The Hygiene Hypothesis – Is Modern Disease Associated With Being Too Clean?

I’m very excited about our guest today. His name is Moises Velasquez-Manoff, and he’s the author of one of the best books I’ve read in a long time and probably one of the best science books I’ve ever read. It’s called An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.

It’s essentially about the hygiene hypothesis, and the idea that there’s a fundamental mismatch between human biology and genetics and the current environment that we’re living in, but this mismatch isn’t always black or white. A lot of modern developments are kind of a double-edged sword.  I invited Moises on the show to discuss the latest research in this area.

In this episode, we cover:

4:00 How Moises got into the hygiene hypothesis
7:23 The difference between the “hygiene hypothesis” and the “old friends hypothesis”
16:13 Why genes that predispose us to disease are selected for?
23:00 Does raw milk protect against asthma?
31:20 Could H. Pylori actually benefit humans?
36:50 Will Fecal Transplant become a common therapy in the future?
43:20 What are the risks associated with Helminthic and Hookworm Therapy?
54:14 How can we put these theories into practice with our children?

Links We Discuss:

• An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases

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Full Text Transcript:

Steve Wright:  Hey everyone, welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com.  I’m your show host, Steve Wright, and my website is SCDLifestyle.com.  With me is integrative medical practitioner and healthy skeptic Chris Kresser.  Chris, how’s the day going out there in California?

Chris Kresser:  Oh, it’s pretty good.  Just busy, busy getting back into the swing of things after PaleoFX.  How are you?

Steve Wright:  Same here.  PaleoFX was a great time, and there was so much work to be done as we got back that my bags are still packed.

Chris Kresser: Haha, right.  So I’m super excited about our guest today.  His name is Moises Velasquez-Manoff, and he’s the author of one of the best books I’ve read in a long time and probably one of the best science books I’ve ever read.  It’s called An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.  And it’s essentially about the hygiene hypothesis, which I’ve mentioned before on the show and I’ve written about.  One of the basic premises of the ancestral health movement is that there’s a fundamental mismatch between human biology and genetics and the current environment that we’re living in, but this mismatch isn’t always black or white.  A lot of modern developments are kind of a double-edged sword.  So for example, antibiotics absolutely prevent infection.  They have reduced rates of infection and have saved lives, and before the invention of antibiotics, a lot of people died that aren’t dying now from acute illness.  But of course, on the other hand, antibiotics may have permanently altered the human gut microbiome, and due to their effect on the gut flora, they can predispose us to a lot of different chronic diseases and cause a lot of problems.  Another example would be C-section, which has certainly reduced infant mortality, particularly in some populations, but a lot of recent research suggests that babies born to C-section may be predisposed to obesity and metabolic disease and other chronic health problems later on in their life.  And then of course, we have modern food processing and distribution that has made starvation a lot less likely, but the ready availability of calories is something that we’re just not really adapted to, and that has probably contributed to the epidemics of obesity and metabolic disease.  So it appears that modern sanitation and hygiene may be another one of these double-edged swords of modern civilization, and that’s what we’re going to talk to Moises about.

Steve Wright:  Yeah, I’m very pumped for this.  I think it’s going to be a great discussion, and we should probably get him on the show.

Chris Kresser:  Let’s do it.

Steve Wright:  OK, well, before we bring Moises on the show, let me first tell the listeners about Beyond Paleo.  If you’re new to the paleo diet or you’re just interested in optimizing your health, you’re going to want to check out what over 30,000 other people have already signed up for.  It’s called Beyond Paleo.  This is Chris’ free 13-part email series on burning fat, boosting energy, and preventing and reversing disease without drugs.  To sign up, go over to ChrisKresser.com and look for the big red box.  Go ahead and put your name and email in that box, and Chris will start sending the first email right away.

Chris Kresser:  All right, so welcome to the show, Moises.  Thanks for joining us.

Moises Velasquez-Manoff:  Thanks for having me.

How Moises Got into the Hygiene Hypothesis

Chris Kresser:  So maybe we can start just by you telling us how you got interested in science writing in the first place.  I’m curious about that since science writing — it seems like it’s been experiencing a renaissance certainly in the past 10 or 15 years, but it’s still maybe not the most common career.

