A Perspective On High Dose Iodine Supplementation – Part XI – Some Thoughts On Dosing And More

Iodine Dosing – Does A Totally Safe Dose Exist Above RDI Levels?

As I have been suggesting, doses of supplemental iodine in the range of 6 -12 mg per day are quite safe in terms of thyroid related side effects for the vast majority of patients.  However, as I suggested in the last installment, some patients who are more prone to iodine-related reactions, such as those patients with pre-existing autoimmune diseases such as celiac disease, may present significant risk even at these doses, which are fairly low in terms of the standards set by Abraham and colleagues.  Nevertheless, even though the risk is low at these doses which some consider minimal, is low good enough?  This is an important question to ask since, in terms of optimizing patient compliance, it is crucial early on in treatment that patients notice no significant adverse reactions to our recommendations.  Assuming the answer is no, we then need to ask another question.  Does a clinically effective dose of supplemental iodine exist above the RDI levels of 150 mcg per day, for which the risk of either thyroid or non-thyroid related reactions is virtually non-existent in almost all patients?  Fortunately, several studies have addressed this question.  In “Intermittent oral administration of potassium iodide solution for the correction of iodine deficiency” by Todd and Dunn (1) 304 children aged 7-13 years from the Hwedza District in east-central Zimbabwe, an area known to have a high prevalence of iodine deficiency disorders, were treated.  Some of these children demonstrated presence of goiter and some did not.  The duration of the study was one year.

The children were divided into five groups ingesting one of the following five supplemental regimens:

  • Group A – 8.7 mg every two weeks (Average daily dose – 0.62 mg)
  • Group B – 29.7 mg every month (Average daily dose – 0.99 mg)
  • Group C – 148.2 mg every 3 months (Average daily dose – 1.63 mg)
  • Group D – 382 mg every 6 months (Average daily dose – 2.09 mg)
  • Group E – 993 mg given one time (Average daily dose on an annualized basis – 2.72 mg)

What were the results in relation to thyroid function?  The authors state:

“After 6 mo, the median blood spot thyroglobulin concentration had decreased in all groups and had normalized in groups A and B to values found in iodine-sufficient populations.  The number of children with elevated thyroid-stimulating hormone concentrations decreased in groups A-C, but the changes were not significant.  Urine iodine concentration generally remained low in all groups but increased in group A.  After 13 mo, mean thyroid volume measured by ultrasound had decreased in groups A and B to values comparable with those in iodine-sufficient areas, and was unchanged in the other groups.”

Based on the fact that only groups A and B improved to levels found in iodine-sufficient populations, Todd and Dunn (1) concluded:

“We conclude that oral potassium iodide is effective for the prophylaxis of iodine deficiency if given as a dose of 30 mg I monthly or 8 mg biweekly.”

What about side effects?  Some were noted, irrespective of the dose and frequency.  Unfortunately, the authors provide information on these side effects that is non-specific in terms of which group had the most significant adverse experiences:

“Some children complained about a sour taste.  One month later, at the first follow-up visit, the children were asked if they experienced any side effects after taking the medicine.  Sore throat, headache, and abdominal pain were reported by few children in all groups.  One child in group E complained of sore cheeks.” 

However, on the positive side in relation to side effects, the authors report a lack of any thyroid-related side effects:

“…no adverse effects of large doses on thyroid function were documented.”

Interestingly, an earlier paper, in contrast to the one just discussed, did report adverse effects on thyroid function at lower daily doses of iodine.  However, one major difference in the subjects being studied must be noted.  In “The effect of small increases in dietary iodine on thyroid function in euthyroid subjects” by Paul et al (2) nine men aged 26 to 56 years with healthy thyroid function were examined whereas the Todd and Dunn (1) study, discussed above, evaluated children, many of whom had documented thyroid dysfunction.  In the Paul et al (2) study, the nine men received either 1500, 500, or 250 mcg of supplemental iodine in the form of sodium iodide daily for 14 days.  What were the results of this protocol?  The authors point out:

“Following the administration of 1500 µg iodine daily, there were small but significant decreases in the serum T4 and T3 concentrations and a small but compensatory increase in serum TSH concentration and the serum TSH response to TRH.  In contrast, no changes in pituitary-thyroid function occurred during the administration of 500 or 250 µg iodine daily. 

