Sunlight has shaped our biology in profound ways, from the structure of our skin to the signals embedded deep in our hormonal and cellular systems. To explore how evolutionary shifts in our light environment affect UV protection and biological adaptation, we spoke with our Chief Science Officer, Dr. Alexander Wunsch, MD, PhD, a leading expert in photobiology and light medicine. 

In this follow-up conversation, Dr. Wunsch explores how early human exposure to forest-filtered light, our loss of visible body hair, and the development of erythema as a biological alarm system all influence how we interact with solar radiation today. The discussion extends from evolutionary adaptations to modern-day strategies for UV defense, including insights on the solar callus, the limits of artificial shade, and  how technologies like BlueSync represent a new frontier in light modulation. 

 

Ra Optics: To start off, let's talk about our evolutionary history. Would it be accurate to say that throughout evolution, we spent the majority of our time in green, forest environments?

 

Dr. Alexander Wunsch

Yes, that's a fair assumption. We can deduce this from the characteristics of our visual reception systems, which align closely with what we see in primate eyes. Most of what we understand about human vision, especially concerning blue light hazard, comes from research on primates like macaques. These studies were ethically permissible in primates, unlike in humans.

One interesting hypothesis is that our visual sensitivity, represented by the V-lambda curve, may have developed in response to the chlorophyll-dominated environments in which our ancestors lived. This makes intuitive sense when you consider the spectral characteristics of forest light.

A key difference between us and primates is our lack of visible body hair, which is significant in terms of UV protection. While we technically still have millions of hair follicles, most are no longer photobiologically active or visible. They no longer offer pigment related protection against sunlight. However, they do retain functionality related to accessory hormonal activity, which is particularly relevant when it comes to UV exposure.

Ra Optics: That’s an important point, especially considering that the chlorophyll spectrum no longer surrounds most people today. Instead, we live among concrete, glass, and reflective surfaces that alter our light environment. Given this shift, how exactly do these remaining hair follicles protect against UV light in a hormonal way?

 

Dr. Alexander Wunsch

To understand that, I recommend making excerpts of Kellogg's "Light Therapeutics" publicly available. It highlights crucial concepts, such as the fact that UV light casts no shadow. Kellogg emphasized that using light therapeutically means contending with many diseases. Sometimes, a therapeutic strategy involves challenging the system maximally, akin to the body hitting reset during a high-stress event like sunburn. But this is a high-risk intervention.

Historically, people were even executed using sunlight. In the Middle Ages, individuals were exposed on sun towers with no shade, and after a few hours of intense solar radiation, death ensued. Sunlight is potent and dangerous without protection.

The body’s first protective reaction against intense, unprotected sun exposure is erythema, skin reddening. But there are two types: thermal erythema, which cools the tissue, and phototoxic erythema, induced by UV-driven photoproduction of reactive oxygen species. The latter typically occurs a few hours after exposure. It's not merely increased blood flow; in cases of UV overdose, blood and even erythrocytes leak into the extracellular matrix to protect deeper layers.

Consider the foundational work of Niels Finsen, who received the Nobel Prize in 1904 for his pioneering research in photobiology. At that time, researchers lacked advanced tools like electron microscopy and had to rely on optical microscopy. Despite the limitations, they sought to understand physiological reactions to light in straightforward, tangible ways.

For example, one can create an effective UV radiation filter by adding a few drops of blood into a bottle of water and shaking it. Hemoglobin in the blood significantly absorbs UV radiation, making blood an efficient UV filter. This property explains why we experience erythema (skin reddening) after UV exposure.

In cases of UV overdose, not only does blood flow increase, but erythrocytes can leak from capillaries into the extracellular matrix. This response acts as a potent first-line defense to protect deeper tissue layers. Key players in this process are sunburn cells, swollen or disrupted keratinocytes in the epidermis, which release substances that trigger inflammation in the dermis.

The epidermis, lacking blood vessels, can vary in thickness depending on skin location. In dark-skinned individuals, the palms and soles are typically lighter because reduced melanin production in these areas is compensated by a thickened epidermis that effectively attenuates short-wavelength UV radiation.

