Dietary Fat, Sunscreen & Skin Photosensitivity: Can Seed Oils Promote Sunburn?
The body's sensitivity to the world depends on what you feed it.
Not medical advice
Podcast episodes that informed this article:
M&M 233: Feel the Burn: Seed Oils, Memes & Oxidative Stress | Brian Kerley
M&M 146: Photobiology, Sunlight, Firelight, Incandescent Bulbs vs. LEDs, Mitochondria, Melatonin, Sunscreen & the Optics of the Body | Scott Zimmerman
M&M 221: Regenerative Energy & the Light Inside You | Jack Kruse
Basic Biology of Oxidative Stress & Sunburns
Reactive oxygen species (ROS) are an inevitable consequence of oxygen-based metabolism. Within our cells, mitochondria are the predominant site of oxygen-based energy and ROS production.
Mitochondria in our cells are always producing ROS at some rate, as a natural consequence of oxygen-based metabolism. Evolution has equipped cells with antioxidant systems that can sense ROS production and quench ROS before they do real damage. As long as ROS production does not exceed antioxidant capacity, there’s not much to worry about.
When ROS production exceeds antioxidant capacity, nucleic acids, proteins, or lipids within our cells take on oxidative damage. In short: ROS break stuff. Minor breaks can be repaired. Major damage requires more substantial repairs, with higher energy cost. Dropped a cup of coffee in the kitchen? Annoying, but no big deal—two minutes to clean up. Threw an all-night rager, and people got wild? The next day, your finite energy budget is spent scrubbing floors and spackling drywall, instead of relaxing. With persistent negligence, things can get worse—the kitchen catches on fire, or the house burns down. Do you have insurance? How much does it cover?
(Side note: there are also reactive Nitrogen Species, RONS. We will simply talk about ROS here, but similar ideas apply: highly reactive molecules break stuff if not properly contained.)
All cells have a finite energy budget, and may or may not be well-insured depending on cell type. The greater the level of oxidative stress cells experience, or the lesser the ability to deal with it, the more likely the damage is to exceed the energetic needs of repair and housekeeping mechanisms. And if the repair mechanisms themselves become damaged, what then? This is part of what underlies aging and senescence—cells are functionally compromised and either can’t or won’t rejuvenate. At some point, core mechanisms of repair and rejuvenation are themselves broken. Grandpa has gone senile.
ROS are not all bad, though. Cells use them to do useful work. Consider how people use fire in their homes: to cook food, heat the home, and so forth. When done on purpose, for some utilitarian reason, fire is contained and regulated—you control where and when flames are ignited, with precautionary systems in place (fire extinguisher, etc.) in the event the flames burn out-of-control. Our cells utilize a certain level of burning to do useful work, with systems that can contain the fire—up to a point, that is.
Endogenously produced ROS are not the only source of flames. Small fires can also be ignited by external physical stimuli, such as UV light, toxic chemicals, etc. The surfaces of our body—both the outer surface (skin), and inner surface (gut lining)—are exposed to these things the most. Naturally, they have evolved to deal with such stressors, up to a point. There’s a reason your skin and gut cells regenerate quickly when damaged: they occupy high-risk real estate within the organism.
Our focus here will be on how the skin deals with light stress, and the ways in which materials that we ingest or apply to the skin surface influences skin’s ability to deal with it.
Skin cells have some natural capacity to absorb and utilize light, as well as natural antioxidant capacity to absorb and utilize some level of ROS. The paler your skin is, the lower its capacity to absorb UV, and the more readily oxidative stress is induced. If this happens enough, it triggers an inflammatory response: pro-inflammatory signals are secreted to attract other cells that will clean up debris and tissue damage. When a building is demolished, you first need to clear our the construction site before new construction can be properly executed. This comes with vasodilation (redness), swelling, and so forth.
To put it more concisely: sunburn is a manifestation of oxidative stress in your dermal tissue. The redness, burning sensations, and skin peeling are symptoms arising from “too much” oxidative stress, which eventually drives cell death and inflammation. Luckily, skin cells have “insurance.” The skin peels, but dead cells are quickly replaced. Inflammation makes way for rejuvenation. Melanogenesis (increased melanin production) can also be stimulated, a light-absorbing pigment that acts as a natural sunscreen, enabling you to tolerate more sunlight exposure in the future.
