Carbotoxicity

BUFFALO, Sept. 3 (P), Sugar is "fuel' for cancer, and its regulation in diet essential for cancer treatment, the American Chemical society was told yesterday. The report came from the cancer research department of the University of Pennsylvania, from work done by Gladys E. Woodward and Edith G. Fry, under direction of Dr. Ellice McDonald. 

"In cancer," said Dr. McDonald, in explaining the technical report, "the essential difference between tumor tissue and normal tissue is the ability of cancer to digest the animal sugar (or glycogen) in a different and more expeditious way than normal. "The greater the amount of sugar there is in the blood of cancer patients, the shorter is the expectation of their lives. There is a greater growth of the cancer when there is a large amount of sugar in the blood. The tumor grows faster, and there are a greater number of dividing cells. Cancer patients with a low blood sugar respond well to treatment and have a better chance of survival, with slow growth of the tumor.

"The amount of the sugar in the blood of cancer patients should be periodically measured, particularly before and after any treatment, for if the blood sugar increases after any treatment of the tumor, this should be corrected before any further treatment is instituted, and any new treatment should be based on the results of the tests. 

"The general conclusion is that cancer patients, particularly those with a high level of blood sugar, should be put on a low carbohydrate diet which should contain little or no sugar."

"The benefit was dramatic, next only to insulin in the minds of its recipients, for it combined greatly increased well-being with escape from the miseries of an endless low carbohydrate diet.

The carbohydrate component soon escalated, and a typical diet prescribed by the Canadian physician Israel Rabinowitch in the mid-1930s might contain 2,230 calories, 400 g of carbohydrate, 50 g of fat and 70 g of protein, with 67% of energy derived from carbohydrate [20]."

Meanwhile, in the interest of showing both sides, a vegan site says this is a good thing:

https://www.wholefoodplantbaseddiet.com/tag/dr-i-m-rabinowitch-and-diabetes/#footnote_1_6199

In a seminal paper published in 1935 2 , Dr Rabinowitch demonstrated that simple dietary changes (increasing the ratio of complex carbohydrates while reducing calorie intake) could reverse type 2 diabetes.

In his summary he states:

“I believe that in the data presented here there is incontrovertible evidence that the high carbohydrate-low calorie diet is more effective in controlling diabetes than all other methods of treatment hitherto reported…it is, therefore, more economical from the point of view of the cost of insulin…”

https://www.crossfit.com/health/ancel-keys-cholesterol-con-part-4

Dr Tim Noakes:

In a previous column (3), I described how already in 1950, John Gofman, MD, had formulated the diet-heart and lipid hypotheses (4) two years before Keys would commandeer the ideas as his own.

Gofman posed as a double challenge for Keys and his future disciples. First, Gofman was far more qualified than Keys to undertake research into the dietary and other factors causing heart disease. But perhaps more importantly, Gofman’s diet-heart hypothesis gave equal weight to dietary fats and dietary carbohydrates as the factors driving atherosclerosis and the development of CHD.

According to Gofman:

What is solidly established is that the Sf° 20-400 lipoprotein levels [i.e., blood triglyceride or VLDL concentrations] on the average, can be raised by increasing the dietary carbohydrate intake and can be lowered by decreasing it. … Furthermore, many individuals who are characterized habitually by some type of error in their metabolism that makes their Sf° 20-400 lipoproteins habitually extremely high will experience a marked reduction in the blood levels of these lipoproteins when the carbohydrate intake is lowered. (5, p. 123, my addition)

Gofman continues:

These same lipoproteins are essentially unaffected, in the average case, by changing from animal to vegetable fats. This information is extremely crucial, for in many individuals the risk of coronary heart disease comes primarily from the Sf° 20-400 lipoproteins [VLDL or triglycerides]. For such individuals, any attempt to lower heart attack risk by shifting from animal fat to vegetable fat in the diet would be illogical. There would be no reason whatever to expect any benefits since one would be changing the diet in a manner directed toward affecting the Sf° 0-20 [LDL] lipoproteins, which is not the problem at hand for these persons. For such individuals, the preventive efforts would have to be directed toward lowering the carbohydrate intake, which will, on the average reduce the Sf° 20-400 lipoprotein levels. With respect to the effect of carbohydrates on the Sf° 20-400 lipoproteins, it is a matter of the amount of carbohydrate that is eaten rather than the total number of calories ingested. For example, if one maintains individuals at exactly the same number of calories per day, so that they do not alter the weight in any way, but takes out some of the carbohydrates in their diet and replaces them by vegetable oil, one finds that the Sf° 20-400 lipoprotein levels will fall. Achievement of this result of lowering the Sf° 20-400 lipoproteins requires neither any alteration in caloric intake nor any alteration in body weight. (5, p. 124, my additions and emphasis)

Subsequently, in 1958 Gofman pointed out a key logical flaw that has since been ignored (6). He noted that a number of studies had found increasing the dietary intake of vegetable oils produced a fall in blood cholesterol concentrations, and this has been interpreted as beneficial. But the addition of vegetable oils also reduced total carbohydrate intake, and since carbohydrate increases the Sf° 20-400 lipoprotein levels, which contain approximately 13% of cholesterol by weight, the shift from a higher- to a lower-carbohydrate diet might be the real reason why increasing the intake of vegetable oils causes a reduction in blood cholesterol concentrations.

Thus, Gofman warned: “No consideration was given by them to the possibility that the lowering of cholesterol levels might have been the result of the simultaneous removal of a large amount of carbohydrate from the diet” (6, p. 277).

Gofman next describes the effects of a low-carbohydrate (100 g/day) diet in a 65-year-old male subject with a previous myocardial infarction (Figure 2).

Figure 2: The effects of a low-carbohydrate diet in a myocardial infarction survivor. Note the low-carbohydrate diet produced a very large decrease in the Sf° 20-400 lipoprotein levels, now known as the VLDL-lipoproteins, which transport predominantly triglycerides. Total blood cholesterol concentration was unaffected by this dietary change. Despite this, the patient’s atherogenic index (AI) had fallen, placing him in a more favorable metabolic state according to Gofman’s understanding. Reproduced from data on Table V in reference 6, p. 279.

As Gofman wrote: “It can be seen from these data that a massive fall in the serum Sf° 20-400 lipoprotein levels occurs on the low-carbohydrate diet, without significant changes in the Sf° 0-20 lipoprotein levels. Accompanying this fall in lipoproteins is a highly marked and favourable reduction in the atherogenic index value” (6, p. 278-279).

Thus, the real originator of the diet-heart and lipid hypotheses stated that a low-carbohydrate, high-fat diet can be used in persons with established coronary atherosclerosis, presumably to reverse that disease.

He continued:

These same principles of carbohydrate restriction have been applied successfully in several types of extreme derangement of lipoprotein level control of the Sf° 20-400 lipoprotein class, namely, in xanthoma tuberosum, essential hyperlipidemia, and in diabetes mellitus … . For such a [post-myocardial infarction] patient, it is quite clear that management of the problem of coronary disease by dietary means involves the use of a low-carbohydrate diet, and not a low-fat, high-carbohydrate diet which is so often prescribed when attention is not paid to the lipoprotein findings. (6, p. 279-280, my emphasis)

The importance of this is that this evidence anticipated Peter Kuo’s “discovery” of carbohydrate-sensitive hyper(tri)glyceridemia (7) and its reversal with a low-carbohydrate diet by nine years (Figures 6 and 7 in reference 8).

In his conclusions Gofman wrote:

The increase in risk of future myocardial infarction associated with elevation of lipoproteins of the Sf° 20-400 lipoprotein classes provides the basis for a rational application of dietary measures in this disease … . Dietary carbohydrate intake is a prime factor controlling the serum level of the Sf° 20-100 and Sf° 100-400 lipoprotein classes. Restriction of dietary carbohydrates can provoke marked falls in the serum level of these lipoproteins … . The serum cholesterol measurement can be a dangerously misleading guide in evaluation of the effect of diet upon the serum lipids … . Rational management of patients with coronary heart disease or of individuals attempting to avoid coronary disease depends upon knowledge of the lipoprotein distribution in the individual patient. (6, p. 282-283)

Elsewhere Gofman wrote: “Neglect of [the carbohydrate factor] can lead to rather serious consequences, first in the failure to correct the diet in some individuals who are very sensitive to the carbohydrate action; and second, by allowing certain individuals sensitive to the carbohydrate action to take too much carbohydrate as a replacement for some of their animal fats” (9, p. 156-157).

