<<Disclaimer: Verify this information before applying it to your situation.>>

Below I share 4 ways that oxalate levels in the body might 
be raised (1. a genetic predisposition, 2. low levels of 
oxalate-degrading bacteria, 3. a vitamin B6 deficit, or 4. 
a bowel dysfunction).

1. The only well-documented way that oxalate levels have 
been shown to become dangerously high is through a genetic 
predisposition:

Genetic hyperoxaluria – disease characterized by 
progressive kidney failure due to renal deposition of 
calcium oxalate. The disease is caused by a deficiency of 
alanine:glyoxylate aminotransferase (AGT) which catalyzes 
the conversion of glyoxylate to glycine. When AGT is 
absent, glyoxylate is converted to oxalate which forms 
insoluble calcium salts that accumulate in the kidney and 
other organs.
Reference: Any medical dictionary. Recent review published 
in Mol Genet Metab. 2004 Sep-Oct;83(1-2):38-46.

2. Some bacteria “eat” (degrade) oxalates, so when an 
antibiotic is administered, the person’s oxalate levels 
may spike. That's why some patients have flare-ups after 
they take an antibiotic.

Oxalate degradation by the anaerobic bacterium Oxalobacter 
formigenes is important for human health, helping to 
prevent hyperoxaluria and disorders such as the 
development of kidney stones. Oxalobacter formigenes and 
Its Potential Role in Human Health
Sylvia H. Duncan et al. Applied and Environmental 
Microbiology, August 2002, p. 3841-3847, Vol. 68, No. 8.

On the up-side, lactobacillus has been shows to degrade 
oxalates in dogs and cats, reference: J.S. Weese et al. / 
Veterinary Microbiology 101 (2004) 161–166.

3. Excess oxalate levels have also been shown to be a 
result of vitamin deficiency (in particular vitamin B6):

Vitamin B6 reference: SAORI NISHIJIMA, KIMIO SUGAYA, 
MAKOTO MOROZUMI, TADASHI HATANO and YOSHIHIDE OGAWA, 
Hepatic Alanine-glyoxylate Aminotransferase Activity and 
Oxalate Metabolism in Vitamin B6 Deficient Rats, The 
Journal of Urology, Volume 169, Issue 2, February 2003, 
Pages 683-686
  
4. According to the recent listserv post referencing Susan 
Owens’ autism work, there is a known link between excess 
oxalates and bowel dysfunction. I don’t doubt this claim, 
makes sense to me, but there is in fact very little 
scientific research to substantiate it.

“Irritable bowel disease (IBD) can increase the risk of 
forming calcium oxalate kidney stones. This observation 
can be explained by the fact that when the gut is 
inflamed, when there is poor fat digestion (steatorrhea), 
when there is a leaky gut, or when there is prolonged 
diarrhea or constipation, excess oxalate from foods can be 
absorbed by the GI tract.” – Susan Owens, MAIS, RA, Autism 
Oxalate Project

References: An interesting paper with few references to 
oxalate research written by Mrs. Susan Owens on leaky gut 
and the low-oxalate diet is available online: 
http://www.usautism.org/USAAA_Newsletter/mechanisms_behind_the_leaky_gut.pdf

Other than Susan’s work, there is little mention in the 
peer-reviewed literature specifically linking high oxalate 
levels to bowel dysfunction except for a few papers on 
short bowel syndrome (SBS) which most commonly results 
after bowel resections for Crohn’s disease, the first of 
which was published in 1992:

Nightingale JMD, Lennard-Jones JE, Gertner DJ, et al. 
Colonic preservation reduces the need for parenteral 
therapy, increases the incidence of renal stones but does 
not change the high prevalence of gallstones in patients 
with a short bowel. Gut 1992;33:1493-1497

In 1980 it was shown that the colon is the presumed site 
of enhanced oxalate absorption in patients with 
steatorrhea (a common symptom of celiac disease): Oxalate 
uptake by everted sacs of rat colon. Biochim Biophys Acta. 
1980 Mar 13;596(3):404-13.

Visit the Celiac Web Page at Http://www.enabling.org/ia/celiac/index.html
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