In this follow-up interview with Glenn Taylor of the Taymount Clinic in the U.K., we discuss the latest developments in fecal microbiota transplant (FMT). Is FMT a panacea? Does everybody get better and live happily ever after? Or are there some people who respond better than others? Or some conditions that respond better than others?
While in the U.K. in late October, I took the opportunity to visit the Taymount Clinic. I was really impressed with what they’re doing and the results that they’re getting. In the U.S., FMT is only FDA-approved for antibiotic-resistant Clostridium difficile. So if someone wants to get an FMT for a different condition, they’re not able to do it in the US, but that is not a limitation in the U.K. I’ve sent some of my own patients there and had a chance to see some really positive clinical responses. I wanted to have Glenn come back onto the show and get an update from him on what he has learned since the last time we talked.
In this episode we cover:
6:18 Is FMT a panacea?
8:40 How well IBD responds to FMT
14:00 How C. difficile, colitis and multiple sclerosis respond to FMT
19:00 How Crohn’s disease responds to FMT
26:10 FMT and weight loss
30:40 FMT’s effect on eczema and allergies
39:38 How to increase species diversity in the gut
48:30 The new Taymount Clinic in the Bahamas
Chris Kresser: Hey, everyone. Welcome to another episode of Revolution Health Radio. This week I’m really excited to welcome back Glenn Taylor, Founder and Co-Director of the Taymount Clinic in the U.K.
Taymount was founded in 2003, and it’s one of the only dedicated FMT (fecal microbiota transplant) clinics in the world, that I’m aware of. Glenn developed Taymount’s donor selection and quarantine safety process, the Taymount Laboratory Stool Processing System, and the treatment delivery program that Taymount uses for FMT. As Taymount’s Director of Science, he oversees the lab team and the entire processing system and supervises the training of the nursing staff to deliver the treatment program.
Glenn’s personal specialty is the human microbiome and microbiology, building on his early training in human biology, biology, and organic chemistry.
Glenn was a guest on the show maybe a year or a year and a half ago. We talked about fecal transplant and the way that they’re applying it over there at Taymount Clinic. I was actually in the U.K. for a couple of weeks, doing some public speaking in late October and early November of last year, and I took the opportunity to head up to Hitchin, which is a little bit outside of London, and meet Glenn and the staff there. I was really impressed with what they’re doing and their professionalism and the results that they’re getting and the way that they’re handling the whole procedure from beginning to end. I’ve referred several patients there because FMT is not available in the US. It’s only FDA approved for antibiotic-resistant Clostridium difficile, or C. diff, so if someone wants to get an FMT for a different condition, they’re not really able to do it in the US, but that is not a limitation in the U.K., so Taymount is a place that I’ve sent a number of patients who I thought FMT would help, and they’re always well taken care of when they go there.
I wanted to have Glenn come back onto the show and kind of get an update from him on what he has learned since we talked last time and what’s new there and what the future plans are, so without any further ado, let’s dive in.
Chris Kresser: Glenn, great to have you back on the show!
Glenn Taylor: Chris, thank you very much for inviting me. It’s good to be back.
Chris Kresser: We talked a while ago—I can’t even remember how long ago it was now, maybe a year or a year and a half ago—about what you’re doing at the Taymount Clinic. There was a great response to that. People are really fascinated by FMT and its potential, and so I thought I’d have you back since a lot of water has passed under the bridge since we first talked, and I know you’ve been really busy over there. I’ve certainly sent some of my own patients there and had a chance to see some really positive clinical responses, and I’d love to just take the opportunity to get an update from you here and chat a little bit about what you’ve learned over the past year and a half since we talked and what you’re up to now and what the future holds.
Glenn Taylor: Great. We’ll pick up on that. A lot of water has passed under the bridge. We’ve learned an awful lot more, and the thing that stands out the most is the striking reality of how much we still don’t know yet.
Chris Kresser: Yeah. I’m glad to hear you say that because it’s such an exciting field, and I think when there’s excitement, there’s a tendency to maybe get a little bit ahead of ourselves in some ways. Actually I was speaking at a symposium at UCSF this weekend, and Justin Sonnenburg was another speaker there, who I’m sure you know.
Glenn Taylor: Yes.
Chris Kresser: He presented some fascinating data, and the title of his presentation was “Could disrupted gut microbiome be at the root of Western disease?” That’s basically the argument that he was making, that certainly there are a lot of environmental and genetic factors that contribute to disease, but his presentation argued that one of the key mechanisms that mediates the effect of all of these various factors is a disruption in the gut microbiome. It was a pretty compelling presentation and a pretty compelling argument, and so after that presentation, as you can imagine, you had a room full of people that were all ready to get an FMT!
Is FMT a panacea?
Chris Kresser: Maybe we can just start with what you’ve learned in terms of patients. Is it a panacea? Does everybody get better and live happily ever after? Or are there some people who respond better than others, or some conditions that respond better than others?