Another study from the same year authored by Gardner et al (3) reported adverse effects on thyroid function at doses ranging from 500 mcg to 4500 mcg per day.  In this study, “Effects of low dose oral iodide supplementation on thyroid function in normal men” the following intervention was performed:

“Thirty normal men aged 22-40 years were randomly assigned to receive 500, 1500, and 4500 micrograms iodide/day for 2 weeks.  Blood was obtained on days 1 and 15 for measurement of serum T4, T3, T3-charcoal uptake, TSH, protein-bound iodide (PBI) and total iodide, and 24 h urine samples were collected on these days for measurement of urinary iodide excretion.”

The following results were noted:

“The mean serum T4 concentration and free T4 index values decreased significantly at 1500 micrograms/day and 4500 micrograms/day doses.  No changes in T3-charcoal uptake or serum T3 concentration occurred at any dose.  Administration of 500 micrograms iodide/day resulted in a significant increase in the serum TSH response to TRH, and the two larger iodide doses resulted in increases in both basal and TRH-stimulated serum TSH concentrations.”

Based on the findings from the papers just reviewed, what can be concluded about iodine dose and side effects?  First, on a population-wide basis where need for iodine supplementation is not being pre-determined, the risk of side effects cannot be totally eliminated even at doses barely above the RDI of 150 mcg per day.  However, with the above in mind, the fact that virtually all of us are treating people who are ailing to the point where they feel they need to seek counsel with us must also be kept in mind.  Assuming that we are performing a quality diagnostic work-up concerning thyroid function and iodine need, as suggested by Todd and Dunn (1), I feel another conclusion can be confidently made.  Milligram dosing of supplemental iodine up to levels just below 3 mg per day appears to pose no risk to thyroid function in those who demonstrate need.  Nevertheless, keep in mind that the risk of non-thyroid related side effects which, in patients’ minds, are probably as significant to their evaluation of the quality of care they are receiving as thyroid-related side effects, exists at virtually all doses above RDI levels, even in patients who demonstrate need from a thyroid function standpoint.

What does the above suggest in terms of policies on clinical application?  For me, it suggests that supplemental iodine, like every other modality we employ, including water, has a benefit:risk ratio.  In turn, as long as we have performed a quality diagnostic work-up that has led us to conclude that the benefits greatly outweigh the risks, and as long as we have accurately and completely informed patients about the benefits and risks that are unique to their specific clinical scenario, I see no reason not to proceed with milligram dosing of supplemental iodine.  In terms of specific numbers, based on the studies I have read and anecdotal feedback I have received from many of you, starting with doses of 1-2 mg per day and ramping up gradually based on clinical need and continued reports of lack of side effects by the patient, seems to me like a prudent course of action.


Looking back at all the information on iodine that I have processed and written about over the last two years, certainly one of the highlights from a clinical standpoint was that which related to breast health.  Why?  In my opinion, the vast store of research on iodine and breast health had, despite its obvious nutritional and clinical value, gone largely ignored by many if not most practitioners not only in the allopathic community but in the nutritional community as well.  Therefore, I was quite excited to discover, thanks to Abraham and colleagues, a modality that not only had a solid scientific backing but had demonstrated, as evidenced by several reliable anecdotal reports, to be of tremendous value clinically, particularly in relation to fibrocystic breast issues.  Interestingly, though, anecdotal reports from many of you did not stop at breast health in relation to milligram dosing of iodine.  Many of you were also suggesting that iodine supplementation was optimizing many other situations where reproductive hormones, especially estrogen, come into play.  With these reports in mind, I decided to perform a literature search, investigating any studies that indicate a relationship between dietary or supplemental iodine and estrogen metabolism.  What were the results of this search?  I found that several relevant studies had been published that, for me, point out that those of you who have been hypothesizing that milligram dosing of supplemental iodine can aid in optimizing issues related to estrogen imbalances were indeed correct.  In turn, I truly believe that you are bringing to our attention a little recognized but extremely important issue from a clinical standpoint.

