Researcher Interactions Video: Science for ME Q&A with Prof Simon Carding, Quadram Institute, June 2019

Andy

Retired committee member


We were delighted that Andy from the forum was able to speak to Prof Simon Carding, of the Quadram Institute in Norwich, about his ME/CFS research work, which focuses on the gut and its microbiome.

You can read more about Prof Carding here, https://quadram.ac.uk/people/simon-carding/

And about the work that he leads at the Quadram institute here, https://quadram.ac.uk/simon-carding/

Donations to support his work can be made here via Invest in ME Research, https://www.justgiving.com/fundraising/letscresearch
 
Thank you @Andy

Really interesting info. I haven't finished viewing yet, but it's interesting (there's that word again), that Prof Carding said IBS can precede ME.

Dr. Bruce Carruthers (lead author of the Canadian Consensus Criteria) said the same thing.

Unfortunately, IBS is treated as benign, and/or some sort of psychological/stress type problem.

Probiotics may help IBS.


Also interesting were Prof Carding's comments about gut viruses and antibiotics being very bad for the microbiome.

We have the theory that enteroviruses may trigger ME.


Although antibiotics are a very needed treatment with bacterial infections, I feel much worse after them - with symptoms effecting more systems than the bacterial infection did.

I have to take a lot of probiotics to get on some sort of balance again - albeit the usual crappy ME balance.

Concerning to hear on the video that it can take years for the microbiome to recover from antibiotics.

If a person has many rounds of antibiotics over a few decades, it seems like their microbiome could be in very bad shape.


We have seen the attitude about antibiotics and probiotics evolve over time.

At first a person may have been seen as odd to say they take probiotics during or after antibiotics.

Now pharmacists and doctors may recommend probiotics, and when to take them in regards to antibiotics.

Thanks very much again, @Andy for organizing this video interview!
 
I almost didn't watch this because the microbiome is something I'd put in the too-hard basket to be figured out in my lifetime, what with all the thousands of microbes, many unidentified, interacting with each other as well as with our own cells - much too complicated for my liking. Plus I guess I'm hoping for treatments with less of a yuck factor than FMT :yuck:

But then I recalled that whenever @Andy does one of his chats there is always something of interest. So I watched - and wasn't disappointed :thumbsup:.

In my dismissal of microbiome studies I'd failed to take into account that sometimes we can treat things without fully understanding them, so the upcoming FMT treatment trials will be interesting.

I was very impressed with the effort and resources Prof Carding is putting into his ME research, basically building his project from scratch. It's a good illustration of what people with sufficient academic standing and influence can do when they set their mind to it. On top of that he's making an excellent effort at improving medical education and links between researchers and clinicians.

A couple of questions that occurred to me while watching that you could ask at your follow up interview. I know it's a while off, just putting them here before I forget.

1
FMT works very well for C.diff but results seem to be more mixed in other conditions, notably there often seems to be an initial response but one that doesn't last. If that turned out to be the case in ME, too, would the solution be repeated, maybe for life, FMTs? Or....?

2
Searches for pathogens in the blood have so far come up with nothing much. Is it a possibility that there is a chronic infection in the gut instead? And that the gut pathogens release something that manages to get into the blood? Or our immune system does as a result of fighting the pathogens in the gut?

This question arose from some puzzling results I had from Ubiome. For reasons nobody, including Ubiome, has been able to explain there is something called 'phagosome' listed as a 'bacterial ability', which makes no sense to me because my understanding of a phagosome is that it is the result of a phagocyte engulfing either a pathogen or cellular debris. If anyone can enlighten me on the phagosome-'bacterial ability' connection I'd be very grateful.


But back to my main point. My 'phagosome' readings rose along with the severity of my ME (while my IBS decreased, maybe or maybe not helped by improved management). Readings are mine compared to All Ubiome Samples (so in y1 mine was much lower than average, but in y3 more than 15 times as high):

year 1: very mild ME, moderate IBS, phagosome 0.28x
year 2: moderate ME, mild-mod IBS, phagosome 13.26x
year 3: moderate-severe ME, mild IBS, phagosome 15.73x

So, using my results as an illustration (not asking for personal advise here), could they be the outcome of a chronic, and worsening, infection, the fighting of which results in a high phagosome and potentially in some particles that can get through the gut barrier into the blood?

