Why We Are Discussing This Now
Over the past month, our nutrition team has received more than a thousand emails from customers taking NMN or NAD+ support products. They all want to understand one practical question:
What should I eat while taking NMN or NAD+?
We believe this question deserves a real answer. That is why this article exists.
NAD+ support is not shaped by capsules alone. Diet, metabolism, inflammation, and age-related enzyme activity all influence the final outcome. Here, we are not talking about adding more supplements. Instead, we are looking at one common food through the lens of public research on NMN, NAD+, CD38, apigenin, food sources, and enzyme-driven NAD+ loss.
If you are taking NMN or NAD+ support products, you need to think beyond intake alone. NAD+ levels are also affected by how actively the body uses and breaks down NAD+. At that point, CD38 is no longer a side detail.
The Missing Half of the NAD+ Story
For many people, the NAD+ conversation begins and ends with NMN.
Take NMN, raise NAD+, support energy, support healthy aging. By now, this version of the story is everywhere: supplement pages, podcasts, newsletters, longevity articles, and short social media clips.
There is real science behind this simplified version. Human studies show that oral NMN and NR can increase circulating NAD+ levels. Newer research also suggests that the gut microbiome and the Preiss–Handler pathway are part of how oral NAD+ precursors may work inside the body.[1]
But what receives far less attention is what happens after the body produces NAD+.
NAD+ is not a storage tank. The body constantly makes it, uses it, recycles it, and breaks it down. It participates in signaling, repair, immune activity, inflammatory response, stress adaptation, and mitochondrial work. In that sense, NAD+ behaves more like a circulating metabolic currency than a backup fuel tank.
That changes how we should ask the question.
We need to ask: What affects NAD+ turnover? CD38 matters because it sits directly in the second half of that story.
What Exactly Is the “NMN Trap”?
The NMN trap is a common mental habit: treating every NAD+ issue as simply a problem of insufficient NAD+ reserves.
At first, that sounds reasonable. If NAD+ is low, give the body more precursor. That is not wrong.
But when we widen the lens and include “NAD+ turnover” as a dynamic process, the core question changes. Inside the body’s internal balance, production and consumption happen at the same time.
In the metabolic map of NAD+, CD38 plays an extremely active role as a breakdown enzyme. If we do not examine these consumption-side factors and only keep adding more input, we often fail to reach the root of the problem.
NAD+ Degradation: The Leak in the Bucket
Think of NAD+ as water in a bucket.
NMN helps pour water in. CD38 is like a leak on the side of the bucket.
This is a simple model, maybe even too simple, but it is still useful. In real life, that “leak” is often connected to demand, inflammation, immune activation, and NAD+-consuming enzymes.
A 2025 review published in npj Metabolic Health and Disease described NAD+ metabolism through this broader framework. NAD+ can be restored through precursor pathways, but it can also be preserved by targeting major NAD+-consuming enzymes, including CD38, PARPs, SARM1, and related degradation systems.[2]
In a younger, more resilient, metabolically flexible body, NAD+ production and NAD+ consumption may stay relatively balanced. With age, stress, inflammation, and metabolic burden, that balance can shift.
That is why CD38 should not be ignored.
CD38: The Enzyme That Breaks Down NAD+
CD38 is a multifunctional enzyme found on many immune cells and other cell types. It is involved in immune signaling, calcium signaling, inflammatory response, and cellular communication.
In the NAD+ conversation, the reason CD38 matters is very direct:
It consumes NAD+.
CD38 has NADase activity, which means it breaks down NAD+.
CD38 should not simply be called a “bad thing.” It has legitimate immune and signaling functions. The real issue is more specific: in aging and chronic immune activation, higher CD38 activity can make it harder to maintain healthy NAD+ levels.
That is the practical reason CD38 appears in this discussion.
Why CD38 Belongs in the Aging Conversation
CD38 connects NAD+ decline with aging, immune activation, and inflammation.
Aging often comes with more inflammatory signaling, more immune noise, and more metabolic pressure.
