Amphetamine Neurotoxicity and Tolerance Reduction/Prevention II

[sekio]

Intravenous supplements = probably a bad idea in the long run

Which ALA are we talking about - alpha-lipoic acid, or alpha-linoleic acid?

Both should be extensively well-absorbed orally. Free acid lipoic acid is very much so, something like 93% bioavailiable orally after 2h. No need to inject it but you can take it as a salt just as easily.

 

[Ksa]

This is a very interesting post, I never knew about it and to see that I have been doing everything that's in there point by point is highly reassuring. I have actually not developed any tolerance to amphetamines for 5 years now. More people should know about this post, I highly vouch it!

It's not just measures that slow down tolerance, like, by 5% or 10%. If you do everything that's in there, you might not develop any tolerance at all. This works guys, at least for me and the OP lol.

For example, I have long felt the need to take 100mg of Tylenol or aspirin with my daily dose. I could not explain it, I just felt it was better. To see it listed there on the first page came as a shock. Does anyone know why this works? I do it because I feel like it works but I don't know why.

 

[Achten]

I just stumbled upon this thread actually... . Could someone elaborate (in layman's terms perhaps) about the danger that may arise from magnesium supplementing ?
I take it when feeling some soreness or tension while tripping. With a regular trip (low/mid dose) it's mostly 300mg or nothing, but when doing larger amounts or releasers (aMT, MDMA, amphetamines too..) that could become 900 or 1200mg. Anything wrong with that? I always drop the compound on empty stomach (or just a piece of fruit) and try to eat fruit and drink lots of water during the trip.

 

[Tussmann]

This is a very interesting post, I never knew about it and to see that I have been doing everything that's in there point by point is highly reassuring. I have actually not developed any tolerance to amphetamines for 5 years now. More people should know about this post, I highly vouch it!

Tolerance, for the majority of users, never occurs to the pro-cognitive effect of amphetamine (due to properties of DA in the prefrontal cortex). For the pro-social, pro-motivational, appetite suppressing, and pro-energetic effects, however, (without drugs and other supplements) tolerance can settle in as few as days.

 

[Ksa]

I just stumbled upon this thread actually... . Could someone elaborate (in layman's terms perhaps) about the danger that may arise from magnesium supplementing ?
I take it when feeling some soreness or tension while tripping. With a regular trip (low/mid dose) it's mostly 300mg or nothing, but when doing larger amounts or releasers (aMT, MDMA, amphetamines too..) that could become 900 or 1200mg. Anything wrong with that? I always drop the compound on empty stomach (or just a piece of fruit) and try to eat fruit and drink lots of water during the trip.

I don't think it's a death risk. Once your blood sugar levels drop below 5mM, you'll blacken out and probably crouch to sit down. You regain vision after 5 or 10 seconds usually because your muscles no longer use glucose, temporarly. Otherwise, you pass out, with memory loss probably. In severe cases, you die but it almost never happens, unless you're being very stupid.

The problem occurs with people who don't know how to get high, read this topic, take magnesium with amphetamines and then pass out. This topic assumes you know how to get high in the first place. If you don't know how to get high, stay away from this topic! You need to take your magnesium when you're not using amphetamines, during the days when you eat and drink thoroughly.

 

[Quercetin]

The problem occurs with people who don't know how to get high, read this topic, take magnesium with amphetamines and then pass out. This topic assumes you know how to get high in the first place. If you don't know how to get high, stay away from this topic!

It must be amazing to know how to get high as much as you.. I wish I had such a skill.. Can you please teach me?

Magnesium can be use while using meth/amphetamine anywhere between 150 to 450mg per serving post-meal, as long as it is not on empty stomach. Magnesium should never be taken on empty stomach while using amph, or mixed with anything causing glucose uptake.

