Vitamin B12 is essential to DNA synthesis, red blood cell formation, neurological integrity, and methylation — the process by which the body converts homocysteine to methionine. Deficiency at any of these levels can produce serious and, if uncorrected, permanent damage: megaloblastic anemia, peripheral neuropathy, spinal cord degeneration, cognitive impairment, and psychiatric symptoms that are frequently misattributed to primary mental illness.
The problem facing both patients and clinicians is that B12-related illness is not a single condition with a single cause. Pernicious anemia (PA) — the best-known cause of B12 deficiency — results from an autoimmune failure of absorption. But a growing body of evidence describes a different category of B12-related illness in which absorption is intact and blood B12 levels appear normal, yet symptoms of deficiency persist. This second category, sometimes called B12 resistance or cellular resistance, reflects failures in transport, cellular uptake, or intracellular conversion after B12 has entered the bloodstream.
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