Or could they be a result of excessive intestinal* autophagy (caused by what?) that maybe weakens the mucus barrier and thereby allows particles to pass into the blood? (A quick google comes up with lots of links between autophagy and one of Prof Carding's areas of interest, IBD.)

* A very quick google shows that mitochondrial autophagy in muscle may be reduced in ME but none of the top results relate to the gut.
phagosome.JPG
 
Thanks, glad you enjoyed it Ravn.

I know you aren't asking me those questions but thought I'd give my thoughts on them anyway.

1. If FMTs turn out to give an initial response that doesn't last then that would, to me, logically seem to strongly suggest that the source of ongoing ME isn't in the gut - that there is something elsewhere that is then affecting the gut, the changed gut microbiome then is the next step in the chain resulting in ME symptoms. If FMTs "only" treat any GI symptoms but otherwise have no effect on patients ME symptoms then we have proof that the gut, while affected, isn't in the causal chain of ME.

2. I think that Prof Carding concedes this possibility? Or at least when I suggest that the "something in the blood" could be something from the gut, released into the bloodstream through a leaky gut barrier, he doesn't shoot the idea down straight away.

And to your phagosome readings, have you talked to a medical practitioner about them? My uneducated layman response is that it would seem to suggest some ongoing infection.
 
1. If FMTs turn out to give an initial response that doesn't last then that would, to me, logically seem to strongly suggest that the source of ongoing ME isn't in the gut - that there is something elsewhere that is then affecting the gut, the changed gut microbiome then is the next step in the chain resulting in ME symptoms.

Depends. If a change in the microbiome is observed that correlates with improvement in symptoms, and the microbiome over time reverts back while the patient relapses back into a pre-FMT symptomatic state, I think that would suggest that the gut is very important. Assuming that there is proper blinding that would allow one to distinguish bias from genuine improvement.

My own experience is that the gut and diet are important.
 
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Depends. If a change in the microbiome is observed that correlates with improvement in symptoms, and the microbiome over time reverts back while the patient relapses back into a pre-FMT symptomatic state, I think that would suggest that the gut is very important. Assuming that there is proper blinding that would allow one to distinguish bias from genuine improvement.

My own experience is that the gut and diet are important.
Yes, I agree, and I don't say that the gut isn't important, just that if there is a reversion then it suggests that the gut isn't the source of ME.
 
I was wishing I'd asked where they get their FM for the FMT in the clinical trials! From healthy relatives? From other people, who've been screened? Is there a future in the 'poop pills' that are being developed?

Even if there's a trial, and it's successful, these issues might affect how replicable the results are.
 
I was wishing I'd asked where they get their FM for the FMT in the clinical trials! From healthy relatives? From other people, who've been screened? Is there a future in the 'poop pills' that are being developed?

Even if there's a trial, and it's successful, these issues might affect how replicable the results are.
Hopefully we'll be able to ask questions like that next time. :)
 
And to your phagosome readings, have you talked to a medical practitioner about them? My uneducated layman response is that it would seem to suggest some ongoing infection.
I have (tried). There've been two types of response, neither very helpful (though one doctor did some sort of stool test which come up clear):

1) The panicky look: I never learned anything about that at med school. Why do I have to get all the difficult patients?

2) The dismissive look: Oh, that load of pop-pseudo-science bollocks again. Why do I have to get all the dumb patients?

I have some sympathy for the first type of reaction, very little for the second. But what's most infuriating is that Ubiome refuse to explain, at least to me, what exactly it is they're measuring, thereby making interpretation impossible.

And here's a third possible future question: Could Ubiome be used for an initial, relatively cheap, big data 'fishing expedition'? Similar to what's been done with 23andme?
 
Part 1
Professor Simon Carding from the Quadram Institute in Norfolk
What they do:
“So let's probably start at the beginning. So it's probably around the
summer of 2014. Invest in ME research charity paid a visit to some senior
people at the University of East Anglia which I'm a member of with the idea of
trying to establish a Research Center based on ME at UEA and I think I was sort of brought in as somebody who might be interested in this because of my interest in immunology.
Gut immunology, and in particular, inflammatory bowel disease which I've
been working on for quite a while and who accompanied me was Professor Tom Mullen who's a biologist. UEA was sort of quite lukewarm I think about trying setting anything up formally, however Tom and myself, after having some discussions and reading a little bit about ME because prior to that, you know, we'd not come across ME.

