Dietary iodide intakes of 750 micrograms/day or more may adversely affect thyroid function, especially in individuals with borderline hypothyroidism.
TSH production is blunted by excessively high blood iodide concentration.
Selenium supplementation (200 microg/day) resulted in significant reduction of serum anti-TPO levels during the first 6 months (by 5.6% and 9.9% at 3 and 6 months, respectively). An overall reduction of 21% was seen after 1 year.
Selenium and Miscarriage
Postpartum thyroid dysfunction and permanent hypothyroidism were significantly lower in the group that received 200 microg/d selenium throughout pregnancy and the postpartum period compared with placebo (28.6 vs. 48.6% and 11.7 vs. 20.3%).
A total of 76 patients with autoimmune thyroiditis, normal or slightly elevated TSH and fT4 within the normal range were divided into two groups: Group 0 was given no treatment while Group 1 was treated with sodium selenite 80 μg/day as a single oral dose for 12 months. RESULTS: No significant variation in TPO-Ab or Tg-Ab levels was observed between the two groups after 6 months, but both values decreased significantly after 12 months in Group 1, and five patients (11%) in this group became negative for TPO-Ab. TSH and FT4 showed no significant variations in either group. CONCLUSIONS: Dietary supplementation with physiological doses of selenium seems to be effective in preventing a reduction in thyroid echogenicity after 6 months of treatment and in reducing TPO-Ab and Tg-Ab after 12 months, but does not modify TSH or FT4.
Selenium supplementation (50-100 microg/day) and thyroxidine therapy resulted in an increase in plasma glutathione peroxidase (GPX3) by 21%. Anti-thyroid peroxidase antibody levels decreased by 76%.
Our objective was to compare the effect of selenomethionine (organic form of selenium available over the counter) on monocyte and lymphocyte cytokine release and systemic inflammation in patients with Hashimoto's thyroiditis. Selenomethionine inhibited lymphocyte release of IL-2, interferon-γ, and TNF-α, which was accompanied by a reduction in plasma C Reactive Protein levels. CONCLUSIONS: Selenomethionine exhibits a systemic antiinflammatory effect in euthyroid females with Hashimoto's thyroiditis. This action, which correlates with a reduction in thyroid peroxidase antibody titers, may be associated with clinical benefits in the prevention and management of Hashimoto's thyroiditis, particularly in subjects receiving both agents.
Patients with Hashimoto disease had lower glutathione peroxidase activities than healthy subjects (glutathione peroxidase activity is dependent on selenium status).
Both deficiency and excess of trace elements (iron, chromium, selenium, manganese, cobalt, copper, nickel, arsenic, and zinc) was shown to be of pathogenetic value in the development of thyroid diseases.
Chemically induced hypothyroid rats reduced plasma thyroxine concentration to 48 to 68% of base line from experimental days 20 to 60. Chemically induced hypothyroidism combined with feeding a manganese-deficient ration significantly reduced plasma thyroxine concentrations to 37% of base line at day 20 and 5% of base line at day 40 in mice.
Groups of mice genetically predisposed to autoimmune disease, beginning at 6 mo of age, were fed a vitamin A-deficient diet or a control diet. The diet contained casein as the protein source and contained adequate levels of trace elements and vitamins. We found that vitamin A-deficient animals manifested more severe hypergammaglobulinemia and an earlier onset of both NTA and IgM anti-erythrocyte autoantibodies than did vitamin A-sufficient mice.
The prevalence of vitamin D insufficiency in Hashimoto's Thyroiditis cases (92%) was significantly higher than that observed in healthy controls (63%). Among Hashimoto's Thyroiditis cases, the prevalence rate of vitamin D insufficiency showed a trend to be higher in patients with overt hypothyroidism (94%) or subclinical hypothyroidism (98%) than in those with euthyroidism (86%), but the differences were not significant. CONCLUSION: Vitamin D insufficiency is associated with Hashimoto's Thyroiditis. Further studies are needed to determine whether vitamin D insufficiency is a casual factor in the pathogenesis of Hashimoto's Thyroiditis or rather a consequence of the disease.
