Photoaging

Photoaging and intrinsic ageing are separable processes in the same tissue. Ultraviolet B, roughly 290 to 320 nanometres, is absorbed largely in the epidermis and causes direct DNA photoproducts; ultraviolet A, 320 to 400 nanometres, reaches the dermis and works mainly through reactive oxygen species. Both activate AP-1, which raises matrix metalloproteinases that cut type one and type three collagen while suppressing new procollagen synthesis. The result is net matrix loss plus solar elastosis in the upper dermis.

Clinically this reads as coarse wrinkling, leathery texture, telangiectasia, mottled pigmentation and actinic keratoses, graded on scales such as the Glogau classification. The most persuasive demonstration is not a trial but a photograph: a widely reproduced 2012 New England Journal of Medicine image of a lorry driver with decades of unilateral window-side exposure, one half of his face markedly more wrinkled and thickened than the other.

That asymmetry sets the interpretive rule for cosmetic evidence. Most visible facial ageing in fair-skinned people is exposure-driven and therefore preventable, so the largest effect in any topical regimen belongs to photoprotection. Topical retinoids are the class with the strongest controlled evidence for partially reversing established photodamage; everything else is measured against that background.

The bite is confounding by co-intervention. Cosmetic peptide studies routinely supply every subject with a daily broad-spectrum sunscreen, then report improvement in the active arm; without a vehicle control the sunscreen alone can produce visible change over twelve weeks. Showing that a peptide suppresses metalloproteinase expression in cultured fibroblasts under ultraviolet is a statement about a dish, not about wrinkle depth.