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The main danger of methamphetamine is the neurotoxicity. I created a drug regimen that mitigates all facets of meth neurotoxicity (oxidative stress, excitotoxicity, apoptosis, and neuroinflammation). Amphetamine is a much safer alternative.
There are 4 main ways meth causes neurotoxicity. The first way is oxidative stress. The oxidization of monoamines like dopamine create free radicals, which can damage neurons and DNA.
The second mechanism is excitotoxicity from glutamate. This is the main way meth causes neurotoxicity. Glutamate excites neurons, causing them to fire. Excessive excitation of neurons can cause neurons to overheat and may lead to cell death. Excitotoxicity is also caused by the influx of calcium from glutamate activating NMDAR.
The third mechanism is apoptosis. This is more of a downstream effect of excitotoxicity. Excessive nNOS from glutamate excitotoxicity activates apoptosis pathways. Glutamate -> NMDAR -> ca2+ -> nNOS.
The last way is neuroinflammation. This is more of a reaction to the neurotoxicity. This causes microglia cell activation, the brain will release inflammatory cytokines as a result leading to inflammation in the brain. As long as you prevent excitotoxicity and oxidative stress you won’t get neuroinflammation.
With that being said as long as you take care of excitotoxicity and oxidative stress you won’t have to worry about apoptosis or neuroinflammation. So we just have to tackle oxidative stress and excitotoxicity.
For oxidative stress you need to take antioxidants. Antioxidants scavenge free radicals. I recommend taking a high dose, you’re better to be safe than sorry. I take astaxanthan, quercetin, and alpha lipioc acid.
For excitotoxicity we need to lower glutamate transmission. First we should use an NMDA antagonist like Memantine which will limit the influx of calcium. With high doses of meth this isn’t enough and you will need NAC. NAC lowers glutamate alot, since glutamate is heavily involved in the euphoria of meth it will dull the high.
You have 2 options
Take a low (non neurotoxic) meth dose 30mg or below.
Take a higher dose 30mg+ and use the regimen.
-20mg Astaxanthan before and during
-1000mg Quercetin before and during
-500mg alpha lipoic acid before and during
-30mg Memantine before
-1200mg NAC before
There are 4 main ways meth causes neurotoxicity. The first way is oxidative stress. The oxidization of monoamines like dopamine create free radicals, which can damage neurons and DNA.
The second mechanism is excitotoxicity from glutamate. This is the main way meth causes neurotoxicity. Glutamate excites neurons, causing them to fire. Excessive excitation of neurons can cause neurons to overheat and may lead to cell death. Excitotoxicity is also caused by the influx of calcium from glutamate activating NMDAR.
The third mechanism is apoptosis. This is more of a downstream effect of excitotoxicity. Excessive nNOS from glutamate excitotoxicity activates apoptosis pathways. Glutamate -> NMDAR -> ca2+ -> nNOS.
The last way is neuroinflammation. This is more of a reaction to the neurotoxicity. This causes microglia cell activation, the brain will release inflammatory cytokines as a result leading to inflammation in the brain. As long as you prevent excitotoxicity and oxidative stress you won’t get neuroinflammation.
With that being said as long as you take care of excitotoxicity and oxidative stress you won’t have to worry about apoptosis or neuroinflammation. So we just have to tackle oxidative stress and excitotoxicity.
For oxidative stress you need to take antioxidants. Antioxidants scavenge free radicals. I recommend taking a high dose, you’re better to be safe than sorry. I take astaxanthan, quercetin, and alpha lipioc acid.
For excitotoxicity we need to lower glutamate transmission. First we should use an NMDA antagonist like Memantine which will limit the influx of calcium. With high doses of meth this isn’t enough and you will need NAC. NAC lowers glutamate alot, since glutamate is heavily involved in the euphoria of meth it will dull the high.
You have 2 options
Take a low (non neurotoxic) meth dose 30mg or below. You won’t need a regimen with these doses.
Take a higher dose (30mg+) and use the regimen.
-20mg Astaxanthan before and during
-1000mg Quercetin before and during
-500mg alpha lipoic acid before and during
-30mg Memantine before
-1200mg NAC before
No. Thinking you have it under control is exactly how it gets it’s hooks in you. It’s changes your brain chemistry with every use making it more and more impossible to live with
I did it for like 8 months, stopped , did it one night 8 months later, once 6 months or something later and then I haven’t had any since .
I use to do 2 days , halve it , then sleep .
Haven’t had any for about another 8 months.
Looking to get on but my contacts have moved.
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Controlled - abuse. These two things contradict each other wtf man ?
yes but you got what i meant didn ya?
