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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

the condition, with its links to a specific conflict, offers a more defined trigger, likely due to exposure to toxic agents such as organophosphates, nerve agents, and pyridostigmine bromide

This implies people with MCAS may spend a good portion of their lives without a proper diagnosis

Autoimmun Rev (2021) 20(2):102736