indicate a correlation between fat reduction and a decrease in coronary heart disease mortality also document a concurrent increase in deaths from cancer, brain hemorrhage, suicide and violent death.6

The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost 150 million dollars, is the study most often cited by the experts to justify lowfat diets. Actually, dietary cholesterol and saturated fat were not tested in this study as all subjects were given a low-cholesterol, low-saturated-fat diet.

Instead, the study tested the effects of a cholesterol-lowering drug. Their statistical analysis of the results implied a 24% reduction in the rate of coronary heart disease in the group taking the drug compared with the placebo group; however, nonheart disease deaths in the drug group increased-deaths from cancer, stroke, violence and suicide.7

Even the conclusion that lowering cholesterol reduces heart disease is suspect.

Independent researchers who tabulated the results of this study found no significant statistical difference in coronary heart disease death rates between the two groups.8 However, both the popular press and medical journals touted the LRC-CPPT as the long-sought proof that animal fats are the cause of heart disease, America's number one killer.

Studies That Challenge The Lipid Hypothesis

While it is true that researchers have induced heart disease in some animals by giving them extremely large dosages of oxidized or rancid cholesterol-amounts ten times that found in the ordinary human diet-several population studies squarely contradict the cholesterol-heart disease connection.

A survey of 1700 patients with hardening of the arteries, conducted by the famous heart surgeon Michael DeBakey, found no relationship between the level of cholesterol in the blood and the incidence of atherosclerosis.9

A survey of South Carolina adults found no correlation of blood cholesterol levels with "bad" dietary habits, such as use of red meat, animal fats, fried foods, butter, eggs, whole milk, bacon, sausage and cheese.10 A Medical Research Council survey showed that men eating butter ran half the risk of developing heart disease as those using margarine.11

Mother's milk provides a higher proportion of cholesterol than almost any other food. It also contains over 50% of its calories as fat, much of it saturated fat. Both cholesterol and saturated fat are essential for growth in babies and children, especially the development of the brain.12 Yet, the American Heart Association is now recommending a low-cholesterol, lowfat diet for children! Commercial formulas are low in saturated fats and soy formulas are devoid of cholesterol. A recent study linked lowfat diets with failure to thrive in children.13

Numerous surveys of traditional populations have yielded information that is an embarrassment to the Diet Dictocrats. For example, a study comparing Jews when they lived in Yemen, whose diets contained fats solely of animal origin, to Yemenite Jews living in Israel, whose diets contained margarine and vegetable oils, revealed little heart disease or diabetes in the former group but high levels of both diseases in the latter.14 (The study also noted that the Yemenite Jews consumed no sugar but those in Israel consumed sugar in amounts equaling 25-30% of total carbohydrate intake.)

A comparison of populations in northern and southern India revealed a similar pattern. People in northern India consume 17 times more animal fat but have an incidence of coronary heart disease seven times lower than people in southern India.15 The Masai and kindred tribes of Africa subsist largely on milk, blood and beef. They are free from coronary heart disease and have excellent blood cholesterol levels.16

Eskimos eat liberally of animal fats from fish and marine animals. On their native diet they are free of disease and exceptionally hardy.17 An extensive study of diet and disease patterns in China found that the region in which the populace consumes large amounts of whole milk had half the rate of heart disease as several districts in which only small amounts of animal products are consumed.18

Several Mediterranean societies have low rates of heart disease even though fat-including highly saturated fat from lamb, sausage and goat cheese-comprises up to 70% of their caloric intake. The inhabitants of Crete, for example, are remarkable for their good health and longevity.19 A study of Puerto Ricans revealed that, although they consume large amounts of animal fat, they have a very low incidence of colon and breast cancer.20

A study of the long-lived inhabitants of Soviet Georgia revealed that those who eat the most fatty meat live the longest.21 In Okinawa, where the average life span for women is 84 years-longer than in Japan-the inhabitants eat generous amounts of pork and seafood and do all their cooking in lard.22 None of these studies is mentioned by those urging restriction of saturated fats.

The relative good health of the Japanese, who have the longest life span of any nation in the world, is generally attributed to a lowfat diet. Although the Japanese eat few dairy fats, the notion that their diet is low in fat is a myth; rather, it contains moderate amounts of animal fats from eggs, pork, chicken, beef, seafood and organ meats. With their fondness for shellfish and fish broth, eaten on a daily basis, the Japanese probably consume more cholesterol than most Americans.

What they do not consume is a lot of vegetable oil, white flour or processed food (although they do eat white rice.) The life span of the Japanese has increased since World War II with an increase in animal fat and protein in the diet.23 Those who point to Japanese statistics to promote the lowfat diet fail to mention that the Swiss live almost as long on one of the fattiest diets in the world. Tied for third in the longevity stakes are Austria and Greece-both with high-fat diets.24

As a final example, let us consider the French. Anyone who has eaten his way across France has observed that the French diet is just loaded with saturated fats in the form of butter, eggs, cheese, cream, liver, meats and rich patés. Yet the French have a lower rate of coronary heart disease than many other western countries.

In the United States, 315 of every 100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. In the Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkably low 80 per 100,000.25 This phenomenon has recently gained international attention as the French Paradox. (The French do suffer from many degenerative diseases, however. They eat large amounts of sugar and white flour and in recent years have succumbed to the timesaving temptations of processed foods.)

A chorus of establishment voices, including the American Cancer Society, the National Cancer Institute and the Senate Committee on Nutrition and Human Needs, claims that animal fat is linked not only with heart disease but also with cancers of various types. Yet when researchers from the University of Maryland analyzed the data they used to make such claims, they found that vegetable fat consumption was correlated with cancer and animal fat was not.26

Understanding The Chemistry Of Fats

Clearly something is wrong with the theories we read in the popular press-and used to bolster sales of lowfat concoctions and cholesterol-free foods. The notion that saturated fats per se cause heart disease as well as cancer is not only facile, it is just plain wrong. But it is true that some fats are bad for us. In order to understand which ones, we must know something about the chemistry of fats.

Fats-or lipids-are a class of organic substances that are not soluble in water. In simple terms, fatty acids are chains of carbon atoms with hydrogen atoms filling the available bonds. Most fat in our bodies and in the food we eat is in the form of triglycerides, that is, three fatty-acid chains attached to a glycerol molecule.

levated triglycerides in the blood have been positively linked to proneness to heart disease, but these triglycerides do not come directly from dietary fats; they are made in the liver from any excess sugars that have not been used for energy. The source of these excess sugars is any food containing carbohydrates, particularly refined sugar and white flour.

Fatty Acid Classifications By Saturation

Fatty acids are classified in the following way:

Saturated: A fatty acid is saturated when all available carbon bonds are occupied by a hydrogen atom. They are highly stable, because all the carbon-atom linkages are filled-or saturated-with hydrogen. This means that they do not normally go rancid, even when heated for cooking purposes. They are straight in form and hence pack together easily, so that they form a solid or semisolid fat at room temperature. Your body makes saturated fatty acids from carbohydrates and they are found in animal fats and tropical oils.

Monounsaturated: Monounsaturated fatty acids have one double bond in the form of two carbon atoms double-bonded to each other and, therefore, lack two hydrogen atoms. Your body makes monounsaturated fatty acids from saturated fatty acids and uses them in a number of ways.

Monounsaturated fats have a kink or bend at the position of the double bond so that they do not pack together as easily as saturated fats and, therefore, tend to be liquid at room temperature. Like saturated fats, they are relatively stable. They do not go rancid easily and hence can be used in cooking. The monounsaturated fatty acid most commonly found in our food is oleic acid, the main component of olive oil as well as the oils from almonds, pecans, cashews, peanuts and avocados.

Polyunsaturated: Polyunsaturated fatty acids have two or more pairs of double bonds and, therefore, lack four or more hydrogen atoms. The two polyunsaturated fatty acids found most frequently in our foods are double unsaturated linoleic acid, with two double bonds-also called omega-6; and triple unsaturated linolenic acid, with three double bonds-also called omega-3. (The omega number indicates the position of the first double bond.)

Your body cannot make these fatty acids and hence they are called "essential." We must obtain our essential fatty acids or EFA's from the foods we eat. The polyunsaturated fatty acids have kinks or turns at the position of the double bond and hence do not pack together easily. They are liquid, even when refrigerated.

The unpaired electrons at the double bonds makes these oils highly reactive.

They go rancid easily, particularly omega-3 linolenic acid, and must be treated with care. Polyunsaturated oils should never be heated or used in cooking. In nature, the polyunsaturated fatty acids are usually found in the cis form, which means that both hydrogen atoms at the double bond are on the same side.

All fats and oils, whether of vegetable or animal origin, are some combination of saturated fatty acids, monounsaturated fatty acids and polyunsaturated linoleic acid and linolenic acid. In general, animal fats such as butter, lard and tallow contain about 40-60% saturated fat and are solid at room temperature.

Vegetable oils from northern climates contain a preponderance of polyunsaturated fatty acids and are liquid at room temperature. But vegetable oils from the tropics are highly saturated. Coconut oil, for example, is 92% saturated. These fats are liquid in the tropics but hard as butter in northern climes. Vegetable oils are more saturated in hot climates because the increased saturation helps maintain stiffness in plant leaves. Olive oil with its preponderance of oleic acid is the product of a temperate climate. It is liquid at warm temperatures but hardens when refrigerated


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## Cookie

THE BENEFITS OF HIGH CHOLESTEROL

By Uffe Ravnskov,MD,PHD

People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.

But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.

High Cholesterol Protects Against Infection

Many studies have found that low cholesterol is in certain respects worse than high cholesterol. For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3

Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.

Low Cholesterol and HIV/AIDS

Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. The Minnesota researchers, now led by Dr. Ami Claxton, followed such individuals for 7-8 years. After having excluded those who became HIV-positive during the first four years, they ended up with a group of 2446 men. At the end of the study, 140 of these people tested positive for HIV; those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6

Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240.7

Cholesterol and Chronic Heart Failure

Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Patients with severe heart failure become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure.

There are many indications that bacteria or other microorganisms play an important role in chronic heart failure. For instance, patients with severe chronic heart failure have high levels of endotoxin and various types of cytokines in their blood. Endotoxin, also named lipopolysaccharide, is the most toxic substance produced by Gram-negative bacteria such as Escherichia coli, Klebsiella, Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted by white blood cells in their battle with microorganisms; high levels of cytokines in the blood indicate that inflammatory processes are going on somewhere in the body.

The role of infections in chronic heart failure has been studied by Dr. Mathias Rauchhaus and his team at the Medical Department, Martin-Luther-University in Halle, Germany (Universitätsklinik und Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle). They found that the strongest predictor of death for patients with chronic heart failure was the concentration of cytokines in the blood, in particular in patients with heart failure due to coronary heart disease.8 To explain their finding they suggested that bacteria from the gut may more easily penetrate into the tissues when the pressure in the abdominal veins is increased because of heart failure. In accordance with this theory, they found more endotoxin in the blood of patients with congestive heart failure and edema than in patients with non-congestive heart failure without edema, and endotoxin concentrations decreased significantly when the heart's function was improved by medical treatment.9

A simple way to test the functional state of the immune system is to inject antigens from microorganisms that most people have been exposed to, under the skin. If the immune system is normal, an induration (hard spot) will appear about 48 hours later at the place of the injection. If the induration is very small, with a diameter of less than a few millimeters, this indicates the presence of "anergy," a reduction in or failure of response to recognize antigens. In accordance, anergy has been found associated with an increased risk of infection and mortality in healthy elderly individuals, in surgical patients and in heart transplant patients.10

Dr. Donna Vredevoe and her group from the School of Nursery and the School of Medicine, University of California at Los Angeles tested more than 200 patients with severe heart failure with five different antigens and followed them for twelve months. The cause of heart failure was coronary heart disease in half of them and other types of heart disease (such as congenital or infectious valvular heart disease, various cardiomyopathies and endocarditis) in the rest. Almost half of all the patients were anergic, and those who were anergic and had coronary heart disease had a much higher mortality than the rest.10

Now to the salient point: to their surprise the researchers found that mortality was higher, not only in the patients with anergy, but also in the patients with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL-cholesterol as well as triglycerides.

The latter finding was confirmed by Dr. Rauchhaus, this time in co-operation with researchers at several German and British university hospitals. They found that the risk of dying for patients with chronic heart failure was strongly and inversely associated with total cholesterol, LDL-cholesterol and also triglycerides; those with high lipid values lived much longer than those with low values.11,12

Other researchers have made similar observations. The largest study has been performed by Professor Gregg C. Fonorow and his team at the UCLA Department of Medicine and Cardiomyopathy Center in Los Angeles.13 The study, led by Dr. Tamara Horwich, included more than a thousand patients with severe heart failure. After five years 62 percent of the patients with cholesterol below 129 mg/l had died, but only half as many of the patients with cholesterol above 223 mg/l.

