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Please note: All of the physicians on this site are in agreement that low thyroid is under-diagnosed. This article by Michael Gerber, MD, HMD is a reprint from The Townsend Letter for Doctors.

Epidemic Hypothyroidism

In Part 1 of 2, I visited 118 peer-reviewed, journal articles that cast serious concerns about the accuracy of standard blood tests which determine thyroid status, TSH and T4 especially. Equally disturbing are the plethora of epigenetic, environmental and genetic conditions which disturb thyroid activity in each of our 100 trillion cells. Although an exhaustive review of thyroid metabolism is beyond the scope of this article, I hope some of the major issues can help guide our understanding of the delicate relationship to thyroid hormone production, receptivity and elimination.

Thyroid in Every PMN Leukocyte

All polymorphonuclear leukocytes (PMN) utilize T4 to convert to T3 and generate iodide via type 3 deiodinase bacteria undergo phagocytosis into PMNs which then release an oxidative burst of myeloperoxidase, H2O2 and iodide, chloride, bromide, or thiocyanate ions. Oxidation of iodide results in the formation of hypoiodite, and the subsequent iodination of bacteria by hypoiodite promotes killing and degradation of the ingested bacteria. A clear relationship was observed between iodination of the ingested bacterial kill capacity of PMN, suggesting that iodination is essential for their bacterial killing capacity.1 Chronic infectious conditions seem to benefit from thyroid supplementation.

Thyroid Hormone Action is Disrupted by Bisphenol A

Endocrine disruptors have emerged as a major public health issue. Bisphenol A (BPA) is a monomer of plastic materials that are widely used in daily life. BPA is detectable in our environment and is present in drinking water, canned goods, and even in milk bottles. Recently, it was shown that BPA contaminates not only human plasma, but also fetal tissues. Many reports have shown that BPA has a weak effect to stimulate estrogen receptors (ERs). BPA can disturb thyroid hormone function by reducing T3 binding to the nuclear thyroid receptors (TRs) and recruited nuclear corepressors (N-CoRs) to the TR resulting in transcriptional inhibition. The chemical structures of BPA and T3 are remarkably similar2.

Halides that Block Iodine Absorption:  Fluoride, Bromide, Chlorine, Perchlorate

There is a plethora of data regarding the blocking power of these halides to block iodine absorption and thyroid function. Fluoride in toothpaste and dental treatments and the water supply; bromide in baking oils; and chlorine as an antiseptic in water treatment; along with rocket fuel in some 43 locales nationwide. These all block thyroid function and disturb our most basic relationships with thyroid function3.

Mercury Exposure Linked to Increase of Thyroid Antibody

Women with high mercury exposures are more than twice as likely to have higher levels of antibodies that are associated with autoimmune disorders. Scientists analyzed data collected from 4,047 women between 2007 and 2008 during a large study in the United States – the National Health and Nutrition Examination Survey (NHANES). They compared total mercury levels in blood and autoantibodies – immune system factors that fight the body’s own cells and indicate autoimmune disease. Patients with autoimmune diseases – such as lupus, rheumatoid arthritis and fibromyalgia – often have elevated concentrations of these antibodies. They found that women with the highest blood mercury levels were more than twice as likely to have elevated levels of thyroglobulin antibody, as compared to women with the lowest mercury levels. Overall, the study provides new evidence for the emerging role of mercury in autoimmune disease4.

Goitrogens in Foods

There are two general categories of foods that have been associated with disrupted thyroid hormone production in humans – soybean-related foods and cruciferous vegetables. In addition, there are a few other foods not included in these categories – such as peaches, strawberries, peanuts, radishes, spinach, and millet – that also contain goitrogens.

Isoflavones are naturally occurring substances that belong to the flavonoid family of nutrients. The link between isoflavones and decreased thyroid function is one of the few areas in which flavonoid intake has been called into question as problematic. Isoflavones, like genistein, appear to reduce thyroid hormone output by blocking activity of thyroid peroxidase. This enzyme is responsible for adding iodine onto the thyroid hormones.

A second category of foods associated with disrupted thyroid hormone production is the cruciferous food family. “Crucifers” including broccoli, cauliflower, brussel sprouts, cabbage, mustard, rutabagas, kohlrabi, kale, and turnips contain isothiocyanates, which also reduce thyroid peroxidase and thyroid hormone formation. Heating and cooking of these vegetables helps to inactivate the goitrogenic isothiocyanates5.

Post-Partum Thyroiditis

Post-partum thyroiditis occurs within the first year after delivery. Although classically it may begin with hyperthyroid symptoms, in my experience, it usually is a hypothyroid response to the pregnancy – with fatigue, depression, poor memory, feeling cold, constipation, muscle cramps and difficulty losing weight. Approximately 25% to 30% of women who have postpartum thyroiditis eventually develop permanent hypothyroidism. As many as 30% to 50% of women who have TPOab during the first trimester of pregnancy will develop postpartum thyroiditis. Of these, 19% developed hyperthyroidism symptoms followed by recovery, and 49% developed hypothyroidism not preceded by hyperthyroidism. This research confirmed many studies indicating an increased incidence of postpartum depression among women who were found to be positive for TPOab6.

Gluten

Gluten sensitivity has been linked to Hashimoto’s thyroiditis, autoimmune thyroid disease (AITD)7. The molecular structure of gluten/gliadin is similar to thyroid tissue and can cause cross-reactive destruction of the thyroid. Genetically engineered wheat in the United States contains five times more gluten than European wheat. Our family reacts much differently to wheat in Germany and Austria. This increased protein content causes more difficulty in digestion and a greater tendency to intestinal permeability. When the autoimmune attack is begun on the thyroid, it is difficult to turn it off. Some authors suggest that gluten can affect the body for six months after ingestion8. The gluten-free diet is important for patients with AITD.

