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+ | ====== Presentation - Vitamin D induced dysregulation of nuclear receptors may account for higher prevalence of some autoimmune diseases in women ====== | ||
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+ | **Type:** Conference presentation\\ | ||
+ | **Presenter: | ||
+ | **Conference: | ||
+ | **Location: | ||
+ | **Date: | ||
+ | **See also:** [[https:// | ||
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+ | {{ vimeo> | ||
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+ | ===== Transcript ===== | ||
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+ | I'm going to examine why autoimmune diseases such as Hashimoto' | ||
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+ | What might be going on? Well, one obvious difference between the sexes is that they express hormones at different levels. | ||
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+ | As Professor Marshall and other researchers have shown, the VDR controls important components of innate immunity, particularly the transcription of the cathelecidin and beta Defensin antimicrobial peptides.(({{pmid> | ||
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+ | Vigano' | ||
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+ | The endometrium may have evolved to express the VDR and produce 1,25-D in an effort to offset the drop in cell mediated immunity that occurs during the weeks before menstruation, | ||
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+ | But increasing evidence indicates that at some point in the history of man, a microbiota composed largely of intraphagocytic and biofilm bacteria evolved a way to take advantage of the innate immune response by creating ligands that dysregulate VDR activity. | ||
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+ | And unfortunately, | ||
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+ | Marshall' | ||
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+ | Here is the emulation of the alpha thyroid nuclear receptor (ThRa). | ||
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+ | So, when 1,25-D displaces T3, the genes with alpha thyroid promoters can no longer be transcribed. | ||
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+ | And as I mentioned before, this same pattern is be repeated when it comes to several of the body's other nuclear receptors. | ||
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+ | An additional effect is also of importance. | ||
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+ | So disabling the VDR with flow on effects to glucocorticoid, | ||
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+ | It comes as little surprise then that hormonal dysregulation is so intricately connected to autoimmune disease. | ||
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+ | We now have a pathway in the molecular biology showing how these apparently diverse physiological conditions can interact. Essentially, | ||
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+ | This model may also explain why women with autoimmune disease often find their symptoms escalate after pregnancy. | ||
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+ | I should also add that Marshall has shown that 25-D, which is derived from supplemental vitamin D is able to displace exogenous ligands from the nuclear receptors just as easily as 1,25-D - marking yet another way in which it is able to suppress the innate immune response. | ||
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+ | So it may indeed be possible that VDR dysregulation plays a significant role in the higher incidence of autoimmune disease observed among women, and that vitamin D supplementation could further account for the skew in incidence. | ||
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+ | Finally, I would like to add one more thing. When it comes to correlating disease incidence with low levels of vitamin D, it's also incredibly important to consider the alternate hypothesis, which is that the low levels of vitamin D may not be causing the disease but may simply be a result of the disease process. So, a low level of vitamin D correlated with an illness may simply be an indicator that the disease process has taken an effect in that patient. | ||
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+ | Thank you, and I appreciate your time. | ||
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+ | {{tag> | ||
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+ | ===== References ===== | ||
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