The Anthropology of Light and Darkness — Why I Deliberately Go Out Into the Sun, and Why This Is Not a Matter of Personal Preference but of Biological Necessity

Why I Deliberately Go Out Into the Sun, and Why This Is Not a Matter of Personal Preference but of Biological Necessity

I was nursing my morning coffee the way you do when the world is still quiet and your thoughts have room to move, and I was turning over a question that has stayed with me for years, a question that sounds simple but isn’t. Why are diseases increasing that barely existed in this form across the evolutionary history of our species? Why are we seeing a concentration of metabolic disorders, chronic inflammation, autoimmune conditions, sleep disruption, depression, and neurodegenerative processes at a rate that genetic drift alone cannot explain, a rate that coincides temporally with a radical change in human environmental conditions?

Conventional medicine delivers precise partial answers to many of these conditions. It describes molecular mechanisms, genetic predispositions, and biochemical signaling pathways with a detail that would have been unimaginable a generation ago. What it rarely answers is the more fundamental question of what has changed so profoundly in the human environment that the organism is coming under increasing pressure. When you follow that question through to its conclusion, you arrive inevitably at a factor so obvious and so ubiquitous that it has been almost systematically overlooked in medical discussion.

Light. More precisely: the relationship between light and darkness, the timing of each, the spectrum, the intensity, and the fact that we as a species have completely inverted this relationship within a historically brief period of time.

Homo sapiens Is Not an Indoor Organism

The human being did not evolve under artificial light. That sentence sounds banal, and that is precisely the problem, because it is not banal. Homo sapiens is a biological system that developed over hundreds of thousands of years under open sky, whose physiology, hormonal systems, and neural processes did not arise by accident but through direct adaptation to an environment defined by a clear and unchanging rhythm, namely daylight and darkness. This rhythm was not variable, not optional. It was constant and compulsory: bright morning light, daylight on the skin, decreasing brightness in the evening, complete or near-complete darkness through the night.

This alternation was not background scenery. It was the control signal. Light determined when hormones were released, when the body was active, when it regenerated, and when cellular repair processes ran that were not possible under daytime light conditions. The retina functioned not only as a visual organ but as a precise sensor for time and season. Through specialized ganglion cells that use melanopsin as their photopigment and respond exclusively to short-wavelength blue light, the suprachiasmatic nucleus of the hypothalamus is synchronized, the biological pacemaker that coordinates virtually all physiological processes from cortisol secretion to core body temperature to immune activity.

Today the human being spends the overwhelming majority of waking life indoors. Daylight is filtered through glass, altered in its spectrum, and substantially reduced in intensity, because a typical office workstation delivers 200 to 500 lux, while outdoor daylight even on cloudy days reaches 10,000 to 25,000 lux and on clear summer days exceeds 100,000 lux, a difference that is biologically anything but trivial. At the same time, we are permanently exposed to artificial light at night, whose spectrum, particularly the high proportion of short-wavelength blue light from modern LED technology and all display-based devices, covers exactly the portion of the light spectrum that has the strongest influence on the circadian system.

The result is a systemic inversion. The day is spent in relative darkness, the night is artificially illuminated, and the biological system calibrated over thousands of years to the contrast between the two loses its primary time-giver.

88,000 People, 13 Million Hours, and an Alarming Finding

How severely this inversion actually shortens life was demonstrated by a prospective study from 2024 that has received far less public attention than its methodological rigor and its findings deserve. Windred and colleagues at Flinders University and Monash University in Melbourne analyzed light exposure data from 88,905 participants in the UK Biobank, each of whom wore wrist-mounted light sensors for one week, generating approximately 13 million hours of measured personal light exposure, and then followed these individuals for an average of eight years (Windred, D. P., et al., 2024, Brighter nights and darker days predict higher mortality risk: A prospective analysis of personal light exposure in >88,000 individuals, Proceedings of the National Academy of Sciences, 121(43), e2405924121).

The result was unambiguous. People with high nighttime light exposure combined with low daytime light exposure showed a significantly elevated mortality risk, and the circadian disruption model calculated from the light data explained a substantial portion of this risk. The association was particularly pronounced for cardiovascular and cardiometabolic causes of death. Exposure modeling confirmed that myocardial infarction, stroke, and type 2 diabetes were more common among people with chronically inverted light-dark patterns, independent of other lifestyle factors.

