Dr. Ruscio interviews UCLA professor Dr. Aaron Blaisdell, Ph. D. They discuss controversies in gut evolution in attempts to determine your ideal carbohydrate consumption. Dr. Blaisdell provides a very interesting account of evolution of the gut. Dr. Ruscio proposes a theory that connects gut types with risk of SIBO after eating Neolithic foods.
Aaron Blaisdell, Ph. D, Professor UCLA Department of Psychology & Brain Research Institute
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Latitudinal discrepancies of carbohydrate intake…..6:00
Fluctuations in microbiota…..11:30
Herbal antimicrobial compounds…..16:13
Evolution of the gut…..21:56
Microbiota as a marker of health…..29:31
Shortening of the gut, carbohydrate intake and brain growth…..35:19
Dr. Ruscio’s theory on carbohydrate intake and the gut…..43:35
Neolithic gut vs. hunter-gatherer gut and carbohydrates…..46:57
Practical application to determine carbohydrate intake…..54:03
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Gut evolution to determine carbohydrate intake with guest Aaron Blaisdell, Ph.D
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The following discussion is for educational purposes only, and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking to your doctor.
Now, let’s head to the show!
Dr. Michael Ruscio: Hey, everyone. This is Dr. Ruscio. In today’s podcast I had the fortune to interview Aaron Blaisdell, who is a Ph.D. He’s a professor at the UCLA Department of Psychology, Brain Research Institute, supersmart guy, really nice guys, generous for taking time out to speak with me. We discuss gut evolution and attempts to help you determine what your ideal carbohydrate intake is. I’ve heard some conflicting things regarding we should eat more or less carbs, and I’ve seen some people mis-reference some data, and so I wanted to bring on expert to help us get the story straight. He does a great job of helping us sort through the information, also provides a really interesting narrative on gut evolution. I propose a theory that connects, or may connect, certain types of guts – so certain gut types that we’ll talk about, and the consumption of certain Neolithic foods in potentially provocating or causing SIBO. So, I think that will be really interesting. When I was trying to articulate this idea, there was a leaf blower going outside, which may be want to jump out the window and tackle the person doing the leaf blowing, but I couldn’t do anything about it. So I get a little thrown off in terms of my focus; it doesn’t really throw off the recording too, too much, but that was the only kind of snafu with today’s recording. So, we will jump into the interview. And, again, I hope this helps you have a better understanding of the evolutionary context of carbohydrate consumption and how that may help you steer your current decision on how much carbohydrate to consume. OK? Hope you enjoy it.
Dr. Ruscio: Hey, folks. This is Michael Ruscio, and I’m here with Aaron Blaisdell. Hey, Aaron, welcome to the show.
Aaron Blaisdell, Ph.D.: Hi, Michael. I’m glad to be here.
DR: So, Aaron is a professor at the UCLA Department of Psychology, Brain Research. Recently, I came across his work when we were both presenting at the Ancestral Health Symposium this year at UC Berkeley. And, I didn’t catch his talk live, but I caught the recording afterward, and there was some really great information that he had regarding the gut, gut evolution. So, I reached out to him because I wanted to discuss something that I think a lot of people are struggling with right now, which, I guess to put it basically is how much carbs should you eat? The evolutionary or ancestral context that I look at through is: There are kind of two competing views regarding the gut, gut evolution and how much carbs you should eat. On the one hand, we have this kind of modern carbohydrate Renaissance that essentially states ‘You should eat carbs – carbs feed bacteria (and) a more diverse microbiota is healthier for you.’ And, I think there’s definitely some grains of truth there, but I also have seen some of the developmental data be somewhat misrepresented, so I wanted to talk about that a little bit. And then, on the other side of the coin, there’s this theory that our guts actually became less microbially diverse and we started to eat less carbohydrate-rich foods to allow us to absorb more energy from our food and to spawn brain growth. And that kind of hints toward a lower carbohydrate diet. That’s kind of the question I wanted to discuss with Aaron today. And I have a few things I’d like to outline. But before I jump in, Aaron, do you have any thoughts-at-large on this whole subject?
AB: Really, I guess it’s that none of us are real experts in this because it’s such a diverse area of research – of sets of research – that I don’t think there’s anybody currently on the planet who really kind of has an overarching grasp of everything, including all of the minutia. That’s reflective with how even in the scientific literature, we are finding new studies that are published everyday it seems like, showing more bits of pieces of the puzzle. At the same time, there’s more commentary about being cautious about each new bit of the piece of the puzzle. So I think that we have to go into it fully realizing that, you know, we are humble, finite beings and to recognize that, and trying to have a peaceful discourse about this stuff, while, at the same time, we also have to figure out action plans for our own health.
