I've been doing some reading lately about oxalates, kidney stones etc which I struggle with. It turns out there is a harmless Gram-negative anaerobic bacterium living in our guts, Oxalobacter formigenes, which degrades oxalate in the intestine. Colonisation with this bacterium is associated with a lower likelihood of developing calcium oxalate stones.
The independent researcher Susan Costen Owens has done an enormous amount of work on oxalates, particularly in autism. Some of this is summarised on her website
www.lowoxalate.info and a lot more is scattered through files in the associated Yahoo group, Trying Low Oxalates. I made a summary of many of the pertinent points for another purpose, so I'll upload the document for you to look at.
As you note, many people have problems with the oxalates in food because antibiotics have wiped out the gut bacterium
Oxalobacter formigenes which preferentially digests oxalate. Currently it is not available as a probiotic, though clinical trials are underway. Some strains of
Lactobacillus and
Bifidobacterium can step into the breech, though it is not their preferred food. VSL 3 is one probiotic that has been shown to be able to digest oxalate. Undigested oxalate is taken up into the body further along the colon and it can accumulate throughout. It is a metabolic poison and the body tries to get rid of it by simply dumping it into the skin, bowel and urine, but it travels down a concentration gradient, so blood levels need to fall before this can happen. Interestingly there appears to be some sensing mechanism whereby cells will not dump their accumulated oxalate into the gut unless there are oxalate-digesting bacteria present. Thus a compounding problem can arise as the body accumulates this metabolic poison for want of appropriate dispersing mechanisms in the gut.
There are a couple of rare genetic conditions where oxalate is manufactured endogenously because of defects in a couple of enzymes. However what Susan Owens and others have discovered is the much more common situation where people become endogenous producers despite having normal enzymes. The predisposing condition appears to be prolonged oxidative stress which damages the B6 dependant enzymes involved and sets up a self-perpetuating process of oxalate accumulation. Everyone on this board should be very thoughtful about this possible consequence of prolonged oxidative stress.
Once oxalate starts accumulating, then many B6, B1 and biotin dependant enzyme systems become compromised and a cascading array of other metabolic pathways get deranged, most notably energy pathways, methylation, trans-sulfuration, glutathione recycling, to name just a few.
Oxalates on an OAT test often reflect the body's handling of dietary oxalate and the normal process of dumping of accumulated material. Only the OAT test done by Great Plains Laboratory looks at three oxalate markers (glyceric and glycolic acids, as well as oxalate) and is capable of giving insight into whether endogenous oxalate production has become an issue (though Susan doesn't necessarily think that they interpret it properly).
Food for thought for all.
With best wishes
Alice
