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08-30-2016, 12:14 PM   #781
wildbill_52280
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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.
These are studies linking antibiotics to increasing the risk of developing IBD in other words "causing" the disease.

2004
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774910/
2010
http://www.ncbi.nlm.nih.gov/pubmed/20700115
2011
http://faculty.vet.upenn.edu/gastro/...jg2011304a.pdf
2012
http://pediatrics.aappublications.or...30/4/e794.full
2013
http://journals.lww.com/ibdjournal/A...w_Onset.4.aspx

While It's hard to say antibiotics alone can cause IBD because many people take antibiotic's and do not develop IBD, it can depends on the type of antibiotic, how many times you have taken it, the length of time etc, and other risk factors that are present like diet etc. But when you look at all the scientific evidence that exists, damage to the microbiome and the correction of this damage with restoration of missing bacteria with Fecal transplants, you can see it all starts to come together and make more sense, maybe we are on the right track here, I believe we are.



More evidence that suggests a link between antibiotics as a cause of IBD and destruction of microbiome:

Antibiotic Associated Hemorrhagic Colitis: The Need to Distinguish
from Clostridium difficile Colitis!
http://www.practicalgastro.com/pdf/J...janArticle.pdf
(this case report strongly showing the ability of antibiotics to promote diarrhea and colitis(colonic inflammation),so to make a small analogical leap and suggest antibiotics could also cause chronic colitis such as in IBD, doesn't sound so far fetched now)


Here is another study of someone with antibiotics associated diarrhea. Quote "Antibiotic administration was associated with distinct changes in the diversity of the gut microbiota, including a marked decrease in the prevalence of butyrate-producing bacteria." (Is it just a coincidence that IBD patients are lacking in diversity of beneficial clostridia which are butyrate producing bacteria)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC356823/

Another study of microbiome changes during antibiotic associated diarrhea of someone taking amoxicillin-clavulanic acid. Clostridia species were so inhibited by antibiotics they undetectable, but grew back after removal of antibiotics. (this is the antibiotic I took before my health changed in a serious way one year later I was diagnosed with crohn's disease.)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC356823/

Clinical onset of the Crohn's disease after eradication therapy of Helicobacteria pylori infection. Does Helicobacter pylori infection interact with natural history of inflammatory bowel diseases?(this is an anecdotal report, but i think it was the amoxicillin that cause the crohn's and certain antibiotics can make a similar pattern of bacterial changes in people? i suggest some people may recover, and some may not)
http://www.ncbi.nlm.nih.gov/pubmed/11208510


Is Crohn's disease caused by antibiotics?
http://www.ncbi.nlm.nih.gov/pubmed/7721242
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Last edited by wildbill_52280; 08-30-2016 at 01:38 PM.
09-01-2016, 07:00 PM   #782
Scipio
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Apparently just a few days in the ICU is enough to wreck the microbiome:

http://www.medicalnewstoday.com/releases/312656.php
09-02-2016, 06:53 AM   #783
mf15
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Here is another new one, when I was a kid back in the 50's they mostly used
penicillins and in the form of shots.
So since then they have pretty much switched from narrow spectrum to wide spectrum antibiotics.
But even this does not quite explain the increase in IBD from say around
1920 ish.
Old Mike
http://medicalxpress.com/news/2016-0...re-higher.html
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09-05-2016, 03:00 PM   #784
wildbill_52280
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Two recent videos on FMT.
https://www.youtube.com/watch?v=yD--XThDJyE
https://www.youtube.com/watch?v=e_dF1N-Ckbw
09-06-2016, 05:19 AM   #785
Spooky1
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Can't watch the second one as it is unavailable in the UK. the first was interesting, thanks
09-20-2016, 11:27 PM   #786
wildbill_52280
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As part of its international microbiome series, Global Engage is pleased to announce the co-located 4th Microbiome R&D and Business Collaboration
Forum: USA and Probiotics Congress: USA which will be held on 3-4 October 2016 at the San Diego Marriott La Jolla.

http://www.globalengage.co.uk/microb...Agenda2016.pdf
10-02-2016, 04:27 PM   #787
wildbill_52280
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Increased Intestinal Microbial Diversity Following Fecal Microbiota Transplant for Active Crohn's Disease.

