The sun’s ultraviolet (UV) rays are a double-edged sword: while they are essential for vitamin D production, prolonged or unprotected exposure can severely damage the skin. This damage is not uniform; it varies significantly depending on skin type (largely determined by melanin levels) and age.

1. Understanding UV Radiation and DNA Damage

UV radiation comes in three main types: UVA (long-wave), UVB (medium-wave), and UVC (short-wave). Among these, UVB is the primary cause of sunburn and DNA damage, while UVA contributes to aging and indirect DNA harm through free radicals . When UVB penetrates the skin, it triggers chemical reactions in DNA molecules, forming cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). These are abnormal bonds between adjacent DNA bases that distort the DNA structure, disrupting normal cell function and increasing cancer risk. 

2. Skin Type: The Role of Melanin

Human skin types are classified using the Fitzpatrick scale, which ranges from Type I (very fair, always burns) to Type VI (very dark, rarely burns). The key difference lies in melanin, the pigment produced by melanocytes. Darker skin (Type IV-VI) contains more melanin, which acts as a natural sunscreen by absorbing UV rays and reducing DNA damage .

Evidence from Studies

• Sheehan et al. (2002) exposed skin Type II (fair) and Type IV (dark) to repeated suberythemal (non-burning) UV doses. Both groups showed similar reductions in DNA damage and redness (erythema), but Type IV skin repaired DNA faster . This suggests melanin not only absorbs UV but also enhances repair mechanisms.

• Zamudio Díaz et al. (2025) found that even at suberythemal doses, darker skin (Type IV) had shorter-lasting DNA damage compared to lighter skin (Type II). This indicates melanin provides continuous protection beyond just preventing burns .

• Young et al. (1991) observed that Type IV skin required 1.8 times higher UV doses to cause the same DNA damage as Type II skin. Melanin’s ability to scatter and absorb UV radiation was the primary reason .

3. Age: Declining Defense Mechanisms

As people age, their skin becomes more vulnerable to UV damage due to reduced repair efficiency and structural changes. The outer layer (epidermis) thins, collagen production decreases, and blood supply to the skin declines, weakening its ability to heal .

Key Findings

• Kemp et al. (2017) studied how aging affects DNA repair. They found that older skin (over 60 years) had 30% less IGF-1 (insulin-like growth factor-1), a protein critical for cell repair. Without sufficient IGF-1, cells struggle to fix UV-induced DNA damage, leading to higher mutation rates .

• Busch et al. (2023) compared UVB and Far-UVC (222 nm) exposure in young and old skin. While Far-UVC caused less DNA damage, older skin still showed slower repair for both UV types. This suggests age-related decline affects multiple repair pathways .

• Del Bino et al. (2006) noted that aging reduces the skin’s ability to tan, further diminishing its natural protection. Older individuals with Type II skin, for example, may develop more persistent DNA damage after UV exposure compared to younger counterparts .

4. Combined Effects: Skin Type and Age

The interaction between skin type and age is complex. While darker skin offers inherent protection, aging can blunt this advantage.

Research Insights

• Zamudio Díaz et al. (2025) observed that even in Type IV skin, older individuals had longer-lasting DNA damage at suberythemal UV doses. This indicates that while melanin slows initial damage, aging weakens the long-term repair capacity .

• Sheehan et al. (2002) found that repeated UV exposure improved protection in both Type II and IV skin, but Type IV skin maintained faster repair rates regardless of age. This suggests melanin’s benefits persist even as repair processes decline with age .

• Kemp et al. (2017) highlighted that older individuals with lighter skin (Type I-II) face the highest risk of UV-induced mutations. Their skin lacks both melanin protection and efficient repair mechanisms .

5. Practical Implications and Prevention

Understanding these factors is crucial for tailored sun protection. Here’s how to reduce risk:

For People with Lighter Skin (Type I-II):

• Daily sunscreen with SPF 30+ is essential, even on cloudy days. Reapply every 2 hours outdoors .

• Physical barriers like wide-brimmed hats and UV-blocking clothing provide extra protection.

For People with Darker Skin (Type IV-VI):

• While melanin offers natural protection, unprotected UV exposure still increases skin cancer risk. Use sunscreen with SPF 15+ and avoid prolonged midday sun .

• Monitor skin regularly for unusual moles or growths, as darker skin cancers are often diagnosed at later stages.

For Older Adults:

• Prioritize repair support: Topical creams with IGF-1 or retinoids may boost collagen production and repair .

• Avoid peak UV hours (10 AM–4 PM) and seek shade whenever possible.

6. Conclusion

UV radiation poses a significant threat to skin health, but the risk varies widely based on skin type and age. Darker skin benefits from melanin’s protective effects and faster repair, while lighter skin and aging both weaken defense mechanisms. By understanding these differences, individuals can adopt targeted strategies to minimize damage and maintain healthier skin. Remember: prevention is key, and no skin type is immune to the long-term effects of UV exposure. 

References

1. Zamudio Díaz DF, Schleusener J, Pacagnelli Infante VH, et al. Prolonged DNA damage at suberythemal UV dose – Dependency on skin type and age. J Photochem Photobiol B. 2025;270:113206. doi:10.1016/j.jphotobiol.2025.113206.

2. Sheehan JM, Cragg N, Chadwick CA, et al. Repeated ultraviolet exposure affords the same protection against DNA photodamage and erythema in human skin types II and IV but is associated with faster DNA repair in skin type IV. J Invest Dermatol. 2002;118(5):825-829. doi:10.1046/j.1523-1747.2002.01681.x.

3. Busch L, Kröger M, Zamudio Díaz DF, et al. Far-UVC- and UVB-induced DNA damage depending on skin type. Exp Dermatol. 2023;32(9):1582-1587. doi:10.1111/exd.14902.

4. Kemp MG, Spandau DF, Travers JB. Impact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin. Molecules. 2017;22(3):356. doi:10.3390/molecules22030356.

5. Young AR, Potten CS, Chadwick CA, et al. Photoprotection and 5-MOP photochemoprotection from UVR-induced DNA damage in humans: the role of skin type. J Invest Dermatol. 1991;97(5):942-948. doi:10.1111/1523-1747.ep12491807.

6. Del Bino S, Sok J, Bessac E, Bernerd F. Relationship between skin response to ultraviolet exposure and skin color type. Pigment Cell Res. 2006;19(6):606-614. doi:10.1111/j.1600-0749.2006.00338.x.