Hypothesis-level exploration of how selenium deficiency, thyroid autoimmunity, and insulin resistance impact reproductive-age women with PCOS, suggesting critical health implications.
Polycystic ovary syndrome affects 6-20% of reproductive-age women and is characterized by hyperandrogenism, ovulatory dysfunction, and insulin resistance. Oxidative stress is a core pathophysiological feature across all PCOS phenotypes. This paper proposes that PCOS creates a compounded failure of the Selenium-Iodine-Kidney (SIK) axis through three concurrent mechanisms: documented selenium deficiency impairing both GPx3-mediated renal antioxidant defense and deiodinase-mediated T3 production; elevated prevalence of thyroid autoimmunity independently disrupting thyroid hormone synthesis; and insulin resistance-driven suppression of NRF2 pathway activity, depleting both antioxidant amplification and mitochondrial biogenesis signaling via PGC-1alpha. All claims are hypothesis-level and require prospective clinical confirmation.
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Grace Ann (2026) studied this question.
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