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A therapeutic dose of a long acting drug in combination with an abused drug for HR?

MeDieViL

Bluelighter
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Feb 11, 2007
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A well known example of this is methadone, however its used as substitution, now i am wondering wheter something simular could be done for people that still abuse their drugs.

I came on this idea because of my use of desoxypipradol, its a very long acting stimulant wich people generally dont feel the urge to redose on, also there doesnt seem to be any craving when it slowly wears off.
now ive been trying MDPV today and noticed the following benefits:
- MDPV works alot stronger and synergizes perfectly with desoxy
- I dont notice mdpv wear off, there's no sudden drop off not any craving afterwards so i cant be bothered at times just waiting hours to redose
- It feels very smooth during the day, i never really notice anything wear off, great for therapeutic use, mdpv if you need a extra boost or for some recreational effects or whatever youd like.
- It seems with desoxy as base like pretty much all drugs work perfectly on it, tried some flephedrone on it, worked like a charm and again a smooth transition to desoxy, also desoxy stayed as powerfull even if i took other drugs before it.

This is just an example for stims, i bet the same can be done with phenibut and GBL (if being carefull) (actually a girl i know allways combined them and never had any withdrawal issues, till i tolled her to stop phen as i tought the combo was bad that time wich resulted in full blown addiction.

klonopin and some xanax for recreation added to it.

Tolerance may be a issue as your receptors are constantly agonized but there's memantine for that.

AMT also is a smooth base for things like mdma, flephedrone etc.

Anyway the point of this thread is, could be this be a way to reduce harm in addiction as:
- no cravings when coming down, no need to go to extreme lenghts for more money, you wont feel absolute shit youd just be like a non addict wanting some shit.
- Substitution therapy has been shown to have a good effect on the harms caused by heroin addiction look at methadone.
- It will be easier to stop an addiction, just stay on the maintenance somewhere.

Those that know me know that im allways extremely optimistic, wich often turned out right but i might be too optimistic on this shit, but worth the discussion atleast id say.
 
Its possible it would induce massive tolerance due to chronic activation of certain receptors but i beleive mem would be the solution for that, and some small courses of ibogaine but the anecdotes on that are too limited.

Being skeptic? haha thats the way to miss out on many good solutions, i remember that everyone said it was impossible to block tolerance with dxm and mem till i made a thread with anecdotes where time after time it was confirmed to work.

Offcourse allways assuming something will work would be stupid, but being stupid leads to alot of things that do work (and alotthat dont obviously)
 
I think that combining two stimulants (one short-acting, one much longer) is a terrible idea. Sure, the short-term effects of the comedown of e.g. MDPV are going to be masked, but after you discontinue both drugs you'll feel much worse than trying to detox from either alone. In reality you're not migitating any of the harm done by stimulants, you're just making it harder to percieve.

I also don't believe that memantine is the miracle wonder drug people tout it to be. It certainly won't prevent the development of tolerance to dopaminergic stimulants.
 
In my experience mem works well enough it also absolutely does magic for the comedown, one big trick however is too is to never let the doses escalate, rather take a short day break wich with mem is enough to let tolerance drop again.

Also it depends wheter youd want to be on the maintenance drug forever or for years, SSRI's downregulate receptors just as well just read all the withdrawal horror story's.

Another trick for crashes is the use of a drug with another mechanism, like use G for a few days, this is the wonder trick for withdrawals too, 2 weeks of benzo's and g withdrawals are painless, 2 weeks of G and you withdrawal painlessly from opiates.

If you ask me its foolisch to go trough pains of withdrawals and comedowns when you can just take something while the receptors upregulate.
 
I also don't believe that memantine is the miracle wonder drug people tout it to be.
Id call this "negative skeptism" as it may very well work, positive skeptism would be saying i have my doubts but hey lets try, or admitting it may work.
 
That said desoxy could also be used in the way methadon is used, just give a amp addict it and hell function fine on it, wont miss he's amp much and once and awhile can get high on top of it.

The other option is enduring extreme craving wich is just terrible, heck i think it would be silly to crave and battle addiction my whole life while id be allright on desoxy, i still want my recreationals but feel fine the days without them just like non addicts.
 
but after you discontinue both drugs you'll feel much worse than trying to detox from either alone..
I completely disagree, youd take half the dose of both wich wont cause any worse withdrawals.

I also don't believe that memantine is the miracle wonder drug people tout it to be. It certainly won't prevent the development of tolerance to dopaminergic stimulants.
http://www.bluelight.ru/vb/threads/...lection-of-the-evidence-and-anecdotal-reports

Shitload of ahttp://www.bluelight.ru/vb/threads/501875-NMDA-antagonists-for-tolerance-a-collection-of-the-evidence-and-anecdotal-reports

Shitload of anecdotes prove you wrong.
 
