Dr. Michael Ruscio, DC is a clinician, Naturopathic Practitioner, clinical researcher, author, and adjunct professor at the University of Bridgeport. His work has been published in peer-reviewed medical journals and he speaks at conferences around the globe.
Can you manipulate your microbiota to lose weight? Is there a direct cause and effect between the microbiota and obesity? Let’s take a look at what the research really shows.
If you need help with your microbiota or weight, click here.
Dr. R’s Fast Facts
Please see transcript below for full references.
The best scientific data to date shows there is no consistent correlation between obesity and the microbiota.
High-level data also suggests the microbiota does not cause obesity.
This means microbiota testing has little value in treating obesity.
This is supported by the clinical data showing poor results when manipulating the microbiota in attempts to treat overweight/obesity:
The best results achieved was 2.3 pounds of weight loss.
2.2 lbs. w/ Lactobacillus gasseri
3.7 lbs. w/ Lactobacillus rhamnosus CGMCC1.3724.
One review showed fiber’s average weight loss effect was 4.2 lbs.
Fecal Microbiota Transplant (FMT):
A study was performed where the feces of lean men was transplanted into recipients who were overweight and had high blood sugar levels. Unfortunately, there was no change in weight or body fat.
Most of the confusion about the microbiota in obesity comes from:
Misinterpreting human data. For example, thinking those in the US should have the same microbiota as Africans; the microbiota that helps African’s may make those in the US constipated and fat.
Over-extrapolation of data from animal studies.
Examining only one side of the data.
The small intestine is not tested in current microbiota testing. The small intestine is responsible for 90% of caloric absorption and represents over 56% of the digestive tract. The small intestine is also more prone to leaky gut and likely has the largest impact on your immune system.
Topics: Fast Facts…..0:42 Episode information…..3:05 The Research – The high-level data…..7:07 The Research – Clinical trials…..12:45 The Research – Animal studies…..27:49 The reasons why we see little connection between microbiota and 0besity…..37:39 Are probiotics recommended?…..40:52 Episode wrap-up…..43:40
(7:22) There is currently no consensus as to whether the gut microbiota plays a causative role in obesity or is modulated in response to the obese state itself or the diet in obesity. http://www.ncbi.nlm.nih.gov/pubmed/21559992
(22:20) A study was performed where the feces of lean men was transplanted into recipients who were overweight and had high blood sugar levels. Unfortunately, there was no change in weight or body fat. http://www.ncbi.nlm.nih.gov/pubmed/22728514
(38:33) Carbohydrate intake might be primary way to influence small intestine microbiota; this might be why carbohydrate is important for GI health and for metabolism. Small intestine also has highest density of immune cells in entire body; GALT and Peyer’s patches http://www.ncbi.nlm.nih.gov/pubmed/25308830
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Now, let’s head to the show!
Dr. Michael Ruscio: Hey, everyone. This is Dr. Ruscio. Just wanted to give you your fast facts for today’s show, which is on the microbiota and obesity.
The best science to date shows there’s no consistent relationship between obesity and the microbiota.
High-level data also suggests that the microbiota does not cause obesity and is more so a reaction to the obesity state. This means microbiota testing has very little value in treating obesity, at least right now. This is supported by clinical data showing poor results when manipulating the microbiota in attempts to treat overweight or obesity.
In prebiotics, we see the best weight loss of 2.3 pounds; in probiotics, we see the best weight loss of 2.2 and 3.7 pounds; with fiber, we see an average weight loss of 4.2 pound; and with fecal microbiotal transplant therapy, or FMT, we see no change in weight or body composition.
Now, you’ve probably heard things that are different than what I just said. Most of the confusion about the microbiota, in my opinion, comes from misinterpreting human data, for example, thinking those in the US should have the same microbiota as those in Africa. The microbiota that helps Africans may make those in the US constipated and fat. We elaborate in the episode. Also because of over-extrapolation from animal studies.
Additionally, potentially this comes from examining only one side of the data, and finally, the confusion here or the inconsistency in results or the lack of really great results may come or stem from the fact that the small intestine is not tested in current microbiota testing. This is relevant because the small intestine is responsible for 90 percent of caloric absorption and represents 56 percent of the digestive tract—56. The small intestine is also more prone to leaky gut and likely has the largest impact on your immune system because it contains the highest density of immune cells in the entire body, known as the gastrointestinal associated lymphoid tissue and Peyer’s patches.
So that’s the brief rundown on today’s show. I think you will hopefully find it very insightful and informative, and we will jump in now. Thanks a lot.
