Iodine. a century of medical fraud Kathryn Alexander Kathryn Alexander 2012

Transcription

1 Iodine a century of medical fraud Kathryn Alexander Kathryn Alexander

2 Kathryn Alexander SHARING THE KNOWLEDGE OF WHAT WORKS Iodine: A Century of Medical Fraud 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: Iodine, in the form of Lugol s solution, was routinely used in both hypo- and hyperthyroidism during the decades before the advent of thyroxine and thyroid suppressing drugs. 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 s) 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 the surgical removal of the gland, which remained an option in those small number of cases which remained refractory to treatment. 2

3 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 Synthetic thyroxine replaced natural thyroid extract following a hoax batch of thyroid extract undermined medical confidence in the viability of natural thyroid extract. 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 mg/day pre-surgery to achieve the anti-thyroid effects and to prevent thyroid storm following surgery.) 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 When the thyroid gland is sufficiently iodated, then it is protected against radioactive iodine. 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 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 In 1965, The National Institute of Health, evaluated the amount of iodine on an average diet to be 0.726mg. 9 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 Bromide, used as a bread improver, displaces iodine in the thyroid gland. On an iodine deficient diet, this can have disastrous consequences and lead to hypothyroidism and goitre. 3

4 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 from 6mg - 55mg/day ( times the RDA), I have come under pressure from the medical fraternity. If there is an existing autoimmune thyroid condition, the application of Lugol s can upset the gland, but the effects are reversible, and under these circumstances it would be unwise to supplement the Lugol s solution without thyroid hormone (as is prescribed on the Gerson Therapy ). However, I have not seen any incidence of iodine-induced hypothyroidism or hyperthyroidism at these doses when the gland is normal; 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 (0.075mg or 75µg) 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 part of the 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:

5 Iodine: a link between breast & thyroid disease? IODINE AND THE THYROID GLAND Iodine, as we know, is important for the manufacture of thyroid hormones. Traditionally inorganic iodine in the form of Lugol s solution was prescribed for all thyroid disorders both over- and underactivity - but was discarded when irradiation, surgery, toxic organic iodine-containing drugs and thyroid hormone replacement therapy became available. However, we are now beginning to understand that the role of iodine in the thyroid is much greater than merely supplying a raw material for hormone production: it is the single-most protective element against autoimmune disease and cancer of the thyroid gland. The thyroid gland is capable of concentrating up to 50mg of iodine. However, the mean value in the population lies at around 10mg. Much lower concentrations occur in patients with autoimmune thyroiditis where mean iodine levels fall to 4.8mg in euthyroid patients (where the thyroid hormone is still being produced) and 2.3mg in the hypothyroid gland. Furthermore, both irradiation of the gland and ingestion of thyroid hormones for three months or more directly result in further iodine depletion from the gland. 10 In the initial stage of iodine depletion, the gland is stimulated by the pituitary hormone, thyroidstimulating hormone (TSH), to increase its number of iodine receptors (sodium-iodide symporters [NIS]) in order to trap as much iodine as possible from the circulation. This leads to an enlargement of the gland (diffuse goitre) or the growth of nodules (nodular goitre). Minute quantities of iodine were believed sufficient to prevent goitre (0.075mg/day which may be obtained from 10g iodised salt), but these amounts are woefully inadequate to reverse iodine depletion. The gland can only begin to concentrate inorganic iodide when serum iodine levels approach 0.65mg 1.3mg/L or the equivalent of taking 37.5mg 50mg iodine daily (500 times more than the current recommended intake) which correlates with amounts traditionally used to reverse thyroid dysfunction. Autoimmune thyroiditis When the gland is iodine deficient it becomes very sensitive to pituitary stimulation. Although the exact aetiology of autoimmunity remains unclear, we do know that this type of persistent stimulation increases enzyme activity (thyroid peroxidase [TPO]) and the production of hydrogen peroxide, a highly reactive oxidant. In the absence of adequate selenium to mop up the oxidants, free radicals will attack DNA increasing the vulnerability to malignant change, or attack enzymes and their substrates involved in the manufacture of thyroid hormone. It is believed that an autoimmune response to the damaged tissue then ensues, and depending upon tissue-specificity will determine the type of thyroiditis, which may manifest either as a hyper- or hypothyroid state. 11 The hypothesis that iodine-deficiency is the primary cause of autoimmune thyroiditis and thyroid cancer may explain why these conditions were almost unheard of prior to the 1920s when treatment for all thyroid problems relied on securing iodine sufficiency through appropriate dosage of inorganic iodine. Iodine depletion in the thyroid gland can be measured against 50mg in the replete gland, to 2.3mg in the hypothyroid gland. In order to achieve repletion it is necessary to apply up to 50mg/day of iodine as Lugol s solution. Prolonged iodine deficiency appears to precede the onset of autoimmune thyroid conditions. Long-term stimulation of the gland by TSH causes oxidative stress followed by an autoimmune response to the damaged tissues. More recently, in 2002, The Iodine Project, undertaken by Guy Abraham, M.D. in the USA, evaluated the therapeutic dose for supplemental inorganic iodine in 4,000 women to be between 12.5mg 50mg daily. 12 Their research revealed that iodine-deficient patients took three months to become iodine sufficient on a daily dose of 50mg, but up to a year to reach sufficiency at the lower dose of 12.5mg. Patients were rigorously monitored; no patients developed suppression of the gland, and any transient increases in TSH in the presence of normal thyroid hormone readings were identified as a marker for increased iodine uptake and not the onset of hypothyroidism. IODINE AND BREAST CANCER Since the early 1970s a strong association became apparent between the incidence of breast cancer and thyroid disease: the prevalence of both goitre and autoimmune thyroiditis was doubled in breast cancer groups over controls. Research indicates that the common link may be iodine deficiency. Both breast tissue and the thyroid gland take up and utilize dietary iodine via the same symporter system There is a significant correlative link between iodine deficiency, thyroid disease and breast cancer. Deficiencies of iodine stimulate proliferative breast tissue disorders, including breast cancer. 5

