Did you know that some of the bacteria living inside us are essential for our health? Gastroenterologist Ari Grinspan delves into the complex world of the microbiome in the human digestive system, and explains how transplanting bacteria from healthy people to patients with a debilitating, sometimes lethal, disease has had astonishing success—despite a method of transfer that might be a little surprising. This SciCafe took place at the American Museum of Natural History on January 4, 2018.
Podcast: Download | RSS | iTunes (1 hour, 59.1MB)
SciCafe: The Power of Poop — Podcast Transcript
MODERATOR: It is my pleasure to first introduce Dr. Susan Perkins, who will be introducing our speaker tonight. Susan in a microbiologist and curator here at the museum in the division of Invertebrate Zoology. She’s also the curator of the Inside You exhibition which you can check out in our Akeley Galley Hall. So please join me in welcoming Dr. Perkins.
SUSAN PERKINS: Before I get into my story to preface our speaker tonight, let me first say Happy New Year, everybody. We are looking forward to a great new 2018, and we’re happy you chose to start it here with us.
So back in November of 2015, we just opened the Secret World Inside You exhibit. My Colleague Rob DeSalle and I curated it. And in the process of developing it, we had a lot of laughs with our exhibit designers and interactive designers about how we were going to translate tonight’s topic, fecal transplants, to our public. And in the end, we all really loved this pinball-style game that we developed where you could shoot poop into a person’s gut and try to resolve their illness, and I know that our visitors loved it a lot, too. I used to spy on them.
But in a short time after the exhibit opened, that experience became very real and very personal to me. A few months after, my aunt, who had Alzheimer’s, it got too serious for her to be able to stay safely on her own. And so my family and I made the very difficult decision to find an assisted living center for her. And we found one that we thought was very well maintained, and the staff were friendly and engaging, and she was moved into it.
But a few months later, like so many people that are in managed medical facilities, she acquired an infection of clostridium difficile, or C. diff, as it’s usually called, and you’ll hear a lot more about it in just a minute. The C. diff infections are horrible. It’s like the worst weed you could ever imagine growing in a garden. It’s aggressive, it takes over your gut, and it gives people that have it a really horrific diarrhea several times a day. And it’s frequently resistant to antibiotics, which makes it extremely hard to treat.
And so when she got sick the facility quarantined my aunt, and in doing so, didn’t give her the right care. And a few weeks later, she collapsed from dehydration and was sent to the hospital.
And it was then that I had one of the hardest, strangest phone calls of my life from her doctor. He said to me, “That’s just how Alzheimer’s patients die.” And I said, “Haven’t you guys ever heard of fecal transplants?” And he said he’d never heard of them before. I felt flabbergasted and I felt helpless. And then a good colleague and friend here heard about my situation and put me in touch with someone that she thought might be able to help: tonight’s speaker.
So I contacted Ari and he helped me identify some people down in Florida that might be able to help consult. But at the same time, my dad fired her doctor, and a new, competent team took over. She responded really well to their treatment, she got discharged to a rehabilitation center, and I went down to see her as she recovered and very happily watched her start to eat food again, and she was even flirting with her very handsome, young physical therapist. It was a little embarrassing. He was cute, though.
The whole experience, though, I’m very sad to say, had taken its toll, and she suffered a stroke a few days after I left, and we lost her.
She was one of thousands of patients who die every year from C. diff, and the Centers for Disease Control estimated that in 2014, half-a-million people in the U.S. had this affliction. And the numbers seem to have improved, but it’s probably temporary, because, as we know, antibiotic resistance doesn’t usually go away.
All right. I’ve dragged the mood down a little, and I managed to do that without crying, so let me try to transform some of these sad feelings into ones of, I hope are motivation and empowerment. And that’s because we have microbiome science as a brand new and exciting field, and every day, researchers like tonight’s speaker are finding new links into how microbiomes in humans and other organisms are shaping their health. And they’re really shaking up these paradigms and changing science as we’ve known it.
Our previous president really saw that, and in his last year in office, he announced the National Microbiome Initiative, which was a bold partnership with federal, industry, and academic participation. And, for instance, as Kiera said, tonight’s SciCafe is sponsored by a grant from the National Institutes of Health where we’re trying to do something similar: linking biodiversity, including those of our smallest organisms on the planet, with human health. However recently, there have been proposed cuts to funding to entities like NIH and the CDC and numerous vacant positions across the system.
Jo Handelsman was the amazing woman scientist and the former director of biology in the Office of Science and Technology Policy, and it was her love for the microbiome and her understanding of its importance that really transitioned the president’s thinking in initiating this initiative. She left that position last January, and it remains unfilled. There is no current Presidential Science Advisor, and if you go to the OSTP websites, most positions say vacant. So if no one’s steering our national scientific ship, where is science going to go in the U.S.? And when will someone that you love’s life depend on that science?
Okay. Enough of my hardship, here. I’m really happy though, that there are people out there fighting the fight, fighting back, pushing on funding, getting that funding, and doing the cutting-edge stuff that we need to actually transform it. And tonight’s speaker is one of those people helping push back that darkness.
Ari Grinspan is an assistant professor of medicine and the director of GI Microbial Therapeutics at the Mount Sinai Medical Center. He is helping patients fight back against those C. diff infections using this bold new technology of fecal transplants, and he’s also exploring the potential for similar treatments of other diseases. Happy New Year. Please help me welcome him to the stage.
ARI GRINSPAN (Gastroenterologist):
Happy New Year. Thank you to the wonderful folks here at the American Museum of Natural History to invite me to talk about my passion: shit. My mother’s very proud.
These floating things that you’re seeing here are bacteria. Bacteria have a really bad reputation. So a hundred years ago, if you lived anywhere in the world, you were going to die most likely by one of these bacteria: an infection. Whether it was pneumonia, whether it was the flu, whether it was tuberculosis or another infection of the gut, like some sort of dysentery, an infection was going to get you. Now, 2018, an infection is not even in the top 10 reasons why we die. Other things get us: cancers, heart disease, strokes. But the idea of a bacteria still sits inside of us as, ooh, we should kill that. We don’t want that to be in our system. Take that antibiotic.
Well, turns out that’s one of the worst things you can do for yourself, because these bacteria are vital for our health. We grew up with these bacteria. We evolved with these bacteria. They help us and we help them. It’s a very symbiotic relationship. So my microbiome... And let me preface that. What is the microbiome? Microbiome is a complex connection, interaction, structure of these bacteria within a habitat. And I will be focusing on the gut microbiome; the collection of these bacteria; the proteins that they produce; the DNA that they have and how that interacts with us, and it is so incredibly important for our survival.