The oldest paper I could find that suggested a relationship between iodine and estrogen metabolism was “Dietary iodine and risk of breast, endometrial, and ovarian cancer” that was published in 1976 (4).  In this epidemiologic report the author states:

“Geographic differences in the rates of breast, endometrial, and ovarian cancer appear to be inversely correlated with dietary iodine intake.  Endocrinological considerations suggest that a low dietary iodine intake may produce a state of increased effective gonadotrophin stimulation, which in turn may produce a hypooestrogenic state characterized by relatively high production of oestrone and oestradiol and a relatively low oestriol to oestrone plus oestradiol ratio.  This altered endocrine state may increase the risk of breast, endometrial, and ovarian cancer.  Increasing dietary iodine intake may reduce the risk of these cancers.”

Of course, many of you will probably recognize the above mentioned ratio as being the “Estrogen Quotient” that has been popularized by Jonathan Wright, MD (5)  This relationship between iodine and estrogen was expanded to include hypothyroid function in a hypothesis paper by Clur (6) published in 1988:

“Oestrogen receptor density may be increased in hypothyroidism as is certain monoamine receptor density.  This would amplify the effect of high circulation oestrogen levels in hypothyroidism and may help explain why hypothyroidism and low iodine intake are risk factors for breast, uterine and ovarian cancer.”

In addition to the above, we now know that increased risk of estrogen-related adverse sequelae can also be well defined by understanding how estrogen forms such as estrone are metabolized in the body.  Many of you are aware of the increasingly popular urine test where the ratio of 2-hydroxyestrone to 16a-hydroxyestrone can be measured.  As suggested by Lord et al (7):

“Numerous studies have shown pre- and postmenopausal women with urinary 2/16a ratios above 2.0 have reduced risk for estrogen-sensitive cancers.”

With this relationship in mind, we now recognize that 2-hydroxyestrone is the “good” metabolite in that it tends not to be linked with adverse metabolic changes, as noted by Ursin et al (8):

“There are some data suggesting that 2-hydroxylated compounds are less biologically active than 16a-hydroxylated compounds, and that women metabolizing more estrone (E1) through the 16a pathway may have a prolonged estrogenic effect of E1.”

Furthermore, it is now being suggested that metabolites formed through the 2-hydroxy pathway may not be considered “good” just because they are less reactive.  In fact, they may have significant antiproliferative properties.  Stoddard et al state (9):

“…data suggests that 2-OH-E2 can be metabolized to 2-methoxyestradiol, an estrogen metabolite with anti-proliferative effects.”

Finally, we now know that there is another major family of estrogen metabolites that pose an even greater risk than the 16a-hydroxy family.  This is the 4-hydroxy family.  Rogan et al (10) note:

“Several lines of evidence…led to the recognition that the 4-hydroxylated estrogens play a major role in the genotoxic properties of estrogens.”

Of course, by now you may be wondering what all of this has to do with iodine.  While it may appear that I am wandering from this central question, please be aware that this foundational discussion of estrogen metabolism is part of the answer to this question.  Thus, with your indulgence, I would like to return to my focus on estrogen metabolic pathways.

Another key issue to understand about formation of the 2-, 4-, and 16a hydroxylated estrogens is the enzymes involved in the formation of these different estrogen metabolite families.  Interestingly, the enzymes involved are some of the same phase I detoxification enzymes that are involved in metabolism and elimination of environmental chemicals.  Specifically, CYP1A1 is instrumental in the creation of the “good” 2-hydroxy metabolites and CYP1B1 is instrumental in the creation of the “bad” 4-hydroxy metabolites.  In relation to a positive effect on estrogen metabolism, this is where iodine comes into play.  Stoddard et al (9) point out that treatment with iodine and iodide increases the ratio between CYP1A1 and CYP1B1:

“Data presented suggests that iodine/iodide may inhibit the estrogen response through…up-regulating proteins involved in estrogen metabolism (specifically through increasing the CYP1A1/1B1 ratio)…”

Another way that iodine can have a positive impact on estrogen metabolism in relation to adverse tissue changes has to do with BRCA1 activity.  As you may know, this transcription factor has received a good deal of publicity in relation to women who have a polymorphism that renders this transcription factor inactive.  Specifically, what is the function of BRCA1?  According to Stoddard et al (9), it inhibits transcription of estrogen receptor alpha, which, in turn, can promote adverse cellular changes in breast tissue.  According to the authors, iodine/iodide plays the following important role in BRCA1 function:

“Data presented suggests that iodine/iodide may inhibit the estrogen response through…decreasing BRCA1 inhibition thus permitting its inhibition of estrogen responsive transcription.”

