The History of Iodine
in Medicine Part III:
Thyroid Fixation and Medical Iodophobia
by Guy E. Abraham, MD
The thyroid gland-iodine connection was known just a few years following the discovery of iodine in seaweed in 1811. Only eight years after this discovery, iodine was used effectively in the treatment of simple goiter. However, the medical uses of iodine during the first century since the discovery of iodine were not restricted to diseases of the thyroid gland only but covered a wide range of clinical conditions.1
In the early 1920s, Marine reported a positive effect from iodide supplementation at 9 mg/day in the prevention of simple goiter among adolescent girls.2,3 That amount of iodine was based on research performed on farm and laboratory animals regarding the effect of iodine on thyroid function and also overall performance. However, in Marine’s studies on adolescent girls, the only parameter assessed was the presence of goiter. Following Marine’s studies, iodine sufficiency became associated with the absence of goiter, not overall performance such as grades in classes, number of absences due to sickness, etc.
As a public measure to control goiter, iodization of table salt was implemented successfully in the US between 1917 and 1924. That is, iodization of table salt was successful in decreasing markedly the incidence of simple goiter in the supplemented population. Keep in mind that the amount of bioavailable iodine (0.05 mg/day) needed to prevent cretinism, endemic goiter, and hypothyroidism is 60 times less than the amount of iodide (9 mg/day) used by Marine2,3 in the original studies. Thyroidologists assumed that, with iodization of table salt, iodine deficiency became a thing of the past. That was the beginning of thyroid fixation.
Prior to the iodization program, the public was relying on iodine preparations from apothecaries for their iodine needs. The recommended daily amount of iodine was 0.1-0.3 ml Lugol containing 12.5-37.5 mg elemental iodine.4 This is exactly the amount of iodine needed for whole body sufficiency, based on a recently reported iodine/iodide loading test by the author.4 Some propaganda was used following iodization of salt to discourage the public from using the iodine preparations, such as Lugol solution, and to rely instead on iodized salt for their iodine needs. In 1926, physician C.L. Hartsock, from Cleveland, Ohio,5 wrote: “Iodized salt is now being very much more extensively used by the public than other forms of iodine, such as sodium iodide, iodostarine and compound solution of iodine (Lugol’s solution), probably because of the propaganda to insure its use …”
Iodized salt was unfortunately used as substitute for the previously recommended forms of iodine/iodide. The bioavailable iodide from iodized salt is only 10% of the estimated 0.75 mg iodide in iodized salt consumed per day.6 That amount, 0.075 mg of bioavailable iodide, represents less than 1% of the amount of iodide used in Marine’s study2,3 (i.e., 9 mg) and also less than 1% of the recommended daily intake of iodine from Lugol solution. Implementation of iodization of salt was associated with an increased incidence of autoimmune thyroiditis.4
Instead of iodized salt, Hartsock5 recommended the use of a tablet of iodine/iodide in known and fixed amounts as the best form of supplementation, just like the most popular form of supplementation used today for vitamins, minerals, and trace elements: “Tablets containing definite amounts of iodine seemed to be the method of choice.”
With the availability of thyroid hormones in the 1930s, iodine was completely ignored by thyroidologists in the treatment of iodine deficiency-induced goiter and hypothyroidism. A textbook, Diagnosis and Treatment of Diseases of the Thyroid, edited by Amy Rowland and published in 1932, contained chapters from 24 thyroidologists of that time.7 Although the most common cause of hypothyroidism and simple goiter worldwide is iodine deficiency, the recommended treatment of hypothyroidism was summarized in two sentences: “The treatment of hypothyroidism of any type consists merely in the substitution of thyroid extract for the deficient secretion. Any form of prepared gland or the active principle, thyroxin, may be used.”
Iodine neglect in the 1930s by thyroidologists progressed to medical iodophobia in the late 1940s and early 1950s. Following World War II, there was a systematic attempt to remove iodine from the food supply of America. Iodophobic misinformation permeated all textbooks of medicine and the subspecialties. From books written by physicians for physicians and for the consumers, iodophobia, which has reached pandemic proportions, trickled down to books written by lay persons for consumers.4,9
A new syndrome, medical iodophobia, was recently reported.4 Medicoiodophobes suffer from: 1) split personality which results in iodophobia within the orthoiodosupplementation range previously used safely and successfully in medical practice and iodophylia for megadoses of iodide (up to 12 g/day); 2) double standards which render those physicians intolerant to the minor side effects of the inorganic forms and extremely tolerant toward severe side effects of the radioactive and organic forms; 3) amnesia toward the inorganic, non-radioactive forms when making therapeutic decisions; 4) confusion, attributing the severe side effects of organic iodine containing drugs to inorganic iodine/iodide; and 5) altered state of consciousness, allowing doublethink, doublespeak, and contradictory logic to become acceptable.