Keratinocytes and mast cells have evolved to secrete signaling substances that induce and control erythema in the papillary dermis, where protective structures housing nerve fibers and capillary loops reside. These reactions are primarily triggered by short-wavelength UV; mainly UVB and, in artificial settings, UVC.

In natural sunlight, we are exposed only to UVB and UVA, with erythema largely driven by the UVB portion of the spectrum. Now, consider this question: how much more UVA radiation is required to induce erythema compared to UVB?

The answer is striking—it takes 500 to 1,000 times more UVA to produce the same erythema effect as UVB. This dramatic difference once led researchers to underestimate UVA's relevance. However, it is now understood that while UVB damage is rapid and obvious, usually over a 24-hour period, UVA’s effects accumulate over decades contributing significantly to long-term damage.

UVB-induced sunburn is a delayed response; by the time it becomes noticeable, excessive exposure has already occurred. That’s why our bodies developed proactive adaptations, like increased erythema receptivity in spring for populations far from the equator. This early warning prepares the skin for higher solar intensity in summer.

So, in healthy individuals, how much blood can be directed into the dermal capillaries as part of this protective response? Surprisingly, up to 60% of total blood volume can enter the dermal capillary system in extreme cases, risking circulatory shock. The catecholamines, the stress hormones like adrenaline and cortisol help mitigate this risk, cortisol by reducing inflammation, and others by maintaining blood pressure.

Crucially, these hormones are not only produced in the pituitary gland. Each hair follicle, even the invisible ones, can produce these hormones: catecholamines, glucocorticoids, mineralocorticoids, and melanocyte-stimulating hormones. This is why the hair follicle is still a functional player in our defense system.

Ra Optics: It sounds like erythema is a protective mechanism our body uses against UVB, but as you’ve described, it can also be quite harmful due to the massive influx of blood into the dermis, which risks circulatory imbalance. So ideally, we would want to avoid reaching that point altogether. What would be the best forms of protection to prevent this kind of overexposure? Could you walk us through the range of protective strategies—from building a biological defense like a solar callus, to environmental approaches such as seeking shade? And finally, how does BlueSync factor into this picture of UV protection?

 

Dr. Alexander Wunsch

First, it's essential to understand, there is no shade for UV. This is a core message from Light Therapeutics. Many assume that sitting in the shade is sufficient protection from ultraviolet radiation, but that’s not the case. While shade can block visible light, UV radiation still reaches you because it scatters and reflects from all directions.

Ra Optics: But surely there’s still a reduction in UV compared to standing in direct sunlight?

 

Dr. Alexander Wunsch

Yes, but it depends on the type of shade. If you’re under a dense leaf canopy, such as in a forest, you do get some significant shielding from UV. However, typical artificial shade, like an umbrella or the side of a building, doesn’t offer the same protection. In those scenarios, UV exposure is still relevant. 

Ra Optics: So if I’m standing under a complete tree canopy with the sun directly overhead, am I still significantly exposed?

 

Dr. Alexander Wunsch

While chlorophyll-rich plant canopies can reduce UV radiation by more than 90% due to pigment absorption and surface scattering, most artificial shade structures—such as umbrellas, canopies, or open mesh fabrics—typically offer a UVB reduction in the range of 60 to 90%, depending on the material, color, weave, and presence of UV-stabilizing coatings.

Ra Optics: And in a dense forest, could it be more like 95 percent or even higher?

 

Dr. Alexander Wunsch

Even up to 99%. But I’m cautious about assigning exact numbers. First, I’d need to consult the data. Second, it varies greatly depending on the environment. When people hear numbers like that, they often misuse them, thinking they’re universally applicable.

 

UVB Reduction by Shade Type – Comparative Table

Table 1. UVB Percent Reduction by Shade Type
Natural canopies, UV-stabilized materials, and solid barriers block most UVB (>90%), while lighter fabrics, umbrellas, and mesh structures allow significantly more exposure.

 

So the real takeaway is this: as long as you're outside during daylight hours, you should be aware of the presence of UV radiation. And in some cases, being indoors doesn’t help much either. For example, modern windows block UVB but still allow in about 80% of UVA. The problem here is that the UVB, which provides signaling effects critical for protective adaptations, is removed, while the aging and damaging UVA still reaches you.

The UVB transmission through standard glass is very low, while UVA passes through much more readily.

