27 replies to this topic

[bgwithadd]

It seems to make sense and is maybe an obvious/stupid question, but I was wondering if anyone had some personal experience with this effect.

[luv2increase]

It seems to make sense and is maybe an obvious/stupid question, but I was wondering if anyone had some personal experience with this effect.

I don't know if it will help with tolerance or not, but taking neuroprotective agents is general a good thing to do for your health and longevity.


1mg Selegiline twice a week
5mg Methyl-b12 EOD
adaptogens
vitamin c
& others should be on your list.

[FunkOdyssey]

Search "memantine + amphetamine" or "memantine + tolerance" on both this board and Mind & Muscle.

[bgwithadd]

Well, I can't really get memantine and am not sure I would take that. Living in the US I am not so sure it's possible to get Selegine either, thought hat's something I'm interested in trying. Does it help with actual tolerance, though?

I was thinking more like general neuroprotectants such as the racetams, idebenone, etc. and wondering if that effect would help.

I am reading up on the methyl b12. Thanks so much for pointing that out, I had no idea what it was before now. The SAMe stuff works for me if I use a high dose but it's so fucking expensive. Even with doctor visits included adderal works out to be so much cheaper. I had no idea there was a SAMe precursor.

[luv2increase]

You can get selegiline in the US with a prescription from your doctor or over the internet without a prescription. It is not a controlled substance, so you cannot get in trouble buying it or possessing it. It is perfectly legal.


SAMe is some good stuff, but you should be careful taking it with amphetamines because of the chance of excess serotonin levels.



Get methyl b12. It is cheap. The best is Jarrows MethylB12 lozenges. It comes in 1mg or 5mg. I take a 5mg EOD held under my tongue on an empty stomach first thing in the morning about an hour before I eat any food.

[bgwithadd]

Next time I go to my regular doc I will get the selegine, then. My psych does not seem too keen on lots of supplementation (and sort of understandably so, since some people overdo it).

[luv2increase]

Next time I go to my regular doc I will get the selegine

Go to this page http://www.emsam.com...UseBVCookie=Yes and print it off. Take it to your GP or psychiatrist and tell him/her that you are depressed, and one of your family members is having great success with Emsam for their depression, and you'd like to try it as well. Also, I hope you have good insurance because I believe the patches run close to $500 for a 30 day supply :(


You are going to have to go the Emsam route if you want to get it prescribed because transdermal selegiline (Emsam) is the only one approved for treating depression in the US. You probably won't be able to get the others because they aren't approved for depression unless you have a great doctor.



You could also do like I am many other people here do which is to get the liquid selegiline. 1mg ED would cost you $60 for 300 days going that route.

[FunkOdyssey]

There are open-minded, forward thinking psychiatrists out there willing to experiment with memantine off-label for amphetamine tolerance. If you are unwilling to order memantine yourself from overseas, you have the option of finding one of those doctors.

[inmostleaf]

SAMe is some good stuff, but you should be careful taking it with amphetamines because of the chance of excess serotonin levels.

What is this?

How would SAMe + Amph = excess serotonin levels?

If you respond please cite your reference.

[inmostleaf]

I agree with FunkOdyssey that you should head to Mind & Muscle and even Dr. Bobs with this question. I mean, I could answer it but in a roundabout way it would be from there.

So with that being said I'd ask Graaatch or Section 8.

You know, Graaatch used to post here but he got sick and tired of luv2increase prevaricating with this own understanding so he stopped.

Regardless, good luck!

[luv2increase]

I just thought since they could both increase serotonin levels in the brain, one may want to be careful taking them concurrently.

Edited by luv2increase, 10 October 2008 - 02:55 AM.

[Jacovis]

Memantine appears to have potential in reducing any neurotoxicity from amphetamines as well (not just preventing tolerance) according to these three Spanish rodent studies dealing with Meth and MDMA...

1: Neurotoxicology. 2008 Jan;29(1):179-83. Epub 2007 Sep 22. Links
Memantine prevents MDMA-induced neurotoxicity.
Chipana C, Camarasa J, Pubill D, Escubedo E.
Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Nucli Universitari de Pedralbes, Universitat de Barcelona, Av. Joan XXIII s/n, 08028 Barcelona, Spain.