In one of his last publications, a 1960 editorial, he again emphasized his concern about the carbohydrate factor:

Several investigators have shown that a low-fat high-carbohydrate diet produces opposite trends in the blood cholesterol and the blood lipid levels. The cholesterol level falls because the low fat diet depresses the level of the cholesterol rich Sf° 0-20 lipoproteins. The triglyceride level rises because the high carbohydrate intake elevates the level of the triglyceride-rich Sf° 20-400 lipoproteins. Both the triglyceride-bearing and cholesterol-bearing lipoproteins have been associated with the development of coronary disease. It therefore behoves the physician utilizing the dietary approach to understand the likelihood that a focus on the fat intake without an appreciation of the effect of carbohydrate intake will not lower all the blood lipids associated with the development of coronary heart disease. (10, p. 83)

Blood lipids and human atherosclerosis

page 213

The Eskimo used to hunt only what he needed--bear, seal, caribou.

The little foxes--Tiriganiak--he despised. In the old days the Copper Eskimo hardly recognized the existence of the fox. If he met one on the trail he might risk an arrow on him, just to try his skill, but never because he wanted the animal. Fox meat makes poor eating, and fox fur is too frail for anything but baby clothes.

But fashionable women in Paris and New York did not share the Inuk's contempt for the fox. They regarded Tiriganiak's silvery fur as a perfect complement to their gleaming shoulders. What women want, men will get, and so the white man came to the Arctic after foxes and dinned into the Eskimo's ear the value of fox pelts.

"Do you want a rifle, eh, Inuk? Ammunition? Then go and get us foxes, plenty of foxes. Plenty of foxes."

The Eskimo wanted the white man's rifle, steel knife, fish net, boat. So he went after foxes. And soon he found he was so busy getting the miserable little animals that he had no time left in which to hunt for real meat--for bear and caribou. Observing the white traders, he saw them eating bread and jam, and tea with sugar. The new food was no good. It had no taste, and certainly didn't stay with one on the trail. But the Inuk wanted to imitate the Krabloonak. He ate the white man's sugar, and soon it became a habit. He found that he could not do without it. 

"Sugar!" he says. "The Eyebrows offered it to us for nothing, just to try, and we threw it away. The taste of that sand was so bad. Now we have got to like it, but they no longer give it to us. They sell it, and dearly. Mamianar! Calamity!"

Systematically, the white traders ensared the Eskimos, making them slaves to commodities of which they had felt no need before the Eyebrows came, unnecessary luxuries such as flour, silk, sugar, even chewing gum. All these things the Inuit paid for--by giving up his healthy, free life in exchange for trivial luxuries. He ceased to be a hunter, in many cases, and became a trapper, a slave to the little foxes he despised. Thus Tiriganiak--the smallest of all--revolutionized the Eskimo's life, at least the lives of those Eskimos close enough to the traders' posts to come under their influence.

Not too long ago, all Eskimos hunted to clothe and feed themselves. Now they go after foxes, with which to buy some jam, or a Micky Mouse watch, or a cheap, tinny-sounding phonograph. They haven't time to hunt fo seal to provide oil for their lamps, so they buy the white man's kerosene. More foxes. There is no caribou meat on hand, so he eats the white man's flour. More foxes. Soon he lives in a vicious circle, like a knifegrinder's dog in his wheel cage.