 

Table 2. UV Transmission and Blocking by Ordinary Soda-Lime Glass
Standard soda-lime glass blocks most UVB radiation but transmits substantial UVA.

 

Only special laminated, tinted, or UV-coated glass significantly reduces UVA.

 

Updated Table Entry for Car Window:

Table 3. Transmission and Blocking of UV Radiation by Ordinary and Treated Glass 

Ordinary glass blocks most UVB radiation but transmits a large portion of UVA. Only UV-treated or laminated glass provides substantial UVA protection.

 

Five hours behind a window can give you the equivalent of a four-hour UVA dose, contributing to premature skin aging, wrinkles, solar elastosis, and actinic keratosis.

The crucial point is that our long-term UV protective mechanisms are not only driven by hormones. They are also based on cellular adaptations, such as the development of a solar callus. 

 

Dr. Alexander Wunsch

But what does it really mean to build up a solar callus?

At the base of the epidermis, in the basal membrane, we have basal cells, essentially stem cells, that continually generate new keratinocytes. This is because the primary role of the epidermis is to defend against ultraviolet radiation, and it is biologically equipped to do so.

Now, when new keratinocytes are needed, how are they formed? Through cell division. It is the only way cells multiply. And with each round of division, what do we get? A thicker epidermis, more layers of living keratinocytes, and ultimately, a buildup of corneocytes, the outermost, dead skin cells.

The transition from keratinocyte to corneocyte is a form of pre-programmed deactivation. It resembles apoptosis but is not quite the same. In true apoptosis, the cell is entirely dismantled without harming neighboring cells. Here, we see the metabolic shutdown of a once-active keratinocyte as it transforms into a protective barrier.

There is a common misconception in dermatology. Some believe they can assess UV damage by counting DNA strand breaks in keratinocytes. But this view overlooks an essential function of that DNA. Even in cells destined to become corneocytes, the DNA continues to serve as a potent photoprotective agent. It can absorb ultraviolet radiation and convert it almost instantaneously into harmless molecular heat, much like melanin.

So in the epidermis, we have two primary systems for photoprotection: degrading DNA and melanin, particularly eumelanin. Both play critical roles in shielding underlying tissues from UV damage.

And how long does a keratinocyte live?

Generally, four to six weeks from its creation in the basal layer to its shedding as a corneocyte. However, problems arise when keratinocytes live too long or are not properly shed. If they sustain UV-induced damage and do not undergo adequate repair, they can become problematic, potentially even malignant.

Another important factor is that increasing the number of keratinocyte layers also means increasing the number of cell divisions in the basal layer. And with each division, telomeres, the protective caps on our chromosomes, shorten. Once they become critically short, the likelihood of errors in DNA replication increases, particularly in the genes responsible for repairing DNA. This is how the risk of malignant transformation rises.

This regenerative adaptation was likely sufficient for early humans with lifespans of 20 to 30 years. But in today’s world, where we often live into our 60s, 70s, 80s, or beyond, cumulative UV damage presents a greater concern.

I can often tell, just by looking at some of my friends, whether they were sun worshippers in their youth. Their skin reflects the story. This is not to say that everyone who spent time in the sun will age prematurely. Some individuals have better genetic “tools” than others.

 

Ra Optics: When you say “tools,” are you referring to things like DNA repair mechanisms?

Dr. Alexander Wunsch 

Precisely. DNA repair capabilities, the balance between eumelanin and pheomelanin, and other genetic variants that influence resilience to UV. Some people in their twenties already show signs of advanced skin aging, while others appear far younger than their chronological age. But outward appearance does not always reveal what is going on inside. The capacity to repair or buffer damage varies from person to person.

Suppose someone is already dealing with illness and wants to leverage sunlight therapeutically. In that case, they can afford to tap into their repair reserves, but this has to be done cautiously and with guidance. For instance, Auguste Rollier understood how to do this effectively. He knew how to guide his patients through safe, individualized heliotherapeutic practices.

This is why simplistic recommendations are so dangerous. UV-induced biological mechanisms exist not because UV is inherently good, but because it is a potent environmental stressor. The adaptations we see, like the solar callus or vitamin D synthesis, are survival strategies in response to that threat.

