trainman04
Bluelighter
- Joined
- Dec 18, 2017
- Messages
- 189
So whats the purpose of anandamide besides activating CB1? also what about 2-AG does FAAH inhibitors increase that? (edit) oh nevermind MAGL inhibitor? increase 2-ag right? do u know of any MAGL inhibitors? otc or drugs? also are there any other important endocannabinoid receptor or stuff im forgetting?
so THC can make New CB 1 receptors? but long term THC usage decreases cb1?.... I saw a comment on reddit "Less CB1 receptors = less places for THC to attach to = a weaker high." Me already having less cb1 receptors accordin to the snp but they also dont get disentized... I need more cb1 receptors tho.
what antidepressant drugs create/activate cb1?
wats the diff between 2-ag and 2-age ? 2-ag turns into 2-age?? both are agonist on cb1 also what is N-Arachidonoyl dopamine ? Is dopamine itself an agonist on cb1?
so all these (2ag/2age/anandimide/NADA etc) produce anti anxiety effect by increasing cb1?
is
2- ag degraded by FAAH or MAGL OR Both?
maca - https://www.ncbi.nlm.nih.gov/pubmed/23853040
pterostilbene http://www.fasebj.org/doi/abs/10.1096/fasebj.28.1_supplement.1144.10
pterostilbene is better absorbed by the body than reservatol
black pepper im a little confused dont know what it does think it activates cb1
https://www.ncbi.nlm.nih.gov/pubmed/28942644
what is the CRHR1-IT1 (CRHR1 intronic transcript 1) & MGC57346-CRHR1 gene ? I have risk alles with these but theres no description about them anywhere.
I already eat healthy and excercise 5 days a week its not working
random study
so THC can make New CB 1 receptors? but long term THC usage decreases cb1?.... I saw a comment on reddit "Less CB1 receptors = less places for THC to attach to = a weaker high." Me already having less cb1 receptors accordin to the snp but they also dont get disentized... I need more cb1 receptors tho.
what antidepressant drugs create/activate cb1?
wats the diff between 2-ag and 2-age ? 2-ag turns into 2-age?? both are agonist on cb1 also what is N-Arachidonoyl dopamine ? Is dopamine itself an agonist on cb1?
so all these (2ag/2age/anandimide/NADA etc) produce anti anxiety effect by increasing cb1?
is
2- ag degraded by FAAH or MAGL OR Both?
maca - https://www.ncbi.nlm.nih.gov/pubmed/23853040
pterostilbene http://www.fasebj.org/doi/abs/10.1096/fasebj.28.1_supplement.1144.10
pterostilbene is better absorbed by the body than reservatol
black pepper im a little confused dont know what it does think it activates cb1
https://www.ncbi.nlm.nih.gov/pubmed/28942644
what is the CRHR1-IT1 (CRHR1 intronic transcript 1) & MGC57346-CRHR1 gene ? I have risk alles with these but theres no description about them anywhere.
I already eat healthy and excercise 5 days a week its not working
random study
These rats exhibit a mutation in a gene called Crhr1 that increases CRF (type 1) receptor signaling.
increased CRF signaling led to elevated activity of the anandamide clearance enzyme fatty acid amide hydrolase (FAAH). Increased CRF was also associated with drops in anandamide levels in the central nucleus of the amygdala. Together, increased FAAH activity and decreased anandamide with low cb1 the signaling reduce inhibitory control of excitatory neurotransmission in this critical region, and lower the brain’s ability to regulate stress and anxiety.
[1] CB1 stimulation helps hold anxiety in check.
[1] CB1 stimulation helps hold anxiety in check.
CB1 Receptors control stress-mediating circuits by inhibiting neurotransmitter release — a sort of gating mechanism to keep anxiety in check.
[2] CRF increases our stress response
corticotropin-releasing factor (CRF) activates the stress response and promotes increased sensitivity to stress and anxiety when activated over and over again.
[3] Too much CRF in the Amygdala and probably the Nucleus Accumbens can shut down this stress releaving system and leave you in a state of constant anxiety.
overactive CRF signaling in this region produces a wide range of effects that override the stress-reducing capabilities of a major eCB called N-arachidonoylethanolamine (anandamide), turning chronic stress into unchecked, or pathological, anxiety.
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