In the last installment of this series I examined in detail how iodine finds it way into the thyroid. As you may recall, this process is largely regulated by a mechanism called the sodium iodide symporter (NIS). Given its complexity, though, why exactly is it important that we understand the NIS and the whole process of transport into the thyroid? The reason, as I suggested, is the fact that, despite all the very positive (iodine and breast health) and negative information I have presented on iodine so far, the main controversy underlying the issue of milligram iodine dosing is the impact high dosing has on the thyroid. Is it harmful to the thyroid? As I have suggested throughout this series, it is indeed unfortunate that this question seems to have divided the nutrition community into two passionate and somewhat confrontational camps. One camp very often answers the question with a self-righteous, self-assured, all-encompassing “No”. The other camp, in turn, answers “Yes” with equal fervor. Nevertheless, for me, as I have suggested all along, the passion that each camp has for positions that are diametrically opposed leaves me with more confusion, not less. Of course, this confusion was partially ameliorated when we learned that Abraham’s claim that high levels of dietary iodine had no adverse effect on the Japanese was incorrect. In fact, a significant volume of literature suggests that a small but significant portion of the Japanese population has suffered thyroid problems due to high levels of dietary iodine. However, is this epidemiologic association enough to confidently and, with absolute assurance, answer the question mentioned above that has created so much passion and controversy? In my opinion, no.
Ultimately, I do believe that if we are ever to take this question out of the realm of fanaticism and passion and into a world of logic and dispassionate evaluation, we must have a much better understanding of what exactly happens when the thyroid first encounters milligram doses of iodine. For me, this understanding can only come when the workings of the NIS are fully appreciated.
Based on part VI of this series, what do we know about the NIS? First, because of large fluctuations in the amount of iodine to which we are exposed in the food supply, the NIS is a necessary “checkpoint” to keep the amount of iodine entering into the thyroid fairly constant. Second, genetic aberrations plus a series of environmental factors such as toxicity and inflammation can adversely affect the ability of the NIS to do its job correctly. Before continuing, I would like to elaborate a bit on this aspect of NIS function. On the surface, knowing that functional medicine issues such as inflammation and toxicity can affect the rate of iodine flow into the thyroid may seem relatively insignificant. However, I do feel that once this relationship is fully appreciated, our attitudes on this controversy of milligram dosing of supplemental iodine must be profoundly altered. In turn, the simple question of whether high dose iodine is “good” or “bad” for the patient becomes completely inappropriate. Instead, we must now ask whether certain unique aspects of the patient’s overall biochemistry and physiology are causing the patient to react negatively or positively to high dose iodine. If this is true, we can no longer simply condemn or praise iodine when bad or good things happen after iodine administration. In particular, if something bad happens, we must now ask, in addition to the question of whether high dose iodine per se is causing problems, whether something else in the patient’s unique biochemical/physiologic profile is contributing to a negative reaction to iodine. Next, if we find that this is true, we must make efforts to correct the underlying biochemical/physiologic imbalances first before just reflexively condemning milligram dosing of supplemental iodine.
Of course, even with the above in mind, evidence presented in part VI does suggest that, independent of any other functional factors such as toxicity or inflammation, high levels of iodine exposure in and of itself can potentially have an adverse impact on NIS function. While this adverse impact, as I mentioned in the previous installment, can take several different pathways, the most notorious and well known is The Wolff-Chaikoff Effect. As you might expect, given that Abraham fervently believes that milligram dosing of iodine is almost totally devoid of any adverse effects on the thyroid, he has been quite adamant in his assertions that, in reality, the Wolff-Chaikoff effect does not exist. Therefore, I would now like to explore the Wolff-Chaikoff effect in detail so that you can make an intelligent and informed decision on this key aspect of the high dose supplemental iodine debate.
