Fluoride Action Network

Health Warning: The Thyroid and Fluoride

Fluoride Action Network | September 21, 2003 | By Paul Connett, PhD

The literature dealing with the interaction between fluoride and the thyroid gland has a very long history, stretching back to a paper written in 1854 by Maumene who linked goiter in dogs with exposure to fluoride. The following URL links to a summary of that history: http://www.bruha.com/pfpc/html/thyroid_history.html.

I do not pretend to know enough about either this history or the detailed functioning of the thyroid gland to offer much insight into this issue. However, it is an extremely important area and it warrants far more attention from governments promoting fluoridation than it currently receives, which is practically zero! Millions of Americans are impacted by thyroid dysfunction, and if only a small fraction of these have their condition caused by, or worsened by, fluoride it is a very serious matter indeed.

There are four important lines of evidence that fluoride interferes with the thyroid gland.

1) The condition known as “goiter” which involves a gross swelling of the thyroid gland, which in turn produces very marked swellings in the neck, is known to be caused by iodine deficiency. However, it has also been found to occur in areas where there are adequate supplies of iodine, but where there’s an excess fluoride in the water.

2) Starting in the 1930s and continuing through to the 1950s sodium fluoride was used to lower the activity of the thyroid gland for those suffering from hyperthyroidism (i.e. over active thyroid gland). The obvious question then becomes, if fluoride lowers the activity of an overactive thyroid gland what does it do to a normal or underactive thyroid gland?

3) It has been known for a long time that one of the consequences of iodine deficiency in mothers is an increased risk of mental retardation in their children. With the advent of iodized salt, this is a less frequent occurrence in industrialized countries. However, studies from China indicate that even a moderate amount of fluoride exposure can exacerbate the effects of low iodide’s impacts on the developing brain.

4) It has been known for a long time that fluoride mimics the action of the thyroid stimulating hormone (TSH). Because TSH sends its message across the cell membrane of the thyroid gland via G-proteins, a candidate mechanism for fluoride’s action would be fluoride’s well established ability (See reviews by Strunecka & Patocka, 1999; and Li, 2003), in the presence of a trace amount of aluminum, to switch on G-proteins.

Taking these lines of evidence one at a time:

1) Endemic Goiter (also spelled goitre) and fluoride.

In a 90 page report entitled “Endemic Goitre in the Union of South Africa and some Neighbouring Territories,” prepared for the Department of Nutrition for the South African government, Dr. Douw Steyn and colleagues concluded that there were two separate causes for endemic goiter. In their summary, they state:

“In the Union of South Africa endemic goitre is caused by: (1) a primary iodine deficiency in the drinking water and soil, and most probably in the food; and (2) excessive quantities of fluorine in subterranean drinking-water in spite of super sufficiency of iodine in the waters.”

The areas with endemic goiter caused by excess fluoride were located in the Northwest part of South Africa. In 1999, Jooste et al repeated Steyn’s findings when they reported endemic goiter in the absence of iodine deficiency in schoolchildren of the Northern Cape Province. A similar relationship between excess fluoride exposure and goiter has been reported in England (Wilson 1941), in the Punjab region of India (Wilson 1941), in Nepal (Day and Powell-Jackson, 1972), in Kenja (Obel 1982), and in Gujarat, India (Desai 1993). Other studies, however, have failed to find this relationship (see Burgi 1984).

2) Treating hyperthyroidism with sodium fluoride tablets.

What is striking about the doses of fluoride used to treat hyperthyroidism is how small they were. Galletti and Joyet (1958) found that a daily dose of just 2 to 10 mg of fluoride per day was enough to reduce the basal metabolism rate (BMR) of hyperthyroid patients and alleviate their condition. This is within the range of doses that many people living in fluoridated areas will ingest. The US Department of Health and Human Services (DHHS,1991) estimates that an adult in a fluoridated community receives between 1.6 and 6.6 mg of fluoride per day from all sources combined.

In a World Health Organization review (Fluoride and Health, WHO, 1970), Semole cites evidence from Korrodi et al (1956) that, in normal human subjects, fluorides have no effect on the thyroid. He then asks:

“Why does sodium fluoride exert a mild antithyroidal effect in hyperthyroidic patients if it is inactive in normal persons? Nobody knows.”

