This editorial
sparked an interesting debate. . .
Recently, a growing number of doctors
have been using iodine supplements in fairly
large doses in their practices. The treatment typically consists
of 12 to 50 mg per day of a combination of iodine and iodide, which
is 80 to 333 times the RDA of 150 mcg (0.15 mg) per day. Case reports1,2 suggest
that iodine therapy can improve energy levels, overall well-being,
sleep, digestive problems, and headaches. People with hypothyroidism
who experienced only partial improvement with thyroid hormone therapy
are said to do better when they start taking iodine.3 In
addition, fibrocystic breast disease responds well to iodine therapy,
an observation
that has been documented previously.4 The reported beneficial
effects of iodine suggest that some people have a higher-than-normal
requirement
for this mineral, or that it favorably influences certain types of
metabolic dysfunction.
While iodine therapy shows promise, I am concerned that two concepts
being put forth could lead to overzealous prescribing of this potentially
toxic mineral. First is the notion that the optimal dietary iodine
intake for humans is around 13.8 mg per day, which is about 90 times
the RDA and more than 13 times the "safe upper limit" of
1 mg per day established by the World Health Organization. Second is
the claim that a newly developed iodine-load test can be used as a
reliable tool to identify iodine deficiency.
Is the optimal human requirement 13.8 mg per day?
The argument, developed by one investigator,5 that the optimal human
iodine intake is around 90 times the RDA is based mainly on two points.
The first point is that the average iodine intake of adults living
in Japan is 13.8 mg per day, and the Japanese are among the healthiest
people in the world, with low rates of cancer. The second point is
in regard to the amount of oral iodine that it takes to saturate
the thyroid tissues.
The idea that Japanese people consume 13.8 mg of iodine per day appears
to have arisen from a misinterpretation of a 1967 paper.6 In that paper,
the average intake of seaweed in Japan was listed as 4.6 g (4,600 mg)
per day, and seaweed was said to contain 0.3% iodine. The figure of
13.8 mg comes from multiplying 4,600 mg by 0.003. However, the 4.6
g of seaweed consumed per day was expressed as wet weight, whereas
the 0.3%-iodine figure was based on dry weight. Since many vegetables
contain at least 90% water, 13.8 mg per day is a significant overestimate
of iodine intake. In studies that have specifically looked at iodine
intake among Japanese people, the mean dietary intake (estimated from
urinary iodine excretion) was in the range of 330 to 500 mcg per day,7,8
which is at least 25-fold lower than 13.8 mg per day.
The other argument being proposed to support a high iodine requirement
is that it takes somewhere between 6 and 14 mg of oral iodine per day
to keep the thyroid gland fully saturated with iodine. Whether or not
that is true, it is not clear that loading the thyroid gland or other
tissues with all the iodine they can hold is necessarily a good thing.
Since emerging from the iodine-rich oceans to become mammals, we have
evolved in an iodine-poor environment. Our thyroid glands have developed
a powerful mechanism to concentrate iodine, and some thyroid glands
(or other tissues) might not function as well after a sudden 90-fold
increase in the intake of this mineral. As I will explain later, relatively
small increases in dietary iodine intake have been reported to cause
hypothyroidism or other thyroid abnormalities in some people.
It has also been observed that iodine supplementation promotes the
urinary excretion of potentially toxic halogens such as bromide and
fluoride. While that effect might be beneficial for some people, it
is not clear to what extent it would shift the risk-benefit ratio of
megadose iodine therapy for the general population.
Is the iodine-load test valid?
For the iodine-load test, the patient ingests 50 mg of a combination
of iodine and iodide and the urine is collected for the next 24 hours.
The patient is considered to be iodine-deficient if less than 90%
of the administered dose is excreted in the urine, on the premise
that a deficient person will retain iodine in the tissues, rather
than excrete it in the urine. According to one doctor who uses the
test and a laboratory that offers it, 92% to 98% of patients who
have taken the iodine-load test were found to be deficient in iodine.
However, the validity of the test depends on the assumption that the
average person can absorb at least 90% of a 50-mg dose. It may be that
people are failing to excrete 90% of the iodine in the urine not because
their tissues are soaking it up, but because a lot of the iodine is
coming out in the feces. There is no reason to assume that a 50-mg
dose of iodine, which is at least 250 times the typical daily intake,
can be almost completely absorbed by the average person. While this
issue has not apparently been studied in humans, cows fed supraphysiological
doses of iodine (72 to 161 mg per day) excreted approximately 50% of
the administered dose in the feces.9
Proponents of the iodine-load test argue that the less-than-90% urinary
excretion seen in most patients is probably not due to incomplete intestinal
absorption. They point out that the percent urinary excretion increases
progressively (usually over a period of months) with continued high-dose
iodine administration, and that this increase occurs because the body
retains less of each successive dose as it becomes more saturated with
iodine. However, an alternative explanation for the progressive increase
in urinary iodine excretion is that repeated dosing leads to increases
in the percent absorbed. That could conceivably occur in a number of
different ways. As an antimicrobial agent, iodine might enhance overall
nutrient absorption by killing certain pathogens in the gastrointestinal
tract. Supplementing with large doses of iodine might also induce the
proliferation of an intestinal iodine-transporter molecule, thereby
increasing iodine absorption capacity. A third possibility is that
an enterohepatic circulation exists for iodine. Repeated dosing with
50 mg of iodine might overload the enterohepatic circulation system,
resulting in less iodine being dumped back into the intestine to be
excreted in the feces, and more excreted in the urine. Before the iodine-load
test can be considered a reliable indicator of tissue iodine levels,
it needs to be demonstrated that only negligible amounts of iodine
are excreted in the feces after an oral iodine load.