Learn more about mitochondria & oxidative stress:
M&M 70: Mitochondria, Aging, Cellular Energy, Metabolism, Gray Hair Reversal & Brain-Body Communication | Martin Picard
M&M 220: Cell Death, Oxidative Stress, PUFAs & Antioxidants | Pamela Maher
Ultraviolet, Non-UV Light & Oxidative Stress
UV light is a major driver of sunburn, but other wavelengths also contribute to oxidative stress. Longer wavelengths of light, including visible light, penetrate our skin more deeply than UV. If you cover your skin in commercial sunscreens, they block UV wavelengths, enabling you to stay in direct sunlight for longer without your senses tell you to seek shade. And as long as you do, longer non-UV wavelengths penetrate your skin.
Obviously, the more time you spend under direct UV, the more likely your skin is to eventually sunburn. Everyone has a different tolerance level based on things like melanin content, but oxidative stress cannot be completely avoided. No one is totally immune from the sun, despite large differences in tolerance levels.
To repeat: nobody can withstand an arbitrary amount of sunlight, especially intense sunlight, without sustaining tissue damage. There is variation and plasticity in tolerance levels, however, allowing skin to adapt to light conditions, up to a point. The pattern and frequency of sunlight exposures you have modulates informs biological adaptations, such as melanin production, that alter your skins’ propensity to sunburn.
Skin’s propensity for sunburn can change as a function of how much pigment it produces. Does it also change as a function of the fatty acid composition of your lipids?
Let’s briefly review how dietary PUFAs related to oxidative stress, which will help us think about how they might tie into dermal photosensitivity.
Learn more about skin and photobiology:
M&M 104: Benefits & Risks of UV Radiation & Sunlight, Skin Health, Vitamin D, Nitric Oxide, Evolution of Skin Color | Richard Weller
M&M 146: Photobiology, Sunlight, Firelight, Incandescent Bulbs vs. LEDs, Mitochondria, Melatonin, Sunscreen & the Optics of the Body | Scott Zimmerman
Dietary PUFAs, Oxidative Stress & Skin Photosensitivity
Like other cells, skin cells have a phospholipid bilayer membrane filled with fatty acids. The fatty acids vary in length and degree of saturation. In any given tissue there is some distribution of fatty acids in lipid membranes. Diet is an important factor influencing the specific fatty acid profile that membranes have.
Polyunsaturated fatty acids (PUFAs) are inherently easier to oxidize than monounsaturated or saturated fatty acids, which makes them more sensitive to ROS. More carbon-carbon double bonds means higher ROS sensitivity. The higher the PUFA concentration in your cell membranes, the more likely they are to “light on fire” if ROS levels exceed antioxidant capacity and start reacting with membrane lipids.This can ultimately drive forms of cell death (e.g. ferroptosis).
The idea is that higher PUFA concentrations in your skin cell membranes make you more sensitive to sunburn. If there’s less dry kindling to burn, your cells will be able to tolerate more “small fires” ignited by UV light before the house burns down (skin cells die). Eventually, if skin cells are exposed to enough UV light, they’re just going to burn no matter how high your tolerance level is. The question is how much they can tolerate.
That’s the idea, anyway. But is it true in practice? And significant enough for your sunburn propensity to noticeable change with a dietary shift?
Does changing the fat you put into your body actually affect your sensitivity and tolerance to sunburn? Some say that it does and that by minimizing seed oil consumption you decrease your sensitivity to sunburn and therefore tolerate more sun exposure before burning. The less dry kindling in your membranes, the more energy it takes to light the house on fire. Others find this idea preposterous.
Before directly examining the question of whether dietary PUFAs from seed oils can affect dermal photosensitivity and sunburn potential, let’s look at how other substances impact skin photosensitivity, either when put on the skin surface or ingested. This will give us a sense for what’s possible and the ways in which our skin’s photosensitivity can be changed. We will consider:
Natural “sunscreens” like melanin in relation to tanning and sunburn.
