NAD/NADH Ratio Test

Your cells run on a molecule called NAD+ (nicotinamide adenine dinucleotide). It is involved in hundreds of chemical reactions that extract energy from food, repair damaged DNA, and regulate the genes that influence how fast you age. The ratio between its active, oxidized form (NAD+) and its spent, reduced form (NADH) acts like a fuel gauge for your cellular metabolism. When the ratio tilts toward NAD+, your cells are in a state of active, efficient energy production. When it tilts toward NADH, something is slowing them down.

What makes this ratio uniquely valuable is that it sits upstream of many of the diseases people fear most. Declining NAD+ levels and a shifting ratio have been linked to heart disease, diabetes, neurodegeneration, and the aging process itself. Standard blood panels do not capture this information. By the time conventional markers like fasting glucose or cholesterol start moving, your NAD+/NADH balance may have been deteriorating for years.

What NAD+ Actually Does in Your Body

NAD+ and NADH are small molecules, not proteins or hormones, that function as electron shuttles. Every cell in your body makes them through multiple pathways, including one that starts with the amino acid tryptophan and several that recycle vitamin B3 precursors (nicotinamide, nicotinic acid, and nicotinamide riboside). The ratio between these two forms controls glycolysis (how your cells break down sugar), mitochondrial respiration (how your cells convert food into usable energy), and fatty acid oxidation (how your cells burn fat).

Beyond energy production, NAD+ is consumed as fuel by three families of signaling enzymes. Sirtuins use NAD+ to regulate gene expression and metabolic health. PARPs use it to repair broken DNA. CD38, an enzyme on the surface of immune cells, breaks it down as part of inflammatory signaling. Each of these enzymes destroys NAD+ in the process of doing its job, so demand can outstrip supply when your body is under stress, fighting inflammation, or simply getting older.

Your cells maintain separate NAD+/NADH pools in three distinct compartments: the cytosol (the main cellular fluid), the mitochondria (your cellular power plants), and the nucleus (where your DNA lives). Each compartment's ratio reflects different metabolic realities, which is one reason measuring this biomarker is more nuanced than a simple cholesterol test.

Heart Disease and Cardiovascular Risk

Abnormal NAD+/NADH ratios are linked to several cardiovascular conditions, including ischemia (restricted blood flow), heart failure, hypertension, and atherosclerosis. In diabetic cardiomyopathy, a decreased mitochondrial NAD+/NADH ratio impairs the heart's ability to generate energy and promotes oxidative stress, which damages cardiac tissue over time. A study of cardiac patients found that blood NAD+ was significantly lower in people with moderate to severe heart failure (13 micromolar) compared to healthy controls (18 micromolar).

The American Heart Association has recognized that abnormal redox status, including altered NAD+/NADH ratios, is a feature of ischemia-reperfusion injury, sepsis, and vascular disease. For someone tracking cardiovascular health, this ratio adds a layer of metabolic insight that standard lipid panels and blood pressure readings cannot provide.

Metabolic Disease and Insulin Resistance

A low NAD+/NADH ratio contributes to insulin resistance, type 2 diabetes, and obesity through several connected mechanisms. When the ratio drops, a mitochondrial enzyme complex called complex I cannot function properly, which disrupts energy production and fat burning. At the same time, a protective enzyme called sirtuin-3 loses its activity because it depends on NAD+ to work. The result is a metabolic bottleneck: too many electrons piling up with nowhere to go, generating harmful byproducts.

The Jidong Community Study, which examined whole blood NAD+ levels in 1,394 adults, found a striking dose-response relationship between NAD+ and metabolic health. Compared to people with the lowest NAD+ levels, those in the highest quarter were about 3 times as likely to already have metabolic disease (adjusted odds ratio 3.01). People with 3 to 6 metabolic risk components showed an even stronger association, with roughly 4.3 times the odds (adjusted odds ratio 4.30). This cross-sectional study measured total NAD+ rather than the ratio directly, but it reinforces the connection between NAD+ status and metabolic dysfunction.

Brain Health and Neurodegeneration

NAD+ depletion and altered ratios are implicated in Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions. When NAD+ falls short in brain cells, the consequences cascade: impaired DNA repair, weakened neuronal plasticity (the brain's ability to form new connections), and accelerated cellular senescence (a state where cells stop dividing and start secreting inflammatory signals).

Brain imaging studies using magnetic resonance spectroscopy have documented age-dependent reductions in the brain's NAD+ content and redox potential, with NADH increasing and NAD+ decreasing as people get older. This shift is not just a bystander effect of aging. It appears to actively contribute to the brain's declining ability to handle stress and maintain normal function.