The prevalence of vitamin D deficiency was significantly higher in patients with autoimmune thyroid disease compared with healthy individuals (72% versus 30.6%), as well as in patients with autoimmune thyroid disease compared to patients with non-autoimmune thyroid disease (79% versus 52%). Vitamin D deficiency also correlated to the presence of antithyroid antibodies and abnormal thyroid function tests. Significantly low levels of vitamin D were documented in patients with autoimmune thyroid disease that were related to the presence of anti thyroid antibodies and abnormal thyroid function tests, suggesting the involvement of vitamin D in the pathogenesis of autoimmune thyroid disease and the advisability of supplementation.
Our objective was to assess the relationship between serum vitamin D levels and thyroid autoimmunity. The mean serum vitamin D of the study subjects was 17.5 nmol/l with 87 % having values < or = 25 nmol/l. TPOAb positivity was observed in 21 % of subjects. The relationship between vitamin D and TPOAb (present in Hashimoto's) showed significant inverse correlation when adjusted for age. Further studies in vitamin D-sufficient populations with wider range of serum vitamin D levels are required to substantiate the findings of the current study.
Rats were randomly divided into 4 groups, namely the prevention group treated with vitamin D from 0 to the 6th week, treatment group with vitamin D treatment from the 2nd to the 8th week after immune sensitization, positive control group and the negative control group. RESULTS: The thyroid gland remained structurally intact in the negative control group. In the positive control group, the thyroid showed obvious inflammatory change with structural disruption and even disappearance of the thyroid follicle. The structure of the thyroid gland follicles was intact in the prevention group and treatment group. No significant differences were found in the autoantibody and cytokine levels between the prevention group and negative control group. Compared with the positive control groups, the autoantibody and IFN-gamma and IL-12 levels decreased significantly in the treatment group, while the levels of IL-4 and IL-10 were markedly increased. CONCLUSION: Vitamin D given before the establishment of the experimental autoimmune thyroiditis model helps maintain structural integrity of the thyroid gland and normal levels of the antibodies and cytokines in rats. Vitamin D can ameliorate the pathological changes of the thyroid gland and correct the cytokine disequilibrium in rats with experimental autoimmune thyroiditis.
CYP27B1 hydroxylase catalyzes the conversion of 25 hydroxyvitamin D(3) (25OHD(3)) to 1,25(OH)(2)D(3), the most active natural vitamin D metabolite, which plays a role in the regulation of immunity and cell proliferation. We therefore investigated two single nucleotide polymorphisms in the CYP27B1 hydroxylase gene for an association with Hashimoto's thyroiditis and Graves' disease. RESULTS: A significant association was found between allelic variation of the promoter (-1260) C/A polymorphism and Hashimoto's thyroiditis and Graves' disease. Significant differences were also observed for the intron 6 (+2838) C/T polymorphism in Hashimoto's thyroiditis but not for the other autoimmune endocrine diseases. CONCLUSIONS: The CYP27B1 promoter (-1260) C/A polymorphism appears to be associated with endocrine autoimmune diseases but the CYP27B1 intron 6 (+2838) C/T polymorphism appears to be associated only with Hashimoto's thyroiditis. These results imply a regulatory difference of the CYP27B1 hydroxylase to predispose to endocrine autoimmunity.
In patients with normal thyroid, zinc levels were significantly positively correlated with free T3 levels. In the nodular goiter group, thyroid volume was negatively correlated with TSH and circulating zinc levels. In the autoimmune thyroid disease group, thyroid autoantibodies and zinc were significantly positively correlated.
The mean BMI change from 49 to 32 kg/m2 after bariatric surgery was associated with a mean reduction in the TSH level from 4.5 to 1.9 μU/mL. Before bariatric surgery, 10.5% of the subjects had laboratory values consistent with subclinical hypothyroidism. After bariatric surgery, 100% of these patients experienced significant weight reduction with simultaneous resolution of their subclinical hypothyroidism. Conclusion: The results of our study have demonstrated a statistically significant positive association between serum TSH within the normal range and BMI. Weight loss after bariatric surgery improved or normalized thyroid hormone levels.
