I got my results and ran it through knowyourgenetics and found out I have these issues to focus on.
COMT V158M +/+
COMT H62H +/+
VDR Taq TT +/+
SHMT C1420T +/-
I understand what COMT is and what it does, but I am a bit unclear about the VDR and SHMT. Mainly the VDR because I had a feeling I have been having issues regarding vitamin D. How does this +/+ in VDR Taq effect my comt issues? Is this like a vitamin D deficiency? Would getting more vitamin D help speed up my comt activity? Any insight greatly appreciated.
One thing to keep in mind is that it shows
possible mutations. But this does not mean that those are actually turned on. Epigenetics vs genetics. So take the results with some salt. Since it is such a small slice of info, often inaccurate and certainly incomplete, I would be careful making drastic decisions based on them.
Some notes I had on VDR, SHMT:
Serine hydroxymethyltransferase (SHMT1) is important for linked reactions. The first is the conversion of tetrahydrofolate to 5,10-methylenetetrahydrofolate. The second is the conversion of L-serine to glycine. It also has a role in mediating the synthesis of dTMP and SAM. It preferentially selects for dTMP biosynthesis which is the precursor to the nucleic acid thiamine. Mutations in this enzyme may cause elevations in uracil which can build up when dTMP synthesis in impaired. Uracil is marker 40 in the OAT.
Vitamin D receptor (VDR) is a nuclear hormone receptor for vitamin D3. Vitamin D3 interacts with this receptor to influence multiple biological activities by regulating gene transcription. Vitamin D3 is associated with maintenance of calcium distribution. More recently, it has been implicated in inflammatory processes, vascular integrity, and collagen formation. Mutations in VDR have been linked to metabolic syndrome. Individuals with VDR mutations have greater propensity for insulin insensitivity, higher triglycerides, and lower HDL levels. Vitamin D receptor mutations can also lead to vitamin-D-dependent rickets type 2.