The Dilemma of "Low Inhib" Substances and a Potential Solution

Cope

Cope

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As appealing as it may seem, taking an agonist such as Phenibut, benzodiazepines, Cabergoline, amphetamines, etc. just isn't that simple. Sure, you will achieve that short term relief of reduced inhibition. But in the end, your mental health will suffer more than it's worth. I have figured out a theoretical solution to this, but first let's take a brief look at some biochemistry.

Neurotransmitters are created and stored in the pre-synaptic neurons, and once released, they're absorbed by the post-synaptic neurons. Both pre-synaptic and post-synaptic neurons contain receptors that regulate how much a neurotransmitter is released and how much is absorbed. When a neurotransmitter is flooded into a synapse, it will uptake any excess of that said neurotransmitter back into the pre-synaptic receptor. These powerful agonists I mentioned, however, prevent this reuptake. The pharmacodynamics of the jewish antidepressants work a bit differently, but they operate similarly enough that they are referred to as selective serotonin reuptake inhibitors. This is significant because this is when the dreaded downregulation of these neurotransmitters occurs. You will end up having to take more of said drugs in order to achieve the desired effect because baseline levels of the neurotransmitters used will decrease due to this downregulation. The brain is autistic and wants to constantly maintain homeostasis. This applies even if the stimulation comes from the most trivial activities.

So the solution to this would be to take substances that upregulate these neurotransmitters. In reference to lowering inhibition, the two neurotransmitters I would focus on upregulating are GABA and dopamine. Both kava kava and bacopa monnieri have been shown to upregulate the GABA-A receptor. If you plan on using a primarily GABA-A agonist such as alcohol and benzodiazepines, I would supplement these adaptogens on your off days. If you plan on using a GABA-B agonist like Phenibut, I would supplement with Fasoracetam on the off days to mitigate tolerance since it upregulates GABA-B receptors. For dopamine agonists such as Cabergoline and amphetamines, I would take uridine, CDP-choline, and potentially DHA since they upregulate dopamine. I will provide a more thorough protocol in a future thread as I'm still experimenting with this. Keep in mind this is theoretical and your mileage may vary. Jumping straight to using these very GABAergic and dopaminergic compounds is still very risky even if you use the accompanying nootropics I mentioned.

But essentially I have figured out a way to completely destroy inhibition without having to deal with the negative side effects or building tolerance.
 
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just stop being a pussy theory
 
Interesting...what about for weed smokers?
 
Any studies to back it up?
 
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Both kava kava and bacopa monnieri have been shown to upregulate the GABA-A receptor.

"it was concluded that the pharmacological activities of kava were not due to direct interactions with the benzodiazepine or GABAA receptors, but rather that the lipophilic kavalactones were incorporated into the lipid membranes, leading to a nonspecific modification of the GABAA receptor conformation."

If you plan on using a primarily GABA-A agonist such as alcohol and benzodiazepines, I would supplement these adaptogens on your off days.

I feel like, due to the MoA posted above, it wold be more beneficial to use Kava Kava the day(s) after consumption as this is when you are going to suffer from the depletion of whatever neurotransmitter so the enhanced binding of ligands (neurotransmitters in this case) is going to compensate for the lack in quantity thereof.

am shit at neuro tho
 
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Good thread OP
 
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Enjoyed reading that OP, gave you a like.
 
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wish paulie_walnuts were here to discuss this with you, but sadly, im sticking on cabergoline, overall, i think i might go balls deep on kava kava and bacopa to see if there is something wrong, dont want to be drugged op.
 
Is that shit true about kava I’m low key addicted to clonopin and want to use something else
 
Any studies to back it up?
Kava Kava

Bacopa monnieri

Fasoracetam

Uridine

CDP-Choline

wish paulie_walnuts were here to discuss this with you, but sadly, im sticking on cabergoline, overall, i think i might go balls deep on kava kava and bacopa to see if there is something wrong, dont want to be drugged op.
Yea, he definitely inspired me to take neurochemistry more seriously.
 
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Kava Kava

Bacopa monnieri

Fasoracetam

Uridine

CDP-Choline


Yea, he definitely inspired me to take neurochemistry more seriously.
Have you looked into sodium butyrate?
 
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As appealing as it may seem, taking an agonist such as Phenibut, benzodiazepines, Cabergoline, amphetamines, etc. just isn't that simple. Sure, you will achieve that short term relief of reduced inhibition. But in the end, your mental health will suffer more than it's worth. I have figured out a theoretical solution to this, but first let's take a brief look at some biochemistry.