Topical commercial sunscreens in relation to light absorption and oxidative stress.
Prescription drugs and food components that change skin photosensitivity.
Effects of topical cholesterol and PUFAs on skin photosensitivity.
With an understanding how all these things relate to light absorption, oxidative stress, and dermal photosensitivity, we will be in a better position to reason about whether changing your dietary fat intake is likely to impact your skin’s light sensitivity.
Let’s start with the basics on skin plasticity and melanin production to help us think about how and why our skin’s photosensitivity can change in response to the physical environment.
Learn more about PUFAs, lipid peroxidation, and cell death:
Podcast | Cell Death, Oxidative Stress, PUFAs & Antioxidants | Pamela Maher
Article | PUFAs & The Palisades: Lipid Peroxidation, Oxidative Stress & Cell Death
Basics of Melanin Biology & Skin Plasticity
The amount of melanin in one’s skin and hair sets limits on how much direct sun exposure of a given intensity one can tolerate before detrimental outcomes manifest. Approximations for the major skin and hair color types of humans:
In simplified terms, the basic way compounds like melanin or those found in chemical sunscreens work is that, based on chemical structure, they are able to absorb photons within a certain range of wavelengths (colors). Notice that the structure of melanin contains conjugated rings with multiple double-bonds:
Chemical structures like this have electrons that can be excited by photons, enabling the molecule to capture light. The key thing here is simply that the melanin concentration of skin effectively determines “UV tolerance,” which is basically how much UV you can handle before oxidative damage begins to “overflow” beyond what antioxidant systems can handle. The more melanin in your skin, the less oxidative stress per unit time in sunlight, because some of that UV will be absorbed by melanin instead of causing direct damage or generating reactive oxygen species (ROS).
(Note: Sunlight can also stimulate antioxidant production, not just oxidative stress. The pattern and intensity of wavelengths matters. For example, red and near-infrared light can stimulate mitochondria function the body, as these wavelengths penetrate beyond the skin. This can influence things like melatonin production, which is a potent natural antioxidant. See M&M 146.)
Melanin in human skin primarily exists as eumelanin and pheomelanin, with eumelanin being the dominant form in most people. Each is synthesized from amino acid precursors:
Eumelanin: A brown-black pigment, highly effective at absorbing UV radiation, providing photoprotection. It is the primary contributor to darker skin tones.
Pheomelanin: A reddish-yellow pigment, less effective at UV absorption, found in higher proportions in lighter skin and red hair. It may contribute to UV-induced damage due to its photochemical properties.
Melanin is synthesized by melanocytes in the epidermis and stored in organelles called melanosomes, which are transferred to surrounding keratinocytes. The size, number, and distribution of melanosomes influence skin pigmentation.
A diagram to help you appreciate the complexity of pathways linking UV exposure and DNA damage to ROS production and melanin synthesis.
The melanin absorption spectrum is broad, spanning UV, visible, and near-infrared, with stronger absorption at shorter wavelengths. By absorbing external UV light, melanin can protect skin by:
Dissipating UV energy as heat, reducing DNA damage.
Scavenging reactive oxygen species (ROS) generated by UV.
Eumelanin is more efficient at photoprotection than pheomelanin. Pheomelanin can actually elevate ROS production, triggering things like lipid peroxidation or DNA damage. This why red-headed individuals are very sensitive to light-induced oxidative skin damage, as they produce higher levels of pheomelanin compared to eumelanin.
Getting intermittent sunlight exposure such that eumelanin is boosted results in greater sun tolerance. Increased melanin levels mean that more UV will be absorbed and dissipated rather than doing direct damage. Melanin also scavenges ROS, helping prevent them from doing damage or triggering lipid peroxidation in cell membranes which would generate more toxic molecules. As a result, a given amount of direct sun exposure produces less overall oxidative stress than it would for someone with lower eumelanin levels (all other things being equal).