When proponents of the cholesterol hypothesis are confronted with findings showing a bad outcome associated with low cholesterol-and there are many such observations-they usually argue that severely ill patients are often malnourished, and malnourishment is therefore said to cause low cholesterol. However, the mortality of the patients in this study was independent of their degree of nourishment; low cholesterol predicted early mortality whether the patients were malnourished or not.

Smith-Lemli-Opitz Syndrome

As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true.

Children with the Smith-Lemli-Opitz syndrome have very low cholesterol because the enzyme that is necessary for the last step in the body's synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14

Laboratory Evidence

Laboratory studies are crucial for learning more about the mechanisms by which the lipids exert their protective function. One of the first to study this phenomenon was Dr Sucharit Bhakdi from the Institute of Medical Microbiology, University of Giessen (Institut für Medizinsche Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with his team of researchers from various institutions in Germany and Denmark.15

Staphylococcus aureus α-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy a wide variety of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in 0.9 percent saline, the blood is hemolyzed, that is the membranes of the red blood cells burst and hemoglobin from the interior of the red blood cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified α-toxin with human serum (the fluid in which the blood cells reside) and saw that 90 percent of its hemolyzing effect disappeared. By various complicated methods they identified the protective substance as LDL, the carrier of the so-called bad cholesterol. In accordance, no hemolysis occurred when they mixed α-toxin with purified human LDL, whereas HDL or other plasma constituents were ineffective in this respect.

Dr. Willy Flegel and his co-workers at the Department of Transfusion Medicine, University of Ulm, and the Institute of Immunology and Genetics at the German Cancer Research Center in Heidelberg, Germany (DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin, Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg) studied endotoxin in another way.16 As mentioned, one of the effects of endotoxin is that white blood cells are stimulated to produce cytokines. The German researchers found that the cytokine-stimulating effect of endotoxin on the white blood cells disappeared almost completely if the endotoxin was mixed with human serum for 24 hours before they added the white blood cells to the test tubes. In a subsequent study17 they found that purified LDL from patients with familial hypercholesterolemia had the same inhibitory effect as the serum.

LDL may not only bind and inactivate dangerous bacterial toxins; it seems to have a direct beneficial influence on the immune system also, possibly explaining the observed relationship between low cholesterol and various chronic diseases. This was the starting point for a study by Professor Matthew Muldoon and his team at the University of Pittsburgh, Pennsylvania. They studied healthy young and middle-aged men and found that the total number of white blood cells and the number of various types of white blood cells were significantly lower in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The researchers cautiously concluded that there were immune system differences between men with low and high cholesterol, but that it was too early to state whether these differences had any importance for human health. Now, seven years later with many of the results discussed here, we are allowed to state that the immune-supporting properties of LDL-cholesterol do indeed play an important role in human health.

Animal Experiments

The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold at the Department of Medicine, University of California, San Francisco, and his group have published several interesting results from such research. In one of them they lowered LDL-cholesterol in rats by giving them either a drug that prevents the liver from secreting lipoproteins, or a drug that increases their disappearance. In both models, injection of endotoxin was followed by a much higher mortality in the low-cholesterol rats compared with normal rats. The high mortality was not due to the drugs because, if the drug-treated animals were injected with lipoproteins just before the injection of endotoxin, their mortality was reduced to normal.19

Dr. Mihai Netea and his team from the Departments of Internal and Nuclear Medicine at the University Hospital in Nijmegen, The Netherlands, injected purified endotoxin into normal mice, and into mice with familial hypercholesterolemia that had LDL-cholesterol four times higher than normal. Whereas all normal mice died, they had to inject eight times as much endotoxin to kill the mice with familial hypercholesterolemia. In another experiment they injected live bacteria and found that twice as many mice with familial hypercholesterolemia survived compared with normal mice.20

Other Protecting Lipids

As seen from the above, many of the roles played by LDL-cholesterol are shared by HDL. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.

Triglycerides, molecules consisting of three fatty acids linked to glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by a lipoprotein named VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of emulsified triglycerides appearing in large amounts after a fat-rich meal, particularly in the blood that flows from the gut to the liver.

For many years it has been known that sepsis, a life-threatening condition caused by bacterial growth in the blood, is associated with a high level of triglycerides. The serious symptoms of sepsis are due to endotoxin, most often produced by gut bacteria. In a number of studies, Professor Hobart W. Harris at the Surgical Research Laboratory at San Francisco General Hospital and his team found that solutions rich in triglycerides but with practically no cholesterol were able to protect experimental animals from the toxic effects of endotoxin and they concluded that the high level of triglycerides seen in sepsis is a normal immune response to infection.21 Usually the bacteria responsible for sepsis come from the gut. It is therefore fortunate that the blood draining the gut is especially rich in triglycerides.

Exceptions

So far, animal experiments have confirmed the hypothesis that high cholesterol protects against infection, at least against infections caused by bacteria. In a similar experiment using injections of Candida albicans, a common fungus, Dr. Netea and his team found that mice with familial hypercholesterolemia died more easily than normal mice.22 Serious infections caused by Candida albicans are rare in normal human beings; however, they are mainly seen in patients treated with immunosuppressive drugs, but the finding shows that we need more knowledge in this area. However, the many findings mentioned above indicate that the protective effects of the blood lipids against infections in human beings seem to be greater than any possible adverse effects.

Cholesterol as a Risk Factor

Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body's need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.

Response to Injury

In 1976 one of the most promising theories about the cause of atherosclerosis was the Response-to-Injury Hypothesis, presented by Russell Ross, a professor of pathology, and John Glomset, a professor of biochemistry and medicine at the Medical School, University of Washington in Seattle.23,24 They suggested that atherosclerosis is the consequence of an inflammatory process, where the first step is a localized injury to the thin layer of cells lining the inside of the arteries, the intima. The injury causes inflammation and the raised plaques that form are simply healing lesions.

Their idea is not new. In 1911, two American pathologists from the Pathological Laboratories, University of Pittsburgh, Pennsylvania, Oskar Klotz and M.F. Manning, published a summary of their studies of the human arteries and concluded that "there is every indication that the production of tissue in the intima is the result of a direct irritation of that tissue by the presence of infection or toxins or the stimulation by the products of a primary degeneration in that layer."25 Other researchers have presented similar theories.26

Researchers have proposed many potential causes of vascular injury, including mechanical stress, exposure to tobacco fumes, high LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic consequences of diabetes, iron overload, copper deficiency, deficiencies of vitamins A and D, consumption of trans fatty acids, microorganisms and many more. With one exception, there is evidence to support roles for all of these factors, but the degree to which each of them participates remains uncertain. The exception is of course LDL-cholesterol. Much research allows us to exclude high LDL-cholesterol from the list. Whether we look directly with the naked eye at the inside of the arteries at autopsy, or we do it indirectly in living people using x-rays, ultrasound or electron beams, no association worth mentioning has ever been found between the amount of lipid in the blood and the degree of atherosclerosis in the arteries. Also, whether cholesterol goes up or down, by itself or due to medical intervention, the changes of cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response. Proponents of the cholesterol campaign often claim that the trials indeed have found dose-response, but here they refer to calculations between the mean changes of the different trials with the outcome of the whole treatment group. However, true dose-response demands that the individual changes of the putative causal factor are followed by parallel, individual changes of the disease outcome, and this has never occurred in the trials where researchers have calculated true dose-response.

A detailed discussion of the many factors accused of harming the arterial endothelium is beyond the scope of this article. However, the protective role of the blood lipids against infections obviously demands a closer look at the alleged role of one of the alleged causes, the microorganisms.

Is Atherosclerosis an Infectious Disease?

For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Chlamydia pneumonia (also named TWAR bacteria) participate in the development of atherosclerosis. Research within this area has exploded during the last decade and by January 2004, at least 200 reviews of the issue have been published in medical journals. Due to the widespread preoccupation with cholesterol and other lipids, there has been little general interest in the subject, however, and few doctors know much about it. Here I shall mention some of the most interesting findings.26

Electron microscopy, immunofluorescence microscopy and other advanced techniques have allowed us to detect microorganisms and their DNA in the atherosclerotic lesions in a large proportion of patients. Bacterial toxins and cytokines, hormones secreted by the white blood cells during infections, are seen more often in the blood from patients with recent heart disease and stroke, in particular during and after an acute cardiovascular event, and some of them are strong predictors of cardiovascular disease. The same is valid for bacterial and viral antibodies, and a protein secreted by the liver during infections, named C-reactive protein (CRP), is a much stronger risk factor for coronary heart disease than cholesterol.

Clinical evidence also supports this theory. During the weeks preceding an acute cardiovascular attack many patients have had a bacterial or viral infection. For instance, Dr. Armin J. Grau from the Department of Neurology at the University of Heidelberg and his team asked 166 patients with acute stroke, 166 patients hospitalized for other neurological diseases and 166 healthy individuals matched individually for age and sex about recent infectious disease. Within the first week before the stroke, 37 of the stroke patients, but only 14 of the control individuals had had an infectious disease. In half of the patients the infection was of bacterial origin, in the other half of viral origin.27

Similar observations have been made by many others, for patients with acute myocardial infarction (heart attack). For instance, Dr. Kimmo J. Mattila at the Department of Medicine, Helsinki University Hospital, Finland, found that 11 of 40 male patients with an acute heart attack before age 50 had an influenza-like infection with fever within 36 hours prior to admittance to hospital, but only 4 out of 41 patients with chronic coronary disease (such as recurrent angina or pervious myocardial infarction) and 4 out of 40 control individuals without chronic disease randomly selected from the general population.28

Attempts have been made to prevent cardiovascular disease by treatment with antibiotics. In five trials treatment of patients with coronary heart disease using azithromyzin or roxithromyzin, antibiotics that are effective against Chlamydia pneumonia,yielded successful results; a total of 104 cardiovascular events occurred among the 412 non-treated patients, but only 61 events among the 410 patients in the treatment groups.28a-e In one further trial a significant decreased progression of atherosclerosis in the carotid arteries occurred with antibiotic treatment.28f However, in four other trials,30a-d one of which included more than 7000 patients,28d antibiotic treatment had no significant effect.

The reason for these inconsistent results may be that the treatment was too short (in one of the trials treatment lasted only five days). Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate inside human cells and when located in white blood cells they are resistant to antibiotics.31 Treatment may also have been ineffective because the antibiotics used have no effect on viruses. In this connection it is interesting to mention a controlled trial performed by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in Buenos Aires, Argentina.32 They vaccinated half of 301 patients with coronary heart disease against influenza, a viral disease. After six months 8 percent of the control patients had died, but only 2 percent of the vaccinated patients. It is worth mentioning that this effect was much better than that achieved by any statin trial, and in a much shorter time.

Does High Cholesterol Protect Against Cardiovascular Disease?

Apparently, microorganisms play a role in cardiovascular disease. They may be one of the factors that start the process by injuring the arterial endothelium. A secondary role may be inferred from the association between acute cardiovascular disease and infection. The infectious agent may preferably become located in parts of the arterial walls that have been previously damaged by other agents, initiating local coagulation and the creation of a thrombus (clot) and in this way cause obstruction of the blood flow. But if so, high cholesterol may protect against cardiovascular disease instead of being the cause!

In any case, the diet-heart idea, with its demonizing of high cholesterol, is obviously in conflict with the idea that high cholesterol protects against infections. Both ideas cannot be true. Let me summarize the many facts that conflict with the idea that high cholesterol is bad.

If high cholesterol were the most important cause of atherosclerosis, people with high cholesterol should be more atherosclerotic than people with low cholesterol. But as you know by now this is very far from the truth.

If high cholesterol were the most important cause of atherosclerosis, lowering of cholesterol should influence the atherosclerotic process in proportion to the degree of its lowering.

But as you know by now, this does not happen.

If high cholesterol were the most important cause of cardiovascular disease, it should be a risk factor in all populations, in both sexes, at all ages, in all disease categories, and for both heart disease and stroke. But as you know by now, this is not the case

I have only two arguments for the idea that high cholesterol is good for the blood vessels, but in contrast to the arguments claiming the opposite they are very strong. The first one stems from the statin trials. If high cholesterol were the most important cause of cardiovascular disease, the greatest effect of statin treatment should have been seen in patients with the highest cholesterol, and in patients whose cholesterol was lowered the most. Lack of dose-response cannot be attributed to the knowledge that the statins have other effects on plaque stabilization, as this would not have masked the effect of cholesterol-lowering considering the pronounced lowering that was achieved. On the contrary, if a drug that effectively lowers the concentration of a molecule assumed to be harmful to the cardiovascular system and at the same time exerts several beneficial effects on the same system, a pronounced dose-response should be seen.

On the other hand, if high cholesterol has a protective function, as suggested, its lowering would counterbalance the beneficial effects of the statins and thus work against a dose-response, which would be more in accord with the results from the various trials.

