The more and more I study this stuff, the more convincing I'...

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Kind-1 (TextNote)

2026-06-29T23:12:02Z

↳ Reply to 010df0c9... (npub1qyxlpj2gl6dt2nfvkl4yyrl6pr2hjkycrdh2dr5r42n7ktwn7pdqrdmu7u)

Can't wait to hear how this goes. Definitely not convinced by the influencers who say it doesn't matter* *source I said so.

The more and more I study this stuff, the more convincing I'm finding it, mechanistically, that massive amounts of lipid particle "pressure" - even if they're large and fluffy pattern A particles and you're as low-inflammation/oxidation/etc as you can get - still may cause plaques to form over the long run. It's the "MAY" part that I'm willing to have some respect for. We just don't know for sure yet. The mainstream claims to be certain - I think they're wrong. The fringe also seems to be certain - I'm not convinced enough that they're right.

That doesn't make it UNTRUE that smaller, denser particles are worse; inflammatory environment is worse; insulin sensitivity is important; etc. etc. - all the main arguments from the high-fat/low-carb crowd are still true. But going so far as to say that "ApoB and LDL just don't matter" is sloppy. Maybe at the numbers that a non-hyper-responder sees, that might be "close enough" that it doesn't matter for most people for most of their life.
But if you hyper-respond to the diet, and it's true that obscene numbers of particles (perhaps by some yet-unknown mechanism - see: https://drmalcolmkendrick.org/2026/06/02/transcytosis-what-is-it-and-does-it-matter/ ....) will cause some to be taken in by endothelial cells, then it's in your best interest, operating partially in the dark, to attempt to lower particle count while holding all those other good things high.

...remains to be seen whether that's possible.
And I maintain that the best case would be CCTA scans every 6 months with sky-high particles to watch for soft plaques which may or may not ever form!

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