Another interesting way that iodine can have an impact on female reproductive health was discussed by Slebodzinski (11) who noted that, in terms of ovarian function, iodine can have an adverse impact.  To fully understand this relationship, the author first makes this important point:

“Since 1928, the iodine concentration in the ovary has been known to be higher than in every other organ except the thyroid.  The ovarian iodide uptake varies with sexual activities, is enhanced by estrogens and a hypothyroid state and blocked by goitrogens.”

Of course, the key question that needs to be asked is whether enhanced uptake of iodine by the ovary is a good thing or a bad thing.  As suggested by Slebodzinski (11), it is bad:

“There is an increase in ovarian iodide uptake during hypothyroidism induced by thiouracil.  The hypothyroid state is characterized by an absolute or relative depletion of thyroid hormones (TH), altered by sensitivity and ovarian response to gonadotrophins leading to a rise in the content of mucopolysaccharides, followed by a tendency in some species towards the development of polycystic ovaries.  In fact, ovarian cyst formation is greatly intensified in women with primary hypothyroidism…”

With this in mind, though, an important question needs to be asked.  If the hypothyroidism is due to iodine deficiency, would iodine administration lead to increased iodine uptake by the thyroid and lower iodine uptake by the ovary?  Unfortunately, the paper by Slebodzinski (11) does not provide an answer to this question.  Therefore, I would certainly appreciate any thoughts you might have on this matter.

In closing the discussion on this topic, I do want to point out that I realize what I have presented concerning the relationship between  estrogen and iodine is far from complete and, as I have suggested, certainly leaves many questions unanswered.  However, I do believe that what I have presented makes it abundantly clear that the claims made by so many of you that estrogen-related issues have optimized upon administration of iodine supplementation are not merely questionable theories that have the placebo effect as their basis.  In turn, I do hope that those of you who are using iodine supplementation with patients demonstrating estrogen-related imbalances will continue to report to me your findings and, when possible, send me any research documentation that comes your way.


Since I began this newsletter series, several of you have suggested an interesting hypothesis to explain the etiology of side effects that occur with administration of milligram dosing of supplemental iodine.  Briefly, this hypothesis revolves around the idea that, due to significant exposure to bromide and fluoride from various environmental sources, most especially brominated bread and fluoridated water, major accumulations of bromide and fluoride in the thyroid has occurred in many patients.  In turn, given that iodine, bromide, and fluoride are halogens, administration of supplemental iodine displaces stores of bromide and fluoride in the thyroid.  Then, as this bromide and fluoride are released into the circulation to ultimately be excreted in the urine, the bromide and fluoride induce the side effects we have conventionally associated with excess iodine intake.  Hopefully I have demonstrated in this series that there is ample evidence to suggest that ingestion of milligram levels of iodine daily has the ability to induce significant symptomatology directly without the involvement of bromide or fluoride.  Nevertheless, as you will see, a significant body of research does suggest that this hypothesis has validity.  Therefore, I would now like to review several publications which, even though they fall short of providing absolute proof of this hypothesis, provide enough support to warrant our objective evaluation.

As you might expect, Abraham has played a major role in popularizing the fact that exposure to bromide and fluoride can have an adverse impact on thyroid and iodine metabolism.  In “Iodine supplementation markedly increases urinary excretion of fluoride and bromide” Abraham (12) presents a review of several papers that demonstrate an adverse effect of bromide and fluoride on both thyroid and iodine metabolism.  In addition, he presents a research project he conducted that provides evidence that milligram dosing of supplemental iodine increases excretion of bromide and fluoride in the urine.  To evaluate the credibility of this paper, I would first like to examine some of the references presented by Abraham (12) plus other references that indicate bromide and fluoride present a significant threat to optimal thyroid and iodine metabolism.  Then I will review Abraham’s experiment that employs supplemental iodine to raise urinary bromide and fluoride levels and offer comments.


