There are several studies in which supplementation with CN-Cbl or OHCbl has not proven to be effective in altering Hcy or MMA in some (generally around 50%) of the patients. The problem with this is that in patients who are riboflavin deficient (very common) MTRR cannot work to reduce Co(III) to Co(I) so that CN-Cbl or OH-Cbl can be converted to MeCbl and AdoCbl. This would effectively mean that patients who are significantly B2 deficient won't respond to treatment. Further, Hcy should normally be removed by CBS, but in B2 deficiency there is a lack of conversion of B6 to P5P and also there is reduced production of heme, thus CBS has reduced activity. In essence Hcy should not really be elevated unless CBS doesn't work. Further, elevated Hcy only occurs if there is elevated SAM production, but elevated SAM production turns on CBS, inferring that in elevated Hcy, there is actually a problem with CBS.
Article Anemia, serum vitamin B12, and folic acid in patients with r...
As far I understand a combination of Mecbl and Adocbl is preferred. Riboflavin is a cofactor for mthfr not mtrr.
Hi Kirshna,
No MTRR uses FAD as a co-factor as well. Whilst you have said MeCbl and AdoCbl are preferred, the question was which form was used? Further, what was the functional FAD activity of the subjects?
Greg
The world of micronutrients still has many gaps, and the specific case of vitamin b12 is particularly complex given the clinical importance of its levels, which are low, but also high. In this sense, in complement to the debate question, I want to share with you the following manuscript detailing the aspects associated with high levels of vitamin b12
Article Hipervitaminosis B12 una mirada desde la atención primaria