Microbiome Myths and Misconceptions [transcript]

Written by Christopher Kelly

April 10, 2020


Christopher:    Well, Lucy, thank you so much for joining me this morning. I very much appreciate you. How’s it’s going over in Chicago right now for you?

Lucy:    Good. Thanks. Just focusing on work now and getting some exercise in every now and then. How’s everything out there?

Christopher:    The sun’s finally come out in Santa Cruz a little bit. It’s been a week of isolation and rain which is I think lack of sunshine is worse than the isolation phase. Super happy to see that fiery thing in the sky again today.

    Let’s talk about the microbiome. Why would anyone care about the microbiome? Can you give us the potted version of why anyone should care about the gut microbiome?

Lucy:    Yeah, sure. I actually personally got interested in the microbiome through my own struggles with skin issues. It was many years of seeing dermatologists and not getting real answers for my health condition and it was finally when I realized that my diet and the gut microbiome had implications for a wide range of chronic diseases including skin health.

    That’s really when I started to do my deep dive into microbiome and realizing that it really had implications for the health of all of our organs and our body as a whole. It just really, really went from there and we’ve had a boom in microbiome research h the last ten, 20 years, just learning so much about how it impacts our digestion, repelling pathogens in the gut, so it’s got all these local actions in the gut but it also has this wide spread effect on the physiology of the entire body.

Christopher:    The last time we’ve talked, you’re on a path to become an MD-PhD. Tell us about how things have changed for you.

Lucy:    Yeah. It’s been quite a ride last year. I think we actually talked last August when I had just finished my PhD at the University of Illinois. I decided to take a gap year before starting my MD.

    I think part of the rationale in taking that gap year was juts to have that break between, but part of it was also really questioning whether med school is really the right path for me. I actually think I remember you starting off that podcast by asking why the heck I wanted to go to med school.

Christopher:    This is nothing to do with me, I promise.

Lucy:    No. It was really a great question though. I think I gave the standard answer I’ve been giving for four years which was I want to change healthcare. I think an MD, doing it from the inside is the way to do it. I think we need someone with those credentials.

    I think in great part, that was kind of the story I kept telling myself was I need the background of the conventional system to make an impact, to be able to work with patients and over the last year, I did a lot of travelling, a lot of reflecting on that and that slowly started to fall apart that I really needed the MD to be able to make the impact that I want to make. 

    Yeah, it was quite a journey, a lot of self-discovery along the way, but I’m really excited that I’ve decided to do full-time blogging now and independent research and just continue to piece together gut research from a wide variety of areas and really synthesize it into something that can actually help people.

Christopher:    Oh, I love that. I love that. Was there anything in particular that was helpful in making that decision?

Lucy:    It was a lot of things. I would say getting into meditation and mindfulness was really key and kind of being able to separate from my own ego and realizing that a lot of it was my long standing need to achieve to feel worthy of something or to have the standard credentials instead of making the impact and to finding success for myself. 

    I think that was a big part of it. Then also, I’d come across on schooling before but I kind of came across it in a number of different ways this year again, which of course is the idea of more self-directed learning instead of learning within an educational institution.

    Coming across that idea again made me realize that I said I wanted to go to med school to learn all these things, but then looking at the entirety of the med school curriculum made me realize that there were a lot of things that I was never really going to use in the work that I wanted to do and things that weren’t included in that that I would’ve wanted to take a deeper dive on.

    That idea just really led me to the idea that self-directed learning and me just taking the topics that I’m naturally curious about and learning more about that will allow me to learn a lot of aspects of medicine that I can use in my work, but with a much greater retention and an output that can potentially create value for people.

Christopher:    That’s fantastic. I’ve got a book recommendation for you that I think generalizes these ideas very beautifully that I just finished reading. It’s called the Carpenter and the Gardener by Alison Gopnik.

Lucy:    Interesting. I’ll write that down.

Christopher:    She’s a researcher at UC Berkeley. Yeah, it’s a fantastic metaphor and I’ll resist the temptation to get into it now. But I think it’s a very useful metaphor for thinking about any time we interact with a complex system including the gut ecosystem. 


    In carpentry, it’s about very goal-directed behavior, like you’re building something from a blueprint and it’s very obvious when you build it to specifications or not, whereas in gardening, it’s really just about keeping out the weeds and you never really know what you’re going to get. 

    What Alison Gopnik argues is that parenting shouldn’t be an activity with a capital P. It should be more like gardening. You’re not a carpenter as a parent, you’re a gardener. You just need to keep the weeds out. The kids, they’re really good at self-directing towards the activities that are best for learning for them at that time. Of course, Josh has been really good in talking about this on the podcast before, but Alison Gopnik is a researcher and she’s done a ton of really interesting experiments that show all this.

    She’s written a bunch of New York Times pieces and for The Wall Street Journal, really, really good stuff. I’ll bet you’ll enjoy that book.

Lucy:    Okay, great. I’ll check that out for sure.

Christopher:    Let’s go into microbiome misconceptions. I’m sad I didn’t get to see you give this presentation in person at UC San Francisco but obviously, due to the recent cordon sanitaire, that was definitely not happening. I think I’m right in thinking that people can watch the video replay if they so wish without having anything to do with the UCSF. Is that right? Is this available publicly online?

Lucy:    Yeah. I believe it’s still publicly posted on their Facebook page. I think it’ll be there indefinitely so I can go back and watch there.

Christopher:    Excellent. Well, Elaine does a fantastic job of finding all the citations for the show notes so we’ll surely have it linked there. If not, at least you have slides for that talk because those are very helpful too. You give most of the citations in the slides as well, right?

Lucy:    Yup.

Christopher:    Well, I love this. It’s so helpful to have somebody point out the problems like the problems are always where my interest lie. That’s where you might progress is by paying close attention to problems. As you went through these misconceptions, I was trying to think if there was any that I didn’t fall for at some point along the way like the last six years.

    I don’t think there really is. Maybe exercise. I didn’t quite fall for that. I never thought that more was better with exercise but I think for the most part, I fell for every single one of these misconceptions so I’m just really excited to have you on today to talk about some of them.

Lucy:    Yeah. That’s great. I’m hopeful that I slipped in enough answers in there that I didn’t just talk about the problems but I think yeah, I think there’s a lot of things that can be misleading about the gut microbiome and a lot of misinformation out there, and Dr. Kiel specifically asked me to talk on this after seeing my talk at ancestral health last year and asked me to kind of expand on that because he thought it would be most enlightening.

