Opioids Does Kratom interfere with Vivitrol (causing pwd)?

[Hodor]

Would you agree with them?

And if Kratom is a full agonist, though others on here have told me it's a partial agonist, then would you not agree that it is not as strong as suboxone, and if not, then how could suboxone be a stronger opioid than kratom?

My doctor wanted to give me suboxone to wean me off kratom and i think i wisely refused because EVERYONE on here says that suboxone is a stronger high than kratom, so if you agree that subs are stronger than kratom but are still a partial agonist, then how would you account for that, or do you really think kratom gets one higher than suboxone?

Opioid strength is not just related to efficacy (i.e. antagonism/partial agonism/full agonism) but also binding affinity. Buprenorphine (the active compound in suboxone) has an insanely high binding affinity; it is structurally related to the ultra-powerful full agonist elephant tranquilizer etorphine. However, it also shares naltrexone's N-methylcyclopropyl group, which is presumably responsible for decreasing its efficacy to the point where it is only a partial agonist (this is of course a grossly simplified explanation of opioid receptor structure-activity-relationships; please don't quote me on that).

At low doses, the binding affinity easily makes up for the low efficacy, meaning that bupe is approximately 40 times as strong as morphine. But once you increase the dose, you eventually reach a point where almost all your opioid receptors are saturated with buprenorphine. At this point, the high affinity no longers works in its favor, because it can no longer make up for the low efficacy by just binding to more receptors at the same time (since they're all already occupied), so the effects cannot get more intense. You've reached what is generally referred to as the "ceiling", and increasing your dose from 8 to 16 or 24 mg or even beyond that is not going to get you any higher.

In terms of opioid receptors getting activated, this "ceiling" for bupe is probably higher than what you'd get from taking just a few grams of kratom per day. However, if you're one of the people who goes through more than a half-ounce of kratom per day, your opioid tolerance may very well be so high that you'd get sick from suboxone.

 

[Mycophile]

Opioid strength is not just related to efficacy (i.e. antagonism/partial agonism/full agonism) but also binding affinity. Buprenorphine (the active compound in suboxone) has an insanely high binding affinity; it is structurally related to the ultra-powerful full agonist elephant tranquilizer etorphine. However, it also shares naltrexone's N-methylcyclopropyl group, which is presumably responsible for decreasing its efficacy to the point where it is only a partial agonist (this is of course a grossly simplified explanation of opioid receptor structure-activity-relationships; please don't quote me on that).

At low doses, the binding affinity easily makes up for the low efficacy, meaning that bupe is approximately 40 times as strong as morphine. But once you increase the dose, you eventually reach a point where almost all your opioid receptors are saturated with buprenorphine. At this point, the high affinity no longers works in its favor, because it can no longer make up for the low efficacy by just binding to more receptors at the same time (since they're all already occupied), so the effects cannot get more intense. You've reached what is generally referred to as the "ceiling", and increasing your dose from 8 to 16 or 24 mg or even beyond that is not going to get you any higher.

In terms of opioid receptors getting activated, this "ceiling" for bupe is probably higher than what you'd get from taking just a few grams of kratom per day. However, if you're one of the people who goes through more than a half-ounce of kratom per day, your opioid tolerance may very well be so high that you'd get sick from suboxone.

Well, i'm not taking kratom right now and just, at least temporarily, taking naltrexone for that and alcohol, but really just to help me more easily abstain for a good long while, because i have managed to stop both for a long time by myself, and my plans are not necessarily permanent abstainance.

But because your explanation is a bit complex, let me just ask you a few simple questions;

1--I had a tolerance of 12 grams per dose of plain leaf kratom to feel really good but was COMPLETELY naive of all other opioids and have only used oxycodone or vicodin years ago for a month or 2 for surgeries, so do you think I would have gotten higher from the 2mgs of suboxone that my doctor wanted to prescribe, and have been going in the wrong direction as many here asserted, or that suboxone really is weaker than kratom ?

2-- do you think a completely opiate naive person will get higher from an approximate amount of suboxone or plain leaf kratom and have a harder time withdrawing from a small amount of plan leaf kratom....meaning they take that daily, or a small amount of suboxone?


3----if you were a doctor and had a kratom addict as a patient, would you sooner recommend them to very slowly taper that plain leaf kratom, or would you switch them to suboxone as my doctor wanted to do with me?


I still insist i made the right choice and will refuse suboxone unless i was ever addicted to a stronger opioid like hydrocodone, oxy, etc.

I take klonopin too, which helps greatly with kratom wd, and all i ever need is about 5 days of feeling tired and crappy to get off kratom, and i think suboxone would have been overkill.

 

[somnilicious]

Well, i'm not taking kratom right now and just, at least temporarily, taking naltrexone for that and alcohol, but really just to help me more easily abstain for a good long while, because i have managed to stop both for a long time by myself, and my plans are not necessarily permanent abstainance.