DR: Hey, folks. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio, and I am with here with the lovely Susan McCauley. Hey, Susan!
Susan McCauley: Hey, Dr. R! What’s going on? What do you have on tap for us today?
DR: Well, I thought today we could revisit and maybe expand upon the microbiota in obesity.
SM: I think that’s awesome because I have to tell you I was on one of my Facebook groups yesterday, and it was a Facebook group for a specific diet protocol. I belong to the group, and I kind of follow their program a little bit.
SM: I don’t want to give names or anything, but somebody was asking questions about this program and said, “Well, maybe I should just focus on changing my microbiota to lose weight instead of, like, just, I don’t know, eating real food.”
SM: And I was like, “What?!” I said, “Once you dig into the research, there’s not a lot there,” and then you pinged me and said this is our topic, and I said, “Perfect.”
DR: Sweet. So we’re in synch. Yeah, I definitely cringe a little bit at hearing someone make that remark because just like you said—and I know we’ve had a lot of off-air discussions about this—when you really dig into the research and the literature and the studies, you see there’s very little there that can really recommend any kind of microbiotal manipulation or testing in the endpoint of obesity. I think it’s really important for us to have this dialogue because what we don’t want to do is find one study and support a clinical recommendation off one study, especially if it’s an animal study or a mechanism study, because that’s just not how one derives human recommendations.
There’s a lot to discuss in this regard because I want to provide people with a responsible narrative on this topic, and admittedly, I have been a bit critical of others regarding microbiota research, but I only am critical because I see the patients walking into my door who have wasted money or tried microbiotal treatments and been very frustrated at the lack of results that they’ve seen and have been astonished when they find out that the science behind X, Y, or Z is very sparse and they were really kind of led astray. So I’m critical because I care about people, and I think we really, in all things, need to be careful with the recommendations we make.
The good thing about this space is also one of the bad things about this space, which is there are a lot of excited people that want to get the information out there. That’s great! But it also can be problematic when people don’t do their due diligence and fact check and take the time to really understand what they’re talking about and to understand if they’re making a qualified, quality recommendation.
SM: Right. And I think people fall into one of two camps when they… I don’t want to say “fall” for these things, or when they do these things. They’re either really, really sick and they’re desperate or they’re looking for a quick fix.
SM: They’re very polar opposites. People in the middle of the road don’t tend to go down these avenues.
DR: Right. And sometimes there is a quick fix and something there’s a great treatment for someone that’s really, really sick, but it’s unfortunate that the people like you described at both ends of the spectrum are almost grasping for straws and sometimes that’s taken advantage of.
SM: Right. I agree.
DR: So let’s jump into the topic of what we can say—what we can confidently and reasonably say—about the microbiota as it is related to obesity. Let’s start with what the high-level scientific data shows, and then we’ll talk about what the clinical trials show, and then we’ll talk about some underlying mechanistic stuff.
The research – the high-level data
DR: There is no consistent consensus or association between the microbiota and obesity, and I’ll just quote one paper here. “There is currently no consensus as to whether the gut microbiota plays a causative role in obesity or is modulated in response to the obese state itself or the diet in obesity.” (1a)
SM: I think the keyword there is “cause,” right?
DR: Right. The keyword is “cause.” Yes.
DR: We see that there is no causative association or even a consistent association established between obesity and the microbiota, and that’s according to one review. Review papers are high-level scientific evidence. There are also two other review papers that have reinforced this (2a) (2b), and maybe the most impressive is a recent systemic review with meta-analysis. Again, this is where we go through a number of, usually, randomized controlled trials and try to look at all the available randomized controlled trials or at least other high-level data and summate that to find what the majority of the data shows, because as I’ve said before, one study does not a case make. We shouldn’t be overly confident in recommending something if one study finds something, but if we look through the breadth of available studies and we see a trend or a consistency, now we’re starting to firm something up, now we can start making a recommendation in confidence.
So we have three review papers, one meta-analysis with systemic review (3a), and this meta-analysis has shown, for example, some studies, yes, do show that the Firmicutes-to-Bacteroidetes ratio does tie with obesity, but as I’ve said before, there’s an equal amount of studies that show there’s no association between the Firmicutes:Bacteroidetes ratio in obesity and even some studies showing the opposite trend, that having high levels of Firmicutes actually makes you skinny. The erroneous assumption is that Firmicutes makes you fat, but that’s not been well borne out when we look at the human studies. When we look at the animal studies, we can very easily be misled. It’s important for people to know that because you may go somewhere else and hear someone really jazzed about this, and I guarantee you they’re referencing either a few of the human studies or the animal studies, but we have to look at all the evidence as a whole, because if we don’t, then we’re just cherry-picking data to reinforce our previous opinion.
