My apologies if this has been discussed at length in other threads. But my PR site search proved fruitless for the specific questions I'm about to ask our resident experts. Can anyone explain what Dr Weyrich is referring to in these two paragraphs about elevated arabinose in the OAT: http://drweyrich.weyrich.com/disorders/autism.html "It is not clear whether elevated urinary levels of arabinose detected in by the Organic Acid Test" are simply a marker for yeast dysbiosis, or are pathogenic in their own right. In some cases, it appears that a metabolic defect in the processing of pentose sugars such as arabinose may be the cause, since it is reported that in some children, eating fruits rich in arabinose (apples and pears) rapidly induces an exacerbation of autistic symptoms [Shaw2008]." I'm asking about this "metabolic defect" because my latest OAT results show elevated arabinose like I had two years ago, but without elevation in the other yeast markers, tartaric and carboxcitric. Those were hugely elevated two years ago, but are now in the normal range. In fact, carboxcitric barely registers; it's near zero. Quick background: OAT test from 2013 showed high elevation for tartaric (14; s/b < 4.5), arabinose (70; s/b < 29), and carboxycitric (113; s/b < 29). Genova fecal testing showed high levels of fungus in gut at the time. Fast forward to 2015 after many months of Nystatin therapy. Fungus now gone per Genova repeat testing. Latest OAT test shows normal tartaric (3.6) and carboxycitric (0.41). But arabinose is actually higher (77). I should also note that I went on off high arabinose foods before testing (apples, pears, grapes). Actually, I don't eat these anymore, nor their juice products, so it wasn't a problem. I've also returned to NADH and D-Ribose supplements for the past three months, which I stopped taking five years ago. D-Ribose helps to lower my blood sugar, but I don't really notice much energy improvement (which is why I originally stopped taking them). If someone has a pentose metabolism defect… will D-Ribose not be assimilated properly and potentially drive arabinose higher? Is that possible? And how, exactly, does the pentose metabolic defect affect someone? The fungus in my gut is gone yet the arabinose continues merrily on. It doesn't add up, at least to me.