A Perspective on High Dose Iodine Supplementation Part IV – Iodine and Breast Health

As I mentioned at the end of part III of this series, I do feel that one of greatest services provided by Guy Abraham’s writings on iodine was emphasizing to the professional nutrition community that iodine is much more than just “the thyroid nutrient.”  In fact, a large body of research which has been almost totally ignored by most of us until Abraham brought it to our attention makes a very strong argument that iodine is as much “a breast nutrient” as it is “a thyroid nutrient.”

In closing the last installment of this series, I presented the intriguing title of a paper by Aceves et al (1), “Is iodine a gatekeeper of the integrity of the mammary gland.”  While this title is certainly very dramatic given the distinct lack of attention the iodine/breast relationship has received over the years, is it deserved?  Based on the body of literature I am about to present, I hope we can agree that the answer to this question is certainly in the affirmative.  However, according to Abraham, this relationship is only part of the story.  As you may recall, Abraham recommends a supplement that is composed of both molecular iodine (I2) and iodide (I) in the form of potassium iodide.  Why?  As I mentioned in part II, one major reason is that he feels that different organs have preferential uptake of different forms of iodine.  In particular, according to Abraham, the breast seems to favor molecular iodine.  As I hope you will also see from the literature I am about to present, this claim by Abraham certainly has merit.  However, before delving into this specific facet of iodine’s relationship with the breast, I would like to present some introductory information that explains why the relationship exists at all.

SOME BACKGROUND INFORMATION ON THE IODINE/BREAST CONNECTION

Why do we need iodine at all?  Venturi et al (2) proposes an interesting evolutionary perspective to this question:

“Over three billion years ago, algae, which contain the highest amount of iodine, were the first living cells to produce oxygen, which was toxic at that time, in the terrestrial atmosphere.  So, algal cells required a protective antioxidant action in which iodides might have had a specific role.  In fact, iodides are greatly present and available in seawaters, where algal phytoplankton acts as a biological accumulator of iodides.”

Venturi et al (2) continue:

“When primitive marine vertebrates started to emerge from the iodine-rich sea and transferred to iodine-deficient fresh water and finally land, their diet became iodine deficient and also harboured vegetable iodide-competitors such as nitrates, nitrites, thiocyanates, and some glycosides.”

With this evolutionary perspective in mind, what role does iodine play in cellular metabolism?  The authors state:

“We may chronologically differentiate on the basis of the phylogenesis and embryogenesis three ways of action of iodine: 1) an ancient and direct action, on endodermal fore-gut and stomach and on ectodermal epidermis, where inorganic iodides probably act as antioxidants. 2) a recent and direct action, on fetal prehormonal thyroid and on salivary and mammary glands, thymus, ovary and on nervous, arterial and skeletal systems, where inorganic iodides are active. 3) a recent and indirect action on the thyroid and its iodinated hormones, on all vertebrate cells, which makes use of specific organic iodine-compounds: thyroxine (T4) and triiodothyronine (T3), which act in very small quantities and utilize T3-receptors.  Indeed, thyroid hormones contain less than 1 mg of iodine and less than 1/30 – 1/50 of total iodine amount.”

Thus, as I hope you can see, Abraham’s claims that iodine has varied functions throughout the body beyond those relating to thyroid hormones is certainly supported by other peer-reviewed papers.  Furthermore, other researchers certainly seem to support Abraham’s assertion that, from a quantitative standpoint, the role of the thyroid in relationship to total body iodine levels is fairly minor.

Moving on from this general description of iodine partitioning in the body, I would like to present an interesting quote from Venturi et al (2) that presents an evolutionary hypothesis why iodine is involved with the breast:

“Thyroid cells phylogenetically derived from primitive iodide-concentrating gastroenteric cells which, during evolution, migrated and specialized in uptake of iodides and storage and elaboration of iodine compounds, in order to adapt to iodine-deficient terrestrial life.  Mammary cells embryologically derived from primitive iodide-concentrating ectoderma too.”