But because your explanation is a bit complex, let me just ask you a few simple questions;

1--I had a tolerance of 12 grams per dose of plain leaf kratom to feel really good but was COMPLETELY naive of all other opioids and have only used oxycodone or vicodin years ago for a month or 2 for surgeries, so do you think I would have gotten higher from the 2mgs of suboxone that my doctor wanted to prescribe, and have been going in the wrong direction as many here asserted, or that suboxone really is weaker than kratom ?

2-- do you think a completely opiate naive person will get higher from an approximate amount of suboxone or plain leaf kratom and have a harder time withdrawing from a small amount of plan leaf kratom....meaning they take that daily, or a small amount of suboxone?


3----if you were a doctor and had a kratom addict as a patient, would you sooner recommend them to very slowly taper that plain leaf kratom, or would you switch them to suboxone as my doctor wanted to do with me?


I still insist i made the right choice and will refuse suboxone unless i was ever addicted to a stronger opioid like hydrocodone, oxy, etc.

I take klonopin too, which helps greatly with kratom wd, and all i ever need is about 5 days of feeling tired and crappy to get off kratom, and i think suboxone would have been overkill.

I can't really comment much to the science, as much of it is very conflicting and not very well understood by the scientific community and much less by myself but you definitely made the right decision. Suboxone would have been a much heavier and drawn out withdrawal compared to kratom. When it comes to kratom effect and strength there is so much at play because kratom has 40+ alkaloids.... Calcium channel blockers, muscle relaxers, 5-ht2a antagonists, adrenergic compounds, Mu, delta and kappa opiod receptor agonists, partial agonists and antagonists all competing for the receptors and from what I understand much of this interplay is what causes the ceiling effect with kratom because, the antagonists and partial agonists, which are smaller constituents of kratom will be able to compete at higher dosages.

I have seen were it was said that Mitragynine, (which is said to metabolize into 7-OH) and 7-OH were full agonists and then I have seen where they were said to be partial agonists, which one is it. I guess the general consensus is that they are now full agonists. Opiod strength is affected by different factors because there are so many different receptors. Then you also have binding affinity and efficacy. Affinity as I understand it is the strength at which the alkaloid binds to the receptor, kind of akin to its magnetic pull to the receptor. Efficacy is the strength it has in lighting up or activating that receptor once it bound, which I am guessing is similar to full or partial agonists descriptions but there are varying degrees of both binding and efficacy.

I would actually like to know more on the subject. I also believe that the degree to which the different opiate receptors are bound to and activated would also change the overall effect of the substance. Such as simultaneous Mu agonism and kappa antagonism and to what degree the molecule binds to which receptor and the overall efficacy for each respective receptor. So as you can see it becomes a very complicated subject when we are talking about the subtle interplay between dozens of competing agonists, partial agonists and antagonist, all with varying binding affinity and efficacy for different opiate receptor subtypes combined with calcium channel blocking, andrenergic, serotonergic, and muscle relaxing properties.

Regardless, you made the right decision because suboxone dependence and withdrawal is a big step above kratom. Especially if you just have 5 kind of uncomfortable days.

 

[Mycophile]

I can't really comment much to the science, as much of it is very conflicting and not very well understood by the scientific community and much less by myself but you definitely made the right decision. Suboxone would have been a much heavier and drawn out withdrawal compared to kratom. When it comes to kratom effect and strength there is so much at play because kratom has 40+ alkaloids.... Calcium channel blockers, muscle relaxers, 5-ht2a antagonists, adrenergic compounds, Mu, delta and kappa opiod receptor agonists, partial agonists and antagonists all competing for the receptors and from what I understand much of this interplay is what causes the ceiling effect with kratom because, the antagonists and partial agonists, which are smaller constituents of kratom will be able to compete at higher dosages.

I have seen were it was said that Mitragynine, (which is said to metabolize into 7-OH) and 7-OH were full agonists and then I have seen where they were said to be partial agonists, which one is it. I guess the general consensus is that they are now full agonists. Opiod strength is affected by different factors because there are so many different receptors. Then you also have binding affinity and efficacy. Affinity as I understand it is the strength at which the alkaloid binds to the receptor, kind of akin to its magnetic pull to the receptor. Efficacy is the strength it has in lighting up or activating that receptor once it bound, which I am guessing is similar to full or partial agonists descriptions but there are varying degrees of both binding and efficacy.

I would actually like to know more on the subject. I also believe that the degree to which the different opiate receptors are bound to and activated would also change the overall effect of the substance. Such as simultaneous Mu agonism and kappa antagonism and to what degree the molecule binds to which receptor and the overall efficacy for each respective receptor. So as you can see it becomes a very complicated subject when we are talking about the subtle interplay between dozens of competing agonists, partial agonists and antagonist, all with varying binding affinity and efficacy for different opiate receptor subtypes combined with calcium channel blocking, andrenergic, serotonergic, and muscle relaxing properties.

