Beyond UV: Visible Light and Pigmentation.

Abstract

Background: Melasma and post-inflammatory hyperpigmentation (PIH) are common dermatologic conditions disproportionately affecting individuals with darker skin phototypes, carrying substantial psychosocial burden and reduced quality of life. Emerging evidence increasingly implicates visible light (VL), particularly high energy visible (HEV) light, as a significant but underappreciated driver of disease appearance and progression.

Aims and methods: This narrative review integrates mechanistic and clinical evidence to examine VL's pathogenic role in melasma and PIH, synthesising data on opsin-mediated melanocyte activation, clinical trial outcomes of VL protective interventions and patient adherence barriers to photoprotection strategies.

Results and discussion: HEV (400-450 nm) activates opsin-3 on melanocytes, triggering calcium-dependent signaling that increases melanogenesis in a wavelength-specific manner. Clinical studies confirm that blue-violet light induces dose-dependent hyperpigmentation whereas red light produces none. Notably, pigmentation induced by high-energy visible (HEV) light can be substantial and persist over time. Protection against VL significantly enhances melasma treatment outcomes: melasma patients using iron oxide-containing sunscreen achieved 15% greater Melasma Area and Severity Index (MASI) improvement, 28% greater lightening on colorimetry and 4% greater histologic reduction in melanin than patients using an otherwise similar UV-only sunscreen. VL also seems to be involved in PIH, as suggested by a suction blister PIH model in which light-blocked sites healed without hyperpigmentation by Day 29, unlike ambient light-exposed sites that showed colorimetric and histologic darkening. Adherence to photoprotection in general remains suboptimal. Fewer than two-thirds of patients with hyperpigmentation use sunscreen and fewer than 10% reapply appropriately, with worse habits observed in skin of color, the population at greatest risk. Shade incompatibility of tinted formulations represents a key additional barrier to the use of VL-specific photoprotection.

Conclusion: This review establishes VL as a clinically significant driver of melasma and PIH pathogenesis. Standardising VL photoprotection metrics and integrating these into sunscreen development is essential. Incorporating VL protective strategies into treatment recommendations is critical to improving outcomes, particularly in darker skin individuals where disease burden is greatest and treatment most challenging.