6 (NIS), and in iodine deficiency, TSH acts as a proliferative stimulus not only at the thyroid gland but also in breast tissue. In fact NIS mrna is strongly positive in human breast cancer tissues with positive staining of NIS in 88% of ductal carcinomas in situ (DCIS) and 76% of invasive carcinomas. Many studies support the hypothesis that iodine deficiency predisposes to breast cancer. For example, demographic studies in Japan and Iceland revealed that both countries have a high intake of iodine and low incidences of goitre and breast cancer. (Japanese women consume on average 13.5mg of dietary iodine daily on their traditional diet. However, the incidence of breast cancer increases in emigrated groups, indicating environmental rather than genetic as causative factors.) Conversely, in Mexico and Thailand, where iodine intake is low, there is a high incidence of goitre and breast cancer. Experimental findings showed that the administration of Lugol s or iodine-rich Wakame seaweed to rats with chemically-induced (DMBA) breast tumours, suppressed tumoural development. A further experiment by the same group showed that seaweed induced apoptosis (programmed cell death) in human breast cancer cells with greater potency that the chemotherapeutic agent fluorouracil. 13 Analysis of iodine concentration in breast tissue in both benign and malignant tumours and fibrocystic breast disease is found to be much lower than in controls. In the early 1990s, Ghent undertook a clinical study involving women with fibrocystic breast disease (a strong risk factor for breast cancer) supplementing inorganic iodine at 5mg/day. He found that in the majority of cases the symptoms were reversible over a period of time. 14 Abraham improved these results by supplementing up to 50mg inorganic iodine daily. Fibrocystic breast disease responds well to iodine supplementation. Although it is poorly understood how iodine protects against breast cancer, it is hypothesized that iodine acts as an anti-proliferative agent both indirectly, by ensuring adequate thyroid hormone production and thereby reducing TSH (and by default NIS and TPO activity), and directly due to iodine s capacity to detoxify reactive oxygen species such as hydrogen peroxide. (Selenium taken in conjunction with iodine forms the best anti-cancer duo for both the thyroid and breast.) If this were the case, it would explain the increased risk of breast cancer in women with hypothyroidism treated with thyroxine. Supplementing with the hormone suppresses TSH and therefore reduces the uptake of iodine both by the thyroid and breast tissue, which exacerbates any existing iodine deficiency. Statistics indicate that women on thyroid hormone replacement for 15 years showed a 19.5% incidence of breast cancer whereas women who have taken thyroid hormone for 5 years had only a 10% incidence of breast cancer. 15 Iodine may also play a pivotal role in fertility. Next to the thyroid gland, the ovaries accumulate the highest levels of iodine. They also share the same symporter mechanisms for the uptake of iodine as breast tissue and the thyroid. The developing follicle has the capacity to generate active thyroid hormone (T3) from its precursor (T4) and it is strongly suggested that thyroid hormone plays a direct role in follicular development. 16 Interestingly, clinical evidence supporting these findings occurred during Abraham s iodine project when women with polycystic ovarian syndrome (PCOS) undergoing iodine supplementation resumed regular menses with the shrinkage of cysts on their ovaries. It is highly likely that iodine will also be protective against ovarian cancer. Supplementing with thyroid hormone does not reduce the risk for breast cancer as this medication suppresses the uptake of iodine by both the thyroid gland and breast tissue. Helpful tips Avoid bromine, chlorine and fluoride as these are all goitrogens (anti-thyroid) and inhibit the utilization of iodine. Chlorine competes with iodine for absorption in the digestive tract, and fluoride damages the transporter sites (NIS) leading to reduced iodine uptake by the thyroid, breasts and ovaries. Bromine is the most potent goitrogen and is found in fumigants, dyes, leaded petrol, fire-retardants, used for water purification, in agents for photography, as brominates in vegetable oil, and as an emulsifier in many citrus-flavoured soft drinks. Fortunately, its use as a cheap agricultural pesticide is now restricted due to its effects on global ozone depletion. Avoid calcium supplementation as calcium not only inhibits the absorption of iodine but also exacerbates magnesium deficiency. Magnesium is more important than supplemental calcium in calcium homeostasis, and is required to support iodine metabolism. Avoid soy products: soy contains the isoflavone genistein which is both goitrogenic, and therefore will exacerbate hypothyroidism, and oestrogenic. In iodine deficiency oestrogen receptor density is increased in breast tissue and therefore more sensitive to oestrogens, including phyto-oestrogens. Under these circumstances genistein may act a cancer promotor. 6

