(This rebuttal: online publication only)

The Iodine Debate so far. . .

Editorial: Iodine: A Lot to Swallow
by Alan Gaby, MD
(Aug/Sept 2005)

A Rebuttal of Dr. Gaby's Editorial on Iodine
by Guy E. Abraham, MD and David Brownstein, MD
Online publication only. . .
(October 2005)

Alan R. Gaby, MD's Response to:
A Rebuttal of Dr. Gaby's Editorial on Iodine
Online publication only. . .
(November 2005)

Iodine Debate Continues: Rebuttal #2
by Guy E. Abraham, MD and David Brownstein, MD
Online publication only. . .
(April 2006)

Alan R. Gaby's Response to Rebuttal #2
Online publication only. . .
(April 2006)

Alan R. Gaby's Response to (this) Rebuttal #3
Online publication only. . .
(July 2006)

We would like to submit a third rebuttal to Gaby's second counter-rebuttal, regarding the safety of iodine at the levels used in the orthoiodosupplementation program.^1,2 Since Gaby's last iodophobic escapade contains only three paragraphs, we will comment on every paragraph.

Gaby:
"Drs. Abraham and Brownstein argue that it is seaweed, not the iodine in it, that causes thyroid disorders. However, a main aspect of their iodine hypothesis is that Japanese people are healthy because they eat a lot of iodine, which in the Japanese diet comes mainly from seaweed. This seems like a contradiction."

Comment:
Gaby created a contradiction where there was none by misquoting what we previously wrote:

1) For those who use the RDA for iodine (0.15 mg/day) as their gold standard, the average daily intake of iodine by mainland Japanese (100-fold higher than the RDA) would be considered excessive and toxic. But statistics show that these mainland Japanese represent one of the healthiest nations on earth.³

2) There is no contradiction. A high incidence of euthyroid goiter was observed in an area of Japan, Hokaido. Suzuki et al⁴ who first reported the high incidence of goiter with normal thyroid function in the area of Hokaido, did not think that iodine in seaweed was the cause because subjects in Tokyo excreted similar levels of iodine in their urine (20-30 mg/day) but did not experience goiter. Also, Suzuki reasoned that the widespread use of iodine in large amounts has not resulted in an increased incidence of goiter. Suzuki proposed that something else in the seaweed of Hokaido was the cause. To quote Suzuki et al:⁴"Considering the paucity of reported cases of iodine goiter with the wide spread usage of iodine medication, we cannot exclude factors other than excessive intake of dietary iodine as a cause of the goiter."

For Gaby's erudition and using the evolutionist viewpoint, we point out that there are many kinds of seaweeds that evolved over billions of years into different types. Some are more selective in concentrating iodide than others. For example, the oceans contain 1400 times more bromide than iodide. To keep toxic goitrogenic bromide out of seaweed, the iodide uptake mechanism must be very selective. The levels of heavy metals in seaweed vary, depending on the kind of seaweeds and on industrial dumping of toxic waste in the areas where seaweeds are harvested.

During the first 40 years following the discovery of iodine in seaweed, France was the sole producer of iodine from seaweed. Therefore, France has a lot of experience with iodine in seaweeds. Currently, there are brands of iodized salt in France where seaweed is used in table salt as a source of iodine.⁵ One brand, Algosel Le Paludier, contains 470 ug iodine/gm of salt. With an average daily intake of ten grams of salt, the daily intake of iodine from that source alone is 4.7 mg, or 4700 micrograms, 31 times the RDA standard of 150 ug.

French legislation requires that the type of seaweeds used in table salt should contain low levels of toxic metals such as lead, mercury, and cadmium. All seaweeds were not created equal. From an evolutionist's point of view, seaweeds evolved over billions of years into different types with different properties.

Gaby:
"Questioning whether Drs. Abraham and Brownstein have meticulously monitored their patients for adverse effects is completely different that suggesting that poor medical care was given, which I did not suggest. What I said was, 'Before one could confidently conclude that high-dose iodine is safe for 99% of the population (as stated by Abraham and Brownstein), it seems that a systematic toxicity study would be necessary.'"

Comment:
Based on 180 years of experience with the safe and effective use of inorganic, non-radioactive iodine in amounts 2:4 order of magnitude greater than the RDA in several clinical conditions,⁶ inorganic, non-radioactive iodine is extremely safe. A clear distinction is made between organic vs. inorganic and stable vs. radioactive iodine (See Table 1). We proposed that, based on the concept of orthoiodosupplementation, only mainland Japanese consume adequate amounts of iodine and that 99% of the world population are deficient in inorganic, non-radioactive iodine; that is, they have not reached whole-body sufficiency for that essential element.