Glenn Taylor: Yeah, all of the above. One of the first things I have to do is to rein in enthusiasm. People are picking up a huge amount of information and at the same time, an equal dose of misinformation off the internet. They’re starting to think that, despite all the papers being written now, despite all the case studies that are now available, a little bit of overenthusiasm is going on, and by the time people get on the phone to me, they’re absolutely convinced that FMT is the panacea to all ills and 21st century answers to medicine. I have to kind of rein that enthusiasm back in a little bit because our evidence is quite clearly it’s a significant part of that—there is absolutely no doubt—but it’s not as huge as everybody might think it is because it’s a mosaic. The gut microbiome plays a vitally important part.
You were talking about the presentation as to whether the gut microbiome is the cornerstone of all health, and, yeah, put me in front of a room full of medical people, and I will talk for two hours and make a fairly compelling argument on what we’ve seen, but I equally have to put in a measure of caution in terms of expectation, particularly when people end up having looked at everything else, having been made so many promises by medicine, and by the time they reach us, sadly some of them are just too late.
There’s a very eminent guy in the U.K. He’s a gastroenterologist by the name of Jeremy Sanderson, who focuses on Crohn’s. Mr. Crohn’s Europe, he’s known.
Chris Kresser: Yes.
Glenn Taylor: He said to me the other day, “Glenn, I’m sorry, but there’ll be times—there will be times—when surgery is the only option because it’s just too late.”
How well IBD responds to FMT
Chris Kresser: Yeah, that’s really interesting that you mention Crohn’s and inflammatory bowel disease, in general, because someone asked Justin after his talk, one of the questions was, “I’m really interested in this for a patient I have.” It was mostly medical professionals at the seminar, and they said, “I have a patient with inflammatory bowel disease. Can we expect FMT to work well in that situation?” Justin is not a clinician, and he’s not working on the frontlines with FMT as you are, but he has some experience with the research, and what he said was something that I would tend to agree with, from what I’ve seen from the research—and I’m curious to hear your experience with this—which is that, although some patients with IBD do respond, others don’t, and still others may actually even have a flare-up after the procedure.
Justin’s speculation was that once the chronic inflammatory process and autoimmune process is active, as it is in IBD, introducing a large number of bacteria, even if they’re healthy bacteria, can really kind of stir things up, and it may be that we need to figure out a way to quell the inflammation and get the patient in remission before an FMT can help. Or perhaps there’s something else that we don’t yet understand, but I’m curious to hear your take on that.
Glenn Taylor: You just might have given me the answer! That’s exactly what I would say.
Chris Kresser: Mm-hmm.
Glenn Taylor: I was giving a talk at a prominent London hospital by the name of St. Thomas’, and the talk was addressed to immunologists. Professor Simon Murch came over after my presentation to talk specifically about the autoimmunity side of what we’re doing and trying to make sense of what happened when bacteria go in and try and re-communicate. Simon was telling me how a lot of his work on both allergies and inappropriate expressions of the immune system was based on the fact that with inflammatory bowel disease, obviously those who suffer from it know that there’s a massive disruption at the epithelial layer. Now, one of the features of our healing process is the moment we detect inflammation, we make masses and masses of immature stem cells and send them directly to the site of the inflammation to replace the broken cells, the ones that have been torn to pieces by the immune system.
Now, one problem here is that immature stem cells on their own are actually proinflammatory. They turn up at a site of inflammation, which isn’t too helpful sometimes, but on it’s own, it can be coped with. If we were then to introduce FMT or attempt a fecal transplant, bacteria are proinflammatory, so if you keep compounding the level of inflammatory agents on a site that’s undergoing inflammation, what do you expect to happen?! We have to stop patients coming in. They are desperate. “I’ve got a flare going on!” Great. Go back to your doctor. Bring it under control. “No, no! I need FMT!” No, no. You don’t.
Chris Kresser: Yes.
Glenn Taylor: What you need is to use whatever methodology is available to you medically to bring your inflammatory markers back right down to rock bottom so that you don’t have inflammation going on, albeit temporarily, albeit artificially, but you need to reduce your inflammation because when we put these little bacteria in, they will elevate the immune response.
Chris Kresser: Right.
Glenn Taylor: They just do. Even for patients without inflammatory bowel disease, we’ve got something that we call dip-day Thursday, Chris. Monday: Patients come in and start their process. We have the first implant on Monday after the initial cleansing process. Tuesday and Wednesday: Now the bacteria are starting to make their presence known, and there’s an elevation of immune markers. We see inflammation starting, only a small amount, but sufficiently that the patient notices, and they come in in terms, with almost flu or cold-like symptoms, now starting to really doubt if they’ve done the right thing, wondering about the wisdom of this whole treatment, beginning to panic. They’ve traveled a huge distance. They’ve paid a lot of money. “Oh, what have we done?!” And then we have to talk them in off the window ledge to translate that we didn’t tell you beforehand because you would then manifest it to happen, but everybody undergoes the little dip, and it always happens right about Thursday. Welcome to dip-day Thursday.
