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Archived Comments for: Introduction of oral vitamin D supplementation and the rise of the allergy pandemic

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  1. Mechanisms for immune activity of oral vitamin D

    Amy Proal, Murdoch University

    25 November 2009

    Matthias Wjst has identified a time-related correlation between vitamin D consumption and higher rates of asthma (sometimes called the vitamin hypothesis). Our own molecular and clinical work supports his findings. Marshall has shown how 25-hydroxyvitamin-D slows innate immune activity by decreasing activity of a key receptor, the VDR.[1] This immunosuppressive property of oral vitamin D has led to its use as a palliative in autoimmune conditions.[2] Yet at the same time, a large body of metagenomic research has linked inflammatory conditions, including asthma, to the presence of persistent microbes.[3, 4] For example, Bisgaard et al. found that newborns who harbor certain types of bacteria in their throats, including Streptococcus pneumoniae and Haemophilus influenzae are at increased risk for developing recurrent wheeze or asthma early in life.[5] Vitamin D consumption slows the ability of the innate immune system to kill such pathogens, easing their proliferation and persistence.

    The contention that vitamin D deficiency causes rickets has been weakened by several recent studies that attribute development of the condition to hypophosphatemia.[6] Nigerian children with rickets have been cured by administration of calcium alone.[7] Bouillon et al. found that VDR null mice administered diets high in calcium and phosphorous did not develop rickets.[8]

    We are currently observing patients on a therapy that uses a VDR agonist and oral vitamin D restriction in order to re-activate innate immunity in autoimmune disease.[9] Many patients are reporting improvement and recovery.[10] Although we focused on autoimmune diagnoses, we have observed that asthmatic comorbidities are resolving as well. In addition, we have shown how the low levels of 25-D often reported in patients with asthma and other inflammatory diagnoses may be the result rather than the cause of the disease process.[4]

    Works Cited
    1. Marshall, T.G., Vitamin D discovery outpaces FDA decision making. BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology, 2008. 30(2): p. 173-82.
    2. Arnson, Y., H. Amital, and Y. Shoenfeld, Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis, 2007. 66(9): p. 1137-42.
    3. Proal, A.D., P.J. Albert, and T. Marshall, Autoimmune disease in the era of the metagenome. Autoimmunity Reviews, 2009. 8(8): p. 677-681.
    4. Albert, P.J., A.D. Proal, and T.G. Marshall, Vitamin D: the alternative hypothesis. Autoimmunity Reviews, 2009. 8(8): p. 639-644.
    5. Bisgaard, H., et al., Childhood asthma after bacterial colonization of the airway in neonates. The New England journal of medicine, 2007. 357(15): p. 1487-95.
    6. Demay, M.B., Y. Sabbagh, and T.O. Carpenter, Calcium and vitamin D: what is known about the effects on growing bone. Pediatrics, 2007. 119 Suppl 2: p. S141-4-S141-4.
    7. Graff, M., et al., Calcium absorption in Nigerian children with rickets. Am J Clin Nutr, 2004. 80(5): p. 1415-1421.
    8. Bouillon, R., et al., Vitamin D and human health: lessons from vitamin D receptor null mice. Endocr Rev, 2008. 29(6): p. 726-76.
    9. Blaney, G.P., P.J. Albert, and A.D. Proal, Vitamin D metabolites as clinical markers in autoimmune and chronic disease. Ann N Y Acad Sci, 2009. 1173: p. 384-90.
    10. Perez, T. MP Study Results. in 6th International Congress on Autoimmunity. 2008. Porto, Portugal. Available from:

    Competing interests

    None declared