I get asked about retinol more than any other ingredient. Usually by someone who has just been told, by a dermatologist or a friend or the internet, that it is the only anti-aging ingredient with real evidence behind it.
They are not wrong about the evidence.
That is the part people expect me to argue with, and I am not going to. Retinoids work. The clinical literature on them is deep, it goes back decades, and any formulator who tells you otherwise is either uninformed or selling something.
We still do not use it. In any form. Including the ones marketed as natural.
I want to walk you through exactly why, because the reasoning matters more than the conclusion, and because I would rather you disagreed with me having understood the argument than agreed with me on vibes.
One thing first. I am not a patient person. I have stood in my own lab holding something I formulated, knowing precisely which lever would make it work faster, and wanted to pull it. I know how to pull it. I have chosen not to, repeatedly, and it has never once felt good in the moment.
The question for me is what I am willing to trade.
What retinol actually does
Retinol is not the active molecule. It is a precursor.
When you apply it, your skin converts it in two steps. Retinol becomes retinaldehyde, retinaldehyde becomes retinoic acid. Retinoic acid is the thing that does the work, and each conversion step loses you some material, which is why retinol is weaker than prescription tretinoin, which arrives as retinoic acid already.
Retinoic acid then binds to nuclear receptors inside your skin cells, the retinoic acid receptors and retinoid X receptors. These are transcription factors. They sit on your DNA and change which genes get read.
Three things follow.
Your fibroblasts increase production of procollagen types I and III.
Your skin suppresses matrix metalloproteinases, the enzymes that cut existing collagen apart.
Your keratinocytes divide and turn over faster, so the surface renews more quickly.
That is a real mechanism. It is elegant, it is well mapped, and it is why the results are real.
Nothing in that list involves irritation. The receptor signaling is the engine. The peeling, the stinging, the flaking that people call retinization and are told to push through, that rides alongside the mechanism. It is not the mechanism.
The internet is not precise about this, and the case against retinol does not need the exaggeration.
The price of admission
Here is what comes with it.
Retinoids accelerate keratinocyte turnover, which thins the stratum corneum, the outermost compacted layer that does most of your barrier work. A thinner stratum corneum loses water faster and admits more UV.
So you become more sun sensitive. Not for a day. For as long as you are using it, and then for however long your skin takes to rebuild that layer after you stop. Retinol itself also degrades under UV, which is why every instruction on every bottle tells you to apply it at night.
As a system, that is self-defeating. You are using an ingredient to repair photoaging, and while you use it, you are more vulnerable to the exact thing that caused the photoaging. The whole strategy runs on daily filter application, indefinitely and without a missed day, just to hold the ground you are gaining. It takes your own defenses down and asks a bottle to stand in for them.
Then there is the irritation itself. Redness, peeling, stinging, a compromised barrier for weeks. People are told this is the ingredient working. It is the ingredient costing.
And a barrier under stress does not simply feel uncomfortable. It produces more oil to compensate, it inflames more readily, and inflammation degrades collagen. You can end up paying with one hand for what you are buying with the other.
The safety question, stated accurately
This is where I want to be careful, because the internet version of this argument is overstated and gets dismissed for good reason.
The US National Toxicology Program ran a photocarcinogenesis study, published as Technical Report 568. Retinoic acid and retinyl palmitate were applied topically to hairless SKH-1 mice under simulated solar light. Skin tumors developed faster and in greater numbers in the treated groups than in the controls.
Now the caveats, because you deserve them.
It required concurrent UV exposure. It was done in hairless albino mice, which are far more UV vulnerable than human skin. And the conclusions were formally challenged through the NIH information quality process, so this is contested science rather than settled science.
It does not prove that retinol causes cancer in people, and I will not present it as though it does.
What it is, is the closest thing we have to a long-term safety investigation of topical retinoids, and it found something worth pausing on. The equivalent study has never been run in humans over decades, because nobody is going to fund forty years of that, and nobody is required to.
Which leaves us here. An ingredient class whose oral form is a confirmed teratogen. Whose topical form has never been tested across a human lifetime. Where the one long-term animal model we have raised a flag under UV. And the standing recommendation is nightly use, indefinitely, starting in your twenties.
