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Interview: Ian Lipkin’s Million Dollar Appeal for Microbiome Study

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Simon McGrath recently secured an interview with the world famous Dr Ian Lipkin – a scientist who continues to believe that ME/CFS has a physical cause – to discover more about his plans for a major study of the gut microbiome and to find out why he's asking the patient community for its support…


Dr W. Ian Lipkin has demonstrated a clear commitment to ME/CFS research. First came his study looking at Borna virus in the 1990′s, and then the landmark study that ruled out XMRV as a cause, and most recently we have heard about the huge pathogen and immune study – a vast collaboration with many key clinicians and researchers, including Dr Dan Peterson and Professor Jose Montoya.

That research had already found clear signs of immune activation in patients and, when I spoke to him, Lipkin was clearly excited about the very latest results to emerge from the study - I wish I could reveal more, but a paper has just been submitted and details are embargoed until publication.

Lipkin believes that immune activation may be responsible for driving the symptoms associated with ME/CFS. And that the immune activation and could itself be triggered by bugs, not in the blood, but found in the vast ecosystem of bacteria, viruses and fungi, that constitute the gut microbiome.

However, he doesn’t have the funds to pursue this research and so he’s appealing to the patient community for the one million dollars he needs to get the work done. The payoff? A better understanding of the illness and the possibility of new treatments.

Dr Lipkin on ME/CFS

Lipkin made a splash in the world of ME/CFS when he led the XMRV study that both disproved its role in the illness and also managed to unite the patient community. At the press conference for that study he said his first brush with CFS was a large study in the 1990s that demonstrated no connection between the Borna virus (one of many viruses he’s discovered) and CFS. But he stressed that their findings in the same study of B-cell activation in CFS patients was a clear sign that this was not a psychosomatic disorder. The findings in his new study have only confirmed his views:

“There is no question in my mind that this is a physical disorder. The fact that we haven‘t been smart enough or invested enough in it to sort that, doesn’t mean that this is anything else.”

The smoking gun

The immune activation he’s found could explain fatigue – it’s almost a universal symptom of infections like flu, and is actually a consequence of immune activation rather than caused by pathogens themselves.

The same could be true of other ME/CFS symptoms including disturbed sleep and brain dysfunction which again are typical symptoms of immune activation.

Lipkin is eager to build on this work. He believes the immune activation is a smoking gun and now wants to track down who or what pulled the trigger.

“I am more keen than ever … to see if we can identify the trigger”
- all quotes are from Dr Lipkin

There are several credible places to look for the culprits triggering the activation. One is white blood cells: some viruses could be hiding out in cells and so wouldn’t have been found by the initial search in the blood plasma – and Lipkin already has a white blood cell study lined up.

However, his attention is particularly focused on the microbiome, the large ecosystem of bugs that live on our skin and within our ‘inner tube‘ that leads from mouth to bottom.

There are at least one trillion bugs in the gut microbiome – and there are more immune cells in the gut than anywhere else: it’s a great place to hunt for bugs that might be triggering immune activation.

Microbiome problems are increasingly being linked to serious illness. The most striking example is the superbug Clostridium Difficile (C. diff), which has become a major problem in hospitals. C. diff lives in most of our guts harmlessly at low levels, but it can take over (particularly if ‘good’ bacteria are killed off) – causing diarrhoea and even death. Happily, doctors have discovered that severe C. diff cases can be treated relatively easily by restoring the microbiome; unhappily, this involves a faecal transplant.

The potential to treat disease by restoring the microbiome is one reason this area of research is attracting so much attention. This recent article explains more about the microbiome, how it might link to ME/CFS and looks at other research being performed.