Regardless, you made the right decision because suboxone dependence and withdrawal is a big step above kratom. Especially if you just have 5 kind of uncomfortable days.

Thanks.

So, then though, IF Kratom really IS a full agonist and Suboxone is a partial one, then to what would you attribute your belief that suboxone is overall the stronger opioid, the one that gets people higher and the one that is harder to withdraw from?

Your explanation of affinity and efficacy was pretty good, simple enough for even me to understand haha, so could it be that suboxone has stronger EFFICACY for the receptors it does light up than kratom does?

And what exactly do ''partial agonist'' and ''full agonist'' really mean?

My doctor basically stated it as a given that because kratom is a full agonist and suboxone a partial one that there is no possible way that suboxone could be stronger, and she says she and her colleagues have weaned many kratom users off using suboxone!!

I don't know, that just boggles my mind, and it doesn't sound right to me even if it worked.

I know I don't know much about this stuff, but I just don't think suboxone is meant to be used for something as weak as kratom and cannot see why a slow kratom taper, perhaps one even going down to stem and vein which is weaker, is not the better option than suboxone, which i think is meant for harder opioids.

Everyone here told me that if I have never used many opioids other than kratom that i was going to get HIGH AS HELL off a few mgs of suboxone, so i opted not to make that choice.

It kind of sounds like maybe you are saying that a full agonist would have greater affinity for more receptors than a partial one, is that correct?

So perhaps maybe Kratom would bind to more receptors than Suboxone, but have a weaker affinity and ''light them up'' less, whereas suboxone would bind to fewer but REALLY get them going strong?

I mean i have no idea.

You are talking to a guy who never took chemistry, physics or any kind of neuroscience or anything like that in school, only biology and earth science.

It's kind of a pet peeve of mine that a lot of posters on this forum will go off on these really complex, or at least complex sounding to me, explanations of how all these drugs work and the receptors and all of that without realizing that a lot of us have absolutely no idea what they are saying hahhaahha.

I know that a good portion of this forum is educated when it comes to neuroscience and chemistry and all that, but i think a good portion also is not, so i think that it's better that posters should speak in simpler ways about this stuff and expect that the person they are talking to may not know much about science unless they already know that that person does, but your explanation of affinity and efficacy was good for someone like me who never knew what those terms meant.

 

[Hodor]

So, then though, IF Kratom really IS a full agonist and Suboxone is a partial one, then to what would you attribute your belief that suboxone is overall the stronger opioid, the one that gets people higher and the one that is harder to withdraw from?

Your explanation of affinity and efficacy was pretty good, simple enough for even me to understand haha, so could it be that suboxone has stronger EFFICACY for the receptors it does light up than kratom does?

And what exactly do ''partial agonist'' and ''full agonist'' really mean?

Full agonist: A compound with high efficacy at the receptor, i.e. it can activate it to its full extent, just like the endogenous ligand.

Antagonist: Can bind to your receptors, but does not activate them (i.e. close to zero efficacy); often used to block the receptor from being activated by other substances (assuming it has a higher binding affinity).

Partial agonist: Can bind to your receptors, but not fully activate them due to its lower efficacy. Just like an antagonist, if its binding affinity is high enough, it can also be used to block other substances from activating the receptor, while also keeping it activated to an extent that is therapeutically beneficial (ex.: abilify blocking dopamine when it would make you psychotic, while keeping enough receptors active to prevent you from turning into an apathetic zombie; suboxone keeping enough opioid receptors active to stop cravings, while simultaneously preventing the patient from getting high on full-agonist opioids like heroin).

My doctor basically stated it as a given that because kratom is a full agonist and suboxone a partial one that there is no possible way that suboxone could be stronger, and she says she and her colleagues have weaned many kratom users off using suboxone!!

The first part of the sentence is both true and false. It is entirely possible for a partial agonist to be "stronger" at clinically relevant doses, especially if it has an insane binding affinity like buprenorphine does. On the other hand, given a sufficiently high dose (a *really* high dose), a weak full agonist may eventually produce a stronger high than the high-affinity full agonist.
This is why I keep stressing the importance of one's tolerance levels. Many users of kratom are only taking a few grams per day. These people might not need suboxone, and may very well be better off tapering. However, there are also plenty of users doing a half-ounce to an ounce per day; out of this group of users, many have probably struggled with opioid addiction in the past. In that case, suboxone would probably be the best option.

That said, opioid discontinuation isn't just about getting the exact right amount of receptors activated, it is also about being able to stick to a taper schedule.

Kratom may not be particularly addictive as far as opioids go (which isn't saying much, since opioids are generally highly addictive substances), but when the next shipment of a pound of kratom is just a few clicks away, it can be *very* easy to slip up and mess up your taper, especially if you're predisposed toward opioid addiction.
With suboxone, on the other hand, you are forced to work with a medical professional, who will try to ensure you stick with the taper plan. It also has the great benefit of blocking other opioids, so you are pretty much restricted to sating your opioid cravings with suboxone and unable to get high on other opioids. Even if someone stays on the same dose of suboxone for an extended period of time without starting a taper, this can still be immensely beneficial to a subgroup of patients who are unable to hold down a job or otherwise lead a stable life because they are prone to drug binges. Lastly, buprenorphine is also effective as an antagonist at the kappa opioid receptor, a subtype of opioid receptor responsible for several negative effects, such as paranoia and nausea; consequently, buprenorphine has antidepressant/anti-anxiety effects beyond those resulting from simple mu opioid receptor activation, and has been investigated as a basis for future drugs against treatment-resistant depression.

 

[Mycophile]

Full agonist: A compound with high efficacy at the receptor, i.e. it can activate it to its full extent, just like the endogenous ligand.

Antagonist: Can bind to your receptors, but does not activate them (i.e. close to zero efficacy); often used to block the receptor from being activated by other substances (assuming it has a higher binding affinity).

Partial agonist: Can bind to your receptors, but not fully activate them due to its lower efficacy. Just like an antagonist, if its binding affinity is high enough, it can also be used to block other substances from activating the receptor, while also keeping it activated to an extent that is therapeutically beneficial (ex.: abilify blocking dopamine when it would make you psychotic, while keeping enough receptors active to prevent you from turning into an apathetic zombie; suboxone keeping enough opioid receptors active to stop cravings, while simultaneously preventing the patient from getting high on full-agonist opioids like heroin).



The first part of the sentence is both true and false. It is entirely possible for a partial agonist to be "stronger" at clinically relevant doses, especially if it has an insane binding affinity like buprenorphine does. On the other hand, given a sufficiently high dose (a *really* high dose), a weak full agonist may eventually produce a stronger high than the high-affinity full agonist.
This is why I keep stressing the importance of one's tolerance levels. Many users of kratom are only taking a few grams per day. These people might not need suboxone, and may very well be better off tapering. However, there are also plenty of users doing a half-ounce to an ounce per day; out of this group of users, many have probably struggled with opioid addiction in the past. In that case, suboxone would probably be the best option.

That said, opioid discontinuation isn't just about getting the exact right amount of receptors activated, it is also about being able to stick to a taper schedule.

Kratom may not be particularly addictive as far as opioids go (which isn't saying much, since opioids are generally highly addictive substances), but when the next shipment of a pound of kratom is just a few clicks away, it can be *very* easy to slip up and mess up your taper, especially if you're predisposed toward opioid addiction.
With suboxone, on the other hand, you are forced to work with a medical professional, who will try to ensure you stick with the taper plan. It also has the great benefit of blocking other opioids, so you are pretty much restricted to sating your opioid cravings with suboxone and unable to get high on other opioids. Even if someone stays on the same dose of suboxone for an extended period of time without starting a taper, this can still be immensely beneficial to a subgroup of patients who are unable to hold down a job or otherwise lead a stable life because they are prone to drug binges. Lastly, buprenorphine is also effective as an antagonist at the kappa opioid receptor, a subtype of opioid receptor responsible for several negative effects, such as paranoia and nausea; consequently, buprenorphine has antidepressant/anti-anxiety effects beyond those resulting from simple mu opioid receptor activation, and has been investigated as a basis for future drugs against treatment-resistant depression.

Thanks for such a good explanation.

That's the kind that works for someone like me who doesn't have a great understanding of this stuff but you made it all very clear.

I can see that another reason my doctor also wanted to try me on suboxone is because i do also have depression and anxiety, but to be honest, Kratom works really really well for those, and I'm not sure that suboxone would have worked better, nor were we talking about keeping me on suboxone, so the idea of using something only for a very short term for depression, as in my case since she was really wanting to use it mainly to taper me off kratom, would seem to make little sense.

I certainly would not have wanted paranoia, and when looking up the side effects that suboxone has I see MANY more than I have ever experienced from suboxone.

I guess the answer is complicated as to which is really ''stronger'', but I know i made the right choice because i already take Klonopin which I had been unaware of till recently is probably the main reason why it's always so easy for me to get off of kratom and never takes more than 3-5 days of feeling tired and sleeping a lot and probably entirely explains why i have never gotten restless leg syndrome while in kratom WD, because Klonopin works for that.

So that being said, i cannot know how bad my kratom wd ever would have been in the past without klonopin, but my doctor also knew i take klonopin and was the one who really fully informed me that it would help with the wds, so I think her reasoning was even more incorrect.