I have already mentioned my second argument, but it can't be said too often: High cholesterol is associated with longevity in old people. It is difficult to explain away the fact that during the period of life in which most cardiovascular disease occurs and from which most people die (and most of us die from cardiovascular disease), high cholesterol occurs most often in people with the lowest mortality. How is it possible that high cholesterol is harmful to the artery walls and causes fatal coronary heart disease, the commonest cause of death, if those whose cholesterol is the highest, live longer than those whose cholesterol is low?

To the public and the scientific community I say, "Wake up!"


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THE SKINNY ON FATS

BY MARY ENIG,PHD & SALLY FALLON

Fats from animal and vegetable sources provide a concentrated source of energy in the diet; they also provide the building blocks for cell membranes and a variety of hormones and hormonelike substances. Fats as part of a meal slow down absorption so that we can go longer without feeling hungry. In addition, they act as carriers for important fat-soluble vitamins A, D, E and K. Dietary fats are needed for the conversion of carotene to vitamin A, for mineral absorption and for a host of other processes.

Politically Correct Nutrition is based on the assumption that we should reduce our intake of fats, particularly saturated fats from animal sources. Fats from animal sources also contain cholesterol, presented as the twin villain of the civilized diet. *The Lipid Hypothesis*

The theory-called the lipid hypothesis-that there is a direct relationship between the amount of saturated fat and cholesterol in the diet and the incidence of coronary heart disease was proposed by a researcher named Ancel Keys in the late 1950's. Numerous subsequent studies have questioned his data and conclusions. Nevertheless, Keys' articles received far more publicity than those presenting alternate views. The vegetable oil and food processing industries, the main beneficiaries of any research that found fault with competing traditional foods, began promoting and funding further research designed to support the lipid hypothesis.

The most well-known advocate of the lowfat diet was Nathan Pritikin. Actually, Pritikin advocated elimination of sugar, white flour and all processed foods from the diet and recommended the use of fresh raw foods, whole grains and a strenuous exercise program; but it was the lowfat aspects of his regime that received the most attention in the media. Adherents found that they lost weight and that their blood cholesterol levels and blood pressure declined. The success of the Pritikin diet was probably due to a number of factors having nothing to do with reduction in dietary fat-weight loss alone, for example, will precipitate a reduction in blood cholesterol levels-but Pritikin soon found that the fat-free diet presented many problems, not the least of which was the fact that people just could not stay on it. Those who possessed enough will power to remain fat-free for any length of time developed a variety of health problems including low energy, difficulty in concentration, depression, weight gain and mineral deficiencies.1 Pritikin may have saved himself from heart disease but his lowfat diet did not spare him from cancer. He died, in the prime of life, of suicide when he realized that his Spartan regime was not curing his leukemia. We shouldn't have to die of either heart disease or cancer-or consume a diet that makes us depressed.

When problems with the no-fat regime became apparent, Pritikin introduced a small amount of fat from vegetable sources into his diet-something like 10% of the total caloric intake. Today the Diet Dictocrats advise us to limit fats to 25-30% of the caloric intake, which is about 2 1/2 ounces or 5 tablespoons per day for a diet of 2400 calories. A careful reckoning of fat intake and avoidance of animal fats, they say, is the key to perfect health. *The "evidence" supporting the Lipid Hypothesis*

These "experts" assure us that the lipid hypothesis is backed by incontrovertible scientific proof. Most people would be surprised to learn that there is, in fact, very little evidence to support the contention that a diet low in cholesterol and saturated fat actually reduces death from heart disease or in any way increases one's life span. Consider the following:

Before 1920 coronary heart disease was rare in America; so rare that when a young internist named Paul Dudley White introduced the German electrocardiograph to his colleagues at Harvard University, they advised him to concentrate on a more profitable branch of medicine. The new machine revealed the presence of arterial blockages, thus permitting early diagnosis of coronary heart disease. But in those days clogged arteries were a medical rarity, and White had to search for patients who could benefit from his new technology. During the next forty years, however, the incidence of coronary heart disease rose dramatically, so much so that by the mid fifties heart disease was the leading cause of death among Americans. Today heart disease causes at least 40% of all US deaths. If, as we have been told, heart disease results from the consumption of saturated fats, one would expect to find a corresponding increase in animal fat in the American diet. Actually, the reverse is true. During the sixty-year period from 1910 to 1970, the proportion of traditional animal fat in the American diet declined from 83% to 62%, and butter consumption plummeted from eighteen pounds per person per year to four. During the past eighty years, dietary cholesterol intake has increased only 1%. During the same period the percentage of dietary vegetable oils in the form of margarine, shortening and refined oils increased about 400% while the consumption of sugar and processed foods increased about 60%.2

The Framingham Heart Study is often cited as proof of the lipid hypothesis. This study began in 1948 and involved some 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals-those who consumed little cholesterol and saturated fat and those who consumed large amounts. After 40 years, the director of this study had to admit: "In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . . we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."3 The study did show that those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease; but weight gain and cholesterol levels had an inverse correlation with fat and cholesterol intake in the diet.4

In a multi-year British study involving several thousand men, half were asked to reduce saturated fat and cholesterol in their diets, to stop smoking and to increase the amounts of unsaturated oils such as margarine and vegetable oils. After one year, those on the "good" diet had 100% more deaths than those on the "bad" diet, in spite of the fact that those men on the "bad" diet continued to smoke! But in describing the study, the author ignored these results in favor of the politically correct conclusion: "The implication for public health policy in the U.K. is that a preventive programme such as we evaluated in this trial is probably effective. . . ."5

The U.S. Multiple Risk Factor Intervention Trial, (MRFIT) sponsored by the National Heart, Lung and Blood Institute, compared mortality rates and eating habits of over 12,000 men. Those with "good" dietary habits (reduced saturated fat and cholesterol, reduced smoking, etc.) showed a marginal reduction in total coronary heart disease, but their overall mortality from all causes was higher. Similar results have been obtained in several other studies. The few studies that indicate a correlation between fat reduction and a decrease in coronary heart disease mortality also document a concurrent increase in deaths from cancer, brain hemorrhage, suicide and violent death.6

The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost 150 million dollars, is the study most often cited by the experts to justify lowfat diets. Actually, dietary cholesterol and saturated fat were not tested in this study as all subjects were given a low-cholesterol, low-saturated-fat diet. Instead, the study tested the effects of a cholesterol-lowering drug. Their statistical analysis of the results implied a 24% reduction in the rate of coronary heart disease in the group taking the drug compared with the placebo group; however, nonheart disease deaths in the drug group increased-deaths from cancer, stroke, violence and suicide.7 Even the conclusion that lowering cholesterol reduces heart disease is suspect. Independent researchers who tabulated the results of this study found no significant statistical difference in coronary heart disease death rates between the two groups.8 However, both the popular press and medical journals touted the LRC-CPPT as the long-sought proof that animal fats are the cause of heart disease, America's number one killer. *Studies that challenge the Lipid Hypothesis*

While it is true that researchers have induced heart disease in some animals by giving them extremely large dosages of oxidized or rancid cholesterol-amounts ten times that found in the ordinary human diet-several population studies squarely contradict the cholesterol-heart disease connection. A survey of 1700 patients with hardening of the arteries, conducted by the famous heart surgeon Michael DeBakey, found no relationship between the level of cholesterol in the blood and the incidence of atherosclerosis.9 A survey of South Carolina adults found no correlation of blood cholesterol levels with "bad" dietary habits, such as use of red meat, animal fats, fried foods, butter, eggs, whole milk, bacon, sausage and cheese.10 A Medical Research Council survey showed that men eating butter ran half the risk of developing heart disease as those using margarine.11

Mother's milk provides a higher proportion of cholesterol than almost any other food. It also contains over 50% of its calories as fat, much of it saturated fat. Both cholesterol and saturated fat are essential for growth in babies and children, especially the development of the brain.12 Yet, the American Heart Association is now recommending a low-cholesterol, lowfat diet for children! Commercial formulas are low in saturated fats and soy formulas are devoid of cholesterol. A recent study linked lowfat diets with failure to thrive in children.13

Numerous surveys of traditional populations have yielded information that is an embarrassment to the Diet Dictocrats. For example, a study comparing Jews when they lived in Yemen, whose diets contained fats solely of animal origin, to Yemenite Jews living in Israel, whose diets contained margarine and vegetable oils, revealed little heart disease or diabetes in the former group but high levels of both diseases in the latter.14 (The study also noted that the Yemenite Jews consumed no sugar but those in Israel consumed sugar in amounts equaling 25-30% of total carbohydrate intake.) A comparison of populations in northern and southern India revealed a similar pattern. People in northern India consume 17 times more animal fat but have an incidence of coronary heart disease seven times lower than people in southern India.15 The Masai and kindred tribes of Africa subsist largely on milk, blood and beef. They are free from coronary heart disease and have excellent blood cholesterol levels.16 Eskimos eat liberally of animal fats from fish and marine animals. On their native diet they are free of disease and exceptionally hardy.17 An extensive study of diet and disease patterns in China found that the region in which the populace consumes large amounts of whole milk had half the rate of heart disease as several districts in which only small amounts of animal products are consumed.18 Several Mediterranean societies have low rates of heart disease even though fat-including highly saturated fat from lamb, sausage and goat cheese-comprises up to 70% of their caloric intake. The inhabitants of Crete, for example, are remarkable for their good health and longevity.19 A study of Puerto Ricans revealed that, although they consume large amounts of animal fat, they have a very low incidence of colon and breast cancer.20 A study of the long-lived inhabitants of Soviet Georgia revealed that those who eat the most fatty meat live the longest.21 In Okinawa, where the average life span for women is 84 years-longer than in Japan-the inhabitants eat generous amounts of pork and seafood and do all their cooking in lard.22 None of these studies is mentioned by those urging restriction of saturated fats.

The relative good health of the Japanese, who have the longest life span of any nation in the world, is generally attributed to a lowfat diet. Although the Japanese eat few dairy fats, the notion that their diet is low in fat is a myth; rather, it contains moderate amounts of animal fats from eggs, pork, chicken, beef, seafood and organ meats. With their fondness for shellfish and fish broth, eaten on a daily basis, the Japanese probably consume more cholesterol than most Americans. What they do not consume is a lot of vegetable oil, white flour or processed food (although they do eat white rice.) The life span of the Japanese has increased since World War II with an increase in animal fat and protein in the diet.23 Those who point to Japanese statistics to promote the lowfat diet fail to mention that the Swiss live almost as long on one of the fattiest diets in the world. Tied for third in the longevity stakes are Austria and Greece-both with high-fat diets.24

As a final example, let us consider the French. Anyone who has eaten his way across France has observed that the French diet is just loaded with saturated fats in the form of butter, eggs, cheese, cream, liver, meats and rich patés. Yet the French have a lower rate of coronary heart disease than many other western countries. In the United States, 315 of every 100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. In the Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkably low 80 per 100,000.25 This phenomenon has recently gained international attention as the French Paradox. (The French do suffer from many degenerative diseases, however. They eat large amounts of sugar and white flour and in recent years have succumbed to the timesaving temptations of processed foods.)

A chorus of establishment voices, including the American Cancer Society, the National Cancer Institute and the Senate Committee on Nutrition and Human Needs, claims that animal fat is linked not only with heart disease but also with cancers of various types. Yet when researchers from the University of Maryland analyzed the data they used to make such claims, they found that vegetable fat consumption was correlated with cancer and animal fat was not.26 *Understanding the chemistry of fats*

Clearly something is wrong with the theories we read in the popular press-and used to bolster sales of lowfat concoctions and cholesterol-free foods. The notion that saturated fats per se cause heart disease as well as cancer is not only facile, it is just plain wrong. But it is true that some fats are bad for us. In order to understand which ones, we must know something about the chemistry of fats.

Fats-or lipids-are a class of organic substances that are not soluble in water. In simple terms, fatty acids are chains of carbon atoms with hydrogen atoms filling the available bonds. Most fat in our bodies and in the food we eat is in the form of triglycerides, that is, three fatty-acid chains attached to a glycerol molecule. Elevated triglycerides in the blood have been positively linked to proneness to heart disease, but these triglycerides do not come directly from dietary fats; they are made in the liver from any excess sugars that have not been used for energy. The source of these excess sugars is any food containing carbohydrates, particularly refined sugar and white flour. *Fatty acid classifications by saturation*

Fatty acids are classified in the following way:

*Saturated:* A fatty acid is saturated when all available carbon bonds are occupied by a hydrogen atom. They are highly stable, because all the carbon-atom linkages are filled-or saturated-with hydrogen. This means that they do not normally go rancid, even when heated for cooking purposes. They are straight in form and hence pack together easily, so that they form a solid or semisolid fat at room temperature. Your body makes saturated fatty acids from carbohydrates and they are found in animal fats and tropical oils.