The Wolff-Chaikoff effect – What it is based on published research on the subject
As you will see, the vast preponderance of researchers in the area of iodine and thyroid physiology suggest, without a doubt, that the Wolff-Chaikoff effect does, in actuality, exist. However, what is even more interesting, given Abraham’s aggressive condemnation of those who believe in the existence of this effect, is that most of these researchers, as you will see, feel that, overall, the Wolff-Chaikoff effect plays a minor role in the relationship between iodine and thyroid function. Therefore, I must admit that I am truly mystified why Abraham would make this such a major point of contention. Nevertheless, I will explore Abraham’s point of view in detail in the next installment so that you can decide for yourself if Abraham’s anger and venom is warranted.
To begin my examination of the Wolff-Chaikoff effect, I would first like to consider it from a historical perspective. Eng et al (1) note the following concerning its discovery:
“Autoregulation in the thyroid refers to the regulation of iodine metabolism within the thyroid gland, independent of TSH. It was first reported by Morton et al. in 1944, who observed that large amounts of iodide inhibited the formation of thyroid hormones by incubated sheep thyroid slices. Wolff and Chaikoff then reported that organic binding of iodide with the rat thyroid was blocked when the plasma iodide level achieved a critical threshold. This inhibition defines the Wolff-Chaikoff effect. They next demonstrated that this inhibitory effect of excess iodide was transient, lasting from 26-50 h, and that the thyroid escaped or adapted to prolonged iodide excess, resuming near-normal hormone synthesis.”
Why does the Wolff-Chaikoff effect last for only a short period of time? Eng et al (1) continue:
“Braverman and Ingbar suggested that adaptation to the acute Wolff-Chaikoff effect was caused by a decrease in iodide transport into the thyroid, which reduced the intrathyroidal iodide to concentrations that were insufficient to sustain the decreased organification of iodide.”
Could this decrease of iodide transport into the thyroid be mediated by the NIS? This is exactly what Eng et al (1) found in their experiments:
“It had been postulated in 1963 that the adaptation to or escape from the acute Wolff-Chaikoff effect was caused by a decrease in the active transport of iodide from the plasma into the thyroid, thereby decreasing the high concentrations of intrathyroidal iodide that inhibit hormone synthesis. We have now reinvestigated this postulate by determining the level of NIS mRNA and protein in the thyroids of iodide-exposed rats. The level of NIS mRNA significantly decreased after 1 and 6 days of iodide ingestion. The decrease in NIS protein was even more dramatic, decreasing to approximately 23% of the control values at both time points. The decrease in NIS occurred in the absence of a significant increase in TSH…”
From these findings the authors concluded:
“In summary, we have shown that excess iodide, given to rats, chronically or acutely decreases both thyroid NIS mRNA and protein. Our findings are consistent with the hypothesis that the escape from the Wolff-Chaikoff effect is caused by a down-regulation of the NIS, resulting in decreased iodide transport into the thyroid.”
More detail on the Wolff-Chaikoff effect, including doses of iodide needed to produce the effect, can be found in the paper by Anguiano et al (2):
“…the thyroid gland has regulatory mechanisms that maintain normal synthesis and secretion of thyroid hormone over a wide range of iodine availability. Currently, the recommended daily iodine intake is 150 Âµg/day, and the safe upper limit (UL) is 1.1 mg/day which comes from the Braverman group’s studies in humans, in which more than 1.5 mg of I– daily induced small but significant decreases in serum thyroxine (T4) and triiodothyronine (T3) concentrations and a significant increase in the thyrotrophin (thyroid-stimulating hormone, TSH) concentration. When moderately high amounts (3-10 times the UL) of I– are given to euthyroid subjects, a transient decrease in the synthesis of TH occurs for 24-48 hours. This inhibition of TH synthesis is called ‘the acute Wolff-Chaikoff effect,’ and is due to increased intrathyroid iodine concentrations which inhibit the iodination of tyrosyl residues of thyroglobulin (Tg) by thyroperoxidase (TPO). After 48 hours of I– excess, the thyroid gland escapes from this effect by an adaptation that decreases the thyroid iodine trap, thereby decreasing intrathyroid iodine concentration. Excess I– inhibits the expression of the mRNA and protein of the sodium/iodide symporter (NIS) and other thyroid functions, as well as TPO mRNA expression, Tg proteolysis, hormone secretion, thyroid blood flow, glucose and amino acid transport, and thyroid growth.”
