Hypothyroidism

Hypothyroidism is a condition in which the thyroid gland doesn't produce adequate levels of thyroid hormones, resulting in symptoms such as lethargy and weight gain. It affects perhaps 5% of the adult American population, most of whom are women with subclinical symptoms.

With so much of the American population overweight and with lethargy having so many possible causes, it was inevitable that some woo meisters would claim that hypothyroidism is an "epidemic" and that you probably have it.[1] Or, if you've been diagnosed with hypothyroidism and you still feel tired and fat on the medication, that your hypothyroidism must not be adequately treated yet.

What mainstream medicine says

In the ancient past, iodine deficiency was the primary cause of hypothyroidism. In the modern developed world, though, iodine deficiency is very rare, and the primary cause of hypothyroidism is an autoimmune disorder called Hashimoto's thyroiditis.File:Wikipedia's W.svg[note 1] The only treatment is thyroid hormone supplements. The first such treatment was desiccated thyroid extract — ground up cow and pig thyroid glands, originally sold by the Armour meat packing company (eventually Forest Labs took over the Armour Thyroid brand name). By the 1950s, the individual hormones involved in thyroid function had been identified, and the pharmaceutical industry soon developed synthetic levothyroxine (T4, sold as Synthroid by Abbot Labs) and synthetic triiodothyronine (T3, sold as Cytomel by King Pharmaceuticals).

The American Association of Clinical Endocrinologists published their most recent guidelines for the diagnosis and treatment of hypothyroidism in November 2012.[2] While these standards are not cut-and-dried absolutes, they basically boil down to this:

  • Hypothyroidism should be diagnosed by measuring the level of Thyroid Stimulating Hormone (TSH) in the blood. If it's above 5 μIU/mL, and symptoms of hypothyroidism are present, the patient is probably hypothyroid.[note 2]
  • Hypothyroidism should be treated by prescription T4.
  • The dose of T4 should be adjusted until the patient's TSH level is brought down within the therapeutic target range of 0.45[3] to 4.12 μIU/mL. (Or a tad lower if the patient is preggers.)

T4, T3, and Reverse T3: Questionable claims

T4 is technically a "prohormone" — it isn't biologically active until it's deiodinated into T3. Two enzymes (D1 and D2) turn T4 into as much T3 as the body thinks it needs; D1 and another enzyme (D3) turn the rest of the T4 into Reverse T3 (rT3), which is inert. Mainstream endocrinologists tend to prefer prescribing synthetic T4 over synthetic T3 or desiccated thyroid extract (which contains some T3) for two reasons: (1) In the vast majority of hypothyroid cases, the only dysfunction is in the production of T4, not in the conversion of T4 to T3; and (2) having too much T4 in your blood isn't nearly as bad as having too much T3.

Unfortunately, treating hypothyroidism won't always get rid of the all the symptoms that can be associated with hypothyroidism — depression, fatigue, weight gain, intolerance of cold, dry and scaly skin, etc.. And that's where the woo peddlers come in.

ClaimWhy it's questionable

Your body isn't turning enough T4 into the biologically active T3, or is turning too much T4 into the biologically inactive Reverse T3. Therefore, you should be taking less T4 and more T3.

 While stress, or at least TNF which can be released by stress, may decrease the conversion of T4 to T3,[4], and at least one study does show a potential quality-of-life benefit for replacing some T4 with T3,[5] no conclusive benefit has been shown for adding T3 to an existing T4 regimen in general.[6][7]


Testing your TSH level is misleading, you need to test Free T3 / Total T3 / Reverse T3 / your Free-T3-to-Reverse-T3 ratio.

TSH is an indirect indicator of thyroid hormone levels. The hypothalamus senses the level of circulating thyroid hormones, and produces TRH if the level is too low. The pituitary responds to the TRH by producing TSH. A (healthy) thyroid gland, in turn, responds to the TSH by producing thyroid hormones (mostly T4 with a little bit of T3). If the thyroid is underproducing, the TSH level will be elevated. Clinical studies have repeatedly shown that, for the general population, testing the TSH level is the most reliable way to gauge thyroid function.

