Vitamin D
Vitamin D (formally calciferol) is not a classical vitamin. It is a secosteroid hormone that your body can produce on its own, provided it has two things: UVB radiation from the sun and cholesterol in the skin. Vitamin D influences the expression of more than 1,000 genes, regulates immunity, supports mitochondrial function, and is essential for the health of bones, muscles, the brain, and the cardiovascular system. Despite this, the majority of the population in Central Europe is deficient.
- Why vitamin D is not a vitamin but a hormone
- How your skin produces vitamin D from cholesterol and UVB light
- What the relationship is between vitamin D and mitochondria
- Why vitamin D deficiency is nearly universal in northern latitudes from October to March
- Why the solar callus and gradual UV tolerance building are essential
- How to support vitamin D production naturally and safely
- What is vitamin D and why is it actually a hormone?
- How is vitamin D produced in the skin?
- What are the forms of vitamin D and how is it activated?
- How does vitamin D affect mitochondria?
- Why is almost everyone in northern latitudes deficient?
- Why is cholesterol essential for vitamin D?
- What is a solar callus and why is it important?
- How to support vitamin D levels naturally?
What is vitamin D and why is it actually a hormone?
Vitamin D was discovered in 1922 and given the name "vitamin" because scientists believed it had to be obtained exclusively from food. Today we know that is not true. Your body synthesizes vitamin D on its own when UVB radiation strikes cholesterol in the skin. That is the definition of a hormone, not a vitamin.
Bikle (2025) described in his comprehensive review in StatPearls that vitamin D3 (cholecalciferol) is formed in the skin from 7-dehydrocholesterol through the action of UVB radiation, which cleaves the B-ring of the steroid molecule and creates previtamin D3. This then isomerizes into vitamin D3 (Bikle, 2025).
Vitamin D influences the expression of more than 1,000 genes in the human body. It regulates calcium and phosphorus metabolism, modulates the immune system, affects muscle function, the cardiovascular system, the brain, and even mitochondrial energetics. That is why calling it a "vitamin" is misleading. It is a full-fledged steroid hormone.
How is vitamin D produced in the skin?
Vitamin D synthesis is an elegant photochemical process that occurs in several steps:
- UVB radiation (wavelengths 290 to 315 nm) strikes exposed skin
- The epidermis (outer layer of the skin) contains 7-dehydrocholesterol (7-DHC), a derivative of cholesterol
- UVB photons cleave the B-ring of 7-DHC and create previtamin D3
- Previtamin D3 is converted by thermal isomerization (body heat) into vitamin D3 (cholecalciferol)
- Vitamin D3 binds to a transport protein (DBP) and travels through the bloodstream to the liver
The entire process depends on UVB intensity, which is determined by the angle of the sun's rays. At latitudes around 45 to 55 degrees north (covering most of Central and Northern Europe, as well as much of the northern United States and Canada), UVB intensity is sufficient for vitamin D synthesis only from late February to October, and only when the sun is high enough above the horizon (approximately from 10:00 AM to 3:00 PM). During winter months (November through February), the sun angle is too low and the atmosphere filters out virtually all UVB.
Chalcraft et al. (2020) showed in their study that just 30 minutes of sun exposure (15 minutes on the back and 15 minutes on the front of the body) in summer can significantly increase blood levels of vitamin D3 (Chalcraft et al., 2020).
What are the forms of vitamin D and how is it activated?
Vitamin D exists in several forms, each with a different function:
- Vitamin D3 (cholecalciferol) – the form produced in the skin by UVB or obtained from animal sources (fatty fish, egg yolks, butter). This is the "raw material."
- Vitamin D2 (ergocalciferol) – the plant form, less effective. It is produced by the action of UV on ergosterol in mushrooms and yeast.
- 25(OH)D (calcidiol) – formed in the liver by hydroxylation of vitamin D3. This is the form measured in blood tests. It is the storage form and the best indicator of overall vitamin D status in the body.
- 1,25(OH)₂D (calcitriol) – the active hormonal form. It is created by a second hydroxylation in the kidneys (and locally in many tissues). This is the form that binds to the vitamin D receptor (VDR) and regulates gene expression.