MDMA (ecstasy) is an illicit drug causing long-term neurotoxicity. Previous studies demonstrated the interaction of MDMA with alpha-7 nicotinic acetylcholine receptor (nAChR) in mouse brain membranes and the involvement of alpha-7 nicotinic acetylcholine receptors (nAChR) in dopaminergic neurotoxicity induced by MDMA in mice. The aim of the present study was to investigate the utility of memantine (MEM), an alpha-7 nAChR antagonist used for treatment of Alzheimer's disease patients, to prevent neurotoxicity induced by MDMA in rats and the oxidative effect of this amphetamine derivative in mice striatal synaptosomes. In isolated mouse striatal synaptosomes (an in vitro model of MDMA neurotoxicity of dopaminergic origin), MDMA (50 microM)-induced reactive oxygen species (ROS) production that was fully inhibited by MEM (0.3 microM). This effect of MEM was fully prevented by PNU 282987 (0.5 microM), a specific agonist of alpha-7 nAChR. The preventive effect of MEM on this oxidative effect can be attributed to a direct antagonism between MDMA (acting probably as agonist) and MEM (acting as antagonist) at the alpha-7 nAChR. In Dark Agouti rats (an in vivo model of MDMA neurotoxicity of serotonergic origin), a single dose of MDMA (18 mg/kg) induced persistent hyperthermia, which was not affected by MEM pre-treatment. [(3)H]Paroxetine binding (a marker of serotonergic injury) was measured in the hippocampus of animals killed at 24h and 7 days after treatment. MDMA induced a significant reduction in [(3)H]paroxetine binding sites at both times of sacrifice that was fully prevented by pre-treatment with MEM. Since previous studies demonstrate that increased glutamate activity is not involved in the neurotoxic action of MDMA, it can be concluded that the effectiveness of MEM against MDMA-induced neurotoxicity would be the result of blockade of alpha-7 nAChR, although an indirect mechanism based on the interplay among the various neurotransmission systems leading to an increase in basal acetylcholine release should also be taken into account.

PMID: 17980434 [PubMed - indexed for MEDLINE]


1: Neuropharmacology. 2008 Jun;54(8):1254-63. Epub 2008 Apr 9. Links
Memantine protects against amphetamine derivatives-induced neurotoxic damage in rodents.
Chipana C, Torres I, Camarasa J, Pubill D, Escubedo E.
Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Universitat de Barcelona, Avda Joan XXIII s/n, Zona Universitaria Pedralbes, 08028 Barcelona, Spain.

We hypothesize that 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH) interact with alpha-7 nicotinic receptors (nAChR). Here we examine whether memantine (MEM), an antagonist of NMDAR and alpha-7 nAChR, prevents MDMA and METH neurotoxicity. MEM prevented both serotonergic injury induced by MDMA in rat and dopaminergic lesion by METH in mice. MEM has a better protective effect in front of MDMA- and METH-induced neurotoxicity than methyllycaconitine (MLA), a specific alpha-7 nAChR antagonist. The double antagonism that MEM exerts on NMDA receptor and on alpha-7 nAChR, probably contributes to its effectiveness. MEM inhibited reactive oxygen species production induced by MDMA or METH in synaptosomes. This effect was not modified by NMDA receptor antagonists, but reversed by alpha-7 nAChR agonist (PNU 282987), demonstrating a preventive effect of MEM as a result of it blocking alpha-7 nAChR. In synaptosomes, MDMA decreased 5-HT uptake by about 40%. This decrease was prevented by MEM and by MLA but enhanced by PNU 282987. A similar pattern was observed when we measured the dopamine transport inhibited by METH. The inhibition of both transporters by amphetamine derivatives seems to be regulated by the calcium incorporation after activation of alpha-7 nAChR. MDMA competitively displaces [(3)H]MLA from rat brain membranes. MEM and METH also displace [(3)H]MLA with non-competitive displacement profiles that fit a two-site model. We conclude that MEM prevents MDMA and METH effects in rodents. MEM may offer neuroprotection against neurotoxicity induced by MDMA and METH by preventing the deleterious effects of these amphetamine derivatives on their respective transporters.