Saying that the TSH test shouldn't be trusted provides a convenient excuse to recommend a higher prescription dose. Proponents often cite a study on elderly men from 2005,[8] which showed that high T4 and rT3 levels were associated with reduced physical functioning in the test subjects. The problem is, T3 has a rather short half-life in vivo, and serum T3 levels can vary over the course of a day depending on a number of factors. Worse, Reverse T3 has a different half-life in vivo than T3 does, and so the ratio could theoretically vary over the course of a day as T3 is broken down by the liver but Reverse T3 isn't, or vice-versa.


All clinical lab tests for hypothyroidism are flawed, and you need to look exclusively at the patient's symptoms.

 This is a favorite of the I-don't-feel-adequately-treated online-support-group crowd. It's also potentially dangerous, in that seeking out an alternative medicine practitioner or fast-and-loose endocrinologist who'll up your dose because you're not feeling good can end up overmedicating you, or mask other potential causes for your symptoms.


The pituitary (or the hypothalamus) preferentially senses T4 over T3. This means that your TSH level will go down in response to taking T4, even if inadequate T3 is still being produced. Therefore, you should be taking less T4 and more T3.

 This claim runs contrary to the evidence. A March 2013 study states: "Given that the TSHB and TRH genes are negatively regulated by T3 (and not T4), it is crucial that T4 be converted to T3 in order to activate the negative feedback mechanism."[9] (Of course, if this conversion is only happening at a high rate locally within the brain, near the hypothalamus and pituitary, and isn't happening at the same rate elsewhere in the body, the subject could theoretically still have both low circulating T3 levels and a TSH level within the normal range. And in fact, nearly half of the intracellular T3 in the pituitary is created via local deiodination.[10][11][12])


Reverse T3 interferes with the D2 enzyme, preventing it from turning T4 into T3. Therefore, you should be taking less T4 and more T3.

 Although rT3 has been shown to interfere with the conversion of T4 into T3 in vitro[13], the minimum concentration at which this effect has been detected is 100 pmol/L of free rT3. The median normal serum concentration of free rT3 is 0.59 pmol/L.[14] (Note: The most common blood test for rT3 measures the total rT3 in the blood, including the rT3 bound to TBG. This is typically hundreds of times higher than the free rT3 level.)


Reverse T3 acts as a T3 antagonist, by blocking or "clogging up" the cellular T3 receptors[15], producing "tissue resistance" to T3[16][17] which results in reduced response even when your T3 levels should be adequate. Therefore, you should be taking less T4 and more T3.

Of course, still others have claimed the opposite.[18][19][20] According to two sources[21][22], Reverse T3 does compete with T3 at the nuclear receptors, but only very weakly; the rT3 concentration has to be 10 to 1000 times higher than the T3 concentration before the number of receptors bound to T3 is halved. In a normal patient, serum concentrations of total T3 are anywhere from 2.5 to 18 times higher than rT3.[23]

Interestingly, actual receptors for Reverse T3 do exist in rats, but their function is not yet known.[24]


If the evil mainstream medical establishment duped you into taking T4, all that awful Reverse T3 will have to be cleansed from your system. You should take an elevated dose of T3 for some weeks.

 Even if Reverse T3 does block T3 receptors, Reverse T3 has a half life in vivo of only a few hours.[25] There might be a "hidden pool" of Reverse T3 lurking somewhere in the body, which could result in extra rT3 being introduced into the blood after the circulating rT3 has cleared.[26]


Desiccated thyroid extract is what we used to use before Big Pharma pushed that awful artificial Synthetic T4 on us, and we should go back to using it.

 It was abandoned because it came from ground up cow and pig thyroids, which have a different ratio of T3 to T4 than is normal for a human. It also contains T2 and T1, which have never been proven helpful in treating hypothyroidism but which desiccated thyroid proponents claim makes it "better." Also, until the last couple of decades, desiccated thyroid preparations had an alarming variation in dose from one batch to the other; and even with tightened USP requirements, the FDA issued a recall of over half a million bottles of desiccated thyroid in 2005 due to unstable concentrations of thyroid hormones.[27]


T4 causes lung cancer![28]

 The study in question, an abstract of which can be found here, is a population study. It looks at 18 different regions in Italy and tries to see if there's any correlation between sales of levothyroxine and various types of cancer. It happened to find one such correlation with lung cancer, but failed to find any correlation with breast, colorectal or gastric cancers. In other words, they were P-value fishing.


