Fluoride & Thyroid Cancer

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"The doctor of the future will give no medicine, but will interest his patients in the care of the human frame, in diet and in the cause and prevention of disease."
- Thomas Edison

Cancer is a political problem more than it is a medical problem.

See also the following pages:

Nationwide call for congressional hearings on fluoridation of drinking water.

Canadian government report questions value of fluoridation.

The case against fluoride.

Fluoridation and cancer.

Fluoride and thyroid cancer.

Fluoridation of drinking water.

American Dental Association health fraud re: fluoride.

Ingested fluoride does not strengthen teeth.
- Journal of the American Dental Association, July 2000.

The toothpaste we use is called Tooth Builder and contains xylitol which is found to reduce tooth decay. Tooth Builder toothpaste is fluoride-free.

 

PFPC NEWSLETTER #7 - "Fluoride & Thyroid Cancer"
©2000 PFPC (Feel free to distribute)
December 20, 2000

IN THIS ISSUE:

1) INTRODUCTION
2) WHAT IS CANCER?
3) WHAT ARE G PROTEINS?
4) HOW DO G PROTEINS ACTIVATE CANCER CELLS?
5) WHAT IS ADENYL CYCLASE?
6) ADENYL CYCLASE, TSH AND THE THYROID
7) EVIDENCE: FLUORIDE ACTIVITY
8) FLUORIDE AND I131 UPTAKE
9) FINAL COMMENT
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Hi everyone,

   This is our last Newsletter for the year. It deals with fluoride and thyroid cancer. For us this is a very important issue as we have some parents in our group whose children were overexposed to fluorides in infancy (formula, too much toothpaste, supplements etc.) and who subsequently suffered from hypothyroidism and were diagnosed with thyroid cancer in their teens. Needless to say, they also suffer from dental fluorosis.

   There is just so much evidence available here that the continued denial of the fluoride/thyroid cancer connection by public health officials, dental organizations, and "scientific reviews" will surely one day prove more embarasing than the denial by cigarette manufacturers that smoking causes lung cancer.

   We thank you all for your past support - despite our angry outbursts at times. We wish we could have more patience, but it often proves hard for us to put up with the ignorance and seemingly purposeful falsifying of information. This so-called "dental health success" has greatly harmed our children's health, and is killing millions of children worldwide.

Thank you for your understanding.

Blessings to all, and best wishes for a safe and happy holiday season!

Andreas Schuld
Parents of Fluoride Poisoned Children (PFPC)
Vancouver, BC, Canada
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1) INTRODUCTION

   "A report in the 1955 New England Journal of Medicine shows a 400 percent increase in thyroid cancer in San Francisco during the period that the city has had fluoridated drinking water", so report Gladys Caldwell and Philip Zanfagna, MD, in their 1974 book  "Fluoridation and Truth Decay" (1).

   In 1974 Leo Kinlen of Oxford compared the occurrence of cancers in fluoridated and non-fluoridated areas (2, 2a).  100 thyroid cancer cases were observed compared to 81 expected ones, an 18% increase. Unbelievably, the authors then contradicted their own findings and stated that "there is no significant excess of cancer of any site in fluoridated areas as compared with nearby fluoridated areas." Those familiar with the recent York Review might remember similar words.

   In China fluoride is openly acknowledged as cause of thyroid cancer and government programs have re-settled many thousands of farmers living in fluoride-contaminated areas (3).

   In 1997 the US Federal Register published the petition of Bayer to establish new residue tolerance levels for products imported into the US for a pesticide called Tolylfluanid, a pesticide which is illegal in the US but applied almost everywhere else in the world - and therefore therefore makes its way into North America in many foods, i.e. tomato products from Italy, grape juices from from Africa, or apple juice from South America. The apple juice issue is of particular and urgent concern as apple juice is the first juice beverage for most infants, and 60% of all apple juice is imported (4, 5).

   Tolylfluanid had been banned for use in the US largely because it had caused thyroid tumors (adenomas) in rats, in a non-linear fashion (-> not dose/concentration-related). Kidney damage occured "probably attributable to the effects of fluoride on renal tubules." Regarding the thyroid adenomas the Bayer petition further stated that, "..Mechanistic studies with tolylfluanid have shown that these tumors are induced through a nonlinear threshold mechanism similar to that discussed in EPA's thyroid policy document."(6)

All should know that IF this thyroid policy were to be properly applied to the vast data available on fluoride compounds and thyroid function, fluoride in all forms would be immediately banned! Repeated efforts have been made by the PFPC within the last two years to have the fluoride issue assessed according to this thyroid policy, and we have asked the EPA, and also the NTEU to investigate this vital issue,  but to no avail to date.]