*Monounsaturated:* Monounsaturated fatty acids have one double bond in the form of two carbon atoms double-bonded to each other and, therefore, lack two hydrogen atoms. Your body makes monounsaturated fatty acids from saturated fatty acids and uses them in a number of ways. Monounsaturated fats have a kink or bend at the position of the double bond so that they do not pack together as easily as saturated fats and, therefore, tend to be liquid at room temperature. Like saturated fats, they are relatively stable. They do not go rancid easily and hence can be used in cooking. The monounsaturated fatty acid most commonly found in our food is oleic acid, the main component of olive oil as well as the oils from almonds, pecans, cashews, peanuts and avocados.

*Polyunsaturated:* Polyunsaturated fatty acids have two or more pairs of double bonds and, therefore, lack four or more hydrogen atoms. The two polyunsaturated fatty acids found most frequently in our foods are double unsaturated linoleic acid, with two double bonds-also called omega-6; and triple unsaturated linolenic acid, with three double bonds-also called omega-3. (The omega number indicates the position of the first double bond.) Your body cannot make these fatty acids and hence they are called "essential." We must obtain our essential fatty acids or EFA's from the foods we eat. The polyunsaturated fatty acids have kinks or turns at the position of the double bond and hence do not pack together easily. They are liquid, even when refrigerated. The unpaired electrons at the double bonds makes these oils highly reactive. They go rancid easily, particularly omega-3 linolenic acid, and must be treated with care. Polyunsaturated oils should never be heated or used in cooking. In nature, the polyunsaturated fatty acids are usually found in the cis form, which means that both hydrogen atoms at the double bond are on the same side.

All fats and oils, whether of vegetable or animal origin, are some combination of saturated fatty acids, monounsaturated fatty acids and polyunsaturated linoleic acid and linolenic acid. In general, animal fats such as butter, lard and tallow contain about 40-60% saturated fat and are solid at room temperature. Vegetable oils from northern climates contain a preponderance of polyunsaturated fatty acids and are liquid at room temperature. But vegetable oils from the tropics are highly saturated. Coconut oil, for example, is 92% saturated. These fats are liquid in the tropics but hard as butter in northern climes. Vegetable oils are more saturated in hot climates because the increased saturation helps maintain stiffness in plant leaves. Olive oil with its preponderance of oleic acid is the product of a temperate climate. It is liquid at warm temperatures but hardens when refrigerated. *Classification of fatty acids by length*

Researchers classify fatty acids not only according to their degree of saturation but also by their length.

*Short-chain* fatty acids have four to six carbon atoms. These fats are always saturated. Four-carbon butyric acid is found mostly in butterfat from cows, and six-carbon capric acid is found mostly in butterfat from goats. These fatty acids have antimicrobial properties-that is, they protect us from viruses, yeasts and pathogenic bacteria in the gut. They do not need to be acted on by the bile salts but are directly absorbed for quick energy. For this reason, they are less likely to cause weight gain than olive oil or commercial vegetable oils.27 Short-chain fatty acids also contribute to the health of the immune system.28

*Medium-chain* fatty acids have eight to twelve carbon atoms and are found mostly in butterfat and the tropical oils. Like the short-chain fatty acids, these fats have antimicrobial properties; are absorbed directly for quick energy; and contribute to the health of the immune system.

*Long-chain* fatty acids have from 14 to 18 carbon atoms and can be either saturated, monounsaturated or polyunsaturated. Stearic acid is an 18-carbon saturated fatty acid found chiefly in beef and mutton tallows. Oleic acid is an 18-carbon monounsaturated fat which is the chief component of olive oil. Another monounsaturated fatty acid is the 16-carbon palmitoleic acid which has strong antimicrobial properties. It is found almost exclusively in animal fats. The two essential fatty acids are also long chain, each 18 carbons in length. Another important long-chain fatty acid is gamma-linolenic acid (GLA) which has 18 carbons and three double bonds. It is found in evening primrose, borage and black currant oils. Your body makes GLA out of omega-6 linoleic acid and uses it in the production of substances called prostaglandins, localized tissue hormones that regulate many processes at the cellular level. Very-long-chain fatty acids have 20 to 24 carbon atoms. They tend to be highly unsaturated, with four, five or six double bonds. Some people can make these fatty acids from EFA's, but others, particularly those whose ancestors ate a lot of fish, lack enzymes to produce them. These "obligate carnivores" must obtain them from animal foods such as organ meats, egg yolks, butter and fish oils. The most important very-long-chain fatty acids are dihomo-gamma-linolenic acid (DGLA) with 20 carbons and three double bonds; arachidonic acid (AA) with 20 carbons and four double bonds; eicosapentaenoic acid (EPA) with 20 carbons and five double bonds; and docosahexaenoic acid (DHA) with 22 carbons and six double bonds. All of these except DHA are used in the production of prostaglandins, localized tissue hormones that direct many processes in the cells. In addition, AA and DHA play important roles in the function of the nervous system.29


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The dangers of polyunsaturates

The public has been fed a great deal of misinformation about the relative virtues of saturated fats versus polyunsaturated oils. Politically correct dietary gurus tell us that the polyunsaturated oils are good for us and that the saturated fats cause cancer and heart disease. The result is that fundamental changes have occurred in the Western diet. At the turn of the century, most of the fatty acids in the diet were either saturated or monounsaturated, primarily from butter, lard, tallows, coconut oil and small amounts of olive oil. Today most of the fats in the diet are polyunsaturated from vegetable oils derived mostly from soy, as well as from corn, safflower and canola.

Modern diets can contain as much as 30% of calories as polyunsaturated oils, but scientific research indicates that this amount is far too high. The best evidence indicates that our intake of polyunsaturates should not be much greater than 4% of the caloric total, in approximate proportions of 1 1/2 % omega-3 linolenic acid and 2 1/2 % omega-6 linoleic acid.30 EFA consumption in this range is found in native populations in temperate and tropical regions whose intake of polyunsaturated oils comes from the small amounts found in legumes, grains, nuts, green vegetables, fish, olive oil and animal fats but not from commercial vegetable oils.

Excess consumption of polyunsaturated oils has been shown to contribute to a large number of disease conditions including increased cancer and heart disease; immune system dysfunction; damage to the liver, reproductive organs and lungs; digestive disorders; depressed learning ability; impaired growth; and weight gain.31

One reason the polyunsaturates cause so many health problems is that they tend to become oxidized or rancid when subjected to heat, oxygen and moisture as in cooking and processing. Rancid oils are characterized by free radicals-that is, single atoms or clusters with an unpaired electron in an outer orbit. These compounds are extremely reactive chemically. They have been characterized as "marauders" in the body for they attack cell membranes and red blood cells and cause damage in DNA/RNA strands, thus triggering mutations in tissue, blood vessels and skin. Free radical damage to the skin causes wrinkles and premature aging; free radical damage to the tissues and organs sets the stage for tumors; free radical damage in the blood vessels initiates the buildup of plaque. Is it any wonder that tests and studies have repeatedly shown a high correlation between cancer and heart disease with the consumption of polyunsaturates?32 New evidence links exposure to free radicals with premature aging, with autoimmune diseases such as arthritis and with Parkinson's disease, Lou Gehrig's disease, Alzheimer's and cataracts.33

Too much Omega-6

Problems associated with an excess of polyunsaturates are exacerbated by the fact that most polyunsaturates in commercial vegetable oils are in the form of double unsaturated omega-6 linoleic acid, with very little of vital triple unsaturated omega-3 linolenic acid. Recent research has revealed that too much omega-6 in the diet creates an imbalance that can interfere with production of important prostaglandins.34 This disruption can result in increased tendency to form blood clots, inflammation, high blood pressure, irritation of the digestive tract, depressed immune function, sterility, cell proliferation, cancer and weight gain.35

Too little Omega-3

A number of researchers have argued that along with a surfeit of omega-6 fatty acids the American diet is deficient in the more unsaturated omega-3 linolenic acid. This fatty acid is necessary for cell oxidation, for metabolizing important sulphur-containing amino acids and for maintaining proper balance in prostaglandin production. Deficiencies have been associated with asthma, heart disease and learning deficiencies.36 Most commercial vegetable oils contain very little omega-3 linolenic acid and large amounts of the omega-6 linoleic acid. In addition, modern agricultural and industrial practices have reduced the amount of omega-3 fatty acids in commercially available vegetables, eggs, fish and meat. For example, organic eggs from hens allowed to feed on insects and green plants can contain omega-6 and omega-3 fatty acids in the beneficial ratio of approximately one-to-one; but commercial supermarket eggs can contain as much as nineteen times more omega-6 than omega-3!37

The benefits of saturated fats

The much-maligned saturated fats-which Americans are trying to avoid-are not the cause of our modern diseases. In fact, they play many important roles in the body chemistry:

Saturated fatty acids constitute at least 50% of the cell membranes. They are what gives our cells necessary stiffness and integrity.

They play a vital role in the health of our bones. For calcium to be effectively incorporated into the skeletal structure, at least 50% of the dietary fats should be saturated.38

They lower Lp(a), a substance in the blood that indicates proneness to heart disease.39 They protect the liver from alcohol and other toxins, such as Tylenol.40

They enhance the immune system.41

They are needed for the proper utilization of essential fatty acids.

Elongated omega-3 fatty acids are better retained in the tissues when the diet is rich in saturated fats. 42

Saturated 18-carbon stearic acid and 16-carbon palmitic acid are the preferred foods for the heart, which is why the fat around the heart muscle is highly saturated.43 The heart draws on this reserve of fat in times of stress.

Short- and medium-chain saturated fatty acids have important antimicrobial properties. They protect us against harmful microorganisms in the digestive tract.

The scientific evidence, honestly evaluated, does not support the assertion that "artery-clogging" saturated fats cause heart disease.44 Actually, evaluation of the fat in artery clogs reveals that only about 26% is saturated. The rest is unsaturated, of which more than half is polyunsaturated.45

What about cholesterol?

And what about cholesterol? Here, too, the public has been misinformed. Our blood vessels can become damaged in a number of ways-through irritations caused by free radicals or viruses, or because they are structurally weak-and when this happens, the body's natural healing substance steps in to repair the damage. That substance is cholesterol. Cholesterol is a high-molecular-weight alcohol that is manufactured in the liver and in most human cells. Like saturated fats, the cholesterol we make and consume plays many vital roles:

Along with saturated fats, cholesterol in the cell membrane gives our cells necessary stiffness and stability. When the diet contains an excess of polyunsaturated fatty acids, these replace saturated fatty acids in the cell membrane, so that the cell walls actually become flabby. When this happens, cholesterol from the blood is "driven" into the tissues to give them structural integrity. This is why serum cholesterol levels may go down temporarily when we replace saturated fats with polyunsaturated oils in the diet.46

Cholesterol acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone.

Cholesterol is a precursor to vitamin D, a very important fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function.

The bile salts are made from cholesterol. Bile is vital for digestion and assimilation of fats in the diet.

Recent research shows that cholesterol acts as an antioxidant.47 This is the likely explanation for the fact that cholesterol levels go up with age. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer.

Cholesterol is needed for proper function of serotonin receptors in the brain.48 Serotonin is the body's natural "feel-good" chemical. Low cholesterol levels have been linked to aggressive and violent behavior, depression and suicidal tendencies.

Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system.

Dietary cholesterol plays an important role in maintaining the health of the intestinal wall.49 This is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.

Cholesterol is not the cause of heart disease but rather a potent antioxidant weapon against free radicals in the blood, and a repair substance that helps heal arterial damage (although the arterial plaques themselves contain very little cholesterol.) However, like fats, cholesterol may be damaged by exposure to heat and oxygen. This damaged or oxidized cholesterol seems to promote both injury to the arterial cells as well as a pathological buildup of plaque in the arteries.50 Damaged cholesterol is found in powdered eggs, in powdered milk (added to reduced-fat milks to give them body) and in meats and fats that have been heated to high temperatures in frying and other high-temperature processes.

High serum cholesterol levels often indicate that the body needs cholesterol to protect itself from high levels of altered, free-radical-containing fats. Just as a large police force is needed in a locality where crime occurs frequently, so cholesterol is needed in a poorly nourished body to protect the individual from a tendency to heart disease and cancer. Blaming coronary heart disease on cholesterol is like blaming the police for murder and theft in a high crime area.

Poor thyroid function (hypothyroidism) will often result in high cholesterol levels. When thyroid function is poor, usually due to a diet high in sugar and low in usable iodine, fat-soluble vitamins and other nutrients, the body floods the blood with cholesterol as an adaptive and protective mechanism, providing a superabundance of materials needed to heal tissues and produce protective steroids. Hypothyroid individuals are particularly susceptible to infections, heart disease and cancer.51

The cause and treatment of heart disease

The cause of heart disease is not animal fats and cholesterol but rather a number of factors inherent in modern diets, including excess consumption of vegetables oils and hydrogenated fats; excess consumption of refined carbohydrates in the form of sugar and white flour; mineral deficiencies, particularly low levels of protective magnesium and iodine; deficiencies of vitamins, particularly of vitamin C, needed for the integrity of the blood vessel walls, and of antioxidants like selenium and vitamin E, which protect us from free radicals; and, finally, the disappearance of antimicrobial fats from the food supply, namely, animal fats and tropical oils.52 These once protected us against the kinds of viruses and bacteria that have been associated with the onset of pathogenic plaque leading to heart disease.

