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Published On: Sep 1, 2015
Last Updated On: Jul 15, 2021
The recent epidemic of atopic disorders, including asthma, allergic rhinitis, and atopic dermatitis (AD), is associated with the shift of human populations from life in a largely rural, agrarian society to ever-more crowded, urban settings.
While there is no doubt that rural life is protective, the usual explanation for the “immune hypothesis” may not be completely correct. This theory suggests that rural children get exposed early in life to microorganisms and antigens that induce immune tolerance, protecting them from developing the characteristic Th2-dominant (allergic- type) inflammation that is seen in most patients with AD.
But the shift from a rural to a more crowded, urban environment is associated not only with less exposure to tolerance-inducing, environmental antigens, but also a dramatic decrease in sun exposure. The studies that support this new paradigm are included in this article’s references for those who want to explore this subject in greater depth.
It seems obvious that children living in urban settings receive much less light than do their rural counterparts. Recent work from Korea has shown that moderate (suberythemal) doses of UV-B, which do not burn the skin, improve barrier function and antimicrobial defense (note: higher, sunburn-inducing doses, however, exert an opposite, deleterious effect). In fact, much of the evidence for the immune hypothesis can be explained instead by differences in sun exposure in rural vs. urban populations.
Moreover, moderate doses of UV-B irradiation could provide several other benefits for patients with AD, which are illustrated in Figure 1. For example, UV-B stimulates vitamin D production in the skin, which is beneficial not only for the barrier, but also for antimicrobial defense (vitamin D stimulates the production of an important antimicrobial peptide, LL-37, which combats skin infections).
Patients with AD experience problems with both their permeability barriers and antimicrobial defense, and problems with the barrier appear to be the underlying cause of AD, regardless of the specific gene that is mutated (filaggrin is only one of several that are now associated with AD).
My colleague, Dr. Jacob Thyssen (of Copenhagen, Denmark) and I wrote a Perspective article for the Journal of Allergy and Clinical Immunology. In this article, we summarize evidence in support of this new hypothesis; i.e., that an insufficiency of exposure to moderate UV-B irradiation could be a major contributor to the current AD epidemic.
But most importantly for AD patients are the therapeutic implications; during late spring, summer and early autumn, regular exposure to moderate doses of sunlight could provide large benefits for AD patients. (To receive the benefits of UV-B, exposure should be in midday, or at least between the hours of 10:00 a.m. and 3:00 p.m.). Since very little UV-B makes it through the atmosphere during late fall, winter and early spring, regular light treatments in a doctor’s office, or with a home light box should be considered.
Dr. Elias is Professor (Emeritus) of Dermatology at UC San Francisco, and a Staff Physician at the San Francisco Veterans Administration Medical Center. His laboratory is located at the new UCSF Medical Center at Mission Bay. Dr. Elias earned his undergraduate degree at Stanford University and then went to UCSF Medical School, followed by a dermatology residency in the Harvard-Massachusetts General Hospital program.