drob31
Senior Member
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I'm curious to see the breakdown for ME/CFS people.
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If C677T is already homozygous, then the status of A1298C is insignificant.Someone selected Compound Homozygous C677T and A1298C. I know that's really rare. I was more interested in the breakdown of MTHFR mutations versus if they had one or didn't have one.
I don't see the choice, but I don't have either of the common MTHFR mutations.
Sushi
@drob31 My new CFS doctor told me that 30% of regular population has these mutations but about 95% of the CFS population has them. I am compound heterozygous and assumed that is what he meant?
Here's the 23andMe data I have for the SNPs which Yasko tests for, for 18 ME patients and 18 controls matched by maternal haplogroup (as an approximation of ethnicity). The Yasko SNPs where everyone has exactly the same version as each other are excluded (2 SNPs), as well as duplicate SNPs where everyone has the same result for multiple SNPs (3 SNPs).
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It's possible that there are MTHFR SNPs which aren't tested by 23andMe that are having an impact. It's also possible that other genes involved with folate or B12 are malfunctioning in different places for different ME patients.So, according to your data MTHFR isn't the right place to look. I guess if someone wanted to cover all aspects, however, they could still take the supplements for MTHFR, but while investigating other areas.
Yeah, good call. Is there a way we can add a none option to the poll, or is it too late?
According to Valentijn, there isn't much a statistical difference. I guess my poll is lacking allot of data without the "none" option.
It's possible that there are MTHFR SNPs which aren't tested by 23andMe that are having an impact. It's also possible that other genes involved with folate or B12 are malfunctioning in different places for different ME patients.
But those are just possibilities - the data which I currently have access to simply doesn't support the possibility of MTHFR or methylation being a major factor in ME/CFS.
Yeah, to be honest I really do not know or understand much about this area. I just got an e-mail from 23andMe that my raw data is in but have not had a chance to look at it yet. Maybe my CFS doctor meant that 95% of the patients he had seen had the compound heterogyzous on MTHFR like me. I really am not sure and don't want to quote him wrong!
Possibly, but unlikely. I wouldn't know where the overlap is between people I have data for and those who are voting. And I prefer to specify that I'm looking at results of ME patients - people who have or have had PEM.Interesting, well maybe this poll could add to your data in some way if enough people vote?
How so? Yasko has the slow version as the "risk" factor, as it implies less tolerance for methyl groups when supplementing B12. But the slow version is also the common version. It's also important to remember that any involvement by VDR, MAOA, and COMT are peripheral to methylation at best - they don't effect how well you methylate, merely how well you supposedly tolerate methylB12.Looking at your chart, MAO looks suspect.
If someone is heterozygous for both on 23andMe results, there's only a 50% chance that they are functionally compound heterozygous. If both mutations are on the same strand, then the other strand picks up the slack and it's just the same as if someone were only heterozygous for C677T - 65% functionality. But if both mutations are on opposite strands, then there is no normal strand to compensate for the mutations, and functionality is down to 30% just as it would be if homozygous for C677T.You can run it through geneticgenie.com to get your detox/methylation profiles for free. I'm compound hetero as well. I keep seeing ALOT of people say they are compound hetero. Even Ben Lynch is compound hetero.
If someone is heterozygous for both on 23andMe results, there's only a 50% that they are functionally compound heterozygous. If both mutations are on the same strand, then the other strand picks up the slack and it's just the same as if someone were only heterozygous for C677T - 65% functionality. But if both mutations are on opposite strands, then there is no normal strand to compensate for the mutations, and functionality is down to 30% just as it would be if homozygous for C677T.
If you have 23andMe results from one or both of your parents, you might be able to figure out if you're actually compound heterozygous, but otherwise it's just a 50/50 possibility. However a high-veggie diet or normal methylfolate supplementation has been shown to completely correct for both folate levels and associated disease risk in either case.