Chris Kresser: Right. Got it. Yeah, that makes a lot of sense. We’re dealing with something that’s almost equivalent to an organ transplant, and it’s been argued that it could be considered that. I mean, it’s not from a medical perspective, but we’re talking about infusing trillions of microbes into a dynamic environment that probably comprises 80 percent of our immune system.
Glenn Taylor: Yeah.
How C. difficile, colitis and multiple sclerosis respond to FMT
Chris Kresser: So it’s no surprise that there would be a significant response in an immune inflammatory disease.
Let’s look at the other side of the coin, though. If you had to pick a few conditions that you’ve seen over the years respond particularly well, in general—of course, everyone should understand that doesn’t mean it guarantees a response in their situation—but if there are certain conditions that tend to respond better than others, what would those be?
Glenn Taylor: OK, starting at the top, everybody knows about Clostridium difficile. We’ve developed a method of treatment, a treatment program, that not only gets rid of Clostridium difficile, but absolutely prevents a recurrence, and it simply was just doing it again and again.
One implant. Oh, look! We’re getting a 65 or 70 percent success rate! Really? What happens if we put two in? Oh, I don’t know! It’s never been done before. How about giving it a go?
The second one in. We now get 75 or 80 percent. Ah! That’s astonishing! That’s brilliant! Let’s call it a day. Really?!
You carry on until you get to the figure that you are looking for as an outcome. I want 100 percent. Five days implant—are you listening out there?!—five days implant doesn’t just displaces the Clostridium difficile, but also recreates the underlying microbiota with the essential diversity and density without which caused the problem with Clostridium difficile in the first place. For C. diff, that’s the easy falling off a log.
I would then say the next ones that are most common to us are that many doctors are referring their patients to us after a course of life-saving antibiotics and watching what goes on in their gut and going, “Whoops! I’ve saved their life, but I’ve set up another problem.”
Chris Kresser: Mm-hmm.
Glenn Taylor: So patients come in, and we restore their microflora, and that’s extraordinarily successful.
Then you move on to what most people are expecting us to begin with: IBDs, Crohn’s, colitis. We’re doing quite well on colitis, actually. The longer we’re allowed to treat the patient, the better the results, a little bit like Jack Nicklaus said. “The harder I practice, the luckier I get.” The point is that it’s not just, “Here’s the treatment program. It stops. If it works for you, great. If it doesn’t, oops.” There are conditions where we keep going. We have this built into the program, a communication with the patient where we’re continuing to supply updated implants for them to do self-treatment in their own environment.
Chris Kresser: Mm-hmm.
Glenn Taylor: We have some patients where we’re getting to one or two years before they start to see complete remission. And when I say “complete remission,” when we get a report back from their gastroenterologist who has just completed their last endoscopy, the camera going in, and then saying to the patient, “If I hadn’t known you’ve had colitis for the past 15 years, I would never have been able to tell. I can’t see a single sign of it when I go and have a look.”
Chris Kresser: Wow.
Glenn Taylor: That I call remission, and there are scales of it up until then. We don’t know. The immune system is one of the most difficult to understand and poorly understood systems in the human body. If we understood the immune system, life would be easy. But we don’t, so we have no clue how each and every patient is going to respond, not just that they have one type of disease, but everybody goes home to a different environment, and in that environment they’re exposed to a lot of environmental challenges. We don’t know what all those challenges are going to be. We don’t know how they’re going to respond. We don’t know whether they’re going to be able to stick to it as they should, compliance, so a lot of things are out of our control, and we sometimes have to just keep helping, keep helping, keep helping.
I have an MS patient who has been coming to us now for three and a half or maybe four years. Every six months, he comes in for a single implant just because he wants to make sure that everything is functioning correctly. He hasn’t seen a major reversal, but he had a progressive disease. We’ve arrested the progression. You can imagine he’s thrilled.
Chris Kresser: Absolutely.
Glenn Taylor: He’s working. He’s useful. He just created a brand-new family. He said, “This is my insurance policy. I’m going to keep going.”
Chris Kresser: Yeah.
Glenn Taylor: Now, we haven’t seen a resolution. What we’ve seen is a method of coping with it. And there may be patients out there who may have to go on a long-term program. For others, five, six, eight, ten days and it’s all over and done with, completely gone.
How Crohn’s disease responds to FMT
Glenn Taylor: Crohn’s is trickier. It always has been trickier, and of course, Crohn’s comes in and out of fashion with its triggers and the etiology, the basis of it. The origin of the disease is not really understood terribly well, and every once in awhile, somebody flies down a different track and says, “Oh, every third patient that I test has a bacterium that nobody else has, and this month it’s going to be called Mycobacterium avium subspecies paratuberculosis,” or something like that, where they’re going, “No, no, it’s the bacterium that’s causing it.” Well, I don’t know. I’m not sure if it is. It may have just turned up because its competitive good guy was missing, because you know they’re all antagonistic. If you take one out, there’s a vacuum and its friends don’t necessarily fill the void. It might be a pathogenic non-commensal that can now enter into the system because you’ve made space, you’ve taken away its competitor. So all these things are going on, and we still don’t fully understand.
