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Archive for the ‘Iodine’ Category

Written by John – April 27, 1999

From here: Iodine

Selenium and iodine are two minerals which are critically important in the proper functioning of the thyroid. While the importance of iodine has been known a long time, the importance of selenium has only been discovered and explored since 1990. Much research is presently being conducted on the functions of these two minerals in thyroid function and it is becoming clear that there is an interaction between the two. Iodine has a seemingly simple role in the thyroid-it is incorporated into the thyroid hormone molecule.

A deficiency of iodine will cause hypothyroidism and if this is severe and occurs during pregnancy, the offspring will be mentally damaged and is called a cretin. Cretinism, or myxeodematous cretinism as it is sometimes called, is not only caused by an iodine deficiency, but is also influenced by a selenium deficiency. Iodine apparently has just one function in the body-in the thyroid.

Selenium, on the other hand, performs many functions. At the beginning of the 1990s it was discovered that the deiodinase enzymes which convert T4 (thyroxin, the thyroid prohormone) into T3 (triiodothyronine, the cellularly active hormone) and also convert T3 into T2, thereby degrading it, are selenium enzymes (formed with the amino acid cysteine). This discovery has led to a lot of research studies on the effects of selenium, iodine, and their interactions.

Selenium also performs other important roles in the body. The most important of these is probably as its role as the body’s best antioxidant (anti-peroxidant). It performs this role as part of glutathione peroxidase (GSHPx or GPX). As part of GPX, selenium prevents lipids and fats from being peroxidized (oxidized), which literally means that it prevents fats from going rancid (this can be seen on your skin as “age spots” or “liver spots” (autopsies show that skin “liver spots” are accompanied by similar spots of peroxidized fats in the liver.) Therefore selenium protects all of the cellular membranes, which are made up of fats, from peroxidation. Peroxidation of cellular membranes reduces the ability of the membrane to pass nutrients including minerals and vitamins, so selenium deficiency is the first step toward developing the many problems caused by nutrient deficiencies.

Joel Wallach considers a selenium deficiency combined with high intake of vegetable oils (salad dressings, margarine, cooking oils) as the “quickest route to a heart attack and cancer.” It seems that the body uses a lot of selenium to protect the fats from peroxidation. Polyunsaturated fats which are hydrogenated or heated become the same as rancid fats and large amounts of selenium are then needed to protect the body. Consumption of these dietary fats can thus lead to a selenium deficiency.

Selenium is also essential for the production of estrogen sulfotranserfase which is the enzyme which breaks down estrogen. A deficiency of selenium can thus lead to excessive amounts of estrogen, which may depress thyroid function, and also upset the progesterone-estrogen balance.

Wallach also lists other effects of selenium deficiency: anemia (red blood cell fragility), fatigue, muscular weakness, myalgia (muscle pain), muscular dystrophy (white muscle disease in animals), cardiomyopathy (sudden death in athletes), heart palpitations, irregular heartbeat, liver cirrhosis, pancreatitis, Lou Gehrig’s and Parkinson’s diseases (mercury toxicity), Alzheimer’s Disease (high intake of vegetable oil), sudden infant death syndrome (and possibly “breathlessness” in adults, jj), cancer, multiple sclerosis, and sickle cell anemia.

Selenium is essential for the production of testosterone. A deficiency seems to be involved in osteoarthritis. I’ve found studies linking selenium deficiency to alopecia (hair loss) and to degeneration of the knee joint (seen in Kashin-Beck disease). Since selenium is necessary to produce GPX which is a major detoxifier of man-made and environmental toxins, selenium deficiency can lead to chemical and drug sensitivities.

These are some of the non-thyroidal effects of selenium deficiency. The effects of selenium deficiency on thyroidal health is even more interesting. One study I read indicated that in experimental animals, selenium deficiency will increase T3 in the heart. This may be the reason that selenium deficiency causes heart palpitations and rapid heart beat, which is common in thyroid disease.

While we’ve seen that selenium deficiency will interfere with T4 to T3 conversion and lead to functional hypothyroidism (low T3 phenomenon), selenium plays another vital role in the thyroid as part of GPX. During the production of thyroid hormone, hydrogen peroxide (H2O2) is produced. H2O2 is important for the production of thyroid hormone, but excessive amounts lead to high production of thyroxin (T4) and also damage to the cells of the thyroid. GPX plays the extremely vital role of degrading H2O2 and thereby limiting hormone production and preventing damage to the thyroid cells. This seems to be the main way in which selenium protects the thyroid from sustaining damage which can lead ultimately to cancer.