 

[Quercetin]

I just stumbled upon this thread actually... . Could someone elaborate (in layman's terms perhaps) about the danger that may arise from magnesium supplementing ?
I take it when feeling some soreness or tension while tripping. With a regular trip (low/mid dose) it's mostly 300mg or nothing, but when doing larger amounts or releasers (aMT, MDMA, amphetamines too..) that could become 900 or 1200mg. Anything wrong with that? I always drop the compound on empty stomach (or just a piece of fruit) and try to eat fruit and drink lots of water during the trip.

Why do you use drugs on an empty stomach? It sound risky to me.

 

[Epsilon Alpha]

I think we both know what this means, just watch your blood sugar on heroic doses of stims. A meal would enhance Mg uptake anyways

 

[Quercetin]

I think we both know what this means, just watch your blood sugar on heroic doses of stims. A meal would enhance Mg uptake anyways

heroic doses of stims.. Is that the amount needed to see into the future?

 

[avcpl]

Why do you use drugs on an empty stomach? It sound risky to me.

It's pretty standard practice for MDMA users to drop on an empty stomach. I have no idea where this came from, but if there is a better pre-roll intake that won't affect the roll (because really that is the most important thing! lol) please share?!!!

 

[Quercetin]

It's pretty standard practice for MDMA users to drop on an empty stomach. I have no idea where this came from, but if there is a better pre-roll intake that won't affect the roll (because really that is the most important thing! lol) please share?!!!

Why would a large meal affect the roll?

 

[avcpl]

Why would a large meal affect the roll?

I think the thinking is that food in the stomach will cause a slower absorption rate of the mdma and not reach the saturation levels needed to "flip the switch" ...



.

 

[Quercetin]

I think the thinking is that food in the stomach will cause a slower absorption rate of the mdma and not reach the saturation levels needed to "flip the switch" ...
.

I really don't know what to say. I would eat the mdma and eat after.. I mean.. its such a small difference..

 

[Epsilon Alpha]

http://www.ncbi.nlm.nih.gov/m/pubmed/9128836/
Saw this on reddit, perhaps inhibiting a relevant P450 enzyme could be a way to prevent the formation of toxic metabolites assuming amphetamine undergoes a similar transformation.

 

[MobiusDick]

Quick comment about a few aspects of post: recent studies have shown that in at least 1/3 of people, 81 mgs of aspirin is a sub-therapeutic dose of the thrombolytic /antithromboembolic (the most common term for these medications is anticoagulant, but it is technically incorrect ; a compound like vampirin, which comes from the vampire bat, is an anticoagulant-the strongest one known, in fact, as it must be washed away before its activity stops). The full 325 mg dose is the ED₅₀ for this subset of patients.

One of the reasons I want to comment on this is because I personally continue to witness too many cases of MI, CVA or other thromboembolic event that has resulted in mortality/morbidity due to the treating physician's lack of understanding of the concept of rebound phenomenon from drug discontinuation (I have heard this called bradyphylaxis, which is completely incorrect. Bradyphylaxis is the technical term for sensitization; tachyphylaxis is the technical term for habituation.) Patients should always be weaned off of thrombolytics when necessary (e.g., prior to elective surgery), including low dose aspirin; even Vitamin E ot Gingko should not be abruptly discontinued because almost all drugs have a period of excessive contra-efficacy when suddenly stopped. Thrombolytics have a period of hypercoagulability after discontinuation for 1-3 weeks depending on the drug, serious enough to be the primary cause of morbidity/mortality. The ME often rules theses death's primary causes as MI or CVA, when in fact, it was secondary to the primary cause of death, rebound phenomenon due to abrupt thrombolytic discontinuation.

Our physicians today, in general, have a very poor understanding of pharmaceutical science and are jeopardizing the lives of too many people by not keeping up with their reading and with CE credits resulting from ridiculously over-simplified course work designed more for the layman than a person the public goes to for their supposed medical, the average physician is far too often killing their patients by the medication they prescribe, and no one ever even realizes the patient was killed by their physician's ignorence

 

[Epsilon Alpha]

Quick comment about a few aspects of post: recent studies have shown that in at least 1/3 of people, 81 mgs of aspirin is a sub-therapeutic dose of the thrombolytic /antithromboembolic (the most common term for these medications is anticoagulant, but it is technically incorrect ; a compound like vampirin, which comes from the vampire bat, is an anticoagulant-the strongest one known, in fact, as it must be washed away before its activity stops). The full 325 mg dose is the ED₅₀ for this subset of patients.

