@alphagruis: Voila! Par example...http://inhumanexperiment.blogspot.com/2009/10/fats-and-ages-pufas-are-even-worse-than.html (Juissance!) This is of course just a blog post commentary on studies, but it makes one wonder about AA oxidation in high meats...Does anyone know how dietary AA is metabolised, given that it's a PUFA?
Thanks MrBBQ for the link though I had read this blog post before.
I do not agree with it because:
-It's definitely absurd IMO to demonize any normal component of the living organisms such as glucose, PUFA's, other carbs etc... They are indispensable.
No living cell can function properly without a substantial amount of PUFAs even if these fatty acids are much more prone to oxidation There are necessarily mechanisms that prevent PUFAs oxidation in healthy cells or in vivo. In vitro experiments (with metal catalysts !!!) cannot tell us much in this respect.
-We must carefully distinguish between heated solvent extracted and virgin cold pressed oils or fats rich in PUFAs. The former are highly toxic indeed for many reasons but there is AFAIK absolutely no evidence that the latter have any adverse effects. Experiments carried out on rodents fed high PUFA diets use nothing but denatured processed oils and tell us essentially nothing in this respect.
- It's definitely not true that endogenous AGEs formation is more important than the exogeneous one. The latter must be by far dominant simply because non enzymatic glycation is a thermally activated process i.e. a process where the reaction rate is many orders of magnitude larger at cooking temperatures than at body or room temperatures. If in graphs shown in your link data on CML formation at boiling water temperature were presented too they would completely dominate the other room temperature data hardly visible at this scale in the graph.
Topic: Dr. William Davis on AGEs (Read 11624 times)