UVA and vitamin D: all of the cost, none of the benefit

"Sunlight is good for you, it gives you vitamin D" is true of a remarkably narrow slice of sunlight. The reaction that starts vitamin D synthesis responds to a band about twenty nanometres wide in the UVB, and it is completely deaf to UVA. That single fact reframes a lot of everyday sun exposure — because the situations where UVA dominates are exactly the situations that produce no vitamin D at all.

The photochemistry

Vitamin D3 is not absorbed from sunlight; it is manufactured in your skin. The sequence is:

1. 7-dehydrocholesterol, present in the membranes of keratinocytes in the epidermis, absorbs an ultraviolet photon.
2. The absorbed energy breaks open one ring of the steroid structure, producing previtamin D3.
3. Previtamin D3 isomerises thermally — driven by body heat, not light — into vitamin D3 (cholecalciferol) over some hours.
4. The liver hydroxylates it to 25-hydroxyvitamin D, the form measured in a blood test, and the kidney converts that to the active hormone.

Only step one requires light, and its efficiency is governed by the action spectrum for previtamin D3 formation. That spectrum rises through the UVB, peaks around 295–300 nm, and collapses to negligible values by about 315 nm — which is precisely where UVA starts.

There is a squeeze built into that table. The wavelengths that make vitamin D most efficiently are the ones ozone removes most aggressively, so useful synthesis depends on a narrow window at the edge of what the atmosphere lets through — and that window closes whenever the sun's path through the atmosphere lengthens. UVA, absorbed only weakly by ozone, carries on regardless. The full contrast is in UVA vs UVB.

The three situations where the trade is worst

Behind glass

Ordinary window glass removes essentially all UVB and transmits a substantial fraction of UVA. A sunny desk by a window, or a long drive with sun through the side window, therefore delivers UVA exposure with mathematically zero vitamin D return. It is the cleanest example of the asymmetry, and the reason does glass block UVA matters more than it first appears.

Winter, at higher latitudes

Above roughly 35–40° of latitude there is a period each year — commonly called the vitamin D winter — during which the sun never climbs high enough for meaningful UVB to reach the ground at all. In much of northern Europe and Canada that runs from around October to March.

Vitamin D synthesis stops completely in those months. UVA does not: it falls, but far less, because the long slant path that strips out UVB leaves UVA comparatively intact. Seasonal UVA works through the arithmetic, and the practical result is that winter sunlight is disproportionately UVA — the season with the least benefit has the highest ratio of ageing dose to vitamin D dose in the year.

Sunbeds

Sunbed spectra are deliberately shifted toward UVA to maximise cosmetic tanning per unit of burning. That same shift makes them inefficient vitamin D producers relative to the ultraviolet dose they deliver — while placing them in IARC Group 1. "Sunbeds for vitamin D" is the worst available route to a nutrient you can buy in a bottle for pennies.

How much sun do you actually need?

A reasonable rule of thumb used by several public health bodies is that meaningful synthesis requires a UV Index of about 3 or above — which is not a coincidence, since the UV Index is erythemally weighted and therefore serves as a rough proxy for UVB availability. It is the one job the UV Index does that the UVA Index cannot.

Beyond that threshold, the commonly cited guidance is short, frequent, unprotected exposure of a moderate area of skin — arms and legs for something in the region of ten to thirty minutes around the middle of the day, several times a week, with the duration rising substantially for deeper skin tones, since melanin competes for the same photons.

Does sunscreen cause vitamin D deficiency?

This is the objection that keeps people from using sunscreen, and the real-world evidence does not support it. In theory a correctly applied broad-spectrum SPF 30 absorbs the great majority of incident UVB and should reduce synthesis substantially. In practice:

• People apply roughly a quarter to a half of the tested density, so real UVB attenuation is far below the label figure — the same arithmetic described in how much sunscreen you actually need.
• Coverage is incomplete, and the vitamin D response saturates easily, so small unprotected areas contribute disproportionately.
• Trials and systematic reviews of everyday sunscreen use have not found clinically meaningful reductions in 25-hydroxyvitamin D. In the Queensland trial where adults used broad-spectrum sunscreen daily for four and a half years, vitamin D status was maintained.

There is also some evidence that high UVA exposure may itself be associated with lower circulating vitamin D — a plausible but not settled finding, and not something to plan around. What is settled is that if vitamin D is your concern, an oral supplement resolves it completely, cheaply and without any ultraviolet dose. There is no version of the vitamin D argument that justifies seeking UVA.

The one-line version

UVB is the band with a benefit attached and a built-in warning signal. UVA has neither. Any circumstance that filters out UVB while leaving UVA — a window, a winter, a cloud, a sunbed — converts sunlight from a mixed proposition into a pure cost, and none of those circumstances feel different from the outside. That is what the UVA Index is for.