just the simple presence of a duplicate CYP2D6 genes does not mean anything due to it's highly polymorphic properties. The reason being is that for as many people who have fully functional duplicate genes, approximately as many people have duplicate CYP2D6 genes that are mutated null allele genes which are inherited meaning that they almost completely lack CYP2D6 enzyme activity and have exactly the opposite problem that SWIY has.
The problem is the fact that it mutates, and if gene duplication events take place then if it has a fully functional allele you have a problem similar to what you describe. But if able to figure out all this on your own, SWIM
probably didn't tell you anything you didn't already know.
However, the medical world does not stand still. "Until recently, detection of multiplicate CYP2D6 genes required the use of restriction fragment length polymorphism (RFLP) analyses."
How long has it been since SWIY gave up on doctors?
About 10 years ago "more simple and rapid PCR-based methods for efficient genotyping of UMs were developed." UM = ultra-rapid metabolizers (whether it be by mutated gene, duplicate gene, or whatever.
Identification of people who have would be classified as an "ultra-rapid metabolizer" is very very important for adjustment of doses in drug therapy, as well as to avoid misidentification of noncompliance.
Tests can prove this! Ask for the tests to be performed, then you would have conclusive evidence that you are in fact telling the truth. SWIM thinks your doctors would definitely work with you if you can document this condition.
Also as stated in the above post, 2C19 would have only considerable inducing effect on diazepam
, naproxen, nirvanol, omeprazole, propranolol, and S-mephenytoin. But diazepam itself has an active metabolite, nordiazepam which accounts for it's longer half life. So an inducing effect on diazepam would not necessarily reduce it ineffective. And also 2D6 induces metabolism of codeine
as also stated in the above post which is this particular case is a good thing as the faster and more rapid metabolism of codeine, the more of it would be converted to morphine
compared to a regular person. As far as the MASSIVE amounts of acetaminophen
SWIY consumed via the 30mg codeine/ 300mg APAP
and no liver damage after 8 years... acetaminophen is metabolized by 1A2, 2E1 and 3A4 and to a lesser extent 3A5... Actually it is 3A4 that accounts for metabolism of over 50% of commonly prescribed as well as THC.
I took 100 Tylenol/w codeine a day for 8 years and my liver is fine; so, the Mayo Clinic doctor didn't believe me. I was in pain for 30 years, and all any doctor needed to do was believe I was I was telling the truth. The only way I'd goto a doctor about this is if I had something to go on. If whatever is going on is that complex, then I need a theory to present to a doctor. Otherwise, I know where this will go.
again you are confusng SWIM. Explain please how SWIY can be 31 years old and have been in pain for 30 years? Do you remeber being 1 years old? Again not trying to argue but can you explain how this is so? Was SWIY born into this world and immediately needed to be treated for pain? That can be the case perhaps, but I don't know many people that can remember being 1 year old. Just trying to get to the bottom of this and some answers to some questions.