On this page you will learn what this compound is, what human studies do and do not show, which doses have been tested and how it compares with NMN and NAD+<\/sup>. Want the background on mitochondria and cellular ageing first? Read our page on longevity at the cellular level<\/a>.<\/p>\n Urolithin A is a so-called postbiotic: a compound that is not present in food itself but is formed when gut bacteria convert something from your diet. The raw material is ellagitannin, a polyphenol found in pomegranate, walnuts, pecans, strawberries and raspberries.<\/p>\n In the gut, ellagitannins are first converted into ellagic acid. Certain bacteria then convert this step by step into various urolithins, of which the A variant has been studied most. After absorption, the compound enters the bloodstream, mostly in conjugated form (for example as a glucuronide).<\/p>\n The conversion depends on which bacteria live in your gut. Researchers speak of metabotypes: some people produce a lot of this metabolite from food, others little or almost none. Research by Singh and colleagues (2021)<\/a> found that blood levels after eating pomegranate or nuts varied widely between individuals, while direct supplementation with the pure compound produced much more consistent levels.<\/p>\n Age, diet and gut health appear to play a role. This is also why supplements exist that deliver the metabolite directly rather than only its precursors.<\/p>\n Mitochondria are the structures in your cells that produce much of the energy carrier ATP. Like other parts of a cell, they become damaged over time. Cells therefore have a clean-up system: mitophagy. Poorly functioning mitochondria are broken down, making room for new ones.<\/p>\n With ageing, this clean-up system appears to become less efficient. Mitochondrial dysfunction is listed as one of the hallmarks of ageing in the scientific framework of the same name. In 2016, Ryu and colleagues reported in Nature Medicine<\/a> that the compound activated mitophagy in worms and rodents, with a longer lifespan in worms and better endurance in older mice.<\/p>\n Important: results in worms and mice do not translate directly to humans. They explain why researchers find this metabolite interesting, but prove nothing about effects in people.<\/p>\n Urolithin A and NMN are often mentioned in the same breath, but they act on different processes. NMN is a precursor of NAD+<\/sup>, a coenzyme required for energy metabolism and enzymatic reactions. This metabolite targets the maintenance of the mitochondria themselves. Think of it as the difference between supplying fuel and servicing the engine. Read more about that first route on our page what is NMN<\/a>, or go straight to our NMN capsules<\/a>.<\/p>\n Human research on this compound is young and mostly conducted with one specific ingredient (Mitopure) and with involvement of the manufacturer. That does not make the studies unreliable, but independent replication matters. These are the three most important randomized trials.<\/p>\n In a phase 1 study by Andreux and colleagues<\/a>, 60 healthy, sedentary older adults received single doses or four weeks of daily 250, 500 or 1000 mg of the compound or a placebo. It was well tolerated. In muscle biopsies, the researchers saw altered expression of genes related to mitochondria and mitophagy, and certain acylcarnitines in the blood decreased. Functional outcomes such as strength were not a primary goal in this short study.<\/p>\nKey points<\/h2>\n
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What is urolithin A?<\/h2>\n
Why doesn\u2019t everyone produce urolithin A?<\/h3>\n
How does urolithin A work in the cell?<\/h2>\n
Mitophagy versus NAD+<\/sup><\/h3>\n
What does research on urolithin A in humans show?<\/h2>\n
1. First study in older adults (Nature Metabolism, 2019)<\/h3>\n
2. Adults aged 65 to 90 (JAMA Network Open, 2022)<\/h3>\n