“If the answer were simple, it would be done by now”

Irritable Bowel Disease is another example – here inflammation is believed to result from changes in the microbiome. Lipkin’s team have just been studying women in sub-saharan Africa and found that certain bacteria in the vaginal microbiome increase the risk of HIV infection. Lipkin thinks the gut microbiome could be playing a similarly important role in ME/CFS:

“By analogy with animals and human situations, we see that different populations of fungi, bacteria and viruses in the colon can have an impact on the immune system and give rise to cytokine activation which could cause the symptom complexes we see in ME/CFS”

in other words:

changes in microbiome > immune activation > symptoms of ME/CFS

I asked Lipkin if this meant particular bugs causing inflammation and he said that is certainly possible. But, he added, another route to illness is that an overgrowth of ‘’bad’’ bacteria could form a film, preventing ‘’good’’ bacteria from interacting positively with the immune system (see this article for more) – an indirect way of causing immune dysfunction.

The exact role that microorganisms in the gut play in health and in the development of disease is complex and still being determined. There are many plausible hypotheses, says Lipkin, and only research can show which (if any) are right.

If the microbiome is the cause, is it treatable?

If the microbiome is the cause (or a cause, or even a contributor) of ME/CFS, it might be relatively easy to treat, perhaps with probiotics, restriction diets, drugs, or even faecal transplants.

Cause or effect?
Of course, the first step in this process is demonstrating a strong link between the microbiome and ME/CFS. If one is found then the next step is to look for evidence it plays a causal role: i.e. do microbiome changes cause immune dysfunction, as opposed to being a consequence of or simply associated with immune dysfunction?

Lipkin says one option is to use an animal model: the idea would be to introduce the microbes suspected of triggering ME/CFS into the gut microbiome of animals, to see if this leads to similar symptoms and immune activation as seen in humans. Something that has been used to study Metabolic syndrome.

Personalised medicine
If there is evidence of a causal role, Lipkin says they would look to establish clinical trials of treatments that could include probiotics, antibiotics followed by prebiotics, restriction diets and possibly even faecal transplants. He believes that there would not be a single microbiome cause of the illness, but different types – potentially fungal, bacterial and viral problems causing three separate types of immune dysfunction.

Lipkin calls these different types ‘endophenotypes’ and it could lead to personalised medicine, where the particular treatment depends on the specific form of the illness. There will be endophenotypes beyond those in the gut, such as genetics endophenotypes, and it is highly unlikely that the microbiome would account for all forms of ME/CFS – but this approach could tackle a very substantial proportion of cases.

The study breakdown

Lipkin’s proposed study will look at all three trees of life: bacteria, fungi and viruses in the microbiome of 100 patients and 100 controls recruited for a previous NIH study. It will cost a cool million dollars:

1. Sample collection: $150,000
Collection of faecal (and blood) samples from patients, including checking the initial ME/CFS diagnosis remains valid and shipping chilled samples back to the labs at Columbia.

2. Faecal Microbiome sequencing and Analysis: $317,000
- Separate, purify and perform high-throughput sequencing of viruses, fungi and bacteria
- Complete sequencing of viruses; partial sequencing to identify bacteria (using 16S rRNA) and fungi (using ITS, the ‘fungal barcode’)
- Generate microbiome profile for each patient, one each for bacteria, fungi and viruses​

Comparison of patient and control microbiomes: bacteria, fungi and viruses that differ in prevalence between CFS subjects and controls will be considered candidates for contributing to either health or disease.

3. Development of highly-accurate real-time PCR assays to confirm findings and levels of microbes: $328,000
This will quantify how much there is of each bug of interest (the main high throughput sequencing approach gives an indication of quantity but is less accurate than real-time PCR).

It’s possible, that the most important thing isn’t the presence or absence of a microbe, but the amount of it – as with C.Difficile. These assays will also be used to check that key microbes haven’t been missed in any patient or controls who were negative for them in initial sequencing, as PCR assays are far more sensitive than high-throughput sequencing.

4. Cytokine analysis: $86,000
The study will again measure cytokines in blood and undertake data analysis to see if there is an association between cytokine profiles and immune profiles. It would then provide strong evidence of an important relationship between the microbiome and immune dysfunction – the hypothesis driving this study. Sophisticated analysis will be required on the vast amount of data generated by microbiome and cytokine profiling; happily, Lipkin’s Center for Infection and Immunity have a team of biostatisticians dedicated to such work.

5. Development of antibody tests for important bugs identified by the microbiome work: $249,000
It could be a few individual species or particular groups of microbes, but antibody tests will be developed by Lipkin’s lab to allow much easier testing to see if the same problems in this sample are found in the wider patient population.

As well as guiding treatments, the PCR assays and antibody tests developed here could both provide a diagnostic test for ME/CFS.

Lipkin’s record



Featured in the New York Times, described by Discovery magazine as the world’s foremost virus hunter, and consultant to a successful Hollywood movie, Dr W. Ian Lipkin has a higher profile than most researchers. But this profile is built on a stellar scientific reputation.

He’s discovered more viruses than anyone else. He’s part of the World Health Organization (WHO) diagnostic discovery and surveillance programme designed to catch pandemics as they arise. And the Chinese recruited him play a leading role in their fight against SARS.

Amongst other things he is John Snow Professor of Epidemiology and Director, Center for Infection and Immunity at Columbia University. Full biography.

He is passionate about communicating science to a wider audience but is insistent the science is right.

Lipkin only agreed to consult on Contagion, a movie about the terrifying potential of epidemics, because of director Steven Soderbergh’s desire to make a film that was true to the science – having turned down offers to advise on several movies with somewhat wilder plots.

When Lipkin was shown a near-final version of the film he threw up his hands at the scene near the climax where a scientist injects herself in the leg with the new vaccine, through her tights – a poor practice that could easily introduce an infection.

This might seem a small detail given everything else the film had right, but Lipkin was adamant it had to go: cue a $100,000 reshoot.

This near-obsession with getting things right is a Lipkin hallmark. The very first point he made to me about this study, before discussing any details, was the need for real, robust findings – because there have been too many false dawns in this field.

At the end of the interview he emphasised the need of crisp, rigorous data. Whatever the findings from this new study – positive or even negative, we should be able to rely on them.​


Scientist in a hurry for answers

Dr Lipkin is a scientist in a hurry for answers. That’s true both in his work trying to stop a new pandemic in its tracks, and in his work on ME/CFS.

He wants to follow up as many promising leads as possible, as soon as possible – rather than waiting for the results of a single study before planning a new one if the first draws a blank.

That’s why he set up a huge study looking for specific pathogens such as EBV, but also used deep sequencing alongside that to search for any other pathogen, known or unknown.

He’s looked in blood plasma for pathogens but is also about to look for them in white blood cells too.

He set the study up to look at immune markers including cytokines as well as for pathogens – and the significant findings of immune activation show the value of backing more than one horse.

On top of all this, Lipkin has invested in a gene expression study using samples from the same study, with results expected shortly that could throw up new leads in epigenetics and genomics.

Dr Lipkin has committed a huge amount of his 60-strong institution’s time to pursuing numerous studies, all aiming to uncover what’s really going on in ME/CFS

Too much, too soon?
However, it may be that the NIH is not in such a hurry as it has declined to fund the study at this time.

But then the NIH has only ever committed relatively small amounts of funding to ME/CFS – around $5 million a year, compared with around $115 annually for MS and $284m for Asthma.

Its funding record firmly suggests the NIH’s priorities lie elsewhere.

So, as Lipkin says, “we are stuck”. It’s possible that the NIH will fund this work in the future, and possible they won’t.

The question is, do we want to wait?

“We are already well behind where we should be”

Dr Lipkin has now appealed to patients to fund his latest study that aims to hunt in the gut microbiome for the ‘trigger’ of the immune activation his study found in ME/CFS. And he needs a cool million dollars to pay for the study outlined above.

Actually, the study comes to a bit over a million dollars (see above) - $1.13 million, to which another $140,000 of costs for maintaining the high-tech equipment used and general lab costs making $1.27 million in total. However, the initial target has been set at $1 million.

In his CDC telecast to patients last September, Lipkin explained the microbiome project was being held up by this lack of funds, and urged patients to contact their representatives in Congress.

He also appealed directly to patients who could afford to do so, to invest in research:

“it may not be appropriate to pass the hat, but that is exactly what I am doing”

How long will it take for the results? “Within a year”, said Lipkin

The man is in a hurry, and the study is all set up and ready to go – once funding is available.

