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Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease.
Proc Nutr Soc 2019; 78(1):34-44PN

Abstract

Hashimoto's thyroiditis (HT) and Graves' disease (GD) are examples of autoimmune thyroid disease (AITD), the commonest autoimmune condition. Antibodies to thyroid peroxidase (TPO), the enzyme that catalyses thyroid-hormone production and antibodies to the receptor for the thyroid-stimulating hormone, are characteristic of HT and GD, respectively. It is presently accepted that genetic susceptibility, environmental factors, including nutritional factors and immune disorders contribute to the development of AITD. Aiming to investigate the effect of iodine, iron and selenium in the risk, pathogenesis and treatment of thyroid disease, PubMed and the Cochrane Library were searched for relevant publications to provide a narrative review. Iodine: chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly-iodinated thyroglobulin (Tg) is more immunogenic. The recent introduction of universal salt iodisation can have a similar, although transient, effect. Iron: iron deficiency impairs thyroid metabolism. TPO is a haem enzyme that becomes active only after binding haem. AITD patients are frequently iron-deficient since autoimmune gastritis, which reduces iron absorption and coeliac disease which causes iron loss, are frequent co-morbidities. In two-thirds of women with persistent symptoms of hypothyroidism despite appropriate levothyroxine therapy, restoration of serum ferritin above 100 µg/l ameliorated symptoms. Selenium: selenoproteins are essential to thyroid action. In particular, the glutathione peroxidases remove excessive hydrogen peroxide produced there for the iodination of Tg to form thyroid hormones. There is evidence from observational studies and randomised controlled trials that selenium, probably as selenoproteins, can reduce TPO-antibody concentration, hypothyroidism and postpartum thyroiditis. Appropriate status of iodine, iron and selenium is crucial to thyroid health.

Authors+Show Affiliations

Department of Nutritional Sciences,Faculty of Health and Medical Sciences,University of Surrey,Guildford GU2 7XH,UK.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

30208979

Citation

Rayman, Margaret P.. "Multiple Nutritional Factors and Thyroid Disease, With Particular Reference to Autoimmune Thyroid Disease." The Proceedings of the Nutrition Society, vol. 78, no. 1, 2019, pp. 34-44.
Rayman MP. Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. Proc Nutr Soc. 2019;78(1):34-44.
Rayman, M. P. (2019). Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. The Proceedings of the Nutrition Society, 78(1), pp. 34-44. doi:10.1017/S0029665118001192.
Rayman MP. Multiple Nutritional Factors and Thyroid Disease, With Particular Reference to Autoimmune Thyroid Disease. Proc Nutr Soc. 2019;78(1):34-44. PubMed PMID: 30208979.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. A1 - Rayman,Margaret P, Y1 - 2018/09/13/ PY - 2018/9/14/pubmed PY - 2019/5/2/medline PY - 2018/9/14/entrez KW - AITD autoimmune thyroid disease KW - DIO deiodinases KW - GD Graves’ disease KW - GPX glutathione peroxidases KW - HT Hashimoto's thyroiditis KW - ID iron deficiency KW - L-T4 levothyroxine KW - RCT randomised controlled trial KW - T3 tri-iodothyronine; T4 KW - TPO thyroid peroxidase KW - TSH thyroid-stimulating hormone KW - Tg thyroglobulin KW - thyroxine KW - Autoimmune thyroid disease KW - Autoimmune thyroiditis KW - Iodine KW - Iron KW - Nutrition KW - Selenium SP - 34 EP - 44 JF - The Proceedings of the Nutrition Society JO - Proc Nutr Soc VL - 78 IS - 1 N2 - Hashimoto's thyroiditis (HT) and Graves' disease (GD) are examples of autoimmune thyroid disease (AITD), the commonest autoimmune condition. Antibodies to thyroid peroxidase (TPO), the enzyme that catalyses thyroid-hormone production and antibodies to the receptor for the thyroid-stimulating hormone, are characteristic of HT and GD, respectively. It is presently accepted that genetic susceptibility, environmental factors, including nutritional factors and immune disorders contribute to the development of AITD. Aiming to investigate the effect of iodine, iron and selenium in the risk, pathogenesis and treatment of thyroid disease, PubMed and the Cochrane Library were searched for relevant publications to provide a narrative review. Iodine: chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly-iodinated thyroglobulin (Tg) is more immunogenic. The recent introduction of universal salt iodisation can have a similar, although transient, effect. Iron: iron deficiency impairs thyroid metabolism. TPO is a haem enzyme that becomes active only after binding haem. AITD patients are frequently iron-deficient since autoimmune gastritis, which reduces iron absorption and coeliac disease which causes iron loss, are frequent co-morbidities. In two-thirds of women with persistent symptoms of hypothyroidism despite appropriate levothyroxine therapy, restoration of serum ferritin above 100 µg/l ameliorated symptoms. Selenium: selenoproteins are essential to thyroid action. In particular, the glutathione peroxidases remove excessive hydrogen peroxide produced there for the iodination of Tg to form thyroid hormones. There is evidence from observational studies and randomised controlled trials that selenium, probably as selenoproteins, can reduce TPO-antibody concentration, hypothyroidism and postpartum thyroiditis. Appropriate status of iodine, iron and selenium is crucial to thyroid health. SN - 1475-2719 UR - https://www.unboundmedicine.com/medline/citation/30208979/Multiple_nutritional_factors_and_thyroid_disease_with_particular_reference_to_autoimmune_thyroid_disease_ L2 - https://www.cambridge.org/core/product/identifier/S0029665118001192/type/journal_article DB - PRIME DP - Unbound Medicine ER -