PMID: 18455739 [PubMed - indexed for MEDLINE]


1: Eur J Pharmacol. 2008 Jul 28;589(1-3):132-9. Epub 2008 May 20. Links
Memantine prevents the cognitive impairment induced by 3,4-methylenedioxymethamphetamine in rats.
Camarasa J, Marimón JM, Rodrigo T, Escubedo E, Pubill D.
Laboratory of Pharmacology and Pharmacognosy, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain. jcamarasa@ub.edu <jcamarasa@ub.edu>

Amphetamine abuse is an important risk factor for the development of cognitive impairment involving learning and memory. Since in previous studies we have demonstrated the effectiveness of alpha-7 nicotinic receptor antagonists in preventing the neurotoxicity induced by amphetamine derivatives, the present paper seeks to determine whether pre-treatment with memantine (MEM) (an antagonist of both nicotinic and NMDA receptors) counteracts the memory impairment induced by 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) administration in male Long Evans rats. In mice, MDMA and MEM induced a locomotor stimulant response but with a different profile. Moreover, MEM inhibited the rearing and thygmotaxis behaviour induced by MDMA. Non-spatial memory was tested in the object recognition test and the spatial learning and memory was tested in the Morris water maze. In our experimental conditions, rats receiving MEM pre-treatment recovered the ability to discriminate between the familiar and the novel object that had been abolished by MDMA treatment. Animals treated with MDMA showed impaired learning in the Morris water maze. Results of the probe trial demonstrated that MDMA-treated rats did not remember the location of the platform, but this memory impairment was also prevented by the MEM pre-treatment. Moreover, MEM alone improved the learning task. No differences were observed between the different groups as regards swim speed. In conclusion, MEM significantly improved the learning and memory impairment induced by MDMA and constitutes the first approach to the treatment of the long-term cognitive deficits found in ecstasy users.

PMID: 18582864 [PubMed - in process]

[inmostleaf]

Memantine appears to have potential in reducing any neurotoxicity from amphetamines as well (not just preventing tolerance) according to these three Spanish rodent studies dealing with Meth and MDMA...

1: Neurotoxicology. 2008 Jan;29(1):179-83. Epub 2007 Sep 22. Links
Memantine prevents MDMA-induced neurotoxicity.
Chipana C, Camarasa J, Pubill D, Escubedo E.
Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Nucli Universitari de Pedralbes, Universitat de Barcelona, Av. Joan XXIII s/n, 08028 Barcelona, Spain.

MDMA (ecstasy) is an illicit drug causing long-term neurotoxicity. Previous studies demonstrated the interaction of MDMA with alpha-7 nicotinic acetylcholine receptor (nAChR) in mouse brain membranes and the involvement of alpha-7 nicotinic acetylcholine receptors (nAChR) in dopaminergic neurotoxicity induced by MDMA in mice. The aim of the present study was to investigate the utility of memantine (MEM), an alpha-7 nAChR antagonist used for treatment of Alzheimer's disease patients, to prevent neurotoxicity induced by MDMA in rats and the oxidative effect of this amphetamine derivative in mice striatal synaptosomes. In isolated mouse striatal synaptosomes (an in vitro model of MDMA neurotoxicity of dopaminergic origin), MDMA (50 microM)-induced reactive oxygen species (ROS) production that was fully inhibited by MEM (0.3 microM). This effect of MEM was fully prevented by PNU 282987 (0.5 microM), a specific agonist of alpha-7 nAChR. The preventive effect of MEM on this oxidative effect can be attributed to a direct antagonism between MDMA (acting probably as agonist) and MEM (acting as antagonist) at the alpha-7 nAChR. In Dark Agouti rats (an in vivo model of MDMA neurotoxicity of serotonergic origin), a single dose of MDMA (18 mg/kg) induced persistent hyperthermia, which was not affected by MEM pre-treatment. [(3)H]Paroxetine binding (a marker of serotonergic injury) was measured in the hippocampus of animals killed at 24h and 7 days after treatment. MDMA induced a significant reduction in [(3)H]paroxetine binding sites at both times of sacrifice that was fully prevented by pre-treatment with MEM. Since previous studies demonstrate that increased glutamate activity is not involved in the neurotoxic action of MDMA, it can be concluded that the effectiveness of MEM against MDMA-induced neurotoxicity would be the result of blockade of alpha-7 nAChR, although an indirect mechanism based on the interplay among the various neurotransmission systems leading to an increase in basal acetylcholine release should also be taken into account.

PMID: 17980434 [PubMed - indexed for MEDLINE]


1: Neuropharmacology. 2008 Jun;54(8):1254-63. Epub 2008 Apr 9. Links
Memantine protects against amphetamine derivatives-induced neurotoxic damage in rodents.
Chipana C, Torres I, Camarasa J, Pubill D, Escubedo E.
Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Universitat de Barcelona, Avda Joan XXIII s/n, Zona Universitaria Pedralbes, 08028 Barcelona, Spain.

