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Natural Treatments for Hashimoto’s Thyroiditis: A Different View on a Common Disease.

I’ve written this paper to review current information on a common autoimmune condition, Hashimoto’s Disease – this is by far the most common autoimmune disease I treat in my practice. Natural treatments for Hashimoto’s Thyroiditis will be discussed, and I’ll also include a unique functional medicine view of how the condition may develop. This information is based on the most recent research into autoimmune disease, and since this field is consistently evolving, we expect that this information will change in time.

This paper was originally published in Naturopathic Currents an evidence-based publication for the Naturopathic profession in April 2014.

Hashimoto’s thyroiditis is an autoimmune disease that is characterized by an infiltration and destruction of the thyroid gland by the immune system. In this condition, immune cells produce antibodies against a key enzyme that is required for thyroid hormone production — thyroid peroxidase — and/or against thyroglobulin, which is the building block of thyroid hormones.[1] Hashimoto’s is believed to be the most common cause of hypothyroidism in North America, and is among the most common causes of goiter in areas of the world where iodine intake is considered sufficient.[2] An average of 1.5 out of 1000 people have this disease, it is 7 times more common in women than in men, and is most prevalent in those between the ages of 45 and 65.

Risk factors for Hashimoto’s include a family history of thyroid disorders, as well as specific environmental triggers. Several genetic polymorphisms (for example, changes to the HLA-DR gene) have been associated with autoimmune thyroiditis.[3] In addition, infectious diseases, excessively high iodine intake, selenium deficiency, and certain medications may also trigger this condition in those who have a genetic predisposition.

Hashimoto’s is a disease process characterized by progressive destruction of the thyroid gland resulting in hypothyroidism. It can be diagnosed by any of the following: 1) enlargement of the thyroid gland / goiter, 2) high levels of antibodies against thyroid peroxidase or thyroglobulin, 3) fine-needle aspiration of the thyroid showing immune-cell infiltration of the gland, 4) an ultrasound showing an enlarged thyroid, or 5) radioactive iodine uptake scan showing a specific pattern of diffuse iodine uptake.

People with Hashimoto’s often experience different symptoms, of varying severity. Some patients may experience no symptoms at all, whereas those experienced by others may be quite severe. As the condition results in progressive destruction, symptoms of hypothyroidism gradually appear.

These symptoms include:

  • Fatigue;
  • Weight gain;
  • Constipation;
  • Depression;
  • Dry skin;
  • Hair loss;
  • Sensitivity to cold;
  • Goiter.

These symptoms often worsen over time, as the gland is progressively destroyed. Another aspect of Hashimoto’s is that patients may experience temporary symptoms of hyperthyroidism — this is known as “Hashitoxicosis”(4).

The symptoms of Hashitoxicosis include:

  • Anxiety;
  • Weight loss;
  • Tremor;
  • Sweating;
  • Insomnia;
  • Palpitations and rapid heart rate;
  • Goiter;
  • Thinning skin.

Hashitoxicosis occurs as a result of disturbance of the thyroid follicles, which causes the release of excessive thyroid hormone. However, as the disease progresses, the predominant symptomatology becomes more one of hypothyroidism.

This article will discuss the underlying causes of autoimmune thyroiditis, the relationship of the intestinal microbiology and gut barrier in provoking and aggravating the disease. Celiac disease and the role of gluten in Hashimoto’s, and nutritional relationships between iodine and selenium in this disease will also be discussed.

Hashimoto’s and the Gut

In recent years, the intestinal immune system and bacterial flora have been found to play a key role in many different autoimmune diseases, such as rheumatoid arthritis.[5] The intestine is in continuous contact with a wide variety of antigens from both food and microorganisms. Beneficial microorganisms in the intestine provide great benefit by forming protective barriers, aiding in the digestion and assimilation of nutrients, and in the development of the intestinal immune system. Fermentation products of intestinal bacteria also may inhibit inflammatory chemicals such as TNF-alpha, IL-6, and NF-kB[6, 7]that can be part of autoimmune destruction. Overall, a well-balanced gut flora is important when considering autoimmune diseases such as Hashimoto’s.

