He made a post on carbs producing oxalates but it's paywalled

oxalate levels within the normal range inhibits the Krebs cycle by about 50%

if anyone here is subscribed could you give a summary

here's the link:
https://chrismasterjohnphd.substack.com/p/are-sugar-and-xylitol-behind-your

What are some caloric foods (other than plain sugar, OJ & pomegranate juice) that don't feed gut bacteria (starches/soluble fiber) or contain bacteria (fermented, dried, etc..)?

Has anyone here had experiences with either of them for Endotoxemia?

Is there a specific blood level to aim for, if so then based on half-life/route of administration/etc how could that be achieved?

When Haidut mentions HED dosages (quotations below) is he referring to oral or topical administration? (I know at least Pregnenolone has about 10x higher oral doses than topical for the same effects, idk about Progesterone & DHEA)

*Georgi's quotes (bolding added by me) on them from his blog:

"HED 1mg/kg progesterone was remarkably protective against endotoxin inflammation and lethality, but it also suggests that progesterone may react directly with endotoxin and form a covalent bond. This progesterone-endotoxin complex is apparently inactive, which suggests that a significant portion of progesterone's (and likely pregnenolone's) protective effects against endotoxin may stem from a direct deactivation effects. If true, it would put steroids like pregnenolone/progesterone on par with charcoal as there are very few other known direct binders/deactivators of endotoxin. This effect is on top of the TLR4/histamine/serotonin/prostaglandin/etc antagonism that these steroids are already known to possess, and suggests that it is the physical properties of C-21 steroids rather than their "receptor" effects that may be responsible for some of their benefits."

"a single HED dose of as little as 5mg - 7mg [of DHEA] daramatically increased survival from a lethal dose of endotoxin (LPS). Higher doses were even more beneficial but I think the cap should be at about 20mg per dose given the estrogenicity of DHEA in higher doses (in humans vs. mice), which can increase the lethality of endotoxin."