NAD+ Levels by Age: What Human Studies Actually Show

Do NAD+ levels decline with age? The short answer

NAD+ levels by age: what the human evidence actually shows

The clearest way to read this field is to stop treating every NAD result as the same measurement. Blood is not muscle. Plasma is not brain. NAD+ is not the same endpoint as total NAD or NAD(H).

What are normal NAD+ levels by age?

There is no validated clinical NAD+ range that tells a healthy adult what their level should be at 30, 40, 50 or 60.

Researchers can measure NAD+. The hard part is comparing the numbers.

Whole blood is not plasma. Plasma is not muscle. Brain studies use different tools from blood studies. Some papers measure NAD+. Others measure NADH, total NAD, combined NAD(H), or a ratio between them.

A large meta-analysis of NAD measurement studies shows how wide the gap can be. The authors screened 4,890 records and used 205 studies in their quantitative analysis across mammalian tissues; about 30% of the included studies were human. They found substantial variation across studies, including within the same measurement method, which limits direct numerical comparisons between experiments.^[18]

That is why a clean table such as “20 years old = 100%, 40 = 50%, 60 = 20%” gives a level of certainty the research does not have.

Whole blood is where the old NAD+ age story gets harder to defend

Blood is easy to collect, so it is often used as a stand-in for what is happening across the body. The human evidence does not support that shortcut.

The 2026 multi-cohort study found no clear age decline

Trętowicz and colleagues built a whole-blood NAD+ test using UHPLC-HRMS with a stable-isotope internal standard. They then applied it across seven independent human cohorts totaling more than 300 people.^[2]

For the cleanest age comparison, they tested 20 adults under 30 and 20 adults over 60. Whole-blood NAD+ did not differ significantly between the groups.^[2]

A second cohort included 26 people aged 28 to 73. Again, there was no age association. The researchers also measured 70 adults aged 63 to 87 from the Leiden Longevity Study, where NAD+ stayed stable across that age range.^[2]

Exercise and diet programs in frail older adults did not produce a clear whole-blood NAD+ change either.^[2]

There was a useful check built into the paper. In a separate group of 24 adults who took nicotinamide riboside, or NR, for five months, the same assay detected a large rise in whole-blood NAD+.^[2] The test could see a biological change when one occurred.

That responsiveness is not unique to NR. Separate randomized human studies using other assays have also shown clear whole-blood NAD+ increases with NMN, including at 500 mg/day and in a 2026 head-to-head comparison with NR.^[5][21]

This does not prove that age has exactly zero effect on whole-blood NAD+. The cohorts were moderate in size, most age data were cross-sectional, and they were not all general-population samples: CardioHT included adults at elevated cardiovascular risk, two intervention cohorts involved frail older adults, and the Leiden sample came from a longevity-family study. The dedicated young-versus-old comparison was 20 people per group; under the authors' variance model, a design of that size had about 80% power to detect a difference around 7 nmol/mL when one freeze-thaw cycle was included, so smaller effects could have gone undetected. What the study does show is that the large, steady decline shown in many age charts was not present in these cohorts.^[2]

A study of 151 healthy blood donors was almost flat

Breton and colleagues measured total NAD, not NAD+ alone, in 151 healthy blood donors aged 19 to 68.^[3]

Across the full group, there was no significant link between age and total blood NAD. The fitted line was:

NAD = -0.0045 × age + 23.609

The R² was about 0.0006. In this healthy donor group, age explained almost none of the variation in total blood NAD.^[3]

The sex results were less simple. Men showed a downward trend, but it did not reach statistical significance. Women did not show a decline. The male and female regression lines did differ from each other.^[3]

The same paper included 19 people aged 75 to 101 whose mean total NAD was lower than in the healthy blood donors.^[3] It is tempting to turn that into a late-life age effect. We should not.

Those 19 people were in hospital with decompensated heart failure. Many also had high blood pressure, atrial fibrillation, diabetes or other health problems. They were older and much sicker.^[3]

The comparison tells us that very old hospital patients with heart failure had lower total blood NAD than healthy blood donors. It cannot tell us how much NAD a healthy person loses simply by reaching 80 or 90.

The largest blood cohort found a small, sex-linked pattern

Yang and colleagues studied 1,518 adults and measured whole-blood NAD+.^[4] The group mean was 33.0 ± 5.5 µmol/L, and men had higher values than women on average.

The age pattern did not form a steady staircase downward. In the full sample, the 40 to 49 group was modestly lower than the group aged 29 or younger after adjustment. The 50 to 59 and 60+ groups were not significantly lower in the same overall analysis.^[4]

When the researchers split the data by sex, men aged 60 and over had a significant adjusted difference of -2.16 µmol/L compared with the youngest male group. Women did not show the same age trend.^[4]

This is evidence that age can relate to whole-blood NAD+ in part of a population. It is not evidence for one fixed percentage loss that applies to everyone.

Other blood studies found clearer age differences

Wang and colleagues used a 5 µL fingerstick assay and found lower whole-blood NAD+ in adults aged 50 to 85 than in adults aged 18 to 50, in both men and women.^[5] The study also found a sex difference before age 50.

Chaleckis and colleagues used metabolomics in just 15 young and 15 older adults. NAD+ was among the blood metabolites that were lower in the older group.^[6] It is useful evidence, but the study was small and exploratory.

Put the blood papers side by side and the fair conclusion is not “NAD+ never falls with age.” It is that whole-blood evidence is mixed, and the newest multi-cohort data do not support a large, universal age decline.

Plasma does not give us a clean age curve either

Plasma is the liquid part of blood. It contains far less NAD+ than whole blood because most blood NAD+ sits inside cells.

Schwarzmann and colleagues measured plasma NAD in 205 adults aged 18 to 83.^[7] Median total plasma NAD was 1.34 µM. There was no general age decline in total NAD or in the NAD+/NADH ratio. Women had a higher ratio than men earlier in adult life, but that sex difference became smaller with age.^[7]

Clement and colleagues found something different in a much smaller group of 29 adults aged 20 to 87.^[8] Plasma NAD+ and NADP+ fell with age, while NAAD showed a non-significant downward trend and several other NAD-related metabolites rose.

Those papers differ in sample size, endpoints and assay methods. Their values should not be merged into one plasma age curve.

The 2026 whole-blood paper adds a practical warning. With that study's assay, plasma NAD+ was about 50 to 100 times lower than whole-blood NAD+ and fell below the assay's limit for reliable quantification.^[2] That does not make all plasma research invalid. It shows why “blood NAD” is too vague a phrase for a careful comparison.

Muscle shows a clearer age signal, with a twist

Human skeletal muscle looks different from whole blood.

Janssens and colleagues compared muscle from young adults with older adults who were trained, normally active or physically impaired.^[10] NAD+ was lower in older muscle. The physically impaired group was lower again, while trained older adults had NAD+ levels closer to the young group. Across the study group, higher muscle NAD+ also went with more daily steps and better measures of muscle and mitochondrial function.^[10]

This was a cross-sectional study. It cannot tell us that exercise caused the higher NAD+ profile. People who stay highly trained into older age may differ from less active adults in many ways, and the physically impaired older group was small.

These data do not let us separate the effect of age from training, fitness, body composition or other differences between people. But they do show that older adults do not all have the same muscle NAD+ profile.

Older adults can show different muscle NAD+ profiles

Mevenkamp and colleagues compared 13 trained older adults with 15 normally active older adults using 31P-MRS.^[11]

The published NAD+/γ-ATP ratio (mean ± SEM) was 5.58 ± 0.22 in the trained group and 4.42 ± 0.17 in the normally active group (p = 0.0003).^[11] The trained group also had lower NADH and a higher NAD+/NADH ratio.

This was a cross-sectional comparison, not an exercise trial. The groups differed in more than training status, including fitness and average BMI. The study therefore cannot show that training caused the NAD+ difference.^[11]

Migliavacca and colleagues provide another comparison among older adults. Men with sarcopenia showed lower muscle NAD+ and weaker NAD+ biosynthesis than age-matched controls.^[12] Direct NAD+ measurements came from only about 4 to 6 men per group in one biopsy subset, so the quantitative estimate is based on a very small sample.

Red blood cells point in a similar direction

Pospieszna and colleagues measured NAD+ and NADP+ in red blood cells from male endurance athletes, sprinters and untrained controls across a wide adult age range.^[9]

NAD+ and NADP+ fell with age in all three groups. Across the sample, the athletic groups had higher erythrocyte NAD(P)+ concentrations than untrained controls, with the strongest profile in sprinters.^[9]

This was cross-sectional, so it cannot show that years of training caused the difference. It does support the same broad point seen in muscle: an age effect can exist alongside large differences tied to physical state.

Technical note: the published abstract and main Methods section report different counts for the endurance-runner subgroup. We do not use that disputed subgroup count here.

Brain studies are mixed, and the samples are small

Healthy brain tissue cannot be sampled like blood, so researchers have used magnetic resonance spectroscopy.

Zhu and colleagues studied 17 healthy adults with 7-T 31P-MRS of the occipital lobe.^[13] The participants were clustered into ages 21 to 26 (n=7), 33 to 36 (n=4), and 59 to 68 (n=6), rather than being evenly spread across adulthood. NAD+ fell with age. NADH rose. Total NAD fell, and the NAD+/NADH redox state shifted. The individual correlations were fairly strong inside this small sample, but 17 people cannot define a population reference curve.

Cuenoud and colleagues later studied 50 healthy adults, with a younger group averaging 27.1 years and a middle-aged group averaging 56.4 years.^[14] None of the NAD variables was significantly associated with age. NAD+ and total NAD showed negative trends (p = 0.063 and p = 0.069), while the NAD+/NADH ratio did not show a significant age association. The study did find links between NAD, ATP and energy-production measures.

The wording matters. The brain evidence is mixed: one small study found a clear age association, while the larger study found only a non-significant trend. Neither gives us a universal percentage decline for everyone.

Skin, liver and cerebrospinal fluid add clues, not a body-wide curve

Massudi and colleagues studied pelvic skin samples from 49 people spanning infancy to older adulthood.^[15] NAD+ was negatively linked with age in both men and women. The samples came from people having surgery, and two authors disclosed ties to an NAD-focused biotech company. This is useful human tissue evidence, but it is still one small study.

Human liver data are thinner. Zhou and colleagues compared non-pathological liver tissue from six middle-aged and six older surgical patients.^[16] Hepatic NAD+ was lower in the older group. Six people per group is nowhere near enough to build a normal liver NAD+ chart by age.

Guest and colleagues studied cerebrospinal fluid from 70 adults aged 24 to 91.^[17] People over 45 had lower combined NAD(H) than younger participants. The endpoint was not NAD+ alone. In an exploratory alcohol analysis, the group drinking more than one standard drink per day (n=8) had lower CSF NAD(H) than abstainers, but this association did not remain significant after stratifying by age and sex. Again, there is a signal, but not a universal age curve.

The way a sample is handled can change the NAD+ result

There is one more reason to be careful when old and new studies are put on the same chart. NAD+ can change before the sample reaches the machine.

The 2026 Trętowicz study tested this in detail.^[2] Their whole-blood assay had an intra-assay coefficient of variation of about 12.5% and an inter-assay value of about 16.1%.

Conventional freezing reduced measured NAD+. Repeated freeze-thaw cycles changed it further. Sample volume and the way blood was preserved also mattered.^[2]

In one fresh-versus-frozen experiment, the handling-related difference had a standard deviation of 3.5 nmol/mL. The team then modeled what that variation meant for a typical age study. With 20 people per group and one freeze-thaw cycle included in the variance model, a difference of roughly 7 nmol/mL was needed for 80% power.^[2]

This does not prove that older studies showing an age effect were wrong. Different papers used different protocols. It means small differences deserve care when sample handling and lab methods are not the same.

Azouaoui and colleagues reached the same broad warning from a much larger survey of mammalian NAD(P)(H) data. They found substantial variation across studies and within measurement methods, alongside wide differences in pre-analytical conditions.^[18]

Can blood NAD+ tell you your biological age?

No validated test can currently turn one blood NAD+ result into a biological age.

The evidence is too inconsistent for that. Trętowicz found little age signal across several whole-blood cohorts.^[2] Breton found almost no overall age association in healthy donors, although that study measured total NAD rather than NAD+ alone.^[3] Yang found a modest, sex-dependent pattern.^[4] Wang and Chaleckis found clearer age differences.^[5][6]

That is interesting biology. It is not a clinical age clock.

If you want to understand the tools that are actually used to estimate biological age, see How to Test Your Biological Age: The Options.

Blood also cannot be assumed to report what is happening in muscle, brain, skin or liver. The tissue studies make that clear.

For a deeper look at what a blood result can and cannot tell you, read NAD+ Blood Test: Can You Measure Your Levels?

Can NAD+ levels be raised?

Yes. At least some interventions can raise measured blood NAD+.

Nicotinamide mononucleotide (NMN) has multiple randomized human studies showing that it can raise blood NAD+. In a double-blind, placebo-controlled study in adults aged 55 to 70, 500 mg/day of NMN resulted in an average whole-blood NAD+ level of 41.7 µmol/L after 30 days, compared with 23.8 µmol/L with placebo.^[5]

A separate 12-week randomized, double-blind trial at 250 mg/day also found a significant increase in whole-blood NAD+.^[20] More recently, a 2026 randomized, open-label, placebo-controlled head-to-head study found that 14 days of NMN and NR each increased baseline whole-blood NAD+ by roughly twofold compared with placebo.^[21]

Some human trials have also reported improvements in walking-related measures (as secondary outcomes) or general-health scores during NMN supplementation.^[19][22] However, pooled physical-function evidence is mixed: one meta-analysis reported a gait-speed signal, while another found no significant effect on gait speed or several other muscle-function outcomes.^[23][24] These findings do not establish that raising blood NAD+ itself caused the functional changes. 

In the 2026 study, 24 adults took nicotinamide riboside (NR) for five months and whole-blood NAD+ rose clearly.^[2]

That answers one narrow question: blood NAD+ can move.

It does not prove that every older adult starts with an NAD+ deficiency. It also does not prove that raising a blood marker reverses aging or leads to a set health benefit. Those are separate claims and need separate evidence.

For the human evidence on NAD precursors, see NAD+ Supplements: What Actually Works?

For the separate question of what higher NAD+ may mean for health outcomes, see NAD+ Benefits: What the Science Actually Says.

What are NAD+ levels, exactly?

NAD mainly exists in two linked forms.

NAD+ is the oxidized form. It accepts electrons during many metabolic reactions.

NADH is the reduced form. It carries those electrons into other reactions tied to energy use.

Researchers may also report total NAD, NAD(H) or the NAD+/NADH ratio. Those terms should not be swapped.

Breton measured total blood NAD.^[3] Trętowicz measured NAD+ in whole blood.^[2] Guest measured combined NAD(H) in cerebrospinal fluid.^[17] Mevenkamp reported muscle NAD+ relative to γ-ATP with magnetic resonance spectroscopy.^[11]

Putting all four values into the same “NAD level” chart would create a comparison none of those studies made.

If you want the chemistry in plain English, see NAD vs NAD+ vs NADH: What’s the Difference?. For the wider primer on the coenzyme itself, see What Is NAD+? The Coenzyme Behind Cellular Energy.

If you want the wider aging framework around cellular energy and metabolism, see The 12 Hallmarks of Aging, Explained Simply.

How CELLSHE reviewed the evidence

This article is a structured review and secondary analysis of published human research. It is not a new clinical study, a registered systematic review or a pooled meta-analysis.

We focused on human studies that directly measured NAD+, total NAD, NAD(H), or a closely related NAD measure in relation to age, or that compared physical and health states within older adults.

• Whole blood was kept separate from plasma and red blood cells.
• Muscle was kept separate from brain, skin, liver and CSF.
• NAD+ was kept separate from NADH, total NAD and NAD(H).
• Healthy aging was kept separate from disease comparisons.
• Animal studies were not used to build the human age map. Reference [18] includes animal and human studies and is used only for measurement-methodology context, not as evidence for a human age decline.
• Absolute concentrations from different assays were not pooled.
• Cross-sectional age slopes were not treated as the rate at which one person's NAD+ falls over time.

When studies use different tissues, assays or units, CELLSHE does not convert them onto one shared numerical scale. Comparisons are kept within the original study and reported using the endpoint the researchers actually measured.

We also checked sample size, sex, health state, study design, sample handling and disclosed conflicts where they could change how much weight a result deserves.

You can see the wider research framework on The Science and the rules CELLSHE uses for sourcing and claim review on Our Standard.

So what really happens to NAD+ as we age?

Human NAD+ biology changes with age. What the evidence does not show is one neat, whole-body decline that can be turned into a universal chart for your 20s, 30s, 40s, 50s and 60s.

Whole blood looks much more stable than the common market story suggests, and the blood studies that do find an age effect do not agree on one fixed rate of decline.^{[2][3][4][5][6]}

Muscle shows a clearer age-related pattern, with physical function and health state tied to the result.^[10][11][12] Brain evidence is mixed: one small 7-T study found age-related changes, while a larger MRS study found only a non-significant downward trend.^[13][14] One small skin study found an inverse age association.^[15] Plasma is mixed.^[7][8] Human liver and CSF data are too thin for broad age claims.^[16][17]

None of this means NAD+ is fixed or that precursor supplementation is biologically inactive. Randomized human trials show that oral NMN can raise whole-blood NAD+, including at 500 mg/day, even though chronological age does not define a universal blood NAD+ deficiency.^[5][20][21] The more cautious question is what that biomarker change means for long-term health, where the human outcome evidence is still developing.

So if someone tells you that a healthy 50-year-old has a set percentage less NAD+ than a healthy 20-year-old, ask four things:

1. Where was NAD measured?
2. Which form of NAD was measured?
3. Who was studied?
4. Which method was used?

Until those questions have clear answers, a precise NAD+ percentage by age gives us more certainty than the human science does.

That is why CELLSHE does not use one.

For the practical side of healthy aging, our How to Age Gracefully guide looks at the habits with the strongest human evidence.

Frequently asked questions about NAD+ levels by age

At what age do NAD+ levels start to decline?

There is no proven age when NAD+ begins to fall across the whole human body. Some tissues show age-related changes. The newest whole-blood data do not show a clear starting point for a decline.^{[2][10][13][15]}

How much NAD+ do you lose by age 40?

There is no validated human percentage that applies to everyone at age 40. A fixed “percentage left” chart is not a clinical reference range and is not supported as a universal human curve.^[1][2]

How much NAD+ do you lose by age 50 or 60?

There is no single percentage for age 50 or 60 either. Human results change with tissue, sex, health state and measurement method.^[1][18]

Are NAD+ levels lower in older people?

Sometimes. Lower NAD+ or related measures have been reported in muscle, brain, skin, red blood cells, liver and CSF.^{[9][10][13][15][16][17]} Whole-blood studies are mixed.^{[2][3][4][5][6]}

What is a normal NAD+ level?

There is no validated clinical NAD+ range by decade for healthy adults in the studies reviewed here. Research values depend heavily on the sample, endpoint and method used.^[18]

Does exercise increase NAD+?

Human studies show higher NAD-related measures in some trained groups than in less active groups.^[9][10][11] Most of those comparisons are cross-sectional, so they cannot prove that exercise caused the difference.

Can NMN raise NAD+?

Yes. Multiple randomized human studies show that oral NMN can raise blood NAD+. In one double-blind, placebo-controlled study, 500 mg/day for 30 days resulted in average whole-blood NAD+ of 41.7 µmol/L versus 23.8 µmol/L with placebo.^[5] A separate 12-week trial at 250 mg/day also increased whole-blood NAD+, and a 2026 head-to-head study found a comparable NAD+-raising effect from NMN and NR after 14 days.^[20][21]

Can NR raise NAD+?

Yes. Human supplementation studies show that NR can raise blood NAD-related measures. In the 2026 Trętowicz study, whole-blood NAD+ rose after five months of NR use in 24 adults.^[2] A higher blood marker does not by itself prove an anti-aging effect.

Scientific references

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2. Trętowicz MM, et al. (2026). Human whole-blood NAD+ levels do not vary with age or lifestyle interventions. Nature Metabolism. PMID: 42135539. DOI: 10.1038/s42255-026-01537-5.
3. Breton M, Costemale-Lacoste JF, Li Z, et al. (2020). Blood NAD levels are reduced in very old patients hospitalized for heart failure. Experimental Gerontology. PMID: 32783906. DOI: 10.1016/j.exger.2020.111051.
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10. Janssens GE, Grevendonk L, Zapata Perez R, et al. (2022). Healthy aging and muscle function are positively associated with NAD+ abundance in humans. Nature Aging. PMID: 37118369. DOI: 10.1038/s43587-022-00174-3.
11. Mevenkamp J, Bruls YMH, Mancilla R, et al. (2024). Development of a 31P magnetic resonance spectroscopy technique to quantify NADH and NAD+ at 3 T. Nature Communications. PMID: 39443469. Read the full text.
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15. Massudi H, Grant R, Braidy N, Guest J, Farnsworth B, Guillemin GJ. (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLOS ONE. PMID: 22848760. Read the full text.
16. Zhou CC, Yang X, Hua X, et al. (2016). Hepatic NAD+ deficiency as a therapeutic target for non-alcoholic fatty liver disease in ageing. British Journal of Pharmacology. PMID: 27174364. Read the full text.
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19. Yi L, Maier AB, Tao R, et al. (2023). The efficacy and safety of β-nicotinamide mononucleotide (NMN) supplementation in healthy middle-aged adults: a randomized, multicenter, double-blind, placebo-controlled, parallel-group, dose-dependent clinical trial. GeroScience. PMID: 36482258. DOI: 10.1007/s11357-022-00705-1.
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22. Morifuji M, Higashi S, Ebihara S, Nagata M. (2024). Ingestion of β-nicotinamide mononucleotide increased blood NAD levels, maintained walking speed, and improved sleep quality in older adults in a double-blind randomized, placebo-controlled study. GeroScience. PMID: 38789831. DOI: 10.1007/s11357-024-01204-1.
23. Wang JP, Wang L, Wang T, et al. (2025). Effects of Nicotinamide Mononucleotide Supplementation on Muscle and Liver Functions Among the Middle-aged and Elderly: A Systematic Review and Meta-analysis of Randomized Controlled Trials. Current Pharmaceutical Biotechnology. PMID: 39185644. DOI: 10.2174/0113892010306242240808094303.
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