We hypothesize that 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH) interact with alpha-7 nicotinic receptors (nAChR). Here we examine whether memantine (MEM), an antagonist of NMDAR and alpha-7 nAChR, prevents MDMA and METH neurotoxicity. MEM prevented both serotonergic injury induced by MDMA in rat and dopaminergic lesion by METH in mice. MEM has a better protective effect in front of MDMA- and METH-induced neurotoxicity than methyllycaconitine (MLA), a specific alpha-7 nAChR antagonist. The double antagonism that MEM exerts on NMDA receptor and on alpha-7 nAChR, probably contributes to its effectiveness. MEM inhibited reactive oxygen species production induced by MDMA or METH in synaptosomes. This effect was not modified by NMDA receptor antagonists, but reversed by alpha-7 nAChR agonist (PNU 282987), demonstrating a preventive effect of MEM as a result of it blocking alpha-7 nAChR. In synaptosomes, MDMA decreased 5-HT uptake by about 40%. This decrease was prevented by MEM and by MLA but enhanced by PNU 282987. A similar pattern was observed when we measured the dopamine transport inhibited by METH. The inhibition of both transporters by amphetamine derivatives seems to be regulated by the calcium incorporation after activation of alpha-7 nAChR. MDMA competitively displaces [(3)H]MLA from rat brain membranes. MEM and METH also displace [(3)H]MLA with non-competitive displacement profiles that fit a two-site model. We conclude that MEM prevents MDMA and METH effects in rodents. MEM may offer neuroprotection against neurotoxicity induced by MDMA and METH by preventing the deleterious effects of these amphetamine derivatives on their respective transporters.

PMID: 18455739 [PubMed - indexed for MEDLINE]


1: Eur J Pharmacol. 2008 Jul 28;589(1-3):132-9. Epub 2008 May 20. Links
Memantine prevents the cognitive impairment induced by 3,4-methylenedioxymethamphetamine in rats.
Camarasa J, Marimón JM, Rodrigo T, Escubedo E, Pubill D.
Laboratory of Pharmacology and Pharmacognosy, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain. jcamarasa@ub.edu <jcamarasa@ub.edu>

Amphetamine abuse is an important risk factor for the development of cognitive impairment involving learning and memory. Since in previous studies we have demonstrated the effectiveness of alpha-7 nicotinic receptor antagonists in preventing the neurotoxicity induced by amphetamine derivatives, the present paper seeks to determine whether pre-treatment with memantine (MEM) (an antagonist of both nicotinic and NMDA receptors) counteracts the memory impairment induced by 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) administration in male Long Evans rats. In mice, MDMA and MEM induced a locomotor stimulant response but with a different profile. Moreover, MEM inhibited the rearing and thygmotaxis behaviour induced by MDMA. Non-spatial memory was tested in the object recognition test and the spatial learning and memory was tested in the Morris water maze. In our experimental conditions, rats receiving MEM pre-treatment recovered the ability to discriminate between the familiar and the novel object that had been abolished by MDMA treatment. Animals treated with MDMA showed impaired learning in the Morris water maze. Results of the probe trial demonstrated that MDMA-treated rats did not remember the location of the platform, but this memory impairment was also prevented by the MEM pre-treatment. Moreover, MEM alone improved the learning task. No differences were observed between the different groups as regards swim speed. In conclusion, MEM significantly improved the learning and memory impairment induced by MDMA and constitutes the first approach to the treatment of the long-term cognitive deficits found in ecstasy users.

PMID: 18582864 [PubMed - in process]

At therapeutic dosages "neurotoxicity" shouldn't be a concern.

[Jacovis]

Search "memantine + amphetamine" or "memantine + tolerance" on both this board and Mind & Muscle.

There are open-minded, forward thinking psychiatrists out there willing to experiment with memantine off-label for amphetamine tolerance. If you are unwilling to order memantine yourself from overseas, you have the option of finding one of those doctors.

Funk (or Graatch),
what do you think Prevagen (Aequorin) would do when taken concurrently with therapeutic dosages of Amphetamines?