Probably the first order of business is to specifically define the difference between bromine and bromide.  This definition was provided by Pavelka (13):

“Bromine is one of the most abundant and ubiquitous of the recognized trace elements in the biosphere.  However, bromine has not been conclusively shown to perform any essential function in plants, microorganisms or animals.  In nature, bromine is found mostly bound to metals in the form of inorganic salts – the bromides.”

How prevalent are bromides?  As noted by Pavelka (13), they have become increasingly prevalent in the food supply due to their use in agriculture:

“Bromide is the main degradation product of brominated hydrocarbons (e.g. methyl bromide) excessively used in agriculture for pre-planting fumigation of soils and post-harvest fumigation of commodities as grains, spices, nuts, fruits and tobacco; as well as of other bromine compounds (e.g. ethylene dibromide) applied on a large scale in industry.  In the course of the 20th century bromide has been introduced increasingly into the environment as a salt-mining waste and degradation product of fumigants.  Therefore, at present the general population will mainly be exposed to bromide via their food.  The new role of bromide as a residue of food and water necessitated its broad toxicological evaluation.”

Of course, as noted often by Abraham in his papers, another major source of bromide is brominated flour that has been used in the food supply for at least 50-60 years.  Kurokawa et al (14) give specific information on the use of bromide in flour:

“Potassium bromate (KBrO3) has been used primarily as a maturing agent for flour and as a dough conditioner in bread-making process for over 50 years, and this application is now used worldwide.  Food additive-grade KBrO3is specified to contain KBrO3 at levels of 99.0 to 101.0% after drying.”

Concerning toxicity and carcinogenicity, the vast majority of research on bromine/bromide has been performed on animals.  Abraham (12), in his paper on the subject mentioned above, references several papers that highlight the adverse impact that bromine/bromide has on thyroid and iodine metabolism.  In “Toxicity of sodium bromide in rats: effects on endocrine system and reproduction” by van Leeuwen et al (15), the authors state the following:

“It is suggested that bromide exerts an inhibitory effect on the thyroid, resulting in an increased hormonal stimulation of this organ by the pituitary gland.”

Concerning iodine Vobecky and Babicky (16) point out:

“It was found that with increased bromide intake the bromine concentration in the thyroid gland increased with simultaneous decrease in iodine concentration.”

What is the impact of bromide on thyroid hormones?  Velicky et al (17) note the following after adding potassium bromide to the diet of rats:

“The concentration of bromine in the thyroid increased with the amount of bromine intake, while at the same time the molar ratio of iodine/bromine decreased.  The plasma level of T4 was lowered after both 16 and 66 days of treatment, but the T3 level only after 66 days of treatment.  The level of TSH did not exhibit any significant change.  The observed changes, which have a parenchymatous goiter-like character, may have a direct relevance for human medicine, since the concentrations of bromide chosen in these experiments are readily encountered in the environment.”

Interestingly, as you will see, the conclusion in the above quote about human relevance has been surprisingly difficult to prove, as noted in the paper by Sangster et al (18) that was also used as a reference by Abraham (12).  In their study, Sanger et al (18) administered either 0, 4, or 9 mg Br/kg/day in the form of sodium bromide to seven males for 12 weeks and seven non-pregnant females over three full cycles.  The results of this study were the following:

“Plasma half-life was about 10 days.  In the females taking 9 mg Br/kg/day (but in no other group) there was a significant increase in serum thyroxine and triiodothyronine between the start and end of the study but all other concentrations remained within normal limits.  No changes were observed in serum concentrations of free thyroxine, thyroxine-binding globulin, cortisol, oestradiol, progesterone or testosterone, or of thyrotrophin, prolactin, luteinizing hormone (LH) and follicle-stimulating hormone before or after the administration of thyrotrophin-releasing hormone and LH-releasing hormone.  Analysis of neurophysiological data (EEG and visual evoked response) showed a decrease in delta 1- and delta 2-activities and increases in beta-activities and in mean frequency (Mobility parameter) in the groups on 9 mg Br/kg/day, but all the findings were within normal limits.”

As you can see, while there were adverse effects of sodium bromide administration, they were minimal and noted only at the highest level of intake in women.  Interestingly, a similar study was performed a year earlier by Sangster et al (19) employing only 1 mg per kg daily of sodium bromide in 11 non-pregnant females and 10 males for 8 weeks or 2 full cycles.  Despite significant elevations in plasma bromide, no changes occurred in any of the parameters measured, which are the same as those measured in the previous study discussed.