Inflamm Bowel Dis. 2016 Sep;22
Abstract

BACKGROUND:
The microbiota in the lumen of patients with Crohn's disease (CD) is characterized by reduced diversity, particularly Firmicutes and Bacteroidetes. It is unknown whether the introduction of the intestinal microbiota from healthy individuals could correct this dysbiosis and reverse mucosal inflammation. We investigated the response to fecal microbial transplantation (FMT) from healthy individuals to subjects with active CD.

METHODS:
We performed a prospective open-label study (uncontrolled) of FMT from healthy donors to subjects with active CD. A single FMT was performed by colonoscopy. Recipients' microbial diversity, mucosal T-cell phenotypes, and clinical and inflammatory parameters were measured over 12 weeks, and safety over 26 weeks.

RESULTS:
Nineteen subjects were treated with FMT and completed the study follow-up. Fifty-eight percent (11/19) demonstrated a clinical response (Harvey-Bradshaw Index decrease >3) following FMT. Fifteen subjects had sufficient pre/postfecal samples for analysis. A significant increase in microbial diversity occurred after FMT (P = 0.02). This was greater in clinical responders than nonresponders. Patients who experienced a clinical response demonstrated a significant shift in fecal microbial composition toward their donor's profile as assessed by the Bray-Curtis index at 4 weeks (P = 0.003). An increase in regulatory T cells (CD4CD25CD127lo) was also noted in recipients' lamina propria following FMT. No serious adverse events were noted over the 26-week study period.

CONCLUSIONS:
In this open-label study, FMT led to an expansion in microbial bacterial diversity in patients with active CD. FMT was overall safe, although the clinical response was variable. Determining donor microbial factors that influence clinical response is needed before randomized clinical trials of FMT in CD.

https://www.ncbi.nlm.nih.gov/pubmed/27542133

Last edited by wildbill_52280; 10-03-2016 at 12:21 AM.
10-04-2016, 03:04 PM   #788
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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?
__________________
*Son (9 years) with severe Crohn's diagnosed at the age of 26 months, currently UC or Crohn's colitis
*Current mediacation: IVIG, Humira, Azathpriorine, Eusaprim
(Tested but failed: Modulen IBD, Neocate advance, Budenofalk, Remicade, Azathpriorine, MTX, Jerusalem cocktail, cycklosporine, pentasa,...)
10-05-2016, 02:24 AM   #789
wildbill_52280
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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?
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.
10-06-2016, 02:22 PM   #790
wildbill_52280
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SO which came first? The dysbiosis or the inflammation? A new study shows it looks like the dysbiosis came first.
This evidence could further support the concept that dysbiosis is the first step in IBD development, and that could mean that it is also the cause of the disease itself and restoring dysbiosis with Fecal Microbiota transplant could be the cure.

If 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.
http://www.sciencedirect.com/science...52345X16301060

I also recall a study examining the microbiome in crohn's patients who were in remission and on immunosuppressant therapy, a dysbiotic state was still evident when inflammation was suppressed, suggesting that the inflammatory response is not the sole cause of a dysbiotic state. But inflammation does have a strong influence on dysbiosis, so inhibiting inflammation does improve things just doesn't seem to correct things completely, I'll have to find that study though.
10-06-2016, 05:23 PM   #791
Scipio
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SO which came first? The dysbiosis or the 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.
10-07-2016, 03:14 PM   #792
wildbill_52280
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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.
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.
Generally speaking my position is that 90% of IBD cases are not genetically determined and the condition is reversible, through a FMT. Whether dysbiosis is a cause of inflammation of inflammation is a cause of dysbiosis, I would say that these questions are important because this evidence would point to the correction of the microbiome as a therapeutic strategy, rather then the prevailing paradigm of suppressing the inflammation or immune system to influence symptoms.

I would say at this point the evidence is really good to justify treating the state of dysbiosis, perhaps affecting symptoms through that variable/pathway instead, and I do believe it will lead to the cure. I really don't know what is taking so long to get these FMT pill studies for crohn's going though, the evidence has been here for a while now, we can do it now. The colonoscopic enemas and home enemas are unreliable way of studying this, we are beyond that by now.

Last edited by wildbill_52280; 10-08-2016 at 12:19 AM.
10-11-2016, 07:56 AM   #793
Scipio
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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.
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.

