fungus have even been shown to have an influence on IBD, bacteria most likely play the biggest role, as ~99% of the organisms that exist are bacteria, as far as I understand at the moment.
fungus have even been shown to have an influence on IBD, bacteria most likely play the biggest role, as ~99% of the organisms that exist are bacteria, as far as I understand at the moment.
http://www.theverge.com/2016/5/4/11...ransplant-josiah-zayner-microbiome-ibs-c-diffThat’s not to say Zayner is dubious of science — in fact, he’s a scientist himself. In 2013, he earned a PhD in Biophysics from the University of Chicago and subsequently served as a postdoc researcher at NASA’s Ames Research Center for two years.
Hi, this is great. If crohn's was just an autoimmune disease - I dont think fmt would work because your not altering the immune system - so there must be more to itResults of a new study On U.C. using Fecal Microbiota transplants.
http://www.medscape.com/viewarticle/860690
My thoughts:
I'm just really waiting for FMT pills to be used in IBD, but this study helps give the idea of FMT more merit because it was a placebo controlled study and demonstrated much greater efficacy compared to placebo. Supposedly these are some of the best ways to demonstrate the effectiveness of any therapy, but even in some single case studies FMT has shown such a dramatic effect, it's hard to ignore, but this study will always help further the cause.
This is very interesting, thank you! I do think fecal transplants are a big piece of the puzzle as will other methods to help clear out any existing pathogens in the system. It is nice that people are researching the CAUSE of the disease now as a trend, rather than the symptoms.Here is link to a recent study covering the dizzying complexity of trying to answer the question of whether microbiome alterations/disruptions are the cause or the result of IBD. It is now clear that there are major alterations in the microbiome, we just don't fully understand the implications and meaning of this data. It seems it is still possible the microbiome could be the sole cause if IBD as opposed to genetic mutations/heredity. Attempting to normalize the altered microbiome in IBD patients to appear more normal/healthy to improve or cure the disease is what Fecal Microbiota Transplants are all about.
Microbiota Alterations in Inflammatory Bowel Diseases: From Correlation to Causality
Published Online: May 14, 2016
http://www.cmghjournal.org/article/S2352-345X(16)30040-6/fulltext
Scared1, you may be interested in the site thepowerofpoop.com whose original curator was somewhat of a pioneer in bringing together a lot of information regarding FMT to the web. And in particular, given the sort of companies you're linking, you might be interested in the listings on this page, where a lot of the companies that were/are doing next-generation FMT research (e.g. poop in a pill) are listed. You'll see Seres, Enterome, Second Genome, Vedanta and some other less known names. And many of these companies are now backed by the giants of the Pharma industry. True, it's an exciting field, but so far, definitely promising research in recurrent CDI, and to some extent UC, but I haven't seen anything too exciting yet for CD. I'm keeping my fingers crossed though.This is very interesting - has to do with UC but a version is also being made for Crohn's based on the website....
http://www.serestherapeutics.com/clinical-trials/overview/ser-287-seres-101-study
I'm pretty sure this is in this thread somewhere, but it doesnt hurt to bring it up again because it is awesome. There is also a synthetic FMT pill being studied right now for crohn's. The pills are usually a selected mixture of different types of good bacteria.This is very interesting - has to do with UC but a version is also being made for Crohn's based on the website....
http://www.serestherapeutics.com/clinical-trials/overview/ser-287-seres-101-study
Yeah, I didn't see it anywhere. I find this very interesting and I hope it leads to something in the next few years. I know there is a version for the pill - except the website just talks about the UC one but they are doing the same thing.I'm pretty sure this is in this thread somewhere, but it doesnt hurt to bring it up again because it is awesome. There is also a synthetic FMT pill being studied right now for crohn's. The pills are usually a selected mixture of different types of good bacteria.
This article mentions an FMT pill for crohn's being studied, third paragraph from the bottom.Yeah, I didn't see it anywhere. I find this very interesting and I hope it leads to something in the next few years. I know there is a version for the pill - except the website just talks about the UC one but they are doing the same thing.
I really think the whole dysbiosis is a piece of it - not the whole piece to the puzzle. But, with that said, its a BIG piece of it and I am following so many trials and news on a daily basis (weird, it has become part of my morning coffee routine - sit and literally look at any postings/news/etc from the prior 24 hours), and it helps seeing that there are some interesting things in the pipeline
I know! All antibiotics - here is a "layman version" per the website abstract:Wow, that's even more antibiotics than AMAT! Shorter duration though. Not thrilled about the PEG.