Although the factors involved in medical iodophobia are still unknown, decreased cognition seems involved. Since low iodine intake is associated with intellectual impairment, deficiency of this essential element cannot be ruled out and, if present, would create a self-perpetuating phenomenon. Needless to say that medical iodophobia is contagious and can be transmitted to patients and other physicians (iatrogenic iodophobia). Although there is yet no official report from the Center for Disease Control regarding the prevalence of medical iodophobia in the US medical community, it is likely that this syndrome has reached pandemic proportion.
Medical iodophobia will remain a syndrome until the causes are discovered and effective therapy implemented. The disastrous effect on the US population of the zombification of the medical profession through iodine deprivation is already evident. Implementation of the orthoiodosupplementation program in the medical community is highly recommended. The increased cognition of health care professionals, resulting from orthoiodosupplementation, will eventually trickle down to patients in the form of a more enlightened approach to patient care.
Before World War II, non-radioactive forms of inorganic iodine were considered a panacea for all human ills,10 but today, they are avoided by physicians like leprosy. Who and/or what killed iodine?
The first nail in the iodine coffin was the publication by Wolff and Chaikoff from UC Berkley in 1948,11 describing their findings in rats administered iodide in increasing amounts by intraperitoneal injection. When serum inorganic iodide levels reached 0.2 mg/L, that is 10-6M, radioiodide uptake by the thyroid gland became undetectable. The correct interpretation would be: Iodide sufficiency of the thyroid gland was achieved when serum inorganic iodide levels reach 10-6M, as we previously discussed.9 But Wolff and Chaikoff concluded that serum inorganic iodide levels at a concentration of 10-6M blocks the synthesis of thyroid hormones, resulting in hypothyroidism and goiter. These authors did not measure thyroid hormones in the rats studied. Hypothyroidism and goiter were not observed in those rats. This fictitious phenomenon became known as the Wolff-Chaikoff effect.12
The second and final nail in the iodine coffin was hammered in by Wolff in 1969.12 By 1969, Dr. Wolff had moved to the National Institute of Health. He arbitrarily defined four levels of “iodine excess.” The first level of excess started with intake above 0.2 mg/day, and iodide intake of 2 mg or more was considered “excessive and potentially harmful.” By the 1970s, physicians concluded that one must avoid inorganic, non-radioactive iodine like leprosy, unless it was incorporated into toxic, organic iodine-containing drugs. Then iodine could be tolerated because iodine could be blamed for the toxicity of these drugs.
Whereas the first wave of medical iodophobia was initiated in 1910 by the pen of one man, Swiss surgeon, Nobel laureate, Professor Theodore Kocher and lasted some 15 years (1910-1925),1 the second wave of medical iodophobia initiated in 1948 by the pen of two men, Wolff and Chaikoff, is alive and well even after some 60 years of existence.
As unbelievable as it may sound, the Kocher iodophobic effect was initiated by a report from Kocher one year after he received the Nobel Prize, stating that he had experienced symptoms of hyperthyroidism following ingestion of potassium iodide. One man, reporting his experience using iodine on himself initiated the first wave of medical iodophobia. After 15 years of intimidation, preventing the widespread effective use of iodine, due to the Kocher iodophobic effect, physicians were able to escape from the Kocher inhibition because of poor synchronization of iodophobic publications and a small nucleus of enlightened members of the medical profession. The amazing success and long duration of the Wolff-Chaikoff iodophobic effect on the medical community is most likely due to the well-synchronized timing of a series of iodophobic publications and also due to iodine deprived and zombified physicians who were unable to escape from the Wolff-Chaikoff effect. The rats used in the Wolff-Chaikoff experiment were successful in escaping the Wolff-Chaikoff effect because they received significant amounts of iodine, improving their cognition.