7 Take foods from the sea kelp, seaweed and fish. Take a selenium supplement mcg is the therapeutic dose. Both selenium and iodine protect against thyroid and breast cancer. Selenium is also required for the conversion of inactive thyroid hormone (T4) to its active state (T3). For menopausal women, or those with oestrogen-dominance, ensure that your diet is high in cruciferous vegetables (broccoli, Brussels sprouts, red cabbage) as these promote conversion of oestrogens to their anti-cancer form. If you are taking thyroid hormone replacement be mindful of iodine deficiency and seek professional advice on supplementation. Inorganic iodine in the form of Lugol s solution will provide both potassium iodide (preferred by the thyroid) and elemental iodine (preferred by breast tissue). However, doses should be monitored by a professional, as the thyroid gland can be unpredictable in its reaction to iodine hence the wide variations in dose of Lugol s in its earlier application. Do not use other iodine medications. Inorganic iodine, not only guards against abnormal tissue changes, but has the capacity to reverse organic change if the doses are within the therapeutic range. One drop of Lugol s solution is equivalent to 6.25mg elemental inorganic iodine. Cruciferous vegetables are goitrogenic and should not be taken in quantity by those with sub-clinical hypothyroidism. In Part 3 we will explore the role of iodine in diabetes, insulin-resistance, hypertension, heavy metal detoxification, depression and ADHD. 7