That much should be intuitive. Now ask yourself: what other biological “knobs” can be changed in our cells to decrease light-induced oxidative stress, other than boosting melanin levels? In other words, what else would lower the overal oxidative stress burden of a light-exposed cell?
(Hint: if there’s lower PUFA density in cell membranes, fewer toxins can be produced from lipid peroxidation—less “flammable material” will be lying around, so ROS will have lower odds of setting the house on fire).
Skin’s ability to change melanin levels in response to sunlight exposure enables our sunlight sensitivity, including sunburn propensity, to change in response to environmental conditions. Melanin is basically a natural sunscreen produced within the skin. In comparison, how to artificial sunscreens applied to the skin surface work?
Artificial Sunscreens: Do they Enable More Oxidative Stress in Skin?
Artificial sunscreens come in two general varieties. “Chemical sunscreens” contain molecules that absorb UV photons; “physical sunscreens” contain minerals that reflect photons. Many natural biomolecules can absorb photons as well. The most famous in this regard is melanin (discussed above).
Light-absorbing molecules often contain multiple aromatic ring structures. For our purposes here, just know that light absorption depends on chemical structure, and aromatic ring structures tend to be good at this. A diagram showing how oxybenzone, a common commercial sunscreen molecule, absorbs UV light:
Here’s the thing: most popular chemical sunscreens only block a narrow band of sunlight from your skin, mostly just UV. At first blush, that might not seem problematic. After all, UV light can be mutagenic to DNA, induce oxidative stress, and eventually result in sunburn. While true, many overlook that non-UV light can also induce oxidative stress.
In essence, commercial sunscreens help prevent you from UV-induced sunburns, allowing you to stay in strong, direct sunlight for longer. In doing so, your skin is exposed to more sunlight overall, including oxidative stress-inducing wavelengths that your sunscreen does not block.
End result: it’s possible to generate as much or more overall oxidative stress while wearing sunscreen and staying in direct sunlight for long periods, despite blocking UV photons. I discussed this with a photobiology researcher on M&M 146:
Scott Zimmerman: In [classic] work by Zastrow, who was in the cosmetics industry, he measured the amount of free radical generation as a function of wavelength throughout the visible spectrum and into the near-infrared. Some modern sunscreen is mainly [blocking] UVA, UVB, and UVC, and then there’s a cutoff.
What Zastrow showed was that, if you take skin and measure the free radicals, with exposure to the UV portion of the light spectrum, you get X [some amount of free radical production]. If you then take skin, block UV but exposing it to visible light, you get X again. There’s equal amounts of free radicals being generated from the visible light.
So what ends up happening when people use sunscreen? [It mostly blocks UV light,] the portion that actually gives you sunburn, which would tell [your senses], “Hey dummy, it’s time to get out of the sun.” Well, now you block that and you stay outside longer, increasing your exposure to the visible portion of the spectrum.
NJ: And that’s also generating oxidative stress. So is what you’re saying that most sunscreens actually make it easier for people to expose themselves to more overall oxidative stress because they can stay out in the sun for longer?
SZ: Yes.
Note: The reason many commercial sunscreens don’t block out a wider band of light is that doing so would cause your skin to be colored when you apply it. Covering yourself in mud works, for example, but nobody wants to do that. Even mineral sunscreens that leave a visible white residue often turn people off. Hence, the multibillion-dollar commercial sunscreen industry is geared towards chemical sunscreens that block narrow bands of sunlight and aren’t visible to the eye, driven by consumer spending patterns.
Here is an excerpt from some of the research done by Zastrow et al., referred to above:
In the absence of sunburn as an unmistakable warning, applicants use to over-exposing themselves to solar radiation, sometimes up to 10 times longer. As the standard commercial sunscreens, however, provide no protection in the VIS/IR spectral region, the free radicals being formed in this spectral region can easily overcome the critical radical concentration (FRTV). Thus, it is not surprising that skin cancer incidence is still rising although the use of sunscreens exhibiting high SPF values has become increasingly popular.