That nighttime light exposure produces circadian disruption was already established. That this disruption is measurably associated with shortened lifespan, at a magnitude that claims clinical relevance, is a finding that has not yet reached preventive medicine practice. A Swedish cohort study with more than 29,000 women had already shown that sun avoidance increased mortality to a degree comparable to smoking, with the decisive difference that the association ran in the opposite direction, not as a risk factor for a harmful behavior, but as a protective factor whose absence becomes pathological (Lindqvist, P. G., et al., 2016, Avoidance of sun exposure as a risk factor for major causes of death: A competing risk analysis of the Melanoma in Southern Sweden cohort, Journal of Internal Medicine, 280(4), 375-387). Anyone skeptical of this conclusion should consider that the mechanisms through which this effect operates are now substantially better understood than they were a decade ago.

The Narrowing of Sunlight to Vitamin D Was a Category Error

A narrative has established itself over years that treats sunlight primarily as a vitamin D source and explains its health significance almost exclusively through this one mechanism. This view is not wrong, but it is incomplete in a way that has real consequences for how prevention recommendations are formulated.

Vitamin D genuinely plays an important role in immune function and bone metabolism. That supplementation reduces the risk of acute respiratory infections, particularly in people with severe deficiency, is well established (Martineau, A. R., et al., 2017, Vitamin D supplementation to prevent acute respiratory tract infections: Systematic review and meta-analysis of individual participant data, BMJ, 356, i6583). That vitamin D supplementation reduces autoimmune disease was also shown in a 2022 randomized trial (Hahn, J., et al., 2022, Vitamin D and marine omega-3 fatty acid supplementation and incident autoimmune disease, BMJ, 376, e066452). The evidence is solid.

But it does not answer the decisive question of whether vitamin D is the causal factor or whether it functions partly as a marker for something more comprehensive. People with high vitamin D levels are frequently people who spend regular time outdoors. In doing so, they expose themselves not to a single active compound but to a complex spectrum of electromagnetic radiation that encompasses, alongside UV-B light, UV-A light, visible light across all frequencies, and infrared radiation, and there are good reasons to believe that each of these components produces its own biological effects that cannot be replicated by swallowing a vitamin D capsule.

The most compelling evidence for this comes from a direction one might not initially expect, namely the cardiovascular system and a molecule that is not vitamin D.

Nitric Oxide: The Secret in the Skin’s Reserve

The skin is not a passive organ. It is the largest organ in the human body, and it contains large stores of nitric oxide precursors, particularly S-nitrosothiols and nitrites, that are released upon UV-A irradiation and exert direct cardiovascular effects entirely independent of vitamin D.

Liu and colleagues demonstrated in a controlled experiment as early as 2014 that brief UV-A exposure produced a measurable and statistically significant reduction in blood pressure, combined with an increase in circulating nitrites and improved blood flow in forearm vessels, and that these effects were not associated with any change in vitamin D levels, unambiguously attributing the mechanism to nitric oxide (Liu, D., et al., 2014, UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase or prostanoids, Journal of Investigative Dermatology, 134(7), 1839-1846). A 2023 review confirmed that UV radiation reduces the risk of cardiovascular and metabolic disorders through NO-dependent mechanisms, including hypertension, obesity, and type 2 diabetes, and that these effects exceed vitamin D as the sole explanatory factor (Quan, Q.-L., et al., 2023, Impact of ultraviolet radiation on cardiovascular and metabolic disorders: The role of nitric oxide and vitamin D, Photodermatology, Photoimmunology and Photomedicine, 39(6), 573-581).

This is not a footnote. It is a standalone mechanism that explains why populations who regularly spend time in sunlight have not only better vitamin D status but also lower blood pressure, fewer heart attacks, and a differently calibrated immune system. And it is a mechanism that oral supplementation cannot replicate, because the NO is released from skin stores that require UV-A irradiation. You cannot swallow your way to this effect.

What Red Light Does Inside the Mitochondrion

The second mechanism that conventional sun protection discourse ignores entirely concerns a different part of the solar spectrum: red and near-infrared light, the spectral range between approximately 630 and 900 nanometers, which accounts for the majority of solar energy reaching the earth’s surface and which the human eye perceives as deep red or not at all.

Within this spectral range lies a phenomenon that science has come to describe as photobiomodulation. Specific wavelengths of red and near-infrared light are absorbed by cytochrome C oxidase, the fourth complex of the mitochondrial respiratory chain, and there modulate mitochondrial activity in a way that increases ATP production, reduces reactive oxygen species, and dampens inflammatory responses. Cytochrome C oxidase is not just any enzyme. It is the actual engine of cellular energy production, and its activity largely determines how efficiently a cell responds to stress, damage, and aging.

