Not sure why you are getting so defensive
No, not defensive in the slightest. I was simply astounded by what you seemed to be saying.
I am a tolerant and patient person and try to understand the point of view of others but your statements were just too much for me. I was expressing my astonishment.
Adding the qualification that a bad environment as well as degree of sickness might influence "expression of a SNP" (to use your terminology, but one I wholly disagree with) doesn't really help. You are still invoking magic.
So your and her position is that SNPs barely matter at all?
Some do nothing at all (probably most), a few seem to have very significant effects (usually because they completely disable a critical enzyme) and some have a small effect.
This latter group includes most of the SNPs that get discussed over and over again on PR. The internet discussion of SNPs has completely distorted the significance of these small effects and convinced people that they have serious mutations that directly cause their health problems. There have been many scientific studies of many SNPs and they simply don't support this idea.
Well done association studies (not the early ones with small sample groups and inadequate statistics) do show a degree of association of some SNP combinations with various disease states, but the genetic contribution is small.
This doesn't mean I think SNPs are irrelevant. If I did I wouldn't have bothered to do a 23andme test nor spent considerable amounts of time understanding at least some of my SNPs.
Fortunately I don't seem to have any of the really serious SNPs but do have a mixture of ones known to have a small effect.
I see knowledge of these as something of an insurance policy - ie it is knowledge of potential weak points.
In healthy people who are eating well, they probably don't matter much. But we are not healthy and many of us are forced into very restricted diets because of food intolerances. Both of these circumstances (and especially the widespread metabolic derangements which seem to be associated with this disease) place our systems under strain and here weak points might manifest themselves. So if there is anything I can do to bolster the weak points I will do it.
This is not so very different from your idea that being sick has made a difference. Where I differ is that I don't attribute symptoms and sensitivities to particular SNPs, I don't single out some SNP as being the cause of some problem, particularly when there is no evidence for it and plenty of evidence to the contrary. I recognise that the endpoints that we perceive as symptoms have complex inputs, only one of which might be a small genetic contribution from various SNPs.
Where there is good reason to think that my combinations of SNPs might be contributing to slowing of an important metabolic pathway, and particularly when this is backed by functional data from an OAT, then I might decide to supplement cofactors for the affected enzymes and/or end products of the pathways, to help my struggling system.
I have COMT and MAO-A and definitely have problems with neurotransmitters
As already discussed, the MAO A variant makes a protein identical to the wildtype - ie the SNP has no effect. If you persist in ignoring things like this then you can't expect people to take you seriously.
Here is a post from Jack Kruse that might help explain it better
Jack Kruse is a neurosurgeon (? former) so I readily accept that he knows far more about the nervous system and related clinical matters than I do.
As for what he said in the quotes, this doesn't flow from that expertise so I don't just accept it. I want to know what it is based on. For example he makes claims for A1298C arising in equatorial regions, most particularly the East Africa rift zone or Mediterranean basin, in response to environmental conditions there. He goes on to say that we should look to the origins of our mitochondrial DNA to see if they accord with this.
I have this SNP and my heritage is almost exclusively from northern Europe (English and Irish). There is a tiny component from west-central Africa, presumably dating from more than 70,000 years ago before the African exodus.
So not especially convincing for me, though I could be persuaded to take him more seriously if he presented some genetic data about the incidence of this SNP, particularly among ancestral populations in East Africa.
So sorry, Jack Kruse doesn't help me much in accepting that COMT causes your methylfolate sensitivity.