This paper reviews the current scientific literature regarding the effects of fluoride exposure on thyroid function. The article also highlights the need for further research to fully elucidate the complex interplay between fluoride exposure and thyroid health.

Fluoride and Thyroid Function

Fluoride, a naturally occurring element found in soil, water, and certain foods, has garnered significant attention due to its role in dental health [1]. However, concerns have emerged regarding the potential effects of fluoride exposure beyond its benefits in preventing dental caries. The thyroid gland, a crucial regulator of metabolism, is a sensitive target for endocrine-disrupting chemicals, and fluoride has been identified as a potential disruptor of its normal function [2]. This article aims to synthesise the current scientific understanding of how fluoride exposure may impact the thyroid gland, focusing on mechanisms of action and potential consequences for human health.

Mechanisms of Thyroid Disruption by Fluoride

Several mechanisms have been proposed through which fluoride can interfere with thyroid function:

1. Iodine Uptake Inhibition: The thyroid gland relies on iodine to synthesise thyroid hormones (T3 and T4). Due to their similar ionic radius to iodine, fluoride ions can compete with iodine for uptake by the sodium-iodide symporter (NIS) located on the basolateral membrane of thyroid follicular cells [3]. This competitive inhibition can lead to decreased iodine availability within the thyroid gland, ultimately reducing the production of thyroid hormones.
2. Thyroid Peroxidase (TPO) Inhibition: Thyroid peroxidase (TPO) is a key enzyme involved in the synthesis of thyroid hormones, specifically in the iodination of thyroglobulin. Fluoride has been shown to inhibit TPO activity [4]. This inhibition further hinders the production of T3 and T4, contributing to hypothyroidism.
3. Alteration of Thyroid Hormone Receptor Binding: Studies suggest that fluoride may alter the binding of thyroid hormones to their receptors in target tissues [5]. Such interference could impair thyroid hormone action even if normal hormone levels are present in the bloodstream, leading to tissue-level hypothyroidism.
4. Effects on TRH and TSH: The hypothalamus releases Thyroid Releasing Hormone (TRH), which stimulates the thyroid to release Thyroid Stimulating Hormone (TSH). Studies have shown that fluoride may disrupt the normal signalling of TRH and TSH, resulting in changes in the release of thyroid hormones [6].

Consequences of Fluoride-Induced Thyroid Dysfunction

The mechanisms described above can lead to a range of health consequences:

1. Hypothyroidism: A deficiency in thyroid hormones can result in hypothyroidism. Clinical signs can include fatigue, weight gain, depression, cold intolerance, and cognitive impairment [7]. 
2. Goitre: Compensatory mechanisms in response to decreased thyroid hormone production can lead to an enlargement of the thyroid gland, known as a goitre [8]. This is often a result of increased TSH stimulation.
3. Metabolic Disturbances: Thyroid hormones play a crucial role in regulating metabolism. Fluoride-induced thyroid dysfunction can therefore lead to disturbances in lipid metabolism, glucose homeostasis, and overall energy expenditure [9].
4. Developmental Effects: Thyroid hormones are critical for normal fetal development. Maternal fluoride exposure during pregnancy can potentially affect fetal thyroid function, with possible consequences for neurological and skeletal development [10].

Discussion

1. The cumulative evidence presented in this paper demonstrates a clear potential for fluoride to disrupt thyroid function through multiple mechanisms.
2. While fluoride's benefits for dental health are well-established, these findings raise concerns that excessive or prolonged fluoride exposure could pose a risk to thyroid health.
3. It is important to note that the effects of fluoride on thyroid function can be influenced by several factors, such as the route, dose, duration of exposure, iodine status, and individual susceptibility [11].

Disclaimer: The views and opinions expressed in this article are those of the author and do not necessarily reflect the official policy or position of M3 India.

About the author of this article: Dr Partha Ghosh, BNYS, MD(YS), is a general physician and a medical writer from Siliguri, Darjeeling.