Also, let me ask you this as per the bolded parts;

I spoke to about 12-15 posters on here, all of whom had used HIGH doses of quality kratom, suboxone at different doses, and other opioids AND EVERY SINGLE ONE told me that even 2mgs of suboxone would likely get me MUCH MUCH higher than the 12 gram doses of plain leaf i was taking, since OTHER than kratom i do not use other opioids and have only used oxy or hydro a handful of times for surgery.

But where I get confused is that yes, I was one of those users, till i stopped a month ago, who would dose 12 grams, 2-3 times per day because my tolerance is that high, but KRATOM HAS A CEILING EFFECT, so that I found your quote where you said ''given a high enough dosage a weak full agonist will produce a stronger high than the high-affinity full agonist.''

So for me, because a few years ago I started taking too much kratom, i pretty much permanently ruined my tolerance so that no matter how long i go without, even though my tolerance will at first go back to 3 grams, i need only break that dose a few times before it shoots back up to 12 grams doses, but no matter how much I take....pretty much anything higher than 14 grams is not going to get me any higher and will only make me feel like crap, so that's why i don't necessarily know if i buy that idea in comparing kratom to suboxone, if it is in fact true that kratom is a full agonist and not a partial one.

And then, the thing is, for me 12 grams would have the same effect that 3 grams would for someone else, so other than negative side effects with increased dose, isn't 3 grams for them and 12 grams for me the same difference?

Given kratom's celiing effect and what many suboxone users here have told me about how highly abusable it has been for them and how high they have gotten off of it, i have a hard time imagining any amount of PLAIN LEAF kratom getting anyone higher than the highest amount of bupe.

Granted, doctors won't usually prescribe just any amount of bupe for that reason, but my doctor was talking about starting me on EIGHT MGS of Suboxone and weaning me to 2mgs, and i have VERY hard time believing that 8mgs of suboxone would not have gotten me higher and more opioid dependent than kratom.

Also, and this is the REAL kicker.....and I DO think she's a good doctor, but not in this way.......

......So, i just started taking naltrexone and at first i thought it was making me tired but now i realize it's not really and mostly my klonopin, but when i first told her that she said ''well, we might want to switch to suboxone then if it's making you tired''.....ISN'T THAT CRAZY?!?

Here I am NOT ANY LONGER DEPENDENT ON KRATOM or any opioid AT ALL....and she was wanting to give me suboxone because she thought it might help me for my cravings for kratom and just put me on subs so i wouldn't go back to kratom!!!!

I'm sorry, but I thought that was straight up NUTS.

Kratom is not that bad an opioid that if that is the ONLY recreational opioid one uses that I believe they should be put on suboxone maintainence so as not to go back to kratom.

I said ''sorry, but I'd sooner go back to Kratom than go on suboxone. I like being opioid free and i don't need that.''

And she said ''ok, i understand.''


I mean, i think that is just overkill completely and many posters on here agreed.

The thing is, I am not some kind of bad addict, I just have anxiety and depression and i have an addictive personality so when things aren't going well I'll take about an ounce of kratom a day and drink a bottle of wine 4-5 days a week and was taking about 20mgs of dexadrine a day, but that was it.

Sure, i was overdoing it, but i have pulled myself back from binges like that, sometimes also including weed and a little phenibut and nitrous here and there, many many times all by myself, and this time i just wanted to try out naltrexone to see what it was like because I figured it would give me more control in terms of choosing to abstain or even moderate, and it has so far proven successful.

It's not like i'm a heroin addict or someone drinking a bottle of whisky a day, who, no offense to any of them, are the types i would think need subs. maintainance, but while i really like this doctor overall and think she'll prove helpful in other areas of my life, i don't think she realizes that i am not in need of such heavy duty treatment, which is what i feel suboxone kind of is IMO, ESPECIALLY to the point of suggesting it to me AFTER i was already off kratom for cravings which, honestly.....I haven't even had barely any of, and i have still skipped the naltrexone many days and have plenty of kratom in my closet, but just knowing that i have the naltrexone and can immediately swallow it should i have an urge to take kratom or drink has stopped me.

Anyways, rant over lol.

 

[Realmccoy]

Kratom is going to have mostly mitragynine as an active component, there isn't a massive variation in alkaloid content between varieties, at least from my first-hand analysis (GCMS of chlorofor:ethanol extract of kratom leaf). A recent study showed that most of the activity actually comes from metabolic activation of mitragynine to 7-OH-mitragynine.

Kratom is not a partial agonist, it is a full agonist. One of the classic 'proofs' that showed that mitragynine was indeed an opioid was that its effects were reversed by naloxone. Naltrexone would do the same. It just has a much longer duration of action. At best you'd be left with a mild adrenergic stimulant along the lines of low dose yohimbine - probably not very pleasant or useful.

