From brou@istar.ca Tue Nov 2 19:00:50 1999 Date: Mon, 1 Nov 1999 15:32:18 -0700 From: Andreas Schuld PFPC NEWSLETTER #1, Nov. 1, 1999 1999/PFPC IN THIS ISSUE: 1) WELCOME & INTRODUCTION 2) HOW DO FLUORIDES INTERFERE WITH THYROID HORMONES?(BRIEF OVERVIEW) 3) "ONE A DAY" 4) BRIEF HISTORY OF FLUORIDE - IODINE ANTAGONISM 5) WHAT DO THYROID HORMONES DO? 1)WELCOME Hello everyone. Welcome to the first edition of our newsletter. The main purpose of this newsletter is to shed light on issues surrounding fluoride and the effects on thyroid function and related disorders. Format will be fine-tuned as we go along. Suggestions, questions, queries, points to ponder are always welcome and encouraged. We realize that this is a complex issue, so don't hesitate to send us any questions you might have. We will compile them and put up a special page in the virtual library. Whenever possible we will supply links to the library for more info. The last few months have been something of frustrating experience for us, as far as dealing with anti-fluoridation groups are concerned. The anti-fluoridation movement consists of many dedicated individuals, but efforts are very fragmented, and no cohesive undertakings are in place, making it much easier for the dental profession/industry/public health to continue the most fraudulent promotion of fluorides as a health benefit. Perhaps part of the problem stems from our conviction that the F- problem is not just water fluoridation. We shudder every time we read on a website that Europe is only 2% fluoridated and when this claim is being used in attempts to convince municipalities to stop water fluoridation. Although these figures might be close to being true, it is of no real relevance, because other supplementation programs exist in many of those countries, making it easy for the ADA and like-minded organizations to defeat such arguments. We have reports of a teaspoon of salt in Germany containing 0.6 mg of fluoride. Fluoridated salt is equally as worrisome as water fluoridation. It soon makes its way into all foods that are prepared with such salt, resulting in excessive intake. Such foods travel freely across all borders. The fact that it can reduce thyroid activity while bathing in water and being absorbed by the skin, make the sanctioned hydrogen fluoride emissions by industry and coal burning power plants a very great concern. In our opinion the toxicity of fluorides from ALL SOURCES must be properly addressed on a global level, because they all contribute highly to a severe problem affecting ALL of our lives, dentists, politicians, and polluters included. Appropriate action to address this problem must be initated on all sides. Here in Canada we have well known anti-fluoridationists appearing on National TV, declaring that's it's okay to use toothpaste for children after they are 4 or 5 years old. It makes us crinch, knowing that some of our own children, who live in non-fluoridated areas, experienced dramatic health improvements after elimination of fluoridated toothpaste. In addition such crucial periods as puberty are just around the corner, a period of highly sensitivity to any thyroid hormone disruption. We believe this misinformation is a direct result of a lack of knowledge concerning fluoride's effects on the thyroid, which is probably the most overlooked organ in the entire body, according to both orthodox and alternative medical journals. Thus this newsletter and other attempts to inform. We hope that by making our research available to all, a common ground in this movement can be found, and effective action initiated. If anti-fluoridationists spend some time researching this issue, they will see that this info can be used effectively to stop all municipal water fluoridation programs, for the anti-thyroid ability of fluorides can be demonstrated in great detail, combined with the pharmacological data stemming from it's use as affective anti-thyroid medication. We are not talking _preventative medicine_ any longer. All documented symptoms of fluoride poisoning so far can be correlated to thyroid dysfunction, which is no small feat considering the many associations, even the more obscure ones. The mechanism involved in many can actually be described in great detail. A most disturbing realization was when we learned that the major iodine deficient areas are identical to endemic fluorosis areas. We learned that in some endemic fluorosis areas hypothyroidism as a result of iodine deficiency affected over 50% of all children. We learned that at least one child dies every minute due to complications associated with this "fluorine - induced" iodine deficiency, and