Reduced diversity and altered composition of the gut microbiome in individuals with ME/CFS

[Snow Leopard]

I asked Ariana to change the headline to "chronic fatigue syndrome"...

The whole headline is messed up "All in your head" is a slur too.

 

[viggster]

The whole headline is messed up "All in your head" is a slur too.

Yes, I cringed.

 

[Bob]

@viggster, I love your metaphor!

In the past, you've shown a soft spot for certain orphan diseases. Well, the history of ME is akin to having locked an entire orphanage in a cellar and bulldozing the house.

 

[Comet]

The whole headline is messed up "All in your head" is a slur too.

I hear you, but don't most of them say something like that? Along the lines of "CF might actually be real" or "New study shows CF isn't just all in your head".

Not that this is a good thing, but it could be a whole lot worse (in my opinion, of course).

Hopefully as we see more articles, they won't have to debunk the "Hey, maybe it's real" nonsense and will just report news on our disease.

At least a girl can dream...

 

[BurnA]

It got the "ridiculous concept" quote in from Maureen Hanson too:

It's amazing how much more powerful and effective the word ridiculous is in this context.Take it out and it's just an opinion, add it in and a reader woukd feel stupid for even considering that concept.

 

[BurnA]

The whole headline is messed up "All in your head" is a slur too.

Yes, I cringed

It's the word 'just'.

Implies it is in your head but not just, it might be in the gut too. Amazing how this happens time and time again, even on 'good' articles.

 

[Bob]

https://twitter.com/i/web/status/748611324930891777

 

[viggster]

Looks like they are changing the headline but the terrible photo is staying for reasons that are too tedious to explain.

 

[duncan]

Question: Wonder which parts of an article pulls the reader in and then grabs her?

Answer: Headline, picture, first paragraph.

I appreciate the author tried, but, it's the impression that matters. You get the impression wrong in any of those three, you not only possibly lose the reader, you send him off with the wrong perspective.

It's a hard thing for any non-pwME to know about how small words or images can mean so much, and I certainly am thankful for the intent of this writer, but this stuff matters.

 

[Comet]

@viggster, you rock! New headline:

"New study shows chronic fatigue syndrome may have to do with gut microbes"

 

[acouchy]

I was listening to a science podcast (TWIS) last night and I was shocked when I heard them talk about this study.

They reported the facts and I did not hear anything negative. Made me happy. Maybe things really are beginning to change.

Anyways, you can find the podcast webpage here... http://www.twis.org/2016/07/01/1974/ . The talk about the study starts around 47:40.

 

[Forbin]

If you don't want to download the entire podcast, here is a link to the the youtube video of this discussion: Jump to 48:00.

[There are a couple of unfortunate written comments under the video from someone who doesn't seem to grasp the difference between "chronic fatigue" and chronic fatigue syndrome. He also totally misses the distinction between finding a biomarker and finding a cause.]

 

[bertiedog]

What I'm dying to know, is what's causing translocation of bacterial components out of the gut.

It's very interesting that hsCRP is not elevated. Is that a new finding? Was the purpose of including that to provide evidence that this is not a typical IBS condition arisen from inflammation of the GI tract?

I am pretty certain from all the research that I have done is that leaky gut causes all this problems and one reason for the leaky gut is eating any gluten. I heard last week on the Webinar on Hashimotos that some recent studies have shown that eating gluten causes a leaky gut in everyone. Gluten is the main culprit but other substances can do this too, dairy being the most obvious. They describe molecular mimicry as to why this happens which I know a certain doctor here doesn't believe in.

The explanation as to what happens then is that the immune system is attacking these proteins and this causes inflammation and any number of other symptoms like fatigue, pain, bloating, brain fog, memory/balance problems etc.

I have been so convinced by this that I gave up gluten 2 months ago and my energy starting coming back within 2 weeks and I have had to cut back on my thyroid medication and adrenal meds. It's like a have a new brain! For me I am also sensitive to dairy so I have cut that out too and eating alternatives so my skin is improved too.

It really is very simple, what you eat can cause all sorts of huge problems and the immune system is the problem.

Pam

 

[M Paine]

Are there any papers apart from the Mae's paper which give more information about dairy and gluten and their role in leaky gut? Why is it that they get included in leaky gut diets?

 

[M Paine]

Also, it seems that leaky gut would be letting molecules that normally cannot be endocytosed by epithelial cells, into the bloodstream. I wonder what sort of problems that may be causing.

