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Evil Genius

Nicotine withdrawal and Kratom

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Hi Everyone,

according to personal experiences, i ask myself if other peoples recognized the Impact of Kratom on the desire to smoke tabacum.

I mentioned that i have absolutely no desire to smoke when using Kratom. I heard this too from other Peoples. Besides Kratom seems to be able to inhibit the nicotin Flash, which normally occurs when smoking a huge amount tabacum at once.

Maybe someone has an idea why. Is it possible that Kratom lowers the speed the nicotine needs to flood the Brain? I heard that Kratoms docks at opiate antagonists. Is this true and could that have any influence on consisting dependencies? Iboga seems to have a positive influence on H-Addicts too and i heard that it is also going to be used for fighting withdrawl symptoms. Do you think there are any connections between the effect of these two different plants? I think it might be possible to use Kratom for teraphy purposes to heal addictions or to simply stop smoking. I´m very interested in your thoughts! BestRegs EG

[ 20. August 2005, 01:06: Message edited by: Evil Genius ]

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Evil Genius:

according to personal experiences, i ask myself if other peoples recognized the Impact of Kratom on the desire to smoke tabacum.

Yep I had that back when it was legal, but it occurred for me with lower doses only. It was very effective tho. At higher doses it only used to reduce nicotine intake, not alleviate the overall desire for it

I heard that Kratoms docks at opiate antagonists.

According to my references, it selectively fills the opiod delta sites first, then when they're all full it overspills to the opiod mu receptors. That's why it has a stimulatory effect at lower doses and a sedative effect at higher doses ( making it an opiod agonist- those two terms sometimes get mixed up )- tolerance and batch allowing of course

Apparantly lower doses might be good for treating symptoms of Parkinsonism, because they give a stimulant using receptors other than dopamine, and its dopamine receptors that die off in some parts of the brain over time in Parkinson's patients, making standard medications less effective.

Have you seen Murple's FAQ on kratom? I believe he was working on an upgraded version. That's a good place to start

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They add Ammonia to cigarettes, and adjust the pH, and various other chemical actions, to make the Nicotine 'hit' you faster, as more of a rush.

Just basic chemistry to make it more easily absorbed. Just like we do with our lime paste, lemon juice, etc, in our various plant concoctions.

Perhaps the Kratom inhibits some of these actions and so the nicotine comes on more naturally?

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sound quite positive, but they've gone and made kratom illegal, i never even got a chance to grow it when it was legal and now i cant

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Yeah, it´s sad! Your Country unfortunately was one of the first who listed Kratom but i assume that more will follow. If the less effective Bogus Material hadn´t been available for that long, it probably would have been allready scheduled in a lot countries. Most Cultures aren´t willing to tolerate more than one effective herbal.

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It's more than sad, it's fucken criminal. We were in a unique position to do as much kratom research as we wanted, having had sterile culture material from a confirmed active clone and a host of seriously gifted people who were prepared to donate time and considerable facilities. Now we can't, and it's left in the hands of pharmagiants who are probably the only people who can afford to work around the S9 scheduling

Wonder how much a formal study on receptor binding sites would cost at the local uni? Probably shitloads more than the shitloads it would have cost, what with the extra layers of beaurocracy and security precautions they'd need. If I had a zillion dollars... or even a few dozen thousand... Coming up with something that might be of use would be the biggest buzz...

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Wellbutrin/Zyban (bupropion) acts upon dopamine/norepinephrine levels and other than it's use as an antidepressant, it is known to help cut the pain of withdrawal from both cocaine and tobacco addiction. Someone at the Nook wrote that Kratom acts upon norepinephrine as well as binding to mu receptors. I asked for references so I could learn more, but the author of that comment did not respond. So I do not know whether Kratom has norepinephrine boosting properties or not, but if it did, it may account for some of the withdrawal symptom reduction.

Who knows, Kratom may even help those unfortunate enough to have gotten themselves addicted to methamphetamine as well as cocaine and tobacco, as former meth addicts have very few alternatives other than experiencing nasty withdrawal followed by long term pain/craving, after quitting, in many instances.

It is pure nuts for any government to impose a ban on a plant like Kratom which has not yet been proven significantly dangerous, but we have been there before.

Oddly enough, as I walk down the local roads or forest trails near here, I pass by hundreds of the deadly poisonous Monkshood/Wolfsbane flowers, Pheasants Eye flowers, and Circuta sp flowers.

[ 20. August 2005, 03:52: Message edited by: hoodoo ]

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quote:

According to my references, it selectively fills the opiod delta sites first, then when they're all full it overspills to the opiod mu receptors. That's why it has a stimulatory effect at lower doses and a sedative effect at higher doses

Do you have a reference from the scientific literature about the "spillover" effect Darklight?

The only mention of it I've seen is in Murple's FAQ.

The concept is not explained properly and the FAQ was not written by a pharmacogist, but I'm not aware of a mechanism which fits the description given having been described for any other drug (acting at opiate or any other receptors).

Without seeing a real reference I'd suspect either poorly informed speculation or a misunderstanding

At any rate, the qualitative change in effect with increasing dose could not be explained purely by a change in delta vs mu stimulation. Agonism at both receptor types produces very similiar subjective effects, typical of opioids, (though mu agonists are stronger), so only increasing opioid effects would be expected.

I have not seen it confirmed, but a more likely explanation is that the affinity for norepinephrine receptors is higher than for opioid receptors, so a small dose mainly occupies NE receptors.

Increasing doses would then linearly increase mu (& delta?) receptor occupany, whereas binding to NE receptors would begin to plateau as full occupancy was approached.

This would explain the observed stimulation-sedation transition, though it is likely that differential affinity for, and activity at, the many NE receptors, transporters etc plays some role.

Please post any relevant references(not just on "spillover"), I'm very interested in Kratom's pharmacology but the only molecular studies I've been able to find just measured opioid/NE receptor affinities.

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Tryptameanie:

Do you have a reference from the scientific literature about the "spillover" effect Darklight?

Damn you're gunna make me look But its fair enough, I'll have a dig around. Good point too, glad you asked it.

All my organised references are TC refs, the rest is an orrible jumble. But I'll start checking them and put a list up here of any that look good.

I'm the least chemically knowledgable person here so it's good you come up with more substantial data and knowledge, in fact its great :D

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The only stuff on my puter seems to be direct or indirect repeats of Murple's FAQ, I'll have to delve through my books. I'm sure I've seen something to back that statement up but it could also have been me simply re-reading the same doc in another form ( it looked different so my memory recorded it as different, which is no substitute for checking the source documents ).

Have you asked Murple where he got his info from?

Have you seen these Trypt? I don't have copies of any of these on my computer, will have to check hardcopies

L.T. Yamamoto, S. Horie, H. Takayama, N. Aimi, S. Sakai, S. Yano, J. Shan, P.K.T. Pang, D. Ponglux, K. Watanabe. Opioid receptor agonistic characteristics of mitragynine pseudoindoxyl in comparison with mitragynine derived from Thai medicinal plant (Mitragyna speciosa). Gen. Pharmacol. 33, 73-81 (1999)

Central antinociceptive effects of mitragynine in mice: contribution of

descending noradrenergic and serotonergic systems

Kinzo Matsumoto a, Maho Mizowaki a, Thongpradichote Suchitra a, Yukihisa Murakami a,

Hiromitsu Takayama b, Shin-ichiro Sakai b, Norio Aimi b, Hiroshi Watanabe

Received 20 June 1996; revised 29 August 1996; accepted 3 September 1996

The above might not be what you're looking for but may have a biblio of interest which points you somewhere relevant. If you find anything of interest it would be great if you could interpret it for us

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This is bugging me now. I wrote my page before murple wrote the faq, so chances are he copied that bit from me. This is many years ago though, so I don't remember how it all came about or in which order it came about. Normally I have all references I use to write my pages stored in a folder for that species, so tracing the source is pretty easy. I've just read them all and cannot find a mention of this.

