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420chan is Getting Overhauled - Changelog/Bug Report/Request Thread (Updated July 26)

does kratom block heroin

- Thu, 18 Jul 2019 03:15:06 EST Tr7vQ+lJ No.608224
File: 1563434106668.png -(129900B / 126.86KB, 288x300) Thumbnail displayed, click image for full size. does kratom block heroin
I do like 10g or more of kratom a day and i got some heroin today and didnt get very high from it if at all, did i get bad gear or does kratom block opiates like suboxone does?
Phoebe Nuttingtag - Thu, 18 Jul 2019 06:56:26 EST aALRdKDy No.608226 Reply
I'm not sure man, I dont think Kratom would block H like bupe does - but it does increase general Opi tolerance for sure. My guess would be the H was fairly weak, or the dose was low compared to where your tolerance currently is - but this is all purely my own opinion and not in any way scientifically based. I'm pretty sure that Kratom does not have a higher binding affinity to opiate receptors than H though, which is why I came to that conclusion...
hsn - Thu, 18 Jul 2019 10:22:40 EST cA+802PK No.608227 Reply
some people claim it does but I’ve never had an issue. You most likely have a shitty batch of dope. It’s no where near suboxone s binding affinity so heroin should be able to break through kratoms antagonistic effects no prob.
dr. m - Thu, 18 Jul 2019 14:51:49 EST 1qKXc0ke No.608229 Reply

It appears that it's very likely that not only does kratom raise cross tolerance, but also likely does have at least partial agonists and possibly full on antagonists at the MORs that block at least some of the effects of other middle of the road affinity opioids like the condones and presumably morphine/heroin. I've never actually studied the MOR binding affinities of common opioids...just Narcan, bupe, naltrexone, and genuine fentanyl hcl.

I just stole the following copy pasta from a circlejerk poster who seemed to know their shit and had a good quality posting history. Bear in mind I couldn't access the actual paper quoted, and yes I actually tried.

...[So the different alkaloids do different things this is from two papers: Mitragynine and the oxidized analogue 7-hydroxymitragynine, are partial agonists of the human mu-opioid receptor and competitive antagonists at the kappa- and delta-opioid receptors. Mitragynine pseudoindoxyl and its corresponding corynantheidine analogs show promise as potent analgesics with a mechanism of action that includes mu opioid receptor agonism/delta opioid receptor antagonism and mitragynin pseudonoxl antagonizes kappa.

The following is taken from a table testing agonism or antagonism with their EC50 and IC50 values. Number in brackets are antagonism, all values are in micromolar concentrations:

mu kappa delta
mitragynine 0.339 ± 0.178 [8.5 ± 7.6 (1.4)] [>10]

paynantheine [2.2 ± 10] [>10] [>10]

speciogynine [5.7 ± 2.8] [>10] [>10]

speciociliatine [4.2 ± 1.6] [>10] [>10]

7-OH 0.0345 ± 0.0045 [7.9 ± 3.7] [>10]

I cannot access the paper to see the numbers for Mitragynine pseudoindoxyl.

Pretty much you want nanomolar concentrations as when you start getting above 5 micromolar the effect is pretty weak and not as relevant. So mitragynine is a potent agonist of mu at 339 nanomolar, but not a significant antagonist at kappa and delta. Paynantheine and speciogynine have modest antagonism at mu, but about 100X less potent than mitragynine agonism. 7-OH has the most potent agonism at mu with 34.5 nanomolar and modest antagonism at kappa. If I remember, I saw the paper on Mitragynine pseudoindoxyl and it was a potent enough for mu agonism and kappa and delta antagonism but I don't know the numbers.

Edit, sorry can't get the table to format correctly, but you can see the numbers for mu first, kappa second, delta 3rd.]

So, first off I honestly don't know what IC50 and EC50 values represent or how they're related. I assume it's a different type of measurement than Ki affinity values.

Yo nodson, can you make heads or tails of this science speak? What say ye resident kratomfag?

Also I forgot your answer to my question about the recommended strain or 2-3 strains from your favorite vendor you mentioned. Which strain is the most potent (preferably red or at least green instead of white vein), and which strain is least stimulating regardless of potency? I'm ordering a few sample packs today and need to know what to get for my old people.