In another paper authored solely by Venturi (3), the author provides more detailed information than what was presented above on a major function of iodine that, as you will see, plays a significant role in the explaining why iodine is important to breast health:

“We have recently hypothesized that iodide might have an ancestral antioxidant function in all iodide-concentrating cells.  In these cells iodide acts as an electron donor in the presence of H2O2 and peroxidase, and the remaining iodine atom readily iodinates tyrosine, histidine or certain specific lipids.  In fact, iodine can add to double bonds of some polyunsaturated fatty acids of cellular membranes, making them less reactive to free oxygen radicals.”

Thus, iodine, in reality, has two important functions in the body.  One, of which we are all aware, pertains to thyroid function.  The other, which is probably much less recognized by most of us but just as important, pertains to reduction of oxidant stress.  However, as noted in the following quote by Venturi (3), both have an impact on breast health:

“But what role does iodide play in mammary cells?  We may chronologically differentiate on the basis of the phylogenesis and embryogenesis two possible mechanisms of action of iodine: 1) the first is more ancient acting directly on mammary cells which embryologically originate from iodide-concentrating ectoderma and epidermis, with iodide in mammary cells acting probably as an antioxidant, 2) the second mechanism of action is more modern, with iodine acting indirectly via thyroid hormones and their specific receptors.”

In “Hypothesis: iodine, selenium and the development of breast cancer” by Cann et al (4), the authors point other aspects of the unusual and vastly under appreciated relationship between iodine and breast health.  First, while iodine can be found in several organs, only the thyroid and breast store the element:

“Although a number of tissues have iodine-concentrating capabilities (i.e., salivary glands, stomach, cervix, etc.), only in the thyroid and breast is iodine organified for storage.  In the thyroid this occurs via thyroperoxidase oxidation of iodide (I), which subsequently binds to tyrosyl residues.  In an analogous manner, lactoperoxidase organifies iodine in the breast – a process particularly active during pregnancy and lactation.”

To what is iodide (I) organified?  Molecular iodine (I2).  As I suggested in the beginning of this newsletter, I will discuss the significance of molecular iodine (I2) in the breast shortly.

Cann et al (4) also point out an interesting and little known relationship between iodine and reproductive hormones in the breast.  The authors state:

“In estradiol-treated rats, iodine deficiency has been shown to lead to pathological changes similar to those seen in benign breast disease – cystic changes, periductal fibrosis and lobular hyperplasia.  Conversely, dietary iodine reintroduction has been shown to reverse these pathological changes.  Thus, iodine deficiency appears to enhance mammary-tissue sensitivity to estrogens.”

Concerning progesterone and its relationship to iodine in the breast, the authors note:

“In dimethylbenz(a)anthracene-induced mammary carcinoma in rats, iodine supplementation has been shown to have a suppressive effect on the development of this disease.  This suppressive activity was enhanced when iodine treatment was combined with progesterone (medroxy-progesterone acetate).  The suppressed tumors were found to have a significantly higher mean iodine content than nonsuppressed tumors, with uptake apparently enhanced by progesterone.”

Of course, as I suggested in the beginning of this newsletter, there is more to the iodine-breast connection that just the fact that healthy breast tissue has a significant affinity for iodine.  As I have also suggested, the form of iodine also appears to be an important factor in determining the ultimate benefit of iodine to breast tissue.  Given that, as was stated above, the breast is one of only two organs that enzymatically convert iodide (I) to molecular iodine (I2), this important aspect of the iodine/breast relationship should not be surprising.

IODIDE (I-) OR MOLECULAR IODINE (I2) – WHICH IS BEST FOR THE BREAST?

