Dr. Weeks’ Comment: We doctors were all taught that the omega 6 pathways was bad and the omega 3 pathway was good and many of us swallowed that hook, line and sinker. Now we have the opportunity to rethink that dogma.
We know that the body is comprised primarily of omega 6 fatty acids. For example: the skin has 1000x more omega 6 than omega 3 fatty acids. The nervous tissue has 100x more omega 6 than omega 3. And the lipid bi-layer membrane of each cell features more omega 6 than omega 3. We know for example that the parent essential oils (PEO) are the brick-and-mortar of each cell which allows for cellular respiration and detoxification. (This is significant because whereas omega 6 fatty acids can transport oxygen into the cell, the omega 3 fatty acids suffocate the cell.)
And yet were all believed that arachidonic acid (in the omega 6 pathway) is pro-inflammatory whereas the omega-3 metabolites DHA and EPA were anti-inflammatory. Again we should look more closely. GLA gamma linolenic acid in the omega 6 series metabolizes to arachidonic acid and then to the body’s most powerful anti-inflammatory substance prostaglandin E1 (PGE1).
How can we understand this apparent paradox? Well all the damning studies on arachidonic acid were done using already oxidized, rancid, hydrogenated, adulterated seed oils so of course the end products were toxic. if you use unadulterated omega 6 oils – we see the benefits of seed oils.
More convincing data follows. Now Eat the Seed to oxygenate your cells and feel your best!
Anti-inflammatory effects of prostaglandin E1: in vivo modulation of the formyl peptide chemotactic receptor on the rat neutrophil.
The local generation of chemotactic factors at sites of acute inflammation is thought to be responsible for the recruitment of polymorphonuclear leukocytes (PMN) from the intravascular compartment to the site of tissue injury (1). Many of these potent phlogistic mediators have also been shown to activate PMN resulting in degranulation of lysosomal granules with release of hydrolytic enzymes into the extracellular environment and the generation of superoxide anion (O2-) and other toxic metabolites (reviewed in Reference 2). Several in vitro studies have shown that treatment of PMN with specific prostaglandins will inhibit both soluble mediator- and particulate material-induced neutrophil lysosomal enzyme release and chemotaxis (3, 4). In vivo studies have demonstrated potent anti-inflammatory activity of prostaglandins of the E series (5-7). Systemic administration of prostaglandin E1 (PGE1) or its stable analog 15-(S)-15-methyl-PGE1 (15-M-PGE1) will inhibit neutrophil dependent immune complex tissue injury in a dose-dependent manner (8). In addition, i.v. infusion of PGE1 into humans has been shown to inhibit formyl-methionyl-leucyl-phenylalanine- (FMLP) induced lysosomal enzyme release from PMN (9). This study was undertaken to examine the effects of in vivo systemic treatment of rats with 15-M-PGE1 on FMLP-induced neutrophil lysosomal enzyme release and O2- secretion. As we will show, the modulation of FMLP-induced neutrophil function is correlated with a decrease in binding affinity for formyl-methionyl-leucyl-(3H)phenylalanine ((3H)-FMLP) to its specific receptor on the neutrophil plasma membrane. The data suggest a novel mechanism for the anti-inflammatory effects of prostaglandins of the E series.
Mechanisms of anti-ischemic action of prostaglandin E1 in peripheral arterial occlusive disease.
The mechanisms of anti-ischemic effects of PGE1 in patients with peripheral arterial occlusive disease (PAD) are probably complex and clearly not limited to a direct vasodilator action. In addition to the known effects on blood flow, viscosity, fibrinolysis and platelet aggregation, the compound also inhibits monocyte and neutrophil function, suggesting that PGE1 will also have anti-inflammatory effects. Recent research has detected additional actions of PGE1 and prostacyclin analogs which might be relevant to its clinical efficacy. This includes inhibition of expression of adhesion molecules (E-selectin, ICAM-1, and VCAM-1), release of inflammatory cytokines (TNFalpha, MCP-1), matrix components and generation and release of growth factors (CYR61, CTGF). These actions may also contribute to the long-term effects of PGE1, particularly in more advanced stages of PAD. Gene-expression experiments with chemically stable prostacyclins and PGE1 suggest that several genes in vascular smooth muscle cells and fibroblasts are modified by prostaglandins at the transcriptional level. This includes TNFalpha-induced VCAM expression in vascular smooth muscle cells which appears to be inhibited via the prostaglandin EP2 receptor as well as IL-1-induced expression of the type-1 collagen gene in fibroblasts. Thus, regulation of gene transcription by PGE1 may contribute to tissue protection in critical ischemia of the lower limbs.