T3's antidepressant properties

The questionable push for T3 over T4 may be related to the fact that T3 has had some benefit in treating depression. Some depression sufferers that don't respond well enough to conventional antidepressants have shown improvement when T3 was added to their antidepressant regimen.[29][30]. It's possible that many of these hypothyroid patients, who still show symptoms when their TSH levels are brought within the normal range by T4 and who swear up-and-down that they feel better with T3 (or with desiccated thyroid extract, which contains some T3), may in fact be suffering from undiagnosed depression.

Listen, Damn You!

Suppose a hypothyroid patient is taking a prescription for synthetic T4, and the patient's TSH levels are now down within the therapeutic target range, but the patient still feels lethargic, fat, and unhappy. It could be because the T3 levels are inadequate, but it might also have nothing to do with hypothyroidism. A good endocrinologist might be willing to test for T3 levels, or adjust the dose of T4 to target the low end of the normal TSH range instead of the high end, or even try supplementing the T4 with a small amount of T3 — but (s)he should also be wary of overmedicating his/her patient all the way into the hyperthyroid range.[note 3]

As a result, books like Stop the Thyroid Madness scream up-and-down about the need to get your doctor to LISTEN!! to you. By which they mean, if your doctor isn't giving you exactly the drugs you tell them to, then they are an evil dupe in the hip pocket of Abbot Laboratories and you should keep looking for one until you find one that will rubber-stamp your prescription mandates. The fact that you couldn't be bothered to either listen to your endocrinologist or read the fucking label, which clearly says to take on an empty stomach and even defines exactly what this means, couldn't possibly be the issue; improper administration be dammed, there must be a conspiracy at work.

T4 vs. Desiccated Thyroid: A False dichotomy

Since desiccated thyroid is derived from ground up animal glands, it is therefore "natural", and must therefore inherently be better than that wicked, man-made synthetic T4.

The book Stop the Thyroid Madness, by Janie A. Bowthorpe, seems to imply that the only two courses of treatment available to a hypothyroid patient are an evil corporate-sponsored dose of synthetic T4 and only synthetic T4, or the "natural alternative" of desiccated thyroid (which she dubiously calls "Armour thyroid"). Almost no mention is made anywhere in the book of the existence of synthetic T3. Nowhere is the suggestion made of asking ones doctor to add synthetic T3 into the prescription mix, if you're not feeling fully treated on T4 alone. The few places that do mention people who have been prescribed synthetic T3 are quick to remind the reader: "But Armour Thyroid contains everything, so you should use that instead!"

She also claims that "mainstream" endocrinologists are receiving kickbacks from Abbot Laboratories, the makers of Synthroid (the first and most-recognized brand of synthetic T4). It is not known whether Ms. Bowthorpe is receiving kickbacks from Forest Labs.

Bowthorpe's book isn't the only hypothyroidism information source to present this false dichotomy. This about.com article, for example, also touts the virtues of desiccated thyroid extract over a regimen of pure synthetic T4, while neglecting to mention the synthetic T3 option except in an off-the-cuff remark about inflexible endocrinologists.

Quackwatch now recommends that you be wary of doctors who prescribe desiccated thyroid extract.[31]

Synthetic T4 shelf life

According to an FDA press release from 2007[32], synthetic T4 can break down if stored in a hot or humid environment (like, say, a bathroom with a working tub or shower).

As of 2008, the FDA[33] and USP[34] now mandate that synthetic T4 must meet a 95%-105% potency specification throughout its shelf life. All formulations sold by pharmacies since that time are required to meet these standards against degradation.

To desiccated thyroid proponents, such degradation with storage time was one more reason not to trust synthetic T4. To more sane individuals, though, it brings up the question of whether the natural T4 in desiccated thyroid doesn't also break down if stored in a hot or humid environment.