The idea that iodine in general and molecular iodine (I2) in particular might be clinically useful for dysplastic breast tissue began in earnest with the landmark paper by Ghent (5) that, as I have mentioned in previous installments of this series, is frequently referenced by Abraham.  This paper is actually a combination of three studies on women with fibrocystic breast disease that occurred from 1975 to 1989.  In study #1, 233 patients received sodium iodide for 2 years and 588 received protein-bound iodide for 5 years.  In study #2, 145 patients from study #1 who were treated with protein-bound iodine but still had symptoms were switched to molecular iodine (I2).  Also, during study #2, 108 new patients were treated with molecular iodine (i2).  Dosage of molecular iodine (I2) during study #2 was 0.08 mg/kg body weight (Approximately 5.5 mg for a 150 lb. Individual).  As study #2 progressed, more patients were added so that, by 1989, 1365 patients were being treated with molecular iodine (I2).  In study #3, 23 patients were treated with molecular iodine (I2) at a dose of 0.07 to 0.09 mg/kg body weight.  In addition, during this final study 33 patients received an aqueous mixture of brown vegetable dye and quinine.  What were the results of these studies?  Ghent (5) states:

“Study 1: 70% of subjects treated with sodium iodide had clinical improvement in their breast disease, but the rate of side effects was high; 40% of patients treated with protein-bound iodide had clinical improvement.  Study 2: 74% of patients in the crossover series had clinical improvement, and objective improvement was noted in 72% of those who received molecular iodine initially.  Study 3: in the treatment group 65% had subjective and objective improvement: in the control group there was a subjective placebo effect in 33% and an objective deterioration of 3%.”

These findings led Ghent et al (5) to conclude:

“The fibrocystic breast reacts differently to sodium iodide, protein-bound iodide and molecular iodine.  Molecular iodine is nonthyrotropic and was the most beneficial.”

Before leaving this discussion of the Ghent et al (5) studies, you may want to know the typical length of treatment time.  While this was not noted is the abstract of the paper, Kessler (6) points out:

“Ghent and Eskin report that 6 months of therapy with iodine is minimally required to effectively reduce modularity and that the optimum response requires 18 months of treatment.” 

With the findings of Ghent et al (5) in mind, I would now like to review the paper by Aceves et al (1) so that the reasons why superior results were seen with molecular iodine (I2) can be fully appreciated.

As I have suggested, Aceves et al (1) strongly believe that supplementation of molecular iodine (I2) to women with dysplastic breast tissue will yield much better results than other iodine forms:

“…I2 is distinctly more effective in diminishing mammary dysplasia and atypia secondary to iodine deficiency.”

What follows is an overview of the review of the literature conducted by the authors that led them to this strong assertion.  While some of what I am about to present has already been stated earlier in this newsletter, I hope you will agree with me that repetition will be helpful to more fully understand this important but almost universally neglected relationship.

Iodine utilization in the healthy mammary gland

In discussing the specifics of the iodine/breast tissue relationship, Aceves et al (1) begin by focusing on iodine and healthy breast tissue.  Interestingly, in contrast to what I stated above concerning unhealthy, dysplastic breast tissue, the healthy breast during pregnancy and lactation seems to favor iodide as opposed to molecular iodine.  The authors note:

“A large body of data has demonstrated that the mammary gland during pregnancy and lactation is highly effective in capturing iodide, even more efficiently than the thyroid gland.”

Why would iodide by favored in this instance?  Aceves et al (1) continue:

“The physiological significance of this mammary I avidity has been explained as a vital evolutionary mechanism to provide the neonate with iodine to make his/her own thyroid hormones necessary to normal neural development.”

Of course, knowing the above relationship brings up an interesting question that was not posed by Aceves et al (1).  Could the competition for iodide between the fetus and pregnant mother provide at least a partial explanation why pregnant women are more susceptible to encountering hypothyroid function?  Furthermore, if the answer to this question is in the affirmative, should we place a more central focus than we have in the past on determining iodide need in our pregnant patients?  I look forward to your thoughts on this interesting question.

Next, Aceves et al (1) discuss iodine physiology in non-pregnancy, non-lactating situations.  As you will see, in these situations, molecular iodine (I2) predominates:

“…it has been demonstrated that iodine contributes to the maintenance of the normal integrity of the mammary gland.  Eskin et al showed that an iodine deficiency alters the structure and function of mammary gland in virgin rats, and that I2 is effective in diminishing ductal hyperplasia and perilobular fibrosis secondary to this iodine deficiency.”  