Neurotransmitters are created and stored in the pre-synaptic neurons, and once released, they're absorbed by the post-synaptic neurons. Both pre-synaptic and post-synaptic neurons contain receptors that regulate how much a neurotransmitter is released and how much is absorbed. When a neurotransmitter is flooded into a synapse, it will uptake any excess of that said neurotransmitter back into the pre-synaptic receptor. These powerful agonists I mentioned, however, prevent this reuptake. The pharmacodynamics of the jewish antidepressants work a bit differently, but they operate similarly enough that they are referred to as selective serotonin reuptake inhibitors. This is significant because this is when the dreaded downregulation of these neurotransmitters occurs. You will end up having to take more of said drugs in order to achieve the desired effect because baseline levels of the neurotransmitters used will decrease due to this downregulation. The brain is autistic and wants to constantly maintain homeostasis. This applies even if the stimulation comes from the most trivial activities.

So the solution to this would be to take substances that upregulate these neurotransmitters. In reference to lowering inhibition, the two neurotransmitters I would focus on upregulating are GABA and dopamine. Both kava kava and bacopa monnieri have been shown to upregulate the GABA-A receptor. If you plan on using a primarily GABA-A agonist such as alcohol and benzodiazepines, I would supplement these adaptogens on your off days. If you plan on using a GABA-B agonist like Phenibut, I would supplement with Fasoracetam on the off days to mitigate tolerance since it upregulates GABA-B receptors. For dopamine agonists such as Cabergoline and amphetamines, I would take uridine, CDP-choline, and potentially DHA since they upregulate dopamine. I will provide a more thorough protocol in a future thread as I'm still experimenting with this. Keep in mind this is theoretical and your mileage may vary. Jumping straight to using these very GABAergic and dopaminergic compounds is still very risky even if you use the accompanying nootropics I mentioned.

But essentially I have figured out a way to completely destroy inhibition without having to deal with the negative side effects or building tolerance.
Black bla bla bla bla

Just run hard liqour game till your buzzed but not drunk then you'll be low inhib
 
Have you looked into sodium butyrate?
Never heard of it, seems like the mechanism of action works better for addiction not so much for increasing receptor density.
 
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Black bla bla bla bla

Just run hard liqour game till your buzzed but not drunk then you'll be low inhib

just fuck up your liver, brain, skin and t theory
 
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Wouldnt upregulating a receptor increase your sensitivity to the drug? I am no expert tbh but couldn't that cause unwanted consequences?
 
high iq tbh
 
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Wouldnt upregulating a receptor increase your sensitivity to the drug? I am no expert tbh but couldn't that cause unwanted consequences?
Drugs that operate as powerful agonists will exponentially desensitize the receptor, so taking the substances needed for upregulation without agonists may be unnecessary (unless you already have an issue with low GABA/dopamine signaling). Also the nootropics I mentioned should be of a low concentration, so unless you're consistently taking ridiculously high dosages than it shouldn't be an issue. Start with low dosages.

Like I said, the brain wants to maintain homeostasis so it will automatically compensate for these exogenous changes on its own.
just fuck up your liver, brain, skin and t theory
Honestly I think alcohol might be worse for the skin than smoking nicotine. Not only does it make you low T, but it's very estrogenic as well.
 
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Drugs that operate as powerful agonists will exponentially desensitize the receptor, so taking the substances needed for upregulation without agonists may be unnecessary (unless you already have an issue with low GABA/dopamine signaling). Also the nootropics I mentioned should be of a low concentration, so unless you're consistently taking ridiculously high dosages than it shouldn't be an issue. Start with low dosages.


Honestly I think alcohol might be worse for the skin than smoking nicotine. Not only does it make you low T, but it's very estrogenic as well.
Wdyt of gut flora replacement surgery for being nt
 
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fuck amphetamines make me soooo low inhib.

Do you have a method to stay as long as possible in phase 1 and 2 thats described in this thread?
 
Why do we care about lowering inhibiton by chemical means?

If you have understood anything from this site, it would be that your behavior is determined by your looks. You are low inhib because you are ugly and people are mean when ugly people call attention to themselves. So by Pavlovian conditioning you try your best to avoid attention to ourself and are thus low inhib. You must address the fundamental cause of your behavior: your LOOKS.
 
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Why do we care about lowering inhibiton by chemical means?

If you have understood anything from this site, it would be that your behavior is determined by your looks. You are low inhib because you are ugly and people are mean when ugly people call attention to themselves. So by Pavlovian conditioning you try your best to avoid attention to ourself and are thus low inhib. You must address the fundamental cause of your behavior: your LOOKS.
This. Nobody would be a high inhib pussy if he had 6'5 height and a big frame.
 
Why do we care about lowering inhibiton by chemical means?

If you have understood anything from this site, it would be that your behavior is determined by your looks. You are low inhib because you are ugly and people are mean when ugly people call attention to themselves. So by Pavlovian conditioning you try your best to avoid attention to ourself and are thus low inhib. You must address the fundamental cause of your behavior: your LOOKS.
ok hold my beer and lemme looksmax to Chad real quick
 
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You don’t even have to get scientific with it, if you use a substance to be low inhib you either become a slave to it, or you only use it a few times and it trading really good neurons for the now but you’ll have to pay for that later on
 
fuck amphetamines make me soooo low inhib.

Do you have a method to stay as long as possible in phase 1 and 2 thats described in this thread?

Apparently NMDA antagonists, specifically DXM, are good for this but imo it's very difficult to relive those initial experiences we get with those drugs. But perhaps if you combined both methods it could work.
 
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Apparently NMDA antagonists, specifically DXM, are good for this but imo it's very difficult to relive those initial experiences we get with those drugs. But perhaps if you combined both methods it could work.
yeah, for example from ritalin I don't get cravings at all to do it again for a long time, but from mdma I get cravings for a whole month, brain telling me to use it again

I take breaks from mdma for at least 3 months

I was thinking of using ritalin every 1-2 months? Just to let the brain cool down from it and use it on special evenings
 
As appealing as it may seem, taking an agonist such as Phenibut, benzodiazepines, Cabergoline, amphetamines, etc. just isn't that simple. Sure, you will achieve that short term relief of reduced inhibition. But in the end, your mental health will suffer more than it's worth. I have figured out a theoretical solution to this, but first let's take a brief look at some biochemistry.

Neurotransmitters are created and stored in the pre-synaptic neurons, and once released, they're absorbed by the post-synaptic neurons. Both pre-synaptic and post-synaptic neurons contain receptors that regulate how much a neurotransmitter is released and how much is absorbed. When a neurotransmitter is flooded into a synapse, it will uptake any excess of that said neurotransmitter back into the pre-synaptic receptor. These powerful agonists I mentioned, however, prevent this reuptake. The pharmacodynamics of the jewish antidepressants work a bit differently, but they operate similarly enough that they are referred to as selective serotonin reuptake inhibitors. This is significant because this is when the dreaded downregulation of these neurotransmitters occurs. You will end up having to take more of said drugs in order to achieve the desired effect because baseline levels of the neurotransmitters used will decrease due to this downregulation. The brain is autistic and wants to constantly maintain homeostasis. This applies even if the stimulation comes from the most trivial activities.

So the solution to this would be to take substances that upregulate these neurotransmitters. In reference to lowering inhibition, the two neurotransmitters I would focus on upregulating are GABA and dopamine. Both kava kava and bacopa monnieri have been shown to upregulate the GABA-A receptor. If you plan on using a primarily GABA-A agonist such as alcohol and benzodiazepines, I would supplement these adaptogens on your off days. If you plan on using a GABA-B agonist like Phenibut, I would supplement with Fasoracetam on the off days to mitigate tolerance since it upregulates GABA-B receptors. For dopamine agonists such as Cabergoline and amphetamines, I would take uridine, CDP-choline, and potentially DHA since they upregulate dopamine. I will provide a more thorough protocol in a future thread as I'm still experimenting with this. Keep in mind this is theoretical and your mileage may vary. Jumping straight to using these very GABAergic and dopaminergic compounds is still very risky even if you use the accompanying nootropics I mentioned.

But essentially I have figured out a way to completely destroy inhibition without having to deal with the negative side effects or building tolerance.

Did read but just stop being a pussy
 
that's absolutely bizarre because MDMA is meant to be non-addictive because it has so little dopaminergic activity
yh don't know why it felt so addictive to me. It's even worser than nicotine, those cravings. meanwhile with ritalin/speed I don't get cravings.

maybe cuz it was ecstasy last time and it could've been mixed with meth or something. no idea
 
I’m new to all of this substance stuff, I only really use caffeine and alcohol to be more NT/low inhib lol

How do you guys get a hold of these other substances?
 
holy shit yeah you probably got cut with meth. how long were you awake / stimulated for after taking it?
first 180mg 11:50pm
redose 150mg ~ 2am
last redose around 80mg at 4am
Could sleep at 9am without problems and I had good afterglow that day
Bad comedown for 2 days, prolly cuz I redosed twice

I had days where I only thought about this substance, browsing mdma reddit non-stop just craving it again
Last time I used was february and those cravings were gone after a month

I’m new to all of this substance stuff, I only really use caffeine and alcohol to be more NT/low inhib lol

How do you guys get a hold of these other substances?
dealers
 
I know this thread old af but i just ordered everything except uridine. Anyone else went for it?
 

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