Peter 0:00
What are your thoughts?
Dr. Wu 0:01
You know, I feel like I should know what this is, like got seeds in it […] I don’t think it’s a cherry. I don’t know- I think the closest I can get to it’s a some type of strawberry jam type of thing.
Peter 0:15
Yeah, that was right on the money […] It was a raspberry covered in strawberry yogurt. I chose the raspberry because I went to the Mayo Clinic website, and I was looking up foods that were high in fiber and I didn’t know this but a cup of raspberries has about eight grams of fiber in it, while an apple which we think of kind of like an apple a day keeps the doctor away as kind of the main fiber fruit which only has about 3.5 grams of fiber in it.
Dr. Wu 0:38
You know, in our studies a vegan eats about 30 grams of fiber a day. But if you’re in Africa, living in rural Africa, they’ve done these studies [that show that they are] eating greater than 50 grams of fiber a day. That’s a lot of raspberries.
Peter 1:01
Hi, and welcome back to season two of The Gastronauts Podcast. My name is Peter and I’ll be your host. For those who have listened to season one thank you so much, and we hope you’re ready for another great season. If you like what you’ve heard, we’d love it if you could leave a review on whatever platform you listen to us on! For those who are new, thanks for joining us and we’re excited to have you. Here at Gastronauts, we are committed to exploring communication in the body, and in particular, how our gut talks to our brain. We will be inviting leading gut brain scientists to share both their incredible research and their captivating life stories. So come join me as we explore the steps that go into shaping a scientist on The Gastronauts Podcast.
Today we have Dr. Gary Wu. The Ferdinand G Weisbrod Professor in Gastroenterology at the Perelman School of Medicine at the University of Pennsylvania. He is the director and chair of the scientific advisory board for the American Gastroenterological Association Center for Gut Microbiome Research and Education. He is also an elected member of both the American Society for Clinical Investigation and the American Association of Physicians. A bit about Dr. Wu’s career path, he completed medical school at Northwestern, his residency at the University of Minnesota hospital, his fellowship in gastroenterology at the University of Michigan Ann Arbor. And his research really focuses on the interplay between the gut microbiome, or the aggregates of microbes that reside within our intestines, and this gut intestinal tissue. So right off the bat, I want to ask a little bit about the inspiration behind your decision to study the microbiome. When was the first time you heard about this term and when did you realize this is a field you wanted to pursue?
Dr. Wu 3:05
Well, you know […] there was some serendipity involved in this. We’ve always sort of been interested in microbes in the gut, because I’m a gastroenterologist. And this is something from a practical standpoint that we […] do in my clinical practice. But for a while, we had been interested in how microbes in the gut could change host physiology, meaning gene expression in the intestinal tract. And a long time ago, we had made an observation that there were certain genes in the intestinal tract that were regulated by bacteria. So we actually deleted that gene with the notion that perhaps it might change bacteria in our gut in some way, because this gene led to a secreted product. And because it was in the gut lumen with all the bacteria we thought it might have an effect on bacteria. So we went through very antiquated types of technologies basically to try to visualize a difference in the composition of bacteria in the gut by looking at stool samples. And in mice, we really couldn’t see anything, which was no real surprise [since] by visually inspecting things, you’re just not going to see anything. But that was around the time that high-throughput sequencing technologies were being applied to studying microbial communities […] and it just turned out that there was a scientist, a very good scientist at Penn, Rick Bushman, who’s now the chair of microbiology at the University of Pennsylvania that was actually at the forefront of that technology. So I basically met up with him and and we began a collaboration. And we found some very interesting things with this. And around that time, the NIH had the first call for the Human Microbiome Project grant applications. And so that’s how we got started in the whole area.
Peter 4:59
So yeah, for me, the microbiome has [moved] to the popular press, and it’s a very commonplace topic nowadays. We hear about it in the news. We hear about it in the foods that we eat. So I was wondering, did you have any interest in the microbiome before you decided to pursue a career in gastroenterology or did that happen later?
