UV Radiation, Skin Damage, and the Case for Serious Sun Protection
UV Radiation, Skin Damage, and the Case for Serious Sun Protection
Ultraviolet radiation is the single most significant preventable cause of skin ageing and skin cancer. Here is an honest account of what it actually does to the skin — and what the evidence says about protecting against it.
The most important sentence in skincare
If a patient asked us to identify the single with the greatest evidence base for preventing skin ageing, the answer would not be a retinoid, a biostimulator, or any of the topical ingredients we have examined elsewhere in this series.
It would be daily, broad-spectrum, high-factor sun protection, applied consistently, without exception, regardless of weather or season. Everything else in a skincare regimen is built on that foundation. Without it, the value of everything else is significantly compromised.
This is not a novel or controversial observation. It has been supported by decades of peer-reviewed research.
What is worth examining in clinical detail is :
What ultraviolet radiation does to the skin at a cellular and molecular level.
Why the damage is cumulative and largely irreversible.
What the evidence says about the role of both SPF and antioxidants in an evidence-based protection strategy.
UVA and UVB — two distinct mechanisms of damage
Ultraviolet radiation reaches the skin in two primary forms, and understanding their distinct mechanisms helps to explain why broad-spectrum protection, covering both UVB, is the only clinically appropriate standard.
UVB radiation — the shorter wavelength component — acts primarily on the epidermis. It is the principal driver of sunburn, and its most significant long-term consequence is direct DNA damage. UVB are absorbed by DNA bases, producing characteristic lesions known as dimers (CPDs). These are structural distortions in the DNA double helix that, if not repaired before the cell divides, can result in the mutations that underlie cell carcinoma and . UVB causes DNA mutations, increasing the risk of cancer, while UVA penetrates deep into the dermis, promoting collagen .
UVA radiation — the longer wavelength component — penetrates considerably deeper than UVB, reaching the dermis where collagen, elastin, and fibroblasts reside. Its primary mechanism of damage is indirect — the generation of reactive oxygen species (ROS) through photosensitisation reactions in the tissue. Overexposure to UV radiation increases the of ROS, which at higher concentrations can damage the main proteins that make up the skin, collagen and elastin. ROS activate the expression of matrix metalloproteinases, which cause of collagen fibers, leading to the appearance of wrinkles and skin ageing.
The two mechanisms work in concert to what is clinically recognised as photoageing; a process distinct from chronological ageing in its character, its distribution, and its rate. Photoaged skin has a different histological appearance from chronologically aged skin: solar elastosis, in which the dermis is infiltrated by abnormal, disorganised elastic replacing degraded collagen, is a characteristic and essentially pathognomonic finding. It does not occur in sun-protected skin of equivalent chronological age.
The MMP cascade — how UV destroys collagen
The matrix metalloproteinase pathway is worth understanding in some detail, because it explains both the mechanism of UV-mediated collagen destruction and the rationale for the protective strategies we advocate.
One of the main effects of UV radiation on the skin is an increase in expression of MMPs, which are responsible for the degradation of extracellular matrix proteins such as collagen, fibronectin, elastin, and proteoglycans. Excessive degradation of these proteins caused by excessive production of MMP-1, MMP-3, and MMP-9 to the photoageing of the skin and thus to the formation of thick wrinkles and sagging through photodestruction, phototransformation, and photooxidation of collagen and elastin.
The ROS generated by UV exposure activates the mitogen-activated protein kinase (MAPK) pathway, which in turn upregulates activator protein-1 (AP-1) — a transcription factor that drives MMP expression. Simultaneously, AP-1 inhibits TGF-beta signalling, which is responsible for regulating pro-collagen type I synthesis.
The result is a double assault on the dermal collagen matrix: its breakdown is accelerated and its synthesis is suppressed simultaneously. This dual mechanism why even moderate cumulative UV exposure has consequences that exceed what chronological ageing would produce over the same period.
