oska_blnn
Iron
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- Oct 28, 2024
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I am genuinely surprised that almost nobody here has ever brought up Meclizine in the context of skeletal growth. The entire community seems focused on GH, IGF-1, CNP analogues, and other well-known interventions, yet Meclizine appears to have slipped completely under the radar.
Mechanistically, it is fascinating. Meclizine is an old antihistamine prescribed for motion sickness, but beyond its H1 receptor blockade, it has a very specific off-target effect: it downregulates FGFR3 signaling in growth plate chondrocytes. For context, FGFR3 is the single most important negative regulator of longitudinal bone growth. High FGFR3 activity suppresses chondrocyte proliferation and hypertrophy, thereby reducing the efficiency of endochondral ossification.
By attenuating FGFR3, Meclizine essentially removes part of the “brake” on the growth plate. The implications:
• Wider proliferative zones in the physis.
• Greater hypertrophic chondrocyte size.
• Increased longitudinal growth velocity while the plates remain open.
Crucially, this has nothing to do with accelerating epiphyseal closure. That process is primarily driven by estrogen exposure and senescence within the growth plate, not FGFR3 signaling. In other words, Meclizine cannot extend the lifespan of the growth plate, but it can plausibly increase the amount of growth achieved during its remaining lifespan.
Animal models support this: in achondroplasia mouse studies, Meclizine treatment partially rescued longitudinal bone growth by counteracting overactive FGFR3. Yet, for some reason, this compound remains almost entirely unmentioned in discussions on height optimization.
I cannot help but feel that Meclizine is one of the most gatekept drugs in this space. Readily available, mechanistically sound, supported by preclinical data — yet absent from virtually every conversation. Perhaps I am among the very few drawing attention to it here, but it seems to me like an overlooked key in the growth optimization puzzle.
Has anyone else seriously considered or experimented with this? I would be very interested to hear perspectives and reasons why it’s not as good as i’m saying it is.
Chatgpt wrote it for me cuz ion wanna write but trust me y’all meclizine is fucking op
please bump.
Mechanistically, it is fascinating. Meclizine is an old antihistamine prescribed for motion sickness, but beyond its H1 receptor blockade, it has a very specific off-target effect: it downregulates FGFR3 signaling in growth plate chondrocytes. For context, FGFR3 is the single most important negative regulator of longitudinal bone growth. High FGFR3 activity suppresses chondrocyte proliferation and hypertrophy, thereby reducing the efficiency of endochondral ossification.
By attenuating FGFR3, Meclizine essentially removes part of the “brake” on the growth plate. The implications:
• Wider proliferative zones in the physis.
• Greater hypertrophic chondrocyte size.
• Increased longitudinal growth velocity while the plates remain open.
Crucially, this has nothing to do with accelerating epiphyseal closure. That process is primarily driven by estrogen exposure and senescence within the growth plate, not FGFR3 signaling. In other words, Meclizine cannot extend the lifespan of the growth plate, but it can plausibly increase the amount of growth achieved during its remaining lifespan.
Animal models support this: in achondroplasia mouse studies, Meclizine treatment partially rescued longitudinal bone growth by counteracting overactive FGFR3. Yet, for some reason, this compound remains almost entirely unmentioned in discussions on height optimization.
I cannot help but feel that Meclizine is one of the most gatekept drugs in this space. Readily available, mechanistically sound, supported by preclinical data — yet absent from virtually every conversation. Perhaps I am among the very few drawing attention to it here, but it seems to me like an overlooked key in the growth optimization puzzle.
Has anyone else seriously considered or experimented with this? I would be very interested to hear perspectives and reasons why it’s not as good as i’m saying it is.
Chatgpt wrote it for me cuz ion wanna write but trust me y’all meclizine is fucking op
please bump.
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