Potential side effects of iodine
Fairly modest increases in iodine intake
have been reported to cause thyroid dysfunction, particularly hypothyroidism.
In a study of 33
Japanese patients with hypothyroidism, the median serum TSH level
decreased from 21.9 mU/L to 5.3 mU/L (indicating an improvement in
the hypothyroidism), and one-third became euthyroid, when the patients
stopped eating seaweed and other high-iodine foods for 1–2
months.10 In a survey of 3,300 children aged 6–12
years from 5 continents, thyroid glands were twice as large in children
with
high dietary iodine intake (about 750 mcg per day), compared with
children with more normal iodine intake.11 While the significance
of that finding is not clear, it suggests the possibility of iodine-induced
goiter. In addition, there is epidemiological evidence that populations
with "sufficient" or "high normal" dietary
iodine intake have a higher prevalence of autoimmune thyroiditis,
compared with populations with deficient iodine intake.12 In a study
of children in a mountainous area of Greece with a high prevalence
of goiter, public-health measures taken to eliminate iodine deficiency
were followed by a three-fold increase in the prevalence of autoimmune
thyroiditis.13 In addition, modest increases in dietary iodine have
been suspected to cause hyperthyroidism in some people,14 an effect
that is known to occur with larger doses of iodine.
Other well-known side effects of excessive iodine intake include acne,
headaches, allergic reactions, metallic taste in the mouth, and parotid
gland swelling. While the doses of iodine reported to causes those
side effects have often been higher than those currently being recommended,
some people appear to be especially sensitive to the adverse effects
of iodine.
Practitioners who are using iodine therapy report that these side effects,
including thyroid problems, are very uncommon. The relative absence
of side effects may be due to the use of iodine as part of a comprehensive
nutritional program. One might also speculate that the iodine/iodide
combination causes fewer adverse effects on thyroid function than does
iodide alone (which is the type of iodine present in iodized salt).
Conclusion
The possibility that high-dose iodine/iodide can relieve certain common
conditions is intriguing. Considering the positive anecdotal reports,
an empirical trial of iodine/iodide therapy, based on the clinical
picture, seems reasonable. The case has not been made, however, that
the average person should markedly increase his or her iodine intake
in an attempt to saturate the tissues with iodine. Nor has the case
been made that the iodine-load test can provide reliable guidance
regarding the need for iodine therapy. Thyroid function should be
monitored in patients receiving more than 1 mg of iodine per day.
Alan R. Gaby, MD
References
1. Brownstein D. Iodine:
why you need it, why you can't live without it. Medical
Alternatives Press, West Bloomfield, MI, 2004.
2. Abraham GE, et al. Orthoiodosupplementation: Iodine sufficiency
of the whole human body. http://www.optimox.com/pics/Iodine/IOD-02/IOD-02.htm#2.
(Note: Several other articles on iodine by Abraham GE et al are
posted at this website).
3. Brownstein D. op.cit.
4. Ghent WR, et al. Iodine replacement in fibrocystic disease of
the breast. Can J Surg 1993;36:453–460.
5. Abraham GE, et al. op. cit.
6. Nagataki S, et al. Thyroid function in chronic excess iodide
ingestion: comparison of thyroidal absolute iodine uptake and degradation
of
thyroxine in euthyroid Japanese subjects. J Clin Endocrinol
Metab 1967;27:638–647.
7. Ishizuki Y, et al. [The variation of Japanese urinary excretion
of iodine in different decades of age]. [Article in Japanese].
Nippon Naibunpi Gakkai Zasshi 1994;70:1093–1100.
8. Ishizuki Y, et al. [Urinary iodide excretion in Japanese people
and thyroid dysfunction]. [Article in Japanese]. Nippon
Naibunpi Gakkai Zasshi 1992;68:550–556.
9. Crout NM, Voigt G. Modeling the dynamics of radioiodine in dairy
cows. J Dairy Sci 1996;79:254–9.
10. Kasagi K, et al. Effect of iodine restriction on thyroid function
in patients with primary hypothyroidism. Thyroid 2003;13:561–567.
11. Zimmermann MB, et al. High thyroid volume in children with
excess dietary iodine intakes. Am J Clin Nutr 2005;81:840–844.
12. Schumm-Draeger PM. [Iodine and thyroid autoimmunity] [Article
in German]. Z Arztl Fortbild Qualitatssich 2004;98
Suppl 5:73–6.
13. Zois C, et al. High prevalence of autoimmune thyroiditis in
schoolchildren after elimination of iodine deficiency in northwestern
Greece. Thyroid 2003;13:485–9.
14. Stewart JC, Vidor GI. Thyrotoxicosis induced by iodine contamination
of food: a common unrecognized condition? Br Med J 1976;1:372–375.
Iodine Debate Continues. . .
Editorial:
Iodine: A Lot to Swallow (this article)
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
by Guy E. Abraham, MD and David Brownstein,
MD
Online publication only. . .
(April 2006)
Gaby Responds to Rebuttal #2
by Alan R. Gaby, MD
Online publication only. . .
(April
2006)
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