Second-guessing the consensus on vitamin D

[Sushi]

Interesting. How long do you have to stay on GcMAF?

That is very individualized. Depends on how your immune system responds.

Sushi

 

[Symptomatic]

Here's a PDF file re Sarc and Vitamin D deficiency -- he suggests raising d slowly -- but the lists 50,000Ius(!) of D2 (!!!) as part of his treatment. Anyway...for your curiosity:

http://www.ildcare.nl/Downloads/ildcaretoday/engels/april_2012_Sharma.pdf

But he also says in that article:

"Sarcoidosis patients who have hypercalcemia should be treated first for their high calcium levels and hen their vitamin D levels be cautiously corrected (see also table 1)."

And the abtract for this article (also by Sharma) is below (big bold font is mine): http://journal.publications.chestnet.org/article.aspx?articleid=1069447

Abstract
Hypercalcemia occurs in about 10% of the patients with sarcoidosis; hypercalciuria is about three times more frequent. These abnormalities of calcium metabolism are due to dysregulated production of 1,25-(OH)2-D3 (calcitriol) by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation. Undetected hypercalcemia and hypercalciuria can cause nephrocalcinosis, renal stones, and renal failure. Corticosteroids cause prompt reversal of the metabolic defect. Chloroquine, hydroxychloroqune, and ketoconazole are the drugs that should be used if the patient fails to respond or develops dangerous side effects to corticosteroid therapy.

So you ultimately have to decide (if you have hypercalcemia caused by sarc or something along those lines) whether to buy into standard medicine (e.g. Sharma) and go with prednisone or the above-mentioned drugs. I opted not to go that way, as I've never read that anyone was cured, only treated (and the side effects are pretty nasty). For me, the MP-like approach offered a way to possibly get at the underlying infection, and avoid corticosteroids. Since it is working for me, I'm sticking with it. I will never go on prednisone.

 

[Symptomatic]

Have you looked into any biofilm busting agents like haritaki?

Also, does the KMAF help lower your 1,25-d calcium, or is it mainly for infections?

I haven't heard of haritaki, but will do some Googling. It isn't part of my current plan. In fact, I'm currently systematically eliminating drugs until I figure out which one is inhibiting the good effects of Benicar I was experiencing, and keeping it out of my regimen.

While I disagree with the MP folks in their strict adherence to the protocol, there is something to be said for limiting the scope of what you're taking. If I was only on MP meds, I doubt I would be having the inhibition I'm experiencing. But I feel I need to explore every possible path that might work for me.

My doctor and I decided to add KMAF because I have high nagalase and known viral infections (and because he saw that it related to VitD/VDR, which I obviously have issues with). I've only recently been reading (in the GcMAF section of the forums) that some folks have experienced normalization of 1,25D levels while on various MAF products. So it would be an added bonus if it had that effect for me, but it's early and it sounds like different people are having different effects with respect to GcMAF and 1,25D.

 

[dannybex]

Yeah, I too try to avoid drugs as much as possible, so that's I guess also one of the reasons I'm searching for alternatives. I'd never take corticosteroids -- too many disasterous side effects -- but I'll be willing to go with Benicar if I have to, to address both the 1,25-d (if that's what it does), and my moderately high systolic BP*. Will be talking to the doc -- hopefully on Wednesday, her last day before a long holiday break.

*Another confusing thing for me is that both Benicar and vitamin D lower BP by helping to block angiostensin II...

Complicated.

Thanks again,

Dan

p.s. If blood calcium is high, then how do you lower it?

 

[Symptomatic]

-- but I'll be willing to go with Benicar if I have to, to address both the 1,25-d (if that's what it does), and my moderately high systolic BP*.

*Another confusing thing for me is that both Benicar and vitamin D lower BP by helping to block angiostensin II...

p.s. If blood calcium is high, then how do you lower it?

Lots to cover here. I also had BP that was inching up, and had resisted meds for it as well until the other info came out about my hypercalcemia and 1,25D. Ironically, it was my Googling to see if my "low Vitamin D" could be causing my high BP that eventually led me to my current treatment plan (not before trying 5000 IU/day VitD for a month in May 2011 though).

To resolve hypercalcemia, you first have to determine what's causing it. This page at Norman's website gives a rundown of most causes: http://parathyroid.com/high-calcium.htm According to him, 99.6% (or more) of hypercalcemia is caused by hyperparathyroidism (which isn't all that common) - have no idea how valid that stat is. He also has a very thorough explanation of why low Vit D (meaning 25D) cannot *cause* high calcium: http://parathyroid.com/low-vitamin-d.htm I'm in the blue area on his graph, yet he personally told me I do not have hyperparathyroidism.

I have been tested for everything on that list, by my very thorough endocrinologist. The only "maybes" left are hyperparathyroidism (but as discussed, 1) Norman's clinic themselves told me I didn't have it, 2) negative sestabmibi and parathyroid ultrasound by experienced lab said I didn't have it, and 3) when my 1,25D is not high, my calcium is normal and PTH is normal = don't have it; and sarc (but I had a negative chest x-ray, which isn't really definitive). Everything else was definitively ruled out.

