A recent multi-center, randomized, controlled trial (RCT) investigated the effects of oral vitamin D3 supplementation on atopic dermatitis:
Hata TR, Audish D, Kotol P, et al. A randomized controlled double-blind investigation of the effects of vitamin D dietary supplementation in subjects with atopic dermatitis. J Eur Acad Dermatol Venereol. 2013; [Epub ahead of print]
Atopic dermatitis (AD), or eczema, is a chronic, itchy skin rash. The condition is thought to have a genetic basis and is often, but not always, accompanied by asthma and hay fever. It is not contagious.
Persons with AD have an increased susceptibility to skin infections due to deficiencies in the innate immune system, including a lessened production of antimicrobial peptides (AMPS) and defects in skin barrier function. They display less AMPs in inflamed skin than would otherwise be expected. Because activated vitamin D is known to increase the production of cathelicidin, a key AMP, researchers hypothesized that supplementation with oral vitamin D might positively alter the course of AD in affected individuals.
76 total subjects were included in this multi-center RCT:
The psoriatic individuals were included to explore the possibility that alterations in AMPs similar to those seen in individuals with AD play a role in their skin condition.
Subjects were randomized to either 4,000 IU of vitamin D3 per day or a placebo for 21 days. Serum calcium, creatinine, parathyroid, IgE, 25(OH)D, cathelicidin and other AMPs, and IL-13 levels were obtained at baseline along with skin biopsies.
Subjects with AD had a mean baseline 25(OH)D serum level of 28.4 ng/mL. There was no statistically significant difference between baseline serum 25(OH)D levels in subjects with AD and the other groups. However, serum IgE at baseline was elevated in AD subjects compared to the other groups.
After three weeks of oral D3 supplementation, mean 25(OH)D levels in the AD subjects had risen to 39.5 ng/mL. A similar change was observed in the control group, but no statistically significant rise in serum vitamin D was seen in the subjects with psoriasis. One possible explanation for this observation offered by the researchers is that the average BMI of the psoriasis group was higher than the other groups, and it is well established that higher BMIs correlate with lower 25(OH)D levels.
While no change in cathelicidin or other AMPs from baseline was noted in any of the groups, the authors noted a promising “weak, negative correlation” between serum vitamin D levels and IL-13, a TH2 cytokine. TH2 cytokine involvement is an established element in the pathophysiology of AD and can lead to the suppression of AMPs, initiating a cascade of events that culminates in the secondary infections of AD.
The authors noted small sample size and short duration of vitamin D therapy as major limitations to their study. Because previous, similar studies yielded mixed results, they cited an urgent need for replication of this study with more subjects for a longer period of time to determine the role of vitamin D in AD.
This exciting new research in the form of a RCT may have uncovered a mechanism that explains how vitamin D can help in AD. While observational studies have suggested that vitamin D may be of benefit to people with AD, future clinical trials are necessary clarify whether or not vitamin D is useful in this skin disorder. Currently, vitamin D analogs and UV lamps are used to treat a variety of skin disorders, but it is unknown if nutritional vitamin D offers the same benefits. If it does, AD sufferers would have a safe and inexpensive therapy to combat the symptoms of an often stubborn skin condition.