NAD (NAD+) Test

Your body runs on a molecule most people have never heard of. NAD+ (nicotinamide adenine dinucleotide) sits at the center of hundreds of reactions that keep your cells producing energy, fixing broken DNA, and switching genes on and off at the right time. When NAD+ levels drop, those processes slow down. Mitochondria sputter. DNA damage accumulates. The cellular machinery that keeps you resilient starts to degrade.

What makes this biomarker compelling from a longevity perspective is that NAD+ levels decline with age, and that decline is linked to many of the diseases people fear most: heart failure, type 2 diabetes, neurodegenerative disease, and age-related muscle loss. Measuring your NAD+ gives you a window into how well your cells are holding up under the cumulative stress of living.

What NAD+ Actually Does in Your Body

NAD+ wears two hats. First, it acts as a shuttle in the energy production chain, carrying electrons between reactions that convert the food you eat into the cellular energy currency called ATP. Every time your mitochondria generate energy, NAD+ is involved. Second, it serves as a raw material consumed by several families of enzymes that do essential maintenance work.

The most studied of these enzyme families are the sirtuins, a group of proteins that regulate gene expression, circadian rhythms, and cellular stress responses. Sirtuins can only function when NAD+ is available to fuel them. Another family, the PARPs, uses NAD+ to repair broken DNA strands. A third enzyme, CD38, consumes NAD+ during immune signaling. The tension between these consumers and the body's ability to produce NAD+ determines your cellular NAD+ status.

Your body makes NAD+ through two main routes. The liver produces it from scratch using the amino acid tryptophan, then exports the building blocks to other tissues. Every other tissue recycles NAD+ through what is called the salvage pathway, which depends on an enzyme called NAMPT. The heart maintains the highest NAD+ levels of any organ because of its relentless energy demands.

How NAD+ Changes with Age

NAD+ levels do not stay constant throughout life. Studies in human skin tissue show a strong inverse relationship between age and NAD+ levels, with a correlation of -0.706 in males and -0.537 in females (where -1.0 would mean a perfect inverse relationship). The decline appears to be driven by both increased consumption, as DNA damage and chronic inflammation activate NAD+-consuming enzymes, and decreased production, as salvage pathway activity slows.

Men and women experience this decline differently. Before age 50, men tend to have higher whole blood NAD+ than women. A large community study of over 1,500 adults found average whole blood NAD+ of 34.5 micromoles per liter in men versus 31.3 in women. After age 50, this sex gap narrows. In men, a significant drop becomes apparent after age 60, while women's levels remain comparatively stable across age groups.

Heart Disease and Cardiovascular Risk

The heart is particularly vulnerable to NAD+ depletion because of its enormous metabolic demands. People with moderate to severe heart failure (classified as NYHA class II to III) have significantly lower blood NAD+ than healthy controls, averaging about 13 micromoles per liter compared to 18 in controls. Very old adults hospitalized for heart failure show even lower levels, averaging 20.7 micromoles per liter compared to 23.4 in healthy blood donors of mixed ages.

NAD+ depletion contributes to cardiovascular damage through several mechanisms: impaired mitochondrial function in heart muscle cells, reduced sirtuin activity that would otherwise protect blood vessels, and increased oxidative stress from weakened antioxidant defenses. Early human data suggests that boosting NAD+ may modestly improve blood pressure and lipid profiles, though large clinical trials confirming cardiovascular outcomes are still needed.

Metabolic Disease and Diabetes

The relationship between NAD+ and metabolic disease is more complex than a simple "low is bad" story. A cross-sectional study of about 1,400 adults from the Jidong community found that people in the highest NAD+ group (above 37.8 micromoles per liter) were roughly 3 times more likely to have metabolic disease than those in the lowest group (below 29.4 micromoles per liter), with the risk beginning to climb at levels around 31.0 micromoles per liter.