    I was a little bit hesitant to give that talk mostly just because I feel it is kind of criticizing the field quite a bit or criticizing the myths out there in the blogosphere, but I do think it’s important that we have the true evidence especially when so many people are trying to self-treat in this area.

Christopher:    Right, absolutely. Yeah. I mean myself included. We’ve run culture-based stool tests for example in our practice for many years but I like to think as soon as I found out that’s not a very useful thing to do, I put my hand up and say hey, we found something better now. Just really look over here.

    That’s the way to handle that change rather than saying, “She’s wrong. Stool culture is the gold standard of microbiology, has been for decades.” That’s kind of I think the wrong way to go about it.

Lucy:    Yeah. Definitely. I think that’s -- I mean I can say the same thing as well. When I was sick dealing with my chronic eczema four years ago, I was definitely throwing every herbal you know, at my gut trying to fix it. I didn’t do so with the nuance that I think we need and that I’m speaking for today knowing better.

    I think we all have room to evolve and continue to follow where the new evidence takes us.

Christopher:    Well, let’s get into it. Tell us, why are culture-based stool testing -- why is it not accurate?

Lucy:    This is a big one. I think we may have even touched on this last time I was on the podcast but basically, for decades, study of gut microbes did rely on culture which is basically streaking out fecal sample on a petri dish, staining that and then looking at it under a microscope.

    The problem is only a small fraction of the microbes in the gut are actually culturable. The culture also skews the abundance of microbes. If you have, for example five -- just for simplicity’s sake, you have five microbes in a stool sample, obviously there’s much more than that.

    But if you streak those out on a plate, and that plate has a certain growth media to try to promote the growth of microbes, it’s naturally going to skew the abundance towards whichever microbe grows really well on that media, and it’s not necessarily going to be the same microbe that was growing well in the gut. It’s hard to replicate the gut environment in a petri dish and so that culture dramatically skews the abundance that’s in the gut.


    I’ve run a number of samples side by side where I’ve sent the same sample to culture-based analysis and to for example, 16S rRNA sequencing which is a DNA-based analysis, you can see clearly that less than about 4% of gut bacteria that live in our guts are actually captured on the culture-based test. I’m just saying like 95% to 96% of the ecosystem and we’re skewing the abundance. It’s basing treatment on 5% of the ecosystem is it’s not giving us accurate information.

Christopher:    What your suggestion said, so the 16S, I mean we lost uBiome. It’s gone. I don’t think there’s going to be anyone doing that anytime soon, right, at that price point? I think the venture capitalists were paying for you to sequence your gut microbiome and they may not be up for doing that anymore. Do you think are anyone around that might be replacing uBiome anytime soon that you’ve heard of?

Lucy:    Yeah. There are a couple of other companies using 16S. Thryve is one of them, Biome is also doing 16S along with 18S and ITS which gets at the archaea and the fungi as well. But the problem is neither of those, even before uBiome went away, neither of those compared with uBiome. If you ran a uBiome and a Thryve next to each other, there were huge discrepancies. Most of the clinical knowledge was built around uBiome, at least my clinical knowledge, I know Dr. Jason Hawrelak’s clinical knowledge was based on uBiome.

    It’s really I found it you know, when uBiome went away, I definitely looked at these other ones but I had trouble transferring any knowledge that we knew from the uBiome to the other ones.

    It’s not that they’re necessarily inaccurate, it’s just with 16S, it depends on the primers that you use and the database that you then match the sequences up against. It’s not that they’re not using sound methodology, it’s that they’re just -- it’s slightly different methodology and it’s leading to such different results that we can’t compare apples and apples anymore.

Christopher:    Right. That’s sad. I wonder what Jason Hawrelak is using now. I don’t know the answer to that because I know that yeah, it seemed like his practice was quite heavily invested in that technology.

Lucy:    Yeah. I’m not sure. I know that you know, for a while, I was using GI-MAP and uBiome as well and I’ve had some concerns with GI-MAP lately. They were using quantitative PCR but I had a practitioner friend who sent a split sample to them, and got widely different results from two different GI-MAPs. It was not reconcilable, the differences.

    For example, one came back with two parasites and the calprotectin which is a marker of gut inflammation of 415 which is off the charts. I mean if you have a 415 calprotectin, you should probably go get a colonoscopy and be checked for IBD.

    Whereas the other report from the same sample said no parasites which sometimes, there’s false positives and small negatives for those but the calprotectin was one. 

Christopher:    Oh, wow. That’s a huge discrepancy.

Lucy:    Huge discrepancy and I -- yeah, I just kind of lost faith in GI-MAP and it’s really unfortunate because I felt like they had the best panel in terms of providing PCR for all of these different microbes and also providing the clinical markers. It’s not to say that the entirety of the GI-MAP report is not trustworthy but it’s hard to know what to trust when you see results like that.

Christopher:    Right. Did GI-MAP Diagnostic Solutions reran hundreds, maybe even a thousand of those panels too, were they ever given an opportunity to try and explain that because humans are in a loop here, and so it could’ve been a machine that needed calibrating or maybe someone who was hungover. Stuff happens, right? If you can explain it, and fix it then maybe that’s okay.

Lucy:    Sure, yeah. They really didn’t have a good explanation for it. They did respond and didn’t really have much to say for it. I know that they did -- I believe they used to run their analysis in quadruplicate and then went down to duplicate. That may have been losing some of their internal reproducibility tests, not to get too much in the weeds here, but reproducibility is one of the key criteria for determining whether a test is useful.

    If we can’t send the same thing, the same sample, and get at least close to the same results then we really can’t be relying on it to make clinical decisions.

Christopher:    Right. You’ve been moving more towards the metagenomics. Are you working with clients at the moment? Are you running stool panels on clients at the moment?

Lucy:    My clients are getting -- often, they’re doing Onegevity for metagenomics currently, which I’ve been exploring more. I really like the raw data from Onegevity. Their reports definitely still need some work, but I’m in communication with the CEOs there. I know that they’re actively working on those.

    I’ve also been exploring Doctors Data and Genova which for a long time, only used the culture-based test, have now added PCR to their tests, so I’m also exploring those and comparing them to the metagenomics. I think that’s where we need to be moving.


Christopher:    Did you know that there used to be a lab called Metametrix and Genova bought the, and they killed the qPCR test. I’m pretty sure that happened around about the time that I came on the scene, maybe 2013 or something. It’s kind of sad that it went away. But yeah, that’s interesting that Genova are going back there.

Lucy:    Yeah, definitely. I think they’ve even introduced some subtyping for blastocystis which is really interesting.

