Health Salon

Your Source for Cutting Edge Information in Alternative Health Care thats hard to find.

  • Subscribe

    • AddThis Feed Button


Iodine Research

17th September 2007 by Arrow Durfee Posted in Uncategorized


Iodine is essential for the formation of thyroid hormone and a deficiency will cause goiter and primary hypothyroidism. In countries where iodine is deficient in the soil, rates of hypothyroidism and goiter from iodine deficiency are very high. In developed countries, however, because iodine is added to salt, iodine deficiencies are rare. It’s possible to get iodine deficient, but it takes work. You would have to eat non-iodized salt, stay away from processed foods, and not eat iodine rich foods like seafoods.

However, there may be interactions between eating certain foods and marginal iodine deficiency which could lead to goiter and hypothyroidism. The following study indicates that this might happen with high consumption of soybeans (or other beans) which are known to be high in copper.

This study shows that both defatted soybean consumption and iodine deficiency decrease thyroid hormone production and cause an increase in thyroid gland size. However there is a very significant synergism between soybean consumption and iodine deficiency. Look at the thyroid gland weights. While iodine deficiency caused a doubling of thyroid gland weight (from 8.4 to 15.5), iodine deficiency combined with soy intake caused the weight to nearly increase 10-fold!! (from 8.4 to 81.7).

Carcinogenesis 2000 Apr;21(4):707-13

Dramatic synergism between excess soybean intake and iodine deficiency on the development of rat thyroid hyperplasia.

Ikeda T, Nishikawa A, Imazawa T, Kimura S, Hirose M

Division of Pathology, National Institute of Health Sciences,1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan.

The effects of defatted soybean and/or iodine-deficient diet feeding were investigated in female F344 rats. Rats were divided into four groups, each consisting of 10 animals, and fed basal AIN-93G diet in which the protein was exchanged for 20% gluten (Group 1), iodine-deficient gluten (Group 2), 20% defatted soybean (Group 3) and iodine-deficient defatted soybean (Group 4). At week 10, relative thyroid gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 2 (15.5 +/- 1.3) and 4 (81.7 +/- 8.6) than in Group 1 (8.4 +/- 2.0) and pituitary gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 3 (9.1 +/- 0. 6) and 4 (9.7 +/- 1.5) than in Group 1 (6.5 +/- 1.5). Serum biochemical assays revealed thyroxine to be significantly (P < 0.05) lower in Groups 2 and 4 than in Group 1. On the other hand, serum thyroid-stimulating hormone (TSH) was significantly (P < 0.01) higher in Groups 3 and 4 than in Group 1. This was particularly striking for TSH (ng/ml) at week 10 in Group 4 (126 +/- 11) as compared with Groups 1 (4.36 +/- 0.30), 2 (4.84 +/- 0.80) and 3 (5. 78 +/- 0.80). Histologically, marked diffuse follicular hyperplasia of the thyroid was evident in Group 4 rats. Proliferating cell nuclear antigen labeling indices (%) were significantly higher (P < 0.05) in Groups 2 (4.8 +/- 2.5) and 4 (13.2 +/- 1.1) than in Group 1 (0.4 +/- 0.5). Ultrastructurally, severe disorganization and disarrangement of mitochondria were apparent in thyroid follicular cells of Group 4. In the anterior pituitary, dilated rough surfaced endoplasmic reticulum and increased secretory granules were remarkable in this group. Our results thus strongly suggest that dietary defatted soybean synergistically stimulates the growth of rat thyroid with iodine deficiency, partly through a pituitary-dependent pathway.

Here is the rough file:

Eur J Endocrinol 2000 Oct;143(4):485-91

Comparative study of thyroid function and types of thyroid dysfunction in two areas in Denmark with slightly different iodine status.

Knudsen N, Bulow I, Jorgensen T, Laurberg P, Ovesen L, Perrild H.

Department of Internal Medicine I, Bispebjerg Hospital, DK 2400, Copenhagen, Denmark.

OBJECTIVE: The pattern of thyroid dysfunction seems to depend on the iodine status of the population. Prevalence of thyroid dysfunction could be a parameter to consider when evaluating iodine deficiency disorders in a population. DESIGN: Comparative cross-sectional investigation in two regions in Denmark with marginally different iodine excretion. METHODS: A random selection of 4649 participants from the Civil Registration System in Denmark in age groups between 18 and 65 years were examined. Thyroid dysfunction was evaluated from blood samples and questionnaires, and compared with results from ultrasonography. RESULTS: Median iodine excretion was 53 microg/l inAalborg and 68 microg/l in Copenhagen. Previously diagnosed thyroid dysfunction was found with the same prevalence in the regions. Serum TSH was lower in Aalborg than in Copenhagen (P=0. 003) and declined with age in Aalborg, but not in Copenhagen. Not previously diagnosed hyperthyroidism was found with the same overall prevalence in the regions, but in age >40 years hyperthyroidism was more prevalent in Aalborg (1.3 vs 0.5%, P=0.017). Not previously diagnosed hypothyroidism was found more frequently in Aalborg (0.6 vs 0.2%, P=0.03). Hyperthyroidism was more often associated with macronodular thyroid structure at ultrasound in Aalborg and hypothyroidism was more often associated with patchy thyroid structure in Copenhagen. CONCLUSIONS: Significant differences in thyroid dysfunction were found between the regions with a minor difference in iodine excretion. The findings are in agreement with a higher prevalence of thyroid autonomy among the elderly in the most iodine-deficient region.

J Clin Endocrinol Metab 2000 Apr;85(4):1513-7

The changing incidence and spectrum of thyroid carcinoma in Tasmania (1978-1998) during a transition from iodine sufficiency to iodine deficiency.

Burgess JR, Dwyer T, McArdle K, Tucker P, Shugg D.

Department of Diabetes and Endocrine Services, Royal Hobart Hospital, Australia.

