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Does NAD⁺ really decline because we get older-and does raising it actually slow aging?

NAD⁺ has become one of the hottest topics in anti-aging and longevity.

You may have heard that NAD⁺ levels naturally fall as we get older. From there, the story often goes something like this:

NAD⁺ declines with age → low NAD⁺ contributes to aging → raise NAD⁺ → slow aging.

That sounds logical.

It has also helped create a growing market for nicotinamide mononucleotide (NMN), nicotinamide riboside (NR), NAD⁺ products, and other supplements designed to increase NAD⁺.

But before we accept that entire story, there is a basic question we should ask:

What does the human research actually show?

NAD⁺ is absolutely important. It is naturally produced in the human body and is found in virtually every living cell. Our cells have systems for making NAD⁺, using it, and then reusing some of its parts to make NAD⁺ again. Scientists sometimes refer to this as recycling NAD⁺.

In other words, your body doesn’t always have to start from scratch every time it needs more NAD⁺.

Certain supplements can also increase NAD⁺ measurements in humans.

But none of those facts, by themselves, prove that NAD⁺ inevitably declines simply because we get older. And they certainly don’t prove that raising NAD⁺ will slow human aging or help us live longer.

In fact, some of the newest research is making the NAD⁺ story much more interesting.

NAD⁺ Is Already Part of Your Biology

NAD⁺ stands for nicotinamide adenine dinucleotide.

The name sounds complicated, but the basic idea doesn’t have to be.

NAD⁺ is an essential molecule found in virtually every living cell in the human body. Our cells need it to carry out many of the basic jobs that keep us alive.

One of NAD⁺’s most important roles involves energy metabolism. It helps cells take energy from the foods we eat and use that energy to perform their jobs.

NAD⁺ is also involved in hundreds of chemical reactions and plays roles in DNA repair, cellular signaling, mitochondrial function, and how our cells respond to stress.[1]

So, let’s establish something important from the beginning:

NAD⁺ is not hype. NAD⁺ is essential to human biology.

The questions begin when we move from understanding NAD⁺ biology to making claims about anti-aging.

Your Body Naturally Makes NAD⁺

Your body does not simply wait for you to take an NAD⁺ supplement.

Your cells already have ways to make NAD⁺.

Some of the raw materials they use come from the foods we eat.

One important nutrient is vitamin B3.

Niacin and nicotinamide are forms of vitamin B3 that the body can use as building blocks for NAD⁺.[1,2]

Another important nutrient is tryptophan.

Tryptophan is an essential amino acid. “Essential” means your body cannot make enough of it on its own, so you need to get it from food.

Tryptophan is found in many protein-containing foods, including poultry, fish, meat, eggs, dairy products, soy, nuts, and seeds.

Through a series of steps, the body can use tryptophan to eventually produce NAD⁺. Scientists call this the de novo pathway.

You don’t need to remember that name.

The important point is simple:

Food provides some of the building blocks your body can use to make NAD⁺.

Your Body Can Reuse Parts of NAD⁺

Now let’s explain what scientists mean when they talk about recycling NAD⁺.

Your cells make NAD⁺ and use it.

When NAD⁺ is used by certain enzymes, parts of the molecule can be recovered instead of simply being thrown away.

One of those parts is nicotinamide, a form of vitamin B3.

Your cells can take that nicotinamide and use it as a building block to make NAD⁺ again.

This recycling system is called the salvage pathway.

Again, don’t worry about memorizing the scientific name.

Think of it this way:

MAKE NAD⁺ → USE NAD⁺ → RECOVER PARTS → MAKE NAD⁺ AGAIN

Your body has an ongoing system for producing, using, and rebuilding NAD⁺.

That is an important part of the NAD⁺ story that can get lost when the conversation focuses only on taking something to “boost” NAD⁺.

There Isn’t Just One NAD⁺ Level

There is another important piece of the puzzle.

When someone says:

“Your NAD⁺ level is low,”

what exactly do they mean?

NAD⁺ is not stored in one big tank somewhere inside your body.

Different tissues have their own NAD⁺ biology.

Your blood is different from your skeletal muscle.

Your skeletal muscle is different from your liver.

Your liver is different from your brain.

Even within many cells, NAD⁺ exists in different areas, including the cytosol, nucleus, and mitochondria. These different NAD⁺ pools can be controlled differently.[1]

That means measuring NAD⁺ in one place does not necessarily tell us exactly what is happening everywhere else in the body.

This becomes very important when we start talking about aging.

Does NAD⁺ Really Decline Because We Get Older?

You’ve probably heard this statement:

“NAD⁺ declines as we age.”

It is repeated so often that it can sound like settled human science.

But we need to be careful.

A major 2025 review published in Nature Metabolism examined the human evidence surrounding NAD⁺ and aging. The researchers reported that consistent evidence of an age-related NAD⁺ decline in humans had been demonstrated in only a limited number of studies. They also pointed out that data from different human tissues remain limited.[1]

This does not mean researchers have proven that NAD⁺ doesn’t decline with age.

They haven’t.

There is evidence of lower NAD⁺ in certain human tissues and populations.

But that is different from saying:

Every human inevitably loses NAD⁺ simply by getting older.

Current human evidence does not allow us to make that statement with the certainty with which it is sometimes presented.

Much of the Early NAD⁺ Aging Story Came from Animals

So where did this idea come from?

Much of the early excitement surrounding NAD⁺ and aging came from laboratory and animal research.

One influential study was published in Cell in 2013.

Researchers studying aging mice reported lower NAD⁺ and changes involving communication between the cell nucleus and mitochondria. When researchers increased NAD⁺ in older mice, aspects of mitochondrial function improved.[3]

This was important research.

It helped scientists develop new ideas about NAD⁺ and aging.

But there is an important distinction:

The subjects were mice—not humans.

Animal research is extremely valuable.

Scientists can use mice, worms, and other laboratory models to discover biological mechanisms and develop ideas that can later be tested in people.

But finding something in a mouse does not automatically prove that the same thing happens in the same way in humans.

A scientific idea that begins with mice should eventually face the most important test:

Does it hold up in people?

Even the Mouse Story Became More Complicated

Later research made the story even more interesting.

In 2021, scientists used a method called isotope tracing to examine NAD⁺ metabolism in aging mice.[4]

Think of isotope tracing as giving researchers a way to follow where molecules come from and where they go.

The older mice had lower NAD⁺ concentrations in many tissues. Across tissues, the median decrease was about 30%.[4]

At first, that seems to support the familiar story:

Older animal → less NAD⁺.

But then the researchers asked a different question:

Were the older animals actually making less NAD⁺?

The answer was surprising.

Whole-body NAD⁺ synthesis was not impaired in the older mice. In most tissues, the amount of new NAD⁺ being produced was maintained even though the total amount of NAD⁺ present was lower.[4]

In simple language:

The older mice could still make NAD⁺.

The researchers found evidence suggesting that increased use or consumption of NAD⁺ could help explain why the amount present was lower.

Here’s an easy way to understand this.

Imagine a bathtub filled with water.

You notice that the water level is getting lower.

Your first thought might be:

“The faucet isn’t putting out enough water.”

But what if the faucet is working normally?

What if the drain is simply letting water out faster?

The water level would still fall.

The same basic idea helps us understand why an NAD⁺ measurement doesn’t necessarily tell us how much NAD⁺ the body is producing.

Lower NAD⁺ does not automatically mean lower NAD⁺ production.

That distinction is extremely important.

New Human Research Challenges the Simple Aging Story

Now we come to some of the newest research.

In 2026, researchers published a study in Nature Metabolism that examined whole-blood NAD⁺ across seven independent human groups.[5]

The researchers used a carefully tested method for measuring NAD⁺.

What did they find?

Whole-blood NAD⁺ remained remarkably stable across age.[5]

That finding deserves attention.

But it also needs to be interpreted correctly.

It does not prove that NAD⁺ never declines anywhere in the human body.

Remember:

Blood is not skeletal muscle.

Skeletal muscle is not the brain.

The brain is not the liver.

Different tissues may behave differently.

But this study does challenge the idea that an age-related decline in NAD⁺ is simple, universal, and easily measured throughout the human body.

If NAD⁺ inevitably declines with age, why was no clear decline observed in whole blood across these seven human groups?

That’s a reasonable scientific question.

Human Skeletal Muscle Tells Us Something Different

Now let’s look at actual human skeletal muscle.

This is particularly interesting because researchers can obtain a small sample of skeletal muscle through a muscle biopsy and study what is happening directly in the tissue.

A 2022 study published in Nature Aging compared younger adults with several groups of older adults.[6]

The older adults included people who were:

• exercise-trained,
• normally physically active, and
• physically impaired.

Researchers found lower NAD⁺ in older skeletal muscle overall.

So yes, there is human evidence showing age-related differences in NAD⁺ in skeletal muscle.

But here’s where the study becomes fascinating.

Exercise-trained older adults had skeletal muscle NAD⁺ levels more similar to younger adults.[6]

The physically impaired older adults had an even greater reduction in NAD⁺.

NAD⁺ abundance was also positively associated with daily steps, mitochondrial function, and skeletal muscle function.[6]

This doesn’t prove that exercise is the only factor controlling NAD⁺.

But it makes the story much more interesting than:

“You’re older, therefore your NAD⁺ is lower.”

It leads to another question.

Is It Aging—or How We Are Aging?

Think about what commonly happens as people get older.

Many people move less.

They lose skeletal muscle.

Their cardiorespiratory fitness declines.

Insulin resistance becomes more common.

Chronic diseases become more common.

Inflammation may increase.

Mitochondrial function may change.

Then researchers compare a 70-year-old with an active 25-year-old and discover biological differences.

It can be tempting to label every difference:

AGING.

But chronological age may not explain everything.

Two people can both be 70 years old and have dramatically different levels of physical activity, skeletal muscle function, cardiorespiratory fitness, metabolic health, inflammation, and disease.

That’s why the findings in exercise-trained older adults are so interesting.

They raise the possibility that some biological changes we commonly associate with getting older may also be influenced by how we are aging.

When it comes to NAD⁺, the picture may involve:

chronological age + tissue type + physical activity + fitness + metabolic health + disease + NAD⁺ production + NAD⁺ use + NAD⁺ recycling.

We still don’t know how much each factor contributes.

And that’s exactly the point.

Can NMN and NR Raise NAD⁺?

Yes.

This is where scientific accuracy works both ways.

Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) are NAD⁺ precursors.

A precursor is simply something the body can use as a starting material to make something else.

Human clinical studies show that NMN and NR can increase measures of NAD⁺.[1,7]

So, it would be inaccurate to say:

“NMN and NR don’t raise NAD⁺.”

They can.

But that answers only one question:

Can we make an NAD⁺ measurement go up?

The anti-aging question is much bigger:

What happens to the human being when NAD⁺ goes up?

Does Raising NAD⁺ Slow Human Aging?

This is where several different scientific ideas can accidentally get blended together.

Let’s separate them.

NAD⁺ is essential.

True.

Your body naturally produces NAD⁺.

True.

Your body can reuse parts of consumed NAD⁺ to make NAD⁺ again.

True.

NAD⁺ biology can change with age, health, activity, and tissue type.

True.

NMN and NR can increase NAD⁺ measurements.

True.

But none of those facts automatically proves:

Increasing NAD⁺ slows human aging.

They don’t prove:

Increasing NAD⁺ extends human healthspan.

And they don’t prove:

Increasing NAD⁺ extends human lifespan.

Those are separate scientific questions.

Each one requires evidence.

The 2025 Nature Metabolism review concluded that while results from laboratory and animal studies involving NAD⁺ precursors have often been promising, human clinical trials have shown limited effectiveness for aging-related outcomes.[1]

That doesn’t mean NAD⁺ precursors will never prove useful.

Future research may identify certain people, health conditions, doses, or situations where increasing NAD⁺ provides meaningful benefits.

But we shouldn’t turn what might happen into what has already been proven to happen.

Raising a Biomarker Is Not the Same as Improving a Person

This may be one of the most important lessons in the entire NAD⁺ discussion.

Raising a biomarker is not the same as improving a human outcome.

A biomarker is something we can measure in the body.

Blood glucose is a biomarker.

Cholesterol is a biomarker.

NAD⁺ can also be measured.

Imagine someone takes NMN or NR and their NAD⁺ measurement increases.

That tells us the supplement had a biological effect.

But if the reason for taking it is anti-aging, we need to ask much bigger questions.

Did the person become stronger?

Did their insulin sensitivity improve?

Did their physical function improve?

Did their risk of age-related disease decrease?

Did they remain independent longer?

Did their biological aging slow?

Did their healthspan increase?

Did they live longer?

Those are human outcomes.

And they are not the same thing as making an NAD⁺ measurement increase.

A 2025 systematic review and meta-analysis examined randomized controlled trials of NMN and NR in older adults.[8]

Researchers looked at skeletal muscle and physical function.

The analysis did not find significant improvements from NMN in outcomes such as skeletal muscle index, handgrip strength, gait speed, and five-time chair-stand performance.[8]

Again, that does not prove that these compounds can never provide benefits.

It tells us what the evidence has—and has not—demonstrated so far.

 

NAD⁺ Isn’t the Problem—Overstating the Evidence Is

This conversation should not be framed as:

NAD⁺ versus NAD⁺ supplements.

NAD⁺ is essential human biology.

NMN and NR are legitimate subjects of scientific research.

The real issue is how confidently we communicate what the research actually shows.

It is reasonable to say:

“NAD⁺ has been linked to aging biology, and researchers are studying whether changing NAD⁺ metabolism could improve human health.”

That’s accurate.

But telling a healthy older person:

“You’re older, so your NAD⁺ has declined. You need to raise it to slow aging.”

is a much stronger statement.

Before making that statement, we would need answers to several questions.

Is this person’s NAD⁺ actually low?

Where is it low?

Blood?

Skeletal muscle?

Another tissue?

Is the body making less NAD⁺?

Is it using NAD⁺ faster?

Is its ability to reuse the building blocks changing?

Is physical inactivity contributing?

Is metabolic health involved?

And most importantly:

If we raise NAD⁺, what meaningful health outcome improves?

Those questions matter.

Exercise May Be More Important Than We Realize

The exercise findings deserve special attention.

Exercise-trained older adults having skeletal muscle NAD⁺ levels more similar to younger adults does not prove that exercise is the master regulator of NAD⁺.[6]

But it gives us an important clue.

Perhaps before asking:

“What supplement can I take to raise my NAD⁺?”

we should also ask:

“What can I do to support my body’s natural NAD⁺ biology?”

Exercise deserves to be part of that conversation.

So does maintaining skeletal muscle.

So does nutrition.

So may metabolic health, mitochondrial health, inflammation, sleep, and disease prevention.

And here’s what makes exercise especially interesting.

We don’t need to speculate about whether exercise is good for healthy aging.

Decades of human research already show that regular physical activity can improve cardiorespiratory fitness, skeletal muscle function, insulin sensitivity, mobility, and many other outcomes that matter to healthspan.

So if exercise also supports healthier NAD⁺ biology, that is another reason to take physical activity seriously as we age.

What Can We Say with Confidence?

After looking at the research, several conclusions seem reasonable.

NAD⁺ is naturally produced in the human body.

NAD⁺ is found in virtually every living human cell.

NAD⁺ is essential for normal cellular metabolism.

Our cells have multiple ways to produce NAD⁺.

The body can reuse parts of consumed NAD⁺ to make NAD⁺ again.

Vitamin B3 and tryptophan can provide nutritional building blocks for NAD⁺ production.

NAD⁺ biology can differ depending on the tissue being measured.

Some human skeletal muscle research shows lower NAD⁺ with age.

Exercise-trained older adults can have skeletal muscle NAD⁺ levels more similar to younger adults.

A 2026 study across seven human groups found that whole-blood NAD⁺ remained stable across age.

NMN and NR can increase NAD⁺ measurements in humans.

But we cannot currently conclude that simply raising NAD⁺ has been proven to:

reverse human aging,

slow human aging,

extend human healthspan,

or

extend human lifespan.

That distinction is important.

Follow the Science Wherever It Goes

This is not an argument against NAD⁺ supplements.

It is an argument for scientific accuracy.

The early animal research was important. It gave scientists new hypotheses and helped launch an exciting area of aging research.

Some of those hypotheses may ultimately prove correct.

Others may change as better human research becomes available.

That’s how science is supposed to work.

But a hypothesis should not quietly become a fact simply because it gets repeated enough times.

And changing a biomarker should not automatically be called anti-aging until we demonstrate that it meaningfully changes aging.

The current evidence does not allow us to conclusively say:

“NAD⁺ never declines as humans age.”

But the human evidence also does not justify conclusively telling everyone:

“Your NAD⁺ inevitably declines simply because you’re getting older.”

The reality appears to be more complicated.

Perhaps one of the most important questions going forward isn’t:

“How do I raise my NAD⁺?”

Maybe we should first ask:

“What determines healthy NAD⁺ levels and metabolism in the first place?”

Physical activity appears to be an important part of that conversation, especially in skeletal muscle.

So may nutrition, skeletal muscle health, metabolic health, inflammation, mitochondrial function, disease status, NAD⁺ production, NAD⁺ use, and the body’s ability to reuse the parts needed to make NAD⁺ again.

And if someone chooses to take something that raises NAD⁺, there is still one question that matters most:

What meaningful human outcome are we improving by raising it?

Until science answers that question, we should be careful not to confuse an interesting biological mechanism with a proven anti-aging intervention.

That’s not being for or against NAD⁺ supplementation.

That’s following the evidence.

References

1. 1. Vinten, K. T., Trętowicz, M. M., Coskun, E., van Weeghel, M., Cantó, C., Zapata-Pérez, R., Janssens, G. E., & Houtkooper, R. H. (2025). NAD⁺ precursor supplementation in human ageing: Clinical evidence and challenges. Nature Metabolism, 7, 1974–1990. DOI: 10.1038/s42255-025-01387-7.  
   2. National Institutes of Health, Office of Dietary Supplements. (2022). Niacin: Fact sheet for health professionals.
   3. Gomes, A. P., Price, N. L., Ling, A. J. Y., et al. (2013). Declining NAD⁺ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624–1638. DOI: 10.1016/j.cell.2013.11.037.
   4. McReynolds, M. R., Chellappa, K., Chiles, E., et al. (2021). NAD⁺ flux is maintained in aged mice despite lower tissue concentrations. Cell Systems, 12(12), 1160–1172.e4. DOI: 10.1016/j.cels.2021.09.001.
   5. Trętowicz, M. M., Scantlebery, A. M. L., Schomakers, B. V., et al. (2026). Human whole-blood NAD⁺ levels do not vary with age or lifestyle interventions. Nature Metabolism, 8, 1282–1290. DOI: 10.1038/s42255-026-01537-5.
   6. Janssens, G. E., Grevendonk, L., Zapata-Pérez, R., et al. (2022). Healthy aging and muscle function are positively associated with NAD⁺ abundance in humans. Nature Aging, 2, 254–263. DOI: 10.1038/s43587-022-00174-3.
   7. Dellinger, R. W., Santos, S. R., Morris, M., et al. (2017). Repeat dose NRPT increases NAD⁺ levels in humans safely and sustainably: A randomized, double-blind, placebo-controlled study. npj Aging and Mechanisms of Disease, 3, 17. DOI: 10.1038/s41514-017-0016-9.
   8. Prokopidis, K., Moriarty, F., Bahat, G., et al. (2025). The effect of nicotinamide mononucleotide and riboside on skeletal muscle mass and function: A systematic review and meta-analysis. Journal of Cachexia, Sarcopenia and Muscle, 16(3), e13799. DOI: 10.1002/jcsm.13799.

__________
Robert Ferguson is a California- and Florida-based single father of two daughters, clinical nutritionist, Omega Balancing Coach™, researcher, best-selling author, speaker, podcast and television host, health advisor, NAACP Image Award Nominee, creator of the Diet Free Life methodology, and Chief Nutrition Officer for iCoura Health. He also serves on the Presidential Task Force on Obesity for the National Medical Association and the Health and Product Advisory Board for Zinzino, Inc.

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