We decided there may be something worth investigating here and based on our
expertise in viruses, gut immunology, gut microbiology we thought there would be an interesting hypothesis if we were to investigate the causes of ME being in the GI tract in the gut and in particular due to disturbances in the populations of microbes that normally reside in the gut. And changes in these microbes causing a change to the permeability of the gut barrier and this would cause leaky gut and this would then allow things that normally don't get into the body to get access our immune system which would stimulate the immune system in a chronic manner.

And, as a consequence of that, we get some of the manifestations of them here so that was our starting point in 2014. And we then went back to the charity and we also had a conversation with UEA and we got an agreement - for the charity and UEA to co-invest in a PhD studentship.

So this was very new to the University and certainly was very new to the charity but from that small beginning we now have three joint funded PhD students with the University and the charity. The first one of the students graduated this year we've got manuscripts that have been submitted and under review now. So we'll get some output from that.


And we've got other students who are continuing on the track of trying to identify whether or not there are any abnormalities that link up microbes in any patients and if the patient's response to this generate abnormal immune responses that are targeting the gut microbes and that is analogous to what we believe to be the cause and functionalities. So we're looking at another potential role of gut microbes triggering an autoimmune reaction. But in ME patients, of course, it’s not inflammatory bowel disease but ME.

From my reading of ME literature is that a majority of patients with ME do have GI
symptoms, more commonly irritable bowel syndrome. From what we know about irritable bowel syndrome, is that there's probably an active role for gut microbes in triggering or making that disease worse. So again there's the overlap there and abnormalities have got microbes causing an adverse response in the patient which can be immune mediated causing allergies. And we also believe gut microbes might be actually associated with about 90% of all human diseases.

Now a lot of that is purely association because for some of the diseases there does seem to be a solid link between the gut microbes changing their behaviour and that's then related to causing on triggering disease. So that's the pathway
or the guide that we have for our ME studies.

We're looking for similar evidence from that. It's very difficult to dissociate cause and effect because if you were to think of it in a purely scientific way you would want to take out what you think the causative agent is from patient, and put that into another individual to see if it causes disease.

Now those experiments are unethical in humans, we can't do that. But you can do that using experimental animals. So you can take what you believe to be the cause of the disease for a patient put it into an animal. Does it cause the same symptoms? If it's yes then you've got causative agent, potential causative agent.
If it doesn't then that still doesn't rule it out completely. Maybe you haven't got the animal model right or whatever.

Unfortunately, in ME we do not have a good animal model of the disease so it's very difficult to actually do those studies. So what we're left with is trying to tease out what might cause the changes in gut microbes and where that occurs, when that occurs in the timeline for a patient to develop the disease . So the best way we can do that with patients is to do what we call longitudinal studies.

So we follow an individual for a period of time taking lots of samples and really
looking for where, when does the trigger point occur in disease onset and
is that preceded by distinct changes in the makeup of microbe populations.
Most of our research is based on the longitudinal studies where we can get a clear timeline for some of these events and then trying to link them more strongly with disease onset or disease progression.

The other confounds we have to worry about with the microbiome is we now know that some of the major factors which cause changes in your gut microbes are to do with lifestyle and behaviour so genetics is a small component. But how you live, where you live, really become major determinants that could shape and change.
I've got two good examples; medications antibiotics, how long, how strong and
infections, gi infections. So you get food poisoning or you can get a viral infection from contaminated food or things you drink. The infections can cause long-term changes in your gut microbes. Medications can have the same effect if you take lots of courses of antibiotics and the very strong ones, it could take your gut microbe years to recover from that.

Diet is also a modifier of your microbiome but it’s less severe.
So your microbes will change quickly to your diet and it adapts very well to it.


Everybody's gut microbes are distinct. It's like a fingerprint, you have a microbial fingerprint and it's constantly changing in response to how you're living, what you consume, what you eat, what you get exposed to. So it's very difficult from one single sample to determine all that's your normal microbiome. People fluctuate and we do not yet know what a healthy gut is. We know what a diseased gut is, and so all the vast majority of studies done so far to try and identify what a healthy one is is based on comparing a disease gut to some healthy non-affected individual and then we could say ‘well this is a healthy one, and this is a diseased one’. But we've got no way of knowing that that healthy gut in that person was analyzed the same for everyone. It's very difficult. So what it comes down to is to be able to get a clear picture of what a healthy gut is for one person is to do lots of samples and look at how it fluctuates.