One of the reasons I want to comment on this is because I personally continue to witness too many cases of MI, CVA or other thromboembolic event that has resulted in mortality/morbidity due to the treating physician's lack of understanding of the concept of rebound phenomenon from drug discontinuation (I have heard this called bradyphylaxis, which is completely incorrect. Bradyphylaxis is the technical term for sensitization; tachyphylaxis is the technical term for habituation.) Patients should always be weaned off of thrombolytics when necessary (e.g., prior to elective surgery), including low dose aspirin; even Vitamin E ot Gingko should not be abruptly discontinued because almost all drugs have a period of excessive contra-efficacy when suddenly stopped. Thrombolytics have a period of hypercoagulability after discontinuation for 1-3 weeks depending on the drug, serious enough to be the primary cause of morbidity/mortality. The ME often rules theses death's primary causes as MI or CVA, when in fact, it was secondary to the primary cause of death, rebound phenomenon due to abrupt thrombolytic discontinuation.

Our physicians today, in general, have a very poor understanding of pharmaceutical science and are jeopardizing the lives of too many people by not keeping up with their reading and with CE credits resulting from ridiculously over-simplified course work designed more for the layman than a person the public goes to for their supposed medical, the average physician is far too often killing their patients by the medication they prescribe, and no one ever even realizes the patient was killed by their physician's ignorence

I've been looking at the NSAID bit too, it shows a lot of promise in non-human trials for various neurotoxic measures but fuck if I know the appropriate dose. I'd rather be too low than too high on something that inhibits bleeding.

But, thats good to know that if someone has been taking ASA for quite some time that they should ween themselves off rather than cold turkey it. Thanks man

 

[Quercetin]

Lets talk about histamine!

Drug interaction between methamphetamine and antihistamines: behavioral changes and tissue concentrations of methamphetamine in rats.
Methamphetamine is a psychomotor stimulant, whereas first generation antihistamines cause sedation. Several studies have demonstrated that first generation antihistamines potentiate methamphetamine-induced psychomotor activation and two possible mechanisms have been postulated. One is blockage of the central histaminergic neuron system and the other is inhibition of dopamine reuptake. However, the exact mechanism is still controversial. In this study, we examined in behavioral tests the effects of selected antihistamines on methamphetamine-induced psychomotor activation in rats, and measured plasma and brain tissue concentrations of methamphetamine. We found that some antihistamines significantly potentiate methamphetamine-induced psychomotor activation in rats and that plasma and brain tissue concentrations of methamphetamine in rats treated with methamphetamine in combination with D-chlorpheniramine were markedly higher than those in rats treated with methamphetamine alone. These results suggest that the potentiating effects of antihistamines are due to not only central effects but also the alteration of the pharmacokinetics of methamphetamine.

 

[atrollappears]

Hey everyone, it's been a while xD

Lets talk about histamine!

Drug interaction between methamphetamine and antihistamines: behavioral changes and tissue concentrations of methamphetamine in rats.
Methamphetamine is a psychomotor stimulant, whereas first generation antihistamines cause sedation. Several studies have demonstrated that first generation antihistamines potentiate methamphetamine-induced psychomotor activation and two possible mechanisms have been postulated. One is blockage of the central histaminergic neuron system and the other is inhibition of dopamine reuptake. However, the exact mechanism is still controversial. In this study, we examined in behavioral tests the effects of selected antihistamines on methamphetamine-induced psychomotor activation in rats, and measured plasma and brain tissue concentrations of methamphetamine. We found that some antihistamines significantly potentiate methamphetamine-induced psychomotor activation in rats and that plasma and brain tissue concentrations of methamphetamine in rats treated with methamphetamine in combination with D-chlorpheniramine were markedly higher than those in rats treated with methamphetamine alone. These results suggest that the potentiating effects of antihistamines are due to not only central effects but also the alteration of the pharmacokinetics of methamphetamine.

