A short, evidence-grounded conversation about CD38 and its place in longevity science.
Speaker 1
...and this is key, because CD38 is a major NAD⁺-consuming enzyme. As we age, its activity rises, effectively draining our NAD⁺ reserves.
Speaker 2
Right. So, the theory is, if you can inhibit CD38, you could slow that NAD⁺ breakdown and help preserve those vital levels. And this is where apigenin comes into the conversation.
Speaker 1
Exactly. Pre-clinical work, like the study in Nature Metabolism from 2020, showed apigenin can indeed inhibit CD38. It’s a promising mechanism.
Speaker 2
Promising, yes, but that’s often the point where the hype can outpace the human evidence. What do the actual clinical trials in humans show about apigenin's effect on NAD⁺ or even longevity markers?
Speaker 1
That's a crucial distinction. While the mechanism in a petri dish or in animal models suggests a pathway, direct human evidence for apigenin raising NAD⁺ levels or translating into human longevity benefits is still largely unproven. We simply don't have large-scale, placebo-controlled human trials demonstrating that yet.
Speaker 2
So, for all the excitement around apigenin’s ability to inhibit CD38, we still don’t know if that translates into a measurable, beneficial increase in NAD⁺ in people, or if it impacts health in the way we hope.
Speaker 1
Precisely. The in vitro and animal data are compelling for the mechanism, but the human evidence for clinical outcomes, or even just NAD⁺ levels, remains to be established. It’s an active area of research, but for now, it's more about potential than proven results in humans.
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.