In addition to the microbes that live in the intestine, the intestinal lining itself is coming more to the forefront of research in autoimmune disease. The intestinal lining provides a barrier that prevents both pathogenic and nonpathogenic bacteria from entering into highly immunoreactive areas of the body, such as the bloodstream. If this mucosal barrier is disrupted, the immune cells of the intestine can become exposed to bacterial and dietary compounds that would normally be kept out. This in turn can lead to activation of the immune system and the development of autoimmune diseases.[7, 8] When this happens, intestinal cells change, and the overall permeability of the intestine increases. This has been demonstrated in conditions such as autoimmune type 1 diabetes, and similar changes in intestinal structure have also been detected in patients with Hashimoto’s disease.[9, 10]

A concept known as “molecular mimicry” has also been implicated in Hashimoto’s and other autoimmune diseases. For example, Yersinia enterocolitica is an intestinal pathogen that can be transmitted to humans through pets and domestic animals, including pigs, with infections acquired via ingestion of contaminated food or water. There have been several studies correlating Yersinia infection with thyroid autoimmunity, including a trial reported in Clinical Microbiology and Infection, which claimed that the prevalence of antibodies to Yersinia was 14 times higher in people with Hashimoto’s than in those within a control group.[11] The researchers concluded that there may be a strong causative relationship between this pathogen and autoimmune thyroiditis.

One important point to consider is that although probiotic flora may be beneficial, the choice of strains is crucial. Some probiotic strains have anti-inflammatory effects and provide benefit in autoimmune disease, whereas other strains may aggravate autoimmunity. For instance, a study conducted in Denmark found that specific strains of Lactobacillus acidophilus and Bifidobacterium bifidum reduced regulatory T-cell activity, which could increase inflammation and aggravate Hashimoto’s,[12] whereas another study found that Lactobacillus rhamnosus HN001 and Bifidobacterium lactis HN019 reduced inflammation without affecting Hashimoto’s antibodies.[13]

Celiac Disease, Gluten, and Hashimoto’s Celiac Disease, Gluten, and Hashimoto’s

There have been several studies correlating celiac disease and Hashimoto’s thyroiditis. As these are both autoimmune conditions, the topic has been the subject of much research, which has found a clear link between the two.

In a Dutch study on 104 people with Hashimoto’s,[14] it was found that there was a significantly increased chance of having markers of celiac disease, including antibodies to gliadin and/or damage to the small intestine. Nearly 50% of the Hashimoto’s patients had the genes for celiac disease (HLA-DQ2). In a separate test within the same study, 184 patients with celiac disease were tested for Hashimoto’s antibodies, and it was found that 21% of them were positive. In some patients with celiac disease, avoidance of gluten may actually eliminate thyroid specific antibodies.[15]

Gluten and Zonulin — Effects on the Gut Gluten and Zonulin — Effects on the Gut

Zonulin is a fascinating intestinal protein that was recently discovered by Dr. Allessio Fasano. Its main function is to regulate the passage of materials from the intestine to the bloodstream. Tight junctions are the areas in which adjacent intestinal cells come into contact with each other, forming an impermeable barrier. They are crucial in that they prevent foreign particles, microbes, and improperly digested food from entering the body. When too much zonulin is released, the tight junctions can become leaky, and as described in the previous section, allow immunologically reactive molecules such as food antigens and microbes to enter into the bloodstream,[16] causing inflammatory activation.

Interestingly, even in people who do not have celiac disease, consuming gliadin (a component of gluten) increases the release of zonulin and temporarily causes “leakiness” in the intestinal barrier, also known as “leaky gut”.[17] In people who carry the HLA-DQ gene (approximately 30% of the population, and around 50% of Hashimoto’s patients) an excessive amount of zonulin is released when gliadin is consumed. For these patients, gut permeability is even more intensive. Once particles can enter the bloodstream through this leaky barrier, we are again faced with antigens entering the bloodstream, leading to aggravation or triggering of autoimmunity.[18]

Hashimoto’s Thyroiditis — Selenium and Iodine Hashimoto’s Thyroiditis — Selenium and Iodine

Iodine is a key nutrient for thyroid function. It combines with thyroglobulin to make the key thyroid hormones T3 and T4, so as you can imagine, its balance is crucial for the function of the gland.

It is well known that the intake of excessive iodine is linked to triggering Hashimoto’s thyroiditis.[19] The literature is full of cases of iodine-induced autoimmune thyroid disease, with many studies correlating the increased incidence of Hashimoto’s in countries where iodine intake is higher. The high doses of iodine in patients with a predisposition to Hashimoto’s seem to trigger the production of T lymphocytes,[20] and these immune cells then turn on the thyroid gland itself, resulting in decreased overall thyroid function over time.