The proper terminology for the Wolff-Chaikoff effect is “The Wolff-Chaikoff Iodophobic Domino Effect.” I will give one example, just one example, of the iodophobic domino effect of the Wolff-Chaikoff 1948 publication,11 resulting in the removal of iodine from a very important staple food in the US, that is our daily bread which contained the full RDA of 0.15 mg per slice for a period of about 20 years between 1960 to 1980.4,9
In the early 1960s, potassium iodate was added to bread as a dough conditioner. Iodate was added with the purpose of oxidizing sulfhydryl groups of flour proteins and thereby improving the rheological properties of the dough. By oxidizing sulfhydryl groups, iodate is reduced already during mixing of the dough, and it reaches the consumer as iodide.13 As mentioned previously, one slice of bread contained the full RDA of 150 µg.14,15 This amount of the dezombifier iodine in a major staple food of America could not be tolerated for long. Something had to be done and fast. The Wolff-Chaikoff Domino Effect was used to deiodize bread, concomitant with an increased concentration of the goitrogenic, carcinogenic, and zombifying bromate in our food and water supplies.8 The following describes the sequence of events in this domino effect:
Because of isotope dilution effect, the percent of radioiodide uptake by the thyroid gland decreased from 20-30% to 10-20%, following iodization of bread. In 1965, London,16 et al, from the National Institute of Health, evaluated the amount of iodine present in 32 bakery products from 12 different commercial bakeries. They reported that a typical diet contributed to approximately 1 mg/day of iodine and 726 µg came from bakery products. Concern was expressed over the inhibition of thyroid hormone synthesis in thyrotoxic patients at those levels of iodine. The last sentence of their publication read: “One milligram of iodine will suppress the uptake of radioactive iodine by the normal thyroid gland, probably by simple dilution of the dose, and may considerably reduce organic binding of iodine in the thyroid glands of thyrotoxic persons.”8 The seventh reference of their manuscript is a study published in 1949 by Stanley17 one year after the Wolff-Chaikoff effect was reported in rats.11 The first paragraph of Stanley’s manuscript stated the objective: “The interest of thyroidologists was recently aroused by the demonstration by Wolff and Chaikoff2 that, with levels of serum iodide higher than 20 to 30 micrograms per cent, organic binding of iodine in the rat thyroid was inhibited. Extension of these observations to man was undertaken …”
The interest of thyroidologists could not have been aroused so quickly by the publication of Wolff and Chaikoff in The Journal of Biological Chemistry,11 a journal involved in publishing research in the basic sciences, not clinical medicine. The thyroidologist with aroused interest was Stanley, himself, who obviously had insider’s information in order to publish his manuscript within a year following the Wolff-Chaikoff publication, considering the fact that it takes several months for the review process in peer review journals, and that it would have required several months for him to design and perform his experiments after reading the Wolff-Chaikoff paper. During the year Stanley published his “extension of the Wolff-Chaikoff effect to man,” he co-authored a paper with Astwood on the use of goitrogens in the management of patients with Graves’ disease as an alternative to inorganic iodine/iodide.
It is a strange coincidence that the investigators who authored the iodophobic publications, regarding the so-called inhibition of organic binding of radioactive iodide in the thyroid gland by the administration of inorganic, non-radioactive iodide, were also involved in testing goitrogens in laboratory animals and in normal human subjects and in implementing the use of these goitrogens as an alternative to inorganic iodine/iodide in patients with Graves’ disease.4
Some four years after London’s publication,16 Pittman,14 et al, reported in 1969, on the negative impact of iodization of bread, that is, as far as Pittman,14 et al, appraised it. Remember this is the same year Wolff published his iodophobic review.12 Again, timing and synchronization of iodophobic misinformation is critical. Events that seem unrelated but well-synchronized for maximum effect is a key ingredient for the successful outcome of deception.
Pittman,14 et al, compared the mean value of the 24-hour radioiodide uptake by the thyroid gland in a group of 63 euthyroid subjects prior to iodization of bread with another group of 53 euthyroid subjects following the use of potassium iodate in bread. These investigators also measured 24-hour urine iodide levels and serum inorganic iodide in some subjects of both groups. The 24-hour radioiodide uptake by the thyroid gland for both groups were (+SD): pre-iodization of bread — 28.6+6.5%; and post-iodization of bread — 15.4+6.8%. We have previously reported the correlation between 24-hour radioiodide uptake by the thyroid gland with the average daily intake of iodine, based on a review of the published literature.9 The data simplified is displayed in Figure 1. Thyroid gland sufficiency for iodide is achieved with a daily intake of 6 mg. For whole body sufficiency, 12.5-50 mg is required daily.4
Pittman,14 et al, estimated a mean daily intake of 680 µg, that is 0.68 mg iodine in the group studied post-iodization of bread. These investigators were alarmed by such unexpectedly “excessive” intake of iodine, resulting in these subjects being “heavily loaded with iodine.” The following is a quote from the discussion section of their publication:
“Evaluation of several aspects of iodine kinetics in 30 of our euthyroid subjects revealed them to be heavily loaded with iodine. We had anticipated that local subjects probably ingested liberal quantities of iodine, but we had not expected to find such high values as 680 µg per day for the urinary iodine excretion or 1.9 µg per 100 ml for the plasma inorganic iodide concentration (PII). These values are far in excess of most in the literature and approach those found in groups ingesting diets unusually rich in iodine.”