DR: I think that’s a great opening thought, because, yeah, I would strongly agree with you that the more we learn about this topic, the more we learn we don’t know. So, yeah, I think caution, caution in making strong conclusions is key. So, a couple of things I want discuss with you because I… to frame the question from a practical standpoint for people, how much carbs should you eat? I think that’s one of the major take-homes people are looking to take away from this discussion. Now, one of things that I’ve noticed is, with many of the modern studies looking at microbiota, there tends to be a little bit of what I call latitudinal bias, meaning most of the studies are done or performed in populations are somewhat equatorial. And, I haven’t really seen much good data looking at points that are more toward the poles. Certainly it’s been well established that there’s somewhat of a latitudinal discrepancy of the macronutrient composition of a diet, meaning the closer to the equator you go, generally speaking, it seems that more of a carbohydrate-rich diet was. And the closer to the poles you go, there’s a little more reliance on animal foods and a little less on carbohydrates consumption. There are multiple studies I’ve examine support that view – it is, kind of, one of the main underpinnings of the metabolic typing diet, which tries to steer your macronutrients based upon your genetics. So, that’s something that I’ve observed. Do you have any commentary or take on that specifically?
AB: It’s interesting that you mention the latitude. And you are right – now that you mention it, most of the studies of microbiom are done in either in ‘civilized’ people, westernized populations in the United States, Europe, Asia, places like that, some in Africa, or this recent work on Khoisan hunter-gatherer group, and getting a fix on their microbial population. And, yeah, I guess if we are looking at more traditional living people, including contemporary hunter-gatherers, mostly what’s been studied are the ones that are more equatorial.
DR: Right, and my take away from that is because we are looking at the population that is a higher carbohydrate consumption, you could very easily be misled into thinking that is kind of the diet you should eat because we’ve seen four studies, and they’ve all been somewhat equatorial and they’ve all shown that these populations eat a somewhat higher carbohydrate diet, have healthy microbiota, and it’s easy to conclude from that, ‘OK, well maybe we should all be eating this higher-carbohydrate diet’ unless you contextualize it to the fact that we’re maybe getting a little biased sample. Would you agree with that?
AB: Yeah, I think the caution is definitely warranted. In fact, I would say…there was even a commentary recently I just saw it came out. I can’t remember whom or where – I’ve been reading too many things all at once.
AB: Occupational hazard. But, the commentary basically said – what was the name of the guy right now living with the Khoisan and just gave himself…
AB: Jeff Leach, yeah, just gave himself a fecal transplant from a donor from the Khoisan to see how it’s going to affect the change in his hindgut microbial colonization. The Khoisan eat a particular type of diet. And it turns out that, by living among them, he’s been able to shift his diet, his microbes somewhat because of eating a similar diet to them, living among them. But, not to the degree that it matches their microbial colony. So, he was taking this other measure to see if he can completely transform his gut microbe colony.
AB: And that’s a very interesting experiment – I think it’s fascinating. I think it really ought to be done, and I’m glad he’s doing it. And I am really fascinated and excited to see the results. But, the caveat, and this was… somebody else was commenting on this somewhere recently: Even if it shows that he is able to do that, does that mean that he’s now shifted it to a healthier colony…
AB: …compared to where he started? We still don’t know. We are starting to find out a lot about the correlations between different microbial colonies, different genera that populate our guts, our hindguts, especially, and health and disease states. We are starting to get a handle on that, but we still know so little. We have to be cautious. Maybe it could be that people who have been eating a Western diet have the mix of bugs they have that tend to be associated with poor health, because our Western diet and style of living are more associated with that. But, maybe the shifts that we’ve seen are a way that the microbial organization are trying to adapt to it in a way that actually improves our health. I mean, we really don’t know enough yet about that except some interesting clues from case reports in individuals starting to try and tweak their own colony with probiotics and perbiotics. But, we really don’t have enough data to know what is really a healthy and what’s an unhealthy microbial population at ecosystem level.
DR: Sure, sure. And a few different things that come to mind as you’re having that discussion: There was one study in a Korean population where they performed serial microbiota analyses, and they showed pretty wild fluctuation in the levels of the microbiota in the same person from month to month to month to month to month. So, there’s Firmicutes Bacteroidetes ratio – that’s a pretty popular kind of measure. Some of these people literally had an inversion of their ratios from month-to-month. And so, kind of to your point, one of the real challenges is – you do a stool test, you come back with certain microbiota reading, but what kind of clinical intervention can you make from that because that may change quite a bit in the next 30 days even if he did nothing at all?
AB: Right, that’s an important point. If we had better baseline data to know how things change, fluctuate versus what don’t fluctuate, and what are the conditions under which populations will fluctuate versus won’t fluctuate. You are right. We need to get a better handle on all of these relationships before we can start understanding what’s causing, what’s resulting, and what kind of health affect or not. It’s too complex right now…it’s fascinating, we really need this, but…I also want to caution people from jumping the gun to try to do more about it than they really can or maybe should at this point.
DR: Yes, that’s an incredibly important point that you’re making, and I agree with 100 percent. There’s one popular lab right now that offers this PCR-based analysis of the microbiota. And they give you a readout of the levels and is available through commercial lab, so many different clinicians are going to be doing this testing with their patients, and what I’m doing with my patients just to get a look at it. But, I want to echo what you said, which is we really have to be careful with getting that reading and then saying, ‘OK, we should manipulate your diet in this way based on these findings.’ Because, really to put it bluntly, we have no clue what a lot of this means just yet.
DR: It’s certainly possible and, as a question myself that I treat patients on a daily basis, I certainly see those sorts of improvements routinely, where people will have vast improvements in their ability to handle foods they couldn’t handle before, and people who come in absolutely savaged guts that get much, much healthier. So, I see those things routinely in clinical practice. What I’m little bit cautious about is the thinking that highly specific manipulations of different probiotics and prebiotics are going to make a huge difference from one person to the other. I’m definitely open to it, but…at my presentation at AHS, I did a very, very detailed examination of the literature on different probiotics and different gestural–intestinal conditions, different prebiotics and different gestural–intestinal conditions. I can’t say that there’s a lot of great results out there, especially when we look at the high level, high-quality scientific data – the peer-reviewed data. So, I’m certainly open to as a possibility. What I’ve noticed to be the most effective clinically is actually interventions that can help get rid of bacterial overgrowth, and that’s something that I see. I think this is where there’s a much larger body of peer-reviewed medical literature to reinforce is that the interventions actually get rid of overgrowth or growth of potentially pathogenic microbes tends to be much, much, more effective. Although I am certainly open to this slightly difference probiotic/prebiotic-based intervention style. I haven’t seen a lot that reinforces that in the published literature in my clinical experience, although I do have a little bias. I think that interventions that rely more heavily on identifying things that shouldn’t be there and eliminating those things in conjunction with good dietary practices, has had more effectiveness at least from my vantage point. So, again, there’s this caution, I guess, because there are all different sorts of opinions and findings, right?
AB: So, a question for you then: When you refer to targeting the potentially pathogenic species or strains, are you talking about an antibiotic approach?
DR: So, one of the things that we use somewhat routinely are different sorts of herbal antibiotic compounds – things like oregano, berberine, grapefruit seed extract, artemisinin, things like that. I’ve seen very, very good results using those. And then, of course, we oftentimes – almost every patient, actually – will use a probiotic and a prebiotic, and potentially some kind of digestive enzyme at a later date. I’m sorry, not at a later date – oftentimes we’ll use the prebiotics, once we’ve gotten rid of the pathogenic bacteria, we’ll then bring in the probiotics. I’ve seen very, very good results with that sort of protocol. I’ve experimented with probiotics and different prebiotics, and I can’t say, for the most part, I’ve seen one make a huge difference compared to other in terms of the prebiotics – or the probiotics. But where I have seen some real benefit is using different antimicrobials – especially the antimicrobials that are also anti-inflammatory, so…
DR: … artemisinin has been used tor to induce remission in inflammatory bowel disease, but it can also be used to clear different protozoal infections.
AB: Oh, interesting.
DR: So I would caution people – Don’t go out there and just put yourself on artemisinin because you can develop resistance if you use it too much. I’m really a fan of the approach of identifying if anything is there that shouldn’t be there?
DR: And then eradicating that. And then some basic principles for encouraging healthy growth. I’m a bit tenuous about the thinking that we can make highly specific recommendations for modulating the microbriota based upon testing – like the microbial testing with PCR, and based upon the prebiotics and probiotics. That being said, I do think there are certain things that can successfully used for everyone, like soil-based organisms, certain spore-forming probiotics. And then, some prebiotics including resistant starch. Kind of a noncommittal answer there, but…
AB: And I do some of that too. I take proscriptakis, a soil-based organism, as well as playing around with some of the prebiotics. I know I tolerate inulin, which I guess is found in onions and garlic. Very well, I’ve never had a problem with onions and garlic. But I tried some of that raw potato starch when that was first raising its head on the blogosphere about a year ago. And that just knocked me out, I mean. I was doing great with my low-carb, cyclical ketogenic diet. But then I just tried introducing some of that along with taking probiotics, and man, I couldn’t handle it.
AB: So, it’s funny there are different triggers, depending on what the intestinal microbes are. Actually, I have a thought here. This brings me back to what you were hinting at or maybe even more explicitly saying earlier – you see all this divergence and diversity of gut microbes among different people within a population, and same person across season across different populations, to what degree are they showing up as problems? Or, to what degree is it possible that really, if you could get yourself into a state of feeling good. For example, by just playing around with food quality and macronutrient ratios, which are very easy to manipulate for an individual, rather than all these targeted specifics – to what that be just good enough? And get you to a point of health where all this extra stuff is icing on the cake, or addressing something that may not need to be addressed?
