A new paper discussing that very common issue - iron.
I've only glanced at it so please comment freely.
Iron: Not Just a Passive Bystander in AITD
by Michał Szklarz
Katarzyna Gontarz-Nowak
Wojciech Matuszewski
Elżbieta Bandurska-Stankiewicz
Clinic of Endocrinology, Diabetology and Internal Medicine, School of Medicine, Collegium Medicum, University of Warmia and Mazury in Olsztyn, 10-957 Olsztyn, Poland
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Academic Editors: Roberto Iacone and Gladys Oluyemisi Latunde-Dada
Nutrients 2022, 14(21), 4682; doi.org/10.3390/nu14214682
Received: 30 September 2022/ Revised: 27 October 2022/ Accepted: 3 November 2022/ Published: 5 November 2022
(This article belongs to the Section Micronutrients and Human Health)
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Abstract
Autoimmune thyroid disease (AITD) is the most prevalent autoimmune disease all over the world and the most frequent cause of hypothyroidism in areas of iodine sufficiency. The pathogenesis of AITD is multifactorial and depends on complex interactions between genetic and environmental factors, with epigenetics being the crucial link. Iron deficiency (ID) can reduce the activities of thyroid peroxidase and 5′-deiodinase, inhibit binding of triiodothyronine to its nuclear receptor, and cause slower utilization of T3 from the serum pool. Moreover, ID can disturb the functioning of the immune system, increasing the risk of autoimmune disorders. ID can be responsible for residual symptoms that may persist in patients with AITD, even if their thyrometabolic status has been controlled. The human lifestyle in the 21st century is inevitably associated with exposure to chemical compounds, pathogens, and stress, which implies an increased risk of autoimmune disorders and thyroid dysfunction. To summarize, in our paper we discuss how iron deficiency can impair the functions of the immune system, cause epigenetic changes in human DNA, and potentiate tissue damage by chemicals acting as thyroid disruptors.
Keywords: AITD; thyroid; iron deficiency
Full paper freely accessible here: