The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
essentially we are a gas tank and all of our body will store the oils that we eat so if you drink corn oil or you are taking two tablespoons or four tablespoons of corn oil every day in your diet you are storing that corn oil in your cells and that corn oil is if that polyunsaturated PUFA is eventually going to get oxidized in a process called beta oxidation
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
What we're talking about here is that you see that when you look at the lipid peroxidation index of patients with atherosclerosis compared to healthy controls this is looking at two age groups age 36 to 47 and people who are older age 69 to 94 and in both age groups there was a 20 to 30 and 100f fold increase in the products of oxidative oxidation of linolic acid in those with atherosclerosis the hypothesis that we're generating here is similar to the first paper I showed and that is exactly that the more more our LDL gets enriched with linolic acid the more oxidized it becomes the more susceptible to oxidation it becomes
whereas with the monounsaturated fat susceptibility of LDL to oxidative stress is lower
we know that these polyan citrate fats are much easily much more easily oxidized we consume them and then they take up resonance in our tissues they take resonance in LDL we know that that increases susceptibility of oxidation for the LDL we see that oxidized LDL in plaques and arteries