SM: Right. It’s the same thing like today. I don’t know if it happened to you, but I was bombarded with the whole red meat thing again today, and it’s like, this is one study—one study. When there’s just one study or even one or two studies, we need to look at the whole body of work, and that’s why these review papers and meta-analyses are so important to look at.
DR: This is really good science, and it’s something that I’ve learned over my career of segueing now into research where we just got our IRB approved for the clinical trial we’ll be doing through my office, and we have two others—maybe even a third study—that will be coming out of my office hopefully within the next year, and I’ve been spending so much more time in the literature over the past few years, I really have noticed my own maturation as a researcher and a scientist, where I used to fall into that very trap of finding a mechanism study or finding an animal study and really just getting jazzed about that and running with it, and now I’ve learned that before I make an opinion or a recommendation, I really have to take some time to look into this stuff more broadly because, yeah, just like you said, we shouldn’t be making recommendations based upon one study. That’s an easy way to make a non-quality recommendation.
There are a couple of other things from that meta-analysis I wanted to show or to highlight, which is that diversity, according to this meta-analysis, also does not show a consistent correlation with obesity.
Now, there is one finding here that we start seeing substantiated, and this is a little bit off the topic, but I just want to make this note that microbiotal assays may be a potential screening tool for inflammatory bowel disease, like Crohn’s and ulcerative colitis. It doesn’t mean that we have a treatment based upon this, but it may be a screening tool.
That’s most of the high-level scientific data on this, but there’s one other review that I’d like to quote also. This review essentially came to the conclusion or suggested the conclusion that “changes in the gut microbiota are an association with rather than the cause of obesity” (4a). We’ll put the links to all five of these studies in the show notes, but I want to reiterate for people that this is the highest level of scientific evidence that we have. Systemic reviews and meta-analyses of randomized controlled trials are the highest-level scientific data that we have, and we see a consensus in these various high-level scientific reports that there is no association, no causation, and maybe even that the microbiota is skewed—even though it’s not skewed consistently—may be skewed in a response to obesity rather than as a cause of obesity.
The research – clinical trials
DR: And now we are going to transition to the clinical trials where we’ve done studies to manipulate the microbiota to see if we can produce weight loss, and we do not see great weight loss being garnered. I hate not to have a super “Hey! Rah, rah, rah! The microbiota! Let’s all jump on the bandwagon and start doing this!” but I want to give people the truth. Trust me—if there was anyone that would be hoping there would be a microbiotal key to obesity, it would me, because this is my field and I would love to start offering this to my patients and doing more with this. But we just don’t see that, so let’s now transition to the clinical trials where we try to manipulate the microbiota in order to produce weight loss. What do these trials show with obesity?
And before I transition there, Susan, anything that you want to add in?
SM: No. I think I’ll have questions when we get to the clinical trials, but just to reiterate what you said was that changes in the microbiota are associated with rather than the cause of obesity, so I go back to my chicken-and-egg scenario. It looks like the person became obese, and the microbiota shifted because of that.
DR: Exactly. That’s what we’re starting to think, anyway, because of the inconsistent findings regarding the microbiota in obesity and the poor results of the clinical trials.
SM: Right. The microbiota shifted, and therefore, the person became obese, whether they extracted more calories from their food or they were hungrier or whatever that was—that we don’t think is the case now.
DR: Exactly. To put it simply, what we’re thinking might be the case—and again, we don’t have definitive proof on this—but what we’re thinking might be the case is that you become obese and then your microbiota shifts because of the obesity.
SM: That makes so much sense.
DR: And the high-level science we just went through summarizes the clinical data that we’ll select a few studies and talk about now, but essentially the reasons why the systemic reviews and the meta-analyses come to the conclusion is in large part based upon the clinical trials that we’ll discuss now, so let’s discuss what happens with the handful of most powerful interventions we have to manipulate the microbiota. We have prebiotics, we have probiotics, we have fiber, and we have fecal microbiotal transplant therapy, or FMT.
What do the randomized controlled trials show us with prebiotics? The best weight loss achieved in a clinical trial with prebiotics is 2.3 pounds of weight loss (5a), and I’ll put the link for that study in here. Now, it’s very important for me to say there are other studies that I’ve seen misreferenced where people have changed their diet, started exercising, and gone on a prebiotic, where more weight loss has been garnered, and that has been cited that, “You can lose 12 pounds from using a prebiotic! Look at this study!” And I always say, “Oh, great! I hope this is true.” I look at the study, and then I see that this study did not isolate for prebiotics, and when we look at the studies that did isolate for prebiotics, meaning prebiotics are the only treatment given, we see the best results are 2.3 pounds of weight loss.
SM: Which isn’t a lot.
DR: I mean, that’s something, but it’s not a ton, and especially when you keep in mind that many of these trials are on people that are already overweight.
SM: Right, and 2.3 pounds could just be water weight. For somebody that’s overweight, that’s not a lot of weight to change compared to the results you and I both see with clients and patients that transition to a paleo diet, and just that in itself, the weight loss could be much, much, much greater.
DR: Right. Exactly. Now, in probiotics, we see the best two trials are 2.2 pounds using Lactobacillus gasseri (6a) and 3.7 pounds using Lactobacillus rhamnosus CGMCC1.3724, the name of the probiotic (7a). We’ll just put it in the links for you. It’s essentially a lactobacillus probiotic. And here’s something that’s very interesting and food for thought for people: These lactobacillus probiotics are part of the Firmicutes phylum. So this is a direct contradiction to the “Firmicutes makes you fat” line of thinking.
SM: Oh, wow.
DR: And as I’ve said before, “Firmicutes makes you fat,” is not supported in the scientific literature. It is not supported in the scientific literature. It does not have an accurate or a consistent association in the human studies, and here we see admonition of a very strong contradiction to that philosophy, where the best weight loss with probiotics is by giving Firmicutes phylum probiotics. Again, more support for why that is not true—or at least based upon the best scientific evidence that we have right now, which is fairly good.
Now, looking at fiber, the best results with fiber have been with a fiber called glucomannan at 7 grams a day, showing 8.3 pounds of weight loss when combined with a low-calorie diet (8a). Again, it’s important to mention that “combined with a low-calorie diet,” and that might be why we see this higher jump compared to the other studies, and this was compared when they put people on the glucomannan fiber and a low-calorie diet compared to people just on the low-calorie diet. People on the fiber and the low-calorie diet lost 8.3 pounds more than the other group. So we’re seeing something that I think is a little bit meaningful here now, so that might be something for people to think about.
Now, again, I said earlier that one study does not a scientific case make. One review paper looking at multiple clinical trials on fiber’s effect for weight loss found that 4.2 pounds was the average weight loss (9a), and this seems like a reasonable expectation for people from using fiber. Also when selecting a fiber, a fiber that’s more viscous or gets more gelatinous when you mix it with water, may be preferential for weight loss (10a).
SM: Would that be soluble fiber versus insoluble?
DR: I don’t believe that the solubility always determines the viscosity.
SM: Oh, OK.
DR: But a simple way for people to know this is if you mix it with water and it still seems very much like water, then it’s not a viscous fiber. If it starts to get gelatinous, thicker, than that’s a more viscous fiber. And this probably has to do with satiation, and it may also have to do with how the viscous fibers may slow down absorption of carbohydrates and calories as they go through the intestinal tract.
SM: Right, and it probably also with the satiation helps people adhere to that calorie restriction.
DR: It’s certainly possible, yeah.
SM: So quick question before we move on to FMT, when you’re saying the first one 2.3 pounds’ weight loss, 2.2, and so on and so on, what’s the average time period? Because I’m sure people are saying, “Oh, if that’s in a week, that’s awesome,” but is it two weeks, six weeks, twelve weeks?
DR: Great question. Usually these trials average, I would loosely say, between three to six weeks.
DR: These are not short-term interventions. That’s a very, very important point you make, Susan. Thank you for asking that question.
SM: Right, because a lot of times when people start a new intervention—say, they go paleo or they go low carb or they go low fat, low calorie—that first week they lose, like, 5 pounds.
SM: Because your body’s changing with the low carb, you’re probably losing a lot of water weight, and so when you look at these numbers in respect of maybe six weeks, then that’s probably not very much, unless you’re looking at the fiber study, which actually is a decent amount.
DR: Yeah. I want people just to be aware of what they can expect, because what people might be confronted with is a program like you were talking about online, and I’m sure it’s going to be a few hundred dollars for the supplements, a few hundred dollars for testing if there’s any testing done along with this. If people want to spend money on their healthcare, I think that they should, but what I don’t want to happen to people is that they get fed misleading claims or false hopes in order to get them to buy into a program.
SM: Right, exactly.
DR: I think we should just be honest and transparent. So if you have a program that you want to promote about manipulating the microbiota for weight loss, be honest with people and tell them this is what we’ve found. I mean, gosh, if you could get 2 pounds from a probiotic, 2 pounds from a prebiotic, 4 pounds from a fiber supplement—yeah, if these things all worked synergistically and added on top of each other, then that might be significant, but we don’t know if they do. We truly do not know that.
Let’s look at FMT now. There has only been one study to date, and in this study they took the feces of lean men and transplanted it into another group of men that were overweight and had high blood sugar, and there was no change in body weight or fat (11a) and, in my opinion, no change in blood sugar. I’ll put the link to this study and also a link to a video with full transcript where I review this study (11a). I was critical of the conclusion because the authors concluded that FMT shows promise for essentially treating blood sugar or helping with diabetes, and the main reason they say that is because they reference improvement in one obscure glucose kinetic marker. What I like to do is fact check stuff, and so I went into the raw data of this study, and when you look something like fasting blood glucose and hemoglobin A1c, really valid clinical markers of blood sugar, there was no change in these, no change at all. But I think the researchers here were reaching for straws in terms of, “How can we spin this as a positive study?” And it may be because researchers are under publication pressure to publish studies that show a benefit because there’s an unfortunate pressure sometimes in science to show positive findings rather than a null finding or a negative finding. But for whatever the reason, the researchers, I think, came up with a very misleading conclusion because they referenced a non-clinically relevant marker of glucose absorption, and when we look at the most important markers—fasting blood glucose and hemoglobin A1c—and I believe they also looked at insulin, and there was no change in insulin either, although I’m not positive on that—we don’t see any change in addition to no change in fat mass and no change in weight loss.
SM: All the things that you care about when it comes to somebody with insulin resistance, right?!
DR: Right. So this is another way in which we see confusion start to grow. And not to get too on my soapbox here, but this reminds me of I saw a Facebook post, and the title of the Facebook post was “Cure Asthma in the First Four Months of Life.” And then when I read the study, I read the person’s—I think it was a blogger—I read her summary of the study, and she talks about how in mice the mice were given these four types of probiotics and then the mice did not form asthma that were getting the treatment, which is great, and then she recommends that everyone should take probiotics, which I don’t necessarily disagree with, but the title and the overall posit of the study is extremely misleading when we look at all of the studies using probiotics in humans to prevent asthma and we show dismal results. Now, there have been probiotics that have shown positive impacts when used perinatally or in infants on different diseases, and I go through this in a very detailed fashion in the eBook, but unfortunately asthma is not one that has shown to have a benefit from probiotic therapy. There’s this title taken from a mouse study that completely contradicts the human evidence, and it’s probably because this person is looking for a catchy title.
SM: I was just going to say that. We have to realize that with the internet it’s like you have to draw people in to click. It’s click bait.
DR: Right. I really think we all need to stop doing that because this confuses the bejesus out of the consumer. I mean, we don’t want to turn the online healthcare community into, like, a Walmart where there are flashing red lights and crazy signs. If you think about advertising, most affluent communities have restrictions on advertising where you can’t have huge neon signs and you can’t do all this, and it’s more pleasant to be in those communities because of that because you’re not spammed all the time.
DR: I’d like to see the same thing happen in the online healthcare community on the internet, where we don’t turn into this spammy, flashing-red-sign-with-crazy-claims sort of advertising, but I think I have lofty expectations!
SM: We could have a whole other discussion about that.
SM: I’m the same way. I look at websites, and it there are ads popping up and there’s this and there’s that, I really take a look at what they’re writing and think, well, what is it really saying? Or is it just trying to get me to click so I click on something else once I’m on their website?
DR: Right. And the other thing I should mention, too, which is equally as important to mention, regarding the science of this claim in the study, is that the probiotics that were given to these mice are not probiotics that are available for human consumption. I mean, it’s just like c’mon!
Anyway, I need to get off my soapbox and get back to the point!
DR: The next question: Where does this confusion come from? Why are there people saying that the microbiota has strong implications in obesity and we should treat the microbiota or try to modulate the microbiota in attempts to cure or treat your obesity or overweight? Well, like we talked about, from the animal studies.
The research – animal studies
DR: The animal studies are where we see the most support for the Firmicutes:Bacteroides ratio, and I’ll put a link in here. I really pick this apart in the eBook, and I’m not going to put all the references in here, in the transcript or the show notes, because it’s just a little bit too robust, but I will put one reference in here that shows that alterations in the Firmicutes is seen in many types of dysbiosis (12a). Firmicutes is not only implicated in obesity. There are other conditions that it associated with, so I just want people to remember that Firmicutes isn’t only responsible for energy regulation, and I’ll put a link for that in here. But maybe more importantly, when we’re talking about energy regulation or absorbing calories from the gut, where does this confusion come from? One of the posits is that potentially when you have the higher Firmicutes, that could be responsible for increased calorie absorption in the gut, and I think part of this comes from the animal studies, but part of this also comes from human observational studies (13a).
