What Doctors Are Saying


What Doctors Are Saying About Iodine Deficiencies


Dr. Broda O. Barnes (M.D., Ph.D.) – Perhaps The Most Eminent Endocrinologist Ever On Hypothyroidism:

– “The average iodine intake of a normal adult on an ordinary diet in a nongoiter region is about 0.03 milligrams, or 0.0000001 ounce, a day. This tiny amount is only about one-seventh of what is needed for daily thyroid hormone production,…” “In goiter regions, not even the 0.03 milligram per day is available in the food and water. Goiter regions are to be found all over the world. No continet is free of them .” (source: Hypothyroidism: The Unsuspected Illness by Broda O. Barnes, M.D. and Lawrence Galton, publ. Harper & Rowe Publishers. ©1976 by Broda O. Barnes and Lawrence Galton)

Dr. Mark Starr (M.D. – Diplomate of the American Board of Pain Medicine:

– “Adequate supplementation of iodine… are necessary for proper thyroid and steroid hormone function.” (source: Hypothyrodism Type 2, by Mark Starr, M.D. publ. Mark Starr Trust. ©2005, 2007 by Mark Starr Trust)

Dr. David Brownstein (M.D.) – One Of The Most Outspoken Proponents For Revising Iodine RDA Upward:

– “In a state of iodine deficiency, the thyroid gland (or any endocrine gland) will not function properly.” “The RDA for iodine is insufficient to meet the thyroid gland’s needs as well as the body’s need for iodine. Iodine levels should be measured and appropriate supplementation begun in a deficient state. Recent research has found that approximately 12.5mg per day of iodine/day… will adequately supply the body’s needs.” (source: Overcoming Thyroid Disorders, by David Brownstein, M.D. publ. Medical Alternative Press. ©2002, 2004 by David Brownstein, M.D.)

Dr. James K. Rone (M.D.) – Board-certified Endocrinologist:

– “How important is the thyroid? …the thyroid is the largest pure endocrine gland, …its hormone acts directly on DNA, … it is the first endocrine organ to form in the human embryo, starting a mere twenty-four days after conception …in adulats, the thyroid receives, gram for gram, 50 percent more blood flow than the kidneys.” “The dietary nutrient iodine is needed to make thyroid hormone. Follicular cells trap it from the blood, making the thyroid, en effect, a powerful iodine sponge.” (source: The Thyroid Paradox, by James K. Rone, M.D. publ. Basic Health Publications, Inc. ©2007 by James K. Rone, M.D.)

Dr. Ken Blanchard (M.D., Ph.D.) – Board-certified Endocrinologist:

– “Insufficient iodine leads to a decrease in thyroid hormones. The manifestations of low iodine levels are grouped together under the name Iodine Deficiency Disorder (IDD). These disorders include goiter (enlarged thyroid gland), hypothyroidism, mental retardation, reproductive problems, and a wide range of neurological and physical disorders. The body does not produce iodine; it must be consumed in the diet. IDD arises when there is not enough iodine in the soil, which impacts the water we drink (groundwater leaches iodine), the crops we eat (food grown in iodine-poor soil), and meats we consume (from animals grazing on the land).” “Soy is known as a phytoestrogen and goitrogen (an iodine blocking agent). …, soy can contribute to hypothroidism.” (source: What Your Doctor May Not Tell You About Hypothyroidism by Ken Blanchard, M.D., Ph.D. with Marietta Abrams Brill. publ. Werner Wellness. ©2004 by Ken Blanchard, M.D. and Marietta Abrams Brill)

Dr. Stephen E. Langer (M.D.) – president of the American Nutritional Medical Association:

– “The Recommended Daily Allowance (RDA) of iodine is 100 micrograms (mcg) for women and 120 mcg for men, although up to ten times that amount has not produced toxic effects in persons with a normal thyroid. Residents of Japan thrive on nearly four thousand times as much iodine as Americans, all from large amounts of seafood, kelp, dulse, and sea lettuce.” “Iodine deficiency has also been known to reduce the capacity to learn adn remember. Now, we find that an iodine deficient can undermine the desire to succeed, as demonstrated in a study conducted in India.” “Numerous studies show that the low-sodium diet does little to prevent heart disease.” (but heavily contributes to lowered daily iodine intake) “In a number of studies, sulfa drugs and antidiabetic agents interfered with the formation of thyroid hormones by inhibiting iodine uptake.” (source: Solved – The Riddle of Illness, by Stephen E. Langer, M.D. and James F. Scheer. publ. McGraw-Hill. ©2006 by the McGraw-Hill Companies)

Dr. Jorge Flechas (M.D.):

– “We first need to note that the body produces no iodine, and there is no organ other than the thyroid that can store large quantities of iodine. In some areas of the US, including mountain regions, the Mississippi River Valley, the Ohio River Valley, and the Great Lakes regions, the soil has always had a very low iodine content. But even in other areas of once iodine-rich soil, over farming has frequently depleted this iodine content. Hence, we no longer get adequate iodine via the plants we consume. To compensate for this, iodine was added to salt, bread, and milk. Today iodine is no longer added to bread or to milk, and the amount of iodine added to salt has steadily declined over the years. All of these factors contribute to the current prevalence of iodine deficiency in the United States.” “Another misconception that is out on the market is that high consumption of iodized salt helps prevent iodine deficiency. The fact is that iodized salt contains 74meg of iodine per gram of salt. The purpose of iodization of salt was to prevent goiter and cretinism and was never meant for optimal iodine requirements by the human body.” (source: posted at: www.helpmythyroid.com. by Jorge Flechas, M.D. publ. Fleshas Family Practice. ©2004-2005 Flechas Family Practice)

Dr. Kenezy Gyula Korhaz (M.D.):

–  [Iodine deficiency in cardiovascular diseases] Molnár I, Magyari M, Stief L.Kenézy Gyula Kórház, Debrecen, III. Belgyógyászat. The thyroid hormone deficiency on cardiovascular function can be characterized with decreased myocardial contractility and increased peripheral vascular resistance as well as with the changes in lipid metabolism. 42 patients with cardiovascular disease (mean age 65 +/- 13 yr, 16 males) were investigated if iodine insufficiency can play a role as a risk factor for the cardiovascular diseases. The patients were divided in 5 subgroups on the ground of the presence of hypertension, congestive heart failure, cardiomyopathy, coronary disfunction and arrhythmia. Urine iodine concentration (5.29 +/- 4.52 micrograms/dl) was detected with Sandell-Kolthoff colorimetric reaction. The most decreased urine iodine concentration was detected in the subgroups with arrhythmia and congestive heart failure (4.7 +/- 4.94 micrograms/dl and 4.9 +/- 4.81 micrograms/dl, respectively). An elevated TSH level was found by 3 patients (5.3 +/- 1.4 mlU/l). An elevation in lipid metabolism (cholesterol, triglyceride) associated with all subgroups without arrhythmia. In conclusion, the occurrence of iodine deficiency in cardiovascular disease is frequent. Iodine supplementation might prevent the worsing effect of iodine deficiency on cardiovascular disease. (Dr. Kenezy Gyula Korhaz also has stated that iodine chelates heavy metals such as mercury, lead, cadmium and aluminum and halogens such as fluoride and bromide, thus decreasing their iodine inhibiting effects[vii] especially of the halogens. Iodine has the highest atomic weight of all the common halogens (126.9). Iodine is the only option when it comes to removing these toxic haloids from the thyroid and even the pineal gland where fluoride concentrates, especially when there is a deficiency in iodine in the body. In an age of increasing radioactivity and toxic poisoning specifically with fluoride, chlorine and bromide, and even mercury, iodine is a necessary mineral to protect us from harm for immediately these toxic substances will increasingly flow out of the body in the urine.) (source: PMID: 9755626 [PubMed - indexed for MEDLINE])

Dr. M. Knobel (M.D.):