Dr. Wu 5:15
You know, I think it sort of happened later. As a physician. We see this in clinical practice a lot. We get a lot of questions about probiotics, prebiotics, about fermented food, what’s good, what’s bad. So from a clinical standpoint, it’s actually a very relevant topic that the patients bring up very often. Unfortunately, we don’t have a lot of real strong evidence that our current probiotics have a real strong effect on either preventing and or treating disease. There is a little bit of evidence to suggest maybe they do something. And […] there are individuals that swear they feel better when they take these probiotics, and I can’t deny the fact that it probably on a case by case basis it may provide some type of benefit. But it’s the notion that as a physician, I’ve sort of known about this because I’ve been in training for a very long period of time, before I became a gastroenterologist. And so now that I’m in the GI field, and it just sort of makes sense that it will come back full circle to what I sort of known about in a clinical entity with patients that now we can actually study it scientifically because we have these types of technologies.
Peter 6:27
Certainly. So I was wondering what sparked your decision to pursue research? Had you always been conducting research while you were a medical student or while you were a resident? Or was there something about the microbiome that really drew you towards that field? And do you feel that your medical training had prepared you to go into the field of research?
Dr. Wu 6:42
Yeah, it’s a good question. So I did a lot of research when I was an undergraduate at Cornell as a chemistry major, and I really didn’t do a lot of research after that. And in medical school, I knew that I was interested in internal medicine. So I did a residency in internal medicine. I decided to go into the field of gastroenterology more because I liked the clinical practice of gastroenterology. I like doing procedures. I like what gastroenterologists do: make a diagnosis, make interventions. So it’s more from a clinical standpoint that I ended up in gastroenterology. And more by just opportunity, when we train as fellows in a sub specialty, [we] have opportunities to do a research track or a clinical track, [where you] take care of more patients. I just by opportunity [found] a research position that was open at the University of Michigan where I did my fellowship. And that’s just what I’ve been doing ever since. I mean, I really liked clinical medicine. I like taking care of patients. But I like doing basic science research because
[it]opened my eyes to so many other things that physicians can do. It’s a very rare rewarding experience to take care of patients, as well as think about questions that you might be able to explore in the laboratory that might ultimately have an impact on the types of things and patients that you see every day in the clinical setting.
Peter 8:16
So now that you are a relatively established physician scientist, what qualities do you feel are important for some younger students who wish to be someone who follows in your path?
Dr. Wu 8:25
You know, I think it takes a lot of different qualities. It takes a lot of perseverance. It takes resilience. But one of the traits that I find in common with individuals that are successful scientists, is creativity. So when people work with me or I talk to other investigators, it’s those individuals that come into the laboratory- they may not have had a lot of laboratory experience, but [they’re] just full of ideas, full of questions and I think some of the best scientists in the world are just deeply creative people. They can come up with ideas, they can see and envision things that the average person cannot actually see. So I, for example, have a lot of admiration for artists, or painters, for musicians who can create things that other people cannot actually conceive of. And it’s the same thing for a scientist, it’s just a little bit different because you’re using science as sort of an output for your creativity. So it’s not as if you know, people that are not innately as creative would not be successful in science, I think that you can learn to explore questions and open your mind to things. In a broader sense it’s something that you can develop over time. But I think innately, there are just people that that are just sort of hard-wired to be incredibly creative. And I think those types of individuals really push the field forward.
Peter 9:58
That’s really interesting. Is there a way to foster creativity? Do you kind of encourage art projects in your laboratory to […] stimulate a different part of your mind to be more creative? Or is there an impetus in your laboratory to try and hone in and develop this creative process?