DR: Exactly. The more time I spend in clinical practice the more I come to find that is true. If things are overly complex – at least from my prospective; I’m open if people have a different interpretation on this – in my experience and also in talking with some other highly revered, highly successful clinicians that really respect and very well respected, that highly, highly complicated approach isn’t really there. I have a hard time thinking that we’re going to have this highly robust, detailed, meticulous treatment for the microbiota. It’s so incredibly complex that I don’t think there’s anyway we could ever make a treatment program that is tailored to the complexity. But rather, we’re going to have to find some fundamentals that work well. The example would be the paleo diet. There are just some fundamentals that we stick to, and those work well. Instead of trying to create this incredibly, crazily detailed diet, we just have a general ballpark you want to be in. We do some self-experimentation, and we find the ideal approach within that general vicinity.
AB: Right. Yeah, I feel that’s a great way to go.
DR: I have a couple thoughts I want to close with a little bit later that I think will help people navigate how to find their ideal carbohydrate ratio.
But there were one or two things I wanted to cover regarding the evolution of the gut, because there’s been more discussion lately about gut evolution. And I think there’s been more searching for data points that substantiate a higher carbohydrate diet – which, again, I’m open to. There is one comparison I heard recently that I wanted to address. I’m not sure if this something you have a lot of familiarity or not. It was looking at two different hominid predecessors – one was homo habilis and one was panthropus (sic) boisei.
AB: Paranthropus (boisei).
DR: I’ve never heard that one pronounced before, so thank you. (laughter)
So we can say it’s habilis versus boisei. And my understanding is boisei was almost a little bit more like a gorilla – very stocky animal, incredibly powerful jaws, and submitted on a high amount of carbohydrate, a high amount of vegetation, a high amount of roots. That point in time when boisei and habilis were inhabiting the earth at the same time, boisei was doing very well because there was an abundance of these tough roots. They had these powerful jaws and highly complex microbial compartments in their digestive track to break down these complex carbohydrates. I’ve heard this particular hominid referenced as support for eating more resistant starch.
DR: However, what struck me about that was, boisei as I understand it, later died because when the environment changed, they were a specialist. They could only eat that sort of food. Whereas habilis was more omnivorous, and they were eating some carbohydrates and some animal foods, and when the climate changed, it was actually habilis that didn’t go extinct and lived on because of their more omnivorous nature. Any commentary on that?
AB: You basically captured that pretty accurately based upon what the anthropologists have also been teaching. Actually, I was an anthropology major in college and learned about boisei and the other robustus australopithecines. As contrast to the gracile hominids, which are the more…homo habilis and later homo erectus. The way they talked about it was that the robustus australopithecines like paranthropus boisei and paranthropus robustus. They jokingly referred to the as ‘Nutcracker Man’ because their heads looked like with these huge sagittal crests for the attachment of the chewing muscles. That large, flat teeth for breaking into…either breaking down tough fiber and roots, and also nuts and seeds, potentially. And yeah, that was kind of specialist adaptation. With the drying out of the east African area, you would have more that dry, dense vegetation and their seeds and their underground storage organs. It seemed like, yeah, the robustus australopithecines were going down an evolutionary pathway of being specialized for those kinds of diets.
In parallel to that, what eventually became homo habilis was a separate trajectory of hominid evolution that was leading to a more open-ended omnivore. Homo habilis was the first associated with tool use.
DR: Right, right.
AB: So, same stone assemblages in Olduvai Gorge in East Africa, where you have the remains of homo habilis and you have the remains of bones with cut marks on it. And you have the remains of the actual stone tools and the debris making those stone tools, all in the same assemblages. There is an associative pattern there. It indicates homo habilis was moving on toward a more carvings form of omnivorie compared to that of other apes.
DR: Well, OK, I’m glad you said that because evolution is kind of a pet of mine, and I follow it pretty closely. And I was struck when I heard boisei used as a reference point for supporting the consumption of more resistant starch. I remember hearing that and scratching my head and saying, ‘Yeah, but he died.’
AB: If we were decendents of boise then that might make a lot of sense. But, as far as we can tell, we are not decedents. We’re just piecing together clues from these evolutionary, archaeological, paleo-anthopological remnants. But the picture that emerges is that they were an offshoot early on, after the early australopithecines. That was an offshoot that did not lead to the homo genus. That was separate. Whereas the separate branch lead to the genius homo.
DR: Right, right. And so, I hope this is helping people because I am always trying to find what information is the most factual. Hopefully that will help people a little bit with the conversation, because I have heard boisei mentioned as something that we should replicate their diet. As far as we know – and there is no way to know for sure I suppose from fossilized remains – but as far as we understand, he wasn’t really our ancestor because of a lack of the ability to have that metabolic flexibility or dietary flexibility, if you will, right?
