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How arabinose can cause hypoglycemia and glutathione deficiency !
Saturday, March 02 2002 - Filed under: General
Candida and/or other yeasts can produce arabinose (boosted when carbs are available).
In autism-patients arabinose levels are severely elevated.
In my case, on a very low-carb diet the arabinose levels are still 58 mmol/mol creatine (ref 0-115).
This doesn't seem like that high, but wait what happens when I eat some carbs. I suspect that these figures fly skyhigh..
It then causes functional B6, biotin and lipoic acid deficiences, which then also affects many other antioxidants and amino acids...
It's apparent that I do have a functional B6 deficiency (due to imbalanced amino acids), so I also assume that biotin and lipoic acid deficiency are probable.
What also happens is the following:
The high concentration of the unusual yeast sugar arabinose may inhibit gluconeogenesis. Indeed, an autistic child with the highest arabinose (40 times the normal limit) was severely hypoglycemic (blood glucose 20-50 mg %; normal is 100 mg %) almost all of the time. This child had been completely normal until being treated for strep throat at nine months of age. Severe hypoglycemia can markedly impair neurological function. In addition the arabinose may have other unknown toxic roles..
Since I suffer from hypoglycemia, even though I've been low-carbing for almost a year (should be cured in half a year) and have supplemented magnesium (which should cure insulin resistance), I'm more and more thinking that arabinose-producting yeasts are the primary cause of my remaining symptoms...
Perhaps the functional lipoic acid (ALA) deficiency then causes the glutathione deficiency, which then causes CFS-like symptoms...
Antioxidants depend on eachother, so when one or more of them get disabled, the entire antioxidant chain is disrupted..
>The ALA stimulates the production of glutathione (described in the book). Both have the property of having stable oxidized and reduced states and can penetrate cell walls. They can be oxidized by oxidative species and then reduced again by a reduced species. Once oxidized they can be reduced by vitamin C which also has a stable oxidized and reduced state. This regenerates the reduced ALA. The vitamin C is soluble in the aqueaous phase of the cell, the cytoplasm, and diffuses freely there. It diffuses to the cell wall. Vitamin E is soluble in the cell wall and also has a stable oxidized and reduced state. The oxidized vitamin C oxidizes the vitamin E in the cell wall, regenerating the reduced vitamin C. The oxidized vitamin E can then pass this on to vitamin C on the other side of the cell wall. Eventually, the oxidized vitamin C reaches the inner membrane of the mitochondria where it delivers its oxidation potential to CoQ10 dissolved in that membrane. This is where the final stage of aerobic metabolism takes place and the CoQ10 is reduced by a process that produces useful biochemical energy in the Respiratory Chain stage of aerobic metabolism. Without this sequence, the oxidized ALA would not be regenerated and it would be ineffective as an antioxidant
While studying I also found this site, which has very nice pictures, especially the one of the alternative view of human gut microflora:
Human Gut microflora:
Imagine this: I've now only covered one single yeast metabolite. One single metabolite that can cause such havoc on the health.. Amazing..
Let me know if you have some remarks or interesting info,