I'll respond in
bold below (thanks AJ
):
AJ_ wrote:
Yes, they would be accounted for, or I should say reflected, in the published half-lives,
Okay
but something that inhibits the metabolism of Nal will increase its half life, and the extent to which it does that will be based on these factors. The effective half-life for 6-b-Nal may also increase as new 6-b-Nal is introduced via the metabolism of Nal. I don't know whether the published figure takes this into account, but if it does then it will also change as it would then be partly dependent on the rate 6-b-Nal is produced via the metabolism of nal, which would have changed.
The whole point of this thread was to show that benzo users have nothing to worry about when it comes to this subject. Virgil was concerned because of the study he came across so I looked into it and found the effects to be minimal. Refer to the Nal+Diazepam graph, at worst their blockade might last 20 hours instead of 24. All of the very good points you are bringing up only make this situation better and more insignificant for benzo users. You have consensus with me in just about everything you're saying.
In many situations it is only the drug that has the therapeutic effect, not the metabolites. That is why you will often read in leaflets that you may need to take a smaller dose if you have acute liver disease or kidney disease, not because the drug will actually damage your liver or kidneys, just that with those conditions, the drug may be metabolised or excreted slower, and so your effective dose of the drug doesn't need to be as high. Some if not many drug interactions are focused on a similar issue - that the combination may slow the metabolism of one or both drugs, and therefore the dose needs to be reduced, not because the particular combination is inherently dangerous.
Sometimes only the metabolite has the therapeutic effect, and the pro-drug doesn't. The present situation is complicated because both the parent drug and the metabolite have the desired effect of receptor blockade. Would the increase in Nal availability and half-life outweigh the inhibited production of 6-b-Nal? We don't know. To answer either way would be merely conjecture, and the graphs can't tell us because we don't have all the required information. I also don't know what model of decay you have used, but with drugs it is rarely if ever exponential decay (i.e. a drugs often have different half-lifes at different concentrations, and the published half-life is the half-life of the average maximum concentration from a typical dose). Different people will also metabolise drugs differently, and at different rates.
Good question, and yeah to try to answer it would be merely conjecture.
The equation I used for half-life was 1/2^n where n is the number of half-lives elapsed. That's interesting about the different half-lives at different concentrations and I suspected as much with Nal. Why would a 100mg dose last longer than a 50mg dose (as is purported)?...they would last equally long using a half life model.
Finally, different people metabolize drugs at different rates. This is especially true with Nal.
With all of these unknowns, its probably best if one doesn't read read too much into the study.
I completely disagree. Everything we've elucidated here seems to show that Benzo use does not inhibit Naltrexone potency in any meaningful way, and it could very possibly even enhance it.
People who aren't seeing results have considered increasing their dosage, but I don't think this study should be used by people on say diazapam to increase their Nal dose prematurely. That being said, there is no evidence that 100mg is more harmful, just more expensive, so its a personal decision as to how soon people increase the dose.
I agree, and see no reason to even mention an increase in dosage, and even less of a reason in light of your points. thanks AJ -E
Virgil, I think you're response is in there^^
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