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.
just as we discussed metformin can do it but how does it do it by giving another step but still inhibits one of these steps and they want to get a buildup of lactate because the metabolic precursions is going to build up and eventually peruid will build up and that results in a buildup of lactate
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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.
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and why do you see it rest 3.5 Mill for 3 m of lactate and by the way is their fat oxidation commensurately suppressed because when you when you metabolically uh test them on the cart do you see in that individual a very very low fat oxidation if if not it might suggest that that that lactate level of two or three Millo is is an artifact but doesn't really speak to what's happening in the mitochondria right
i mean i think having more circulating lactate can be you know a bit of a challenge for clearing fat right because they have some sort of competition so from that perspective i think you know being in a a lower state might have some benefits but then you know lactate is a valuable fuel as long as it's not getting to too high levels so i i'm not sure how that all plays out in terms of long-term health
with metformin uh if we give metformin and there's an increase in lactate uh in the plasma is that uh due to um production outstripping removal or is are we actually increasing the oxidation the oxidative disposal of um glucose or is the glucose H High because of increased glucogenesis we could answer all of these things with our combination of tracers
it would be interesting to see the difference in lactate production uh in those two uh individuals and it would be interesting to also see if there was a way quantify this osy production