Wilson's Syndrome

Wilson's Temperature Syndrome, more commonly known as Wilson's Syndrome (and not to be confused with Wilson's disease), is a commonly pushed for thyroid diagnosis in the alternative medicine community,[35] though it has never been recognized as a valid diagnosis within the established medical community.[36][37][38] Originally proposed in 1990 by Dr. E. Denis Wilson (the syndrome's namesake), the premise of the Wilson's pushers is that, if you have non-specific symptoms similar to hypothyroidism, you must have hypothyroidism regardless of what the blood tests say your thyroid count is. Among the nonspecific symptoms seen as "definitive" for hypothyroidism is a body temperature below 98.6°F, so apparently the Wilson's folks feel that playing in the snow will make you hypothyroid.

Even more dangerously, the cranks who support treating Wilson's Syndrome often prescribe T3 as its treatment. Unsurprisingly, it was treating a phony diagnosis with T3 that led to a patient dying of a heart attack and to the subsequent disciplinary actions against Dr. Wilson by the Florida Board of Medicine.[39]

Hypothyroid diet

Not content with a choice between modern synthetic treatments that have been proven to work, and the older ground-up-thyroid gland that was also proven to work in its own time, various woo peddlers have chimed in with the claim that you can cure your hypothyroidism by diet.

There are some legitimate dietary concerns if you have hypothyroidism:

  • There are some foods known to be goitrogenic,File:Wikipedia's W.svg such as soybean protein and cauliflower; these foods contain isoflavones that can interfere with thyroid peroxidase (TPO), thereby reducing the thyroid gland's ability to manufacture T4 -- but only in cases of iodine deficiency.[40] A reasonable recommendation would be to limit your intake of goitrogenic foodstuffs.
  • In patients with Hashimoto's thyroiditis, there's some evidence that increasing your iodine intake can sometimes make the condition worse,[41][42] perhaps because it can result in elevated levels of TPO (which the Hashimoto's patient's anti-TPO antibodies attack).[43] A reasonable recommendation would be to ensure that your iodine intake is appropriate and not excessive. (Remembering to take the amount of iodine in your thyroid hormone drugs into account.)
  • Conversion of T4 to T3 may be impaired in cases of selenium deficiency.[44] A reasonable recommendation would be to ensure that your selenium level is adequate.
  • People with Hashimoto's thyroiditis have a greater incidence of celiac disease than the general population.[45] A reasonable recommendation would be to get checked for subclinical celiac disease.

However, the diet woo meisters go far beyond these reasonable recommendations.[46][47][48][49][50][51] You'll see claims that you need to completely avoid all foods that might be goitrogenic, completely avoid all foods that have so much as a milligram of iodine in them (including iodized salt), go gluten-free, and (of course) try their new and improved diet program guaranteed to make you feel less hypothyroid in just 21 days or your money back.

The Mayo Clinic says there's no evidence for dietary control of hypothyroidism, outside of ensuring that the patient doesn't eat certain foodstuffs too soon after taking hormone supplements.[52]

Hypothyroidism treatments as weight loss gimmicks

One of the possible symptoms of hypothyroidism is weight gain. One of the possible symptoms of hyperthyroidism is weight loss. It didn't take long for those desperate to find an easy weight loss gimmick to think of deliberately taking thyroid hormones even when thyroid function is normal.

The American Thyroid Association has this to say about the subject:

“”Thyroid hormones have been used as a weight loss tool in the past. Many studies have shown that excess thyroid hormone treatment can help produce more weight loss than can be achieved by dieting alone. However, once the excess thyroid hormone is stopped, the excess weight loss is usually regained. Furthermore, there may be significant negative consequences from the use of thyroid hormone to help with weight loss, such as the loss of muscle protein in addition to any loss of body fat. Pushing the thyroid hormone dose to cause thyroid hormone levels to be elevated is unlikely to significantly change weight and may result in other metabolic problems.
—Thyroid and Weight (PDF), American Thyroid Association

In addition, Cytomel (prescription synthetic T3) is required by the FDA to come with this warning:

“”Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.
—Cytomel (Liothyronine Sodium) Drug Information: Warnings and Precautions - Prescribing Information at RxList, retrieved on 14-April-2014

Dietary supplements used to be sold which contained actual thyroid hormones. Today, however, legal access to these drugs is impossible without a prescription. That hasn't stopped certain unscrupulous manufacturers from giving "thyroidally suggestive" names to their dietary supplements, like "T-3"[53], even though they contain no triiodothyronine.

