Fatty Acid Modulation Of The Endocannabinoid System

[in vivo]

Abstract

Endocannabinoids and their G-protein coupled receptors (GPCR) are a current research focus in the area of obesity due to the system’s role in food intake and glucose and lipid metabolism. Importantly, overweight and obese individuals often have higher circulating levels of the arachidonic acid-derived endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) and an altered pattern of receptor expression. Consequently, this leads to an increase in orexigenic stimuli, changes in fatty acid synthesis, insulin sensitivity, and glucose utilisation, with preferential energy storage in adipose tissue. As endocannabinoids are products of dietary fats, modification of dietary intake may modulate their levels, with eicosapentaenoic and docosahexaenoic acid based endocannabinoids being able to displace arachidonic acid from cell membranes, reducing AEA and 2-AG production. Similarly, oleoyl ethanolamide, a product of oleic acid, induces satiety, decreases circulating fatty acid concentrations, increases the capacity for β-oxidation, and is capable of inhibiting the action of AEA and 2-AG in adipose tissue. Thus, understanding how dietary fats alter endocannabinoid system activity is a pertinent area of research due to public health messages promoting a shift towards plant-derived fats, which are rich sources of AEA and 2-AG precursor fatty acids, possibly encouraging excessive energy intake and weight gain.

 

http://www.hindawi.com/journals/ije/2013/361895/

 

 

This paper focuses on food intake and metabolism, but the therapeutic implications of modulating your endogenous cannabinoid levels are far reaching. This is an example of reducing AEA and 2-AG, but it's also safe to assume that consumption of these are likely to decrease the efficiency of THC treatments, and increase the efficiency of CBD treatments.

 

Modulating exogenous cannabinoids is a form of cannabinoid treatment all unto itself, and seems worthy of exploration.