Ich würde mir zumindest ein paar mehr Meinungen einholen, bevor ich solche Mengen Jod schlucke. Ich halte Jod Supplementierung weiterhin für alles andere als unbedenklich.
Saudi Med J. 2007 Jul;28(7):1034-8.
The effect of iodine prophylaxis on the frequency of thyroiditis and thyroid
tumors in Southwest, Iran.
Soveid M, Monabbati A, Sooratchi L, Dahti S.
Department of Internal Medicine, Shiraz University of Medical Sciences, Nemazee Hospital, Shiraz, Iran.
msoveid@sums.ac.ir
OBJECTIVE: To investigate the effect of the salt iodization program, which was initiated in 1989 on frequencies of thyroiditis and papillary carcinoma in Fars province of Iran, which was previously an iodine deficient area. METHODS: Four hundred and eighty-two thyroidectomy specimens belonging to the pre-iodization period from 1983 to 1988, and 466 post iodization specimens from 1998 to 2003 were re-examined for presence of lymphocytic infiltration and types of thyroid tumors. This study was carried out in Shiraz University of Medical Sciences,
Iran.
RESULTS: The frequency of lymphocytic infiltration in non-neoplastic specimens increased from 30-60.5% after salt iodization (p<0.001). Background of lymphocytic infiltration in neoplastic specimens also increased from 18.5-61% after iodine prophylaxis (p<0.001). The frequency of papillary carcinoma in neoplastic specimens increased from 15-43% (p=0.01) and that of follicular adenoma decreased from 69-32.5% (p<0.0001). CONCLUSION:
Salt iodization is associated with an increased occurrence of histologic thyroiditis and papillary
carcinoma.
Endocr Pathol. 2002 Fall;13(3):175-81.
Thyroid cancer and thyroiditis in Salta, Argentina: a 40-yr study in relation to iodine prophylaxis.
Harach HR, Escalante DA, Day ES.
Services of Pathology, Dr A Oñativia Endocrinology and Metabolism Hospital, Salta, Argentina.
rubenharach@ciudad.com.ar
The natural history of thyroid cancer and thyroiditis in relation to iodine
prophylaxis in the region of Salta, Argentina, where goiter is common was
investigated over a time span of 40 yr. For analysis of thyroid cancer, the
specimens were divided into two periods. The first 15 yr (59 cases), including 5 yr before prophylaxis, was compared with the second 25 yr (182 cases), a period well after salt iodination. Papillary carcinomas formed the largest group of tumors in both periods, with a significant increase in their proportion in the second period (44 vs 60%, chi(2): p < 0.05), while the percentage of follicular and undifferentiated carcinomas decreased and medullary carcinoma remained about the same. The ratio of papillary to follicular carcinoma rose from 1.7:1 in the
irst period to 3.1:1 in the second. Four thyroid lymphomas of non-Hodgkin's B-cell type occurred in the second period in females over age 50. A severe lymphoid thyroiditis was present in the two cases with assessable background thyroid tissue. The frequency of moderate to severe lymphoid infiltrate in females rose from 2 of 12 (16.6%) in the preprophylaxis period to 34 of 114 (28.0%) in the last 25 yr after prophylaxis. After salt prophylaxis, thyroiditis was more frequent in patients with papillary carcinoma (36.2%) than in those with
nonpapillary tumors (14.7%) (chi(2), p < 0.02).
These observations indicate that a high dietary intake of iodine may be associated with a high frequency of papillary carcinoma and thyroiditis, and that thyroiditis is more commonly associated with papillary carcinoma than with other thyroid tumors. The occurrence of non-Hodgkin's lymphomas only in the postprophylaxis period may be linked to an increase in thyroiditis.
Enhanced iodination of thyroglobulin facilitates processing and presentation of a cryptic pathogenic peptide. Dai YD, Rao VP, Carayanniotis G.
Division of Endocrinology, Faculty of Medicine, Memorial University of
Newfoundland, St. John's, Newfoundland, Canada.
Increased iodine intake has been associated with the development of experimental autoimmune thyroiditis (EAT), but the biological basis for this association remains poorly understood. One hypothesis has been that enhanced incorporation of iodine in thyroglobulin (Tg) promotes the generation of pathogenic T cell determinants. In this study we sought to test this by using the pathogenic nondominant A(s)-binding Tg peptides p2495 and p2694 as model Ags. SJL mice
challenged with highly iodinated Tg (I-Tg) developed EAT of higher severity than Tg-primed controls, and lymph node cells (LNC) from I-Tg-primed hosts showed a higher proliferation in response to I-Tg in vitro than Tg-primed LNC reacting to Tg. Interestingly, I-Tg-primed LNC proliferated strongly in vitro against p2495, but not p2694, indicating efficient and selective priming with p2495 following processing of I-Tg in vivo. Tg-primed LNC did not respond to either peptide.
Similarly, the p2495-specific, IL-2-secreting T cell hybridoma clone 5E8 was activated when I-Tg-pulsed, but not Tg-pulsed, splenocytes were used as APC, whereas the p2694-specific T cell hybridoma clone 6E10 remained unresponsive to splenic APC pulsed with Tg or I-Tg. The selective in vitro generation of p2495 was observed in macrophages or dendritic cells, but not in B cells, suggesting differential processing of I-Tg among various APC. These data demonstrate that enhanced iodination of Tg facilitates the selective processing and presentation of a cryptic pathogenic peptide in vivo or in vitro and suggest a mechanism that
can at least in part account for the
association of high iodine intake and the development of EAT.