Exposure to ionizing radiation, changing levels of iodine nutrition, and increased pathologic diagnosis of clinically unimportant thyroid neoplasia have all been proposed as explanations for a worldwide rise in the incidence of thyroid carcinoma (TC) over the past 6 decades. Tasmania is geographically an area of endemic iodine deficiency. In this report, we describe the spectrum of TC in a population averaging 450,000 persons during a 21-yr period that spans the communities transition from iodine sufficiency to iodine deficiency after discontinuation of universal iodine prophylaxis in the mid 1980s. The Tasmanian Cancer Register was used to ascertain all cases of TC diagnosed in Tasmania between 1978 and 1998. Histopathological and demographic data were reviewed. A total of 289 cases of TC were identified. Papillary TC (PTC), follicular TC, medullary TC, and other species accounted for 62%, 23%, 4%, and 11% of cases, respectively. The age standardized incidence rate for total TC increased from 2.45 to 5.33 per 100,000 for females and 0.75 to 1.76 per 100,000 for males between 1978 and 1984 and 1992 and 1998, respectively. A rise in the incidence of PTC by 4.5-fold (P < 0.05) in females and 2.1-fold in males (not significant) was the dominant change over this period. In parallel, the proportion of follicular TC relative to PTC fell from 0.35 to 0.17 during these years (P < 0.05). The rise in PTC incidence was, in part, due to an increase in the occurrence of tumors 1cm or less in diameter. Nonetheless, a 3-fold rise in incidence of larger lesions was also observed during the study period. Forty-three (24%) PTC cases had multifocal disease, 17 (40%) of whom had bilateral tumors. Familial (autosomal dominant) PTC was identified in nine (5%) total PTC cases. Prior studies have linked iodine prophylaxis to a rise in the proportion of differentiated TC, particularly PTC. Our data suggest a complex relationship between iodine nutrition and thyroid tumorigenesis. Factors such as a long latency between changes in iodine nutrition and thyroid tumorigenesis, a dose threshold for the effect of iodine nutrition on thyroid tumorigenesis, and an interaction between iodine nutrition and thyroidal sensitivity to ionizing radiation may all play a role.

Iodine deficiency leads to a decrease in the activity of deiodinase enzyme and consequently to lower levels of T3. selenium--high intake does not lead to high D-I.doc

"Inhabitants of many severe endemic goiter areas have low serum T4 and high circulating TSH, despite normal levels of T3. This situation may be produced experimentally chronically feeding rats a low iodine diet (LID). We fed rats a Remington-type LID and gave them 1% NaClO4 in their drinking water for 2 days. After this, the animals were divided into three groups. One group was fed LID, supplemented with 5 micrograms I/ and was used as the control group. Another group was fed LID alone. The third group was fed LID and given 1% NaClO4 to drink. The latter treatment was used to induce severe hypothyroidism. Animals were killed 1, 2, 3, and 5 weeks after the onset of these treatment schedules. The following measurements were made on some or all groups of animals: body and thyroid weights; thyroidal I content; soluble labeled iodoprotein profile; thyroidal labeled iodoamino acid distribution pattern; plasma T4, T3, and TSH; pituitary GH content; and liver intramitochondrial alpha-glycerophosphate dehydrogenase and cytosolic malic enzyme activities. T4 and T3 concentrations were also measured in liver nuclei of the animals killed 5 weeks after the onset of treatment. As assessed from various indices of thyroid function, the LID rats became iodine deficient, although not as markedly as those given LID and ClO4-, The plasma T4 decreased to undetectable levels, and plasma TSH increased, whereas circulating T3 remained normal throughout in the LID rats. In rats given LID and ClO4-, plasma T4 decreased sooner than in rats given LID alone; plasma T3 levels also became undetectable, and TSH increased more markedly and sooner than in rats given LID alone. As measured at the end of 5 weeks of treatment, pituitary GH content, and liver alpha-glycerophosphate dehydrogenase and malic enzyme activities were lower in rats given LID than in the euthyroid LID- and I--treated controls. They were not, however, as markedly reduced as in the severely hypothyroid LID- and ClO4--treated rats. In spite of normal plasma T3 levels, the concentration of T3 in liver nuclei of the rats given LID alone was significantly lower than that of the LID- and I--treated controls. The results show that the thyrotrophs, somatotrophs, and livers of rats given LID alone are not like those of euthyroid rats despite normal circulating T3 levels. In iodine-deficient rats, there is a discrepancy between the measured indices of thyroid hormone action in the liver and the circulating T3 level, but not between biological activity and liver nuclear T3 concentration. It remains to be seen whether the same is true in the anterior pituitary." iodine deficient rats.doc

Three patients with subclinical hyperthyroid goitre, women aged 63, 72 and 75 years following intravenous administration of an iodinated contrast medium developed hyperthyroidism with a marked rise of the concentration of free T4. Thyreostatic agents were unsuccessful in two patients, the third was left untreated. Hyperthyroidism improved spontaneously in all three. Iodine-induced hyperthyroidism is rare and is usually encountered in patients with a pre-existent autonomous thyroid function. Treatment of iodine-induced hyperthyroidism is essentially exclusively symptomatic. Prophylaxis with sodium perchlorate should be considered in cardiac patients with a goitre and a subnormal level of thyroid-stimulating hormone (TSH). iodine induced hyperT.doc

The high prevalence of goiter and hyperthyroidism with low prevalence of hypothyroidism probably resulted from the combined effects of food goitrogens and iodine deficiency in Ethiopia, with the latter playing only a minor role. Neither factor was in effect after arrival in Israel. Genetic and hormonal factors may contribute to the low prevalence of both goiter and hypothyroidism in the adult males. In view of the high prevalence of hyperthyroidism, iodine enrichment is not recommended for Ethiopian immigrants. iodine enrichment in goitrous people can lead to hyperT.doc

