Understanding melanin biology in Fitzpatrick III-V skin
Indian skin spans Fitzpatrick types III through V, which means higher baseline melanocyte activity and greater density of melanosomes distributed throughout the epidermis. Unlike Fitzpatrick I-II skin where melanosomes are clustered and degraded quickly, melanosomes in Indian skin are individually dispersed and persist longer in keratinocytes. This fundamental biological difference means that any inflammatory trigger — acne, friction, sun exposure, hormonal shifts — results in prolonged and more visible hyperpigmentation. The tyrosinase enzyme, which catalyses the rate-limiting step of melanin synthesis, is constitutively more active in darker skin tones. This is not a defect but an evolutionary adaptation for UV protection. However, it means that treatments must address not just existing pigmentation but the ongoing enzymatic overproduction that makes Indian skin prone to recurrence. Post-inflammatory hyperpigmentation (PIH) affects 94% of Indian acne patients compared to 48% of European patients with equivalent acne severity, making pigment management an inseparable component of any acne treatment protocol in the Indian context.