David Sinclair· PhD
This led us in 2001-2003 to show in Nature that an NAD biosynthesis gene called PNC1 (Nampt in humans) controls yeast lifespan in response to cell adversity, consistent with the hormesis hypothesis of aging
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.
This led us in 2001-2003 to show in Nature that an NAD biosynthesis gene called PNC1 (Nampt in humans) controls yeast lifespan in response to cell adversity, consistent with the hormesis hypothesis of aging
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.
in yeast what it does is this gene is turned on by too much heat not enough food not enough sugar pretty much anything that doesn't kill a yeast cell will make it live longer but you need this PN C 1 gene what PN C one does in yeast and the equivalent in humans is recycle nad
we could over express give more copies of a gene that made nad and this is called an MPT which is the equivalent of the PNC one gene in yeast which we found was important for lifespan in those organisms so we were over expressing least amputee cells had more ne D hit them with the toxin they'd survive better than regular cells