ReviewNutrients2022
Iron: Not Just a Passive Bystander in AITD.
Review in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Functional Medicine Approach to Autoimmune Hypothyroidism: A Case Report.Integrative medicine (Encinitas, Calif.) · 2026Article
- Effects of essential metals (iron, zinc, and copper) on thyroid diseases - a narrative review.Frontiers in medicine · 2026Review
- Population-based national incidence of thyroid dysfunction in Spain.Scientific reports · 2025Observational
- Epigenetic Mechanisms in Autoimmune Thyroid Diseases: Bridging Research and Clinical Applications.International journal of molecular sciences · 2025Review
- Shared Immunopathogenic Mechanisms in Chronic Spontaneous Urticaria, Vitiligo, and Hashimoto's Thyroiditis: The Role of Oxidative Stress and Vitamin D.Life (Basel, Switzerland) · 2025Review
- Effects of Trace Elements on Endocrine Function and Pathogenesis of Thyroid Diseases-A Literature Review.Nutrients · 2025Review
- Zinc and Ferritin Levels and Their Associations with Functional Disorders and/or Thyroid Autoimmunity: A Population-Based Case-Control Study.International journal of molecular sciences · 2024Article
- A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response.Scientific reports · 2024Article
- Impact of Vitamin D on Immunopathology of Hashimoto's Thyroiditis: From Theory to Practice.Nutrients · 2023Review
- Selenium, Iodine and Iron-Essential Trace Elements for Thyroid Hormone Synthesis and Metabolism.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.