Dr. Wu 10:15
Yeah, it’s a very interesting question. Part of that is, I think part of being a good mentor. So when people start out in the laboratory, especially if they haven’t done a lot of basic science research, it’s basically you just have to learn these techniques. And so part of the laboratory experience is a two part process. One is technology, you’re going to have to be able to put your hands on and do an experiment because even if you have the best ideas in the world, if you can’t do the experiment, then you really can’t get anything done. The other part is to think like a scientist, and that’s where the creativity comes in. And that’s a much more difficult thing to teach. You can teach people how to do things technically, but to become creative, it’s much more difficult. But I think that you could learn from example, you could learn from reading the literature, learn how people think. And then also look at other great scientists. You go to talks, and you get inspired by what other people do and how people think about problems. I’ll give you an example. Many years ago, I went to a fabulous talk by a really world renowned scientist [who studied] nuclear hormone receptors. And he said that he had a graduate student that knocked out a gene for some type of pathway. And the graduate student at that time, this many years ago, spent a long time making that knockout mouse. And at the end of the day, it had no phenotype. And the graduate student was absolutely devastated because he had spent so much time making this knockout mouse. But the scientist was just elated. He said, You just don’t understand what this actually means. Everything we know about this gene product suggests that there should have been a phenotype. The fact there is no phenotype is a really fabulous discovery. And it turns out that he had the foresight to think about what alternative mechanisms might be available through this model system. And they ended up publishing it in a very high profile magazine. And that’s just another example where maybe an average individual would also be very disappointed. But a very seasoned scientist who’s very creative can see beyond it, and say, well, this is absolutely fabulous. And we can […] think of a way that you can go about trying to answer this question. So being creative, getting inspiration from other people looking at how people approach different types of experiments. I think that to a certain degree, you can learn those types of skills over time and [for] a lot of people, it’s probably within them, but they’ve never been challenged to develop that part of their armamentarium. And so given the opportunity, people can sort of grow into that. I think over time, we’ve given the right types of exposures in the environment.
Peter 12:58
Yeah, that’s really neat. I hadn’t thought of that before. Being creative in sciences [is] interpreting your results that are very different than your initial hypothesis. And being able to posit alternative mechanisms or different approaches when something doesn’t quite go the right way you think it should be going.
Dr. Wu 13:13
Exactly. I mean, I think that we all try to do hypothesis driven research. And at the end of the day, if you do an experiment, and it didn’t answer your hypothesis one way or the other, then you probably didn’t design it correctly as long as technically there was no flaw. But at the end of the day, you’re going to get an answer if you did the experiment correctly, and maybe it doesn’t agree with your initial hypothesis. You can’t change the results, but you can change your hypothesis, right? And so then you come up with an alternative hypothesis and you begin to chase it down. But that’s exactly it; that’s the scientific method.
Peter 14:06
That’s really great advice. Thank you. I wanted to talk a little bit about some of your early research. And I know I’ve mentioned this earlier, the microbiome field has really grown kind of at a breathtaking pace. Eight years ago, you published some landmark work on long term dietary patterns with the microbiota in the gut. And [you] were the first to show that consumption of specific diets of a known composition could not only rapidly change the microbiota composition and as quickly as 24 hours, but result in stable changes for up to 10 days. It’s been a decade almost since then, and I was wondering how you feel about our ability to utilize diet as an intervention to treat diseases of dysbiosis or imbalances in our gut microbes?
Dr. Wu 14:47
Yeah, I think one of the things that we’ve learned over time that we actually saw in our initial publication a number of years ago is that the human microbiota is actually very resilient to dietary influences and so you can see consistent and maybe somewhat larger effects by using very extreme diets, like the ketogenic diet lacking any carbohydrates or an herbivorous diet. But still one of the largest sources of variance in the composition of the microbiota is inter-subject variability, how different we are from each other. So the usual influence of a diet on the composition of the microbiota actually is smaller that how different we are from each other, demonstrating that again that the human microbiota is actually quite resilient to change induced by diet. In a way, that’s good, because you know, every time you eat, you don’t want your microbiota changing in some type of wild way. Alternatively, if you want to engineer the microbiota into a different types of configuration, it may be more difficult than initially conceived. But there’s another way to think about it. It’s not just the composition of the microbiota, but it’s the metabolites that they actually make. So you may not change the configuration dramatically, but if you feed your microbiota something different, you provide a different type of substrate, you still may have an effect, not by the change in a composition that types of microbes but the products that they actually make. So an example of this would be equine production by the microbiota. So microbes can make a non-steroidal estrogen that is a hormone that has biological activity. And the substrate for that is soy. So in individuals that eat very little soy, there is very little production of equine that you detect in the plasma. But people that eat high levels of soy, in the United States, about 40% of those individuals will have equine. It’s actually interesting that if you’re in Asia, you’re in Japan, about 80% of people will produce equine. So part of it is the amount of soy that you’re actually eating, but part of it is also culturally based different ethnicities will have different compositions of the microbiota, different types of functionality, even independent of diet. So there are constraints. But I think that there are still meaningful outcomes that diet can have and influence the microbiota, particularly through metabolite production.