Christopher:    Oh, my favorite subject. We’re going to jump around a bit now, but let’s talk about blastocystis. I’ve been following this with interest as well. It’s so tempting, isn’t it, when you’ve got a client that’s not feeling good and that have got a bunch of gut symptoms and you run a stool test. 

    It comes back and here’s blastocystis which is supposedly some parasite potentially pathogenic. You’re like, I found it. We went on a fishing trip and we found something or we caught something is perhaps a better word.

    Of course, you try treating it and if you’re lucky, it goes away, and who knows it went away because of the accuracy of the testing as we just talked about, or whether you really got it, but was it the cause of the person’s underlying symptoms? Really questionable at this time, right?

Lucy:    Right. It’s tricky. The problem is we don’t have an animal model so most of the studies are correlational, basically saying, comparing people who have IBS versus controls. Do people with IBS have more prevalence, higher prevalence of blastocystis infection than controls, and trying to do those comparisons and you know, we don’t have any solid evidence to say that it definitely is pathogenic.

    We have those correlational studies and then we also have a few case reports where you have someone who has blastocystis and has some symptom for example, like chronic urticaria is one that’s been commonly associated with blastocystis so you have a case report where you have someone who has that and they treat it with Flagyl, and it gets rid of the blastocystis, and their symptoms resolve, but was that really clearing the blastocystis or was that something that the Flagyl did because it’s changing the entire ecosystem?

    That’s why blastocystis and dientamoeba fragilis which is a similar parasite/commensal has been so tricky, is because we don’t have the animal models and we’re relying on those association studies and the case reports.

Christopher:    Right, right. Again, Jason Hawrelak has been super good here. I did his course on blastocystis and dientamoeba recently. I thought it was very good and he cited some of the research I’ve already read by Christen Stensvold, is it? The blastocystic.net. I’ve read his book and some of his original research.

    But I mean some of the clues that made me think twice about this is I’m pretty sure there’s some studies where they just grab  people in an airport and start taking samples and they find 50% in some cases that people have blastocystis, and it’s like okay, it’s like H. pylor over again. I think there’s something more to it than that.

Lucy:    Right, yeah. The prevalence is quite high. The other interesting thing is that I recently found an article where they -- blastocystis is thought to be an anaerobe so it doesn’t use oxygen for a long time. That’s what they thought, and then they recently found an enzyme called an alternative oxidase in blastocystis and found that it can actually respire oxygen and so it may actually buffer transient oxygen fluctuations in the gut. 

    I think I mentioned this last time on the podcast but one of the classic signs of dysbiosis from research that’s come out of Dr. Andreas Bäumler’s lab at UC Davis and Dr. Sebastian Winter at UT Southwestern that dysbiosis is characterized by this influx of oxygen, leaking into the gut and feeding opportunistic pathogens that can survive on oxygen. 

    This newest research on blastocystis suggest that it might actually buffer that oxygen fluctuation coming in so if it’s buffering it, maybe it’s preventing the overgrowth of other pathogens. If you get rid of that blastocystis, maybe your gut profile changes and now you have an overgrowth of proteobacteria. We just don’t know.

Christopher:    Right. Well, that’s going to be my next question. I realize we’re not going to get all the 12 myths at this rate, but that's okay. We can just refer people to the video replay of the talk. But yeah, I mean that’s still then the question is if not blastocystis then what? I think you’ve just given us the answer.

Lucy:    Yeah. I mean we just really don’t know what happens. There’s been some studies trying to look at is blastocystis -- does it lead to like -- does the rest of your gut profile look healthier when you have blastocystis and there’s kind of mixed results there. Some studies have found that when you're colonized with blastocystis, you tend to have a higher bacterial diversity, whereas others have found the opposite. It’s possible, it may depend on that subtype. We just don’t know yet.

Christopher:    Well, this leads us nicely into myth number two, what a healthy gut microbiome looks like. I’ve been reading some of your blog posts on this recently. I think you’ve been really good, and it kind of goes back to the Gopnik stuff like the difference between the carpenter and the gardener.


    Another good metaphor is the map versus the terrain, Richard Feynman once famously said, that knowing the name of something is not the same as knowing something, right?

Lucy:    Right, yeah. Definitely. I think this is a huge misconception is that we know what a healthy gut microbiome looks like and if we just do enough things to yours, we can make it look like one. The problem is it is a little bit different when we’re talking about does your specific individual gut microbiome look healthy and do we know in general what constitutes a healthy gut microbiome like population level?

    I think we know a little bit more when we look at an individual gut microbiome profile on a stool test. We know if you’ve got 10% proteobacteria that something’s going on there. 

    There are some keys we know looking at an individual that seem to be associated with health or disease and that is kind of on the higher level looking more at functions, so like proteobacteria, those like oxygen, we know that having more butyrate, that’s definitely a good thing. But on kind of a population level, we really can’t say like this is what a healthy gut microbiome looks like across people. 

    Part of that is that on average, two people share only about a third of their gut microbiome. The other two-thirds depend on a lot of different factors – our genetics, a lot of different environmental exposures, your diet, lifestyle, geography, early life exposures, those kinds of things.

    There’s really no core group of species that make up the healthy microbiome across individuals. The other thing is that we’ve really been, for the last ten years, with all these advances and technology, we’ve been really excited about the opportunity to do all these omics, right? Microbiomics, metogenomics, proteomics, it’s just gotten more and more complex. We’re just saying we need to just go more granular, get more and more data and we’ll finally be able to make progress, we’ll finally understand what a healthy gut microbiome is.

    But that’s just totally lack of framework for putting it together into anything useful.

Christopher:    So it’s understanding the ecosystem and the interactions and the interactions with the host and all that kind of stuff is what’s important.

Lucy:    Right. I think we need more of that systems thinking than just producing more volumes of data. And fortunately, a lot of researchers are starting to do that.

Christopher:    Do you think it’s possible to do it the other way around then? If we can’t say what a healthy gut microbiome is, can you say what it isn’t? A Via Negativa style, right? You just gave me a rule, right? So 10% proteobacteria is probably not good. Are there any other rules like that?

Lucy:    It’s hard to create hard and fast rules or reference ranges, but we do think that it’s a little more clear, starting to become a little more clear what dysbiosis is, and there does seem to be this signature of gut dysbiosis where in a healthy gut, most of the microbiome is predominantly they’re called obligate anaerobes, and that means they really can only grow and reproduce in an environment that’s really largely devoid of oxygen.

    That includes a number of beneficial bacteria like those that produce short-chain fatty acids like butyrate from fermenting dietary fiber. It has a really low abundance of facultative anaerobes. These are microbes that are capable of growing and reproducing an environment with or without oxygen.

