January 25, 2010

In working with iodine deficiency since early 2006, I’ve
also had cause to study the issue of dietary salt intake. Approximately
1/3rd of the patients I treat with Iodine begin to detoxify (with symptoms)
from excessive levels of bromine in the body. Excreting bromine (with
significant relief of symptoms) is much more rapid in the presence of
salt (not from the sodium, but from the chloride anion).

I have learned much about salt that is contradictory to what I was taught
in medical school. For the purposes of this paper, I have borrowed heavily
from a book by David Brownstein, M.D., entitled Salt Your Way to Health,
which is available at Medical Alternatives Press, 4173 Fieldbrook, West
Bloomfield, Michigan, 48323 (tel 248 8513372) and also through at
This and his other excellent books (including one on Iodine), can also
be ordered from There is much more in this book than
I will summarize below, and I would highly recommend that you obtain
it and read it. He also has an article published which is available online, by clicking here.

Salt and Hypertension: The most common belief is that increased dietary
salt causes high blood pressure. It is true that for people who already
have high blood pressure, there is a greater reduction in blood pressure
with salt restriction than is seen in the normal population (those without
blood pressure problems). The effect is modest, however, with reductions
in blood pressure of approximately 5/2.5 (mm mercury, systolic/diastolic)
(reference 1).

Not all hypertensive patients are salt sensitive (e.g. develop higher
blood pressure with increased salt intake). Some, particularly the elderly,
may be sensitive. A review of 56 clinical trials showed that a low-salt
diet had a minimal effect on blood pressure in the vast majority of
people studied (average decrease in blood pressure approximately 4/1)
(reference 2).
In general, medical research does not indicate that low-salt diets lower
blood pressure (reference 3,4,5). It is easy enough to monitor blood
pressure, in any case, to see if any particular individual has a problem
with increased salt intake.

Adverse effects of Low salt diets: In one study of nearly 3000 hypertensive
patients, the group with the lowest salt intake had a 430% increase
in heart attack compared to the group with the highest salt intake (reference
6). Low salt diets have also been shown to cause increases (over 10%)
in both total cholesterol and in LDL cholesterol (reference 7).

Other issues:
Unrefined Sea Salt (“grey salt”) is a good source of essential
trace elements that have been removed from “table salt”
through processing. In addition, ordinary “table salt” has
aluminum and other impurities added to it.

The use of unrefined sea salt has also been used with positive effects
in holistic medical practices (please see Dr. Brownstein’s book
for more details).

Dr. Brownstein recommends ¼ tsp unrefined sea salt daily for
each quart of liquid consumed. Unrefined sea salt should have an “off”
color, indicating that it has not been bleached, nor had all the trace
minerals refined out of it. Brands that are known to have good levels
of trace minerals (they have been independently tested) include Celtic
salt and Himalayan salt.

Salt load procedure: If, while taking Iodine, we suspect bromine toxicity
(bad taste in mouth, acne-like eruptions, fatigue, irritability, difficulty
concentrating or with memory, emotional instability, or depression),
follow the following procedure (“salt load”):

1. Drink ¼ tsp of unrefined sea salt in about ½ cup
of warm water, or simply place it on your tongue, and chase it with
16 ounces of water.

2. Repeat this in 30-45 minutes, and then once again, in order to
start urinating a good amount. The chloride in the salt flushes the
bromine into the urine, and if this relieves the symptoms, then we
are most probably dealing with bromine toxicity.

3. If I have you do this for more than one day, you do the 3 repetitions,
as in 1. and 2. above, each day.

4. Report the results to me. I may adjust the iodine dose.

It is only fair to mention that even in Asian populations, who have
otherwise much lower rates of heart disease and stroke, that higher
salt intakes are associated with higher rates of those illnesses. I
suspect that what has happened in this country  over the past several
decades is that a diet high in prepared, processed foods (canned soups,
etc.) with high salt content  has resulted in a diet which  promotes high blood pressure, heart disease, and stroke.
But those of us who do not consume such foods, and who consider that
salt intake should be limited may wind up with inadequate salt intake.
This, in combination with excessive environmental bromine exposure and
iodine deficiency, is a bad combination.

It is important to understand that I am not advocating a “high
salt diet.” I have the strong impression that people who do not
eat much highly salted foods (bacon, ham, anchovies, seaweeds, salted
cheeses (like feta), etc., and who also do not add salt in cooking
and/or at the table, thinking that salt is “bad” for you
are actually getting less than the currently recognized “adequate”
dose of salt.

The current medical  guidelines for daily salt (sodium) intake are
as follows:

1. Adequate intake (we should not eat less than this amount): 1500
milligrams for young and middle-aged adults, 1300 milligrams for those
over 50, and 1200 milligrams for those over 70. Note that 1 tsp of salt
is 2400 milligrams of sodium, so that the equivalent of 1/2 tsp of salt
is recommended for those over 70.

2. The upper recommended limit is 2300 milligrams (just under 1 tsp
salt). Nutritional studies indicate that most Americans exceed this
level. (this data from the Health and Nutrition Newsletter, Tufts University,
April 2004)

A list of the sodium content of common foods can be found at

Potassium — this is another very basic and vital mineral, which works in conjunction with Sodium in a large number of biochemical reactions.  Most Americans eat too little potassium (found primarily in fruits and vegetables).  Daily intake should be 4700 mg.  A listing of potassium rich foods can be found at

For those who need to do a salt load, but cannot tolerate the sodium load, Potassium chloride (chemically written as KCl) serves as well as salt (as it is the chloride that flushes bromine into the urine).  KCl is commonly available in 99 mg tablets, with approximately 38 mg of chloride per tablet.  To get the equivalent of 1/4 teaspoon of salt (sodium chloride), it would be necessary to take 8 KCL tablets (which would then also give almost 500 mg of potassium, well within the daily requirement.