Fluoride

Several alternative medicine sources claim that fluoridation can impair thyroid function.[54][55][56][51] Fluoride was, at one point, even prescribed as a possible treatment for hyperthyroidism.[57][58]

However, a review of the literature published in Klinische Wochenschrift in 1984 found that "Published data failed to support the view that fluoride, in doses recommended for caries prevention, adversely affects the thyroid."[59] A population study in 2015 found "diease clusters" of hypothyroidism in areas of England with fluoridated water[60], but such population studies are notorious for finding dubious associations.[61] (And even if the association is solid, WebMD points out that correlation does not imply causation.[62])

gollark: <@151391317740486657> ***USE RUST***
gollark: Just "quite similar".
gollark: Not "literally the same".
gollark: C ftl (for the lose).
gollark: RUSTUST

Notes
  1. Other common causes of hypothyroidism include pregnancy, and getting your thyroid gland surgically removed or destroyed due to cancer. In Hashimoto's thyroiditis, the patient creates antibodies that attack her own thyroid peroxidase (TPO) enzymes; it can be tested for by looking for anti-TPO antibodies in the patient's blood, but since not all people with Hashimoto's thyroiditis develop hypothyroidism, such a test isn't definitive for diagnosing hypothyroidism.
  2. A test for the anti-TPO antibodies caused by Hashimoto's Thyroiditis is also recommended in pregnant patients with a history of Graves’ disease who were treated with radioactive iodine or thyroidectomy prior to pregnancy. (c.f. Recommendation 5 in the PDF file).
  3. Technically, it's only called hyperthyroidism if the patient's own thyroid produces the excessive hormones. The clinical term for excessive thyroid hormone levels due to oversupplementation is thyrotoxicosis. Symptoms of thyrotoxicosis include nervousness, irritability, increased perspiration, heart racing, hand tremors, anxiety, difficulty sleeping, thinning of the skin, fine brittle hair, and muscular weakness—especially in the upper arms and thighs.