Peter 17:24
I wanted to touch upon your comment on creativity earlier, what if, in your previous work when you were looking at the effects of diet on microbiota composition, you hadn’t found an effect on the different diet compositions on rapid changes in the gut microbiota and sustained changes? How would you have been able to […] posit a response to that? Could it have just been the metabolites that had been different or what would be an alternative hypothesis if you did not find changes in microbiota composition following diet?
Dr. Wu 17:53
Well, you know, one obvious issues we didn’t study the right diet, right? And so maybe it was was the composition of the diet. Maybe it was the duration of the diet, or maybe it was the type of subjects that we actually had in the study, right? Maybe a vegan would respond differently than an omnivore. Or maybe it was age dependent. There are many different variables that could explain differences. And that’s one of the challenges when doing human subject research. So we do mouse research, because genetically, they’re inbred. And they’re living in very similar types of environments. And there’s a very high signal-to-noise ratio. [But in] doing human subject research, they’re free living individuals, genetically diverse eating many different types of things. So we do these controlled feeding experiments and in the hospital setting to try to control as many variables as possible. But when we don’t see some type of effect that we anticipate and see, well, maybe that’s just normal physiology and normal human biology. But it also brings the point that in fact, humans are intrinsically very noisy, and there may have been an effect, but maybe we didn’t see it because we didn’t do a robust enough type of intervention. So two lessons that we have learned during human subject research is that we try to think about interventions that are going to be reasonably robust that will exceed the noise level that we see in individuals. And we try to do longitudinal prospective studies, where we’re not just looking at cross sectional or looking at one time, we’re looking at an individual over time. And so each individual may be different. But within that individual, there might be changes that are consistent. And so there are two important lessons that we’ve learned over time by doing these types of human subjects studies.
Peter 19:41
How do you define your timeframe for a longitudinal study? How long do you typically look for?
Dr. Wu 19:47
You know, it depends on what your outcome is, right? And so we know that in terms of change in the microbiota, it’s relatively rapid, and our notion is a lot of the metabolites that are produced by the microbiota are also relatively rapid. So a couple of days might be enough and our first study was 10 days. On the other hand, if you’re looking at other inputs, development of obesity, metabolic syndrome, cardiovascular disease, that that takes a long time. That takes decades to do. But I think the opportunity in the microbiome field or metabolites from microbes may be their surrogate biomarkers, intermediate biomarkers, where they actually track with the development, eventually a disease. For example, high blood pressure, you know, high blood pressure is a biomarker and a causative factor in development of heart disease many decades later, but do you know that it’s a good biomarker? So maybe the gut microbiota could be a signature that you would see relatively early on, that may predispose or be associated with disease at a much later time point. So again, it depends on what the question is.
Peter 20:57
In one of your talks, you were mentioning how inflammatory bowel disease has been primarily treated with kind of anti-inflammatory medications. But we’re starting to realize the effects of industrialization on the increase of inflammatory bowel disease and the effect of environment on IBD, or inflammatory bowel disease. Do we have an idea of what gut microbes are triggering kind of this auto-inflammatory response? Or do we believe that the inflamed environment of the gut leads to different bacterial populations? I think piggybacking off […] my question earlier on, how long should you be looking at the microbiome for development of IBD? Or do we even have an idea of kind of this correlation?