Knowing this, the following fact, often overlooked and usually surprising to people, should make sense: melanoma, the most deadly form of skin cancer, is not actually linked to sunlight exposure. Many, including dermatologists, presume that it is. The evidence is thin. The more common and far less deadly form of skin cancer, basal cell carcinoma, is correlated with UV/sunlight exposure, but you might be surprised at what the data actually shows for other skin cancers, especially for melanoma. A short excerpt from this excellent article:
What’s critically important to understand about melanoma is that while it’s widely considered to be linked to sunlight exposure—it’s not. For example:
Patients with solar elastosis, a sign of sun exposure, were 60% less likely to die from melanoma.
Melanoma predominantly occurs in areas of the body with minimal sunlight exposure, unlike SCC and BCC, which are linked to sun-exposed regions.
Outdoor workers, despite significantly higher UV exposure, have lower rates of melanoma compared to indoor workers.
Many sunscreens contain toxic carcinogens (to the point Hawaii banned them to protect coral reefs). Conversely, existing research indicates widespread sunscreen use has not reduced skin cancer rates.
•A mouse study designed to study malignant melanoma found mice kept under simulated daylight develop tumors at a slower and diminished rate compared to those under cool white fluorescent light.
There has been a significant increase in many areas from melanoma, something which argues against sunlight being the primary issue as it has not significantly changed in the last few decades. For instance, consider this data from Norway’s cancer registry on malignant melanoma.
Here is the data from that last bullet point, showing that melanoma deaths have been either flat or increasing for decades, depending on age group. Keep in mind that since the mid-1900s people have been spending more time indoors overall, and buying more and more sunscreen products, over this entire interval. The data comes from Norway, where it is known there has been no increase in UV radiation in this timespan.
I can’t find sunscreen data going back to the mid-20th century, but sales patterns since the 2000s, industry projections, and common sense all point to the same basic observation: commercial sunscreen use has increased ever since they were invented, and the trend is likely to continue.
Perhaps we’ve forgotten that humans, like other creatures, have had to manage their sunlight exposure for a hell of a lot longer than commercial sunscreens have been available for purchase. How do animals, including humans, regulate sun exposure under natural conditions? Well… they use their senses, including the largest sensory organ of the body: skin. In fact, our species evolved to be largely hairless, which has probably given us especially sensitive skin-based sensory abilities.
Modern humans have scrambled our ability to use this exquisite sensory system by covering it up with chemicals. Should you look to the future, and keep relying on the newer, “better” product innovations? Or should you look to the past, and come back to your senses?
Under pre-industrial conditions, humans in traditional societies had a couple of basic, common sense options for dealing with intense daytime sun:
Make intermittent use of shade when your senses tell you to (skin gets hot, starts to turn red).
Cover yourself in mud or something, or wear breathable sun-blocking garments.
Today, the “official” strategic advice from medical institutions is that the best approach to human-sunlight interaction is the minimize direct contact of your bodily surfaces with sunlight, at all times and at all costs. Alternative viewpoints are expressed in the two podcasts below. For our purposes in this article, just keep in mind that commercial sunscreens do not block all wavelengths—even with sunscreen, you will still be experiencing some level of oxidative stress in the skin.
To learn more human photobiology and the effects of sunlight:
M&M 221: Regenerative Energy & the Light Inside You | Jack Kruse
M&M 146: Photobiology, Sunlight, Firelight, Incandescent Bulbs vs. LEDs, Mitochondria, Melatonin, Sunscreen & the Optics of the Body | Scott Zimmerman
If your use of sunscreen causes you to stay in intense, direct sunlight for far longer stretches of time than you would otherwise, then you may very well be taking on more overall oxidative stress within your tissues over time, compared to if you used natural sensory feedback and intermittent sun-shade-seeking, rather than multi-hour stint of direct sun exposure while wearing. sunscreen.
So, applying certain molecules to the body’s outer surface can modulate photosensitivity and “sun tolerance,” as does changing the concentration of light-absorbing molecules like melanin within the skin.
What about molecules you absorb into your body? As it turns out, certain medications and food components can affect skin photosensitivity.
Prescription Drugs, Food Components & Skin Photosensitivity
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