Successful FMT could indeed prove to be a useful tool to break this vicious cycle and restore good health, but there is no particular reason think that disruption of the microbiome is only way the process can get started in the first place.
10-11-2016, 01:37 PM   #794
wildbill_52280
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Healing effect of fecal microbiota transplantation lasts for long
October 11, 2016
https://www.sciencedaily.com/release...1011085352.htm

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.
10-18-2016, 10:32 AM   #795
wildbill_52280
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Tapping the Human Gut Microbiome
The Next Frontier for Novel Therapeutics
October 17, 2016

Part 1
http://www.genengnews.com/insight-an...art-1/77900760

Part 2
http://www.genengnews.com/gen-exclus...art-2/77900761
10-27-2016, 12:27 PM   #796
wildbill_52280
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My father's poo saved my life': Woman who could not leave her bed due to her agonising chronic constipation reveals how a VERY personal transplant saved her life
October 23rd 2016


http://www.dailymail.co.uk/femail/ar...nt-father.html
11-02-2016, 09:49 AM   #797
Scared1
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Great progress:
http://www.news-medical.net/news/201...l-disease.aspx
11-02-2016, 06:17 PM   #798
wildbill_52280
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ARE YOU READY TO SWALLOW A PILL FULL OF POOP?
11.02.16

https://www.wired.com/2016/11/microb...plants-better/

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
11-09-2016, 02:00 PM   #799
wildbill_52280
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Pectin fiber(for example from an apple)makes Fecal Transplants more effective.
For the sake of interpreting this abstract, a lower number on the MAYO score indicates lower amount of symptoms in U.C. This was a very small study though but since good results were observed larger studies would likely be replicated in the future and anything that makes FMT more effective is a great step forward.

BMC Microbiol. 2016 Nov 3;16(1):255.
Pectin enhances the effect of fecal microbiota transplantation in ulcerative colitis by delaying the loss of diversity of gut flora.

Abstract

BACKGROUND:
Fecal microbiota transplantation (FMT) induces remission in ulcerative colitis (UC). However, the treatment effect of FMT diminishes over time. Maintaining the diversity of the gut flora for long periods may improve the effects of FMT in UC. Pectin, which can be fermented by gut microbiota into short-chain fatty acids, is postulated to shape the composition and maintain the balance of gut microbiota following transplantation. This study investigated whether pectin could enhance the effects of FMT in UC patients.

RESULTS:
Three FMT patients and four FMTP(FMT plus Pectin fiber) patients achieved the primary outcome. The Mayo scores of the FMTP group were lower than those of the FMT group at weeks 4 and 12 (P = 0.042 and P = 0.042, respectively). There were no differences in the diversity of the gut flora between the two groups at weeks 4 and 12; however, the composition of the gut flora of the FMTP group was more similar than the FMT group to that of the donor at all-time points post-treatment.

CONCLUSIONS:
Pectin decreased the Mayo score by preserving the diversity of the gut flora following FMT for UC.

Last edited by wildbill_52280; 11-10-2016 at 11:11 AM.
11-09-2016, 02:04 PM   #800
wildbill_52280
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WOW!!

Crit Care. 2016 Oct 18;20(1):332.
Successful treatment with fecal microbiota transplantation in patients with multiple organ dysfunction syndrome and diarrhea following severe sepsis.
Abstract
BACKGROUND:
The dysbiosis of intestinal microbiota plays an important role in the development of gut-derived infections, making it a potential therapeutic target against multiple organ dysfunction syndrome (MODS) after sepsis. However, the effectiveness of fecal microbiota transplantation (FMT) in treating this disease has been rarely investigated.

METHODS:
Two male patients, a 65-year-old and an 84-year-old, were initially diagnosed with cerebellar hemorrhage and cerebral infarction, respectively, after admission. During the course of hospitalization, both patients developed MODS, septic shock, and severe watery diarrhea. Demographic and clinical data were collected. Intestinal dysbiosis was confirmed by 16S rDNA-based molecular analysis of microbiota composition in fecal samples from the two patients. The two patients each received a single nasogastric infusion of sterile-filtered, pathogen-free feces from a healthy donor. Fecal samples were collected every two days post infusion to monitor changes in microbiota composition in response to treatment.

