Oh my gosh, listening to him was like hearing fingernails on a blackboard. How annoying! I have to counter with Dr. Abraham's article on Autoimmune Thyroiditis.
Facts about Iodine and Autoimmune Thyroiditis
by Guy E. Abraham, MD
Since the 2006 publication by Tang, et al,1 reporting a positive association between iodization of salt in China and autoimmune thyroiditis (AIT), I have received a lot of calls and e-mails questioning the use of iodine in patients with autoimmune thyroiditis. Iodophobes were elated with this publication, which vindicated their iodophobic viewpoint. However, a year later in 2007, the same authors, using the same data2 retracted their original statement and concluded that: “Chronic iodine excess does not apparently increase the risk of autoimmune thyroiditis.”
In 1912, pathologist H. Hashimoto published in a German medical journal,3 his histological findings in four thyroid glands removed at surgery: numerous lymphoid follicles; extensive connective tissue formation; diffuse round cell infiltration; and significant changes of the acinar epithelium. He called this pathology of the thyroid “struma lymphomatosa”, but it became popular under the name “Hashimoto thyroiditis”. At the time of Hashimoto’s publication, autoimmune thyroiditis was not observed in the US population until the iodization of salt. Hashimoto’s thyroiditis is now classified as goitrous AIT because the gland is enlarged, in distinction to atrophic AIT where atrophy and fibrosis are predominant. Both conditions are chronic, progressing over time to hypothyroidism in a significant percentage of patients.4
In several communities worldwide, an increased incidence of AIT was reported following implementation of iodization of sodium chloride.5 In areas of the US where this relationship has been studied, mainly in the Great Lakes Region, a similar trend was reported. In 1966 and 1968, Weaver, et al,6,7 from Ann Arbor, Michigan reported: “The salient histopathological feature of the thyroid glands, removed at operation in a five-year period before iodine prophylaxis (1915-1920), was the paucity of lymphocytes in their parenchyma and, more importantly, the absence of thyroiditis of any form … It should be emphasized that the thyroid glands prior to the use of iodized salt were devoid of lymphocytes, and nodular colloid goiters with dense lymphocytic infiltrates were found after the introduction of iodized salt in 1924.”
Furszyfer, et al,8 from the Mayo Clinic, studied the average annual incidence of Hashimoto’s thyroiditis among women of Olmsted County, Minnesota, during three consecutive periods covering 33 years of observation, from 1935 to 1967. They found the incidence to be higher in women 40 years and older versus women 39 years and younger. However, in both groups, there was a progressive increase in the incidence of Hashimoto’s thyroiditis over time. During the three periods evaluated — 1935-1944; 1945-1954; 1955-1967 — the average annual incidence of Hashimoto’s per 100,000 population were 2.1, 17.9, and 54.1 for women 39 years and less. For women 40 years and older, the average annual incidence over the same three periods were 16.4, 27.4, and 94.1.
It is important to point out that the Mayo Clinic study started 10-15 years after implementation of iodization of salt in the area. Therefore, even during the first decade of observation, the prevalence of AIT was already significant. Again, it must be emphasized that prior to the implementation of iodized salt as observed by Weaver, et al,6,7 this pathology of the thyroid gland was not reported in the US, even though Lugol solution and potassium iodide were used extensively in medical practice at that time in daily amounts two orders of magnitude greater than the average intake of iodide from table salt.4 This suggests that inadequate iodide intake aggravated by goitrogens, not excess iodide, was the cause of this condition. To be discussed later, AIT cannot be induced by inorganic iodide in laboratory animals unless combined with goitrogens, therefore inducing iodine deficiency.
The pathophysiology of AIT is poorly understood. Experimentally induced autoimmune thyroiditis in laboratory animals by acutely administered iodide required the use of antithyroid drugs, essentially goitrogens, to produce these effects.9-12 These goitrogens induced thyroid hyperplasia and iodide deficiency. Antioxidants either reduced or prevented the acute iodide-induced thyroiditis in chicks13 and mice.14 Bagchi, et al,13 and Many, et al,14 proposed that the thyroid injury induced by the combined use of iodide and goitrogens occurs through the generation of reactive oxygen species.
We have previously proposed a mechanism for the oxidative damage caused by low levels of iodide combined. with antithyroid drugs:2 Inadequate iodide supply to the thyroid gland, aggravated by goitrogens, activates the thyroid peroxydase (TPO) system through elevated TSH, low levels of iodinated lipids, and high cytosolic free calcium, resulting in excess production of H2O2. The excess H2O2 production is evidenced by the fact that antioxidants used in Bagchi’s experiments did not interfere with the oxidation and organification of iodide and therefore neutralized only the excess oxidant.11 This H2O2 production is above normal due to a deficient feedback system, caused by high cytosolic calcium due to magnesium deficiency and low levels of iodinated lipids which requires for their synthesis iodide levels two orders of magnitude greater than the RDA for iodine.4 Once the low iodide supply is depleted, TPO in the presence of H2O2 and organic substrate reverts to its peroxydase function, which is the primary function of haloperoxydases, causing oxidative damage to molecules nearest to the site of action: TPO and the substrate thyroglobulin (Tg). Oxidized TPO and Tg elicit an autoimmune reaction with production of antibodies against these altered proteins with subsequent damage to the apical membrane of the thyroid cells, resulting in the lymphocytic infiltration and in the clinical manifestations of Hashimoto’s thyroiditis. Eventually, the oxidative damage to the TPO results in deficient H2O2 production. Hypothyroidism occurs in AIT when oxidation and organification of iodide in the thyroid gland become deficient enough to affect synthesis of thyroid hormones.