Dr. Wu 21:36
Yeah, yeah. So there […] are a lot of insightful questions and in what you just said […] We think the environment is important, because there’s a rapid, really increasing incidence of many different inflammatory diseases associated with industrialization. So that’s an environmental effect, but it’s a complex process. So inflammatory bowel disease, like a lot of complex disease states, is part genetic part environment. In inflammatory bowel disease, there’s a genetic influence. It’s relatively modest, but it’s very important. Otherwise we’d all have inflammatory bowel disease. So there’s a genetic predisposition that’s actually in most cases necessary to a certain degree, that imparts a risk to fully developed that phenotype. Unfortunately, for inflammatory bowel disease, we do think environmental factors are important. And there’s just so much data in animal models and what we know about immunology and physiology, that gut microbes are just fundamentally important the development of inflammatory bowel disease. The issue is cause and effect […] we actually cause the dysbiosis; we cause those different structure in the microbiota because inflammation of our intestinal tract, based on work of a lot of people, is an environmental stress that changes the composition of the microbiota. But in return that dysbiotic, or different type of configuration, […] helps perpetuate inflammatory bowel disease based on animal model systems, where we take those organisms that are more abundant in inflammatory bowel disease and put them in an animal model, it tends to be disadvantageous lead to inflammation in animal models. And we even have a little evidence in humans, that fecal microbiota transplantation taking fecal material from a healthy individual transplant again, and people with inflammatory bowel disease, particularly all sort of colitis, can lead to a modest yet meaningful response. Now, I caution people that are listening to this podcast. I’m not saying that fecal transplantation is a treatment for inflammatory bowel disease. It’s too early yet to say that definitively. But there are some intriguing results and in several clinical studies to suggest that on the horizon maybe changing the microbiota significantly, and I’m not even excluding fecal transplantation, might have some utility in the future, not now. Because I would say now it’s still highly experimental. The most important aspect of this is that people are quite interested in preventing disease. And so the notion is that if you were genetically predisposed to development of inflammatory bowel disease, based on your pedigree, you have a family history of inflammatory bowel disease is there something that you could do earlier in age, or stay away from something or do something to your microbiota or your environment that would prevent you from getting disease? That’s the Holy Grail. There are studies ongoing where they’re actually tracking individuals before they get inflammatory bowel disease to ask, (well, unfortunately, some of those people will get inflammatory bowel disease but they will have collected biospecimens before they got disease) what did it look like before and could we have predicted that person would get inflammatory bowel disease and maybe you if you had changed something, maybe you can prevent That the development of laboratory policies prevention is so much more impactful. But it’s very difficult to prove, takes a lot of time, takes a large number of individuals, but ultimately, that’s the holy grail prevent the development of disease.
Peter 25:16
You were mentioning fecal microbiota transplant earlier as not necessarily a treatment for inflammatory bowel disease. But in my medical school courses, we have been taught that FMT or fecal microbiota transplant is a treatment for clostridium difficile colitis. How did someone come about with this idea? Or do you even know the history of how FMT came about and how people thought of this as a possible treatment?
Dr. Wu 25:41
Yeah, you know, transplantation of fecal material actually, historically, I think originated in like 3000 BC in China. As I understand […] this yellow soup where they would take fecal material and make something edible out of it. In the livestock industry transplantation has been used for a long period of time in livestock, I think it was several decades ago and I think it was by a surgeon that actually published an article about, about transfer of fecal material. So you know, it’s been out there for a while, and more recently, based on some initial observations and a pivotal clinical study that ended up in a New England Journal of Medicine that really provided I think, reasonable evidence that fecal microbiota transplantation is an effective modality of treatment for our clostridiodes difficile infection with a with a cure rate 80 to 90% in certain populations.
Peter 26:48
Yeah, that’s really incredible. Do we have any idea of what the needle in the haystack of the fecal microbiota transplant is or do we have any idea of a particular microbe that could [provide] the causative effect of this or is it just completely unknown right now?
Dr. Wu 27:05
Yeah, I think that based on animal model systems, there are a number of different hypotheses. One is is competitive niche exclusion so basically you inoculate somebody that has clostridiodes difficile with a complete community and it basically crowds out that organism closes off the niche so the clostridiodes difficile and will not be as abundant and stop producing toxin. Other ideas are that bile acids are really important. In clostridiodes difficile biology. Primary bile acids, which basically come out of your liver in the small intestine, are germinant for clostridiodes difficile
[and]will cause them to start to grow. But then your microbiota will convert those primary bile acids into secondary bile acids in your colon. The secondary bile acids are actually toxic to clostridiodes difficile [and] will actually kill those organisms. So one of the notions is that the risk factor for the development of C. difficile is actually use of antibiotics. So Eric Pamer(?) and other people have shown that when you take certain types of antibiotics, you can reduce the representation of certain types of bacteria that make the conversion from primary to secondary bile acids. If you reduce secondary bile acids, then you’re not going to be killing off the C diff and [preventing] overgrowth.
Peter 28:34
Are secondary bile acids produced by the human at all or is it solely produced by bacteria?
