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.
when your mitochondria break down a saturated fat like palmitate or stearic acid which are long chain fatty acids they produce more fadh2 relative to nadh2 and those mitochondria actually get what is called reverse electron transport which leads to production of reactive oxygen species and that is how the cell signals insulin resistance
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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.
the reverse is saturated fat which has a higher f2n ratio because of beta oxidation the fadh2 to nadh and that causes our adipocytes to become insulin resistant they don't grow they never expand you never get to this pathological spewing of free fatty acids which essentially leads to underlying metabolic dysfunction
that is what saturated fats are supposed to signal in your body by generating reactive oxygen species