Now, it’s the neurologicals that really have me interested. That’s hugely interesting.
Chris Kresser: Glenn, before we go on, I just want to ask you one question about Crohn’s. With ulcerative colitis—just for the listeners who aren’t aware—by definition, the disease is in the colon, but with Crohn’s disease—and this is one of the key differences between Crohn’s and ulcerative colitis—the disease can be anywhere in the digestive tract, starting in the mouth, going all the way down to the rectum. So do you see a difference in response in patients that have maybe Crohn’s in the small intestine versus Crohn’s in the large intestine?
Glenn Taylor: It comes back down to that magic word, the “etiology” of it. What is the cause? I know gastroenterologists specializing in Crohn’s whose first question to the patient is, did you or do you anytime get mouth ulcers, as a first indicator. Then can you stretch your thumb down to touch your wrist? You know how kids used to do this at school? It’d look gross.
Chris Kresser: Right!
Glenn Taylor: Or can you actually sort of bend your elbows out straight and it goes the opposite way, these hyperextensive joints, because they’ve made a very strong correlation between extended ligaments and Crohn’s. It seems to work as a marker.
With Crohn’s, as you know, Chris, there are three primary types, and our experience is that if we’re dealing with what is, I think, the most common, the ulcerating type of Crohn’s disease, which, as you correctly said, can appear in the ileum, the small intestine, and the duodenum, as opposed to stricturing, which is like somebody has put a rubberband around your gut and is closing it off. That’s a stricture, a closure. Or fistulating, where your gut is basically trying to find a second way out. It tries to bore a hole out from the wall at the epithelium. A tube starts to wander off in different directions, not always in the right direction. Now, these are all different methodologies or ways that clients present.
Back to the ulcerating thing, with ulcerating we get a better crack at it. We get a better response, but it’s still a tricky one, and I would say of our Crohn’s patients, it’s probably no better than 50 percent that respond. That’s because it’s autoimmune and we’re looking at how the immune system is attacking itself. We know in the gut it’s simply that cells aren’t recognizing each other and attacking each other, causing ulceration.
Now, whether bacteria need to be on site to stop those cells or whether we simply need to be changing the bacteria and utilizing the immune cells that are traveling through the bloodstream and getting close to where the bacteria are in the large intestine, where specific species of bacteria talk to T cells, T reg cells, and regulate their immune responses. I oversimplify things sometimes too much because I try to describe the bacteria in our gut. I’ll talk in terms of Apple Macs here because that’s what I use, and those of you on PC will just have to… well, you should have gotten a Mac!
Chris Kresser: Right!
Glenn Taylor: Your computer, your laptop, whatever, is you, and your immune system is the software that lives on that computer. That’s the software that makes it function. Now, that software is only good whilst it knows what’s going on. Every once in awhile, the software is out of date because stuff changes and there are new bits added on, or viruses get into systems and stuff has to be adjusted, and new programming has to be built. Well, bacteria are like the upgrade. Bacteria are OS 10.1.6. No, wait a minute, 1.7. Oh, hang on a second. They just thought of a workaround for that problem. It’s now 1.8.
Chris Kresser: Yeah.
Glenn Taylor: The bacteria, of course, rapidly replicate. They’re little bugs that grow in size, split in half, and are nearly almost identical to each other every time—almost. Every once in awhile, something changes and they mutate, but most of the time they’re making another one just like themselves. As their environment changes, so any little mistake, the mutation, if the mutation gives them a benefit in that environment, yeah, then it’s of really good use to them. If it doesn’t give any use whatsoever, it disappears off into history and nobody ever knows about it.
Stuff goes on around us. Our environment is literally changing by the second, and our immune systems can’t keep up. It’s as simple as that. They don’t know how to. They’re not replicating. They don’t know what they don’t know. So bacteria, being out in the world, seeing things, knowing what to do, constantly replicating, they turn up in the gut and go, “Hey, guys! I’ve just come from outside, and do you know what everybody else is now doing?” This is how it teaches the immune system. “By the way, this is what we’re going to do now because this is how we deal with it.”
So we have us, the computer; we have the immune system, the operating system; and the bacteria are today’s upgrade to the system. Does that kind of make sense?
FMT and weight loss
Chris Kresser: It makes perfect sense. I want to ask you a couple more questions about conditions that you’ve seen respond well or not respond, and then I want to go back and talk a little bit about bacterial diversity.
One thing, I’m sure, that’s on many people’s mind is that by now this has been so mainstream, this connection between obesity and the gut microflora. There were articles, I think, in Time Magazine, The New York Times. There have been popular books about it. There have been now some studies investigating FMT in humans, clinical trials to determine whether FMT can lead to weight loss in people who are overweight, so I’m just curious to hear what your own internal experience has been with that. First of all, have patients come to you with weight loss as their primary goal? And second of all, even if it’s not their primary goal and the main reason they’re coming to you is for a different condition, are they seeing any weight loss after FMT?
