Sun: how to protect skin from the inside and outside?

Internal photoprotection relies on a set of mechanisms integrated into the skin’s structure and function.

It combines three major lines of defence: the stratum corneum’s physical barrier, melanin-based pigmentation, and cellular DNA repair systems. These defences vary in effectiveness across phototypes, age groups, and body sites, yet they form the first biological response to solar exposure.

The stratum corneum: a first physical barrier against the sun.

The stratum corneum, the outermost epidermal layer, acts as a first line of defence against solar radiation. It has a dual photoprotective function: the stratum corneum reflects part of the light in visible and infrared wavelengths and absorbs some UV. The effectiveness of this barrier at protecting the body from the sun varies with its thickness, which differs across the body. Indeed, the stratum corneum on the soles of the feet averages 1.5 mm thick, compared with less than 0.1 mm for the eye contour. Photoprotective capacity also depends on skin phototype: it is greater in darker skin due to the diffuse presence of melanin granules. The stratum corneum blocks most UVB, unlike the more penetrating UVA.

Melanin: a potent biological filter.

Melanin is the primary element of internal photoprotection. It is produced by melanocytes located in the basal layer of the epidermis during the process of melanogenesis, it absorbs over 90% of UV radiation that penetrates the stratum corneum. Melanin protects epidermal melanocytes and keratinocytes by neutralising photon-induced free radicals and limiting DNA damage. Contrary to certain assumptions, melanocyte number remains relatively constant across individuals of all phototypes. Melanosome size, density and distribution – the organelles that contain melanin – vary considerably. In darker skin, melanosomes are larger, present throughout the epidermis and reach the stratum corneum, which increases photoprotective capacity.

At the molecular level, melanin synthesis is regulated by a complex network of cellular signals. The key enzyme in this process is tyrosinase, which catalyzes the initial steps in converting tyrosine to melanin. Its activity is modulated by associated proteins, such as tyrosinase-related protein 1 (TRP1) and dopachrome tautomerase (DCT), both expressed by melanocytes. These pigment cells are also influenced by surrounding keratinocytes, which release paracrine signals, especially under UV exposure. A major hormonal regulator is melanocyte-stimulating hormone (MSH), which activates the MC1R receptor on the surface of melanocytes. This receptor directs synthesis toward eumelanin—a brown-black photoprotective pigment—or pheomelanin—a red-yellow pigment that is less efficient and potentially pro-oxidant under UV radiation. Genetic variations in the MC1R gene are responsible for specific phenotypes (very fair skin, freckles) and increased sun sensitivity.

Dark and light skin do not benefit from the same natural photoprotection: it is estimated that the average SPF for black skin is 13.4 compared to 3.4 for white skin.

Cellular repair systems to correct UV-induced damage.

When UV rays penetrate skin layers, they interact with chromophores and generate reactive oxygen species and DNA photoproducts, including pyrimidine dimers. These changes can be mutagenic. In response, the skin activates several cellular repair systems to preserve genomic integrity. The photoreactivation mechanism, for example, uses an enzyme, photolyase, to restore thymine-thymine dimers under visible light. However, the efficiency of cellular repair pathways declines with age, increasing skin cancer risk in older individuals or those with high exposure.

Some molecules found in our diet or available as dietary supplements have shown a modest photoprotective effect in research. However, the magnitude of this effect, its duration, and above all its clinical significance remain under debate. While a varied, balanced diet is recommended, we advise consulting a physician before starting supplementation.

Vitamins C and E: a moderate photoprotective synergy.

Individually, neither vitamin C (ascorbic acid) nor vitamin E (α-tocopherol) has shown a convincing photoprotective effect in vivo. However, their oral combination appears to induce a slight increase in the minimal erythema dose (MED), indicating enhanced skin resistance to UVB rays. Three controlled studies reported a modest but significant increase in MED, ranging from 16.5 to 80 mJ/cm2, attributed to vitamin C’s ability to regenerate oxidized vitamin E within cell membranes. For example, one of these studies involved 45 volunteers with phototypes II to IV divided into three groups. Over one week, the first group received 805 mg of α-tocopherol daily, the second received 2 g of ascorbic acid, and the third received 805 mg of α-tocopherol plus 2 g of ascorbic acid. The following results showed a slight MED increase in groups 1 and 3.

