I'm compound hetero for MTHFR. I know Valentijn says it may not be relevant, but it seems like allot of people have this on here.
It certainly is relevant. The uncertainty comes in because 23andMe results make it impossible to know if the mutations are actually compound, because they report alleles in alphabetic order instead of by DNA strand. Hence you usually can't tell if you got one bad allele from each parent, or both from the same parent, in the case of MTHFR C677T +/- and MTHFR A1298C +/-.
But since
@ReneeN's mother was also tested, and her mother only had one, she must have gotten the other one from her father. While it's possible she got both from her father, that's somewhat less likely. So compound heterozygous does seem like the more likely possibility in her case, and she's probably producing active folate at about 30% of the normal rate.
But all of that aside, it really doesn't look like MTHFR is at all relevant to causing ME/CFS, since we do have mutations at about the same rate as the general public.
I've also been compiling a new report, somewhat in the Yasko/Genetic Genie manner, but with all of the SNPs included based on research, more relevant SNPs and genes included, and with indications of how much impact each genotype has. When looking at 31 patients and controls, our BHMT function is 2.5% better, our MTHFR is 1% better, our MTRR is 1% worse, and there's less than 1% of difference for AHCY, MAT, and MTR.
Most interesting, the average impairment for the controls is approximately -32% functioning of MTHFR and -38% functioning for MTRR. So it seems to be extremely normal to have some significant mutations on those genes, though of course it's probably still a very good idea to supplement a bit to compensate, especially when quite ill for other reasons.