i wanted to add that I am experimenting with different prebiotics. I've gone back to the drawing board with the aim of finding a way to make this approach to displacing organisms much more tolerable. I continue to believe this problem has a microbial solution and likely involves enhancing the expansion of butyrate-synthesizing clostridial species. Unfortunately, the inter-relationships among the predominant commensals and the complexity of this dynamic allows for only guesswork, so I apologize for how speculative this is.
With that said, if one wanted to minimize bacterial dislocation/translocation, I think they may want to simultaneously seek to stimulate the growth of butyrate producing species while temporarily avoiding aggressive enhancement of bifidobacterial species. While the latter genus is likely essential, and its effects participate in enhancing intestinal integrity, its ability to displace pathogens in the colon is very pronounced. Some species may just be too potent with marked intestinal permeability because one of the consequences of rapidly expanding a particular bifidobacterial species can be a transient escalation of lipopolysaccharide in the GIT, which itself increases colonic permeability. I continue to think these species are just as likely to be implicated in the perpetuation of the condition, but perhaps there is an order of operations that would prove to be more tolerable.
While the displacement of bacteria via cell lysis can dramatically raise extra-intestinal LPS concentrations, this is a consequence of both the pre-existing deficiency of structural integrity and the temporary inflammatory response created by the endotoxin displacement in the bowel. In effect, each time we try to displace bacteria there will be a transient, but highly significant increase in permeability. It's one of those "two steps forward, one step back" situations where a pathogen load is diminished and the epithelial layer gradually improves, but at a price. So, while there is obviously no way to wholly separate the good from the bad and individually micromanage such a complex ecological community, I do think a more targeted approach may be worthwhile. What we can most readily control includes the direct supplementation of the desired organisms, or those prebiotics upon which the organisms utilize.
I think providing conditions more favorable for butyrate synthesis and de-emphasizing bifidobacterial organisms may be one way of easing the extra-intestinal endotoxin burden. @anne_likes_red is using a clostrial butyrate-synthesizing species with apparent benefits. I think this is a sound strategy, but my experience with this is too limited to draw any conclusions. It may have variable effects, in part depending upon the other environmental conditions. One concern I have is that there are reasons that these organisms have not gained a foothold or maintained prominence, and these could be numerous, including, pH, oxidizing conditions, or a host of other reasons. The one I am predominantly focused on is acetate availability. These organisms need acetate for growth, and they can get this from Bifidobacteria species, which are dramatically stimulated by potato starch supplementation; i was considering an alternative source of acetate.
@Gestalt may have found a way of enhancing clostrial butyrate synthesis without Bifidobacterial-synthesized acetate by using larch arabinogalactan, and this may represent another effective strategy. While I haven't been able to fully explore this yet, it looks like Bacteroides species may be able to preferentially access this combination of arabinose and galactose to yield acetate over Bifidobacterial species. (Don't take my word for this, this is simply my initial conclusion).
I am getting good, albeit very preliminary, results from this. It seems this has already lessened P.E.M., and it has also rapidly increased my ability to tolerate proteins. This is exactly what would be expected from butyrate enhancement as it should bolster the synthesis of all fatty acids and increase the efficiency of the glutamine metabolism, which I think represents the core disease process.
I hate to render a conclusion so quickly, and I honestly can only speculate about what is happening, but I think this may have potential to direct the carbon flux towards acetate and butyrate synthesis without so much extra-intestinal endotoxin displacement. At the very least, it seems that selectively stimulating different organisms may provide some benefits given the likely microbial diversity that exists. I will report back in a week or two.
With that said, if one wanted to minimize bacterial dislocation/translocation, I think they may want to simultaneously seek to stimulate the growth of butyrate producing species while temporarily avoiding aggressive enhancement of bifidobacterial species. While the latter genus is likely essential, and its effects participate in enhancing intestinal integrity, its ability to displace pathogens in the colon is very pronounced. Some species may just be too potent with marked intestinal permeability because one of the consequences of rapidly expanding a particular bifidobacterial species can be a transient escalation of lipopolysaccharide in the GIT, which itself increases colonic permeability. I continue to think these species are just as likely to be implicated in the perpetuation of the condition, but perhaps there is an order of operations that would prove to be more tolerable.
While the displacement of bacteria via cell lysis can dramatically raise extra-intestinal LPS concentrations, this is a consequence of both the pre-existing deficiency of structural integrity and the temporary inflammatory response created by the endotoxin displacement in the bowel. In effect, each time we try to displace bacteria there will be a transient, but highly significant increase in permeability. It's one of those "two steps forward, one step back" situations where a pathogen load is diminished and the epithelial layer gradually improves, but at a price. So, while there is obviously no way to wholly separate the good from the bad and individually micromanage such a complex ecological community, I do think a more targeted approach may be worthwhile. What we can most readily control includes the direct supplementation of the desired organisms, or those prebiotics upon which the organisms utilize.
I think providing conditions more favorable for butyrate synthesis and de-emphasizing bifidobacterial organisms may be one way of easing the extra-intestinal endotoxin burden. @anne_likes_red is using a clostrial butyrate-synthesizing species with apparent benefits. I think this is a sound strategy, but my experience with this is too limited to draw any conclusions. It may have variable effects, in part depending upon the other environmental conditions. One concern I have is that there are reasons that these organisms have not gained a foothold or maintained prominence, and these could be numerous, including, pH, oxidizing conditions, or a host of other reasons. The one I am predominantly focused on is acetate availability. These organisms need acetate for growth, and they can get this from Bifidobacteria species, which are dramatically stimulated by potato starch supplementation; i was considering an alternative source of acetate.
@Gestalt may have found a way of enhancing clostrial butyrate synthesis without Bifidobacterial-synthesized acetate by using larch arabinogalactan, and this may represent another effective strategy. While I haven't been able to fully explore this yet, it looks like Bacteroides species may be able to preferentially access this combination of arabinose and galactose to yield acetate over Bifidobacterial species. (Don't take my word for this, this is simply my initial conclusion).
I am getting good, albeit very preliminary, results from this. It seems this has already lessened P.E.M., and it has also rapidly increased my ability to tolerate proteins. This is exactly what would be expected from butyrate enhancement as it should bolster the synthesis of all fatty acids and increase the efficiency of the glutamine metabolism, which I think represents the core disease process.
I hate to render a conclusion so quickly, and I honestly can only speculate about what is happening, but I think this may have potential to direct the carbon flux towards acetate and butyrate synthesis without so much extra-intestinal endotoxin displacement. At the very least, it seems that selectively stimulating different organisms may provide some benefits given the likely microbial diversity that exists. I will report back in a week or two.
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