More on iodine and the pregnant lactating breast

In the next section of their paper, Aceves et al (1) go into more detail on the relationship between iodine and the pregnant and lactating breast:

“…it has been observed that during pregnancy and lactation, hormonal stimulation of mammary gland leads to glandular differentiation that dramatically enhance both iodide absorption and local generation of free iodine by deiodination.”

Could this enhanced affinity for iodine during pregnancy and lactation have an impact on breast health later on?  The authors state:

“A high iodine concentration in breast tissue may also explain the reduction in nodularity and tissue density that are often observed following pregnancy and lactation.  Thus a link may exist between enhanced breast iodine content during pregnancy/lactation and subsequent reduction in breast cancer risk.”

Iodine and breast abnormalities

Concerning iodine and abnormal breast growth, Aceves et al (1) make several key statements.  First, consider the following:

“…I2 treatment of patients with benign breast disease is accompanied by a significant bilateral reduction in breast size, in addition to causing a remission of disease symptoms, which is not observed when I or protein-bound iodine is administered.”

Please note again in this quote that only molecular iodine (I2) was effective in optimizing breast health.  In contrast, iodide, the form of iodine used in most supplements, was not effective.  The authors continue with their discussion of this important distinction:

“The importance of I2 in the treatments for mammary gland dysfunction has been corroborated in human and animal models.”

What are good food sources of molecular iodine (I2)?  Aceves et al (1) point out:

“Seaweeds, such as wakame, nori, or mekabu (used in sushi, soup, salads, and in powdered form as a condiment), are widely consumed in Asian countries and contain high quantities of iodine in several chemical forms, (i.e. I, I2, IO3), and protein-associated.”

Next, the authors point out some epidemiologic data that supports the idea that iodine optimizes breast health:

“This element has been associated with the low incidence of benign and malignant breast disease in Japanese women (iodine average consumption in the Japanese population is 5,280 µg/day versus 166-209 µg/day in the UK and USA, respectively).”

By the way, before continuing, did you notice in the above quote that Aceves et al (1) are stating that the average amount of iodine consumed daily by the Japanese population is significantly lower than the consumed amount claimed by Abraham?  I will be addressing this major controversy a bit later.

Why would molecular iodine (I2) be more effective in optimizing breast health than iodide (I)?  To begin to answer this fairly complicated question, I would like to present a quote from the paper “The thyroid, iodine and breast cancer” by Smyth (7).  As you will see, this quote notes how the thyroid and the breast compare in terms of iodine metabolism:

“Both organs require a method of oxidizing I to I2 (organification) in order to produce iodoproteins.  This involves the presence of H2O2 as an oxidizing agent catalyzed by thyroid peroxidase (TPO) in the thyroid and by lactoperoxidase (LPO) in the breast.”

According to Aceves et al (1), based on research in virgin rats, LPO is present in the breast only during pregnancy and lactation.  How might a relative inability to convert iodide (I) to molecular iodine (I2) during times other than pregnancy and lactation most directly affect breast health?  As you will see, the answer lies with the relatively little known aspect of iodine that was mentioned above, its ability to act as an antioxidant.  The authors point out:

“…we demonstrated that in mammary gland homogenates from virgin rats, the addition of I2, but not potassium iodide (KI), significantly decreases lipoperoxidation measured by the thiobarbituric acid reaction and expressed as malondialdehyde (MDA).”

Thus, it appears that, based on research by Aceves et al (1), molecular iodine (I2) but not iodide (I) can quench lipid-based free radicals in the breast that, left unchecked, might lead to maladapative breast tissue formation.  Since, the non-pregnant, non-lactating breast cannot readily convert iodide (I) to molecular iodine (I2), it would certainly follow that administration of the latter would lead to superior results.

The impact of iodine on mammary gland neoplasia

Next, Aceves et al (1) discuss the impact that iodine has on breast neoplasia.  As an introduction to this section, the authors discuss how breast neoplasia might form:

“In mammary cancer from humans or animals the cell oxidative status is disrupted.  It has also been postulated that reactive oxygen species (ROS) such as single oxygen (O2), superoxide anions (O2), hydrogen peroxide (H2O2) are intimately related in the etiology of cancer.”