   In 1998 the late great John Yiamouyiannis sent us the results of the National Toxicology Program cancer bioassay on sodium fluoride (7). Again, the data showed incidences of thyroid adenomas, as well as the same "nonlinear" mechanism as had been observed with tolylfluanid. However - as is well-known by now - the final published version of the NTP report downgraded  the "clear evidence of carcinogenicity " to "equivocal evidence of carcinogenicity".  It was this change in classification which prompted Dr. William Marcus, who was then Senior Science Adviser and Toxicologist in the Office of Drinking Water, to blow the whistle about the issue, which led to his firing by the U.S. Environmental Protection Agency (EPA).  Dr. Marcus sued the EPA, won his case and was reinstated with back pay, benefits and compensatory damages.(8) However, the issue itself - fluoride CAUSING cancers as identified by Dr. Marcus and others - remains denied to this date.

   Between 1975 and 1996 the incidence of thyroid cancer rose 42.1% in the United States, and incidence of diagnosed thyroid cancer has now climbed up to 8.0 per 100,000. Canada reports a yearly 6% increase in thyroid cancer.

   The most prevalent carcinomas in US children and adolescents younger than 20 years are now thyroid carcinomas (35.5%); more prevalent than the more publicized melanomas (30.9%). Approximately 75% of the thyroid carcinomas occurred in adolescents aged 15 -19 years of age (9).

   Thyroid cancer in most cases is a slow-progressing cancer - in children average time from onset to diagnosis is thought to be 15 years. It is therefore clear that onset occurs during infancy and early childhood.

   In the elderly, thyroid disease is very common. Upon autopsy, the find of a "normal thyroid gland" is rare, testifying to the incredible high prevalence of thyroid disorders among the elderly. Fleischman in 1999 reviewed over 800 autopsies and only found 25% of thyroids to be "normal".

   Fluorides cause thyroid cancer. All common anti-thyroid agents are thought to be cancer causing, as they influence the natural feedback mechanism which regulates the thyroid-pituitary axis and cause increased levels of thyrotropin, the thyroid-stimulating- hormone (TSH),  which then in turn activates cancer cells by activating an enzyme system called adenyl cyclase.

   Propylthiouracil (PTU), which replaced fluoride compounds in the treatment of hyperthyroidism in the early 1940s, is  now considered a carcinogenic for the same reason (10).

   PTU administered in the drinking water induced increased incidences of thyroid carcinomas and adenomas in rats of both sexes, identical to the findings by the NTP regarding fluoride (7).

   The FDA regulates the use of propylthiouracil as a pharmaceutical to treat hyperthyroidism under the Food, Drug, and Cosmetic Act (FD&CA).

Why NOT fluoride?

   WHY is fluoride, although it had been used as most-effective anti-thyroid medication for more than three decades - either alone or  with PTU - NOT declared a carcinogenic?
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2) WHAT IS CANCER?
by Bob Johannsen

   Cancer is the popular general term used to describe over 100 diseases that are characterized by the uncontrolled growth and spread of abnormal cells in the body. Cancerous masses can grow and develop from a single abnormal cell in any tissue of the body. These abnormal cells are often called "mutations". The name given to a particular cancer stems from the tissue in which it originated, for example a hepatocellular carcinoma is called a liver cancer. Cancer cells can spread locally or through the bloodstream and lymphatic system to other parts of the body. Dissemination of cancer cells throughout the body will allow secondary tumors or neoplasms to be established in other organs. This process is known as metastases.

   Normally cells reproduce and divide in an orderly fashion through the cell cycle. This enables the body to grow, and to repair worn out or damaged tissue.  Every cell in the body has the potential to form a new growth. This occurs not only in humans but in all living organisms (plants and animals),  simply because all living organisms are made up of cells. Cells grow by dividing in half, such that one cell will become two, two become four, and so on. These new cells are then called "daughter cells".

   Cancer is a direct consequence of the loss of the cell cycle control. Most of the genetic events that lead to cancer occur over the lifetime of an individual and often originate in childhood.

   The realization of the stepwise progression of cancer has been the most significant contribution to the understanding of the cancer disease process since U.S. President Nixon first declared the so-called "War on Cancer" back in 1971.