Gaby pontificates, "It seems that a systematic toxicity study would be necessary." Systematic toxicity studies on an essential element used extensively, safely and effectively in medical practice for over 180 years in daily amounts 2:4 orders of magnitude greater than the RDA?^1,3,6 Where are the systemic toxicity studies for many other alternative therapies using nutrients several orders of magnitude greater than the RDA, which Dr. Gaby has endorsed, such as the Meyers IV cocktail?

Gaby:
"I suggested that such a study should include serial testing of all patients to identify the appearance of thyroid antibodies during treatment with iodine, since iodine supplementation has been reported to increase the incidence of thyroiditis [italics added]. Thyroid-antibody measurements may not be necessary as a component of routine medical care, but they would seem to be necessary before one could confidently claim that high-dose iodine supplementation does not increase the incidence of autoimmune thyroiditis. I asked in my rebuttal how many of the iodine-treated patients had had thyroid-antibody tests, but Drs. Abraham and Brownstein did not answer my question."

Comment:
We have already responded to Gaby's statement that iodine supplementation has been reported to increase the incidence of thyroiditis. From the literature review previously discussed in our second rebuttal, the references Gaby supplied to support the above statement either used organic iodine containing drugs or iodized salt. There were no autoimmune thyroiditis reported in the US before iodization of salt, at a time when Lugol solution and other forms of inorganic iodine were widely used in the US at levels two orders of magnitude greater than the RDA.¹

Stable iodide content of the thyroid gland measured by X-ray fluorescence scanning revealed that autoimmune thyroiditis is associated with low stable iodide levels in the thyroid. For the US population, Okerlund⁷ reported a mean value of 10 mg iodine/thyroid. In 56 patients with autoimmune thyroiditis but with normal thyroid function, he observed a mean value of 4.8 mg iodine/thyroid. In 13 patients with autoimmune thyroiditis and hypothyroidism, the mean value for thyroid iodine was lower at 2.3 mg/thyroid. In patients on amiodarone, a toxic, sustained-release form of iodine, patients suffering from thyroid dysfunctions as side effects of amiodarone had much lower levels of thyroid iodine than patients without thyroid dysfunction: 30.5 ± 9.2 mg/thyroid in 12 patients without thyroid dysfunction compared to levels four to ten times lower in five patients with hyper- or hypothyroidism following amiodarone.⁸ We do not feel that the data available justifies performing antibodies titers against TPO, TG, TSH-R, and others in every patient unless the thyroid function tests are abnormal in the initial evaluation.

We previously presented evidence that autoimmune thyroiditis is due to iodine and magnesium deficiency, not iodine excess, and patients with autoimmune thyroiditis have responded to this nutritional program.¹ Besides, inorganic non-radioactive iodine is an essential element that has been in clinical use for 180 years. It is not a drug that is new on the block. Therefore, people using iodine in the orthoiodosupplementation ranges are not "guinea pigs," as proposed by Gaby's advocate Doctor Lonsdale.⁹

In Dr. Brownstein's practice, every patient placed on iodine therapy had thyroid antibody levels tested before and after beginning iodine therapy. Dr. Brownstein's experience has been consistent: the use of inorganic nonradioactive iodine has not resulted in a higher incidence of autoimmune thyroid disorders.

Gaby:
"Concerning the report of deaths due to high-dose iodine, here is the pertinent reference:
Sterling JB, Heymann WR. Potassium iodide in dermatology: a 19th century drug for the 21st century – uses, pharmacology, adverse effects, and contraindications. J Am Acad Dermatol. 2000;43:691-697.

In this review article, the authors state that in the 1920s and 1930s, when potassium iodide (KI) was widely used, many patients died of KI-induced side effects, particularly pulmonary edema and associated heart failure."

Comment:
In Gaby's first counter rebuttal, he stated:

"High-dose iodine therapy is of great value in some circumstances. We should not forget, however, that this treatment was abandoned in the past, because it caused many deaths from heart failure, as well as a long list of other side effects" [Italics added].

There were no references to support this statement. So, we requested validation. In his second counter-rebuttal, Gaby gave one reference.¹⁰ The title of this publication, "Potassium Iodide in Dermatology: A 19th Century Drug for the 21st Century – Uses, Pharmacology, Adverse Effects, and Contraindications," strongly suggests that the authors were in favor of a 21st century revival of the 19th century uses of iodide for some severe dermatological conditions, not responsive to any other treatment modalities. Under the section of "Indications," we read:

In 1976, Schulz and Whiting repopularized the use of KI after reporting that 24 to 28 patients with erythema nodosum and 16 to 17 patients with nodular vasculitis (crythema induratum), responded to KI. Relief of symptoms occurred within 2 days, with most lesions clearing within 2 weeks. The doses of KI used by Schulz and Whiting ranged from 360 to 900 mg daily [Italics added].

