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Cannabinoid System

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Why do you think you are qualified to self diagnose if you lack understanding of the most basic stuff ?
 
CBD, particularly in solution, is not fully stable; it needs to be stored at temperatures below 8C and protected from light. Under acidic conditions, CBD can be converted (isomerized) to THC and other cannabinoids.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510776/

Trainman, please consider using the internet to answer those questions, how do you think I'm doing this? Dosages for THC can be found on Erowid and you can learn more about ananadamide and FAAH on Wikipedia.
 
The acidic conversion of CBD to THC....CBD oil is now available OTC in the UK. This would be akin to the process known as 'isomerization' that is sometimes performed using conc H2SO4 on hash oil would it not?
 
The T allele may cause lower CB1 receptor numbers and less CB1 activation . The T allele of rs1049353 may cause lower receptor numbers and less activation. With this variation, the receptors also don't become significantly less sensitive when activated (R) - i.e. you don't build up tolerance

Can someone tell me what the last sentence means when my CB1 receptors dont get less sensitive? dont build tolerance to what? I tried google but i suck at it cant find anything
 
This would be akin to the process known as 'isomerization' that is sometimes performed using conc H2SO4 on hash oil would it not?
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It's the very same.

Can someone tell me what the last sentence means when my CB1 receptors dont get less sensitive?
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It means what it says - the receptors are less likely to be desensitized when they are stimulated excessively. (e.g. tolerance to the effects of cannabinoids will develop slower)
 
I know anandamide decreases stress but wtf does AA, MAG , 2-ag and faah do? increase stress? (english is my 3rd language so I dont understand the wikipedia explanation that well )
 
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The article for anandamide on wikipedia has 22 different translations into varying languages availaible.

Anandamide is the brain's natural cannabinoid neurotransmitter. FAAH is the enzyme that breaks it down. Blocking FAAH results in elevated anandamide concentrations and typical cannabinoid effects but there are no approved drugs that act as FAAH inhibitors... yet.

AA is arachidonic acid which is the breakdown product of anandamide and also a polyunsaturated fatty acid. 2-AG and MAG are "monoacylglycerols" which are also cannabinoid agonists.

The issue with anadamide and its friends (2-AG etc) are that they are not orally bioavailiable and hence cannot be taken directly as drugs.
 
sekio said:
The article for anandamide on wikipedia has 22 different translations into varying languages availaible.

Anandamide is the brain's natural cannabinoid neurotransmitter. FAAH is the enzyme that breaks it down. Blocking FAAH results in elevated anandamide concentrations and typical cannabinoid effects but there are no approved drugs that act as FAAH inhibitors... yet.

AA is arachidonic acid which is the breakdown product of anandamide and also a polyunsaturated fatty acid. 2-AG and MAG are "monoacylglycerols" which are also cannabinoid agonists.

The issue with anadamide and its friends (2-AG etc) are that they are not orally bioavailiable and hence cannot be taken directly as drugs.
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so Increasing the CB receptors 1 and 2 with Marijuana can Increase all the other stuff too? Also why does Increasing CB1 cause a high with THC? Since THC mainly increases CB1 and CBD mainly increases CB2 but doesent cause a high.- Like why does increasing cb1 cause you to get high?
btw this is my last 2 questions :D been bothering you guys enough now
someone told me Maca is a FAAH-inhibitor so I might try that.
 
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You're confusing activation of receptors with creation of new receptors. THC/CBD activate cannabinoid receptors, they do not create more of them.

SO I have 3 different mutations (bad low) in my cannabinoid system?
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Yes, but there's no reason your body cannot adapt to such conditions.
 
hmmm so if marijuana only activates it and there are no FAAH inhibitors im basically doomed. Unless this pure NMDA I ordered works im doomed for life .
 
For fucks sake throw that NMDA OUT man. It WON'T help. And proglutamatergic compounds like that, even in doses that would be less than those required to cause excitotoxicity (are there such doses with orthosteric glutamatergic ionotropic receptor agonists? not that I'd take one, just curious to know if such a thing exists), they would CAUSE the fear, anxiety etc. that you seek to repress.

You are confusing NMDA with NMDA receptor antagonists. NMDA itself is an AGONIST at the receptor, and as such is an excitotoxic poison. It is well known to be one.
 
Limpet_Chicken said:
For fucks sake throw that NMDA OUT man. It WON'T help. And proglutamatergic compounds like that, even in doses that would be less than those required to cause excitotoxicity (are there such doses with orthosteric glutamatergic ionotropic receptor agonists? not that I'd take one, just curious to know if such a thing exists), they would CAUSE the fear, anxiety etc. that you seek to repress.

You are confusing NMDA with NMDA receptor antagonists. NMDA itself is an AGONIST at the receptor, and as such is an excitotoxic poison. It is well known to be one.
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in the study that caused excitotoxic it was only when directly injected into the brain . Theres no study that shows Oral can cause excitotoxicty.
besides the NMDA hasnt arrived yet and Iwhen it does im trying it.
NMDA when activated surpressed the amygdala. Im not confusing it with NMDA antagonists . Im not that stupid.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263393/
 
trainman04 said:
in the study that caused excitotoxic it was only when directly injected into the brain . Theres no study that shows Oral can cause excitotoxicty.
besides the NMDA hasnt arrived yet and Iwhen it does im trying it.
NMDA when activated surpressed the amygdala. Im not confusing it with NMDA antagonists . Im not that stupid.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263393/
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The study you linked to speaks to the action of D-cycloserine, an agonist at the glycine recognition site - NMDA itself is an agonist at the glutamate binding site. This isn't going to have the effect you're anticipating.

Oral dosing vs injection into the brain doesn't make the difference, it is a matter of dose.
 
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Moxious said:
The study you linked to speaks to the action of D-cycloserine, an agonist at the glycine recognition site - NMDA itself is an agonist at the glutamate binding site. This isn't going to have the effect you're anticipating.

Oral dosing vs injection into the brain doesn't make the difference, it is a matter of dose.
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NMDA is an agonist on the glutamate which is the main site that controls everything else so activating that will affect all other sites too.
yes i think it matter if its injected directly vs if its taken orally.. If its taken orally there is the BBB.
 
NMDA is an agonist on the glutamate which is the main site that controls everything else so activating that will affect all other sites too.
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This is almost laughably wrong. Where are you learning this from?
 
sekio said:
This is almost laughably wrong. Where are you learning this from?
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idk i just made that up . but does it really matter what site it binds to? nmda is nmda. and what about the guy that said NMDA heavily surpresses the amygdala? what he made that up?
 
OP, keep in mind D-cycloserine is a partial agonist at NMDA receptors as well (at the glycine site). There was a study showing that D-cycloserine given during cognitive behavioral therapy/exposure therapy can enhance fear extinction but I really think that sort of beneficial effect is very separate from a full agonist.

Heed the other's warnings about the adverse effects of taking NMDA. Hopefully none of it makes it to your brain.
 
trainman04 said:
idk i just made that up . but does it really matter what site it binds to? nmda is nmda. and what about the guy that said NMDA heavily surpresses the amygdala? what he made that up?
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I suppose a lot of people make things up nowadays.

Pop sci is really just that, popularized and oversimplified, usually blatantly incorrect at many points
 
Seriously dude, throw away the NMDA. What makes you think you know better than the others here who have repeatedly warned you not to take it (or any other NMDA agonist for that matter)? The consensus is clear on this.

Almost think you're trolling at this point.
 
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