Cope
- Joined
- Apr 7, 2019
- Posts
- 3,261
- Reputation
- 5,283
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.
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.
Last edited: