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The OAT interpretation guide states that mineral conjugate base forms of oxalic acid are also byproducts of molds such as Aspergillus and Penicillium. Can high levels of aflatoxin or ochratoxin contribute to oxalate load? Are these toxins converted to oxalic acid or do you need fungal colonization in the GI tract or elsewhere in the body to produce oxalates? What is the route of oxalate production?
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