Thus, a significant body of research seems to suggest that the Wolff-Chaikoff effect is a legitimate phenomenon that can be induced by only a few milligrams of supplemental iodide and is physiologically mediated by inhibition of the NIS. However, just knowing that the Wolff-Chaikoff effect exists does not really tell us what we truly want to know. I would assume that what we all really want to know is whether the Wolff-Chaikoff effect is a clinically relevant concern in deciding whether to supplement patients with milligram doses of iodine. To begin to address this, I want to note an important but subtle point, the importance of which will become more apparent when I discuss Abraham’s comments on the Wolff-Chaikoff effect. Hopefully you have noticed that none of the authors who issued the quotes above appear to be “freaking out” about the Wolff-Chaikoff effect. Rather, the tone of the quotes seem to suggest that, while we need to be aware of the existence of the effect, there is no need to issue sweeping prohibitions against doses of iodine higher than the RDA because the duration of the effect is fairly short. In fact, this positive attitude towards milligram dosing of supplemental iodine in spite of the existence of the Wolff-Chaikoff effect is particularly evident in papers that discuss the use of supplemental iodine with patients who have issues of breast health. As you may recall from part IV of this series, Kessler reported in the paper “The effect of supraphysiologic levels of iodine on patients with cyclic mastalgia” that supplementation of 3-6 mg molecular iodine produced very positive findings in patients suffering from breast pain. While Kessler did not mention the Wolff-Chaikoff effect directly, he did point out that some patients did demonstrate adverse effects on the thyroid but were not clinically significant:
“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.”
More specifically, Kessler noted the following thyroid related effects:
“The largest mean change from baseline to the maximum value in TSH at any time point was 1.2 mU/ml for the 6.0 mg/day treatment group. Low TSH levels were observed for eight subjects receiving molecular iodine; these returned to normal in all but one of the subjects within several months after discontinuation of therapy.”
To me, these quotes suggest that while milligram dosing of iodine can have adverse effects on thyroid function consistent with the Wolff-Chaikoff effect, this effect is not profound enough to contraindicate the use of 3-6 mg of molecular iodine per day in selected patients under controlled circumstances.
Why is the Wolff-Chaikoff effect of minimal concern clinically to researchers using milligram dosing of molecular iodine with women suffering from suboptimal breast health?
If the Wolff-Chaikoff effect truly does exist, why is it that certain iodine researchers seem to minimize its impact clinically? This question was addressed in a fascinating paper entitled “Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland: Evidence that chronic administration has no harmful effects” by Anguiano et al (2). As you will see, the central premise of the paper revolves around an important but little recognized point about iodine nutriture that was made in the last installment of this series, the form of iodine being supplemented is an extremely important clinical consideration. Specifically, the actions of supplemental iodide (I–) are very different physiologically than the actions of molecular iodine (I2). As a review of this key issue, consider this quote from the first paragraph of the paper by Anguiano (2):
“…it has been demonstrated that iodine distribution in the organism depends on the chemical form of iodine ingested, and that molecular iodine (I2) is not totally reduced to iodide (I–) in the blood before it is absorbed systemically from the gastrointestinal tract. Indeed, in iodine deficiency conditions, I– appears to be more efficient than I2 in restoring the thyroid gland to normal from a goitrous state, whereas I2 is distinctly more effective in diminishing mammary dysplasia and atypia resulting from iodine deficiency.”
Of course, Anguiano et al (2) acknowledge that many have viewed these findings using iodine to improve breast health with caution due to concerns about an adverse impact on thyroid function:
“Nevertheless, these findings have been viewed with caution because exposure to moderate or high iodine is thought to be potential risk to thyroid physiology (leading to hypothyroidism or autoimmune disease) as well as to general health (retinal damage).”