So my microbiome is very different than yours and different from the person next to you; different from a person in China or rural India or in Westchester. Our microbiome began at birth. So when you were in utero, there was no bacteria in you. The first contact you had with bacteria was with how were you delivered? Were you a C-section baby, or did you come down the birth canal? That will determine what the first bacteria you have, and there are very clear differences. You can tell, just in the microbiome, you can separate C-section babies from vaginal delivery babies, and that can last for a long period of time.
Up until the age of three, your microbiome can change depending on what you eat, were you breast-fed, were you a bottle baby, did you get an antibiotic for an ear infection? That will dramatically alter your microbiome. And then at the age of three, things sort of stabilize for a long, long period of time. Now, don’t get me wrong. If you go to Mexico City, if you go to some place and you come back with a little Montezuma Revenge, your microbiome will be different for a period of time, but then it usually comes back to its homeostasis.
Because your bacteria are a community, and they like to support one another. They support you by helping you digest certain foods. They support you by telling you, ooh, there’s a bad bug, here. This doesn’t belong in our community, and you can prevent it from causing a problem. So they protect us, and we protect these bacteria. We feed them every day multiple times a day, and they love it. And we give them a habitat to live in that’s protected from the bomb cyclone that’s coming tomorrow.
I am—well, I think I am—an average human being. I have about a trillion cells, human cells that make up me. But in my gut, I have 10 trillion bacteria who are not all bad. So I am 10% human and 90% bacteria. It gets a little bit more complicated, because the blueprint of human life is DNA. So if you take the DNA that is within me and look at it, you’ll find that 1% of the DNA in me is human, and 99% is bacteria. This relationship is incredibly important, and we’re just beginning to investigate it. For a long period of time we ignored it, because we didn’t really know that it even existed. Oh, but it exists, and it’s incredibly, incredibly important. Because when things go awry in the microbiome, it can affect you and it can cause problems.
I’m going to talk about the posterchild for how to look at the microbiome. It’s an infection called C. diff that Susan mentioned to you just a moment ago. It is a very bad bug. This is the human colon. This is, actually, this is a beautiful-looking human colon. I mean, I would eat off this colon. No, too much. Too much. This is a beautiful colon. It is healthy, it is vibrant, and there are trillions of bacteria that you cannot see floating around and [attached] sort of to the lining. C. diff, when it gets inside of the colon, causes that. Yeah. That is a sick colon. In fact, I don’t even want to look at it. It’s pretty gross.
So how does C. diff even get there? So you have 10 trillion bacteria, and the most important thing about this 10 trillion is that it’s diverse. You’ve got bacteria coming from different species, different phylum, different everything, and they all come together as one unit, and that unit is there to protect you. The problem happens when you get an antibiotic to treat a pneumonia or a urinary tract infection, or maybe your doctor gave you a CPAP for that sniffle that you got.
Okay, if it’s a pneumonia or if it’s a urinary tract infection, that bacteria that’s causing it is causing you harm, so the antibiotic is appropriate. Get rid of the infection, and you’ll get better. But it doesn’t just kill the bad bacteria. It kills a lot of the microbiome in your gut, and you get a contraction of this rich, diverse microbiome. You could lose the diversity. You lose the richness, and then you become susceptible to certain things. In this case, C. diff.
Now, the problem with C. diff is I can treat it with antibiotics, I can control it, but your microbiome is still so not where it should be. It’s contracted. So if I get rid of the infection and your microbiome is still in this low state, the C. diff comes right back, and it comes back again and again and again, and it’s a classic story. We call it recurrent C. diff. It causes 30,000 deaths per year just in this country. It costs $4 billion in extra healthcare costs to take care of patients who have recurrent C. diff. It’s a bad bug. It’s an expensive bug.
So then there is something called... So if the antibiotics don’t work, what can we do? Well that’s where fecal transplant comes to be. Fecal transplant is the idea is, okay, I’m going to take somebody else’s healthy microbiome, and I’m going to transfer it to the patient with the low microbiome—with the no diversity, the lack of richness—and I’m going to expand their microbiome. And hopefully that will cure the infection. It turns out it does it so remarkably well that it blows everybody’s mind. Antibiotics work for this recurrent C. diff infection maybe 30 to 50 percent of the time. A fecal transplant cures it more than 90% of the time. We don’t see these dramatic differences in modern medicine: 90-plus percent versus 30 to 50 percent for standard of care. This is dramatic. But it’s a little icky.
So when I first starting doing this, five, six years ago and patients would come to my office for C. diff and I’d be like, “You need a fecal transplant,” and they’re like, “You want to do what? You’re going to put what in my butt?” And I said, “No, no, no.”
So I don’t use shades of brown when I’m talking about this. I use shades of green. It’s life. It’s wonderful. Look at that lawn. You could eat off that lawn. Okay. Imagine that healthy lawn as your microbiome. Every blade of grass is a healthy microbe. It’s beautiful. Well, something happened to you. You got an antibiotic. You had a contraction, a decrease in your microbiome; less diverse, less rich. Then you get these dandelions. You got C. diff. Now, I don’t know how many of us actually have lawns, being in New York, but if you did have a lawn, you would try to kill that dandelion with weed killer. You spray the weed killer at it, but the dandelions keep coming back. You throw the antibiotics at the C. diff, but the C. diff keeps coming back. So the idea behind a fecal transplant is we need to re-sod your soil. We need to repopulate your gut. Re-poop-ulate your gut. I wish I coined that term. I didn’t, dammit. Re-poop-ulate your gut to bring it back to health, and that’s the idea behind a fecal transplant.
Now, there’s nothing new here. Fecal transplant is an old therapy. It was first done in fourth-century China. The Chinese physicians would use a fecal slurry, give to patients to treat anything from diarrhea, constipation, abdominal pain, and my favorite, nausea and vomiting, and they actually had success.
Now, it lost favor for a long period of time, and then it showed up in the English literature in 1958, where a professor in Denver used it to treat patients who had this in their colon. Now, he didn’t know it was C. diff. He just saw this, the patients weren’t getting better with antibiotics, and so he looked in where most doctors look about how to treat things we don’t know: in the veterinary literature. Nobody actually does that. But he did, and he found that horses who had dysentery and similar findings, if you feed them healthy horse manure, they get better. So he took the spouses of these patients, and he gave them fecal enemas from the spouse, and all four of those patients got better. It made a small splash in 1958 and then lost favor, because people were like, that’s ridiculous.
And in the ‘80s and ‘90s and even the early 2000s, it remained on the fringes of medicine until the landmark paper in The New England Journal of Medicine showed that fecal transplant: 90% cure rate, and standard of care of antibiotics: 30% cure rate. Again, you don’t see these kind of things in modern medicine. And then all of the sudden like, whoa, whoa, whoa. Yeah, fecal transplant, of course. Of course. We’ve known it all along. Now, it took a long time for people to really get on board with this.
Now, is that what we’re doing, here? So how does this whole process work? Is it just me re-poop-ulating the gut with healthy bacteria? So this is what our patient with C. diff looks like before their transplant. This is their bacteria. This is what we call microbiota disarray. And this is the donor. This healthy swab of orange is healthy bacteroides; these wonderful, healthy bacteria that we all consider to be a normal part of our gut. And so we give this to the patient, and this is what the patient looks like two weeks later: remarkably similar to the donor. If you look at that patient a month after their transplant, they look like this. So not like the donor, they share some similarities, but the patient is healthy. No C. diff. Feeling great. Playing tennis.
What we don’t know is, is this what the patient looked like before C. diff, or is this their new normal? We don’t have that information. How much of this donor stool, these donor microbes, how many of them stayed in the patient? We don’t have that information. And then it begs the question, well, who’s going to be your donor? So I get that question all the time. Okay, I want to do a fecal transplant, they sign up, okay, okay, great. Wait, whose shit are you going to use? And then I say, well, whose shit do you trust?
So we used to ask the patients, all right, do you got a brother or sister or mother, a spouse, family friend, the guy at your office who goes to the bathroom like clockwork every day? Like who do you want to use? So they’d have to give me a donor, I’d have to screen them, make sure that they were safe, so similar to as if you were going to be a blood donor, and then some. I had to make sure that they are healthy, they don’t have diabetes. They can’t be too big, they can’t be too small. It’s gotta be Goldilocks poop, or something like that.
They’d come, they’d have to produce the sample—the drug—on the day of the procedure. Now, you’ve heard of stage fright. Imagine me [unintelligible] like, hey, I got things to do, man. You gotta... That gets a little problematic. Well then they’d have to produce it, I then take it across the street, and make what we call the dirtiest martini. And then I bring it back, I do a colonoscopy to administer the drug; the fecal slurry. Because the problem is in the colon, I want to deliver it exactly there.
Would you like to see it? [Guard] your loins. Again, sick C. diff colon. What you’re going to see is a fecal transplant in action. So it’s moving because the patient is breathing—that’s good—and here it is. Boom. That’s the money shot. Too much? Too much. So this is wonderful. This is happy. This patient was in the hospital three times over six months with C. diff. Went to hospital to hospital, got multiple courses of antibiotics before coming to Mount Sinai. A young woman with ovarian cancer, she couldn’t function for the past six months prior to this. And this is what she looked like a month later. She walked out of the hospital. She was an avid tennis player, she was able to play tennis, and she is picture perfect health. Pretty remarkable.
But the whole process is pretty cumbersome. We don’t like to screen donors over and over again, so we don’t do that anymore. I import my poop. You’ve heard of blood banks, you’ve heard of sperm banks, but have you heard of stool banks? They exist, and they do all the things for me. They screen the donors, they make sure that they’re healthy, they make sure that there’s no diseases, they process the stool, they put it into a nice little canister, they freeze it for me—I don’t know if you know this, but fresh poop is just as good as frozen poop—they ship it to me via UPS. What can brown do for you? And I have a treasure trove in a freezer in my unit that I can use when it is required. So they always ask me, “So, wait, wait, wait. Where is this bank?” And I tell them, “It’s in Boston, and they usually screen Harvard and MIT students, so it’s smart shit. You’re welcome.”
But again, this whole thing is cumbersome. I still have to do a colonoscopy, it’s invasive, there’s anesthesia, you have to take a bowel prep, and people with C. diff, they don’t want to take anything that’s going to give them more issues.
So the future of this is the crap-sule. It shouldn’t be brown. We should probably fix that. But this is developed. We have this. It’s not quite ready for primetime, because there’s a lot of technology that goes into delivering this product. First of all, you don’t want it to release too soon. That would be a bad burp, oof. Again, I crossed a line. Too much, okay. But I don’t know what I’m supposed to put in it. Do I put the entire microbiome like I do via colonoscopy, or do I just take sections of the microbiome; some of the species; some of the bacteria? And that’s what we’re trying to figure out.
For C. diff, this bad infection, fecal transplant is a homerun. It’s rare in medicine that you find something for such a bad disease that just knocks it out of the park, and fecal transplant does that. And so if fecal transplant can be so remarkably effective for C. diff, where we think that the issue is with the microbiome being... we just need to restore the microbiome, can we take that to other disease processes?
Now, there have been a number of diseases that have been associated with changes in the microbiome. But association does not mean causation. And I don’t know if that change in the microbiome may have led to the disease state or if the disease state led to the changes in the microbiome. You name a disease, and there’s somebody who can show that there’s changes in the microbiome. Notably autism, multiple sclerosis, heart disease, diabetes, obesity, liver disease, inflammatory bowel disease—which is what I focus on—including Crohn’s disease, ulcerative colitis, and a number of other conditions.
But again, I don’t know—and nobody knows—is if the microbiome led to that problem. C. diff is easy. It’s a bug. The infection. Get rid of the bug, you’ve cured the disease. But all the things I just mentioned to you, there’s no single infection, single bug that causes these diseases. It’s multifactorial. Maybe the microbiome has a role. Maybe. But there’s genetics, there’s the environment, there’s your immune system—whether it’s overactive or underactive—among other things. So it gets all very complicated. So while the association may be there, I don’t know if we can be—and I doubt—that we’re going to have a homerun by changing the microbiome to affect the other disease process that I just mentioned.
But with the research by investigating the microbiome, and we’re at this explosion of research that’s going on, maybe we won’t find a new therapy for some of these conditions, but maybe we can prognosticate. Maybe we can identify people who are going to be susceptible to certain diseases later in life and potentially enact prevention strategies to prevent that disease from coming on later. That would be a wonderful outcome from all of this.
The microbiome is incredible, and there are so many secrets that we have yet to uncover. There’s all this crosstalk between the bacteria that are floating in our gut and in lining of the intestine. Now, we don’t have Rosetta Stone yet. I don’t know what they’re talking about. We’re trying to figure that out. And maybe what we can do is, once we figure out the conversation, maybe there will be ways that we can manipulate the microbiome to change the conversation; to change maybe some of the outcomes of certain diseases. That would be another wonderful outcome.
I’m going to leave you with three things before I stop the talk. Number one, don’t do this at home, okay? Don’t treat your headache, don’t treat your hangnail, don’t treat your abdominal discomfort with a fecal transplant. Leave that to the professionals. I need the business. I’m kidding.
Fiber. Fiber is your friend. If you want to promote a healthy microbiome, if you want to augment your microbiome for a health purpose, fiber is your friend. Don’t go to the local drugstore and buy all of the probiotics off the shelf, okay? That’s not going to do it. Fiber is your friend.
And number three, as my father always says, wear your seatbelt. Thank you very much.
Now, I’m very happy to answer questions, but let’s not make this personal. And I don’t want to hear about your “friend.” We know it’s you.
