UV radiation and photo-ageing: the science of sun damage

UVB: DNA damage and sunburn

UVB rays (280 to 315 nm) are primarily absorbed by the epidermis. They cause direct DNA damage by inducing the formation of cyclobutane pyrimidine dimers (CPDs), which are abnormal bonds between adjacent thymine bases in the DNA strand. If not repaired efficiently by nucleotide excision repair mechanisms, these dimers result in mutation accumulation that drives both carcinogenesis and chronic tissue dysfunction.

UVB is responsible for sunburn, and its intensity varies significantly with season, latitude, and time of day. However, the absence of sunburn does not indicate the absence of UV-induced damage, because UVA operates on a different and more continuous basis.

UVA: the deeper and more constant threat

UVA rays (315 to 400 nm) account for approximately 95% of UV radiation reaching the Earth’s surface. Unlike UVB, UVA intensity is relatively constant throughout the day, across seasons, and penetrates clouds and glass. UVA penetrates significantly deeper than UVB, reaching the dermis, where collagen and elastin are located.

UVA causes indirect DNA damage primarily through the generation of reactive oxygen species (ROS). It also directly activates enzymes called matrix metalloproteinases (MMPs) in dermal fibroblasts, the primary mechanism behind UVA-driven photo-ageing: progressive enzymatic dismantling of the dermis’s structural scaffold.

Risk profiles compared

The risk profile of neuromodulators is well-characterised and limited primarily to localised effects: temporary asymmetry if product migrates slightly, mild bruising at injection sites, and in rare cases transient ptosis (drooping) of a brow or eyelid that resolves as the protein metabolises. These are temporary and require no intervention.

Fillers carry a distinct and broader set of risks. Vascular occlusion, where filler material enters or compresses a blood vessel, is rare but potentially serious, and can result in tissue necrosis or, in extreme cases, vision impairment. Chronic foreign body inflammatory response produces low-grade tissue reactions in some patients. Product migration is documented particularly with repeated treatment over time. Tyndall effect (a bluish discolouration visible through the skin from superficially placed HA) requires dissolving. These risks require different clinical skills and emergency protocols to manage.

Treatments that stimulate collagen synthesis, polynucleotides, PRP, microneedling, are substantially more effective when ongoing UV-driven collagen degradation is minimised. Daily SPF is not aftercare formality; it is a prerequisite for sustaining the structural improvements treatments create.

The SPF evidence

Broad-spectrum SPF 30+ blocks approximately 97% of UVB radiation. True broad-spectrum products also attenuate UVA. In Europe, the UVA PF is required to be at least one-third of the SPF value. SPF is only as effective as its application. The standard SPF test uses 2mg/cm², however most people apply less than half this amount. Applying generously and reapplying every two hours in direct sun is not excessive; it reflects how the product was tested.

SPF does not meaningfully block infrared radiation (IR-A), which also penetrates to the dermis and generates ROS. Topical antioxidants (Vitamin C, E, ferulic acid) extend photoprotection by neutralising ROS that SPF does not prevent, making them a meaningful complement, not a substitute.

Photoprotective supplements

Polypodium leucotomos (tropical fern extract) is the most studied oral photoprotective agent. It reduces UV-induced erythema, limits CPD formation, and attenuates MMP activation in controlled studies. Typically dosed at 240 to 480mg before UV exposure. It supplements but does not replace topical SPF.

Astaxanthin (a carotenoid from algae) has evidence for reducing UV-induced ROS, protecting skin lipids from oxidative degradation, and supporting collagen integrity under UV stress. Typical effective dose 4 to 8mg daily with a fat-containing meal.

Vitamin C + Vitamin E in combination provide synergistic antioxidant photoprotection. Vitamin C regenerates oxidised Vitamin E, maintaining antioxidant activity under UV stress. The combination has stronger evidence than either alone. Commonly dosed at 500mg Vitamin C + 200 IU Vitamin E daily.