Could vitamin D3 overdosing may be contributing to autoimmune diseases including CFS?

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The mechanism for L-form bacteria's sensitivity to D3 is theorized to be equivalent to smoking's nicotine addiction:

1. Try smoking. Toxin exposure causes nausea.
2. Try smoking again. Liver upregulates detox pathways to clear toxins faster, side effect is better nicotine tolerance and less toxin accumulation.
3. Nicotine blood levels from smoking increase causing euphoria due to dopamine increase.
4. Overstimulation of dopamine receptors causes decreases in the number of receptors causing the high to wear off.
5. Now dopamine receptors are desensitized so smokers feel less pleasure unless they smoke.

For L-form infection:

1. Viral infection decreases number of vitamin D receptors (VDR).
2. L-form bacteria exposure and colonizes, further decreases receptors.
3. Body responds to infection by maximizing production of 1,25D (D3) causing an overdose.
4. Overstimulation of VDR receptors causes decreases in the number of receptors causing the cells to stop receiving signals to make antibacterial peptides.
5. D3 is now in a vicious cycle where tolerance causes less effect until eventually no effect.

I found some interesting research regarding supplementation in Navy submariners. Doses of 400 IU daily D3 did not prevent bone turnover. I"m wondering if the problem could be due to decreased absorption due to overly frequent dosing; something we often see occurring with other supplements. Moreover, because D3 is the active form (1,25 D cholecalciferol) the body can't regulate its stores through feedback and it would be prone to overdose). You need 2000 IU/day D3 to overcome the resistance effect. This looks suspiciously similar to the above theorized D3 resistance and makes me suspect that daily dosing of D3 is unhealthy.

The submariner paper also quoted studies showing that VDRs are located on monocytes and lymphocytes47 and seem to promote self tolerance which is the ability of the immune system to not attack host tissues.48,49 This loss of autoimmunity may be a factor in CFS with a presentation similar to myastheia gravis where autoantibodies attack acetylcholine neurotransmitters. (Gertner, J. Vitamin D Supplementation in Submariners. December 2, 2008. Naval Submarine Medical Research Laboratory. NSMRL/50210/TR--2008-1267. http://www.dtic.mil/cgi-bin/GetTRDoc?Location=U2&doc=GetTRDoc.pdf&AD=ADA498140)
Here's the basic theory quoted from my comments in another thread.

I just found more evidence for a link between autoimmune disease and cell receptor changes due to uv light like what we see in D3 ingestion:

For years weve been warned that too much sun exposure increases the risk of skin cancer and can turn the soft, supple skin of youth into a weathered and leathered topography. But now it turns out the suns dangers are more than skin deep. The suns rays particularly deep-penetrating ultraviolet-A (UVA) rays can damage the DNA within the nuclei of the bodys cells, inhibiting their ability to control how and when cells grow and divide. While the most obvious threat is skin damage, the suns rays also can wreak havoc for many people with lupus, as well as those taking certain arthritis medications. And recent research has connected UV radiation with the development of cancer of lymphoid tissues, including Hodgkins disease, non-Hodgkins lymphoma and leukemia. (Dunkin, MA. Do you have an autoimmune disease? Why you should stay out of the sun. accessed 10/23/2010. http://www.arthritis.org/sun-and-the-immune-system.php)


No one understands what, specifically, the UVA rays do to immune system cells in people with lupus, but a large percentage of people with lupus have problems with the sun, says Robert Brodell, MD, professor of medicine in the dermatology section at Northeastern Ohio Universities College of Medicine in Rootstown. Problems can range from an immediate redness, burning and stinging of the skin to a systemic flare of the disease, characterized by inflammation of the joints, blood vessels and internal organs.

People with scleroderma, too, can be affected by sun exposure, says Frederick Wigley, MD, director of the Johns Hopkins Scleroderma Center in Baltimore. While they dont have the same blistering or flares associated with lupus, the sun can cause further damage to skin already hardened and damaged by the disease, he says. Also, some people with scleroderma have hyperpigmentation of the skin that is made worse by sun exposure.

