And a jolly good one at that!.........Sarah

Incredible papers, Marie. I have been taking only 2400 units a day. I was wrong I think and will increase both of us. Thank you.

Rica EDSS 6.7 at beginning - now 2
Ignorance is voluntary bad luck. Lauritz S. A true Viking
If you come to a fork in the road, take it. Yogi Berra

An abstract for a new study on Vitamin Di and infectionsi can be found at:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&lis...

It seems that D can act like an antibiotic.

Raven

CAP since 8-05 for Cpn and Mycoplasma P. for MSi and/or CFS

This is a great find, and good addition to the importance of Vitamin Di supplementation for many of us.

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei & Fibromyalgiai- Currently: 150mg INHi, Doxycyclinei/Zithromycin, Tinidazolei pulses. Northern Ohio, USA

 

Apologies if this this has been posted before but I found it very interesting

http://www.sciencenews.org/articles/20061111/bob9.asp

 

Elinor from England, UK..... on Wheldon protocol for ME/lyme borreliosis , positive for borrelia and Cpn. Started Aug 05, stopped Jan06, started again Oct 06.

Vitamin Di can reduce NFkB activity thereby reducing inflammation.

http://ndt.oxfordjournals.org/cgi/content/abstract/21/4/889

 

This is interesting as I recently noticed a reduction in overall inflammation after an hour in the sun. In next few days when I felt inflammation coming on, I took about 4000 iu of D and felt inflammation was smoothed out in a matter of 10 to 15 minutes.

Raven

CAP since 8-05 for Cpn and Mycoplasma P. for MSi and/or CFS. Now treating for EBVi with Valtrex. Calif. USA

 

 

I am so confused about the D issue. When I first got sick I spent two years reading the Marshall Protocol website and his papers - but didn't do the protocol (I'm not sure about the high doses of Benicar and its effects on the body). Had my D tests done. It is true, all of us with infectionsi have low D. But that is because the bugs convert it to the hormone 1,25 D. So we have low D, but high 1,25 D. The more D we ingest (fortified D foods, supplementsii) the higher our 1,25 D hormone goes and the more inflammationi we have. Apparently a high 1,25 D hormone suppresses the immunei system. D foods and supplements will make us feel better, but prevent us from getting well. At least thats what his science says, and I hate to argue, but the science seems sound. Marshall has sinced backed off the sunlight issue (only D foods and supplements can lead to 1,25 D toxicity) and only recommends avoiding because of herx problems with the Benicar, but it is not necessary to stay out of sun. He only recommends avoiding D enriched foods. I think he may be right on this one. Think about it. Ever since D-fortified foods hit the market these diseasesi have gone through the roof. Don't get me wrong, I am on the CAP protocol, but am not sold on overloading myself with D supplements. If you all check your 1,25 D I think you will find it to be too high. Once the infection is reduced, however I don't any of us will have this problem. Didn't mean to stir things up, but have been thinking about this for a while. If any Dr's out there could sort this out for me I would love to hear from you! Be well all. Chris CAP since 11/06 for CFS. Cpn, Myco P, CMV, HHV-6 infections. Zithi 250mg MWF. Will add Minocin in Deccember. All supplements.

The effects of 1,25-D are more complicated than just "suppressing the immunei system". In some cases they boost it; one study found that 1,25-D caused white blood cells to kill tuberculosis germs residing inside themselves. (This was mentioned on Marshall's website; but he has since censored the post, so you will no longer find it there.) A better characterization is that 1,25-D is an immune system signaling hormone, for which Vitamin Di is the raw material. Most of the 1,25-D is made and used locally; it never hits the bloodstream. Its precise effects are still being explored; but human biochemistry evolved running around naked in Africa, with loads and loads of Vitamin D always at hand. That is the condition nature has optimized us for. Whatever its precise role, deliberately depriving the body of this signaling hormone is likely to work about as well as ripping out all the red-colored wires in an electrical circuit works.

The Harvard study which examined vitamin Di supplementation and incidence of MSi is persuasive [Munger KL, Zhang SM, O'Reilly E, et al., Vitamin D intake and incidence of multiple sclerosisi. Neurology. 2004 Jan 13;62(1):60-5.] link. The authors conclude that vitamin D supplementation reduces the risk of developing MS.