I think this is a horrible idea to give someone all these antibiotics when we already suspect the destruction of the natural microbiota to be the cause of many diseases. If anything, they should try to select antibiotics specific to a certain group of pathogens and also try to verify the good bacteria will not be affected by the antibiotics.Has anyone hears about this trial? I came across it it today and thought it was interesting - it is not yet recruiting and in phase 2 and last updated and entered in this month...
https://clinicaltrials.gov/ct2/show/NCT02765256
I wouldn't rule it out - I mean, I am just curious to see what the reasoning is - perhaps they are trying to aggressively kill of the bad bacteria and these antibiotics were selected for a reason - too soon to tell. At least they are trying to look at the CAUSE as opposed to another symptom focused treatment. I do think that this is a step in the right direction from that regards, whether or not the reasoning is as sound right now - I can't tell, too premature without further data. I always check those clinical trials - I like to see what the status is and it gives you a nice overview. Interesting, I was looking at historical archives of PUD (Peptic Ulcer Disease) and here is some clips I found in scientific articles at the time (this is an article from 1985):I think this is a horrible idea to give someone all these antibiotics when we already suspect the destruction of the natural microbiota to be the cause of many diseases. If anything, they should try to select antibiotics specific to a certain group of pathogens and also try to verify the good bacteria will not be affected by the antibiotics.
If I were to approve such a study those would be the only criteria under which something like this would be tried. Also start in mice and rats first as usual for any groups of chemicals, and only after that perhaps on only a few patients because who knows what could happen.
The topics of Map and the microbiome are not that much different. One of the main purposes of the natural bacteria(microbiome) in our guts is to defend against pathogens, like MAP. This defense provided by the good bacteria is called colonization resistance, the creation of short chain fattys acids is one main purpose of the bacteria when they ferment fiber from our food. This lowers intestinal PH to inhibit pathogens. other molecules are created as well like antibacterials AKA biocins. So theoretically the main cause could be a damaged microbiome that could allow map to persist in the gut.I at least like that they are moving away from immunosuppresives! I kind of agree partly with Wildbill, in that I'd be curious to see which microbes they're targeting and with what meds. I worry about damaging things with AMAT, but at least I know I am specifically targeting something that I have tested culture positive for. It's likely killing more, and I may be on to fecal transplants after AMAT, but since I feel so well and that has corresponded with a large drop in my mycobacteria culture load, I deal. I still think some of this microbiota research, while super interesting, is destracting to the debate of MAP. Wish they'd just fund the full MAP research and give us proof once and for all! Then we can move on to looking for other harmful pathogens.
http://www.worldgastroenterology.org/UserFiles/file/e-wgn/e-wgn-2014-july.pdfFMT: Quality Control and Feasibility
It would be ideal to standardize FMT. If the purification of fecal microbiota
can be technically controlled it might be more available; otherwise
its application in the world would be restricted by health policy if there is
no quality control. The best solution for this problem
is to allow the procedures to be performed automatically with
machines, GenFMTer. The latest news, from my team cooperating with
Dr. Youquan Zhao and Dr. Huiquan Wang at Tianjin University Precision
Instrument College in China, is the successful development of a new
automatic system for purification of fecal microbiota from fresh feces. This
will advance the standardized FMT from a bio-safety cabinet to automatic
instruments. The operator only needs to press the buttons related to the
designated processes and all procedures can be done in less than a half
an hour. Since we do not know the changing of fecal viable organism after
the feces is expulsed from the colon, it may be the best way to transplant
those microbiota back to the gut as soon as possible.