In response to these concerns the authors point out:
“Careful examination shows that pathological responses occurred at low or moderate iodine intake in patients with underlying or evident thyroid pathology (e.g., Hashimoto’s thyroiditis, history of treated Graves’ diseases, etc.) or in normal subjects only with excessively high doses of iodine or I– (>20 mg/day). In contrast, no damaging effects were reported in either the human or animal studies that used therapeutic I2 concentrations (3-15 mg/day).”
Could the reason for these differences in the way I– and I2 affect thyroid function be related to differences in the Wolff-Chaikoff effect? This is exactly what Anguiano et al (2) found with their experiments. On one hand, I–generated a classical Wolf-Chaikoff effect:
“Exposure of the thyroid gland to high levels of I– results in the acute Wolff-Chaikoff effect, in which thyroid hormone synthesis is inhibited. This inhibition is transient, lasting from 24 to 48 hours, after which the thyroid has adapted to prolonged iodine excess, resuming near-normal hormone synthesis.”
More specifically, the authors detected the following changes in thyroid function with IÂ– supplementation:
“In relation to the effect of I– excess, our data corroborated the earlier report that thyroid gland exhibits the classical inhibition of NIS and thyroid peroxidase expression, as well as the transient decrease in T4 and T3 circulating levels. In addition, we found that both the mRNA and activity of thyroid deiodinase type 1 and the expression of pendrin mRNA also decrease, suggesting that the I– effect on the thyroid machinery includes, besides reducing I– uptake, a decrease in the generation of thyroid hormone.”
In contrast, while I2 still generates a Wolff-Chaikoff effect, the overall impact is not nearly as profound:
“…a moderately high concentration of I2 triggers the Wolff-Chaikoff effect in the thyroid gland, that is, diminished NIS, thyroid peroxidase, and deiodinase type 1 expression, but without the typical transient decrease in the levels of circulating thyroid hormones…”
From these findings, Anguiano et al (2) conclude:
“These data indicate that the uptake and metabolism of iodine are organ-specific and differ depending on the chemical form in which it is ingested, and they provide additional evidence that a chronic, moderately high I2supplement causes no harmful secondary effects on health (e.g., body weight, thyroid economy, or reproductive cycle). Thus, we propose that I2 supplementation should be considered for use in clinical trials of breast cancer therapies.”
What can be concluded about the Wolf-Chaikoff effect based on the information presented thus far?
- A large amount of published information seems to make it clear that the Wolf-Chaikoff effect indeed occurs in both animals and humans.
- The existence of this effect does not preclude the idea that iodine supplementation can be used both safely and effectively in doses higher than RDA levels.
- The clinical impact of the Wolff-Chaikoff effect can be greatly minimized when careful attention is given to both the dose and the form of iodine supplementation. In fact, under these circumstances, doses up to 15 mg per day appear to be quite safe for the majority of patients.
Of course, I would suspect by now you may be wondering, given what I have just stated, why, as reported in part V of this series, so many Japanese experienced adverse thyroid-related reactions to similar doses of iodine from seaweed ingestion. To me, the first reason is fairly obvious. Unlike the controlled circumstances of administration advocated in the breast health studies discussed so far, Japanese populations have been ingesting comparable doses of iodine under circumstances where no controls exist in terms of duration. However, the second reason, based on what I have presented above, probably provides the most obvious reason why so many reactions occurred. According to Hou et al (3) in their study “Determination of chemical species of iodine in some seaweeds” most of the iodine in seaweed occurs in the I– form:
“In leachates of marine algae, 61-93% of soluble iodine exists as I–…”
Before closing this discussion, I do want to report that a claim made previously in this series may have been in error. In part IV of this series I did discuss a study by Aceves et al(4) that suggested seaweed is a good source of molecular iodine. The paper by Hou et al (3) now makes it clear that this claim is most likely in error. I apologize for any confusion I may have created and thank you for your understanding as I continue to try to make sense of all the divergent claims and different studies on iodine.
