anandamide

Anandamide, generally referred to as AEA, is one of the cannabinoids that the human body makes naturally.

The endocannabinoids alkylamides and anandamide (AEA) are found in echinacea, bind to the CB2 receptor and, like the THC cannabinoid, greatly inhibits inflammation.

Cannabidiol also inhibits an enzyme that metabolizes the endocannabinoid anandamide, which are neurotransmitters produced throughout the central nervous system, including the brain.

This enzyme is responsible for the degradation of endocannabinoids and is encoded by its homonym gene FAAH which presents a missense SNP (rs324420/C385A) that reduces the expression and the activity of that enzyme, resulting in increased anandamide levels (Chiang, Gerber, Sipe, & Cravatt, 2004; Dincheva et al, 2015).

It is a simple fatty acid amide that is structurally related to the endogenous cannabinoid transmitter, anandamide (AEA).

Sheep cheese naturally enriched in [alpha]-linolenic, conjugated linoleic and vaccenic acids improves the lipid profile and reduces anandamide in the plasma of hypercholesterolaemic subjects.

All human beings have an endocannabinoid system, which naturally produces cannabis-like compounds, the main ones being anandamide and 2-arachidonoylglycerol (2-AG) that bind to their receptors to produce beneficial effects.

(31-32) In addition, CBD increases the availability of the endogenous cannabinoid anandamide, which may have antipsychotic properties.

CBD stimulates the body to release anandamide, a neurotransmitter produced in the brain.

There exist also endogenous cannabinoids eg., arachidonoyl ethanolamide or anandamide and arachidonoylglycerol.

Combining CBD with chocolate helps prolong and double the effect of anandamide, a cannabinoid found in dark chocolate that works as the body's own antidepressant and pain reliever, resulting in a calm, soothing effect.

Anandamide (N-aracuidonoyl etanolamine) and 2-aracuidonoyl glycerol both belong to the group of endocanabinnoids that are synthesized by neurons in the brain (MASSI et al., 2012; BRUCKI et al., 2015; LESSA et al., 2016) and are released by excitatory synaptic stimuli (BRUCKI et al., 2015).