PFPC Fluoride Education Project

The past 30 years have witnessed dramatic changes in the concepts of thyroid hormone activity. The 1970s brought the recognition of the central role of triiodothyronine (T3) in mediating thyroid hormone action, establishing T3 as the "active" thyroid hormone. The same decade shattered the long-held belief that all thyroid hormones entered the cell by "diffusion" and brought the first evidence that the uptake of T3 was energy-dependent. In the 1980s and 1990s, the cloning of receptors and the discovery of G proteins further enabled investigators to undertake detailed analyses of the biochemical events which underlie the physiological and pathological action of thyroid hormones.

The laboratory discovery of fluoride as a "universal G protein activator" contributes greatly to the understanding of fluoride effects upon thyroid hormone activity and helped define the role of thyrotropin, the thyroid-stimulating hormone (TSH), and its function in activating thyroid cancer cells. Fluoride directly imitates the effects of the TSH receptor, the only G-protein-coupled receptor known so far to be able to activate all G protein families, thus displaying unprecedented diversity indicative of complex, multi-functioning signaling throughout the body.

When the new findings from the field of endocrinology are applied to the vast amount of historical data on fluoride as an effective anti-thyroid agent, a new picture of fluoride toxicity emerges, calling for an urgent reassessment of our understanding of "fluorosis." The toxic effects of fluoride in humans are dependent upon the individual's thyroid status. Opposing effects are observed when fluoride is given to hypothyroid or hyperthyroid patients.

Keywords: G-proteins, Thyroid function, Triiodothyronine, TSH-receptor.