I highly recommend the herb rhodiola to get you off of stimulants completely. It's a supplemental adrenal adaptogen used to treat depression so it has some effect on modulating the serotonin system, but it has zero side effects. In your case I would go above the usual dose and take 300-400mg per day, once in the morning. It will last the entire day in your body, and being an adaptogen, it will moderate your cortisol levels so that you have energy when you need it but it will help you chill out completely when you need to rest. I've used rhodiola to treat downers after stimulant use and it works wonders.

I know you've read lots of anecdotal reports and feel strongly about it, but my gut tells me that using MDPV or another stimulant to get off a stimulant seems like a bad idea. It's true that there are drug therapies used to get you off the drugs, but the secondary assistant usually needs to have some therapeutic value in order to aid the actual recovery. That's why I recommend rhodiola. It's stimulating but nutritive.
 
I highly recommend the herb rhodiola to get you off of stimulants completely. It's a supplemental adrenal adaptogen used to treat depression so it has some effect on modulating the serotonin system, but it has zero side effects. In your case I would go above the usual dose and take 300-400mg per day, once in the morning. It will last the entire day in your body, and being an adaptogen, it will moderate your cortisol levels so that you have energy when you need it but it will help you chill out completely when you need to rest. I've used rhodiola to treat downers after stimulant use and it works wonders.

I know you've read lots of anecdotal reports and feel strongly about it, but my gut tells me that using MDPV or another stimulant to get off a stimulant seems like a bad idea. It's true that there are drug therapies used to get you off the drugs, but the secondary assistant usually needs to have some therapeutic value in order to aid the actual recovery. That's why I recommend rhodiola. It's stimulating but nutritive.
Its not to get off stims, im not addicted to stims, just use them several times a week, i never get withdrawals comedowns for some reason wich is nice:) I do take rhodiola togheter with st johns wort, quercetine (wich i use for tolerance, it lowers nitric oxide wich works like nmda antagonists), phenibut and aniracetam.

I dont see why its a bad idea, it SOUnDS like a bad idea however if you half the dose of both its not.
 
I take 500mg twice a day.

anecdotally, i often forget to redose mdpv on desoxy, often take a dose in the morning and only redose in the evening, works great.
 
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I'd also like to throw in I'm not a fan of negative skepticism either, if there's no danger in trying something then by all means try it and don't keep telling yourself it won't work. Some psychiatrists will even prescribe memantine and stimulants for the purpose of keeping tolerance low.
 
no idea why but this combo i dont abuse unlike all other stim releasers or things like ritalin or ethylphenidate, prob just me but... interesting

Ill try desoxy with other stuff, must be the background stim keeping me "satisfied" i think.
trying alphapvp with it next.

Cannabinoids def increase addictive behavor and abolish the combo's ability to not constantly chase a high, ur-144 in this case.

Low doses of desoxy have simular benefits with ethylphenidate wich im testing now for awhile instead of MDPV.

Update: works like a charm again, dramatically reduced ethyl abuse.

MDPV and desoxy are far more selective for da then ne compared with releasers like amp, perhaps that explains my positive therapeutic response and much lower tendency to abuse, who knows...
 
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I would not be suprised if some non-monoaminergic mechanism modulates this - desoxypipradol is pretty similar in structure to dirty simple drugs like PCP, cyclizine, etc.

More selectivity for dopamine does not make sense that it would result in reduced abuse, generally the more selective for DA the more problems with self administration the drug has. Not to say NE release does not play a part (NET knockout rats don't respond normally to MDMA) but I don't think MDPV is "less prone to abuse than amphetamines".
 
Its more prone to abuse id say, i was just referring to my particular brain chemistry. Im the only one here that finds mdpv far less addictive then most other stims.
 
There are studies that do point towards memantine as a cognitive protector. Studies do show memantine to reduce neurotoxicity with Amp. and MDMA use.
Recent research has demonstrated that blockade of a7 nicotinic acetylcholine receptors (nAChR) inhibits METH- and MDMA-induced ROS production in striatal synaptosomes which is dependent on calcium and on NO-synthase activation. Moreover, a7 nAChR antagonists (methyllycaconitine and memantine) attenuated in vivo the neurotoxicity induced by METH and MDMA, and memantine prevented the cognitive impairment induced by these drugs

Neuronal Nicotinic Receptors as New Targets for Amphetamine-Induced Oxidative Damage and Neurotoxicity
- David Pubill, Sara Garcia-Ratés, Jordi Camarasa and Elena Escubedo

