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The gap between the marketed mechanism (localized IGF-1 receptor activation driving hyperplasia) and lived experience (systemic effects including lethargy, joint pain, and unpredictable blood glucose swings) is what makes community discussion essential

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[5] It has been hypothesized to act through GH-mediated pathways on the osteoblasts (bone-forming cells), possibly leading to increased proliferation, development, and differentiation of the osteoblasts