A 2022 study from Yale and Johns Hopkins identified an additional pathway, the aryl hydrocarbon receptor (AhR) axis, through which UVB-generated photo-metabolites directly activate MMP-2 and MMP-11, enzymes implicated in type IV collagen degradation. This finding adds an new dimension to the photoageing mechanism that is independent of the ROS pathway and that conventional antioxidant strategies may not fully address — suggesting that the molecular complexity of UV damage continues to be even now
The cumulative and irreversible nature of photodamage
One of the most important aspects of UV damage is its cumulative and largely irreversible . Each episode of unprotected UV exposure adds to an accumulating burden of DNA damage, collagen degradation, and fibroblast senescence that the skin’s repair mechanisms cannot fully correct.
Excessive exposure of the skin to UV radiation accelerates the ageing process and leads to a photoageing state which involves similar pathological alterations to those occurring in chronological ageing. UV radiation oxidative stress and a leakage of double-stranded DNA from nuclei and mitochondria into the cytoplasm, triggering cellular senescence and a chronic inflammatory state in the skin.
The concept of cellular senescence is particularly relevant. Senescent fibroblasts, cells that have permanently exited the cell cycle in response to damage, accumulate in photoaged dermis and contribute to a chronic low-grade inflammatory state known as the senescence-associated secretory phenotype (SASP). Senescent fibroblasts not only fail to produce collagen themselves but actively promote further collagen degradation in the surrounding tissue through the cytokines and MMPs they secrete. The damage, in other words, is self-perpetuating once established.
This is the biological basis for the clinical observation that photoaged skin, in a patient who continues to receive UV exposure, deteriorates faster than in a patient who adopts rigorous photoprotection — even after significant photodamage has already accumulated. It is never too late to benefit from sun protection. The mechanism of ongoing damage continues regardless of what has already occurred, and interrupting it at any point reduces the rate of further deterioration.
SPF — what it is and what it is not
The sun protection factor is a measure of a sunscreen’s ability to protect against UVB-induced erythema, the visible reddening of the skin that signals UV damage to the epidermis. An SPF of 50 allows 1/50th of the UVB that would otherwise reach the skin to penetrate, theoretically permitting the wearer to remain in the sun fifty times longer than they could protection before burning.
In practice, this calculation depends entirely on the product being applied in the quantity tested, typically 2mg per cm² of skin surface, which is considerably more than most people apply in daily use. The practical protection offered by a well-applied SPF 30 is meaningfully less than the theoretical protection of its rating, and applying a higher SPF partially compensates for habitual .
Broad-spectrum designation, covering both UVA and UVB, is not optional. A that protects only against UVB prevents sunburn but allows the deeper-penetrating UVA to continue driving collagen degradation and ROS generation in the dermis unimpeded. Broad-spectrum protection is the only clinically meaningful standard for photoprotection in the context of skin health rather than simply sunburn prevention.
The SPF rating system has limitations that are worth acknowledging honestly. It measures a single endpoint — redness — and does not directly quantify protection against DNA damage, collagen degradation, immunosuppression, or carcinogenesis. High-SPF formulations provide additional protection against these endpoints, and the evidence supports the use of SPF 50 or above as the appropriate daily standard for patients who are serious about photoprotection.
The role of antioxidants — a complementary layer of protection
Sunscreen filters — chemical or mineral — work by absorbing or UV photons before they penetrate the skin. They do not capture every photon, and even beneath an effective sunscreen, some ROS are generated. This is where antioxidants — both topical and endogenous — a complementary protective function.
The skin has multiple antioxidant defence systems, including enzymatic systems such as the glutathione-peroxidase-reductase enzyme system and superoxide dismutase, and non-enzymatic systems including vitamin C, vitamin E, glutathione, and coenzyme Q10. Topical antioxidants can potentially improve the intrinsic defence systems of the skin and boost the photoprotective function of UV .