Several medications that people take for those and other inflammatory diseases, including rheumatoid arthritis (RA), can also cause sun sensitivity and lead to problems such as skin rash or rapid burning. Some of the most common culprits are nonsteroidal anti-inflammatory drugs (NSAIDs) and some disease-modifying antirheumatic drugs (DMARDs), including hydroxychloroquine (Plaquenil), methotrexate and sulfasalazine (Azulfidine). Tetracycline antibiotics, some antidepressants and diuretics can cause sun sensitivity too.

Minimizing sun effects as well as reducing risks of cancers means protecting your skin from harmful rays.

Fluorescent Light & Lupus: May Be a Dangerous ComboThe sun isnt the only light source that gives off ultraviolet-A (UVA) rays. Most people dont know that fluorescent bulbs do too. For people with lupus who are extremely sensitive to UVA rays, the rays given off by fluorescent lights may cause a burn or trigger a flare. If you have fluorescent lights in your home, replace them. If you work in an office with fluorescent lighting, be sure to wear sunscreen to work. Ask to have the bulbs in your immediate work area removed or simply keep them turned off, if possible and use an incandescent desk lamp instead.
If you think about the way people have managed D3 in the past thousand years, there was no D3 available orally so what would happen is that people would get sun exposure for 3/4 of the year then in the winter be deprived-allowing the levels to go down. Now because there is supplementation in the food supply people lack that wean down period and overdose. Additionally, the daily dosing desensitizes the receptors to lower their activity.

I think the solution is to use vitamin D2 dosed weekly rather than D3 daily. This allows the body to use its feedback control mechanisms to control the D3 levels.
 

garcia

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Moreover, because D3 is the active form (1,25 D cholecalciferol) the body can't regulate its stores through feedback and it would be prone to overdose)
Your argument is full of basic errors. For example D3 is not the active form 1,25 D as you state.
 
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I doubt your assertion that these errors exist and easily found a source that shows your statement that D3 isn't the active form of vitamin D to be false.


Calcitriol (INN) (pronounced /ˌklsɨˈtraɪ.ɒl/ or English pronunciation: /klˈsɪtri.ɒl/), also called 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin D3, is the hormonally active form of vitamin D with three hydroxyl groups (abbreviated 1,25-(OH)2D3 or simply 1,25(OH)2D).[1]

-Nomenclature of Vitamin D. Recomendations 1981. IUPAC-IUB Joint Commission on Biochemical Nomenclature (JCBN)" reproduced at the Queen Mary University of London website. Retrieved 21 March 2010.
(http://en.wikipedia.org/wiki/1,25-Dihydroxycholecalciferol)
You are also wrong because the Marshall Protocol explicity bans all vitamin D and doesn't discriminate between ergocalciferol (25D) and cholecalciferol (1,25D) because it erronously believes 25D inhibits the VDR in any amount and dosing schedule.

Please refrain from posting more false information in the future.
 

garcia

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I doubt your assertion that these errors exist and easily found a source that shows your statement that D3 isn't the active form of vitamin D to be false.

I doubt your assertion that these errors exist and easily found a source that shows your statement that D3 isn't the active form of vitamin D to be false.


Calcitriol (INN) (pronounced /ˌklsɨˈtraɪ.ɒl/ or English pronunciation: /klˈsɪtri.ɒl/), also called 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin D3, is the hormonally active form of vitamin D with three hydroxyl groups (abbreviated 1,25-(OH)2D3 or simply 1,25(OH)2D).[1]

-Nomenclature of Vitamin D. Recomendations 1981. IUPAC-IUB Joint Commission on Biochemical Nomenclature (JCBN)" reproduced at the Queen Mary University of London website. Retrieved 21 March 2010.
(http://en.wikipedia.org/wiki/1,25-Di...holecalciferol)



You are also wrong because the Marshall Protocol explicity bans all vitamin D and doesn't discriminate between ergocalciferol (25D) and cholecalciferol (1,25D) because it erronously believes 25D inhibits the VDR in any amount and dosing schedule.
Ok I grant that you are saying something different from the Marshalites (as you say they say to avoid all Vitamin D, where as you are saying avoid D3 only).

But I repeat Vitamin D3 is *not* the same thing as 1,25-D.

