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Understanding the connection between MTHFR and longevity requires moving past the standard homocysteine narrative to the full mechanistic picture: how reduced methylation capacity accelerates the epigenetic aging clock, how it depletes the glutathione substrate pool, how it uncouples eNOS and accelerates vascular aging, how it impairs DNA repair through uracil misincorporation, and how it reduces the methylation-dependent gene regulation that FOXO3 and SIRT1 require to execute their longevity programs

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Also, prostate cancer mouse models showed progression from androgen-dependence to androgen-independence to be associated with an increase in IGF-I and decrease in IGFBP-3, further suggesting their role in cancer aggressiveness (128)

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