6 replies to this topic

[Lufega]

This study says Zinc is needed by Borrelia Burg. for growth and it also inhibits a key neutrophil protein that kills it. To lower or not to lower zinc, that is the question. Manganese is also needed by BB. In both these cases, copper and magnesium can antagonize the cations. Would this lead to a positive outcome in treatment?

Calprotectin, an abundant cytosolic protein from human polymorphonuclear leukocytes, inhibits the growth of Borrelia burgdorferi.Lusitani D, Malawista SE, Montgomery RR.

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.

<H3 class=abstract_label>Abstract</H3>We previously showed that numerous polymorphonuclear leukocyte (PMN) granule components efficiently kill Borrelia burgdorferi, the agent of Lyme disease. In addition, motile, granule-poor cytoplasts (U-Cyt) from human blood PMN can exert anti-Borrelia activity against opsonized B. burgdorferi independently of oxidative mechanisms. Here we show that lysates of U-Cyt also possess anti-Borrelia activity, a portion of which comes from the abundant cytosolic protein calprotectin. The anti-Borrelia activity of U-Cyt lysates and recombinant calprotectin was partially or completely reversed by specific antibody to calprotectin and by Zn(2+), a cation essential for the growth of B. burgdorferi and known to inhibit the antimicrobial activity of calprotectin. Quantitative microscopic and regrowth assays revealed that calprotectin acted in a bacteriostatic fashion against B. burgdorferi. We conclude that calprotectin, a potent bacteriostatic agent from a cell primarily recognized for its oxidative and granular antibacterial mechanisms, may play a modulatory role in infection by the Lyme spirochete, particularly at sites of acute inflammation.

Full study http://www.ncbi.nlm....21/pdf/0455.pdf

Edited by Lufega, 29 May 2010 - 11:13 PM.

[Lufega]

Found a study where they did just that in bacteria. Full version is available from the link.

Metal chelation and inhibition of bacterial growth in tissue abscesses.
Corbin BD, Seeley EH, Raab A, Feldmann J, Miller MR, Torres VJ, Anderson KL, Dattilo BM, Dunman PM, Gerads R, Caprioli RM, Nacken W, Chazin WJ, Skaar EP.

Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Comment in:

Science. 2008 Feb 15;319(5865):910-1.

Abstract
Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.

PMID: 18276893 [PubMed - indexed for MEDLINE]

[rwac]

You can't deprive yourself of all the things that Lyme needs to grow. You will starve yourself way before you starve the bug out, and feel miserable throughout to boot.

Edited by rwac, 29 May 2010 - 11:25 PM.

[Lufega]

One method of enhancing calprotectin release..exercise !

Calprotectin is released from human skeletal muscle tissue during exercise.
Mortensen OH, Andersen K, Fischer C, Nielsen AR, Nielsen S, Akerström T, Aastrøm MB, Borup R, Pedersen BK.

Centre of Inflammation and Metabolism at Department of Infectious, Diseases and Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Denmark.

Abstract
Skeletal muscle has been identified as a secretory organ. We hypothesized that IL-6, a cytokine secreted from skeletal muscle during exercise, could induce production of other secreted factors in skeletal muscle. IL-6 was infused for 3 h into healthy young males (n = 7) and muscle biopsies obtained at time points 0, 3 and 6 h in these individuals and in resting controls. Affymetrix microarray analysis of gene expression changes in skeletal muscle biopsies identified a small set of genes changed by IL-6 infusion. RT-PCR validation confirmed that S100A8 and S100A9 mRNA were up-regulated 3-fold in skeletal muscle following IL-6 infusion compared to controls. Furthermore, S100A8 and S100A9 mRNA levels were up-regulated 5-fold in human skeletal muscle following cycle ergometer exercise for 3 h at approximately 60% of in young healthy males (n = 8). S100A8 and S100A9 form calprotectin, which is known as an acute phase reactant. Plasma calprotectin increased 5-fold following acute cycle ergometer exercise in humans, but not following IL-6 infusion. To identify the source of calprotectin, healthy males (n = 7) performed two-legged dynamic knee extensor exercise for 3 h with a work load of approximately 50% of peak power output and arterial-femoral venous differences were obtained. Arterial plasma concentrations for calprotectin increased 2-fold compared to rest and there was a net release of calprotectin from the working muscle. In conclusion, IL-6 infusion and muscle contractions induce expression of S100A8 and S100A9 in skeletal muscle. However, IL-6 alone is not a sufficient stimulus to facilitate release of calprotectin from skeletal muscle.

[Lufega]

You can't deprive yourself of all the things that Lyme needs to grow. You will starve yourself way before you starve the bug out, and feel miserable throughout to boot.

That's a good point. The idea though, is to starve it long enough to help the antibiotics. This is done in cancer as well; chelation therapy, anti-folates, etc. I bet it must feel like &^% to do this but if you have Lyme (or cancer for that matter), you already feel miserable enough. A little more suffering for the sake of cure is warranted.

For example, Manganese is conditionally needed by BB. There is an antagonistic relationship between magnanese and mangesium. Elevating magnesium levels significantly while concurrently undergoing heavy antibiotics might improve the outcome. Ofcourse, that's given that Mg does interfere with the antibiotic.

Magnesium-manganese interactions caused by magnesium deficiency in rats

Department of Physiology, School of Pharmacy and Institute of Nutrition and Food Technology, University of Granada, Spain.

OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the nutritive utilization and tissue distribution of manganese (Mn). METHODS: Wistar rats were fed a Mg-deficient diet (56 mg/kg) for 70 day. Absorbed Mn, Mn balance and Mn content in plasma, whole blood, skeletal muscle, heart, kidney, liver, femoral bone and sternum were determined after 21, 35 and 70 days.
RESULTS: The Mg-deficient diet significantly increased Mn apparent absorption and Mn balance from week five until the end of the experimental period. This effect was accompanied by a significant increase in the concentration of Mn in heart at all three time points. Whole blood, skeletal muscle and kidney Mn were significantly increased from day 35, and femur Mn content was increased only at the end of the study (day 70). However, Mn concentration in the sternum decreased significantly from day 35. No changes were found in liver Mn content. CONCLUSION: Mg deficiency increased Mn absorbed, and this favored the deposition of Mn in all tissues studied except the liver and trabecular bone. The lack of response by the liver to increased Mn absorption may have led to the redistribution of this ion to other tissues.

PMID: 10511330 [PubMed - indexed for MEDLINE]

Full study http://www.jacn.org/...eprint/18/5/475

Either way, make sure you are getting enough Mg. According to the above study, low Mg status increases Mn and might feed the problem.

Edited by Lufega, 29 May 2010 - 11:51 PM.

[Lufega]

I also want to point out that many antibiotics work, partly, by disrupting biochemical processes in the body involving minerals and vitamins. Examples of this are metronidazole (thiamin), Tetracycline (magnesium), Cipro (whole bunch of minerals). Essentially, they are starving bacteria (and you!) of essential nutrients and produce side effects as a result. I.e. Tendon rupture seen in Cipro by chelating magnesium.

Edited by Lufega, 30 May 2010 - 12:05 AM.

[rwac]

That's a good point. The idea though, is to starve it long enough to help the antibiotics. This is done in cancer as well; chelation therapy, anti-folates, etc. I bet it must feel like &^% to do this but if you have Lyme (or cancer for that matter), you already feel miserable enough. A little more suffering for the sake of cure is warranted.

Thing is, you're not going to be able to kill lyme quickly. Expect atleast a year or so of antibiotics.