Atopic dermatitis is a chronic, pruritic, relapsing skin disorder that is thought to have an immunologic basis, often with a personal or family history of atopic conditions such as asthma or hayfever. The etiology however is not established, and has been linked to a number of factors including nutrient deficiencies and dietary allergens. (Berkow 1992; Spagnola 2005)
The clinical presentation can vary to a large degree, from a mild, itchy rash to severe, red crusting legions that can cover progressively larger regions of the body, and in children can interfere with normal growth and development. With repeated scratching the condition can worsen and secondary bacterial infections can appear. Very often the term eczema is used interchangeably with atopic dermatitis, however, eczema is a less precise term of which atopic dermatitis is a specific form, along with other sub-classifications that include allergic, irritant and seborrheic contact dermatitis. (Berkow 1992; Spagnola 2005)
The pathology of atopic dermatitis relates to a variety of IgE-mediated inflammatory response involving mast cells, lymphocytes, and leukocytes. The most prominent theory for this cause is an imbalance between Th1 and Th2 helper cell activities. Depending upon the antigenic substance, either Th1 or Th2 cells rise from the original T helper cell that interfaces with the antigen presenting cells. Th2 cells secrete cytokines in response to allergens, which in turn promotes the synthesis of immunoglobulin E (IgE). In contrast, Th1 is normally activated during infection with bacteria or parasites – the hygiene hypothesis states that the failure to acquire a normal flora both within and without the body suppresses Th1 response, and allows Th2 activities to function out of control. (Berkow 1992; Spagnola 2005)
Another prominent theory underlying the etiology of atopic dermatitis is either a deficiency of the essential omega-3 and omega-6 fatty acids, or a failure to properly metabolize them. This is clearly demonstrated in bottle-fed infants fed a formula lacking in either omega-6 or omega-3 fatty acids, which have a significantly higher incidence of atopic dermatitis than their breast-fed counterparts. Omega-3 acids specifically also promote the synthesis of eicosanoids that down regulates Th2 activity, and restores a balance between these paired T helper cells. Problems of essential fatty acid metabolism are thought to related to a potential hereditary deficiency of delta-6-desaturase, a key enzyme in the biotransformation of the essential fatty acids. Environmental factors that promote a deficiency of delta-6-desaturase include a diet rich in transfatty acids, aging, chronic disease and emotional stress. True omega-6 deficiencies are not as common as omega-3 deficiencies however, as omega-6 fatty acids are over consumed in the modern diet by a ratio as high as 20:1, when in reality the ratio should be closer to 2:1. (Berkow 1992; Spagnola 2005)
Another important factor to take into consideration is the role of food allergens and food intolerances in atopic dermatitis. Although generally not acknowledged as a major etiological factor by many medical professionals, at least on an anecdotal and clinical basis the removal of common food allergens including dairy, wheat, egg whites, soy, fish, shellfish and peanuts are often accompanied by significant improvements.
Atopic dermatitis can begin during infancy (i.e. ‘infantile eczema’), and can be relatively severe, with red, weeping, and crusting lesions over the entire body, particularly the face and scalp. In children the manifestations are typically less acute, more chronic lesions characterized by erythema and lichenification in typical areas such as inside the elbow or knee. In many people the condition goes into remission during puberty or adulthood, sometimes with periodic exacerbations. In many cases there is a concomitanthypersensitivity to numerous environmental factors, including changes in temperature or humidity, certain fragrances, fabric softeners, and wool. Given the embryonic link between the nervous and integumentary systems it is perhaps no surprise that emotional stress can promote atopic dermatitis. (Berkow 1992; Spagnola 2005)
The mainstay of the medical treatment of atopic dermatitis are topical corticosteroids, often used in increasing strength after simpler measures such as OTC creams, moisturizers and lotions have been tried to rehydrate the skin and relieve itching. In severe or particularly recalcitrant cases systemic corticoids may be used, and if the condition is refractive to steroids, immunosuppressives such as cyclosporine. Topical and systemic antipuritics are another important component of medical therapy, such as pramoxine, which acts to blocks nerve conduction and impulses by inhibiting depolarization of neurons, and doxepin, which is an antihistamine. Antibiotics are used both topically and systemically to deal with secondary bacterial infection.