References
  1. Quackwatch lists hypothyroidism among the Fad Diagnoses prevalent in the past.
  2. American Association of Clinical Endocrinologists (November/December 2012). "Clinical Practice Guidelines for Hypothyroidism in Adults" (PDF). Endocrine Practice 18 (6): 988-1028.
  3. According to this 2010 article, it may be safe to go as low as 0.04 μIU/mL, at least as far as your risk of heart disease, abnormal heart patterns, and bone fractures go. That doesn't mean you'll be safe from other risk factors at such a low TSH level, though, which is why the AACE still recommends a low end of 0.45 μIU/mL.
  4. Ongphiphadhanakul, B; Fang, SL; Tang, KT; Patwardhan, NA; Braverman, LE (1994). "Tumor necrosis factor-alpha decreases thyrotropin-induced 5'-deiodinase activity in FRTL-5 thyroid cells". European journal of endocrinology 130 (5): 502–7. PMID 8180680.
  5. Nygaard et al., Effect of combination therapy with thyroxine (T4) and 3,5,3′-triiodothyronine versus T4 monotherapy in patients with hypothyroidism, a double-blind, randomised cross-over study, European Journal of Endocrinology, vol. 161 no. 6 (December 2009), pp. 895-902
  6. Escobar-Morreale, H. F.; Botella-Carretero, JI; Escobar Del Rey, F; Morreale De Escobar, G (2005). "Treatment of Hypothyroidism with Combinations of Levothyroxine plus Liothyronine". Journal of Clinical Endocrinology & Metabolism 90 (8): 4946–54. PMID 15928247.
  7. Joffe, R. T.; Brimacombe, M.; Levitt, A. J.; Stagnaro-Green, A. (2007). "Treatment of Clinical Hypothyroidism With Thyroxine and Triiodothyronine: A Literature Review and Metaanalysis". Psychosomatics 48 (5): 379–84. PMID 17878495.
  8. van den Beld et al., Thyroid Hormone Concentrations, Disease, Physical Function, and Mortality in Elderly Men, The Journal of Clinical Endocrinology & Metabolism, vol. 90 no. 12 (1-Dec-2005), pp. 6403-6409
  9. Fonseca et al., Coordination of hypothalamic and pituitary T3 production regulates TSH expression, The Journal of Clinical Investigation, vol. 123 no. 4 (1-April-2013), pp. 1492–1500
  10. Silva and Larsen, Contributions of Plasma Triiodothyronine and Local Thyroxine Monodeiodination to Triiodothyronine to Nuclear Triiodothyronine Receptor Saturation in Pituitary, Liver, and Kidney of Hypothyroid Rats, Journal of Clinical Investigation, vol. 61 no. 5 (May 1978), pp. 1247-1259
  11. Silva et al., The contribution of local tissue thyroxine monodeiodination to the nuclear 3,5,3'-triiodothyronine in pituitary, liver, and kidney of euthyroid rats., Endocrinology, vol. 103 no. 4 (Oct. 1978), pp. 1196-207
  12. Larsen et al., Inhibition of intrapituitary thyroxine to 3.5.3'-triiodothyronine conversion prevents the acute suppression of thyrotropin release by thyroxine in hypothyroid rats., Journal of Clinical Investigation, vol. 64 no. 1 (July 1979), pp. 117-128
  13. Han et al., 3,3',5'-Triiodothyronine inhibits iodothyronine-5'-deiodinating activity induced by 3,5,3'-triiodothyronine at equimolar concentrations in cultured fetal mouse liver, Endocrinology, vol. 119 no. 3 (Sept. 1986), pp. 1076-82
  14. Faber et al., Serum free T4, T3, rT3, 3,3'-diiodothyronine and 3',5'-diiodothyronine measured by ultrafiltration, Acta Endocrinologica, vol. 107 no. 3 (Nov. 1984), pp. 357-65
  15. The Role of Reverse T3 Testing in Thyroid Treatment, by Mary Shomon on about.com
  16. http://www.thyroid-rt3.com/whatdo.htm
  17. http://nahypothyroidism.org/deiodinases/ , section "Deiodinase type III (D3)"
  18. http://tiredthyroid.com/rt3.html
  19. Venkatraman, Lefebvre. Multiple thyroid hormone binding sites on male rat liver nuclear matrices, Biochemical and Biophysical Research Communications, Volume 148, Issue 3, 13 November 1987, Pages 1496–1502
  20. Wiersinga WM, Chopra IJ, Solomon DH, Specific nuclear binding sites of triiodothyronine and reverse triiodothyronine in rat and pork liver: similarities and discrepancies, Endocrinology. 1982 Jun;110(6):2052-8
  21. Molecular Basis of Thyroid Hormone Action, page 93
  22. Papavasiliou et al., Thyroid Hormonelike Actions of 3,3′,5′-l-Triiodothyronine and 3,3′-Diiodothyronine, The Journal of Clinical Investigation, vol. 60 no. 6 (Dec 1977), pp. 1230-1239
  23. http://www.globalrph.com/labs_t.htm
  24. Specific 3,3',5'-triiodothyronine (reverse T3) binding sites on rat liver plasma membranes: comparison with thyroxine (T4) binding sites, Journal of Receptor Research, vol. 3 no. 3 (1983), pp. 393-407
