(This rebuttal: online publication only)
The Iodine Debate so far. . .
Iodine: A Lot to Swallow
by Alan Gaby, MD
Rebuttal of Dr. Gaby's Editorial on Iodine
by Guy E. Abraham, MD and David Brownstein,
Online publication only. . .
R. Gaby, MD's Response to:
A Rebuttal of Dr. Gaby's Editorial on Iodine
Online publication only. . .
Continues: Rebuttal #2
by Guy E. Abraham, MD and David Brownstein,
Online publication only. . .
R. Gaby's Response to Rebuttal #2
Online publication only. . .
R. Gaby's Response to (this) Rebuttal #3
Online publication only. . .
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.
"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."
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
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
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
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
"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.'"
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
greater than the RDA, which Dr. Gaby has endorsed, such as the Meyers
"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."
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
"Concerning the report of deaths due to high-dose iodine, here is the pertinent
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.
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
effects, particularly pulmonary edema and associated heart failure."
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
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
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
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
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
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
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
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
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 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
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.
E. Abraham, MD and David Brownstein, MD
Center for Holistic Medicine
5821 W. Maple Road
W. Bloomfield, Michigan 48322
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
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
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.
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.