that this is a problem affecting almost a third of the population, perhaps more. Because ALL studies that we looked at - which measured _both_ the fluorine and iodine levels - showed that iodine levels are reduced directly corresponding to increasing F- intake, the obvious conclusion must be that it is the excessive fluoride intake in those areas which is primary cause of this iodine deficiency and all related consequences. These findings clearly take this matter out of the dental domain and make it a health issue of great global concern, demanding all of our attention as a global community. The urgency cannot be over-emphasized. IDD is called the "hidden hunger" for a reason. When Roholm conducted his classic studies on cryolite workers in the 1930's, which still serve as the basis for the definition of fluorosis, the field of endocrinology was yet to be recognized. We strongly believe that if Roholm would be alive today, his conclusions would be very similar to ours. Fluoride poisoning IS thyroid dysfunction. Some news: as a result of the York submissions, enthusiasm has been created in our organizations, which hosts a few artists involved in all aspects of the entertainment industry. This is due to the quite obvious attempt by a reknown institution to approach a review from a entirely unscientific position. Their highly visible attempt to reclassify a halogen described in high school textbooks as something new, and re-writing a protocol to avoid submitted information - in direct contradiction to stated minutes - and hiding behind a "review process", shows how utterly twisted things have become. We have decided to produce documentaries, professional 'info-mercials' (25 min interviews) as well as commercials for both TV and radio. All work will be highly professional. They will all be preproduced and offered as public service to all radio and media. We have well known actors on board, and are also talking to popular children's entertainers as spokespersons. Legal consultation is also being sought. It's going to change. It must change. The truth has become self-evident. We are doing what we can with our means. We all must act. What can you do? The best to all, Andreas Schuld Head, Parents of Fluoride Poisoned Children Vancouver, BC, Canada --------------------------------------------------------------------------- 2)HOW DO FLUORIDES INTERFERE WITH THYROID FUNCTION? (BRIEF TSH OVERVIEW) Several concepts of interference in hormone synthesis have been put forward and documented. The fact that fluorides have been used as treatment, specifically to reduce thyroid function, has been mentioned numerous times in the articles to the York Review, and can be verified with the references supplied.(See also article #4 below) http://www.bruha.com/fluoride/html/uk_review.htm For the purpose of this brief article we will concentrate on the thyroid-stimulating-hormone (TSH), for here the mechanisms of fluoride's effects can be most easily identified and verified. The process of producing thyroid hormones is controlled by a *feedback mechanism*. The process starts in the hypothalamus, a portion of the brain. It releases TRH (thyrotropin releasing hormone) which, in turn, stimulates the pituitary gland, another part of the brain, to secrete TSH, the thyroid stimulating hormone(TSH). TSH stimulates the thyroid gland to produce the thyroid hormones T4 and T3, which are released into the bloodstream. (As the name implies, T4 carries 4 iodine molecules, T3 carries 3.) T4 and T3 circulate in the blood to all the organs of the body, including teeth and brain. When the pituitary gland senses a drop in thyroid hormone levels in the blood, it releases more TSH to stimulate the thyroid gland, and the cycle of thyroid hormone production continues. If the pituitary gland detects too much thyroid hormone in the blood,it will decrease production of TSH, which then, in turn, reduces the production thyroid hormone in the normal thyroid gland. In addition to stimulating the thyroid gland to make thyroid hormone, TSH causes the thyroid gland to grow. As stated above, if there is not enough thyroid hormone in the body, the pituitary gland will increase production of TSH in an attempt to stimulate the thyroid gland to make more thyroid hormone. When patients are hypothyroid due to iodine deficiency, their thyroid gland cannot make enough thyroid hormones, and the pituitary gland continues to produce TSH. Therefore, because of this continued elevation of TSH, the thyroid gland may enlarge. This enlarged thyroid gland is called a goiter. The leading cause of goiters worldwide is a lack of iodine in the system. Thyroid hormone