By The Fluoride Action Network

It has been established that fluoride has the ability to alter your endocrine function, yet this fact is being ignored by the agencies and associations that continue to promote the practice of water fluoridation. According to a 2006 report by the National Research Council of the National Academies¹ , fluoride is "an endocrine disruptor in the broad sense of altering normal endocrine function."

This altered function can involve your thyroid, parathyroid, and pineal glands, as well as your adrenals, pancreas, and pituitary.

Your thyroid gland and its associated hormones are responsible for maintaining your body's overall metabolic rate, and for regulating normal growth and development. As all metabolically active cells require thyroid hormone for proper functioning, disruption of this system can have a wide range of effects on virtually every system of your body. Thyroid dysfunction is considered among the most prevalent of endocrine diseases in the United States.

Historical Use of Fluoride as a Medical Intervention for Hyperthyroid

Up until the 1970s, scientists in Europe prescribed fluoride to reduce the basal metabolism rate in patients with an over-active thyroid gland. One published clinical study from this period reported that doses of just 2 to 3 milligrams of fluoride—a dose that many, if not most, Americans now receive on a regular basis—were sufficient to reduce thyroid activity in hyperthyroid patients.

The use of fluoride as an anti-thyroid treatment was prompted by research beginning in the 1800s² linking fluoride ingestion to goiter, a swelling of the thyroid gland resulting from a hypothyroid condition.

In its 2006 report Fluoride in Drinking Water: A Scientific Review of EPA's Standards, the National Research Council (NRC) reported that "several lines of information indicate an effect of fluoride on thyroid function."

Specifically, the report discussed research showing that:

"fluoride exposure in humans is associated with elevated TSH concentrations, increased goiter prevalence, and altered T4 and T3 concentrations" with "similar effects on T4 and T3…reported in experimental animals."

In addition, the NRC discussed research linking fluoride to impacts on parathyroid activity, impairment of glucose tolerance, and possibly the timing of sexual maturity.

In light of these findings, the NRC panel recommended that the "effects of fluoride on various aspects of endocrine function should be examined further, particularly with respect to a possible role in the development of several diseases or mental states in the United States"³. Despite this, proponents of fluoridation continue to ignore the scientific literature concerning the detrimental effects that fluoride has on the endocrine system.

Surprisingly Tiny l Amounts of Fluoride Changes Your Thyroid Function

Altered thyroid function is associated with fluoride intakes as low as 0.05-0.1 mg fluoride per kilogram body weight per day (mg/kg/day), or 0.03 mg/kg/day with iodine deficiency. Increased prevalence of goiter (>20 percent) is associated with fluoride intakes of 0.07-0.13 mg/kg/day, or 0.01 mg/kg/day with iodine deficiency.⁴

For a 70 kg (154 pound) adult, this means that 3.5 mg fluoride per day (or 0.7 mg fluoride per day with iodine deficiency) could result in thyroid dysfunction. The most recent exposure analysis by the U.S. Environmental Protection Agency⁵ estimates that the average American adult is consuming nearly 3 mg fluoride on a daily basis, and some are routinely ingesting 6 mg per day or more.

Even more concerning, however, are the doses of fluoride in children.

For a 14 kg (30 pound) child, fluoride intakes greater than 0.7 mg per day (or 0.14 mg per day with iodine deficiency) puts the child at risk for endocrine dysfunction. The EPA (2010) estimates children within this weight range (1-3 year-olds) consume over 1.5 mg fluoride each day, or more than twice the amount necessary to induce altered thyroid function, even with an adequate iodine intake.

These chronic exposures could have profound and life-long effects on the intellectual, social, sexual and overall physical development of children.

Numerous studies have found a relationship between relatively low to moderate levels of fluoride exposure and reduced IQ in children⁶ . Even fluoride levels of less than 1.0 mg/L have been associated with reduced IQ and increased frequency of hypothyroidism in children experiencing iodine deficiency⁷.

Iodine Deficiency, Fluoride, and Thyroid Disease

Iodine is necessary for proper functioning of your thyroid gland. As your body cannot produce its own iodine, it must be obtained from your diet. Iodine is sequestered into your thyroid gland, where it is incorporated into the thyroid hormones thyroxine (T4) or triiodothyronine (T3). In healthy individuals these hormones are precisely regulated by thyroid-stimulating hormone (TSH), and are required by all metabolically active cells in your body.

