Oleocanthal, a Phenolic Derived from Virgin Olive Oil: A Review of the Beneficial Effects on Inflammatory Disease
- oleocanthal not only mimics the mode of ibuprofen inflammatory activity, but inhibits COX 1 and COX 2 enzymes significantly more at equimolar concentrations...
- This adds further weight to oleocanthal as a potential factor in the health benefits associated with a traditional Mediterranean Diet. Assuming approximately 70% absorption, then 50 mL/day [Olive oil] corresponds to approximately 10% the current Ibuprofen pain relieving dose...
- The inflammatory enzymes attenuated by oleocanthal, COX 1 and COX 2, are responsible for the conversion of arachidonic acid to prostaglandins and thromboxane, which are produced in response to inflammatory or toxic stimuli...
- oleocanthal encourages cell apoptosis by activating caspase-3 and poly-adenosine diphosphate-ribose polymerase, phosphorylates p53...
- unusual effect of oleocanthal on heat shock protein 90 (Hsp90) [49]. Hsp90 is a chaperone protein that stabilizes a number of proteins that are required for tumor growth. Therefore Hsp90 inhibitors are investigated as anti-cancer drugs...oleocanthal significantly reduce two Hsp90 proteins, Akt and Cdk4 without actually influencing Hsp90 regulation...
- Furthermore oleocanthal had a pro-apoptotic effect on cancer cells...
- oleocanthal inhibits NO production in J774 macrophages and inhibits both IL-6 and MIP-1α in both ATDC5 chrondocytes and J774 macrophages [57]. These inflammatory cytokines are both implicated in the inflammatory process and cartilage destruction of inflammatory arthropathies...
- oleocanthal decreased expression of other pro-inflammatory markers Interleukin 1 (IL-1), tumour neurosis Factor (TNFα), and granulocyte-macrophage colony-stimulating factor (GM-CFS)...
- oleocanthal inhibits tau fibrillization in vitro by forming an adduct with PHF6 peptide. PHF6, is a VQIXXK motif that resides in the microtubule binding region [59]. Common lesions that are observed in neuro-degenerative disease (i.e., Alzheimer’s disease) are hyperphosphorylated tangles of tau and the PHF6 peptide enables the phosphorylation of tau. Therefore as oleocanthal modifies the PHF6 peptide it then disturbs tau-tau interaction and the subsequent fibril formation.
- the mechanism by which oleocanthal reacts with the tau protein ...covalently modifies the construct of tau referred to as K18 in biologically relevant conditions. Oleocanthal cross linked with two lysine residues and the end result was the rearrangement of the skeleton producing a more stable piridinium like complex...
- Derived from Aβ are diffusible ligands (ADDLs) which are neurotoxic factors believed to initiate the onset of Alzheimer’s disease. In vitro evidence suggests that oleocanthal alters the structure of ADDLs and augments antibody clearance of ADDLs, therefore protecting hippocampal neurons from ADDL toxicity...
- in vivo data indicating that oleocanthal enhances the clearance of Aβ by up regulating P-glycoprotein (P-gp) and also LDL lipoprotein receptor related protein-1 (LRPI)...
http://www.ncbi.nlm....les/PMC4139846/
These effects, and their downstream effects, are familiar to anyone who has been following C60oo's anecdotal reports etc.
Perhaps C60 most enhances the bioavailability of Oleocanthal?
Could C60 be binding to the same point in the Oleocanthal, hydroxytyrosol, etc molecules that is normally bound to by the substances that metabolise them...?
Very interesting!
I do find it ironic that it inhibits GMCSF, because this stuff activates the microglia to collect extraneuronal protein aggregates, for example, tau fibrils. Rheumatoid arthritis releases a lot of it, which is why that condition is associated with a lower risk of dementia, despite being an inflammatory process. However, it sounds as though oleocanthal intervenes at an early stage in the aggregation and fibrilization process, during which it shuts down the chain reaction which would otherwise result in those end products. Amyloid aggregation has already been shown, at least in primitive worms, to be a protein misfolding viral process analogous to prion diseases; tau phosphorylation is suspected of the same. So anything which could interrupt that chain reaction would be very valuable indeed. In other words, idiopathic tau phosphorylation is survivable via neuroplasticity, but viral phosphorylation leads to terminal cognitive decline.
It bears repeating: the longest lived person, Jean Calment, was an olive oil addict. She even used it topically as a sort of cosmetic treatment. Granted, she's only one data point, but one hell of a data point! Then of course it has also been said, with good statistical backing, that the EVOO in c60oo was responsible for most of its life extensive benefits in the Moussa study.
What do you know... there's a good Scientific American article, predating the above paper, on the inverse correlation of EVOO consumption and Alzheimer's. (They used the Med diet as a proxy for EVOO, which means there's probably more to gain because the Med diet is also loaded with pasta and white bread: "A recent study of 1,880 elderly people living in New York City, for example, showed that those who strongly adhered to a Mediterranean diet over the study's 14-year span had a 32 to 40 percent lower incidence of Alzheimer's compared with those who did not.") Perhaps the most useful insight is that it's apparently the oleocanthal which causes the throat burn for which EVOO is so infamous. So there's one rough way to gauge concentration. Rather than wait for a prescription drug based on oleocanthal, I think it's time to eat an egg drowned in olive and coconut oil...