    That includes a number of opportunistic pathogens, mostly in salmonella, pseudomonas, E. coli, desulfovibrio. What we see in dysbiosis is really a state of total organ dysfunction where you’re leaking oxygen into the gut because your gut barrier has essentially become inflamed. The metabolism has broken down. That leads to this oxygen influx into the gut, and then expansion of those opportunistic pathogens in the phylum proteobacteria, so family.

    Those are known to be highly pro-inflammatory. A lot of them have lipopolysaccharide that’s highly inflammatory to the gut and if it leaks into systemic circulation can definitely cause systemic inflammation as well. 

    We’re starting to see that microbial signature of gut dysbiosis, the kind of high proteobacteria and low abundance of those butyrate-producing and other important metabolic producing obligate anaerobes, and we see that across a number of chronic diseases now in which the microbiome’s been characterized including inflammatory bowel disease, colorectal cancer, IBS, diabetes, obesity.

    It does seem that while we’re struggling to determine what a healthy gut microbiome is, we’ve gotten closer to understanding that this is one common pattern of dysbiosis that seems to occur in a lot of different conditions.

Christopher:    Have you thought about any ways in which you could test that hypothesis, the oxygen leakage hypothesis directly? I’m thinking about those pill cams. Do they measure the gases, the various different points inside of the gut? Is that a possibility?


Lucy:    I believe those already are designed to detect the oxygen level as a way of determining where it is in the gut. I’m not sure how sensitive that is, the oxygen sensing as to whether it could pick up my new changes in the colon for example versus distinguishing between the oxygen levels in the stomach versus the small intestine versus the large intestine which is the most anaerobic environment of the three.

    But yeah, that would be amazing if we could start to examine that, although I got to say. It is a lot easier to just look on a stool panel and if you’ve got this overgrowth of the facultative anaerobes, it’s likely that that’s going on. It’s weighing the utility of that invasive procedure although, with the capsule, it’s a little less.

Christopher:    Right. Maybe the proxy’s good enough. Well, maybe that leads us into our next question which is does everybody need comprehensive gut testing? As athletes and optimizers, I love the idea that you could peek inside and find a problem that’s easily fixable and that somehow might improve your health or performance but do you think that’s just not possible at this time with the available comprehensive gut testing?

Lucy:    I think for some people, it can be motivating especially for people who struggle to maintain a healthy lifestyle for themselves. Sometimes, if they see that there’s improvement to make in their gut microbiome, perhaps they’re more likely to exercise or eat healthy or that kind of thing, but for a lot of people, again, we don’t fully understand what a healthy gut microbiome looks like and there’s a lot of variation in what constitutes healthy.

    Plenty of healthy people could get a stool test and kind of falsely think that they have an unhealthy gut microbiota. I kind of think of this sort of like genetic testing. You can think you have all these bad snps and maybe that’s worse than having the bad snps, and maybe that’s worse than having the bad snps.

    I don’t think it’s necessary if you’re healthy unless you really like -- you just really want to geek out about your microbiome and want to understand what’s there from more of like an education standpoint but I don’t think really think it’s necessarily going to lead to any action.

    If it does, there’s plenty of healthy people that for example, might see blastocystis and think oh, that’s a parasite. I’ve got to treat that, and yet they’re asymptomatic.

Christopher:    Right. You got to think theory. What am I going to do with the result? How will I respond if I see this thing that is potentially a pathogen? There’s been some really good discussions recently with Malcolm Kendrick and Ivor Cummins about the coronary artery calcium scan for this exact reason.

    Why are you doing the tests if you don’t intend to change anything based on the results and knowing that you have a non-zero amount of calcium could potentially hurt you, stress you out, then what are you doing it for? It’s like, I’m not sure I know what the answer is but it’s certainly interesting to think about.

Lucy:    I think we have a tendency and I mean myself definitely included to think that more data is always better. I think in a lot of cases, that is true to have more data about your health, but it’s important to think about how different results might lead to what actions and whether those are warranted.

Christopher:    Let’s talk about breath testing as a reliable way for assessing SIBO.

Lucy:    Sure. I’ve talked and written about this quite extensively. It’s probably one of the most controversial topics out there, but really, I just did a deep dive of the literature and I don’t think that we can rely on breath testing to test for SIBO.

    Part of that is because for years, we’ve been in the research, we’ve been looking at breath tests and comparing them to culture as the gold standard. We take the gold standard for SIBO diagnosis is doing an upper endoscopy, taking a small aspirate of the small intestine and then taking out that aspirate and culturing it in a petri dish and seeing how many colonies grow in that culture.

    There’s a certain threshold for SIBO diagnosis. If you meet that threshold in the culture, you’re considered positive for SIBO. Of course, we already discussed on the stool testing, many species that live in the small intestine can’t be effectively cultured. So the number of colonies you’re detecting in the sample is going to depend on your individual gut microbiome in the small intestine and the growth media that they choose to culture it.

    Issue number one is that breath testing has always been related back to culture as determining whether it’s reliable. That’s a huge issue. There’s been a number of studies that have confirmed that these culture-based methods actually underestimate the number of bacteria in the small intestine by about a hundredfold. 

    If you do that aspirate and you take it, and you do DNA-based methods like PCR, to see how many bacteria are there, you get nearly a hundred times more bacteria showing up than you did by that culture. That’s a real issue.


    Then it really comes down to a number of differences in your physiology. For example, the breath testing is basically -- for those who might not be familiar, you ingest a define amount of carbohydrate usually glucose or lactulose, and then you measure gases released in the breath over two to three hours. Usually, you’re measuring hydrogen and methane.

    The diagnostic interpretation is that if you have a rise of hydrogen before 90 minutes, that’s greater than 20 parts per million then that’s considered a positive test for SIBO. The major problem with this is that there’s a measure called orocecal transit time, and that’s a fancy word basically means that the time for the carbohydrate to get from your mouth to your cecum, which is the end of your small intestine.

    There was a study that basically administered radioisotope along with the lactulose carbohydrate and also did a breath test. They’re basically tracking this this radioisotope through the gut and they’re also tracking the hydrogen in breath, and they found that this orocecal transit time, the time it takes to get to the end of the small intestine which is supposed to be 90 minutes, right? It actually in IBS patients ranges from ten to 220 minutes.

Christopher:    Ten minutes, holy cow. That is fast.