– [Disorders associated to chronic iodine deficiency] Knobel M, Medeiros-Neto G. Unidade de Tiróide, Departamento de Clínica Médica, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP. The thyroid gland promotes its adaptation to iodine deficiency inducing an increase in the iodine uptake followed by a substantial increase in the thyroid gland mass (goiter). Simultaneously, there is a preferential T3 secretion by the follicular cell and a persistently elevated serum TSH. Laboratory tests, isotopic methods and imaging are routinely used to verify the altered thyroid pathophysiology. In certain populations the presence of goitrogenic natural substances, present in the locally consumed staple food, were found and may add to the pathogenic process. (source: PMID: 15611818 [PubMed - indexed for MEDLINE])

JT Dunn (M.D.):

– [Iodine should be routinely added to complementary foods] Department of Medicine, University of Virginia Health System and International Council for the Control of Iodine Deficiency Disorders, Charlottesville, VA 22908, USA. jtd@virginia.edu. Iodine deficiency has major health consequences for the fetus and infant. Most individuals can tolerate fairly high intakes of iodine without problems. The Western Hemisphere has made great progress towards correcting its iodine deficiency, but pockets of deficiency remain and fragile monitoring systems endanger sustainability. Because the consequences of iodine deficiency are severe and the risks of excess treatment with modest supplements are minimal, we recommend the regular addition of 90 microg of iodine daily to complementary foods for children and 150 micro g for pregnant or lactating women, accompanied by effective monitoring of urinary iodine concentration in the population. (source: PMID: 12949401 [PubMed - indexed for MEDLINE])

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A Contrary View by J. Borak (M.D.)

– [Adequacy of iodine nutrition in the United States] Borak J. Yale School of Medicine, New Haven, CT, USA. jborak@jborak.com. “Concerns have been raised about the adequacy of iodine nutrition in the United States despite recent NHANES III data indicating that iodine intake remains generally adequate. Such concerns probably reflect misunderstanding of definitions of iodine deficiency. We review current criteria for iodine deficiency, the reasons for variability of urine iodine determinations, and their relation to interpretations of NHANES data. Although NHANES data indicate that iodine nutrition in the United States is adequate, the possibility remains that those who adhere to restricted diets may have reduced intake of iodine. Because of such possibilities, patients’ diets and use of dietary supplements should be explicitly considered as a part of routine medical care.” (source: PMID: 15779603 [PubMed - indexed for MEDLIN])