Without selenium, the thyroid gland becomes damaged and it is through this mechanism that the main selenium and iodine interactions are found. An iodine deficiency will cause goiter, an enlargement of the thyroid gland produced by the body in an attempt to increase hormone production from limited amount of iodine. Selenium deficiency increases the weight of the thyroid in experimental animals, and a selenium deficiency combined with an iodine deficiency leads to a further increase in thyroidal weight (bigger goiter). In African countries like Zaire, there are areas where both iodine and selenium are very scarce in the soil (these deficiencies seem to run parallel in most areas). Consequently a high percentage of the people have goiters and hypothyroidism. An experimental attempt was made to correct the selenium deficiency and the result was that the hypothyroidism was made WORSE in the hypos and it produced hypothyroidism in some euthroid subjects. This was entirely unexpected and the experimenters issued a warning about supplementing with selenium (and not iodine) when both deficiencies exist concurrently.

The body has a compensatory mechanism to maintain T3 levels when iodine is deficient–it increases the production of the deiodinase Type I enzyme (DI-I). This is not a small increase, but has been shown in cattle to be an increase of 10-12 times. This increase in ID-I increases the conversion of the existing T4 to T3 to maintain T3 levels, but also increases the conversion of T3 to T2 (the degraded by-product of T3). Because of the iodine deficiency, T4 is not replenished and T3 ultimately decreases from the lack of sufficient T4 leading to a worsening of the hypothyroidism.

This result is made worse by another phenomenon which hasn’t been thoroughly studied: a selenium deficiency causes an iodine deficiency to get worse. This may be a protective adaptation by the body to limit the damage caused to the thyroid when selenium is deficient and iodine is adequate. Let’s examine this part of the interaction.

We’ve all heard that many doctors tell hypo patients, especially those with Hashimoto’s thyroiditis, not to take iodine because it can aggravate their condition. The reason seems to be that selenium protects the thyroid gland from oxidative damage and this damage can increase significantly if iodine is supplemented. Taking iodine will increase thyroid hormone production and the production of H2O2 which damages the thyroidal cells. The lack of selenium prevents GPX from being able to protect the cells from this oxidative damage. While I doubt if most doctors realize why iodine should be restricted (it certainly seemed counter-intuitive to me at first), they have learned through experience that iodine can increase the thyroid damage in Hashimoto’s. The information that selenium should be supplemented along with iodine is so new that most of them are unaware of it.

Here’s what we have: Studies have shown that if iodine is low, selenium must also be kept low to prevent the hypothyroidism from becoming worse (from increased DI-I and T4 depletion, as explained above.) So if both minerals are low, then the person is hypo and gets a goiter, but the damage to the thyroid is kept to a minimum. More severe problems happen when either selenium or iodine is high and the other is low. If selenium is high and iodine low, then T4 to T3 to T2 conversion is accelerated without T4 being replenished, leading to a worsening of the hypoT. If iodine is high and selenium is low, then H2O2 is not degraded by GPX. Since H2O2 drives the thyroid hormone production, then the thyroid over-produces thyroid hormone (Grave’s hyperthyroidism), the thyroid is damaged from the oxidation by the H2O2, and the end result is that the damaged thyroid ultimately decreases activity and hypothyroidism results (Hashimoto’s thyroiditis). This could explain the observed progression of Grave’s to Hashimoto’s.

If a selenium deficiency causes an iodine deficiency, leaving you both selenium and iodine deficient, and supplementing with either selenium or iodine causes severe problems, then the only solution is to supplement both selenium and iodine simultaneously and gradually. Even then you could experience an immediate boost (from increased conversion of T4 to T3) with a subsequent letdown (lack of T4 production because of insufficient iodine or other necessary nutrient). You have to be prepared to ride out the tough times and continue increasing the selenium and iodine until those two deficiencies are corrected and the respective metabolic pathways are back working properly.

Everything that I’ve read about selenium indicates that it is absolutely essential for proper functioning of the thyroid. A deficiency of selenium may lead to either hyperthyroidism or hypothyroidism. I’ve always wondered if high intake of selenium can lead to hyperthyroidism and finally found someone who did the experiment. They found that a high intake of selenium will not increase T4 production and lead to hyperthyroidism.

If a person has hyperT, then it looks like taking selenium without iodine will result in a decrease in production of T4 (although there may be an initial transient increase in T4 to T3 conversion and hence higher T3). I would suggest to start with a small amount of selenium methionine (about 50 mcg) and gradually increase it. I cannot see any way that thyroid function can be normalized without selenium.

For hypos the important message is that a selenium deficiency may cause an iodine deficiency, so that even though you are taking iodine you may not be assimilating it unless selenium is also being taken. This would explain how people can have iodine deficiencies even though salt and many foods have iodine added. Supplement with both iodine and selenium. I would recommend starting with 100 mcg of selenium and one kelp tablet and gradually work up to 400-600 mcg of selenium and 2-4 tablets of kelp.

