Why I’m Not Blaming the Sun for My Melasma and Sun Spots (Anymore)

Let me just say upfront: this isn’t a dermatology post. It’s not a list of serums or a pitch for a miracle acid peel. It’s my current working theory of what melasma is—and more importantly, why it landed on my face when it did, and why it hasn’t left yet. It’s personal, but I think it might resonate with anyone who’s ever stood in front of the mirror and asked: why here? why now?

The Bigger Picture: Pigmentation Isn’t Just a Cosmetic Issue

Before we dive deeper into my story, let’s zoom out and define the landscape. There’s a whole category of skin changes that get brushed off as cosmetic or “just aging.” But they’re messengers of something deeper—hormonal shifts, mitochondrial stress, light mismatch, and nutrient imbalance.

Here’s a quick breakdown of the most common pigmentation issues:

Category	Name	Common Triggers	Key Characteristics	Root Cause (Quantum/Functional View)
Hormonal Pigmentation	Melasma	Hormonal shifts (pregnancy, birth control), blue light, sunscreen, circadian mismatch	Symmetrical patches on cheeks, upper lip, forehead; worsens with light exposure	Dysfunctional melanin processing due to poor redox and vitamin A photo-oxidation
Hormonal Pigmentation	Chloasma	Same as melasma; often used interchangeably, especially in pregnancy	Pregnancy-associated melasma; “mask of pregnancy”	Same as melasma; vitamin A handling + mitochondrial stress
Sun-Related Pigmentation	Solar Lentigo (Sun Spots)	Cumulative sun exposure, especially in lighter skin tones over time	Flat, brown or black spots on sun-exposed areas (face, hands, arms)	Impaired melanin due to long-term UV exposure + blue light dominance + circadian mismatch
Sun-Related Pigmentation	Age Spots / Liver Spots	Aging, oxidative stress, light damage, and lipofuscin buildup	Often seen in older adults, linked to mitochondrial dysfunction and damaged pigment	Accumulation of lipofuscin (oxidized trash pigment) due to aging, PUFA exposure, and light stress

Now that we’ve set the stage, let’s rewind to where this all began for me.

The Beginning: My Cheekbones, First Pregnancy, and a Whole Lot of Sunscreen

The first time I noticed melasma, I was pregnant with my first baby. It crept in on my cheekbones like a soft, stubborn shadow. Not a freckle, not a burn—just a new pigment pattern that didn’t fade with the season.

At the time, I was working in an office—fluorescent lights overhead, screens all day. Summers were my “sunscreen era.” I mean slathered, religiously. I was also keto (cue pork rinds and nuts), under-slept, and trying to be productive despite everything in my body begging for a nap and a steak.

Years later, that melasma is still on my cheeks. But it hasn’t worsened. I haven’t worn sunscreen since. I haven’t returned to an office. I soak up the summer sun like it’s my job, and yet… those cheekbone patches linger. So, I started asking deeper questions.

What Causes Melasma? (Hint: It’s Not Just the Sun)

Melasma is often described as “hyperpigmentation triggered by sun exposure and hormones.” That’s the standard story. But let’s look at what might really be going on, especially if you’re viewing skin through a quantum lens like I am these days.

Melasma shows up when the body’s light-handling systems break down. Specifically, when melanin stops doing its job well.

Melanin is meant to be your skin’s semiconductor—it captures, stores, and re-routes solar energy. But when melanin gets overwhelmed, degraded, or hijacked (think: blue light, EMFs, mitochondrial stress), it starts producing lipofuscin instead. That’s the junk pigment. The one that can’t handle ROS. The one that builds up like rust. And the skin? It pushes it where the light hits most: cheeks, upper lip, forehead. Not because of the sun—but because those are the zones meant to handle solar information. When they can’t, they offload dysfunction instead.

Why It Shows Up Where It Does

The cheekbones, forehead, and upper lip aren’t random targets. These are areas designed to sense and respond to light. They’re home to melanocytes, melanopsin, and photoreceptors. In a healthy system, they’d be decoding the light signal and turning it into internal instructions—like, “Make dopamine. Calm inflammation. Repair mitochondria.” But when those systems are offline (think indoor winter life, overuse of sunscreen, blue light dominance, or high PUFA intake), that incoming signal turns into noise.

Melasma is where light meets broken code.

