Vitamin D3 is essential to human health. Its absence leads to a variety of ailments, most notably the bent limbs and weak bones characteristic of rickets. While vitamin D3 can be obtained through diet, the human body synthesizes it through exposure to sunlight. But how exactly does this happen?
The process was first detailed in a 1980 study by M. F. Holick and colleagues that used rat skin as a model for human skin. Vitamin D synthesis begins with 7-dehydrocholesterol (7-DHC), a molecule present throughout the skin but most highly concentrated in the lowest layers of the epidermis, the stratum basale and especially the stratum spinosum. Ultraviolet B radiation (wavelength 280-315 nanometers) penetrates through the skin, converting 7-DHC into an isomer—same chemical formula, but different spatial configuration of atoms—of vitamin D3 called preD3.
The final stage, isomerization, or converting preD3 into vitamin D3 is dependent on the temperature within the skin. To keep the reaction going, a protein—the descriptively named vitamin D binding protein—binds to the newly created vitamin D3 and transports it into the blood, via capillaries located where the epidermis meets the lower skin layer, the dermis. If D3, the product of the isomerization, becomes overconcentrated, the reaction may be forced into equilibrium, stopping vitamin D3 synthesis. Vitamin D binding protein ensures that synthesis proceeds as efficiently as possible.
At temperatures at or near body temperature, the reaction can proceed for around three days, continuing even after sun exposure ends. Moderate sun exposure is sufficient to produce enough vitamin D3, assuming otherwise good health and nutrition.
What's Your Quick Question?
For this monthly series from JSTOR Daily, we invite readers to submit their burning questions. If we choose your question, it will be published alongside related research housed on JSTOR.