A short, evidence-grounded conversation about CD38 and its place in longevity science.
Speaker 1
...and this is really interesting when we talk about NAD⁺. We know NAD⁺ levels decline with age, and that's linked to a host of age-related issues. But why do they decline?
Speaker 2
Exactly. One major player in that decline seems to be an enzyme called CD38. Research, like a study in Nature Metabolism in 2020, indicates that CD38 activity rises significantly as we get older.
Speaker 1
And what does CD38 do? It’s a huge consumer of NAD⁺. So, as CD38 activity ramps up, it’s essentially draining the NAD⁺ pool faster than the body can replenish it. It's like having a leak in your bucket that gets bigger over time.
Speaker 2
Right. Now, there’s a lot of buzz around compounds that might inhibit CD38. Apigenin, for example, is one that’s been identified. The idea is that by slowing CD38’s breakdown of NAD⁺, you could help preserve those crucial NAD⁺ levels.
Speaker 1
That’s the theory, and it's compelling. But what’s still genuinely unknown? While we see this relationship in cells and animal models, the direct, long-term impact of CD38 inhibition on human longevity and healthspan, using something like apigenin, is still being actively researched.
Speaker 2
Yes, exactly. We know apigenin inhibits CD38, and CD38 consumes NAD⁺. But definitively proving that apigenin directly translates to improved human healthy aging outcomes by this specific mechanism, in large-scale human trials, is still an open question. We're connecting the dots, but some of those dots are bigger than others.
Educational research discussion only — not medical advice. Statements have not been
evaluated by the FDA. Nothing here is intended to diagnose, treat, cure or prevent any disease.
Talk to a qualified clinician before changing any treatment.