@Púca Rebellion I'm not really sure what you mean when you say that Methadone causes intestinal obstruction. Constipation is one of the archetypal Opioid symptoms along with stuff like itching (pruritus) and miosis (narrowed pupils). Otherwise, an intestinal obstruction would be something like a foreign body becoming stuck in the the digestive tract. I am not aware of "Methadose" causing any side effects that are significantly different than any other form of Methadone. Granted, there are people who are sensitive to certain dyes and binders that are used in pharmaceuticals, though this is not what you're describing.
I definitely would disagree that "Methdose" produces a withdrawal of "greater intensity". I could be wrong, I just can't imagine how this could be the case.
Methadone is a generic drug. Methadone clinics, just like hospitals and pharmacies have the ability to choose where they buy their drugs from. "Methadose" is just one example of a commonly used brand name, though this is not at all a uniform thing across the country. I am not convinced that the issues you are describing with "Methadose" are accurate. I would ask you to throw down some references for these claims so we can further the debate.
@4DQSAR First off, the Buprenorphine tends to bind to the Mu Opioid Receptor (MOR) with a slightly higher affinity than that of Naloxone. What this means is that Naloxone will play a negligible role in how the combination of Buprenorphine/Naloxone actually effects a person. The biggest crime of Pharma here is just this, that they marketed a drug at significantly higher cost during a huge wave of Opioid addiction. Buprenorphine was already a relatively cheap generic drug by this point. Pharma manufacturers would go on to convince the powers that be of Suboxone's decreased abusability as the result of the Naloxone. This led to a practice of only prescribing Suboxone due to the perceived risk of standalone Buprenorphine.
Even despite the mounting evidence that the Naloxone found in "Suboxone" has practically no effect whatsoever (it's more common to encounter folks who are allergic to Naloxone than anything else, even these cases are a very small percentage of the whole) the practice of prescribing "Suboxone" has continued in America and the myth of its requirement mostly persists among doctors too stupid or lazy to read into it.
Also, you were discussing Precipitated Withdrawal. First off, we know that the Naloxone in "Suboxone" does not cause precipitated withdrawal due to the above-mentioned competition for binding affinity with Buprenorphine. Naloxone will not produce a mild form of precipitated withdrawal on a completely open-ended basis when a person is maintained on "Suboxone".
Next, Precipitated Withdrawal is not a phenomenon that works "both ways" as you're describing. Buprenorphine basically unseats other Opioids from your MOR's and takes their place. This is a pretty simplistic explanation, but it's accurate. This "unseating" is also why Buprenorphine is able to block the effects of these same Opioids. To be clear, Buprenorphine produces precipitated withdrawal in an Opioid-dependent individual. If that same individual then takes an Opioid agonist like Morphine, the effects of the Morphine will just be blocked as opposed to producing precipitated withdrawal.
Now back to the original objective of this post, discussing the relative potency of Methadone compared to other common Opioid agonists. I believe that the numbers used in the "mainstream" i.e. dose conversion charts/calculators are probably as close to accurate as we can easily get.
If we are comparing to say Morphine/Heroin, Oxycodone, Hydrocodone to name a few, Methadone is well-known for a greater variability/lower predictability regarding how a given dose will effect a specific person. Methadone is highly effected by enzymes of the P450 family, whereas the others I have listed here are negligibly effected. When the numbers for bioavailability are listed as between 40%-80%, they are doing their best to account for this variability and keep people safe.
Furthermore, people consume other pharmaceuticals, foods and supplements that can have significant effects on the enzymes I have listed above. What's more, there is evidence that a more alkaline stomach environment can have a positive effect on bioavailability of Methadone. So, at the end of the day, there is a ton of potential variability with this drug specifically that makes it really hard to pin down a universal dosing guideline.
You can only use the established guidelines as a good place to start. The only person who will really know for sure is you when you take the drug though.
I saw some folks talking about the chirality of Methadone. I'm not positive if this is needed, but here is a small tidbit. Methadone is chiral and only one enantiomer is a potent Opioid agonist, that being Levomethadone. Dextromethadone has effects of its own, though they are mild by comparison and not predicated on Opioid agonism.
In certain parts of Europe and elsewhere, only the Levomethadone is used. Germany for instance, uses this stuff a lot. Racemic Methadone is cheaper to produce as the resolution of the molecule is not needed, saving a costly last step in the synthesis process. However, as we know that Dextromethadone produces potentially unwanted and complicating side effects, it's easy to see how this is just as unethical as the purposeless inclusion of Naloxone in the product "Suboxone"
Here we have examples of Pharma using opposite sides of the same idea to fuck with the health of the populace. With Suboxone, they add a useless substance to make more money and with Racemic Methadone they don't do the work of removing a useless substance from the Methadone, also to save money.