Where I go further than the evidence
Everything above is what can be shown. What follows is what I think, and I want the line between the two to be unmistakable.
I suspect retinol is carcinogenic.
Not proven. Suspected. I cannot demonstrate it, and neither can anyone else in either direction, which is rather the point.
But I have spent a long time with this chemistry, and here is the shape of the thing that bothers me. An ingredient that drives cells to divide faster. That thins the layer standing between ultraviolet light and the dividing cells underneath. That accelerated tumor formation in the one long-term animal study anybody ran, under UV. And that has never been tested across a human lifetime, and never will be, because no one will fund forty years of it and no one is required to.
None of those facts is damning on its own. Together they are a pattern I am not comfortable with.
That is a suspicion, and it deserves the weight of one. I would rather tell you plainly what I believe and label it clearly than imply it through careful wording and let you infer something I have not earned the right to state.
And here is what makes the suspicion easy to act on, which is the part that actually decides it.
I do not need retinol.
If the choice were between retinol and nothing, I would think about this much harder, and I would probably land somewhere more forgiving. But I have an ingredient that reaches a comparable place in a head-to-head trial, without irritating the barrier and without raising your UV vulnerability while it works.
When a better option exists, an unresolved question stops being a dilemma and becomes an easy no.
What bakuchiol is, and what it is not
Bakuchiol comes from Psoralea corylifolia, a plant called babchi in Ayurveda and Unani medicine and bu gu zhi in Chinese medicine. Its use for skin disease, including vitiligo and leprosy, runs through all three traditions and is documented across the ethnobotanical literature. That is not a story the beauty industry invented in 2018.
Here is the part almost every brand writing about bakuchiol gets wrong, and it is the part that matters most.
Babchi seed oil and bakuchiol are not the same thing.
Babchi seed oil contains psoralens: psoralen itself, isopsoralen, bakuchicin. Psoralens are phototoxic. They slot into DNA and, when they absorb UVA, they form cross-links. That is the entire basis of PUVA therapy, where dermatologists use psoralens plus UVA deliberately to treat psoriasis and vitiligo. It works because it is a controlled injury.
So babchi oil on your face before sunlight is a genuinely bad idea, and the plant's ancient reputation was built partly on that phototoxic effect.
Bakuchiol is a different thing. It is a meroterpene phenol, isolated and purified out of the plant. It is not a psoralen. It does not carry that phototoxicity with it.
Which is why the grade you buy is not a detail. A cheap bakuchiol that is really a crude babchi extract brings the psoralens along with it. We use Sytenol A, the purified isolate, the most refined form commercially available and considerably more expensive than the alternatives. It is also the material the published research was conducted on, so when I cite a study, I am citing work done on the ingredient that is actually in the bottle.
Buying the cheap version and calling it bakuchiol is the most common failure in this whole category.
What the evidence says
Bakuchiol is not structurally a retinoid. It bears no chemical resemblance to vitamin A at all. What it has is functional overlap.
Chaudhuri and Bojanowski published gene expression profiling in the International Journal of Cosmetic Science in 2014 showing that bakuchiol upregulates a similar set of genes to retinol, including collagen types I, III and IV, while also acting on targets retinol does not touch. Different key, similar lock.
Then in 2019, Dhaliwal and colleagues published a prospective, randomized, double-blind trial in the British Journal of Dermatology comparing 0.5% bakuchiol against 0.5% retinol over twelve weeks for facial photoaging. Both significantly reduced wrinkle surface area and hyperpigmentation, with no statistically significant difference between them on those measures.
The difference showed up in the side effects. The retinol group reported more facial scaling and more stinging.
That is head to head, blinded, and published in a serious dermatology journal. It is the study I would point at if I were only allowed one.
What it does not tell you is what either ingredient does over thirty years, because it ran for twelve weeks. Bakuchiol has no decades of longitudinal human safety data. Neither does retinol. The difference is that bakuchiol is not asking you to compromise your barrier and raise your UV vulnerability while you wait to find out.
