Hydroxycobalamin is not the same as methylcobalamin. As alicec said, many of us do not convert.
Not quite. If we take methylcobalamin, it is not used directly. Instead, once taken into the cell, the methyl group is removed and the cobalamin is directed to MTR and MUT according to need. A methyl group is added at MTR and adenosyl at MUT.
Other forms such as hydroxy are processed in the same way. The fate of the cobalamin is not influenced by the original ligand on the cobalamin since the first processing step is its removal.
In other words, all forms are theoretically equivalent.
It is not clear why some people respond differently to different forms, but it is likely to reflect individual differences in uptake and/or processing - ie removal of the upper axial ligand - not "that we can't convert". There is no direct conversion. The critical step after uptake is removal. This is done by MMACHC, the enzyme that goes wrong in cblC disease.
The only study that I am aware of that specifically addressed the mechanism for different responses to different forms compared only hydroxy and cyano. It looked at known MMACHC variant proteins and showed that the defective variants were better able to bind the hydroxy form and hence were more efficient in removing the upper axial ligand.
The cyano form did not bind as well to MMACHC, the cyano group was not removed and so the cobalamin was unable to be used by the cell. This was the basis of the more favourable response of the patients from whom the variant MMACHC proteins were derived to hydroxyB12 compared with cyanoB12. The critical event was the efficient removal of the upper axial ligand.
Possibly there is more individual difference in MMACHC binding than we are aware of and so the reason that some forms are better for some people is that their MMACHC is better able to remove the upper axial ligand from that particular form.
Of course differences in initial uptake from the gut or from the blood may also be relevant. We just don't have the studies yet to explain it all.