Additional information on environmental factors that can adversely affect NIS function
Hopefully, I have made a plausible case for the idea that supplemental iodine can inhibit NIS activity and this inhibition is not the same for all forms of supplemental iodine. However, as I mentioned, Abraham passionately disagrees with the idea that iodine supplementation can create the Wolff-Chaikoff effect. Therefore, I will be reviewing Abraham’s point of view on this issue in great detail. For now, though, I would like to round out this discussion on NIS function by going into more detail on factors that can have an adverse impact on NIS function. In turn, I hope to present a convincing hypothesis that, when patients have adverse thyroid-related reactions to iodine supplementation, the best answer may not always be related to adjustments in the iodine supplementation. In contrast, the answer may depend on optimization of NIS function via the use of functional medicine modalities that can correct or eliminate environmental factors that adversely affect NIS function.
Other toxins besides perchlorate that can inhibit NIS function
Thiocyanate – According to Erdogan (5), the following can be stated about thiocyanate (SCN–):
“SCN–…is a potent inhibitor of iodide transport…”
Where can thiocyanates be found? The author states:
“Consumption of naturally occurring goitrogens, certain environmental toxins and cigarette smoke can significantly increase SCN– concentrations to levels potentially capable of affecting the thyroid gland. Certain other foodstuffs like almonds, cabbage, turnip, mustard and cow-milk are potential sources of SCN–.”
Where else can thiocyanates be found? Roman (6) states the following:
“…thiocyanates is found in Brassicae plants including cabbage, cauliflower, kale, rutabaga, and kohlrabi, as well as in tropical plants such as cassava, lima beans, linseed, bamboo shoots, and sweet potatoes.”
Certain flavonoid compounds can also inhibit NIS activity. Schroder-van der Elst et al (7) point out:
“…for the population in general, with apigenin and luteolin or other flavonoids in megadose intake, it has to be taken into account that in normal thyroids the iodide uptake is lowered and goiter will develop.”
Before, leaving the discussion on natural substances that inhibit NIS activity, I do realize these quotes suggest that foods that we consider to be some of the healthiest appear to be a major part of the problem. Therefore, it is important to keep in mind the word “megadose” contained in the last quote. My interpretation of almost all the literature on this subject suggests that NIS suppression with these substances is only a concern with patients who are ingesting the massive amounts that would be found in “fad” diets such as the cabbage juice diet, etc.
Bromide – According to Wolff (8):
“…large concentrations of bromide are required to inhibit thyroid iodide accumulation and these may be toxic…”
Because of the large quantities required, Wolff (8) feels that bromide is not a significant NIS inhibitor. However, Abraham, due to the presence of brominated flour in the diet of many Americans, takes an opposing position stating that the average American is ingesting enough brominated flour to have an adverse impact on NIS activity.
Pharmaceuticals – According to Shen et al (9), several pharmaceuticals that are often ingested by patients can either increase or decrease NIS function:
“Many drugs may affect thyroid NIS status by modulating its expression. Hydrocortisone, dexamethasone, sex steroids, RU486, amiodarone, bromide, and ketoconazole are known to decrease thyroidal iodide uptake or NIS expression.”
Concerning upregulation of NIS function, the authors state the following:
“In contrast, adenosine and retinoic acid increase thyroidal iodide uptake and NIS expression.”
Finally, Shen et al (9) point out that the commonly used antipsychotic lithium can down regulate iodine uptake into the thyroid and ethanol can upregulate iodine uptake.
Hopefully, with the above in mind, you can see that providing standard iodine dosing to patients without any awareness of patient history that might affect NIS activity can create ample opportunity for adverse, thyroid related side effects.
How can nutritional/functional medicine practitioners minimize NIS dysfunction that can lead to the Wolff-Chaikoff effect and other adverse reactions to iodine supplementation?
As I have been suggesting, it appears from an overall standpoint that even though milligram dosing of iodine can adversely affect function of the sodium/iodide symporter (NIS), leading to the Wolff-Chaikoff effect and other disturbances in thyroid function, milligram dosing of iodine can still be safely used in many if not most patients since the NIS is designed to accommodate large variations in iodine dosage. However, I feel it is also very obvious that, due to a variety of environmental factors, the NIS can be adversely affected so that it loses its ability to optimally protect the thyroid from any adverse affects that might occur during variations in iodine dosage. With this reality in mind, then, how can we as nutritional/functional medicine practitioners optimize NIS function so as to create the widest margin of safety possible? Based on what I have presented so far, I would like to make some suggestions concerning ways that we can create the lowest possible risk for adverse reactions to iodine supplementation:
Determine whether the following functional medicine factors are present that would create suboptimal NIS function:
- Check for genetic predisposition to thyroid disorders and/or reactions to iodine supplementation. The best way clinically to determine genetic predisposition is learning about family history.
