Type I collagen is the primary structural protein of the dermis. COL1A1 and COL1A2 variants affect collagen fiber strength, skin elasticity, and wound healing rate. These variants determine both baseline skin structural quality and the rate at which collagen density declines with age — informing targeted collagen support protocols.
MMP1 encodes collagenase-1, an enzyme that breaks down skin collagen. The 2G allele at the -1607 promoter polymorphism increases MMP1 expression — accelerating collagen degradation under UV exposure and oxidative stress. Carriers benefit more from UV protection and antioxidant supplementation than the population average.
Melanin is the skin's primary UV protection. SLC45A2 and TYR variants determine melanin synthesis efficiency — affecting baseline photoprotection capacity and the threshold at which UV-induced DNA damage occurs. Genotypically low-melanin individuals require proportionally higher SPF and more aggressive photoprotection protocols.
SOD2 (superoxide dismutase 2) and CAT (catalase) are key antioxidant enzymes protecting skin cells from oxidative damage. Reduced-activity variants increase ROS-driven skin aging — accelerating photoaging, pigmentation irregularity, and wrinkle formation in proportion to sun exposure and metabolic stress.
Skin inflammation is a core driver of accelerated aging. IL6 and TNF variants that increase baseline inflammatory tone also increase the skin's inflammatory response to environmental stressors — relevant to acne tendency, wound healing speed, and the efficacy of anti-inflammatory skincare interventions.
Vitamin C is essential for collagen synthesis via prolyl and lysyl hydroxylases. SLC23A2 variants affect intracellular vitamin C transport — determining the endogenous vitamin C concentration available for collagen production. Low-transport variants increase the benefit of topical and supplemental vitamin C for skin quality.
Genotype-matched collagen supplementation and dietary recommendations — based on COL1A1/COL1A2 structural genetics and MMP1 degradation rate. The specific case for or against collagen peptides, vitamin C, and proline supplementation for a given individual.
Melanin genetics-driven photoprotection recommendations — a genotypically informed SPF framework rather than generic sun safety advice. Combined with MMP1 and oxidative stress variants, this provides a personalized UV damage risk profile.
A structured multi-variant aging risk profile — covering collagen degradation rate, oxidative stress capacity, UV sensitivity, and inflammatory tone. The genetic context that makes anti-aging interventions targeted rather than speculative.
Genotype-specific recommendations for antioxidant supplementation (vitamin C, vitamin E, CoQ10, astaxanthin), collagen support, and anti-inflammatory protocols — grounded in the specific variants that determine benefit from each approach.
Whether you're a skincare brand, a beauty supplement company, or a personalized wellness product — tell us about your use case and we'll show you what genomic intelligence adds.