While serum cholesterol levels provide an inaccurate indication of future heart disease, a high level of a substance called homocysteine in the blood has been positively correlated with pathological buildup of plaque in the arteries and the tendency to form clots-a deadly combination. Folic acid, vitamin B6, vitamin B12 and choline are nutrients that lower serum homocysteine levels.53 These nutrients are found mostly in animal foods.

The best way to treat heart disease, then, is not to focus on lowering cholesterol-either by drugs or diet-but to consume a diet that provides animal foods rich in vitamins B6 and B12; to bolster thyroid function by daily use of natural sea salt, a good source of usable iodine; to avoid vitamin and mineral deficiencies that make the artery walls more prone to ruptures and the buildup of plaque; to include the antimicrobial fats in the diet; and to eliminate processed foods containing refined carbohydrates, oxidized cholesterol and free-radical-containing vegetable oils that cause the body to need constant repair.

Modern methods of processing fats

It is important to understand that, of all substances ingested by the body, it is polyunsaturated oils that are most easily rendered dangerous by food processing, especially unstable omega-3 linolenic acid. Consider the following processes inflicted upon naturally occurring fatty acids before they appear on our tables:

Extraction: Oils naturally occurring in fruits, nuts and seeds must first be extracted. In the old days this extraction was achieved by slow-moving stone presses. But oils processed in large factories are obtained by crushing the oil-bearing seeds and heating them to 230 degrees. The oil is then squeezed out at pressures from 10 to 20 tons per inch, thereby generating more heat. During this process the oils are exposed to damaging light and oxygen. In order to extract the last 10% or so of the oil from crushed seeds, processors treat the pulp with one of a number of solvents-usually hexane. The solvent is then boiled off, although up to 100 parts per million may remain in the oil. Such solvents, themselves toxic, also retain the toxic pesticides adhering to seeds and grains before processing begins.

High-temperature processing causes the weak carbon bonds of unsaturated fatty acids, especially triple unsaturated linolenic acid, to break apart, thereby creating dangerous free radicals. In addition, antioxidants, such as fat-soluble vitamin E, which protect the body from the ravages of free radicals, are neutralized or destroyed by high temperatures and pressures. BHT and BHA, both suspected of causing cancer and brain damage, are often added to these oils to replace vitamin E and other natural preservatives destroyed by heat.

There is a safe modern technique for extraction that drills into the seeds and extracts the oil and its precious cargo of antioxidants under low temperatures, with minimal exposure to light and oxygen. These expeller-expressed, unrefined oils will remain fresh for a long time if stored in the refrigerator in dark bottles. Extra virgin olive oil is produced by crushing olives between stone or steel rollers. This process is a gentle one that preserves the integrity of the fatty acids and the numerous natural preservatives in olive oil. If olive oil is packaged in opaque containers, it will retain its freshness and precious store of antioxidants for many years.

Hydrogenation: This is the process that turns polyunsaturates, normally liquid at room temperature, into fats that are solid at room temperature-margarine and shortening. To produce them, manufacturers begin with the cheapest oils-soy, corn, cottonseed or canola, already rancid from the extraction process-and mix them with tiny metal particles-usually nickel oxide. The oil with its nickel catalyst is then subjected to hydrogen gas in a high-pressure, high-temperature reactor. Next, soap-like emulsifiers and starch are squeezed into the mixture to give it a better consistency; the oil is yet again subjected to high temperatures when it is steam-cleaned. This removes its unpleasant odor. Margarine's natural color, an unappetizing grey, is removed by bleach. Dyes and strong flavors must then be added to make it resemble butter. Finally, the mixture is compressed and packaged in blocks or tubs and sold as a health food.

Partially hydrogenated margarines and shortenings are even worse for you than the highly refined vegetable oils from which they are made because of chemical changes that occur during the hydrogenation process. Under high temperatures, the nickel catalyst causes the hydrogen atoms to change position on the fatty acid chain. Before hydrogenation, pairs of hydrogen atoms occur together on the chain, causing the chain to bend slightly and creating a concentration of electrons at the site of the double bond. This is called the cis formation, the configuration most commonly found in nature. With hydrogenation, one hydrogen atom of the pair is moved to the other side so that the molecule straightens. This is called the trans formation, rarely found in nature. Most of these man-made trans fats are toxins to the body, but unfortunately your digestive system does not recognize them as such. Instead of being eliminated, trans fats are incorporated into cell membranes as if they were cis fats-your cells actually become partially hydrogenated! Once in place, trans fatty acids with their misplaced hydrogen atoms wreak havoc in cell metabolism because chemical reactions can only take place when electrons in the cell membranes are in certain arrangements or patterns, which the hydrogenation process has disturbed.

In the 1940's, researchers found a strong correlation between cancer and the consumption of fat-the fats used were hydrogenated fats although the results were presented as though the culprit were saturated fats.54 In fact, until recently saturated fats were usually lumped together with trans fats in the various U.S. data bases that researchers use to correlate dietary trends with disease conditions.55 Thus, natural saturated fats were tarred with the black brush of unnatural hydrogenated vegetable oils.

Altered partially hydrogenated fats made from vegetable oils actually block utilization of essential fatty acids, causing many deleterious effects including sexual dysfunction, increased blood cholesterol and paralysis of the immune system.56 Consumption of hydrogenated fats is associated with a host of other serious diseases, not only cancer but also atherosclerosis, diabetes, obesity, immune system dysfunction, low-birth-weight babies, birth defects, decreased visual acuity, sterility, difficulty in lactation and problems with bones and tendons.57 Yet hydrogenated fats continue to be promoted as health foods. The popularity of partially hydrogenated margarine over butter represents a triumph of advertising duplicity over common sense. Your best defense is to avoid it like the plague.

Homogenization: This is the process whereby the fat particles of cream are strained through tiny pores under great pressure. The resulting fat particles are so small that they stay in suspension rather than rise to the top of the milk. This makes the fat and cholesterol more susceptible to rancidity and oxidation, and some research indicates that homogenized fats may contribute to heart disease.58

The media's constant attack on saturated fats is extremely suspect. Claims that butter causes chronic high cholesterol values have not been substantiated by research-although some studies show that butter consumption causes a small, temporary rise-while other studies have shown that stearic acid, the main component of beef fat, actually lowers cholesterol.59 Margarine, on the other hand, provokes chronic high levels of cholesterol and has been linked to both heart disease and cancer.60 The new soft margarines or tub spreads, while lower in hydrogenated fats, are still produced from rancid vegetable oils and contain many additives.

The Diet Dictocrats have succeeded in convincing Americans that butter is dangerous, when in fact it is a valued component of many traditional diets and a source of the following nutrients:


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Nutrition of fats

Fat-Soluble Vitamins: These include true vitamin A or retinol, vitamin D, vitamin K and vitamin E as well as all their naturally occurring cofactors needed to obtain maximum effect. Butter is America's best source of these important nutrients. In fact, vitamin A is more easily absorbed and utilized from butter than from other sources.61 Fortunately, these fat-soluble vitamins are relatively stable and survive the pasteurization process.

When Dr. Weston Price studied isolated traditional peoples around the world, he found that butter was a staple in many native diets. (He did not find any isolated peoples who consumed polyunsaturated oils.) The groups he studied particularly valued the deep yellow butter produced by cows feeding on rapidly growing green grass. Their natural intuition told them that its life-giving qualities were especially beneficial for children and expectant mothers. When Dr. Price analyzed this deep yellow butter he found that it was exceptionally high in all fat-soluble vitamins, particularly vitamin A. He called these vitamins "catalysts" or "activators." Without them, according to Dr. Price, we are not able to utilize the minerals we ingest, no matter how abundant they may be in our diets. He also believed the fat-soluble vitamins to be necessary for absorption of the water-soluble vitamins. Vitamins A and D are essential for growth, for healthy bones, for proper development of the brain and nervous systems and for normal sexual development. Many studies have shown the importance of butterfat for reproduction; its absence results in "nutritional castration," the failure to bring out male and female sexual characteristics. As butter consumption in America has declined, sterility rates and problems with sexual development have increased. In calves, butter substitutes are unable to promote growth or sustain reproduction.62

Not all the societies Dr. Price studied ate butter; but all the groups he observed went to great lengths to obtain foods high in fat-soluble vitamins-fish, shellfish, fish eggs, organ meats, blubber of sea animals and insects. Without knowing the names of the vitamins contained in these foods, isolated traditional societies recognized their importance in the diet and liberally ate the animal products containing them. They rightly believed such foods to be necessary for fertility and the optimum development of children. Dr. Price analyzed the nutrient content of native diets and found that they consistently provided about ten times more fat soluble vitamins than the American diet of the 1930's. This ratio is probably more extreme today as Americans have deliberately reduced animal fat consumption. Dr. Price realized that these fat-soluble vitamins promoted the beautiful bone structure, wide palate, flawless uncrowded teeth and handsome, well-proportioned faces that characterized members of isolated traditional groups. American children in general do not eat fish or organ meats, at least not to any great extent, and blubber and insects are not a part of the western diet; many will not eat eggs. The only good source of fat-soluble vitamins in the American diet, one sure to be eaten, is butterfat. Butter added to vegetables and spread on bread, and cream added to soups and sauces, ensure proper assimilation of the minerals and water-soluble vitamins in vegetables, grains and meat.

The Wulzen Factor: Called the "antistiffness" factor, this compound is present in raw animal fat. Researcher Rosalind Wulzen discovered that this substance protects humans and animals from calcification of the joints-degenerative arthritis. It also protects against hardening of the arteries, cataracts and calcification of the pineal gland.63 Calves fed pasteurized milk or skim milk develop joint stiffness and do not thrive. Their symptoms are reversed when raw butterfat is added to the diet. Pasteurization destroys the Wulzen factor-it is present only in raw butter, cream and whole milk.

The Price Factor or Activator X: Discovered by Dr. Price, Activator X is a powerful catalyst which, like vitamins A and D, helps the body absorb and utilize minerals. It is found in organ meats from grazing animals and some sea food. Butter can be an especially rich source of Activator X when it comes from cows eating rapidly growing grass in the spring and fall seasons. It disappears in cows fed cottonseed meal or high protein soy-based feeds.64 Fortunately, Activator X is not destroyed by pasteurization.

Arachidonic Acid: A 20-carbon polyunsaturate containing four double bonds, found in small amounts only in animal fats. Arachidonic acid (AA) plays a role in the function of the brain, is a vital component of the cell membranes and is a precursor to important prostaglandins. Some dietary gurus warn against eating foods rich in AA, claiming that it contributes to the production of "bad" prostaglandins, ones that cause inflammation. But prostaglandins that counteract inflammation are also made from AA.

Short- and Medium-Chain Fatty Acids: Butter contains about 12-15% short- and medium-chain fatty acids. This type of saturated fat does not need to be emulsified by bile salts but is absorbed directly from the small intestine to the liver, where it is converted into quick energy. These fatty acids also have antimicrobial, antitumor and immune-system-supporting properties, especially 12-carbon lauric acid, a medium-chain fatty acid not found in other animal fats. Highly protective lauric acid should be called a conditionally essential fatty acid because it is made only by the mammary gland and not in the liver like other saturated fats.65 We must obtain it from one of two dietary sources-small amounts in butterfat or large amounts in coconut oil. Four-carbon butyric acid is all but unique to butter. It has antifungal properties as well as antitumor effects.66

Omega-6 and Omega-3 Essential Fatty Acids: These occur in butter in small but nearly equal amounts. This excellent balance between linoleic and linolenic acid prevents the kind of problems associated with overconsumption of omega-6 fatty acids.

Conjugated Linoleic Acid: Butter from pasture-fed cows also contains a form of rearranged linoleic acid called CLA, which has strong anticancer properties. It also encourages the buildup of muscle and prevents weight gain. CLA disappears when cows are fed dry hay or processed feed.67

Lecithin: Lecithin is a natural component of butter that assists in the proper assimilation and metabolization of cholesterol and other fat constituents.

Cholesterol: Mother's milk is high in cholesterol because it is essential for growth and development. Cholesterol is also needed to produce a variety of steroids that protect against cancer, heart disease and mental illness.

Glycosphingolipids: This type of fat protects against gastrointestinal infections, especially in the very young and the elderly. For this reason, children who drink skimmed milk have diarrhea at rates three to five times greater than children who drink whole milk.68

Trace Minerals: Many trace minerals are incorporated into the fat globule membrane of butterfat, including manganese, zinc, chromium and iodine. In mountainous areas far from the sea, iodine in butter protects against goiter. Butter is extremely rich in selenium, a trace mineral with antioxidant properties, containing more per gram than herring or wheat germ.