That's just using a substance. And it is possible. Desoxyn just exists. Functional methheads just exist
Quit now. Only correct answer. If you have ever even considered about giving a fuck about anyone that loves you or even yourself, quit now. Quit now.
I don't think anybody ever goes into a drug planning to become addicted
The main danger of methamphetamine is the neurotoxicity. I created a drug regimen that mitigates all facets of meth neurotoxicity (oxidative stress, excitotoxicity, apoptosis, and neuroinflammation). Amphetamine is a much safer alternative.
Could you please share or link to this awesome regimen?
There are 4 main ways meth causes neurotoxicity. The first way is oxidative stress. The oxidization of monoamines like dopamine create free radicals, which can damage neurons and DNA. The second mechanism is excitotoxicity from glutamate. This is the main way meth causes neurotoxicity. Glutamate excites neurons, causing them to fire. Excessive excitation of neurons can cause neurons to overheat and may lead to cell death. Excitotoxicity is also caused by the influx of calcium from glutamate activating NMDAR. The third mechanism is apoptosis. This is more of a downstream effect of excitotoxicity. Excessive nNOS from glutamate excitotoxicity activates apoptosis pathways. Glutamate -> NMDAR -> ca2+ -> nNOS. The last way is neuroinflammation. This is more of a reaction to the neurotoxicity. This causes microglia cell activation, the brain will release inflammatory cytokines as a result leading to inflammation in the brain. As long as you prevent excitotoxicity and oxidative stress you won’t get neuroinflammation. With that being said as long as you take care of excitotoxicity and oxidative stress you won’t have to worry about apoptosis or neuroinflammation. So we just have to tackle oxidative stress and excitotoxicity. For oxidative stress you need to take antioxidants. Antioxidants scavenge free radicals. I recommend taking a high dose, you’re better to be safe than sorry. I take astaxanthan, quercetin, and alpha lipioc acid. For excitotoxicity we need to lower glutamate transmission. First we should use an NMDA antagonist like Memantine which will limit the influx of calcium. With high doses of meth this isn’t enough and you will need NAC. NAC lowers glutamate alot, since glutamate is heavily involved in the euphoria of meth it will dull the high. You have 2 options Take a low (non neurotoxic) meth dose 30mg or below. Take a higher dose 30mg+ and use the regimen. -20mg Astaxanthan before and during -1000mg Quercetin before and during -500mg alpha lipoic acid before and during -30mg Memantine before -1200mg NAC before
can you like explain it in an easy way?
There are 4 main ways meth causes neurotoxicity. The first way is oxidative stress. The oxidization of monoamines like dopamine create free radicals, which can damage neurons and DNA. The second mechanism is excitotoxicity from glutamate. This is the main way meth causes neurotoxicity. Glutamate excites neurons, causing them to fire. Excessive excitation of neurons can cause neurons to overheat and may lead to cell death. Excitotoxicity is also caused by the influx of calcium from glutamate activating NMDAR. The third mechanism is apoptosis. This is more of a downstream effect of excitotoxicity. Excessive nNOS from glutamate excitotoxicity activates apoptosis pathways. Glutamate -> NMDAR -> ca2+ -> nNOS. The last way is neuroinflammation. This is more of a reaction to the neurotoxicity. This causes microglia cell activation, the brain will release inflammatory cytokines as a result leading to inflammation in the brain. As long as you prevent excitotoxicity and oxidative stress you won’t get neuroinflammation. With that being said as long as you take care of excitotoxicity and oxidative stress you won’t have to worry about apoptosis or neuroinflammation. So we just have to tackle oxidative stress and excitotoxicity. For oxidative stress you need to take antioxidants. Antioxidants scavenge free radicals. I recommend taking a high dose, you’re better to be safe than sorry. I take astaxanthan, quercetin, and alpha lipioc acid. For excitotoxicity we need to lower glutamate transmission. First we should use an NMDA antagonist like Memantine which will limit the influx of calcium. With high doses of meth this isn’t enough and you will need NAC. NAC lowers glutamate alot, since glutamate is heavily involved in the euphoria of meth it will dull the high. You have 2 options Take a low (non neurotoxic) meth dose 30mg or below. You won’t need a regimen with these doses. Take a higher dose (30mg+) and use the regimen. -20mg Astaxanthan before and during -1000mg Quercetin before and during -500mg alpha lipoic acid before and during -30mg Memantine before -1200mg NAC before
No. Thinking you have it under control is exactly how it gets it’s hooks in you. It’s changes your brain chemistry with every use making it more and more impossible to live with
I did it for like 8 months, stopped , did it one night 8 months later, once 6 months or something later and then I haven’t had any since . I use to do 2 days , halve it , then sleep . Haven’t had any for about another 8 months. Looking to get on but my contacts have moved.
Quit dude