Filaggrin

Filaggrin is stored as a large precursor, profilaggrin, in the granular layer of the epidermis. As a cell moves upward it is cut into filaggrin units, and those units bundle keratin filaments together — the name is a contraction of filament aggregating protein. The result is the flattened, densely packed corneocyte that acts as the brick in the brick-and-mortar picture of the barrier.

Then it does a second job. Higher in the stratum corneum the protein is broken down again, this time into free amino acids and their derivatives: pyrrolidone carboxylic acid, urocanic acid and the rest of what is collectively called natural moisturizing factor. These hold water inside the corneocyte, and urocanic acid contributes to the acidity of the surface. So one protein both builds the wall and supplies the humectant inside it. Its breakdown is sensitive to the air around the skin — dry conditions accelerate it, which is one mechanism by which winter changes how skin behaves.

This is also the clearest place where genetics shows up in skin. Loss-of-function variants in the filaggrin gene are the strongest known inherited risk factor for atopic dermatitis, and are also behind ichthyosis vulgaris. Someone carrying them makes less filaggrin and therefore less natural moisturizing factor, with a drier, more permeable stratum corneum from birth.

No cosmetic changes that. Products marketed as filaggrin boosters are not supported by anything that would justify the phrase. What a routine can do is replace what the deficit costs: humectants that stand in for natural moisturizing factor, an occlusive layer to slow water loss, a low-pH gentle cleanser, and less of everything that strips. A persistent itchy rash is a diagnosis, not a formulation problem.