8 Iodine: a link between thyroid, diabetes & depression? HYPOTHYROIDISM AND DIABETES If I mention the symptoms of fatigue, weight gain, high cholesterol and depression, would it surprise you to learn that these symptoms are common to both low thyroid function (hypothyroidism) and diabetes? Not only do these conditions share symptoms, but also they are often found together. Simply put, people with diabetes are also more likely to have poor thyroid function; there is a higher than normal prevalence of thyroid disorders in patients with type 2 diabetes (insulin-resistant diabetes, NIIDM) and a staggering 33% incidence of autoimmune thyroid disease with the autoimmune type 1 diabetes (insulin dependent diabetes, IDDM). Medically, our experts are puzzled as to why this relationship exists, but simply give the assurance that people with one kind of autoimmune disease are at risk of developing another type. 17 So we must look for a common factor. They are both endocrine disorders one of insulin metabolism, and the other of thyroid metabolism. They both govern energy: thyroid hormone sets the metabolic rate and insulin ensures the uptake of glucose by the cells to make energy. They both govern cholesterol metabolism: in insulin resistance, excess insulin stimulates cholesterol synthesis and with hypothyroidism, insufficient thyroid hormone makes the liver inefficient in its cholesterol clearance. Each condition increases the risk factors for heart disease. If you have both conditions, then you may well double your risk. Sadly, sub-clinical hypothyroidism remains largely undiagnosed and untreated, and other drug-related treatments are recommended for both cholesterol reduction and the management of diabetes. It would pay to test for iodine deficiency in diabetes, as making good deficiencies would likely improve any health outcome and could reduce drug-dependency The breakthrough for a possible explanation to the link between both conditions came during the clinical study involving 4,000 women with fibrocystic breast disease (FBD) who were treated with inorganic iodine in amounts up to 50mg/day over a prolonged period. Some of these women also presented with diabetes. It was found that patients with diabetes needed to monitor their blood sugar levels more closely as the condition became more easily controlled on the iodine supplementation. This led to a clinical study of 12 diabetics, where all the patients were able to lower their medications with six cases being weaned off drugs completely, their blood indicators for diabetes being maintained within normal parameters. 18 The researchers then began looking at the role of hormone receptors as there is a similarity in the families of receptors for thyroid hormone, the steroid hormones, insulin and the hypothalamus and pituitary stimulating hormones. These receptors require specific tyrosine residues without which the receptor fails to relay the signal from the hormone into the nucleus of the cell. It was postulated that the binding of iodine to the tyrosine residue made it functional. Two events highlighted this possibility: in patients on iodine supplementation there was reduction in insulin resistance and therefore better control of diabetes, and secondly, in hypothyroid patients, there was improved thyroid hormone activity on lower doses of thyroid supplementation. For me, what clinched this possibility was that patients diagnosed with insulin dependent diabetes (pancreatic failure to produce insulin) but still capable of producing insulin (C-peptide is measurable), when supplemented with inorganic iodine, started to produce insulin. It is the insulin signal via the receptors at the pancreas which relays the instructions for the pancreas to make more insulin; if the receptors cannot receive the signal (insulin resistance) then the pancreas will not synthesise insulin. This gives the features of type 1 diabetes (IDDM). Similarly, insulin signals at the liver indicate to the liver that there is plenty of glucose in the circulation; if these signals fail, the liver goes into glucose production overdrive which leads to type 2 diabetes (NIDDM). If supplementation of iodine starts to reverse these conditions, then the common factor between diabetes and hypothyroidism may well be a primary iodine deficiency. Insulin signals the pancreas to produce more insulin and the liver to stop releasing glucose. If the insulin receptors require iodine to function, then supplementing with iodine in iodine deficient states could reverse insulin resistance at the liver and pancreas and improve the clinical outcome for diabetics. HYPOTHYROIDISM & DEPRESSION, INSOMNIA AND ADHD We all know of the serotonin connection with depression; low serotonin equals depression and poor concentration. Perhaps what is not so well known is that tryptophan (an amino acid) is the precursor 8