Lucy:    Yeah. If it’s ten minutes and you’re seeing a rise in hydrogen at 30 minutes, then you might think that person’s going to be diagnosed with SIBO because that’s before the diagnostic threshold of 90 minutes, but for that person, that carbohydrate has already reached the colon. What you’re seeing is a signal of colonic fermentation not small intestinal fermentation.

Christopher:    Wow. But does this ultimately limit the clinical utility of the test? I was thinking about this. Is this why you know, certain practitioners who I won’t mention continue to promote the labs that make these tests and use them in their practice. Is that wise? Maybe it doesn’t work the way that they think it works, but it still works, right?

Lucy:    I mean perhaps, but colonic fermentation is a normal thing though. If we’re seeing this rise in hydrogen and interpreting it as small intestinal fermentation when indeed, it’s not, then we’re going to think there’s bacterial overgrowth in the small intestine, we need to kill that overgrowth. 

    I think that we can talk about the issues with that paradigm as well. Yes, there are potentially cases where especially if you were to do this radioisotope study in patients where you can actually see where it is and when you’re getting that rise in hydrogen perhaps, but there’s been a number of -- there’s one study that actually did a bunch of calculations and estimated that bacterial overgrowth at the level considered positive for SIBO is not even likely to produce enough hydrogen to result in a positive breath test.

    In most cases, except for post-surgical patients, any positive breath test signal in hydrogen is likely the result of fermentation in the large intestine not the small intestine.

Christopher:    Right. So you're getting all kinds of false positives and negatives. I’ve actually heard some of these practitioners. I think we’ve seen it. We’ve not run many of these tests, we’ve run a few and we’ve already seen it. I’ve heard practitioners talk about it on other podcasts is that quite often you’ll get a positive retest that the client or patient can’t reconcile with the life experience. 

    It’s like I made all these changes and I feel so much better so I’m really excited about redoing the SIBO breath test and the result comes back and it’s still positive. What’s up with that? Am I still broken? Could I be feeling better? The answer is it’s probably the test is broken.

Lucy:    Right. I think that’s true in a lot of cases. It goes back to what are we hoping to get from the test. I always give -- I think testing in general, having more data is generally useful. I think the best test of all is, are you feeling better?

Christopher:    Right, your subjective life experience.

Lucy:    If your microbiome profile improves but you’re feeling so much worse, I’m not sure I care what your microbiome is doing because we don’t know all of the variables in the system even with a stool test. Only 50% of the sequences in the gut are matched up to microbes. We don’t even know what the other 50% is often. There’s such enough that we don’t know that I do use some testing with my clients but I really rely on symptom changes more than anything else.

Christopher:    Right. Well, that leads us nicely on to your next myth or misconception. Most bloating distension gases from SIBO, we need to kill the overgrowth. I think the emphasis is on the word overgrowth there, right?

Lucy:    Right. There was a really interesting paper that came out last year in Nature Communications. This research group found that small intestinal dysbiosis, not bacterial overgrowth is what underlies a lot of those symptoms – gas, bloating, abdominal pain. In other words, it’s not the bacterial number in the small intestine but it’s a shift in the types and functions of bacteria in the small intestine that are contributing to the symptoms that we think of as SIBO symptoms.


    I think this kind of comes back to thinking of -- the need to think of the gut as a complex system because if we just assume oh, it’s just too many bacteria, we can just kill those off, we’re not really thinking about how that’s influencing the entire system. 

Christopher:    Yeah. It’s such a good point, isn’t it? Is this just a natural byproduct of the way that the system has been investigated, right? We’re just giving things names. Then when it doesn’t work the way that you hope, because you don’t have any real understanding of how the system is working with it’s complex interactions, you just think well, it must be too much of the thing and then let’s just kill it off, see what that does, right? It’s just a fundamental misunderstanding of a complex system.

Lucy:    Right. It was born out of good intentions. The original research on SIBO came from Mark Pimentel’s group. I mean they were instrumental in even identifying bacteria as the cause of irritable bowel syndrome. They were just a little bit misguided as to the fact that it was too much bacteria, it was overgrowth instead of the fact that it seems to be dysbiosis, kind of a shift I the ecosystem.

    I’m of the belief that we need kind of more supportive interventions to support the gut environment kind of, and then the -- basically, our gut barrier and our gut immune system, that whole system is set up to make our gut microbiome beneficial for us. Over thousands of years, our microbiome has evolved within the confines or our gut.

    If we can support our gut barrier or our gut environment, the terrane, it often is going to top-down select for the microbes that are beneficial to the host.

Christopher:    How do we do that? Minimizing mismatch, species appropriate diets, all that kind of stuff.

Lucy:    I think it comes back to all of those major health behaviors certainly, and then there are certainly some things on top of that we can potentially do to support that gut ecosystem so one supplement I didn’t mention in my talk that could be particularly beneficial in supporting the gut immune system that’s come out recently is serum bovine immunoglobulins. This are basically kind of like added immune support for the gut until it can recover.

    I’ve seen a lot of benefits with those especially in people with the small intestinal dysbiosis. But certainly, it really starts with the healthy diet and lifestyle. Interestingly in this study that they found where they found that the dysbiosis is what underlies functional GI symptoms.

    They actually found that the symptomatic patients, they had lower bacterial diversity but they also had an enrichment of bacterial pathways associated with the metabolism of simple sugars suggesting that maybe they’re really being fed in a lot of cases by people consuming simple sugar. It’s possible that even just trying to shift the ecosystem, perhaps get a little bit more fiber in the diet if it’s tolerated, can really be beneficial for shifting the ecosystem back.

Christopher:    I believe Megan has had good results with clients with the serum immunoglobulins, the SBI Protect I think is the product that she’s been using, and you can search the forum for that, and you’ll find all the references.

    Well, let’s talk about something that I know is going to be important for my listeners. A high-fat diet is bad for the gut.

Lucy:    Yeah. I feel like this is a very common thing in the blogosphere is that a ketogenic or a high-fat diet is going to ruin your gut. If you don’t have those whole grains and legumes, then you can’t possibly have enough butyrate from the fermentation of those to feed the gut lining.

    I think there’s a lot of misconceptions in this are in particular. A lot of that comes back to the fact that in the literature, there’s a lot of studies on a high-fat diet in the literature for animal studies. The problem is these studies are really misleading. A rodent high-fat diet is really a diet that’s high in refined soybean oil and refined sugar and low in fiber.

    We’re using that as a comparison to humans that are eating a ketogenic diet that’s rich in high quality meats and vegetables and high quality fats. I think that that’s one major problem and also that the lab mice of choice that are used with that high-fat diet in the literature are actually selected or weight gain. Weight gain we know has a corresponding response in the gut microbiome.