One frequently voiced objection to the consumption of butter and other animal fats is that they tend to accumulate environmental poisons. Fat-soluble poisons such as DDT do accumulate in fats; but water-soluble poisons, such as antibiotics and growth hormones, accumulate in the water fraction of milk and meats. Vegetables and grains also accumulate poisons. The average plant crop receives ten applications of pesticides-from planting to storage-while cows generally graze on pasture that is unsprayed. Aflatoxin, a fungus that grows on grain, is one of the most powerful carcinogens known. It is correct to assume that all of our foods, whether of vegetable or animal origin, may be contaminated. The solution to environmental poisons is not to eliminate animal fats-so essential to growth, reproduction and overall health-but to seek out organic meats and butter from pasture-fed cows, as well as organic vegetables and grains. These are becoming increasingly available in health food stores and supermarkets and through mail order and cooperatives.

Composition of different fats

Before leaving this complex but vital subject of fats, it is worthwhile examining the composition of vegetable oils and other animal fats in order to determine their usefulness and appropriateness in food preparation:

Duck and Goose Fat are semisolid at room temperature, containing about 35% saturated fat, 52% monounsaturated fat (including small amounts of antimicrobial palmitoleic acid) and about 13% polyunsaturated fat. The proportion of omega-6 to omega-3 fatty acids depends on what the birds have eaten. Duck and goose fat are quite stable and are highly prized in Europe for frying potatoes.

Chicken Fat is about 31% saturated, 49% monounsaturated (including moderate amounts of antimicrobial palmitoleic acid) and 20% polyunsaturated, most of which is omega-6 linoleic acid, although the amount of omega-3 can be raised by feeding chickens flax or fish meal, or allowing them to range free and eat insects. Although widely used for frying in kosher kitchens, it is inferior to duck and goose fat, which were traditionally preferred to chicken fat in Jewish cooking.

Lard or pork fat is about 40% saturated, 48% monounsaturated (including small amounts of antimicrobial palmitoleic acid) and 12% polyunsaturated. Like the fat of birds, the amount of omega-6 and omega-3 fatty acids will vary in lard according to what has been fed to the pigs. In the tropics, lard may also be a source of lauric acid if the pigs have eaten coconuts. Like duck and goose fat, lard is stable and a preferred fat for frying. It was widely used in America at the turn of the century. It is a good source of vitamin D, especially in third-world countries where other animal foods are likely to be expensive. Some researchers believe that pork products should be avoided because they may contribute to cancer. Others suggest that only pork meat presents a problem and that pig fat in the form of lard is safe and healthy.

Beef and Mutton Tallows are 50-55% saturated, about 40% monounsaturated and contain small amounts of the polyunsaturates, usually less than 3%. Suet, which is the fat from the cavity of the animal, is 70-80% saturated. Suet and tallow are very stable fats and can be used for frying. Traditional cultures valued these fats for their health benefits. They are a good source of antimicrobial palmitoleic acid.

Olive Oil contains 75% oleic acid, the stable monounsaturated fat, along with 13% saturated fat, 10% omega-6 linoleic acid and 2% omega-3 linolenic acid. The high percentage of oleic acid makes olive oil ideal for salads and for cooking at moderate temperatures. Extra virgin olive oil is also rich in antioxidants. It should be cloudy, indicating that it has not been filtered, and have a golden yellow color, indicating that it is made from fully ripened olives. Olive oil has withstood the test of time; it is the safest vegetable oil you can use, but don't overdo. The longer chain fatty acids found in olive oil are more likely to contribute to the buildup of body fat than the short- and medium-chain fatty acids found in butter, coconut oil or palm kernel oil.

Peanut Oil contains 48% oleic acid, 18% saturated fat and 34% omega-6 linoleic acid. Like olive oil, peanut oil is relatively stable and, therefore, appropriate for stir-frys on occasion. But the high percentage of omega-6 presents a potential danger, so use of peanut oil should be strictly limited.

Sesame Oil contains 42% oleic acid, 15% saturated fat, and 43% omega-6 linoleic acid. Sesame oil is similar in composition to peanut oil. It can be used for frying because it contains unique antioxidants that are not destroyed by heat. However, the high percentage of omega-6 militates against exclusive use.

Safflower, Corn, Sunflower, Soybean and Cottonseed Oils all contain over 50% omega-6 and, except for soybean oil, only minimal amounts of omega-3. Safflower oil contains almost 80% omega-6. Researchers are just beginning to discover the dangers of excess omega-6 oils in the diet, whether rancid or not. Use of these oils should be strictly limited. They should never be consumed after they have been heated, as in cooking, frying or baking. High oleic safflower and sunflower oils, produced from hybrid plants, have a composition similar to olive oil, namely, high amounts of oleic acid and only small amounts of polyunsaturated fatty acids and, thus, are more stable than traditional varieties. However, it is difficult to find truly cold-pressed versions of these oils.

Canola Oil contains 5% saturated fat, 57% oleic acid, 23% omega-6 and 10%-15% omega-3. The newest oil on the market, canola oil was developed from the rape seed, a member of the mustard family. Rape seed is unsuited to human consumption because it contains a very-long-chain fatty acid called erucic acid, which under some circumstances is associated with fibrotic heart lesions. Canola oil was bred to contain little if any erucic acid and has drawn the attention of nutritionists because of its high oleic acid content. But there are some indications that canola oil presents dangers of its own. It has a high sulphur content and goes rancid easily. Baked goods made with canola oil develop mold very quickly. During the deodorizing process, the omega-3 fatty acids of processed canola oil are transformed into trans fatty acids, similar to those in margarine and possibly more dangerous.69 A recent study indicates that "heart healthy" canola oil actually creates a deficiency of vitamin E, a vitamin required for a healthy cardiovascular system.70 Other studies indicate that even low-erucic-acid canola oil causes heart lesions, particularly when the diet is low in saturated fat.71

Flax Seed Oil contains 9% saturated fatty acids, 18% oleic acid, 16% omega-6 and 57% omega-3. With its extremely high omega-3 content, flax seed oil provides a remedy for the omega-6/omega-3 imbalance so prevalent in America today. Not surprisingly, Scandinavian folk lore values flax seed oil as a health food. New extraction and bottling methods have minimized rancidity problems. It should always be kept refrigerated, never heated, and consumed in small amounts in salad dressings and spreads. Tropical Oils are more saturated than other vegetable oils. Palm oil is about 50% saturated, with 41% oleic acid and about 9% linoleic acid. Coconut oil is 92% saturated with over two-thirds of the saturated fat in the form of medium-chain fatty acids (often called medium-chain triglycerides). Of particular interest is lauric acid, found in large quantities in both coconut oil and in mother's milk. This fatty acid has strong antifungal and antimicrobial properties. Coconut oil protects tropical populations from bacteria and fungus so prevalent in their food supply; as third-world nations in tropical areas have switched to polyunsaturated vegetable oils, the incidence of intestinal disorders and immune deficiency diseases has increased dramatically. Because coconut oil contains lauric acid, it is often used in baby formulas. Palm kernel oil, used primarily in candy coatings, also contains high levels of lauric acid. These oils are extremely stable and can be kept at room temperature for many months without becoming rancid. Highly saturated tropical oils do not contribute to heart disease but have nourished healthy populations for millennia.72 It is a shame we do not use these oils for cooking and baking-the bad rap they have received is the result of intense lobbying by the domestic vegetable oil industry.73 Red palm oil has a strong taste that most will find disagreeable-although it is used extensively throughout Africa-but clarified palm oil, which is tasteless and white in color, was formerly used as shortening and in the production of commercial French fries, while coconut oil was used in cookies, crackers and pastries. The saturated fat scare has forced manufacturers to abandon these safe and healthy oils in favor of hydrogenated soybean, corn, canola and cottonseed oils.

In summary, our choice of fats and oils is one of extreme importance. Most people, especially infants and growing children, benefit from more fat in the diet rather than less. But the fats we eat must be chosen with care. Avoid all processed foods containing newfangled hydrogenated fats and polyunsaturated oils. Instead, use traditional vegetable oils like extra virgin olive oil and small amounts of unrefined flax seed oil. Acquaint yourself with the merits of coconut oil for baking and with animal fats for occasional frying. Eat egg yolks and other animal fats with the proteins to which they are attached. And, finally, use as much good quality butter as you like, with the happy assurance that it is a wholesome-indeed, an essential-food for you and your whole family.

Organic butter, extra virgin olive oil, and expeller-expressed flax oil in opaque containers are available in health food stores and gourmet markets. Edible coconut oil can be found in Indian or Caribbean markets. (See Sources for good quality fats and oils by mail order.)


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THE IMPORTANCE OF SATURATED FATS FOR BIOLOGICAL FUNCTIONS

By Mary G. Enig, PhD

Many people recognize that saturated fats are needed for energy, hormone production, cellular membranes and for organ padding. You may be surprised to learn that certain saturated fatty acids are also needed for important signaling and stabilization processes in the body.

Signaling processes work in the cells at the level of the membrane proteins, many of which are called G-protein receptors. The G-protein receptors become stimulated by different molecules and can be turned off or on in a manner similar to a binary light switch, which remains on for a limited time and then flips itself off until it is stimulated again.

The saturated fatty acids that play important roles in these processes are the 16-carbon palmitic acid, the 14-carbon myristic acid and the 12-carbon lauric acid. These saturated fatty acids are found in certain food fats. Palmitic acid, for example, comprises 45 percent of palm oil and about 25 percent of animal and dairy fats. Furthermore, the body makes palmitic acid out of excess carbohydrates and excess protein.

A biochemical process called palmitoylation, in which the body uses palmitic acid in stabilization processes, although not very well known, is very important to our health.

When these important saturated fatty acids are not readily available, certain growth factors in the cells and organs will not be properly aligned. This is because the various receptors, such as G-protein receptors, need to be coupled with lipids in order to provide localization of function.

The messages that are sent from the outside of the cell to the inner part of the cell control many functions including those activated by, for example, adrenaline in the primitive mammalian fight/flight reactions. When the adrenal gland produces adrenaline and the adrenaline (beta-adrenergic) receptor communicates with the G-protein and its signal cascade, the parts of the body are alerted to the need for action; the heart beats faster, the blood flow to the gut decreases while the blood flow to the muscles increases and the production of glucose is stimulated.

The G-proteins come in different forms; the alpha subunit is covalently linked to myristic acid and the function of this subunit is important for turning on and off the binding to an enzyme called adenylate cyclase and thus the amplification of important hormone signals.

When researchers looked at the fatty acid composition of the phospholipids in the T-cells (white blood cells), from both young and old donors, they found that a loss of saturated fatty acids in the lymphocytes was responsible for age-related declines in white blood cell function. They found that they could correct cellular deficiencies in palmitic acid and myristic acid by adding these saturated fatty acids.

Most Westerners consume very little myristic acid because it is provided by coconut oil and dairy fats, both of which we are told to avoid. But myristic acid is a very important fatty acid, which the body uses to stabilize many different proteins, including proteins used in the immune system and to fight tumors. This function is called myristoylation; it occurs when myristic acid is attached to the protein in a specific position where it functions usefully. For example, the body has the ability to suppress production of tumors from lung cancer cells if a certain genetically determined suppressor gene is available. This gene is called fus1 and is a protein that has been modified with covalent addition of the saturated fatty acid myristic acid. Thus, the loss of myristic acid from the diet can have unfortunate consequences, including cancer and immune system dysfunction.

Lauric acid has several functions. It is an antimicrobial fatty acid on its own and as a monoglyceride. It also has the function of stabilization when it is attached to certain proteins in a similar fashion to myristic acid and palmitic acid.

Stearic acid is the 18-carbon saturated fatty acid. The main sources are animal tallows, which contain about 20-25 percent stearic acid, and chocolate, which contains about 35 percent stearic acid. In other foods it occurs only on levels of 1-2 percent.

How much total saturated do we need? During the 1970s, researchers from Canada found that animals fed rapeseed oil and canola oil developed heart lesions. This problem was corrected when they added saturated fat to the animals diets. On the basis of this and other research, they ultimately determined that the diet should contain at least 25 percent of fat as saturated fat. Among the food fats that they tested, the one found to have the best proportion of saturated fat was lard, the very fat we are told to avoid under all circumstances!

These are some of the complex but vital reasons we need to include palm oil, coconut oil, butter and lard in our diets.


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## hackskii

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Keep up the good work.


