classical symptoms
Home

Stephen Cooter found that the description of an acute polio virus infection is almost identical to vitamin B1 deficiency caused damage, Beriberi. This is commonly caused by dextrose and alcohol as well as eating white rice. DrMcCormick pointed out that the first case of polio was reported in Vienna one year after roller-mill white flour was first sold there. He calls poliothe form of beriberi that follows the use of de-germinated flour.

Polioencephalomalacia, thiamine deficiency, or PEM is a neurological problem seen in ruminants that is due to a lack of thiamine (B1) to the brain resulting in brain swelling and pressure necrosis of brain tissue.  Caused most often by diet changes that alter gut flora populations so that the new gut bugs produce a thiaminase that deactivates the dietary thiamine. Thiamine is indispensable for the vital functioning of the brain if thiamine is unavailable or its required level is decreased, the brain cortex degenerates.  http://www.saanendoah.com/basicme3.html

Klenner, Southern Medicine & Surgery, April, 1951
"... review[ing] the findings of McCormick in 50 confirmed cases of poliomyelitis in and around Toronto, Canada, during the epidemic of 1949...families eating brown bread who came down with poliomyelitis did not develop paralysis; whereas in those families eating white bread many of the children having poliomyelitis did develop paralysis. The point here is that brown bread has 28 times more vitamin B1 than does white bread. Obviously, then, the paralysis which complicates acute poliomyelitis appears to be due to aB1 avitaminosis." http://www.seanet.com/~alexs/ascorbate/

Paralytic Polio Linked To Vaccinations

 

"The early triple vaccine against diphtheria, whooping cough and tetanus had also been shown beyond doubt to cause paralytic polio in some children to whom it was administered. The incidence of polio in children recently vaccinated against diphtheria was statistically greater than in unvaccinated children, symptoms showing in the vaccinated limb within 28 days of the initial injection. This scandal broke in Britain during 1949, an epidemic year for polio, other reports soon following from Australia. Papers dealing with this topic are plentiful. One, British, gives details of 17 cases of polio which followed 28 days or less after various injections. (129) Another, Australian, gives details of 340 cases of polio, 211 of which had been previously vaccinated against whooping cough and/or diphtheria. Of these, 35 had been vaccinated within the preceeding 3 months and a further 30 within the previous year. (130) Dr. Geffen reported similar findings from the London Borough of St. Pancras, where 30 children under the age of 5 developed polio within four weeks of being immunized against diphtheria or whooping cough or both, 'the paralysis affecting, in particular, the limb of injection. In 7 other recently vaccinated cases,
paralysis occured but not in the limb that had received the injection'. (131) Two medical statisticians at the London School of Hygiene and Tropical Medicine examined these reports and concluded that:

 

"'In the 1949 epidemic of poliomyelitis in this country cases of paralysis were occuring which were associated with inoculation procedures carried out within the month preceding the recorded date of onset of the illness'. (132)

 

"Dr. Arthur Gale of the Ministry of Health reported 65 cases from the Midlands, where paralysis followed about two weeks after an injection; in 49 of these, paralysis occurred in the injected limb. (133) Then it was reported that of 112 cases of paralysis admitted to the Park Hospital, London, during 1947-1949, 14 were paralyzed in the limb which had received one or more of a course of immunizing injections within the previous two months. In the majority of cases, the interval between the last injection and the onset of paralysis was between 9 and 14 days. Again, combined whooping cough, diphtheria and tetanus injections were involved. This outbreak of polio followed an intensive immunization campaign during that time, 1947-49. (134) Following these findings, the Ministry of Health recommended that diphtheria and triple vaccines should not be used in areas where polio was naturally present. From that time onwards, the incidence of paralytic polio decreased rapidly in Britain, even prior to the advent of Salk vaccination..."

(Bill Bingham, Diphtheria - Part Two, The Campaigners' Handbook: The Infectious Diseases series, National Anti-Vivisection Society, 261 Goldhawk Rd, London W12 9PE, England, May 1988.)

"The medical profession has been aware of the damaging effects of vaccines on the immune system since their introduction. For example, the ability of pertussis and DTP vaccines to stimulate the onset of paralytic polio was first noted in 1909. In every polio epidemic since then DTP injections have caused the onset of polio disease.

"In 1950, two careful studies were conducted in the state of New York to evaluate the reports of an association between the onset of paralytic polio and recent injections. Investigators contacted the families of all children who contracted polio during that year, a total of 1,300 cases in New York City and 2,137 cases in the remainder of New York State. A history of vaccinations received in the previous two months was obtained on each child and from a group of matched controls in the same population. Those studies discovered that children with polio were twice as likely to have received a DTP vaccination
in the two months preceding the onset of polio than were the control children (Korns et al., 1952; Greenberg et al., 1952).

"The association of vaccines with the onset of polio continues in the modern age. During a recent polio epidemic in Oman, DTP vaccination again caused the onset of paralytic polio. In that epidemic, 70 children 5 to 24 months old contracted paralytic polio during the period 1988-1989. When compared to a control group of children without polio, it was found that a significantly higher percentage of these children had received a DTP shot within 30 days of the onset of polio, 43 percent of polio victims compared to 28 percent of controls (Sutter et al., 1992). The DTP vaccine suppresses the body's ability to fight off the polio virus."

(Dr Randall Neustaedter, The Vaccine Guide: Making an Informed Choice, North Atlantic Books, 2800 Woolsey Street, Berkeley, California 94705, United States, 1996. Neustaedter's web site at www.healthy.net/vaccine, which contains a forum for vaccine questions.)


References to NAVS article:

129. Martin, J.K. 1950. "Local paralysis in children after injections" Arch. Dis. Childhood, March 1950, pp 1-5.

130. McCloskey, B.P. 1950. "The relation of prophylactic inoculations to the onset of poliomyelitis". Lancet, April 8th, pp
659-663.

131. Geffan, D.H. 1950. "The Incidence of Paralysis Ocurring in London Children Within Four Weeks After Immunisation".
Medical Officer, April 8th, pp 137-140.

132. Bradford Hill, A., Knoweldon, J. 1950. "Inoculation and Poliomyelitis". BMJ, July 1st, pp 1-6.

133. Gale, A.H. 1950. Daily Express, April 10th.

134. BMJ., July 29th, 1950.

Sugar Increases Polio Risk -- Lessons For Other Viral Infections


http://www.mercola.com/article/Diet/sugar/polio_sugar.htm

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.

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

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.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 quick-acting 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 manís diet with its sugar and starch.  It is true that the Eskimoís 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. Diet Prevents Polio, by Benjamin P.  Sandler, M.D., and published in 1951 by The Lee Foundation for Nutritional Research, Milwaukee, WI

 Back to page