AB: It’s hard to say what their real diet was. If you really want to talk to someone who knows, who is an expert in this field, I would talk to Peter Unger, who is at Arkansas, I think. He was a postdoc at SUNY Stony Brook in the anthropology department while I undergraduate there, so I knew him personally back then. He was a Ph.D. student of Fred Ryan, who pioneered a lot of the techniques for using electron microscopes to analyze in minute detail the teeth of these extinct species of hominid, including boisei and those types. So, Peter Unger has continued to do that kind of work and he’s the current reigning expert in early hominid diet.
AB: He’d be even better to talk to, if you can get him on the show, to really pick apart the details of this stuff.
DR: Sure, yeah, maybe he’ll be a follow-up to this. And thank you for sharing this – Peter Unger, you said?
AB: Unger, yeah. U-N-G-E-R I think.
DR: So, I think the discussion has been great, and hopefully it is helping some people with kind of figuring out, or piecing all this together. Something else I just kind of wanted to chime in. This is something that when I read a lot of the microbiota literature, you hear so much about, and I think it’s been somewhat consistently shown that a more diverse microbiota is usually associated with health. Again, I don’t say causal – I say associated, because I don’t think we can say causal, per say. Interestingly, so much of today’s clinical interventions are geared at ridding the body of too much bacteria, like small intestinal bacterial overgrowth, or candele overgrowth, or an h-pylori infection, which, in non-Westernized countries, if you contract h-pylori earlier in life, it seems like it’s protective. But, oftentimes in Westernized countries we won’t have that early colonization – we will have a late colonization, which has been correlated with things like autoimmunity. Studies have also show that treating h-pylori can help lower, for example, thyroid autoimmunity. While a lot of the microbiota literature suggests more bacteria, more bacteria, more bacteria, a lot of today’s best clinical interventions are geared at getting rid of bacteria. And, I know you’re not a clinician, but do you have any commentary on that?
AB: The only commentary I could think of that I’ve got enough knowledge to talk about with this is that, as you said, a diverse microbe colony is a sign or marker of health. Just like being lean is a maker of health. And eating a poor diet can cause obesity, but that doesn’t mean that obesity itself is then the cause of all the other diseases – it could be like a blood sugar diseases, and things like that. It could be a marker as well of those other diseases. So, in the same way, if you somehow are healthy because of the right ancestry ontogeny, that is you’re development and everything, then you are likely to have a more diverse microbial colony. Whereas if you’ve gotten an illness, or you’ve gotten an infection, or some malnutrition during development or other event during early development that (has) essentially de-canalized your developmental process, that can cause disease states as well as, potentially your microbiome could less diverse as a result of that rather than causing that. So, you’re right – it’s a maker associated with…So, I think that gets back to it. If you can do interventions that improve health that are easier for somebody as an individual to manage, like going on a paleo diet, maybe a low-carb one with maybe some ketogenic diet thrown in to help rescue some loss of metabolic function. If you improve your health dramatically that way, you might find that you’re microbial organization – I don’t know, this is actually an open question – might actually improve in its diversity or its makeup.
DR: Right, and some studies have shown when patients have gone on low-carbohydrate diets, we’ve seen a bolstering of some of the bacterial populations that are associated with health. Like with this faecal bacteria prazniki, which potentially has anti-inflammatory bowel disease characteristics, was shown to increase when patients went on a low-carb diet. But, again, every time I find one of these studies that shows…like, there recently was one with arcameacia mucenaphilia I believe it is pronounced. I was a single presenter I think it was with Grenoble Lab showing how this bacteria may have anti-obesity properties. I was excited. I said, “Great, let me dive in and let me vet this.” And I went in and I found an equivalent amount of studies showing that it had the ability to lose weight as it could cause a weight gain. So, it’s kind of a crap shoot (laughter), pardon my candor, because to find data that is re-enforcing one another is really hard. And to echo one of the themes of this call, there is so much that we don’t know that it’s, I think, almost impossible to say we need to increase this one bacterial population or decrease this other bacterial population within the microbiota to have a health benefit. We just really don’t know – with the exception of things that are established pathogens, right? So, if you have giardia infection, sure, yeah, we definitely don’t want giardia there. But, when it comes down to the commensal bacteria, the bacteria that should be there, manipulating those to achieve desired health outcomes I think right now is just something we just really don’t know much about at all.
AB: Right. I guess the one place where – and you already identified this – it depends also on when in the person’s lifetime. Early on, for example, having h-pylori exposure seems to be non-harmful at all – perhaps even beneficial. Who knows? Whereas, if it’s not until later that it shows up, it could be detrimental. A lot of pathogens turn out be like that.
