Iodine: Its Use in the Treatment and Prevention of Poliomyelitis and Allied Diseases

By J.F. Edward, MD

Summary: Writing in a Canadian medical journal, this physician gives voice to his observations on the role of iodine in the prevention of viral disease and “central nervous system fevers” such as polio. From Manitoba Medical Review, 1954. Lee Foundation for Nutritional Research reprint 76.

[The following is a transcription of the original Archives document. To view or download the original document, click here.]


Iodine: Its Use in the Treatment and Prevention of Poliomyelitis and Allied Diseases

According to British law, an individual is innocent until proven guilty. [Let us apply] the same legal dictum to poliomyelitis. Its cause was adjudged between 1905 and 1911 to be contagious and infectious—this in the absence of a knowledge of its cause of spread; its only proven crime being that it could become epidemic. It was declared to be viral in origin.

This implication by the public health laws of many of the provinces of Canada and of the States of the Union made poliomyelitis legally an infectious, contagious disease and thereby opened the door for research considering the disease as such and closed the door to research along lines other than [the one] that has been publicized and financed by endowment for the past forty years.

This situation finds the medical profession, in this year of our lord 1954, in a position to declare, “We have no treatment for poliomyelitis.” Truly, nursing care has improved—dating from the initiation of the Kenny Method of therapy—but methods of treatment or prevention of the disease are conspicuous by their absence.

Viewing the disease from a clinical standpoint, one notes in Manitoba’s epidemics of 1952 and 1953 the following:

  1. Few of our cases had a history of contact with an earlier case.
  2. Few of our cases transmitted the disease to family contacts.
  3. Few of medical personnel in attendance on polio patients acquired the disease or transmitted it to their families.
  4. A state of fatigue frequently preceded the [victim’s] attack, yet many medical personnel working with these patients to a point of their exhaustion did not fall victim to the disease.
  5. The disease is seasonal and may be geographical.

Animal experimentation has truly shown the disease to be transmissible, but no single means of transmission in the human animal has been proven.

The fact that polio is a seasonal disease that occurs in late spring and summer places it in a class apart from practically all other infectious diseases, which are most prevalent in those seasons in which humans are confined within doors and congregate in groups. And the fact that [polio] epidemics fall off with the advent of cool fall days and nights leaves one to consider whether the then existing protection is not linked with body function—probably with stimulation of thyroid function.

An overall geographic picture of epidemics would place Winnipeg as the Canadian polio capital and St. Louis the American capital. A similar map drawn for encephalitis in horses would correspond favorably with the polio map.

Viewing the problem of spread from the geographic angle, one is not a little surprised to see it compares favorably with our goiter area. Could iodine deficiency link in with polio’s so-called infection? Assuming this to be a fact—and after confirming the assumption in animal virus diseases—I treated in 1952 three Bulbar polio patients with intravenous sodium iodide. In these three control of the disease was found to be most rapid, and convalescence was surprisingly brief.

I was [before] that time convinced that iodides acted as a virucide, but the virucide theory was hardly tenable since the quantity used (7.5 grains) was hardly ample and the dosage was never given more than twice, and then three days apart. Further consideration and discussion brought forth from one of my confreres the suggestion that with the intravenous injection of iodide I was stimulating a defense mechanism, the iodides acting as a catalyst.

The 1953 epidemic was entered with this theory in mind. Numbers and the varying severity of the disease forbade intravenous therapy, so I administered iodides orally, depending on clinical examination for diagnosis, having concluded in 1952 that spinal puncture only added insult to injury with nothing gained.

The season advanced; gamma globulin stocks became exhausted, and my patients clamored for protection. Carrying the defense mechanism theory a step farther, [I reasoned], “If I could control, why could I not protect?” Of those seeking protection, I formed an experimental group, giving 1 to 3 minims, according to age, of ss potassium iodide in milk daily for ten days (equivalent to 1.7 to 5 grains KI).

The season finally ended. I had seen some sixty cases. Two were sent to King George Municipal Hospital because of the possibility of respiratory difficulties and lack of nursing care. The remainder were treated at home. Only one on home care developed paralysis—a paralysis that did not advance after oral iodide administration. None of 200 contacts on prophylactic therapy developed polio. There were no deaths.

Can this theory fit our endemic cases and our Eskimo group? I believe it may. These people may be so low in iodine requirement as to have little or no defense against the invader if such there be.

The use of iodide in the control of known virus diseases affecting the central nervous system is by no means new.

1. Manson, of England (1825), advocated its use in palsies, many of which cases must have been polio.

2. Coplan (1850) reports benefits in palsy derived from potassium iodide in dosages as small as 1 grain in 24 hours.

3. Brown-Sequard (1861) recommended potassium iodide as the only known remedy that could be used without danger for various forms of paraplegia.

4. Sinkler (1875) reported the treatment of an asthmatic with potassium iodide. The patient, who also had polio, improved with the therapy.