Vitamin C (ascorbic OnabotulinumtoxinAAbobotulinumtoxinAIncobotulinumtoxinAPrabotulinumtoxinALetibotulinumtoxinARimabotulinumtoxinBHyaluronic Acid FillersCalcium Hydroxylapatite FillersPoly-L-lactic Acid FillersPolymethylmethacrylate FillersAutologous Fat GraftingForehead Lines TreatmentGlabellar Frown Lines TreatmentCrow’s Feet TreatmentBunny Lines TreatmentChemical Brow LiftLip FlipGummy Smile CorrectionMasseter ReductionJaw SlimmingDimpled Chin SmoothingCobblestone Chin SmoothingNefertiti Neck LiftMicro-BotoxMesotoxHyperhidrosis TreatmentChronic Migraine ReliefBruxism TreatmentTMJ TreatmentNeck Spasm TreatmentBlepharospasm TreatmentLip AugmentationLip ContouringCheekbone EnhancementTear Trough FillersNasolabial Fold SofteningMarionette Line FillersLiquid RhinoplastyNon-Surgical Nose JobJawline ContouringJawline DefinitionChin VolumisingHand RejuvenationAcne Scar Subcision Filling – londonbiolab.com -) is the most clinically significant topical antioxidant in the context of photoprotection. It is a potent water-soluble free radical scavenger, and its role in collagen synthesis — as an essential for the hydroxylation of proline and lysine residues in procollagen — means that it both the oxidative and the structural of UV damage simultaneously. Vitamin C and retinol prevent the breakdown of collagen and stimulate its growth, which prevents and repairs photodamaged skin. Application of vitamin C prior to sunscreen in the morning is most advantageous. The sequencing matters: vitamin C applied beneath SPF creates a dual protective layer that reduces both the ROS generated by UV photons that penetrate the filter and the oxidative damage to collagen that follows.
Vitamin E (alpha-tocopherol) is the lipid-soluble antioxidant in the skin, protecting cell membranes and lipid structures from oxidative damage. It works with vitamin C — the two regenerating each other’s antioxidant capacity in a cycle that produces greater combined protection than either achieves in isolation. Vitamin E has been employed in combination with vitamin C, revealing significant protection against sunburn and erythema, indicating potential against skin cancer and photoageing.
Niacinamide (vitamin B3) contributes to photoprotection through a different mechanism — inhibiting the transfer of melanosomes that would otherwise produce UV-induced pigmentation, and DNA repair pathways that reduce the persistence of UV-induced lesions. Its anti-inflammatory properties further reduce the chronic inflammatory component of photodamage.
The practical protocol
The clinical evidence converges on a photoprotection that is straightforward in principle even if its consistent execution requires genuine habit formation.
A topical vitamin C serum applied immediately before the SPF enhances the antioxidant defence against ROS generated by the UV that penetrates the filter.
A broad-spectrum SPF 50 or above, applied to all sun-exposed areas as the final morning skincare step, provides the primary barrier against UV damage.
In the evening, a retinoid, the most comprehensively evidenced agent for repairing existing photodamage and preventing further structural deterioration addresses the collagen synthesis deficit that UV exposure drives during the day. Read our exploration of the beneficial effects of
This trilogy of vitamin C in the morning, SPF as the final step, and retinoid in the evening represents the most evidence-based daily photoprotection and anti-photoageing protocol currently . Everything else — biostimulators, fillers, advanced topical ingredients — produce better results, and last longer, in patients who have this foundation consistently in place.
A final observation
It is worth stating plainly something that the skincare industry tends to underemphasise relative to its commercial interest in selling a wide range of products. The most effective anti-ageing intervention available does not come in a premium serum or a novel biostimulator. It costs considerably less than most treatments, it needs to be applied once a day, and its mechanism of action is the most thoroughly documented in all of dermatology. It is sunscreen. Used daily, consistently, and at adequate SPF, from as early in life as possible, it prevents more skin ageing than any other single measure available. The rest is supplementary.
The views expressed in Clinical Perspectives are the Dr Forrester’s own and reflect his personal and professional experience in aesthetic medicine.
References
Brar GS et al. A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin. PMC. 2025.
Pawlak A et al. The impact of ultraviolet radiation on skin photoaging — review of in vitro studies. Journal of Cosmetic Dermatology. 2021.
Kim DJ et al. UVB-mediated DNA damage induces matrix to promote photoaging in an AhR- and SP1-dependent manner. JCI Insight. 2022.
Ferreira MS et al. Photoaging: UV radiation-induced cGAS-STING signaling promotes the aging in skin by remodelling the immune . Biogerontology. 2025.
Jesus A et al. Antioxidants in Sunscreens: Which and What For? Molecules. 2023.
Ball S et al. Vitamin C, Topical Retinoids, and Sunscreen in Clinical Practice. ACOFP Journal. 2024.
Abdel Azim AA et al. Sunscreens part 1: Mechanisms and efficacy. Journal of the American Academy of Dermatology. 2024.
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