Going on that you can actually find out what the core healthy microbiome is for that individual. So we have to go beyond looking at populations, groups of people to individuals. And of course that's very time consuming. It's very expensive.
So we have to start looking at this from an individual perspective and this sort of fits in with the current buzzword of personalized medicine.

Drugs
And you know you need to give the patient the right drugs in the right amount.
The thing to remember about drugs, very interesting, is that most drugs we take are oral medications, so of course your gut microbe doesn't distinguish a drug from food.
It will process them and metabolize them just as if it were food. Now that
can be good because some drugs we take are called pro drugs which need gut
microbes to process to make them active drugs. A good example is metronidazole.

But there are some drugs which will get metabolised by your gut microbes to make them toxic and that's bad obviously, that's a bad consequence. So again you don't want to give those sort of drugs to people with the particular microbes that will make toxic products from them.

So I think medicine is slowly coming to realise the importance of gut microbes and that we have to factor in an individual's gut microbes as to which drugs we give them. And there's some interesting studies coming out showing that anti-cancer drugs work in only some people with a certain type of gut microbes. In others there's no effect at all. And it’s the same for cancer drugs it's also the same for anti-hiv medications. How well they work depends on the patient's microbes.
So we're moving towards a personalised medicine and gut microbes, and your microbiota is an integral part of that in determining what sort of disease you have, but also what's the best means of treating that disease for you.
The particular cancer drugs we are talking about are called ‘checkpoint inhibitors’.

Clinical subgroups

We define ME based on symptom severity. That's a convenient way certainly for research, that is you know our patients are mild or moderate. Now I've always wondered what demarks somebody with mild symptoms from moderate symptoms.
I mean on a day-to-day basis they can be moderate they could be mild, they could be severe so and that's not particularly good but then severe ones seem to be far more easy category.
And so we focused on the severely affected because we thought, well, the disease phenotype, the features would be more consistent and robust because the patient's clearly are so severely affected. And I think some of the research is coming up in the mild to moderate group of patients and we’re finding some consistencies but there are also ambiguities and differences and again when you look at how the patients have been diagnosed what criteria they use. If you delve into the data and sort of categorise the data for patient subtypes symptom severity duration etc even male/female, I think it's becoming more apparent that there are clinical subgroups within ME.

How many there are? I don't know. But severes can be clearly distinct from more moderate and within that you may have three, four or more subtypes. So again in trying to group all these individually to one group to look for a cause you may just lose the real signal in all the noise because you’ve mixed everybody up with different symptoms, different duration of symptoms etc. So I think we've got to be much better at segregating patients according to lots of different criteria
to get a clearer picture of the underlying causes. And of course this all relates back to diagnosis.


Diagnosis
Patients can take five years or more to get a clear diagnosis.
What's been happening in those five years. Have their symptoms fluctuated, have they got better or worse or is the same?

We need to go all the way back I think to GPS or whoever makes the initial diagnosis and they need to be better informed about how do we diagnose ME.

Not just sending them off for CBT or GET. We actually want to know what actually is the pathological cause of it and not just pass them off to psychiatrists, psychologists or physical therapists.


Recruiting patients and the GP fellowship scheme.
We've been trying to recruit severely affected ME patients in Norfolk. Our Hospital the Norwich University Hospital does not have a clinical service for ME.

There are two major GP practices in Norfolk where a lot of patients get referred to and one of these is in Great Yarmouth/ Lowestoft area and the Clinical Commissioning group there we've been involved in trying to get them to help us identify patients and recruit them into our research projects. That's proven to be difficult, I think because, again we're asking for a new process to be put in place that didn't exist previously. We need to get somebody who's medically trained to go out with us to see patients to allow us to get samples. That's just not in existence before. It's physiotherapists doing the visiting patients not clinically trained people that can take blood samples for example. So we've had to invent processes with the CCG and in the course of that they've now sort of realised they have a research outlet through the Quadram. And so about six months ago they approached us with the idea of this GP fellowship scheme.

This is for a newly recruited GP to work in the practice out there but to spend one day a week for a year at the Quadram and getting involved in our research. So this is biomedical research; we're not training them to do CBT or GET that's outside of my remit. It's to get them an understanding of what biomedical research is and so when they go back to their GP practice they have an idea about explaining to patients what research is being done, if there are new avenues of research, new treatments potentially that are coming along so they can serve as, if you like, a champion for ME research. And it's biomedical research.