Thanks! This is encouraging - I don't know if its me because I have just been looking into this since April (my husband's diagnosis), but it seems a lot has been going on with research regarding IBDs in general. Sorry if this is a stupid question - but for those that have had Crohn's for a long time (10+), how do you feel that research has changed and/or GI's methods personally during your treatments? My husband's GI made a statement that when he started practice, there were no options and through his lifetime, he has seen so many changes....so I wonder from your guy's perspective, have you always seen this much research/interest in this area or is this just me having been involved now in this disease that it SEEMS that way?Vedanta biosciences gets 50 million to continue developing Fecal transplant pills for IBD and other health conditions.
http://www.forbes.com/sites/luketim...ionally-defined-bugs-into-drugs/#64702ff46e03
Thanks for the article! Its time like this I love this forum - sharing knowledge and at the same time hope based on actual evidence Thank you!Fecal transplants can be used to clear antibiotic-resistant bacteria out of the gut:
Colonization of the gastrointestinal tract with multidrug-resistant (MDR) bacteria is a consequence of gut dysbiosis. We describe the successful utilization of fecal microbiota transplantation to inhibit Klebsiella pneumoniae MBL+ and Escherichia coli ESBL+ gut colonization in the immunocompromised host as a novel tool in the battle against MDR microorganisms.
http://link.springer.com/article/10.1007/s00005-016-0387-9
I also took antibiotics for years for acne, I never went ahead with accutane though because I read on forums of people taking 3-6 courses and still having acne I decided doctors don't fully understand this disease, and when I eliminated milk and reduced sugar and other dietary improvements my skin improved. But it was learning about the emerging studies on antibiotics and IBD that I made the connection the years of doxycycline most likely contributed to Crohn's diagnoses. Below is a link to one of many studies that show a connection. This study was also done to explore the theory that antibiotics were a confounding(hidden) variable which made the studies connecting accutane use to IBD and that the real culprit is antibiotics not accutane because almost everyone who had been on accutane already were given lots of antibiotics by their dermatologist.Hi ppk,
Upon my first skimming of the article this seems very interesting - will need to -re-read and digest. But honestly, I do think that with any treatment down the line - any of the vaccine initiatives (MAP, SSI for AEIC, and some of the pending trials about using antibiotics directed at AEIC), that fecal transplants will be a part of the therapy to a cure. I do believe that antibiotics could lead to the dysbiosis - my husband was on antibiotics for three years (minocycline, and prior those three years, another few years of accutane), so I do believe that contributed. He may have the genetic predisposition but no one in his entire family has every had crohn's - so he would be the first. So at a certain point, I think this fecal transplant will become more of a standard treatment down the line (complimenting other therapies as well).
This here touches on the topic you mention, and it has a lot of good references to related papers.Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification? The sheer variability of this disease makes it such a trial and error issue - which is probably one of the most annoying things about it. I wonder if anyone has tried to research this at least for treatment recommendation's sake...
I don't recall there being 5 types of crohn's but levels of severity sure, but I have read studies which say they could classify the disease into different types in the future. I dont think we are at the point where we know exactly what causes what type or severity, because there are still so many factors that can cause IBD. Like vitamin d, dietary fiber, antibiotics, artificial sweeteners, animal fat, omega 6 fats, etc, and any combination of the above, but i think they will be able to classify the types by the bacterial makeup. If you looked hard enough and collected most of the latest studies you might be able to piece some of that information together, but I'm pretty sure we don't have enough studies yet, getting closer though.Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification? The sheer variability of this disease makes it such a trial and error issue - which is probably one of the most annoying things about it. I wonder if anyone has tried to research this at least for treatment recommendation's sake...
Thanks for the article! I do think that FT are going to be a piece of the puzzle - the more I think about this dysbiosis caused by whatever the underlying reason in immune deficient hosts (i.e. my husband) due to antibiotics, a pathogen, etc.... I think once that underlying cause is gone - i.e. pathogen, then they would need to replenish or repopulate the microbiome and FT would be the way to go about it. For my husband, I think he would prefer a FT every 2 years rather than daily pills, symptoms, etc....that would be much a more ideal maintenance regime than many of the medications and their potential side effects.Here is a really old study i forgot about that is like a super risky form of a fecal transplant.
They tried to eliminate as much gut bacteria as they could and repopulate the IBD patients gut with just a few good bacteria. Apparently it seemed to help.
http://www.currenttherapeuticres.com/article/S0011-393X(97)80067-7/pdf
This is true, the research has a way to go yet. Doing it yourself requires an understanding of the process and the risks involved. But there is even an FMT recently done by professionals that went wrong because they didn't follow proper donor selection criteria, http://ofid.oxfordjournals.org/content/2/1/ofv004.fullHere is an interesting article summary from this year - very recent entitled:
Fecal transplantation: any real hope for inflammatory bowel disease?
