• Select Your Topic Then Scroll Down
    Alcohol Bupe Benzos
    Cocaine Heroin Opioids
    RCs Stimulants Misc
    Harm Reduction All Topics Gabapentinoids
    Tired of your habit? Struggling to cope?
    Want to regain control or get sober?
    Visit our Recovery Support Forums

Stimulants How to prevent dopamine depletion from meth?

Dr Jekyll

Greenlighter
Joined
Feb 16, 2019
Messages
42
I've been taking meth in reasonable doses (30-40mg) a day to address my ADHD. It works well for this purpose; but, I'm entering the grey territory between therapeutic doses (25mg) a day and recreational doses.

I've researched quite a fair share of ways to prevent sensitization (lithium); but, can't find any substances that would prevent persistent depletion of dopamine in nerve terminals. I have also considered selegiline; but, a study points out that its ineffective for this goal.

Any info on how to minimize the risks associated with continual methamphetamine use would be appreciated.
 
Well I hate to break it to you but there really isnt too much you can do about the depletion. Your body only has so much to give and amphetamines just take and take til there is nothing left.
You can try eating food that are rich in tyrosine and other dopamine precursors, or take supplements that wont really work well, but those are about it in regards to maintaining adequate dopamine levels, but it still won't touch how much dopamine the math is taking
 
magnesium...ndma antagonists in general reduce neurotoxicity (i think) but might play a role in preventing sensitization as well
 
The only 100% reliable way to avoid DA depletion is keep doses low and stay well fed/hydrated.

Maybe consider dividing your dose; ~20mg twice daily will produce lower peak concentrations than a 40mg dose.
 

Berberine prevents nigrostriatal dopaminergic neuronal loss and suppresses hippocampal apoptosis in mice with Parkinson's disease.
Kim M1, Cho KH1, Shin MS2, Lee JM2, Cho HS2, Kim CJ2, Shin DH3, Yang HJ4.
Author information

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of nigral dopaminergic neurons and a reduction in striatal dopaminergic fibers, which result in tremors, rigidity, bradykinesia and gait disturbance. In addition to motor dysfunction, dementia is a widely recognized symptom of patients with PD. Berberine, an isoquinoline alkaloid isolated from Berberis vulgaris L., is known to exert anxiolytic, analgesic, anti-inflammatory, antipsychotic, antidepressant and anti-amnesic effects. In the present study, we investigated the effects of berberine on short-term memory in relation to dopamine depletion and hippocampal neurogenesis using a mouse model of PD, induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/P) treatment. Mice in the berberine-treated groups were orally administered berberine once a day for a total of 5 weeks. Our results revealed that the injection of MPTP/P induced dopaminergic neuronal death in the substantia nigra and fiber loss in the striatum. This resulted in impaired motor balance and coordination, as assessed by the beam walking test. We further demonstrated that MPTP/P-induced apoptosis in the hippocampus deteriorated short-term memory, as shown by the step-down avoidance task. By contrast, neurogenesis in the hippocampal dentate gyrus, which is a compensatory adaptive response to excessive apoptosis, was increased upon PD induction. However, treatment with berberine enhanced motor balance and coordination by preventing dopaminergic neuronal damage. Treatment with berberine also improved short-term memory by inhibiting apoptosis in the hippocampus. Berberine demonstrated maximal potency at 50 mg/kg. Based on these data, treatment with berberine may serve as a potential therapeutic strategy for the alleviation of memory impairment and motor dysfunction in patients with PD.


So, berberine it is.
 
The only 100% reliable way to avoid DA depletion is keep doses low and stay well fed/hydrated.

Maybe consider dividing your dose; ~20mg twice daily will produce lower peak concentrations than a 40mg dose.


Yeah, I'm looking at potentiating the meth with something like atomoxetine and selegiline.
 
If you potentiate your meth you will just be slowly draining more dopamine than you are already. You are essentially using a lower dose of speed with a compound that releases dopamine or inhibits reuptake of it. You will still lose just as much, if not more, dopamine.
 