So I think the CCG are currently advertising for this fellow and we would hope to have one in place pending interviews etc certainly by the end of the year if not sooner and with the clinical trial that we're trying to get started some ideal opportunities to get the GP, the GP practice, involved in that. If not just to help us recruit patients for the trial.

I think that's an important activity because you know we are trying through research to get a little bit more awareness of ME and the sort of condition that it is at the biological level in the frontline, the GP practices. So hopefully that will feed into a better and more quickly, more accurate diagnosis, treatment pathway hopefully for ME patients. At least in that GP practice. And if it works I think the model could be extended to other GP practices and maybe other centres as well across the UK.

This is a three partner investment in the GP scheme. So the GP practice obviously Quadram and Invest in ME Research are the partners investors so we're putting funding in to help this happen.

Educating medical students about ME
So the other thing we're trying to do is to try and make change in the medical school curriculum. Again here at UEA I teach medical students Tom Mullen teaches medical students. We asked medical students how much exposure do you get in your medical education to ME and it's virtually nothing. So Tom and I are, through a particular scheme that the medical students have which is called Researched Learning; so they spend a period of time studying a research project and make presentations. Tom and I are trying to get more ME focused research there for the students to sort of investigate/ present to increase awareness.

We also have medical students that come and do research projects anywhere from three months to a year in the lab; again this gives them exposure to ME patients as well because they come out with us to visit patients. So we try to make inroads into the educational deficit as well for ME but it's very, very difficult because the medical school curriculum is so prescriptive, as prescribed by the General Medical Council.

There's no scope or room to sort of expand and give special series of lectures or anything. So Tom and I are trying to do it through their curriculum when they get exposed to doing research projects. We can bring ME research into it that way.

New clinical trial
From our gut microbes and looking at the abnormal gut microbiota we've looked at ways of restoring or replacing an abnormal gut microbiota to patients with a new one with a healthy one and what we're proposing to do is a feasibility clinical trial to do a fecal microbiota transplant therapy in ME patients.
This is not new. There's a Professor Borodi(?) in Sydney who's been doing this
for quite a while who claims some quite striking effects of giving patients with ME an FMT and microbiota transplant.
So he's been advising us on developing the trial he's been very helpful.

Invest in ME Research raised a lot of money towards this and still trying to fundraise to get all the money we need to do the trial. We're developping a facility within the Quadram to be able to do FMT because the MHRA the medical medicines and health regulatory agency said FMT is to be treated as a medicine, as a drug, so that means it has to be prepared on the very stringent conditions in a licensed room, by licensed practitioners. So we're investing in a facility to do this in the Quadram and we hope that the first FMT trial we will do is in a ME patients. So if everything goes well we get the rest of the money we're looking to probably start the trial about this time next year.

Taking part in the trial/recruitment
We have a long-standing relationship with the clinic fatigue service at Saint Helier and Epsom Hospital and until recently the head of that facility was Dr. Amolak Bansal who's now sort of moved away from that. He's still active but he's no longer the head of that institute. So the arrangement is still that we will utilise Dr. Bansal as a source of patients. He's still seeing ME patients at St. Anthony's Hospital primarily, but he will identify the patients that are best suited for our clinical trial. And so he has contacts and details and access to a large number of patients from St Helier, he has still strong links, works one day a week I believe at St Helier, so we would envision that that would be the route by which we would recruit patients.

So we at Quadram would not be involved in identifying or selecting patients. That would come from the clinical service using the criteria that they've used for a long time to diagnose and assess ME.
 
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part 2
Re ‘test for Leaky Gut’
I should say that there is no gold standard for diagnosing leaky gut.
It's indirect measures. The NHS doesn't endorse or accept any test at the moment as indicating leaky gut so we are reliant on surrogate markers and as I've said I think earlier that if we can detect microbes or microbial products in the blood that's usually a pretty good indication of a leaky gut. Because most of the microbes we think come from the gut.
Now there are some sugar based solutions that people can use. In America they
have lactulose mannitol test which is a drink that people take and then in the
urine sample, if one or more of those sugars is in the urine, then that's an indication of leakiness of the gut. But there's no gold standard of that.