Thus, in those areas where the traders hold sway, the happy hunter of old has become a kind of clerk. Once fierce and independent, ignoring tomorrow and contemptuous of anyone who mentioned it, now he is always in debt, as badly off as a petty office worker caught in the clutches of the race-track bookmaker. Once his life was diversified--today hunting, tomorrow sealing, the next day fishing--whatever satisifed the whim of the moment. Now he must turn all his energies toward the capture of the fox. And the supreme irony, of which he is aware, is in the fact that he, the Agun, the male, must outstrip himself to satisfy the desires of the scorned Arna--the woman. And the Krabloonak's woman, at that.

Along the coast, noawadays, one often hears from the Eskimos a bitter, disillusioned cry. "Kakertogot taima"..."We are always hungry now."

Of course they were hungry. The Eskimo is a carnivore. His body craves meat--seal, bear, caribou, fish--and the climate and his hard life aren't satisfied by anything else. Half a grapefruit and a couple of pieces of toast are not the breakfast for the Inuk at all, but for another class of people.

Yet the Inuk counts on the little foxes to provide his sustenance all the year round, and sometimes the foxes don't turn up. Then he's in trouble. Then there is famine. And it is usually too late before the Inuit resign themselves to going out on the ice after seals, as they should have done early in the winter. They starve. At Coppermine, in 1948, for example the whole Eskimo colony kept alive only by eating old skins, boots, and other rubbish--and this not fifteen miles from a white man's settlement.

You might blame the traders themselves, and it is true that some are mightily unscrupulous, but it is not the individuals who should be blamed, but the system, and the government that encourages it. I am told that such tragedy is not known among the Eskimos in Greenland, under Danish rule, though it matches the colonial pattern elsewhere--in the sugar islands of the Caribbean, for eample, where the natives were persuaded to forego their food crops in order to plant sugar cane, and where starvation results when the sugar crop is poor or when the market drops and the price breaks. 

The Eskimos have never heard of the seven lean kine. A trapper may bag three hundred foxes in one year and three the next, but it never occurs to him to store provisions against a bad season. Of course, we must blame him for his improvidence. But must we not also blame the white men who profit vilely from the Eskimo's ignorance, who take advantage of a good fox season by importing diamond rings, gold watches, silk dresses, chronometers, and similar goods? Of what use is a diamond ring to a woman who's going to wear it for cutting seal blubber, if she's lucky enough to have a seal to cut up? What good is a chronometer, complete with sweep second hand, to a man who doesn't care a whit for time? Of what use is a silk dress under a greasy caribou parka?

With melancholy one must watch a venal civilization displace the old Eskimo style. The white man is as devious as Sila. He takes much, and gives little. He talks big, and the rewards look inviting, but when the season is over he has the foxes and what has Inuk?

An empty belly. A forlorn view of the future. The precious watch will soon be opened to see what makes it tick and ruined by snow or water. The elegant dress will soon because a greasy snot-stained rag. The diamong ring will not be worn long before it is lost down a seals' hole. Alas!

The following is a chapter from the book Diet Prevents Polio written by Benjamin P. Sandler, M.D., and published in 1951, at the height of the polio epidemic. Dr. Sandler received his degree in medicine at New York University in 1931. He interned at Morrisania city hospital in the Bronx, New York and later was on the staff there as well as Polyclinic and Montefiore hospitals in New York City. From July, 1941, until February, 1947, he was in the U. S. naval medical corps, attaining the rank of commander. He has done considerable research in polio and the relationship between diet and disease. He has published six papers on the latter subject, as well as papers on other medical subjects including research on glucose and tuberculosis. His research includes a period assisting the research staff at Willard Parker hospital in New York City during the epidemic there in 1931, and independent research later, when he “gave” polio to a rhesus monkey, transmitted it to a rabbit, and then to another monkey. 

Diet Prevents Polio by Benjamin P. Sandler, M.D., and published in 1951 by the Lee Foundation for Nutritional Research, Milwaukee, WI 

Chapter 2: Low Blood Sugar and Susceptibility to Polio 

During my research I observed a large number of patients who had symptoms that were caused by low blood sugar. They complained of the symptoms previously described, namely: 

• headache

• dizziness

• weakness

• fatigue

• abdominal pain

• nervousness

• palpitation

• frequent sweats

• occasional fainting spells 

Most of these patients were malnourished, which, physiologically, meant subnormal liver glycogen storage. Their diet was deficient in protein and consisted largely of the cheaper starchy foods. 

