5 replies to this topic

[male_1978]

I just stumbeled across this video with David Sinclair.

 

https://www.youtube....SL3g1Hg#t=26m37

 

 

Summary about what Sinclair said:

 

 

Oleic acid is produced when we are hungry by a breakdown of fat and it activates SIRT1 just as Resveratrol does. Olive Oil, Avocados and wal nuts have this oil

 

This means, that oleic acid just like resveratrol are mimicing fasting.

 

David Sinclair said it is about 10 times or 100 times more potent than resveratrol

 

 

Your oppinions on this?

 

 

 

Edited by male_1978, 18 February 2020 - 09:38 AM.

[Justin BoBustinBananaFanaF]

I think we need someone with a strong science background on this one.

 

Studies that seem to agree:

https://www.ncbi.nlm...pubmed/23329830

 

Studies that seem to disagree:

https://www.ncbi.nlm...pubmed/27072559

[anothercanuck]

I think Dr. Sinclair may be referring to this paper titled "Lipid Droplet-Derived Monounsaturated Fatty Acids Traffic via PLIN5 to Allosterically Activate SIRT1".

[Oakman]

So taking olive oil and R together is counterproductive if they use the same receptors. I wounder what the equivalence between them is in terms of how much oleic acid = how much R as far as SIRT1 up regulation?.

[Castiel]

it is sirt1 activation for oleic acid.  There have been papers suggesting resveratrol activates multiple other sirtuins as well.

[thompson92]

Chromatin and metabolic states both influence lifespan, but how they interact in lifespan regulation is largely unknown. The COMPASS chromatin complex, which trimethylates lysine 4 on histone H3 (H3K4me3), regulates lifespan in Caenorhabditis elegans. However, the mechanism by which H3K4me3 modifiers affect longevity, and whether this mechanism involves metabolic changes, remain unclear. Here we show that a deficiency in H3K4me3 methyltransferase, which extends lifespan, promotes fat accumulation in worms with a specific enrichment of mono-unsaturated fatty acids (MUFAs). This fat metabolism switch in H3K4me3 methyltransferase-deficient worms is mediated at least in part by the downregulation of germline targets, including S6 kinase, and by the activation of an intestinal transcriptional network that upregulates delta-9 fatty acid desaturases. Notably, the accumulation of MUFAs is necessary for the lifespan extension of H3K4me3 methyltransferase-deficient worms, and dietary MUFAs are sufficient to extend lifespan. Given the conservation of lipid metabolism, dietary or endogenous MUFAs could extend lifespan and healthspan in other species, including mammals.

 

  Han, S., Schroeder, E., Silva-García, C., Hebestreit, K., Mair, W., & Brunet, A. (2017). Mono-unsaturated fatty acids link H3K4me3 modifiers to C. elegans lifespan. Nature, 544(7649), 185-190. doi:10.1038/nature21686

https://www.ncbi.nlm...pubmed/28379943