See attached.
Fermented foods are full of LABs, so this might be a problem. I could perhaps try the SBOs. I might also try to up my R-ALA dose (taking 100mg now).
Thanks. I'm looking at the energy metabolism, especially the Krebs cycle, in an attempt to establish what processes are inhibited to prevent further oxidative stress and thus protect you from killing yourself. While there are nutrient deficiencies that impair the ETC and likely bacterial interference, explaining, in part, why someone may benefit from B2 supplementation, for example, it has to be directly connected to redox sensitive genes that will inhibit energy generation. (I love run-on sentences) It can't be just about nutrient availability, I don't think. It is necessarily tied to your capacity to suppress oxidative stress and thus the competency of your immune system, which are essentially integrated. I have been thinking about the "roadblocks" in the Krebs cycle observed with ME/CFS and am mostly interested in those areas that most closely interact with SCFA production, acetylation, CoQ-10 biosynthesis, succinate production, etc. Stuff that gets back to what I think is necessary to maintain intestinal integrity and by extension, energy metabolism. While it sounds implausible that so much energy could be lost from the GIT, the mechanisms are there. If as they say, 80% or so of the immune response is integrated in the GIT, then it follows that the energy metabolism is similarly connected.
The TCA metabolites always fall off after a dehydrogenation reaction. I see you have no detectable fumarate, which is on the other side of succinate and of course is a product of a dehydrogenation reaction. Need to think about this more, and will ask you some questions off line; when I can.
Regarding the lactate elevation, though, I think this is really more of a feature of not having species that can efficiently carry out lactate dehydrogenation combined with the lack of SCFA's and the effects this produces, probably more of the latter as I'm not aware of a huge contribution from bacterial lactate dehydrogenation. We do know though, that most people with huge concentrations of LAB, an overpopulation, if you will, do not develop elevated lactate. Elevated lactate is a grossly abnormal finding and I don't think can be compatible with good health. Without a intrinsic (host) mechanism for D-lactate metabolism, there has to be a microbial explanation. Sorry, lots of parts to this, I'm sort of thinking out loud.
I do think the problem is less about what organisms you have, and has more to do with what you don't have, specifically those in the lower bowel. Honestly, I think a concentration on restoring SCFA with RS, provided you have some colonizing bifidobacterial strains in place, is going to represent the most effective strategy; you may just have to do this more slowly. The RS does appear to be more efficient at correcting the problems, than the provision of organisms themselves, provided you have some. I can't discount the importance of the bifidobacterial strains because these are critical and are really driving much of what is happening, but I also can't argue with results. I wish I had some data, but my presumption is that butyrate-producing species must have come up because my own inflammatory response is diminished yet I have increased energy. This is what I would predict would happen if intestinal energetics improved.
ALA is going to have a more dramatic effect on dehydrogenation than any supplement I have studied, but I think correcting the lower bowel alkalinity and SCFA deficiency is going to produce much more rapid effects. No reason you couldn't take the ALA, but after my Mercury experience, you would have to understand that I am going to advise everyone against taking this intermittently, and instead, suggesting it be used in accordance with it's half-life. (Even though I'm assuming you have used this in the past without problem) I don't have a problem with the R isomer.
What are you thinking is going to be most effective for you, with regard to the the gut?