Pittman, et al, were referring to mainland Japanese who consume a daily average of 13.8 mg (13,800 µg) of iodine from seaweed when they mentioned “groups ingesting diet unusually rich with iodine.” Based on statistics generated some 20 years ago, mainland Japanese represent one of the healthiest nations on earth.4,9 At the time of Pittman’s publication, iodophobic misinformation from the Wolff-Chaikoff domino effect was so widespread that bread makers were already looking for an alternative to iodates as dough conditioners. They first considered azodicarbonamide, but it was too toxic, so they settled for bromate, a goitrogen with carcinogenic and zombifying potentials.4 Pittman,14 et al, were elated with this move by bakers to replace iodates with azodicarbonamide. They stated: “Bread makers are using a new organic agent, azodicarbonamide, to an increasing extent to replace the halogens. If this trend continues, dietary iodine from this source may fall to low levels.”
To recapitulate on the iodophobic domino effect of the Wolff-Chaikoff forgery:
•1948: Wolff-Chaikoff (W-C) forgery is published.11
•1949 Stanley supposedly extended the fictitious W-C effect observed in rats to humans.17
1965: London,16 et al, from the National Institute of Health quoted Stanley’s forgery to alarm their readers about their findings of “large quantities” of iodine in bread.
1969: Pittman,14 et al, confirmed London’s findings of “excessive iodine” in bread.
1969: Wolff publishes iodophobic review.12
Late 1970s to early 1980s: Bakers replace iodate with bromate as a dough conditioner. Bromate is a goitrogen, carcinogen, and a zombifying agent.4
1980-2000: Prevalence of obesity, diabetes, hypertension, and cancer of the breast and thyroid glands increases in the US.4
We have previously presented evidence that iodophobic misinformation in medical textbooks may have contributed to the high prevalence of breast cancer in the US female population.4,9 Unfortunately, the latest edition (ninth) of Werner & Ingbar’s The Thyroid,18 published in 2005 contains the same iodophobic misinformation promulgated in the eighth edition published in 2000.19 In the eighth and ninth editions, Roti and Vagenakis wrote the section on “Effect of Excess Iodide.”20,21 The following are quotes from the eighth edition:
“Strong evidence indicates that excess iodide can induce thyroid dysfunction, and these iodine-induced abnormalities in thyroid function are the subject of this subchapter.”
“Occasionally drinking water may be a source of excess iodine intake, such as in some Chinese countries where the drinking water has an iodine concentration of 300-462 µg/L. The population residing in those areas has a urinary iodine excretion rate as high as 900 µg/L.”
These authors used micrograms instead of milligrams to make the numbers appear “excessive”. They considered iodide concentrations of 300-462 µg/L (0.3-0.46 mg/L) in drinking water as excessive. Yet, studies performed in the US for five years in a prison inmate population consuming drinking water containing 1-2 mg/L (1,000 to 2,000 µg/L) of iodine22 reported no complication.
“Because of the increasing difficulty experienced by many communities in achieving satisfactory disinfection of public water supplies with acceptable concentrations of chlorine, a feasibility study on the use of iodine for this purpose was undertaken ... The effectiveness, ease of administration and palatability were prime reasons for considering iodine as a disinfectant of community water supplies ... effective bacteriological control of the water was maintained by all concentrations of iodine used in this study … At an iodine concentration of 1 mg/liter (1 ppm), the water met all standards for safety and palatability (1962 USPHS Drinking Water Standards) ... During the five years in which this study was conducted no instances of urticaria or iodism were observed … for serum thyroxine were unaffected by iodination of the water supply … None of the prison inmates developed clinical evidence of hyperthyroidism or hypothyroidism throughout this study.”
Several other studies confirmed the safety of inorganic, non-radioactive iodine in daily amounts greater than the amount Roti and Vagenakis considered toxic. For example, Clement23 in Tasmania, reported that a daily intake of 1.4 mg of potassium iodide (10 times the RDA) by infants and children for 16 years resulted in reduction in the prevalence of goiter, but in some regions, that amount of iodine was not sufficient enough to have a significant effect on the rates of goiter.