   The discovery of G-proteins has helped tremendously in understanding cancer and its progress.

3) WHAT ARE G PROTEINS?

   In essence, G proteins are "On/Off" switches which regulate cellular communication  - relaying  information received from outside the cell to the inside, or from one cell to another.

   This process of cell communication is called "signal transduction", a term first applied in molecular biology by Martin Rodbell, who with Alfred Gilman received the 1994 Nobel Prize in medicine and physiology for their independent work leading to the discovery of G proteins.

   As G proteins are vital in all cell communication, uncontrolled G protein signaling can often lead to cancer in humans. Over 30% of all cancers are now thought to be caused by G protein mutations.

   For example, the ras oncogene (member of the G protein subfamily)  was first found in human bladder cancer cells and is now also thought to be also responsible for up to 40% of all colon cancers, as well as 90% of pancreatic cancers. Studer et al (11) identified ALL thyroid goiter nodules examined to contain areas where the epithelial cells were morphologically grossly altered and heavily loaded with p21ras, which has now further been identified in breast, bladder and prostate cancers.

Fluoride compounds are known and established p21ras pathway activators (12-23).

4) HOW DO G PROTEINS ACTIVATE CANCER CELLS?

   G proteins regulate an enzyme system called adenyl cyclase. This system is at the convergence of multiple neuronal, hormonal, and environmental inputs.  Permanently ("constitutively") activated adenyl cyclase will lead to abnormal cell growth - thus to cancer.

There are two broad groups of G proteins : stimulating ones -> G(s), and inhibiting ones, ->G(i) .

   G(s) describes a G protein which STIMULATES the activation of adenyl cyclase (AC). For example, when it is stimulated in the heart muscle, cardiac output increases. In the case of cholera, a G(s) protein remains stuck in its active "ON" state, so AC and thus cAMP is overproduced, leading to massive sodium water transport across intestinal epithelial cells; hence diarrhea and the often life-threatening loss of water and salts.

   By contrast pertussis toxin (whooping cough) does the same thing to G(i), preventing its interaction with AC, so that the cells cannot INHIBIT the cyclase activity, resulting in the accumulation of pulmonary fluid as seen in whooping cough.

G protein dysfunction or mutations involve either gain or loss of function.

5) WHAT IS ADENYL CYCLASE?

   The adenyl cyclase is as a multi-component system embedded in the lipid bilayer of the plasma membrane which serves as a signal transduction system in apparently every cell type of higher organisms (24).

   The complete system consists of various receptor molecules, which sensitize the external ligands, the effector enzyme adenylate cyclase, which catalyzes the formation of cyclicAMP from ATP, and two G proteins, which transduce the signals from the receptors to the adenylate cyclase. Depending on the receptor type activated by a ligand, stimulatory or inhibitory, either the stimulatory or the inhibitory G protein is activated and induces stimulation or inhibition of adenylate cyclase with subsequent increase or decrease in cellular cyclic AMP levels  (25).

   Anything that activates AC is thought to be a cancer promoter for elevation can cause increase in cancer cell growth. Patients with constitutively active adenyl cyclase  (permanently "ON") have what are called hyperactive or overfunctioning tumors, such as are seen in the fluoride-related literature.

   While knowledge of G proteins is virtually non-existent not only among the general public, but also among most general practitioners, research on G proteins has been one of the hottest biological pursuits of the past decade, mainly because of the experience gained from advanced investigations into G proteins as "programmable messengers", as Rodbell had called them. Pharmacologists estimate that up to 60% of all medicines used today exert their effects through G protein signaling pathways (26). This industry frenzy had been forecasted by Gilman who - in a 1992 Scientific American article on G proteins authored together with Maurice Linder - had predicted that scientists would eventually diagram the cellular players involved in communication and be able to predict how those cells will operate in response to different combinations of signals.

"For those who would hope to develop drug therapies such discoveries would be like giving a thief a wiring diagram to the alarm system at a bank", the authors wrote (27).

Gilman further said,  "The ultimate dream is to design drugs that will prevent aberrant G-protein action."

   In a press conference in Maryland following the announcement of the 1994 Nobel Prize, Rodbell had critized the current state of the commercialization of science. . ."The tenor is changed, the world ain't the same, everything is targeted, everything is bottom line, how to make a buck, " he said,  adding that it is crucial to "capture knowledge for its own sake and for humanity" (28).

Indeed.