Glenn Taylor: Actually, yes. It’s unintentional, as well. Patients are reporting that. But then again, some patients who have not been able to eat correctly are managing to put a lot of weight back on.
Chris Kresser: Sure.
Glenn Taylor: That big story that everybody knows about, the press about the rather slim mother who acquired Clostridium difficile and chose her daughter to be her donor. The problem was her daughter was actually clinically obese. Or, no, she was morbidly obese, even worse.
Chris Kresser: Yes.
Glenn Taylor: And within a short term, one, it rectified the problem. Her Clostridium difficile was eradicated, and it saved her life. But the mix of bacteria that her daughter was carrying around created its own set of problems, particularly with the recipient who had previously had a really nice balance of her two large classes, the firmicutes and the bacteroidetes, which cascading down, there are many genera and species that come from those. The ratio between them is critical, and the daughter had the wrong balance because she had pre-existing obesity, and she gave those bacteria to the mother, who then struggled like crazy to bring her weight gain back under control.
Now, we already chose many years ago, many years before this incident, that we weren’t going to play around with the ratio between firmicutes and bacteroidetes, and we only chose donors who had pretty much a lifetime of natural slimness and they weren’t artificially trying to manipulate their body weight, because we knew the ratio ordered right there, so all our donors are actually really slim, lithe, athletic, and naturally so. That was the safe way to progress forward.
Chris Kresser: Sure.
Glenn Taylor: But the stories keep coming out. You almost have to consider choosing a professional donor, if that makes sense, or at least one that has been selected by a very, very careful process, and that will kind of help the situation.
Now, there is a lab in Paris. I was at a meeting last Tuesday, a week ago, where there are two specific species. They named them at the time, and I wouldn’t be able to repeat them now because I’ve been asked not to, but there are two specific species that are directly related to obesity. There’s manipulation of these two species going on at the moment in mouse studies again to make sure that now they’ve isolated those, that they can get reproducible results. That’s the key, that we still get the same results every single time. That should be quite big. These friends of mine in Paris are currently working on that, and I eagerly await that. Glenn Gibson is doing the same thing at Reading University.
Chris Kresser: Right.
Glenn Taylor: He’s the head of microsciences there. Glenn is also trying to make sense about “fat” bacteria.
Chris Kresser: Right. Creator of the word “prebiotic.”
Glenn Taylor: Exactly! My mate, Glenn Gibson!
Chris Kresser: Big guy in the field, for sure.
Glenn Taylor: Oh, absolutely huge. I keep tempting him to try and join us. Maybe sooner or later.
Chris Kresser: Good luck with that!
Glenn Taylor: We’ll see.
FMT and eczema and allergies
Chris Kresser: The last question I have about conditions is atopic conditions, so things like eczema, allergies. That’s another one we might predict could go either way, given that it’s immune dysregulation, so the same reason that it’s not always successful in Crohn’s could apply here, but what do you see with these kinds of conditions?
Glenn Taylor: Very frequently people with a gut dysbiosis, and let’s be honest, that’s what they arrive at our door with, all of them pretty much with that.
Chris Kresser: Yeah.
Glenn Taylor: They tend to talk about their skin conditions, saying, “What can be done?” And I say, well, at one point, I’m sure we’re going to do a controlled study on this, but at the moment, all I can tell you is it’s very, very common. Many, many patients turn up—perhaps the majority—turn up with some kind of skin condition, and as much as we try to advise them that this is not a cure for eczema, it’s not a cure for whatever you may be expressing with, but I have to say that we have an extraordinarily high level of remission. It’s one of those serendipitous moments. We don’t aim to do it, but the patients come in and say, “Look at the size of the patch on my skin! It’s half the size! Look! It’s stopped getting all flaky! It’s now just red!”
Chris Kresser: Yeah.
Glenn Taylor: We see that from days, weeks, months. There’s no real pattern. We can’t predict that yet. There are no markers that help us to translate that to the patient to give them the encouragement they’re looking for.
Chris Kresser: Well, that makes a lot of sense. One of my kind of pet areas of research over the past few years has been the gut-brain-skin connection. As a clinician, it’s common for me to see symptoms manifest in that triad. If someone comes in and they have depression or anxiety, they have eczema or psoriasis or acne, the first thing I’m going to be thinking about is testing their gut. For most of my patients, it’s not a surprise because they’ve been following my work and they expect that, but occasionally I’ll get a person who says, “What are you talking about, test my gut? I’m here for my skin or my mood problem.” But it is really remarkable to see that connection, and it’s not surprising, therefore, to hear about your experience with that.
