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One possibly obvious one: Fasting in mice turns on SIRT3 which requires NAD+ and this newly discovered gene SLC25A51 is involved in transporting NAD+ to SIRT3.

One possibly obvious one: Fasting in mice turns on SIRT3 which requires NAD+ and this newly discovered gene SLC25A51 is involved in transporting NAD+ to SIRT3. There's plenty of data that shows mice can live 30% longer when calorie-restricted due to sirtuins being activated.. Anyone who's ever listed to Dr. David Sinclair speak about longevity, he almost always talks about how NAD+ is possibly the most important chemical in the human body, since we'd be "dead in 30 seconds" without it. Sirtuins are the longevity genes that are activated when organisms are under duress, which can be simulated by fasting. Your body doesn't know when you're going to eat again, so the sirtuins get activated. I wouldn't be surprised if researchers and labs are looking for ways to activate SLC25A51 chemically to get the NAD+ flowing to SIRT3 without requiring fasting. You can listen to David Sinclair and Rhonda Patrick get into the details of how all of this works: https://www.foundmyfitness.com/episodes/david-sinclair https://www.foundmyfitness.com/episodes/david-sinclair

ChrstnBonanno 4y ago
Polymorphisms in SLC25A51 might be linked to chronic fatigue or other mitochondria disorders. So that is pretty important. Sinclair, IMHO, is all protein and zero enzyme and that is his problem. Without enough zinc NMNAT will not function and will slow the SIRT cycle. And increasing SIRT activity by shoving NAD in the cell with out zinc will end up depleting zinc.
TedDoesntTalk 4y ago
Rhonda Patrick is amazing. Been a subscriber to her posts podcast for 3 years. But she has tons of free content on YouTube and elsewhere. It was disappointing to hear David Sinclair makes his own resveratrol… can’t get it
deleted 4y ago
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rsync 4y ago
"I wouldn't be surprised if researchers and labs are looking for ways to activate SLC25A51 chemically to get the NAD+ flowing to SIRT3 without requiring fasting." To what end ? Fasting would be cheaper, easier and less time-consuming and would include all of the related, broad-spectrum effects that we also believe fasting may produce. I guess if you're a pharma investor or existing, entrenched player it makes sense to go that direction. As a consumer, however, I wonder why (pills that might convey a subset of the benefits of fasting) would be interesting in any way.
- TedDoesntTalk 4y ago
  > As a consumer, however, I wonder why Because fasting is hard?

ChrstnBonanno 4y ago

Polymorphisms in SLC25A51 might be linked to chronic fatigue or other mitochondria disorders. So that is pretty important. Sinclair, IMHO, is all protein and zero enzyme and that is his problem. Without enough zinc NMNAT will not function and will slow the SIRT cycle. And increasing SIRT activity by shoving NAD in the cell with out zinc will end up depleting zinc.

TedDoesntTalk 4y ago

Rhonda Patrick is amazing. Been a subscriber to her posts podcast for 3 years. But she has tons of free content on YouTube and elsewhere. It was disappointing to hear David Sinclair makes his own resveratrol… can’t get it

deleted 4y ago

[deleted]

rsync 4y ago

"I wouldn't be surprised if researchers and labs are looking for ways to activate SLC25A51 chemically to get the NAD+ flowing to SIRT3 without requiring fasting." To what end ? Fasting would be cheaper, easier and less time-consuming and would include all of the related, broad-spectrum effects that we also believe fasting may produce. I guess if you're a pharma investor or existing, entrenched player it makes sense to go that direction. As a consumer, however, I wonder why (pills that might convey a subset of the benefits of fasting) would be interesting in any way.

TedDoesntTalk 4y ago
> As a consumer, however, I wonder why Because fasting is hard?