How Does Sunlight Affect Vitamin D's Structure?

December 10, 2025 •

2 min read

An estimated one billion people worldwide have vitamin D deficiency, despite the potent role of sunlight in its production. The chemical process that begins when ultraviolet B (UVB) radiation from the sun hits the skin is key to understanding how sunlight affects vitamin D's structure.

Quick Summary

The process begins with UVB light penetrating the epidermis and striking 7-dehydrocholesterol, initiating a photolysis reaction that opens its B-ring. This forms previtamin D3, which then undergoes a temperature-dependent rearrangement to become vitamin D3.

Key Points

UVB Radiation is Key: Only ultraviolet B (UVB) radiation, not UVA, possesses the specific energy required to trigger the photochemical conversion in the skin.
Precursor Molecule is 7-DHC: Vitamin D synthesis starts with 7-dehydrocholesterol (7-DHC), a cholesterol derivative present in the skin's epidermis.
Photolysis and Ring-Opening: When UVB strikes 7-DHC, it causes the B-ring of the steroid structure to break open in a process called photolysis, forming previtamin D3.
Thermal Isomerization: Previtamin D3 is unstable and undergoes a temperature-dependent rearrangement, or isomerization, into the more stable vitamin D3.
Self-Regulation Prevents Toxicity: Continued sun exposure leads to the conversion of excess previtamin D3 and vitamin D3 into biologically inactive photoproducts, preventing toxic levels from accumulating.
Factors Influence Synthesis: Melanin, latitude, season, age, sunscreen, and clothing all affect the efficiency of vitamin D production from sunlight.

The Photochemical Transformation of 7-Dehydrocholesterol

Vitamin D synthesis in the skin starts with 7-dehydrocholesterol (7-DHC), a cholesterol derivative located in the epidermis. Exposure to sunlight, specifically UVB radiation (290-315 nm), provides the energy absorbed by 7-DHC. This triggers a photolysis reaction that breaks a carbon-carbon bond in the B-ring of the 7-DHC steroid structure. This ring-opening results in the formation of previtamin D3 (pre-D3), a secosteroid with a split B-ring and a flexible, reactive structure.

Thermal Isomerization into Vitamin D3

Previtamin D3 is unstable and undergoes a thermal isomerization, driven by body heat, to form the more stable vitamin D3 (cholecalciferol). This process does not require further sun exposure and can take several hours. Once converted, vitamin D3 enters the bloodstream bound to a vitamin D-binding protein.

Natural Self-Regulation to Prevent Toxicity

The body has a natural mechanism to prevent vitamin D toxicity from excessive sun exposure. This involves the photoisomerization of both previtamin D3 and vitamin D3 into inactive photoproducts, preventing an accumulation of active vitamin D forms.

Inactive Photoproducts

Extended sun exposure can convert previtamin D3 into inactive compounds like lumisterol3 and tachysterol3. Similarly, vitamin D3 can be transformed into inactive products such as suprasterols and 5,6-trans-vitamin D3. These inactive products are then cleared from the skin, ensuring that excessive sun exposure does not lead to dangerously high levels of active vitamin D.

Factors Influencing Synthesis

Several factors affect vitamin D synthesis in the skin:

Skin Pigmentation: Melanin in darker skin competes with 7-DHC for UVB absorption, requiring more sun exposure for vitamin D production.
Latitude and Season: Less UVB reaches the Earth at higher latitudes and during winter, impacting synthesis.
Age: Older adults have lower levels of 7-DHC in their skin, reducing their capacity for vitamin D production from sun exposure.
Sunscreen and Clothing: These block or filter UVB, significantly reducing vitamin D synthesis.

Synthesis in the Skin vs. Dietary Intake: A Comparison


Feature	Sunlight-Mediated Synthesis (In-Skin)	Dietary Intake / Supplements (Oral)
Initial Form	7-Dehydrocholesterol (7-DHC) in skin	Vitamin D2 (ergocalciferol) or D3 (cholecalciferol)
Activation Step 1	Photolysis by UVB to form previtamin D3	Absorption from the digestive tract
Activation Step 2	Thermal isomerization to vitamin D3	Transported to the liver for 25-hydroxylation
Toxicity Risk	Extremely low due to self-regulation mechanisms	Potential for toxicity with excessive supplementation
Transport	Released into bloodstream and bound to DBP	Incorporated into chylomicrons and transported via the lymphatic system
Binding Efficiency	100% bound to vitamin D-binding protein	Approximately 60% bound to DBP

Conclusion

Sunlight initiates a non-enzymatic, two-step chemical process in the skin that transforms 7-dehydrocholesterol into vitamin D3. UVB radiation breaks the B-ring of 7-DHC, creating previtamin D3. Body heat then converts previtamin D3 into the stable vitamin D3. A natural self-regulating mechanism prevents toxicity by converting excess vitamin D forms into inactive products. This process is influenced by factors like skin pigmentation, location, age, and sun protection. Understanding these structural changes highlights a vital natural process for health, complementing dietary sources and supplements.

Frequently Asked Questions

The ultraviolet B (UVB) component of sunlight is responsible for vitamin D production. Specifically, UVB radiation with wavelengths between 290 and 315 nanometers triggers the necessary photochemical reaction in the skin.

No, prolonged sun exposure does not cause vitamin D toxicity. The body has a self-regulating mechanism where excess previtamin D3 and vitamin D3 are converted into biologically inactive photoproducts, which prevents overproduction.

People with darker skin have more melanin, a pigment that absorbs UV radiation and protects against sun damage. This competition for UV rays means that less UVB penetrates to the 7-dehydrocholesterol, requiring longer sun exposure to synthesize the same amount of vitamin D as lighter-skinned individuals.

Sunscreen is designed to filter out and block UVB rays, which are necessary for vitamin D synthesis. The use of sunscreen with a sun protection factor (SPF) of 8 can reduce the production of vitamin D in the skin by over 95%.

7-dehydrocholesterol (7-DHC) is the precursor molecule, or provitamin D3, present in the skin's epidermis. It is the compound that absorbs UVB radiation and is structurally modified to begin the synthesis of previtamin D3.

After previtamin D3 is formed by UVB radiation, it undergoes a temperature-dependent thermal isomerization process. This converts it into the more stable and biologically useful form, vitamin D3.

Aging reduces the capacity to produce vitamin D from sunlight because the concentration of the precursor molecule, 7-dehydrocholesterol, decreases in the skin with age.