In areas with relatively high iodine intake, the incidence rate of hypothyroidism is several-fold higher than that of hyperthyroidism. Recently, we found a similarly high prevalence rate of subclinical hypothyroidism compared with hyperthyroidism in a high iodine intake area, while a relatively low prevalence of subclinical hypothyroidism was observed in a low iodine intake area. In the present study we compared the incidence rate (newly diagnosed in primary care and at hospital) of overt hypothyroidism with that of hyperthyroidism in a well-defined geographical area in Jutland, Denmark, with an iodine intake around 60 microg/day. The number of personsxyears studied was 569,108. Data on hyperthyroidism have been published previously. The overall incidence of hypothyroidism was 13.5/100,000 per year (F/M 22.9/3.6), hyperthyroidism 38.7/100.000 per year (F/M 63.0/13.0). The incidence of hypothyroidism was steadily increasing with age up to 80/100,000 per year in subjects older than 70 years of age, but apart from congenital hypothyroidism it was lower than that of hyperthyroidism at all ages. The majority of patients (79%) was diagnosed to have spontaneous autoimmune hypothyroidism (16% with goiter, 84% with no thyroid visible or palpable). In conclusion, in an area with moderately low iodine intake, hypothyroidism was considerably less common than hyperthyroidism. This is in contrast to findings in high iodine intake areas. The iodine intake of an area seems to be of major importance for the pattern of thyroid disorders observed.iodine low in soil--hypoT low and hyperT high.doc

Groups of 6-wk-old male F344/NCr rats received a single i.v. injection of either vehicle or N-nitrosomethylurea (Cas: 684-93-5) (MNU) at a dose of 41.2 mg/kg body weight. Two wk later, groups of rats were placed on iodine-deficient, iodine-adequate, or commercial (Wayne Lab Blox) diets, or one of these diets and without previous MNU injection. Animals were sacrificed at either 52 or 77 wk, or when they became moribund. Carcinogen-treated rats on the iodine-deficient diet for up to 52 wk had significantly increased thyroid gland weights and increased incidences of both thyroid follicular cell carcinoma (90%) and diffuse pituitary thyrotroph hyperplasia (90%) at 52 wk. The majority of the follicular carcinomas were transplantable and invasive into the mammary fat pad of weanling F344/NCr rats. No other tumors induced by MNU were affected by the iodine-deficient diets. Rats fed the iodine-deficient diet without MNU injection had a 40% incidence of thyroid follicular adenomas at 52 wk and 60% at 77 wk, and a 10% incidence of follicular carcinomas at 77 wk. Thus this experiment provided evidence that the iodine-deficient diet is a potent promoter of thyroid tumors initiated by MNU and carcinogenic by itself. In addition, pituitary tumors were found in 29 of the 58 rats treated with the carcinogen alone, compared to only 3 of the 20 rats in the control groups. The vast majority of these pituitary tumors contained prolactin that was demonstrable by the avidin:biotin:peroxidase complex immunocytochemical technique.iodine deficiency contributes to thyroid cancer.doc

About 90% of all functional thyroid autonomies (FTA) are euthyroid for a prolonged period of time. It is estimated that more than 10% of goiter patients in iodine deficient regions and less than 10% in iodine rich areas have evidence of FTA. After the age of 40, the risk of hyperthyroidism decompensation gradually increases. This risk rises with increasing thyroid volume, nodularity and patient age. In the elderly, hyperthyroidism also occurs in the absence of goiter. After decades of iodine deficiency, especially the intake of unphysiologically high iodine concentrations may result in increased frequencies of hyperthyroidism. In iodine deficient regions, almost half of all cases of hyperthyroidism are FTA related. Following elimination of iodine deficiency, the rate of hyperthyroidism may be reduced below 10%. This will not affect the prevalence of immunogenic hyperthyroidism.iodine can cause hyperT in iodine deficient populations.doc

JJ: There is literature suggesting that an iodine deficiency can lead to thyroid cancer. Research this because hypers who control their hyperT by iodine restriction might be subject to this risk.

A cross-sectional study in two stages consisted of healthy children to assess the effect of iodine supplementation on a pediatric population with mild iodine deficiency in an ongoing program in the Province of Pontevedra, northwestern Spain. In the first survey (1984), 1565 schoolchildren and in the second survey (1995) 907 schoolchildren were randomly selected from the population. In January 1985, a mandatory consumption of iodized salt in our region was begun. In both surveys we studied prevalence of goiter, urinary iodine excretion, and prevalence of thyroid dysfunction. Similar prevalences of goiter were observed in both surveys, 3.7% versus 3.9%; however, significantly lower prevalence of Ib and II degree goiters were observed in the second survey. The mean iodine excretion was 88.6 +/- 73 microg/L (median 66.3) and 146.4 +/- 99 microg/L (median 115.7), p < 0.01 for the first and second surveys, respectively. Finally, the overall prevalence of thyroid dysfunction was similar in both surveys, 9.2% versus 7.0%; however, significantly lower prevalence of suppressed serum thyrotropin (TSH), considered as a marker of subclinical hyperthyroidism, was observed in the second survey when compared to the first, 0.1% versus 2%, p < 0.01. Our results are in agreement with the recent data from Denmark, where the prevention of subclinical hyperthyroidism occurring in the elderly as a consequence of longstanding mild iodine deficiency is the reason that the Danish finally started iodine supplementation on a national basis. In conclusion, long-term correction of mild iodine deficiency in a pediatric population has beneficial effects on the prevalence of high-degree goiters, and this correction reduces significantly the prevalence of subclinical hyperthyroidism. The present observation constitutes a strong argument for correcting even mild iodine deficiency.iodine supplementation reduces rate of hyperT.doc