That light in this wavelength range produces biological effects is not speculative. A randomized controlled trial from 2024 showed that fifteen minutes of whole-body irradiation with 670-nanometer light reduced blood glucose levels following a glucose challenge by 27.7 percent integrated over two hours, with the maximum glucose peak reduced by 7.5 percent (Powner, M. B., et al., 2024, Light stimulation of mitochondria reduces blood glucose levels, Journal of Biophotonics, 17(2), e202300521). The mechanism is direct: red light activates cytochrome C oxidase, increases the mitochondrial membrane potential, and with it the glucose turnover in peripheral tissues. This is photobiology, not wellness marketing.

The National Institute on Aging in the United States convened a dedicated workshop on this mechanism in 2023, because photobiomodulation is being discussed as a promising strategy against age-associated mitochondrial dysfunction, not as a treatment for exotic conditions, but as a counterforce to the ubiquitous mitochondrial deterioration that accompanies aging and that is associated with diabetes, cardiovascular disease, and neurodegenerative processes.

Sunlight contains this red and near-infrared light in substantial amounts, particularly pronounced in the morning and evening hours when the sun is low on the horizon and atmospheric filtering absorbs blue light while letting red and infrared through. Anyone who lives primarily indoors and uses a screen as their primary light source does not receive the portion of the solar spectrum that mediates this mitochondrial activation.

Melatonin as Antioxidant, Not Sleeping Pill

Melatonin is discussed in public discourse almost exclusively as a sleep hormone, as the chemical signal that tells the body night has arrived and that can be supplemented when sleep is disturbed. This reduction is a category error that conceals the molecule’s actual significance.

Melatonin is one of the most potent endogenous antioxidants known in nature. It protects mitochondria directly against oxidative stress, it penetrates all biological membranes without transport proteins, it accumulates in mitochondria at concentrations far exceeding plasma levels, and it activates antioxidant enzymes there that govern the mitochondrial maintenance process (Tan, D.-X., and Reiter, R. J., 2019, An evolutionary view of melatonin synthesis and metabolism related to its biological functions, Melatonin Research, 2(4), 1-13). More recent work discusses the possibility that melatonin may also be synthesized within the mitochondria themselves in response to near-infrared light, independently of the pineal gland, which gives solar spectrum a significance for mitochondrial melatonin synthesis that has not yet entered mainstream medical awareness (Tan, D.-X., et al., 2023, Melatonin: A potent, endogenous mitochondrial antioxidant, Antioxidants, 12(8), 1573).

The implication for modern lifestyle is direct. Anyone who sits in front of a screen at night is not merely suppressing a sleep hormone. They are suppressing one of the most potent endogenous antioxidants in their organism at precisely the moment when its regenerative function is most needed. That this has consequences for cellular aging processes, oxidative stress, and long-term mitochondrial health is not a hypothesis. It is a logical consequence of the biochemistry.

The Balance We Have Lost

I go out into the sun deliberately. Not from a romantic impulse, not because it is pleasant, though it is, but because I am convinced that my organism depends on it, on the full spectrum of solar radiation, on the timing of that exposure, on the darkness that follows the light phase, and on the consistency of the rhythm that connects the two.

This does not mean ignoring risks. UV radiation can cause skin damage at excessive or unprotected exposure levels and increase the risk of certain forms of skin cancer. That is biologically real and clinically relevant. But as with most biological factors, the truth lies not at the extreme but in the balance. Complete avoidance of sun exposure is no more biologically sensible than uncontrolled exposure, and the recommendation to categorically avoid sunlight imposes on the body a light deprivation that was never experienced in the course of human evolution, whose consequences we are only now beginning to measure.

Equally, the significance of genuine darkness should not be underestimated, because it has become rare in the modern environment. Even low light intensities of five to ten lux at night can measurably suppress melatonin production. The standby indicators on televisions, routers, and charging devices can, under certain sleeping conditions, be physiologically relevant. Restoring a natural light-dark rhythm is therefore not an esoteric concept and not a retreat to a romanticized past. It is a logical consequence of understanding human biology.