I noted that these patients also had poor resistance to infections such as colds, sore throat, grippe, influenza, bronchitis, and pneumonia. By increasing the protein content of their diet and by reducing the sugar and starch content, they improved considerably. They became stronger, more vigorous and buoyant, and had fewer infections. 

A few of these patients had had polio in childhood. Observations of these patients over a long period of time led me to suspect that their susceptibility to infection was possibly due to their poor diet with its high sugar and starch content.  

Their increased resistance to infection with a better diet confirmed this suspicion. It then occurred to me that their susceptibility to polio could be explained on a similar dietary basis. 

Specifically, I suspected that children and adults contracted polio because of low blood sugar brought on by a diet containing sugar and starch. 

I reasoned that the polio virus was able to cross tissue barriers, reach the brain and spinal cord, invade the nerve cells, damage or destroy them and cause paralysis. And I further reasoned that if the blood sugar never fell below 80 mg polio could never result. I suspected that during a polio epidemic only those children and adults who experienced periods of low blood sugar would contract the disease and that those individuals who were in actual contact with the virus but who maintained normal blood sugar levels would not contract the disease. Thus, it remained to prove that low blood sugar could be a factor in susceptibility to polio. And, after this had been proved, the following questions had to be answered: 

• What causes low blood sugar in humans?

• How can low blood sugar be prevented?

The prevention of low blood sugar would thus mean the prevention of polio. Before describing the experiments performed, I should like to make a preliminary summary and state without reserve that: 

1. 1. Low blood sugar is a factor of susceptibility to polio. 

2. 2. Low blood sugar occurs frequently in children and adults and is caused chiefly by a dietary error, namely, the consumption of sugar and starch 

3. 3. Correction of this dietary error will prevent low blood sugar and thus prevent polio. 

