Peter Attia· MD
when you do that you still see a very dramatic difference in things like fatty liver and insulin resistance
The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
when you do that you still see a very dramatic difference in things like fatty liver and insulin resistance
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
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.
if we knock out fructokinase just in the liver we can protect animals from obesity and diabetes and high blood pressure
these animals do not uh develop insulin resistance they do not develop fatty liver they do not you know they're really protected from the metabolic syndrome and they and they gain much less weight and have less fat than a normal animal
what happens is these animals do not uh develop insulin resistance they do not develop fatty liver they do not you know they're really protected from the metabolic syndrome and they and they gain much less weight and have less fat than
but um but most of the fructose you know it gets ends up getting metabolized in the liver and the liver seems to be the primary place that drives the metabolic syndrome and obesity and diabetes and if we knock out fructokinase just in the liver we can protect animals from obesity and diabetes and high blood pressure
uh i have a small company we're trying to develop fructokinase inhibitors uh for the treatment of metabolic syndrome and uh and other uh conditions associated with fructose but there are also several large pharma that are actively uh working on making fructokinase inhibitors and eli lilly for example is one that's actively trying to make fructokinase inhibitors
what happens is it continues to keep its ciao low so even though it's eating drinking a lot of glucose the the chow stays low so that the overall energy intake is only very
the amount a mouse that just gets glucose alone really gains weight a mouse that gets glucose in which they cannot metabolize fructose it's dramatically less but it's still a little bit more than normal