Why People Blame the Sun—and Why I Don’t (Anymore)

It’s easy to blame the sun because that’s when melasma seems to “darken.” And yes, UV light does interact with pigment. But here’s the catch: if your pigment system (melanin) is dysfunctional to begin with—either overloaded with ROS, swapped out for lipofuscin, or unable to handle iron—then of course UV will trigger a response. But the root problem isn’t the light. It’s the system receiving it.

I had my worst flare while indoors all day under blue light, living on pork rinds and almond flour. My mitochondria were likely drowning in omega-6s, my dopamine was bottomed out, and I was blocking the very signals (UVA/IR-A) that stimulate the POMC-melanin pathway to repair the skin. Sunscreen may have blocked a burn, but it also blocked a repair mechanism.

Let’s Talk About Vitamin A and PUFAs

Here’s where things get messy.

Vitamin A is a tricky beast. It’s vital for photoreceptor function, retinoid signaling, and skin renewal. But in excess—or when stored improperly due to low redox—it becomes a phototoxic liability. In Kruse’s world, vitamin A derivatives in a low-light, high-EMF environment can create toxic retinoid byproducts that accumulate as—you guessed it—lipofuscin.

Now layer in polyunsaturated fats (PUFAs), which are prone to peroxidation under light and stress. These fats, especially from industrial seed oils or even “healthy” keto snacks like pork rinds and nut butters, embed into your cell membranes and make your skin literally more fragile under light exposure.

So what happens when you combine overloaded vitamin A, PUFA-rich membranes, sunscreen blocking UV repair pathways, and mitochondrial stress? You get oxidized pigment where you’re supposed to have melanin wisdom.

That was me in my office summers. Eating oxidized fats, blocking healing frequencies, and staring into blue-lit screens wondering why my face felt… off.

So, What Actually Helps?

This is the part where I tell you it’s not fast. This is a long game. But it’s also deeply hopeful—because melasma isn’t a curse. It’s communication.

Here’s what I’m doing now—and what I’d recommend if you’re walking a similar path:

1. Fix the light environment
   Morning sun. No sunglasses. No sunscreen. Red light before blue. Minimize artificial light at night. Basically: reverse engineer how light used to touch your ancestors’ faces.

2. Nourish with saturated fats, not PUFA bombs
   Grass-finished tallow. Butter. Raw milk. Egg yolks. Let your membranes rebuild with fat that can take the light.

3. Support mitochondrial cleanup
   Cold exposure. Natural movement. Adequate sleep. Strategic fasting. Your melanin needs ATP and redox to do its job.

4. Avoid excess vitamin A unless it’s earned
   Get it from food, not synthetic supps. Respect your redox. Respect the sun.

5. Rebuild your solar callus
   This isn’t a tan. This is your skin learning how to speak light fluently again. It takes time.

And How Long Will It Take?

I wish I had a number for you. I’m two pregnancies and many lifestyle shifts in, and I still see those cheekbone marks. But they haven’t worsened. And I know now that every summer I spend in the sun without sunscreen, every bowl of raw cream instead of almond milk, every morning walk instead of screen scroll—that’s a vote for healing.

This isn’t a sprint. It’s a seasonally-aware, mitochondria-first, skin-as-an-interface kind of experiment. And yeah, I might be wrong about parts of it. But I’d rather explore the wrong path consciously than keep repeating the blind one that got me here.

Disclaimer

This isn’t medical advice. It’s a story, a theory, and a work in progress. Melasma has many possible roots—some of which may be medical, hormonal, or genetic. Always consult your own intuition and your trusted practitioner. What I’ve shared here is meant to offer perspective, not prescription.

 

REFERENCES:

• CPC #9: HASHIMOTO’S AND MELASMA – GATEWAY DISEASES

• CPC #32: KRUSE LONGEVITY Rx FOR SKIN – Psoriasis, Rosacea, Atopic Dermatitis, Vitiligo, & Actinic Keratosis

• HYPOXIA #15: BLUE LIGHT CAUSES IRREVERSIBLE HYPOXIA IN ALL CELLS

• MY 2023 CHRISTMAS LIST FOR MY TRIBE

• QUANTUM ENGINEERING #27: WHY SUNSCREEN AND SUNGLASSES ARE HARMFUL

• QUANTUM ENGINEERING #34: OUTING A “LONGEVITY EXPERT” IN MY RECENT MALIBU PODCAST

• QUANTUM ENGINEERING #51: LIPOFUSCIN DEPOSITION IS A DEFECT IN MELANIN

• REALITY #21: 1ST MEXICAN MITOHACK OF 2018