As you might expect by now, because it can function as an antioxidant, molecular iodine (I2) has a significant impact on the formation of ROS in the breast?  The authors elaborate:

“…we and others postulate that I2 or other oxidized iodine species (I.), either act in competition with ROS for different cellular components, or neutralize .OH radicals by the formation of HOI, resulting in less cellular damage.”

From this the authors conclude:

“Thus, assuming that iodine may exert this antioxidant effect, it is evident that carcinogenetic mechanisms may involve the turning off of genes related to the local generation of oxidized iodine components.”

Why would iodide not have the same effect?  Again, the reason has to do with lack of lactoperoxidase (LPO):

“Although in a wide variety of primary or immortalized mammary tumors, cells…are capable of taking up I, effectively, the LPO necessary to oxidize it is not present.”

Next, Aceves et al (1) present more epidemiologic data to support their point of view in relationship to iodine and breast neoplasia:

“The notion that oxidized iodine is the active chemical form with a tumor suppressive effect is strongly supported by data showing that anticarcinogenic effects of seaweeds or iodine supplements contain in both cases a portion of oxidized iodine.  Previously, we mentioned that seaweeds contain iodine in several chemical forms although the exact proportion is not known.”

The authors then discuss breast cancer research that employs iodine supplements containing molecular iodine (I2):

“In mammary carcinomas induced by dimethylbenzanthracene (DMBA) in rats, Lugol’s solution (mixture of Iand I2) supplementation exerts a suppressive effect on the development and size of the neoplasias.”

Interestingly, Aceves et al (1) note that this effect, as was mentioned above, is enhanced when progesterone is administered concurrently.  The authors then discuss additional research that lends credence to this molecular iodine (I2) connection:

“Data generated in our laboratory have shown that chronic administration of I2 exhibits a potent protective effect (70%) on mammary cancer induced by the carcinogen N-methyl-N-nitrosourea (MNU).  This effect is exerted only by I2 but not by KI or T4.  The suppression by I2 treatment is accompanied by the development of latent mammary cancers that do not progress to overt cancers, suggesting that the mechanism of action of I2­ is due to a decrease in carcinogenesis at the promotion level.”

A clinical study on the impact of molecular iodine on breast pain related to fibrocystic breasts

Given that most of the research cited by Aceves et al (1) was animal studies, only one paper presented so far in this installment, the Ghent et al (5) study, has actually focused on the clinical environment.  Therefore, I wanted to next present an overview of a recently published study that has clinical outcome as its primary focus.  In “The effect of supraphysiologic levels of iodine on patients with cyclic mastalgia” by Kessler (6), 111 euthryoid women aged 18 to 50 years with a history of breast pain were evaluated.  In the introduction to this study, the author does point out that clinical studies on the use of iodine with breast dysfunction do exist (Most notably, the Ghent et al study discussed above).  However, none of these studies, including the Ghent et al (5) study, employed control groups.  Kessler (6) elaborates:

“The literature suggests that daily administration of supraphysiologic levels of iodine for 6 months can remediate breast pain in a majority of women with clinical cyclic mastalgia associated with fibrocystic breasts.  However, to date, there has not been a controlled multicenter trial with a well-characterized dosage form of iodine to determine whether there are benefits to patients over and above placebo effects.”

Furthermore, in affirming an ongoing theme of this newsletter series, Kessler (6) points out that little research is available concerning optimal dose levels:

“In addition, if iodine is shown to be beneficial, there are no clinical studies that provide information concerning the optimal dose of iodine for treating breast pain.”

With the above in mind, consider the author’s hypotheses for the study:

“The primary hypotheses for this study are (a) patients treated with iodine will exhibit a greater decrease in breast pain than women treated with placebo; (b) there will be a dose-related effect for iodine, such that patients treated with lower doses will report less benefit than those treated with higher doses; and (c) any reductions in nodularity will be associated with pain relief and require at least 3/mg/day of iodine.”

Concerning the goal of determining optimal dosing and safety, Kessler (6) states the following:

“In addition to testing the above hypotheses, this study determined the specific dose of iodine that produces the largest decrease in breast pain severity, as well as the safety of iodine as a treatment for breast pain.”

