The Supreme Court on Thursday rejected a controversial settlement that would have sent billions of dollars to treatment programs and victims of the nation’s opioid epidemic but that also shielded the Sackler family from future lawsuits despite the fact that it made its fortune selling prescription opioids.
I don’t know vyvanse xr method of action off the top of my head…
But for opioids the difference in in enzymatic breakdown is already problematic.
Even for non XR, some people just burn thru it at different rates.
Personally I don’t have enough of a couple of the L enzymes and that means most opioids barely do anything to me. Some people have too much and will burn thru a Vicodin in half as much time, leaving them unmedicated for half the time.
There’s just too much human variation for a one sized fits all approach.
The point I’m making is, while I’m aware of people being fast or slow metabolizers, that should only factor in when it comes to active ingredient that is fully mechanically released and available for metabolism.
It cannot metabolize that which has not either been a) mechanically released or b) that which is pharmacodynamically inertt since it requires cleaving off the other binding substance (like l-lysine in Vyvanse) before the underlying active drug can be mechanically available to metabolize if that makes sense.
Vyvanse cannot be injected or administered in basically any other ROA than oral like normal dex because it (lis-dexamferamine—not dextroamphetamine) is inert until it has undergone the uncleaving of lysine from the active drug. Doesn’t matter how fast one metabolizes dextro, nobody metabolizes lis as a straight stimulant, it is inert until made not so thru the blood or whatever.
Also, doesn’t that mostly apply to codeine and morphine, wasn’t aware of that extending to oxy and hydro?
I don’t know vyvanse xr method of action off the top of my head…
But for opioids the difference in in enzymatic breakdown is already problematic.
Even for non XR, some people just burn thru it at different rates.
Personally I don’t have enough of a couple of the L enzymes and that means most opioids barely do anything to me. Some people have too much and will burn thru a Vicodin in half as much time, leaving them unmedicated for half the time.
There’s just too much human variation for a one sized fits all approach.
The point I’m making is, while I’m aware of people being fast or slow metabolizers, that should only factor in when it comes to active ingredient that is fully mechanically released and available for metabolism.
It cannot metabolize that which has not either been a) mechanically released or b) that which is pharmacodynamically inertt since it requires cleaving off the other binding substance (like l-lysine in Vyvanse) before the underlying active drug can be mechanically available to metabolize if that makes sense.
Vyvanse cannot be injected or administered in basically any other ROA than oral like normal dex because it (lis-dexamferamine—not dextroamphetamine) is inert until it has undergone the uncleaving of lysine from the active drug. Doesn’t matter how fast one metabolizes dextro, nobody metabolizes lis as a straight stimulant, it is inert until made not so thru the blood or whatever.
Also, doesn’t that mostly apply to codeine and morphine, wasn’t aware of that extending to oxy and hydro?
Morphine (not sure about codeine) are/is one of the few options that are direct acting.
Oxy, Vicodin, and all the rest first get broken down I to an active metobalite. Even if they’re not XR. XR just compounds the issue