Purpose of review: Fecal microbiota transplant (FMT) has emerged as an important treatment for antibiotic resistant or recurrent Clostridium difficile infection. There has been a great deal of media coverage of the efficacy of FMT, and patients with inflammatory bowel disease (IBD) understandably wonder if this approach would also work for them. There are also instructions on ‘do it yourself’ FMT therapy on the web. It is important to understand whether there is evidence that this approach is effective in IBD so that we can advise our patients appropriately.
Recent findings: Systematic reviews have identified four case series involving 27 ulcerative colitis patients with a pooled remission rate of 24% (95% confidence interval (CI) = 11–45%). Two randomized controlled trials evaluating a total of 123 active ulcerative colitis patients have given conflicting results but the pooled data do suggest benefit with a number needed to treat of 6 (95% CI = 3–33). There are four case series involving 38 patients with Crohn's disease with a clinical response in 60.5% (95% CI = 28–86%). There are no randomized trials in Crohn's disease.
Summary: At present there are insufficient data to recommend FMT in IBD, and patients certainly should not be administering this themselves. This remains an interesting approach to treating IBD and more studies are needed to establish the optimal method of delivery as well as randomized, placebo controlled trials to establish the efficacy of FMT.
Yes, there is an interesting and very recent publication on this very question, although they looked in terms of gene expression across all of IBD and not just Crohn's. And they found that IBD really consists of three distinct diseases instead of the usual two. Instead of the usual CD/UC breakdown, their genetic data indicates that IBD should really be classified as either UC, or Colonic Crohn's, or Ileal Crohn's.Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification?
All good theory aside, the most dramatic and effective FMT's performed to date have been through a nasogastric tube and this was in crohn's disease, in some cases just one fmt makes a big difference. FMT enemas or through colonoscope have been labor intensive and take a long time like 30-60 enemas.Fecal transplants are a bit of a paradox to me in regards to Crohn's. And I'm talking about small bowel disease. The small intestine bacterial density is orders of magnitude less than the large bowel composition. The species are markedly different as well. Upper small bowel are primarily gram-positive aerobes. At the terminal ileum the composition transitions more toward a 50/50 areobes/anaerobes, and in the colon (large intestine), the bacterial diversity explodes with anaerobes. It seems at odds with nature's design to introduce fecal species into the upper gut. She wouldn't have spent millions of years evolving the the illececal valve in vertabrae if she didn't mind the mixing of small and large bowel contents. Most animals don't go around eating each other's poops.
I'll apologize in advance if my views don't align with yours. Just saying FMT may have therapeutic value for disease in the large bowel, which doesn't really cover Crohn's spectrum completely.
You may find this interesting.Most animals don't go around eating each other's poops.
http://www.eurekalert.org/pub_releases/2016-06/bcom-ass061516.phpBuffington next tested whether the specific differences in the microbiome were causative factors underlying the social impairments in offspring of mothers fed a high-fat diet. Because mice eat each other's poop, the researchers housed the animals together so that they would acquire microbiota from their cagemates. When socially impaired three-week-old mice born to mothers on a high-fat diet were paired with normal mice, a full restoration of the gut microbiome and a concurrent improvement in behavior was observed within four weeks.
Read the first post of this thread. This study is in the list of studies being done on FMT. results? not sure.A study going on - not sure if this was completed and if any results were posted somewhere?
https://clinicaltrials.gov/ct2/show/NCT02097797?term=crohn's+fecal&rank=1
Thanks for posting Lady Organic! I definitely agree - I am so happy for that family!Not sure if this case report has been posted before in the thread. FMT on a child failing big drugs and who was on way to colectomy. stories of this kind bring tears to me eyes... Im so happy for this child and his family, I feel so hopeful on day we could all make it...:
''Repeated fecal microbiota transplantation in a child with ulcerative colitis.''
http://www.ncbi.nlm.nih.gov/pubmed/27324973
thanks Lady Organic, I don't think we have seen this before so this is a good contribution to this thread. There is a study that was posted before that similarly used FMT orally in 30 patients with refractory crohn's that didn't respond well to med's. Amazing stuff. http://www.ncbi.nlm.nih.gov/pubmed/25168749Not sure if this case report has been posted before in the thread. FMT on a child failing big drugs and who was on way to colectomy. stories of this kind bring tears to me eyes... Im so happy for this child and his family, I feel so hopeful on day we could all make it...:
''Repeated fecal microbiota transplantation in a child with ulcerative colitis.''
