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Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage that begins with an inability to produce myelin and is followed by gradual degeneration of the axon and nerve head

While it is not possible to roll back the clock, deeper understanding of the biological pathways and mechanisms through which adverse childhood experiences produce a lifelong vulnerability to altered mitochondrial metabolism and the related pathways can provide a path for compensatory plasticity toward more positive health directions

Furthermore, mutation of site B in mice resulted in reduced retention of apoB100 in the artery wall and reduced atherosclerosis, providing in vivo support for the response to retention hypothesis (232)