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Meg Mangin R.N.
Former Team Member
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Posted: Thu Dec 16th, 2004 07:03 |
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The Importance of Reducing 25-D
"The 25-D seems to be the most critical factor as to whether the immune system is able to start working. Any level of 25-D above about 20ng/ml is likely to be acting as an immunosuppressant, with an action very similar to that of corticosteroids."
The goal of avoiding all ingested Vitamin D while on the MP is to get your 25-hydroxyvitamin D as low as possible, and keep it there. The human body does not need any ingested vitamin D at all, it is counterproductive as the body generates as much active hormone as it needs. If your 25-D level cannot be detected by the lab, then that is excellent, and most of our cohort manage to get their levels undetectable. This should be everybody's goal. Give your body's metabolism a chance to do its job again."
Dr. Trevor Marshall, Ph.D.
Vitamin D is converted to 25-D and 25-D is immunosuppressive. It acts on the steroid receptors and that hinders the immune system from killing pathogens, just as the corticosteroids do.
Since 25-D has no function but to enable 1,25-D to be produced, if you have enough 1,25-D, then you do not need any 25-D. See You do not need to ingest Vitamin D to be healthy
Persons with Th1 inflammation produce excess 1,25-D directly within the kerotinocytes in the skin. No 25-D is necessary for this production.
Will the body generate active vitamin D hormone without light, dietary sources of vitamin D and vitamin D stores?
the opposite is true. In mammals other than man you don't find these ridiculous theories about sunlight and supplements advanced.
For example, the Lamprey (fish-like) has a VDR, and its population recently swelled to epidemic proportions in the Great Lakes. Where does it get its UVB from in that environment? Canadians are always being told that they need to sunbathe. That is just plain stupid. It has no basis in science or species evolution.
How do the nocturnal mammals get their supposed need for "vitamin" D?
If you look at Figure 1 of my most recent paper you will find that the human body can take care of every ounce of its production of activated Vitamin D, and it is at its best when exogenous or supplementary steroid is not forced upon it.
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
Ingested vitamin D
"I know of no reason the body needs ingested Vitamin D (25-D) provided that the 1,25-D stays within a reasonable range (above approx 12pg/ml). Most of the early adopters have kept their 25-D below 5 ng/ml (the lower limit of the testing in the USA) during the 2-3 years they have been on the MP, without any adverse effects.
Vitamin D feeds the inflamation, as it is converted to 25-D and 1,25-D in the mitochondria of the macrophages at an accelerated rate. One paper said that Gamma-interferon (from the bacterial reaction) increased the production of 1,25-D 30 times. IMO, if there already is enough 1,25-D then you just don't need any more (25-D).
High concentrations of 25-D (above 20ng/ml) will displace 1,25-D from the Vitamin D Receptor {VDR} and thus shut down the immune system's ability to mount a Th1 response in a concentration-dependent manner.
It is not possible for a person to control whether their D metabolism is working correctly or not. Supplementation with exogenous Vitamin D, 25-D; 1,25-D; or the pharmaceutical analogues, has not proven very satisfactory, as the body has such exquisite control over the D-metabolism, which regulates its primary defence against pathogens, termed 'innate immunity' by immunologists.
I have seen no evidence that the body cannot create its entire needs of 1,25-D by conversion from 7-dehydro-cholesterol. Exogenous Vitamin-D; and exogenous 25-D; both displace 1,25-D from performing its vital functions in the VDR.
All of the D metabolites are seco-steroids, and they affect the nuclear receptors in much the same way as cortico-steroids do.
As the level of vitamin D itself, or its metabolite 25-D, rises in the bloodstream some of them will enter the phagocytes, and, if the concentration of cholecalciferol or 25-D is high enough, they will displace 1,25-D from the VDR and inactivate it.
This means that they have disabled the body's last line of defense against intracellular pathogens which is not good. I think that a level of 25-D above 20ng/ml is totally suppressive of VDR activation, and therefore of innate immunity, and that levels of 25-D below 12 ng/ml seem to allow it to function moderately well."
Dr. Trevor Marshall, Ph.D.
25-D and photosensitivity
Natural light has very little effect on 25-D. A small amount of 25-D may be generated by exposure to sunlight. Sunlight catalyzes the production of the Vitamins D from 7-dehydro-cholesterol in the skin. In healthy folks a significant amount of 25-D will be generated, but in folks with Th1 disease that will energetically be converted to 1,25-D by the disease process, and 1,25-D is thus the resulting primary product. In healthy folks there will be remanent 25-D generated.
1,25-D is directly synthesized from 7-dehydrocholesterol when sunlight falls on the keratinocytes of the skin. Because the keratinocytes of Th1 patients are parasitized by CWD bacteria, they produce interferon-gamma (which is part of the bacterial defense mechanism) and TNF-alpha. These cytokines cause the cells of Th1 patients to produce much more 1,25-D in their skin than healthy folks. In patients with Th1 inflammation, the production, by sunlight, of 1,25-D in the skin predominates the production of 25-D. Studies show that all 25-D produced in the skin from sunlight is hydroxylated directly into 1,25-D, leaving no 25-D to be stored.
"The keratinocytes of the skin can, by comparison, make 1,25-D directly from 7-dehydro-cholesterol, and they do this when exposed to sunlight. Because the final stage of this reaction is also catalyzed by any Interferon-gamma from any inflammation paracrine to the keratinocytes, any and all 25-D which is made from sunlight is energetically converted to 1,25-D (OK, well, NEARLY all  ). Thus sunlight is not usually a significant contributor to the 25-D levels of Th1 patients. " ..Trevor..
Therefore, you cannot judge your level of photosensitivity by your level of 25-D.
The effect of sunscreen on 25-D
For some people, 25D may be raised by sun exposure, and, in fact, using Nizoral (ketoconazole cream) would not help that but might increase that tendency, since it blocks the conversion of 25D to 1,25D. So, the 25D is formed, but then goes into the blood stream instead of going straight to the 1,25D form.
It would probably be worth trying a switch to zinc oxide sunscreen or a combination of zinc oxide sunscreen and the keto cream. The zinc oxide seems to be able to block the 25D production. Probably one of the sunscreens with a higher level of zinc would be best -- like Kabana or UV Natural. Or covering up more is even better, if you can (like gloves etc..). ~Joyce Waterhouse, Ph.D.
When it's might be safe to resume eating foods high in vitamin D
Ingested Vitamin D is not something I would suggest, until your endogenous 25-D starts to regulate itself into the teens. That is likely to be 5+ years into the MP. Obviously, if there is nothing else to eat, then you have no choice, but, when given the choice, you should opt to continue staying away from mushrooms, fish, etc, until you are well beyond the risk of relapse. ..Trevor..
See also:
Vitamin D-Basic Information
Last edited on Fri Jun 13th, 2008 07:39 by Meg Mangin R.N.
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