“As long as I can do it, I will do it. I‘m eager to start, I‘m optimistic it will bear fruit, it‘s not just an academic exercise, it could lead to treatment”
When I mentioned to Dr Mady Hornig, the Principal Investigator on this study, that I was interviewing Dr Lipkin she added: “Terrific – we need the resources to get this done”.

Crowdsourcing: Together we can make it happen

I do think we are very lucky to have Dr Lipkin on our case and believe that we should back his new study, which will be performed at his Center for Infection and Immunity, Columbia University – the world’s largest and most advanced academic center in microbe discovery, identification and diagnosis.

“Why don‘t we crowdsource this, we are all losing valuable time in our lives?”
Vanessa Li, Phoenix Rising member and fundraiser

ME/CFS patient, Vanessa Li, responded to Lipkin’’s call last year, by contacting his office and suggesting crowdsourcing in a similar way to MEandYou, which through the efforts of Dr Maria Gjerpe had raised an astonishing $0.5 million towards the Norwegian Rituximab trial in 90 days.

Lipkin was a physician in San Francisco at the start of the AIDS epidemic and commented how, when the government was reluctant to pay, much of the important early work was funded by private donors so he’s very open to this possibility. He continued to seek funds for his work from institutions, but as that hasn’t worked he is now asking patients if they can make the study happen - and has given this interview to launch the million dollar appeal.

Donate to the the ME/CFS microbiome study
I have just donated and hope many other patients will do too. Just click on the button below and follow the instructions. The option is to donate to CFS research, but in the next page you can add ‘special instructions’ such as ‘for the microbiome study’.

We need only for every US patient to donate $1. Or one in ten patients to donate $10.


If people want to do more to help – and this is a big target – they can help to promote this crowdsourcing initiative at this new group, or email Vanessa Li. I will give her the last word:

The CDC says there are more than one million ME/CFS patients today in the US alone. There is no reason why, if every patient were made aware of Dr. Lipkin’s appeal and donated $1, that we should fail to raise the $1 million. An esteemed researcher doing high-caliber work is taking a serious interest in finding out the cause of our desperately under-researched illness. Now is the time to act!​

Simon McGrath tweets on ME/CFS research:


Phoenix Rising is a registered 501 c.(3) non profit. We support ME/CFS and NEID patients through rigorous reporting, reliable information, effective advocacy and the provision of online services which empower patients and help them to cope with their isolation.

There are many ways you can help Phoenix Rising to continue its work. If you feel able to offer your time and talent, we could really use some more authors, proof-readers, fundraisers, technicians etc. and we’d love to expand our Board of Directors. So, if you think you can help then please contact Mark through the Forum.

And don’t forget: you can always support our efforts at no cost to yourself as you shop online! To find out more, visit Phoenix Rising’s Donate page by clicking the button below.


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Comments

(@Ember Dr Lipkin said he's planning to use a NIH cohort - pretty sure that was the one recruited for the XMRV study but made available for other studies too and I thought that used CCC - but presume you would know.)
This may be the one:
Enrollees have consented to future use and the samples are accompanied with a code so that many characteristics can be matched with each. Inclusion requirements for cases were:

1. Established diagnosis of CFS
2. Meet both 1994 Fukuda and Canadian case definitions
3. Unable to work due to illness
4. Report “viral-like” prodrome
5. Report >/= 2 of the following (SF-36 criteria): vitality <35, social functioning subscale <62.5, role-physical subscale <50
6. Be between 18 and 70 years of age at time of informed consent
7. Ineligible if pregnant, <3 months postpartum or lactating.
 
Go here:

https://giving.columbia.edu/giveonline/?schoolstyle=5881&alloc=21677

and enter the amount you want to give, and click 'Next'. On the next page there's a message box - say there that it's 'For the microbiome study'.
Not trying to rain on this parade of "happiness", but did anyone ask Columbia how the donation you make will flow through Columbia. In other words, how much of the donation goes to overhead and how much goes to the actual research? Also, does Columbia take a cut of the donation for a general Columbia University donation account.

