Androgenetic alopecia (AGA), the most common cause of hair loss in men and women, involves progressive follicular miniaturization and reduced hair density. Emerging evidence implicates the scalp microbiome as a potential modifier of this process. Preliminary evidence suggests alterations in microbial communities in patients with AGA compared to the general population, with the most robust finding being an enrichment of Cutibacterium acnes, particularly in males. Increases in Malassezia and reductions in Lawsonella and Corynebacterium have also been described, though results are less consistent across studies, while Staphylococcus displays variable patterns. These microbial shifts parallel alterations in scalp sebum composition, such as elevated triglycerides and palmitic acid, that may favor growth of lipophilic microbes. Mechanistic insights from in vitro studies and related inflammatory skin conditions indicate that C. acnes and Malassezia spp. are capable of generating free fatty acids and activating innate immune pathways, such as TLR2- and NLRP3-associated signaling, leading to pro-inflammatory cytokine production, potentially contributing to follicular stem cell apoptosis and hair follicle miniaturization. Although findings remain heterogenous, emerging evidence suggests microbial-lipid-immune interactions may contribute to AGA pathogenesis, providing a rationale for exploring treatments like ketoconazole or other lipid-modulating interventions.
Gupta et al. (Fri,) studied this question.