Horio et al.¹⁵ confirmed the finding of Schulz and Whitting and also found KI effective for Behcet's syndrome, erythema multiforme, and Sweet's syndrome. Using a dose of 300 mg 3 times daily, they observed relief of subjective symptoms such as lesional tenderness, fever, and arthralgias within 24 hours. Complete remission of lesions 10 to 14 days after administration of KI was noted in 11 of 15 patients with erythema nodosum, 7 of 10 patients with nodular vasculitis, 1 of 4 patients with leg lesions of Behcet's syndrome, 14 of 16 cases of erythema muliforme, including those with concomitant herpes simplex, and 7 of 8 cases of Sweet's syndrome. The best response was noted in those patients with erythema modosum associated with systemic symptoms and a positive C reactive protein, and in those patients to whom the medication was administered shortly after the onset of illness.^1,15 A rapid response to KI has also been reported in a case of subacute nodular migratory panniculitis (erythema nodosum migrans)¹⁶ and in a case of neutrophil-poor Sweet's syndrome, in which KI was tried after oral prednisolone, dapsone, and minocycline failed.¹⁷

Cabezas et al. in 1996 performed a randomized, nonblinded study on 57 patients with culture-confirmed cutaneous or lymphocutaneous sporotrichosis to compare the safety and efficacy of one-daily versus 3-times-daily dosing in the pediatric population. Patients (mean age, 7 years) received KI in the form of SSKI that began at 150 mg/day and increased rapidly over approximately 11 days to a maximum of 160 mg/kg daily in both groups. Mild side effects, most frequently nausea, were common in both groups (61% in the once-daily and 42% in the 3-times-daily group). Three patients had to discontinue therapy because of side effects; one patient in each group discontinued therapy because of a severe urticarial rash, and one patient in the once-daily group discontinued therapy after experiencing erythema nodosum leprosum…Of interest, Rafal and Rasmusen in 1991 reported using KI to treat an 84-day-old patient with fixed cutaneous sporotrichosis. They used a dose of 3 drops of SSKI 3 times daily (approximately 450 mg/day) for 3 months with complete response. They claimed that this was the youngest patient reported to have sporotrichosis.

Under the section, "Side Effects and Contraindications," Sterling et al.¹⁰ commented:

During the widespread use of KI in the 1920s and 1930s, many patients died because of the side effects associated with KI [italics added], most notably pulmonary edema and associated heart failure.⁵³ However, most of the above-mentioned side effects regress rapidly with discontinuation of KI. If necessary, corticostcroids can be used to control these side effects.

Reference 53 of Sterling's paper contains a review of the literature in 1936 by Hollander et al.¹¹ on fatal iododermia observed in patients with advanced stages of syphilis treated with potassium iodide. They reported one case of fatal iododermia and a review of the literature revealed ten more cases, 11 cases of fatal iododermia in how many thousands of patients treated successfully over the past 180 years, we are not told. A careful review of the reported case study by Hollander¹¹ showed that the patient had not taken any iodine for many months before he was admitted to the hospital where his death took place. It appears that this patient died from tertiary syphilis, not iododermia. Only two of the ten cases of fatal iododermia due to potassium iodide were published. The other eight cases were anecdotal reports. These results do not justify Sterling's statement: "During the widespread use of KI in the 1920s and 1930s, many patients died because of the side effects associated with KI…"

Also, these data do not justify Gaby's statement in his first rebuttal: "This treatment was abandoned in the past, because it caused many deaths from heart failure, as well as a long list of other side effects," or Gaby's statement in his second counter-rebuttal: "In this review article, the authors state that in the 1920s and 1930s when potassium iodide (KI) was widely used, many patients died of KI-induced side effects, particularly pulmonary edema and associated heart failure."

Gaby proposed that iodine was abandoned in the past due to many deaths. Yet, only 11 cases involving tertiary syphilis when iodide was the only effective treatment at that time for more than a century. Since potassium iodide reintroduction for dermatological conditions in 1976, Sterling and Heymen¹⁰ did not report any fatality caused by this treatment.

In a monograph published in 1940 by the Harvard University Press, reviewing the history of iodine in medicine with 588 references, the author, William Thomas Salter¹² expressed his amazement at the surprisingly good results obtained with the widespread use of potassium iodide in tertiary luetic (syphilitic) lesions and arteriosclerosis using daily amounts (grams) of iodide for long periods of time and without any evidence of complications:

After the discovery of iodine by Courtois in 1811, there was a great vogue for iodine therapy. … Likewise, in the 1820s, it was first introduced in the treatment of syphilis, and that use of the medication has continued since. It still is employed in the treatment of various granulomata such as actinomycosis, blastinomycosis, and odd skin disturbances like lupus erythematosus. Occasionally, even today, a gumma is found and the response of such a tertiary luetic lesion to iodide therapy is very surprising, … The dosage used in these disturbances is often very high. Doses of several grams a day have not infrequently been administered for considerable periods. … This form of therapy, however, still remains important in the treatment of sclerotic lesions of the aorta due to syphilis and has even been used over long periods for the treatment of generalized arteriosclerosis.