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## Cookie

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## Cookie

POLYUNSATURATED OILS AND CANCER

Up to the 19th-century, fat was relatively expensive and butter was a luxury. The poor lived mainly on potatoes and bread, which were cheap, supplemented whenever possible with whatever source of protein and fat they could afford. Not surprisingly, mortality was high amongst the poorer classes. To fill the gap in the market cheap substitutes for butter began to be produced in the last quarter of the Victorian era. Made from cheaper fats and coloured yellow to mimic the look, if not the taste of butter, they were called margarine. And this started, quite slowly at first, a radical change in the types of fat we, as a nation, ate.

Originally margarines were made of beef suet, milk and water. Later the recipes changed to include lard, whale oil and the oils of olive, coconut, ground nut and cottonseed. By the middle of the 20th-century an emulsion of soya bean and water was substituted for the milk and margarines could be made entirely of inexpensive oils from vegetable sources. In all these forms, margarine was the poor relation to butter.

In the 1920s a new disease had suddenly 'taken off' all over the industrialised world. By the 1940s it had become a leading cause of premature death - and nobody knew why. In 1950, an American scientists hypothesised that cholesterol might be to blame. (1) In 1953, another American, Ancel Keys, compared levels of this disease in seven countries with the amounts of fat in those countries. (2) And so was born the 'Diet-Heart' hypothesis, for the new disease was coronary heart disease.

To reduce the risk of a heart attack, Ancel Keys recommended cutting down on the vegetable oils and margarines. However, it was discovered that vegetable oils, which are composed largely of unsaturated fats and oils, tended to lower blood cholesterol levels, while saturated fats tended to raise them. And by that time, it had been decided, largely by majority vote, (3) that raised cholesterol increased the risk of a heart attack. With the advent of the 'Prudent Diet' in the USA in 1982, and COMA's introduction of 'healthy eating' in Britain two years later, the fats in our diet changed even more dramatically: we were told to avoid animal fats such as butter and lard, which have a larger proportion of saturated fats, in favour of largely polyunsaturated vegetable margarines and cooking oils. Now margarines could be priced to rival butter. Recently, margarines have been developed specifically to lower cholesterol levels, and prices have risen again. Benecol, made from tree bark is considerably more expensive than butter.

Margarine - a natural food?

The polyunsaturated fats used to make margarine are generally obtained from vegetable sources: sunflower seed, cottonseed, and soybean. As such they might be thought of as natural foods. Usually, however, they are pressed on the public in the form of highly processed margarines, spreads and oils and, as such, they are anything but natural.

In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion. This was enough to cause Perrier to be removed from supermarket shelves. The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents. Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product. That is 700 times as much as fourteen parts per billion.

The oils then go through more than ten other processes: degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, . . . that include heat treatment at 140-160C with a solution of caustic soda; the use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product; the addition of antioxidants such as butylated hydroxyanisol (E320). These antioxidants are again usually petroleum based and are widely believed to cause cancer.

The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.

The heat treatment alone is enough to render these margarines nutritionally inadequate. When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.

You may be interested in a list of the ingredients that may be present in butter and margarine:

Butter:

milk fat (cream),

a little salt,

Margarine:

Edible oils,

edible fats,

salt or potassium chloride,

ascorbyl palmitate,

butylated hydroxyanisole,

phospholipids,

tert-butylhydroquinone,

mono- and di-glycerides of fat-forming fatty acids,

disodium guanylate,

diacetyltartaric and fatty acid esters of glycerol,

Propyl, octyl or dodecyl gallate (or mixtures thereof),

tocopherols,

propylene glycol mono- and di-esters,

sucrose esters of fatty acids,

curcumin,

annatto extracts,

tartaric acid,

3,5,trimethylhexanal,

ß-apo-carotenoic acid methyl or ethyl ester,

skim milk powder,

xanthophylls,

canthaxanthin,

vitamins A and D.

Dietary fat patterns

The total amount of fats in our diet today, according to the MAFF National Food Survey, is almost the same as it was at the beginning of this century. What has changed, to some extent, is the types of fats eaten. At the turn of the century we ate mainly animal fats that are largely saturated and monounsaturated. Now we are tending to eat more polyunsaturated fats - it's what we are advised to do. In 1991, two studies, from USA (4) and Canada, (5) found that linoleic acid, the major polyunsaturated fatty acid found in vegetable oils, increased the risk of breast tumours. This, it seems, was responsible for the rise in the cancers noted in previous studies. Experiments with a variety of fats showed that saturated fats did not cause tumours but, when small amounts of polyunsaturated vegetable oil or linoleic acid itself was added, this greatly increased the promotion of breast cancer.

Body cell walls are made of cholesterol, protein and fats. The graph below demonstrates that the human body's fat make-up is largely of saturated and monounsaturated fatty acids. We contain very little polyunsaturated fat. Cell walls have to allow the various nutrients that body cells need from the blood, but stop harmful pathogens. They must be stable. An intake of large quantities of polyunsaturated fatty acids changes the constituency of cholesterol and body fat. Cell walls become softer and more unstable.

Polyunsaturated fats suppress the immune system

Polyunsaturated fats (PUFs) are greatly immunosuppressive, and anything that suppresses the immune system is likely to cause cancer. The first person to suggest that polyunsaturated fats cause cancer was Dr R A Newsholme of Oxford University, England. (6) What Newsholme wrote was that when our bodies get sufficient nutrition, our diet includes immunosuppressive PUFs which make us prone to infection by bacteria and viruses. When we are starved, however, our body stores of PUFs are depleted. This allows our bodies' immune systems to recover which, in turn, allows us to fight existing infection and prevent other infections. He was making the point that the immunosuppressive effects of PUFs in sunflower seeds are useful in treating autoimmune diseases such as multiple sclerosis, (7) and that the same fatty acids could be used to suppress the immune system to prevent rejection of kidney transplants.

It was during the early days of kidney transplantation that doctors first encountered the problem of tissue rejection as their patients' bodies destroyed the alien transplanted kidneys. If transplantation were to be a success, they had to find a way to suppress the immune system. Newsholme had said that there was no better way to immunosuppress a renal patient than with sunflower seed oil. So kidney transplant doctors fed their patients linoleic acid. (8) (Linoleic acid is the major polyunsaturated fatty acid in vegetable oils.) But the transplant doctors were then astonished to see how quickly their patients developed cancers: some cancers were up to twenty times as frequent as was expected.

This was in line with heart trials using diets that were high in PUFs which, reported an excess of cancer deaths from as early as 1971. (9)

By the early 1980s, we were being exhorted by doctors and nutritionists to eat more PUFs because they were 'good for us' despite the fact that Oncology Times carried a paper in January 1980 from the University of California at Davis that mice fet PUFs were more prone to develop melanoma. In May 1980, the same publication carried a similar report from Oregon State University which said that PUFs fed to cancer-prone mice increased the numbers of cancers formed.

In 1989 there was a report of a ten-year trial at a Veterans' Administration Hospital in Los Angeles. In this trial half the patients were fed a diet which had double the amount of PUFs as compared to saturated fats. In the half of the patients on the high PUF diet there was a fifteen percent increase in cancer deaths compared to the saturated fat group. (10) The authors of the report said that the PUFs had been the cause of the increase in cancer deaths. The British Medical Journal carried an editorial in its 6 October 1973 issue which asked if PUFs were carcinogenic. It came to the conclusion that they were.

Wayne Martin likes to tell a story which suggests just how cancer-causing are PUFs. In 1930 in the USA, eighty percent of men smoked cigarettes and the tar content of cigarettes was much higher than it is today. The death rate at that time from lung cancer was very low. In 1955 doctors decided that PUFs were good in terms of heart disease protection. After this lung cancer deaths increased so dramatically. By 1980 although the number of American men who smoked had dropped to only thirty percent, three times as much PUF was being eaten - and there were sixty times as many lung cancer deaths. (11)

In 1990, Martin called Newsholme's Oxford University office but by then Newsholme had retired. Martin spoke to his successor to find that they were still treating autoimmune diseases with PUFs. By then they were using fish oil. The doctor said the reason for the fish oil was that the degree of immunosuppression increased with the degree of unsaturation and fish oil was much more unsaturated than sunflower oil. Martin asked the doctor why they were not talking about PUFs causing cancer. The doctor replied that if he did that he would be run out of Oxford.

Carcinogens - background radiation, ultraviolet radiation from the sun, particles in the air we breathe and the food we eat - continually attack us all. Normally, the immune system deals with any small focus of cancer cells so formed and that is the end of it. But linoleic acid suppresses the immune system. With a high intake of margarine, therefore, a tumour may grow too rapidly for the weakened immune system to cope thus increasing our risk of a cancer.

Polyunsaturated fats cause cancer

Since 1974, the increase of polyunsaturated fats has been blamed for the alarming increase in malignant melanoma (skin cancer) in Australia. (12) We are all told that the sun causes it. Are Australians going out in the sun any more now than they were fifty years ago? They are certainly eating more polyunsaturated oils: in Australia in 1995 I saw that even the cream on milk was removed and replaced with vegetable oil. Victims of the disease have been found to have polyunsaturated oils in their skin cells. Polyunsaturated oils are oxidised readily by ultra-violet radiation from the sun and form harmful 'free radicals'. These are known to damage the cell's DNA and this can lead to the deregulation we call cancer. Saturated fats are stable. They do not oxidise and form free radicals.

Malignant melanoma is also said to be increasing in this country. Does the sun cause this? In Britain the number of sufferers is so small as to be relatively insignificant. Even so, it is not likely that the sun is to blame since all the significant increase is in the over-seventy-five-year-olds. People in this age group tend to get very little sun.

That the sun is not to blame is confirmed by other findings:

Melanoma occurs ten times as often in Orkney and Shetland than it does on Mediterranean islands.

It also occurs more frequently on areas that are not exposed to the sun.

In Scotland, for example, there are five times as many melanomas on the feet as on the hands;

and in Japan, forty per cent of pedal melanomas are on the soles of the feet . (13)

Polyunsaturated fats promote cancer

Many laboratories have shown that diets high in polyunsaturated fatty acids promote tumours. Cancer promotion is not the same as cancer causing. The subject is complex; suffice to say here that promoters are substances that help to speed up reproduction of existing cancer cells.

It has been known since the early 1970s that it is linoleic acid that is the major culprit. As Professor Raymond Kearney of Sydney University put it in 1987: 'Many laboratories have shown that a greater proportion of polyunsaturated fats are superior to diets rich in saturated fats in promoting the yield of experimental mammary tumours. In such studies, omega-6 linoleic acid appeared to be the crucial fatty acid . . .' and 'Vegetable oils (eg Corn oil and sunflower oil) which are rich in linoleic acid are potent promoters of tumour growth.' (14)

Polyunsaturated fats and breast cancer

A study of 61,471 women aged forty to seventy-six, conducted in Sweden, looked into the relation of different fats and breast cancer. The results were published in January 1998. This study found an inverse association with monounsaturated fat and a positive association with polyunsaturated fat. In other words, monounsaturated fats protected against breast cancer and polyunsaturated fats increased the risk. Saturated fats were neutral. (15)

Flora margarine, the brand leader, is thirty-nine percent linoleic acid; Vitalite and other 'own brand' polyunsaturated margarines are similar. Of cooking oils, sunflower oil is fifty percent and safflower oil seventy-two percent linoleic acid. Butter, on the other hand, has only a mere two percent and lard is just nine percent linoleic acid. Linoleic acid is one of the essential fatty acids. We must eat some to live, but we do not need much. The amount in animal fats is quite sufficient.

Because of the heart disease risk from trans-fats in margarines, in 1994 the manufacturers of Flora changed its formula to cut out the trans fats and other manufacturers have since followed. But that still leaves the linoleic acid.

The anti-cancer fat

Linoleic acid is one of the essential fatty acids that our bodies need but cannot synthesise. We must eat some to survive. Fortunately there is one form of linoleic acid that is beneficial. Conjugated linoleic acid (CLA) differs from the normal form of linoleic acid only in the position of two of the bonds that join its atoms. But this small difference has been shown to give it powerful anti-cancer properties. Scientists at the Department of Surgical Oncology, Roswell Park Cancer Institute, New York (16) and the Department of Biochemistry and Molecular Biology, New Jersey Medical School, (17) showed that even at concentrations of less than one percent, CLA in the diet is protective against several cancers including breast cancer, colorectal cancer and malignant melanoma.

Conjugated linoleic acid has one other difference from the usual form - it is not found in vegetables but in the fat of ruminant animals. The best sources are dairy products and the fat on red meat, principally beef. (18)

It has been suggested that the consumption of red meat increases the risk of colon cancer, yet in Britain there is no evidence to support this. (19) It is interesting that all the evidence implicating red meat in cancer comes from the USA - where they cut the fat off.

Conclusions

Saturated fats and animal fats are usually blamed for all manner of diseases in Western society. But look at the facts:

In the 19th-century, when animal fats were all that was available, cancers were rare (as was heart disease).

Polyunsaturated fats and oils are used to suppress the immune system, such immunosuppression is known to cause cancers to start and promote cancer.