MODERATOR: So a huge thank you again to Dr. Grinspan. As I had mentioned to Ari previously, he’s way too cool for stool, and we’re so happy to have him here.
GRINSPAN: Thank you.
MODERATOR: So as always, we have two roaming mics, and we’ll try to get to as many questions as possible. We’ll also be taking some Twitter questions, #AMNHSciCafe.
AUDIENCE QUESTION: I’m curious, what other cures from veterinary medicine have helped humans?
GRINSPAN: I am not aware of much. Well, smallpox. That was a... So cowpox, we got the vaccination for smallpox from cowpox. So perhaps that. But beyond that, not my forte. I stay with the humans as much as I possibly can.
AUDIENCE QUESTION: So I rarely take antibiotics, but I know people take probiotics, and I’ve heard that, once it gets in your gut, it doesn’t get to where it needs to go. So if you do end up needing to take antibiotics, how can you rebuild your microbiome in a good way?
GRINSPAN: Well, I think there’s two important questions in there. She’s asking, people take probiotics and it maybe not gets to the right place. And if you take an antibiotic, how can you then restore your microbiome?
So regarding the probiotics, I think that’s an important question. I’m sure a lot of people have questions about that. Depends on why you’re taking the probiotic. So a lot of people take probiotics just for general health, and I have no idea why you’re doing that. Don’t waste your money. If you’re okay and you’re normal, to take a probiotic. I don’t think it’s dong much for you.
There’s been a lot of data out there looking at the role of probiotics in certain diseases. One of them is antibiotic-associated diarrhea, and that is an indication where I would recommend a probiotic. If you’re going to take an antibiotic, take a probiotic. It’s certainly not going to hurt you, and it may prevent you from having... Frequently people get diarrhea when they take antibiotics, and it can help prevent that.
A lot of people take probiotics for irritable bowel-type syndromes, whether it’s abdominal discomfort, bloating, diarrhea, constipation. And maybe there’s a role there, but the data is very weak. We typically do recommend it because it’s something that you can do, and I’ll tell you from my experience, there’s a very large placebo effect there. I can tell you that upfront.
The probiotics that you take, that you buy over the counter, a lot of them contain lactobacillus: lacto-bacillus. It was grown in milk. Do you have milk in your colon? No. You do not have a lot of lactobacillus in your colon, so it’s just not the right probiotic to take to reestablish your gut flora. There are some other ones on the market that might be a little bit better, but a lot of them are not designed from human gut. They’re designed from other sources that you’re trying to sort of just put in there.
So probiotics, there’s a lot of press about it. The most important thing about probiotics is that they are medical foods. They are not governed by the FDA. They are not drugs, so they don’t go through that regulatory process. So you can take one lactobacillus from company, and it’s completely different from what another company might produce. So choose cautiously if you’re going to go down that route.
AUDIENCE QUESTION: Hi. I was just wondering, we talked about a lot of the pros of the fecal transplant, and I was wondering if there were any risks associated with it.
GRINSPAN: So if you read the early literature, there’s like no risks whatsoever associated with a fecal transplant. Well, that’s not true. Currently, we’re giving fecal transplant via colonoscopy, so all the risks that are associated with a colonoscopy also go along with the risk of giving a fecal transplant, because you have to—at least at this point in time—the vast majority of people who are doing this are doing it via colonoscopy. So those risks apply. The most common things that we see after a fecal transplant are abdominal bloating and either diarrhea or constipation. And the most common thing that we come across is something called post-infection irritable bowel syndrome.
So when C. diff, it causes problems in the gut. Your microbiome gets in complete disarray, and it could cause functional issues with how your colon works. So it’s not uncommon that people will develop IBS after any kind of gastrointestinal infection. Very, very common. And the same applies with C. diff. So when we get rid of the C. diff via fecal transplant, we see 20, 25 percent of patients who will have altered bowel habits for a period of time. Now, it’s hard to separate, is that from the C. diff or is that from the transplant? Unclear.
The microbiome has been associated with all these different medical conditions, so if there’s alterations in the microbiome that could potentially lead to other disease states, if I transmit the fecal matter—the fecal microbiota—from one patient, one person to another, do I also bring with it all the susceptibilities of that donor? So if a donor in 10 years was going to get diabetes or high blood pressure or cancer, do I then transmit that risk from the donor to the patient? We don’t know. We haven’t seen it, but it doesn’t meant that it’s not going to come up in the future.
And so there’s actually the AGA, the American Gastroenterology Association, we’re starting a 10-year follow up. So every patient who gets a fecal transplant, we’re going to follow them for 10 years and see if anything happens to them along the way that we could then attribute to potentially the microbiome transfer.
AUDIENCE QUESTION: Hi. Is there any research being done on whether fecal transplants would have an impact on some of the other diseases we talked about, particularly the gut diseases like Crohn’s disease or colitis?
GRINSPAN: So that’s my research. So we partnered with a group in Australia who, frankly, they don’t have an FDA in Australia, so they can do all these very cool things, and then we can take their samples and take a look and see what happens. So we’ve partnered with a group in Australia, and we just published an article earlier this year about ulcerative colitis.
And what we found is that in this population of people who had moderate disease, 25% of them we could put into clinical and endoscopic remission, meaning there was no evidence of disease after they got series of fecal transplants. And in this one cohort, they got 40 of them. They were done by enemas. Forty enemas over eight weeks. That’s a lot of poop. No one is ever going to redo that trial. It’s just way too hard to do. But if you compare that to a couple trials that were done over the past two or three years, that 25% sort of holds true.
So the interesting thing is, why 25%? Why not 50? Why not 75%? What is it about the 25% of patients with ulcerative colitis that we could improve their symptoms? And that’s what we’re trying to figure out. Is it something about the host? About the person with the ulcerative colitis, that that’s the reason they responded; something about them? Or was it something about the stool that they got? So that is what we’re working on next.
Beyond ulcerative colitis, it gets very, very wishy-washy.
AUDIENCE QUESTION: Hi. Isn’t it true that C. diff is present in all First World humans, and it’s not just presence, but abundance, that causes the infection?
GRINSPAN: Good question. So C. diff is everywhere. It’s on the floors, it’s in the ground, it’s on our skin, it hangs out everywhere. We find more of it in First World countries probably because we’re using antibiotics more. But in the early 2000s, there was sort of an explosion of C. diff. Thirty years ago we knew about C. diff, but it wasn’t like the biggest deal in the world. But there was this hyper-virulent strain that hit Europe, Canada, United States in the late ‘90s, early 2000s, and the rates of C. diff skyrocketed, and it was a very bad strain and it caused a lot of disease. So we see a lot more of it in the developed countries. Whether or not we see it less or we just don’t hear about it so much in the other countries, that, I can’t give you an answer on.
And in terms of abundance, the bug itself, C. diff, it doesn’t hurt you. The bug itself doesn’t hurt you. If it creates a toxin, it’s the toxin that causes the diarrhea. It’s the toxin that causes that massive inflammatory process that you saw in that picture. The bug itself, it’s okay. Don’t treat just the bug. But if the bug makes a toxin, then absolutely you have to treat it.
So it’s less about abundance and more about if it’s making toxin or not.
MODERATOR: So we have our first Twitter question for you. The Twitterverse wants to know what your favorite source of fiber is.
GRINSPAN: I’m a kimchi boy. Love me some kimchi. Fiber comes in many different forms. Any kind of fruit, vegetable, grain, bran, you get a rich source of fiber. Some of them will, if you eat too much of them, can be a little gas producing. And there’s something called a FODMAP diet, I don’t know if many of you have heard of it, but the FODMAP diet tries to incorporate fiber into your diet without getting that unfortunate gassy symptom. But again, for me, I like cabbage. I like kimchi.
AUDIENCE QUESTION: Hi. So I have two kind of unrelated questions that I couldn’t choose between, so I’m going to ask you both of them.
The first is, have there been studies where you’ve taken patients with inflammatory bowel disease, let’s say ulcerative colitis, and just analyze their stool and just get huge banks of information to see what’s in the stool of a person who has inflammatory bowel disease, just to understand their makeup so that maybe we wouldn’t have to rely on the fecal transplant—which I think is phenomenally fascinating—but rather isolate what it is that’s so interesting, or what we can identify that is their makeup so that we don’t run the risk of potentially opening up risks for other medical conditions that may not have manifested yet in the donor that we don’t know that we’re transmitting to a patient who is getting the immediate benefit but maybe some changes in their own microbiome down the road?
So the first question is, are we studying patients that may not be really sick but have underlying conditions to see what their makeup is so we can maybe more target the transplants?
And then the second question is, do you have any thoughts about SIBO? So it’s kind of this small, intestinal bacterial overgrowth, and we measure this and we are treating this now with antibiotics very often. And so we’re talking about this tremendous—all the bacteria that’s so valuable inside of our intestines, and then we’re saying that some people have too much of it, and we’re going to treat it with antibiotics to make them better. And do you have any thoughts about that?
GRINSPAN: So two good questions. One is about inflammatory bowel disease. So Crohn’s disease and ulcerative colitis, that’s what makes up inflammatory bowel disease. And those patients have tremendous amounts of diarrhea, abdominal pain, and bleeding. It’s a very common disease, and it’s something that I specialize in.
So we have looked at the microbiome of patients with IBD, with inflammatory bowel disease, and there’s clear differences between those with IBD and those without IBD.
It’s hard to find the patients who are not on treatment. So the medications that we use to treat IBD can also affect the microbiome. But if you look at naïve—so patients who have not have any medications, naïve to medications, they have IBD—you can detect there’s clear, what we call, dysbiosis. You have a lack of diversity, and there’s enrichment of certain species that are associated with pathogenicity. The problem is is, how do you remove those? And is it remove those bugs, or do I need to put different bugs in? And what is the community structure? It’s very complicated.
And so computational biologists are looking at that, to look at the structure of the microbiome to see how we can manipulate it to change the overall function of the microbiome to health as opposed to one that favors inflammation. It’s hard. People are actively looking at it, but there’s so much data, and right now, it’s just data. It’s hard to actually analyze it to make any sense of it. But that is the future. And the future’s going to be a designer FMT. I’m not going to give you the whole thing; I’m going to give you what you’re missing, the functions of the microbiome that you’re missing, as opposed to just this species, like a probiotic. So that’s the future.
Your second question: small, intestinal bacterial overgrowth. This is a condition where you’ve got a lot of bacteria in the small intestine; not the large intestine. A big in the small intestine, and your small intestine can’t really stretch so much. And so you get a lot of gas that’s being produced in the small intestine. It can cause a lot of bloating and discomfort.
The mainstay treatment is to give antibiotics. So you’re going to wipe out all that excessive bacteria in the small intestine, and people get better. The problem is is that frequently the underlying problem hasn’t been fixed, and so the bacteria just grow back up again, and then you need to give them another couple of courses of antibiotics every few months, or whatever it’s going to be.
So I don’t like to treat SIBO. I like to use other ways, dietary modifications to try to reduce the bacterial load. Changing their fiber intake might actually be very helpful, and I find that working with a nutritionist is actually the best way to do that; one who actually knows how to handle small intestinal bacterial overgrowth.
There’s actually been some reports that fecal transplant can help, oh, but maybe it can worsen SIBO. So the jury is out on that, and I do not recommend using fecal transplant for that purpose, but good questions.
AUDIENCE QUESTION: First off, thank you very much. First question: so if what we eat matters with regards to fiber, would that also be true with, say diets and people who have maybe less diversity in what they eat? So for example, indigenous communities, vegetarians, vegans, strictly meat eaters, which you might see in different groups around the country or around the world? So should my friend, who might be a vegetarian—
GRINSPAN: Yes, yes. Your friend.
AUDIENCE QUESTION: —have to worry about diversity with this? Or like my friend might have to worry about, say, other vitamins and other things we might get from our diet? So that’s the first question.
And the second question would be basically, is there a way to adjust this over time? So if my friend has been a vegetarian for, say, 33 years, can my friend reverse anything that might come from this? Is this something that we should be mindful of?
GRINSPAN: “My friend” has a lot of medical problems. “My friend” always has the worst stuff. The key to the microbiome... So let me give you an example. There’s a great example in mice, because that’s where we can do all these crazy microbiome studies, and you can really control the diet of a mouse. If you change the diet of a mouse from a balanced diet of protein and fiber and you take away all their fiber, or just give them just a touch and you make it almost all protein, those mice die pretty quickly. They lose a tremendous amount of weight Atkins style. Kidding. Don’t do that. They lose a tremendous amount of weight, they get inflammation of their gut, and they die. If you look at the microbiome, what happens is you see a... it like falls off a cliff. You get a dramatic reduction of the microbiome in these patients—or in these mice, I’m sorry.
It’s very hard to do that in humans. Controlling a human diet requires them to be in a hospital setting where you control exactly what they’re getting. And even then, they still cheat. Their friend brings them a Snicker bar or a celery stick. I’ve seen it. It’s ridiculous. Who brings a celery stick to a friend in the hospital? I don’t...
But to your point about being a vegetarian, as long as you’re getting... So clearly you’re getting fiber. And as long as you’re getting protein from non-meat products, then you’re going to be okay. Even if you are a vegan, as long as you can get the protein, you’re going to be fine. It’s all about finding your balance. There are plenty of people who are vegans or vegetarians or whatever the newest rage is, raw vegans—I don’t even know... I don’t even know what that is anymore—that they’re okay. The problem is, it’s hard to study their microbiome, because yeah, they can sneak things in that they don’t even realize, and then it completely will change the outcome of the study.
AUDIENCE QUESTION: You mentioned one of your favorite fiber sources is kimchi. It’s somewhat trendy now to eat things that are fermented or supposedly alive: beer and wine, kimchi, sour kraut, yogurt. Is it anything particularly good about those things, or is that just kind of a trend without much support?
GRINSPAN: So when you eat kimchi—where are we going? I know a place. When you eat kimchi or these fermentable foods... Okay, so you drink beer, right? You drink beer? You know how we make beer. You take wheat and yeast. The yeast goes onto the wheat, the yeast ferments the wheat, you get alcohol—yay—but you also get that natural carbonation. Beer is naturally carbonate, not like seltzer when we’re pumping the CO2 in, okay? So fermentable foods tend to be ones that the bacteria go after. They are the ones that ferment the kimchi and ferment the cabbage and ferment the cauliflower and the broccoli and all of those gas-producing foods that may make you feel a little gassy and bloated after the delicious meal.
So that’s why they are considered good for the microbiome, because they are fermentable, and that’s how these bacterial will get their food supply.
AUDIENCE QUESTION: My question’s actually related to a previously SciCafe we had on the microbiome. And specifically, it gave examples of microbiomes of hunter-gatherer populations, of subsistence farmers, and then people from the First World.
And I’ve got two questions, which is first of all, given that there’s a much restricted microbiome in first world populations, is anything of what you’re doing trying to reintroduce some of the lost strands of species of microbiomes from First World populations that still exist in hunter-gatherer and subsistence farmers?
And then the second one I was wondering was, within the First World population, are there differences based on diet as processed food versus sort of more regular food that would be more similar to what subsistence farmers would eat, and also within populations that were more recently migrated to the first world? So, I don’t know, somebody from the Andes or Somalia or something, versus somebody who’s been in the U.S. eating processed food for, not generations, but you know, one or two generations.
GRINSPAN: So there’s clear differences between different populations about what they eat, where they are, and what they’re being exposed to. So they have the 23andMe where you can see if you’re actually from Ireland or if you’re actually Jewish or all these things. You can do similar type things based on what species of bacteria are, and you can sort of say, oh, you must come from someplace over here. But it’s not perfect.
And your microbiome, while even, you get up to the age of three, it’s sort of stable. Only 50% of it or so is stable. The other 50% sort of fluctuates depending on what you ate yesterday, where you travel to, did you get an antibiotic? Did you get a new pet, okay? Your microbiome, that 50% can change. But the bottom part is going to be pretty stable.
Now, when people transfer, when they move... So there’s this guy who tracked his microbiome like on a daily basis for years. And he traveled, I think, I don’t know if he went to Thailand or Vietnam, and he was there for a period of time, and you can see his microbiome was dramatically different. Then he got sick, and his microbiome changed again. And then he went back to California—lived in San Diego—and after a very short period of time, his microbiome went right back to where it was before.
So you can get these perturbations, absolutely, but usually your microbiome wants to stay where it has been. And a lot of it’s going to depend on what happened to you in the first three years of your life. That’s what’s going to sort of shape your microbiome for the future.
So when you move and you have children in a new environment, that new environment’s going to dictate what their microbiome’s going to look like.
MODERATOR: And we’re going to end on a Twitter question which is, what about that study where they removed the bacteria from the fecal transplant?
GRINSPAN: Shit. You got me.
MODERATOR: This might require a backstory, I don’t know.
GRINSPAN: Okay. So I gave you this whole talk about how the microbiome is everything. Maybe it’s nothing. See you next month at SciCafe: The Virome.
There was a group in Germany who took patients with C. diff, and they said, okay, great. Fecal transplant works. But what if we take the bacteria out and just give the... whatever’s left to patients? So they did that with five patients. They filtered out all of the bacteria. It was sterile. They tried to grow bacteria in this sterile stuff and nothing grew. And they gave that to five patients with C. diff, and all five of them were cured. Their C. diff was gone.
What? What did we... What is happening? Well, we don’t know. It was five patients. But it made massive headlines in the fecal transplant community, because we’re like, what are we supposed to do with this information? So we’re trying to figure out what it is that’s... The bottom line is the mechanism of action of a fecal transplant is unclear.
The interesting thing about that study in Germany is that they looked at the viruses, and there was viral changes that—basically the viruses that are in the biome in these patients look similar to the viruses that were in the donors.
So have you guys—do you guys know what a bacteriophage is? Hopefully no, because it has a bad connotation. Eastern Europeans tried to use it as chemical biological warfare. Viruses typically attack human cells. A bacteriophage is a virus that attacks a bacteria. So in the country of Georgia and other places, they don’t use classic antibiotics. They use phages to kill bacteria.
Well, it’s possible that it’s a phage, a virus that we’re transmitting from a donor to the patient, and that is what’s actually killing the C. diff. Has that been proven? No. Has anything I’ve been telling you about has been proven? Not really. Do people still come to me to get put shit up their ass? All the time. Because it works. We just need to understand why, and we don’t know the why. And it’s so important before we start doing it for other things, because the “why” is... that’s everything.
And on that note, we’re going to call this the end.
Subscribe to the Science@AMNH Podcast on iTunes, Soundcloud, or wherever you get your podcasts.
Watch a video version here:
SciCafe: The Power of Poop — Video Transcript
ARI GRINSPAN (Gastroenterologist):
Happy New Year. Thank you to the wonderful folks here at the American Museum of Natural History to invite me to talk about my passion: shit. My mother’s very proud.
These floating things that you’re seeing here are bacteria. Bacteria have a really bad reputation. So a hundred years ago, if you lived anywhere in the world, you were going to die most likely by one of these bacteria: an infection. Whether it was pneumonia, whether it was the flu, whether it was tuberculosis or another infection of the gut, like some sort of dysentery, an infection was going to get you. Now, 2018, an infection is not even in the top 10 reasons why we die. Other things get us: cancers, heart disease, strokes. But the idea of a bacteria still sits inside of us as, ooh, we should kill that. We don’t want that to be in our system. Take that antibiotic.
Well, turns out that’s one of the worst things you can do for yourself, because these bacteria are vital for our health. We grew up with these bacteria. We evolved with these bacteria. They help us and we help them. It’s a very symbiotic relationship. So my microbiome... And let me preface that. What is the microbiome? Microbiome is a complex connection, interaction, structure of these bacteria within a habitat. And I will be focusing on the gut microbiome; the collection of these bacteria; the proteins that they produce; the DNA that they have and how that interacts with us, and it is so incredibly important for our survival.
So my microbiome is very different than yours and different from the person next to you; different from a person in China or rural India or in Westchester. Our microbiome began at birth. So when you were in utero, there was no bacteria in you. The first contact you had with bacteria was with how were you delivered? Were you a C-section baby, or did you come down the birth canal? That will determine what the first bacteria you have, and there are very clear differences. You can tell, just in the microbiome, you can separate C-section babies from vaginal delivery babies, and that can last for a long period of time.