  25. Peeters et al., Serum 3,3′,5′-Triiodothyronine (rT3) and 3,5,3′-Triiodothyronine/rT3 Are Prognostic Markers in Critically Ill Patients and Are Associated with Postmortem Tissue Deiodinase Activities, Journal of Clinical Endocrinology & Metabolism, vol. 90, issue 8, page 4559 (August 2005)
  26. LoPresti et al., Does a hidden pool of reverse triiodothyronine (rT3) production contribute to total thyroxine (T4) disposal in high T4 states in man., Journal of Clinical Endocrinology and Metabolism, vol. 70 no. 5 (1990), pp. 1479-84
  27. Enforcement Report for May 11, 2005, from the FDA's site. Note that this page lists all recalls issued on 11-May-2005, not just those recalls issued for desiccated thyroid extract. Note also that the Class II recall of desiccated thyroid shown at the top was later downgraded to a Class III recall.
  28. More BAD news if you are on T4-only like Synthroid?: it can cause Lung Cancer, says a study!, stopthethyroidmadness.com, 12-Aug-2013
  29. The Treatment of Depression with T3, Evolutionary Psychiatry, Feb. 2012
  30. Abraham et al., T3 augmentation of SSRI resistant depression, Journal of Affective Disorders, April 2006
  31. Desiccated Thyroid: Be Wary of Doctors Who Prescribe It, Quackwatch, last revised 10-Sept-2013
  32. Thyroid Drug Potency is Being Tightened: FDA Changes Specs for Levothyroxine
  33. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm161266.htm
  34. http://www.usp.org/usp-nf/notices/retired-compendial-notices/usp-announces-revised-monograph-levothyroxine-sodium-tablets
  35. , a major Wilson's crankery website
  36. Is Wilson's syndrome a legitimate ailment?, From the Mayo Clinic
  37. The American Thyroid Association's Statement on “Wilson’s Syndrome”
  38. Wilson's Syndrome also appears on Quackwatch's list of fad diagnoses.
  39. Doctor's syndrome a sham, board says
  40. Doerge DR, Sheehan DM (June 2002). "Goitrogenic and estrogenic activity of soy isoflavones". Environ. Health Perspect. 110 Suppl 3: 349–53. PMC 1241182. PMID 12060828.
  41. Effect of small doses of iodine on thyroid function in patients with Hashimoto's thyroiditis residing in an area of mild iodine deficiency, European Journal of Endocrinology, vol. 139 no. 1 (July 1998), pp. 23-28
  42. Yoon et al., The Effect of Iodine Restriction on Thyroid Function in Patients with Hypothyroidism Due to Hashimoto's Thyroiditis (PDF file), Yonsei Medical Journal, vol. 44 no. 2 (2003), pp. 227-235
  43. According to this article in Biological trace elements research, excessive iodine intake actually reduces TPO activity, rather than elevating TPO levels.
  44. Type I iodothyronine deiodinase is a selenocysteine-containing enzyme, Nature, vol. 349, pp. 438-440 (31 January 1991)
  45. Akçay et al., The presence of the antigliadin antibodies in autoimmune thyroid diseases, Hepato-gastroenterology, 2003 Dec; 50 Suppl 2: cclxxix-cclxxx
  46. Smart Foods For Hypothyroidism
  47. LiveStrong hypothyroidism diet -- at least this one doesn't recommend you use a diet instead of taking thyroid hormone medications.
  48. The HypoThyroid Diet: Lose Weight and Beat Fatigue in 21 Days
  49. The Thyroid Diet: Manage Your Metabolism for Lasting Weight Loss; some sound advice mixed in with herbal supplement woo
  50. The Gluten-Thyroid Connection
  51. Midlife plight: my thyroid or my teeth?, by Jennifer Berman, writer and sign language interpreter (rebuttal in Forbes)
  52. Is there any truth to the hypothyroidism diet? Can certain foods increase thyroid function?
  53. S.A.N. T-3
  54. Fluoride and your Thyroid
  55. The Daily Activity Every Middle Aged Woman Should Beware of, on Joseph Mercola's site
  56. Thyroid, on the Fluoride Action Network
  57. [http://www.fluoridealert.org/wp-content/uploads/galletti-1958.pdf Effect of Fluorine on Thyroidal Iodine Metabilism in Hyperthyroidism] (PDF), Galletti and Joyet, 1958
  58. The Merck Index (PDF), 8th Edition (1968), p. 959
  59. Bürgi et al., Fluorine and thyroid gland function: a review of the literature, Klin Wochenschr. 1984 Jun 15;62(12):564-9.
  60. Peckham et al., 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, Journal of Epidemiology & Community Health (impact factor: 3.2), February 2015
  61. Experts Criticize Thyroid Study, American Academy of Pediatrics campaign for dental health, 2-March-2015
  62. Alan Mozes, Fluoride in Water and Underactive Thyroid Rates, WebMD, 25-Feb-2015
This article is issued from Rationalwiki. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.