Well, we already know that H3 antagonists (H3 being an autoreceptor expresses exclusively in the brain) can potentiate methamphetamine induced monoamine release and subsequent hyperactivity. Judging by the fact that in that case an increase in histamine signaling is increasing the effect of methamphetamine (which isn't surprising, considering H3 antagonists increase monoamine release on their own), I'm willing to chalk this up to a H3 antagonistic effect of chlorpheniramine.

Now, that bit about the tissue concentration is pretty interesting. I wonder: is methamphetamine degraded more quickly in the intracellular or extracellular environment? If there is a difference, would an increase or decrease in methamphetamine uptake affect the rate of change of the tissue concentration?

 

[atrollappears]

Oh, also, I recently came across something while reading about Olney's lesions which I thought might be relevant to this thread. The popular opinion on Olney's lesions at this point seems to be that the mouse studies in which Olney's lesions were discovered do not apply to humans. One of the justifications for this is that the metabolic rate of the mouse is higher, so the mouse mitochondria are much more liable to lose their proton gradient in response to toxic insults and/or release more free radicals upon losing their proton gradient. Considering that excitotoxic/oxidative damage definitely plays a role in amph neurotoxicity, I wonder if this same principle means that mouse studies overestimate the neurotoxicity of amphetamines?

 

[blight12]

Wow thank you all for this thread, went through it all and while not understanding any technical stuff, simply reading between the lines, conclusions, logic, assumptions based on recurring themes etc ensured i gained a ton of knowledge and insight and i would never have thought possible before actually going ahead and trying to interpret as much as possible. Firstly awesome insights as a recent high dose meth user and secondary:

I have been fascinated with Glutathione and direct supplementation, even just posted a new thread which was justly shut down due to no references and my overly enthusiastic claims/hopes etc. I was glad to see it mentioned often in this thread and to see known precursors to be highly valued, indicating that my conclusion of its value on topic seems justified. What i noticed was that the precursors (like NAC and ALA) where usually given credit for benefits directly and not increase in GSH itself. Is this accurate? Does NAC for example hold separate value beyond that provided by increased GSH?

I also noted a few comments where high levels would be negative. This seems very strange to me. My understanding of its value is antioxidant effects (the master antioxidant they call it), some sort of control over lesser antioxidants, a major role in the immune system and therefore noteworthy benefits in terms of autoimmune conditions as well as inflammatory conditions. My understanding that supplementation directly held major benefits as a deficiency here could be directly linked to aging and related issues. I reviewed many unconfirmed testimonials relating to massive benefits to difficult to treat diseases like many autoimmune concerns, cancers, parkinsons, altzhimers and many others.

I know the major consumer products with the most info and testimonials are based on increasing levels via precursors, the number 1 product via supplementing bonded cystine etc through undenatued whey and the other through a combination of NAC/ALA etc. Then recently I have seen liposomial delivered glutathione supplements as well.

Apparently maximizing blood GSH levels where possible, beyond the normal levels and also where levels are below the norm could produce some "amazing" results with claims against cancer and other things.

So really, i wanted to say that im a business, marketing persona and dont know the technical specifics and would really value confirmation, comments, etc of the above claims, inadequacies etc. I need the truth from you guys in the know, as i had planned to build a business around this product based on the claimed potential. results etc.

Appreciate any feedback, the more technical the better. Im certain this chemical has value but some of the claims are hard to believe, not matter how much i want to.

And then ofcourse the purpose of my other post and this one is determining any value to drug users through direct supplementation with the goal to maximize levels as it was understood that the more the better and low levels where closely linked to many illnesses and thus increasing levels could be the solution.