In the 2005 edition,21 Roti and Vagenakis repeated the same iodophobic misinformation promulgated in the 2000 edition and added a new one: “A group of American volunteers working in West Africa had a median urinary iodide excretion of 5.048 µg/L, due to a faulty iodination system, and some developed goiter and subclinical hypothyroidism.”26
A review of their 26th reference revealed that this manuscript was poorly documented and should not have qualified for publication in the Journal of Clinical Endocrinology & Metabolism unless some heavyweight coauthor threw his weight around to get it through. In the manuscript, entitled “Effects of chronic iodine excess in a cohort of long-term American workers in West Africa,” by Pearce,24 et al, 102 Peace Corps volunteers were evaluated during and 30 weeks after they ceased to ingest water from filters containing organic-iodine iodophores. During the period the subjects were using the iodine-containing filters, the urinary concentrations of iodide had a mean value of 5 mg/L. Serum iodide levels had a mean value of 0.29 mg/L. Based on renal clearance of iodide, that is 43.5 L/day,6 the average daily intake of iodine in these subjects calculated from the mean serum iodide level is 12.6 mg/day (0.29 mg/L × 43.5 L/day). This is the average daily intake of 60 million mainland Japanese,4,9 one of the healthiest populations on the planet. The following quotes from Pearce’s publication are evidence of a faulty experimental design. It is very surprising that such a mediocre manuscript made it through just because it is iodophobic.
“Corps volunteers were authorized to receive a follow-up evaluation by an endocrinologist after returning from Niger. Some follow-up evaluations were incomplete, as some of the subjects chose not to visit an endocrinologist upon returning, and different endocrinologists obtained different follow-up laboratory studies … Ultrasound evaluation was not performed … No volunteers had overt symptoms of thyroid dysfunction as evaluated clinically.”
In the discussion section of their publication, Pearce, et al, did not fail to mention the fictitious Wolff-Chaikoff effect as if it was a proven fact. More than 50 years after the Wolff-Chaikoff forgery, it is still quoted in iodophobic publications: “Acute excess iodine ingestion has long been known to result in a transient decrease in iodine organification, termed the acute Wolff-Chaikoff effect.”
Attempts to reproduce the Wolff-Chaikoff experiments in rats by other investigators were unsuccessful. In vitro studies revealed that concentrations of iodide as high as 10-2M were required to interfere with the mechanisms involved in cellular uptake and organification of iodide.25 These amounts are four orders of magnitude greater than the 10-6M serum iodide proposed by Wolff and Chaikoff to cause inhibition of organification of iodide by the thyroid gland. Yet, thyroidologists refer to these in vitro studies to confirm the Wolff-Chaikoff effect. They must think we are really stupid. Daily intake of 50 g (50,000,000 µg) iodide would be required to achieve these peripheral levels of 10-2M in the adult human subject,4 a heroic amount by any standard.
In the eighth edition of The Thyroid, Meier and Burger26 called iodine a contaminant that interferes with the destructive effect of goitrogens. Obviously, thyroidologists hate the thyroid gland. “There is a marked competition between iodide and the thionamides for the active site of TPO … In situations of severe iodine contamination, these are the two major mechanisms leading to the loss of efficiency of these drugs. It is also likely that iodine contamination reduces the capacity of the thyroid to concentrate the thionamides.”
However, in the ninth edition, they were kinder and gentler to iodine; they stopped calling iodine a contaminant.27 They just wrote that it is “excess” iodine that is the problem. The amount of daily intake of iodine that protects the thyroid gland from the harmful effects of iodine inhibitors is called by these thyroidologists “severe iodine excess.” They have gone berserk!
“There is a marked competition between iodide and the thionamides for the active site of TPO … In situations of severe iodine excess, these are the two major mechanisms leading to the loss of efficiency of these drugs. It is also likely that iodine excess reduces the capacity of the thyroid to concentrate the thionamides.”
Keep in mind that these drugs block the uptake of iodide not only by the thyroid gland but also by every target organ of the human body. Why would anyone in his/her right mind want to concentrate iodine-blocking agents in the thyroid gland and the rest of the body because of iodine-deficiency induced hyperthyroidism? These patients need more iodine, not iodine blocking agents.
Thyroidologists have become so destructive that some of them recommend radioiodine ablation of the thyroid to allow the reintroduction of the toxic, organic iodine-containing drug, amiodarone in patients with a prior history of amiodarone-induced thyrotoxicosis. To quote Hormida,28 et al: “… However, hypothyroidism should be viewed as a goal, rather than a complication of treatment in these patients.”
Farwell,29 et al, recommend “near total thyroidectomy” in cases of “resistant amiodarone-induced thyrotoxicosis: “…We suggest that near-total thyroidectomy warrants considerations as definitive treatment for resistant amiodarone-induced thyrotoxicosis.”