That said, many practitioners do use iodine therapy with Hashimoto’s patients. This part of the article will discuss the critical balance between two key thyroid nutrients, iodine and selenium. I also have another article with information on the use of iodine in patients who are trying to conceive or are suffering with infertility and Hashimoto’s.

Much of the research about using iodine for patients with Hashimoto’s involves the effect of optimal selenium status. Selenium is a mineral that is found in high concentration in the thyroid, and the selenoproteins in that gland are involved in antioxidant defense; specifically in the action of glutathione peroxidase [21] — a major cellular protector. These antioxidant defense mechanisms protect the thyroid from the reactive oxygen species that are produced as a byproduct of thyroid hormone synthesis. The three key enzymes involved in the activation and inactivation of thyroid hormones are also selenium-based in structure.

There are numerous studies finding that selenium supplementation reduces thyroid autoimmune antibodies. A study of 80 women with Hashimoto’s disease found that supplementation of 200 mcg of selenomethionine reduced anti-TPO antibodies by 21%,[22] and many other studies support this finding. Supplementation of selenium is without doubt of great benefit for patients with Hashimoto’s, but what about the balance between iodine and selenium?

An animal study completed in China set out to test the hypothesis that the toxicity induced by excessive iodine intake might actually be induced by selenium deficiency.[23] The study found that when iodine was given in high doses, it decreased the activity of thyroid enzyme thyroid peroxidase, changed the cell structure to a goiter-like appearance, and reduced the protective glutathione in the thyroid gland. However, when selenium was supplemented along with the iodine, these all returned back to control levels.

Another study found something quite similar: three groups of mice were included, including a healthy control group and two groups with iodine-induced Hashimoto’s. One of the thyroiditis groups was given selenium and one was not, but both were given high amounts of iodine. The selenium group had completely reversed the thyroiditis pattern on biopsy after eight weeks of supplementation, despite continuing on the high dose of iodine.[24] In the non-selenium group, the destructive pattern in the thyroid gland remained.

Each of these studies indicates that achieving good selenium status can reverse the stimulation of thyroiditis caused by excessive amounts of iodine. The amount in these studies corresponds to approximately 200–400 mcg per day of selenium. It is important to note that selenium can be toxic, and that supplementing selenium in conditions of iodine deficiency may be harmful for thyroid function.

Another interesting point is that the areas of the world where Hashimotos’ increased after iodization of salt were areas in which selenium deficiency is predominant as well. For example, a study comparing different provinces in China indicated that the provinces with the lowest intakes of iodine also had the lowest incidences of Hashimoto’s.[24] Coincidentally, these provinces were also more deficient in selenium.[24] Thus, we can conclude that selenium status may play a key role in preventing autoimmune thyroiditis, and that the balance between iodine and selenium is important for thyroid function. It is often helpful to check iodine status before supplementing higher doses of iodine. Urinary iodine testing is the most accurate (either a 24-hour urine iodine, or dried urine iodine test).

If you have been diagnosed with or suspect a thyroid problem, we recommend consultation with a licensed naturopathic doctor prior to undertaking high dose iodine or selenium supplementation.