If you potentiate your meth you will just be slowly draining more dopamine than you are already. You are essentially using a lower dose of speed with a compound that releases dopamine or inhibits reuptake of it. You will still lose just as much, if not more, dopamine.

If someone can correct me, METH is a releaser at lower doses, and at higher doses is a reuptake inhibitor. Anyway, atomoxetine would function as a potentiator in the manner of increasing effects in the PFC via reuptake inhibition of NET transporters that also increase DA levels too, rather than in lower brain regions. This would make the meth ore therapeutic rather than rewarding for my purposes. Less dopamine would be required to be released to attain a similar level of efficacy than higher doses.
 
L-Tyrosine. It's in bannanas but they also make supplements as well. It always helped my meth crashes and tured them into "afterglows." It also seemed to make the rush hit harder. I believe this is how I kept my meth tolerance down as well (I also waited until I completely came down before doing another shot). While everyone was graduating to gram slams and half gram slams to deal with tolerance I was able to be consistently satisfied with .1 to .2 shots each day. Idk if its scientifically proven to level your dopamine out but it worked for me. But I had to eat a lot of bannanas. Like A LOT of bannanas. So much to the point to where I got sick of em. Im sure it would work all the better for someone using theraputic doses of meth but a word of caution. Meth is a drug that is very easy to fall into recreational/abusive usage.l as im sure you already know. Your best bet would to be to get some speed paste (racemic amphetamine sulphate) from the dark net or something. Its cheap and bountiful and a lot more useful for theraputic application.

I think there was actually a study on rats that said L-Tyrosine reversed meth neurotoxicity to the dopamine receptors or something like that but don't quote me on that. All I know is it consistently helped me.
 
Atomoxetine does do that, but it inhibits alot of effects and like you said, still releases dopamine, which you are trying to save IIRC. You could easily just drop your dose instead of adding on more compounds on top of a very potent one. These kinds of combos are unnecessary and put alot of strain of the body and brain. For the sake of HR, why dont you try reducing your dose and eating precursor rich foods?
If someone can correct me, METH is a releaser at lower doses, and at higher doses is a reuptake inhibitor. Anyway, atomoxetine would function as a potentiator in the manner of increasing effects in the PFC via reuptake inhibition of NET transporters that also increase DA levels too, rather than in lower brain regions. This would make the meth ore therapeutic rather than rewarding for my purposes. Less dopamine would be required to be released to attain a similar level of efficacy than higher doses.

Atomoxetine does do that, but it inhibits alot of effects and like you said, still releases dopamine, which you are trying to save IIRC. You could easily just drop your dose instead of adding on more compounds on top of a very potent one. These kinds of combos are unnecessary and put alot of strain of the body and brain. For the sake of HR, why dont you try reducing your dose and eating precursor rich foods?
 
If you are looking to prevent depletion of DA then anything that 'potentiates' the meth will also very likely work against you by increasing stimulation of dopamine autoreceptors...
 
If you are looking to prevent depletion of DA then anything that 'potentiates' the meth will also very likely work against you by increasing stimulation of dopamine autoreceptors...

Well, as I said, METH is a releaser at lower dosages and becomes a reuptake inhibitor at higher dosages. Atomoxetine covers everything upward from the threshold of releasing properties to reuptake inhibition. Many users of polypharmacy with Strattera and stimulants find needing a lower dose of the stimulant for therapeutic effects.

Anyway, I think I'm going to have to go through the legal routes of obtaining a script for Adderall XR, 30mg b.i.d. as I am having some kind of psychosomatic dissonance from consuming such a drug with such a bad rep which is causing me distress. A contributing factor to all this is a diagnosis of a psychotic disorder, which I am treating with Zyprexa. But, I've read extensively about the safe use of stimulants with concomitant antipsychotic use. Did I mention that the comedown really sucks? No way around that I suppose.
 
According to this paper methampetamine is slightly more potent as a reuptake inhibitor but not by much - it is almost equipotent as a releasing agent as a reuptake inhibitor. (IC50 at DAT: 14nM / 9nM for racemic / D-meth, and EC50 for dopamine release: 20nM / 11 nM for racemic / D-meth). So any dose that causes reuptake inhibition will necessarily cause release.