Nevertheless, animal research continues to suggest that bromide poses a significant risk to optimal thyroid and iodine metabolism.  In the paper mentioned above by Pavelka (13) entitled “Metabolism of bromide and its interference with the metabolism of iodine,” the results of several studies that suggest risk are reported.  What follows is a select group of quotes that highlight the nature of the risk according to the author.  The first quote I would like to present points out that the chemical similarity of bromine to iodine makes it fairly obvious that significant intake of bromide poses a risk to iodine metabolism:

“Considering the chemical similarity of bromine to iodine…goitrogenic effects of bromide may be assumed.  Indeed, an enhanced bromide intake in the rat could markedly reduce iodide accumulation in the thyroid as well as in the skin.”

However, in reality, bromide toxicity is not just related solely to the levels of bromide intake.  In contrast, iodine deficiency must also exist:

“Buchberger et al studied the effects of chronic administration of large bromide doses on the biosynthesis of thyroid hormones in iodine-deficient rats.  The results of this study indicate that bromide toxicity is dependent on the state of iodine supply in the organism: the signs of hypothyroidism caused by bromide intake were significantly enhanced under the conditions of simultaneous iodine deficiency.”

Pavelka (13) goes on to point out that, as bromide levels in the thyroid increase, production of iodine-based thyroid hormones continues to decrease:

“Most probably, bromine in the thyroid remains in the form of bromide ion and, in proportion to its increasing concentration, the production of iodinated thyronines decreases.”

However, as suggested above in the quote about iodine deficiency and bromide toxicity, there is some good news:

“These results indicate that with sufficient iodine supply in the organism, a stable [I]/[Br] concentration ratio in the thyroid is rapidly established during the exposure of rats to increased concentrations of bromide, while under iodine deficiency iodine atoms in the thyroid are replaced by bromine atoms.”

How much iodine is lost from the thyroid with enhanced intake of bromide?  Vobecky et al (20) note the following:

“Under experimental conditions, more than one-third of the iodine content in the thyroid was replaced by bromine.”

Unfortunately, no mention was made of whether overall iodine deficiency co-existed.

Does any research on bromide exist that is specific to potassium bromate which, as mentioned above, may be the principal form of bromide ingested by humans due to its significant presence in the food supply?  Stasaik et al (21) note the following:

“It has been demonstrated that KBrO(3) triggers thyroid follicular cell tumors in rats.  It has been revealed in our in vivo and in vitro studies that KBrO(3) significantly increases lipid peroxidation in rat and porcine thyroid.”

However, this study also presented some good news.  The authors pointed out that antioxidants such as melatonin “…produce distinct protective effects against lipid peroxidation due to KBrO(3) in the thyroid in vivo.”  These findings were replicated in a study by Karbownik et al (22), who concluded:

“In conclusion, melatonin and indole-3-proprionic acid may be of great value as protective agents under conditions of exposure to KBrO3.”


In contrast to the many papers that suggest a detrimental impact of bromide on iodine and thyroid metabolism, particularly when iodine deficiency exists, I could find little research suggesting a similar relationship between fluoride, iodine, and the thyroid.  However, one paper by Galletti and Joyet (23), which was referenced by Abraham (12), points out the following after prolonged therapeutic administration of a daily dose of 5-10 mg fluoride to patients with hyperthyroidism:

“Thyroidal, blood and urinary radioiodine studies suggest that fluorine inhibits the thyroid iodide-concentrating mechanism.  Fluorine does not impair the capacity of the gland to synthesize thyroid hormone when there is an abundance of iodide in the blood.  However, inhibition of the thyroidal concentrating capacity when the total iodide pool is low will impose a critical limitation of hormonal synthesis, and may explain the therapeutic effect.”

In contrast, a later paper by Burgi et al (24) states the following:

“There is no convincing evidence that fluoride produces true goiters with epithelial hyperplasia in experimental animals.  There are some reports based on casual observations that fluoride is goitrogenic in man.  On the other hand, several good studies with adequate exposed and control populations failed to detect any goitrogenic effect of fluoride in man.  It is noteworthy in particular that fluoride does not potentiate the consequences of iodine deficiency in populations with a borderline or low iodine intake.”