Looking for evidence of exposure of the immune system to gut microbes and their products; what we're using as an indicator of that are the presence of antibodies which would be in the blood that react with microbes in the gut.
So one of the projects that one of my PhDs students is undertaking is looking at
whether or not a patient's blood antibodies react with microbes in their stool.
So now ordinarily you would not expect your immune system to react with your gut microbes so we're trying to ask the question ‘are there gut microbe reactive antibodies in patients?’.
If the answer is yes then ‘what are those antibodies reacting to?’,
‘Can we identify the microbe?’ because if we can identify the microbe then that could be a strong indicator of that microbe causing maybe some of the symptoms. Because we know what the microbe is we can target that microbe to get rid of it kill it whatever ways and various means , antibiotics being one for example.

‘Something in the blood?’ Microvesicles and exosomes.
We are interested in bacterial derived microvesicles. We are about to start a preliminary study using some samples we've obtained from patients to look for the presence of bacterial microvesicles in their serum, in their blood as an indicator of leaky gut, but also may be a source of stimulating the immune system and this may even prove to be useful as a diagnostic tool in ME. We don't know.

So that's something we're just about to start.

But I think it's worth noting that microbes are not directly in contact with your gut cells. So you have this barrier in your gut which is made of epithelial cells but on top of that you've got a sticky gelatinous material called mucus. And bacterial cells cannot get through the mucus so they sit at the surface. So you have like a sterile layer of mucus that separates your epithelial boundary cells from your gut microbes.
So then the question is ‘how do gut microbes communicate with cells of the body? how do they deliver signals?’ and we think there are two ways.
One is through metabolites the small compounds that they secrete; metabolites that can get through the mucus into epithelial cells and maybe the bloodstream.
Second route is through microvesicles. So these are nanometer very, very small spherical particles that bud off from the surface of certain types of bacteria and permeate through the mucus into the epithelial cells and actually could stimulate the immune system.

Now we believe that these microvesicles play an important role in instructing the immune system to not react to gut microbes and food. So we believe the microvesicle is important to instruct the immune system to ignore gut microbes food particles and so they make the immune cells produce what we call tolerance.

So tolerant to everything in the gut. What we've seen in inflammatory bowel disease patients is that the immune cells lose that ability to be tolerant instead they now become super inflammatory immune cells, there's a breakdown there in the communication of these microvesicles with the immune system in IBD.
We're looking for similar evidence in ME patients.
‘Is the immune system in ME patients now abnormally responding to the microvesicles particular those seen in the blood?’.
So microvesicles could be important.

There's another source of microvesicles that us our own cells in the body produces. These are called exosomes, which are very popular in cancer research at the moment. These are vesicles that are in all cells in the body that our body produce, and a lot of them end up in blood, saliva, breast milk any lymphatic fluid, any fluid in the body will contain these exosomes. And we can distinguish exosomes because they are unique to the cell that produces them. So they are, if you like, a signature of the cell that produces them. And we know in cancer that cancer cells produce these exosomes and the exosome promotes the growth of the tumor cell, metastases, spread around the body.

So there is a group in the U.S. that's starting to look at exosomes in the blood of ME patients. ‘Are they unique? Are they distinct? what cells are producing them?’ and ‘are they attributable to any of the causes of pathology of ME?’

So there's a lot of interest at the moment. It's all new research about microvesicles.
We're focused on the bacterial type. There are groups like I said in America that
are looking at exosomes. So all of these are present in the blood, so I
think it's a very interesting avenue of investigation in ME.
And again are other diseases are sort of pointing the way here? Cancer, inflammatory bowel disease. There is a precedent.

Future plans, current work
I hope I haven't given the perception that we work in isolation here in Norwich, that we're not interested to collaborate with anybody else. We do in fact collaborate with a lot so we have extensive collaborations in Sweden, Norway, Denmark other places in the UK, the USA and we're currently involved in an FMT trial which is currently ongoing in ME patients in Norway at the moment. So we are working with them on analysing what's happening in the gut microbiome of patients after they receive an FMT. So we're just about to get our first set of samples. So that's very exciting.

And we're also collecting stool samples from ME patients in Denmark, Iceland and Norway.
So we are sort of becoming a stool repository.
It's all for the benefit of our research and also it shows that there are other countries and other ME research groups, elsewhere in Europe particularly, that are very interested in working with us on this. So it is a sort of multinational research activity that we have, and Norwich, at the moment, is sort of the hub of that. But, hopefully , we'll be able to develop ME research in other countries as well through interacting. “

All monetary donations should be made to Invest in ME Research.
 
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