I'm thinking pantethine might be helpful for countering the negative effects of endotoxins, it seems it inhibits hypercoagulation and protects the BBB:
Protection against cerebral malaria by the low-molecular-weight thiol pantethine
Good suggestion, but I will caution that Pantethine is readily incorporated to form Coenzyme A, which is going to effect some processes that can cause some people, a few problems. The positive contributions are many, especially as it relates to lipid and sterol synthesis.
The tricky part is that Co-A has a sulfhydryl group and can affect some processes that can cause some unfavorable symptoms, in some. By taking Pantethine instead of B5, one would be circumventing a big part of the chemical process, which is rate-limiting for Co-A biosynthesis because one would be directly supplementing pantethine downstream from the rate-limiting phosphorylation reaction. Generally, this is not such a bad thing, because this pathway is very sensitive to lipid oxidation. By this, I mean that the flow will shift towards sterol and lipid synthesis, which should be beneficial. (As you know, Pantethine has also been shown to have fairly strong associations with improving lipid profiles.)
The problem, which can arise is that this influences the cysteine pathways, which produce hydrogen sulfide. The provision of Co-A is thus spares cysteine, which will be available for synthesis of hydrogen sulfide. It seems to do so at a part of the metabolism that significantly influences H2S. H2S of course has a number of useful roles, but if concentrations in the blood rise too high, it produces adverse symptoms. I found that high doses of pantethine, NAC, or MB12 would all produce the exact same effect, terrible, almost debilitating headaches. Of course the commonality is that they raise circulating cysteine or direct more cysteine to H2S synthesis. This is not so much of a problem when cysteine metabolism is limited by other factors, including co-factor availability, cysteine oxidation from ROS/NOS, etc, but this is the reaction that changes over time, with improved redox status and micro-nutrient availability. This is just one of the things people need to look out for as their metabolism starts to become more normal. Symptoms are going to vary as well, since the capacity to produce H2S from cysteine will vary depending upon the tissues where this is synthesized. Of course research into H2S as biomolecule and blood gas messenger is pretty underdeveloped at this time, but it is also of note that high cysteine foods can directly stimulate the synthesis of hydrogen sulfide within the red blood cells. In this regard, high-thiol foods may suggest that there is high H2S bacterial load.
H2S is a very interesting molecule in ME/CFS when we look at it's potential role in mitigating the effects of a bacterial infection. Bacterial H2S appears to have a role in down-regulating the inflammatory response created by exposure to endotoxins. This blood gas can suppress some pro-inflammatory cytokines, so actually having sulfide in the blood likely plays a major role in keeping us alive as it allows us to endure part of the inflammatory response created by the endotoxins. More H2S may translate to severe symptoms, but it also appears that it may be life-sustaining in so far as it suppresses the inflammatory response we otherwise would mount without the H2S. Perhaps, those of us who have high levels of SRB don't want to interfere too much in the cysteine metabolism, and simply work on reducing concentrations indirectly by nurturing our own commensal organisms.
Of course too much H2S is not good, as is too little. I think back to the time that my glucose metabolism started to decline despite the fact that I had no evidence of metabolic disease, and, according to the endocrinologist, had a remarkable sensitivity to insulin. When I withdrew all those fermentable carbohydrates, my glucose metabolism or glycolysis utterly collapsed in a matter of weeks. In retrospect, what likely happened is that Bifidobacterial organisms and Clostridal species collapsed, but I also think about what organisms must have filled the void, and H2S-synthesizing organisms seem to be uniquely qualified to carry out this role.
The preponderance of hydrogen sulfide producing bacteria would seem to be ideally suited to this new, hostile environment since they could passivate an inflammatory response attributable to the presence of gram-negative bacteria. This is of course assuming that other gram-negative organisms predominated in the new and more hostile community that no longer included the same commensal organisms that populated the colon. These H2S emitting organisms are also very efficient at reducing lactate, and I think elevated lactate would be one manifestation of the new, hostile microbiome. Also, H2S producing organisms may have also served to stabilize energy metabolism, or at least carbohydrate metabolism because hydrogen sulfide stimulates glucose transporter molecule (GLUT4). This is protein which transports glucose from the blood to the tissues, and is of considerable interest now in the study of metabolic disease.
Pantethine is probably going to be o.k. for most. I used to love that stuff, it is Bifidogenic, it is useful in many ways. One of the really cool things it can do is boost CoQ-10 biosynthesis since it is used as a co-factor in the TCA at succinate, of course if you have high lactate/pyruvate, it serves as a cofactor here as well. I think it would be used more commonly for lipid lowering, had it been a substance that could be patented. There is just no economic incentive for the drug companies, and we know that medicine is dominated by script writing. It is sort of like the anti-statin in that it improves lipids and CoQ-10 simultaneously. I would take it again myself, if it didn't give me headaches.