The vitamin D receptor (VDR) mediates the cellular actions of vitamin D, which is critical for calcium homeostasis, bone health, and immune function. During menopause, declining estrogen levels impair intestinal calcium absorption and accelerate bone resorption, increasing osteoporosis risk. VDR polymorphisms (e.g., FokI, BsmI, TaqI) may theoretically modulate vitamin D signaling efficiency and thereby influence bone loss or menopausal symptoms like hot flashes. However, the evidence is inconsistent: some studies report associations, others do not. No clinical guidelines currently recommend VDR genotyping for menopause management. Instead, measuring serum 25(OH)D and supplementing accordingly is the evidence-based approach. The role of VDR genetics in menopause remains mechanistic and unclear; it cannot replace established risk assessments such as DXA scans or hormone profiling. Therefore, the evidence level is mechanistic/unclear, and consumer DNA tests claiming to predict menopause-related outcomes via VDR should be viewed with caution.
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