In many aging models, CD38 activity is associated with age-related NAD+ decline. An important study published in Cell Metabolism used the CD38 inhibitor 78c and found that blocking CD38 reversed age-related tissue NAD+ decline and improved several metabolic and physical function markers in mouse models of natural and accelerated aging.[3]
This is one reason the NAD+ field has moved beyond the old, simple precursor story. Raising NAD+ is still very important, but researchers are also asking a more basic question: Why is NAD+ falling in the first place?
Why NMN Alone Is an Incomplete Strategy
NMN is a precursor. Its role is to provide raw material for NAD+ metabolism.
That is also why NMN became popular in longevity circles. It is direct, easy to explain, and easy for the market to communicate.
The blind spot appears when precursor intake is treated as the complete strategy.
If degradation is high, more precursor can help, but the final result depends on the broader metabolic environment. This is also where NMN alone can easily be overestimated.
One Modern Signal: NMN Plus CD38 Control
One of the more interesting recent papers in this field came from Nature Cancer in 2025.
The study examined aging, NAD+ decline, mitochondrial dysfunction, CD38 expression, and CAR-T cell performance. Its core mechanism is not limited to the CAR-T setting: aged T cells showed NAD+ decline and mitochondrial damage, while CD38 was linked to that NAD+ loss.
In the study, combining NMN with the CD38 inhibitor 78c restored NAD+ levels in aged CAR-T cells and improved mitochondrial and functional performance.[4]
Most people are not thinking about CAR-T therapy when buying an NAD+ product. That is obvious. But the mechanism is still worth paying attention to.
This again shows that CD38 cannot be completely bypassed.
CD38 Inhibitors: A Direction NAD+ Science Is Studying
CD38 inhibitors are becoming part of serious NAD+ research because they target one part of the enzyme activity behind NAD+ decline.
The CD38 inhibitor 78c is one of the better-known examples. In aged mouse models, 78c has been shown to raise NAD+ and improve physical and metabolic function.
Another study published in Aging Cell showed that CD38 inhibition with 78c increased median lifespan by about 10% in naturally aged mice and improved exercise performance, endurance, and metabolic function.[5]
This area is still research-focused. It is not a casual supplement recommendation. But that is also why it deserves attention.
Apigenin for NAD+: The Natural CD38 Angle
This is where apigenin becomes interesting.
Apigenin is a natural flavonoid found in foods and botanicals such as parsley, celery, and chamomile. In the NAD+ conversation, it matters because it has been studied as a natural CD38 inhibitor.
A landmark paper published in Diabetes reported that apigenin inhibited CD38 NADase activity, increased intracellular NAD+ levels, and influenced protein acetylation and metabolic markers in experimental models.[6]
That puts apigenin in a different category from NMN.
NMN is a precursor. Apigenin is better understood through its relationship with CD38 activity. This distinction is easy to miss. The market often talks about NAD+ support as if there were only one lane. The science is more layered than that.
Parsley Deserves More Attention Than Celery
When people hear “apigenin,” they often think of celery.
Celery does contain apigenin. But parsley contains much more.
The USDA Selected Foods Flavonoid Content Database, Release 3.3 lists fresh parsley with an average apigenin content of 215.46 mg per 100 g edible portion. The same database lists dried parsley at 4503.50 mg per 100 g edible portion.[7]
That helps explain why parsley and chamomile often appear ahead of ordinary celery in discussions about apigenin food sources.
For someone already taking NMN or NAD+ support products, this matters because parsley offers a simple food-based way to connect diet with the CD38 side of the NAD+ conversation.
Its value mainly comes from the apigenin side.
Why “More NMN” Is Not Always the Smarter Move
When a supplement does not perform as expected, the market usually gives a simple answer: take more.
Higher dose. More capsules. Newer form. More aggressive protocol.
But NAD+ biology is not always linear. Increasing the dose is not always the answer.
That is the simplest form of the NMN trap: assuming the only problem is intake.
