Zinc is an essential nutrient that functions as an important cofactor in cell metabolism and growth pathways.20 One study showed that intracellular erythrocyte zinc levels were significantly lower in AD patients compared to healthy controls (P<.001); however, there was no observed difference in serum zinc levels (P=.148). Furthermore, greater disease severity as determined by the SCORing Atopic Dermatitis (SCORAD) index was negatively correlated with erythrocyte zinc levels (r=−0.791; P<.001).21 Kim et al22 investigated hair zinc levels and the efficacy of oral zinc supplementation in children with mild to moderate AD. Mean (SD) hair zinc levels were lower in the AD group compared to the control group (113.10 [33.6] μg vs 130.90 [36.63] μg [P=.012]). Of 41 AD patients with low zinc levels, 22 were allocated to group A, which received oral zinc oxide 12 mg for 8 weeks, and 19 were allocated to group B, which did not receive any supplementation over the same period. Groups A and B also received oral antihistamines and topical moisturizers. Mean (SD) zinc levels increased significantly in group A from 96.36 (21.05) μg to 131.81 (27.45) μg (P<.001). Furthermore, relative to group B, group A showed significantly greater improvements in eczema area and severity index (P=.044), transepidermal water loss (P=.015), and visual analog scale for pruritus (P<.001) at the end of 8 weeks. The authors concluded that oral zinc supplementation might be an effective adjunctive therapy for AD patients with low hair zinc levels.22
Researchers also have explored the efficacy of fat-soluble vitamins D and E in treating AD. Vitamin D is thought to downregulate IgE-mediated skin reactions and decrease adverse effects of UV light on the skin.23,24 A double-blind, placebo-controlled trial randomized 45 patients with AD to 4 groups: vitamins D and E placebos (n=11), 1600 IU vitamin D3 plus vitamin E placebo (n=12), 600 IU vitamin E (synthetic all-rac-α-tocopherol) plus vitamin D placebo (n=11), and 1600 IU vitamin D3 plus 600 IU vitamin E (synthetic all-rac-α-tocopherol)(n=11).25 After 60 days, the SCORAD index was reduced by 28.9% in the placebo group, 34.8% in the vitamin D3 group, 35.7% in the vitamin E group, and 64.3% in the combined vitamins D and E group (P=.004). Furthermore, prior to intervention, a negative correlation was demonstrated between plasma α-tocopherol concentration and the SCORAD index (r=−.33; P=.025).25 Thus, supplementing vitamins D and E may play a beneficial role in the treatment of AD.
Other emerging studies are investigating the role of the gut microbiome in various pathologies. Prebiotics may alter the gut microbiome and are thought to play a role in reducing intestinal inflammation.26 One randomized, placebo-controlled, parallel study examined the effect of prebiotic oligosaccharide supplementation on the development of AD in at-risk children, defined as having a biological parent with a history of asthma, allergic rhinitis, or AD.27 At 6-month follow-up, 10 infants (9.8%)(95% CI, 5.4%-17.1%) in the intervention group (n=102) and 24 infants (23.1%)(95% CI, 16.0%-32.1%) in the placebo group (n=104) had developed AD. The authors postulated that the prebiotic oligosaccharides might play a role in immune modulation by altering bowel flora and preventing the development of AD in infancy.27
Notably, a 2012 Cochrane review evaluated 11 studies of dietary supplements as possible treatment options for AD. The authors concluded that the evidence was minimal to support the regular use of dietary supplements, especially due to their high cost as well as the possibility that high levels of certain vitamins (eg, vitamin D) may cause long-term complications.26