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Association of fecal microbiota & fecal, blood serum & urine metabolites. Chris Armstrong & co

Messages
78
Location
Melbourne, Australia
New paper by the Bio21 team:

"The association of fecal microbiota and fecal, blood serum and urine metabolites in myalgic encephalomyelitis/chronic fatigue syndrome"

by Chris Armstrong, Neil McGregor, Don Lewis, Henry Butt & Paul Gooley.

Abstract
Introduction
The human gut microbiota has the ability to modulate host metabolism. Metabolic profiling of the microbiota and the host biofluids may determine associations significant of a host–microbe relationship. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a long-term disorder of fatigue that is poorly understood, but has been linked to gut problems and altered microbiota.

Objectives

Find changes in fecal microbiota and metabolites in ME/CFS and determine their association with blood serum and urine metabolites.

Methods

A workflow was developed that correlates microbial counts with fecal, blood serum and urine metabolites quantitated by high-throughput 1H NMR spectroscopy. The study consists of thirty-four females with ME/CFS (34.9 ± 1.8 SE years old) and twenty-five non-ME/CFS female (33.0 ± 1.6 SE years old).

Results

The workflow was validated using the non-ME/CFS cohort where fecal short chain fatty acids (SCFA) were associated with serum and urine metabolites indicative of host metabolism changes enacted by SCFA. In the ME/CFS cohort a decrease in fecal lactate and an increase in fecal butyrate, isovalerate and valerate were observed along with an increase in Clostridiumspp. and a decrease in Bacteroides spp. These differences were consistent with an increase in microbial fermentation of fiber and amino acids to produce SCFA in the gut of ME/CFS patients. Decreased fecal amino acids positively correlated with substrates of gluconeogenesis and purine synthesis in the serum of ME/CFS patients.

Conclusion

Increased production of SCFA by microbial fermentation in the gut of ME/CFS patients may be associated with deleterious effects on the host energy metabolism.

http://link.springer.com/article/10.1007/s11306-016-1145-z
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
That's surprising - I thought that the production of SCFAs was generally supposed to be a good thing, and supportive of the immune system (but I speak as someone pig-ignorant of biology).
 
That's surprising - I thought that the production of SCFAs was generally supposed to be a good thing, and supportive of the immune system (but I speak as someone pig-ignorant of biology).

My guess is
From the study said:
These differences were consistent with an increase in microbial fermentation of fiber and amino acids to produce SCFA in the gut of ME/CFS patients. Decreased fecal amino acids positively correlated with substrates of gluconeogenesis and purine synthesis in the serum of ME/CFS patients.
shows the body trying to generate energy from less efficient sources and the downstream effects. But I'm very foggy at the moment and know almost no biology so what could I possibly get wrong.... ;)
 

roller

wiggle jiggle
Messages
775
a decrease in fecal lactate and
an increase in fecal butyrate, isovalerate and valerate
an increase in
Clostridiumspp.
and a decrease in
Bacteroides spp.

That's surprising - I thought that the production of SCFAs was generally supposed to be a good thing, and supportive of the immune system (but I speak as someone pig-ignorant of biology).

i would like to know this, too.

i eventually gave up searching on this as i thought "treatment" may not lead to anything much.

but the last thing i noted without a source, was that
those (high and negative turning) bacterial scfa-shifts are not a regular product of our body.
we may not produce them.

therefore they may not be oxidized, as usual.
in this case, faik coenzym A should help, i wondered,

this may be all wrong ;)

these high and unbeneficial scfa's are common in helminthic infections.
(and imo may happen with other parasitic infections as well)
 

Kati

Patient in training
Messages
5,497
I have a question for @ChrisArmstrong, who deserves much congratulations and thanks for this body of work. It is much interesting, despite my brain not able to understand everything.

My question is... is this gut issue and bacteria/ metabolomic profile present in other diseases and has the comparison been made?

Thank you. If you have no time for answering, no worries... I am ok with you spending more time in research :):nerd:
 
Last edited:

Gondwanaland

Senior Member
Messages
5,092
Increased production of SCFA by microbial fermentation in the gut of ME/CFS patients may be associated with deleterious effects on the host energy metabolism.
I always feel worse from prebiotic foods, and can't figure out if they increase uric acid production or mobilize uric acid from tissue deposits.
 

FMMM1

Senior Member
Messages
513
Conclusion
Increased production of SCFA by microbial fermentation in the gut of ME/CFS patients may be associated with deleterious effects on the host energy metabolism.


Based on a very brief look, I can't claim to understand this paper but it's still very welcome!

I need to go back to Chris Armstrong's webinar to try to understand this. From memory my understanding is that the hypothesis is that people with ME/CFS have lower levels of stomach/gut acid, caused by their altered metabolism.

Lower stomach acid equals altered gut flora and from this paper (not surprisingly) altered gut flora result in changes in what comes across into the blood stream [i.e. increased levels of short chain fatty acids (SCFA) in the blood]. Linking increases in blood SCFA to
deleterious effects on the host energy metabolism
would be appear to be pretty significant - groundbreaking?

Are there methods which can directly measure the acidity (pH) of the stomach/gut? I.e. to test whether people with ME/CFS have lower levels of stomach/gut acid.

How do we reverse, or reduce the impact of, lower levels of stomach/gut acid? E.g. by supplementing with amino acids (something else to check on the webinar).

Good to see that there are scientists like Chris Armstrong doing this work. How do we influence the decision makers to fund this work?
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
From memory my understanding is that the hypothesis is that people with ME/CFS have lower levels of stomach/gut acid, caused by their altered metabolism.

Lower stomach acid equals altered gut flora and from this paper (not surprisingly) altered gut flora result in changes in what comes across into the blood stream [i.e. increased levels of short chain fatty acids (SCFA) in the blood].
Most of us seem to have higher levels of stomach acid than normal, and we often have almost constant acidosis. (Maybe you've found this now.)
 

FMMM1

Senior Member
Messages
513
Most of us seem to have higher levels of stomach acid than normal, and we often have almost constant acidosis. (Maybe you've found this now.)

Hi, I suggest that you check out Chris's webinar in particular 45.30 to 52.34 minutes. He's proposing a higher pH (i.e. less acid) in the gut.

From Wikipedia: "Acidosis is an increased acidity in the ---- blood plasma". Possibly if you review the webinar then you my find clues re increased "acidity in the ---- blood plasma" if so then please come back to me with the time window. Was the acidosis confirmed by laboratory test (an unusual concept in ME/CFS).

I'm struggling with the concepts presented here, are elevated SCFAs acting as signalling compounds (negatively impacting on metabolism) or are they simply indicative of a poorly functioning digestive system (too little acid) or something else (please specify)?
 

FMMM1

Senior Member
Messages
513
Does anyone have access to the full paper?

*edit: thanks to the person who sent it through

Hi, check out Chris's webinar; he discusses the material in this paper.

If you have the paper or know where I can get it then I'd be grateful for same. I have to say this appears to be pretty complex but most welcome all the same.