On a weight-to-weight basis, there is less chloride in KCl than in sodium chloride (NaCl) as potassium is a heavier element than sodium.

Excessive intake of potassium is not a problem in healthy persons, who simply excrete it in the urine.  In those who are type 1 diabetics, or who have chronic kidney disease, or who take certain “potassium sparing” diuretics, or take non-steroidal anti–inflammatory drugs, or blood pressure pills in the “ACE inhibitor” categor, medical advice should be sought before dramatically increasing one’s intake of potassium.


1.Cutler, JA., An overview of randomized trials of sodium restriction
and blood pressure. Hypertension. 1991;17(suppl 1): I-27 – I-33

2. Midgley, J., et al. Effect of reduced dietary sodium on blood pressure.
JAMA, May 22/29, 1996. Vol. 275 No. 20

3. Smith, WCS, et al. Urinary electrolyte excretion, alcohol consumption,
and blood pressure in the Scottish Heart Health Study. BMJ. 297:320-330,

4. Alderman, M., et al. Dietary sodium intake and mortality: The National
Health and Nutrition Examination Survey (NHANES I). Lancet. Vol. 351,
Issue 9105, March 14, 1998, 781-785

5. Swales, JD. Salt saga continued: Salt has only small importance in
hypertension. BMJ. 1988;297;307-8

6. Alderman, M. Low urinary sodium is associated with greater risk of
myocardial infarction among treated hypertensive men. Hypertension,
19995;25: 1144-1152

7. Rupert, M. et al. Short term dietary sodium restriction increases
serum lipids and insulin in salt-sensitive and salt-resistant normotensive
adults. Klin Wochenschr. 1991;69: (suppl. XXV):51-57

[Original article date: April 2006, most recent revision 12/5/2008]

NOTE: This article is long and somewhat technical.  The issues raised
and discussed are, however, extremely important.  I urge you to struggle
(if necessary) through the article, and to bring questions into our

UPDATE OF 12/5/2008:  I continually monitor the clinical results using supplemental iodine, and they remain extremely positive.  I have had a small number of patients develop new thyroid problems while on iodine, and in most of the cases there is a family history of thyroid disease, and since there are large numbers of people who develop thyroid problems without being on iodine supplementation, I have no clear sense that iodine has actually provoked any issues.  In a few cases, I don’t have a clear explanation yet for what has happened, and I am sharing my experience with other physicians around the country who are also using supplemental iodine, in the hope of developing a greater understanding.

In summary, I think the following points are significant:

1.  If, on supplemental iodine, there are positive changes in well-being, the dose that maintains that improvement is probably in the 1/2 to 1 tablet daily range, and after several months on iodine supplementation, most people would maintain that improvement for months to years even if they stopped supplementation;

2.  There is probably always bromine detoxification when taking iodine (and fluorine, and probably also lead, mercury, arsenic, cadmium, and aluminum).  Approximately 1/3rd of people on supplemental iodine have at least a mildly symptomatic bromine detoxification (one that requires a salt-load procedure to relieve the symptoms).  These detoxifications should be beneficial, even if they are not accompanied by any symptoms.  However, after some months, at least in the case of bromine, substantial detoxification should have taken place and will continue to take place even with a lower dose of iodine.  Again, there is much about this that is yet to be precisely defined;

3.  Research in breast cancer raises the possibility that Iodine supplementation MAY be beneficial, and if a person is at high risk, any such benefit would require higher (4-8 tablets daily) of iodine, and we would want to know that high levels of saturation have occurred (by doing the 24-hour urine iodine loading test).  Much less is known about the effect of iodine in prostate cancer, but in the best-case scenario, where high iodine intakes in Japan are the ONLY reason that prostate cancer is so much less common, because of the relatively small numbers of prostate cancer (122 men per 100,000), we would have to treat 1000 men with iodine to prevent one cancer.

4.  For the 1/3rd of people (including myself) who experience no subjective response to iodine supplementation, AND who start out with no significant fatigue or other difficulty, I think that it is likely that they are genetically well-adapted to a low intake of iodine, and high levels of supplementation are not necessary;

5.  These are the considerations that I am presently using to make decisions as to dosage and general management.  I am less inclined to do a lot of follow-up loading tests, and less inclined in general to maintain doses of 4 tablets per day for long periods of time.

If you have not already read the original article, please do so and then come back to these points (as they will then make more sense).


Over the past several years, I’ve been struck by how common it is to see
hypothyroidism (low thyroid function), particularly in women. One source was
quoted (in 1996) as indicating that there are 1,490,371 adults and 205,159
children in this country with Hashimoto’s thyroiditis, the most common form of
hypothyroidism (Rose and Mackay, 1998, The Autoimmune Diseases, Third Edition).
The American Women’s Medical Association reports that 1 in every 4,000 babies
born in the United States

has congenital hypothyroidism (both these reports are quoted on
This is a serious issue, as for the baby, the consequences of this include
impaired brain development.

Synthetic thyroid hormones (far more often prescribed than products derived
from animal thyroid) were the 7th most frequently drug prescribed in the United
States in 2005 (data from the National Prescription Audit, link no longer
active). In 2006, thyroid hormones were the 5th most commonly prescribed drugs
by family practitioners (Family Practice News, Vol. 37 No. 16, 8/15/07).

In a study published this year, which measured iodine concentrations in
breast milk, investigators concluded that “47% of the women sampled may
have been providing insufficient iodine to meet infant’s requirements.”
(Pearce, et. al., in Breast Milk Iodine and Perchlorate Concentrations in
Lactating Boston-Area Women — Journal of Clinical Endocrinology and Metabolism
Vol. 92, No. 5, pg 1673-77, February 20, 2007).

Furthermore, hypothyroidism is thought by many to be very under-diagnosed by
medical professionals.