To evaluate the importance of trace amounts of elements in thyroid cancer etiology and diagnostics, instrumental neutron activation analysis has been used to estimate Ag, Co, Cr, Fe, Hg, I,Rb, Sb, Sc, Se, and Zn concentrations in malignant and benign thyroid nodules as well as in apparently intact paranodular thyroid tissue. Resected material from 135 patients was obtained from operations. Forty-five cancer cases were diagnosed and the rest were of benign nodules. The thyroid glands of 65 people, 53 male and 12 female, who died and unexpected death or committed suicide, were used as a control group. Trace element contents of the International Atomic Energy Agency reference material H-4 (animal muscle) were analysed simultaneously with the thyroid tissue in order to evaluate the accuracy of the obtained data. No dependence of trace element contents on sex and age (14-80 years) was found for normal thyroids. In paranodular tissue, the Ag, Co, Hg, I and Rb contents were much higher for malignant and benign nodules than they were for the standard. There was also a slight deficiency of Se in the nodules compared with the standard. This result supports the hypothesis that the direct toxic heavy metal influence on thyrocytes plays a major role in thyroid cancer etiology, provided that an adequate level of the defence mechanisms is absent. Iodine concentrations are 15 times lower, on average, in malignant compared with benign nodules. It is also shown that the radio between the iodine concentration in nodular and paranodular tissue can be used for in vivo thyroid cancer diagnostics.iodine low in thyroid cancer.other elements.doc

Geographical distribution patterns of incidence and mortality for a wide variety of diseases display strong positive and negative correlations when analyzed statistically. It is argued that these relationships do not occur by chance, but reflect the causal role of surpluses and/or deficiencies of various bulk and trace elements. This concept is explored for one such "disease family tree", that of iodine. Deficiencies of this essential trace element appear to be associated with many diseases, or birth defects, including goitre, cretinism, multiple sclerosis, amyotrophic lateral sclerosis and cancer of the thyroid and nervous system. Although the evidence is weaker, iodine deficiency may also be implicated in Alzheimer's and Parkinson's diseases. In contrast, too much iodine may be linked to elevated mortality from cancer of the skin and melanoma. Rat studies indicate that iodine deficiencies can cause reduced brain weight, limited myelin formation, retarded neuronal maturation, a lowering of the production of various enzymes and slowing of the rates of protein and R.N.A. synthesis. Similar processes appear to occur in many of the diseases identified above.iodine--diseases of deficiency and excess.doc

In view of the adverse effects of the administration of pharmacological quantities of iodine to euthyroid patients with a history of a wide variety of thyroid disorders, it has been suggested that iodine-containing medications and radioopaque dyes containing iodine should be avoided, if possible, in patients with underlying thyroid disease. We have now prospectively studied the effects of pharmacological doses of a saturated solution of potassium iodide (SSKI) on thyroid function in euthyroid patients with a previous history of hyperthyroid Graves' disease successfully treated with antithyroid drugs. Ten euthyroid women (mean age, 56 yr) who had hyperthyroid Graves' disease successfully treated with methimazole 36.4 +/- 4.7 months earlier were evaluated before, during, and after the administration of 10 drops SSKI daily for 90 days. The following thyroid function tests were obtained: serum T4, T3, TSH, TSH receptor antibody (TSH-RAb), and antithyroid peroxidase antibody (AbTPO) concentrations; TRH tests; and iodine perchlorate discharge tests. Serum T4, T3, basal and TRH-stimulated TSH, and TSH-RAb values were normal before SSKI administration, but serum AbTPO levels were markedly positive in 7 and iodine perchlorate discharge tests were positive in 4 of these 10 women. During SSKI administration, basal and TRH-stimulated serum TSH values increased above normal in 2 women with normal serum T4 and T3 concentrations; thyroid hormone values and TRH tests were normal in the other 8 patients and similar to values observed in 4 euthyroid women without a history of thyroid disease given SSKI. Serum AbTPO increased slightly, but significantly, during SSKI administration in the 7 women with positive values at baseline (P < 0.05). TSH-RAb remained undetectable. After SSKI withdrawal, the 10 women were reevaluated 60 and 120 days later. Two women developed a blunted TSH response to TRH, but normal serum T4 and T3 concentrations, and 2 women developed overt hyperthyroidism, with undetectable basal and TRH-stimulated serum TSH and elevated serum T4 and T3 concentrations, requiring methimazole therapy. All values in the remaining 6 women were similar to those present before SSKI administration. These results suggest that some euthyroid patients with a history of antithyroid drug therapy for Graves' disease may develop thyroid dysfunction during and after excess iodine administration. The development of subclinical hypothyroidism during SSKI administration was not clinically important, but the occurrence of overt hyperthyroidism after SSKI was discontinued did require antithyroid drug therapy. It is advisable, therefore, to avoid iodine-containing substances in euthyroid patients with a history of antithyroid drug therapy for Graves' disease.iodine effects in pts previously treated with ATD for Graves.doc

To evaluate the importance of trace amounts of elements in thyroid cancer etiology and diagnostics, instrumental neutron activation analysis has been used to estimate Ag, Co, Cr, Fe, Hg, I,Rb, Sb, Sc, Se, and Zn concentrations in malignant and benign thyroid nodules as well as in apparently intact paranodular thyroid tissue. Resected material from 135 patients was obtained from operations. Forty-five cancer cases were diagnosed and the rest were of benign nodules. The thyroid glands of 65 people, 53 male and 12 female, who died and unexpected death or committed suicide, were used as a control group. Trace element contents of the International Atomic Energy Agency reference material H-4 (animal muscle) were analysed simultaneously with the thyroid tissue in order to evaluate the accuracy of the obtained data. No dependence of trace element contents on sex and age (14-80 years) was found for normal thyroids. In paranodular tissue, the Ag, Co, Hg, I and Rb contents were much higher for malignant and benign nodules than they were for the standard. There was also a slight deficiency of Se in the nodules compared with the standard. This result supports the hypothesis that the direct toxic heavy metal influence on thyrocytes plays a major role in thyroid cancer etiology, provided that an adequate level of the defence mechanisms is absent. Iodine concentrations are 15 times lower, on average, in malignant compared with benign nodules. It is also shown that the radio between the iodine concentration in nodular and paranodular tissue can be used for in vivo thyroid cancer diagnostics.cancer of thyroid and trace elements.doc

