Dev29 wrote:I am a bit of lurker here but my main question w/ vitamin d is whether or not it impact men and women equally. I don't have any paper reference handy, but that it doesn't "work" in men or at least not as well.
Does anyone here have any information?
Despite the recent expansion in vitamin D research, an immense gap remains in our knowledge of its multiple functions in the variety of cell types where the presence of vitamin D receptors and paracrine production of calcitriol have been established. However, it is now generally accepted that a strong connection between vitamin D and the immune system exists as suggested by several key findings: (a) the presence of VDR in activated human immune cells, (b) the ability of these cells to produce calcitriol, and (c) the ability of calcitriol to inhibit the proliferation of T cells. In addition, it has become increasingly evident in recent years that calcitriol plays a significant role in modulating the function of the immune system. Furthermore, many epidemiological studies strongly suggest that vitamin D deficiency and certain VDR polymorphisms may be linked to immune system related diseases such as multiple sclerosis, SLE, DM type I, alopecia (areata or universalis), and psoriasis.
The immunoregulatory pathways are based on populations of lymphocytes, termed regulatory T cells (Tregs), in which there is currently considerable interest. In the case of infectious disease, such populations may lead to rapid resolution, the establishment of latent or persistent infection or to tissue damage by autoimmune processes . Accordingly, Tregs have been termed ‘a dangerous necessity’ . This term implies that Tregs are neither ‘good’ or ‘bad’ per se but may, according to the overall pattern of responsiveness, participate in appropriate immune reactions leading to resolution of disease or in inappropriate ones resulting in immunopathology.
The temporal sequence of infections, especially initial and early ones, is crucial to the development of patterns of immune reactivity as prior contacts with other antigens may have induced cross-reactive T-helper cells competing with Tregs. As a consequence Tregs normally induced by the second pathogen may be marginalized or even eclipsed. The latter phenomenon, also known as lateral inhibition, has many parallels in biology, particularly in neurology. The locking of an immune response into an eclipsed state seems to involve an active deletion of clones of T-cells occurring as a result of reinfections or reactivations . In the case of MS, infections such as those with HHV-6 [30, 31] and, possibly, with CP [12, 26] occurring before or at the time of initial or reactivated EBV infection could have such an effect.
mrbarlow wrote:I would love to see some definitive research on what effect Vit D has post diagnosis and in respect to progression of disability.
daverestonvirginia wrote:If you have not had your vitamin d level checked, I would do that. I was taking 4000 IU a day also, had my level checked and it was still very low. We should be looking for a vitamin d level of 125nmol/l. Everyone is a little different so the vitamin d level tests are important.
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