Moises Velasquez-Manoff:  Yeah, well, I had always wanted to be a fiction writer, I suppose, of novels and short stories when I was younger, and I did the sort of usual thing where I got a day job to make ends meet and tried to write early in the mornings and dealt with all that fun frustration.  But then I was graphic designing and doing other things, and I decided if I really wanted to make a go of writing, I had to go back to school, so I went back to school.  I specialized in science writing mostly because I think there was one moment where I was covering something political, like in the local sort of New York City politics, and I just realized that everyone was trying to spin everything all the time, and I said, you know, I really don’t want to do this and deal with this kind of stuff all the time.  I want to deal with people who are actually trying to get at some sort of truth.  And that is, of course — at least that’s one interpretation of what science is trying to do.  You create hypotheses and you test them somehow empirically.  And of course, I’m a curious person, I like to know how things work, so science was a natural draw.

Chris Kresser:  Right, and then when did you first become interested in the hygiene hypothesis or old friends, as we’re calling it now?

Moises Velasquez-Manoff:  Well, there was a moment actually in grad school, I think around 2005 or 2006.  I was doing some research, and I came across one article on Joel Weinstock’s work in the journal Science.  You’ve probably read the same article.  It was about his development of the pig whipworm for the treatment of inflammatory bowel disease.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  And I had never come across anything like the hypothesis he presented, which flipped everything that I had learned previously on its head.  Everything else basically argued something along the lines of we’re exposed to some new pollutant or something that’s wreaking havoc on our immune system in the modern world — and there are certainly lots of possible exposures these days — It’s messing with our immune system, thus the increase in these diseases like asthma and various autoimmune diseases.  He was saying the opposite.  He was saying we’re missing something that’s been with us since time immemorial.  It’s been with us so long that it has actually shaped our immune system, and our immune system fails to function correctly in its absence.  And you know, you just follow that hypothesis and that trail of breadcrumbs, and it ends up leading you to some amazing science.

Chris Kresser:  Absolutely.  I mean, I remember being just so blown away when I first came across it.  And I think I was perhaps somewhat open to it as an idea because, of course, a lot of what I write and speak about is this concept that humans now, our biology and genes are somewhat mismatched with the modern environment.  So from that perspective, it seemed like another expression of that mismatch and another sort of double-edge sword, where improvements in modern sanitation and hygiene have certainly saved a lot of lives, but as it turns out, there’s a dark side to this, isn’t there?

Moises Velasquez-Manoff:  Yeah, that’s exactly right.

The Difference between the “Hygiene Hypothesis” and the “Old Friends Hypothesis”

Chris Kresser:  So, can you explain the difference between the hygiene hypothesis and the old friends hypothesis?  What’s the difference in those two perspectives?

Moises Velasquez-Manoff:  Well, I guess it clears it up a little bit to understand the history.  The hygiene hypothesis stems from a study in 1989 on large families showing that younger kids in large families that had many older siblings were relatively protected against allergic disease compared to the older siblings.  The guy who originally formulated it, David Strachan, an epidemiologist, he thought it was infection.  So you’re a young kid, you’re born, you have four older brothers, and they just keep giving you all these nasty infections, and that ends up protecting you.  It turns out that was probably wrong.  There’s not much evidence, or any evidence really, suggesting that acute infections, like the flu or like measles, help in terms of preventing these diseases.  What’s probably more important is that you’re born into this microbially enriched environment.  You have all these older brothers. — And of course, they could be sisters, too.  They’re tracking in mud.  There’s saliva everywhere.  There’s a little poop here and there, fecal bacteria.  And sure enough, these days with improved technology when scientists examine these kinds of environment with lots of children, which also include daycares, they find an enhanced microbial diversity sort of in the dust that accumulates.  That’s probably what’s important because it either, one, stimulates your immune system and sort of hits all these receptors on your immune system in a way that it’s sort of the equivalent of like, say, hearing good music constantly in the background or something.  It just keeps you soothed so you don’t over-respond when someone comes along and claps in your ear or something.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  Or it’s because some of those microbes are actually key species that colonize you, and then when they take up residence in your gastrointestinal tract or elsewhere, they end calibrating your immune system in a way that prevents wheezing and hay fever and eczema.  So the old friends is basically a way of reformulating the hygiene hypothesis, which was focused on infections, refocusing it on what’s probably the true protective factor, which are actually innocuous microbes, possibly symbiotic microbes, as in that they’re native to our body and we need them and so they’re old friends because they’ve been with us for a long time.  Now it turns out that old friends as a category also includes parasites.