While I’ve found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.

I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it’s complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected.

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Validation of the orthoiodosupplementation program:

A Rebuttal of Dr. Gaby’s Editorial on iodine

By: Guy E. Abraham, M.D. and David Brownstein, M.D.

Orthoiodosupplementation is the daily amount of the essential element iodine needed for whole body sufficiency 1 . Whole body sufficiency for iodine is assessed by an iodine/iodide loading test. The test consists of ingesting 4 tablets of a solid dosage form of Lugol (Iodoral®), containing a total of 50 mg iodine/iodide. Then urinary iodide levels are measured in the following 24 hr collection. The iodine/iodide loading test is based on the concept that the normally functioning human body has a mechanism to retain ingested iodine until whole body sufficiency for iodine is achieved. For consistency and uniformity, the same solid dosage form of Lugol (Iodoral®) is used in the loading test and for orthoiodosupplementation. During orthoiodosupplementation, a negative feedback mechanism is triggered that progressively adjusts the excretion of iodine to balance the intake. As the body iodine content increases, the percent of the iodine load retained decreases with a concomitant increase in the amount of iodide excreted in the 24 hr urine collection. When whole body sufficiency for iodine is achieved, the absorbed iodine/iodide is quantitatively excreted as iodide in the urine. At such time, 90% or more of the iodine load is recovered in the 24 hr urine collection, and the body retains approximately 1.5 gm of elemental iodine.

In the August/September 2005 issue of Townsend Letter, Dr. Allen Gaby, M.D. wrote an Editorial on iodine, questioning the validity of the iodine/iodide loading test we use to assess whole body sufficiency for iodine; and the safety and efficacy of the orthoiodosupplementation program in medical practice. Our rebuttal will cover four topics:

1. The safe and effective use of iodine by our medical predecessors.

2. The computation of the average daily intake of iodide from seaweed by mainland Japanese.

3. The validation of the iodine/iodide loading test.

4. The effectiveness and safety of orthoiodosupplementation in current medical practice.

Read it here: A Rebuttal to Dr Gaby’s Editorial on Iodine.

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By Guy E. Abraham, M.D.

In textbooks of medicine, endocrinology and thyroidology, the essential element iodine is mentioned only in connection with the most severe forms of deficiency of this nutrient: cretinism, iodine-deficiency induced goiter and hypothyroidism. Due to thyroid fixation, inhibitors of iodine uptake and utilization by target cells are called goitrogens, that is, substances causing thyroid enlargement, implying that iodine inhibitors only influence thyroid function. Perhaps, there is a restraining order preventing iodine inhibitors from interfering with iodine in extrathyroidal target organs. Many physicians would be surprised to learn that more than a hundred years ago, iodine was called “The Universal Medicine”, and was used in several clinical conditions. Nobel Laureate Albert Szent Györgyi,1 the physician who discovered Vitamin C in 1928, commented:

“When I was a medical student, iodine in the form of KI was the universal medicine. Nobody knew what it did, but it did something and did something good. We students used to sum up the situation in this little rhyme:

If ye don’t know where, what, and why

Prescribe ye then K and I.

Our medical predecessors, …were keen observers and the universal application of iodide might have been not without foundation.”

Continue reading here: Iodine: The Universal Nutrient:.

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The recommended daily allowance (RDA) of elemental iodine by the Food and Nutrition Board of the United States National Academy of Sciences was not established until 1980, and it was not confirmed until 1989.1