Psychotic disorders and stuff like bipolar generally are disqualifiers for stimulant treatment because there is a strong risk of exacerbating the disorder. In fact amphetamine use can be a root cause of psychosis, especially with long-term or high dose usage, or if you're genetically predisposed to it.

Also, treatment with drugs that have antidopaminergic activity, like almost all antipsychotics, will almost certainly reduce the efficacy of dopaminergic stimulants in a dose-dependent manner, especially if they also posess anti-adrenergic effects, like olanzapine.
 
Is there any reason you need to use meth instead of regular amphetamine sulfate e.g. in the form of powder/paste or pharmas like Adderall, Vyvanse, Dexedrine? Meth is far more neurotoxic and potent than normal amphetamine and will cause more tolerance and depletion especially when you're using street drugs of unknown purity. I recommend getting the script stuff if possible especially if you have diagnosed ADHD.
 
Psychotic disorders and stuff like bipolar generally are disqualifiers for stimulant treatment because there is a strong risk of exacerbating the disorder. In fact amphetamine use can be a root cause of psychosis, especially with long-term or high dose usage, or if you're genetically predisposed to it.
This is the old school opinion on the matter. If you do more research, ADHD can be treated in individuals with schizophrenia or other psychotic disorders effectively with concomitant treatment with antipsychotics without exacerbating the condition. Lisdexamphetamine by Shire, is being investigated for effective treatment of negative symptoms of schizophrenia and will soon be approved for that issue.
 
Is there any reason you need to use meth instead of regular amphetamine sulfate e.g. in the form of powder/paste or pharmas like Adderall, Vyvanse, Dexedrine? Meth is far more neurotoxic and potent than normal amphetamine and will cause more tolerance and depletion especially when you're using street drugs of unknown purity. I recommend getting the script stuff if possible especially if you have diagnosed ADHD.
Well, street meth isn't that contaminated. You can find high-quality meth on the DM. The neurotoxicity concerns are blown out of proportion. I mean, yes, if you're going to smoke or inject high doses to get high, then you'll be reaching comparable peak plasma levels in studies on rodents and primates that cause neurotoxicity. However, within the reasonable range of 20mg twice a day, that danger is pretty negligible as far as I understand. Of course, you can further mitigate this concern with stuff like Ibuprofen, ALCAR, selegiline, lithium, etc.
 
Well, street meth isn't that contaminated. You can find high-quality meth on the DM. The neurotoxicity concerns are blown out of proportion. I mean, yes, if you're going to smoke or inject high doses to get high, then you'll be reaching comparable peak plasma levels in studies on rodents and primates that cause neurotoxicity. However, within the reasonable range of 20mg twice a day, that danger is pretty negligible as far as I understand. Of course, you can further mitigate this concern with stuff like Ibuprofen, ALCAR, selegiline, lithium, etc.

I understand the risks are reduced at lower doses of course, but meth just seems like overkill for something that is adequately treated with regular old amphetamine. And since you have easy access to affordable meth I assume you're in the US where getting something like an Adderall script is very easy.
 
I understand the risks are reduced at lower doses of course, but meth just seems like overkill for something that is adequately treated with regular old amphetamine. And since you have easy access to affordable meth I assume you're in the US where getting something like an Adderall script is very easy.

Not that easy given my diagnosis and economic means. My county psych is old school and doesn't want to prescribe me Adderall or Dexedrine out of fear of exacerbating my condition. The meth is just a stop-gap measure in my mind, as I will be likely seeking some private p-doc that is willing to prescribe me Adderall XR. But, as it stands, D-meth is pretty fantastic and highly economical (look up the prices on the DM for meth in the US, it's ridiculous)... The only issue is the comedown. I used to take 2-FMA, the absolute gold standard for treating ADHD; so I might go with that if my plan fails.
 
20mg 2x a day is more than you think if you have very clean product. Desoxyn has a max daily limit of 25mg. And if you are truly using it for therapeutic use, then trying to potentiate it with other medications would be not be advisable. Not to be rude, but your it seems like you are bouncing back and forth between wanting to use it for medical purposes and recreational purposes.
 
Top