---

D W - Myalgia and hypertensioni (typically 155/95.) Began (2003) taking doxycyclinei and macrolide and later adding pulsed metronidazolei. Improved; normotensive

 

Ken Lassensen's site has a number of excellent reviews of the Vitamin Di issues including these links:

http://lassesen.com/cfids/recommended_levels.htm

http://lassesen.com/cfids/vit_d_&_illnesses.htm

 

CAP for Chlamydia pneumonia since 11/04. 25yrs CFS & FMSi- Currently: 150mg INHi, 300mg Rifampin, 200 Doxycyclinei, 500mg mwf Azithromycini, plus 500mg Tinidazolei 2x/day pulses every two weeks. Whew! That's a lot! about 60% recovery. Ohio,

I agree it is confusing that there are two camps apparently effectively ridding people of intracellulari bacteria with diametrically opposed points of view: one encouraging using vit D freely and one limiting it severely. What is similar is that both are using antibiotics so to that extent there is agreement about the need to kill off these bug but the disagreement comes in in relation to the reaction to treatment and the need to ameliorate it with other approaches. Here the focus is on the work done at VU that indicates that there maybe some secondary porphyria related to treatment (see research pages) as well as some common herxheimer type reactions to the LPSi released during treatment. Both are considered manageable by us here, though some people get enough inflammaatory reaction that make the addition of new meds as they ramp up at the start the protocol slowly.

Here is what I know: I was tested for both D analogues and was high normal for BOTH, not the anomaly the Marshall says "will" be there if I have a TH1 disease. Since I have MSi and RAi, I should show the anomaly he says (high 1,25 D caused by immune cells taking more of the 25D and converting it to that active version). I had active disease at the time of D tests, which was in fall pretreatment.

Research does NOT support the idea of 1,25 D causing inflammation. In paper after paper you get evidence it DECREASES it. Examples follow:
Giulietti A, van Etten E, Overbergh L, Stoffels K, Bouillon R, Mathieu C
Monocytes from type 2 diabetic patients have a pro-inflammatory profile 1,25-Dihydroxyvitamin D(3) works as anti-inflammatory.
Diabetes Res Clin Pract. 2006 Nov 15; [Epub ahead of print]
PMID: 17112620
AND THIS ONE
Stio M, Martinesi M, Bruni S, Treves C, Mathieu C, Verstuyf A, d'Albasio G, Bagnoli S, Bonanomi AG. Related Articles, Links
The Vitamin Di analogue TX 527 blocks NF-kappaB activation in peripheral blood mononuclear cells of patients with Crohn's disease.
J Steroid Biochem Mol Biol. 2006 Oct 16; [Epub ahead of print]
PMID: 17049230

Follow the links on the right side of the pubmed page for these and read other related papers also

I cannot find a paper on pubmed that says that vitamin D increases inflammation. This site points out some worrisome information about the quality of the information used to support the MP http://impnvestigator.chat.ru/

Especially worrisome is that the papers written by T. Marshall particularly related to vitamin d and inflammation were rejected by peer reviewed journals, yet the papers are referred to as support for the MP point of view as if they are accepted research. That would be like me referring you to the CPN help handbook on MS stuff that I wrote as if it were authoritative research!

A very recent paper accepted for publication by TM was in a journal for theoretical biological models, the paper makes the case that the vitamin d receptor might be acted upon by angiotenson receptor blockers like benicar as demostrated by his theoretical molecular models. But this proves nothing whatsoever in regards to inflammation or intracellular bacteria, only that in his theoretical model the VDR is strongly blocked by benicar. He makes the case someone should study it directly in the lab now that his model has pointed the way. I agree with that. see it here Theor Biol Med Model. 2006 Jan 10;3:1.
"Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b." Marshall TG, Lee RE, Marshall FE.

Here is another paper, this one importantly a review, on D3 and its immunomodulatory properties. Note that it is mentioned as a positive factor for autoimmune diseases, not as proinflammatory or problematic.
Curr Drug Targets Inflamm Allergy. 2004 Dec;3(4):377-93.
Immunoregulation through 1,25-dihydroxyvitamin D3 and its analogs.May E, Asadullah K, Zugel U.
If you read the related links you will find numerous papers suggesting that D3 agonists--note agonist means opposite of antagonist--decrease inflammation and many that indicate it improves immune function. It is intimately involved with modulation of the immune system in fairly complex ways.

