original editorial is also online, as well as a second
rebuttal by Drs. Abraham and Brownstein.
More on High-dose Iodine
by Alan R. Gaby, M.D.
In an editorial in the Aug/Sept issue of the Townsend
Letter, I expressed
concern about potential adverse effects that might occur with the routine
use of megadose iodine therapy, which is currently being advocated
by some practitioners. I cited research indicating that even modest
increases in dietary iodine intake might increase the incidence of
hypothyroidism, autoimmune thyroiditis, and possibly hyperthyroidism.
In the following issue of the Townsend Letter, Drs.
Abraham and Brownstein wrote a rebuttal to my editorial. They stated that, in Brownstein's
experience with 4,000 patients at the Center for Holistic Medicine
in West Bloomfield, Michigan, these side effects have not occurred;
on the contrary, high-dose iodine has been effective in some cases
as a treatment for these conditions. Although high-dose iodine therapy
has a definite place in clinical medicine, I believe that some of their
remarks warrant comment.
First, it does not seem appropriate
to use the term "orthoiodosupplementation" to
describe the treatment they are recommending. That term is borrowed
from Linus Pauling's "orthomolecular medicine," which refers
to the concept of creating the optimal molecular environment in the
body ("orthomolecular" means "the right molecules").
Defining the optimal dosage range as an amount that is 40 to 320 times
the usual dietary intake obfuscates any debate about whether such a
high intake is desirable or safe. Therefore, until iodine doses of
6.25-50 mg per day are proven to be optimal, it would be more logical
to refer to these doses as "high-dose iodine therapy."
Drs. Abraham and Brownstein stated
that the thyroid disorders I mentioned that resulted from iodine
supplementation occur mainly with "organic
forms" of iodine, such as amiodarone and certain iodine-containing
dyes used in radiology. However, all but one of the references I cited
discussed the adverse effects of inorganic iodine. The other article
concerned the use of an iodophore, which is a surfactant molecule that
slowly releases inorganic iodine. As surfactants would not by themselves
be expected to affect thyroid function, one might presume that the
released inorganic iodine was responsible for the reported adverse
I would also question the statement that our medical predecessors
recommended daily iodine intake of 12.5 to 37.5 mg from Lugol's solution.
While Dr. Lugol did use those doses, they were recommended primarily
to treat infections (iodine is a broad-spectrum antimicrobial agent)
and hyperthyroidism, not as routine nutritional support for the average
Regarding the safety data from the
Michigan clinic, Dr. Brownstein learned about high-dose iodine only
about two years ago, from a letter
written by Dr. Abraham in the Townsend Letter.
For a three-doctor practice to initiate high-dose iodine therapy on
4,000 patients over a two-year
period seems like a daunting endeavor, and one wonders how meticulously
these patients were monitored for adverse effects. How many patients
discontinued the treatment because of side effects and never returned
to the clinic to report their experiences? How many patients who did
return were questioned in detail about potential side effects, including
fatigue and other symptoms of hypothyroidism? How many patients showed
a decline in their serum thyroxine level that was judged to be clinically
insignificant because it remained in the normal range? Abraham has
in fact, observed such decreases in thyroid hormone levels in patients
receiving iodine therapy. One should not automatically assume that
these changes are benign. Research has shown that each person has a
unique "set point" for serum concentrations of T4, T3, and
TSH. Any iodine-induced deviation from these set points may be result
in suboptimal thyroid function for that person, even if all measurements
remain within the normal range.1 How many patients were tested serially
to identify the appearance of thyroid antibodies during treatment with
iodine? 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.
It is also worth considering that the positive
results observed in Michigan might not be reproducible in other geographical
Abraham and Brownstein hypothesized that the beneficial effect of iodine
is due in part to removal of bromine from the body. In 1973-4, several
thousand Michigan dairy farms were contaminated by polybrominated biphenyls
(PBBs) from an industrial accident. This bromine-containing pollutant
is known to persist in the body for long periods of time. Five years
after the accident, 97% of adipose tissue samples taken from Michigan
residents had detectable levels of PBBs,2 and 96% of breast
milk samples from women in densely populated areas of the state contained
up to three years after the accident.3 Because of its exceptionally
long half-life, it is reasonable to assume that many Michigan residents
still have a body burden of PBBs. As thyroid dysfunction is known to
occur in people exposed to PBBs, it is possible that some of the beneficial
effects attributed to iodine therapy were due to a reduction of the
body burden of PBBs.4
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. The doses used then were higher
than those currently being advocated. However, it is premature to assert
that more modest doses do not cause more modest side effects.
1. Andersen S, et al. Narrow individual variations
in serum T4 and T3 in normal subjects: a clue to the understanding
of subclinical thyroid disease. J Clin Endocrinol Metab 2002;87:1068-1072.
2. Wolff MS, et al. Human tissue burdens of halogenated aromatic
chemicals in Michigan. JAMA 1982;247:2112-2116.
3. Brilliant LB, et al. Breast-milk monitoring to measure Michigan's
contamination with polybrominated biphenyls. Lancet 1978;2:643-646.
4. Bahn AK, et al. Hypothyroidism in workers exposed to polybrominated
biphenyls. N Engl J Med 1980;302:31-333.