From brou@istar.ca Thu Mar 23 09:59:56 2000 Date: Wed, 22 Mar 2000 14:24:59 -0800 From: Andreas Schuld PFPC NEWSLETTER #3 - "FLUORIDES: ANTI-THYROID MEDICATION" February 17,2000 (as always, feel free to distribute) IN THIS ISSUE: 1) EARLY PIONEERS 3) GALETTI 3) IODINE DEFICIENCY OR FLUORIDE EXCESS? Hi everyone, Welcome to Newsletter #3. This newsletter features more information on the use of fluorides in the treatment of hyperthyroidism. (Please remember that hyperthyroidism is the opposite condition of hypothyroidism. When anti-thyroid medication is given to a health person (euthyroid), hypothyroidism will obviously result.) Mary Shomon, author and expert on thyroid disease, has written a very informative article on fluoride and thyroid, which can be accessed here: http://thyroid.about.com/health/thyroid/library/weekly/aa020700a.htm Mary has an incredible website with information on thyroid disease, and is never afraid to tackle the "experts". She is always willing to share info. If any of you are dealing with thyroid disease, and require more info for yourself or a loved one, please check out her site: http://thyroid.about.com/health/thyroid/mbody.htm Meanwhile, thank you Mary for doing so much to raise thyroid awareness and for your article! Best wishes to all, Andreas Schuld Parents of Fluoride Poisoned Children Vancouver, BC, Canada -------------------------------------------------------------------------------- ------ 1) EARLY PIONEERS (the following information has been compiled from the references listed at the end of the newsletter) In 1932 Wilhelm May first reported on his findings using sodium fluoride in the treatment of hyperthyroidism. May had been largely inspired by the work of Goldemberg who was based in Buenos Aires and had published extensively between 1919 and 1930 on his findings of applying fluorides as anti-thyroid medication. Goldemberg firmly believed that the occurrence of goiter and cretinism was NOT due to iodine deficiency, but to excessive fluoride intake from air, food and water. Investigating areas then commonly referred to as "goiterous waters" ('Kropfwaesser') and reviewing the work by Repin, Gautier, Clausmann, McCarrison, Parhou and Goldstein, Pighini, Cristiani, Cahages, Houssay, Tappeiner, Schulz, Brandt and Pisotti, Goldemberg became convinced of the fluorine-iodine antagonism and thus began using fluorides in the successful treatment of hyperthyroidism. As a result of Goldemberg's findings, May likewise began with fluoride therapy in preliminary trials involving 39 patients in Germany, publishing the results in 1932. By 1935 he had observed the antagonism successfully in 800 more patients. May - as did Goldemberg before him - reported that the thyroid after fluoride administration developed a similar hyperplasia as were seen in goiter. Like Goldemberg, von Mundy, and Todd, May found that the fluoride-iodine antagonism was most easily observable through fluoride's action on glycolysis in the liver. [Glucose is required to convert thyroxine (T4) to the biologically active triiodothyronine (T3). This occurs mainly in the liver, if glucose is adequate]. According to Dresel and Goldner glycolysis in the liver was to be seen as the FIRST sign of thyroid hormone activity. Abelin had shown that priority in the treatment of hyperthyroidism had to be given to improving the disturbed liver function. Later Stuber and Land reported their findings that glycolysis was inhibited directly correlating with increasing fluoride levels in the blood. First experiments with sodium fluoride, showing inhibitory effects on glycolysis in isolated muscle tissue had been published as early as 1869 [Nasse O - "Beitraege zur Physiologie der contractilen Substanz"; Pfluegers Archiv fuer Physiologie 2: 97-121 (1869)]. Michaelis further reported that fluoride were to be seen as catalyst in the process of calcium binding. Goldemberg had already pointed to increased calcium levels in the blood due to fluoride . According to Saegesser hypercalcemia occurred in hypothyroidism. He showed that this was due to increased calcium levels in the blood, resulting from a reduction in calcium excretion. In hyperthyroidism, therefore, a reverse condition of INCREASED calcium elimination had to be observable, and this was indeed confirmed by May in 1935. In 1937 Dr. Georg Litzka reported on the use of 3-fluorotyrosine in the treatment of hyperthyroidism which was now being used by him and May. IG Farben had brought this product (developed by Schiemann and co-workers) onto the market under the tradename "Pardinon". (IG Farben, of course, was also the notorious and most powerful industry cartel which developed Sarin. ) Schoeller and Gehrke had earlier brought evidence that the specific traits of the fluorine atom were sustained when bound in organic compounds.