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SIBO and ME/CFS similarities ......

EddieB

Senior Member
Messages
633
Location
Northern southern California
Without that, SIBO as the causative agent is just conjecture. Not saying it's wrong. It's just not knowable what role it plays, if any.
That would depend on your symptoms. If you have unexplained digestive issues, it’s worth a look.

As to a root cause, it may never be found. Sibo could simply be the result of any number of other neurological/ functional conditions.

I myself am looking at sibo as a symptom, rather than a root cause. I’m hoping the testing will reveal something informative. If I can (within reason) treat for sibo, and beat it back and feel a bit better, I’d consider that success.
 

lenora

Senior Member
Messages
5,010
Hello @2Cor.12:19. Yes, I know exactly what you mean about getting your hopes up...and then they're dashed, once more. I have to say that old age has befallen me and I now have plenty of other things to worry about. In my case, I have to say that my genetic profile is pretty lousy indeed.

@SwanRonson....It's very hard to prove or disprove something if the main research misses the details. I'm not saying that research shouldn't be done, it's just that we really should bear in mind that until it's proven, it's only a supposition. Like so many other things in life. Wishing both of you well...Yours, Lenora.
 
Messages
82
H2S SIBO can lead to mitochondrial damage:

Although H2S is generated by the host and is increasingly recognized to have a multitude of important beneficial physiologic functions [33], it becomes a potent toxin once its concentration exceeds the detoxifying capacity in the tissue. Specifically, higher amounts of H2S generated in the intestine have the potential to disrupt the gut barrier function, which may be an early and critical initiating event in triggering the onset of UC and the perpetuation of its activity [34]. Traditionally, the H2S toxin hypothesis has focused on the potential injurious effects of sulfide gas on the cellular metabolism of colonocytes, mainly the inhibition of cytochrome c oxidase activity in mitochondria, which induces oxidative stress in a fashion similar to cyanide [35]. Roediger and colleagues demonstrated that H2S inhibits β-oxidation of butyrate by colonocytes, their preferred energy source [36]. Notably, UC mucosa has lower rates of butyrate uptake and oxidation relative to healthy controls [37]. In summary, oxidative stress and energy starvation caused by excessive H2S concentrations may lead to colonocyte death, penetration of the epithelial barrier by the intestinal microbes and their direct interaction with the mucosal immune system. Resulting inflammation leads to further disruption of the gut barrier, decreased butyrate oxidation [37], and decreased mucosal sulfide detoxification and the subsequent perpetuation of inflammation [38].
from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6521024/
 
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