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.
in states of dysbiosis or in states of inflammation and i'll let you kind of piggyback on this and elaborate if the gut is inflamed getting ketones getting beta-hydroxybutyrate from the blood side now we're on the opposite side of the clonic epithelial cell can go into the same metabolic pathway as butyrate and can be fuel for those colon cells
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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.
if there's uh inflammation in the gut mucosa uh those colonic epithelial cells are inflamed then you essentially have impaired uptake of butyrate so if that mucosa is inflamed it's not going to be expressing the transporters to bring butyrate from the lumen into the epithelial cell so in that case it might be beneficial to get ketones from uh you know from the blood instead at least until the gut barrier can repair