Here is a thread on Prevagen (Aequorin):
http://www.imminst.o...showtopic=17541

http://www.msrc.co.u...how/pageid/1848
"...Aequorin is a calcium-binding protein that is similar in structure to its corresponding human protein and by selectively binding calcium, it acts as a “surge protector” preventing excess calcium buildup..."

http://cat.inist.fr/...cpsidt=18066163
"...During pathological activation of the NMDA receptor, memantine blocks excessive calcium entry through the channel and is neuroprotective in in vitro and in vivo models..."

http://www.bluelight...;threadid=97021
"...Amphetamine tolerance is caused by excess Ca++ influx through the NMDA receptor gated calcium channels on the outer membranes of the dopamine cells bodies in the ventral tegental area, one of two areas in the brain with concentrations of dopamine producing neurons.
As alluded to above, taking an appropriate NMDA (partial) antagonist will prevent the development of a tolerance for the effects of an amphetamine or amphetamine-like stimulant. Also, by preventing excess Ca++ influx into the neuron, an NMDA antagonist will prevent associated brain alterations and damage (excitotoxicity).

Studies have indicated that amphetamine tolerance is prevented by exogenous or endogenous agents that are able to inhibit excess Ca++ influx into the neuron through the gated calcium channels on the neuronal membrane that have NMDA subtype glutamate receptors.Glutamate , the body’s major excitatory neurotransmitter, opens the gated calcium ion channels upon attaching to the NMDA receptor. A number of other receptors are also expressed on these calcium channels, which, when stimulated, either facilitate or inhibit glutamate’s action.

It is also important that agents that inhibit calcium channel activity not also cause deficient Ca++ influx. For example, ketamine is a full NMDA receptor antagonist, that prevents excess Ca++ influx and amphetamine tolerance. But being a full NMDA antagonist, ketamine in excessive doses results in deficient Ca++ influx. This could be one of the reasons it leaves K-user in a state of disassociation.

So basically we have following NDMA antagonists:
1. Memantine (Akatinol/Axura)
2. Acamprosate (Campral)
3. Amantadine (Symmetrel/Amantix)
4. Magnesium (supplement)
5. Dextrometorphan/DXM
6. Ketamine
7. PCP
(funny that 5,6,7 are recreational drugs)

Two of them have minimal (or none) side effects and have been identified (and verified by one anecdotal person, which has been taking amphetamine-type stimulants and NDMA antagonist with same beneficial effects for a period of 2 years) as preventing amphetamine tolerance: 1) Memantine and 2) Acamprosate.

1) Memantine is a partial NMDA antagonist that effectively puts an upper limit on Ca++ influx without compromising healthy levels of Ca++ influx. Memantine is not available in the US at this time. It is in stage 3 trials for Alzheimer’s disease. US approval may come within the next 2 years. Memantine is now approved in the European Union for the treatment of Alzheimer’s. It has been marketed in Germany since 1978 for the treatment of dementia and other cognitive disorders. It comes in 10mg tablets. One or two tablets/day are sufficient to prevent amphetamine tolerance, overactivity of the NMDA receptor and consequent free radical stress inside the neuron. The most expensive option though.

2) Acamprosate (n-acetyl-homo-taurine) analogue of the amino acid taurine. Alternatively, it may be termed as a carrier molecule for taurine, that allows taurine to readily cross the blood brain barrier, unlike taurine itself. Taurine is a NMDA receptor antagonist. Acamprosate is an investigational drug in the US, undergoing stage 2 (?) trials for the treatment of alcoholics. It is available in most European countries as a treatment for alcoholism, with great efficiacy. Cheaper than memantine, however efficiacy should be the same.

3) Amantadine, originally used in the treatment and prophylaxis of influenza infection and drug-induced Parkinsonism, also blocks NMDA receptors. Besides it is beneficial in traumatic head injury, dementia, multiple sclerosis,cocaine withdrawal and depression. Amantadine appears to act through several pharmacological mechanisms, none of which have been identified as the one chief mode of action. It is a dopaminergic, noradrenergic and serotonergic substance, blocks monoaminoxidase A and NMDA receptors, and seems to raise beta-endorphin/beta-lipotropin levels. I couldn't find what amount of the drug should be used to block NDMA. Cheaper than Acamprosate. No one has tested it yet, but I think it would be a good choice.

4) Magnesium is also an NMDA antagonist. Most people are deficient in magnesium, and stress reduces magnesium levels. Whether or not one takes amphetamines, magnesium supplementation is very important for mood, general well-being and keeping stress levels under control. It is also important to take magnesium in efficient form, with adequate bioavailability. The best type is magnesium glycinate (chelated) with bioavailability at around 80%. Second best is magnesium carbonate with (I don't remember exactly) bioavailability at little above 30%. Supplemented magnesium should be at 500 mg/day level. Also there is a study which shows that children who use amphetamine-type stimulants have bad magnesium/calcium balance. Calcium levels stay the same with amphetamine usage, but magnesium levels drop.