Up until the age of three, your microbiome can change depending on what you eat, were you breast-fed, were you a bottle baby, did you get an antibiotic for an ear infection? That will dramatically alter your microbiome. And then at the age of three, things sort of stabilize for a long, long period of time. Now, don’t get me wrong. If you go to Mexico City, if you go to some place and you come back with a little Montezuma Revenge, your microbiome will be different for a period of time, but then it usually comes back to its homeostasis.
Because your bacteria are a community, and they like to support one another. They support you by helping you digest certain foods. They support you by telling you, ooh, there’s a bad bug, here. This doesn’t belong in our community, and you can prevent it from causing a problem. So they protect us, and we protect these bacteria. We feed them every day multiple times a day, and they love it. And we give them a habitat to live in that’s protected from the bomb cyclone that’s coming tomorrow.
I am—well, I think I am—an average human being. I have about a trillion cells, human cells that make up me. But in my gut, I have 10 trillion bacteria who are not all bad. So I am 10% human and 90% bacteria. It gets a little bit more complicated, because the blueprint of human life is DNA. So if you take the DNA that is within me and look at it, you’ll find that 1% of the DNA in me is human, and 99% is bacteria. This relationship is incredibly important, and we’re just beginning to investigate it. For a long period of time we ignored it, because we didn’t really know that it even existed. Oh, but it exists, and it’s incredibly, incredibly important. Because when things go awry in the microbiome, it can affect you and it can cause problems.
I’m going to talk about the posterchild for how to look at the microbiome. It’s an infection called C. diff that Susan mentioned to you just a moment ago. It is a very bad bug. This is the human colon. This is, actually, this is a beautiful-looking human colon. I mean, I would eat off this colon. No, too much. Too much. This is a beautiful colon. It is healthy, it is vibrant, and there are trillions of bacteria that you cannot see floating around and [attached] sort of to the lining. C. diff, when it gets inside of the colon, causes that. Yeah. That is a sick colon. In fact, I don’t even want to look at it. It’s pretty gross.
So how does C. diff even get there? So you have 10 trillion bacteria, and the most important thing about this 10 trillion is that it’s diverse. You’ve got bacteria coming from different species, different phylum, different everything, and they all come together as one unit, and that unit is there to protect you. The problem happens when you get an antibiotic to treat a pneumonia or a urinary tract infection, or maybe your doctor gave you a CPAP for that sniffle that you got.
Okay, if it’s a pneumonia or if it’s a urinary tract infection, that bacteria that’s causing it is causing you harm, so the antibiotic is appropriate. Get rid of the infection, and you’ll get better. But it doesn’t just kill the bad bacteria. It kills a lot of the microbiome in your gut, and you get a contraction of this rich, diverse microbiome. You could lose the diversity. You lose the richness, and then you become susceptible to certain things. In this case, C. diff.
Now, the problem with C. diff is I can treat it with antibiotics, I can control it, but your microbiome is still so not where it should be. It’s contracted. So if I get rid of the infection and your microbiome is still in this low state, the C. diff comes right back, and it comes back again and again and again, and it’s a classic story. We call it recurrent C. diff. It causes 30,000 deaths per year just in this country. It costs $4 billion in extra healthcare costs to take care of patients who have recurrent C. diff. It’s a bad bug. It’s an expensive bug.
So then there is something called... So if the antibiotics don’t work, what can we do? Well that’s where fecal transplant comes to be. Fecal transplant is the idea is, okay, I’m going to take somebody else’s healthy microbiome, and I’m going to transfer it to the patient with the low microbiome—with the no diversity, the lack of richness—and I’m going to expand their microbiome. And hopefully that will cure the infection. It turns out it does it so remarkably well that it blows everybody’s mind. Antibiotics work for this recurrent C. diff infection maybe 30 to 50 percent of the time. A fecal transplant cures it more than 90% of the time. We don’t see these dramatic differences in modern medicine: 90-plus percent versus 30 to 50 percent for standard of care. This is dramatic. But it’s a little icky.
So when I first starting doing this, five, six years ago and patients would come to my office for C. diff and I’d be like, “You need a fecal transplant,” and they’re like, “You want to do what? You’re going to put what in my butt?” And I said, “No, no, no.”
So I don’t use shades of brown when I’m talking about this. I use shades of green. It’s life. It’s wonderful. Look at that lawn. You could eat off that lawn. Okay. Imagine that healthy lawn as your microbiome. Every blade of grass is a healthy microbe. It’s beautiful. Well, something happened to you. You got an antibiotic. You had a contraction, a decrease in your microbiome; less diverse, less rich. Then you get these dandelions. You got C. diff. Now, I don’t know how many of us actually have lawns, being in New York, but if you did have a lawn, you would try to kill that dandelion with weed killer. You spray the weed killer at it, but the dandelions keep coming back. You throw the antibiotics at the C. diff, but the C. diff keeps coming back. So the idea behind a fecal transplant is we need to re-sod your soil. We need to repopulate your gut. Re-poop-ulate your gut. I wish I coined that term. I didn’t, dammit. Re-poop-ulate your gut to bring it back to health, and that’s the idea behind a fecal transplant.
Now, there’s nothing new here. Fecal transplant is an old therapy. It was first done in fourth-century China. The Chinese physicians would use a fecal slurry, give to patients to treat anything from diarrhea, constipation, abdominal pain, and my favorite, nausea and vomiting, and they actually had success.
Now, it lost favor for a long period of time, and then it showed up in the English literature in 1958, where a professor in Denver used it to treat patients who had this in their colon. Now, he didn’t know it was C. diff. He just saw this, the patients weren’t getting better with antibiotics, and so he looked in where most doctors look about how to treat things we don’t know: in the veterinary literature. Nobody actually does that. But he did, and he found that horses who had dysentery and similar findings, if you feed them healthy horse manure, they get better. So he took the spouses of these patients, and he gave them fecal enemas from the spouse, and all four of those patients got better. It made a small splash in 1958 and then lost favor, because people were like, that’s ridiculous.
And in the ‘80s and ‘90s and even the early 2000s, it remained on the fringes of medicine until the landmark paper in The New England Journal of Medicine showed that fecal transplant: 90% cure rate, and standard of care of antibiotics: 30% cure rate. Again, you don’t see these kind of things in modern medicine. And then all of the sudden like, whoa, whoa, whoa. Yeah, fecal transplant, of course. Of course. We’ve known it all along. Now, it took a long time for people to really get on board with this.
