The Pigment Puzzle—Why Melasma Might Be a Vitamin A Story (and a Light Story, and a Fat Story) (Part 2/2)
In part one, I shared how my melasma showed up during my first pregnancy—cheekbones, office life, keto pork-rind summers, sunscreen slathered like frosting. It hasn’t budged since, but it also hasn’t gotten worse.
Which tells me something interesting: this isn’t a condition that’s getting actively worse. It’s something that was set in motion—by light, by food, by timing—and is now just waiting for a new set of conditions to reverse the signal.
Today I want to dig into the deeper mechanics: Vitamin A, blue light, and the pigment your skin creates when it’s overwhelmed.
Melanin vs. Lipofuscin: The Good Pigment and the Garbage One
Most people think of melanin as just skin pigment. But zoom out, and melanin is actually a high-powered antioxidant and semiconductor that helps your body process light. It scavenges free radicals, supports mitochondrial redox, and even creates dopamine.
But here’s the rub: when the system breaks down—when there's oxidative stress, poor light signaling, and mitochondrial dysfunction—your body stops producing quality melanin and starts hoarding a pigment called lipofuscin instead.
Lipofuscin is not the good kind of pigment. It’s not functional. It’s basically oxidized trash—a mix of damaged fats, proteins, and Vitamin A byproducts that the cell can’t break down. And where does it accumulate? In high-light areas. The face. The cheeks. The skin. The retina. The brain.
Sound familiar?
Vitamin A: The Molecule That Glows (Until It Doesn’t)
Vitamin A is fascinating. It’s the only vitamin that literally emits light—a process called fluorescence. It absorbs UVB (328 nm, for the nerds) and releases energy as longer wavelengths. That light-emitting quality is what makes it essential to your visual cycle and skin photoreception.
But here’s the problem: in a stressed system—especially one full of blue light, poor redox, and PUFA-rich membranes—Vitamin A can photo-oxidize. That’s the word you were looking for.
Photo-oxidation is when a molecule reacts with light (especially blue light) in the presence of oxygen and becomes damaged. Think of it like leaving a piece of fruit out in the sun—it might still technically be “fruit,” but it’s breaking down, fermenting, turning into something else.
In your cells, photo-oxidized Vitamin A creates toxic byproducts that get packaged into lipofuscin. The body doesn’t know what else to do with it. It can’t clear it easily. So it hides it—often in your pigment-producing tissues.
And boom. A new dark spot appears.
Enter: Blue Light and Its Unholy Alliance with Vitamin A
You might’ve noticed your skin gets worse in winter, or in front of screens, or after a plane ride. That’s not a coincidence. Blue light—especially when it's unopposed by the rest of the spectrum (like infrared and UVA)—has a uniquely damaging relationship with Vitamin A.
Here’s how it goes:
-
Blue light alters the weak covalent bond between melanopsin and retinal (a form of Vitamin A).
-
This makes the system unstable. The light signal gets distorted.
-
The result is circadian chaos, oxidative stress, and Vitamin A molecules that have now turned rogue.
-
These damaged retinoids are no longer useful—they’re inflammatory, light-sensitive, and prone to accumulate in skin, eyes, and brain tissue as… yep, lipofuscin.
This is what I now suspect happened during those two years I was working under fluorescent lights, eating oxidized fats, and slathering on sunscreen like it was going to save me. Instead of building melanin, my body was likely shoving damaged retinoids into my cheekbones and calling it a day.
Why the Cheeks? And Why Doesn’t It Fade?
The cheeks are light-receiving zones. They're photoreceptor-rich. Melanin is supposed to live there, not trash pigment. But if the system is off—if your light inputs are wrong, your fats are unstable, and your Vitamin A is photo-oxidizing—your body deposits junk instead of renewing tissue.
And it lingers. Because lipofuscin isn’t easily cleared. It's resistant to autophagy. It doesn’t get flushed out with lymph drainage or a juice cleanse. It’s stuck until you rebuild the systems that should’ve never created it in the first place.
That’s why your melasma might not be spreading—but it’s not going away either. You’re not adding more to the fire, but the ashes are still there.
The Role of Pseudohypoxia (aka Mitochondria Starving for Oxygen Despite Plenty of It)
There’s one more layer worth touching on: pseudohypoxia. This is when your mitochondria act like they’re oxygen-starved even though there’s oxygen all around. It’s like a car with a full tank of gas and a busted spark plug—no combustion.
This happens when:
-
NAD+ is low
-
Lactate is high
-
Thiamine or pyruvate metabolism is off
-
You’ve got too many blue photons hitting your tissues and not enough infrared to balance it
Pseudohypoxia contributes to oxidative stress. Oxidative stress degrades melanin. Degraded melanin can’t handle light. And when you add in unstable fats and vitamin A byproducts?
More lipofuscin.
It’s a tangled web. But once you see the pattern, you can start to reverse-engineer it.
So How Do You Heal It?
This is the part everyone wants: the protocol. And I’ll be honest—there is no neat list. There’s only system support, and the patience to see it through.