In vitro studies with purified fractions of calf thyroid glands by De Groot, et al,15 gave compelling evidence that iodide at 10-5 molar confers protection to TPO against oxidative damage. To achieve peripheral levels of 10-5 molar iodide, a human adult needs a daily amount of 50-100 mg. DeGroot’s findings can be summarized as follows:
• TPO is inactivated by H2O2.
• KI at 10-5 molar protects TPO from oxidative damage.
• Potassium bromide and potassium fluoride do not share this protective effect of KI.
• The protective effect of KI is not due to the covalent binding of iodine to TPO but due to the presence of KI itself in the incubation media.
The concentrations of iodine measured in the thyroid of patients with AIT are the lowest observed. Further, AIT patients with hypothyroidism have significantly lower iodine levels in the thyroid gland than AIT patients with normal thyroid function. For the US population, Okerlund16 reported a mean value of around 10 mg iodine/ thyroid, with a range of 4-19 mg. In 56 patients suffering from autoimmune thyroiditis, but with normal thyroid function, a mean value of 4.8 mg/thyroid was reported. In 13 patients with autoimmune thyroiditis and hypothyroidism, the mean value was 2.3 mg/thyroid.
Based on the above facts, it is obvious that iodine deficiency, not excess, is the cause of AIT.
1) Teng, et al. “Effect of iodine intake on thyroid disease in China.” New England Medical Journal, 2006; 354:2783-93.
2) Yang F, et al. “Chronic iodine does not increase the incidence of hyperthyroidism: A prospective community-based epidemiological survey in China.” Eur J Endocrinol, 2007; 156(4):403-8.
3) Hashimoto H. “Zur Kenntniss der lymphomatosen Veranderung der Schilddruse (Struma lymphomatosa).” Arch Klin Chir, 1912; 97:219-248.
4) Abraham GE. “The safe and effective implementation of orthoiodosupplementation in medical practice.” The Original Internist, 2004; 11(1):17-36.
5) Gaitan E, Nelson NC, and Poole GV. “Endemic goiter and endemic thyroid disorders.” World J Surg, 1991; 15:205-215.
6) Weaver DK, Batsakis JG, and Nishiyama RH. “Relationship of iodine to ‘lymphocytic goiters.’” Arch Surg, 1968; 98:183-186.
7) Weaver DK, Nishiyama RH, et al. “Surgical thyroid disease.” Arch Surg, 1966; 92:796-801.
8) Furszyfer J, Kurland LT, et al. “Hashimoto’s thyroiditis in Olmsted County, Minnesota, 1935 through 1967.” Mayo Clin Proc, 1970; 45:586-596.
9) Weetman AP. “Chronic autoimmune thyroiditis.” In: Werner & Ingbar’s The Thyroid. Braverman LE and Utiger RD, editors. Lippincott Williams & Wilkins, 2000; 721-732.
10) Follis RH. “Further observations on thyroiditis and colloid accumulation in hyperplastic thyroid glands of hamsters receiving excess iodine.” Lab Invest, 1964; 13:1590-1599.
11) Belshaw BE and Becker DV. “Necrosis of follicular cells and discharge of thyroidal iodine induced by administering iodide to iodine-deficient dogs.” J Clin Endocr Metab, 1973; 13:466-474.
12) Mahmoud I, Colin I, et al. “Direct toxic effect of iodine in excess on iodine-deficient thyroid gland: epithelial necrosis and inflammation associated with lipofuscin accumulation.” Exp Mol Pathol, 1986; 44:259-271.
13) Bagchi N, Brown TR, and Sundick RS. “Thyroid cell injury is an initial event in the induction of autoimmune thyroiditis by iodine in obese strain chickens.” Endocrinology, 1995; 136:5054-5060.
14) Many MC, Papadopoulaous J, et al. “Iodine-induced cell damage in mouse hyperplastic thyroid is associated to lipid peroxidation.” In: Progress in Thyroid Research. Gordon A, Gross J, and Hennenian G, editors. Proceedings of the 10th International Thyroid Conference. Balkema, Rotterdam, 1991; 635-638.
15) DeGroot Leslie J, et al. “Studies on an iodinating enzyme from calf thyroid.” Endocrinology, 1965; 76:632-645.
16) Okerlund MD. “The clinical utility of fluorescent scanning of the thyroid.” In: Medical Applications of Fluorescent Excitation Analysis. Kaufman and Price, editors. CRC Press, Boca Raton, Florida, 1979; 149-160.
I used to have a problem with Mg, but not Vit C. Eventually looked at it from the other direction -- not that taking Mg caused diarrhea, but what else might cause diarrhea if Mg were not artificially low and causing a balancing constipation. Came up with candida and/or lack of beneficial flora. I did not know then about the candida/Hg connection. I found I could take one Trenev Trio probiotic per day, and the diarrhea stopped. However, it's made with sunflower oil, and soon my sinuses were completely blocked, so I switched to Culturelle. Two a day also kept the diarrhea in check, and I could take the Mg (and Vit C) I wanted. A solution while I work on the bigger problem, candida & Hg.
I know, I'm always curious, too. My last two fillings have been gone for 2 years. I've stayed steady with about 400 mg Iodoral/SSKI. Currently on 200 mcg selenium, but have taken as much as 1500 mcg until my stock was full. Several years ago I knew I'd topped out at 800 mcg when I started smelling really garlicky. Then I didn't take it for awhile. This time, what with all the detox and balancing with iodine, I never smelled garlic, but my sleep got more restless than usual, and reducing the selenium fixed that. Thinking about it attaching to mercury to usher it out makes me want to be sure selenium is topped off. As for the ALA, I've been taking 300 mg time-released for 14 months. Since I wasn't sure this would have an effect for mercury reduction, I took it at least to support my liver. Hubby had good results with it, and I hoped it would help me as well. Time for a blood test soon.