Skin Barrier Function

The permeability barrier is usually described as bricks and mortar: flattened, keratin-filled corneocytes bound by corneodesmosomes and surrounded by lipid sheets extruded from lamellar bodies in the granular layer. The mortar does the work, and its composition is specific, dominated by ceramides with cholesterol and free fatty acids in roughly equimolar proportion. Filaggrin breakdown products supply the natural moisturising factor and help hold a surface pH near five, which keeps the lipid-processing enzymes active.

Barrier state is measurable rather than notional. Transepidermal water loss indexes permeability, capacitance-based corneometry indexes hydration, and the two are different quantities. Loss-of-function mutations in filaggrin, carried by close to one in ten people of European ancestry, impair the barrier and are among the strongest known genetic risk factors for atopic dermatitis. After tape stripping or solvent damage, lipid synthesis restarts within hours and function usually recovers over one to three days.

This changes how any topical result should be read, because the barrier is simultaneously the thing measured and the thing controlling exposure. An impaired barrier admits more of an active, so one formulation can be well tolerated on intact skin and irritating on eczematous or over-exfoliated skin, and efficacy data generated in compromised skin does not generalise upward.

The measurement trap is immediate post-application testing. Any occlusive or film-forming ingredient lowers transepidermal water loss within minutes by adding a physical layer, which is not repair and will not survive washing; a genuine repair claim needs measurement after a washout with the product absent. Lower water loss alongside unchanged hydration tells you an occlusive was applied, not that lamellar organisation improved.