Omega 3 EPA/DHA

Omega 3 Fatty Acids

Although omega-3 ALA (sourced mainly from plants and organ meats) can be converted to EPA and DHA, research suggests that only a small portion can be converted from this process.
Excessive dietary intake of LA (omega 6 and precursor to Anandamide) induces endocannabinoid hyperactivity and promotes diet induced obesity.
The effects of LA can be offset by consuming sufficient omega-3 EPA and DHA.

EPA/DHA

EPA and DHA omega 3 fatty acids are produced by water plants, such as algae, and are prevalent in marine animals.
DHEA and EPEA activated cannabinoid CB1 and CB2 receptors in vitro with significant potency, suggesting that they are endocannabinoids.
- DHEA and EPEA are derivatives of DHA and EPA, respectively.
Dietary EPA and DHA when esterified to phospholipids (PLs) are more efficiently incorporated into tissue PLs and affect endocannabinoid biosynthesis at much lower doses than EPA and DHA in triglyceride form.
- Most fish oil capsules have omega 3 in triglyceride form and most krill oil delivers it in phospholipid form.
- EPA/DHA has been found to be absorbed better with different foods.

Be aware of differences in farmed and wild seafood and what the farmed seafood is fed.
- A 2013 study showed that Atlantic salmon fed a diet higher in soybean oil versus fish oil was used to study effects on feed in mice. It showed a marked decrease in the EPA and DHA in the liver and erythrocyte phospholipids as well as weight gain and adipose tissue inflammation compared to the mice fed salmon on a fish oil diet.

~EPA is the only nutrient known de-activate muscle breakdown in the human body~

- EPA is anti-catabolic, meaning that it helps to prevent the breakdown of muscle in the human body. It acts through various pathways that work to breakdown muscle in the human body.
- DHA intake has been shown to increase the likelihood of omega 3 fatty acids being metabolized preferentially over omega 6 and omega 9 fatty acids.
- DHA metabolites (remaining chemical structure after broken down) have been shown to activate CB2 receptors. CB2 is a potent anti-inflammatory endocannabinoid receptor.
- There are some farmed fish that are claimed to have higher levels of omega 3 and they may contain lower levels of mercury; however there are questions on the antibiotic and hormone usage.
The omega-3 long chain polyunsaturated fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), elicit anti-proliferative effects in cancer cell lines and in animal models.
- Data shows that the two omega-3 (DHA & EPA) ethanolamides exert anti-proliferative effects by inducing autophagy in breast cancer cells highlighting their potential use as breast cancer preventive and/or therapeutic agents.
DHA has been shown to prevent altered CB1 and GABAA receptor binding densities in rats fed a high saturated fat diet.

DHA/EPA and Cancer

The omega-3 long chain polyunsaturated fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), elicit anti-proliferative effects in cancer cell lines and in animal models.
- Data shows that the two omega-3 (DHA & EPA) ethanolamides exert anti-proliferative effects by inducing autophagy in breast cancer cells highlighting their potential use as breast cancer preventive and/or therapeutic agents.
The omega-3 fatty acid ethanolamides, docosahexaenoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA), displayed greater anti-proliferative potency than their parent omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in LNCaP and PC3 prostate cancer cells.
DHEA is likely metabolised differently from EPA, DHA and EPEA. Alternatively the anti-tumor effect of DHEA may be due to another metabolite of DHEA when it is metabolised by FAAH, which is produced when FAAH is inhibited. These results confirm the anti-proliferative effects of cetain omega 3 fatty acids and suggest a role of cannabinoid receptors and FAAH in breast cancer cells.

The Endocannabinoid Solution (ECS)