Sunscreen alone is only half the story
NAD⁺'s role in repairing UV damage
TA MEDICAL NAD+ RESEARCH · A summer feature on UV exposure and cellular repair
Chances are, sunscreen is already part of your summer without you thinking much about it — tucked into your bag, applied out of habit before you even walk out the door. That's exactly why the next part is easy to miss: even the best sunscreen was never designed to stop every ray of light from reaching your skin. A small amount always gets through, every single time you're outside, no matter how carefully you applied it. What your skin quietly does with that leftover light is one of the more remarkable things happening to you this season, and almost nobody talks about it.
Here's what's actually happening. UV light carries enough energy to cause small amounts of damage to the DNA inside your skin cells — tiny, invisible errors that occur constantly, any time your skin is in the sun. This isn't dangerous by itself, because your cells have a natural repair process that detects this kind of damage and corrects it, usually before it becomes anything more serious. Sunscreen reduces how much UV reaches your skin in the first place. What we want to look at today is what your cells do with the UV that gets through anyway — because that part of the story rarely gets told.
After you apply it,
where does that ingredient go?
Walk down any drugstore aisle in Japan and you'll see the same numbers on bottle after bottle: SPF25, SPF50, PA+++, PA++++. It's natural to read those as a simple scale — higher number, stronger shield, better choice — and reach for whichever bottle promises the most. What the number doesn't tell you is what's actually doing that work, or where it goes after it's on your skin.
That turns out to be a genuinely open question, and it's worth knowing before we go any further into what's happening beneath the surface. Several of the most common chemical UV filters — including avobenzone and oxybenzone — have been shown, in clinical trials funded by the U.S. Food and Drug Administration and led by researcher Dr. Murali Matta, to be absorbed into the bloodstream rather than simply sitting on the surface of the skin.¹ In that research, all six chemical filters tested exceeded the FDA's own safety threshold for blood concentration after just one application, and two of them — homosalate and oxybenzone — were still detectable in more than half of participants' blood a full 21 days after they'd stopped applying it. The researchers were careful to add that this isn't a reason to stop using sunscreen: its protective benefit is well established, and no clear harm has been shown at these levels. What they were saying, more precisely, is that nobody has yet studied what years of daily use actually means, because that long-term research simply hasn't been done.
This isn't a reason to be afraid of your sunscreen — it's simply worth knowing, in the same spirit as everything else in this article. If you'd rather sidestep the question entirely, mineral sunscreens are the alternative already sitting on the same shelf: look for the label “non-chemical”, which means the active ingredient is zinc oxide or titanium dioxide. These work by physically reflecting UV light off the skin's surface rather than absorbing it in, and haven't shown this same pattern of entering the bloodstream. Whichever kind you reach for, it's worth being a label-reader for more than just the SPF number — and now, let's get back to what's happening beneath the surface, because that part of the story doesn't depend on which bottle you chose.
This repair process runs on NAD⁺
When a skin cell detects UV damage to its DNA, a repair enzyme activates immediately, and the fuel it uses to do that job is NAD⁺. The more sun your skin deals with over the course of a day, the more NAD⁺ that repair process uses, right at the site of the damage — it isn't something that happens later, it's active work taking place while you're still outside. At the very same time, your skin is also producing more NAD⁺ to keep up with this demand, which means a sunny afternoon sets off a real balancing act inside your skin: production trying to keep pace with use, for as long as you're in the light.²
Confirming, through experiment,
the reason NAD⁺ dropped
Scientists have measured this directly, in research led by Takeshi Katayoshi and colleagues at DHC Corporation in Japan.² First, they exposed skin cells to UV light. Inside those cells, NAD⁺ levels dropped — in some cases, by more than half. Next, they wanted to prove why. So they blocked the repair enzyme itself, the one that works inside the cell, stopping it from using any NAD⁺ at all. This time, NAD⁺ levels inside the cells stayed high. That told them clearly: it was the repair work happening inside the cell that had been using up the NAD⁺ in the first place. So the finding is simple: skin cells really do spend their own internal NAD⁺ defending against sun damage, and now that's been confirmed directly, not just assumed.
So where does NMN actually fit in?
NMN is one of the raw materials your skin uses to produce NAD⁺, and in that same Japanese research, scientists tested this connection directly: when NMN was added to sun-stressed skin cells, those cells recovered better — consistent with the idea that having more of the raw material on hand helped support the repair process. That's a genuinely exciting result, and it deserves to be treated as one. But it's worth being precise about what it actually shows, because the study was done in cells in a lab dish, not in a living person's skin. What hasn't been tested yet is whether the same thing holds true in real, living human skin day to day — that's a question only a properly designed human trial can answer, and none has been run yet. Given how cleanly the cell-level evidence lines up with what's already known about NAD⁺'s role in this kind of repair, it's exactly the sort of result we're eager to see carried into human trials, and one of the directions in NAD⁺ research we're watching most closely.
None of this changes the basics, and it shouldn't be read as license to spend more time unprotected in the sun. Sunscreen remains the first and most important line of defense, and nothing here is a substitute for it. What we're describing is simply what's already happening beneath the surface — a real, continuous piece of your biology doing its job whether you think about it or not.
The takeaway
Your skin isn't a passive surface sitting out in the sun. Every day, it's catching small UV damage and repairing it on the spot, and NAD⁺ is what makes that possible. Here's why that matters: damage that doesn't get repaired doesn't just disappear — it stays, and it builds up over years. That gradual buildup is one of the most well-established drivers of visible skin aging: the fine lines, uneven tone, and loss of elasticity most people associate with a lifetime of sun exposure. A repair process that keeps working well, day after day, is quietly part of what keeps skin looking and functioning the way it's supposed to, for longer. Wear the sunscreen, wear the hat, and enjoy the season — just maybe with a little more appreciation for what your skin is already doing on your behalf, every time you step outside.
References
1. Matta, M.K., Florian, J., Zusterzeel, R., et al. Effect of Sunscreen Application on Plasma Concentration of Sunscreen Active Ingredients: A Randomized Clinical Trial. JAMA, 2020;323(3):256–267. U.S. Food and Drug Administration, Silver Spring, Maryland, USA.
2. Katayoshi, T., Nakajo, T., & Tsuji-Naito, K. Restoring NAD+ by NAMPT is essential for the SIRT1/p53-mediated survival of UVA- and UVB-irradiated epidermal keratinocytes. Journal of Photochemistry and Photobiology B: Biology, 2021;221:112238. DHC Corporation Laboratories, Chiba, Japan..