Before continuing, please note again that Kessler (6) is hypothesizing that optimal dosing will be considerably less than that recommended by Abraham.  More on that controversy later.  Also, I assume, based on the above discussion, you are wondering by now what form of iodine was used by the author.  As you will see in the quote below, it is a special iodine compound that converts to molecular iodine (I2) in the stomach:

“The active study drug (IoGen) is a novel iodine formulation based on sodium iodide and sodium iodate; these two food additives are generally regarded as safe for general consumption.  The test article generates molecular iodine (I2) in the stomach upon dissolution in gastric fluid.  Molecular iodine was selected as the active iodine species since several studies have demonstrated that molecular iodine is less thyrotoxic than iodide due to a different tissue distribution in mammals.”

What was the basic study protocol?  The author states:

“Subjects were recruited by media and were randomized to receive one tablet per day that delivered 0, 1.5, 3.0, or 6.0 mg of molecular iodine, according to a computer-generated randomization list in blocks of six in a dosing ratio of 1:1:2:2.  The study period included an observational pretreatment menstrual cycle, a run-in menstrual cycle (cycle 1) during which all subjects received placebo tablets, six menstrual cycles of daily dosing with randomized drug (months 1-6), and a follow-up safety assessment 2 months after the last dose of study drug.”

What were the results of the study?  First, the breakdown of those who reported at least a 50% reduction in breast pain was as follows:

“These values ranged from a low of 8.3% for the placebo group to a high of 51.7% for the 6.0 mg/day group at month 6.  The percentage of responders increased with dose at months 3 and 6, and all treatment groups except placebo demonstrated an increase in this variable at month 6 as compared to month 3.”

Concerning three variables (pain, tenderness, and nodularity), twelve subjects improved.  What can be stated about the twelve that improved?  Consider the following:

“Twelve subjects (seven who received 3.0 mg/day and five who received 6.0 mg/day) improved in all three of the physician-assessed categories (pain, tenderness, and nodularity) at the 5-month assessment point, although the difference in the frequency of improvement across groups was not statistically significant.  None of the subjects in the placebo or 1.5 mg/day groups had such an improvement.”

What percentage of women improved with all three parameters based on category?  The author states:

“Of the 80 subjects who had all three clinical findings at baseline and who completed at least 5 months of double-blind therapy, 7 of 28 in the 3.0 mg group and 5 of 27 in the 6.0 mg group exhibited a reduction in all three physician assessed variables compared to no subjects in either the placebo or 1.5 mg group.”

What about side effects?  Several were noted and, with the exception of headaches, the percentages were consistent between dosage groups.  Kessler (6) notes:

“The 10 most frequently reported treatment-emergent adverse events were upper respiratory tract infection (n = 29; 26%), headache (n = 23, 20%), sinusitis (n = 14, 12%), nausea (n = 11, 9.9%), acne (n = 10, 9.0%), back pain (n= 10; 9.0%), diarrhea (= 10, 9.0%), dyspepsia (n =9, 8.1%), rash (n = 9, 8.1%), and abdominal pain (n = 7, 6.3%).”

As I mentioned, concerning headaches, the percentage breakdown was different based on dosage:

“Headaches were the only adverse event that occurred in a different proportion among the treatment groups; 41% of the placebo group reported headaches as compared to 6.3% of the 1.5 mg/day group, 26% of the 3.0 mg/day group, and 12% of the 6.0 mg/day group.”

What about the impact of iodine supplementation on thyroid function?  Kessler (6) states:

“No statistically significant change was observed in any of the five thyroid function tests (T3, T4, T uptake, TSH, and FT3)) for any treatment group, as the mean changes were all within the normal range and considered not clinically significant.”

In the discussion section, the author first points out how the findings of his study greatly parallel those of Ghent et al (5):

“Several aspects of the current study are consistent with previously reported iodine-based trials.  Ghent and Eskin concluded (a) 3.0 to 6.0 mg/day of iodine are needed to provide relief from cyclic mastaglia; (b) the majority of pain relief is observed by month 6; and (c) the maximum reduction in nodularity requires 18 months of therapy, but some improvement is observable after 6 months.”