I went ahead and contacted Columbia to ask these questions for my own due diligence before making a donation and I will share this information here on the Forum unless someone else has already researched all of this. (@Simon - sorry if this was covered in the article you wrote - I have not had a chance to read it all the way through yet.)

Wally
 
Not trying to rain on this parade of "happiness", but did anyone ask Columbia how the donation you make will flow through Columbia. In other words, how much of the donation goes to overhead and how much goes to the actual research? Also, does Columbia take a cut of the donation for a general Columbia University donation account.

I went ahead and contacted Columbia to ask these questions for my own due diligence before making a donation and I will share this information here on the Forum unless someone else has already researched all of this. (@Simon - sorry if this was covered in the article you wrote - I have not had a chance to read it all the way through yet.)
Yes, we did ask this, partly prompted by your questions on another thread and the breakdown was given in the article. I do hope you were persuaded to donate by what CII told you.
Actually, the study comes to a bit over a million dollars (see above) - $1.13 million, to which another $140,000 of costs for maintaining the high-tech equipment used and general lab costs making $1.27 million in total. However, the initial target has been set at $1 million.
I would argue the high tech equipment maintenance costs (about $30k, I think) are actually a direct cost of the study, leaving "admin" which includes providing the building, heating and lab benches, general service costs amounting to around 9%. That struck me as fair enough.

Feel free to publish the detail here (assuming it's the same one page breakdown I had) - I checked with Columbia and they were ok for it to go public (but my article was long enough without includig any more budget detail!).
 
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Yes, we did ask this, partly prompted by your questions on another thread and the breakdown was given in the article. I do hope you were persuaded to donate by what CII told you.
I would argue the high tech equipment costs (about $30k, I think) are actually a direct cost of the study, leaving "admin" which includes providing the building, heating and lab benches, general service costs amounting to around 9%. That struck me as fair enough.

Feel free to publish the detail here (assuming it's the same one page breakdown I had) - I checked with Columbia and they were ok for it to go public (but my article was long enough without includig any more budget detail!).
@Simon - Thanks Simon. I will post if I am provided with any information that is different from what you were provided (which I doubt would happen). I do know that some organizations will take a large cut of any fundraising efforts directly for their general fund (which may be a separate cut over and above overhead costs) and only a portion of the funds raised go to the project the funds were raised for. This is something that people need to be aware of when getting involved with fundraising projects. (Like us lawyers like to say "the devil is in the details":devil:)

I hope to be able to provide more information about the ins and outs of fundraising that might be important for our patient community to know before any commitments are made to a big fundraising event. Just juggling a lot on my plate right now and unfortunately all my plates are currently residing with me in my bed. :ill:
 
I am happily in! Lipkin on ME fulfills my definition of a good cause--as did Maria's Rituxumab venture. I think we are going to have to get used to crowdfunding our research, after seeing where NIH puts there money. Just think how we would feel if Lipkin did find a large part of the answer, and the NIH had to deal with that finding. That would give me pleasure out of all proportion to the pain of giving up a couple of little things.
Chris
 
I think that this research has enormous promise, and crowdfunding is a great idea.

I have one main reservation:

There is likely to be a great deal of interpersonal variability, and we may need very personalised approaches. Presumably the initial part of the research will reveal much of what we need to know about the variability of gut microbiomes.

I cannot see how an animal model will help, if there is so much variability between human patients with regard to genotype, epigenotype (is that a word?), age, environmental factors (e.g. diet and geographic factors), body mass and co-morbidities.

Add to that the substantial differences between humans and other animals: genetics (including different effects of the same genes in different species), natural habits (e.g. diet but also including things such as hygiene with regard to faeces), lifespan, bowel structure and much more, and the very poor record of translatability from animal studies to human patients...

