Blog: Body in Ecstasy
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Autoimmune and Iodine

Cancer AIDS and autoimmune unbalance

Date:   11/2/2007 12:02:16 PM   ( 16 y ) ... viewed 3083 times

Iodine: Part 1 - A Century of Medical Fraud

Kathryn Alexander

After a century of propaganda against the use of inorganic iodine, the lid is finally being lifted – and not before time. Amid recent concerns linking low IQ in our children with widespread iodine deficiency, our food regulators (FSANZ) are considering mandatory plans to force bakers to fortify bread with iodine and replace standard salt with iodised salt. Studies have shown that children born to moderately iodine-deficient mothers have IQs 10 to 15 points lower than other children, more hearing and learning difficulties and an increased risk of ADHD.1

The known effects of iodine deficiency on thyroid function and brain development are not new. Since 1829 iodine deficiency was known to be the cause of endemic goitre (enlarged thyroid gland with low function [hypothyroidism]) in areas where soils were poor in iodine. For over a century the treatment was inorganic iodine in the form of Lugol’s solution, a mix of inorganic iodine and potassium iodide, at a dose between 12.5mg – 37.5mg daily (2-6 drops). Lugol’s was routinely applied in other conditions when patients failed to respond to treatment. Nobel Laureate Albert Szent Györgyi, the physician who discovered Vitamin C in 1928, commented: “When I was a medical student, iodine in the form of KI [potassium iodide] 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. 2

So why do we have this crisis in iodine deficiency two centuries later? How come the safest, most effective and cheapest medicine has become so feared by the medical fraternity? And how come our iodine intake has been regulated almost out of the food chain? Iodine, once heralded for its universal beneficial effects, has now become a leper.

Reading through the volumes of literature it appears that the “iodophobia” generated by the scientific fraternity ranks as one of the worst cases of fraud, and was based on hypothetical conclusions drawn from the results of various experiments on rats, which were never tested in a clinical setting. As these published results were synchronized with the launch of a new drug and had the effect of persuading physicians to exchange their clinically-proven safe and effective treatments for the more toxic treatments (organic and radioactive iodine), one can only assume that this was part of the pharmaceutical propaganda machine. Obviously, as thyroid conditions provide an opportunity for big business, a lot was at stake.

For over a century (1830s - 1930s) both low thyroid function (hypothyroidism) and hyperthyroidism were treated with Lugol’s solution, at lower or higher doses, respectively. The medical consensus on treatment and dosage was reached over three generations of clinical observation where therapeutic application of Lugol’s was seen to balance the gland. For example, a study in 1923 involving adolescent girls at risk from goitre, showed a positive response on a daily dose of 9mg of inorganic iodine.3 Similarly, in 1924, a study involving patients with thyrotoxicosis (hyperthyroid) revealed a 92% remission, with no requirement for surgery, on a daily dose of 90mg inorganic iodine. 4

The first wave of propaganda began in 1910 when Professor Kocher, who had won the Nobel Prize for his work on thyroid surgery, urged medics to drop Lugol’s in favour of surgical removal of the gland. This message was expedited by his own timely and much-publicized sudden onset of hyperthyroidism which he blamed on the ingestion of inorganic iodine. However, most physicians still preferred Lugol’s as a first line treatment instead of to surgical removal of the gland, which remained an option in those small number of cases which remained refractory to treatment.

In the 1930s, the active compound, thyroxine, was isolated from the thyroid gland and thyroid disorders suddenly became a disease rather than a deficiency-state. The manufacture of thyroid hormone products began, initially derived from the desiccated gland of a sheep’s thyroid and later, by 1952, the synthetic form of thyroxine was perfected. Physicians were slow to make the switch preferring to prescribe Lugol’s or the desiccated gland. With a little help they were persuaded to change their allegiance. In 1963 a hoax batch of thyroid extract, containing only iodine, was shipped to Europe and the US. There was widespread concern that the effects of this “drug” were not consistent with previous clinical experience and so thyroid extract was labelled “unreliable”. Although the hoax was uncovered 7 years later and a medical letter in 1973 maintained that thyroid extract had never been unreliable, mud sticks and physicians started using synthetic thyroxine in droves. 5

With the iodisation of salt (mandated around 1924) and the use of thyroid hormones, goitre and hypothyroidism was medically dealt with. However, this didn’t address hyperthyroidism (thyrotoxicosis). As we have seen, physicians were getting outstanding results with high dose Lugol’s solution, without the requirement for surgery. Even current medical texts concur that potassium iodide is the “most rapidly acting anti-thyroid drug” but adds a proviso “it has no place as an anti-thyroid drug except pre-surgery or in the management of thyrotoxic crisis.” 6 (Inorganic iodine is prescribed at between 120-180mg/day pre-surgery to achieve the anti-thyroid effects.)