5. Elliott (1885) employed and recommended potassium iodide in combination with other medications for polio. Similar therapy was employed by Erb, Charcot, and Hammond.

6. Webber (1885) recommended [potassium iodide] use in polio.

7. Ridley (1925) employed tincture of iodine in the treatment of beriberi, a paralytic disease genetically related, according to Braddon (8), to poliomyelitis. Beriberi was at one time declared, like pellagra, to be a viral disease.

9. Sir Thomas Horder (1927) reported the use of colloidal iodine intravenously in the treatment of poliomyelitis. He recommended its early use.

10. Breuil and Dartiguenave (1937), after trial with chemotherapy failed for polio, reported improvement using iodine therapy.

11. Maberly (1939) reported complete recovery of four cases of polio on iodine therapy.

12. Mazzitelli (1939) gave a teaspoon of iodine-and-tannic-acid syrup twice a day for several days to children in families with cases of poliomyelitis or in contact with them. None of these children who had preventive therapy developed poliomyelitis in that epidemic or in future ones. (Syrupus iodo-tannicus contains 1 percent iodine.)

13. Scoby (1946) suggested the use of iodine in the prevention and treatment of polio, and (14) in 1948 pointed out that iodine combined with ascorbic acid and calcium produced improvement in some cases in 24 hours.

The present writer in 1944 discussed with Dr. Fahrni of Winnipeg the possibilities of using intravenous sodium iodide in polio. Dr. Fahrni was then using sodium iodide, 15 grains in 10 mL distilled water (Parke-Davis), intravenously in thyroid crisis. Dr. Fahrni assured me that if given slowly it would at worst do no harm. Not until 1952 did the opportunity arise to use it, with the previously recorded results.

15. In 1948 I reported to the Canadian Medical Association Journal a report of a number of experiments with iodine on humans and animals.

Iodine Therapy in Herpes Zoster

16. Head and Campbell (1900) described herpes zoster as “acute posterior horn poliomyelitis.” In this disease the anterior horn cells have not infrequently been involved and paralytic manifestations and atrophy have been observed. Epidemics of herpes zoster have been reported. These epidemics have sometimes paralleled polio epidemics.

17. Ruggles (1931) and (18) Beers (1939) reported early and dramatic relief of herpes zoster with intravenous sodium iodide.

19. Beckman (1953) approves the use of sodium iodide for herpes zoster—2 g in 30 mL water intravenously at two day intervals for four or five treatments.

Iodine in the Treatment of Encephalitis and Central Nervous System Diseases of Animals and Fowl

20. Lewitis (1935) states that iodides have been used with surprising results in cases of inflammation involving the spinal cord and brain.

21. Brinton (1931), a poultry man, reported that leg weakness in his flock following the feeding of excess wheat was cured with iodized buttermilk. Later, he prevented the leg weakness and also coccidiosis with said buttermilk.

22. Grey (1940) used a 10 percent solution of potassium iodide in distilled water in the treatment of fowl paralysis (lymphomatosis). After the first injection, the birds became brighter; after the second, muscular tone was restored and the birds rapidly progressed to normal.

23. Radeleff (1946) employed intravenous sodium iodide in the treatment of equine encephalitis. In his group so treated, the mortality rate was less than 10 percent, with no “dummies.” (Dummies are animals that survive but have permanent brain damage.) In his control group, the mortality rate was 40 to 50 percent. He reports rapid recovery and short convalescence in his iodide-treated group.

McLoughry, a Manitoban veterinarian, during the epidemic of encephalitis in the late 1930s and early ’40s, paralleled Radeleff’s findings. He employed potassium iodide. His success prompted my experiment reported in 1948 on the prophylaxis of equine encephalitis.

It is worthy of note that a number of workers, including (24) von Economo (1931), employed iodine in the treatment of human encephalitis with favorable results.

Last summer, Dr. Archie Kiteley of Nipawin, Saskatchewan, drew my attention to the fact that his area had no cases of human encephalitis during or since the epidemic years. This, he argues, may be due to the fact that in the early days, while we farmers were battling our stock breeding problems, he and his confrere Dr. Max Scott, recognizing the deficiency of iodides, prescribed sodium iodide in practically every prescription they wrote. Is it possible epidemics of polio were suppressed by this very means?

25. In an editorial in the Journal of the American Veterinary Association, the reports on the treatment and prophylaxis of equine encephalitis by Radeleff and myself are reviewed. In that editorial it is pointed out that (26) Holtman (1946) has made known his belief that there may be a relationship between the level of thyroid secretion and susceptibility to human poliomyelitis and encephalitis, due to the fact that these diseases occur in warm weather, when natural secretions of the thyroid are the lowest.

Within our midst we may shortly have definite information to prove or disprove Holtman’s belief. Dr. Brereton Sr. is finding some startling data on thyroid function in children. And Dr. Elliott is conducting a survey in those areas of Manitoba that the Department of Health supplies with iodides to prevent goiter to determine the incidence of polio in those children on iodides.