In this last century there has been a change in favour of polyunsaturated fats and oils - and cancer rates have soared.

Unfortunately, as polyunsaturated fatty acids are also essential to the body; we must have some. So a proper balance must be struck. Whether the dramatic increase in the numbers of cancers in the last century was as a result of a similarly dramatic rise in our intake of polyunsaturated vegetable oils is not known - but the evidence strongly favours such a conclusion.

Under the circumstances, it seems prudent to get what linoleic acid we need from animal sources. Or to restrict polyunsaturated oil consumption so that linoleic acid is no more than three percent of the total fat intake.


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## Cookie

Explanation of terms

Fat is a substance which contains one or more fatty acids and is the principal form in which the body stores energy. It is also used as an insulating material both just beneath the skin and around some of the internal organs. Fat is essential in the diet to supply an adequate amount of essential fatty acids and for the absorption of the fat-soluble vitamins: A, D, E and K.

The chemical and physical properties of a fat are determined by the relative amounts of the various fatty acids of which it is composed. Generally, the more saturated the fatty acid content, the harder the fat will be at room temperature; the more unsaturated its content, the runnier it will be. All fats are a mixture of different fatty acids.

Fatty Acids

All fats are composed of fatty acids, of which there are dozens in nature. A fatty acid is an organic acid having a chain of carbon atoms coupled to hydrogen atoms at the side and a carboxyl radicle at one end. The carbon atoms are joined together with mainly a single bond plus a number of 'double bonds'. It is the difference between these that differentiates the various fatty acids.

Saturated fatty acids have no double bonds and this makes them stable.

H H H H H H H H H H H H H H H H H

| | | | | | | | | | | | | | | | |

H-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-COOH

| | | | | | | | | | | | | | | | |

H H H H H H H H H H H H H H H H H

The diagram above is of Stearic acid . It has 18 carbon atoms and no double bonds. It is designated 18:0 . Because all the carbon atoms are surrounded by hydrogen atoms, it is called saturated . As the hydrogen atoms are all close together, it is difficult to bend. It is this resistance to bending that makes most saturated fats solid at room temperature.

Unsaturated fatty acids are those where two or more of their carbon atoms are connected with 'double bonds'.

Mono- unsaturated fatty acids are unsaturated fatty acids with one double bond.

H H H H H H H H H H H H H H H H H

| | | | | | | | | | | | | | | | |

H-C-C-C-C-C-C-C-C-C=C-C-C-C-C-C-C-C-COOH

| | | | | | | | | | | | | | |

H H H H H H H H H H H H H H H

Here we have another 18 carbon fatty acid: Oleic acid , the major fatty acid in olive oil. This has one ' double bond ' in the middle. Fatty acids with one double bond are called mono -unsaturated. It is designated by the term 18:1 . Because of the double bond this fatty acid can bend and is liquid at room temperature. Oleic acid is also the most abundant fatty acid in animal fats and in human fat.

Poly- unsaturated fatty acids are those with two or more double bonds.

H H H H H H H H H H H H H H H H H

| | | | | | | | | | | | | | | | |

H-C-C-C-C-C-C=C-C-C=C-C-C-C-C-C-C-C-COOH

| | | | | | | | | | | | |

H H H H H H H H H H H H H

The one above is Linoleic acid , the most abundant fatty acid in vegetable seed oils such as sunflower, safflower, soya and corn oils. This has two double bonds, the first after the sixth carbon atom. This makes it an Omega-6 fatty acid. If the first double bond follows the third carbon atom, the fatty acid is an Omega-3 fatty acid. The shorthand for linoleic acid is 18:2.

Some fatty acids come in two configurations: Omega-3 and Omega-6. Linolenic acid , an 18-carbon molecule with three double bonds, is an example. Alpha-linolenic acid is Omega-3 , while Gamma-linolenic acid is Omega-6 .

All polyunsaturated fatty acids are liquid at room temperature.

The unsaturated fatty acids are not stable; they react gradually with oxygen in the air and become rancid. This oxygenation process produces molecules known as free radicals which are known to have undesirable effects on the body. The more unsaturated a fatty acid is, the more liable it is to oxidation. This is why polyunsaturated margarines must be kept refrigerated.

Cis and trans bonds

Generally, in Nature, fatty acids' double bonds are as shown above with the single hydrogen atoms at a double bond on the same side of the molecule. This is called a cis configuration. However, in the process of margarine manufacture, liquid oils are not much good. They have to be made more solid. The process which does this is called hydrogenation . During hydrogenation, some of the double bonds are twisted so that the hydrogen atoms lie on opposite sides, as in the diagram below. This configuration is called trans.

H H H H H H H H H H H H H H H

| | | | | | | | | | | | | | |

H-C-C-C-C-C-C=C-C-C=C-C-C-C-C-C-C-C-COOH

| | | | | | | | | | | | | | |

H H H H H H H H H H H H H H H

(In the diagram of linoleic acid above, both double bonds are shown as trans bonds.)

Fats are attacked by oxygen. Just like iron left out in the rain, fats oxydise (rust). But oxygen can only attack fats where there are double bonds. This is why saturated fats don't spoil but polyunsaturated margarines must be kept in the fridge. And the more double bonds a fatty acid has, the more it oxydises and the more ' free radicals ' it throws off.

Fats

All fats contain a mixture of different fatty acids, both saturated and unsaturated. The fatty acid content of some typical foods are tabled below. The total percentages are less than 100% because of the glycerol and other compounds that are present. Note that, although animal fats are generally thought of as being saturated fats, most are less than fifty percent saturated.

Table : Fatty acid content of typical foods

Percentage of fat

% Fat Sat Mono Poly

Milk cow's 3.9 64 28 3

human 4.1 50 39 9

Cheese, Cheddar 33.5 63 27 4

Eggs 10.9 31 39 11

Beef 27.4 41 47 4

Pork 25.5 35 42 15

Chicken 12.8 30 45 20

Liver, lamb's 6.2 28 29 15

Mackerel 22.9 20 49 20

Butter 76.9 50 34 3

Lard 95.5 39 45 11

Margarine hard 81.0 39 47 10

polyunsaturated 81.0 17 27 52

Blended cooking oil 99.9 13 25 58

Peanuts, roasted 49.0 12 38 37

Chocolate, milk 30.3 58 33 4


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## hackskii

Good read.

I kindof dont get the ratios of the % none of them add to 100%


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## Killerkeane

i have read 5, having trouble digesting the remaining few....Cookie thats a lot of information mate, brilliant idea to put it one place.


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## Cookie

Thanks glad your enjoying it,

TONS more to come


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## Cookie

New Cholesterol More Dangerous Than LDL?

Past studies have shown that one of the contributing factors to heart attacks and strokes is low-density lipoprotein. (LDL cholesterol) Now, researchers have found another type of cholesterol that may be just as, if not more, dangerous: Chylomicrons.

Chylomicrons, a class of lipoproteins, are defined as metabolized balls of fat and cholesterol. They enter the blood stream through the intestines after a meal and accumulate on arterial walls. Doctors find it difficult to measure chylomicrons due to how quickly they process. For example, when a patient gives a blood sample after fasting for 12 or more hours, chylomicron cholesterol will usually include only three percent of all the cholesterols present in the sample. The bulk of the sample (70 percent) will be comprised of LDL.

It is for this reason that most researchers are led to believe that LDL is the leading cause of the development of coronary artery disease. However, these findings have prompted a question of contradictory proportions: Why is it that 40 percent of people prone to suffering from a stroke or heart attack have low or normal LDL levels?

Some researchers believe understanding chylomicrons and their metabolism may answer this question and the role it plays in the development of:

Diabetes

Obesity

Other cardiovascular diseases


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## Cookie

A new study suggests that level of triglyceride in the blood may help predict heart attack risk as well as other more well-known blood fats such as LDL and HDL cholesterol. High triglycerides alone increased the risk of heart attack nearly three-fold, according to a report in the current issue of Circulation. And people with the highest ratio of triglycerides to HDL -- the "good" cholesterol -- had 16 times the risk of heart attack as those with the lowest ratio of triglycerides to HDL in the study of 340 heart attack patients and 340 of their healthy, same age counterparts. The ratio of triglycerides to HDL was the strongest predictor of a heart attack, even more accurate than the LDL/HDL ratio," reported Harvard lead study author.

Triglycerides, a mixture of fatty acids and glycerol that make up the principle fats in the blood, bind to carrier proteins, forming compounds known as lipoproteins. Other types of lipoproteins that carry cholesterol, such as LDL and HDL, are known to be related to the risk of heart disease because of their propensity to deposit -- or not deposit -- fat in coronary arteries. However, it has not been clear if triglyceride level could predict heart attack risk, despite years of research.


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## Cookie

Reduce Grains and Sugar to Lose Weight and Improve Health

For several million years, humans existed on a diet of animals and vegetation. It was only with the advent of agriculture a mere 10,000 years ago - a fraction of a second in evolutionary time - that humans began ingesting large amounts of sugar and starch in the form of grains (and potatoes) into their diets. Indeed, 99.99% of our genes were formed before the advent of agriculture; in biological terms, our bodies are still those of hunter-gatherers.

While the human shift to agriculture produced indisputable gains for man - modern civilization is based on this epoch - societies where the transition from a primarily meat/vegetation diet to one high in cereals show a reduced lifespan and stature, increases in infant mortality and infectious disease, and higher nutritional deficiencies.

Contemporary humans have not suddenly evolved mechanisms to incorporate the high carbohydrates from starch- and sugar-rich foods into their diet. In short, we are consuming far too much bread, cereal, pasta, corn (a grain, not a vegetable), rice, potatoes and Little Debbie snack cakes, with very grave consequences to our health. Making matters worse, most of these carbohydrates we consume come in the form of processed food.

That 65% of Americans are overweight, and 27% clinically obese, in a nation addicted to sesame seed buns for that hamburger, with a side of French fries and a Coke, is no coincidence. It is not the fat in the foods we eat but, far more, the excess carbohydrates from our starch- and sugar-loaded diet that is making people fat and unhealthy, and leading to epidemic levels of a host of diseases such as diabetes.

If you are experiencing any of the following symptoms, chances are very good that the excess carbohydrates in your body are, in part or whole, to blame:

Excess weight

Fatigue and frequent sleepiness

Depression

Brain fogginess

Bloating

Low blood sugar

High blood pressure

High triglycerides

We all need a certain amount of carbohydrates, of course, but, through our addiction to grains, potatoes, sweets and other starchy and sugary foods, we are consuming far too many. The body's storage capacity for carbohydrates is quite limited, though, so here's what happens to all the excess: they are converted, via insulin, into fat and stored in the adipose, or fatty, tissue.

Any meal or snack high in carbohydrates generates a rapid rise in blood glucose. To adjust for this rise, the pancreas secretes the hormone insulin into the bloodstream, which lowers the glucose. Insulin is, though, essentially a storage hormone, evolved over those millions of years of humans prior to the agricultural age, to store the excess calories from carbohydrates in the form of fat in case of famine.

Insulin, stimulated by the excess carbohydrates in our overabundant consumption of grains, starches and sweets, is responsible for all those bulging stomachs and fat rolls in thighs and chins.

Even worse, high insulin levels suppress two other important hormones - glucagons and growth hormones - that are responsible for burning fat and sugar and promoting muscle development, respectively. So insulin from excess carbohydrates promotes fat, and then wards off the body's ability to lose that fat.

Excess weight and obesity lead to heart disease and a wide variety of other diseases. But the ill effect of grains and sugars does not end there. They suppress the immune system, contributing to allergies, and they are responsible for a host of digestive disorders. They contribute to depression, and their excess consumption is, in fact, associated with many of the chronic diseases in our nation, such as cancer and diabetes.

The bottom line is this: Americans need to reduce their intake of grains, including corn-based foods, and all sweets and potatoes, dramatically.


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## Vernon

Stop

you are driving yourself made its all about finding the calorie and understanding it.

and getting back to our anscertral diet we have a changed our lives to fast and once we have lost ancient foods and replaced them **** maufactured and marketed foodstuffs especially sugar ..you seen how thats sticted into us ..what is it 150lbs per person per year i worked it at 500 cals day!!

vern


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## ChefX

Vern, you still have yet to answer those questions I posted for you.


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## Tatyana

BUMP to read Cookie's stuff!

Love those big right click left click postings! NOW that I am done UNI for the summer! JOY

x

x

x

T


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## bozz

when we were cavemen we did eat much animalfat, but didtn live longer then now.. now we live 3times longer even with alot of grains and carbs.


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## gymlady




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## Love2DL

Thumb hurts from scrolling.


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## purplemule

bozz said:


> when we were cavemen we did eat much animalfat, but didtn live longer then now.. now we live 3times longer even with alot of grains and carbs.


Nice bump, terrible input. Medication, living conditions and understanding illnesses play a huge part in life expectancy now.


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