- Evaluate for the presence of systemic inflammation that could adversely affect NIS activity using modalities such as clinical examination, white cell count, differential, and C-reactive protein. If present, use functional medicine modalities to reduce inflammation as much as possible.
- Evaluate for the presence of metal or chemical toxicity. In particular, gain information about the following:
- Bromide intake (This issue will be more fully explored when I review Abraham’s view on the NIS).
- Perchlorate exposure
- Tobacco use (A significant source of thiocyanate)
- Significant intake of natural sources of thiocyanates such as vegetables in the brassica family and foods such as cassava, lima beans, linseed, bamboo shoots, and sweet potatoes.
- Alcohol use
- Commonly used pharmaceuticals such as cortisone, testosterone, estrogen, and lithium.
Before leaving this section on toxins and NIS activity, please keep in mind the following key points concerning clinical management:
- Many patients will be ingesting various combinations of the factors listed above. Unfortunately, the cumulative effect on NIS activity is largely unknown.
- Any changes in usage of the environmental factors listed above during iodine treatment could possibly create a situation where a dosage that is currently being well tolerated changes to one that is linked with thyroid-related symptoms.
- Ideally, to increase the predictability that patients will not experience adverse thyroid related reactions to a given dose of iodine, efforts to reduce toxin exposure and to detoxify should be initiated before commencing with milligram dosing of supplemental iodine. In contrast, Abraham strongly feels that supplemental iodine itself can act as a powerful detoxifier. More on that perspective in the next issue.
Can NIS activity be measured clinically?
As I mentioned in the last issue, it has been suggested that a laboratory test exists that can measure NIS activity. This test, the saliva/serum iodide ratio, has traditionally been used to help determine the presence of hereditary and congenital defects in iodide transport. However, in “The saliva/serum iodide ratio as an index of sodium/iodide symporter efficiency” by Abraham et al (10) the authors suggest that the ratio can also be used to detect milder forms of NIS dysfunction that might occur in our patients:
“Measurement of stable iodide in serum and saliva under standardized conditions seems the ideal procedure for fine tuning the assessment of the iodide transport efficiency, and it is the least invasive way to assess response of the symporter function following intervention.”
The authors continue:
“A ratio near unity would indicate a severe defect/damage/inhibition of the symporter function. An increase in the ratio following intervention would reflect an improvement in the symporter function.”
Whereas traditional testing to detect congenital/hereditary transport defects employed radioactive iodine, Abraham et al (10) suggest that an iodine load similar to what is used in the loading test mentioned previously could be used as a suitable replacement:
“Assessing whole body iodine sufficiency and iodide symporter function can be performed following the same loading test. A 24 hr urine collection is initiated after 50 mg iodine is ingested. Twenty-four hours after the load, serum and saliva samples are obtained.
To ascertain the validity of this hypothesis, the authors conducted some preliminary human studies. In the first, 14 normal subjects who had ingested supplemental iodine until they were determined to have ideal iodine levels were evaluated. As you may recall, ideal levels, according to Abraham, occur when at least 90% of a 50 mg loading dose of iodine/iodide are excreted in the urine within 24 hours. The specifics of this experiment are as follows:
“We first established a normal range of values based on data obtained in 14 normal subjects (5 males and 9 females) who achieved whole body sufficiency for iodine. The mean + standard deviation for the saliva/serum ratios of iodide in these 14 subjects was 44.2 + 13.7 with a range of 28 to 74.
According to Abraham et al, (10) normal and abnormal results for the ratio are as follows:
“…a ratio above 10 is considered normal; between 3 and 10, borderline; and below 3 is considered abnormal.”