Now, is that what we’re doing, here? So how does this whole process work? Is it just me re-poop-ulating the gut with healthy bacteria? So this is what our patient with C. diff looks like before their transplant. This is their bacteria. This is what we call microbiota disarray. And this is the donor. This healthy swab of orange is healthy bacteroides; these wonderful, healthy bacteria that we all consider to be a normal part of our gut. And so we give this to the patient, and this is what the patient looks like two weeks later: remarkably similar to the donor. If you look at that patient a month after their transplant, they look like this. So not like the donor, they share some similarities, but the patient is healthy. No C. diff. Feeling great. Playing tennis.
What we don’t know is, is this what the patient looked like before C. diff, or is this their new normal? We don’t have that information. How much of this donor stool, these donor microbes, how many of them stayed in the patient? We don’t have that information. And then it begs the question, well, who’s going to be your donor? So I get that question all the time. Okay, I want to do a fecal transplant, they sign up, okay, okay, great. Wait, whose shit are you going to use? And then I say, well, whose shit do you trust?
So we used to ask the patients, all right, do you got a brother or sister or mother, a spouse, family friend, the guy at your office who goes to the bathroom like clockwork every day? Like who do you want to use? So they’d have to give me a donor, I’d have to screen them, make sure that they were safe, so similar to as if you were going to be a blood donor, and then some. I had to make sure that they are healthy, they don’t have diabetes. They can’t be too big, they can’t be too small. It’s gotta be Goldilocks poop, or something like that.
They’d come, they’d have to produce the sample—the drug—on the day of the procedure. Now, you’ve heard of stage fright. Imagine me [unintelligible] like, hey, I got things to do, man. You gotta... That gets a little problematic. Well then they’d have to produce it, I then take it across the street, and make what we call the dirtiest martini. And then I bring it back, I do a colonoscopy to administer the drug; the fecal slurry. Because the problem is in the colon, I want to deliver it exactly there.
Would you like to see it? [Guard] your loins. Again, sick C. diff colon. What you’re going to see is a fecal transplant in action. So it’s moving because the patient is breathing—that’s good—and here it is. Boom. That’s the money shot. Too much? Too much. So this is wonderful. This is happy. This patient was in the hospital three times over six months with C. diff. Went to hospital to hospital, got multiple courses of antibiotics before coming to Mount Sinai. A young woman with ovarian cancer, she couldn’t function for the past six months prior to this. And this is what she looked like a month later. She walked out of the hospital. She was an avid tennis player, she was able to play tennis, and she is picture perfect health. Pretty remarkable.
But the whole process is pretty cumbersome. We don’t like to screen donors over and over again, so we don’t do that anymore. I import my poop. You’ve heard of blood banks, you’ve heard of sperm banks, but have you heard of stool banks? They exist, and they do all the things for me. They screen the donors, they make sure that they’re healthy, they make sure that there’s no diseases, they process the stool, they put it into a nice little canister, they freeze it for me—I don’t know if you know this, but fresh poop is just as good as frozen poop—they ship it to me via UPS. What can brown do for you? And I have a treasure trove in a freezer in my unit that I can use when it is required. So they always ask me, “So, wait, wait, wait. Where is this bank?” And I tell them, “It’s in Boston, and they usually screen Harvard and MIT students, so it’s smart shit. You’re welcome.”
But again, this whole thing is cumbersome. I still have to do a colonoscopy, it’s invasive, there’s anesthesia, you have to take a bowel prep, and people with C. diff, they don’t want to take anything that’s going to give them more issues.
So the future of this is the crap-sule. It shouldn’t be brown. We should probably fix that. But this is developed. We have this. It’s not quite ready for primetime, because there’s a lot of technology that goes into delivering this product. First of all, you don’t want it to release too soon. That would be a bad burp, oof. Again, I crossed a line. Too much, okay. But I don’t know what I’m supposed to put in it. Do I put the entire microbiome like I do via colonoscopy, or do I just take sections of the microbiome; some of the species; some of the bacteria? And that’s what we’re trying to figure out.
For C. diff, this bad infection, fecal transplant is a homerun. It’s rare in medicine that you find something for such a bad disease that just knocks it out of the park, and fecal transplant does that. And so if fecal transplant can be so remarkably effective for C. diff, where we think that the issue is with the microbiome being... we just need to restore the microbiome, can we take that to other disease processes?
Now, there have been a number of diseases that have been associated with changes in the microbiome. But association does not mean causation. And I don’t know if that change in the microbiome may have led to the disease state or if the disease state led to the changes in the microbiome. You name a disease, and there’s somebody who can show that there’s changes in the microbiome. Notably autism, multiple sclerosis, heart disease, diabetes, obesity, liver disease, inflammatory bowel disease—which is what I focus on—including Crohn’s disease, ulcerative colitis, and a number of other conditions.
But again, I don’t know—and nobody knows—is if the microbiome led to that problem. C. diff is easy. It’s a bug. The infection. Get rid of the bug, you’ve cured the disease. But all the things I just mentioned to you, there’s no single infection, single bug that causes these diseases. It’s multifactorial. Maybe the microbiome has a role. Maybe. But there’s genetics, there’s the environment, there’s your immune system—whether it’s overactive or underactive—among other things. So it gets all very complicated. So while the association may be there, I don’t know if we can be—and I doubt—that we’re going to have a homerun by changing the microbiome to affect the other disease process that I just mentioned.
But with the research by investigating the microbiome, and we’re at this explosion of research that’s going on, maybe we won’t find a new therapy for some of these conditions, but maybe we can prognosticate. Maybe we can identify people who are going to be susceptible to certain diseases later in life and potentially enact prevention strategies to prevent that disease from coming on later. That would be a wonderful outcome from all of this.
The microbiome is incredible, and there are so many secrets that we have yet to uncover. There’s all this crosstalk between the bacteria that are floating in our gut and in lining of the intestine. Now, we don’t have Rosetta Stone yet. I don’t know what they’re talking about. We’re trying to figure that out. And maybe what we can do is, once we figure out the conversation, maybe there will be ways that we can manipulate the microbiome to change the conversation; to change maybe some of the outcomes of certain diseases. That would be another wonderful outcome.
I’m going to leave you with three things before I stop the talk. Number one, don’t do this at home, okay? Don’t treat your headache, don’t treat your hangnail, don’t treat your abdominal discomfort with a fecal transplant. Leave that to the professionals. I need the business. I’m kidding.
Fiber. Fiber is your friend. If you want to promote a healthy microbiome, if you want to augment your microbiome for a health purpose, fiber is your friend. Don’t go to the local drugstore and buy all of the probiotics off the shelf, okay? That’s not going to do it. Fiber is your friend.
And number three, as my father always says, wear your seatbelt. Thank you very much.
The Scicafe Series is proudly sponsored by Judy and Josh Weston.
SciCafe: The Power of Poop and related activities are generously supported by the Science Education Partnership Award (SEPA) program of the National Institute of Health (NIH).