    There’s some major issues around animal studies and people often say well, we have to rely in the animal studies because we don’t have human studies, but there actually was one done in 2014 where thy basically put people on a plant-based diet for a few days and then they put them on an animal-based diet for a few days, and then back again. 

    They showed that the diet alter the gut microbiome composition within 48 hours. That was kind of the major finding that was touted from the study that diet rapidly and reproducively shifts the gut microbiome.


    But what a lot of people don’t look at in this study is that if you look deep in the supplementary data, the animal-based diet was actually ketogenic. This is kind of the study that people are saying we don’t have of the ketogenic diet on the gut in humans and granted, it was a very short-term study but I think in general, it just points to the metabolic flexibility of our gut microbiome and the ability to shift with adapting dietary pressures across our evolution with our gut microbes.

Christopher:    This certainly makes sense when you think about it from -- I mean humans are everywhere and they eat everything. Perhaps, the reason they’re everywhere is because they can eat anything. It makes sense that the whole thing would be flexible and be able to adapt to different diets.

Lucy:    Yeah, definitely. That’s actually been shown in for example, the Hadza hunter-gatherer groups has been -- their microbiota has been shown to isolate with the seasons depending on what they’re eating and what’s available during that season. Many of the microbial taxa that dropped undetectable levels in one season are actually those that flourish most in the next season.

    Some of those same microbes are rare or absent in industrialized populations. It’s possible that that metabolic flexibility is actually enhancing diversity. I haven’t seen any studies like this in a western context where it’d be really interesting to put people for example on cyclical keto and see if it has any influence on overall diversity. 

    I haven’t really seen anything like that but certainly, these hunter-gatherer studies kind of suggest that maybe we’re missing seasonality in the modern world and the influence it has on our gut microbiome.

Christopher:    You’re not worried about postprandial inflammation that might be the result of a high-fat meal either through endotoxin or just the increase of plasma-free fatty acids. That’s something that’s been discussed in office hours and on the forum recently.

Lucy:    I’m certainly not an expert in those areas. I do think that there is some increased LPS absorption typically with a high-fat meal but I think if you have ongoing gut inflammation and intestinal permeability, then the amount of LPS that you’re going to be getting from that continuously, chronically, is probably much more significant than the amount you would get, the increased absorption you would get through chylomicrons from a high-fat meal.

    I’d like to see more studies on this, but I think it’s quite likely that ketones actually support gut barrier function, and so yes, we might be getting slightly more LPS absorption from the high-fat meal helping to translocate LPS, but perhaps that’s even helping with its detoxification in the liver, there’s some studies to suggest that a little bit of that might be going on.

    That might even help with gut inflammation if it’s transporting those out of the gut for detoxification, perhaps it’s helping support the gut lining. I think we need more studies in that are before I can say that that’s not significant. But there are plenty of examples we have of ancestral populations who ate a high-fat diet. I certainly don’t think that they were overcome by LPS from their high-fat meals, right?  Populations like the Inuit. They certainly have very low levels of chronic disease.

Christopher:    It’s hard for me to not draw comparisons with what people have said about LDL, right? It’s like, it’s not the LDL. It’s the barrier function. You need to worry about your endothelial health and I wonder if the same is true here. It’s not the LPS, it’s the endothelial function. You need to worry about the barrier, not the thing that’s there anyway, right?

Lucy:    Right. Yeah, definitely. I think it’s quite possible that ketones could actually help to tighten up the gut barrier, so they actually feed into the same pathway as butyrate and so it’s possible that for some people, they might get improved gut barrier function on a high-fat ketogenic diet that might significantly reduce the amount of that LPS that’s getting into circulation, even if they’re getting some translocation with the fat.

Christopher:    Well, talk about exercise. That’s definitely something that’s going to be of concern to my listeners. I guess the question -- I mean so the myth or misconception of more exercise is better, I’m not sure if anyone listening really believes that. They know that if they do a certain duration or intensity, especially over subsequent days that can often lead to GI distress. I’m not sure that that’s maybe something we want to cover. 

    What might be of interest is like well, how much is too much? Is there a way for people to figure that out or is it just -- you just have to like notice the symptoms?

Lucy:    Yeah. That’s tricky. I think it really is symptoms because I think too much for one person is not the same as too much for another. It depends on your level of training. We’ve got some preliminary data from our lab that suggests that you might be actually train the gut barrier. 

    For example, after significant hard aerobic exercise, you do get acute intestinal permeability and you do get some LPS in the blood stream especially after a marathon. Most marathon runners do have endotoxemia after they run. But actually, with exercise training, you may actually reduce that LPS translocation that occurs during aerobic exercise. It’s almost like you’re strengthening the gut much like you’re strengthening your cardio-respiratory system, your muscles. 


    I think there’s going to be great variation in what constitutes too much exercise. Someone with colitis for example is going to be able to tolerate a lot less exercise likely than someone who’s healthy and does not have any GI symptoms.

Christopher:    I wonder as well, is if it would be a mistake to try and counter that increased intestinal permeability, is that part of the training response? Is that how we get stronger is this hormesis? I don’t know.

Lucy:    That’s a great question. There have been some studies looking at for example, taking zinc carnosine before exercise, can you blunt that acute permeability that occurs? But you’re right, perhaps that is blunting the training response, much like antioxidants could blunt muscle adaptation.

Christopher:    What happened with the zinc carnosine? Were they able to stop the intestinal permeability?

Lucy:    It’s been a while since I looked at that study but it definitely significantly attenuated it.

Christopher:    Okay. Let’s skip over a couple of here. I’ll refer people to my interview with Jason Hawrelak and with you and to your talk. You talked about do probiotics recede the gut microbiota and the probiotic strain doesn’t matter. I think we’ve talked about those before and I think you did a really a good job in your talk. Let’s skip over those.

    There’s an important one here. You should always take probiotics after antibiotics. I think I’ve been guilty of saying that too as well.

Lucy:    Yeah. This is a big one and one that I was fooled by for a long time. It seems really intuitive that when we take antibiotics, we’re basically clearing out our gut system, so why not put some beneficial bacteria back in there? Even a lot of doctors are prescribing probiotics after antibiotics now.

    To use an analogy that I used in the talk, it’s kind of like back to thinking about your gut as an ecosystem. Before antibiotics, you’ve got this dense rainforest of hundreds of species in the interactions. Then after antibiotics, those species have been knocked down and the terrane’s all depleted, maybe you’ve got a few seeds left in the soil.

