aquariusgirl
Senior Member
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For those of you interested in the role of oxolates in our illness, I wanted to draw your attention to this paper & to point out the authors' assertion that glucose is converted to oxolate in the presence of copper 2 and iron 3.
https://www.hindawi.com/journals/au/2012/819202/
Also, if you check out Fig 1 in the paper, you will notice that copper 2 is essential for 2 pathways that wind up generating oxolate.
William Shaw at Great Plains has talked about ascorbate converting to oxolate in the presence of free copper but I haven't heard anything about this other pathway & I wonder if this ties in with the findings of Fluge & Mella & the australians with respect to pyruvate dehydrogenase.
I'm assuming that results in elevated glucose if a person keeps eating carbs. So my clumsy guesswork is ...elevated glucose in the presence of free copper & iron = lots & lots of oxolates.
So I wonder if we need a low glucose diet, not a low oxolate diet, as well as therapies to lower ROS, to stop our cells turning into oxolate factories?
Quotes from the paper:
The biochemical pathways involved in oxalate production are poorly understood despite decades of research.However, it is clear that glyoxylate is the major precursor of oxalate [1].
We hypothesize that glyoxal is one of the most important sources of endogenous oxalate synthesis in humans.
In addition to the many exogenous sources of glyoxal, it is endogenously produced via autoxidation of carbohydrates and ascorbate, degradation of glycated proteins and lipid peroxidation [9].
Glyoxal can be formed through various pathways as illustrated in Figure 1.
It is created directly from glucose via retroaldol condensation, and it is formed indirectly from glucose via a glycoaldehyde intermediate that undergoes autoxidation. The autoxidation reaction is promoted by the presence of phosphate buffer and trace metal ions (Fe3+ and Cu2+) in solution.
Manini et al. have demonstrated that glyoxal cannot only be formed from glucose but from many other carbohydrates as well, including galactose, mannose, fructose, ribose, arabinose, ribulose, glyceraldehyde, acetone, adenosine, mannitol, and glycerol [12].
https://www.hindawi.com/journals/au/2012/819202/
Also, if you check out Fig 1 in the paper, you will notice that copper 2 is essential for 2 pathways that wind up generating oxolate.
William Shaw at Great Plains has talked about ascorbate converting to oxolate in the presence of free copper but I haven't heard anything about this other pathway & I wonder if this ties in with the findings of Fluge & Mella & the australians with respect to pyruvate dehydrogenase.
I'm assuming that results in elevated glucose if a person keeps eating carbs. So my clumsy guesswork is ...elevated glucose in the presence of free copper & iron = lots & lots of oxolates.
So I wonder if we need a low glucose diet, not a low oxolate diet, as well as therapies to lower ROS, to stop our cells turning into oxolate factories?
Quotes from the paper:
The biochemical pathways involved in oxalate production are poorly understood despite decades of research.However, it is clear that glyoxylate is the major precursor of oxalate [1].
We hypothesize that glyoxal is one of the most important sources of endogenous oxalate synthesis in humans.
In addition to the many exogenous sources of glyoxal, it is endogenously produced via autoxidation of carbohydrates and ascorbate, degradation of glycated proteins and lipid peroxidation [9].
Glyoxal can be formed through various pathways as illustrated in Figure 1.
It is created directly from glucose via retroaldol condensation, and it is formed indirectly from glucose via a glycoaldehyde intermediate that undergoes autoxidation. The autoxidation reaction is promoted by the presence of phosphate buffer and trace metal ions (Fe3+ and Cu2+) in solution.
Manini et al. have demonstrated that glyoxal cannot only be formed from glucose but from many other carbohydrates as well, including galactose, mannose, fructose, ribose, arabinose, ribulose, glyceraldehyde, acetone, adenosine, mannitol, and glycerol [12].