If Dr Lipkin were to state categorically that he would not use animal studies, I would seriously consider donating, as would some other people I know.
You make a lot of good points regarding the potential implementation of an animal study as a part of this larger initiative and I just wanted to record my own opinion on the matter. I recently read a study regarding certain animal species (I believe elephants were one of them) which are born without an established microbiome and rectify this through consuming the feces of healthy adult animals, it sounds awfully similar a process to the fecal transplants discussed in this article so it's interesting to see as a presumably innate behavior exhibited in certain species. This really stands out to me as indicating just how important the microbiome may indeed be.

We know that, in general, animal models have a lot of problems alongside their potential benefits. For quite a while it has been very popular to use animal models - usually mice - to try and simulate human diseases before testing any hypotheses the researchers may or may not have. The obvious problem this brings is that the disease they are studying is not actually the condition from which humans suffer but an analogue produced for the sole intention of being studied, this logically seems a little odd to understand as in many cases since we manufacture the disease using the knowledge we have so you'd think we stand to learn little about the condition other than the response the immune system that particular animal produces which while interesting is more often than not unrelatable to the human immune response.

We do however stand to learn a lot about diseases in which the disease processes are very similar between the animal being studied and within humans. These tend to be diseases which effect bodily organs, tissues or reaction processes that have not changed much throughout evolution - good examples being diseases which affect the organs such as with heart disease, the glands such as hypo and hyperthyroidism and vital biological processes such as respiration and the many diseases which can cause problems here.

As I see it this study is truly investigating two things, the gut microbiome and the immune response that changes in the biome can trigger. It has to be said that we know little about the microbiome overall, its importance is only very recently becoming clear, we do however know that the immune responses in many animals differ to those of humans in certain aspects so that could be a potential problem as this study progresses but it's very difficult to predict given that we know very little of how the gut microbiome and immune system interact with one another. The question then is are microbiomes in animals similar enough to humans to allow us to learn anything from this study and I think that with the little we know it's hard to say but it stands to reason that the gut microbiome is likely fairly unique to each animal, a logical assumption given their diets are very different, points which you have pricked up on and quite rightly so. I do however suspect that the basic mechanisms in place for the interaction between the microbiome and the immune system are likely to have remained a fairly similar process throughout evolution, given how accommodating the gut microbiome is to beneficial microbes I suspect there is a degree of co-evolution between the organism and the microbiome to allow the immune system to be more even more accommodating of these helpful microbes. I do however believe there must be a degree of allowing new microbes to grow in the microbiome as some of these could potentially confer advantages to the organism, whether that be allowing them to digest a previously undigestable food source or otherwise. This openess is something I suspect may lend itself to being quite a consistent feature in many organisms.

While the likely difference in the gut microbiome and different functioning of the immune system seem to imply that the animals model is of little use in this case, I believe that we stand to learn a lot about the intermediate stage of the process; studying the mechanism of the interaction between the two distinct systems. If we can learn more about the processes as they are intended to occur, it makes it a lot easier to spot when something goes wrong as is being hypothesised by Lipkin.

Overall I think this study is very ambitious in nature and we stand to learn a lot from it, not just about the potential importance of the microbiome in ME/CFS but how problems in the microbiome may cause a distinct form of disease. The animal model does have problems as they always tend to, but it seems to me that it plays a relatively small role in this study overall. From a personal standpoint I'm not yet convinced that this is where the true problem in ME/CFS lies, but I think it's certainly worth studying further and I couldn't think of many researchers better to do it than Prof. Lipkin.
 
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Hi, all. I've just donated from Australia. My very first symptoms were atypical gut problems, followed by all my other symptoms. I've just recently benefited from a course of Rifaxamin. At first I didn't think it had worked, but now, 6 months later, I'm finding I can eat lots of food I haven't been able to eat for 17 years—even garlic! So I think the gut is an important area to research. I'll donate again if it looks like getting up through crowd sourcing. Way to go!

cheers, Lynne
 
Donated. Seems like this research has great potential as a starting point not only for ME/CFS but for a lot of the other poorly defined, but presumed-to-be-autoimmune, illnesses that kind of look like ME/CFS (but aren't) and frequently seem to "travel along with" GI problems.