How come cardiologists never considered inorganic, non-radioactive iodine as first line of therapy in cardiac arrhythmias instead of the toxic, sustained-release iodine drug, amiodarone? A careful review of published data on amiodarone suggests that this organic iodine-containing drug is a sustained-release form of iodine. The iodine released is the active agent with the drug itself being the cause of its toxicity.30 Inorganic, non-radioactive iodine is the treatment of choice in those clinical conditions currently treated with amiodarone.
In their 2001 publication, Martino,31 et al, reported a list of side effects and complications of amiodarone: corneal microdeposits in 100% of the cases; anorexia, nausea in 80%; skin photosensitivity and discoloration in 55-75%; neurological symptoms in 48%; abnormal liver tests in 25%; thyroid dysfunction in 14-18%; and lung dysfunction in 10-13%. The pulmonary toxicity is the most serious complication of amiodarone therapy, with a fatal outcome in 9% of the patients experiencing this side effect of amiodarone.32
It is hard to believe that such a drug is widely used by US physicians in medical conditions where inorganic, non-radioactive iodine has never been tested. Connolly33 in his 1999 review of amiodarone efficacy and safety reported: “On the basis of the number of prescriptions filled in retail pharmacies, amiodarone was the most often prescribed antiarrhythmic agent, accounting for 24.1% of the total antiarrhythmic prescriptions in 1998.”
He further commented that amiodarone accounted for 33-74% of prescriptions in Europe, North and South America, compared to 0.3% in Japan, which is 100 times less than the other countries mentioned. It is of interest that mainland Japanese consume at least 100 times the RDA for iodine.9,34 That is at least 100 times more iodine than countries with 100 times more prescriptions for amiodarone. Regarding the evidence –based analysis of amiodarone efficacy and safety, Connolly stated: “The general view that amiodarone is the most useful drug for VT and VF, notwithstanding the rather modest evidence from randomized trials, led to its being adopted as the standard medical therapy in several recent randomized secondary prevention trials evaluating the ICD … A meta-analysis of these trials based on individual patient data yielded a relative risk reduction in all-case mortality of 13-15%, which was of borderline statistical significance (P=0.03 or 0.06 depending on analytical method used).”
When endocrinologists from India reported the presence of biologically active sodium/iodide symporter (NIS) in breast tissue from women with intraductal carcinoma,35 they totally ignored the obvious implications for the therapeutic use of inorganic non-radioactive iodine in patients with breast cancer. They showed their preference for the systemic use of radioiodide. This form of therapy would expose every organ of the body to the carcinogenic and cytotoxic radioiodide. They have gone berserk!
“The unequivocal demonstration of NIS expression, its functionality and retention of iodine by organification further provides supportive evidence for use of radioiodine as an additional treatment modality of human breast carcinoma.”35
After 60 years in the Dark Ages, following the second wave of medical iodophobia, inaugurated by the Wolff-Chaikoff iodophobic effect,11,12 iodine is emerging recently as an important nutrient for protection against breast cancer and the degenerative diseases of the Western World.4,6,8,9,36-45 For the first time, a simple loading test became available to assess whole body sufficiency for iodine.4 For the first time, a simple test became available to asses the efficiency of cellular iodide uptake system using the saliva/serum stable iodide ratio.44 For the first time, the detoxifying effect of iodine at 50 mg/day on the toxic halides fluoride and bromide was reported.40 For the first time, evidence for an enterohepatic circulation of inorganic iodine was presented.41
For the first time, a mechanism used by the human body to prevent iodine overload was reported:4,38 In cases of whole body deficiency, the ingested iodine/iodide is retained by the body in proportion to the degree of deficiency. At sufficiency, the amount of iodine absorbed is quantitatively excreted in the urine as iodide, therefore protecting the body against iodine overload. In the adult, 1,500 mg of iodine was retained at sufficiency,41 an amount 50 times higher than the amount of total body iodine reported in medical textbooks. We have confirmed38 the observation of our medical predecessors46 that iodine detoxifies the body from the heavy metals lead and mercury.
For the first time, evidence that the administration of vitamin C improves a defective cellular transport system for iodine was reported.39 So far, every case of iodine transport inefficiency we had studied, has responded to a complete nutritional program, including several grams of vitamin C. Iodine alone in daily amounts of 50 mg or more is also effective in cases of iodide symport inefficiency.