Also there's a lot of signalling hormone and neurotransmitters in the gut. The first thing that comes to mind is norepinephrine (noradrenaline). Could that be a source of hormone entering the bloodstream that normally would be contained within the gut?

 

[M Paine]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810492/

Adrenergic signaling in bacteria.
Adrenaline and NA are the most abundant catecholamines in the human body and are primarily involved in the fight-or-flight response. Adrenaline and NA contribute important functions to intestinal physiology, including modulation of intestinal smooth muscle contraction, submucosal blood flow, and chloride and potassium secretion (9). Several sources contribute to the pool of intestinal adrenaline and NA, which can reach micromolar concentrations (10). In addition to the central nervous system and adrenal medulla, the adrenergic neurons that are present in the enteric nervous system are major sources of NA in the intestine (11,12). Furthermore, the resident microbiota, as well as pathogens, influences adrenaline/NA concentrations in the colon. The resident commensal microbiota stimulates the production of NA and, to some extent, adrenaline in the GI tract through an as-yet-unknown mechanism (13). Additionally, T cells, macrophages, and neutrophils generate and secrete adrenaline and NA (14). Therefore, pathogens may augment adrenaline and NA concentrations in the GI tract, not only because of the stress of infection but also by stimulating an immune response.

Personally, when I've had that manic feeling of adrenaline during PEM, my hunch would be the source of that is from hormones entering the blood stream from the gut

 

[rosie26]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810492/



Personally, when I've had that manic feeling of adrenaline during PEM, my hunch would be the source of that is from hormones entering the blood stream from the gut

I had that full-on at severe onset and it took a long time (years) to ease up. An intolerable symptom. Prednisone made it worse for me. I'm not sure if this symptom was connected to the intolerable poisoned feeling I also had in those years.

 

[M Paine]

I'm not sure if this symptom was connected to the intolerable poisoned feeling I also had in those years.

I know the poisoned feeling you mean. Almost like the worst hangover will give you, a kind of 'my liver isn't working properly' kind of feeling that permeates through the whole body. It wouldn't surprise me if it's related to the contents of the gut spilling into the bloodstream unchecked

 

[lansbergen]

The hangover feeling.

When I still sometimes forgot to take the immunemodulator I got a huge hangover the next morning.

 

[kangaSue]

What I'm dying to know, is what's causing translocation of bacterial components out of the gut.

It's very interesting that hsCRP is not elevated. Is that a new finding? Was the purpose of including that to provide evidence that this is not a typical IBS condition arisen from inflammation of the GI tract?

Impaired blood flow to the bowel is another reason for intestinal permeability. The mucosal layer requires a three-fold increase in demand for blood flow during the digestion process and will suffer varying degrees of breakdown if the supply is insufficient and can result in chronic intestinal ischemia when this is occurring regularly and damage to the mucosal barrier becomes more extensive. This then allows toxic products to come in contact with the bowel wall and leak into circulation.

There are rarely any regular blood pathology findings to indicate intestinal ischemia until the bowel starts to turn necrotic but there are a couple of markers that might at least indicate intestinal permeability;
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980675/

[Translocation of bacteria and their products
Breakdown of the mucosal barrier potentially leads to translocation of microbiota or their toxic products. Two promising plasma markers, reflecting translocation of bacteria or their products, are D-lactate and endotoxin lipopolysaccharide (LPS), which are metabolic products or components of the commensal bacteria of the gastrointestinal tract. D-lactate is only produced by bacteria as a product of bacterial fermentation[10]. Baseline levels of D-lactate in healthy subjects are very low. Increased levels of D-lactate have been correlated with conditions in which the number of bacteria elevates rapidly, including in patients with bacterial overgrowth due to infection, short bowel syndrome, and mesenteric ischaemia[11]. LPS, the major constituent of the outer membrane of Gram-negative bacteria, is released by Gram-negative bacteria when replicating or dying. Increased circulating LPS levels have been related to an impaired mucosal barrier. The presence of LPS can be measured directly in blood, e.g. by the Limulus Amoebocyte Lysate assay[12]. In addition, anti-LPS antibodies can be measured by endotoxin-core antibody (EndoCAb), an indirect measurement of LPS leakage into the circulation[13]. A drop in levels of circulating anti-LPS antibodies is considered to indicate consumption of antibodies to LPS by exposure to LPS[14].]