Comment

A summary is here presented of the uses of iodine in treating poliomyelitis and other central nervous system fevers in man, animals, and birds. Its use in polio is viewed with definite doubt by a large portion of the medical profession and with reason—for so many theories of therapy have failed, even our hopeful gamma globulin being questioned, not without reason.

My personal opinion is that iodine restores to normal a function, probably thyroid in origin, that produces a chain reaction of defense, and the patient is made to develop his own gamma globulin or its counterpart.

I do not ask you to accept my theory without reserve until I have delivered further proof. I am planning, should Manitoba have a polio epidemic in 1954, to place an experimental group of 10,000 [individuals] on prophylactic therapy. May I ask your sympathetic observation and your extension of the experiment if you see fit.

I am in my own mind convinced that iodine constitutes a prophylactic means against polio, and that its use in the treatment of polio tends to restore muscle tone early and reduces convalescence to a minimum. Its use as a prophylactic could be extended to large areas by using the present system employed by provincial health [institutions] in goiter areas. This would bring the “third halogen,” iodine, into the field of preventive medicine, along with chlorine and fluorine.

Appreciations

27. To Dr. R.R. Scobey, 1411 South Salina St., Syracuse, NY, I extend my appreciation. I have used his article in the Archives of Pediatrics (vol. 68, 1951) as my guide in tracing the medical uses of iodides in human therapy. I have indulged possibly in plagiarism in my quotations from his article. My only regret is that he does not quote his own cases. He may have been in a position not dissimilar to my own from 1944 to 1952, when I had no cases.

To Dr. Isa of the Veterinary Department of the University of Manitoba, I am indebted for the research of veterinary medical literature.

To Dr. Ormerod of the Manitoba School of Medicine, I am indebted for discussion and constructive criticism. He is responsible for the formulation of the protective mechanism theory.

To my best of all wives, I am indebted for her patience in reviewing my records and assisting in my experiments. Her observations were most valuable.

To my patients who submitted to experimental therapy, I am indeed indebted.

By J.F. Edward, MD. Reprinted from the Manitoba Medical Review, Vol. 34, No. 6., pp. 337–339, June/July 1954, by the Lee Foundation for Nutritional Research.

References

1. Manson, Alexander. Medical Researches of the Effects of Iodine in Bronchocele, Paralysis, Chorea, Scrofula, Fistula Lachrymalis, Deafness, Dysphagia, White Swelling, and Distortion of the Spine. London, 1825.
2. Coplan, James. On the Cause, Nature, and Treatment of Palsy and Apoplexy. Lea and Blanchard, Philadelphia, 1850.
3. Brown-Sequard, C.E. Lectures on the Diagnosis and Treatment of the Principle Forms of Paralysis of the Lower Extremities. J.P. Lippincott and Co., 1861.
4. Sinkler, W. Am. J. Med. Sc., 69:348–365, April 1875.
5. Elliott, G. Am. J. Med. Sc., 89:138–146, January 1885.
6. Webber, S.G. A Treatise on Nervous Diseases—Their Symptoms and Treatment, p. 200, 1885.
7. Ridley, H.W. J. Trop. M. and Hyg., 28:102–103, March 2, 1925.
8. Braddon, W.L. The Causes and Prevention of Beriberi, 1907.
9. Horder, Sir Thomas. Lancet, 1:340–341, February 12, 1927.
10. Breuil and Dartiguenave. Bull. Soc. Med. Chir. de L’Indochine, 15:803, August/September 1937.
11. Maberly, J. The Health of the Nation and Deficiency Diseases, 1938.
12. Mazzitelli, M. Studium, 29:73, April 1, 1939.
13. Scobey, R.R. Arch. Pediat., 63:322–354, July 1946.
14. Scobey, R.R. Arch. Pediat., 65:131–166, March 1948.
15. Edward, J.F. Can. M.A.J., 58:210, February 1948.
16. Head, H., and Campbell, A.W. Brain, 23:23, 1900.
17. Ruggles, E.W. Arch. Dermat and Syph., 23:472–476, March 1931.
18. Beers, N.T. J.A.M.A., 112:2553, June 17, 1939.
19. Beckman, H. Pharmacology in Clinical Practice, p. 257, 1953.
20. Lewitus, Victor. Vet. Med., 31:29–33, January 1936.
21. Brinton, W.R. Quoted by Chidester, F.E., Ashworth, A.M., Ashworth, G.A., and Wiles, I.A. International Clin., 3:63–72, September 1934.
22. Gray, E. Vet. J., 96:28–34, 1940.
23. Radeleff, R.D. J. Am. Vet. M.A., 109:129–132, August 1946.
24. von Economo. Encephalitis Lythargica. London, 1931.
25. Editorial, Vet. Med., 37:6, January 1942.
26. Holtman, F. Science, 104:50–51, July 1946.
27. Scobey, R.R. Arch. Pediat., 68:309–321.

Reprint No. 76
Lee Foundation for Nutritional Research
Milwaukee, Wisconsin 53201

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