In genetically predisposed individuals, autoimmune lymphocytic thyroiditis (LT) is potentiated by excess dietary iodine (I). There have been data which suggest that oxidative stress may have a role in iodine-induced LT. These in vivo studies were undertaken to examine the effect of iodine on intrathyroidal levels of the potent antioxidant glutathione (GSH) and see if the thyroids of LT-prone BB/Wor rats have aberrant GSH responses after iodine-loading. LT-prone BB/Wor, non LT-prone BB/Wor and Wistar rats were randomized to receive either 0.05% I (as Nal) or tap water. Thyroid and liver homogenates were assayed individually for GSH. Following the administration of 0.05% iodine water overnight, all of the animals demonstrated a rise in intrathyroidal GSH regardless of LT-proneness. To determine whether this was a dose-dependent response, Wis rats were randomized to receive tap, 0.0125%, 0.025%, 0.05%, or 0.075% I, overnight. Intrathyroidal GSH levels rose with increasing iodine concentrations peaking at 0.025% I. Hepatic GSH levels were unaltered by iodine treatment. Ten days of 0.05% I water did not result in any difference between the GSH levels of thyroids from treated and control rats. Frozen sections of the thyroids and livers from iodine-treated rats were compared to tap-water controls after staining with Mercury Orange for GSH and Schiff's reagent for evidence of lipid peroxidation. Iodine-treated thyroids had an apparent shift of GSH staining from the apical border to the cytoplasm. However, there was no Schiff's staining indicative of lipid peroxidation in the iodine-treated thyroids.iodine ingestion increases intrathyroidal glutathione.doc

Iodine-induced thyrotoxicosis or "jodbasedow phenomenon" has been reported throughout the world since iodine has been administered to treat endemic goitre. Nowadays, iodinated radiocontrast agents and the antiarrhythmic drug amiodarone are the most common sources of excess iodine load subsequently leading to iodine-induced thyrotoxicosis, especially in elderly patients with underlying goitre. The aim of the study was to identify the number of cases of iodine-induced thyrotoxicosis among patients with thyrotoxicosis in a large urban hospital. Over an 18-month period thyrotoxicosis has been diagnosed in a total of 39 patients. Eight patients with iodine-induced thyrotoxicosis (5 female, 3 male; mean age 60.6 years) have been identified (20%). In all patients with iodine-induced thyrotoxicosis, iodine exposure with a mean iodine dose of 21.5 g was documented 2 to 16 weeks before diagnosis (iodinated radiocontrast agents in 5 patients, amiodarone in 2 patients, kelp tablets in 1 patient). Clinical features were predominantly tachyarrhythmias and heart failure, while 6 of 8 patients had goitre (thyroid volume 31 to 193 ml). Thyroid antibodies were not detected. Diagnosis was confirmed in 5 of 8 patients with increased urinary iodine concentrations (3436 to > 6000 nmol/24 h), and in 3 of 8 patients with a low tracer uptake in thyroid scintigraphy (1 to 4%). Treatment consisted of methimazole in all patients, additional tional beta-blockers and lithium in 4 patients, and prednisone in 5 patients. The mean treatment ment duration was 9.2 months, and patients became euthyroid after a mean treatment duration of 6.4 weeks. One patient (with still elevated free thyroxine levels) died of myocardial infarction 4 weeks after antithyroid drug therapy had been installed. The incidence, mechanisms and features of iodine-induced thyrotoxicosis are discussed. Iodine-induced thyrotoxicosis is a common disease, and the recognition and treatment of iodine-induced thyrotoxicosis, particularly in elderly patients and patients with goitre, are of clinical importance.iodine-induced hyperthyroidism.doc

Iodine is a requisite substrate for the synthesis of the thyroid hormones, the minimum daily requirement being about 50 micrograms. An autoregulatory mechanism within the thyroid serves as the first line of defense against fluctuations in the supply of iodine and also permits escape from the inhibition of hormone synthesis that a very large quantity of iodine induces (Wolff-Chaikoff effect and escape therefrom). Environmental iodine deficiency continues to be a significant public health problem worldwide, compounded in some geographic regions by the presence of other goitrogens in some staple foods. The pathologic consequences of severe iodine deficiency include endemic goiter, endemic cretinism, increased fetal and infant mortality, and an increased prevalence in the community of cognitive and neuromotor disabilities. The implementation of an iodization program prevents endemic cretinism and reduces the frequency of the other pathologic consequences of iodine deficiency. Iodine excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. The pathologic consequences of iodine excess will ensue only when thyroid autoregulation is defective, in that escape from the Wolff-Chaikoff effect cannot occur, or when autoregulation is absent. Defective autoregulation characterizes the fetal and neonatal thyroid, Hashimoto’s thyroiditis, radioiodine or surgically treated Graves’ hyperthyroidism, the thyroid of patients with cystic fibrosis, and the thyroid that has been exposed to weak inhibitors of the organic binding of iodine. In these circumstances, the provision of excess iodine may lead to iodide goiter with or without hypothyroidism. Absent autoregulation may be a feature of longstanding multinodular goiter, and the provision of excess iodine in this circumstance may induce thyrotoxicosis (Jod-Basedow disease). The pathologic consequences of iodine excess will resolve when the source of iodine has been dissipated. In addition to its role in reversing iodine deficiency, iodine is used as adjunctive therapy for hyperthyroidism. By inhibiting the proteolytic release of iodothyronines from thyroglobulin, it induces a prompt slowing of thyroid hormone secretion. This effect is exploited in the treatment of thyrotoxic crisis or severe thyrocardiac disease. Iodine also reduces thyroid cellularity and vascularity and therefore is used in the preparation of the patient for thyroidectomy. Finally, by exploiting the failure of escape from the Wolff-Chaikoff effect, iodine may also be used in the early management of radioiodine-treated Graves’ hyperthyroidism.iodine and thyroid disease.doc