contains molecules of iodine, and, when there is not enough iodine, this goiter and/or hypothyroidism can develop. Iodine deficiency is rarely the cause of goiters in North America because iodine is added to salt and other foods. The common cause of goiter/hypothyroidism in America is thought to be an increase in thyroid stimulating hormone (TSH) in _response to a defect in normal hormone synthesis within the thyroid gland._ TSH hormone is responsible for activating the many G proteins in the body. G proteins function essentially as "Off" and "ON" switches for cellular signaling, with TSH as the power source, if you will. Normally, the binding of TSH to its receptor activates G protein, which stimulates the effector systems and then quickly becomes inactive. The end result of this signal-transduction process in the thyroid gland is stimulation of thyroid hormone synthesis and thyroid growth. Without TSH, G proteins are _inactive_. Fluorides behave like TSH in their ability to activate those Off/On switches. They are now known as universal G protein activators, which means they can activate all G proteins in the body. However, signal production is not controlled by the normal thyroid feedback system. As a result, the thyroid gland function as well as feedback mechanism are seriously disturbed. Not only can fluorides activate the TSH receptor to cause profound excitation or inhibition, by raising cyclicAMP (cAMP) it causes de-senitization of the TSH receptor, thereby causing hypothyroidism, for now the signal is inhibited and thyroid hormone production depressed. Some labs we have contacted have reported indication of hypothyroidism in 90% of blood tests. Secretin receptor, opioid receptor, oxytocin receptor, dopamine receptor,TRH-thyrotropin-releasing-hormone receptor, TSH-thyroid-stimulating-hormone receptor, stress inducers, etc., are all coupled to Off/On switches and are responsive to fluoride as activators, sometimes even prefer them to the natural activator, TSH. ------------------------------------------------------------------ Here are some links for more info on G proteins. G PROTEINS IN MEDICINE The New England Journal of Medicine -- January 19, 1995 -- Vol. 332, No.3 http://www.nejm.org/content/1995/0332/0003/0186.asp FIGURE:HOW G PROTEINS WORK (On/Off) http://www.nejm.org/content/figs/1995/0332/0003/0186.asp?section=F1 SOME DISEASES CAUSED BY G PROTEIN COUPLED RECEPTORS http://www.gcrdb.uthscsa.edu/GCRs-disease.html RECEPTOR LISTING: http://www.le.ac.uk/csn/e56/GPCR-listing.html G COUPLED RECEPTORS POINT MUTATIONS DATABASE http://tinygrap.uit.no/GRAP/ligrecsub.html LIGANDS OF G PROTEIN COUPLED RECEPTORS http://www.gcrdb.uthscsa.edu/GCR_Ligand.html SUSA REVIEW (1999) "Heterotrimeric G proteins as fluoride targets in bone (Review)."Int J Mol Med 3(2):115-126 (1999) http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9917518&form=6&db=m&Dopt =b Strunecká, A; Patocka, J - "Aluminofluoride complexes: new phosphate analogues for laboratory investigations and potential danger for living organisms" http://www.cadvision.com/fluoride/brain3.htm Thyrotropin-Receptor Mutations and Thyroid Dysfunction The New England Journal of Medicine -- January 19, 1995 -- Vol. 332, No. 3 http://www.nejm.org/content/1995/0332/0003/0183.asp Defs: G-PROTEINS http://www.graylab.ac.uk/cgi-bin/omd?query=G+proteins&action=Search+OMD G-PROTEIN COUPLED RECEPTOR http://www.graylab.ac.uk/cgi-bin/omd?G+protein+coupled+receptor GTP BINDING RECEPTOR http://www.graylab.ac.uk/cgi-bin/omd?GTP+binding+protein -------------------------------------------------------------------- #3: "ONE A DAY" by Bob Johannsen Every day millions of Americans take a small pill to compensate for a lack of thyroid hormone (iodine deficiency) in their bloodstream, which causes a condition called hypothyroidism. Hypothyroidism is related to over 150 diseases. The drug of choice for the treatment of this thyroid disorder is synthetic levothyroxine sodium. Physicians and scientists may use different scientific names for levothyroxine, such as L-thyroxine, thyroxine, and T4; however, all of these terms refer to the same chemical. Checking the prescribed drugs in the United States during 1996, 36,000,000 prescriptions of synthetic levothyroxine were filled. In 1958, the first synthetic levothyroxine tablets were marketed in the United States. Because thyroid hormones were on the market before the Food and Drug Administration (FDA)laws were in place, manufacturers of these hormones were not required to meet the extensive testing requirements of safety and effectiveness required of all new drugs introduced after 1938. In other words, thyroid