Remy
Administrator
More research on the benefits of CBD/cannabidiol coming out.
Cannabidiol looks to be an inhibitor of anandamide deactivation, similar to low dose amisulpride that @Hip has written about in the past, but with much fewer side effects. Plus it's a supplement whereas amisupride is an rx...another reason to be vigilant about the DEA's attempts to regulate CBD out of availability).
Boosting levels of anandamide looks to be helpful in PTSD and general anxiety states as well as in psychosis.
http://www.nature.com/tp/journal/v2/n3/full/tp201215a.html
https://www.sciencedaily.com/releases/2017/02/170213131201.htm
Cannabidiol looks to be an inhibitor of anandamide deactivation, similar to low dose amisulpride that @Hip has written about in the past, but with much fewer side effects. Plus it's a supplement whereas amisupride is an rx...another reason to be vigilant about the DEA's attempts to regulate CBD out of availability).
Boosting levels of anandamide looks to be helpful in PTSD and general anxiety states as well as in psychosis.
http://www.nature.com/tp/journal/v2/n3/full/tp201215a.html
Cannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid anandamide.
We previously reported that an elevation of anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms.
Furthermore, enhanced anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition.
In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement.
The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.
https://www.sciencedaily.com/releases/2017/02/170213131201.htm
In the new study, published in the journal Biological Psychiatry, the researchers investigated the interaction between the stress-promoting (CRF) and stress-constraining (eCBs) mechanisms in the central nucleus of the amygdala, a critical brain region involved in mediating emotional reactions. The findings suggest that 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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