Abstract: Amphetamine derivatives such as methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, “ecstasy”) are widely abused drugs in a recreational context. This has led to concern because of the evidence that they are neurotoxic in animal models and cognitive impairments have been described in heavy abusers. The main targets of these drugs are plasmalemmal and vesicular monoamine transporters, leading to reverse transport and increased monoamine efflux to the synapse. As far as neurotoxicity is concerned, increased reactive oxygen species (ROS) production seems to be one of the main causes. Recent research has demonstrated that blockade of a7 nicotinic acetylcholine receptors (nAChR) inhibits METH- and MDMA-induced ROS production in striatal synaptosomes which is dependent on calcium and on NO-synthase activation. Moreover, a7 nAChR antagonists (methyllycaconitine and memantine) attenuated in vivo the neurotoxicity induced by METH and MDMA, and memantine prevented the cognitive impairment induced by these drugs. Radioligand binding experiments demonstrated that both drugs have affinity to a7 and heteromeric nAChR, with MDMA showing lower Ki values, while fluorescence calcium experiments indicated that MDMA behaves as a partial agonist on a7 and as an antagonist on heteromeric nAChR. Sustained Ca increase led to calpain and caspase-3 activation. In addition, modulatory effects of MDMA on a7 and heteromeric nAChR populations have been found.

Also with the PDF-
http://www.mdpi.com/journal/pharmaceuticals/special_issues/drug_abuse
 
Ooh that sounds like a recipe for pure depression - a short acting stimulant inside of a long acting one! A comedown inside a comedown ... inception !

I wonder if the comedown sparing effect you notice from the 'pip is competion and the 'pip knocks the MDPV off the receptor due to higher affinity.

It frankly blows my mind that people knowingly CHOOSE to use MDPV .
 
I also don't believe that memantine is the miracle wonder drug people tout it to be. It certainly won't prevent the development of tolerance to dopaminergic stimulants.

This is a pretty bold statement. Why are you so certain?
 
There are studies that do point towards memantine as a cognitive protector. Studies do show memantine to reduce neurotoxicity with Amp. and MDMA use.


Neuronal Nicotinic Receptors as New Targets for Amphetamine-Induced Oxidative Damage and Neurotoxicity
- David Pubill, Sara Garcia-Ratés, Jordi Camarasa and Elena Escubedo

Abstract: Amphetamine derivatives such as methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, “ecstasy”) are widely abused drugs in a recreational context. This has led to concern because of the evidence that they are neurotoxic in animal models and cognitive impairments have been described in heavy abusers. The main targets of these drugs are plasmalemmal and vesicular monoamine transporters, leading to reverse transport and increased monoamine efflux to the synapse. As far as neurotoxicity is concerned, increased reactive oxygen species (ROS) production seems to be one of the main causes. Recent research has demonstrated that blockade of a7 nicotinic acetylcholine receptors (nAChR) inhibits METH- and MDMA-induced ROS production in striatal synaptosomes which is dependent on calcium and on NO-synthase activation. Moreover, a7 nAChR antagonists (methyllycaconitine and memantine) attenuated in vivo the neurotoxicity induced by METH and MDMA, and memantine prevented the cognitive impairment induced by these drugs. Radioligand binding experiments demonstrated that both drugs have affinity to a7 and heteromeric nAChR, with MDMA showing lower Ki values, while fluorescence calcium experiments indicated that MDMA behaves as a partial agonist on a7 and as an antagonist on heteromeric nAChR. Sustained Ca increase led to calpain and caspase-3 activation. In addition, modulatory effects of MDMA on a7 and heteromeric nAChR populations have been found.

Also with the PDF-
http://www.mdpi.com/journal/pharmaceuticals/special_issues/drug_abuse

The first few days it just blocks those drugs from releasing monoamines, this doesnt proof anything.

Ooh that sounds like a recipe for pure depression - a short acting stimulant inside of a long acting one! A comedown inside a comedown ... inception !

I wonder if the comedown sparing effect you notice from the 'pip is competion and the 'pip knocks the MDPV off the receptor due to higher affinity.

It frankly blows my mind that people knowingly CHOOSE to use MDPV .

A comedown in a comedown? That doesnt make any sense, unless people here miss the point and dont half the doses of both stims there shouldnt be more comedowns.

As an aside doesnt seem this works long term without breaks, i developped full tolerance to desoxy, even 60mg in a day doesnt keep me awake lol, so it also stopped me using other stims a ton less and just as much as without.
If you can take breaks then it should be a very good solution tough.
 
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