References for this article

  1. Dayan, C.M. and G.H. Daniels GH. “Chronic autoimmune thyroiditis”. N Engl J Med. Vol. 335, No. 2 (1996): 99-107.
  2. Kumar, V. The Endocrine System. Robbins and Cotran Pathologic Mechanisms of Disease, 8th ed. Philadelphia, PA: Elsevier, 2010: 1111–1205.
  3. Jabrocka-Hybel, A., et al. “How far are we from understanding the genetic basis of Hashimoto’s thyroiditis?” International Reviews of Immunology Vol. 32, No. 3 (2013): 337–354.
  4. Nabhan, Z.M., N.C. Kreher, and E.A. Eugster. “Hashitoxicosis in children: clinical features and natural history”. The Journal of Pediatrics Vol. 146, No. 4 (2005): 533–536.
  5. Ebringer, A. and T. Rashid. “Rheumatoid arthritis is caused by a Proteus urinary tract infection”. APMIS: Acta Pathologica, Microbiologica, et Immunologica Scandinavica 2013 Aug 29. [Epub ahead of print]
  6. Segain, J.-P., et al. “Butyrate inhibits inflammatory responses through NFkB inhibition: implications for Crohn’s disease”. Gut Vol. 47, No. 3 (2000): 397–403.
  7. Macdonald, T.T. and G. Monteleone. “Immunity, inflammation, and allergy in the gut”. Science Vol. 307, No. 5717 (2005): 1920–1925.
  8. Vaarala, O., M.A. Atkinson, and J. Neu. “The ‘perfect storm’ for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity”. Diabetes Vol. 57, No. 10 (2008): 2555–2562.
  9. Cindoruk, M., et al. “Increased colonic intraepithelial lymphocytes in patients with Hashimoto’s thyroiditis”. Journal of Clinical Gastroenterology Vol. 34, No. 3 (2000): 237–239.
  10. Sasso, F.C., et al. “Ultrastructural changes in enterocytes in subjects with Hashimoto’s thyroiditis”. Gut Vol. 53, No. 12 (2004): 1878–1880.
  11. Chatzipanagiotou, S., et al. “Prevalence of Yersinia plasmid-encoded outer protein (Yop) class-specific antibodies in patients with Hashimoto’s thyroiditis”. Clinical Microbiology and Infection Vol. 7, No. 3 (2001): 138–143.
  12. Schmidt, E.G.W., et al. “Antigen-presenting cells exposed to Lactobacillus acidophilus NCFM, Bifidobacterium bifidum BI-98, and BI-504 reduce regulatory T cell activity”. Inflammatory Bowel Diseases Vol. 16, No. 3 (2010): 390–400.
  13. Zhou, J.S. and H.S. Gill. “Immunostimulatory probiotic Lactobacillus rhamnosus HN001 and Bifidobacterium lactis HN019 do not induce pathological inflammation in mouse model of experimental autoimmune thyroiditis”. International Journal of Food Microbiology Vol. 103, No. 1 (2005): 97–104.
  14. Hadithi, M., et al. “Coeliac disease in Dutch patients with Hashimoto’s thyroiditis and vice versa”. World Journal of Gastroenterology Vol. 13, No. 11 (2007): 1715–1722.
  15. Chen, X., et al. “Effect of excessive iodine on immune function of lymphocytes and intervention with selenium”. Journal of Huazhong University of Science and Technology. Medical Sciences Vol. 27, No. 4 (2007): 422–425.
  16. Fasano, A. “Zonulin, regulation of tight junctions, and autoimmune diseases”. Annals of the New York Academy of Sciences Vol. 1258 (2012): 25–33.
  17. Drago, S., et al. “Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines”. Scandinavian Journal of Gastroenterology Vol. 41, No. 4 (2006): 408–19.
  18. Fasano, A. “Leaky gut and autoimmune disease”. Clinical Reviews in Allergy & Immunology Vol. 42, No. 1 (2012): 71–78.
  19. Mazokopakis, E.E., et al. “Effects of 12 months treatment with l-selenomethionine on serum anti-TPO levels in patients with Hashimoto’s thyroiditis”. Thyroid Vol. 17, No. 7 (2007): 609–612.
  20. Xu, J., et al. “Supplemental selenium alleviates the toxic effects of excessive iodine on thyroid”. Biological Trace Element Research Vol. 141, No. 1–3 (2011): 110–118.
  21. Xue, H., et al. “Selenium upregulates CD4+CD25+ regulatory T cells in iodine-induced autoimmune thyroiditis model of NOD.H-2h4 mice”. Endocrine Journal Vol. 57, No. 7 (2010): 595–601.
  22. Contempre, B., et al. “Effect of selenium supplementation in hypothyroid subjects of an iodine and selenium deficient area: the possible danger
  23. of indiscriminate supplementation of iodine-deficient subjects with selenium”. The Journal of Clinical Endocrinology and Metabolism Vol. 73, No. 1 (1991): 213–215.
  24. Chong, W., et al. “[Multifactor analysis of relationship between the biological exposure to iodine and hypothyroidism]” (article in Chinese). Zhonghua Yi Xue Za Zhi Vol. 84, No. 14 (2004): 1171–1174.
  25. Tong, Y.J., et al. “[An epidemiological study on the relationship between selenium and thyroid function in areas with different iodine intake]” (article in Chinese). Zhonghua Yi Xue Za Zhi Vol. 83, No. 23 (2003): 2036–2039.

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