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The mechanism is not entirely clear but it is hypothesized that the reduction in homocysteine from B vitamin supplementation may exert favorable and protective effects on nerve demyelination (31), and may attenuate the neurotoxic effects of homocysteine and N-methyl-D-aspartate (NMDA) agonists (32)

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Perhaps this is because of the iron-overloaded environment in ectopic tissue cells [101]

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