The thing that confused me was whether I was looking at the positive or negative strand for all this, and then, after figuring that out, it turns out that it's a haplotype-issue: individual SNPs don't make as much difference as what combinations you have. The same PMID article said:
Yes, I was wondering the same thing about that NAT2PRED tool. When I input my 23andme results (as is), I get:
Slow = 0.997581. When I look at haplotypes, I think I'm probably *6A/*6A.
I found this a while ago:
http://www.ncbi.nlm.nih.gov/pubmed/24221535
“We identified an 'ultra-slow' acetylator phenotype based on combined *6A/*6A, *6A/*7B and *7B/*7B genotypes containing the homozygous minor alleles of C282T (rs1041983, *6A, *7B) and G590A (rs1799930, *6A).”
I have both of those homozygous snps.
I don't understand this gene. Does it affect your ability to produce acetyl groups? That sounds pretty important to me, since it will affect cognition and the ability to detoxify carcinogens and a whole lot of drugs.
In another thread,
@caledonia said "In addition, you have to balance methyl groups with acetyl groups in order to balance reuptake of neurotransmitters. The relative levels of neurotransmitters are not nearly as important as the reuptake functioning."
http://forums.phoenixrising.me/inde...-in-a-way-i-can-understand.34707/#post-541118
Does this point to a need to take acetyl-containing supplements? Which ones? How do we boost acetylation?
I'm really scratching my foggy-groggy head about this. Why is my brain function so bad lately on the B12 protocol? Something's really out of whack. Is it methyl/acetyl equilibrium?
Can someone help?
@Valentijn, do you know?