The iodine/iodide loading test to assess whole body sufficiency for iodine becomes more accurate by implementing a complete nutritional program for one month prior to the loading test. In cases of iodine transport inefficiency, the high urinary excretion of iodide would give the false impression of iodine sufficiency.38,39 By correcting this inefficiency of the iodine transport system through nutritional intervention38,39 prior to performing the loading test, this test becomes more accurate. The loading test is not reliable in patients on antithyroid drugs which inhibit oxidation and organification of symported iodide in the target cells. This results in a high urinary excretion of iodide, giving the false impression of whole body sufficiency.
About the Author
Guy E. Abraham, MD, is a former Professor of Obstetrics, Gynecology, and Endocrinology at the UCLA School of Medicine. Some 35 years ago, he pioneered the development of assays to measure minute quantities of steroid hormones in biological fluids. He has been honored as follows: General Diagnostic Award from the Canadian Association of Clinical Chemists, 1974; the Medaille d’Honneur from the University of Liege, Belgium, 1976; the Senior Investigator Award of Pharmacia, Sweden, 1980. The applications of Dr. Abraham’s techniques to a variety of female disorders have brought a notable improvement to the understanding and management of these disorders.
Twenty-five years ago, Dr. Abraham developed nutritional programs for women with premenstrual tension syndrome and post-menopausal osteoporosis. They are now the most commonly used dietary programs by American obstetricians and gynecologists. Dr. Abraham’s current research interests include the development of assays for the measurement of iodide and the other halides in biological fluids and their applications to the implementation of orthoiodosupplementation in medical practice.
1 Abraham GE. “The history of iodine in medicine. Part 1: From discovery to essentiality.” The Original Internist, 2006; 13(1):29-36.
2 Marine D and Kimball BS. “The prevention of simple goiter in man.” J Lab Clin Med, 1917; 3:40-48.
3 Marine D. “Prevention and treatment of simple goiter.” Atl Med J, 1923; 26:437-442.
4 Abraham GE. “The safe and effective implementation of orthoiodosupplementation in medical practice.” The Original Internist, 2004; 11(1):17-36.
5 Hartsock CL. “Iodized salt in the prevention of goiter.” JAMA, 1926; 86:1334-1338.
6 Abraham GE. “The concept of orthoiodosupplementation and its clinical implications.” The Original Internist, 11(2):29-38, 2004.
7 Diagnosis and Treatment of Diseases of the Thyroid Gland. Rowland AF, editor. W.B. Saunders Company, 1932; 98.
8 Abraham GE. “The Wolff-Chaikoff effect: Crying wolf?” The Original Internist, 2005; 12(3):112-118.
9 Abraham GE, Flechas JD, and Hakala JC. “Orthoiodosupplementation: Iodine sufficiency of the whole human body.” The Original Internist, 2002; 9(4):30-41.
10 Kelly FC. “Iodine in medicine and pharmacy since its discovery – 1811-1961.” Proc R Soc Med, 1961; 54:831-836.
11 Wolff J and Chaikoff IL. “Plasma inorganic iodide as a homeostatic regulator of thyroid function.” J Biol Chem, 1948; 174:555-564.
12 Wolff J. “Iodide goiter and the pharmacologic effects of excess iodide.” Am J Med, 47:101-124, 1969.
13 Burgi H, Schaffner Th, and Seller JP. “The toxicology of iodate: A review of the literature.” Thyroid, 2001; 11:449-456.
14 Pittman, et al. “Thyroidal radioiodine uptake.” NEJM, 1969; 280:1431-1434.
15 Wartofsky L and Ingbar SH. “Estimation of the rate of release of non-thyroxine iodine from the thyroid glands of normal subjects and patients with thyrotoxicosis.” J Clin Endocr, 1971; 33:488-500.
16 London WT, Vought RL, and Brown FA. “Bread — A dietary source of large quantities of iodine.” NEJM, 1965; 273:381.
17 Stanley MM. “The direct estimation of the rate of thyroid hormone formation in man. The effect of the iodide ion on thyroid iodine utilization.” J Clin Endocr, 1949; 9:941-954.
18 Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Ninth edition. Lippincott Williams & Wilkins, 2005.
19 Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Eighth edition. Lippincott Williams & Wilkins, 2000.
20 Roti E and Vagenakis AG. “Effect of excess iodide: Clinical aspects.” In: Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Eighth edition. Lippincott Williams & Wilkins, 2000; 316-329.
21 Roti E and Vagenakis AG. “Effect of excess iodide: Clinical aspects.” In: Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Ninth edition. Lippincott Williams & Wilkins, 2005; 288-305.