In 1990, iodine deficiency affected almost one-third of the world population and was the greatest single cause of preventable brain damage and mental retardation. Following a resolution adopted by the World Summit for Children in 1990. major programmes of iodine supplementation were implemented by the governments of the affected countries with the support of major donors. Iodisation of salt was recognised as the method of choice. Nine years later, by April 1999, 75% of the affected countries had legislation on salt iodisation and 68% of the affected populations had access to iodised salt. The prevalence of iodine deficiency disorders decreased drastically in most countries and the deficiency disappeared completely in some such as Peru. This result constitutes a public heath success unprecedented with a non-infectious disease. However, occasional adverse effects occurred. The principle effect is iodine-induced hyperthyroidism which occurs essentially in older people with autonomous nodular goitres, especially following iodine intake that is too rapid and of too massive an increment. The incidence of the disorder is usually low and reverts spontaneously to the background rate of hyperthyroidism or even below this rate after 1 to 10 years of iodine supplementation. The possible occurrence of iodine-induced thyroiditis in susceptible individuals has not been clearly demonstrated by large epidemiological surveys. Iodine supplementation is followed by an increased prevalence of occult papillary carcinoma of the thyroid discovered at autopsy but the prognosis of thyroid cancer is improved due to a shift towards differentiated forms of thyroid cancer that are diagnosed at earlier stages. Iodine-induced hyperthyroidism and other adverse effects can be almost entirely avoided by adequate and sustained quality control and monitoring of iodine supplementation which should also confirm adequate iodine intake. Available evidence clearly confirms that the benefits of correcting iodine deficiency far outweigh the risks of iodine supplementation.iodine supplementation–benefits outweight risks.doc

After a cure with iodine in Bad Hall (Upper Austria), patients with age-related maculopathy repeatedly reported improvement in visual power: the picture seen seems to be clearer on the whole or more distinct. These statements were checked in 50 patients with beginning age-related macula degeneration (‘dry form’) using the ‘Vision Contrast test system (VCTS 6500)’. The analysis of the results showed that there is indeed a statistically highly significant improvement in contrast sensitivity after the cure (p < 0.0001). The spontaneous observations of the patients were therefore confirmed by the study. iodine improves macular degeneration.doc

After taking a cure with iodine treatments in Bad Hall (Upper Austria), patients with eye diseases repeatedly report improvements in their color vision. They state that colors are once again "more saturated, richer, and more distinct." These statements were checked using the Farnsworth Panel D-15 dicotomous test and the Lanthony desaturated 15 Hue test. The analysis of the results showed that there is indeed a statistically significant improvement in color vision after the cure. The spontaneous observations of the patients were therefore confirmed by the study.iodine improves color vision.doc

Patients must be assessed for iodine allergy prior to indocyanine green administration. A scrupulous injection technique will ensure a safe diagnostic procedure. 2. Indocyanine green dye is used for choroidal angiography to diagnose age-related macular degeneration. 3. Indocyanine green dye has no discernable after effects for the patient. It is nontoxic and wholly removed by the liver. Indocyanine green does not show up as skin discoloration.iodine dye used for macular degeneration angiography.doc

The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2.5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P < 0.01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P < 0.01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P < 0.01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P < 0.01), fractional turnover rate (P < 0.01), absolute disposal rate (P < 0.05), urinary clearance (P < 0.05) and faecal clearance (P < 0.05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH.iodine antagonized by cadmium.doc

Can J Surg 1993 Oct;36(5):453-60

Iodine replacement in fibrocystic disease of the breast.

Ghent WR, Eskin BA, Low DA, Hill LP

Department of Surgery, Queen's University, Hotel Dieu Hospital, Kingston, Ont.

OBJECTIVE: To determine the response of patients with fibrocystic breast disease to iodine replacement therapy. DESIGN: Review of three clinical studies beginning in 1975: an uncontrolled study with sodium iodide and protein-bound iodide; a prospective, control, crossover study from iodide to molecular iodine; and a prospective, control, double-blind study with molecular iodine. SETTING: University affiliated breast-treatment clinics. PATIENTS: Study 1: 233 volunteers received sodium iodide for 2 years and 588 received protein-bound iodide for 5 years. Study 2: the treatment of 145 patients from study 1 treated with protein-bound iodide for several months who still had symptoms was switched to molecular iodine 0.08 mg/kg; 108 volunteers were treated initially with molecular iodine. Study 3: 23 patients received molecular iodine, 0.07 to 0.09 mg/kg body weight; 33 received an aqueous mixture of brown vegetable dye and quinine. The numbers in study 2 increased over the review period so that 1365 volunteers were being treated with molecular iodine by 1989. INTERVENTIONS: All patients in study 3 had pre- and post-treatment mammography and measurement of serum triiodothyronine, thyroxine and thyroid-stimulating hormone levels. MAIN OUTCOME MEASURES: Subjective evaluation--freedom from pain--and objective evaluation--resolution of fibrosis. RESULTS: Study 1: 70% of subjects treated with sodium iodide had clinical improvement in their breast disease, but the rate of side effects was high; 40% of patients treated with protein-bound iodide had clinical improvement. Study 2: 74% of patients in the crossover series had clinical improvement, and objective improvement was noted in 72% of those who received molecular iodine initially. Study 3: in the treatment group 65% had subjective and objective improvement; in the control group there was a subjective placebo effect in 33% and an objective deterioration of 3%. CONCLUSIONS: The fibrocystic breast reacts differently to sodium iodide, protein-bound iodide and molecular iodine. Molecular iodine is nonthyrotropic and was the most beneficial.