Rebuttal to Dr. Borak’s statements: The NHANES iodine nutrition studies (done under the auspicies of the NIH and CDC) determine iodine presence data on a study population group by performing ICP-DRC-MS (Inductively Coupled Plasma Dynamic Reaction Cell Mass Spectroscopy) on test subjects urine. These iodine  studies do not take into consideration that though the urine levels of iodine presence may be considered low, high or within ‘established’ current normal ranges, these tests, as currently interpreted, do not ascertain if iodine is even being ‘utilized’ by the body’s tissues… only the ‘assumption’ that iodine presence somehow mysteriously determines iodine tissue-binding activity. Most disturbing is the fact that the NHANES iodine presence studies referred to do not take the goitrogen factors of the test population into consideration, especially since the ubiquitous presence of the goitrogenic halogen agents – bromine, chlorine and flourine (as flouride) in the drinking water supply, common foods (especially bakery products), beverage and brominated cooking oil products are all so freely available to and consumed by the population at large and will countervail the iodine presence test interpretations. Goitrogen halogens (particularly bromine) mimic iodine with the consequence of displacing and/or blocking the absorption/utilization of iodine into tissues and can cause what little iodine is ingested not being able to be taken up by tissues, and hence being in the urine to be flushed out of the body. In other words, the presence of iodine in the urine not because the body has ‘enough’ iodine but because the iodine is not properly binding to the tissues and hence being taken out of the bloodstream to be flushed out with urine. This factor skews the intended interpretive basis of the NHANES iodine nutrition studies, especially if presence of urine iodine is actually a anti-iodine halogen driven factor. Add to this that the NHANES iodine studies did not factor a concurrent head-to-head bromine urine spillage test to factor in with the iodine urine spillage tests performed. This is huge in relevancy to the study that was done and without that bromine data factored in the urine spillage test for iodine content is flawed. Fact is, regardless of the NHANES iodine studies interpretive basis, it has been and is a well discussed and agreed to premise in many sectors of the scientific and medical fields that the current RDA levels for iodine are actually precipitously low for maintaining ‘normal’ let alone optimal health, since the RDA was originally established only to recommend just barely enough daily iodine intake to stave off the most serious IDD (Iodine Deficiency Disorder) – ‘serious’ iodine deficient caused conditions (that include goiter and cretinism), not to prevent sub-clinical iodine deficiency or take care of all the body’s other needs for iodine. This last point alone renders the ‘established’ and ‘accepted’ NHANES urine iodine presence test interpretation standard questionable and highly suspect, since many times more daily iodine intake is required before a truly ‘normal’ state of health (‘health’ defined as adequate thyroid and systemic tissue saturated levels of iodine) can be considered adequate relative to iodine-related health and defficiency issues. Even so, the 2000 NHANES iodine presence study compared against the same study of 1970 showed a whopping 50% less overall base-line iodine presence in the urine over that 30 year period, indicative in this instance, that much less iodine is being taken in by the body that is not present for the test. In the face of ever increasing iodine deficiency related symptoms and conditions among the population at large, the question begs to be asked, “Has the standard for ‘normal’ or ‘adequate’ urine iodine presence levels, by NHANES “definitions of iodine deficiency,” actually been lowered over that 30 year period (as the now accepted new normal basal temperature was) to meet a predetermined outcome interpretation (considered ‘bad science’ by any measure) for Dr. Borak to actually claim that ‘iodine nutrition in the United States is adequate,’…”?  Or is NHANES , through Dr. Borak as their mouthpiece, simply regurgitating the now discredited 1948 UC Berkeley Wolff-Chaikoff study/1969 Wolff review (of 1948 study) reinforcing the iodine RDA stance, that forensic level reviews have shown to have been manipulated in favor of a conflict-of-interest driven study interpretation/conclusion agenda and that was a scientific forgery of the actual factors that were supposed to be tested for, studied and by ‘objective’ scientific interpretation be determined upon? While the Wolff-Chiakoff study appears to have identified a little understood aspect of mineral salts of iodide initial effects on the thyroid, this aspect was overshadowed by the study’s assertion that the long held to woefully low RDA for daily iodine intake was adequate is what’s in question here. (source: Comments on Dr. Borak’s statements by L. Carl Robinson, MH,TT,CCHt. October 05, 2008. ©2008 Cedar Bear Naturales™)/L. Carl) Robinson)

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THE ‘IODINE LOADING URINE SPILLAGE’ TEST – CLINICIANS, CONSIDER THE FOLLOWING:

Determining how much iodine a person should take on a daily basis is based on a two-fold combination of a person’s health history relative to hyperthyroid/hypothyroid issues and related cardiovascular related issue (including medical procedures history, medications history, etc.), and, that if a person is able to take a daily dose of supplemental iodine then how much is taken being determined through an ‘Iodine Loading Urine Spillage Test.’  Popularized by the ‘Iodine Doctors,’ the ‘Iodine Loading Urine Spillage Test’ protocol is: A - first morning urine is discarded; B - 50 mg of Iodine/Iodide is taken (which would equate to XX ml of XODINE™ being taken); C - 24 hour urine is collected; and D - Iodine excretion is measured.  The assumption being that once an iodine sufficient state is attained, there is 90% excretion of iodine (45 mg (which would be XX ml of XODINE™), of which 90% excretion is supposed to provide the best clinical response for ascertaining daily intake level of iodine for an individual.