http://www.ncbi.nlm.nih.gov/pubmed/27324973
Thanks again! This is great!another case report of long term disease resolved by FMT:
''Coordinated Hospital-Home Fecal Microbiota Transplantation via Percutaneous Endoscopic Cecostomy for Recurrent Steroid-Dependent Ulcerative Colitis.'':
http://www.ncbi.nlm.nih.gov/pubmed/27282271
I think the studies just show there is promise - perhaps more so for UC but I think for Crohn's it will serve as a complimentary therapy to the other prospective treatments out there (SSI Vaccine & MAP Vaccine/Redhill Triple Therapy). It is still nice to hear people get better though - UC or otherwiseI'll give it to you guys. The case for FMT in UC may be there. But it's less convincing in Crohn's.
You all keep posting UC studies.
These days, fecal transplantation is no joke“There is no doubt that poo can save lives,” said Bordenstein. Take the case of the use of fecal transplants to treat Clostridium difficile infections. According to the literature, it has a 95 percent cure rate. “Right now fecal transplants are used as the treatment of last resort, but their effectiveness raises an important question: When will doctors start prescribing them, or some derivative, first?” Bordenstein asked.
Still, it’s often hard to improve on nature. “We’ve tried for decades to make artificial blood, and we ultimately failed,” Dr. Khoruts said. “And so we still have blood banks.”
It may also prove difficult to outdo our own stool. “This is something nature put together over millions and millions of years,” Dr. Khoruts said.
Thanks, I was just about to post on this. disappointing for sure. this pill from seres is just a handfull of bacteria though, spores to be precise. As a comparison a different type of FMT pills used for c diff were "full spectrum" containing a much wider range of bacteria and were just as effective as regular fecal transplants.http://www.cleveland.com/healthfit/index.ssf/2013/10/a_canadian_doctor_is_curing_st.htmlA disappointing failure for the microbiome approach to controlling recurrent C. diff. infections. No better than placebo and in some cases worse.
It looks like this microbiome approach is not going ot be as quick and easy as some have predicted:
http://www.cnbc.com/2016/07/29/gut-...nge-after-microbiome-drug-fails-in-trial.html
The "consultation" with Vendanta will consist almost entirely of haggling over how much the other company must pay for a license to use the technology covered by the patent.Vedanta biosciences issued broad patent for microbiome therapies utilizing clostridia species of bacteria. As far as I know this means any company that wants to use them for any medications must consult with them for a period of time.
http://www.kctv5.com/story/32766682...ome-therapeutics-based-on-bacterial-consortia
I can definitely believe that - my husband took antiobiotics (minocycline for 3-4 years before he was diagnosed), no family history, very healthy, 28 years old, never been to a doctor (literally). Plus, he is overly clean (hygiene hypothesis - not like normal clean, like obssessive). So I definitely believe that part of it.Here is a piece of evidence that supports the concept of damage to the microbiome possibly involved in many diseases and not just C. diff or IBD, in this cases using antibiotics. http://www.nature.com/articles/nmicrobiol2016140
Restoration of the natural microbiome with a fecal microbiota transplant would likely be able to reverse this and that is the hopes we have for the upcoming experiments when applied to humans, many studies are happening right now. There are also 4 studies in the last 5 years linking antibiotics to increased risk of IBD, many of my serious health problems began 2 weeks after taking an antibiotic, within a year i was diagnosed with crohn's.
These are studies linking antibiotics to increasing the risk of developing IBD in other words "causing" the disease.Another anecdote: while I have lots of family with Crohn's and I am of Ashkenazi descent and my family environment was super-clean, my history of getting Crohn's directly follows repeatedly being given 2 week regimens of full-spectrum antibiotics for chronic urinary tract infections when I was in my 20s.
As far as I recall most people who have received FMT for crohn's were refractory and failed most med's. There hasn't been much negative effects from it, some cases people who were stable went into a flare, one guy who did a home FMT with U.C. became much worse but who knows what he was doing without proper guidance. But of course, this is all early info on an experimental but promising treatment. Take the precautions of course if you DIY.My son's diagnosis has changed from Crohn's to UC. He is cortisone dependent (at the moment on 30 mg of prednisolone per day, has been on prednisolone for 9 months now, 30-60 mg day), currently also on Humira and 75 mg of Azathpriorine, IVIG and Eusaprim antibiotics. We are considering FMT. Is he too immunocomprimised to get a FMT? Any risks for serious side effects?
http://www.sciencedirect.com/science/article/pii/S2352345X16301060If a dysbiosis is an instigator, then in principle it should be possible to detect this defect in otherwise healthy populations who are at increased risk for disease, such as healthy relatives of IBD patients.