In 1943, the pharmaceuticals launched their own anti-thyroid drug (Thiouracil), which carries severe side-effects such as uncontrolled infection and bleeding. Reported “results” were promising with a 50-75% remission rate. However, other researchers couldn’t reproduce these results and later studies in 1973 confirmed a woeful 11-16% remission. So by the 1980’s these drugs fell out of favour making way for radioactive iodine – to ablate the gland (kill it off!). Hypothyroidism now became a goal of treatment, rather than an unwanted side-effect, and is achieved in the majority of cases.
It was the propaganda in 1948 that heralded the major wave against inorganic iodine. Two researchers, Wolff and Chaikoff, gave rats a very high dose of inorganic iodine. They then zapped the rats with radioactive iodine and found that there was no radioiodide uptake by the gland. They also observed a transient decrease in thyroid hormone. They did not conclude iodine sufficiency in the gland protected it from radiation (as we now know), but that iodine saturation of the gland inhibited thyroid function! 7
As high doses of Lugol’s were commonly used to suppress the over-active thyroid gland, then these findings were of little consequence. However, their deductions were lethal. They extrapolated this data onto human subjects, indicating that iodide levels above 0.2mg could lead to considerable increase of hormone stores (potential for hyperthyroidism) while doses of 12.5mg iodine/day would block the synthesis of thyroid hormones resulting in hypothyroidism and goitre. None of the rats in their experiment actually developed these conditions, and later, in 1969, Wolff commented, “the rarity of iodide goitre in the face of the extensive exposure of a great many patients to iodide has not been satisfactorily explained.” We now know long-term application at these higher levels of inorganic iodine do not saturate the gland, nor do they inhibit daily thyroidal iodine uptake, or thyroid hormone synthesis. And in the rat experiment, the initial inhibition persisted for a mere 26-40 hours after which normal synthesis of thyroid hormone was resumed.
By now, the daily iodine recommendations became even more conservative, were based on minimal amounts where 10g of table salt would deliver 0.075mg of bio-available iodine – enough to prevent goitre. (If you were to achieve therapeutic levels of iodine at 12.5mg you would need to eat 0.5 kg of salt daily!)

But we couldn’t get away from the statistics. The incidence of autoimmune thyroid disease, which was almost non-existent prior to the iodisation of salt, steadily rose with the USA prevalence of Hashimoto’s thyroiditis (hypoactive), a condition that predominantly affects females over the age of 40, standing at 549 per 100,000 population in 1996. 8

In 1965, The National Institute of Health, 9 evaluated the amount of iodine on an average diet to be 0.726mg. Following the Wolff-Chaikoff lead that daily intakes of iodine greater than 0.2mg were excessive, and more than 2mg, potentially dangerous for inducing hypothyroidism, bakers were encouraged replace potassium iodate with bromide as a bread improver. As one slice of bread would deliver 0.15mg of iodine, the removal of iodate was a severe blow to our iodine status. But interestingly, these same levels of iodine were also being blamed for the outbreaks of “iodine-induced thyrotoxicosis” (hyperthyroidism). However, the scientists remained staunch in their approach and in 1980 the RDA for iodine was set at 0.15mg even though studies had shown that it was impossible to induce either thyrotoxicosis or Hashimoto’s in animals with inorganic iodine.
On a personal note, as a long time practitioner of the Gerson Therapy, which requires Lugol’s solution at doses between 6mg and 55mg/day (30–275 times the RDA), I have come under pressure from the medical fraternity. However, I have not seen any incidence of iodine-induced hypothyroidism or hyperthyroidism at these doses; thyroid hormone output remains stable, and furthermore, I have seen the reversal of pre-existing goitres, both nodular and diffuse, over an average two-year period.

The iodine story is about to unfold further. With increasing iodine deficiency over the last 30 years compounded by an increase of goitrogens (elements that oppose iodine and inhibit thyroid function) in our water (chlorine and fluoride) and our food, particularly bakery products (bromide) and soy products – there has been a concomitant rise in various chronic conditions: the hormone-responsive cancers (breast, ovarian, prostate) and female reproductive disorders, such as fibrocystic breast disease, endometriosis and ovarian cystic syndromes; diabetes (including autoimmune diabetes of the young), obesity, hypertension and depression.

To my mind (and it would appear to some of the government’s health statisticians) there is a clear correlation between the incidence of breast cancer with Hashimoto’s thyroiditis (13.7% incidence with breast cancer; 2% in controls) and the incidence of childhood insulin-dependent diabetes with thyroid antibodies (38% incidence with thyroid antibodies; 6% in controls). To my mind it is not a coincidence that mainland Japanese women, who consume 13.5mg of iodine daily (90 times the current RDA), have the lowest incidence of breast cancer. And it is a simple matter of clinical observation that many of these diseases improve when supplemented with inorganic iodine in therapeutic amounts. As to why there is a lack of scientific evidence to support its use brings us back to the growing problem that medical trials are funded by pharmaceuticals when trying to develop a new product, not by governments to defend a cheap, existing product.

What has transpired is that the amount of iodine required to prevent goitre is insufficient to meet whole body requirements and as a consequence of denying the clinical evidence for nearly a century, we have been plunged into a state of chronic iodine deficiency and, for many, a life of misery.

In the next issue we will explore the evidence linking iodine deficiency to diabetes, insulin-resistance, obesity, depression and the hormone-responsive cancers.

All the studies mentioned in this article are well-referenced in the article by Abraham, G.E., M.D.; The Safe and Effective Implementation of Orthoiodosupplementation in Medical Practice; The Original Internist, March 2004:17-36

1. Push for iodine in bread to boost brains The Australian 18/05/07
2. Abraham, G.E., Iodine: The Universal Nutrient

3. Marine, D., Prevention and Treatment of Simple Goitre J. Am. Med.Assoc., 1926: 86:1334-1338,
4. Starr, P., et al., The effect of iodin in exopthalmic goitre Arch. Int.Med., 1924: 34:355-364
5. Abraham, G.E., The History of Iodine in Medicine Part III: Thyroid fixation and medical iodophobia

6. Davidson’s Principles and Practise of Medicine, 15th Edition 1987:438-440 ISBN 0 443 03824-4
7. Wolff, J. and Chaikoff, I.L., Plasma Inorganic Iodide as a Homeostatic Regulator of Thyroid Function. J.Biol. Chem, 1948: 174:555-564,

9. London et al; Bread – A dietary Source of Large Quantities of Iodine; New Engl. J. Med., 1965: 273:381

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