Vitamin B12 genetic control refers to the influence of inherited genetic variations, or polymorphisms, on the absorption, transport, and metabolic utilization of Vitamin B12 (cobalamin). These genetic factors can affect an individual’s functional requirement for B12, impacting the efficiency of essential metabolic pathways like the methylation cycle. Clinically, understanding this control is vital for personalized supplementation strategies to prevent functional B12 deficiency.
Origin
The term links Vitamin B12, the essential micronutrient, with genetic control, indicating the regulatory role of the genome. This concept is a core component of nutrigenetics, emerging from the identification of specific single nucleotide polymorphisms (SNPs) that impair the function of B12-dependent enzymes.
Mechanism
Key genetic control points involve genes like MTHFR, MTRR, and TCN2. Polymorphisms in the MTRR gene, for example, can reduce the activity of methionine synthase reductase, an enzyme required to maintain the active form of B12 needed for the methylation cycle. Reduced B12 availability impairs the conversion of homocysteine to methionine, which can lead to elevated homocysteine levels and compromised hormonal detoxification pathways.
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