NAD+ Explained (and How Urolithin A Fits In)

NAD+ is one of the most discussed molecules in longevity science, yet it is rarely explained clearly. This guide covers what NAD+ actually does inside your cells, why levels tend to drift downward with age, and how it differs from the very different job urolithin A performs.

What NAD+ actually is

NAD+ stands for nicotinamide adenine dinucleotide. It is a coenzyme, which means it is a small helper molecule that many of your enzymes cannot function without. Nearly every living cell carries it, and it participates in hundreds of reactions. Rather than being a fuel itself, NAD+ is better understood as a shuttle: it accepts and donates electrons, moving them between reactions so that energy can be extracted from the food you eat. When it picks up electrons it becomes NADH, and when it releases them it returns to NAD+. This constant back-and-forth is one of the busiest chemical cycles in human biology.

Because NAD+ sits at the center of so much metabolism, researchers often describe it as a hub molecule. It is not exotic or rare; it is fundamental infrastructure. What has drawn attention over the past decade is the observation that the amount of usable NAD+ in tissues appears to change across the lifespan, and that this shift lines up with several features of biological aging.

What NAD+ does in the body

NAD+ has two broad roles. The first is metabolic: in the mitochondria and cytoplasm, NAD+ helps drive the reactions of glycolysis, the citric acid cycle, and oxidative phosphorylation, the pathways that convert carbohydrates, fats, and protein into usable cellular energy in the form of ATP. Without adequate NAD+ to carry electrons, these pathways slow.

The second role is regulatory. Two families of enzymes consume NAD+ as a raw material while doing their work. Sirtuins use NAD+ to adjust how genes are packaged and expressed and are involved in cellular stress responses. PARPs use NAD+ during DNA repair. Because these enzymes actually spend NAD+ rather than simply borrowing it, heavy demand for DNA repair or stress signaling can draw down the available pool. This dual identity, a metabolic carrier and a consumable signaling substrate, is why NAD+ is studied in the context of both energy and aging.

Why NAD+ tends to decline with age

A recurring theme in the research literature is that tissue NAD+ availability appears to decrease with age in many organisms and tissues. The proposed reasons are not settled, but they generally fall into two buckets: the body may make less NAD+ over time, and it may consume more. On the consumption side, accumulated DNA damage and a low-grade inflammatory tone associated with aging can keep NAD+-spending enzymes busier. On the production side, the machinery that recycles NAD+ may become less efficient. The honest summary is that decline is well documented in preclinical models and increasingly measured in humans, but the exact magnitude, tissue by tissue, and its precise consequences are still being mapped.

How your body makes NAD+

Your cells build NAD+ through several routes. The dominant one is the salvage pathway, which recycles nicotinamide (a form of vitamin B3) back into NAD+ over and over. There is also a route from dietary tryptophan, an amino acid, and routes from other B3 forms such as niacin. Supplement makers have focused on intermediates that feed the salvage pathway quickly.

NAD+ precursors: NMN and NR

The two precursors you will hear about most are NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside). Both are steps on the way to NAD+. The logic is straightforward: rather than trying to deliver NAD+ itself, which is a large and unstable molecule to absorb, you supply a building block the cell can convert. Human trials of oral NMN and NR have generally reported that they are well tolerated and can raise blood NAD+ markers. Whether that measurable rise translates into the functional outcomes people care about, energy, strength, healthspan, is where the evidence is still developing and where careful reading matters. You can go deeper in our NMN explainer and our guide to mitochondrial health.

Where urolithin A fits, and how it differs

It is easy to lump every longevity-adjacent ingredient together, but NAD+ and urolithin A operate through genuinely different mechanisms. NAD+ is about the supply of a coenzyme. Urolithin A is about mitochondrial quality control. Urolithin A is a gut postbiotic: your microbiome produces it from ellagitannins, compounds found in pomegranate, walnuts, and certain berries. Notably, only some people carry the gut bacteria needed to make meaningful amounts, which is one reason a standardized supplement is of interest.

The specific process urolithin A supports is called mitophagy, the cell's routine for identifying and recycling worn-out mitochondria so that newer, better-functioning ones can take their place. Think of NAD+ as keeping the electrical carriers stocked, and mitophagy as maintenance that clears out failing equipment. On the human evidence: Andreux and colleagues (2019, Nature Metabolism) reported in a first-in-human study that urolithin A was safe and well tolerated at doses up to 1,000 mg per day and produced a mitochondrial gene-expression signature. Later randomized human trials, including Singh et al. (2022, Cell Reports Medicine) in middle-aged adults and Liu and D'Amico et al. (2022, JAMA Network Open) in older adults, examined measures of muscle strength, exercise performance, and muscle endurance. A 2025 randomized trial in Nature Aging reported support for immune-cell mitochondrial health in midlife adults. Foundational work such as Ryu et al. (2016, Nature Medicine) established the mitophagy mechanism, but that early work is preclinical (worms and rodents) and should be read as mechanism rather than human proof. A 2024 systematic review in Ageing Research Reviews fairly characterizes the human evidence as still emerging, built on relatively short trials of modest size. For a fuller walk-through, see our urolithin A guide and our roundup of the best urolithin A gummies.

Practical takeaways

If you are trying to make sense of this category, a few grounded points help. First, NAD+ decline with age is real in the research literature, but a single blood number is not a verdict on your health. Second, precursors and urolithin A are not interchangeable; they target different steps, so comparing them head to head as if they do the same thing is misleading. Third, the strongest human data in the urolithin A space centers on muscle and mitochondrial endpoints, and the clinically studied range is 500 to 1,000 mg per day, with 1,000 mg at the top of that range. SOMA HEALTH Urolithin A Gummies deliver 1,000 mg per four-gummy daily serving, are third-party tested, and are sugar-free.

A note on health conditions: NAD+ metabolism intersects with topics like metabolic health, energy, and aging. Nothing here is a treatment for any medical condition. If you have a diagnosed condition, take medication, are pregnant, or have specific concerns, talk with your doctor before starting any supplement.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This guide is educational and is not a substitute for advice from a qualified healthcare provider.