The skin is not a passive surface. It is an active system with a specific function that goes far beyond aesthetics: it is the body's first line of defense against the environment. The concept of "barrier function" – so present in the discourse of advanced dermatology and cosmetics – refers to a very precise biological architecture that can deteriorate, and which has solutions both from the outside and from within.
The barrier function explained in plain language
The stratum corneum – the outermost layer of the epidermis – is composed of corneocytes (flattened dead cells rich in keratin) embedded in an intercellular lipid matrix primarily composed of ceramides, free fatty acids, and cholesterol. This structure, commonly described as "bricks and mortar," has two main functions: preventing water loss from within (TEWL, Trans-Epidermal Water Loss regulation) and blocking the entry of pathogens, irritants, and allergens from the outside.
The Natural Moisturizing Factor (NMF), present inside corneocytes, acts as an additional moisture reservoir: it is composed of amino acids, lactic acid, urea, and other hygroscopic components derived from the degradation of filaggrin.
Signs that your barrier is compromised
A deteriorated skin barrier manifests in several ways: persistent dryness that doesn't respond well to topical hydration, a feeling of tightness especially after cleansing, redness or increased reactivity to products previously well-tolerated, itching without apparent cause, a greater tendency to dermatitis or eczema flare-ups, and an irregular or scaly texture even with regular hydration.
Many people with reactive, sensitive, or atopic eczema-prone skin share a common defect in barrier function – whether genetic, acquired, or aggravated by habits. Recognizing the signs is the first step to addressing them with appropriate strategies.
The 5 most common causes of barrier damage
The most frequent causes of barrier function deterioration are: over-exfoliation (excessive use of AHA, BHA, or retinol in inappropriate concentrations or frequencies), the use of cleansers with aggressive detergents that remove intercellular lipids, unprotected environmental exposure (UV, cold, wind), chronic stress (which increases cortisol and reduces ceramide synthesis), and nutritional deficiencies of zinc, vitamin A, and essential fatty acids.
The role of nutrition in barrier integrity
Ceramide synthesis, filaggrin production (which generates NMF), and the activity of barrier repair enzymes depend on specific nutrients. Zinc is a cofactor for multiple enzymes involved in epidermal protein synthesis. Vitamin A (retinol) regulates keratinocyte differentiation and the expression of barrier proteins. Essential fatty acids are direct precursors of ceramides.
This means that a skin barrier damaged by nutritional causes – zinc, vitamin A, or fatty acid deficiencies – cannot be fully repaired with topical cosmetics alone. Internal nutritional support is part of the solution.
Zinc, vitamin A, and fatty acids: what the evidence says
Zinc has authorized EFSA claims for the maintenance of normal skin. Vitamin A – present in LEVIAL at 800 µg/vial, covering 100% of the NRV – has the EFSA claim: "contributes to the maintenance of normal skin." Omega-3 fatty acids have evidence regarding the reduction of skin inflammatory markers and improved hydration in skin with a compromised barrier.
External care + internal support: the correct logic
Repairing and maintaining barrier function requires acting on two levels simultaneously: externally, with gentle cleansers, occlusive humectants (ceramides, hyaluronic acid, niacinamide), and reduction of aggressive stimuli; internally, with the nutrients the epidermis needs to synthesize its own lipids and structural proteins. Neither level replaces the other: they complement each other.