Presumably if you were on a high enough dosage of kratom, you'd get some sort of precipitated withdrawal. But between the short half-life and comparatively low dose when compared to "recreational" heroin usage, I would think that as little as 24 hours after dosing you should be fine when it comes to opioid antagonists. The only time precipitated withdrawals are a concern is initially, switching from full-agonists to partial-agonists or antagonists. Once you are taking naltrexone on a regular basis, if you "slip" you will not get sick but rather ... nothing will happen.

Naltrexone has been reported to reduce alcohol consumption/cravings as well but I don't think it actually blocks the inebriating effects of alcohol. Maybe some of the rewarding effects will be reduced, but nothing like the total removal of most effects from any opioid.

Kratom is a partial opioid agonist like Suboxone. It’s not a full opioid agonist hence it doesn’t completely fuck you up. Get your facts right!

 

[Shant]

Kratom is a partial opioid agonist like Suboxone. It’s not a full opioid agonist hence it doesn’t completely fuck you up. Get your facts right!

You sure about this? I’ve always heard it’s a full agonist.

 

[Realmccoy]

You sure about this? I’ve always heard it’s a full agonist.

Google it I promise. If it were a full agonist it would be an opiate (opiate is anything derived from the poppy plant either synthetic or natural). An opioid is both partial and full agonist. It’s an opioid but not an opiate. If it were a full agonist it would have killed a lot of people and junkies would be putting it in needles.

 

[Shant]

Ok, I googled it.
“Mitragynine and 7-hydroxymitragynine, the two alkaloids mainly responsible for the effects of kratom, are selective and full agonists of the μ-subtype opioid receptor (MOR).”

Kratom (Mitragyna speciosa) drug profile | www.emcdda.europa.eu

Kratom drug profile Chemistry Physical form Pharmacology Origin Mode of use Other names Analysis Typical potency

www.emcdda.europa.eu

 

[Realmccoy]

It does have full agonist properties but it is predominantly partial agonist, so much so it is referred to as a partial opioid agonist by the majority of the sources I have visited. Theoretical aside, have you ever used a full opioid agonist, and have you ever used a partial opioid agonist like suboxone? Now tell me which one does kratom's effects mimic? Those were rhetorical questions. You are arguing for the sake of arguing. So it has some full agonist effects but it is still a partial opioid agonist.

 

[Realmccoy]

Mitragynine is a Partial Agonist of Human MOR. We isolated the four major alkaloids (Figure 1) from the Thai strain of Mitragyna speciosa and prepared 7-OH by photochemical oxidation of mitragynine (Scheme S1).Jun 1, 2016

Synthetic and Receptor Signaling Explorations of the ...
www.ncbi.nlm.nih.gov › pmc › articles › PMC5189718

 

[Realmccoy]

7-Hydroxymitragynine Is an Active Metabolite of Mitragynine ...
www.ncbi.nlm.nih.gov › pmc › articles › PMC6598159

May 29, 2019 - We have reported that mitragynine and 7-OH are partial agonists of the human μ-opioid receptor (hMOR) in vitro, with 7-OH (EC50 = 34.5 nM; ...
by AC Kruegel - ‎2019 - ‎Cited by 24 - ‎Related articles

People also ask

 

[Realmccoy]

Mitragynine - an overview | ScienceDirect Topics
www.sciencedirect.com › topics › mitragynine


Despite structural similarity to yohimbine, mitragynine acts as a µ-opioid receptor partial agonist. The relatively minor component, the indole alkaloid 7- ...

 

[Realmccoy]

Ok, I googled it.
“Mitragynine and 7-hydroxymitragynine, the two alkaloids mainly responsible for the effects of kratom, are selective and full agonists of the μ-subtype opioid receptor (MOR).”

Kratom (Mitragyna speciosa) drug profile | www.emcdda.europa.eu

Kratom drug profile Chemistry Physical form Pharmacology Origin Mode of use Other names Analysis Typical potency

www.emcdda.europa.eu

Read the bottom three post. You're like 10% right and 90% wrong

 

[Realmccoy]

Read the bottom three post. You're like 10% right and 90% wrong

Kratom has limited full opioid agonist properties but it is predominantly partial and is always referred to as a partial opioid agonist.

 

[Shant]

Ok bud you seem to be the expert, not arguing with you. I’ve simply never heard that it’s a partial agonist and I know a dude who takes it with heroin and there’s no PWD so I dunno what to make of that. Maybe some strains are partial and some aren’t? But to answer your question, suboxone doesn’t make me feel like shit. No euphoria, absolutely zilch. But a K-shot (Kratom) fucks me up.

 

[Shant]

Thanks.

