Vitamin News: Poliomyelitis As A Deficiency Disease

The resemblance of poliomyelitis to beriberi has been recently remarked by McCormick.¹ He suggests that the paralysis of polio may be directly due to vitamin B1 deficiency, and that a virus infection of the nervous tissue involved should be suspected.

As far back as July 9th, 1916, the possible deficiency background of poliomyelitis was suspected by Professor Simon Baruch, who may be quoted: “There is a striking similarity in some of the causes predisposing to infantile paralysis and beriberi. Both occur chiefly in overcrowded localities, in hot weather, and more among males than females. Both are accompanied by fever and paralysis, and both are extremely fatal. Both have prevailed as epidemics, and their fatality has caused terror and despair.”

“Beriberi was formerly regarded as an infectious disease from undiscoverable sources, but is now known to be due chiefly, if not solely, to absence of vitamins in the diet.”

“May not infantile paralysis, which has eluded thus far the most searching investigations, be likewise traceable to some defect in diet that may be discovered? “

“It is not a new idea that beriberi, as well as polio, may develop from an infective agent. In fact, many early experimenters isolated various bacilli from the tissues of beriberi patients and reproduced definite symptoms of beriberi by injecting the cultures into test animals.”² If a virus were present and acted as the real causative agent as a contaminant of invisible nature in each case, it would account for the wrangle among the different early investigators, each of whom were sure that their own variety of bacteria was the cause of the disease, and which disagreement resulted in the abandonment entirely of the whole idea on an infectious cause, and the establishment of the deficiency theory.

Tuberculosis today is accepted as an infectious disease, which has as a primary cause, lowered resistance secondary to malnutrition. Originally, when the bacterial nature of the immediate cause was first discovered, it was assumed that the immediate cause was the primary cause.

In beriberi, it is quite possible that the infective cause has still to be identified, as our knowledge of virus diseases is in its infancy. But in the case of polio, it is pretty well established today that it is actually a virus disease. Burnet tells us that carriers are known (usually children) who are apparently healthy, but continually excrete polio virus by the faecal route.³ This virus then acts to infect susceptible individuals.

The next question is, “Why does the victim become susceptible?” We may find clues in the behavior of other virus diseases, for example, herpes simplex, also discussed by Burnet. This virus is known to continually exist in the patient’s body throughout life, once the subject is inoculated, and the antibody is found in the blood of a constantly higher percentage of patients tested in increasing age levels.

Now it is definitely known that the symptoms of herpes simplex are never exhibited unless the patient has a lowered content of calcium in his tissue fluids. Factors that increase blood calcium at the expense of tissue fluid calcium aggravate herpes: simplex, and factors that accomplish the opposite quickly eliminate herpes simplex. (Vitamers D and F, respectively, accomplish this–D increases blood calcium content and F vitamin reduces it by diffusion into the tissues. These effects are supplementary, rather than antagonistic, and natural sources of vitamer D, such as fish oils, are known to carry definitely active components of the F vitamer. The normal action is for the vitamer D to accelerate intestinal calcium absorption by the blood stream, and for the vitamer F to unload the cargo at the destination.)⁴ The effect of the D without F is usually an aggravation of herpes.

Doctors Reese and Frisch (of Madison, Wisconsin) have promoted a theory that polio virus often enters the subject through tooth cavities, offering as evidence the fact that in a survey of 272 polio victims, cavities were present in 2.6 times the number of a comparable group of non-infected persons. Further, that in communities having fluorine enough in the water to reduce tooth decay to 75% of normal, polio incidence was 22 to 34% less than usual.

This evidence, however, may also be adduced to mean that where more calcium was metabolized, there was not only less tooth disease but less polio, for natural fluoridated water contains calcium fluoride.

Dr. McCormick points out that the demineralization of flour by the roller mill was to be suspected as a major cause of polio. In fact, he points out that the first roller mill to manufacture white degerminated flour was set up in Vienna in 1839, and the first case of polio reported was found there in 1840.

The effect of muscular exercise in precipitating an attack of polio is also explainable, in that the muscle sugar reserves burned up thereby are held as phosphagen, and loss of the sugar component releases phosphorus ions which, in turn, can combine with the diffusible calcium bicarbonate moiety, and lower the diffusible calcium of the tissue fluids below the critical point. This form of calcium seems essential to the control of virus activity.

At this moment it is important that we grasp the full significance of the concept of tissue reaction to malnutrition, by which the receptivity to specific agents is produced. Crotti, in his lifetime study of goiter and thyroid disease, looked for and seems to have unquestionably found a specific micro-organism that exists in all goiters, and which causes goiter, if injected into healthy thyroids. But the presence of this organism does not preclude the accuracy of the conclusion that all goiter is a consequence of deficiency. Crotti found that he could cure goiter with bichloride of mercury about as easy as with iodine.⁵ That certainly does not justify the treatment of goiter with this drug; in similar fashion, malnutrition consequences in general may be successfully treated by various substitutes for the physiological remedy, and medical science has not fully awakened yet to its obligation to see that such mistakes are not too common. A good example of such a mistake is the treatment of infective diseases with sulfa drugs, which accomplish their effects solely by drawing into the blood stream vitamin C, which thereby stimulates the phagocytic elimination of the micro-organisms. It is obvious that the use of sulfa drugs is made necessary only by a deficiency of the vitamin, and a too great deficiency in a patient will cause a failure of the drug, and instead of recovery, death will follow. The vitamin could never cause harm, and should be given first, and the sulfa used only as a last resort.⁶

 

References Cited:

1. McCormick, W. J., M.D., Medical Record, February 4, 1942.
2. McCarrison, Studies in Deficiency Disease, Oxford Press, 1921. 
3. Burnet, F. M., Virus as Organism, Harvard University Press, 1945, p. 60.
4. “Calcium Metabolism,” Lee Foundation for Nutritional Research, Milwaukee, Wisconsin, Report #3.
5. Crotti, Andre, M. D. Diseases of the Thyroid, Parathyroids, and Thymus, Lea & Febiger, 1938.
6. Vitamin News, Vitamin Products Company, Milwaukee, p. 154.