We know that classic eczema (atopic dermatitis), is a chronic skin condition where the skin barrier is weakened or disrupted. This can lead to a cycle of inflammation, redness, and itchiness. Scratching further weakens the skin barrier, which can worsen the condition and lead to infections.

The filaggrin gene (filament aggregating protein) plays an important role in maintaining skin barrier integrity, preventing de-hydration, as well as preventing pathogens and irritants from getting through the skin barrier.  Those with eczema may have fewer copies of the FLG gene, resulting in less functional filaggrin protein in the epidermis, less natural moisturization factor, and a leakier skin barrier. [image reference: DOI 10.1111/bjd.14997] This in turn increases water loss (skin de-hydration) and pH, inhibiting lipid-generating enzymes, which decreases skin cell adhesion (tight junctions/corneodesmosomes), deregulates skin turnover (desquamation), and decreases ceramides (the lipid matrix).