In trying to understand all this, in December of 2005 I came across an
article in Holistic
Primary Care
regarding iodine deficiency, and in particular the work of Guy
Abraham, M.D. Most of his work can be found at the website of, following the link to iodine
research. For those of you who are interested, I’d suggest reading publications
9 and 10, which are more general, and for the technically inclined, starting
the other articles with numbers 5 and 2.

It is well known that iodine deficiency can cause goiter (thyroid
enlargement) and hypothyroidism, and that children born to hypothyroid mothers
are at risk for mental retardation and, in the extreme form, cretinism. 
In the developed world, deemed for the most part to be “iodine
sufficient,” the leading cause of hypothyroidism is said to be autoimmune
disease, rather than iodine deficiency.

The data presented in the article in Holistic Primary Care made a lot
of sense to me, and certainly seemed  plausibly related to the high
incidence of hypothyroidism that is experienced in this country.  The
conventional view is that hypothyroidism in this country is primarily caused by
“auto-immune” thyroid inflammations, which are characterized by the
presence of antibodies against thyroid enzymes.  Dr. Abraham hypothesizes
that iodine deficiency may lead to thyroid cell damage, leading to the
formation of antibodies against thyroid enzymes and thyroid tissues, thereby
beginning the auto-immune reaction.  I am not aware of any proof to this
theory, but it is plausible.  According to him, as of 20 years ago (the
most recent data we have) , auto-immune thyroid disorders were not nearly as
common in Japan as they are in this country.  Antibodies to thyroid components
are much more common in the United Kingdom

than in Japan
(Mittra, I. et. al., “Thyroid and other autoantibodies in British and
Japanese women:  an epidemiogical study of breast cancer” British
Medical Journal
1976, 1, 257-259).

The production of thyroid hormone inside the
cells of the thyroid requires, among other things, hydrogen peroxide. 
Excess hydrogen peroxide (which if unused has a destructive effect) can be
broken down into diatomic oxygen (O2 ), by the enzyme glutathione
peroxidase, which in turn requires the mineral Selenium as a co-factor. 

Selenium deficiency is thought to be fairly common in the United States,
and is possibly worsened by our high exposures to toxic compounds which demand
a lot of glutathione peroxidase for our protection against their harmful
effects.  For this reason, Iodine supplementation should always be
accompanied by adequate Selenium intake (at least 100 micrograms daily, more
probably 200 – 400 micrograms, especially if autoimmune disease or some form of
chemical or mineral toxicity has already been diagnosed.

High levels of calcium relative to magnesium
inside the thyroid and possibly other tissues (such as the female breast)
promote excess production of H2O2 (above the level normally found) in the
thyroid.  Iodine above the RDA is necessary for organification of iodine
into iodolipids which in turn tends to lower the production of H202 (in
addition to their normal functions, which include inducing cell death in
cancerous cells.  Imbalances in these reactions may lead to damage of
thyroid cells and the formation of antibodies to thyrogloblulin (the protein
skeleton of thyroid hormone) and to thyroid peroxidase (the enzyme that
“stitches” iodine into thyroglobulin to make thyroid hormone).  These
antibodies are markers of autoimmune thyroiditis (most notably Hashimoto’s
disease, but are also found in Graves’ disease — hyperthryoidism).

More importantly, however, were the purported links between iodine
deficiency and cancers of the breast, prostate, and other sites, and the possibility
that iodine deficiency was related to chronic digestive disorders (think of
amount of television advertising for heartburn medicines), chronic sinusitis
and other respiratory tract infections, autoimmune disease, diabetes, and many
other illnesses.

The possible relationship between iodine deficiency, hypothyroidism, and
breast cancer has been the subject of much research. The epidemiological and
biochemical evidence to suggest these linkages is presented on the Optimox website. From that site’s home page,
click on the link to “iodine research” and read publication #2.

From that site, the following references are listed:

  • Wiseman, R., Breast cancer
    hypothesis: a single cause for the majority of cases. J Epid Comm Health,
    54:851-858, 2000.
  • Finley, J.W., Bogardus, G.M.,
    Breast cancer and thyroid disease. Quart. Rev. Surg. Obstet. Gynec.
    17:139-147, 1960.
  • Thomas, B.S., Bulbrook, R.D.,
    Russell, M.J., et al, Thyroid function in early breast cancer. Enrop. J.
    Cancer clin, Oncol, 19:1213-1219, 1983.
  • Thomas, B.S., Bulbrook, R.D.,
    Goodman, M.J., Thyroid Function and the Incidence of Breast Cancer in
    Hawaiian, British and Japanese Women. Int. J. Cancer, 38:325-329, 1986.
  • Smyth, P., Thyroid Disease
    and Breast Cancer, J. Endo. Int., 16:396-401, 1993.
  • Eskin B., Bartuska D., Dunn
    M., Jacob G., Dratman M., Mammary Gland Dysplasia in Iodine Deficiency,
    JAMA, 200:115-119, 1967.
  • Eskin, B., Iodine Metabolism
    and Breast Cancer. Trans. New
    York, Acad. of Sciences, 32:911-947, 1970.
  • Eskin B., Iodine and Mammary
    Cancer, Adv. Exp. Med. Biol., 91:293-304, 1977.
  • Ghandrakant, C., Kapdim MD,
    Wolfe, J.N., Breast Cancer. Relationship to Thyroid Supplements for
    Hypothyroidism. JAMA, 238:1124, 1976.
  • Backwinkel, K., Jackson,
    A.S., Some Features of Breast Cancer and Thyroid Deficiency. Cancer
    17:1174-1176, 1964.
  • Ghent, W., Eskin, B., Low,
    D., Hill, L., Iodine Replacement in Fibrocystic Disease of the Breast,
    Can. J. Surg., 36:453-460, 1993.
  • Eskin, B., Grotkowski, C.E.,
    Connolly, C.P., et al, Different Tissue Responses for Iodine and Iodide in
    Rat Thyroid and Mammary Glands. Biological Trace Element Research,
    49:9-19, 1995.