Carotenoids: a protective antioxidant role.

Carotenoids such as lycopene, lutein, zeaxanthin, and provitamin A compounds like β-carotene occur naturally in fruits and vegetables. They accumulate in the epidermis, where they scavenge free radicals and protect cellular structures from UV damage. β-carotene is the most studied carotenoid. Its protective effect was first observed in the 1970s in patients with erythropoietic protoporphyria, a rare genetic disorder that causes skin photosensitivity among other symptoms. In healthy individuals, results are more mixed. Some studies report a modest reduction in minimal erythema dose (MED), but only after six weeks of continuous supplementation at doses above 10 mg/day.

Regarding lycopene, another carotenoid, two clinical studies explored its effect on UVB-induced erythema. In the first, 11 participants received tomato concentrate containing 16 mg of lycopene for 10 weeks. After that, a 40% reduction in erythema on the back of the hand following MED irradiation was observed. In the second study, 36 volunteers were randomized to receive synthetic lycopene, tomato extract, or a lycopene beverage for 12 weeks. All three forms resulted in modest increases in skin lycopene levels and reduced erythema by 38 to 48%. Further research is needed, but lycopene appears to be a promising antioxidant for skin protection.

Nicotinamide: a photoprotective vitamin.

Nicotinamide, or niacinamide, is a precursor of NAD+, a cofactor essential for DNA repair and post-UV immune response. Unlike other vitamins, its photoprotective effects have been assessed in several clinical trials with promising results. A phase III double-blind randomized study enrolled nearly 400 participants who had at least two nonmelanoma skin cancers (basal cell or squamous cell carcinoma) in the past five years. They received 500 mg of nicotinamide twice daily for 12 months or a placebo.

At the end of one year, the nicotinamide group showed a significant 23% reduction in new nonmelanoma skin cancer cases compared with the placebo group. The number of actinic keratoses, precancerous lesions, also decreased significantly by the third month. However, the benefits did not persist after supplementation stopped.

External photoprotection includes clothing-based protection and sun cream application. External photoprotection is often considered the cornerstone of sun protection.

Clothing: a primary physical barrier.

A garment can provide an effective physical barrier against UV radiation. To assess this efficacy, an index has been defined: the ultraviolet protection factor (UPF). The higher this factor, the more the fabric blocks solar radiation, both UVB and UVA. A textile’s capacity to filter UV depends on several parameters: fibre type, weave density, thickness, colour, moisture, and wear condition. For example, a dark blue jean may reach a UPF above 50 and safeguard the skin, whereas a fine white cotton t-shirt will not exceed a UPF of 7 to 10. UPF is regulated by the international standard AS/NZS 4399.

Sun protection products: essentials for shielding skin from ultraviolet radiation.

Sun protection products – whether sticks, mists, sprays, lotions or creams – represent a key strategy to protect skin from the sun. Their efficacy relies on the organic and/or mineral filters they contain. These molecules absorb and reflect UV rays, protecting the skin from harmful effects. The performance of sunscreens is assessed by the SPF (Sun Protection Factor) and the UVA-PF (UVA Protection Factor), indices measured during rigorous, regulated laboratory evaluations. Under European regulation, a sunscreen must offer UVA protection corresponding to at least one third of the UVB protection indicated on the label.

SPF measures protection against erythemal UV radiation (85% UVB and 15% UVA-II), which cause sunburn, while the UVA-PF quantifies protection against UVA rays, which penetrate deeper into the skin and accelerate its ageing.

In practice, the efficacy of a sun protection product depends largely on the amount applied. Whereas the SPF tests are conducted with 2 mg/cm2, users apply on average four times less (≈ 0.5 mg/cm2), which results in a marked reduction in protection. To achieve the labelled protection, you must apply the equivalent of 2.5 finger widths of sunscreen to the face and neck, 8 to the chest and back, 4 to each arm, 1 to each hand, 6 to each leg, and 2 to each foot.

Besides, the application frequency of sunscreen is essential during prolonged exposure. If you spend the day in the sun, reapply sunscreen every two hours. Most UV filters degrade during exposure, reducing skin protection.

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