Some people may be aware of the Italian-versus-Malawian—I can’t pronounce it—Italian-versus-African study, essentially, where they looked at Africans versus Italians. In these studies—and we’ve talked about these before—they found that Africans had healthier weights, had more Bacteroidetes, and consumed higher amounts of carbs and grains, and so therefore, the conclusion derived from this is everyone should now eat more carbs and grains to increase Bacteroidetes to be skinny like the Africans.
To zoom way out, remember they say that high Firmicutes makes you fat, and that’s an erroneous position on this, and here is a study where that may come from, where the Africans—who are skinnier—the Africans had higher of the other family of bacteria called the Bacteroidetes, probably because they consumed higher amounts of grains and carbs. So—this is kind of inverse logic here, or reverse engineering—because of that, if everyone eats more grains and carbs, they will increase their Bacteroidetes and they will be skinny like the Africans.
This is very flawed logic, and there are a few things that people need to realize about this study and this sort of assumptive reasoning. The Africans consumed half the calories the Italians did.
SM: That’s kind of an important thing!
DR: The Africans consumed virtually no processed foods, and presumably the Africans were having far more activity. For example, they had to hand-grind their grains before even being able to eat them. And they had an incredible amount of contact with their environment and with dirt, which we know is a very powerful stimulus for a diverse or healthy microbiota or immune system.
These are all very important things, and another very important thing is that—and I’ll put a link in our notes for this also—in Sub-Saharan Africa, we see the highest colonization with Methanobrevibacter smithii (14a), the type of archaea or the type of organism in the gut that’s responsible for methane-positive SIBO and for constipation. And we’ve even seen in some of the clinical trials and observational trials in Westerners that people that have high levels of this methane bacteria will, yes, have constipation, but then by treating that, it may be able to lower blood sugar and cholesterol levels and may even cause weight loss.
So what’s happening here? Well, here’s what we think. If you’re an African, you only have access to these foods that are very fibrous and hard to break down, some vegetation and some other very fibrous foods like truly whole grains that have been hand-ground and minimally processed. These are very hard to break down, and these are very hard to extract calories from. So if you had a gut microbiota that slowed down motility, it would allow the bacteria in your gut a longer period of time to be able to break down and extract calories from these foods.
SM: And also because calories themselves are probably scarce as well, not just the food that they have, but the quantities of food available.
DR: Right. They don’t necessarily have enough calories, so by allowing the bacteria to grow that would allow you to extract more calories from your food, that is now a survival advantage.
DR: So you take that and you put that in a Westerner, you are likely not going to see the same positive outcomes.
SM: And in fact, you might see a negative outcome!
DR: Yeah! And that’s what we’re starting to see in some of the United States-like, Westernized, industrialized populations, that the high levels Methanobrevibacter smithii are causing methane-positive SIBO, which causes constipation and may even cause weight gain. I should also mention that these highly fibrous, dense plant foods tend to have a laxation effect, so they tend to kind of speed up how stuff moves through the intestinal tract. So again, this is another reason why it would be beneficial for the Africans but not be beneficial for a Westerner. Right?
DR: It’s really important that we look at these things in the context of wherever you live you have a diet and an environment that likely allows a certain bacterial population to thrive. And just because you live in a different society that’s healthier doesn’t mean we can just rip out your bacterial colony and supplant that into someone from a totally different society and upbringing with a totally different immune system and expect to see the beneficial effects that we did from the other population.
SM: I can’t agree with this more. There are so many inputs to the microbiota. Your body is trying to keep you alive, and so all of the things that are shifting in there are responses to things coming from the outside—your sleep, your stress, your food, how many calories you have, what your community is like, what your dirt is like—that to think that you just need to change one thing without changing all the inputs, it doesn’t make sense.
DR: Exactly. These bacteria are there for a reason, and one of the main themes that is threaded throughout my book based upon what the science shows, not based upon my preconceived opinion—my opinion was open going into this period of research and has now been formed by what the science shows—is that in multiple parameters—the environment, your environment, and I mean your sleep, your stress, your hygiene, your inflammation, the external and internal environment you create in your life, if it’s healthy, will allow healthy bacteria to grow and will allow you to be healthy. And if the environment is unhealthy, you will allow unhealthy bacteria to grow, and then you become sick.
SM: Right, and the microbiota of a healthy person in California could be completely different from the microbiota of a healthy person in Africa.