While it cannot be conclusively stated at this time, at least, that there is
a clear causal relationship between breast cancer and iodine deficiency, the
epidemiological evidence is highly suggestive:

  • Finley, J.W., Bogardus, G.M.,
    Breast cancer and thyroid disease. Quart. Rev. Surg. Obstet. Gynec.
    17:139-147, 1960.
  • Thomas, B.S., Bulbrook, R.D.,
    Russell, M.J., et al, Thyroid function in early breast cancer. Enrop. J.
    Cancer clin, Oncol, 19:1213-1219, 1983.
  • Thomas, B.S., Bulbrook, R.D.,
    Goodman, M.J., Thyroid Function and the Incidence of Breast Cancer in
    Hawaiian, British and Japanese Women. Int. J. Cancer, 38:325-329, 1986.

The possible therapeutic role of iodine in the clinical treatment of breast
cancer is suggested by the following:

  • Kato N, Funahashi H, Ando K,
    Takagi H. Suppressive effects of iodine preparations on proliferation of
    DMBA-induced breast cancer in rat. J Jpn Soc Cancer Ther. 1994;29:582–588.
  • Funahashi H, Imai T, Tanaka
    Y, Tobinaga J, Wada M, Morita T, Yamada F, Tsukamura K, Oiwa M, Kikumori
    T, Narita T, Takagi H. Suppressive effect of iodine on DMBA-induced breast
    tumor growth in the rat. J Surgical Oncol. 1996;61:209–213.
  • Funahashi, H., et. al. in
    Jpn. J. Cancer Res. 92, 483–487, May 2001: Does
    Seaweed Prevent Breast Cancer?
  • Stoddard FR, Brooks AD, Eskin BA, Johannes GJ,  Breast Cancer Cell
    Line:  Evidence for an Anti-Estrogen Effect of Iodine  International
    Journal of Medical Sciences  2008 5(4): 189 -196

In the second study by Funahashi and his co-workers, seaweed extract
exerted a strong protective effect in breast cancer prone rats, and also
induced apoptosis (cell death) in human breast cancer cells in tissue culture,
without causing any excess cell death in normal female breast tissue in tissue culture.  This was also seen in the study by Stoddard, available here.

Whatever is true of breast cancer is may also likely to be true for prostate
cancer, which is also rare in societies with high dietary intakes of iodine.  In Japan, for instance, the incidence of prostate cancer 90% lower than in the United States.

Prostate cancer:

  • Men with a diagnosis of thyroid cancer
    have a 31% increased risk of subsequently developing prostate cancer;
  • Men with prostate cancer have a 21%
    increased risk of subsequently developing thryoid cancer; (British Journal
    of Cancer 117: 281-288; 2006)
  •  Japanese prostate cancer 12.6/100,000 vs. American
    124.8/100,000.  Japanese men that move away from Japan have
    higher rates of prostate cancer (British Journal of Cancer 63:963-966,
  • NHANES (The National Health and
    Nutrition Examination Survey) 1 (1970) and Nutrition and Cancer
    58(1): 28-34, 2007 indicate that the highest tertile (1/3rd) of
    the population (in terms of iodine intake) have a 29% reduced risk of
    developing prostate cancer;
  • Hoption SA, et al; in Nutr. Cancer
    58(1): 28-34, 2007, examined the relationship between iodine intake,
    thyroid disease, and prostate cancer;
  •  A history of thyroid disease confers a 2.34 X overall increased
    risk of developing prostate cancer;
  • 10 years after thyroid disease, the
    prostate cancer risk increases 3.38 times.

If hypothyroidism may be due to Iodine deficiency, treating with thyroid
hormone may alleviate the symptoms, but does not correct the underlying problem
that leads to the disease. If, as is proposed by Dr. Abraham and others, that
Iodine serves many other functions, then only giving thyroid hormone is
obviously insufficient to treat the whole person.

Testing for iodine deficiency is primarily done through the urine.
There are two tests involved:

  1. A first morning urinary
    iodine level — this test has been done around the world, for several
    decades. The World Health Organization and UNICEF, in 1994,issued a joint
    statement regarding iodine deficiency. Among the criteria for a country to
    supplement the food supply with iodine is a median value (a number above
    which is found 1/2 the population, with the other half below that number)
    of 0.2 mg/liter. The main value of this test lies in two areas: firstly,
    that there is a lot of data around the world to compare with, and
    secondly, it is primarily a reflection of the amount of iodine consumed in
    the 24 hours prior to collecting the sample.

    In evaluating approximately 300 patients with a first morning urinary
    iodine measurement, over 90% test below this number!

    For this reason, I no longer routinely order this part of the evaluation,
    which also then reduces the cost of the testing.

  2. A 24 hour loading test —
    after collecting the the first morning urine (only if you are also doing
    the spot test, which goes into the blue bottle – otherwise discard the
    first morning urine), 50 mg of iodine is ingested as a single dose, and
    the amount of iodine excreted is measured. All other things being equal,
    the more deficient the body, the greater the absorption (the lower the
    amount excreted). Unfortunately, owing to Bromine accumulation (see
    below), heavy metal toxicity, and perhaps other factors, some of us need
    iodine but don’t utilize it effectively. This discrepancy is detected by
    the tests, and can be helped with a proper nutritional program.

As of this this date (9/29/2008), of the 363 patients I’ve been able to
evaluate after at least 6-8 weeks of supplementation at full doses, 66.9% are
unequivocally improved, another 15.7% feel better but I can’t be sure that it
is solely due to iodine, 13.2% have not noticed any change (most of whom
already felt well, the rest with illnesses not expected to respond directly to
iodine supplementation), and 3.3% were affected negatively and dropped out of
treatment (from, I believe, toxicity of bromine and/or heavy metals, as these
patients had pre-existing multiple chemical sensitivities). An additional 0.8%
dropped out of treatment for various reasons (moving away, philosophical
issues, etc.) Since the first 6 months of beginning the iodine program, and now
that I know how to predict who will have trouble, no one has had to drop out
for reasons of toxicity, although a approximately 20-30 people are on reduced
iodine dosages in order to slow down the bromine detoxification).  Three
people are included in the “dropout” group who actually responded
positively to iodine but for various reasons are no longer on the program.