An experimental method to prove that low blood sugar was a factor of susceptibility to polio was readily available. In 1938, the only laboratory animal that could contract polio by experimental inoculation was the monkey. All other laboratory animals were completely resistant to the polio virus. The rabbit is one of these resistant animals. Without knowing the blood sugar range in the monkey and rabbit, it was suspected that the blood sugar in the monkey reached lower levels than in the rabbit. These suspicions were found to have a basis in fact through the investigations of Drs. Jungeblut and Resnick of Columbia University who studied blood sugar levels in monkeys, and through the investigations of Drs. du Vigneaud and Karr of Cornell University who studied blood sugar levels in rabbits. In monkeys, blood sugar values as low as 50 mg. were observed, whereas in the rabbit, values below 100 mg. were never observed. In numerous determinations made on rabbits I have never obtained values below 100 mg. It was therefore concluded that the susceptibility of the monkey to the polio virus was due to the fact that its blood sugar fell to subnormal values, and that the resistance of the rabbit might be associated with the fact that its blood sugar never fell below 100 mg, and that at this concentration cellular oxidation of glucose in the nervous system and other organs would be maintained at such a level as to enable the cells to protect themselves against invasion by the virus. Physiologists have stated that the normal blood sugar level of 80 mg. holds true for all mammals. The next step was to lower the blood sugar of the rabbit to subnormal values with insulin injections, and then inoculate the rabbit with polio virus. This was done and it was found that the rabbits became infected and developed the disease. The details of these experiments were published in the American Journal of Pathology, January, 1941. Some rabbits showed signs of infection 8 to 10 hours after inoculation. I wish to stress this short period of incubation in the rabbit because it demonstrates that polio can develop in a short period of time. This is important, as we shall learn later, when we discuss the onset of polio in humans within 24 hours after severe physical exertion. The rabbit is also resistant to the dog distemper virus. One of the largest research laboratories has conducted much research with this virus and when I informed the members of the staff about my success in inoculating rabbits with polio virus after  lowering the blood sugar, they inoculated rabbits with the dog distemper virus after insulin and reported to me that they observed signs of infection in the rabbit for the first time. This corroborating experiment indicates that low blood sugar may cause susceptibility to many infections. I was thus satisfied that low blood sugar was a factor of susceptibility to the polio virus in monkeys, and that rabbits could be rendered susceptible after their blood sugar was lowered with insulin (Insulin, as you probably know, is the hormone which diabetics inject into themselves in order to keep their blood sugar within normal range. It is a quickacting drug and can lower the blood sugar within an hour or so after injection). I concluded that the concept that low blood sugar created susceptibility to polio in both monkeys and rabbits could be applied to humans as well. What Causes Low Blood Sugar in Humans? The next step in the solution of the polio problem was to find out the causes of low blood sugar in humans. Fortunately the answer to this problem was already at hand. It has been found that the consumption of sugar and starch and foods containing these substances were the chief causes of low blood sugar. When patients drank a solution of pure glucose they had a period of low blood sugar which began one to two hours after the glucose was taken and which lasted for one to two hours, and longer. This study of the blood sugar is called the "glucose tolerance test" and is employed for the detection of hypoglycemia or hyperglycemia. When they ate a meal containing sugar and starch they also had periods of low blood sugar which came on an hour or so later and which lasted for from one to two hours. The low blood sugar was more marked and lasted for a longer time after the glucose solution than after a meal containing starch. It is an established fact that this paradoxic depressant effect on the blood sugar level is more readily exerted by sugar than it is by starches. I have observed these results in hundreds of cases and similar results have been obtained by other investigators. It is a surprising paradox: the more sugar (and starch) you eat, the more likely you will develop low blood sugar. Drs. E. P. McCullagh and C. R. K. Johnston have shown how the glucose tolerance test is readily influenced by diet. Thus the second problem: What can cause low blood sugar in the human? was solved. How Can Low Blood Sugar be Prevented? The third problem, "How can low blood sugar be prevented?" was the only one left and this, too, was readily solved. It had been found by other investigators that a meal consisting of protein, fat, and carbohydrates, but with no sugar or starch, NEVER caused low blood sugar. The addition of sugar and starch to such a meal could readily produce low blood sugar. Thus I arrived at a simple formula for preventing polio: eliminate from the diet sugar and foods containing sugar, and reduce the consumption of foods containing starch. Since eating sugar and starch during a meal may cause low blood sugar after one to three hours, and since elimination of sugar and starch prevents low blood sugar, the invasion of the body by the polio virus will be prevented by a diet containing no sugar and no starch. Protection against polio would thus begin on the very day such a diet was started and protection would last just as long as such a diet was adhered to. I have found that a diet completely free of sugar and starch and consisting of proteins, fats, and non-starchy vegetables: May be adhered to for years with beneficial effect and absolutely NO harmful effect. There is NO supporting evidence to indicate that sugar and starch are necessary for health or for energy purposes.

 The human is a carnivore and can thrive on protein and fat alone, if necessary. The Eskimos thrive well on meat and fish which yield only protein and fat, and polio is unheard of among them.  American and European explorers in the Arctic regions have lived on meat and fish for as long as 18 months and have maintained perfect health all the time on such a diet. Vilhjalmur Stefansson, the Arctic explorer, has described his existence on such a diet in great detail. He states that he was in perfect health on such a diet which consisted of protein and fat alone. 

Eskimos who live on meat and fish are not susceptible to infectious diseases. They do become susceptible when they live amongst white men and eat the white man’s diet with its sugar and starch. It is true that the Eskimo’s fresh contact with the white man exposes him to infectious diseases to which he (the Eskimo) has not had the opportunity to become immune. The presence of sugar and starch in the Eskimo's new diet is of greater significance. A US public health officer stationed in Alaska has blamed this dietary factor for the great susceptibility of the Eskimo to tuberculosis. A low carbohydrate meal elevates and stabilizes the blood sugar levels. This stabilizing effect is important because some of the symptoms of low blood sugar are due to rapid fall in blood sugar level which accompany wide fluctuations in blood sugar levels following the ingestion of sugar and starch.