Glenn Taylor: Yeah, sooner or later, people are going to start to make sense of this. We’re now getting doctors who are recognizing particularly the behavioral side of it, the depression, as a classic example of a kind of progressive part of IBS. They get to a couple of years of having IBS, and then they start to really worry, and then they’re put on antidepressants, and by the time they reach us, they’re popping antidepressants like crazy. And by changing the gut microflora, suddenly we see everything change. There’s an emotional element to it. There’s an endocrinological element, which I guess you can call emotional as well, where there’s definitely a hormone issue going on. There’s immunological.
Oh! I’ve got to tell you this one. You’ll love this particular case. This was only three months ago. Now, I had never, ever heard of chorioretinopathy. It’s a condition, shotgun chorioretinopathy, in particular. See! I can’t even say it! I had a patient contact me and say, “What can you do? How many patients have you treated with this?” And I said, “I can barely say it. I’ve never heard of it. I’m sorry, but I can’t give you any direct encouragement.” But I knew it was kind of an autoimmune, stroke, neurological thing—mostly neurological—and I said, “Well, before we go into that, can I just go back to my usual?” I have this set of questions I have written down—or I’ll forget them! These questions are, what was your mother’s health like? What was your father’s health like? All your siblings—what was their health like? Generally in the household, were people well? Did you eat well? Did you not eat well? What were the circumstances of your birth? Were you a vaginal birth? Were you birthed by Cesarean section? Were you naturally fed? Were you bottle fed? Were you sick as an infant? Were you sick at school? Were you coming home with everything? The usual kind of indicators that show what the critical acquisition period—the CAP is the first 24 months—to find out whether the child was actually born with the right bugs in the first instance.
Chris Kresser: Yeah.
Glenn Taylor: So I’ve gone through this with her, and she’s ticking every box. Then multiple exposures to antibiotics. She has really had everything and is starting to lose her sight. So she comes in for treatment. We are rectifying her gut microflora. We’re not dealing with her eyesight, not dealing with her neurological conditions. I’ve said I don’t know a thing about that. I’d be interested to record it every single day and take data because every patient is an incredibly valuable source of data for us.
So we get to day four, and she walks through the door. I happened to be in reception when she walked through the door, and she said, “Good morning, everybody! I can see leaves!” Now, it’s fall. We can all see leaves. They’re all coming down. It’s the time of year, so we’re kind of nodding, and she says, “No, no, no. You’ve missed my point. I can see leaves. Yeah, there’s a lot, and it was a bit blurry last night, but when I walk in in the morning to see you, trees are a blur. This morning… I… can… see… leaves.”
Chris Kresser: Wow.
Glenn Taylor: It got that silent in the clinic as well. We all were stunned.
Chris Kresser: Yeah. This is what obviously gets people excited, to see these kinds of reversals and improvements, and at the same time, as you said, there’s still so much we have to learn here.
One of the things that stood out to me about Justin’s presentation and one of the key arguments he was making is that species diversity seems to be one of the key mediating factors between the gut microbiota and illness, meaning the lower the diversity of species observed in the gut, the higher the chances are of modern disease being present. We have limited data on this so far, but it’s growing all the time, and so it seems to me that that’s perhaps one of the benefits of FMT and the way that you do it in some cases, where the FMT is coming from more than one donor, you’re increasing that species diversity.
Glenn Taylor: I am so pleased you slipped that one in! Thank you very much. I was chatting to a friend the other day. He’s one of your countrymen, Jeff Leach. His latest book is Rewild, and he talks a lot about bugs in that one. Jeff is the guy in west Tanzania working with the Hadza tribesmen. Jeff wrote in one of his books that this generation of humans has the worst diversity of microflora of any generation in the entire history of the species, and any hope to restore that microflora from our own number is likely to be a fool’s errand, or words to that effect. I talk to Jeff on a regular basis, and I said, “So when I create a stable of donors, each of whom is particularly good at something,”—because everybody lives in different places, don’t they, Chris? They all do different things. They have kids; they don’t. They exercise at a particular gym. They go running. They do stuff. They work in an office. They work outside. They eat different things because they like different things. Everybody does something different, and that means you remodel your gut microflora specifically to your environment. Some people are really good at some bacteria and not particularly good at others, so what you said about having multiple donors, that’s how it works.
We call our donors super heroes because they’re just nice people and they’re out to help people anyway, but these superheros have particular superhero skills or talents. It’s not x-ray vision or super-strength, but if you look at it in terms of, we have a Hulk, we have a Captain America, we have a Thor, they’re all great at something, but they’re not all good at everything. But when we put all our donors together and give one implant per day to the patients, they get the entire Avengers. Do I have to apologize to Stan Lee for that one?
How to increase species diversity in the gut
Chris Kresser: I don’t think so! But I do want to talk a little bit about some of the other ways of increasing species diversity that don’t involve FMT since, of course, not everyone, unfortunately, will be able to have access to FMT for a variety of reasons.
