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Accessible online at: www.karger.com/journals/ned Multiple sclerosis (MS) has tantalised epidemiologists for half a century. The incidence is consistently higher in females than in males. In general, rates increase with latitude, although there are some noteworthy exceptions to this geographic gradient. Populations migrating between regions of discrepant risk tend to carry their original risk with them if they migrate after adolescence – but not if they migrate early in life, in which case they acquire the risk of their host environment population. Many risk factors have been invoked for MS. These include genetic susceptibility, dietary lipids, certain physicochemical (e.g. solvent) exposures, unusual patterns of childhood viral infectious disease, glandular fever and (reduced) exposure to ultraviolet radiation (UVR). As epidemiological studies have proceeded – comprising descriptive studies over time and place, migrant studies, and, less often, case-control and cohort studies – the pathogenesis of the disease has gradually become clearer. It is now generally agreed that MS entails an autoimmune process that destroys basic myelin protein (and hence blocks conduction) [1, 2]. That autoimmune basis to the disease may facilitate the drawing together of several of the otherwise apparently disparate risk factors. Viral infections, especially those occurring in later childhood and adolescence, can induce self-attack – that is, autoimmunity – when the immune system fails to distinguish between viral protein and myelin protein. The similarity between peptides, of course, is not accidental; it is via this molecular mimicry process that the virus enhances its survival and replication prospects. There is considerable evidence that infection with the Epstein-Barr virus in particular is involved in initiating MS [3–5]. The resultant autoimmune process is presumably modulated by certain factors that have immune-suppressive activity, including dietary polyunsaturated fats (especially the n-3 polyunsaturates, prominent within fish oils) and UVR. That last-mentioned factor, UVR, appears as subject of overlap in the two epidemiological studies of MS published in this issue of the journal. From much animal experimental research and some observations in human studies, it is apparent that UVR exposure has an immunesuppressive effect. The details are not fully resolved, but it seems to encompass both local and systemic immune suppression, including via suppression of Th1 cell activity. Since these cells mediate the attack on ‘self’ that characterises MS, and some other autoimmune diseases, it is plausible that UVR influences some aspect of MS pathogenesis. There are other possibilities too: UVR increases the synthesis of vitamin D3, and that in turn has a known immune-suppressive action. Indeed, a Japanese study has reported that a polymorphism (specifically the b allele) in

Multiple Sclerosis and Ultraviolet Radiation: Time to Shed More Light