Polycystic ovary syndrome (PCOS), affecting 6-20% of reproductive-age women globally, is a complex endocrine-metabolic disorder characterized by oligo-anovulation, hyperandrogenism, and polycystic ovarian morphology (PCOM), frequently accompanied by insulin resistance (IR), dyslipidemia, and heightened cardiovascular risk.This narrative review synthesizes contemporary mechanistic and clinical evidence delineating the role of vitamin D deficiency-now recognized as a global pandemic-as a critical modifier of PCOS pathophysiology.The identification of vitamin D receptors (VDRs) and 1-hydroxylase in reproductive and metabolic tissues has reframed vitamin D as a pleiotropic secosteroid hormone.Epidemiological studies consistently demonstrate a markedly higher prevalence of deficiency in women with PCOS (67-85%) compared with matched controls, independent of body mass index (BMI), though obesity further exacerbates deficiency via sequestration and volumetric dilution.Vitamin D modulates insulin secretion and sensitivity through calcium-dependent -cell function, VDR-mediated insulin gene transcription, PI3K/Akt pathway activation, GLUT4 translocation, and suppression of the renin-angiotensin system.In ovarian tissue, it regulates steroidogenesis by inhibiting CYP17A1, enhancing aromatase activity, increasing sex hormone-binding globulin (SHBG) synthesis, and repressing anti-Mllerian hormone (AMH) transcription, thereby restoring folliculogenesis.Additional anti-inflammatory, mitochondrial, gut-barrier, and microbiome-modulating actions further attenuate metabolic and reproductive dysfunction.Genetic and epigenetic alterations in VDR contribute to functional vitamin D resistance.Collectively, the evidence positions vitamin D deficiency as a critical "second hit" in PCOS, supporting routine screening and therapeutic optimization as a low-risk, cost-effective adjunct in comprehensive management.
Bhattacharyya et al. (Thu,) studied this question.