One thing I agree with Sharma on is that he feels the elevated 1,25D is caused by activated macrophages. I agree, but think that those are caused by infection(s), in my case complicated by an immune system unable to help fight it/them off.

 

[dannybex]

Thanks for your reply Symptomatic. Definitely complicated and complex. And kind of a catch-22 in hindsight -- as I wonder if your low d -- if it had been higher all along -- would have been able to regulate/normalize your immune function (and mine, and a million others as well) so that our current immune function wouldn't be so screwed up? I guess it makes sense that the 1,25 could be high due to the activated macrophages, but what is activating them? I know too many questions.

That being said -- hopefully I can ask just two more questions: Did you/do you have any classical sarc-like symptoms? And has anyone been able to explain why you're in the 10% that has elevated blood calcium rather than low calcium?

THANKS.

 

[Sushi]

Symptomatic

Macrophages can also be activated by LPS--which is apparently a "bad" way to activate them. I was told that this is what my body was doing before GcMAF. I believe that once you supply GcMAF the GcMAF will "override" the LPS mechanism of activation.

Maybe this is related to the high D 1,25?

Sushi

 

[Symptomatic]

I guess it makes sense that the 1,25 could be high due to the activated macrophages, but what is activating them? I know too many questions.

That being said -- hopefully I can ask just two more questions: Did you/do you have any classical sarc-like symptoms? And has anyone been able to explain why you're in the 10% that has elevated blood calcium rather than low calcium?

My opinion is that it's an underlying bacterial/viral/whatever cause that is causing the macrophages to be activated. Body is trying continuously to get rid of it, but since it's not successful it just keeps trying.

As Sushi mentioned, LPS can activate macrophages. LPS is an endotoxin. From Wikipedia's endotoxin entry:

The term endotoxin was coined by Nats Umangay, who distinguished between exotoxin, which he classified as a toxin that is released by bacteria into the environment, and endotoxin, which he considered to be a toxin kept "within" the bacterial cell and to be released only after destruction of the bacterial cell wall. Today, the term 'endotoxin' is used synonymously with the term lipopolysaccharide[citation needed], which is a major constituent of the outer cell membrane of Gram-negative bacteria. Larger amounts of endotoxins can be mobilized if Gram-negative bacteria are killed or destroyed by detergents. The term "endotoxin" came from the discovery that portions of Gram-negative bacteria themselves can cause toxicity, hence the name endotoxin. Studies of endotoxin over the next 50 years revealed that the effects of "endotoxin" are, in fact, due to lipopolysaccharide.
The key effects of endotoxins on vertebrates are mediated by their interaction with specific receptors on immune cells such as monocytes, macrophages, dendritic cells, and others. Upon challenge with endotoxin, these cells form a broad spectrum of immune mediators such as cytokines, nitric oxide, and eicosanoids.[1]


With respect to my own personal situation, nobody has even given me a diagnosis, much less an explanation! I don't think I have any sarc symptoms (I don't even really believe I have sarc - it's just the closest "label" that corresponds to some of my lab data, namely the high 1,25D and hypercalcemia). When I first started researching it last year, I found that others besides Marshall (e.g. Moller and Drake at Vanderbilt) think that sarc may have a bacterial cause, that's why I've decided not to get too caught up in a specific diagnosis, and instead focus on treatment - acting as if it's a bacterial/viral infection. Whether it's technically sarc or not is of no real concern to me since I will pursue the same treatment regardless.

Something else I find interesting in my medical puzzle is that my (now deceased) mother had TB multiple times in her life (or perhaps it was one chronic infection that went on for many many years)...I have to believe that's significant (from an exposure and/or genetic point of view).

 

[dannybex]

Thanks for your replies Sushi and Symptomatic -- sorry for my late reply. I've been getting advice and recommendations from all over the place, which agree and conflict with advice here...but that's how it goes with almost every question we have to deal with, doesn't it?

Interesting regarding the TB connection -- my grandmother had TB twice, once in the 1920's, and then again in the '40's. The treatment back then was to go to a sanitarium (or sanatorium?) where the main treatments were rest, cod liver oil, and sunshine when possible.

 

[dannybex]

Symptomatic -- I just came across this and was wondering if it may possibly play a role in your elevated calcium levels?

This is from a book entitled Manganese in Health and Disease, that I got last spring...was just skimming through parts of it when I saw this:

"After 12 months, the rats fed the low and depleted manganese diets had significantly higher levels of serum calcium and phosphorus and lower levels of serum and femur manganese as compared to normal rats."

Of course not sure if this would apply in humans, although there are studies of supplemental calcium interfering with manganese levels.

Just throwin' it out there. Hope to get my PTH and calcium levels measured before the end of January...(my doc's on vacation).

 

[Symptomatic]

dannybex - thanks for the info

I suspect since my calcium and PTH are fine when my 1,25D is in-range that low manganese is not my issue, but I'll file this "just in case".

Hope you are able to get some labs run soon. If your calcium comes back high, let me know and I'll scan and PM you some correspondence that you might find helpful.

Happy New Year!