Photoaging

Photoaging is skin aging caused by the sun rather than by time, and it accounts for most of what makes a face look old: wrinkles, leathery texture, sun spots and fine broken surface veins. Ultraviolet (UV) light switches on enzymes that break down the skin's collagen and permanently damages the collagen that's left. Regular sunscreen measurably slowed it in a randomised trial.

The best-tested way to slow photoaging is to cut UV: broad-spectrum sunscreen on exposed skin, plus a hat and cover for long stretches outdoors. Oral "skin protection" supplements have only small, short trials behind them, and none measured skin aging.

How much of skin aging is sun

Compare the underside of a 70-year-old's upper arm, which rarely sees the sun, with the back of the same person's hand. The difference is the cumulative UV history.

One study tried to put a number on it. In 298 white women aged 30 to 78, researchers working for a cosmetics company put UV's share of visible facial aging signs at about 80%. The signs differed:

  • Sun spots and uneven pigmentation tracked sun exposure.
  • Wrinkles and texture reflected both sun and age.
  • Sagging tracked age rather than sun.[1]

Sun-damaged skin looks different from naturally aged skin: leathery rather than thin. Underneath, both show the same kind of cumulative damage to collagen.[2] The mechanisms below are settled cell and molecular biology.

What UV does to collagen

UV light triggers an immediate burst of reactive oxygen species (unstable, damaging molecules) in the outer skin and the dermis beneath it. These switch on a stress-signalling chain that ends at two transcription factors, the switches that decide which genes a cell turns on. The result is a set of collagen-degrading enzymes called matrix metalloproteinases (MMPs):

  • MMP-1, a collagenase, makes the first cut in intact collagen, the dermis's main load-bearing protein.
  • MMP-3 breaks down other parts of the supporting matrix and activates further MMPs.
  • MMP-9 finishes off the collagen fragments.

At the same time, the cells that make collagen (fibroblasts) make less of it, so the dermis ends up with a structural deficit.[3]

UV also permanently oxidises the collagen that survives. This changes how fibroblasts grip and contract the matrix.[4] The matrix doesn't just thin; it stops working properly.

The two kinds of UV divide the work. UVA reaches deep into the dermis and is the main driver of these changes. UVB penetrates less but causes most of the direct DNA damage and is the main driver of skin cancer.

Skin type sets the pace

Lighter skin is richer in pheomelanin, a pigment that adds to free-radical damage under UV. Darker skin is richer in eumelanin, which filters UV and acts as an antioxidant. The built-in sun protection factor (SPF) of the palest skin types is about 3.3, against roughly 13.4 for the darkest.[5]

What slows it

Sunscreen, on the one trial that tested it. In a randomised trial in Queensland, Australia, adults under 55 who applied sunscreen daily showed about 24% less skin aging than those who used it at their own discretion.[6] That is a single trial, but it is the only long-term randomised trial of a sun-protection habit against skin aging. See Sunscreen, which also covers the small vitamin D cost of daily high-SPF use and why very dark skin is the exception.

Oral supplements, much less. In small, short, industry-funded trials, a combination of Polypodium leucotomos extract, red orange extract and vitamins raised the UV dose needed to redden the skin by about 24% within the treated group over 8 weeks, with no direct comparison against placebo reported,[7] and in 23 adults astaxanthin raised it compared with placebo.[8] These trials measured the sunburn threshold, not skin aging. A 2025 review of 47 human studies of oral photoprotection judged the evidence limited by small samples and short duration.[9] None of them substitutes for sunscreen.

What to do

  1. Broad-spectrum sunscreen on the face and hands whenever you are out for long, or daily if visible aging matters to you and your skin is not very dark; daily high-SPF users should take oral vitamin D in winter.
  2. A hat and cover for long stretches outdoors, and never burn.
  3. Treat oral "sun protection" supplements as optional extras, not protection.
  4. The wider trade-off, since some sun is still worth having, is on Sun exposure.

Further reading

  • Rittié L, Fisher GJ. Natural and sun-induced aging of human skin. Cold Spring Harb Perspect Med 2015.[10]
  • Feng C et al. Matrix Metalloproteinases on Skin Photoaging. J Cosmet Dermatol 2024.[11]
  • Flament F et al. Effect of the sun on visible clinical signs of aging in Caucasian skin. Clin Cosmet Investig Dermatol 2013.[12]
  • Hughes MC et al. Sunscreen and prevention of skin aging: a randomized trial. Ann Intern Med 2013.[13]
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