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The T833C mutation, frequent in the German population, is observed in vitamin B 6 responders

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In these cases, simply taking a supplement may not fully address the problem

LN: Methodology, Writing original draft

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In animal models, it has been shown preclinically to upregulate growth hormone receptors in tendon fibroblasts, stimulate angiogenesis via the VEGFR2/Akt-eNOS pathway, and modulate nitric oxide signaling, mechanisms that, if they translate to humans, could support tissue repair in a hormonal environment where estrogen-dependent healing capacity is declining