Sun protective, and why that does not mean sunblock
Bakuchiol is a potent antioxidant, and this is where I need to define a term properly, because the distance between these two ideas is the distance between a true statement and a dangerous one.
A filter works before the photon lands. A sunscreen sits on the surface and either absorbs UV radiation or scatters it, so a proportion of it never reaches your living cells. It is tested to a standard, it earns a number, and in the United States it is regulated as an over-the-counter drug, because functionally that is what it is.
Antioxidant photoprotection works after the photon lands. The UV that does get through generates reactive oxygen species inside your skin. Those free radicals are what actually does the damage. They oxidize lipids, they damage DNA, and they switch on the matrix metalloproteinases that dismantle collagen. An antioxidant quenches a portion of that cascade before it finishes.
Dermatology has a name for the second one. It is called non-sunscreen photoprotection, and the published framing is precise: antioxidants add value to a filter. They are not a filter.
So when I say bakuchiol is sun protective, I mean it reduces some of the oxidative damage caused by the UV that reaches you. I do not mean it blocks UV. It has no SPF. It has never been tested for one and it would not earn one. Nobody should read this page, skip cover on a long day in strong sun, and think an antioxidant has them.
Where I land on daily filter use is a longer argument, and it is its own piece. The short of it is that a filter is one half and your skin's own reserves are the other, and the industry built a whole category on the first half.
What matters here is the contrast between these two ingredients. One makes you more vulnerable to UV the entire time you use it, by thinning the layer that was doing the work. The other adds to what your skin can already do. If you live somewhere sunny, and I live in Las Vegas, that difference compounds over years.
Where it sits in our line
F108 The Renewal Accelerator Bio-Serum is the structural one, from $322. It is our most concentrated treatment and it is built for the point where hydration is no longer the problem and the architecture underneath is. It goes on cleansed skin first, directly against the skin, underneath everything else including your root serum. That order is not arbitrary. It is so the concentrated layer reaches skin rather than a film of oil.
Most skin should follow it with a reinforcing cream. Oil-dominant skin can use it alone.
F109 When I Dream Night Cream, from $125, is the gentler entry point. It works overnight, when your skin is in its repair phase rather than its defending phase. Bakuchiol alongside a peptide complex, ceramides and cacao butter, so the barrier is being reinforced at the same time the renewal is being supported.
If firmness and structure are what you are actually after, the firmness and visible aging page lays out the full sequence. And if you are not certain that is your main concern, start from your concern rather than buying the strongest thing on the site.
If you are coming off retinol
Stop. You do not need to taper.
Give your barrier two to four weeks to rebuild before you judge anything, and expect it to look worse before it looks better, because you are seeing your actual skin rather than skin in a state of accelerated turnover.
This is the one window where I would be genuinely careful in the sun, and it is worth knowing why. Your stratum corneum is thin, which means the layer that normally absorbs and scatters UV on your behalf is not there yet. That is a real deficit rather than a general precaution. Keep out of strong sun, cover up, and use a mineral filter on the days you cannot, until the layer is back.
Then start the bakuchiol and give it twelve weeks. Collagen is slow. Anything promising you structural change in three weeks is describing water, not collagen.
The short version
Retinol works. I have said so throughout and I meant it.
It works by changing gene transcription, and it charges you a thinner barrier and heightened UV sensitivity for as long as you use it, on an ingredient whose long-term human safety has never been established because nobody has ever tested it. I suspect it is carcinogenic. I cannot prove that, and I have told you plainly that it is a suspicion.
Bakuchiol reaches a comparable place in a twelve week head to head, with less irritation, no phototoxicity when it is the purified isolate rather than the crude oil, and antioxidant activity that adds to your skin's own defenses rather than removing one of them.
Given both options, I know which one I want on my face every night for the next thirty years.
If you use retinol and love it, I am not going to tell you that you have ruined yourself. You have not. Mind your barrier, be sensible about strong sun while that layer is thin, and go carefully.
And if you want to talk through what switching would actually look like for your skin, write to me. I read them all.