DR: Right, absolutely. And that’s one of the reason that I think those raised in non-hygienic societies are healthier than we are by many parameters because they have that early exposure to a lot of these different microbes.
DR: So, something I’d like to get your take on, and then I have a closing concept for us. Evolution of the gut. You did a great job in your talk AHS discussing this. There is this carbohydrate renaissance right now suggesting that you should eat more carbs because carbs feed growth of the microbiota. However, and this is what I’d like to get your narrative on, it seems like as we evolved, we shortened the gut, made the gut potentially less complex, less microbial diverse, so that we could absorb more food stuffs from animals. And by shortening the gut, saving that energy, we were able to free up energy to grow the brain. I’d like to get your narrative on that, because that was one of the most interesting parts of your talk from AHS.
AB: All right, and this is kind of an idea that actually been – it was first discussed, to my knowledge, in the anthropological literature on the expensive-tissue hypothesis by AIello and Wheeler. Its kind of been going around the paleo-sphere for awhile. I’ve even seen Mike Eades in a blog about this years ago. The basic story is that compared to the rest of the extant Great Apes, as the other Great Apes like chimpanzees, bonobos, gorillas, and orangutans, that our gut is significantly shorter, and particularly our hindgut is over 60 percent shorter than what it should be for an ape of our size. Whereas our brain is three-times larger than a chimpanzee brain is, and three-to-four-times larger than it should be for an ape of our size. The idea is that, during human evolution, there was this tradeoff – that these different metabolically expensive tissues, tissues that are expensive to keep running once you have them. You can only have so much metabolic tissue that is metabolically expensive. There is a limit for your body size of what those can be. Those different tissues are brain, the gut, the liver, kidneys, and the heart. Compared to an ape of our size, our heart is about the right size scaled to what it should be, our kidneys are about the same as what you would expect, and our liver is about the size you’d expect for an ape of our size. Our guts our significantly shorter, and our brains are significantly bigger. So, the idea was that there was this tradeoff that allowed the evolution of larger brains by allowing for the shrinking of the guts, essentially, over evolutionary time.
AB: That tradeoff was driven by – as I talked about in my AHS talk, again, ideas by Aello and Wheeler, and some other anthropologists like Hill and Kaplan, talking about human life history strategy; basically, our lifeway is different from, including our longevity, is different from that of the other Great Apes. The story that seems to be merged from the anthropological literature is that the way that our brains were allowed to be larger, our guts were allowed to be smaller because we shifted from a hindgut fermentation strategy – so, like, chimps eat a lot of leaves and fruits, and they have a long large intestine, where there is a long transit time for those foods once they hit the large intestine. And they have a rich and diverse set of microbes that do a lot of fermentation, and actually provide a lot of free fatty acids to feed the animal. So, a lot of his calories end up coming from what absorbed from the breakdown of microbial fermentation in the hindgut.
AB: Gorillas are even further down the spectrum. They are like the cows of the Great Apes. They are like big bunnies – rabbits are also hindgut fermenters. Gorillas also are hindgut fermenters; they eat ton of foliage. They spend up to eight hours a day eating leaves – they’re grazers. Most of their energy comes from the fatty acids that are released by the microbial breakdown.
AB: Modern humans, extant humans, are different. We have a much smaller hind gut, and actually we have longer small intestine, which is where you breakdown and directly assimilate foods into your bloodstream after you digest it with your aces, your enzymes.
DR: Enzymes, sure.
AB: Protease, lipase, and amylase breaking down the fats, proteins, and sugars, starch, right? So we do extract most of our nutrition through digesting it directly and absorbing it, rather than in the hindgut. There is some in the hindgut, but not nearly as much. And so, for us as species, compared to the other Great Apes, we are much less dependent on hindgut fermentation on the microbiota. They do play an important role, but it’s much reduced relative to the (other) Great Apes. Instead, what we’ve done, and this started with homo habilis and the ability to use stone tools with their hands, and larger brains, more structurally complex and presumably, more cognitively complex brains, we are able to then start manufacturing tools to plan and execute kills of large medium-to-large size mammals to get at more of the fat, the marrow, the tongue and brains, areas that other carnivores couldn’t always get to, but are highly nutritious – they have a lot of nutrition, a lot of calories, and energy. You need to be able to directly break those down with your own enzymes – those are not fermentable kinds of energy. Those are much higher in nutrient quality, and much easier to digest. And so, by switching to that easier-to-digest food, you don’t need the large intestine anymore. That took evolutionary pressure off of growing this large intestine – hindgut – and that could be devoted to fueling the brain – both brain growth and brain metabolic activity.
DR: Sure, sure.