Thyroid. 2001 May;11(5):501-10.
Iodine-Induced hypothyroidism.
Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG.
Department of Medicine, University of Patras Medical School, Greece.
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of
thyroxine (T4) and triiodothyronine (T3) returns.
This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume normal activity. However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with
autoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or
subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-alpha who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term
thereafter because many will develop permanent primary hypothyroidism.
Hokkaido Igaku Zasshi 1994 May;69(3):614-26.
[Screening for thyroid dysfunction in adults residing in Hokkaido Japan: in
relation to urinary iodide concentration and thyroid autoantibodies]
[Article in Japanese]
Konno N, Iizuka N, Kawasaki K, Taguchi H, Miura K, Taguchi S, Murakami S,
Hagiwara K, Noda Y, Ukawa S. Department of Internal Medicine, Hokkaido Central Hospital for Social Health Insurance, Sapporo, Japan.
The prevalence of thyroid dysfunction and its relation to thyroid autoantibodies (TAA) and urinary iodide concentration (UI) was studied in apparently healthy adults in Sapporo (n = 4110) (Sapporo group), and in five coastal areas of Hokkaido (n = 1061) (coastal group) which produce iodine-rich seaweed (kelp).
The frequency of above normal UI (high UI) in the morning urinary samples of coastal group was 10.8%, significantly higher than that of Sapporo group (6.4%) (p < 0.001). Frequency of positive TAA in both groups were similar. In Sapporo group TAA was positive in 6.4% of males and 13.8% of females with an age-related increase.
The overall prevalence of hyperthyroidism (TSH < 0.15 mU/L) in coastal group (0.6%) was similar to that in Sapporo group (1.1%), while that of hypothyroidism (TSH > 5.0 mU/L) in coastal group (3.8%) was significantly higher than that in Sapporo group (1.3%) (P < 0.001). The frequency of high UI correlated significantly with that of hypothyroidism with negative TAA (r =0.829, P < 0.05), but not with positive TAA, or with that of hyperthyroidism. Hypothyroidism was more prevalent in TAA negative subjects with high UI than with normal UI. Moreover, serum TSH and thyroglobulin levels were higher and free T4 level was lower in former than in latter group. These results indicate
that 1) the prevalence of TAA negative hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested, 2) this hypothyroidism is more prevalent and marked in subjects consuming further excess amounts of iodine, and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.
Am J Clin Nutr. 2005 Apr;81(4):840-4.
High thyroid volume in children with excess dietary iodine intakes.
Zimmermann MB, Ito Y, Hess SY, Fujieda K, Molinari L.
Human Nutrition Laboratory, Swiss Federal Institute of Technology, Zurich,
Switzerland.
michael.zimmermann@ilw.agrl.ethz.ch
BACKGROUND: There are few data on the adverse effects of chronic exposure to high iodine intakes, particularly in children. OBJECTIVE: The objective of the study was to ascertain whether high dietary intakes of iodine in children result in high thyroid volume (Tvol), a high risk of goiter, or both. DESIGN: In an international sample of 6-12-y-old children (n = 3319) from 5 continents with iodine intakes ranging from adequate to excessive, Tvol was measured by ultrasound, and the urinary iodine (UI) concentration was measured. Regressions were done on Tvol and goiter including age, body surface area, sex, and UI concentration as covariates. RESULTS: The median UI concentration ranged from 115 microg/L in central Switzerland to 728 microg/L in coastal Hokkaido, Japan.
In the entire sample, 31% of children had UI concentrations >300 microg/L, and 11% had UI concentrations >500 microg/L; in coastal Hokkaido, 59% had UI concentrations >500 microg/L, and 39% had UI concentrations >1000 microg/L. In coastal Hokkaido, the mean age- and body surface area-adjusted Tvol was approximately 2-fold the mean Tvol from the other sites combined (P < 0.0001), and there was a positive correlation between log(UI concentration) and log(Tvol) (r = 0.24, P < 0.0001). In the combined sample, after adjustment for age, sex, and body surface area, log(Tvol) began to rise at a log(UI concentration) >2.7,
which, when transformed back to the linear scale, corresponded to a UI
concentration of approximately 500 microg/L. CONCLUSIONS: Chronic iodine intakes approximately twice those recommended-indicated by UI concentrations in the range of 300-500 microg/L-do not increase Tvol in children.
However, UI concentrations >/=500 microg/L are associated with increasing Tvol, which reflects the adverse effects of chronic iodine excess. Multicenter Study
Clin Immunol Immunopathol 1996 Dec;81(3):287-92
Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice.
Rasooly L, Burek CL, Rose NR.
Department of Molecular Microbiology and Immunology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA. Excess iodine ingestion has been implicated in induction and exacerbation of autoimmune thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R),
spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks.
Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies increased throughout the 8-week iodine ingestion period; however, no correlation
was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA, IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.