Here’s where I am right now:
-
Rebuild melanin with sun, not serums
I use real sun exposure—especially morning UVA and late afternoon IR—to retrain my skin’s light-handling machinery. Think of it as software reinstallation. -
Ditch the PUFAs, deeply
I’ve swapped nuts, pork rinds, and keto snacks for grass-finished tallow, pastured yolks, and raw dairy. You need stable fats to handle solar input. Period. -
Reduce blue light and fake frequency exposure
Fewer screens. More sun. No LED overheads. And ideally, less time indoors during the cold months (still a work in progress). -
Don’t supplement Vitamin A unless you’ve earned it
This isn’t a deficiency problem—it’s a mismanagement problem. More retinol in a body with low redox = more lipofuscin. I trust food sources only, in the context of sunlight and seasonal eating. -
Give it time. Like, years.
If it took two years of indoor living, synthetic sunscreen, and dietary fats that oxidize under light to set this up, it’s going to take time to unwind. But each season I notice something. A softening. A shift. Less intensity. And that’s enough for now.
Final Thoughts: This Is a Theory, Not a Truth
I’m not a dermatologist. I’m a curious founder with stubborn melasma and a deep respect for how the body speaks through the skin. I might be wrong about parts of this. But I’m also not outsourcing this to an industry that told me to fear the sun and slather myself in endocrine disruptors.
Instead, I’m learning to listen to my skin. To rebuild its relationship with light. To give it what it needs to clear the pigment that doesn’t belong.
If you’re reading this with your own version of stubborn skin, know this: it’s not about “correcting” your skin. It’s about restoring the conditions that made healthy skin normal in the first place.
Addendum: Healing Options for Pigmentation Issues
If you’re wondering what to do with all this information—how to actually support the skin from the inside out—here’s a quick look at some functional, long-view strategies that align with the deeper root causes:
| Name | Supportive Actions | Expected Timeline |
| Melasma | Morning sun exposure, rebuild redox with saturated fats, avoid blue light at night, support liver detox, prioritize whole-food Vitamin A | Slow improvement over seasons; 6–24 months with consistency |
| Chloasma | Same as melasma, plus hormone balance through circadian alignment, nutrient-dense prenatal prep | Seasonal support and ongoing nutrient repletion; 3–12 months |
| Solar Lentigo (Sun Spots) | Gradual solar callus building, reduce PUFA intake, support skin with infrared light and mitochondrial support, embrace seasonal outdoor time | Fades slowly once PUFA exposure and light mismatch are resolved; 6–18 months |
| Age Spots / Liver Spots | Autophagy support via fasting and cold exposure, red light therapy, remove processed fats, increase glutathione production, rebuild with nutrient-dense foods | Most stubborn; may take years, but visible softening with long-term redox + mitophagy support |
This isn’t a one-serum fix. It’s a long-view, whole-system recalibration. But each step—each walk outside, each forkful of real food, each skipped sunscreen pump—is a vote for your skin’s ability to remember what it was built to do.
Did you miss part 1/2? Why I’m Not Blaming the Sun for My Melasma and Sun Spots (Anymore) (Part 1/2)
Looking for other blogs on Vitamin A?
-
Non-Vegan Vitamin A (retinol): the most underrated nutrient for your skin, thyroid, and metabolism.
-
Is Vitamin A Really Toxic—Or Are We Just Getting It Wrong?
Disclaimer: This blog is for informational and educational purposes only. It is not intended to diagnose, treat, cure, or prevent any medical condition. Always consult a qualified healthcare provider before making changes to your diet, lifestyle, or skincare routine.
REFERENCES:
-
Dr. Jack Kruse - CPC #9: HASHIMOTO’S AND MELASMA – GATEWAY DISEASES
-
Dr. Jack Kruse - HYPOXIA #15: BLUE LIGHT CAUSES IRREVERSIBLE HYPOXIA IN ALL CELLS
-
Dr. Jack Kruse - MY 2023 CHRISTMAS LIST FOR MY TRIBE (Patreon)
-
Dr. Jack Kruse - QUANTUM ENGINEERING #27: WHY SUNSCREEN AND SUNGLASSES ARE HARMFUL (Patreon)
-
Dr. Jack Kruse - QUANTUM ENGINEERING #34: OUTING A “LONGEVITY EXPERT” IN MY RECENT MALIBU PODCAST (Patreon)
-
Dr. Jack Kruse - QUANTUM ENGINEERING #51: LIPOFUSCIN DEPOSITION IS A DEFECT IN MELANIN (Patreon)
Cites from Kruse's Blogs:
1.Navarrete-Solís J, Castanedo-Cázares JP, Torres-Álvarez B, Oros-Ovalle C, Fuentes-Ahumada C, González FJ, Martínez-Ramírez JD, Moncada B,”A Double-Blind, Randomized Clinical Trial of Niacinamide 4% versus Hydroquinone 4% in the Treatment of Melasma”
2.http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=13152519&ordinalpos=166&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
3.http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9134597&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
4.http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15529025&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
5.http://www.ncbi.nlm.nih.gov/pubmed/22237023
6.http://www.sciencedirect.com/science/article/pii/S030441651100184X
8.Olivarius F. de Fine, H.C. Wulf, P. Therkildsen, et al.Urocanic acid isomers: relation to body site, pigmentation, stratum corneum thickness and photosensitivity Arch Dermatol Res, 289 (1997), pp. 501-505
9.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721001/
10. https://www.sciencedirect.com/science/article/abs/pii/S0306987716304169
11. https://www.sciencedirect.com/science/article/pii/S0022202X15301160
12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3586554/
13. https://onlinelibrary.wiley.com/doi/full/10.1111/exd.12715
14. https://www.ncbi.nlm.nih.gov/pubmed/25645910/
15. https://twitter.com/DrJackKruse/status/1638334680599613440