aimossy
Senior Member
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C Difficile.
You are aware there isn't anything solid in this area, which is why you stated this
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Fecal metagenomic profiles in subgroups of patients with ME/CFS
- Thread starter Kati
- Start date
C Difficile.
You are aware there isn't anything solid in this area, which is why you stated this
C Difficile. You are aware there isn't anything solid in this area, which is why you stated this
Yes, that was the obvious example that I failed to think of.
´Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity.´
Question: do you care how severe your disease is?
arewenearlythereyet
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One of the things that seems to always get missed in these discussions about "pathogens" is that Microbes do need a receptive environment to grow. Our body has several environments within the gut that suit particular micobes etc.
Simply removing the perceived offenders doesn't mean that they will not just re-establish themselves either in the gut or beyond. Predation\population pressure is a factor, but environment is probably more significant. This is why probiotics and antibiotics as solutions will not alter the outcome unless you address the environment that caused the supposed imbalance in the first place.
I think what we need is a fantastic endosope that measures metabolites, pH etc in situ at the same time as taking a sample of the microbiological flora for plating up in vitro. Examining faeces seems a little after the fact?
Simply removing the perceived offenders doesn't mean that they will not just re-establish themselves either in the gut or beyond. Predation\population pressure is a factor, but environment is probably more significant. This is why probiotics and antibiotics as solutions will not alter the outcome unless you address the environment that caused the supposed imbalance in the first place.
I think what we need is a fantastic endosope that measures metabolites, pH etc in situ at the same time as taking a sample of the microbiological flora for plating up in vitro. Examining faeces seems a little after the fact?
Anyway, I think there are some problems with this study. Why not try to look for a connection between microbiota composition and levels of LPS in the plasma? Even this would only be looking at one side of the problem though, since intestinal permeability is determined by the interaction between the microbiota, the gut environment (including diet), and the immune system.
Just wait for someone to test LPS and cytokine levels in people with ME after exercise. I believe we will see a much stronger correlation, with a greater separation between cases and controls.
I was thinking of that one, but as I recall those two observations (increased LPS and altered microbiota) were separate. I meant to say someone should look for a correlation between specific microbiome-types (or even just levels of particular genera or species) and levels of LPS in the plasma. Someone with a better understanding of statistics than me.
This is very Real and very Powerful IMO.
Having said that, all "good" research is welcome, but we are in a hurry !!!!!
I did not intend to diminish the potential for Ron Davis's work.
Marco
Grrrrrrr!
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C Difficile.
You are aware there isn't anything solid in this area, which is why you stated this
Literally
C difficile would fit in with a external pathogen rather than an inbalance in commensal microbiota :
http://pmj.bmj.com/content/81/956/367
Marco
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I know how severe it is.
Manganus
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I really doubt if it's teoretically possible to kill, like, all of a bacterial population. I would guess that regardless of method, there will allways remain a rest population.
The trick, unless I'm mistaken, would hence be to reduce the population that much that other bacteria and/or white blood cells were able to consume the bacterias faster than they reproduced. Usually with the help of antibiotics. In the intestines, one may guess that white blood cells are less important.
An alternative to "killing them all" may be to, one way or another, strengthen or add those kinds of bacteria that may keep the unwanted one within bounds.
Marco
Grrrrrrr!
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I quoted severe heatstroke as one condition where translocation of gut bacteria can ultimately result in death. Extreme exercise is another (related) condition leading to 'leaky gut':
http://www.sciencedirect.com/science/article/pii/S2095254616300163
Where appropriate I feel that exercise (or other stressor) challenge should be mandatory in ME/CFS studies.
Manganus
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Well.. like 25 years ago, I did understand some of what was then known about endothelial cells (and immune system cells).
Very little remains, and meanwhile the scientifical front has moved ahead. I hardly understand anything nowadays.
And in particular, I do not understand how LPS should cause disruption of the tight bonds between outer cells of the intestinal walls.
:/
when will finally banish that horrible term and put it just in history books?
I think the underlying cause-s of an altered microbiome in PWME has to be treated first. I assume a faecal transplant wouldn´t be a cure otherwise. I think it has been tried already with a temporary, good effect.
Yes of course, if we are talking in terms of altered microbiome. That is quite different from what I was talking about which is bacterial translocation - when gut bugs end up in the blood stream. There is really only one way for them to get there - through the intestinal wall/tight junctions. They should definitely NOT be in the blood stream - can lead to sepsis and death and every effort should be made to treat them with antimicrobials, and then attempt to tighten up the junctions in the gut that are letting them through. I wasn't suggesting treating an altered microbiome WITHOUT translocation with nuke level abx.
I know at least one PWME who was made significantly worse from it and has had terrible gastro issues ever since, far worse than the original issue. We should be careful.