Dr. Wu 28:37
It’s a bacterial process. So bacteria have different types of enzymes that can actually transform bile acids and it’s a normal physiology that actually occurs in mammalian systems and clostridiodes difficile infection takes advantage of that. In terms of bile acid physiology, because in part, the use of antibiotics. There’s even a notion that the host immune response may be important. There are individuals that get recurrent clostridiodes difficile infection. Is it because it’s that particular microbe or because their immune response is not able to deal with that particular infection? There’s some interest in developing vaccines for the prevention of C. difficile infection, meaning that it may not just be the bacteria may not just be the environment like bile acids, but it may be the host immune response. So we know a little bit about the pathogenesis of C. difficile infection, but there’s still a lot more that needs to be understood.
Peter 29:42
Are there any therapeutics to stop the production of secondary bile acids?
Dr. Wu 29:46
In bacteria? Yeah, so actually diseases that disrupt the microbiota that lead to dysbiosis actually reduce the conversion from primary to secondary bile acids. So actually in clostridiodes difficile infection is a reduction in conversion from primary to secondary bile acids. And inflammatory bowel disease, there’s a reduction in the conversion of primary to secondary bile acids. And the reason is that the enzymes that are responsible for the conversion from primary to secondary bile acids are not very abundant in the organisms that are associated with dysbiosis. So you get the dysbiosis. And you can’t make that conversion of your bile acids.
Peter 30:36
That’s pretty neat. We’ve been talking about […] this dysbiosis and this change in our microbiota and how different microbes in our gut are able to produce certain metabolites and others aren’t. And we also mentioned earlier that our gut microbiome is relatively stable, it can sustain perturbations from a lot of the foods that we eat. Is there a particular time in life that you think that the gut microbiome is most plastic or most modifiable?
Dr. Wu 31:01
Yeah, I think there’s a lot of interest early on in life. I’m involved in a prospective cohort of infants with a number of […] investigators that are following infants from birth out the several years of age. We have a study ongoing at Children’s Hospital of Philadelphia called I-gram infant growth and Microbiome Project. We track infants from birth, all the way out to two years of age. As an infant, you’re born sterile, and then you become colonized. And that colonization actually occurs in a very systematic way, which begins with a very few number of organisms. And over time, you acquire more and more organisms out to the year, age of two or three, then your microbiota is as rich as an adult. So during the first couple of weeks or months after birth, your microbiota is very plastic and bounces around a lot. There’s a lot of things coming in, moving in and moving out. And the notion is that when you don’t have a lot of things in the environment, that it’s, it’s less resilient. So you think about it as a lawn. Like if you have a really plush, grassy lawn, you don’t have a lot of weeds in it. But if you have a lawn like mine at home that has a lot of holes in it, there are weeds in it, right? And so if you have a very rich microbiota or rich lawn, you don’t have a lot of perturbation, so it’s […] it’s much more stable. So an infant’s microbiota, because it doesn’t contain as many different types of organisms, is more prone to perturbation. And what does perturbation mean? Use of antibiotics […] early on in life. Think about ear infections, the use of antibiotics. There’s an association between antibiotic use and the development of a topic disease later on in life and obesity. These are just associations. The type of feeding, breastfeeding versus formula feeding could have a significant effect on a competition on microbiota because it’s not as resilient and human milk oligosaccharides that you find in breast milk are very bifidogenic, because certain types of bacteria called bifidobacteria […] grow out. Just another example that early life microbiota is less resilient and very malleable to environmental changes.
Peter 33:19
Even the type of delivery: C sections versus vaginal deliveries have been associated with differences.
Dr. Wu 33:22
Now they’re not, at least in our studies, not enormous. But for the first period early on in life, you can find differences between the two, but then eventually those things go away. Otherwise, I’d be up to look at somebody’s fecal sample as an adult and say, well, you were born by C section or by vaginal birth. We can’t do that. Because that difference actually disappears later on.
Peter 33:46
So it is very malleable in the early months.
Dr. Wu 33:50
Yeah. By the age of two or three, Jeff Gordon, and other people have shown that it’s pretty much as rich as an adult.
