Fluoride and Hypothyroidism

One of the things I remember about my grandmother was her crusading against water fluoridation. Her activism seemed rather extreme and based on fear, not facts.

Now, decades later, as I'm looking up recent scientific study reports about hypothyroidism after being asked about it by a sister with a slightly elevated level of thyroid stimulating hormone (TSH), I've come across evidence pointing to a negative effect of public water flouridation. First, there's an observational study out of the United Kingdom, which found evidence indicating a correlation between flouridated water and hypothyroidism.

J Epidemiol Community Health. 2015 Jul;69(7):619-24. doi: 10.1136/jech-2014-204971. Epub 2015 Feb 24.
Are fluoride levels in drinking water associated with hypothyroidism prevalence in England? A large observational study of GP practice data and fluoride levels in drinking water.
Peckham S1, Lowery D1, Spencer S1.Author information

• 1Centre for Health Services Studies, University of Kent, Canterbury, Kent, UK.

Abstract
BACKGROUND:
While previous research has suggested that there is an association between fluorideingestion and the incidence of hypothyroidism, few population level studies have been undertaken. In England, approximately 10% of the population live in areas with community fluoridation schemes andhypothyroidism prevalence can be assessed from general practice data. This observational study examines the association between levels of fluoride in water supplies with practice level hypothyroidism prevalence.METHODS:
We used a cross-sectional study design using secondary data to develop binary logistic regression models of predictive factors for hypothyroidism prevalence at practice level using 2012 data onfluoride levels in drinking water, 2012/2013 Quality and Outcomes Framework (QOF) diagnosedhypothyroidism prevalence data, 2013 General Practitioner registered patient numbers and 2012 practice level Index of Multiple Deprivation scores.FINDINGS:
We found that higher levels of fluoride in drinking water provide a useful contribution for predicting prevalence of hypothyroidism. We found that practices located in the West Midlands (a wholly fluoridated area) are nearly twice as likely to report high hypothyroidism prevalence in comparison to Greater Manchester (non-fluoridated area).INTERPRETATION:
In many areas of the world, hypothyroidism is a major health concern and in addition to other factors-such as iodine deficiency-fluoride exposure should be considered as a contributing factor. The findings of the study raise particular concerns about the validity of community fluoridation as a safe public health measure.

This is far from a denunciation of flouride, but it indicates it could be a factor. Then, while looking up "hypothyroid" and "flouride," I found out that one of the ways scientists induce hypothyroidism in lab rats is by giving them flouride (and GABA--go, sprouts!--appears to help heal the thyroid afterward, interestingly). Further reading revealed that since 1979 it has been apparent that too much flouride in cattle can cause hypothyroidism and anemia.

Several of my female friends and relatives--plus myself for a short time after moving to Colorado from a place where I was drinking distilled water--have been told that they are hypothyroid due to elevated TSH levels and will have to go on synthetic thyroid hormones for the rest of their lives. This is not OK, especially if it is avoidable, for the proper amount of such hormone supplementation can change over time and taking the wrong dosage causes all kinds of serious side effects. Also, it's important that women, who are much more likely to be diagnosed with hypothyroidism, know that hypothyroidism can be transitory and elevated TSH levels don't necessarily require medication when there are no other symptoms:

Prescrire Int. 2015 Oct;24(164):241-4, 246.
Hypothyroidism in adults. Levothyroxine if warranted by clinical and laboratory findings, not for simple TSH elevation.
[No authors listed]
Abstract
Hypothyroidism is a common disorder due to inadequate thyroid hormone secretion. When a patient has signs and symptoms suggestive of hypothyroidism, how is it determined whether thyroid hormone replacement therapy will have a favourable harm-benefit balance? How should treatment be managed? To answer these questions, we conducted a review of the literature using the standard Prescrire methodology. The symptoms of hypothyroidism are due to slow metabolism (constipation, fatigue, sensitivity to cold, weight gain, etc.) and to polysaccharide accumulation in certain tissues, leading to hoarseness, eyelid swelling, etc. A blood TSH concentration of less than 4 or 5 mlU/L rules out peripheral hypothyroidism. TSH levels increase with age. Between 30% and 60% of high TSH levels are not confirmed on a second blood test. In overt hypothyroidism, the TSH level is high and the free T4 (thyroxine) level is low. Most of these patients are symptomatic. So-called subclinical hypothyroidism, which is rarely symptomatic, is characterised by high blood TSH levels and normal free T4 levels. The natural history of hypothyroidism depends on its cause. In chronic autoimmune thyroiditis, the most common form seen in rich countries, hypothyroidism generally worsens over time. However, other situations can lead to transient hypothyroidism that may last several weeks or months. Subclinical hypothyroidism, as the name implies, is usually asymptomatic. The risk of progression to overt hypothyroidism is about 3% to 4% per year overall but increases with the initial TSH level. Treatment guidelines are mainly based on physiological and pharmacological considerations and generally recommend levothyroxine therapy. The adverse effects of levothyroxine are signs of thyrotoxicosis in case of overdose (tachycardia, tremor, sweating, etc.). Even a slight overdose carries a risk of osteoporotic fractures and atrial fibrillation, especially in the elderly. In young adults, levothyroxine is usually started at a dose of about 1.5 microg/kg per day, taken on an empty stomach. Elderly patients and those with coronary artery disease should start at a lower dose: 12.5 to 50 microg per day. Treatment monitoring is based mainly on blood TSH assay. Dose adjustment should only be considered after 6 to 12 weeks, given the long half-life of levothyroxine. Certain drugs, such as iron and calcium, reduce the gastrointestinal absorption of levothyroxine. Enzyme inducers reduce its efficacy. In 2015, there is no robust evidence that levothyroxine therapy has any tangible benefit in patients with subclinical hypothyroidism. Some practice guidelines recommend treatment when the TSH level is above 10 mIU/L, or sometimes trial treatment for a few months for patients with symptoms suggestive of hypothyroidism. In practice, replacement therapy is needed for patients with overt hypothyroidism and a blood TSH concentration above 10 mIU/L. The main challenge is to recognise transient hypothyroidism, which does not require life-long treatment. When the TSH is only slightly elevated, there is a risk of attributing non-specific symptoms to an abnormal laboratory result and prescribing unnecessary treatment. Watchful waiting is an alternative to routine levothyroxine prescription in case of TSH elevation.