AB: And that’s basically the trajectory all through human evolution and the genus homo – from homo habilis to homo erectus to homo sapiens was this march toward larger brains, more complex and sophisticated tools, presumably more complex cognition and planning, and extending life span, doubling to a tripling of the average lifespan compared to a chimpanzee, a much larger period of pre-adult growth, especially brain growth, took a lot longer now for humans than for chimps. All that needs the nutrition from these really high-nutrient dense sources of animal foods.
DR: Sure. I think that’s…there’s actually a few nuggets in there that I’ve never heard of before, so thank you. That was a great overview. And, I guess to recapitulate that in a really simple way, we almost become less cow-like, where we had less of a long, complex gut that could breakdown things like grasses. So we had a less-complex gut. Then we started eating foods that required a less-complex gut to eat, like meat. Because the gut was less complex, and there was less energy needed to run the gut, we could then use the extra energy to grow the brain.
DR: That’s a perfect segue for this novel idea I want to propose to kind of help people reconcile where they fit in to this whole spectrum of more carbs/less carbs. I think a lot of our discussion has, hopefully, helped them to get there already. Walter and Lay are two researchers that I follow in this area. One of the things that they have written about in a couple recent papers is, as we’ve Neolithic foods – so foods that are slightly more modern – Neolithic adaptations to these more modern day, carbohydrate-rich foods are more enzymes that can help break down carbohydrates – amylose and lactose, the higher amlose and lactose genes. And what they propose is that, as we’ve segued from hunter-gatherers to more of Neolithic species, we are eating more of these carbohydrate-rich foods. These carbohydrate-rich foods require more to digest. And so, there are two ways that we can achieve that digestion of these more complex foods: We can secrete more of these enzymes, like amylose and lactose; or we can recruit bacteria to help us digest those. The problem with recruiting bacteria is bacteria are going to consume a lot of that energy, and just give you a little bit of the energy derived. If you can secrete your own enzymes to digest these foods, you’ll maintain more energy per unit of food. So, to zoom out for a quick second, we are eating more carbohydrate-rich foods nowadays. The goal is to be able to extract from those foods as possible. There are two ways that we can extract energy from those foods: We can borrow bacteria to help us break them down – but bacteria are going to keep a lot of the energy; or we can secrete more of these Neolithic enzymes, and so we can keep the energy.
So, that would, of course, be the favorable one, where we evolve our guts to secrete more of these enzymes, so that we can keep more of the energy compared to having more bacteria.
AB: Is that necessarily the case, though? Might it be that could be a problem if we are more efficient at retrieving the energy ourselves, that could lead to dis-regulation of metabolic function?
DR: That might be part of the reason why there’s a lot of obesity and diabetes right now, in terms of what we are seeing in Westernized population. There may be that change that may be occurring maybe spawning that. I agree with you. I think that it may not be a healthy change given our plenty of food. But, here is the final piece I want to tie up back into, and then I definitely want to get more of your thoughts, and maybe we can wrestle this concept to the ground.
So, my speculation on this is, if you have more of a Neolithic gut, then your intestines may be able to excrete more amylose and lactate to help you breakdown these Neolithic foods. And so, if you have a more Neolithic gut, you may be able to eat more of the Neolithic foods because you’ve evolved the ability to secrete enzymes to help you break down those foods. But if you have a little bit more of a hunter-gatherer-type gut, then what may end up happening is, if you eat these Neolithic foods, you have to allow more bacteria to grow, because you don’t secrete the enzymes needed to break them down. So you have to use a bacteria instead, and that may be one of the things that opens the door for some of the small intestinal bacterial overgrowth that we see nowadays, where, if you have the enzymes, you could breakdown these Neolithic foods. But, if you don’t have the enzymes, you have to allow more bacteria into the intestinal tract to help you. And that can manifest as a clinical entity of small intestinal bacterial overgrown, which can be not a nice condition – a condition that you don’t want to have. So, I guess in summery, you have Neolithic adaptations to digestion – you can eat Neolithic foods. If you don’t have those adaptations – if you don’t have the amylose and lactate secretions – then you may not do well with Neolithic foods. So, that’s one of the things that I’ve been trying to piece together to help people individualize this. But, sure, lets discuss holes in that theory, because I am sure there are a couple. (laughter)
AB: It’s interesting. I think you’re definitely onto something. Certainly, evolution didn’t stop with agricultural revolution, and with the Neolithic period. If anything, it sped up. When you have a population that’s been in a particular environment for a long time, and then they move into a very different environment, or something in the environment changes quite a bit, the rate of evolution on many of the traits that those organisms bear will now speed up.
AB: Because, it’s an error-correction process. And I think the 10,000 Year Explosion, the guys who wrote that book, Cochran and Harpending, basically, that’s the thesis of their book. They basically took Jared Diamond’s Guns, Germs, and Steel premise about hunter-gatherers and human evolution and said, ‘Ah.’ But then, with the change with the Agricultural Revolution, we’ve changed our dietary environment, as well as other aspects of our environment, in such a way that it sped up evolution. And now we have signatures of a more-rapid rate of evolution of many of our traits, like metabolic traits, and digestion traits and stuff. I think that fits into what you’re saying. Like, when we compare someone who is more Neolithic-like to someone who is more hunter-gatherer-like.