There are problems with the interpretive basis and assumptions regarding ILUS test results. The biggest problem is that an accurate assertion of ’tissue loading’ of iodine is not possible without also performing a concurrent side-by-side Bromine Urine Spillage test to ascertain how much bromine is being flushed from the body as iodine displaces bromine at the iodine receptor binding sites of tissues, thus better ascertaining tissue iodine loading, that results in bromine displacing and flushing from the body. Added to this is the fact that some individuals experience what appears to be an iodine toxicity crisis during an iodine loading protocol, when it may actually be a bromine toxicity crisis since bromine toxicity symptoms is almost exactly that for iodine toxicity symptoms, hence the added need for a concurrent head-to-head bromine urine spillage being performed side-by-side with an iodine urine spillage test.  

Pureodine™ processed XODINE™ mono-element pico-colloidal triiodide of iodine’s lead-developer, L. Carl Robinson, responds to the interpretive basis and assumptions made for the popularly used Iodine Loading Urine Spillage (ILUS) test as follows – 

“Clinicians should be aware that the ILUS test is only ascertining iodine loading (i.e. ‘saturation’) in the residue urine  fluid of the body – not iodine loading of the tissues (i.e. ‘assimilating/tissue saturated’) of the body per se.’ It is assimilation and saturation of iodine into the body’s tissue’s, not saturation of the body’s residue fluid system with iodine, that is key to normalizing and optimizing iodine related health factors. The fact that an ILUS Test alone does not ascertain ‘actual’ tissue absorption/saturation levels of iodine, as the ILUS test’s outcomes are currently and erroniously interpreted, but only ascertains ‘actual’ residue urine fluid saturation of iodine, is not too dissimilar in its highly specific (and limited) usefulness/interpretation to how a Thyroid Stimulating Hormone (TSH) test can test for TSH levels to specifically ascertain Type 1 Hypothryoid only, but cannot ascertain Type 2 Hypothyroid, also referred to as TSH resistant hypothyroid, a condition that will be completely missed if relying only on a TSH test for erroneously ascertaining all aspects of hypothyroid activity – just like relying only on an ILUS test alone to arbitrarily determine adequate daily iodine intake levels while missing potential tissue ‘iodine resistance’ and/or goitrogen halogen-driven (particularly bromine) iodine displacing issues, resulting from any of a number of causative factors, requiring other dietary, supplemental and clinical considerations for dealing with iodine uptake/tissue saturation and/or iodine resistant issues. These shared observations are excellent examples of where a clinician (and patient/client) is best served by not becoming over dependent on a single lab test protocol to make singularly arbitrarily assessments/determinations and worse yet, highly speculative assumptions concerning daily levels of supplemental iodine intake but instead incorporating more ‘differentially’ based inputs and considerations into making important, and for many individuals, essential life enhancing (or prolonging) assessments/determinations concerning levels of daily supplemental iodine intake. One such additional test done side-by-side with the ILUS test would be a Bromine Urine Spillage test, as this gives a better picture of if tissue iodine receptor sites are releasing bromine in favor of binding with iodine, which would result in raised levels of free bromine residue in the urine to compare against iodine residue levels in the urine. In other words, maybe the bromine urine spillage test is more relevant during an iodine loading protocol for ascertaining tissue iodine loading than the ILUS test done alone.  In the final analysis, the ILUS test, as the test outcomes are currently interpreted, makes an assumption of what is or is not adequate iodine uptake/tissue saturation based solely on iodine spillage consideration only, absent the bromine displacement/flushing/spillage factor. that is not a scientifically sustainable premise for a number of physiological and biochemical reasons. Perform both Iodine Urine Spillage AND Bromine Urine Spillage tests side-by-side to better ascertain the probable or actual tissue iodine loading of an Iodine Loading protocol.”

WARNING: Individuals who have thyroid and/or cardiovascular problems or are on any medications should consult with a physician before using XODINE transformative nanocolloidal mono elemental nascent iodine matrix. Side effects and/or contraindications, if any, would generally be the same as that listed for any other supplemental use and/or topical use based iodine matrix preparation.