Professor Ebers Vit D
Posted: Thu Feb 05, 2009 2:23 pm
I think I posted this in Summer 2007, but given today's research the talk by Professor Ebers may be of interest.
Ian
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Ian
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Hey Robbie...
UV-B The ultraviolet wavelength that stimulates our bodies to produce vitamin D is UV-B.
The reason it is difficult to get adequate vitamin D from sunlight is that while UV-A is present throughout the day, the amount of UV-B present has to do with the angle of the sun's rays. Thus, at higher latitudes, UV-B is present only during midday hours and only has significant intensity in temperate or tropical latitudes. Only 5 percent of the UV-B light range goes through glass and it does not penetrate clouds, smog or fog.
Sun exposure at higher latitudes before 10 am or after 2 pm will cause burning from UV-A before it will supply adequate vitamin D from UV-B. This finding may surprise you, as it did the researchers. It means that sunning must occur between the hours we have been told to avoid. Only sunning between 10 am and 2 pm during summer months (or winter months in southern latitudes) for 20-120 minutes, depending on skin type and color, will form adequate vitamin D before burning occurs.(9)
It takes about 24 hours for UV-B-stimulated vitamin D to show up as maximum levels of vitamin D in the blood. Cholesterol-containing body oils are critical to this absorption process.(10) Because the body needs 30-60 minutes to absorb these vitamin-D-containing oils, it is best to delay showering or bathing for one hour after exposure. The skin oils in which vitamin D is produced can also be removed by chlorine in swimming pools.
If you have symptoms of vitamin D insufficiency or are unable to spend time in the sun, consider adding a supplement of 2,000 IU daily. Higher levels may be needed but should be recommended and monitored by your health care practitioner.
Adequate calcium and magnesium, as well as other minerals, are critical parts of vitamin D therapy. Without calcium and magnesium in sufficient quantities, vitamin D supplementation will withdraw calcium from the bone and will allow the uptake of toxic minerals. Do not supplement vitamin D and do not sunbathe unless you are sure you have sufficient calcium and magnesium to meet your daily needs. Weston Price suggested a minimum of 1,200-2,400 mg of calcium daily. Research suggests that 1,200-1,500 mg is adequate as a supplement for most adults, both men and women. (Magnesium intake should be half that of calcium.)
Jimmy,In my experience, high, infrequent dosing can lead to problems. In one recent study, blood levels rose from low to extremely high, (more than 300 nmol/l) 24 hours after a 50,000 IU oral dose,65 and then slowly returned to pretreatment suboptimal levels. Clearly this must disrupt normal feedback mechanisms in D and calcium regulation
ACA T cell repertoire with millions of specificities provides surveillance against a multitude of foreign pathogens [32]. An inherent danger in recognizing so many foreign proteins is the potential to respond to self-proteins. To circumvent this problem T cells are scrutinised for self-reactivity as they mature in the thymus with deletion of those posing the greatest threat (central deletion) [32]. One constraint on central deletion is the requirement for the relevant autoantigen to be present in the thymus. Whether or not these are expressed as proteins at levels sufficient to induce T cell deletion is not clear. Given the results of this study, variable expression of HLA-DRB1 could affect central deletion of autoreactive T cells. It is plausible that a lack of vitamin D in utero or early childhood can affect the expression of HLA-DRB1 in the thymus, and impacting on central deletion. For MS, in HLA-DRB1*15 bearing individuals, a lack of vitamin D during early life could allow auto reactive T cells to escape thymic deletion and thus increase autoimmune disease risk. Indeed it has been shown that antigen presentation in the thymus of VDR knock-out mice is impaired [33]
You are right, the study discusses what kind of antigene representation in the thymus might be relevant for autoreactive T-cell (ARTC) deletion.cheerleader wrote: Here's what the study says about t-cells, Frank. It's more about the specificity of autoantigen presentation in the "central deletion" process, as opposed to elevated levels of autoreactive t-cells.
--FrankGiven the results of this study, variable expression of HLA-DRB1 could affect central deletion of autoreactive T cells. It is plausible that a lack of vitamin D in utero or early childhood can affect the expression of HLA-DRB1 in the thymus, and impacting on central deletion. For MS, in HLA-DRB1*15 bearing individuals, a lack of vitamin D during early life could allow auto reactive T cells to escape thymic deletion