The vitamin D receptor (VDR) is found in virtually all cells of the body, including immune cells, neurons, muscle cells, and heart cells. This explains why vitamin D has such a broad impact on health.
How does vitamin D affect mitochondria?
Vitamin D is not just a "bone vitamin." It has a direct impact on mitochondrial function. Ryan et al. (2016) demonstrated that the vitamin D receptor (VDR) is essential for proper mitochondrial function. When the VDR is not working, the rate of mitochondrial respiration and ATP production from oxidative phosphorylation declines (Ryan et al., 2016).
Sinha et al. (2022) found that vitamin D status directly modulates the oxidative capacity of mitochondria in muscle cells. Vitamin D deficiency led to reduced ATP production and increased oxidative stress. After supplementation, mitochondrial function improved (Sinha et al., 2022).
From a mitohacking perspective, vitamin D is one of the key factors influencing the efficiency of the electron transport chain. If you are deficient in vitamin D, your mitochondria work more slowly, produce less energy, and generate more free radicals. That is why optimal vitamin D levels are one of the pillars of mitochondrial health.
Why is almost everyone in northern latitudes deficient?
Vitamin D deficiency is nearly universal in Central and Northern Europe, especially from October to March. There are multiple reasons, and they compound each other:
- Latitude. At latitudes above 45 degrees north, UVB intensity is sufficient for vitamin D synthesis only about 7 to 8 months of the year.
- Indoor lifestyle. The average person in modern society spends 90% of their time indoors. Window glass blocks UVB, so even sitting by a window does not help.
- Sunscreen. SPF 30 blocks 97% of UVB radiation. Applying sunscreen practically stops vitamin D synthesis.
- Insufficient cholesterol in the skin. Statins and low intake of animal fats reduce levels of 7-dehydrocholesterol, the raw material for vitamin D.
- Aging. With age, the amount of 7-DHC in the skin decreases. A 70-year-old produces approximately 4 times less vitamin D from the same dose of UVB compared to a 20-year-old.
- Darker skin. Melanin in the skin acts as a natural UVB filter. People with darker skin need more sun exposure to produce the same amount of vitamin D.
Riccio (2024) in his review called vitamin D "the sunshine molecule that makes us strong" and emphasized that vitamin D deficiency is directly linked to the Western lifestyle, insufficient time outdoors, and excessive sun protection (Riccio, 2024).
Why is cholesterol essential for vitamin D?
Cholesterol plays an irreplaceable role in the context of vitamin D. 7-dehydrocholesterol (7-DHC), the precursor to vitamin D3, is a direct derivative of cholesterol. Without sufficient cholesterol in the skin, UVB radiation has nothing from which to produce vitamin D.
This is important to understand because mainstream medicine has demonized cholesterol for decades and promoted lowering it at all costs. From a mitohacking perspective, cholesterol is the fundamental building material for:
- Vitamin D (from 7-DHC in the skin)
- Steroid hormones (testosterone, estrogen, cortisol, progesterone)
- Cell membranes (cholesterol is a structural component)
- Bile acids (needed for fat digestion)
Demonizing cholesterol without understanding its biochemical role is one of the myths we address at Mitochondriak®. Cholesterol is not the enemy. It is the raw material from which your body produces hormones and vitamin D.
What is a solar callus and why is it important?
A solar callus is a term that describes the gradually built tolerance of the skin to UV radiation. Just as the soles of your feet develop a callus from walking barefoot, your skin builds a protective layer through regular, gradual sun exposure.
A solar callus involves several adaptive mechanisms:
- Melanogenesis – production of melanin, the skin's natural UV filter
- Epidermal thickening – an increase in the thickness of the stratum corneum, which scatters UV
- Antioxidant protection – increased levels of antioxidants in the skin (vitamin A, E, carotenoids)
- DNA repair mechanisms – activation of enzymes that repair UV-induced DNA damage
The key is gradual progression. You start with short exposures (5 to 10 minutes) and gradually extend them. You never burn. A sunburn is inflammation that damages DNA and increases the risk of problems. Gradually building a solar callus, on the other hand, is a protective process.