In those days there were really only 3 people I got first hand information about kratom from. This was Giorgio Samorini, Claude Rifat and Karl Jansen. Samorini has everything published, so I don't think it was via him. I still have all of Claude's emails, so I can trawl through these later. But my discussions with Karl Jansen were mostly about his published work on anti addiction treatments via kratom, of which this concept is an integral part. I have the feeling it might have come via him. I will try and find out.

There is also the possibility that it is actually from a hardcopy paper that I did not scan and file (unlikely).

if anyone has asked murple please post the result here.

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Hi,

Darklight i feel bad about the enforced ending of your Kratom Studies. I work on the Mitragyna Species too and i worry it could soon going to become illegal in my country too because that would unfortunately mean that i also have to shut down the work on this very promising plant. If you put a certain amount of money in a Project, you don´t want it getting burried like that!

The scheduling of these plants inhibits serious studies and pharmacological work. I would assume that further work on scheduled substances would lead to very interesting facts about the human brain and it´s complex functions.Like many peoples mentioned, DMT and other tryptamines for example, seem to have a major influence on our daily cognitions, as well as on the very interesting condition what we call Dreaming.It also has impact on serious brain diseases or cluster headaches. The disease schizophrenia seems to have connections to some tryptamines or similar chemicals like serotonin in the Brain.I assume they play an important role in the way our reality is build of. How can you develope a cure for diseases you can´t really understand because you aren´t allowed to look at the causes? I have to think about the very intersting infos y´all posted in this thread. later

hoodoo, i have a package of these zyban at home for a few years now but i didn´t wanted to use them. I only kept it to be a museum piece. A female friend told me that she wanted to strangle her child due to the hallucinogations and psychotic effects triggered by zyban.Definately no stuff you would offer your mom in order to stop smoking :)

I made the experience that high dose Kratom makes me feel drunk like i had too much alcohol. The Native recommendation to use Kratom is to stay at a certain level and to try to keep that level over the day. They said that experienced users can easily prolonge the effects of Kratom over the whole day.Maybe this has something to do with the different agonists used? I would be very interested on the impact of Kratom on these hardy benzo addictions, which are somehow related to alcohol addiction too. I heard in case your are addicted to benzos, you aren´t able to drink alcohol anymore too without falling back into benzo addiction. Not sure if that´s true or myth.

Someone knows what exactly is the active agent in Mitragyna Sp.? Some people had doubts that mitragyne can be the only active agent in the speciosa. I´m not sure what to think about that. I´m asking that because i had no good experiences with extracts but with the herb. But that may also depend on the strain used for making the extract.

[ 20. August 2005, 16:58: Message edited by: Evil Genius ]

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Thanks guys, please post anything more as you find it and I'll do the same :)

 

quote:

I'm the least chemically knowledgable person here so it's good you come up with more substantial data and knowledge, in fact its great

Umm, don't get me wrong, my theory was really just idle speculation, it just sounded more reasonable to me in light of my knowledge of other drugs than the vague and (apparently) unsubstantiated "spillover" idea.

Cheers!

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I'm about 2/3 of the way through my search and can't find anything referring to "spillover". Unlikely I'll locate anything but you'll hear if I do

Thanks Trypt, another myth bites the dust. This is good science :)

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I believe Anodyne is researching Kratom for a uni pharmacology paper, hopefully she'll post a reference list (and maybe her finished paper?)

as well as any insights she might discover, and I'll also look have a look through the refs and translate the interesting bits from Pharmacese to English for you.

[ 27. August 2005, 04:21: Message edited by: Tryptameanie ]

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