Also, since 7-ohm is created through oxidation of mitragyne or w/e, does that mean kratom left in a jar with some extra oxygen for a year will age it positively like fine wine? I'm thinking of buying a kilo or two half kilos before Indonesia bans exporting or the US bans importing kratom from Indonesia, since apparently that country exports 95% of our country's kratom production. If it only gets better the longer it ages, might as well get it now right?

On a side note, I am considering dropping my bupe dose every 5 days from 4>3>2.5>2>1.5>1.25>1>0.8 to 0.1mg 100ug at a time, to 50ug, then switching to kratom+ULDN for a few months to see if it does more good than harm for me, instead of switching to low dose naltrexone.

Still not convinced it's necessarily a good idea or even a step forward, but I'm just considering it. Anyone have any thoughts on the matter? An anon asked me what my endgame was as I'm approaching one year on bupe having started on 24mg/day subbed and currently on 4mg/day snorted/plugged, and apart from definitely dropping down to 2mg/day snorted/plugged within 2-6 months, I really have no idea beyond that. My fear is that kratom is too short acting and way too much work to encapsulate like 5-40 capsules minimum every single day, and that I'd end up mentally addicted again because in theory I should maybe feel something when I dose kratom, which rewires the Pavlovian cause>effect link in my mind. Also, dosing 3-4x aka (every 4-5 hours )per day may not be doable for me with my new career I'm starting in August.

It sounds like I've already answered my own question in that I haven't had more than one day of strong cravings to use per month in the last 5-6 months minimum. It's like I forgot how good it feels/felt. Either way, there's no way using full agonists besides kratom is remotely a good idea for at least 5 years and most likely forever. That ship has sailed and I don't need to lose another spouse or something equally important largely caused directly or indirectly by full agonist opioid use. That shit multiplies depression long term IMO even if you don't get clean.

tl;dr OP IMO it definitely raises cross tolerance and also does partially block oxy/pst/heroin related usage, but IME only really in terms of euphoria for the most part, and only when both your kratom and other opioid dosage/tolerance is high enough that most or all receptors end up occupied. When someone uses lower doses of both opioids regularly, I presume the blocking effect is less of a concern.

If I needed pain relief, I'd still combine them in low doses. With higher doses, I'd wait at least 6 hours after last kratom dose to use another opioid. If you use to get high, wait at least 18-24hr since last kratom dose.
dr. m - Thu, 18 Jul 2019 14:58:46 EST 1qKXc0ke No.608231 Reply

So yeah it appears that 7-OHM is the most likely culprit because it's a partial agonist and appears to have a pretty high binding affinity. There could possibly be others as well.
hsn - Thu, 18 Jul 2019 15:58:31 EST cA+802PK No.608234 Reply
7-OHM is found in such little concentrations that it is unlikely to have any kind of effect. My best guess is that mitragynine’s antagonistic effects are more apparent in certain people if they are hypersensitive to it like with tramadol and it’s seizure causing effects. Personally I’m one of those who are very sensitive to the SNRI effects. It’s a weak mu and delta antagonist but like I said I suspect certain people are just more sensitive to it just like with anything. If this was such a problem, people would be getting thrown into precipitated withdrawal from the kratom competing with your last dose the same way bupe can. I just suspect it’s a small percentage of people like OP who experience this if for some reason it isn’t due to other unknown factors like dope quality and tolerance.

IC50 has to do with how much of of an inhibitor is left after 50% of its max concentration. EC50 is a 50% change in either direction.

This fella put it nicely
“If considering simple receptor-ligand interactions, the IC50 is used to describe the concentration of an inhibitor that results in a half-maximal inhibition of a response (i.e. the concentration that reduces a response to 50% of its maximum). That maximum response being inhibited is due to the action of something else (typically an agonist for the receptor of interest). The EC50 is conceptually similar although it is more inclusive. EC50 can be used for both the inhibition of responses (by an inhibitor) but it is more commonly used to describe the stimulation of responses (such as with an agonist). EC50 is the concentration that results in a 50% change in response, in either direction.“

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