At Mitochondriak®, we recommend starting to build a solar callus in spring, when UVB intensity gradually increases. Ideally in combination with morning sunlight (red and infrared wavelengths prepare the skin for later UV exposure) and with photobiomodulation using red light, which according to studies accelerates DNA repair and reduces inflammatory reactions in the skin.
How to support vitamin D levels naturally?
At Mitochondriak®, we prefer natural vitamin D production over supplementation. Supplementation makes sense in winter or when a deficiency is confirmed, but it can never replace the complex effect of sunlight on the body.
Sun exposure (primary source)
- February through October: 15 to 30 minutes in the sun daily, with exposed arms and legs (or a larger body area), without sunscreen
- Timing: ideally between 10:00 AM and 2:00 PM, when UVB intensity is highest
- Gradual progression: start short and extend. Do not overdo it in the beginning.
- Morning light before UV: 30 minutes of morning sunlight (rich in red and IR) before intense UV exposure prepares the skin
Diet (secondary source)
- Fatty fish (salmon, mackerel, sardines) – the richest dietary source of D3
- Cod liver and fish oil
- Egg yolks (from free-range hens with access to sunlight)
- Butter and animal fats
Panels with UVB (supplementary source)
The Mitochondriak® Maxi UVB panels contain UVA and UVB diodes in addition to red and NIR light. With this panel, you can produce vitamin D in your skin even during the winter months. We always recommend turning on UV light together with red and NIR, because red light prepares the skin and reduces the risk of an inflammatory reaction.
Related glossary terms
- Mitochondria – cellular organelles whose function vitamin D directly influences through the VDR
- ATP – energy whose production depends on adequate vitamin D levels
- Photobiomodulation – red light that prepares the skin for UV and supports DNA repair
- Circadian rhythm – the biological rhythm synchronized by sunlight, which simultaneously triggers vitamin D synthesis
- Melatonin – the nighttime hormone and antioxidant whose production is linked to daytime light exposure
Vitamin D even in winter? Mitochondriak® Maxi UVB panels
Our Maxi UVB panels combine red, infrared, and UV light in a single device. Red and NIR light stimulate mitochondria and prepare the skin, while UVB triggers vitamin D synthesis directly in your skin. Even in January.
- Vitamin D is a secosteroid hormone, not a classical vitamin. Your body produces it from cholesterol and UVB light
- In northern latitudes, UVB is sufficient for vitamin D synthesis only from February to October (10:00 AM to 3:00 PM)
- Vitamin D directly affects mitochondrial function, ATP production, and oxidative stress
- Cholesterol in the skin (7-DHC) is the essential raw material for vitamin D production
- A solar callus is gradually built skin tolerance to UV that enables safe vitamin D synthesis
- The optimal level of 25(OH)D is 40 to 60 ng/ml. In winter, D3 supplementation with K2 is a sensible safeguard
Sources and References
- Bikle, D. D. (2025). Vitamin D: Production, Metabolism, and Mechanism of Action. Endotext / StatPearls. NBK278935
- Sinha, A. et al. (2022). Vitamin D status modulates mitochondrial oxidative capacities in skeletal muscle. Frontiers in Physiology, 13, 1049. PMC9700804
- Ryan, Z. C. et al. (2016). Vitamin D Receptor Is Necessary for Mitochondrial Function and Cell Health. American Journal of Physiology, 311(1), E11–E20. PMC6032156
- Riccio, P. (2024). Vitamin D, the Sunshine Molecule That Makes Us Strong. Nutrients, 16(14), 2232. PMC11243384
- Chalcraft, J. R. et al. (2020). Vitamin D Synthesis Following a Single Bout of Sun Exposure in Older and Younger Men and Women. Nutrients, 12(8), 2237. PMC7468901
- Voiculescu, V. M. et al. (2025). Vitamin D: Beyond Traditional Roles—Insights into Its Protective Effects Against Infectious Diseases. Nutrients, 17(5), 782. PMC11902150
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