In Justin’s presentation, he showed some n=1, self-experiment data, which was really interesting to me. He mentioned that as a scientist when he first started studying this stuff, he was eating… I don’t think it was an unhealthy diet, but he wasn’t really particularly emphasizing his intake of what he calls “microbiota-accessible carbohydrates.” These are the types of carbohydrates that are fermentable by gut bacteria and that increase the amounts of beneficial bacteria that we have in our gut. He said that over time, as he was doing all these experiments in the lab, he just naturally noticed it was influencing how he and his family ate. He was sequencing his own microbiota throughout this entire period, and his species richness went from something like 550 or 600 to 1300 or 1400 over a period of time, where the only changes that he really made were to start consuming some fermented foods like kefir and sauerkraut and then also dramatically—dramatically—increasing his intake of fermentable fiber.
Glenn Taylor: Chris, do you remember the last time you and I went out for a bite to eat? I said something that was diversity on the plate equals diversity in the gut.
Chris Kresser: Absolutely. I sure do.
Glenn Taylor: Exactly that, and we put that to the test. With all our donors, we present to them a little challenge. Again, it was Jeff Leach. We set a little challenge on the basis that the diversity on the plate equals diversity in the gut. We spoke to all our donors because we have such a good working relationship with them, and they understand what we want and what we need. In one of our little bulletins or newsletters we send out to them, we set a challenge. We wanted them to try, based on the fact that the average person on the street eats about 25 different food groups in one calendar month—shocking, really.
Chris Kresser: Yeah.
Glenn Taylor: We asked if they could try to eat 100 different food groups in a month. It was a challenge for them. They went off around the supermarkets, and they were looking for different foods. They were going down different lanes, looking for different things they never picked up before. We had a number of them actually make a hundred or close to it.
Now, what they didn’t know was that we were actually recording the net result. How do we record the net result of our donors increasing the types of foods? Well, we were looking at those who engaged in the process and those who didn’t, and we could tell the ones who didn’t because the amount of microbiota that we can physically harvest and weigh accurately after we’ve put it through the laboratory is literally that. It’s recordable. Now, with those who were eating a broader diversity… and the lab staff didn’t know this because we kind of blinded the study, and we looked at the figures that are produced at the end of each day of the number of implants obtained from a given weight of sample, and we watched it rocket for those who were eating a broader diversity of foods. We were looking at, in some cases, a 60 percent increase in the net weight of the net microflora. That’s the beauty of the Taymount process. We’re not interested in all the other rubbish that gets thrown down the throat. We only want the bacteria. A 60 percent increase in the net weight of the microflora with those who had responded favorably to the challenge and started eating like crazy wild people looking for different foods. There’s our evidence.
Chris Kresser: Yeah, absolutely, and we have similar anecdotal reports from people like Justin Sonnenburg, and I just want this to be a note of encouragement for everybody. You can definitely increase your species diversity by consuming fermented foods, which have a much richer number of species in them than commercial probiotics, generally, even the broad-spectrum ones.
Glenn Taylor: Yeah.
Chris Kresser: And then also feeding those organisms, most of which are transient, but you can feed your own internal milieu of gut bugs by consuming fermentable fibers. I’ve talked about this a lot, and I wrote about it in my book. There’s lots of information out there about it, but one of the biggest differences between ancestral cultures and our cultures is that many of them consumed over a hundred plant species per day, like Glenn was just talking about, and the average American consumes somewhere between maybe eight and ten, if they’re lucky. And probably the average person living in the U.K., in the industrialized world. They’d be things like tomatoes, lettuce—things that go on burgers, probably, for the most part! Maybe carrots and broccoli.
And the other biggest difference, which Justin mentioned and has been mentioned elsewhere, as well, is the overall fiber intake. That is about 15 grams a day in the industrialized world, whereas in traditional hunter-gatherer societies—you mentioned Jeff Leach and his work with the Hadza—Jeff told me that, in his measurements, they consume somewhere between 100 and 150 grams of fermentable fiber a day.
Glenn Taylor: Can you see it’s not what you’ve eaten. It’s what what you’ve eaten eats. You acquire the bacteria at some point through the oral route, and they’re now living in your gut. Now you have to put something else down there. You have to feed them.
Diversity and density of the foods, as well, the things that the bugs are looking for. If you can’t pronounce it. If you’ve looked on the packet and you don’t know what it means on the packet, put… the… packet… back.
Chris Kresser: Exactly! I know the way I’ve said it, too, to my patients is with every bite of food you put into your mouth, you have to ask two questions: how will it nourish you and how will it nourish your gut bugs? It’s not always the same. Some foods will nourish your gut bugs more than they’ll nourish you, and that’s a very valid reason to eat something.
Glenn Taylor: While we’re on processed foods, just remember that bacteria are determined to survive in a difficult world, and the replication rate being super high, super fast, anything like six minutes, means that they’re constantly looking for opportunities to mutate to be able to get around changes in the environment, and that includes foods that are entering into the food chain that are not common to us, brand-new foods that are effectively being manufactured. Under normal circumstances, we wouldn’t expect to find them.