    The real question is how do you restore that rainforest, right? One option could be to plant kale and arugula. Those are beneficial species. But those are going to take up niches meant to be filled by native species. This was actually what was found by a group in 2018 was that when they gave probiotics, lactobacillus, and bifidobacterium blend after antibiotics, it actually delayed the restoration of the native microbiota including delaying a lot of the butyrate producers from coming back.

    Yes, probiotics after antibiotics may have some benefits. It’s possible that in hospitalized settings especially, they could prevent overgrowth of opportunistic bacteria like clostridium difficile, for example, or could prevent antibiotic-associated diarrhea, but I think it’s more nuanced. We need to think about the fact that while we might be mitigating those risks, we are potentially delaying the return of the entire gut ecosystem.

    What I laid out was that the alternative would be to support the health of the soil. We know that a healthy gut environment naturally selects for and supports healthy microbes so if we can support the health of the soil for example with butyrate, we can actually support gut hypoxia.

    One of the things that actually happens after antibiotics -- during and after antibiotics is that oxygen leakage into the gut. That’s one of the major reasons why antibiotics cause loss of gut diversity potentially is because it’s leading to this oxygenation of the gut and leading to overgrowth of opportunistic pathogens. 

    If we can support the gut epithelial cell with butyrate, we can actually potentially prevent that antibiotic associated dysbiosis, and this has been shown in studies to reduce the advantage of some of those pathogenic microbes. I think a better approach is to really support kind of the soil with things like butyrate and then also potentially recede the native species. This would be with autologous fecal transplant, transplanting a bit of all of those original species that you had in your gut back will help it return faster.

    In fact, they showed in this study that I mentioned in 2018 that if you basically banked the participant’s stool samples before they got antibiotics, and then reinoculated them with a personalized fecal transplant after antibiotics, it restored the composition of the gut microbiome all the way down to the mucosal level in less than a single day.

Christopher:    Wow. Who’s going to be the first to do autologous FMT?


Lucy:    Yeah. I don’t know. I think it really has incredible potential to prevent chronic disease. We know that successive rounds of antibiotics especially in early life can potentially lead to increased risk of chronic disease.

    I’d love to see more studies on this that are kind of thinking about this restoration of the gut ecosystem from more of a holistic perspective because I think there’s been too much focus on oh, let’s just do probiotics and that will be enough or that will at least make me feel like I’m doing something for my gut, right? It’s why a lot of people take them.

Christopher:    So to be clear then, you would never recommend taking probiotics during or immediately after a course of antibiotics. Let’s just make it clear that you’re not a medical doctor and this is not medical advice and all of that usual stuff. But say it was you, what would you do? Under what circumstances would you take the probiotics?

Lucy:    Personally, probably only if I was hospitalized and at significant risk for C. diff and then in that case, I would probably take saccharomyces boulardii but I would probably also be taking plenty of butyrate as well to support the gut epithelium.

    I think in a lot of cases, also just thinking about how to support the soil, if you will, support the environment, it’s also just making sure that after antibiotics, you are really being strict with your diet, trying to eat more fiber not eating sugar that’s going to feed the pathogenic microbes to try and help the prebiotics will help restore the healthy gut ecosystem.

Christopher:    Well, let’s talk about prebiotics then. Should we all be taking resistant starch? I think everyone knows the answer to that right now. Is anyone still taking resistant starch? I mean it’s pretty awful, isn’t it? I don’t think anyone takes a supplement for an extended period of time unless it tastes good or it’s having an obvious benefit. Do you know anyone that’s taking potato starch and said, “Oh, this is great. I love the way that this makes me feel,” but I have never met someone like that. Have you?

Lucy:    I can’t say that I’ve met a lot of people who have had a lot of benefits from it. There’s definitely anecdotal reports out there on the internet of people --

Christopher:    Exactly. The blogosphere is like full of those stories but I had just not met many clients in real life that have had great results with it.

Lucy:    I think that’s tricky though because if they’re clients of ours then they’re struggling with their health, if it worked, they wouldn’t be coming to us so I struggle with that because I recognize that the population I’m seeing is probably a bit skewed towards people who have tried the interventions that are well known and they haven’t worked.

    But that being said, I think there are still practitioners out there who are recommending supplementing with resistance starch as a way to correct gut dysbiosis. I think it’s common enough that I wrote an entire blog or article about it recently but I think it really comes down to the fact that first, prebiotic response is really individualized so it really depends on your base line gut microbiota in terms of what response you’re going to get.

    It’s not necessarily -- you’re not necessarily going to get the same gut microbiome response that’s been reported in the literature as the average across a large group of subjects.

    The other thing that I pointed out in my talk, there was a -- actually just last December, just a couple of months ago, there was a study by Dr. Turnbaugh’s group at UCSF where they fed mice in humans raw or cooked tubers and they found that the raw tubers led to lower diversity and increased microbial damage to a similar degree as antibiotics.

    This was really interesting, and I think suggest that maybe some people are getting a benefit from taking raw potato starch, but maybe it’s just because it’s acting almost you know, it’s damaging certain gut microbes and perhaps, it’s even acting sort of like an antibiotic in terms of the fact that it’s clearing out some of the bacteria that are causing them symptoms.

    But I don’t think it’s the way to long-term gut health. I generally recommend avoiding supplementing with raw starches, like potato starch. I think there’s enough studies to suggest that it might be problematic and focusing more on whole food sources of resistant starch for example. Type 3 is the retrograde cooked and cooled resistance starch, from cooked and cooled potatoes, rice. That’s much more evolutionary familiar than just eating raw tubers.

Christopher:    Would you say the same is true of the fructo-oligosaccharides and the galacto-oligosaccharides like inulin for example? I’ve seen a couple of studies with highly variable glycemic responses to that. It’s the refined carbohydrates, what it is, right?

Lucy:    I think the responses are still highly variable. I haven’t seen any studies suggesting that those produce microbial or gut damage, but certainly, just from experience working with clients, there are people who have rampant gut inflammation or bloating and they definitely do not do well implementing inulin and fructo-oligosaccharides especially in higher doses.

    Typically, my approach has been to kind of try and bring down inflammation and reduce symptoms before diversifying in terms of prebiotics and then when we get to that point, doing so more with wholefoods than with isolated supplements because we really don’t know how when you put five grams of isolated inulin, how that’s going to affect your particular system.


Christopher:    Yeah, absolutely. Hopefully, it's first. I mean, that's easy, isn't it? I can definitely do that and then that’s one less supplement to worry about. Okay, so let’s just do one last one. All herbal antimicrobials are safe and effective.