Those who feel improved commonly report improvements in energy, mood, and
clarity of mind. Other changes are improved thyroid function, improvement in
premenstrual syndromes, menopausal syndromes, fibrocystic breast disease,
fibromyalgia, male sexual function, and improved (more easily managed) stress

Obviously, these results are very gratifying. There are some problematic
issues, however:

— I have found 8 confirmed cases of thyroid cancer in this group of patients.
Two other patients are pending surgical confirmation. Thyroid cancer is known
to be more common in the presence of iodine deficiency. For this reason, and
also to detect multinodular goiter, which can (slightly) predispose to mild
(and transient) hyper- or hypothyroidism while on iodine replacement therapy,
ultrasound of the thyroid is usually recommended.

— I have also become aware of several patients with thyroid cancer, who
have already had surgery and radioactive iodine treatment but whose cancers
have persisted or relapsed being treated by other physicians, with Dr.
Abraham’s guidance.  Doses of iodine in the range of 200 mg are being used
in the context of a complete nutritional program and detoxification regimen,
with extremely promising results.  I will continue to follow this as well.

— A few patients known to be hypothyroid, although feeling significantly
better in their energy, clarity of thinking, and even beginning to lose weight
(after previous failures to do so) have had changes in their thyroid test
results suggesting that their thyroid dose is too low. I continue to follow
these patients, and at least in one case the test results have substantially

— One patient, known to be hypothyroid (and who also has chemical
sensitivities) became hyperthyroid while on iodine supplementation. I am not
sure at this time if this was related to iodine, or perhaps to bromine or
fluorine toxicity. After stopping thyroid hormone and iodine supplementation
she improved, but relapsed briefly but notably after taking a liquid multi-mineral
supplement with a very small amount of iodine, fluorine, and bromine in it.
This patient appears to be very sensitive to iodine intake, and after
consulting with an endocrinologist, it is felt that she has both hypothyroidism
and hyperthyroidism. This might have represented a “Jod-Basedow”
effect, which can be related to toxic nodular goiter. However, an ultrasound
done prior to instituting iodine treatment failed to demonstrate any nodules.
She has antibodies typical of Graves’ disease (and so apparently has two forms
of auto-immune thyroiditis. This is rare, but is reported in the medical
literature. As of this writing (10/21/2007) this is the only one of my patients
using iodine supplementation to have shown this effect. Her hyperthyroidism quickly
began to subside when iodine supplementation was stopped although it has not
yet reached normal levels, and she is still being assessed.

— (update of 11/20/2007):  Another patient, with multinodular goiter,
but normal thyroid function, just came in with symptoms of
hyperthyroidism.  I’d treated her with iodine at 50 mg doses for about a
year, with a 40% increase in her iodine saturation, but no subjective
changes.  Two weeks after increasing the iodine dose to 75 milligrams
daily, she began to feel jittery and a rapid heart beat.  Lab studies
confirm that she is hyperthyroid.  Medical texts state that this is a rare
occurrence, that may occur in the setting of iodine deficiency and subsequent
replacement, and primarily in the elderly.  I’ll report further on this
case as I know more.

   update as of 12/3/2007 — she has also been found (by antibody
testing) to have Graves’ disease (autoimmune hyperthyroidism).  The other
possibility would have been that one of the pre-existing nodules had become
“autonomous” and overactive, which is a normal progression of
multinodular goiter.

— In the early days of iodine supplementation of the nation’s food supply
(salt and bread), it was noted that a few people became hyperthyroid, consuming
supplemental iodine. For this reason, it was considered safe to supplement at
low doses, and not at higher doses. Before iodine was removed from commercial
breads, one slice would contain 150 micrograms of iodine. Textbooks on thyroid
disorders now note this to be a “rare” effect, mostly noted in the
elderly with multiple thyroid nodules.  It is still the consensus among
medical experts that the benefits of iodine supplementation of the food supply
for virtually everyone outweighs the small risk that a few individuals may become

   Iodine-induced hyperthyroidism was reviewed by Stanbury (in Thyroid
1998 Jan;8(1):83-100) who noted that this seemed to occur in people with
pre-existent multinodular goiter (which might be too small to be detected) or
in people with Graves’ disease who were too idoine deficient to over-produce
thyroid hormone.  Hyperthyroidism is treatable, but is a more dangerous
condition in the elderly (owing to the strain on the heart).

— bromine is an element close to iodine (in a chemical sense), and which is
ubiquitous in our environment. Dietary sources include soft drinks like Dr.
Pepper, Mountain Dew, and other citrus-flavored soft drinks (some Gatorade
products), vegetables contaminated by the use of methyl bromide used as a
fumigant in agriculture, and seaweeds (which, however, also containing iodine
and large amounts of salt, and so are not problematic, assuming enough iodine
in the system). Environmental sources include methyl bromides from the burning
of unleaded gasoline (reduced now, but still very problematic) but mostly from
the use of bromine in flame retardants, which are used in clothing, mattresses,
building materials, airplane (and presumably automobile) construction,
furniture construction, etc.

Bromine interferes with iodine biochemistry, and is toxic in its own right
(psychological symptoms include disinhibition, self-neglect, fatigue,
difficulty with memory and concentration, irritability, emotional instability,

Iodine supplementation causes bromine to be released from within the tissues
of the body, into the bloodstream, and if this happens rapidly and in
sufficient quantities, produces toxic symptoms. This is treated with salt (the
chloride ion flushes the bromine into the urine) and may necessitate the
reduction of the iodine dosage. Potassium chloride can be used in place of
ordinary salt (table salt, for example) in people who are salt-sensitive.
Coping with bromine issues has necessitated intervention with salt in
approximately 33% of patients. 96 out of 115 people (83% !) who have tried the
“salt load” have felt better from doing so.