DR: Exactly. Now, for people listening, this does not mean that we don’t have ways to improve your gut health. We have tremendous ways of improving your gut health and things that I’m very excited about, and we’ll talk about some more of the clinical interventions that I use for repairing and recovering gut health in the clinical section of the eBook and in posts in the future, but there are definitely things you can do to overcome inflammatory bowel disease, like Crohn’s and ulcerative colitis, like IBS, like SIBO, like constipation, like reflux, like heartburn. There are great clinical interventions that we have for these, but to think that you can test your microbiota and come back with high Firmicutes and then go on some fancy fiber or prebiotic protocol and that’s going to change you from obese to not obese or from IBS to non-IBS, there is no good evidence to support that. I want people to get that because I want to prevent them from going down a road that may not really be helpful for them.
SM: Right. You have to fix all the other inputs as well, not just try one thing. Diet, lifestyle, gut health, sleep, stress—all the other things that we’ve talked about!
DR: Exactly. And we’ve even talked recently about how, for example, sleep has been clearly correlated to weight gain (15a).
DR: When we disrupt sleep in humans and then take their microbiotas and transplant them into mice, we see the mice gain weight. And when we use other humans that have not had their sleep disrupted and transplant their microbiota into mice, we don’t see weight gain. So we’re seeing that the internal environment, the environment that you create, will foster good or bad bacterial growth, and that will have negative or positive impacts on your health.
The reasons why we see little connection between microbiota and obesity
DR: Now, another reason I want to transition us to in terms of why we see so little association or so little causative relationship between the microbiota and different disease points, most specifically with weight gain and obesity, there’s a major, major thing that has been left out of the discussion. Ninety percent of caloric absorption occurs in the small intestine (16a) (16b). When you perform a microbiota test, a fecal test, that is looking at the large intestinal microbiota.
DR: So we are missing 90 percent of where caloric absorption occurs with the current window that we have into the microbiota. Not only that, but the large intestine only represents 20 percent of the digestive tract. The small intestine represents 56 percent of the digestive tract. Not only that, but the small intestine has the largest density of immune cells in the entire body. This is known as the gastrointestinal associated lymphoid tissue and Peyer’s patches (17a). So you have potentially the highest relationship between your immune system and your small intestine because that’s where you have the highest density of immune cells, and the small intestine, because it has a thinner mucous membrane, is much more prone to leaky gut compared to the large intestine.
So I want to reiterate my primary area of specialty is in the gut and in gastrointestinal conditions and through modulating bacteria and trying to fix leaky gut and all of this, and as someone who is predominantly focused on this and looking at this, I want to give people a reasonable narrative on this. I love what we’re doing with the microbiota research, but we are in early stages of research and we’re not at a point yet where we have a ton—or really any—meaningful clinical recommendations that we can make based upon the current knowledge base. Now, this doesn’t mean that you can’t treat an H. pylori infection successfully or successfully overcome IBD or cure your constipation or what have you. Yes, those things can definitely happen, but these are more so from the interventions that we’ve established through clinical medicine and functional medicine rather than the new academic area of microbiota research. It’s super important that we continue to do research so we can learn more, but right now, coming back to the initial comment that you made, Susan, the person who’s thinking about trying to manipulate their microbiota to lose weight, there’s really little to no scientific evidence to support that kind of thing.
SM: Well, that’s fascinating. It’s really fascinating. So I guess the question is, if you’re just a regular person, maybe you don’t have any health conditions—because I know there are a lot of people like that who listen to the show—do you recommend taking a probiotic, a general probiotic? Or do you recommend don’t bother?
Are probiotics recommended?
DR: I think taking a probiotic is a good idea for pretty much everyone. The reason why I think that is because probiotics have little to no negative side effects, and they have a lot of health benefits. They’re also fairly inexpensive, and so I think we can very easily make a rationale that most people should be on a probiotic. There are different types of probiotics available, and I think trying to have the broadest and the best mixture of probiotics that you can possible is really a good idea.
Now, when it comes to people that are not feeling well—so we just talked about people that are generally pretty healthy. I think a probiotic would be a good idea for those people, or probiotic-rich foods. For people that are not healthy and trying to recover their health, I also think these are a good idea, but we get a bit more prescriptive in our recommendations because a lot of people that are not feeling well may have imbalances. And so knowing how to use probiotics along with antimicrobials and/or antiinflammatory agents in a synergistic way is very important. Certain probiotics have been shown to greatly enhance the effectiveness of antimicrobials and of antibiotics. Certain other probiotics may aggravate conditions in children. So knowing how to use these things clinically is important when someone is ill and trying to recover their health.