22 Thomas WC, Black AP, et al. “Iodine disinfection of water.” Arch Environ Health, 1969; 19:124-128.
23 Clements FW. “Goitre prophylaxis by addition of potassium iodate to bread.” The Lancet, 1970; 1:489-492.
24 Pearce EN, et al. “Effects of chronic iodine excess in a cohort of long-term American workers in West Africa.” J Clin Endocr & Metab, 2002; 87:5499-5502.
25 Pitsiavas V, Smerdely P, and Boyages SC. “Amiodarone compared with iodine exhibits a potent and persistent inhibitory effect on TSH-stimulated cAMP production in vitro: a possible mechanism to explain amiodarone-induced hypothyroidism.” European J Endocr, 1999; 140:241-249.
26 Meier CA and Burger AG. “Effects of drugs and other substances on thyroid hormone synthesis and metabolism.” In: Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Eighth edition. Lippincott Williams & Wilkins, 2000; 265-280.
27 Meier CA and Burger AG. “Effects of drugs and other substances on thyroid hormone synthesis and metabolism.” In: Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Ninth edition. Lippincott Williams & Wilkins, 2005; 229-246.
28 Hermida JS, Jarry G, et al. “Radioiodine ablation of the thyroid to allow the reintroduction of amiodarone treatment in patients with a prior history of amiodarone-induced thyrotoxicosis.” Am J Med, 2004; 116:345-348.
29 Farwell AP, Abend SL, et al. “Thyroidectomy for amiodarone-induced thyrotoxicosis.” JAMA, 1990; 263(11):1526-1528.
30 Phillippou G, Koutras DA, et al. “The effect of iodide on serum thyroid hormone levels in normal persons, in hyperthyroid patients, and in hypothyroid patients on thyroxine replacement.” Clin Endocr, 1992; 36:573-578.
31 Martino E, Bartalena L, et al. “The effects of amiodarone on the thyroid.” Endocrine Reviews, 2001; 22(2):240-254.
32 Dusman RE, et al. “Clinical features of amiodarone-induced pulmonary toxicity.” Circulation, 1990; 82:51-59.
33 Connolly SJ. “Evidence-based analysis of amiodarone efficacy and safety.” Circulation, 1999; 100:2025-2034.
34 Abraham GE. “The Wolff-Chaikoff effect: Crying wolf?” The Original Internist, 2005; 12(3):112-118.
35 Upadhyay G, Singh R, et al. “Functional expression of sodium iodide symporter (NIS) in human breast cancer tissue.” Breast Cancer Research and Treatment, 2003; 77:157-165.
34 Abraham GE, Flechas JD, and Hakala JC. “Optimum levels of iodine for greatest mental and physical health.” The Original Internist, 2002; 9(3):5-20.
35 Abraham GE, Flechas JD, and Hakala JC. “Measurement of urinary iodide levels by ion-selective electrode: Improved sensitivity and specificity by chromatography on anion-exchange resin.” The Original Internist, 2004; 11(4):19-32.
36 Abraham GE. “The historical background of the iodine project.” The Original Internist, 2005; 12(2):57-66.
37 Abraham GE and Brownstein D. “Evidence that the administration of vitamin C improves a defective cellular transport mechanism for iodine: A case report.” The Original Internist, 2005; 12(3):125-130.
38 Abraham GE. “Iodine supplementation markedly increases urinary excretion of fluoride and bromide.” Townsend Letter, 2003; 238:108-109.
39 Abraham GE. “Serum inorganic iodide levels following ingestion of a tablet form of Lugol solution: Evidence for an enterohepatic circulation of iodine.” The Original Internist, 2004; 11(3):29-34.
Brownstein D. “Clinical experience with inorganic, non-radioactive iodine/iodide.” The Original Internist, 2005; 12(3):105-108.
41 Flechas JD. “Orthoiodosupplementation in a primary care practice.” The Original Internist, 2005; 12(2):89-96.
42 Abraham GE, Brownstein D, and Flechas JD. “The saliva/serum iodide ratio as an index of sodium/iodide symporter efficiency.” The Original Internist, 2005; 12(4): 152-156.
43 Abraham GE and Brownstein D. “Validation of the orthoiodosupplementation program: A rebuttal of Dr. Gaby’s editorial on iodine.” The Original Internist, 2005; 12(4): 184-194.
44 “Iodine.” In: Encyclopedia Britannica, Vol 11, 1910-1911. u
Thyroid sufficiency is achieved with a daily iodine intake of 6 mg. That is where the slope crosses the X-axis at zero radioiodide intake.
*Modified from Abraham, et al. The Original Internist, 9(4):30-41.
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