What All of This Means

When you bring the evidence together, a picture emerges that was not expressible with this clarity even a decade ago. Sunlight operates through at least three independent biological systems. It synchronizes the circadian rhythm through specialized ganglion cells and thereby coordinates virtually all physiological processes in the body. It releases nitric oxide from skin stores through UV-A radiation and thereby acts directly as a vasodilator, blood pressure reducer, and cardioprotective agent, independent of vitamin D. And it activates cytochrome C oxidase in the mitochondrial membrane through red and near-infrared light and thereby modulates cellular energy production, oxidative stress, and mitochondrial regenerative capacity.

Anyone who discusses sunlight exclusively in terms of vitamin D is describing one out of at least three known mechanisms and a further dozen less well characterized ones. And anyone who avoids summer sun, applies SPF 50, and supplements their vitamin D deficiency with a capsule believes they have solved the problem, while having left three quarters of the problem unaddressed.

Homo sapiens is not an indoor organism. The human body is not designed to function under artificial light, to spend the night with display screens, and to filter the spectrum of solar radiation through glass. The accumulation of modern disease cannot be traced monocausally to this single factor, but the research of the past decade has shown that the human light environment has substantially more biological relevance than the medical establishment has been willing to acknowledge.

Light during the day. Darkness at night. A rhythm that was constant for millions of years before we, within a few generations, began to fundamentally change it.

I go out into the sun. I allow darkness in. Not because I believe I have all the answers. But because I believe that the question itself, why the most natural thing for Homo sapiens has become a deliberate choice, is already part of the answer.

Supplements: Important, but Understood Correctly

I am someone who has tried, over the course of his life, essentially everything that might be relevant to health. High-dose intravenous vitamin C, daily vitamin D, adaptogens, enzyme complexes, mineral profiles. This is not experimentation for its own sake. It is the consistent posture of someone who takes seriously the fundamental question of Homo sapiens: What did our ancestors have ten thousand years ago that modern humans no longer have? What did they consume daily, how did they behave, what did they experience in their environment, and what of this is absent in the life of someone alive today? For me this question is not philosophical. It is methodological. In most cases it is the most direct route to understanding why a particular biological system is under pressure.

And it leads unavoidably to the first recognition: our food simply no longer provides what Homo sapiens requires. The mineral content of fruits and vegetables has declined substantially over the past seven decades of intensive agriculture, because depleted soils transfer fewer minerals into plant material. Magnesium is particularly absent from industrially managed soils. Vitamin D is barely present in meaningful quantities in food at all. And vitamin K2 is a quantité négligeable in the Western diet, because the fermented foods and organ meats in which K2 concentrates have been disappearing from plates for generations. All of this justifies the question of whether and how one should supplement.

Vitamin D, K2, and Magnesium: the logic behind the combination

Supplementing vitamin D without K2 is biochemically incomplete. Vitamin D increases intestinal calcium absorption and raises circulating calcium levels. K2, particularly in its MK-7 form with its long biological half-life of several days, activates matrix Gla protein and osteocalcin, two proteins that direct calcium into bone while simultaneously keeping it out of arterial walls. Anyone taking high-dose vitamin D without sufficient K2 is biochemically routing calcium to places where it does not belong, namely into vascular walls. MK-7 is substantially superior to MK-4 here, because the short half-life of MK-4 does not sustain continuous activity in peripheral tissue.

Magnesium is the most consistently overlooked weak point in this entire system. At least eight magnesium-dependent enzymes are directly involved in vitamin D conversion, from hepatic hydroxylation to 25-hydroxyvitamin D through renal activation to the biologically active 1,25-dihydroxyvitamin D. Anyone supplementing vitamin D without sufficient magnesium is running a synthetic process whose substrates are missing, while simultaneously drawing down existing magnesium reserves, because increased vitamin D activity raises magnesium demand. A 25-OH-D level in laboratory results that remains low despite supplementation is therefore frequently not a signal of insufficient vitamin D intake but of magnesium deficiency as the rate-limiting factor. The problem is hidden in the solution, and it goes undetected because the result is measured but not the bottleneck.

Melatonin spray: useful, but for which mechanism?

A sublingual melatonin spray is superior to an oral capsule because sublingual absorption bypasses hepatic first-pass metabolism and bioavailability is substantially higher. At the correct low dose, in the range of 0.1 to 0.5 milligrams, it delivers a valid timing signal to the suprachiasmatic nucleus: night has begun, please calibrate circadian phase accordingly. This is sensible, particularly when one has been exposed to screens in the evening and blue light has extended physiological melatonin suppression beyond its natural onset.