We will have a section about how I recommend applying all of this in the eBook, and it’s a fairly logical algorithm that we have people work through to navigate all this. I give people the best that I can. You can’t really teach someone what you’ve learned in eight years of clinical practice!
SM: Oh, come on now!
DR: Right?! But I can give people a good “If you’re not feeling well, here are the series of steps I would run through to try to recover your health.” And then if they don’t work, I would get myself to a clinician. The eBook is soon to be released. I’m just starting in on the last section now, so hopefully it won’t be too long. I’m really excited about it because as people can probably tell, I’m very passionate about these issues, and I’ve put an immense amount of time into looking into these things and fact-checking these things and researching these things, and I’m really looking forward to giving people a reasonable and responsible guide to navigating their microbiota.
SM: I can’t wait.
DR: Me neither!
SM: I’m sure you can’t wait for it to be done! I know what it feels like to launch a product.
DR: Yeah, it’s been a lot of work.
SM: You’re eating, breathing, sleeping, dreaming your eBook right now, right?
SM: So any wrap-up? Do you have anything else you want to fascinate us with today?
DR: I think that’s probably the bulk of it, and I hope that people listening to this just kind of have a better understanding of the microbiota. I wish we had a little bit more, I guess, positive news and we could be saying, “Hurray, hurray! Yah, yah! Try this and you’ll lose a bunch of weight and everything in life will be great!” but I’m starting to really believe that in this space, knowing what not to do is equally as important as knowing what to do.
SM: Right, because you can save, first of all, a ton of money and a ton of time.
SM: That you know what to avoid, because I know for me specifically, we had talked about this stuff before we went to a conference, and then I went to a conference and heard somebody talk about how they manipulated their microbiota and now they can eat gluten and dairy, and so I went there and now I knew I didn’t want to waste a bunch of time on trying those things because I can’t eat gluten and dairy. And it would be nice for me to eat gluten! It would make my life a lot easier!
SM: But now I don’t believe you can manipulate your microbiota so then you’re not sensitive to foods.
DR: Right. It’s really inaccurate to say that, in my opinion. What would be accurate to say is that, “I was eating a poor diet, and that poor diet was causing a lot of inflammation, and it also allowed me to have a candidal overgrowth in my intestine, so my gut was a mess. Then I got off of all unhealthy foods, I cleared the candida infection, I gave my body time to heal, I made the environment healthier, and now healthier bacteria are living in my gut and my gut is generally healthier overall, and now I have better digestion overall. I’m more tolerant to dairy. I’m more tolerant to gluten. I’m more tolerant to nuts,” or whatever it is, which is exactly what happened to me and happens to many people, is that when they repair their gut, they have increased food tolerance. That is totally true for many people.
DR: But to say that you specifically manipulated your microbiota is so inaccurate, at least based upon the evidence that we have right now, it’s almost offensive. We can optimize the environment so that we will have optimal expression of the bacterial colony in our gut. Yes. Can we custom manipulate? “Optimize” and “manipulate” are very different. “Optimize” means to create the ideal environment for something to thrive or to grow. “Manipulate” means you are specifically trying to lower this or increase that or what have you, and we cannot do that. I rarely use such strong language, but I think it’s important that I do because the science is clear on this and I really want people to walk away with this with some confidence in this message and in my position because it has been very thoroughly researched and thought out and I hope to prevent people from going down a fictitious route, if you will.
SM: And we’ll have all the links of all the studies he talked about today in the show notes, so you guys can go click on those links and look at the research and make your own decision. If you have a different theory on this, post it in the comments on the blog post. Let us know. If you’ve had a different experience, let us know! Let’s start the conversation.
DR: Yeah, I love for people to comment because certainly I am not dogmatic in any way, shape, or form, and as the evidence here evolves, so will my opinion. So I’m certainly open to any healthy discussion on this, and there will be a number of references in this transcript, and then the eBook, I think, has maybe 300 references right now.
SM: Wow. It’s going to be a book that’s just references!
DR: Yeah, the person whose job it’s going to be to convert every link into, like, a 1 or a 2 or a 3—
SM: Oh, no.
DR: That is going to be a very tedious job!
SM: OK, anything else for this week, Dr. R?
DR: That’s it, guys. Hopefully this will help everyone navigate this topic. More on this to come, and thanks for your time and your attention. Please, if you have thoughts or comments, post those, and we can have a dialogue about this.
SM: We’ll see you guys next week. Thanks for listening.
DR: Thanks, guys.
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