This study basically refers to Thyroiditis, which is an inflammation

of the thyroid gland. I have autoimmune hyperthyroidism (Graves'),

but I have been diagnosed as having "chronic thyroiditis" as well.


(Or go to – and use the “search” feature. Type in

“Linking Iodine with Autoimmune Thyroiditis”)

From another document I obtained:

“The introduction of dietary iodine as a public health measure in

the early twentieth century eliminated endemic goiter in the United

States, but may have spawned another set of problems. The incidence

of autoimmune thyroiditis is increasing concomitantly with

progressively increasing iodine content in the American diet.”

“The effects of high iodine uptake, however, are observed only in

genetically susceptible individuals.”

Carrageenan (sometimes called carragean moss) is ground up seaweed! It’s

also used to do marbling, as it’s useful property is that it thickens. I

should think it’s LOADED with iodine.

Interactions between selenium and iodine
April 27, 1999

Selenium and iodine are two minerals which are critically important in the proper functioning of the thyroid. While the importance of iodine has been known a long time, the importance of selenium has only been discovered and explored since 1990. Much research is presently being conducted on the functions of these two minerals in thyroid function and it is becoming clear that there is an interaction between the two. Iodine has a seemingly simple role in the thyroid-it is incorporated into the thyroid hormone molecule.

A deficiency of iodine will cause hypothyroidism and if this is severe and occurs during pregnancy, the offspring will be mentally damaged and is called a cretin. Cretinism, or myxeodematous cretinism as it is sometimes called, is not only caused by an iodine deficiency, but is also influenced by a selenium deficiency. Iodine apparently has just one function in the body-in the thyroid.

Selenium, on the other hand, performs many functions. At the beginning of the 1990s it was discovered that the deiodinase enzymes which convert T4 (thyroxin, the thyroid prohormone) into T3 (triiodothyronine, the cellularly active hormone) and also convert T3 into T2, thereby degrading it, are selenium enzymes (formed with the amino acid cysteine). This discovery has led to a lot of research studies on the effects of selenium, iodine, and their interactions.

Selenium also performs other important roles in the body. The most important of these is probably as its role as the body’s best antioxidant (anti-peroxidant). It performs this role as part of glutathione peroxidase (GSHPx or GPX). As part of GPX, selenium prevents lipids and fats from being peroxidized (oxidized), which literally means that it prevents fats from going rancid (this can be seen on your skin as “age spots” or “liver spots” (autopsies show that skin “liver spots” are accompanied by similar spots of peroxidized fats in the liver.) Therefore selenium protects all of the cellular membranes, which are made up of fats, from peroxidation. Peroxidation of cellular membranes reduces the ability of the membrane to pass nutrients including minerals and vitamins, so selenium deficiency is the first step toward developing the many problems caused by nutrient deficiencies.

Joel Wallach considers a selenium deficiency combined with high intake of vegetable oils (salad dressings, margarine, cooking oils) as the “quickest route to a heart attack and cancer.” It seems that the body uses a lot of selenium to protect the fats from peroxidation. Polyunsaturated fats which are hydrogenated or heated become the same as rancid fats and large amounts of selenium are then needed to protect the body. Consumption of these dietary fats can thus lead to a selenium deficiency.

Selenium is also essential for the production of estrogen sulfotranserfase which is the enzyme which breaks down estrogen. A deficiency of selenium can thus lead to excessive amounts of estrogen, which may depress thyroid function, and also upset the progesterone-estrogen balance.

Wallach also lists other effects of selenium deficiency: anemia (red blood cell fragility), fatigue, muscular weakness, myalgia (muscle pain), muscular dystrophy (white muscle disease in animals), cardiomyopathy (sudden death in athletes), heart palpitations, irregular heartbeat, liver cirrhosis, pancreatitis, Lou Gehrig’s and Parkinson’s diseases (mercury toxicity), Alzheimer’s Disease (high intake of vegetable oil), sudden infant death syndrome (and possibly “breathlessness” in adults, jj), cancer, multiple sclerosis, and sickle cell anemia.

Selenium is essential for the production of testosterone. A deficiency seems to be involved in osteoarthritis. I’ve found studies linking selenium deficiency to alopecia (hair loss) and to degeneration of the knee joint (seen in Kashin-Beck disease). Since selenium is necessary to produce GPX which is a major detoxifier ofman-made and environmental toxins, selenium deficiency can lead to chemical and drug sensitivities.

These are some of the non-thyroidal effects of selenium deficiency. The effects of selenium deficiency on thyroidal health is even more interesting. One study I read indicated that in experimental animals, selenium deficiency will increase T3 in the heart. This may be the reason that selenium deficiency causes heart palpitations and rapid heart beat, which is common in thyroid disease.

While we’ve seen that selenium deficiency will interfere with T4 to T3 conversion and lead to functional hypothyroidism (low T3 phenomenon), selenium plays another vital role in the thyroid as part of GPX. During the production of thyroid hormone, hydrogen peroxide (H2O2) is produced. H2O2 is important for the production of thyroid hormone, but excessive amounts lead to high production of thyroxin (T4) and also damage to the cells of the thyroid. GPX plays the extremely vital role of degrading H2O2 and thereby limiting hormone production and preventing damage to the thyroid cells. This seems to be the main way in whichselenium protects the thyroid from sustaining damage which can lead ultimately to cancer.

Without selenium, the thyroid gland becomes damaged and it is through this mechanism that the main selenium and iodine interactions are found. An iodine deficiency will cause goiter, an enlargement of the thyroid gland produced by the body in an attempt to increase hormone production from limited amount of iodine. Selenium deficiency increases the weight of the thyroid in experimental animals, and a selenium deficiency combined with an iodine deficiency leads to a further increase in thyroidal weight (bigger goiter). In African countries like Zaire, there are areas where both iodine and selenium are very scarce in the soil (these deficiencies seem to run parallel in most areas). Consequently a high percentage of the people have goiters and hypothyroidism. An experimental attempt was made to correct the selenium deficiency and the result was that the hypothyroidism was made WORSE in the hypos and it produced hypothyroidism in some euthroid subjects. This was entirely unexpected and the experimenters issued a warning about supplementing with selenium (and not iodine) when both deficiencies exist concurrently.