hormone replacements, such as synthetic levothyroxine, were "grandfathered" into the system; consequently, there are no FDA approved procedures or standards for testing these preparations other than specifying that each pill contain between 90% to 110% of the stated chemical content. The majority of patients taking levothyroxine have a permanent form of hypothyroidism and will take one pill, every day, for the rest of their lives. Knoll, the company that makes the most popular thyroid drug, "Synthroid", recently had to pay $42 million to settle allegations of false drug claims. Knoll was accused of claiming its Synthroid drug was superior to others and that competing drugs could not be substituted for it. The drug is used to treat a "thyroid condition that can cause patients to suffer fatigue, irregular heart rate and memory loss". (We call it fluoride poisoning => hypothyroidism) Synthroid is consistently in the top 10 of the 200 most-prescribed-drugs in America, with the next generic brand being in the 80's. Synthroid accounted for more than $300 million of Knoll's sales last year. The study, which was finally published by the Journal of the American Medical Association in 1997, said consumers could save at least $350 million if they had a choice other than Synthroid. Dr. Drummond Rennie, deputy editor of the Journal of the American Medical Association, which published the study, was highly critical of the company for delaying its release for seven years. "If they had received $350 million extra per year for seven years, that means keeping it quiet was the equivalent of $2 billion for the company," Rennie said. "The $42 million they are paying now sounds sort of pathetic by comparison." Rennie said the company made numerous allegations about the quality of the research and engaged in "an astonishing attack on the researchers," whom he said felt "threatened" and "maligned" by Knoll. "The specific allegations were shown to be ridiculous," he said. "Things went wrong with this study when they started finding out that all four preparations were equal." Knoll is still trying to settle a class-action suit brought against the company. The company has agreed to pay up to $135 million to consumers to settle dozens of lawsuits. The proposed settlement is under review by a federal judge in Chicago. The latest settlement comes only a few months after parent company BASF AG of Germany was forced to pay $225 million to settle criminal charges that it conspired to fix vitamin prices with Hoffmann-La Roche for more than a decade. The combined fine of $725 million against the two companies was the largest ever imposed in a federal antitrust case. In iodine-induced, as well as fluorine-induced hypothyroidism, thyroid function may revert to normal with iodine or fluoride restriction alone. Once on "Synthroid", or any other generic brand of levothyroxine, the thyroid gets "lazy" and fails to function properly, causing life-long dependence on the "pill once a day". At current fluoride intake levels being much higher than the dose given once daily specifically to reduce thyroid activity, the solution should be obvious. Reduce all fluoride intake. Stop water fluoridation. Eliminate fluoride in toothpaste. Label foods. Control industry emissions. Think about it. -------------------------------------------------------------- #4) BRIEF HISTORY OF FLUORIDE - IODINE ANTAGONISM In 1854 Maumené feeds sodiumfluoride to a dog and causes a goiter to appear. He is the first to consider fluorides as a cause of goiter. Pighini (1923) is able to cause goiters in rats, dogs and chicken. Goldemberg (1926, 1930) is the first to take advantage of the iodine-fluoride antagonism and begins to use fluorides to cure Basedow's disease (Graves' Disease). May (1935, 1937) follows suit. In 1950 May publishes his findings that addition of thyroxine (T4) raised the iodine level in the blood, while the addition of fluorides lowered the iodine level in blood. Litzka (1937) discusses the mode of action of fluorides in treating patients with Graves' disease: fluoride antagonizes thyroid hormone effects on liver metabolism. Wilson and DeEds (1940) report that dental fluorosis is a result of the synergistic action of fluoride and the thyroid. Results are "strikingly clearcut". Wilson (1941) reports in the Lancet on his findings that mottling of teeth is prevalent in the same areas in the UK which had been previously prevalent with goitre. 