72 subjects (62F/10M), with mean age 39.6 years and mean BMI 53.0 kg/m2 were studied. The prevalence of subclinical hypothyroidism before gastric bypass surgery was 25%. There was a significant post-surgical decrease in BMI in the whole population, as well as in subclinical hypothyroid patients. In the subclinical hypothyroid group and normal TSH group, there was a decrease in TSH and T3, but not in free T4. TSH concentrations reached normal values in all subclinical hypothyroid patients after gastric bypass surgery. CONCLUSION: Our data confirm that severe obesity is associated with increased TSH. The decrease in TSH was independent of BMI, but occurred in all subclinical hypothyroid patients. A putative effect of weight reduction on the improvement of subclinical hypothyroidism in all patients may be an additional benefit of bariatric surgery.
224 patients underwent gastric bypass surgery. 23 of 224 patients (10.3%) were treated preoperatively for hypothyroidism. During a median follow-up of 17 months, hypothyroidism was improved in 10/23 patients (43.5%). 2 patients had complete resolution, and the remaining 8 had reduction (14%-50%) of their thyroxine requirements. Improved thyroid function occurred at a mean follow-up of 8.9 months and at a mean excess weight loss of 57%. 6 of the 8 patients (75%) with improved thyroid function had excess weight loss >90% at last follow-up, compared to 1 out of 15 patients (6.6%) with unchanged thyroid function. CONCLUSION: Improvement of hypothyroidism may be an additional benefit of bariatric surgery that has not been previously reported. http://www.ncbi.nlm.nih.gov/pubmed/15130228
Compared with controls, obese patients had lower free T3 levels and free T4 levels, greater prevalence of hypothyroidism, and higher commonness of antithyroid antibodies. As a marker of autoimmune thyroid disorder, thyroid peroxidase antibodies were more frequent in the obese group. Correlation analysis showed that leptin levels (produced by fat cells and affected by multiple variables) were associated with autoimmune thyroid disease independent of bioanthropometric variables. Multiple logistic regression analysis in pooled groups identified female sex and leptin as significant predictors of autoimmune thyroid disease. CONCLUSIONS: Obesity increases the susceptibility to harbor autoimmune thyroid disease with an emerging role for leptin as a peripheral determinant, which needs to be confirmed in future investigations.
Total T4 and free T4 decreased at higher BMI levels, which is consistent with subclinical hypothyroidism.
Calorie restriction has been shown to improve both immune and thyroid function.
The type of dietary fat dramatically affects the onset of autoimmune disease in lupus-prone female mice. Disease development was strikingly slowed in mice fed a diet containing quantities of omega-3 fatty acids (fish oil). By 10 months of age, 94% of the fish oil mice were still living, whereas all the mice fed a saturated fat diet (lard) were dead. Those mice fed a corn oil diet were intermediate with 35% alive at the 10-month time evaluation. It is likely omega-3 fatty acids of fish oil reduce immune-complex-induced glomerulonephritis through production of prostaglandin metabolites with attenuated activity and/or through altering cell membrane structure and fluidity, which may, in turn, affect the responsiveness of immune cells.
Significantly increased levels of antibodies to beta-casein were found in patients with Type 1 diabetes, coeliac disease and in latent autoimmune diabetes in adults compared to age-matched controls. No differences were observed in beta-casein antibody titres between patients with other disease conditions (multiple sclerosis, and autoimmune thyroid disease) and age-matched controls. The highest antibody response to beta-casein in Type 1 diabetic patients and in patients with coeliac disease could reflect the gut mucosal immune disorders common to Type 1 diabetes and coeliac disease. Furthermore, the elevated beta-casein antibody levels found in latent autoimmune diabetes in adults patients suggest that the antibody response to this protein may be relevant in autoimmune diabetes.
Early diagnosis and dietary treatment with a gluten-free diet might slow down the progression of associated autoimmune diseases in celiac disease, but the data are contradictory. We investigated the course of autoimmune thyroid diseases in newly diagnosed celiac disease patients before and after gluten-free dietary treatment. MATERIAL AND METHODS: Adults with newly diagnosed celiac disease were investigated at the time of diagnosis and after 1 year on gluten-free diet. RESULTS: At the time of diagnosis, the celiac disease patients had more manifest or subclinical thyroid diseases than the controls. During the follow-up, the thyroid volume decreased significantly in the patients with celiac disease compared with the controls, indicating the progression of thyroid gland atrophy despite the gluten-free diet. CONCLUSIONS: Celiac patients had an increased risk of thyroid autoimmune disorders. A gluten-free diet seemed not to prevent the progression of autoimmune process during a follow-up of 1 year.