In that year, 1989, the Executive Director of the International Council for Control of Iodine Deficiency Disorders (that is a very impressive title to say the least), Basil S. Hetzel, published a book entitled The Story of Iodine Deficiency..2 In that book, goiter and cretinism were the only two aspects of iodine deficiency discussed. One would assume that the experts on human requirements for iodine have already figured out the amounts of iodine needed for sufficiency of the human body (i.e., the daily amount of iodine needed for the prevention and control of cretinism and endemic goiter). However, the 1930 statement of Thompson, et al,3 is still valid today: “The normal daily requirement of the body for iodine has never been determined.” In the ninth edition of the classic textbook of nutrition, Modern Nutrition in Health and Disease, edited by Shils, et al, and published in 1999, the section on iodine was written by no less than Basil S. Hetzel and coauthored with Graeme A. Clugston.4 They reported the latest recommended intakes of iodine established in 1996 by the World Health Organization (WHO), based on age and physiological conditions. The highest recommended daily intakes are for pregnant and lactating women — 200 mcg or 0.2 mg. In a subsection entitled “Iodine toxicity,” the authors stated: “Wolff39 has suggested that human intakes of 2,000 mcg I/day should be regarded as excessive or potentially harmful.” Please note, the unit mcg is used instead of 2 mg in order to make the amount appear really “excessive.” For example, if they used the unit ng, that amount would be 2,000,000 ng, a number that would scare just about anybody. Reference 39 in this citation was authored in 1969 by the world famous thyroidologist, I. Wolff,5 coauthor of the world famous Wolff-Chaikoff effect published in 1948.6 There was a fly in the Wolff-Chaikoff ointment, however.
In 1993, Ghent, et al,7 reported that daily intake of iodine at 0.1 mg/kg BW was effective in fibrocystic disease of the breast. The title of the article — “Iodine replacement in fibrocystic disease of the breast” — implies that this abnormality of the breast was due to iodine deficiency and the amount of iodine used, that is 5 mg/day for a 50 kg woman, was within the physiological ranges of iodine intake. Ghent’s study did not confirm Wolff’s prediction that daily iodine intake of 2,000 mcg (2 mg) was “excessive and potentially harmful” as quoted by Hetzel and Clugston.4 Based on academic credentials and reputation, the opinion of thyroidologist Wolff, from the National Institute of Health, would prevail over the findings of Canadian gynecologist Ghent. However, being interested in facts only, not in preconceived opinions of famous thyroidologists, this author initiated an extensive search of the literature on iodine in medicine.

The concept of orthoiodosupplementation is the outcome of this intensive literature search, which started seven years ago, combined with some original clinical research performed by the author. The clinical aspects of this research were performed under contract at the Flechas Family Practice Clinic in Hendersonville, North Carolina under the supervision of Jorge D. Flechas, MD, and funded with grants from Optimox Corporation. The author designed the protocols and monitored the progress and completion of each project. Informed consent was obtained from all the subjects participating in these projects. Pilot studies were performed with tablets containing Lugol solution in amounts per tablet ranging from 1 to 12.5 mg and compounded by John C. Hakala, RPh, from Hakala Apothecary in Lakewood, Colorado. The results of some of these projects have been published,8-12 with Flechas and Hakala as coauthors in two publications.10,11
From a review of the published data, it soon became evident that medical textbooks contain several vital pieces of misinformation about the essential element iodine, which may have caused more human misery and death than both world wars combined.8,9 The purpose of this manuscript is to present some useful information about iodine and to discuss the concept of orthoiodosupplementation in more detail than in previous publications.9,11 This manuscript was written in response to a request from the eclectic and altruistic physician, a recent collaborator on the iodine project, David Brownstein, MD, to expand further on the concept of orthoiodosupplementation with more details than in the previous publication9 in order to help the practicing physician fully appreciate the impact of this concept on their practice. Dr. Brownstein recently wrote a book about his experience with the implementation of orthoiodosupplementation in his practice.1

Continue reading here:IODINE: The Concept of Orthoiodosupplementation and Its Clinical Implications.

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“The essential trace element iodine (I) is the only one required for and in the synthesis of hormones. These I-containing hormones are involved in embryogenesis, differentiation, cognitive development, growth, metabolism, and maintenance of body temperature. I is highly concentrated in one organ, the thyroid gland, which becomes visibly enlarged when there is a deficiency of that element. It is the most deficient trace element in the world with an acknowledged third of mankind functioning below optimal level due to its deficiency (1). Low intake of I is the world’s leading cause of intellectual deficiency (2). Yet, as unbelievable as it may sound, this essential element has suffered from total neglect regarding the amount of it required by the human body for optimal health. In 1930, Thompson et al wrote (3): “The normal daily requirement of the body for iodine has never been determined.” This statement is still true today, more than 70 years later.”

“At the Children’s Summit held in 1990, the United Nations and heads of state assembled for that occasion, pledged to eliminate I deficiency by the year 2000. Commenting on this meeting, John T. Dunn stated in 1993 (4) “The goal is technically feasible, but many obstacles must be overcome before it is realized.” In the list of obstacles, no mention was made of the greatest obstacle of them all: Our total ignorance regarding sufficiency of the whole human body for I. It is obvious that I deficiency has been equated with the simple goiter, cretinism, and I-deficiency disorders related to its role in thyroidal physiology. Supplementation was considered adequate if such amount prevented cretinism, simple goiter and symptoms of hypothyroidism (1,2,4). The assumption that the only role of I as an essential element is in its essentiality for the synthesis of T3 and T4, became a dogma. With the advent of sensitive assays, Thyroid Stimulating Hormones (TSH) was promoted to queen of tests for thyroid functions (5) and I was forgotten altogether as irrelevant to the point where most endocrinologists and other medical practitioners do not request a single test for urine I concentration, during their whole medical career.”

Continue reading here:IODINE: Orthoiodosupplementation: Iodine Sufficiency Of The Whole Human Body

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