RESULTS:
Following FMT, MODS and severe diarrhea were alleviated in both patients. Their stool output and body temperature markedly declined and normalized. Significant modification of microbiota composition, characterized by a profound increase of commensals in the Firmicutes phylum and depletion of opportunistic organisms in the Proteobacteria phylum, was observed in both patients. Furthermore, we identified a reconstituted bacterial community enriched in Firmicutes and depleted of Proteobacteria that was associated with a decrease in the patients' fecal output and in the levels of plasma inflammation markers.

CONCLUSIONS:
The outcome of treating two patients with FMT indicates that restoration of the intestinal microbiota barrier can alleviate the infection and modulate the immune response. These findings warrant further investigation of FMT as a putative new therapy for treating microbiota-related diseases such as MODS.
11-09-2016, 02:16 PM   #801
wildbill_52280
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Medicine (Baltimore). 2016 Jul;95(30):e4055. doi: 10.1097/MD.0000000000004055.

Clinical efficacy maintains patients' positive attitudes toward fecal microbiota transplantation.

Abstract
Few studies have been conducted on the attitudes of patients seeking fecal microbiota transplantation (FMT). This study aimed to investigate the reasons for patients with Crohn's disease (CD) seeking FMT and their attitude changes after FMT.In this prospective study, all included patients were diagnosed with CD for at least 6 months and intended to receive FMT. A questionnaire was designed to investigate the history of medical visits and patients' attitudes toward FMT. Only refractory patients who failed to clinically respond to previous treatment were selected for undergoing FMT. Three months after the first FMT, patients were required to complete the second questionnaire on attitudes toward the first FMT.A total of 207 patients with CD were included for questionnaire survey. In 118 refractory patients, 94.07% sought FMT because they had no other choice. In 89 nonrefractory patients, 78.65% sought FMT for the reason that they wanted to achieve better clinical results or even a cure, although the current treatment was effective for them. In all, 118 refractory patients received FMT. Three months after the first FMT, 88.98% (105/118) patients completed the questionnaire on patients' attitudes toward FMT. Of these 105 patients, 56.19% reported to have satisfactory clinical efficacy and 74.29% were willing to receive the second FMT. Moreover, 89.52% (94/105) showed their willingness to recommend FMT to other patients.In conclusion, this study at least first time demonstrated that patients with CD were willing to accept FMT due to its efficacy.
11-09-2016, 02:25 PM   #802
wildbill_52280
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YouTube Video Published on Nov 4, 2016

Experts from the AGA Center for Gut Microbiome Research and Education share updates on one of the most important medical breakthroughs -- fecal transplants. Drs. Loren Laine, Colleen Kelly, and Gary Wu serve as co-principal investigators on AGA's new FMT national registry
https://www.youtube.com/watch?v=fAUUpP5HiFA
11-11-2016, 05:28 PM   #803
wildbill_52280
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Inflamm Bowel Dis. 2016 Nov 7. [Epub ahead of print]
A Single Species of Clostridium Subcluster XIVa Decreased in Ulcerative Colitis Patients.


Abstract
BACKGROUND:
Imbalance of the intestinal microbiota is associated with gastrointestinal disease and autoimmune disease and metabolic syndrome. Analysis of the intestinal microbiota has recently progressed, and the association with inflammatory bowel disease has been reported at the species level. Such findings suggest that the recovery of homeostasis in the intestinal microbiota could cure inflammatory bowel disease. We aimed to search new probiotic candidates for inflammatory bowel disease through translational research by analysis of ulcerative colitis (UC) patients' intestinal microbiota and clarify the effects of them on inflammation. Here, we focused on Fusicatenibacter saccharivorans, which belongs to Clostridium subcluster XIVa and was successfully isolated and cultured in 2013. We analyzed the association of F. saccharivorans to UC patients' activity and inflammation for the first time.

METHODS:
Feces from UC patients and healthy controls were analyzed by 16S ribosomal RNA gene sequences. F. saccharivorans was administered to murine colitis model. Colitic lamina propria mononuclear cells from UC patients and mice were stimulated with F. saccharivorans.

RESULTS:
The whole fecal bacteria in active UC patients were less than that in quiescent UC patients. Furthermore, F. saccharivorans was decreased in active UC patients and increased in quiescent. The administration of F. saccharivorans improved murine colitis. F. saccharivorans induced interleukin 10 production by lamina propria mononuclear cells from not only colitis model mice but also UC patients.