Lucy:    Yeah, great. This one, I think, you probably talked about herbals a little bit with Dr. Hawrelak as well but I think these really do have great potential to modulate the gut microbiota so we know of many herbs that have been shown to act as prebiotics. They stimulate the growth of beneficial bacteria and they seem to inhibit pathogens at the same time. 

    Some herbs do really seem to be selective in terms of supporting the beneficial ones and inhibiting pathogenic ones. But there’s also a number of supplements that could potentially do a lot of harm.

    For example, actually Jason Hawrelak’s work has shown that at least in vitro, grapefruit seed extract is worse than clindamycin, an antibiotic. This is in terms of its inhibition of beneficial bacteria.

    I think what I discussed in my presentation was that yes, these herbals have great potential but if we use them indiscriminately, even with good intentions, we could potentially be causing long-term damage and loss of gut diversity.

    I think there really need more studies on how these herbals are affecting the gut microbiome. Unfortunately, it’s really hard to get funding for any kind of studies like that with natural products is much more difficult.

Christopher:    Right, and that’s because they’re not patentable, not really a good business model there, how you’re ever going to get the money back for your study. Are there any herbs that you’ve been using in your practice that you found to be useful?

Lucy:    Yeah. There’s quite a few. Basically, since we don’t have a lot of studies on how herbal supplements affect the composition and function of the gut microbiome, I’ve largely relied on herbs that I feel have a lot of evidence behind them in terms of their symptom improvement for various gut conditions so a few of those are Atrantil, which is particularly effective for people with constipation, methanogen overgrowth, and has been shown in studies to improve symptoms of IBS with constipation.

    Iberogast is another one that I like a lot. It’s been studied since 1990 like over a dozen clinical trials and has shown effective reduction of symptoms in IBS and I believe functional dyspepsia. It also interestingly has a number of herbs that kind of support the gut pathways that prevent oxygen influx into the gut as well.

    I like it. It’s a little bit more -- feel like it’s a little bit more of a supportive herbal instead of kind of inhibiting growth of microbes. But again, we don’t have a lot of studies as to how it actually impact microbial composition but I feel much more comfortable using things like this that have been studied for gut issues for various different gut conditions for many years.

    Then the last one that I mentioned in my talk was triphala which has prebiotic properties. It’s an ayurvedic formulation of three dried fruits. Don’t ask me to pronounce them, but it’s been used for a long time as a remedy for GI disorders of various different kinds and there’s some promising animal models that show benefits for that physiology.

    Those are kind of given that that we need kind of things that can modulate the gut microbiome. I’m largely relying on ones like these that I mentioned that have that clinical, efficacy and clinical safety as well because there’s a lot of different herbal blends out there, and a lot of them have only come out in the last three or four years and we just really don’t know what impact they’re having on the gut microbiome. 

Christopher:    I totally agree with that. I mean I would say that we’ve had a lot of success with our clients in our practice with some of these herbal formulas but I would not like to speculate exactly how it is that they’re working. I don’t think I really know.

    I think at least myself personally, that was kind of how I got into this was somebody through the herbal kitchen sink at me, and I deflated like a balloon over the course over the next couple of weeks. I can remember vividly being terrified of stopping all these herbs I was taking because I was sure that the bloating would come right back. It never did. It was obviously incredible.

    I had already made the fundamental changes to my diet at the time, so I’m pretty sure it was just the herbal protocol that was doing that. It’s not like I switched from eating a bunch of pasta after a eating a wholefoods diet at the same time, so I’m pretty sure -- but literally, I took all the herbs. I couldn’t tell you what I did or how it had an effect, but it was really quite incredible.

Lucy:    Right, yeah. I think they are really beneficial for a lot of people. I think we need to be a little bit more careful with what we use, how much we’re using them. I’m certainly a not an herbalist so I don’t want to pretend to understand all the mechanisms of how this work. I don’t even think we know for a lot of them especially things like triphala, it’s just got a long history of use. I think that that supports its use today as well, but yeah, we don’t necessarily know all the mechanisms that they work by.


Christopher:    Well, this has been really helpful. I will of course link to your slide deck plus the full video version of the talk that was given for the UCSF group.

    Tell us. What are you doing now? What are you working on? Are you seeing clients? Are you creating training courses? What are you doing?

Lucy:    Yeah. I’ve got a number of things in the works now that I’m fully independent. I’ve of course got my blogging. I’m going to be ramping up quite a bit. I’m now accepting clients, so excited to work with anyone who would like to. They can go to my website, and check that out.

    I’m also creating a number of advanced gut courses so people can also support my work on Patreon and get free access to those upcoming online courses. In the long-term, I’m also hoping to start podcast and maybe bring back up a citizen science project start-up idea we had last year. Maybe I can come on and talk about that again in the future.

Christopher:    Excellent. I look forward to that, and recording a person -- none of this Zoom nonsense. I will look forward to that.

    Tell us about the training courses. Who are they going to be for? They’re going to be for people like me? Are they going to be more aimed at clinicians? Who are they going to be for?

Lucy:    Hopefully, both. I’m hoping a more similar along the lines of my blog resources, kind of a deep dive into gut health for patients who are pretty gut savvy, so individuals who want to learn more about gut health but also practitioners who are hoping to learn more as well, so hopefully, hitting that middle of the road so it’s understandable across the board.

Christopher:    Yeah. I’m hoping you’ll keep it bite-size, just because I know that people tend to disappear like with this grand vision of some huge training course with a 160 different modules, like and then just never reappear with. If they do, it’s not what everyone hoped for. 

    When I looked at your talk that you gave at UCSF, I thought each one of these 12 things could be -- I would pay, I don’t know, $50 or a hundred dollars or something just for a 30 to 60-minute presentation on just this one topic, just give me the references. That’ll be great. I’ll be super happy with that rather than it being like a 12-module training course that I have to wait two years for.

Lucy:    Well, I’m definitely planning to release each little segment. I’m hoping that overall, it will build a comprehensive course, but I’m definitely planning to release them as I go so actually hoping to have the first one ready in just a couple of weeks.

Christopher:    Okay. What’s the best way for to people to find out if they head over to lucymailingphd.com, they could get on your email list and then you get notified when the courses start coming out?

Lucy:    Yup. It’s just lucymailing.com. Yeah, and I’ll be releasing my courses there or they can join my Patreon, and I’ll certainly announce it there as well.

Christopher:    Excellent. Well, this has been fantastic. Thank you so much, Lucy. I really appreciate it.

Lucy:    Yeah. Thank you so much for having me on again. Great talking to you.

Christopher:    Thank you.

[1:03:30]    End of Audio

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