So, then though, IF Kratom really IS a full agonist and Suboxone is a partial one, then to what would you attribute your belief that suboxone is overall the stronger opioid, the one that gets people higher and the one that is harder to withdraw from?

Your explanation of affinity and efficacy was pretty good, simple enough for even me to understand haha, so could it be that suboxone has stronger EFFICACY for the receptors it does light up than kratom does?

And what exactly do ''partial agonist'' and ''full agonist'' really mean?

My doctor basically stated it as a given that because kratom is a full agonist and suboxone a partial one that there is no possible way that suboxone could be stronger, and she says she and her colleagues have weaned many kratom users off using suboxone!!

I don't know, that just boggles my mind, and it doesn't sound right to me even if it worked.

I know I don't know much about this stuff, but I just don't think suboxone is meant to be used for something as weak as kratom and cannot see why a slow kratom taper, perhaps one even going down to stem and vein which is weaker, is not the better option than suboxone, which i think is meant for harder opioids.

Everyone here told me that if I have never used many opioids other than kratom that i was going to get HIGH AS HELL off a few mgs of suboxone, so i opted not to make that choice.

It kind of sounds like maybe you are saying that a full agonist would have greater affinity for more receptors than a partial one, is that correct?

So perhaps maybe Kratom would bind to more receptors than Suboxone, but have a weaker affinity and ''light them up'' less, whereas suboxone would bind to fewer but REALLY get them going strong?

I mean i have no idea.

You are talking to a guy who never took chemistry, physics or any kind of neuroscience or anything like that in school, only biology and earth science.

It's kind of a pet peeve of mine that a lot of posters on this forum will go off on these really complex, or at least complex sounding to me, explanations of how all these drugs work and the receptors and all of that without realizing that a lot of us have absolutely no idea what they are saying hahhaahha.

I know that a good portion of this forum is educated when it comes to neuroscience and chemistry and all that, but i think a good portion also is not, so i think that it's better that posters should speak in simpler ways about this stuff and expect that the person they are talking to may not know much about science unless they already know that that person does, but your explanation of affinity and efficacy was good for someone like me who never knew what those terms meant.

I’ll give you my 2 cents amigo, as I’ve gone both routes multiple times. Suboxone is better for kicking. For the sheer reason you feel absolutely nothing, which is why it’s good for beating the psychological addiction which any addict knows is 10 times harder to shake than the physical addiction.Suboxone is a strange drug in that you can start at 24mg and ween down to 4mg inside a week, maybe 10 days and not notice a damn thing. Plus it’s got a 37 hour half life which is much longer than Kratom so you can do it once a day or split your dose morning and night and you’re all good. Kratom you’ll be doing a few times a day. It’s unpredictable which is very bad for detoxing.

But that’s not to say you can’t make the Kratom work for you. You can, there’s plenty of people in this forum that have done it. But for me? Beating years of heroin/fentanyl/methadone abuse, suboxone was literally the only thing that gave me half a chance.

 

[Shant]

Thanks for such a good explanation.

That's the kind that works for someone like me who doesn't have a great understanding of this stuff but you made it all very clear.

I can see that another reason my doctor also wanted to try me on suboxone is because i do also have depression and anxiety, but to be honest, Kratom works really really well for those, and I'm not sure that suboxone would have worked better, nor were we talking about keeping me on suboxone, so the idea of using something only for a very short term for depression, as in my case since she was really wanting to use it mainly to taper me off kratom, would seem to make little sense.

I certainly would not have wanted paranoia, and when looking up the side effects that suboxone has I see MANY more than I have ever experienced from suboxone.

I guess the answer is complicated as to which is really ''stronger'', but I know i made the right choice because i already take Klonopin which I had been unaware of till recently is probably the main reason why it's always so easy for me to get off of kratom and never takes more than 3-5 days of feeling tired and sleeping a lot and probably entirely explains why i have never gotten restless leg syndrome while in kratom WD, because Klonopin works for that.

So that being said, i cannot know how bad my kratom wd ever would have been in the past without klonopin, but my doctor also knew i take klonopin and was the one who really fully informed me that it would help with the wds, so I think her reasoning was even more incorrect.

Also, let me ask you this as per the bolded parts;

I spoke to about 12-15 posters on here, all of whom had used HIGH doses of quality kratom, suboxone at different doses, and other opioids AND EVERY SINGLE ONE told me that even 2mgs of suboxone would likely get me MUCH MUCH higher than the 12 gram doses of plain leaf i was taking, since OTHER than kratom i do not use other opioids and have only used oxy or hydro a handful of times for surgery.

But where I get confused is that yes, I was one of those users, till i stopped a month ago, who would dose 12 grams, 2-3 times per day because my tolerance is that high, but KRATOM HAS A CEILING EFFECT, so that I found your quote where you said ''given a high enough dosage a weak full agonist will produce a stronger high than the high-affinity full agonist.''