CONCLUSIONS:
F. saccharivorans decreased in correlation to UC activity and suppresses intestinal inflammation. These results suggest that F. saccharivorans could lead to a novel UC treatment.
11-16-2016, 09:40 PM   #804
Scared1
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Thank you WildBill - all these are very helpful!
11-27-2016, 02:10 PM   #805
wildbill_52280
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I already posted this study but see what I highlighted here. It's nice to hear a scientific article say this straight out, it's rare to hear it but it's high probability for FMT to correct GI microbiome to be a cure for IBD, most articles talk about FMT as a treatment but cure is a real possibilty and some cases people seemed to be cured.

Inflamm Bowel Dis. 2016 Nov 7. [Epub ahead of print]
A Single Species of Clostridium Subcluster XIVa Decreased in Ulcerative Colitis Patients.


Abstract
BACKGROUND:
Imbalance of the intestinal microbiota is associated with gastrointestinal disease and autoimmune disease and metabolic syndrome. Analysis of the intestinal microbiota has recently progressed, and the association with inflammatory bowel disease has been reported at the species level. Such findings suggest that the recovery of homeostasis in the intestinal microbiota could cure inflammatory bowel disease. We aimed to search new probiotic candidates for inflammatory bowel disease through translational research by analysis of ulcerative colitis (UC) patients' intestinal microbiota and clarify the effects of them on inflammation. Here, we focused on Fusicatenibacter saccharivorans, which belongs to Clostridium subcluster XIVa and was successfully isolated and cultured in 2013. We analyzed the association of F. saccharivorans to UC patients' activity and inflammation for the first time.

METHODS:
Feces from UC patients and healthy controls were analyzed by 16S ribosomal RNA gene sequences. F. saccharivorans was administered to murine colitis model. Colitic lamina propria mononuclear cells from UC patients and mice were stimulated with F. saccharivorans.

RESULTS:
The whole fecal bacteria in active UC patients were less than that in quiescent UC patients. Furthermore, F. saccharivorans was decreased in active UC patients and increased in quiescent. The administration of F. saccharivorans improved murine colitis. F. saccharivorans induced interleukin 10 production by lamina propria mononuclear cells from not only colitis model mice but also UC patients.

CONCLUSIONS:
F. saccharivorans decreased in correlation to UC activity and suppresses intestinal inflammation. These results suggest that F. saccharivorans could lead to a novel UC treatment.
12-01-2016, 02:46 PM   #806
wildbill_52280
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new video made about FMT.
https://www.youtube.com/watch?v=eXH3NtEBFe0
12-01-2016, 02:46 PM   #807
wildbill_52280
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New video on FMT.
https://www.youtube.com/watch?v=eXH3NtEBFe0
12-01-2016, 10:26 PM   #808
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I've researched the fecal transplant and don't think I could do it. Probiotics are very helpful. Even if someone seems healthy they could still carry unknown pathogens or parasites. Not only is the idea gross but the risk is incredible.
12-02-2016, 12:56 PM   #809
wildbill_52280
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I've researched the fecal transplant and don't think I could do it. Probiotics are very helpful. Even if someone seems healthy they could still carry unknown pathogens or parasites. Not only is the idea gross but the risk is incredible.
Yes some risks exist, so far studies have shown its pretty safe. I think it's been done at least 1000 times for C. diff infection, very few problems but some events like people developing new autoimmune disease have occured as well as some diseases like parkinsons and multiple sclerosis improving. None of them clearly related to the fecal transplant. This is why screening and knowing your donor is super important. Without a doubt, you just cant choose any random person to become a donor, they have to be very healthy. By way of comparison antibiotics are now known to be very destructive to the microbiome causing 80% of c. difficile cases which can lead to death, but we currently call this "medicine" which is actually is in many cases. Despite these known risks, doctors continue to prescribe them.

Last edited by wildbill_52280; 12-02-2016 at 09:14 PM.
12-06-2016, 06:36 PM   #810
wildbill_52280
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I've researched the fecal transplant and don't think I could do it. Probiotics are very helpful. Even if someone seems healthy they could still carry unknown pathogens or parasites. Not only is the idea gross but the risk is incredible.
A Video from a professor who studies FMT and his opinion on FMT safety.
https://www.youtube.com/watch?v=ot7e9bQO2U8

Last edited by wildbill_52280; 12-06-2016 at 11:48 PM.
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