It was recently reported that metformin has a TSH-lowering effect in hypothyroid patients with diabetes being treated with metformin. The serum levels of TSH and FT(4) were measured before and after a 4-month period of metformin therapy. Results: In the 9 hypothyroid patients with PCOS, the basal median serum levels of TSH (3·2 mIU/l) significantly decreased after a 4-month course of metformin treatment (1·7 mIU/l). No significant change in the serum levels of FT4 was observed in these patients. Conclusions: These results indicate that metformin treatment has a TSH-lowering effect in hypothyroid patients with PCOS, both treated with l-thyroxine and untreated.
In insulin-resistant hypothyroid patients, treatment with metformin (prescribed for insulin resistance) caused suppression of TSH to subnormal levels without clinical symptoms of hyperthyroidism in any patients.
Insulin Resistance and Miscarriage
We selected 45 patients with problems of polycystic ovary syndrome, hypothyroidism and insulin-resistance and divided them into 3 groups. The 15 Group A patients followed a dietetic therapy. The 15 patients of Group B received hormonal therapy. The 15 Group C patients received replacement therapy with laevo-thyroxine. All patients had their thyroid and ovary function checked every six months and a glycoinsulinaemic curve was plotted after glucose loading. RESULTS: A reduction in TSH levels and an increase in the values of circulating thyroid hormones was observed in all patients. The ovary situation underwent both a hormonal and symptomatological improvement with diminution in LH and testosterone levels and an increase in progesterone. The glucose-insulin picture of our patients progressively improved in all 3 groups studied.
Insulin sensitivity and adiponectin were not different at baseline in the subclinical hypothyroidism and euthyroid controls. Plasma soluble intercellular adhesion molecule-1 concentration was significantly higher in the patients with subclinical hypothyroidism. The comparison of lipids profiles revealed that only LDL-cholesterol concentration was higher in the group with subclinical hypothyroidism. After 5 months levothyroxine therapy, we observed an improvement of insulin sensitivity and a decrease of plasma glucose and soluble intercellular adhesion molecule-1, whereas adiponectin concentration remained unchanged. We concluded that L-thyroxine treatment in patients with subclinical hypothyroidism might exert a beneficial effect by reducing cardiovascular risk factors.
The prevalence of anti-thyroid antibodies among euthyroid, infertile patients was 10.5%, similar to the one reported in euthyroid women between 18 and 45 years. Anti-thyroid antibodies positive patients who did not receive any adjuvant treatment showed significantly poorer ovarian responsiveness to stimulation and IVF results than controls. Anti-thyroid antibodies positive patients patients receiving levothyroxin responded better to ovarian stimulation, but had IVF results as poor as untreated anti-thyroid antibodies positive patients women. Patients receiving levothyroxin+aspirin+prednisolone had significantly higher pregnancy and implantation rates than untreated anti-thyroid antibodies positive patients patients (pregnancy 25.6% and implantation rate 17.7% vs. pregnancy 7.5% and implantation rate 4.7%, respectively), and overall IVF results comparable to patients without anti-thyroid antibodies (pregnancy 32.8% and implantation rate 19%). Conclusion: These observations suggest that euthyroid anti-thyroid antibodies positive patients undergoing IVF could have better outcome if given levothyroxin+aspirin+prednisolone as adjuvant treatment.
Insulin and hydrocortisone stimulates thyroglobulin synthesis. (Thyroglobulin is used by the thyroid gland to produce the T4 and T3)
Serum thyroglobulin levels are not affected by estrogen.
Thyroid Peroxidase Test (TPO) will also be positive with pernicious anemia (B12 deficiency), rheumatoid arthritis, Sjogren's syndrome and lupus.
Iodine and tyrosine are used to form both T3 and T4.
The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones.
A genetic defect of the vitamin D receptor gene can predict Hashimoto's.