6) ADENYL CYCLASE, TSH AND THE THYROID

   Stimulation of proliferation, thyroid hormone synthesis, and expression of  thyroid-specific genes are transmitted by the adenyl cyclase system via thyrotropin, the thyroid-stimulating-hormone (TSH).

   It is TSH that mediates iodine, zinc and selenium (29). TSH stimulates all metabolic and cellular processes involved in synthesis which occur in thyroid and peripheral tissue. TSH also stimulates intermediary metabolism and thyroid growth. TSH initiates release of thyroxine (T4) and triiodothyronine (T3) from thyroglobulin. It is TSH excess which ultimately causes goiter.

   TSH is generally accepted to be the main regulator of thyroid growth and function and is considered the "natural" universal G protein activator (30). The TSH receptor belongs to a broad class of receptors known as "seven-loop receptors" because they contain a long stretch of amino acids which cross the cell membrane seven times.

[At this point it is important to realize that TSH receptors are not only found in the thyroid gland, but also in the liver, cardiac muscle, gastrointestinal tract , thymus, peripheral blood mononuclear cells, orbital tissue, fibroblasts, peripheral lymphocytes, fat, cardiac muscle, osteoblasts and osteosarcoma cells, and of course the brain - where they are overexpressed in patients with Down Syndrome or Alzheimer's Disease (31-38)]

   It has been established that even small increases in serum TSH is sufficient to promote thyroid tumors (39, 40). Because of this fact, thyroid cancer survivors are required to keep their TSH levels suppressed, so as not to promote growth and multiplication of any remaining cancerous cells after removal of the cancerous thyroid gland (thyroidectomy).

   Why are these survivors not also advised to "suppress" fluoride intake? The biological effects are identical. Low amounts of fluoride stimulate AC, high doses inhibit AC (41) - effects IDENTICAL to TSH.

   When faced with the fluoride/G protein issue, many pro-fluoridationists serve up a standard reply stating that the amount of fluoride required to activate G proteins are a "thousand times higher" than are seen in the human plasma. They then usually cite some papers where very high amounts of fluorides are used to activate inhibiting G(i) proteins.

  The fact is that low amounts of fluoride activate stimulating G proteins G(s) while high doses activate G(i)  - again, this is identical to TSH effects. Rat experiments have shown that the amount of fluoride required for AC activation in the thyroid  is IDENTICAL to the one at which fluoride causes dental fluorosis (42, 43).

   Therefore - if fluoride activates AC at such low concentrations, it obviously activates G proteins, as activation of AC is absolutely dependent on the regulatory G proteins (44).

It is important that all recognize such statements as the one above as complete scientific nonsense.

Here is some devastating evidence of fluoride effects - on HUMAN thyroid cancers.
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7) EVIDENCE: FLUORIDE ACTIVITY
compiled by Wendy Small

"The adenylcyclase (AC) activity of crude human thyroid plasma membranes were studied in some detail and conditions for optimal cyclic AMP-production established. Membranes from eight "cold" and two "hot" thyroid adenomas were investigated and compared to membranes from corresponding normal, paranodular tissues. The investigated membranes were found to contain similar basal AC activities, which were stimulated three to five times with TSH and ***20--30 times with fluoride***." (!!!)

Walinder O, Karlsson FA, Dahlberg PA - "Adenyl cyclase activity in human thyroid plasma membranes from normal human thyroid tissue and thyroid adenomas" Acta Endocrinol (Copenh) 92(1):95-104 (1979)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=227209form=6&db=m&Dopt=b

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"In the hyperfunctional follicular carcinoma the basal adenylate cyclase is much higher than in control tissue, carcinoma adenylate cyclase does not respond to TSH and prostaglandin E1, ***whereas it responds normally to fluoride****."


Macchia V, Mandato E, Carella C, Pisano G, Biscaglia G - "The adenylate cyclase-cyclic AMP-phosphodiesterase system in pathological human thyroid" J Endocrinol Invest 1(4):337-45 (1978)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=229151form=6&db=m&Dopt=b

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Kalderon AE, Sheth V - "Secretion and adenylate cyclase in thyroid nodules" Arch Pathol Lab Med 102(7):381-86 (1978)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=580872form=6&db=m&Dopt=b

"Thyrotropin (TSH)- and ***sodium fluoride (NaF)-sensitive adenylate cyclase (AC) activity was measured in ten cases of "cold" thyroid nodules and compared with perinodular tissue. Findings were correlated with the ultrastructure of the nodular and perinodular tissue. Comparisons of the results of assay studies revealed an increase of basal and*** NaF- and TSH-stimulated AC activity in cold lesions."
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F- stimulation in normal tissue 3 times higher than TSH:

"We observed an increased adenylate cyclase activity in cold nodules as compared to normal. More importantly, this activity was much more responsive to TSH in cold nodules than in normal ....Also, maximal TSH stimulation was similar to that elucited by ***fluoride in the cold nodules but only one-third in normal tissue...."