Iodine deficiency is known to be responsible for a variety of disorders—including hypothyroidism, goiter, and disturbances of physical and mental development. According to recent research, "normal" dietary intake of iodine is 100-150 mcg per day, however greater amounts of iodine are recommended for pregnant and lactating women, as studies have shown that the most detrimental effects of iodine deficiency occur during fetal and neonatal growth.

The primary sources of iodine are saltwater fish and seaweed, with grains providing trace amounts. An estimated 2.2 billion people worldwide are at risk for iodine deficiency⁸. Many countries have introduced iodine supplements into the food supply to combat deficiencies, such as has been done with table salt in the United States, where iodine deficiency is generally no longer considered a problem.

However, data suggest that iodine intakes have decreased over the past few decades⁹. Although this decline may have stabilized in recent years¹⁰, more than 11 percent of all Americans—and more than 15 percent of American women of child-bearing age—presently have urine iodine levels less than 50 mcg/L¹¹, indicating moderate to severe iodine deficiency. An additional 36 percent of reproductive-aged women in the U.S. are considered mildly iodine deficient (<100 mcg/L urinary iodine).

Considering the importance of iodine for proper functioning of your thyroid gland, and the importance of your thyroid gland for proper functioning of your entire body, any disturbances to this delicate balance must be seriously considered. Your thyroid gland may be the most sensitive tissue in your body to fluoride¹², with more fluoride accumulating in your thyroid than many other soft tissues¹³.

Fluoride may directly or indirectly interfere with proper functioning of your thyroid gland, with potential actions including fluoride's ability to:

• Mimic thyroid-stimulating hormone (TSH)
• Disrupt sensitive G-proteins, which serve as the building blocks of your body's hormone receptors
• Damage the cells of your thyroid gland
• Damage your DNA¹⁴
• Disrupt conversion from the inactive form of the thyroid hormone (T4) to the active form (T3)

Inadequate diet—including deficiencies in iodine, calcium and protein—can play a key role in fluoride-induced thyroid dysfunction. For someone with a deficient diet and/or an already compromised thyroid gland, any of the detrimental effects of fluoride exposure on the thyroid system, and thus the entire body, will likely be compounded. In fact, in one 2005 study, Gas'kov et al.¹⁵ determined that even an increased intake of iodine would not be sufficient to counter the adverse effects of excessive fluoride exposure on the thyroid gland in children.

When the function of your thyroid gland is suppressed, your body cannot produce or maintain adequate levels of T3 and T4, resulting in a condition known as hypothyroidism.

Hypothyroidism is Pervasive Among Women

According to PubMed Health, women over the age of 50 are at the highest risk for developing hypothyroidism, or under-active thyroid. Nearly 4 percent of the U.S. population (over 11 million people) has overt hypothyroidism.¹⁶ Perhaps an additional 10 percent of the general population (21 million people) has subclinical hypothyroidism, which is considered a strong risk factor for later development of overt hypothyroidism.

It is important to understand that even these surprisingly large numbers likely vastly underreport the number of women that are affected as they rely on outdated criteria to diagnose hypothyroidism.

The frequency of hypothyroidism tends to increase with age—one 2010 study estimates that up to 20 percent of older age groups have some form of hypothyroidism. Synthroid and Armour, both pharmaceuticals used to treat hypothyroidism, were the 7^th and 73^rd top selling drugs in the United States in 2009, with over 24 million combined units sold.

Symptoms of hypothyroidism are numerous, and may include:

fatigue, loss of energy, general lethargy	cold intolerance
muscle and/or joint pain	decreased sweating
depression	puffiness
weight gain	coarse or dry skin and hair
hair loss	sleep apnea
carpal tunnel syndrome	forgetfulness, impaired memory, inability to concentrate
carpal tunnel syndrome	bradycardia (reduced heart rate)
menstrual disturbances	decreased appetite
impaired fertility	constipation
fullness in the throat, hoarseness	increased risk of heart disease
increased "bad" cholesterol (LDL)	weakness in extremities
emotional instability	blurred vision
mental impairment	decreased hearing

 

Despite a higher incidence in older populations, the rate of primary (neonatal) congenital hypothyroidism has increased by nearly 75 percent over the past two decades in the United States, now affecting 1 in every 2,370 births¹⁷. Untreated neonatal hypothyroidism can lead to mental retardation, growth retardation, and heart problems. Children with congenital or juvenile hypothyroidism have been reported to have delayed eruption of teeth and/or enamel defects, although the connection between these findings and the impact of fluoride on the thyroid has not been studied¹⁸.