Concerning comparisons between the studies in relation to nodularity and breast pain, Kessler (6) states the following:

“…improvement in physician-assessed nodularity and breast pain was not observed in this study at a dose less than 3.0 mg/day, as previously suggested.”

In concluding this paper, the author presents an overview of how iodine acts to prevent formation of abnormal breast tissue:

“The mammary tissue of women with clinical cyclic mastalgia may actively sequester iodine as a consequence of a subtle imbalance in the dynamic control of prolactin.  Increased levels of iodine, in turn, may lead to formation of iodolipids.  The antiproliferative activity of iodolactones could be the basis for the reported effects of iodine on breast tissue and the effects observed in this trial, as previously suggested.”

More specifically, Kessler (6) suggests the following in terms of the effect of iodolactones on breast tissue:

“Cann et al first suggested that iodolipids may be the basis for iodine-induced suppression of mammary hyperplasia and tumor growth that has been observed in animal models.”

SOME FINAL THOUGHTS ON THE IODINE/BREAST CONNECTION

As I have mentioned, there is no question in my mind that iodine status is a critically important yet vastly under appreciated issue in breast health.  Furthermore, I feel a strong case has been made that the form of iodine being administered to various patients requires serious consideration.  Therefore, I feel Abraham deserves our appreciation for bringing these issues to our attention.  However, other controversies that have been underlying themes in this series remain.  Why?  First, please note again that in the Kessler (6) study, success rates were not enormous for any dosage.  In fact, as was noted, the best result was with breast pain where 6.0 mg per day provided 51.7% pain reduction after six months.  However, even more importantly, the ongoing concern about side effects of milligram dosing of iodine was in no way, at least for me, eased by Kessler’s data.  For, even though the incidence of various side effects was not statistically significant compared to placebo, I felt that the incidence of various side effects was much higher than what is typical of natural substances.  Is this a concern?  I feel it is.  Why?  While the rate of occurrence may not be statistically significant, this rate may be significant in terms of patient management in the routine clinical nutrition setting where insurance coverage is rare and patient skepticism is a common reality.  Therefore, while I feel the papers presented this month affirm Abraham’s contention that iodine has an important clinical role beyond thyroid health and that the forms of iodine being administered need to be considered, they do not even begin to suggest the panacea-like qualities claimed by Abraham.  Therefore, for me, after reviewing the papers discussed above, I feel that the flames of controversy concerning optimal dosing in terms of efficacy and safety have only been intensified.

In the next installment I will be examining key issues where there is much less agreement between Abraham’s claims and what has been reported in both the medical literature and anecdotally from you.  Using the criteria I outlined in part III of this series, I hope to keep bias at a minimum and objectivity at the forefront so that at least a beginning of a much needed consensus on the major controversies relating to dosage and safety of milligram dosing of iodine can be forged.

Moss Nutrition Report #217 – 10/01/2007 – PDF Version

REFERENCES

  1. Aceves C et al. Is iodine a gatekeeper of the integrity of the mammary gland? J Mammary Gland Biol Neoplasia. 2005;10(2):189-96.
  2. Venturi S et al. Role of iodine in evaluation and carcinogenesis of thyroid, breast and stomach. Advances in Clin Path. 2000;4(1):11-17.
  3. Venturi S. Is there a role for iodine in breast diseases? The Breast. 2001;10(5):379-82.
  4. Cann SA et al. Hypothesis: iodine, selenium and the development of breast cancer. Cancer Causes Control. 2000;11(2):121-7.
  5. Ghent W et al. Iodine replacement in fibrocystic disease of the breast. Can J Surg. 1993;36:453-460.
  6. Kessler JH. The effect of supraphysiologic levels of iodine on patients with cyclic mastalgia. Breast J. 2004;10(4):328-36.
  7. Smyth PP. The thyroid, iodine and breast cancer. Breast Cancer Res. 2003;5(5):R110-3.