I am recognizing bromine toxicity symptoms much more commonly than I had,
even several months ago, and now consider that this may be an extremely common

— fluorine, mercury, lead, and cadmium in the body are also potential
sources of difficulty in managing iodine repletion programs, although evidently
much less commonly than bromine.

— another issue relates to the maintenance of iodine stores once iodine
levels have been replenished. The Japanese ingest approximately 43 mg of
Iodine, daily, on average, in their diets, primarily from kelp (see publication
#2 and 5 on the Optimox website).
Unfortunately, seaweeds concentrate heavy metals from polluted seawater, and so
the source of the seaweed is a critical issue. The inhabitants of Iceland, who
grind up the unused parts of fish into meal which is in turn fed to cows, who
then secrete large amounts of iodine into milk, consume milk as an important
part of their diet.

I currently (7/20/2008) think that for maintenance of the positive
subjective responses to iodine, doses of 6 – 12.5 mg (1/2 to 1 tablet of
iodoral) would probably be sufficient for most people.  For the
HYPOTHETICAL preventive effect of iodine on cancer (see next paragraph and
below) higher doses (in the range of 50 – 100 mg/d) appear to be necessary.

— Cancer rates, especially of the breast, are very low in Japan and other
countries with high iodine intakes. The concentration of iodine needed to
demonstrate anti-cancer effects (in animals and in human breast cancer cells in
tissue culture) can theoretically be achieved in humans at doses of 50 – 100 mg
/ day.

In the United States,
and most of the world, it is considered that a small amount of iodine (0.15 mg,
approximately 280 times less than the Japanese intake) is sufficient to
maintain normal thyroid function, and therefore is considered to be the
recommended daily allowance. Again, as discussed above, this logically assumes that
iodine has no other function in the body than that of thyroid function. This is
similar to the argument made that 60 mg. of Vitamin C, an amount sufficient to
prevent Scurvy, is sufficient to maintain the total health of the organism.

That iodine is taken up by many other tissues in the body, besides the
thyroid gland, is well documented in the medical literature. An interesting
slide regarding this can be found in the slide show “Harmful and Healthy
Halogens” on Dr. Miller’s website
A good summary article by Dr. Miller can be found here.

I think that it is only fair to say that the issue of iodine sufficiency in
the doses being recommended by Dr. Abraham and the other physicians using his
recommendations is outside the conventional teaching of the medical community.
These issues are all discussed on the Optimox

Epidemiological studies, such as the low incidence of breast cancer in
societies with high iodine intakes (eg. Japan) establish association, but
not causality. Though suggestive, such studies do not constitute proof of cause
and effect. In the case of iodine and breast cancer, the possibility that
iodine could be preventive and even therapeutic in breast cancer is supported
by the animal studies and tissue culture reports that can be found in the
references above, especially the Funahashi study (see references above). Still,
studies such as these cannot yet be accepted as proof of causality, which in
turn can only be supported by a very large, placebo controlled randomized
double blind clinical trial, which would be extremely expensive and
time-consuming. Such a study is not likely to be done since iodine is not a
patentable medication and the costs of such a study could never be recouped by
the sponsoring company. The government is the only agency which could be
expected to fund such a study.

is also worth noting that no nutritional factor works in isolation. Other nutritional factors which strongly influence
thyroid function and iodine biochemistry include Selenium, Magnesium, Iron,
Vitamin A, Niacin (Vitamin B-3), and Riboflavin (vitamin B-2).  This list
should not be considered to be complete, however.  A good nutritional program
is important.  By far the most important part of any nutritional program
is adequate intake of healthy foods, grown in healthy soils.

The iodine supplementation program therefore rests on the basis of a
“complete nutritional program.” This, in turn, needs to be individualized
in all cases, although the broad outlines pertain to most of us.

As a further consideration, it must be recognized that studying a single
factor (Iodine, in this case), without taking into account the many confounding
factors (bromine exposure, magnesium intake, other environmental toxins, etc.)
can be expected to produce results which can at best be interpreted with

I do not think, at this point (7/20/2008) that iodine supplementation will,
in the short run, prevent the onset of auto-immune thyroid disease.  
That is to say that if the process of auto-immune thyroid disease has already
begun (even if not detectable through symptoms and/or laboratory and imaging
tests), iodine will probably not reverse the process.  Selenium supplementation
has been shown to reduce antibody levels in Hashimoto’s disease, but not to
return them to zero.  It is theoretically possible that with early
attention to adequate selenium levels, iodine levels, proper function of
gluathione peroxidase systems, etc., a genetic tendency to Hashimoto’s disease
may be prevented.

The safety of Iodine — in summary, there are situations in which
iodine supplementation may cause problems:

  — Problems can occur in people who need to detoxify (bromine,
fluorine, mercury, lead, cadmium, etc.).  Some of the detoxification
reactions are strong, especially in people with multiple chemical sensitivity

 — There are also potential difficulties in people with pre-existing
thyroid disease:  This includes multinodular goiter (as discussed above),
but also people with a past history of Graves’s
disease managed with anti-thyroid drugs, and possibly with radioactive iodine
or surgery as well.  There are also rare individuals with one apparent
thyroid disease (such as the two patients discussed above) who may also be
harboring a second thyroid illness at the same time.  These situations
require more frequent monitoring.  Interestingly enough, it appears that
all these thyroid disorders are much more common when there is already iodine

Autoimmune hypothyroidism (Hashimoto’s
disease) was unknown in the United
States prior to the iodination of
salt.  Archives Surgery 1966: 92;796.  Although this might seem to
indicate that iodine could promote Hashimoto’s disease, this is apparently not
the case: Attempts to experimentally induce hypothyroidism with iodized salt
were fruitless unless goitrogens (compounds that induce enlargement of the
thyroid gland by interfering with the function of the gland) are added
(perchlorate [known to contaminate ground water in many areas of this country],
bromine, fluorine, possibly even chlorine ( from sources such as disinfected
waters, dishwasher steam, whiteners and bleaches, swimming pools, and some
artificial sweeteners [sucralose]).