[Schoeller a. Gehrke - Klin. Wochenschr. 1129 (1929)] When tyrosine was bound to fluorine, the action of fluorine were not only sustained, but greatly magnified and a mere 0.1mg/day F- had therapeutic effects on humans. [We have since found much evidence of this in ALL our fluoride-compound investigations, be it tolylfluanid (pesticide), PMSF, Prozac, Paxil, phenothiazine or many other fluorinated medications. The thousands of studies on fluoride-aluminum compounds or beryllium fluoride clearly show this as well by their documented G protein activation, an activity normally reserved for TSH, the thyroid stimulating hormone. TSH controls iodine, selenium and zinc] For May, 3-fluorotyrosine became the treatment of choice in hyperthyroidism. Within 6 to 8 weeks patients became symptom-free, and employment-ready. (1937) Litzka and May were able to document and supply evidence for all claims. Between Jan.1, 1935 and October 1936, May further cured 501 patients successfully with fluorotyrosine. Around the same time (1932) Gorlitzer von Mundy, being aware that fluorides also get absorbed through the skin, began fluoride treatments of hyperthyroid patients in Austria by prescribing 20 minute baths containing 30ccm (0.03l) HF per 200 liters of water. He reported on his successful treatment spanning over 30 years and involving over 600 patients at a 1962 symposium on fluoride toxicity organized by Gordonoff in Bern, which was also attended by other world-leading experts including the great George Waldbott, Steyn, and others. -------------------------------------------------------------------------------- ------ #2) GALETTI We have received several comments from doctors and dentists who we have sent some of our documents to. They claim that fluoride suppresses the thyroid only at high doses, citing the Galetti paper from 1958. This is NOT correct. We wish these folks had a better understanding of thyroid disease and function. It shows how much ignorance relating to thyroid disorders must be overcome first in order to have this issue addressed properly. There is a reason why the thyroid has often been called the most neglected and misunderstood organ in the body... We are concentrating our efforts to bring this information to endocrinologists. It is this field which should be addressing the fluoride issue. The fact is that in ALL cases but 1 fluoride showed reduced plasma bound iodine, even at 0.9 mg/day - a fact of great importance when one considers the current knowledge on sub-clinical hypothyroidism. The critics critics don't bother to analyze the actual data, but tend to concentrate on the author's conclusion which state his doubts about fluoride as an effective anti-thyroid. There is much wrong with that, for if one does not understand thyroid disorders and evaluate the test methods properly, one surely cannot evaluate results correctly. Galetti's conclusions are very much based on knowledge as it was in the year 1958, and he displays severe ignorance about thyroid function and anti-thyroid agents when compared to today's standards. However, it's his DATA that's important. In ALL cases but 1 the Basic Metabolic Rate (BMI) decreased. This was achieved sometimes within 20 days. To evaluate this properly, one needs to understand how anti-thyroid agents work. It is well known in the field of endocrinology that PTU and Methimazole, the two drugs currently used in the treatment of hyperthyroidism, sometimes can take a few months to kick in, due to the thyroid storing large amounts of iodine. Galetti seems to complain about the fact that it took so long, concluding that it was "effective only occasionally among people subjected to massive doses of this substance" (This besides the fact that 6 of 15 patients were completely healed!...average"massive" dose meaning 6mg NaF (2.9 F-) daily, less than half the intake as estimated in 1991 by the US PHS in fluoridated areas => 6.5mg F-) One patient was clinically cured by 2.72 mg F-/day over a period of four month period... -------------------------------------------------------------------------------- - #3)IODINE DEFICIENCY OR FLUORIDE EXCESS? EXCERPTS from WORLD HEALTH ORGANIZATION PRESS RELEASE, May 25, 1999 World Health Organization Sets Out To Elimate Iodine Deficiency Disorders "It affects 740 million people a year. It causes brain disorders, cretinism, miscarriages and goiter. It is the world's single most important and preventable cause of mental retardation. And it is almost unknown...Calling it one 'one of the best kept secrets' the WHO has rededicated itself to eliminating Iodine Deficiency Disorder, or IDD, through an intense programme of salt iodisation