The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
if this scd enzyme is blocked we're going to have an increase in the saturate a decrease in our poa okay but again what we have when we're consuming the high carbohydrates even if they're the again more refined carbohydrates or the less rapidly absorbed carbohydrates this is the path that we wind up going on 16 1 is our 16 0 saturated fat is elevated and it turns on this cascade leading to increase in vldl
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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.
in the liver when you are taking c16 or c18 but let's just keep the discussion simple and start with a saturated c16 it's it's the first committed step is going through scd-1 is an enzyme and it adds that double bond it makes a few more steps along the way but ultimately it is increasing a process of lipogenesis it is making more lipid it is increasing the amount of lipid within the cholesterol ester in the triglyceride it is being exported from the liver
if you go down that pathway what you're basically doing is bundling and packaging fat to leave the liver