Iodine content of thyroid can be measured by
X-ray Fluorescent scanning.  A study was performed to evaluate the iodine
content in individuals with and without autoimmune thyroid disease:

  • Where no autoimmune disease
    was present, a mean value of 10
    mg iodine/thyroid was found;
  • In 56 individuals with autoimmune thyroiditis but normal thyroid
    function a mean of 4.7 mg iodine/thyroid was present;
  • In 13 subjects with autoimmune thyroiditis and reduced thyroid
    function (hypothyroidism) only 2.3 mg iodine/thyroid was found.

This study therefore correlates low thyroid
gland iodine content with the increasing severity of autoimmune hypothyroidism.

Reference:  Okerlund, M., Medical
Applications of Fluorescent Excitation Analysis
, 1979, cited in Abraham,
G., et al. The saliva/serum iodide ratio as an index of sodium/iodide symporter
efficiency (see

Also note that during the time that iodine
intakes (as measured by urinary iodine) in the United States decreased by 50%, the
incidence of thyroid cancer and autoimmune thyroid disease has increased
markedly.  To examine this relationship, studies done at the Mayo Clinic
(Mayo Clinic Proceedings 1970 45:586) looked at 3 time periods, and noted the
respective incidence of autoimmune thyroid disease:

1935 – 1944:  approximately 2/100,000
            1945 –
1954:  approximately 18/100,000

            1955 — 1967: 

Iodine alone is not sufficient to “cause” autoimmune thyroid
disease.  The situation is, however, obviously complicated, and requires
ongoing monitoring.  There are goitrogens (substances that interfere with
thyroid function) in the environment, and rarely, iodine supplementation may induce
thyroid problems:

A study
performed in Denmark
compared the area of Aalborg, with an average first-morning urinary iodine
excretion of 53 micrograms/liter (World Health Organization criteria equates
moderate to severe iodine deficiency with average urinary iodine excretion of
less than 50 micrograms/liter) with the area around Copenhagen (average first morning urinary
iodine excretion of 68 micrograms/liter).  Lower iodine excretions are
generally thought to indicate lower dietary iodine intakes.  The incidence
of autoimmune hyperthyroidism was 2.6 times higher in the area of Aalborg,
suggesting that increased iodine intake (in the Copenhagen area) was protective, rather than
causative (Eur J. Endocr. 2000.  Oct;143(4) 485-91, cited in
Brownstein, D., Iodine – Why You Need it / Why You Can’t Live Without It 3rd

edition 2007).

— I have recently (July 2008) seen two patients, who have noted good
subjective benefit to iodine, go on to develop abnormalities in their thyroid
tests after 18 months of supplementation.  In one case there appears to be
mild autoimmune hypothyroidism, and in the other the TSH level is suppressed,
suggesting hyperthyroidism, although her thyroid hormone levels themselves are
not elevated.  This patient is currently under investigation.


Iodine conference report

I’ve presented my clinical experience with iodine supplementation twice in
2007 (Phoenix in February, and in San Diego in early
October). This last time I was able to report on the status of 287 patients
whom I’ve been able to adequately analyze, to describe some of the difficulties
and problems I’ve encountered (see Iodine
), and most significantly for me, to discuss these issues with my colleagues.

Some of the highlights of the information presented and what I learned in
such discussions are:

  • Guy Abraham MD, who is at the
    forefront of iodine research at this time, presented a several hour review
    of the history of use of iodine in medical practice, discussed the
    (apparently unfounded) aversion of medical authorities to more than very
    small doses of iodine, and presented information on many other issues
    related to the iodine project.
    • He reminded us that
      the Japanese, who eat, on average 100 – 200 times as much iodine as we
      do, have much better health as a population than we do;
    • He discussed and
      refuted the recent
      study from Denmark
      which purported to show an increased incidence of
      hypothyroidism in Denmark
      following a small increase in the dose of iodine used in the food supply;
      • The “increase” was of
        the order of 1 person in 10,000 persons supplemented;
      • Toward the end of the
        several month study period, the incidence was actually dropping, which
        agrees with the experience that I and my colleagues have seen (a
        temporary increase in TSH [thyroid stimulating hormone] which normalizes
        after several months).
  • We all agreed that the issue
    of bromine toxicity is widespread and is responsible for the great
    majority of the difficulties experienced by patients who are supplementing
    iodine in adequate dosages.
  • It can take a good while to
    reduce the body burden of bromine. In one of the cases cited, the initial
    blood level was in the mid-200’s initially (normal is less than 12 mg/L).
    • He felt a definite
      increase in energy and clarity of thinking on iodine supplementation,
      never needed to do a salt load for bromine detoxification reactions
      (presumably because he was already using a good amount of unrefined sea
    • His bromine level then
      stabilized in the range of 150 mg/L for 3-4 years, during which time he
      was unable to get the iodine saturation to go up significantly, despite
      taking 100 mg of Iodine daily.
    • Recent measurement
      showed a level around 50 mg/L, a substantial decrease (but one that I
      have seen be symptomatic in my patients.)
    • The persistence of
      bromine could be related to his high consumption of fruits and vegetables
      (if they are still fumigated with methyl bromide), or possibly to
      continued exposure to brominated flame retardants (an exposure that we
      all share), or some other factor or combinations of factors as yet not
  • It appears that there are no
    sources for accurate testing of bromide in body fluids other than Dr.
    Abraham’s laboratory, with whom I have collaborated, and FFP labs, who
    can, as of the last month, test urine bromides (which unfortunately are
    not a good indicator of total body burden.)
  • There is an extensive body of
    research regarding bromine toxicity in the environmental literature.
    • A series of studies in
      conducted in the 1960’s demonstrated a connection between high levels of
      serum bromine and psychiatric illness requiring hospitalization (see
      Evans, Med.J. Aust.1:498 1955, Fischer, Med.J. Aust. 8:13, 1960, Kessell,
      A., Med.J. Aust. 1:1073-1075, 1960).
    • A strong relationship
      between bromide and thyroid disease was demonstrated by Allain (Allain,
      P., et al. Bromine and thyroid hormone activity. Clin Pathol 46;456-458,
      1993 )
    • Strong toxic effects
      on female rats and their offspring have been repeatedly demonstrated in
      research done by Stanislav
    • Bromine readily
      crosses the placenta, and this must now be considered a potential issue
      for pregnant women (either on or off iodine).
  • There is much more to the
    bromine story than I have time to present here. The good news is that it
    is not difficult to detoxify the body – it requires salt and water (see
    the “salt”
    in Patient Education).
  • The links between iodine
    deficiency and breast cancer was reviewed by more than one of the
    presenters. Bernard Eskin, M.D., a celebrated researcher in female
    endocrinology, who has specifically researched and elucidated iodine
    metabolism in the female breast, both in normal breast tissue and in
    breast cancer tissue, presented a review of his past and current work:
    • He reviewed aspects of
      the link between thyroid disease and breast cancer (see Stoddard and
      Eskin, Iodine Alters Gene Expression Profile in the MCF-7 Breast Cancer
      Cell Line, Thyroid 2006;16(9):894).
    • Although it is not
      definitively understood, he linked the anti-proliferative effect of
      iodine to the effect of iodine on estrogen receptors in the breast, a
      direct effect of iodine on cancer cells, as well as to other aspects of
      iodine metabolism;
      • Recent advances in
        the study of estrogen receptors should, in the near future, improve our
        understanding of their role in breast cancer (approximately 80% of
        breast cancers are “positive” for estrogen receptors);
        • As a footnote, many
          organic chemicals in the environment (most prominently from plastics)
          which migrate into the body, effect the estrogen receptors.
      • Iodine will obviously
        not effect an estrogen receptor mechanism in those tumors which are
        estrogen receptor negative, although other mechanisms of iodine’s
        anti-cancer effect will presumably still play a role.
      • Iodine does not
        effect the initiation of cancer, but rather inhibits its promotion
    • He noted that a new
      study is underway to study the clinical effect of iodine in humans at
      risk for breast cancer. Apparently, because of disclosure rules, he was
      not able to share many details about the study.
    • I did inquire about
      the dosages to be used. Unfortunately, it appears that the dose will be
      barely above the currently recommended minimum intake, and given the
      basic science that we already know, I consider it unlikely that the study
      will show any effect.
    • The “silver lining in
      this cloud,” however, is that at very low doses, I don’t expect the
      researchers to find that the subjects intolerant to iodine (because of
      bromine toxicity, which I doubt has been considered in the study design).
  • Dr. Abraham and Dr.
    Brownstein are currently engaged in a pilot study to further define iodine
    biochemistry, using saliva as the tested body fluid.
  • The other clinicians
    presenting had independently arrived at the same conjecture that I’ve
    entertained: that if we didn’t have the apparently high levels of toxic
    bromine in the environment (and we should add to that list fluoride,
    mercury, lead, cadmium, etc.), if might not be necessary to take iodine at
    the levels that are being recommended in our practices.
  • I picked up a number of
    practical tips at the conference, including the following:
    • In patients with
      Hashimoto’s disease, it has been found to helpful to supplement
      Riboflavin (B-2) and Niacin (B-3) in higher doses than I have been
    • People with
      Hashimoto’s disease (auto-immune hypothyroidism) may have very
      significant reductions in their antibody levels with iodine
      supplementation), but this is unlikely if the disease has been present
      for a long period of time. This is the impression of a couple of
      clinicians with longer experience than my own, but they were not able to
      quantify just what “early” or “late” actually is.
    • Iodine should not be
      considered as a “sole” intervention. Considered solely from a nutritional
      standpoint, it is important to also look at the person’s general
      nutrition, and also to consider Selenium, Magnesium, B-vitamins
      (especially riboflavin and Niacin), Iron, vitamin C, possibly vitamin D,
      glutathione, etc.
    • All the clinicians,
      including myself, confirm that in hypothyroid patients, the initial TSH
      rises, but returns to normal after several months. It is hypothesized
      that the TSH rises to facilitate the transport of Iodine into the cell (a
      known function of TSH).
    • The use of unrefined
      sea salt, in adequate doses, appears to be important, as it includes the
      following health benefits:
      • It tends to restore
        the acid-base balance (pH) of the body to a slightly alkaline state
        (which is normal). Most of our patients are noted to be overly acidic
        (which promotes osteoporosis, among other things). The pH of the body
        can be readily ascertained and monitored at home with commercially
        available pH strips or paper.
      • It contains a large
        number of valuable trace elements which have been removed from commonly
        available “table salts;”
      • The chloride in the
        salt is useful for bromine detoxification (along with adequate intake of
      • People who eat a
        “healthy” diet and do not add salt may not be getting enough
        sodium. All this is covered in my article on salt.
    • I currently estimate
      that in 1/3rd of the patients that I treat with iodine, special attention
      to bromine detoxification is necessary. But I think that we should all be
      using adequate amounts of good quality salt

      (and see Salt Your Way to Health, by David Brownstein, M.D.).

  • An additional highlight was a
    presentation by Stephanie Buist, who described her long and and difficult
    saga with thyroid cancer, including 3 rounds of treatment with radioactive
    iodine, and how her health has changed since beginning therapy with iodine
    supplementation. Her story can be accessed at her blogsite.

I will make copies of the powerpoint presentations available in my waiting
room for those of you that are interested.