Chemical contamination and the thyroid

Industrial chemical contaminants have a variable impact on the hypothalamic-pituitary-thyroid axis, this depending both on their class and on confounding factors. Today, mounting evidence is pointing to the role of environmental factors, and specifically EDCs, in the current distressing upsurge in the incidence of thyroid disease. The unease is warranted. These substances, which are nowadays rife in our environments (including in foodstuffs), have been shown to interfere with thyroid hormone action, biosynthesis, and metabolism, resulting in disruption of tissue homeostasis and/or thyroid function. Importantly, based on the concept of the “nonmonotonic dose–response curve”, the relationship between dose and effect has often been found to be nonlinear. Thus, small doses can induce unpredictable, adverse effects, one case being polychlorinated biphenyls (PCBs), of which congener(s) may centrally inhibit the hypothalamic-pituitary-thyroid axis, or dissociate thyroid receptor and selectively affect thyroid hormone signaling and action. This means that PCBs can act as agonists or antagonists at the receptor level, underlining the complexity of the interaction. This review highlights the multifold activity of chemicals demonstrated to cause thyroid disruption. It also represents a call to action among clinicians to undertake systematic monitoring of thyroid function and registering of the classes of EDs and additionally urges broader scientific collaborations to clarify these chemicals’ molecular mechanisms of action, substances whose prevalence in our environments is disrupting not only the thyroid but all life on earth. © 2014, Springer Science+Business Media New York

Resveratrol and its impact on aging and thyroid function

Resveratrol, the naturally occurring polyphenolic compound characterized by anti-oxidative, anti-inflammatory and apoptotic properties, appears to contribute substantially to cardioprotection and cancer-prevention. In addition, resveratrol is believed to regulate several biological processes, mainly metabolism and aging, by modulating the mammalian silent information regulator 1 (SIRT1) of the sirtuin family. Resveratrol may arrest, among various tumors, cell growth in both papillary and follicular thyroid cancer by activation of the mitogen-activated protein kinase (MAPK) signal transduction pathway as well as increase of p53 and its phosphorylation. Finally, resveratrol also influences thyroid function by enhancing iodide trapping and, by increasing TSH secretion via activation of sirtuins and the phosphatidylinositol-4-phosphate 5 kinase γ (PIP5Kγ) pathway, positively affects metabolism. ©2011, Editrice Kurtis

Selenium and the thyroid: A close-knit connection

Context: The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease. Evidence Acquisition: Clinical reports as well as a large number of biochemical articles linking selenium to thyroid have been considered. Interventional, prospective, randomized, controlled studies, including large observational studies, supplementing selenium in autoimmune thyroid disease, together with review articles published in Medline and Pubmed have undergone scrutiny. The methodological differences and variety of results emerging from these trials have been analyzed. Evidence Synthesis: Evidence in support of selenium supplementation in thyroid autoimmune disease is evaluated, the results herein presented demonstrating the potential effectiveness of selenium in reducing the antithyroid peroxidase titer and improving the echostructure in the ultrasound examination. However, considerable discord remains as to who should comprise target groups for selenium treatment, who will most benefit from such treatment, the precise impact of the basal antithyroid peroxidase level, and the effect of disease duration on the treatment outcome. Clearly, further in-depth studies and evaluation are required concerning the mechanism of action of selenium as well as the choice of supplements or dietary intake. Conclusions: Maintenance of "selenostasis" via optimal intake not only aids preservation of general health but also contributes substantially to the prevention of thyroid disease. Copyright © 2010 by The Endocrine Society

The catalytic role of iodine excess in loss of homeostasis in autoimmune thyroiditis

PURPOSE OF REVIEW: To review the latest developments concerning the role of iodine in the pathophysiology of autoimmune thyroiditis. RECENT FINDINGS: Recent studies have provided evidence that in areas with excess iodine intake, increased incidence of autoimmune thyroiditis marked by high titers of thyroid peroxidase and thyroglobulin antibodies has occurred. Investigations in the NOD.H2h4 mouse, a strain prone to AIT, showed that they are better adapted to the Wolff-Chaikoff effect. SUMMARY: To provide an overview of the studies conducted during the last few years implicating iodine in the development and manifestation of autoimmune thyroiditis