The Vitamin D Receptor (VDR) is a nuclear receptor mediating the effects of vitamin D, expressed in reproductive tissues such as ovaries, endometrium, placenta, and testes. Evidence suggests that common VDR polymorphisms (e.g., FokI, BsmI, TaqI, ApaI) can modulate vitamin D signaling and have been associated with fertility outcomes. In women, links to endometriosis, polycystic ovary syndrome (PCOS), and implantation failure have been reported; in men, associations with sperm quality parameters exist. However, the evidence is predominantly observational and mechanistic, lacking large randomized controlled trials. Vitamin D deficiency is a well-known modifiable risk factor for fertility, but whether VDR genotyping alone provides clinically actionable information remains uncertain. Direct-to-consumer DNA tests often overstate the significance of these variants. Optimizing vitamin D status (target serum 30–50 ng/ml) is prudent, but personalized recommendations based solely on VDR genotype are not supported by current evidence. Caveat: ancestry-specific effects and small effect sizes limit utility; these tests are not diagnostic.
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