Meclizine is sometimes mentioned in growth discussions because it was shown in cell and animal models to inhibit FGFR3, a pathway that negatively regulates chondrocyte proliferation in growth plates. However, meclizine does not target the primary driver of growth plate closure. In humans, epiphyseal fusion is primarily caused by estrogen, not FGFR3 activity. FGFR3 modulates the rate of cartilage growth, but estrogen determines the timing of growth plate senescence and fusion. Meclizine’s effect on FGFR3 is indirect, weak, and non-selective, and there is no human clinical evidence that it meaningfully delays bone age advancement or epiphyseal closure. Also, meclizine’s cognitive dulling and lack of endocrine specificity make it ass for sustained modulation of bone maturation.
If u want to delay growth plates closure use Aromasin it acts directly on the key biological trigger of growth plate closure by inhibiting aromatase, the enzyme responsible for converting androgens into estrogen. Human genetics and clinical endocrinology show that reduced estrogen exposure delays growth plates fusion individuals with aromatase deficiency or impaired estrogen signaling exhibit prolonged linear growth and delayed skeletal maturation. Clinical studies in adolescent males show that aromatase inhibitors slow bone age progression relative to chronological age, directly demonstrating delayed skeletal maturation. While this does not guarantee increased height, it provides human evidence that estrogen suppression can increase the window when growth plates remain open.
Just make sure not to inhibit it too much especially during puberty as it can cause a variety of other issues.
If u want to delay growth plates closure use Aromasin it acts directly on the key biological trigger of growth plate closure by inhibiting aromatase, the enzyme responsible for converting androgens into estrogen. Human genetics and clinical endocrinology show that reduced estrogen exposure delays growth plates fusion individuals with aromatase deficiency or impaired estrogen signaling exhibit prolonged linear growth and delayed skeletal maturation. Clinical studies in adolescent males show that aromatase inhibitors slow bone age progression relative to chronological age, directly demonstrating delayed skeletal maturation. While this does not guarantee increased height, it provides human evidence that estrogen suppression can increase the window when growth plates remain open.
Just make sure not to inhibit it too much especially during puberty as it can cause a variety of other issues.