What the spray does not deliver is critical to understand. The intramitochondrial melatonin that constitutes its own class in the context of photobiomodulation is not replicated by exogenous melatonin. It is synthesized locally within the mitochondria themselves, probably in response to near-infrared light within the cells, and it accumulates there at concentrations that exceed plasma levels by a large multiple. This melatonin is not a sleep hormone in the narrow sense. It is a mitochondrial free radical scavenger that regulates cellular aging processes and oxidative stress directly at their site of origin. The spray addresses the circadian dimension of melatonin biology. The mitochondrial dimension is addressed only by light itself, and specifically the right light at the right time.

Is all of this pointless then? Yes and no.

Vitamin D, K2, magnesium, and a melatonin spray are not useless interventions. They are sensible responses to real deficits in a modern nutritional and living environment in which soils are mineral-depleted, food is processed, nights are illuminated, and days are spent indoors. These supplements address genuine gaps.

But they do not address the gap this entire article is about. No supplement replicates the UVA-induced nitric oxide mechanism that lowers blood pressure and protects vascular walls. No supplement replicates the photobiomodulation by red and near-infrared light that activates cytochrome C oxidase and increases mitochondrial ATP production. No supplement replicates the circadian synchronization delivered by bright morning light that calibrates the suprachiasmatic nucleus to the outside world. These mechanisms have no oral surrogates, because they do not operate through the bloodstream but through light as a direct biological stimulus.

The Homo sapiens of ten thousand years ago had none of these supplements. He had something else: sun on his skin, darkness at night, food from soils that had not yet been depleted, and a body evolutionarily calibrated to benefit from that environment. I keep coming back to this question, and it keeps leading somewhere useful: what did he have that we no longer have? The answer, most of the time, is the key. What can be addressed by oral supplementation today covers part of what is missing. Light cannot be supplemented.

That is the sentence that matters.

References

Hazell, G., Khazova, M., and O’Mahoney, P. (2023). Low-dose daylight exposure induces nitric oxide release and maintains cell viability in vitro. Scientific Reports, 13, 16399. https://doi.org/10.1038/s41598-023-43653-2

Hahn, J., et al. (2022). Vitamin D and marine omega-3 fatty acid supplementation and incident autoimmune disease. BMJ, 376, e066452. https://doi.org/10.1136/bmj-2021-066452

Lindqvist, P. G., et al. (2016). Avoidance of sun exposure as a risk factor for major causes of death: A competing risk analysis of the Melanoma in Southern Sweden cohort. Journal of Internal Medicine, 280(4), 375-387.

Liu, D., et al. (2014). UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase or prostanoids. Journal of Investigative Dermatology, 134(7), 1839-1846.

Martineau, A. R., et al. (2017). Vitamin D supplementation to prevent acute respiratory tract infections: Systematic review and meta-analysis of individual participant data. BMJ, 356, i6583.

Nairuz, T., and Lee, J.-H. (2024). Photobiomodulation therapy on brain: Pioneering an innovative approach to revolutionize cognitive dynamics. Cells, 13(11), 966. https://doi.org/10.3390/cells13110966

Powner, M. B., et al. (2024). Light stimulation of mitochondria reduces blood glucose levels. Journal of Biophotonics, 17(2), e202300521. https://doi.org/10.1002/jbio.202300521

Quan, Q.-L., et al. (2023). Impact of ultraviolet radiation on cardiovascular and metabolic disorders: The role of nitric oxide and vitamin D. Photodermatology, Photoimmunology and Photomedicine, 39(6), 573-581. https://doi.org/10.1111/phpp.12914

Tan, D.-X., and Reiter, R. J. (2019). An evolutionary view of melatonin synthesis and metabolism related to its biological functions. Melatonin Research, 2(4), 1-13.

Tan, D.-X., et al. (2023). Melatonin: A potent, endogenous mitochondrial antioxidant. Antioxidants, 12(8), 1573. https://doi.org/10.3390/antiox12081573

Windred, D. P., Burns, A. C., Lane, J. M., Olivier, P., Rutter, M. K., Saxena, R., Phillips, A. J. K., and Cain, S. W. (2024). Brighter nights and darker days predict higher mortality risk: A prospective analysis of personal light exposure in >88,000 individuals. Proceedings of the National Academy of Sciences, 121(43), e2405924121. https://doi.org/10.1073/pnas.2405924121