Now, one of the problems we’re experiencing is when you eat foods for which no commensal, normal bacteria would be normally breaking it down, other species or subspecies or mutated species will find a way of breaking those foods down. Now, what we don’t know is what those species are going to turn out to do, be, or make. Specifically, when I say “make,” they could, as a byproduct of fermentation, start to make neurotoxins. OK, now there are neurotoxins coming from foods that are not naturally available from the environment, but the bacteria, not knowing what to do, just carry on making stuff, and some of our new foods arriving on our plates that are manufactured compounds are starting to have effects we did not foresee.
Chris Kresser: Yeah.
Glenn Taylor: Be really, really careful with what you eat. When you look at the Israeli studies on sweeteners, artificial sweeteners, and how in place of normal gut microflora we were mutating bacteria that could break the sweeteners down, and in doing so, the sweeteners were creating neurotoxins, or the bacteria that were surviving on the sweeteners were creating neurotoxins.
The new Taymount Clinic in the Bahamas
Chris Kresser: Yeah. It is scary and there’s so much we don’t even know. What we don’t know about it is, in some ways, scarier than what we already do know. What we already do know is scary enough, and there’s so much more that we don’t know.
I know we only have a few minutes left here. Maybe you could tell us a little bit about what’s new for you. I know you guys have recently launched a new arm of the clinic or a new clinic. Tell us a little about that.
Glenn Taylor: Yeah, you mean the one very close to you.
Chris Kresser: Yeah, and in a nice warm place!
Glenn Taylor: We got a call from the Bahamas to ask if they could go into negotiation with us, and we did. Reluctantly we went over to see them.
Chris Kresser: Yeah, I bet. Too bad!
Glenn Taylor: And the net result is today there is a Taymount Clinic in Nassau, Bahamas, 25 minutes from Miami, and it utilizes the material from the U.K. We couldn’t really justify putting a laboratory into an area where the likelihood of finding good donors was just not good enough. So the material flies at -80 degrees centigrade. I know you guys work on Fahrenheit. I can’t, for the life of me, remember what that is.
Chris Kresser: Cold.
Glenn Taylor: It’s cold, very cold, so we keep them absolutely stable, and it takes just 28 hours, on average, from freezer to freezer in a super-freezer case that goes on express air freight over there. It arrives in beautiful condition and goes into storage, and they’re providing all the facilities. What’s more, because it’s in a hospital with all of the support facilities and they have a license from the Bahamian government to be able to apply across a broad range of subjects. When I was there in October we brought on a pediatrician, so they have a license now to treat children. Because we also have a neurologist on board, we now have a license to treat autism in pediatrics.
Chris Kresser: Wow.
Glenn Taylor: That’s huge. That’s what we can deal with over there, which we still can’t quite get to in the U.K. because there are a lot of hoops to jump through.
Chris Kresser: Sure.
Glenn Taylor: That was big. While I’m talking about us sending material over there, I only have a few seconds, but I have to get this out there because it’s critically important: quarantine. Quarantine, quarantine, quarantine. It’s absolutely vitally important. If you seek fecal microbiota transplant, be aware you can test your donor till—in the English expression—the cows come home. You can test and test, but we have some pathogens we harbor inside us that don’t expose themselves to the test until they are just about pathogenic or they’ve gone crazy inside you. You can test a donor and go, “The donor’s fine. They don’t have a disease.” Meanwhile, the disease wasn’t at a detectable phase, but they still have it. So you’ve taken a sample, you’ve processed it, you’ve given it to your patient, and then the patient expresses the disease. So the method that the world should be using is you harvest, you process, you quarantine for three months—magic three months. In three months, the donor will tell you whether they have gotten disease or not, believe me, because all diseases express within three months, all the ones that really matter to us.
Chris Kresser: Yeah.
Glenn Taylor: So whatever you do, ensure that you use safe, quarantined material. And just while we’re on the material thing, I realized from day one that foods in one person don’t work well in another, and I’m not going to use a donor who may have eaten peanuts and use their material in a patient who’s going to go into straight anaphylaxis. So I process out the food. Number one, out went the food. Then I wasn’t interested in whether it was a male or female at the peak of particular hormones or not. Let’s get the hormones out. So they are removed because we’ve had cases reported in the press of a female at the limit of her female testosterone receiving implants from males at the limit of their male testosterone and it having very complicated results for her, endocrinologically speaking. So throw out all the hormones.
Then mucus, all the toxins. Remember, we’re throwing out rubbish via our liver all the time, and if you are immunologically challenged, you do not want the toxins that your donor is throwing out. The essence is you just want the bugs. The microscopic material is the only thing that matters to you. Ensure that wherever you go it’s processed out to just the microbiome, that valuable little group of bacteria and fungi that live happily together, looking after your gut for you.
Chris Kresser: It makes sense. Glenn, it’s always a pleasure to have you. Thanks for taking time out of your busy schedule to join us. We’ll do it again in a couple of years, and I’m sure we’ll have tons more to talk about at that point.
Glenn Taylor: It’s always a pleasure, Chris.
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