A Better NAD+ Framework
A stronger NAD+ framework has four parts.
1. Provide NAD+ Precursors
This is where NMN belongs.
2. Pay Attention to CD38
This is one part of the NAD+ loss side that should not be ignored.
3. Support Mitochondrial Demand
NAD+ is closely tied to mitochondrial function. If mitochondria are under stress, demand rises. If demand rises while degradation also rises, NAD+ comes under more pressure.
4. Lower the Inflammatory Drain
Immune noise and chronic inflammatory signaling can increase NAD+ turnover. CD38 connects part of the inflammatory environment with NAD+ loss. This is more useful than simply taking NMN and hoping the rest of the system cooperates.
So, What Should You Eat With NMN or NAD+?
Start with the basics: build a diet that does not work against your NAD+ strategy.
That means fewer empty calories, fewer inflammatory eating patterns, better protein quality, better micronutrient density, and more polyphenol-rich plant foods.
If the question is specifically about apigenin for NAD+, fresh parsley deserves a real place on the plate.
We do not need to pretend that eating 100 g of parsley every day is normal. That is not the point. The point is that, in this discussion, parsley is not just decoration.
You can add it to salads, blend it into green sauces, use it in soups, fold it into eggs, or add it to tabbouleh-style dishes. When the recipe makes sense, dried parsley can also be used.
If NMN is part of your NAD+ routine, parsley is one of the simplest food-based ways to bring apigenin into the diet.
FAQ
Can NMN Increase NAD+?
Yes, it can.
Why Do People Talk About CD38 in the NAD+ Field?
Because it can consume NAD+.
Is NMN Alone Enough to Support NAD+?
Sometimes, yes. But if NAD+ is being overconsumed, you need to look at what is driving that consumption.
What Causes NAD+ Degradation?
NAD+ can be consumed by several enzyme systems, including CD38, PARPs, and SARM1.
What Are CD38 Inhibitors?
CD38 inhibitors are compounds used to reduce CD38 activity.
Why Is Apigenin Mentioned in an NAD+ Article?
Apigenin is mentioned because its relationship with CD38 activity has been studied. It is considered to have the potential to reduce CD38 activity.
What Food Is High in Apigenin?
Parsley is one of the higher-concentration common food sources listed in the USDA flavonoid database.
Fresh parsley is listed with an average apigenin content of 215.46 mg per 100 g edible portion.[7]
Final Word: Stop Thinking Only About NMN
NMN itself is not the problem. The problem is stopping the discussion there.
NAD+ support is more complicated than simply adding more precursor. CD38 is one NAD+-consuming enzyme inside the larger aging, immune, and inflammation network. When this part of the system is ignored, the NAD+ conversation becomes too narrow.
If you are already taking NMN or NAD+ support products, adding parsley to your plate is a good strategy.
Editorial Note
This article is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. People who are pregnant, nursing, taking medication, or managing a medical condition should consult a qualified healthcare professional before changing their supplement routine.
References
- Christen S. et al. The differential impact of three different NAD+ boosters on circulatory NAD and microbial metabolism in humans. Nature Metabolism. 2026.
- Yusri K. et al. The role of NAD+ metabolism and its modulation of mitochondria in aging and disease. npj Metabolic Health and Disease. 2025.
- Tarragó M. G. et al. A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline. Cell Metabolism. 2018.
- Hope H. C. et al. Age-associated nicotinamide adenine dinucleotide decline drives CAR-T cell failure. Nature Cancer. 2025.
- Peclat T. R. et al. CD38 inhibitor 78c increases mice lifespan and healthspan in a model of chronological aging. Aging Cell. 2022.
- Escande C. et al. Flavonoid apigenin is an inhibitor of the NAD+ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes. 2013.
- Haytowitz D. B., Wu X., Bhagwat S. USDA Database for the Flavonoid Content of Selected Foods, Release 3.3. U.S. Department of Agriculture, Agricultural Research Service. 2018.
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