5) DXM - definitely the cheapest option of all NDMA antagonists, but I'd rather use Memantine or Acamprosate. Although, I've heard anecdotes that doses as low as 70 mg/day are enough to block NDMA - I couldn't find those amounts in abstracts/studies.

6) and 7) I wouldn't use as an amphetamine tolerance prevention. Ketamine for its known effects (you wouldn't want to be in a K-hole during the tweak just for the sake of prevention tolerance)
PCP - this one doesn't need explanation. It has nasty side-effects and I've mentioned it just because it is a NDMA antagonist. I wouldn't touch it even if it was dirt cheap.


So basically combination of partial NDMA antagonist and amphetamines should prevent tolerance. But I'm curious whether NDMA antagonists are able to *reduce* amphetamine tolerance. If yes then my goal would be to reduce it as far as to the point of first speed experience :] Right now, I have high amphetamine tolerance (too much tweaking during short time in the summer) so I will be using Acamprosate to try and reduce my tolerance. I'll post my results here.
And sorry for the length of the post - but I just wanted to write down everything I researched during last few days (I skipped PubMed abstracts).
Take care."

[FunkOdyssey]

Unfortunately, there are no studies that specifically indicate any of these substances have reduced amphetamine tolerance, despite what the poster from bluelight stated. The closest I have found is a study in which memantine increased the enjoyment of cocaine by cocaine abusers.

Anecdotally, memantine has the most positive testimonials to its efficacy for this purpose. DXM has a few, but I would not consider it despite the low cost because it is just an ugly, dirty drug (unscientific opinion). Memantine is not expensive from the sources I've found, so I question the need for less expensive and possibly less effective alternatives. Amantadine and acamprosate do seem like they might work, but I've never read any positive reports about them.

I am not convinced that prevagen does anything in vivo, let alone prevents amphetamine tolerance. If you try it though, let us know how it works for you.

Edited by FunkOdyssey, 21 November 2008 - 05:18 PM.

[Jacovis]

I am not convinced that prevagen does anything in vivo, let alone prevents amphetamine tolerance. If you try it though, let us know how it works for you.

Thanks for your comments/concern man.
Has anyone actually tried combining Prevagen (say at high dosages) with Amphetamines and/or Methylphenidates?
Here is the thread on Prevagen (Aequorin):
http://www.imminst.o...showtopic=17541

http://www.msrc.co.u...how/pageid/1848
"...Aequorin is a calcium-binding protein that is similar in structure to its corresponding human protein and by selectively binding calcium, it acts as a “surge protector” preventing excess calcium buildup..."


And anyone know the result of Gahan's experiments with Agmatine on the mindandmuscle forums (has anyone else tried combining Agmatine with Amphetamines and/or Methylphenidates)?

http://www.mindandmu...p...35579&st=30

gahan (October 13, 2008):
"Okay, at the risk of being premature, I'm going to go ahead and give a preliminary report. A few things in disclaimer first: n=1, I have also been reducing my stim use on an as-needed basis (ex. 20-30mgs instead of 40mgs unless I have a really intense day, also keeping coffe at three cups or below), and I spend a large amount of time and effort doing things best labeled 'internal work'.

Agmatine is the best mentally-oriented supplement I have ever tried.

First: The mood boost from my amphetamine is returning. It isn't close to as powerful as it was at the beginning of my dexedrine treatment, but it is more pronounced in a way that strongly indicates no placebo effect. I'll be walking around on 10mg of dexedrine (so far that day) and be surprised by a sudden breeze of that well-being/optimism vibe that made me fall in love with amphetamine in the first place.

Secondly, this is an incredible anti-anxiety anti-depression compound. I have weird OCD-like anxiety, revolving around intrusive visual images and repetitive behaviors but not of such intensity I feel medication to be warranted. At first amphetamine eliminated this problem, but after tolerance set in the opposite effect became dominant. One of the things I noticed soon after beginning agmatine, and this was an observation that popped into my head at the end of the day, was that these OCD-like symptoms had been almost completely absent.