Look here:
1,25D is also called calcitriol:

http://en.wikipedia.org/wiki/1,25-Dihydroxycholecalciferol

Vitamin D3 is called Cholecalciferol

http://en.wikipedia.org/wiki/Vitamin_D3
 
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It's the same thing. Don't jump to conclusions.

http://en.wikipedia.org/wiki/Vitamin_D3

Vitamin D3 has several forms:

Cholecalciferol, (sometimes called calciol) which is an inactive, unhydroxylated form of vitamin D3)
Calcifediol (also called 25-hydroxyvitamin D3), which is the form measured in the blood to assess vitamin D status[3]
Calcitriol (also called 1,25-dihydroxyvitamin D3), which is the active form of D3.
 

jace

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This exchange shows clearly why I prefer another forum. Constructive debate is far more illuminating.
 

garcia

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It's the same thing. Don't jump to conclusions.
It is not the same thing. "Active form" in this context means chemically it is a different compound, i.e. it has to be converted.

In the same way that T3 is the active form of T4. That doesn't mean that T3 & T4 are the same thing.
 
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Are you saying that wikipedia is wrong? I don't see your point. I think they are just pseudonyms and you are misreading too much into it.
 

garcia

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Are you saying that wikipedia is wrong? I don't see your point.
No, wikipedia is right. The links I posted above were to 2 different wiki articles showing that D3 and 1,25-D are different substances.

They are not pseudonyms. Understanding the difference between the two would help you perhaps refine your theories and see any errors in your argument.
 
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Thanks for the explanations. Actually the supplement I was using, cod liver oil, is D3 (I just learned) so this is moot.

But interestingly, three hours after taking 2000 IU of D3 my body temperature dropped to 95.2 F (was previously 97.8 F) so obviously this is an overdose. This supports what I was saying about there being fewer receptors. I'll be watching to see how long the effect lasts. I didn't have this response yesterday when I dosed 400 IU 2x.

Timing the temperature depression now. So far is on the way quickly back up to 97.2 after 40 minutes with supplement dosing.

I found a citation showing that a period of body temperature depression is common with Jared-Herxheimer reactions.
 
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The only stupid questions are the ones that you don't ask heckler.

I checked with a pharmacist before posting the thread and she was misinformed as well.
 

Martlet

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The only stupid questions are the ones that you don't ask heckler
Moderator: I have been following the posts in this thread and while argument has been strong, have not felt a need to intervene until now. Calling someone a heckler is out of line. Now, I am asking everyone to calm down and get back to the topic at hand without further name-calling, or I will close the discussion.
 
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Martlet do you not see the offensive nature of Bex's comment that I intentionally misinformed the board? That is heckling so there is nothing wrong with calling him out on it.

So far there has been no comment on the main idea of the thread, that sustained overdoses of vitamin D could cause receptor insensitivity and reduced immune response. I think this is a factor in my own bartinella spp infection.
 

rlc

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hi fejal i noticed your strange reaction to vit d and thought this may help, i don't know if you are taking any other medications or have been investigated for other contitions that may cause this but here's alink about it http://www.rxmed.com/b.main/b2.phar...s/CPS- (General Monographs- V)/VITAMIN D.html If anyone is taking or considering taking codliver oil they need to know this if they don't already link http://www.essortment.com/lifestyle/possiblesideef_slyf.htm as for the argument about the marshall protcol i think i'll stay out of it, but i would advise anyone considering it to read this link about the complications of vit d deficiency first http://www.buzzle.com/articles/vitamin-d-deficiency-symptoms.html have fun all the best
 
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I had my MD check out my hyperparathyroid hormone level re: the hypercalcemia but he didn't report anything abnormal which is pretty incredible given I was hypo at 17 for 9 months. I just started supplementing to get it back up so there's no way I can be hyper vit D. Moreover, cod liver oil is D3 not D2 (ergocalciferol).

If someone is infected with an L-form bacteria I do think it is preferable to not take any D because otherwise the active D is so high it demineralizes the bones. I had a lot of tooth erosion before I went hypo D, so going hypo probably saved my teeth.

The solution is to id the bug, supplement to correct blocked apoptotic pathways and then take D.