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Oxalic acid is produced by a variety of fungi, including saprophytic and phytopathogenic species. Some patients with IBD have high oxalate levels. Would the overgrowth of fungi in patients with IBD explain the high oxalate levels? Even if those fungi did not reside in the gut,they would still be able to get the undigested food because of the leaky gut. Many SCD followers report improvements in other parts of their bodies after starting SCD; elimination of eczema is one example.
The most important oxalate degrading flora that is being displaced is the bacteria,O.formigenes. Patients without O. formigenes had higher urinary oxalate than those with it. Patients with IBD and Renal Stones rarely have O. formigenes in their stools as compared with controls. Therefore, "the absence of intestinal oxalate degrading bacteria,Oxalobacter formigenes, may cause hyperoxaluria in IBD".Lactic acid bacteria also degrade oxalates,but they are not as powerful as Oxalobacter formigenes.
Susan Owens has written that there is now evidence that oxalates are being produced in the human gut. Might the oxalate be produced by fungi? Susan Owens posted a research paper claims that there is proof that microorganisms do not produce oxalate in the gut. That article speculated that it was the intestinal mucosal cells themselves that made this conversion. However,one can disagree with this conclusion
The article claims: "That intestinal microorganisms do not synthesize significant amounts of oxalate was indicated by the findings that oral tetracycline had no effect on oxalate excretion and that germ-free rats excreted more oxalate than conventional rats. "
A major question arises here:if microorganisms have no effect on the amounts of oxalate produced,why would the germ free rats excrete more oxalate than the conventional rats? The mystery might be solved if we examine the kind of microorganisms that tetracycline eliminates.
Tetracycline does not kill all microorganisms; it eliminates bacteria but allows fungi to overgrow because their competitors,the bacteria, are gone. This explains why germ-free rats excreted more oxalate than conventional rats: they had more fungi than the conventional rats since their fungi had more room and food after the bacteria were eliminated by the tetracycline.
Whether it is the mucus or the fungi is not important for the relevance of SCD for oxalates since both theories support the role of SCD. Elaine Gottschall wrote that more mucus is produced when the intestinal walls are damaged by the pathogenic microorganisms. SCD heals the gut and helps decrease the mucus as well as the fungi.
Website with information about Tetracycline:
http://www.cfs-recovery.org/antibiot.htm
Most antibiotics kill "friendly bacteria" allowing the overgrowth of Candida and mycoplasma bacterias. Tetracycline has a warning about overgrowth of fungus. It must be noted that no antibiotic is completely safe and many kill "friendly bacteria" to some extent, but some are better than others.
Here is the article that Susan found:
11: J Nutr. 1982 Nov;112(11):2161-9.
Factors affecting endogenous oxalate synthesis and its excretion in feces and urine in rats.
Ribaya JD, Gershoff SN.
It has been observed that the feces as well as urine of rats fed diets supplemented with 3% glycine and 5.2% hydroxyproline contain unexpectedly high amounts of endogenously formed oxalate. That intestinal microorganisms do not synthesize significant amounts of oxalate was indicated by the findings that oral tetracycline had no effect on oxalate excretion and that germ-free rats excreted more oxalate than conventional rats. Since little intraperitoneally injected [14C] oxalate appeared in the feces, and rat intestinal mucosa homogenates were found to produce oxalate from a variety of precursors of which glyoxylic acid was far the most important, it is probable that the intestinal mucosa may be an important source of fecal oxalate observed in these studies. Ninety percent of weanling rats fed complete diets supplemented with glycine and hydroxyproline developed urinary stones in 38 days. It has been concluded that in the treatment of patients with histories of calcium oxalate urolithiasis, more concern than is commonly shown should be directed towards the feeding of diets high in precursors of endogenous oxalate synthesis.
PMID: 7131093 [PubMed - indexed for MEDLINE]
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Proof that oxalic acid is produced by a variety of fungi, including saprophytic and phytopathogenic species:
Dutton, M. V. & Evans, C. S. (1996). Oxalate production by fungi: its role in pathogenicity and ecology in the soil environment. Can J Microbiol 42, 881-895
Unfortunately,there is no online abstract available but there are many online citations inluding the one below where this article is mentioned in
the second paragraph.
http://mic.sgmjournals.org/cgi/content/full/145/9/2569
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There are other oxalate producing fungi besides the Aspergillus species. A person might have other oxalate producing fungi inside their body.
1: Pathol Res Pract. 2005;201(5):363-8.
Aspects of oxalosis associated with aspergillosis in pathology specimens.
Pabuccuoglu U.
School of Medicine, Department of Pathology, Dokuz Eylul University, Inciralti-Izmir, Turkey. ugur.pabuccuoglu@deu.edu.tr
Oxalosis (calcium oxalate deposition) is associated with various conditions, including aspergillosis. Some Aspergillus species produce oxalic acid, which reacts with blood or tissue calcium to precipitate calcium oxalate. Calcium oxalate crystals exhibit various shapes and are strongly birefringent. These occur in cytological specimens, as well as in tissues of patients with Aspergillus infection. Aspergillus species are hyaline septate moulds, and they can be accurately recognized in pathology specimens only if conidial heads (fruiting heads) are present. When these structures are not observed, detection of associated oxalosis in a mould infection supports the pathological diagnosis of aspergillosis. The presence of oxalosis is helpful when microbiological identification or immunohistological techniques for fungi are not available. Calcium oxalate crystals can induce cellular injury by several mechanisms, and there is increasing evidence that oxalosis-induced tissue damage may occasionally lead to a poor clinical outcome. This review discusses the diagnostic value and the potential clinical significance of oxalosis associated with aspergillosis.
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1: J Gastroenterol Hepatol. 2004 Dec;19(12):1403-9.
Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: possible role in renal stone formation.
Kumar R, Ghoshal UC, Singh G, Mittal RD.
Department of Urology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India.
BACKGROUND AND AIM: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD. METHODS: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h. RESULTS: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11-2.09]vs 0.43 [range 0.16-1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14-1.90 vs 0.44 mmol/24 h, range 0.23-0.97; P = 0.008, Mann-Whitney U-test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11-2.09], 0.56 [0.14-1.9] and 0.41 [0.21-0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38-21.00], 6.78 [1.55-20.30] and 4.99 [1.47-9.60] mmol/24 h; P < 0.05, Kruskal-Wallis H-test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50-12.30], 3.60 [0.90-6.35] and 2.49 [0.74-4.80]; P < 0.001, Kruskal-Wallis H-test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls. CONCLUSIONS: Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.
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Here is another pathogen that is involved in kidney formation.
1: Urol Res. 2003 Jun;31(2):47-54. Epub 2003 Mar 27.
Characteristics of nanobacteria and their possible role in stone formation.
Kajander EO, Ciftcioglu N, Aho K, Garcia-Cuerpo E.
Department of Biochemistry, University of Kuopio, PO Box 1627, 70211 Kuopio, Finland. olavi.kajander@uku.fi
Kidney stone formation is a multifactorial disease in which the defence mechanisms and risk factors are imbalanced in favour of stone formation. We have proposed a novel infectious agent, mineral forming nanobacteria (NB), to be active nidi that attach to, invade and damage the urinary epithelium of collecting ducts and papilla forming the calcium phosphate center(s) found in most kidney stones. Stone formation may proceed in urine supersaturated with calcium phosphate, calcium oxalate and uric acid/urate under the influence of crystallization promoters and inhibitors. Our hypothesis underlines the role of active nidi: even supersaturated urine requires nidi for crystallization to appear.
PMID: 12669155 [PubMed - indexed for MEDLINE]
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