The body has a compensatory mechanism to maintain T3 levels when iodine is deficient–it increases the production of the deiodinase Type I enzyme (DI-I). This is not a small increase, but has been shown in cattle to be an increase of 10-12 times. This increase in ID-I increases the conversion of the existing T4 to T3 to maintain T3 levels, but also increases the conversion of T3 to T2 (the degraded by-product of T3). Because of the iodine deficiency, T4 is not replenished and T3 ultimately decreases from the lack of sufficient T4 leading to a worsening of the hypothyroidism.

This result is made worse by another phenomenon which hasn’t been thoroughly studied: a selenium deficiency causes an iodine deficiency to get worse. This may be a protective adaptation by the body to limit the damage caused to the thyroid when selenium is deficient and iodine is adequate. Let’s examine this part of the interaction.

We’ve all heard that many doctors tell hypo patients, especially those with Hashimoto’s thyroiditis, not to take iodine because it can aggravate their condition. The reason seems to be that selenium protects the thyroid gland from oxidative damage and this damage can increase significantly if iodine is supplemented. Taking iodine will increase thyroid hormone production and the production of H2O2 which damages the thyroidal cells. The lack of selenium prevents GPX from being able to protect the cells from this oxidative damage. While I doubt if most doctors realize why iodine should be restricted (it certainly seemed counter-intuitive to me at first), they have learned through experience that iodine can increase the thyroid damage in Hashimoto’s. The information that selenium should be supplemented along with iodine is so new that most of them are unaware of it.

Here’s what we have: Studies have shown that if iodine is low, selenium must also be kept low to prevent the hypothyroidism from becoming worse (from increased DI-I and T4 depletion, as explained above.) So if both minerals are low, then the person is hypo and gets a goiter, but the damage to the thyroid is kept to a minimum. More severe problems happen when either selenium or iodine is high and the other is low. If selenium is high and iodine low, then T4 to T3 to T2 conversion is accelerated without T4 being replenished, leading to a worsening of the hypoT. If iodine is high and selenium is low, then H2O2 is not degraded by GPX. Since H2O2 drives the thyroid hormone production, then the thyroid over-produces thyroid hormone (Grave’s hyperthyroidism), the thyroid is damaged from the oxidation by the H2O2, and the end result is that the damaged thyroid ultimately decreases activity and hypothyroidism results (Hashimoto’s thyroiditis). This could explain the observed progression of Grave’s to Hashimoto’s.

If a selenium deficiency causes an iodine deficiency, leaving you both selenium and iodine deficient, and supplementing with either selenium or iodine causes severe problems, then the only solution is to supplement both selenium and iodine simultaneously and gradually. Even then you could experience an immediate boost (from increased conversion of T4 to T3) with a subsequent letdown (lack of T4 production because of insufficient iodine or other necessary nutrient). You have to be prepared to ride out the tough times and continue increasing the selenium and iodine until those two deficiencies are corrected and the respective metabolic pathways are back working properly.

Everything that I’ve read about selenium indicates that it is absolutely essential for proper functioning of the thyroid. A deficiency of selenium may lead to either hyperthyroidism or hypothyroidism. I’ve always wondered if high intake of selenium can lead to hyperthyroidism and finally found someone who did the experiment. They found that a high intake of selenium will not increase T4 production and lead to hyperthyroidism.

If a person has hyperT, then it looks like taking selenium without iodine will result in a decrease in production of T4 (although there may be an initial transient increase in T4 to T3 conversion and hence higher T3). I would suggest to start with a small amount of selenium methionine (about 50 mcg) and gradually increase it. I cannot see any way that thyroid function can be normalized without selenium.

For hypos the important message is that a selenium deficiency may cause an iodine deficiency, so that even though you are taking iodine you may not be assimilating it unless selenium is also being taken. This would explain how people can have iodine deficiencies even though salt and many foods have iodine added. Supplement with both iodine and selenium. I would recommend starting with 100 mcg of selenium and one kelp tablet and gradually work up to 400-600 mcg of selenium and 2-4 tablets of kelp.

While I’ve found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.

I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it’s complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected. John

Endocr Regul 2000 Jun;34(2):57-63

Anti-goitrous effect of lecithin-bound iodine in propylthiouracil treated rats.

Matsuzaki S, Ma HT, Burikhanov RB

Department of Biochemistry, Dokkyo University School of Medicine, Mibu, Tochig, Japan.

OBJECTIVE: Excess iodine and some iodine-containing compounds are known to affect various parameters of thyroid function. Lecithin-bound iodine (LBI) is a compound which induces involution of an enlarged thyroid. LBI was tested for its ability to affect thyroid ornithine decarboxylase (ODC) activity and apoptosis. METHODS: LBI was given orally to propylthiouracil-pretreated rats and the changes in ODC activity and apoptosis were observed. The thyroid apoptosis was detected by DNA laddering and flow cytometry. RESULTS: LBI suppressed the thyroid ODC activity within one hour after its administration and lowered slightly but significantly the thyroid putrescine levels at 3 h. The DNA cleavage ladder was evident at 3-6 h after LBI treatment. Propylthiouracil induced thyroid enlargement was reduced significantly at 3 days after chronic treatment with LBI. The thyroidal content of putrescine was also decreased after chronic treatment. These effects of LBI were essentially the same as those of excess iodide, while other iodinated compounds including amiodarone, iopanoic acid and erythrosine had no effect on the thyroid ODC activity. CONCLUSIONS: These results suggest that LBI may exert its anti-goitrous effects, consisting of the inhibition of ODC activity and apoptosis, in the form of inorganic iodide in vivo.

Related Posts:

Comments are closed.