The Aging Connection

NAD+ levels decline with age across multiple organs, including the brain, liver, and adipose tissue. This decline is driven by a growing imbalance: the enzymes that consume NAD+ (especially CD38 and PARPs) become more active with age, while the body's ability to synthesize new NAD+ slows down. The salvage pathway, which recycles NAD+ through an enzyme called NAMPT, becomes less efficient.

Plasma metabolomics data from adults aged 20 to 87 showed that NAD+ and NADP+ decline with age, while their reduced counterparts (NADH and NADPH) increase. This progressive redox imbalance is one of the reasons aging researchers have become so interested in NAD+ biology. In animal models, restoring NAD+ levels extends healthspan and, in some cases, lifespan. Whether those results translate to humans is one of the most actively investigated questions in longevity science.

Sex Differences in NAD+/NADH Levels

Your sex affects your baseline NAD+/NADH ratio. A study of 205 healthy German adults found that women had higher plasma NAD+/NADH ratios than men (median 1.33 versus 1.09). This difference narrowed with increasing age, particularly when assessed using biological aging markers rather than calendar age. A separate Chinese study of 1,518 adults found the opposite pattern for total NAD+ levels: men had significantly higher whole blood NAD+ (34.5 micromol/L) than women (31.3 micromol/L), with the sharpest age-related decline occurring in middle-aged men.

These conflicting findings reflect a real complexity. Total NAD+ pool size and the ratio between NAD+ and NADH are distinct measurements that can move independently. Your interpretation of results must account for your sex and age, and ideally, you should compare against sex-specific and age-matched reference values.

Reference Ranges

No medical society has established standardized clinical reference ranges for the NAD+/NADH ratio. The values below come from published research studies and should be treated as orientation points rather than firm diagnostic cutoffs. Assay methods, sample types (plasma versus whole blood versus fingerstick), and laboratory techniques vary enough that comparing results across different labs is unreliable.

These values are drawn from published research using specific assay methods. Your lab may use different techniques and report different units. The most meaningful use of these numbers is not to judge a single reading against a population average, but to establish your own baseline and track your trajectory over time within the same lab.

Why One Reading Is Not Enough

NAD+ metabolism is one of the most dynamic systems in your body. In some tissues, NAD+ has a half-life measured in minutes, and synthesis and breakdown rates vary enormously across organs. Your circadian clock directly regulates NAD+ production through the NAMPT salvage pathway, meaning levels rise and fall throughout the day. A single snapshot cannot capture this complexity.

Serial tracking matters more here than for almost any other biomarker. Get a baseline measurement, then retest in 3 to 6 months, especially if you are making changes to your exercise habits, supplementation, or alcohol intake. After that, annual monitoring gives you a trajectory. A slow downward drift in your NAD+/NADH ratio over several readings is more informative than any single number, and it is the kind of trend that might prompt you to take action years before conventional markers flag a problem.

When comparing results, always use the same lab and the same sample type. Switching between fingerstick and venous blood, or between two labs using different assays, can introduce enough variability to make the comparison meaningless.

When Results Can Be Misleading

The NAD+/NADH ratio is sensitive to several factors that can distort a single reading and lead you to the wrong conclusion. These are not things that change your true NAD+ status over time; they are things that can make one blood draw unrepresentative of your actual metabolic state.

• Recent exercise: Acute exercise substantially alters intracellular NAD+ metabolism within hours, and these changes can persist long enough to affect a blood draw the next day. Avoid intense exercise for at least 48 to 72 hours before testing.
• Fasting status: Fasting causes a reductive shift in the NAD+/NADH ratio in multiple tissues. Whether you ate or fasted before your blood draw can meaningfully change the result.
• Circadian timing: NAD+ biosynthesis follows a circadian rhythm, with distinct fluctuations tied to your sleep-wake cycle. Drawing blood at different times of day can produce different numbers from the same person.
• Sample handling: NAD+ and NADH can interconvert during blood collection and processing. If the lab does not handle the sample properly, NADH and NADPH levels can drop by up to 50% within 24 hours. This is a pre-analytical problem that is invisible to you but can significantly affect your results.

The Measurement Challenge

This biomarker is harder to measure accurately than most standard blood tests. A meta-analysis of NAD measurement methods found significant variability both between and within methods across mammalian tissues, making cross-study comparisons difficult. Current clinical assays cannot reliably distinguish between protein-bound and free NAD/NADH, and the free form is the one that matters most for understanding your metabolic state.

Interindividual variability in response to NAD+ supplementation is also high. One study of nicotinamide mononucleotide supplementation reported coefficients of variation ranging from 29.2% to 113.3% across participants, meaning the same dose can produce wildly different blood NAD+ responses in different people. This reinforces the value of tracking your own trend rather than comparing yourself to population averages.