The reason iodine was abandoned in the past was not due to "many deaths from heart failure, as well as a long list of other side effects," as Gaby misinformed us but due to iodophobic misinformation resulting in medical iodophobia. The first wave of medical iodophobia was started by surgeon Kocher in 1910¹ and the second wave in the late 1940s by Wolff and Chaikoff.¹³ Regarding the Kocher Iodophobic Effect, Redisch and Perloff¹⁴ commented in 1940:

The relationship between iodine and the thyroid gland, particularly as regards function, was recognized as early as the beginning of the last century by Staub (1819) and Coindet (1820). After the syndrome of Flajani was classically described by Graves and von Basedow, iodine became the basis for treatment, with variable degrees of success, until that time when Kocher first described his hyperthyroidism presumably caused by iodine. This conception of the great Swiss surgeon caused such a sensation that the use of iodine was almost completely abandoned [italics added]. Today, however, we are skeptical of the validity of Kocher's conclusions.¹²

Kocher's iodophobic effect lasted some 15 years, from 1910 to 1925, then the pendulum swung back to the safe and effective use of iodine.¹ It is unbelievable that one man, Kocher, could negatively influence the use of iodine in Europe and the US, based on his report in 1910 that he developed hyperthyroidism after ingesting potassium iodide.

The devastating iodophobic domino effect of the Wolff-Chaikoff forgery has been discussed previously.¹³ Synchronization and timing were critical for the success of that grand deception, resulting in the progressive removal of iodine from our food supply. This was associated with an increased prevalence of obesity, diabetes, hypertension, and cancers of the breast and thyroid gland.¹ Will Gaby start a third wave of tsunamic iodophobia powered by a lot of hot air?

Iodophobic bioterrorism is the dissemination of iodophobic misinformation with the goal to deceive the medical profession and the public, preventing them from using effective amounts of the essential element iodine in iodine-responsive medical conditions. As we previously stated,¹³ the most effective way to destroy a nation is to remove iodine from the food supply. Iodophobic bioterrorism is a real threat to our nation, and the enemies within our gates masquerade as protectors of our well-being.

Guy E. Abraham, MD and David Brownstein, MD
Center for Holistic Medicine
5821 W. Maple Road
Suite 192
W. Bloomfield, Michigan 48322

Notes

1) Abraham, GE. The safe and effective implementation of orthoiodosupplementation in medical practice. The Original Internist. 2004;11:17-36.
2) Abraham, GE. The historical background of the Iodine Project. The Original Internist. 2005;12(2):57-66.
3) Abraham, GE, Flechas, JD, Hakala, JC. Orthoiodosupplementation: Iodine sufficiency of the whole human body. The Original Internist. 2002;9:30-41.
4) Suzuki, H, Higuchi, T, Sawa, K, et al. Endemic Coast Goitre in Hokkaido Japan. Acta Endocr. 1965;50:161-176.
5) Aquaron, R, Delange, F, Marchal, P, et al. Bioavailability of Seaweed Iodine in Human Beings. Cell. Mol. Biol. 2002;48(5):563-569.
6) Abraham, GE. The history of iodine in medicine. Part 1: From discovery to essentiality. The Original Internist. 2006;13(1):29-36.
7) Okerlund, MD. The Clinical Utility of Fluorescent Scanning of the Thyroid. In Medical Applications of Fluorescent Excitation Analysis, Eds. Kaufman and Price. Boca Raton, Florida: CRC Press, 1979, pg 149-160.
8) Jonckheer, MH. Amiodarone and the thyroid gland: a review. Acta Cardiologica. 1981;T. XXXVI, (3) pg 199-205.
9) Lonsdale, D. More About iodine. The Townsend Letter. (April) 2006;273:93,.
10) Sterling, JB, Heymann, WR. Potassium iodide in dermatology: A 19th century drug for the 21st century – Uses, pharmacology, adverse effects, and contraindications. J. Am. Acad. Dermatol. 2000;43:691-697.
11) Hollander, L, Fetterman, GH. Fatal iododerma: the eleventh case reported in the literature. Arch Dermatol Syphilol, 34:228-241, 1936.
12) Salter, WT. The Endocrine Function of Iodine. Cambridge, MA: Harvard University Press, 1940, pp 254-255, 261, 268-269.
13) Abraham, GE. The Wolff-Chaikoff effect: Crying wolf? The Original Internist. 2005;12(3):112-118.
14) Redisch, W. Perloff, WH. The medical treatment of hyperthyroidism. Endocrinology. 1940;26:221-228.