9 to serotonin, and that the brain only makes serotonin after we eat carbohydrates. What s the link here? Carbohydrates stimulate the release of insulin, and insulin receptors at the brain stimulate the uptake of tryptophan which is then converted to serotonin! Imagine if you have insulin resistance at the brain how a defective uptake of tryptophan could then affect your mood, concentration and learning. Similarly, melatonin, the sleep chemical, also requires tryptophan. Invariably we see depression linked to insomnia. I have a patient who suffered severe insomnia for seven years; she also had sub-clinical hypothyroidism and heavy metal poisoning. Her urinary iodine test indicated severe iodine deficiency. We tried many methods over the years, but it wasn t until she began iodine supplementation that she started sleeping again, her thyroid became rebalanced and many of her other symptoms reversed. Could iodine deficiency also lead to insulin resistance at the brain? If so this would explain the link between hypothyroidism and depression. There is also a serotonin connection with ADHD. The drugs given to alleviate the symptoms act by elevating serotonin. Interestingly, a study in Sicily which compared two small groups of pregnant women where iodine intakes were either moderately deficient (group A) or marginally sufficient (group B), found that 68% of the children born to group A mothers were diagnosed with ADHD (compared to none in group B) and total IQ scores were also lower in group A. 19 All the children had normal thyroid function, although 50% of mothers in group A had thyroid failure during pregnancy. As the role of maternal thyroid hormone is to develop the brain neurons and terminals in the foetus, and as iodine is required for the synthesis of thyroid hormone, then evidence points yet again to a primary iodine deficiency as a possible key causative factor. DIGESTION, ABSORPTION AND GUT PARASITES Another symptom of hypothyroidism, or more accurately iodine deficiency, is reduced hydrochloric acid (HCl) output which results in poor protein digestion, poor absorption of iron, calcium and B12, and an increased incidence of helicobacter pylori and gut parasites. Stomach cells require iodine which concentrates chloride in the parietal cells ready for output as HCl when food hits the stomach. The acidity generated causes the unfolding of dietary protein and the activation of pepsin a protein digesting enzyme. High acidity also keeps the gut sterile, kills any micro-organisms that may have been ingested or any potentially resident pathogens such as H pylori. Iodine is also a powerful disinfectant and is used by the immune system when infection is present. This is why illness may produce a transient hypothyroid state in patients, as thyroid hormone is broken down to release its iodine which is made available for the immune system. Iodine is a major disinfectant of the gut and keeps pathogenic micro-organisms at bay, including helicobacter pylori. It is the active compound in many of our antiparasitic herbs and medical drugs. Many of our herbs used for gut parasites, such as black walnut hull, contain iodine. Iodine in the gut is hostile to harmful pathogens. Some amoebicidal medications, such as Iodoquinol, contain organic iodine in amounts up to 1,248mg/day this is 25 times the upper amount of inorganic iodine (50mg) recommended. Iodine has been used to disinfect water since the early 1900s and is still the lightest, cheapest and simplest method of water purification. HEAVY METAL TOXICITY Being a halogen, iodine in sufficient doses will displace and remove other more toxic halogens such as bromine, fluorine and chlorine, the levels excreted via the urine increasing proportionally to the amount of iodine ingested. Iodine can also remove heavy metals. Dr Abraham has shown that iodine promotes the excretion of heavy metals such as lead, mercury and cadmium of which excretion rates increased several-fold after just one day of supplementation. Aluminium elimination took longer, being excreted after one month on supplementation. 20 This must be an additional bonus for people whose health problems are compounded by heavy metal toxicity. Simply put, if you are iodine-sufficient, you should not accumulate heavy metals. Iodine sufficiency protects against the accumulation of heavy metals. How can I tell if I am iodine-deficient or hypothyroid? Ask your GP for a urinary iodine test. In most cases this will indicate your iodine status. Determine if you have sub-clinical hypothyroidism. If your temperature on waking is below 36.3º over a few consecutive days, then you may well be hypothyroid. Ask your GP for a thyroid function test; if your TSH (thyroid stimulating hormone) registers over 2.0 then this is an indicator for sub-clinical hypothyroidism even though your levels of circulating thyroid hormones may be normal. 9

