The microbiome hypothesis: Lipkin's collaborative, part 1 (Simon McGrath blog)

New blog at ME/CFS Research Review

The microbiome hypothesis: Dr Ian Lipkin's collaborative, part 1​

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A gut reaction is the problem in ME/CFS – that’s the main idea being pursued by Dr Ian W. Lipkin of the Center for Infection and Immunity at Columbia University. He believes that the body’s response to changes in the gut could be what’s driving ME/CFS for at least some patients.

Lipkin’s collaborative group, the Center for Solutions for ME/CFS, will test this theory as part of a $9.6 million, five-year research programme, which Lipkin was good enough to discuss with me via phone and email.

This huge research programme, which is funded by the National Institutes of Health (NIH), is made up of three main projects. This blog looks at the first two, which will use high-tech approaches to see if changes in the gut are causing changes in the body, particularly in the immune system. The third project, which looks at the biological response to exertion in ME/CFS, will be covered in the next blog.

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Read the full blog

 

https://twitter.com/user/status/1019164709122174977

 

Thank you @Simon M !!

 

Only very quickly skimmed so far, but to me there would be no great surprise at all for a connection between ME/auto-immune/gut issues. My wife has the lot and I suspect is far from alone. Research into this area is very worthwhile I think.

 

It is a big surprise to me that since the Gut and the Liver work very closely together ("enterohepatic circulation","Gut-Liver Axis") , no one is paying attention to the Liver.

Some interesting excerpts from https://www.nature.com/articles/s41575-018-0011-z :


Title : The Gut-Liver Axis and the intersection with the microbiome

Interestingly Dr Lipkin reports the following :

Next, recall that Maureen hanson has found impaired Bile Acids (BAs) Metabolism. Interestingly BAs are very much connected with the Gut Microbiome :

and

There are more reasons for increased gut permeability of course such as impaired N-Linked Glycosylation.


I e-mailed to Ron Davis, Robert Phair, Maureen Hanson and Derya Unutmaz (among others) Fibroscan Results showing Liver Fibrosis.


Also interestingly :

This is a Fibroscan of an ME/CFS patient with F3 Fibrosis and completely normal Liver Function Tests :

 

This 2018 paper found that respiratory viruses can alter the gut microbiome (in mice).

Assuming that something similar can happen in humans, perhaps the non-specific "viral triggers" apparent in many ME cases are actually only important in that the immune response to them disrupts the gut microbiome (even when they're lung infections). A predisposition, or just blind chance, may account for the form that the altered microbiome takes.

 

Anyone have any idea what Lipkin's ' bullish views' might be in relation to ME/CFS that Simon refers to for upcoming blog.... I'm intrigued!!

 

Good to see that the teaser worked . Coming next week

 

Thank you @Simon M . A great explanation and hopefully a silver lining - a crap disease to get now, but hope that things can change soon.

 

https://jaxmecfs.com/2018/07/23/the-microbiome-hypothesis-lipkins-collaborative/

 

cc : @JaimeS

I just had a look to @Simon M 's blog post on Ian Lipkin's Research. As stated in the text :

Also of interest is the following text taken from here:

Referencing the following post, please see below a Network Analysis graph (some more nodes are disclosed here (this is the graph version sent to Ron Davis in October 2017) . Interestingly, Vitamin K, Liver issues (NAFLD), Bile acid-related Metabolism Genes (CYP27A1, CYP7B1) are there. Also it is interesting to see that Choline Deficiency (Ian Lipkin found altered levels) is there. Unfortunately no data about Gut Microbiome was part of the Input at that point in time.






As stated in the document i circulated to Professor Ron Davis in October 2017 (and then Derya Unutmaz, Maureen Hanson and others), there are several Vitamin K-related Genes (GAS6, MERTK, GGCX and others) that have many critical roles potentially relevant to ME/CFS (Hypothesis)

 

@mariovitali -- write a paper and publish it. You've been on this awhile -- you have devoted many, many hours to this. PM me and I'll help you construct and edit it if you want.

 

Thank you @JaimeS , your help is very much appreciated and needed. I will PM you

 

IMHO this is an issue of cause and effect. I can only draw on my own experience and it is subjective and limited evidence from which to extrapolate, besides which I may be one subtype and there may be others. I await empirical illumination with interest.

That said I got ME quickly at the same time as a viral infection which became atypically recurrent. I became strongly allergic to grass pollen at the same time, to my mind this matches Dr Paul Cheney's TH2 shift hypothesis and indicates to me the viral infection was somehow causal due to the evident triggering effect for all the other symptoms.

Consequently I remain open minded on the one hand but doubtful on the other about the microbiome study as a search for a cause, as I think an HSV (on top of previous EBV) triggered my CFIDS, not gut dysbiosis, but I do think dysbiosis developed sometime later and that the microbiome is a very important contributor to the way the disease developes, especially over the longer timescales involved in chronic illness. I think we can learn a lot by studying the microbiome in ME/CFS and perhaps do a lot for the palliative care of ME patients.

I am sorry to say that reports of several serious cases of ME I have read include difficulty with digestion and sensitivity to food, which is no stranger to me either, though I struggle against degradation of my condition as best I can, it strikes me the more we know about this the better.

I agree @mariovitali the liver is an important factor in the affect of ME on digestion and the microbiome, low liver function has long been a helpful working hypothesis for me in dealing with my difficulties with food intolerance and hypersensitivity. The liver needs a lot of energy to function and if energy deprivation is a feature of ME then that might explain a few things. Interestingly the tight junctions between epithelial cells in the gut may also be important. I learned recently (working my way through this) that maintaining the tight junctions is an energy dependent process. Its an obvious speculation that metabolic problems with energy production could potentially have knock on effects on the liver's ability to deal with the load in the hepatic circulation from the bowel and the magnitude of the hepatic load itself through a tendency to exacerbate "leaky gut" by affecting the efficacy of tight junctions.

It seems to me the gut and the microbiome are important to understand in the search to unravel ME. So I wish Dr Lipkin success in his work and thank @Simon M for breaking it down for us into digestible portions in his blog.