Also extremely concerning is the inverse relationship between the severity of subclinical hypothyroidism in pregnant women and the reduced IQ of their children¹⁹. Maternal subclinical hypothyroidism has also been proposed as a cause or contributor in the development of autism²⁰.

Fluoride's potential to impact the thyroid gland highlights, yet again, the need for a precautionary approach to the indiscriminate use of fluorides. The deliberate addition of fluoride to public drinking water supplies is particularly problematic, as it exposes your entire body—not just your teeth—to a biologically-active substance, without regard to individual need or sensitivity, and thereby violates key principles of modern pharmacology.

What You Can Do TODAY!

The Fluoride Action Network has a game plan to END water fluoridation in both Canada and the United States. Our fluoride initiative will primarily focus on Canada since 60 percent of Canada is already non-fluoridated. If we can get Calgary and the rest of Canada to stop fluoridating their water, we believe the U.S. will be forced to follow.

Please, join the anti-fluoride movement in Canada and United States by contacting the representative for your area below.

Contact Information for Canadian Communities:

1. If you live in Ontario, Canada, please join the ongoing effort by contacting Diane Sprules at sprules@cogeco.ca.

2. The point-of-contact for Toronto, Canada is Aliss Terpstra. You may email her at aliss@nutrimom.ca.

Contact Information for American Communities:

We're also going to address three US communities: New York City, Austin, and San Diego:

1. New York City, NY: With the recent victory in Calgary, New York City is the next big emphasis. The anti-fluoridation movement has a great champion in New York City councilor Peter Vallone, Jr. who introduced legislation on January 18 "prohibiting the addition of fluoride to the water supply.” A victory there could signal the beginning of the end of fluoridation in the U.S. If you live in the New York area I beg you to participate in this effort as your contribution could have a MAJOR difference. Remember that one person can make a difference. The point person for this area is Carol Kopf, at the New York Coalition Opposed to Fluoridation (NYSCOF). Email her at NYSCOF@aol.com . Please contact her if you're interested in helping with this effort.

2. Austin, Texas: Join the effort by contacting Rae Nadler-Olenick at either: info@fluoridefreeaustin.com or info@yahoo.com, or by regular mail or telephone:

POB 7486 Austin, Texas 78713 Phone: (512) 371-3786

1. San Diego, California: Contact Patty Ducey-Brooks, publisher of the Presidio Sentinel at pbrooks936@aol.com .

In addition, you can:

• Comment on the EPA’s docket on the proposed ban (just scroll down a bit). It’s open for public comment up to July 5, 2011. They published the proposed ban in the Federal Register and the deadline for comments were extended due to requests from Dow and their allies in the pesticide world (such as American Farm Bureau Federation, National Pest Management Association, North American Millers' Association, and the California Rice Commission). Tell the EPA you expect them to uphold their duty to protect you and your children from this toxic food fumigant.
• Make a generous tax-deductible donation to the Fluoride Action Network, to help them fight for your rights to fluoride-free food and water.
• Check out FAN’s Action Page, as they are working on multiple fronts to rid our food and water supplies of fluoride.
• For timely updates, join the Fluoride Action Network Facebook page.

References:

• ¹ National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press: Washington, DC. 507 pp.
• ² Maumené E. 1854. Compt Rend Acad Sci 39:538.
• May W. 1935. Antagonismus Zwischen Jod und Fluor im Organismus. Klinische Wochenschrift 14:790-92.
• ³ National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press: Washington, DC.
• ⁴ National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press: Washington, DC.
• ⁵ EPA (U.S. Environmental Protection Agency). 2010. Fluoride: Exposure and Relative Source Contribution Analysis. Health and Ecological Criteria Division. Office of Water. Washington, D.C.
• ⁶ Connett P, Beck J, Micklem HS. 2010. The Case Against Fluoride. How Hazardous Waste Ended Up in Our Drinking Water and the Bad Science and Powerful Politics That Keep It There. Chelsea Green Publishing: White River Junction, VT. 372 Pp. / Ding Y, Gao Y, Sun H, et al. 2011. The relationships between low levels of urine fluoride on children's intelligence, dental fluorosis in endemic fluorosis areas in Hulunbuir, Inner Mongolia, China. J Hazard Mater. Feb 28;186(2-3):1942-6. / Xiang Q, Liang Y, Chen B, et al. 2010. Serum fluoride level and children's Intelligence Quotient in two villages in China. Env Health Persp (Online 17 Dec 2010). doi:10.1289/ehp.1003171.
• ⁷ Lin FF, Aihaiti HX, Zhao J, et al. 1991. The relationship of a low-iodine and high-fluoride environment to subclinical cretinism in Xinjiang. IDD Newsletter 7(3):24-25.
• ⁸ ICCIDD (International Council for the Control of Iodine Deficiency Disorders). 2011. Iodine Deficiency.
• ⁹ Hollowell JG, Staehling NW, Hannon WH, et al. 1998. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from NHANES I and III (1971-1974 and 1988-1994). J Clin Endocrin Metab 83(10):3401-8.
• ¹⁰ Lee SL, et al. 2009. Iodine Deficiency. Medscape Reference.
• ¹¹ Caldwell KL, Miller GA, Wang RY, et al. 2008. Iodine status of the U.S. population, National Health and Nutrition Examination Survey 2003-2004. Thyroid. 18(11):1207-14.
• ¹² Shashi A. 1988. Biochemical effects of Fluoride on thyroid gland duringexperimental fluorosis. Fluoride 21:127–130.
• ¹³ Monsour PA, Kruger BJ. 1985. Effect of fluoride on soft tissue in vertebrates. Fluoride 18:53-61. / Call RA, Greenwood DA, LeCheminant H, et al. 1965. Histological and chemical studies in man on effects of fluoride. Pub Health Reports 80(6):529-38.
• ¹⁴ Ge Y, Ning H, Wang S, Wang J. 2005. DNA damage in thyroid gland cells of rats exposed to long-term intake of high fluoride and low iodine. Fluoride 38(4):318-23.
• ¹⁵ Gas'kov A, Savchenkov MF, Lushkov NN. 2005. [The specific features of the development of iodine deficiencies in children living under environmental pollution with fluorine compounds] [in Russian]. Gig Sanit. Nov-Dec (6):53-5.
• ¹⁶ Aoki Y, Belin RM, Clickner R, et al. 2007. Serum TSH and total T4 in the United States population and their association with participant characteristics: National Health and Nutrition Examination Survey (NHANES 1999-2002). Thyroid 17(12):1211-23.
• ¹⁷ Olney RS, Grosse SD, Vogt RF. 2010. Prevalence of Congenital Hypothyroidism—Current Trends and Future Directions: Workshop Summary. Pediatrics 125, May 2010, pp. S31-S36. doi:10.1542/peds.2009-1975C
• ¹⁸ National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press: Washington, DC.
• ¹⁹ Klein RZ, Sargent JD, Larsen PR, et al. 2001. Relation of severity of maternal hypothyroidism to cognitive development in offspring. J Med Screen 8(1):18-20.
• ²⁰ Román GC. 2007. Autism: Transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neuro Sci 262:15-26./ Sullivan KM. 2009. Iodine deficiency as a cause of autism. J. Neuro Sci 276:202.

Additional Sources:

• Andersson M, de Benoist B, Delange F, Zupan J. 2007. Prevention and control of iodine deficiency in pregnant and lactating women and in children less than 2-years-old: conclusions and recommendations of the Technical Consultation. Public Health Nutr 10(12A):1606-11.
• Bharaktiya S, et al., 2010. Hypothyroidism. Medscape Reference.
• Delange F. 2004. Optimal iodine nutrition during pregnancy, lactation and neonatal period. Int J Endocrinol Metab 89:3851.
• Drugs.com. Undated. Top-selling drugs of 2009.
• IOM (Institute of Medicine). 2001. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. A Report of the Panel On Micronutrients, Subcommittees on Upper Reference Levels of Nutrients and of Interpretation and Uses of Dietary Reference Intakes, and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board. National Academy Press: Washington, D.C.
• Larsen PR, Davies TF, Schlumberger MJ, Hay ID. 2002. Thyroid physiology and diagnostic evaluation of patients with thyroid disorders. Pp. 331-373 in Williams Textbook of Endocrinology, 10th Ed. Larsen PR, Krongenberg HM, Melmed S, Polonsky KS, eds. Saunders: Philadelphia, PA.
• PubMed Health. 2009. Neonatal hypothyroidism.
• PubMed Health. 2010. Hypothyroidism.
• Wang H, Yang Z, Zhou B, et al. 2009. Fluoride-induced thyroid dysfunction in rats: roles of dietary protein and calcium level. Toxicol Ind Health 25(1):49-57.
• Zimmermann MB. 2009. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. Am J Clin Nutr 89(2):668S-72S.
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