10 If your TSH is above 4.0 then ask your GP to run tests for any thyroid antibodies to determine if you have an autoimmune condition. What Can I do? Although I like to give self-help advice I have to warn you against supplementing with inorganic iodine (Lugol s solution) unless your thyroid function is being monitored by a professional. If you are hypothyroid and it s due to a simple iodine deficiency, then taking Lugol s solution may fix the problem. But if the gland has any pathology (such as autoimmune thyroiditis or nodules) then taking Lugol s solution, even if you are iodine-deficient, may appear aggravate the condition. Under these circumstances it is important that all thyroid parameters are monitored, which include ft4, ft3 and the thyroid antibodies, to make sure that any changes are transient and not directly affecting the gland. Even if the gland is aggravated, this is reversible once you stop the iodine supplementation. In the meantime, eat fish and seaweed and even take kelp; Ensure adequate selenium supplementation as selenium protects against damage to the thyroid gland in autoimmune conditions, and is also required for the conversion of thyroxine (T4) to its active form (T3); Ensure adequate iron which catalyses the synthesis of thyroxine; If you are hypothyroid then avoid foods which contain goitrogens such as soy products, the cabbage family, millet and peanuts; Ensure a good magnesium status; Avoid calcium supplementation as this inhibits the uptake of magnesium, iron and iodine; and If you are a female, reduce soy intake and avoid calcium supplementation as these may be counter-productive and provide no health benefits References 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: Starr, P., et al., The effect of iodine in exopthalmic goitre Arch. Int.Med., 1924: 34: 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: ISBN Wolff, J. and Chaikoff, I.L., Plasma Inorganic Iodide as a Homeostatic Regulator of Thyroid Function. J.Biol. Chem, 1948: 174: , London et al; Bread A dietary Source of Large Quantities of Iodine; New Engl. J. Med., 1965: 273: Abraham G. E., M.D. The historical Background of the Iodine Project Iodine/IOD-08/IOD_08.htm 11. Abraham G. E., M.D. The Safe and Effective Implementation of Orthoiodosupplementation In Medical Practice Schachter M., M.D. Iodine: Its Role in Health and Disease htm 13. Smyth, P., The thyroid, iodine and breast cancer Breast Cancer Research 2003, 5: breast-cancer-research.com/content/5/5/r Ghent et al, Iodine replacement in Fibrocystic Disease of the Breast. Can. J. Surg., 36: , Howenstine, J., M.D. Thyroid Hormone Therapy Appears to Cause Breast Cancer; NewsWithViews.com Slebodzinski, A.B. Ovarian iodide uptake and triiodothyronine generation in follicular fluid. The enigma of the thyroid ovary interaction. Domest Anim Endocrinol Jul;29(1): Patricia Wu, MD, Thyroid disease and diabetes Clinical Diabetes Vol 18:1 Winter

11 journal.diabetes.org/clinicaldiabetes/v18n12000/pg38.htm 18. Jorge D. Flechas, M.D. Orthoiodosupplementation in a Primary Care Practice com/pics/iodine/iod-10/iod_10.htm 19. F. Vermiglio, et al; Attention Deficit and Hyperactivity Disorders in the Offspring of Mothers Exposed to Mild-Moderate Iodine Deficiency: A Possible Novel Iodine Deficiency Disorder in Developed Countries The Journal of Clinical Endocrinology & Metabolism Vol. 89, No Guy E. Abraham, M.D. The historical background of the Iodine Project Iodine/IOD-08/IOD_08.htm 11