Cannabinoids are compounds that our body creates or that we consume from food and supplement sources that relieve pain, alleviate anxiety, and improve epilepsy symptoms.
These compounds have been getting a lot of press lately, especially in connection to hemp, and specifically to CBD (cannabidiol). But the fact is, many nutrient sources can either help bolster and preserve our own naturally-occurring cannabinoids (endocannabinoids) or provide their own components that interact with specific cannabinoid receptors in the mind and body.
One of the things that determines how well our endocannabinoid system will support us is omega-3 intake and DHA status. But omega-3s aren’t just there as a scaffold for anandamide and other endocannabinoids – they may actually contribute their own.
This research shows that levels of DHA are directly related to a metabolite of the fatty acid called N-Docosahexaenoylethanolamine, or by the more easily-remembered name, synaptamide. As its name implies, synaptamide is involved with developing and protecting brain cells. While we’ve known for some time that DHA levels can be related to cognitive health and mood, this study expands on the ways that DHA has a positive effect and how the endocannabinoid system affects the mind, body, and inflammatory responses.
If you’re not eating three servings of cold-water fish per week, and fish oil supplements just haven’t been your thing, consider trying an omega-3 supplement that is bound to phospholipids for better stability and once-daily dosage levels. It’s a convenient way to get your DHA, EPA, phospholipids, and brain-building peptides and build that “endocannabinoid tone” that all the smart minds are trying for.
Kim HY, Spector AA. N-Docosahexaenoylethanolamine: A neurotrophic and neuroprotective metabolite of docosahexaenoic acid. Mol Aspects Med. 2018 Mar 20.
N-Docosahexaenoylethanolamine (synaptamide) is an endocannabinoid-like metabolite endogenously synthesized from docosahexaenoic acid (DHA, 22:6n-3), the major omega-3 polyunsaturated fatty acid present in the brain. Although its biosynthetic mechanism has yet to be established, there is a closely linked relationship between the levels of synaptamide and its precursor DHA in the brain. Synaptamide at nanomolar concentrations promotes neurogenesis, neurite outgrowth and synaptogenesis in developing neurons. Synaptamide also attenuates the lipopolysaccharide-induced neuroinflammatory response and reduce the deleterious effects of ethanol on neurogenic differentiation of neural stem cells (NSCs). These actions are mediated by a specific target receptor of synaptamide GPR110 (ADGRF1), a G-protein coupled receptor that is highly expressed in NSCs and the brain during development. Synaptamide binding to GPR110 induces cAMP production and phosphorylation of protein kinase A (PKA) and the cAMP response element binding protein (CREB). This signaling pathway leads to the expression of neurogenic and synaptogenic genes and suppresses the expression of proinflammatory genes. The GPR110-dependent cellular effects of synaptamide are recapitulated in animal models, suggesting that synaptamide-derived mechanisms may have translational implications. The synaptamide bioactivity transmitted by newly deorphanized GPR110 provides a novel target for neurodevelopmental and neuroprotective control as well as new insight into mechanisms for DHA's beneficial effects on the central nervous system.
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