David Sinclair Backs NAD Boosting Plus CD38 Inhibition as a Longevity Stack
Sinclair highlights apigenin's role in blocking CD38, the enzyme that degrades NAD+, calling the combined strategy a logical anti-aging approach.
Summary
Harvard aging researcher David Sinclair shared a tweet endorsing a two-pronged NAD+ strategy: boosting NAD+ levels while simultaneously blocking CD38, the enzyme responsible for much of its degradation. He credits Nathan Price, a graduate student in his lab, with discovering that apigenin — a natural flavonoid found in parsley, chamomile, and celery — inhibits CD38. Sinclair notes he has personally followed this approach ever since that discovery. NAD+ is a critical coenzyme involved in energy metabolism, DNA repair, and sirtuins activation, all of which decline with age. CD38 is one of the primary consumers of NAD+ in aging tissues, so inhibiting it may help preserve NAD+ levels more effectively than supplementation alone. This tweet reflects a growing consensus in longevity circles that combining NMN or NR with a CD38 inhibitor like apigenin may be more effective than either approach alone.
Detailed Summary
NAD+ has become one of the most discussed molecules in longevity science, and for good reason. This coenzyme is essential for mitochondrial energy production, DNA damage repair, and the activation of sirtuins — a family of proteins closely linked to healthy aging. The problem is that NAD+ levels decline significantly with age, and simply supplementing with precursors like NMN or NR may not be enough if the molecule is being rapidly degraded.
David Sinclair, a prominent aging researcher at Harvard Medical School, highlighted this issue in a recent tweet, pointing to CD38 as a key culprit. CD38 is an enzyme that increases in activity as we age and is responsible for consuming large amounts of NAD+. Blocking CD38 while simultaneously boosting NAD+ production represents a logical two-pronged strategy to maintain youthful NAD+ levels.
Sinclair credits Nathan Price, a graduate student in his lab, with the discovery that apigenin — a naturally occurring flavonoid abundant in parsley, chamomile tea, and celery — acts as a CD38 inhibitor. This finding opened the door to using a widely available, low-cost plant compound to preserve NAD+ from enzymatic degradation.
Sinclair states he has personally adopted this combined approach ever since the discovery, lending it a degree of real-world credibility from someone deeply embedded in the science. The tweet links to what appears to be supporting research, reinforcing the mechanistic rationale.
The practical implication is that individuals already taking NMN or NR supplements may benefit from adding apigenin to their regimen. However, most supporting evidence remains preclinical, and human clinical trials specifically testing this combination are limited. Clinicians should note that apigenin also has mild estrogenic activity and drug interaction potential, warranting caution in certain populations.
Key Findings
- CD38 is a major NAD+-degrading enzyme that increases with age, undermining supplementation efforts.
- Apigenin, a flavonoid in parsley and chamomile, was discovered in Sinclair's lab to inhibit CD38.
- Combining NAD+ precursors with CD38 inhibition may preserve NAD+ more effectively than either alone.
- Sinclair reports personally using this dual strategy, adding real-world context to the approach.
- Apigenin is widely available as a supplement and in common foods, making this strategy accessible.
Methodology
This content is a tweet from David Sinclair referencing unpublished or previously published lab findings by graduate student Nathan Price. No formal study design, sample size, or peer-reviewed methodology is described in the tweet itself. The linked URL may point to supporting research, but its content was not available for review.
Study Limitations
This summary is based on a tweet and its brief text only — no full study, data, or peer-reviewed paper was available for review. The claim about apigenin inhibiting CD38 is supported by prior published research, but the specific findings referenced in the linked URL could not be verified. Sinclair's personal use of this strategy is anecdotal and should not be interpreted as a clinical recommendation.
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