However, the claim that fluoride has no effect on normal thyroid function may have been premature. According to a study conducted by Bachinskii (1985), prolonged consumption of water with 2.3 ppm fluoride produced changes in thyroid function, not only in people with hyperthyroidism but in people with normal thyroid function as well. Bachinskii writes in the abstract of his paper:

“Altogether 123 persons were examined: 47 healthy persons, 43 patients with thyroid hyperfunction and 33 with thyroid hypofunction. It was established that prolonged consumption of drinking water with a raised fluorine content (122 +/- 5 mumol/l with the normal value of 52 +/- 5 mumol/l) by healthy persons caused tension of function of the pituitary-thyroid system that was expressed in TSH elevated production, a decrease in the T3 concentration and more intense absorption of radioactive iodine by the thyroid as compared to healthy persons who consumed drinking water with the normal fluorine concentration. The results led to a conclusion that excess of fluorine in drinking water was a risk factor of more rapid development of thyroid pathology.”

3. Lowering of IQ in China.

It is well established that the pituitary/thyroid system is important in the early mental development of children thus if fluoride interfered with the thyroid it could, among other things, result in lowered IQ in children. In this respect, the results of a UNICEF sponsored study of mental retardation, IQ and thyroid hormone status in children in areas endemically low in iodide are particularly revealing. Lin et al. (1991) found in one region of China that even a modest amount of fluoride in the water (i.e. 0.91 ppm versus 0.34 ppm) led to an even greater reduction in IQ and the frequency of mental retardation, than simply low iodide by itself.

Yang et al (1994) further investigated the effect of iodide and fluoride on IQ and hormonal status in areas of high iodide and high fluoride. From their study the authors concluded that their results “indicate that high iodine and high fluorine exert severe damage to human body.” Compared to controls, children had higher dental fluorosis rates; markedly lower iodine-131 uptake; higher serum TSH levels, and slightly lower average IQ, with 16.7% placed in a category labeled “low intelligent.”

4. TSH, fluoride and G-proteins.

Just how fluoride impacts the thyroid gland is not clear. We know that, in the presence of a trace amount of aluminum, fluoride switches on G-proteins, thus sending messages normally delivered by water soluble hormones. TSH is one of the water soluble hormones which is mimicked by aluminum fluoride. But the puzzling thing about this is that one would expect that this would lead to an activation of the thyroid gland not deactivation (as in the case of someone with hypothyroidism).

A clue to this puzzle may have come in 1994 in a paper by Tezelman et al. These researchers using Chinese hamster ovary cells, report that fluoride increases intracellular cAMP concentration (the secondary messenger produced as a result of switching on G-proteins), but the end result was desensitization of the receptor for the thyroid stimulating hormone (TSHr). In other words, the fluoride begins by stimulating the cell but the end result was that it led the cell to become less responsive to the normal stimulation by TSH. The authors state that, “Desensitization or decreased response to the same (homologous) or other stimuli (heterologous) is a well known process. Homologous desensitization to TSH has been demonstrated in normal thyroid tissue.”

Various recent government sponsored reviews have given this topic very short shrift. The York Review (McDonagh et al., 2000) looked at only two of the goiter studies (Jooste, 1999 and Gedalia, 1963). They didn’t use a weight of evidence approach, bringing in the clinical and biochemical studies above. The Irish Fluoridation Forum (2002) didn’t do any review of primary studies on health except dental fluorosis and four bone fracture studies. The CDC (1999) reviewed no health studies beyond citing the NRC (1993) review and the NRC(1993) review didn’t consider impacts on the thyroid system, nor did the First draft of the WHO review (Environmental Health Criteria 227: Fluorides, 2002).

I welcome any corrections or comments, especially if readers know of any government review since WH0 (1970) that has discussed fluoride’s impact on the thyroid gland.

* A Minor correction was made to this article in August 2012. Specifically, the statement that fluoride was used to treat hyperthyroidism until the 1970s was changed to “through to the 1950s.” This was based on information from the Merck Index, coupled with the study in 1958 from Galletti & Joyet.


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