In a new study published in this issue of Cellular and Molecular Gastroenterology and Hepatology, Jacobs et al 3 do exactly that. Performing a thorough analysis of fecal microbial profiles from 36 IBD patients in remission (26 with Crohn’s disease and 10 with ulcerative colitis) and 54 healthy first-degree relatives, they showed that it is possible to identify an IBD-like intestinal microbiome in at-risk healthy individuals who do not have clinically detectable inflammation.
My guess (and it's just a guess - no data) is that it's either or both. I'm thinking the dysbiosis and the inflammation form a self-feeding loop, a vicious cycle that can start with either one.SO which came first? The dysbiosis or the inflammation?
Under what natural or semi natural circumstance would that happen though, inflammation is generally a response to bacterial threat, or tissues damage/repair, as far as I know. What circumstance could inflammation be triggered entirely independent of any changes in the microbiome? I'm not arguing any given position just thinking out out loud really.My guess (and it's just a guess - no data) is that it's either or both. I'm thinking the dysbiosis and the inflammation form a self-feeding loop, a vicious cycle that can start with either one.
There are many ways the gut can become directly inflamed without first disrupting the bacterial microbiome - celiac disease, viral enteritis, NSAIDS, all sorts of autoimmune inflammation, etc. And once inflamed the inflammation could easily result in disruption of the microbiome, which in turn could lead to more inflammation. It's a chicken and egg thing.Under what natural or semi natural circumstance would that happen though, inflammation is generally a response to bacterial threat, or tissues damage/repair, as far as I know. What circumstance could inflammation be triggered entirely independent of any changes in the microbiome? I'm not arguing any given position just thinking out out loud really.
The researchers in the University of Helsinki and Helsinki University Hospital have studied in detail the intestinal microbiota of 14 patients treated with a faecal microbiota transplant. The patients suffered from recurrent Clostridium difficile -infection, also known as antibiotic associated diarrhea, and they had not responded to antibiotic treatment. After the faecal microbiota transplantation therapy, the patient's microbiota was followed for a year.
The researchers found out that the patient's intestinal microbiota highly resembled the donor's microbiota and this composition remained stable through-out the 1-year follow-up period.
"Our results suggest that intestinal microbiota can be modified relatively permanently. This opens new possibilities to the use this treatment for other diseases related to microbial dysbiosis," says the Academy Research Fellow Reetta Satokari from the University of Helsinki.
COLLEEN KELLY STARTED using fecal microbiota transplants in 2008—one of the first gastroenterologists in the US to do so. Over the years, she has noticed some strange side effects. One of her C. diff patients, for instance, also suffered from alopecia universalis. He hadn’t been able to grow any hair since he was 16: not on his head, not in his armpits, not even on his eyebrows. But when he got a stool transplant from his sister, he started sprouting fresh patches.
When Kelly told a colleague about the result, she got a second shock: He had seen a fecal transplant recipient regrow hair too. The two doctors were stuck. They didn’t have the resources to analyze their patients’ microbiomes to see what bugs might have been responsible for the change. “You don’t know how bad I wish I had that,” she says.
Tabletop robots sort through fecal samples from around the world, identify species of bacteria, and use those to grow more.
She’s not alone. It’s becoming more and more clear that the microbiome has therapeutic potential beyond the gut. Some patients undergo significant weight changes after a transplant; others say their depression goes away. Yet doctors still can’t figure out how it works.
Which is why, in early August, the National Institutes of Health announced that it would fund a fecal transplant registry, maintained by the American Gastroenterological Association. For the first time, thousands of transplant patients will have their microbiomes sequenced before and after treatment so doctors can have a better shot at identifying not only the bugs that fight C. diff but also what’s causing all those side effects. If Kelly had access to that kind of analysis with her alopecia patient, she might have stumbled onto a new, targeted microbiome therapy—delivering just the right bacteria to trigger hair growth