Translating the Donguibogam concept of body fluids into modern medical terms points directly to our skin's moisture barrier function and internal homeostasis maintenance. Atopic dermatitis goes beyond merely itching from dryness; it is a chronic inflammatory disease caused by a complex interplay of genetic and environmental factors. The stratum corneum, the outermost layer of the skin, is tightly arranged like bricks and mortar, serving as a crucial defense shield that blocks foreign irritants and prevents internal moisture loss. Patients with atopic dermatitis frequently have an impaired defense shield, namely the skin barrier. Mutations in the gene encoding the skin barrier protein filaggrin are common, which loosens adhesion between skin cells and reduces natural moisturizing factor production, leaving the skin easily dried and vulnerable to external stimuli. This aligns with the Donguibogam perspective that a lack of body fluids parches the skin and leaves it easily exposed to external wind.
Modern medicine also explains atopic dermatitis from the perspective of an imbalance in the immune system. While a normal cutaneous immune response defends properly against foreign invaders, the immune system in atopic patients reacts hypersensitively, triggering inflammatory reactions. In particular, excessive activation of Th2 lymphocytes leads to the generation of IgE antibodies and the secretion of inflammatory mediators like histamine, inducing pruritus and skin inflammation. This chronic inflammation further damages the skin barrier, creating a vicious cycle of itch-scratch-worsening. Much like Donguibogam's view that heat dries body fluids and fuels inflammation, modern medicine also sees that chronic inflammation impedes skin hydration and barrier function, intensifying the disease.
Recently, an imbalance in the skin microbiome has gained attention as an important factor in atopic dermatitis. In healthy skin, diverse beneficial bacteria coexist, suppressing harmful bacteria proliferation and modulating skin immunity; however, in atopic skin, specific harmful bacteria such as Staphylococcus aureus tend to overgrow and aggravate inflammation. Furthermore, from a neurological perspective, mechanisms are being elucidated where cutaneous sensory nerves become excessively sensitive, perceiving even minor stimuli as itch, which the brain processes as pain signals, amplifying discomfort. All these elements interact in complex ways to cause chronic atopic dermatitis. Just as Donguibogam emphasized whole-body balance and body fluids, modern medicine likewise recognizes the importance of an integrative approach that goes beyond merely suppressing symptoms to strengthening the skin barrier, modulating immune balance, and managing internal inflammation.