I'm sure it's not going to be the answer to every question we have, nor define every subset. I'm sure there will be additional costs etc above the $1 million. The point is...we have a brilliant scientist who wants to do studies that are likely to give us some answers! Even if they're negative answers, they'll be answers. Hmmm $1 mil for Ian Lipkin's research or $1 mil for the NIH sponsored IOM project. Know where I'm putting my money and support. :)

Thanks Simon and Vanessa for getting this going!:thumbsup:
 
Sounds good, but, what happens to the money if the project fails to meet target? If I recall correctly, Kickstarter projects do not charge you unless the project meets the target. I know that may not be common practice for donations, but I am reluctant to make a relatively large donation without knowing what happens if it fails.
 
@biophile , I am chasing this particular question--a very good one--up with Columbia since you and a few other patients have already raised it. Columbia knows I am trying to get a crowdfunding campaign going, which WILL allow donors to see how much of the target they've reached and to get their money back if it isn't reached etc., but the PR content team decided that @Simon should first get the article out there, so that we can get a sense of how many would be interested in a microbiome study and willing to donate. I also need lots of help should I launch a crowdfunding campaign because I'm just not strong enough, which is why the end of the article urges readers to join the crowdfunding group I started if you have experience and/or are willing to help--my only way of knowing if a campaign can even be launched.

While I wait for Lipkin's office to answer this question, please know that they have assured me that if a campaign is launched, all gifts made at that link will be transferred to the crowdfunding campaign "pot".
 
I think some crowd funding sites don't penalize you for not meeting the target, but I'll admit I'm not an expert.
 
Some more very welcome news:

We heard last night, that Jen Brea from Canary in a Coal Mine has given her support to the project and is very willing to help where she can. This is just the kind of expertise needed and perhaps a further example of how we can all come together to make such research become a reality.

Thanks Jen :balloons:
 
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Just in case this has been missed

Following the requests of quite a number of members, I have made the crowdfunding group into a private one where I have been updating the group on the news about Jen Brea, for instance. Sorry if this creates inconvenience for some people but members have expressed a desire to throw ideas around but not to have them made public.

Thanks a lot.
 
The down side to this crowdfunding efforts is that there is no 'thermometer'- we need to find a way to know how much we've raised so far. It motivates people to give and to ask others to give.
 
The down side to this crowdfunding efforts is that there is no 'thermometer'- we need to find a way to know how much we've raised so far. It motivates people to give and to ask others to give.
The means of donating now, from the article above, Kati is an initial one. It simply allows folk to do something now if they wish to. Vanessa is going to regularly update the total raised by this method, and then hopefully we can launch a proper crowdsourcing effort on social media - with targets and more visible updates etc.

You might like to consider joining the Group and share any ideas you might have. With Jen Brea now also on board and others with the expertise, I think the chances are good that we will see a more visible and global effort before too much time has passed.
 
I agree @Kati --that was what I was trying to say (not very well) before your post. A proper crowdfunding page would have all those features we want--thermometer, with a more staggered approach perhaps where we try to reach the $1 mil goal in several stages, the first being for sample collection and the second for sequencing and analysis and so on--but the article's only been out a day and frankly, we did not know how much interest this project would attract! So again, if you would like to help with putting a campaign together (help that I desperately need!) please join: Lipkin's $1 million dollar appeal
 
1) So far no great animal models have been developed for CFS. It would be great if one could be but not along the lines of what I've seen. A few studies have used rats forced to run or swim to replicate CFS but that model doesn't make sense to me. I and many others did not get sick merely by exercising or doing more activities. Otherwise, we'd lots more people sick. I think lazy people get ME/CFS too -- much like many other medical conditions.

2) I'm glad Lipkin is investigating this but I'd like to hear more from him about why they think the microbiome is a cause. I've not heard a reason yet that makes a lot of sense to me other than statements like the gut makes up a huge amount of the immune system. That is true but so does the skin. It is a non-specific statement.

I do believe that some subset of people do have the gut as a starting point (for example people who started their illness with an enterovirus infection) and others have the gut affected as part of their illness if not the starting point. However, I don't think this will be the origin for others. However, I don't mind being proven wrong at all.