and iodine delivery within the next decade." IDD: The Impact IDD is a significant public health problem in 130 countries, affecting a total of 740 million people. While remarkable measurable progress is being made through universal salt iodization, there are nearly 50 million people estimated to still be affected by some degrees of IDD-related brain damage. One third of the world's population is estimated to be at risk of IDD. Since the passage of a special resolution at the World Health Assembly in 1990 and subsequent resolutions in 1992 and 1996, the Department of Nutrition for Health and Development (NHD) of WHO has worked tirelessly to establish iodisation programmes around the world. The director of the NHD Department, Dr. Graeme Clugston, points out that 'The tragedy is that such a huge global burden of brain damage is still occurring, much of it irreversible, yet less than a single teaspoon of iodine is all a person requires during an entire lifetime.'" ------- Is this really iodine deficiency? Or is Goldemberg right, and it's really caused by excessive fluoride intake through water, food and air and which dose-dependently reduces biologically active iodine in the system and causes biochemical iodine deficiency? We agree with Goldemberg. Let's look at one example - Hong Kong. Water fluoridation was introduced in 1961. Hong Kong is declared an area of Iodine Deficiency. This is completely absurd, as it is in most areas in Asia where sea products are commonly consumed. Both hypo- and hyperthyroidism exist in Hong Kong. A paper was published in 1996 in the European Journal of Clinical Nutrition [Kung AWC, Chan LWL, Low LCK, Robinson JD - "Existence of iodine deficiency in Hong Kong - A coastal city in southern China" Eur J Clin Nutr 50; 8 (1996)] which shows that "as far as IDD is concerned, Hong Kong is just another big city in China."(CCPR) The study shows that although Hong Kong is a non-goitrous area, iodine deficiency exists. Iodine intakes, as reflected in urinary iodine excretion, were found to be marginally deficient. The study was done out of concern because a high percentage of newborns were found to have TSH cord blood values greater than 5mIU/l and a high incidence of transient neonatal hypothyroidism. There is NO "iodine deficiency" in Hong Kong. Here is the more than obvious proof: Responding to another study which had found that Chinese children in Hong Kong have a higher incidence of hyperthyroidism, the Consumer Council took steps to inform the public on the adequacy of iodine intake, and in association with the Chinese University of Hong Kong, examined the iodine content of 146 food products including seafood, salt, seaweed products, meat, vegetables, eggs, soy sauce, milk and butter. The amount of iodine customarily consumed in a meal of some dried seafood, e.g. kelp, mussels, seadragon and seahair was shown to be much higher than the WHO recommended daily intake for children or adults. The average iodine concentration of roasted seaweeds is some 400 times higher than that of vegetables. 6 brands of roasted seaweed were found to contain comparatively high iodine concentration. Consuming 2g (about 7 to 8 small slices or 2 small packages) would have exceeded the WHO recommended daily iodine intake for children under 12 years old. 3 milk products were found to contain a particularly high iodine content. Iodine Deficiency? In the WHO South-east Asia region alone maternal and hence fetal "iodine deficiency" is responsible for 101,800 stillbirths and 93,500 neonatal deaths, each year, in the region's eight member countries, NOT EVEN INCLUDING CHINA! FLUORIDE KILLS! ---------------------------------------------------------------------------- REFERENCES: Galetti, PM;Joyet, G - "Effect of Fluorine On Thyroidal Iodine Metabolism in Hyperthyroidism" J Clin Endocrinol 18:1102-1110 (1958) Gorlitzer von Mundy - "Einfluss von Fluor und Jod auf den Stoffwechsel, insbesondere auf die Schilddrüse" Münch Med Wochenschrift 105:234-247 (1963) Gordonoff, T. - Fluor und die Schilddrüse, Toxikology des Fluors Basel/Stuttgart (1964) May W - "Antagonismus zwischen Jod und Fluor im Organismus" Klin Wochenschr 14:790-792 (1935) May W - "Behandlung der Hypothyreosen einschließlich des schweren genuinen Morbus Basedow mit Fluor" Klin Wochenschr 16:562-564 (1937) May W - Fortschr. Med. No.14 (1932) Litzka G - "Die experimentellen Grundlagen der Behandlung des Morbus Basedow und der Hyperthyreose mittels Fluortyrosin" Med. Wochenschr 63:1037-1040 (1937) ---------------------------------------------------------------------------- To subscribe to the PFPC NEWSLETTER, send message to pfpc@istar.ca and put "subscribe" in subject box. Likewise, to unsubscribe, put "cancel" in subject box.