Not all UV radiation is equivalent for vitamin D synthesis. The action spectrum for cutaneous previtamin D3 production — the relationship between wavelength and photochemical efficiency — peaks at approximately 295-300nm and falls off rapidly on either side. Wavelengths below approximately 280nm are absorbed by the ozone layer and do not reach the Earth's surface in meaningful quantities. Wavelengths above approximately 315nm are too long to be absorbed efficiently by 7-dehydrocholesterol in the skin.
This means that a narrow band of UVB radiation centered at approximately 295-300nm is responsible for essentially all of the vitamin D synthesis that occurs in human skin. This is not incidentally the same band of UV radiation that is most effectively blocked by glass, most effectively reduced by sunscreen, and most effectively attenuated at high latitudes and low sun angles.
Dr. Ann Webb and colleagues at the University of Manchester have published detailed analyses of the solar zenith angle effects on vitamin D-effective UV radiation, documenting that at latitudes above approximately 35°N — which includes most of the contiguous United States, all of the UK, and all of Scandinavia — the vitamin D-effective UV radiation reaching the Earth's surface is essentially zero for several months per year, even on clear days.
The Molecular Cascade: Step by Step
Step one: UVB photons in the 295-315nm range penetrate the epidermis and reach the living keratinocytes and fibroblasts of the lower epidermis and upper dermis. Here they encounter 7-dehydrocholesterol (7-DHC), also called provitamin D3, which is present in cell membranes.
Step two: A photon is absorbed by 7-DHC, causing a [6π] electrocyclic ring-opening reaction. This converts 7-DHC to previtamin D3 — an isomer with an opened B-ring and a different three-dimensional configuration.
Step three: Previtamin D3 is thermally unstable at body temperature. Over the course of hours, it spontaneously undergoes a [1,7] sigmatropic hydrogen shift to form vitamin D3 (cholecalciferol). This reaction is driven simply by body heat — no additional light is required.
Step four: Vitamin D3 diffuses from skin cells into dermal capillaries and is transported in blood bound to vitamin D-binding protein (DBP) to the liver.
Step five: In the liver, vitamin D3 is hydroxylated by the enzyme 25-hydroxylase (CYP2R1 is the primary enzyme) to form 25-hydroxyvitamin D3 (calcidiol, 25(OH)D3). This is the form measured in clinical blood tests and is the primary circulating form of vitamin D.
Step six: In the kidneys (and, importantly, in many peripheral tissues including immune cells and skin), calcidiol is further hydroxylated by 1α-hydroxylase (CYP27B1) to form the biologically active 1,25-dihydroxyvitamin D3 (calcitriol). It is calcitriol that binds to the vitamin D receptor (VDR) and regulates gene expression.
What Determines How Much Vitamin D You Produce
The amount of vitamin D synthesized from a given amount of sun exposure varies considerably between individuals, based on several well-characterized factors.
Skin pigmentation is the most important determinant. Melanin — the pigment responsible for darker skin color — absorbs UV radiation and reduces the amount that reaches the deeper epidermal layers where 7-DHC is located. Individuals with darker skin (higher Fitzpatrick skin type) require approximately three to five times more sun exposure to produce the same amount of vitamin D as individuals with lighter skin.
Age is a second key factor. The concentration of 7-DHC in skin declines with age — a 70-year-old has approximately 25% of the 7-DHC concentration of a 20-year-old, meaning that for the same UV exposure, older individuals synthesize substantially less vitamin D. Dr. Holick's research has documented this age-related decline in detail, with important implications for vitamin D sufficiency in older adults.
Body weight affects bioavailability, not synthesis. Vitamin D is fat-soluble and is sequestered in adipose tissue. In individuals with higher body fat percentage, a greater fraction of synthesized vitamin D is sequestered in fat rather than entering the general circulation, reducing the serum 25(OH)D response to any given dose.
Time of day, season, latitude, and altitude all affect the intensity of vitamin D-effective UV radiation reaching the skin. The 'shadow rule' — if your shadow is longer than you are tall, there is insufficient UV radiation for meaningful vitamin D synthesis — provides a practical heuristic.
Implications for Those in Northern Latitudes
At latitudes above approximately 35°N — covering Chicago, New York, Boston, Seattle, and Minneapolis in the US, and essentially the entire UK and Nordic regions — the sun's angle during winter months is too low for vitamin D-effective UVB to reach the Earth's surface in meaningful quantities. This is not a minor seasonal variation. In Boston (42°N), meaningful vitamin D synthesis from sun exposure is essentially impossible from approximately November through March. In Edinburgh (56°N), this window extends from October through April or longer.
For populations living in these latitudes, maintaining adequate vitamin D levels through sun exposure alone requires aggressive sun-seeking behavior during the summer months — sufficient to build up stores that can sustain winter levels. Most people in these regions do not manage this, which is a primary driver of the endemic vitamin D insufficiency documented in northern populations.
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REFERENCES
• Holick MF et al. Photosynthesis of previtamin D3 in human skin. Science. 1980;210(4466):203-5. PMID: 7414336
• Webb AR et al. Influence of season and latitude on cutaneous synthesis of vitamin D3. J Clin Endocrinol Metab. 1988;67(2):373-8. PMID: 2839537
• Holick MF. Vitamin D: A millenium perspective. J Cell Biochem. 2003;88(2):296-307. PMID: 12520530
• Matsuoka LY et al. Cutaneous vitamin D3 formation in progressive systemic sclerosis. Arch Dermatol. 1992;128(6):753-7. PMID: 1595254
• Wacker M, Holick MF. Sunlight and Vitamin D. Dermatoendocrinol. 2013;5(1):51-108. PMID: 24494042
• Holick MF et al. Age, vitamin D, and solar ultraviolet. Lancet. 1989;2(8671):1104-5. PMID: 2572832
• MacLaughlin J, Holick MF. Aging decreases the capacity of human skin to produce vitamin D3. J Clin Invest. 1985;76(4):1536-8. PMID: 2997282