But then you’re talking about two different ways that one can deal with this change – like an increase in digestible carbohydrates. Perhaps, as oppose to being independent and competing accounts, they could both be going on at the same time. The reason I wonder about that is because I read somewhere that the Hun Chinese have been shown to have longer colons than Europeans.
AB: And, they’ve been on an agricultural diet for a long time. Whereas, many Europeans come from more recent hunter-gatherer backgrounds, depending on what part of Europe their ancestry is from – like the British, much more recent hunter-gatherer.
DR: And you know something that is interesting along the same lines: There was a paper published recently trying to establish the validity of the SIBO breath test within Asian populations. It was not found to be nearly as valid as in more Westernized European populations. Maybe there’s that tie in there.
AB: Yeah, that’s why we named our society the Ancestral Health Society, because it’s not just paleo. It’s the stuff that happened after that in our individual ancestries. Even your development, your upbringing, you ontogenic development is part of your ancestry, so to speak. And even before the Paleolithic period. Most primates’ ancestry was spent as insectivores, before we became fruitivits primates. I’m going on a tangent, and I don’t want to go too much on that tangent. Yeah, there are lots of individual differences, but those might be tied to ancestry in a very interesting way, such that some peoples that have been on an agricultural diets for the longest, might have acquired a set of different adaptations to those, including more copies of the amylose gene, as well as longer colons or more-diverse colons populated with species that do more fermentation and breakdown. It might be kind of a package, a suite of traits that evolved together. Whereas, people who come from an ancestry – I think myself included, based on my own self-diagnosis – I think I come from a herding ancestry, with my Jewish background.
AB: And I tolerate dairy very well, and I do really well on very low-carb, high-animal meat and fat diet. I seem to thrive on that, and I think it fits nicely with the story, with the story I kind of create for myself about my ancestry being more hunter-gatherer-like. But I think there is something to this idea, as you were saying.
DR: Sure, and I hope that the idea that I am throwing forward, or putting forward, helps people realize that there is a spectrum, and it’s not a ‘Hey, right now resistant to starch is en vogue, so everyone needs to be having resistant starch and eating high-resistant starch foods, and having more carbohydrate. Hopefully, people can see through, yeah, there are things that come into vogue and are very popular. But that doesn’t mean that you need to abandon your current health practice and do this one. If it doesn’t feel good to you, or if it doesn’t make sense to you. Yeah, there is this kind of spectrum where you may fit, from the lower-carb end of the spectrum to the higher-carb end of the spectrum. I think, Aaron, I’m a little bit more like you also where I do fine with dairy, and I tend to do better on a lower-carb diet. And I have not responded very well to things like prebiotics. In fact, I gained weight from prebiotics and resistant starch, and not a good weight. So, maybe to bring it home, I’ll throw out the way I like to approach this in the clinic, and please add any additions that you want to throw in. I like to start people on a lower-carb version of either the paleo or autoimmune paleo diet, see how they respond, and then eventually we go through a food reintroduction, where they reintroduce foods they cut out and they note the response. But, along with that, we go through a carbohydrate reintroduction. We help people figure out what threshold of carbohydrate they feel good at. If they starting getting too high, and they start gaining weight or getting bloated, then we scale it back a little bit. It’s just a very simple process of starting clean with the lower-carb paleo/autoimmune paleo, and then slowly work your way outward and see where you feel the best.
AB: Makes perfect sense to me. That’s exactly what I did with myself and I kind of know where I am on my carbohydrate curve, as Mark Sisson in his Primal Blueprint book has a nice carbohydrate curve.
AB: I think that everybody should tinker and figure out where they are on that curve, as long as the rest of their diet avoids processed foods – which pretty much is the key.
DR: I agree. Well, I guess in closing is there anything that you want to share in terms of events you have coming up or anything you want to make people aware of?
AB: Ah, wasn’t even thinking about that (laughter) during our talk. AHS is going to be in Colorado, in Bolder, Colorado next year – I believe the dates are going to be in June, we haven’t nailed it exactly yet, but that’s where were working toward. So, it might be a little earlier next year than it typically is – rather than August. But, stay tuned on the Facebook page – Ancestral Health Symposium, has its own Facebook page that you should go an like it, so that you find out the announcement for when we are going to have the call for abstracts, for giving a presentation, as well as other undated information about the society there.
DR: Well, all right, sir. Thank you so much for taking the time to chat with us. We will hopefully see you at AHS.
AB: Awesome. It was a pleasure being on your show, Michael.
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