So for me, because a few years ago I started taking too much kratom, i pretty much permanently ruined my tolerance so that no matter how long i go without, even though my tolerance will at first go back to 3 grams, i need only break that dose a few times before it shoots back up to 12 grams doses, but no matter how much I take....pretty much anything higher than 14 grams is not going to get me any higher and will only make me feel like crap, so that's why i don't necessarily know if i buy that idea in comparing kratom to suboxone, if it is in fact true that kratom is a full agonist and not a partial one.

And then, the thing is, for me 12 grams would have the same effect that 3 grams would for someone else, so other than negative side effects with increased dose, isn't 3 grams for them and 12 grams for me the same difference?

Given kratom's celiing effect and what many suboxone users here have told me about how highly abusable it has been for them and how high they have gotten off of it, i have a hard time imagining any amount of PLAIN LEAF kratom getting anyone higher than the highest amount of bupe.

Granted, doctors won't usually prescribe just any amount of bupe for that reason, but my doctor was talking about starting me on EIGHT MGS of Suboxone and weaning me to 2mgs, and i have VERY hard time believing that 8mgs of suboxone would not have gotten me higher and more opioid dependent than kratom.

Also, and this is the REAL kicker.....and I DO think she's a good doctor, but not in this way.......

......So, i just started taking naltrexone and at first i thought it was making me tired but now i realize it's not really and mostly my klonopin, but when i first told her that she said ''well, we might want to switch to suboxone then if it's making you tired''.....ISN'T THAT CRAZY?!?

Here I am NOT ANY LONGER DEPENDENT ON KRATOM or any opioid AT ALL....and she was wanting to give me suboxone because she thought it might help me for my cravings for kratom and just put me on subs so i wouldn't go back to kratom!!!!

I'm sorry, but I thought that was straight up NUTS.

Kratom is not that bad an opioid that if that is the ONLY recreational opioid one uses that I believe they should be put on suboxone maintainence so as not to go back to kratom.

I said ''sorry, but I'd sooner go back to Kratom than go on suboxone. I like being opioid free and i don't need that.''

And she said ''ok, i understand.''


I mean, i think that is just overkill completely and many posters on here agreed.

The thing is, I am not some kind of bad addict, I just have anxiety and depression and i have an addictive personality so when things aren't going well I'll take about an ounce of kratom a day and drink a bottle of wine 4-5 days a week and was taking about 20mgs of dexadrine a day, but that was it.

Sure, i was overdoing it, but i have pulled myself back from binges like that, sometimes also including weed and a little phenibut and nitrous here and there, many many times all by myself, and this time i just wanted to try out naltrexone to see what it was like because I figured it would give me more control in terms of choosing to abstain or even moderate, and it has so far proven successful.

It's not like i'm a heroin addict or someone drinking a bottle of whisky a day, who, no offense to any of them, are the types i would think need subs. maintainance, but while i really like this doctor overall and think she'll prove helpful in other areas of my life, i don't think she realizes that i am not in need of such heavy duty treatment, which is what i feel suboxone kind of is IMO, ESPECIALLY to the point of suggesting it to me AFTER i was already off kratom for cravings which, honestly.....I haven't even had barely any of, and i have still skipped the naltrexone many days and have plenty of kratom in my closet, but just knowing that i have the naltrexone and can immediately swallow it should i have an urge to take kratom or drink has stopped me.

Anyways, rant over lol.

And btw you’re right, that doc WAS crazy. If you were already stabilized on naltrexone she’d have to be off her rocker to say “OK let’s switch you to suboxone”...wtf! For starters, as a doctor she should know damn well that naltrexone doesn’t cause fatigue. If you’re on klonopins she couldn’t figure out that those were the cause of your “fatigue”? Anyway I didn’t read this thread from the beginning but I hope you’re still opioid free and still on naltrexone. I’m almost off suboxone and will be transitioning to naltrexone myself.

PS - to all 12 to 15 posters on here who told you that 2mgs of suboxone would get you “MUCH MUCH HIGHER” than Kratom are all liars or fools. You could slip 2mg in the drink of someone who has never done an opiate in their life and they probably wouldn’t even notice.

 

[Realmccoy]

Ok bud you seem to be the expert, not arguing with you. I’ve simply never heard that it’s a partial agonist and I know a dude who takes it with heroin and there’s no PWD so I dunno what to make of that. Maybe some strains are partial and some aren’t? But to answer your question, suboxone doesn’t make me feel like shit. No euphoria, absolutely zilch. But a K-shot (Kratom) fucks me up.

Post acute withdrawal is usually caused by either the naloxone in the Suboxone or the fact that Suboxone has a high affinity for the receptors so it throws the heroin off. Kratom has a much lower affinity.