Abraham’s study examining the impact of milligram dosing of iodine supplementation on urinary excretion of bromide and fluoride

Before reviewing this study in detail, please note the following important points from the above discussion:

  • Administration of significant levels of bromide compounds to rats, particularly when iodine deficiency co-exists, has a major adverse impact on thyroid and iodine metabolism.
  • There is little evidence that bromide delivers a similar impact in humans.
  • Because of the small amount of conflicting research available on the relationship between fluoride and thyroid and iodine metabolism, no definitive conclusions can be made.

Furthermore, there was no suggestion in any of the studies reviewed that iodine administration could lead to significant elimination of bromide and fluoride from the body.  In addition, there was no data presented that would support the hypothesis that what appears to be adverse effects of iodine administration are, in fact, signs and symptoms related to bromide and fluoride toxicity.  With that stated, though, I still feel that Abraham’s experiment on the relationship between iodine administration and bromide and fluoride elimination is very compelling and, in my opinion, warrants our consideration.

In this study 10 healthy women were administered tablets containing a combination of 5 mg iodine and 7.5 mg iodide for three months.  The results of the study are as follows:

“The baseline level of urinary fluoride was very low, but bromide concentration was 18.4 mg/24h, 3 times the ADI recommended by Van Leeuwen et al.  Following supplementation with the iodine/iodide preparation, there was a progressive increase in the excretion of fluoride and bromide.  With 3 tablets, the 24h excretion of fluoride was 17.5 times the baseline level; and for bromide, 18 times baseline level; and for bromide, 18 times baseline level.  These high levels persisted even after one month of supplementation at 3 tablets/day, being 15 times baseline level for fluoride, and 16 times for bromide.  After one month, the estimated total amount of halide excreted was 24 mg fluoride and 8700 mg bromide.”

These results led Abraham (12) to make the following conclusion:

“It is unlikely that such large amounts of halides came from the thyroid gland.  It would seem that the whole body is being detoxified.  Orthoiodo-supplementation could be used under medical supervision to detoxify the body from unwanted halides in a manner similar to the use of EDTA for the detoxification of heavy metals.”

Some final thoughts on Abraham’s experiment

Hopefully, we are in agreement that the results of this study are extremely compelling and warrant our attention.  Of course, there is a concern, as I mentioned, that use of supplemental iodine in this manner has not been suggested in any other published research.  Therefore, while I find the results of Abraham’s findings very exciting, I do feel that we should await additional studies that confirm the outcome presented before making generalized clinical recommendations.

In addition, it also must be emphasized that, while the results are suggestive, we cannot conclude at this time that milligram levels of supplemental iodine solves the primary problem discussed in this section, accumulation of bromide and fluoride in the thyroid.  Finally, it does not add credence to the anecdotal claim made by many of you that any side effects witnessed after administration of milligram levels of supplemental iodine are, in reality, signs and symptoms associated with the elimination of bromide and fluoride.  Why?  One reason is that, in his paper, Abraham (12) steadfastly maintains, as he has done in virtually every other paper of his that I have read, that no one ever experiences any type of side effect when ingesting milligram levels of supplemental iodine:

“There were no adverse effects observed on urinalysis, hematology, blood chemistry, thyroid functions and ultrasound of the thyroid.”

However, in closing, given the highly suggestive nature of all the research discussed above, I remain open-minded to the idea that milligram dosing of supplemental iodine can have a major positive impact on body burdens of bromide and fluoride and that any symptoms experienced upon supplementation are, in many cases, “detox reactions” related to bromide and fluoride elimination.  Therefore, please keep on informing me of any research or personal clinical experiences that relate to iodine administration and its impact on these two halogens.

In what will certainly be the final installment of this two-year exploration of iodine physiology, biochemistry, and clinical application, I will examine in depth the controversy surrounding diagnosis of iodine deficiency.  Also, I will present some overall conclusions from the series as well as recommendations about how all the information presented can by applied clinically.

NOTE:  For  those of you who may have missed any of the earlier iodine newsletters, they are all located at www.mossnutrition.com in the medical research and information section.  You will need your user name and password to access them, though.  Therefore, if you do not have a user name and password, please submit a request.

Moss Nutrition Report #227 – 06/01/2009 – PDF Version


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