This effect ties in with the anti-depressive effects. There is no feeling of being 'chilled out' and really very little mood boosting from agmatine (I've taken it without dexedrine as well), but simply a attenuating of the negative 'noise' that makes it so hard to pull yourself out of a funk. I think this compound may have a lot of potential in the treatment of OCPD, manic depressives, anxiety disorders etc.

It's sort of an enabler to me, in that it stops up the flow of shit to such a degree that I can use things like CBT, meditation, NLP-like techniques etc. The cease of automatic and intrusive thoughts allows mindfulness to be maintained and a constant attitude of self-overcoming adopted. In my case at least, agmatine is an endurance supplement for psychospiritual exercise.

I know none of my posts about it have contained studies or references, but I've been up to my neck in school work lately. I'm planning on starting a new thread with a lot of cites and my further experiences in the near future."

[Jacovis]

sorry double post...

Edited by Visionary7903, 16 January 2009 - 12:10 PM.

[bgwithadd]

Just to update, my tolerance to amphetamines seems to be reducing.

[Pike]

be VERY careful when taking magnesium and theraputic amphetamines (i.e. Dex, Adderall, etc.) simultaneously. the combination can put dangerous amounts of amphetamine in your system with high potentiation due to it effectively eliminating all tolerance whilst on it (and that's in my experience as well).

[bgwithadd]

The issue with magnesium is that some forms of magnesium reduce acidity in the gut, so taking it just before your dose will increase the absorbance of amphetamines dramatically. Taking most forms of magnesium should be fine, and in fact you pretty much have to if you take amphetamines or else you'll probably get a lot of side effects like twitchs, teeth grinding etc.

As for it actually reducing tolerance...maybe. If so, not by a degree easily noted.

[August59]

Unfortunately, there are no studies that specifically indicate any of these substances have reduced amphetamine tolerance, despite what the poster from bluelight stated. The closest I have found is a study in which memantine increased the enjoyment of cocaine by cocaine abusers.

Anecdotally, memantine has the most positive testimonials to its efficacy for this purpose. DXM has a few, but I would not consider it despite the low cost because it is just an ugly, dirty drug (unscientific opinion). Memantine is not expensive from the sources I've found, so I question the need for less expensive and possibly less effective alternatives. Amantadine and acamprosate do seem like they might work, but I've never read any positive reports about them.

I am not convinced that prevagen does anything in vivo, let alone prevents amphetamine tolerance. If you try it though, let us know how it works for you.

Where the best place to order Agmatine? Seems hard to find! Thanks

[kikai93]

The issue with magnesium is that some forms of magnesium reduce acidity in the gut, so taking it just before your dose will increase the absorbance of amphetamines dramatically. Taking most forms of magnesium should be fine, and in fact you pretty much have to if you take amphetamines or else you'll probably get a lot of side effects like twitchs, teeth grinding etc.

As for it actually reducing tolerance...maybe. If so, not by a degree easily noted.

Because of the dramatic increase in absorption of the amphetamine, I'd recommend taking your amphetamine, waiting 30min-1hour, and then taking the magnesium (and whatever other vitamins/minerals you're on) supplement to ameliorate some of the crap side effects of the amphetamine. I have a TON of anecdotal reports of reduced tolerance when coadministrating magnesium with AMPH or D-AMPH, but I suspect its due to the increased absorption mentioned previously, which probably isn't a good thing.

Amphetamines are pretty reactive with other drugs (note the long list of contraindications and food reactions noted in the insert), so caution seems prudent. Funny anecdote: I knew a guy that for about a year had been taking his dex dose with orange juice (he liked OJ). He had gotten up to a 30mg x3 dose, when he developed chronic heartburn and cut out all of his acidic foods and beverages (including the OJ). Saw him a couple of days later and he was flying (standard "tweaker" effect of moderate dosage). Luckily his doctor had a clue and just reduced the dosage to 10mg XR, but damn... this dude housecleaning like a rabid wombat was a sight to see.

[bgwithadd]

I take ionic magneisum so it's not even remotely an issue. It's the type of magnesium in antacids that causes that effect. I also take it at night anyway, since it is calming.

[yoyo]

agmatine isn't just an nmda antagonist, it could be the alpha2 agonism for instanc.e

[bgwithadd]

That's interesting, because guanfacine is an alpha2 agonist, and that is shown to improve concentration.

[purerealm]

how does one get ahold of memantine?

[FunkOdyssey]

1) an exceptionally progressive physician

2) alldaychemist.com

[August59]

Memantine can be picked up at drugdelivery.ca or generics.ws