In contrast, the following was noted in patients who had not followed the above procedure to attain ideal levels of iodine:
“In patients with an inefficient cellular iodide transport mechanism, the absorbed iodine/iodide is rapidly excreted in the urine resulting in low serum iodide levels 24 hours following a load of 50 mg iodine/iodide. In 7 patients not on orthoiodosupplementation and with post 24 hr load serum iodide levels below 0.1 mg/L (normal mean + standard deviation = 0.45 + 0.051 mg/L), the mean + standard deviation of serum/saliva ratio was 4.1 + 1.5.”
Of course, before leaving this discussion, given that Abraham et al (10) provide no third party documentation that affirms the accuracy of the above mentioned testing procedure, I do feel that some discussion is necessary concerning its accuracy and reliability in a routine clinical setting. On the negative side, there is still some question, as I have mentioned previously, about the accuracy of the iodine loading test upon which the testing protocol devised by Abraham et al (10) is based. However, on the positive side, this testing protocol, to me, does seem to be a reasonable extrapolation of a test that is well documented to determine genetic or congenital defects in iodine transport. Therefore, overall, I do feel that, unless further information is presented that suggests otherwise, the saliva/serum iodide ratio as devised by the authors, can be of great assistance to clinicians who are concerned about the presence of suboptimal NIS function in their patients.
SOME CONCLUDING REMARKS
In my opinion, the body of literature supporting the idea that the Wolff-Chaikoff effect exists is very impressive. Equally impressive is the literature supporting the idea that, given the numerous environmental and genetic factors that can individually or in combination alter NIS function, a small group of patients will invariably have negative reactions to any given amount of milligram dosing of supplemental iodine. Furthermore, some patients will invariably have adverse reactions because they were given the wrong form of supplemental iodine. However, if we are going to accept the idea that negative reactions to milligram doses of supplemental iodine are often the result of the wrong form of iodine and/or the types of functional medicine factors that we deal with daily in relation to many other patient concerns, we must also realize that the current, highly publicized “sermons” that would have us believe that patients either NEVER or ALWAYS adversely react to high doses of supplemental iodine, not only lack any relevance but appear to suggest fanaticism rather than intelligence. Furthermore, given that adverse reactions to milligram doses of supplemental iodine appear to be functional medicine issues and issues relating to optimal iodine form, it appears to me that the intelligent way to prevent reactions is to address issues such as toxicology, inflammation, and patient specific iodine needs and then determine the optimal iodine form and dose based on each patient’s unique biochemical, physiological, and genetic presentation.
In the next installment of this series, I will present, in detail, Abraham’s passionately opposing point of view on the Wolff-Chaikoff effect and NIS function in general along with my usual discussion of references so that, hopefully, we can determine, with reasonable assurance, which point of view is correct. This discussion will also include Abraham’s very interesting approach to restoring optimal NIS function.
Moss Nutrition Report #220 – 04/01/2008 – PDF Version
- Eng PHK et al. Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. Endocrinology. 1999;140(8):3404-3410.
- Anguiano B et al. Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland: Evidence that chronic administration has not harmful effects. Thyroid. 2007;17(9):851-859.
- Hou X et al. Determination of chemical species of iodine in some seaweeds. Science of the Total Environment. 1997;204(3):215-221.
- 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.
- Errdogan MF. Thiocyanate overload and thyroid disease. Biofactors. 2003;19:107-111.
- Roman GC. Autism: transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other antithyroid agents. J Neurol Sci. 2007;261(1-2):15-26.
- Schroder-van der Elst JP et al. Dietary flavonoids and iodine metabolism. Biofactors. 2003;19:171-176.
- Wolff J. A miss for NIS? Thyroid. 2002;12(4):295-297.
- Shen DHY et al. Sodium iodide symporter in health and disease. Thyroid. 2001;11(5):415-425.
- Abraham GE et al. The saliva/serum iodide ratio as an index of sodium/iodide symporter efficiency. The Original Internist. 2005;12(4):152-156.