In Western herbal medicine atopic dermatitis is viewed as a manifestation of skin deficiency, and thus measures are taken to address the underlying cause of such, which includes promoting liver anabolism, peripheral vasodilation, and skin and neuroendocrinal trophorestoration. Modifications are made to the diet on the basis that many of the foods commonly consumed in the modern diet are inherently antigenic, the most common culprits being gluten (e.g. wheat) and casein (A1 casein, derived from the milk of Bos taurus).
Initial herbal therapy consists of a mild eliminatory program, enhancing detoxification through the use of alteratives (e.g. Burdock [Arctium lappa], Red Clover [Trifolium pratense], Cleavers [Galium aparine], Nettles [Urtica dioica]), cholagogues (e.g. Yellow Dock [Rumex crispus], Bearberry [Berberis vulgaris], Black Radish [Raphanus sativus], Turmeric [Curcuma longa]), aperients (e.g. Cascara bark [Rhamnus purshiana], Amlavetasa [Rheum emodi], Trivit [Operculina turpethum], Triphala) and diuretics (e.g. Pipsissewa [Chimaphila umbellata], Buchu [Barosma betulina], Parsley leaf [Petroselinum sativum], Gokshura [Tribulus terrestris]). Circulatory stimulants are used to direct the activity of these herbs to the periphery (e.g. Prickly Ash [Zanthoxylum clava-herculis], Ginger [Zingiber officinale],Cayenne [Capsicum minimum], Pippali [Piper longum]). This approach can be followed or used concurrently botanicals that support neuroendocrinal function and down-regulate sympathetic stress (e.g. Licorice [Glycyrrhiza glabra], Damiana [Turnera diffusa], Milky Oats [Avena sativa], Reishi [Ganoderma lucidum], Ashwagandha [Withania somnifera], Skullcap [Scutellaria lateriflora] etc.), as well as botanicals that have a vulnerary activity (e.g. Comfrey [Symphytum officinale], Marigold [Calendula officinalis], Plantain [Plantago spp.], Gotu Kola [Centella asiatica] and Yin Chai Hu [Stellaria dichotoma]).
Trophorestorative nutrients including vitamins A, B, C and E are important, as well as antioxidants (e.g. grape seed extract, MSM, shilajitu), and omega fatty acids (EPA/DHA). In the case of atopic dermatitis in children of breast feeding mothers attention is directed to removing antigenic foods from the diet, the use of “galacto-purifiers” such as Turmeric (Curcuma longa), as well as the supplementation of essential fatty acids and trophorestorative nutrients.
Soaps and detergents are eliminated and replaced by simply using water, along with oatmeal baths and the topical application of Aloe vera juice to alleviate itching. Lesions can be treated directly with the application of baths, fomentations, oils and salves prepared with vulnerary and demulcent herbs such as Comfrey (Symphytum officinale), Marigold (Calendula officinalis), Plantain (Plantago spp), St John’s Wort (Hypericum perforatum), Gotu Kola (Centella asiatica) and Yin Chai Hu (Stellaria dichotoma). In Ayurveda, one traditional remedy for red, inflamed lesions is a medicated ghee preparation called Mahatiktakam ghritam, prepared from a number of herbs including Neem (Azadirachta indica), Turmeric (Curcuma longa), Barberry stem (Berberis nepalensis), Shatavari root (Asparagus racemosa), Guduchi stem (Tinospora cordifolia), and Licorice root (Glycyrrhiza glabra). For weeping, oozing sores a gentle astringents can be applied, such as Oak (Quercus spp.), Witch Hazel (Hamamelis virginiana) and Walnut bark (Juglans nigra), as a bath, fomentation, or as tinctures added to a cream (3-10% v/v). Secondary bacterial infection that may arise from scratching can be treated topically with antibacterial herbs, applying tinctures such as Goldenseal (Hydrastis canadensis), Neem (Azadirachta indica), and Purple Coneflower (Echinacea angustifolia) directly to the skin, several times daily.