Orgiazzi J, Chopra IJ, Solomon DH, Williams DE - "Comparison of the effect of TSH and fluoride on the adenylate cyclase activity of cold thyroid nodules" Ann Endocrinol (Paris) 37(2):107-8 (1976)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1008507form=6&db=m&Dopt=b

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"... The localization of adenylate cyclase and 5'-nucleotidase activities in the follicular cells of adenomatous goiter and normal thyroid was studied by light and electron microscopy. Simultaneous biochemical measurement for both activities was carried out to confirm the histochemical findings. Adenylyl-imidodiphosphate (AMP-PNP) was used as an effective substrate for adenylate cyclase. The specificity of the adenylate cyclase reaction was also examined by adding oxalacetic acid or PCMB as an adenylate cyclase inhibitor, and by adding ***sodium fluoride or TSH*** as an adenylate cyclase stimulator to the reaction mixture...."

Mizukami Y, Matsubara F, Matsukawa S - "Localization of adenylate cyclase and 5'-nucleotidase activities in human thyroid follicular cells" Histochemistry 74(1):9-19(1982)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=6282789form=6&db=m&Dopt=b

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"The adenylate cyclase system was studied in hyperfunctioning autonomous nodules in comparison with normal thyroid tissue. The basal, TSH- and**** NaF-stimulated adenylate cyclase activities were tested in purified plasma membrane preparations..."

Toccafondi RS, Rotella CM, Tanini A, Fani P, Arcangeli P -"Thyrotrophin-responsive adenylate cyclase activity in thyroid toxic adenoma" Acta Endocrinol (Copenh) 92(4):658-68  (1979)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=231370form=6&db=m&Dopt=b

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"Low concentrations of NaF and Gpp(NH)p stimulated AC activity [in human thyroid neoplasms] whereas high concentrations of NaF and Gpp(NH)p assayed either together or separately inhibited AC activity."

Clark OH, Gerend PL - "Thyrotropin regulation of adenylate cyclase activity in human thyroid neoplasms" Surgery 97(5):539-46 (1985)

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2986305form=6&db=m&Dopt=b

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9) FLUORIDE AND I131 UPTAKE

   As if fluoride activity on AC wasn't bad enough, there is one more important factor to consider. Officialy, the only verified cause of thyroid cancer remains ionizing radiation such as radioactive iodine (I131), with children again being at greatest risk. We are currently seeing the aftermath of the Chernobyl disaster and increasing thryoid cancers are now seen in the children affected by the disaster.

   Many studies within the last 50 years have shown that fluoride greatly enhances the uptake of I131 - even when only slightly iodine deficient (45, 46, 47, 48, 49), and at F- in water levels even BELOW the amount deemed "optimal" for caries prevention (48).

10) FINAL COMMENT

    Thyroid cancer cells are not the only ones activated by fluoride. All hormone-related cancers such as breast, ovary, uterine, prostate, testis, thyroid and osteosarcoma, etc. share a unique mechanism of carcinogenesis. These cancerous cells are activated by adenyl cyclase. These cancerous cells are activated by fluoride. This is why there is an increase in osteosarcomas observed in fluoridated areas (50), as is uterine cancer (51), etc..

"Everything causes cancer? Perhaps. Conceivably even a single electron at the other side of the universe. The real question is, how likely is any one particular cause? In point of fact, fluoride causes more human cancer, and causes it faster, than any other chemical."

-  Dean Burk, Chief Chemist Emeritus, U.S. National Cancer Institute
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About Dean Burk:

http://www.bruha.com/fluoride/html/dean_burk.html

THYROID CANCER

http://www.bruha.com/fluoride/html/thyca.html

FLUORIDE & THYROID

http://www.bruha.com/fluoride/html/f___thyroid.html

CANCER

http://www.bruha.com/fluoride/html/cancer_a.html

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For complete list of references, please send message to pfpc@istar.ca and put REFS#7 in subject box
=====================================================
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