1944 editorial in the Journal of the American Dental Association (JADA) states: "We do know that the use of drinking water containing as little as 1.2 to 3ppm of fluorine will cause such developmental disturbances in bones as osteosclerosis, spondylosis and osteopetrosis, as well as goitre". Steyn (1948, 1955) finds that fluoride has a thyrostatic effect. He investigates the incidence of endemic goitre (fluorine -induced) in the North Western Cape Province in South Africa and reports that his findings closely agree with the above JADA editorial. Wespi(1954)finds mottled teeth (dental fluorosis) together with goiters in Italy. Korrodi, Wegmann, Galetti and Held (1955) also verify a fluoride - iodine antagonism, proclaiming that the fluoride ion pushes out the iodine in the thyroid gland. Galetti et al (1957) treats hyperthyroid patients with fluoride, and documents a significant reduction in protein-bound iodine, as well as an overall reduction of iodine and a reduction of iodine uptake by the thyroid gland. Jentzer (1959) further shows reduced iodine levels under the influence of fluorides. In 1960 Gordinoff and Minder describe the results of experiments with radioactive iodine (I131) which show that fluorides remove an iodine atom. Effects were dose-responsive, meaning the higher the fluoride intake the lower the iodine measurements. Steyn writes in 1962 that drinking water containing as little as 1 to 2 ppm of F- can cause serious disturbances of general health and especially in normal thyroid gland function and in the normal processes of calcium-phosphate metabolism (parathyroid function). In 1963 Gorliter von Mundy reports on the [then] current knowledge gained from experiments with I131 as to how the effects of the enzyme responsible for the T4 to T3 conversion were inhibited if a fluorine ion was absorbed before the conversion was supposed to happen. In 1969 Siddiqui shows small visible goiters in persons 14 to 17 years of age in India to be connected directly to high fluoride concentrations in drinking water. Willems et al (1972) document that sodium fluoride blocks thyroid hormone secretion. Also in 1972 Day and Powell-Jackson study 648 people in 13 mountaineous regions in Nepal where the iodine content in the water was low and find a close relationship between fluoride intake and the incidence of goiter. Bobek and Kahl (1976) document that rats on 1.0 mg fluoride daily from drinking water had significantly lowered T4, T3, and free thyroxine index in plasma. In 1978 George Waldbott writes that in most cases of poisoning from fluoridated water in which he had occasion to study the action of the thyroid gland, it's function was low. He cites a case of a 33-year-old male who exhibited typical manifestations of pre-skeletal fluorosis and a basal metabolism rate of -22, indicative of hypothyroidism. Within three months after the man ceased consuming fluoridated water, the thyroid function had returned to normal (BMR=0) In addition, Waldbott writes that "simultaneously, other symptoms associated with low grade fluoride poisoning - including excessive thirst, headaches, blurred vision, arthritis in shoulders, elbows, knees, and gastrointestinal disturbances - also disappeared." [He did not know that many of the symptoms he ascribed to low-grade fluoride poisoning would be likewise considered symptoms of hypothyroidism some 20 years later. See: COMPARISON OF SYMPTOMS:FLUORIDE POISONING/HYPOTHYROIDISM http://www.bruha.com/fluoride/html/symptoms_hypo_f.htm Hillman et al (1979) find that cattle afflicted with fluorosis developed hypothyroidism, anemia, and eosinophilia of leukocytes. [The latter two also now commonly associated with hypothyroidism. Anemias are diagnosed in 20-60% patients with hypothyroidism.] Sidora (1983) finds iodine deficiency and adaptive amplification of the hypophyseal-thyroid system, not ensuring an absolute compensation in the citizens using drinking water with an "enhanced" fluorine content as compared to a "decreased" one, accompanied by an augmented incidence of functional disturbance. Bachinskii et al (1985) document how fluorides at 2.3 ppm in water cause tension of function of the pituitary-thyroid system that is expressed in TSH elevated production, a decrease in the T3 concentration and more intense absorption of radioactive iodine by the thyroid. The results lead to a conclusion that excess of fluorine in drinking water was a risk factor of more rapid development of thyroid pathology. Tokar' and others (1989) in a study on workers exposed to fluorides write that changes in the pituitary-thyroid axis were seen without co-existing clinical manifestations of hypo- or hyperthyroidism, and that those changes were caused by disorders of the regulatory chain and fluorine impact on thyroid hormones' metabolism at the _level of target cells_. Lin Fa-Fuet al (1991) report that a low iodine intake coupled with "high" (0.88ppm) fluoride intake exacerbates the central nervous lesions and the somatic developmental disturbance of iodine deficiency. Tezelmann et al (1994) report that fluoride, by increasing the intracellular cAMP concentration, causes desensitization of the thyroid stimulating hormone receptor (TSHR). No specific thyroid factor(s) other than increased levels of cAMP are required for desensitization. Balabolkin et al (1995) study the thyroid and immune statuses in workers continuously exposed to fluorine. The examinees with euthyroid condition had immune disorders with an allergic tendency (increased number of B-lymphocytes, immunoglobulins A). In workers with subclinical hypothyrosis (T3 reduced in 51%), the immune alterations were more evident, T-lymphocytes count rose, but their functional activity declined, indicating impaired cooperation of immunocytes as a result of imperfect control under low concentrations of T3. Zhao et al (1998) does an extensive study on mice receiving several fluoride-iodine combinations in addition to basal diet. He finds that iodine and fluorine have mutually interacting effects on both goiter and fluorosis in the experimental mice. Jooste et al (1999) show that goiter occurrence in two iodine-sufficient areas in Africa seem to be due to high fluoride water levels. In 1999, as a result of research into molecular biology ("the art of cloning") there are hundreds upon hundreds of studies available documenting the actions of fluorides upon G proteins, the "On" and "Off" switches involved in cellular signal transmission. Fluorides become known as the universal G-protein activator. Although there have been numerous studies before showing that fluorides mimick TSH, the thyroid stimulating hormone, it can now be documented in deep detail, for it is known that G proteins are normally absolutely dependent on TSH and are _inactive_ without it. Too much TSH (speak fluoride) in the system will cause hypothyroidism and other severe thyroid disorders. Because high TSH levels in the system are indicative of hypothyroidism, TSH tests at birth are implementated on a global basis, to avoid severe brain damage and stunted growth resulting from congenital hypothyroidism. --------------------------------------------------------------------- __________________________________________________________________ #5)WHAT DO THYROID HORMONES DO? BODILY MECHANISM - EFFECTS OF THYROID HORMONE CARBOHYDRATE METABOLISM: increases uptake of glucose by the cells, enhances glycolysis, gluconeogenesis, increases rate of absorption from the gastrointestinal tract, increases insulin secretion FAT METABOLISM: increases lipid mobilization from the fat tissue increases free fatty acid concentrations in the plasma, accelerates the oxidation of free fatty acids PLASMA AND LIVER FATS: decreases the quantity of cholesterol, phospholipids, and triglycerides in the plasma, increases the concentrations of cholesterol, phosholipids, and triglycerides in the liver VITAMIN METABOLISM: increases the need for vitamins BASAL METABOLIC RATE: increases basal metabolic rate to 60-100% of normal or if thyroid hormone is not produced, basal metabolic rate falls to half of normal BODY WEIGHT: increased thyroid hormone decreases body weight, decreased production increases weight CARDIOVASCULAR SYSTEM: Blood flow and cardiac output - increased metabolism in the tissues causes greater than normal quantities of metabolic end products to be released from tissues causing vasodilatation (state of increased calibre of the blood vessels) and increased blood flow, cardiac output increases as a consequence of increased blood flow. Heart Rate - affects excitability of the heart which increases heart rate Strength of Heartbeat - increases due to increased enzymatic activity, when thyroid hormone is produced in excess heart muscle strength becomes depressed because of excessive protein catabolism. BLOOD VOLUME: increases secondary to vasodilatation RESPIRATION: increases utilization of oxygen and formation of carbon dioxide GASTROINTESTINAL TRACT: increases the rate of secretion of digestive juices and motility of the GI tract MUSCLES: slight increases in thyroid hormone make muscles react with vigor although excessive hormone production causes muscle weakness due to protein catabolism OTHER ENDOCRINE GLANDS: increases the rate of secretion of most other endocrine glands (pancreas, parathyroid, adrenals), increases metabolic activities related to bone ----------------------------------------------------------------------------- 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.