I should also say that I do know people who have gotten better on the MP, but I suggest it is the antibiotics they use (which do get to regular levels eventually) that accomplishes the goal.

If lowering D were important to treatment we would be having trouble with this protocol, and that is not the case.

I do not know if this helped your concerns but I hope it did
marie

On CAP since Sept '05 for MS, RA, Asthmai, sciatica. EDSS at start 5.5. Currently on: Doxy 200, Azith 3x week, Tini 2x month, all supplementsi.
"Color out side the lines!"

Hi all,

I also recently posted these studies that suggest Cpn may prevent normal cell apoptosisi via upregulation of NF-kappaB and inhibitor of apoptosis protein 2 (cIAP2):

NF-kappaB and inhibitor of apoptosis proteins are required for apoptosis resistance of epithelial cells persistently infected with Chlamydophila pneumoniae

While vitamin D3 has been shown to induce "decreases in levels of antiapoptotic proteins Bcl-2, Bcl-X(L), and Mcl-1, BAG1L, XIAP, cIAP1, and cIAP2 (without altering proapoptotic Bax and Bak) in association with increases in apoptosis" in the following study:

Apoptosis induction by 1alpha,25-dihydroxyvitamin D3 in prostate cancer

I'm not currently taking Vit D supplementsii as I usually get plenty of sun exposure here in SoCal and I'm also doing so well now in treatment, but I've sure thought of trying additional supplementation (and still may in the future)...

 

On Combined Antibiotic Protocol for Cpn in Rosaceaii since 01/06

There is plenty of information about the vitamin Di issue in an article by Mark London. It is a somewhat critical assessment of the reasoning behind the MP (see link).

Mycoplasma1, you may want to try the calcium loading test that is described in that article. Supplement with calcium and see whether your 1,25-D level goes down (as it should if renal production is the main factor) or whether it stays the same (indicative of TH1 production).

There certainly are people who improve on either protocol. So in the end, neither adding nor avoiding vitamin D may strictly be necessary for recovery.

BTW, I've also tested low on 25-D and high normal on 1,25-D.

There have been some very useful posts on this thread. Four observations may be made:

a) Vitamin Di induces the production of cathelicidin peptides.
b) Cathelicidins have antibacterial (including antichlamydial) activity.
c) People with MSi are likely to be borderline deficient in vitamin D
d) People who supplement with Vitamin D are less likely to get MS

Together, these observations support the idea of supplementation with Vitamin D; they also lend support to the idea of MS having an infective origin. Furthermore, cathelicidins have wide-ranging antiviral properties and have been found to be particularly active against Herpes Simplex Virus [Gordon YJ, Huang LC, Romanowski EG, Yates KA, Proske RJ, McDermott AM. Human cathelicidin (LL-37), a multifunctional peptide, is expressed by ocular surface epithelia and has potent antibacterial and antiviral activity. Curr Eye Res. 2005 May;30(5):385-94.] Link. Cathelicidin deficiency has also been found to occur in people with eczema herpeticum in people with atopic dermatitis. Supplementation with Vitamin D may therefore be important in suppressing the posited henchmen viruses in MS and other chronic C pneumoniae infectionsi.

---

D W - [Myalgia and hypertensioni (typically 155/95.) Began (2003) taking doxycyclinei and macrolide and later metronidazolei. Now normotensive.]

 

Thanks for all the work you are doing, Marie; it's much appreciated. I've just come upon this, an excellent paper which reviews Vitamin Di induction of cathelicidin antimicrobial peptide (CAMP) in a very clear way [Gombart AF, Borregaard N, Koeffler HP. Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. FASEB J. 2005 Jul;19(9):1067-77.] Link. It's available as a pdf. The authors found that Vitamin D induced CAMP in bone-marrow cells and in BM-derived macrophages. This could be of key importance as marrow is an organ of filtration and its cells are targets of C. pneumoniae. The authors also point out that CAMP binds to endotoxini and prevent modify induction of pro-inflammatory cytokinesi.

This is relevant work, too: addition of D3 to peripheral blood monocytes and macrophages infected with Mycobacterium bovis resulted in enhanced bacterial killing, probably due to enhanced NO production [Waters WR, Nonnecke BJ, Rahner TE et al., Modulation of Mycobacterium bovis-specific responses of bovine peripheral blood mononuclear cells by 1,25-dihydroxyvitamin D(3). Clin Diagn Lab Immunol. 2001 Nov;8(6):1204-12.] Link. This may be of importance as there are parallels between mycobacterial and chronic C pneumoniae infection: might vitamin D deficiency allow an acute C pneumoniae infection to persist and become chronic?

Well, as this is the middle of winter, I took 8,000 IU D3 yesterday. Today I feel a lot better for it; in fact I feel rather like I did as a boy after a day at the sea-side.

---

D W - [Myalgia and hypertensioni (typically 155/95.) Began (2003) taking doxycyclinei and macrolide and later metronidazolei. Now normotensive.]

 

Gosh I wish it had that effect on me! Although I can't ever remember feeling like a boy...

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Michele: on Wheldon protocol since 1st May 2006 for a variety of long standing ailments, also spokesperson for Ella star

Hi all, I just noticed this finally showed up. I posted it several weeks ago, but it got picked up as spam. Must have been added in the site upgrade...

 

 

On only my 4th day of 4000ius of Vit D3 and so far very impressed with its benefits (skin, sinus, etc), I decided to dig a bit to see what pathogens have been shown to be affected by Vit D3 directly or through LL-37, the human cathelicidin that Vit D3 has been shown in the studies presented above to induce so dramatically. Since the pathogens that are affected by LL-37 don't necessary show up in a search related to Vit D3 directly I decided to list a few of these here:

LL-37 & Candida Albicans

"Treatment of C. albicans with 20 μM LL-37 caused a complete disappearance of the integrity of cellular membranes, as no recognizable ultrastructure could be distinguished"

LL-37 and Bacillus species

" Although, B. anthracis is more resistant to LL-37 than other members of the Bacillus genus, LL-37 was bactericidal for B. anthracis at concentrations greater than 125 µg/ml. Infectionsi with B. anthracis are mediated by spores, which lack protease secretion and, as such, are extremely susceptible to LL-37-mediated killing at this early stage in the infection process."

LL-37 & E. coli

" Our findings clearly show that LL-37 neutralizes the LPSi-induced proinflammatory response. Compared to polymyxin B and the beta-lactams, LL-37 caused the highest inhibition of LPS-induced TNF- and NO production in RAW 264.7 cells, and it was effective in vivo versus all parameters considered, regardless of the animal model utilized. Importantly, intravenous LL-37 produced a significant reduction in TNF- plasma levels, compared to both control and beta-lactam-treated groups. In contrast, compared with polymyxin B, it produced a similar decrease in the concentration of plasma endotoxini. Since polymyxin B is frequently used as the standard against which novel antiendotoxin compounds are measured, it is significant that polymyxin B and LL-37 reduced the plasma levels of LPS to a similar extent and showed similar abilities in blocking induction of TNF in animal models. Models 2 and 3, which also evaluated the in vivo antimicrobial effects of the four compounds, showed that although LL-37 exhibited a somewhat lower antibacterial activity than other drugs, it decreased the rate of lethality at a level similar to those of imipenem and polymyxin B and better than that of piperacillin. It is important to observe in this regard that two key determinants of sepsis survival are bacterial clearance and the inflammatory response to the infection. Finally, comparable data were observed when the drugs were administered at 360 min (model 3)"

LL-37 & M. furfur & Dermatophyes (responsible for tinea infections)

"LL-37 inhibits the growth of fungi with an MIC of 20-30 microM for M. furfur and 12.5 microM for Trichophyton mentagrophytes and T. rubrum. LL-37 also shows fungicidal activity with a minimum fungicidal concentration (MFC) of 12.5 and 25 microM for T. mentagrophytes and T. rubrum, respectively"

LL-37 & Pseudomonas aeruginosa (PA), Staphylococcus aureus (SA), Staphylococcus epidermidis (SE), herpes simplex virus type 1 (HSV-1), and adenovirus (Ad)

"We found LL-37 to have potent antibacterial activity against both a laboratory strain and clinical isolates of PA. Our EC₅₀values of approximately 2-4 μg/ml compare well with published studies of the effectiveness of LL-37 against other PA strains.^{20,27,28,58,59} LL-37 also demonstrated potent antibacterial activity against the most common Gram-positive keratitis-producing organisms: SE (mean EC₅₀1.3 μg/ml) and SA (mean EC₅₀1.6 μg/ml)"

"We report for the first time that LL-37 demonstrates significant antiviral inhibitory activity (>98% inhibition) against HSVi-1, the leading viral cause of corneal blindness in industrialized countries."

"Additionally, we report for the first time that LL- 37 demonstrated statistically significant inhibitory activity in vitro against Ad19, a major cause of conjunctivitis and epidemic keratoconjunctivitis in local and global epidemics."

LL-37 & H. pylori

"LL-37, the C-terminal peptide of LL-37/hCAP18, alone or in synergy with human beta-defensin 1, was bactericidal for several H. pylori strains"

LL-37 and B. Burgdorferi

"B. burgdorferi were killed by the PMNL antimicrobial components elastase, LL-37, bactericidal/permeability-increasing protein, and human neutrophil peptide-1"

LL-37 and group A Streptococcus

"Analysis of anti-microbial activity of this C-terminal peptide against group A Streptococcus revealed that both LL-37 and CRAMP potently inhibited bacterial growth. Action against group A Streptococcus occurred in conditions that typically abolish the activity of anti-microbial peptides against other organisms"

Hope you find this interesting. I sure did...

 

 

 

On Combined Antibiotic Protocol for Cpn in Rosaceaii since 01/06

BTW, the only study that I've been able to find related to human cathelicidins and Cpn is the following, and it seems to suggest that human cathelicidins may not be all that effective against Cpn at least in vitro (see free full text):

Involvement of the antimicrobial peptide LL-37 in human atherosclerosis

"Intriguingly, Chlamydia pneumoniae withstood the antimicrobial activity of LL-37 in vitro, although inflammatory response was induced on infection."

The additional fatigue and stuffiness I'm curently getting (in a bit of a delayed reaction) with the addition of Vit D3 makes me think that this may not really be the case, potentially due Vit D3's interference with the mechanism Cpn seems to use to prevent apoptosisi (see above), the mechanisms DW mentions (see above), or differences between in vivo and in vitro mechanisms. My symptoms could also be due to a die-off of some other pathogen of course (such as Candida, etc)...

Has anyone seen any studies that do suggest human cathelicidins are actually effective directly against Cpn by any chance? I don't really need convincing that Vit D3's important in fighting Cpn, but I'm just curious...

 

On Combined Antibiotic Protocol for Cpn in Rosaceaii since 01/06

Hi everyone! Havent been here for a while for medicale reason. A lot of new things on the site, good things. I am glade to be able to come back and read or trying to keep up with the stories (even thoght I dont respond, I have trouble frasing or explaning my feelings or thats in english. When I read what I wrote, it often dosent say what I wanted to say) Is anyone fallowing me?????? Any way, I have been reading a lot tonight and found this page with all these study's (very interesting but some hard for me to understand). I was looking for something in purticulor and did not find it. So I am asking if someone can give me a answer or lead me to the right direction? For those that dont know, my father has MSi and is on abxii. He wasent taking any vitamine D, witch we added about 3 weeks ago. Since that time, he is having more numness in his arms, hard time to talk, he is less stable, looses his balance more. He was suppossed to star his second pulse, but he waided because of that. But the thing is, it dos not seem to go away. He dos not go outside at all, so we think it is important for him to take this vitamine? Has any one hade a reaction similar to this? and this may sound strange but he noticed that with caffein it get's worse and he feel's it fast, he needs to go for a sleep and the symptomes are amplified. Is that strange????? He has always drink so many coffees in a day, it's just since the Vitamine D. So of course he is trying to cut down on his coffee. We know that we souldent start a pulse when you are not feeling good, but should he cut down the vitamine D and wait, or start his pulse anyway? What is the impact of delaying a pulse for a long period of time?????? As always, "apresheading" your help!(I need to go by my self a english/french dictionnairy) karen b