This paradoxical finding may reflect the body's compensatory response: when metabolic stress increases, the salvage pathway may temporarily ramp up NAD+ production. It is also a single cross-sectional snapshot, meaning it captured who had disease at one point in time rather than tracking who developed it over years. Still, it is a reminder that interpreting NAD+ levels requires context, not just a simple "higher is better" framework.

Neurodegeneration and Brain Health

NAD+ depletion has been linked to Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions in preclinical models. People with demyelinating neurological diseases (conditions where the protective coating around nerves breaks down) show lower blood NAD+ than healthy controls, averaging about 14 micromoles per liter versus 18.

The brain's NAD+ pool is also affected by alcohol and aging independently. Cerebrospinal fluid levels of NAD+ decline in adults over 45, and people who consume more than one standard drink per day show additional reductions. These findings connect NAD+ depletion to some of the most feared aspects of aging, though the clinical field is still working out whether measuring NAD+ in blood accurately reflects what is happening in the brain.

Reference Ranges

No medical society has published standardized reference ranges for NAD+, and values vary substantially depending on the lab method, sample type, and the specific form of NAD being measured. That said, several population studies provide useful orientation. The ranges below are based on whole blood NAD+ measured by enzymatic or mass spectrometry assays.

These tiers are drawn from published research. Your lab may use different assays and cutpoints. Compare your results within the same lab over time for the most meaningful trend. Extracellular NAD+ in plasma is roughly 500 times lower than intracellular NAD+, so plasma and whole blood readings are not interchangeable.

Why One Reading Is Not Enough

NAD+ is one of the most dynamic molecules in your body. In some tissues, it turns over completely in a matter of minutes. Yet individual baseline levels appear remarkably stable over periods of at least 100 days when no intervention is introduced. This combination of rapid turnover with long-term baseline stability makes NAD+ an excellent candidate for serial tracking.

A single reading tells you where you stand today, but it cannot tell you whether your level is climbing, stable, or sliding downward. Get a baseline measurement, then retest in 3 to 6 months if you are making changes (such as starting an NAD+ precursor supplement or a new exercise program). After that, annual testing lets you monitor your trajectory. The trend line over time is far more informative than any isolated number.

Response to NAD+ precursor supplements varies enormously between individuals. One clinical trial found coefficients of variation (a measure of how much results scatter around the average) ranging from 29% to 113% across participants taking the same dose of NMN. Your personal response is something only serial testing can reveal.

When Results Can Be Misleading

The biggest source of error in NAD+ testing is not your biology but the sample handling. If blood sits too long before processing, or if cells rupture during centrifugation, intracellular NAD+ leaks into the plasma fraction and inflates the reading. Prolonged centrifugation beyond five minutes and aggressive braking can both cause this artifact. If your result seems unexpectedly high, ask whether sample handling might explain it.

Acute inflammation drives extracellular NAD+ down, as shown by a negative correlation with C-reactive protein. If you are recovering from an illness or infection, your reading may be artificially low. Similarly, an intense exercise session temporarily shifts NAD+ metabolism in immune cells and muscle, so testing within hours of a hard workout may not reflect your resting baseline. For the most reliable result, draw blood in a rested, non-fasted state at least 24 hours after vigorous exercise and away from any acute illness.

The Gap Between Animal Studies and Human Evidence

Much of the excitement around NAD+ comes from animal research, where boosting NAD+ levels has reversed aspects of aging in mice, improved cardiac function, and protected neurons. The translation to humans has been slower and less dramatic. NAD+ precursor supplements reliably raise blood NAD+ levels in people, but the physiological benefits seen in animal models have not consistently followed.

Several factors may explain this gap. The gut microbiome metabolizes some NAD+ precursors before they reach target tissues. NAD+ is compartmentalized differently inside human cells than in mouse cells. And it remains uncertain whether raising NAD+ in the blood actually replenishes it in the mitochondria and nuclei where it is most needed. These are active areas of research, not settled questions. If you are testing NAD+ and considering supplementation, go in with calibrated expectations: you are likely to see your blood number rise, but the downstream health effects are still being worked out.