Peter 33:58
Really neat. One last question that I wanted to ask was tying this a little bit back to some of the talks that you gave earlier. And I was fortunate to be able to attend both of your seminars, one for Gastronauts and the other one for the Pediatric Obesity Microbiome and Metabolism Mini-symposium. I felt like the two talks had very different flavors, one focusing on […] clinical correlations associated with microbiota and the other one on the impact of physiologic processes, bile salts, urea production and such on the microbiota. I was wondering, how have you been able to teach yourself to effectively communicate to both clinicians and basic scientists?
Dr. Wu 34:35
You know, that’s that’s a really interesting question. I don’t think anybody’s ever asked me that before. I think that it just comes with practice. I mean, I think about it would be people ask me, “How do you think about talking to individuals that don’t have a scientific background? And so you know, I give talks at fundraisers and things like that, and I think about how would I explain what I do to my mom, for example, that might have a passing interest. What I do, but if I explain it for more than five minutes, she’s not really going to care anymore. So what’s that elevator talk? And how can I convey that information in […] reasonable terms that somebody that doesn’t have a scientific background, really understands. Part of it is also I do believe being a physician helps me with this because a physician, you know, our training is based on a scientific method, right, and the first two years of medical school [are] all about basic science, the type of work, but as a good physician, you have to be able to communicate to your patients, and sometimes very complex ideas in ways that they need to understand. Because informed consent is really fundamentally important. People have to understand what the potential benefits and potential risks are. And some of these concepts are very, very difficult. So I do believe at least for myself, that being a physician and I was a physician before I was a scientist, essentially, […] has helped me Me communicate better scientific principles because I’ve essentially had to do it my entire career as a physician in the patients that I take care of.
Peter 36:10
That’s a neat perspective. Do you have any tips on how you think we can improve collaboration between people in the basic sciences and clinicians? Not everyone can be a physician scientist, but can we improve […] collaborations between people who are working in the academic medicine field and people who are doing basic science?
Dr. Wu 36:25
Yeah, I think that a lot of it has to be is sort of respect for each other. I deeply respect clinicians, because I mentioned this earlier today that I think interesting observations by clinicians can sometimes be fundamentally important for us as scientists to think about hypotheses to try to address so for example, […] I’m a basic scientist, but I’m also a clinician when I when I think about trying to start another program, where I’m going to do basic science I have to find a partner. If I’m going to do a translational type of project, I have to find a clinician that really has deep knowledge of that patient population. And it’s very often that I’ll ask them very early on and in the relationship, you tell me, what are some of the most difficult things that you face [with] your patients? Because maybe we can together think about an intervention or an approach in which we might be able to use science to try to address that question, or that need. That’s not an easy thing to do. But it’s a starting point, right, and as a beginning conversation respecting the value of people that take care of patients, because at the end of day, that’s very practical, right? You could do the best science in the world and it’s super exciting, but at the end of the day, when you’re sick and you have a problem, you turn to your physician and physicians get to take care of you,[so] a physician sees the patient side of it, they see human physiology and so I I think that that’s enormously valuable. But at the end of the day also, to move science forward, to be a good physician is also to be a scientist. That’s the way that we’re trained. So they’re actually interdigitated. And I think a lot of it is respect for what each party brings to the table and acknowledging that if you work together, you can move things forward a lot faster than if you were to do it individually.
Peter 38:27
That’s some really great advice. Well, thank you so much for your time. Dr. Wu, it was great having you.
Dr. Wu 38:31
Alright. My pleasure. Thanks a lot.
Peter 38:46
Dr. Wu gave us some really neat insights into the interplay between the microbiome and our gut, as well as a look into where he believes the microbiome field will be. And in order for us to reach the future, he believes budding scientists will need to hone in on their creativity. Only through evaluation and reevaluation of what has been done can we develop new approaches, or methodologies to bring us to the future. Thank you all so much for listening, and we’ll see you on the next episode. If you like what you’ve heard, we’d love it if you could leave us a review. For more of our content, you can follow us on Twitter @Gutbrains or visit our website at thinkgastronauts com. The Gastronauts Podcast would be impossible without the incredible team that we have here. Meredith Schmehl is our producer and theme music composer. And special thanks to the founders of Gastronauts, Dr. Diego Bohórquez, and the Bohórquez laboratory