Medications That Effect Thyroid Function

Medications which change thyroid function tests include: dopamine, levodopa, bromocriptine, glucocorticoids, dexamethasone, hydrocortisone, octreotide and amphetamine. These decrease TSH levels. Metoclopramide, amiodarone, and iodinated contrast media increase TSH. IV furosemide, nonsteroidal agents, salicylates, diclofenac, naproxen, IV heparin, amiodarone, and iodinated contrast media can increase free T4. Phenytoin and carbamazepine decrease free T4.

Inhibition of conversion of T4 to T3 occurs with administration of amiodarone and iodinated contrast media, such as ipodate, iopanoic acid and tyropanoate. Beta blockers and corticosteroids inhibit the peripheral conversion of T4 to T3 minimally. Propranolol (>160 mg/d) and metoprolol produce small reduction in total T3 levels. Large doses of corticosteroids (>4 mg dexamethasone) give reductions in total T3 levels, which are useful in the management of thyroid storm or severe hyperthyroidism.

Lithium induces hypothyroidism in up to 50% of patients taking lithium carbonate. It can cause a smooth, nontender goiter and is observed in up to 60% of those receiving lithium for 5 months to 2 years; hypothyroidism may not be present. As with iodides, lithium is concentrated in the gland and interferes with thyroid hormone synthesis and release. Once lithium is stopped, the goiter and hypothyroidism do not always resolve.

Interferon alpha causes frequent thyroid dysfunction. Symptoms of thyroid dysfunction may take as long as 17 months after stopping therapy to resolve. Thyroid hormones are metabolized primarily by deiodination, but glucuronidation and sulfation are also important routes of elimination. Cytochrome P-450 hepatic enzyme inducers, such as rifampin, rifabutin, phenytoin, carbamazepine, and phenobarbital increase the metabolic elimination of T4 and T3 by 20%.

Serotonin reuptake inhibitors may also alter T4 requirements. In nine patients receiving thyroxin therapy, an elevation in thyrotropin levels and a reduction in free T4 levels were noted after the addition of sertraline hydrochloride. An increase in thyroxine clearance was thought to have occurred9.

Aging and Cognition

Normal thyroid function appears to be an important factor in retaining optimal cognition in human aging. Overall, many studies suggest that there may be a continuum characterizing the impact of thyroid function on cognition in which cognitive dysfunction results from either chronically increased or decreased concentrations of thyroid hormones. Even thyroid hormones and TSH levels within low-normal range appear to influence cognition performance, such that low-normal thyroid function appears associated with cognitive decline over time10.

Pesticide Exposure

Exposures to pesticides may also increase risk of thyroid problems. A study of 16,529 women in Iowa and North Carolina married to pesticide applicators reported that 12.5% had some form of thyroid problems, and 6.9% had clinical hypothyroidism. Exposure to organochlorine pesticides, such as aldrin, chlordane, DDT and lindane; fungicides such as benomyl, captan, maneb; and the fumigant, meth bromide, were associated with significantly higher rates of thyroid problems11.

Selenium, Iodine and Iron Deficiency in Hypothyroidism

Selenium and iodine repletion in hypothyroidism is an evolving art/science. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron deficiency anemia blunts, and iron supplementation improves, the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations, even under conditions of inadequate selenium supply, and expresses many of the known selenocysteine-containing proteins. Among the selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxin reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism12.

In Conclusion

The world of thyroid biochemistry is extremely complex with many lifetimes of research available for our interpretation. Thyroid adequacy at the cellular level is critical for every organelle and chemical reaction. The interplay of thyroid with all the other hormones and the autonomic nervous system leads to a dizzying array of potential breakdown points for our health. If patients look and sound hypothyroid, believe your clinical judgment, and consider gentle thyroid support with dietary and lifestyle modification counseling.

References

  1. Boelen A, Kwakkel J, Fliers E. Beyond low plasma t3: local thyroid hormone metabolism during inflammation and infection. Endocrine Reviews. October 1 2011 vol. 32 no. 5 670-693.
  2. Moriyama K, Tagami T, Akamizu T, Usui T, Saijo M, Kanamoto K, Hataya Y, Shimatsu A, Kuzuya H, Nakao K. Thyroid hormone action is disrupted by bisphenol a as an antagonist. Journal of Clinical Endocrinology & Metabolism. November 1, 2002 vol 87 no. 11 5185-5190.

3.Osansky E. Fluoride, bromide, and thyroid health. www.naturalendocrinesolutions.com. 2013 March. Accessed June 2013.

  1. Karimi R. Mercury exposure linked to ramp up of thyroid antibody. Environmental Health News. 2012 March.
  2. The world’s healthiest foods. www.Whfoods.com. Accessed July 2013.
  3. Thyroid Australia LTD. www.thyroid.org/au. Accessed July 2013.
  4. Akçay MN, Akçay G. The presence of the antigliadin antibodies in autoimmune thyroid Diseases. Hepatogastroenterology. 2003 Dec; 50 Suppl 2:cclxxix-cclxxx.
  5. Mainardi E, Montanelli A, Dotti M, Nano R, Moscato G. Thyroid-related autoantibodies and celiac disease: a role for a gluten-free diet? J Clin Gastroenterol. 2002 Sep;35(3):245-8.
  6. Dong BJ. How medications affect thyroid function. West J Med. 2000 February; 172(2):102-106.
  7. M.E. Begin, et al. Thyroid function and cognition during aging. Current Gerontology and Geriatrics Research Vol. 2008. Article ID 474868.
  8. Curtis L. Pesticide exposure and increased risk of thyroid problems. American Journal of Epidemiology. February 15, 2010.
  9. Zimmerman MB, Köhrle. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid. 2002 Oct; 12(10):867-78.