Proc Soc Exp Biol Med. 1997 Oct;216(1):21-7.Links
Vitamin D and multiple sclerosis.
Hayes CE, Cantorna MT, DeLuca HF.
Recently, it has been clearly demonstrated that exogenous 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent experimental autoimmune encephalomyelitis (EAE), a widely accepted mouse model of human multiple sclerosis (MS). This finding has focused attention on the possible relationship of this disease to vitamin D. Although genetic traits certainly contribute to MS susceptibility, an environmental factor is also clearly involved. It is our hypothesis that one crucial environmental factor is the degree of sunlight exposure catalyzing the production of vitamin D3 in skin, and, further, that the hormonal form of vitamin D3 is a selective immune system regulator inhibiting this autoimmune disease. Thus, under low-sunlight conditions, insufficient vitamin D3 is produced, limiting production of 1,25-dihydroxyvitamin D3, providing a risk for MS. Although the evidence that vitamin D3 is a protective environmental factor against MS is circumstantial, it is compelling. This theory can explain the striking geographic distribution of MS, which is nearly zero in equatorial regions and increases dramatically with latitude in both hemispheres. It can also explain two peculiar geographic anomalies, one in Switzerland with high MS rates at low altitudes and low MS rates at high altitudes, and one in Norway with a high MS prevalence inland and a lower MS prevalence along the coast. Ultraviolet (UV) light intensity is higher at high altitudes, resulting in a greater vitamin D3 synthetic rate, thereby accounting for low MS rates at higher altitudes. On the Norwegian coast, fish is consumed at high rates and fish oils are rich in vitamin D3. Further, experimental work on EAE provides strong support for the importance of vitamin D3 in reducing the risk and susceptibility for MS. If this hypothesis is correct, then 1,25-dihydroxyvitamin D3 or its analogs may have great therapeutic potential in patients with MS. More importantly, current research together with data from migration studies opens the possibility that MS may be preventable in genetically susceptible individuals with early intervention strategies that provide adequate levels of hormonally active 1,25-dihydroxyvitamin D3 or its analogs.
J Chronic Dis. 1983;36(8):551-9.Links
Epidemiology of multiple sclerosis in U.S. veterans: 2. Latitude, climate and the risk of multiple sclerosis.
Norman JE Jr, Kurtzke JF, Beebe GW.
An analysis of ten climatic factors and elevation for the counties of birth of 4371 U.S. white male veterans with multiple sclerosis and matched controls has been made in relation to birthplace latitude. The climatic factors include an air pollution index, concentrations of minerals in ground water, measures of annual solar radiation, both in energy per unit area and in hours of sunshine, mean annual periods of high and low temperatures, and measures of annual rainfall and average humidity. These variables all significantly influence the risk of multiple sclerosis when analyzed alone, but when they are adjusted for latitude, their effect is found to be due to their correlation with this variable.
Does Immunosuppressive UV Radiation Explain the Latitude Gradient for MS?
Multiple sclerosis is regarded as an autoimmune disease. The autoimmune process is thought to be triggered by early-life exposure to viral/bacterial antigens that share key peptide sequences with myelin protein (the target of autoimmune attack in multiple sclerosis). It has long been known that the incidence of multiple sclerosis is positively correlated with latitude, particularly in Caucasian populations. There is no agreed explanation for this latitude gradient, however. Ultraviolet radiation level is negatively correlated with latitude. Recent evidence suggests that ultraviolet-B is immunosuppressive, affecting particularly T-cell activity and delayed-type hypersensitivity. We hypothesize here that the latitude gradient of multiple sclerosis may reflect differential ultraviolet suppression of autoimmune activity, particularly since the autoimmune profile of multiple sclerosis is characterized by disturbances of those T-cell-related activities that are specifically affected by ultraviolet-B. We propose toms specifice tests of this hypothesis.
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