 

Ra Optics: I think we've made it pretty clear how UV light can be biologically damaging, especially in the absence of proper protection. With that context in mind, where does BlueSync fit into this picture? Why is it a solution?

Dr. Alexander Wunsch

To understand this, let’s look at the concept of melanopic efficacy. The alphaopic daylight efficacy ratio is set at 1, which means standard daylight has a baseline influence on melatonin suppression. BlueSync, by comparison, has a melanopic efficacy ratio of 1.3.

 

Ra Optics: So BlueSync increases the potential to suppress melatonin?

Dr. Alexander Wunsch

Exactly. If you were to put on typical blue-light blocking glasses, your melanopic efficacy would drop drastically, possibly down to 0.01. But BlueSync, instead of blocking, selectively modulates. It enhances the effect of light on melatonin suppression by about 30% beyond natural daylight.

 

Ra Optics: And what does melanopic efficacy mean in practical terms?

Dr. Alexander Wunsch

It refers to the ability of light to suppress melatonin, which is critical for regulating circadian rhythm. Suppressing melatonin during the day is necessary for alertness and proper biological signaling. But this is only one side of a broader physiological system.

Melatonin suppression does not happen in isolation. On the other side, we find the activation of the pituitary gland and all of the POMC-derived hormones. This includes stress hormones like catecholamines, cortisol, and mineralocorticoids. 

 

Ra Optics: So melatonin suppression by BlueSync leads to the upregulation of stress hormones?

Dr. Alexander Wunsch

Yes, in a controlled way. Stress hormones are not inherently bad. Without them, we could not function. We would not even be able to get up in the morning. But the key is balance. 

 

Ra Optics: So BlueSync needs to be understood not as a blocker, but as a modulator?

Dr. Alexander Wunsch

Precisely. If you block all blue light, both harmful and beneficial, you create a non-physiological situation. Instead, BlueSync reduces the harmful blue light, specifically high-energy visible light (HEVL), by about two thirds, while reducing the beneficial, chronobiologically significant blue light by only one-third. This makes it a smart, soft modulation.

Dynamic lighting systems often increase the total amount of blue light indiscriminately. For about 40 percent of the population, this can cause problems. With BlueSync, we maintain the circadian signaling by enhancing the spectral quality, not by simply increasing intensity.

This is confirmed by the increase in melanopic efficacy. Daylight is considered to be at 100 percent. With BlueSync, melanopic efficacy rises to 130 percent, while the total intensity of blue light, both beneficial and harmful, is actually reduced.

 

Ra Optics: That seems paradoxical.

Dr. Alexander Wunsch

It does, and that’s why it can be difficult to explain. You're achieving two things at once: enhanced biological signaling with reduced overall exposure. In lighting design, this is already recognized. For example, certain biological effects achieved in sunlight with 50,000 lux can also be achieved with only 1,000 or 2,000 lux in artificial lighting if the spectral composition is optimized.

In the past, the goal was to increase lux. But energy regulations restricted this, so lighting designers started increasing the blue portion of the spectrum. There is even research showing that office workers adjusted their internal clocks more to the lighting indoors than to the brighter, full-spectrum light outside.

 

Ra Optics: So BlueSync achieves similar internal clock alignment, but more safely?

Dr. Alexander Wunsch

Yes. We are altering the relative spectral composition to favor melanopic efficacy, rather than simply increasing blue light indiscriminately. That’s the intelligent approach. It’s a nuanced balance, modulating the spectrum while maintaining biological efficiency. And this is where BlueSync provides a truly meaningful solution.

 

Takeaways 

Our discussion with Dr. Wunsch underscores the intricate interplay between light and biology. From erythema and melanocyte signaling to solar callus formation and telomere shortening, evolutionary adaptations have long helped us cope with solar radiation. But modern environments—full of artificial shade, reflective surfaces, and filtered sunlight—demand a new level of awareness.

Enter BlueSync: a next-generation solution that doesn't only block light but selectively modulates it. By enhancing melanopic efficacy while reducing total blue light exposure, BlueSync supports alertness, circadian alignment, and hormonal balance more intelligently than conventional lighting or blue-blocking glasses. In this nuanced dance between protection and performance, it's not about eliminating stressors like UV or blue light, but understanding and harnessing them wisely.