Chris Kresser:  Right, which aren’t always innocuous, but in the right amount maybe are innocuous and even beneficial.

Moises Velasquez-Manoff:  Yeah, you know, the way I’ve come to think of it is that there’s a gradient of organisms.  Some on one end are the pure mutualists that are purely in a beneficial relationship with you.  You benefit them, they benefit you.  On the other end are the pure pathogens, like the plague.  They benefit basically and you die.  And in the middle there are a whole lot of other organisms.  Medicine has tended to focus on the pathogens so far, but in the middle are the parasites, which they benefit you a little bit just by virtue of the fact that they’ve always been there, right?  So somehow your immune system actually expects them to be there even though take stuff from you.  They hurt.  They’re not always totally benign.

Chris Kresser:  Right, and one of the analogies — I can’t remember if you used it or somebody else.  I don’t think it was in your book. — But if you’re standing and facing someone, and you both have your hands out and you’re leaning into each other, and all of a sudden somebody steps away, you’re going to fall down.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  And it’s kind of like that background tension that these organisms provided, and it gave our immune system to do, essentially.  And then as soon as those organisms are removed from the environment, an adaptation that would have been protective in the presence of those organisms all of a sudden starts attacking self-tissue, and then we have this epidemic of allergic and autoimmune disease.

Moises Velasquez-Manoff:  Yeah, that’s right.

Chris Kresser:  So with the old friends, what are we talking about here?  We’re talking about helminthes, lactobacilli, other soil-based organisms.  What else?

Moises Velasquez-Manoff:  Well, that’s a good question.  I think we’re probably talking about a whole repertoire of heirloom species that are native just to our particular lineage of primate, Homo sapiens.  It turns out the lactobacilli that inhabit a chicken are not the same as the ones that inhabit a pig or that inhabit a human.  That said, it also seems that we inherit sort of at least genetic capabilities from environmental microbes that don’t really colonize us, but as you know, microbes can interchange genetic information.  There’s this study a few years ago on the Japanese microbiome.

Chris Kresser:  Um-hum, the seaweed.

Moises Velasquez-Manoff:  You’re right.  It had this unique ability to break down aspects of seaweed.  And it wasn’t that a microbe from seaweed had colonized Japanese stomachs.  It was that it had imparted this genetic ability to microbes that are already resident in Japanese stomachs.  That implies that our connection with the external microbiome — via food, via even fermentation products, via just inhaling air from a living ecosystem, via water that comes from surface sources — is a constant supply of genetic innovation for a microbiome.  How that might apply to our immune function remains largely unexplored, but it’s hard to imagine that it wouldn’t.

Chris Kresser:  Right.  And it also seems to change the notion — or least push it forward a little bit — of how probiotics and things like fermented foods might benefit us.  I think the typical idea is more like a sort of question of volume, like if your gut microbiome is depleted, you take in some probiotics or fermented foods, and it kind of increases the flora, and that’s how it works, but it seems like now from my reading — and I’d love to hear your thoughts on this — that it’s a lot more sophisticated and complex than that.  These bacteria that we’re consuming are modulating our immune system and creating changes in our gut that probably do influence the composition of the gut flora, but it’s not so much about just filling it back up as it is about the effects that these organisms have on everything from our immunity to our gut genome.

Moises Velasquez-Manoff:  Yeah, well, our gut is basically an immune organ is one of the revelations of all this work.  You know, 70% of our immune activity on a day-to-day basis happens around our gut.  So it’s not really just this thing that absorbs nutrients, period.  It’s this place where our whole immune system is calibrated by our resident microbes.  One other thing that keeps showing up, though, as we mentioned earlier, is diversity.  And what I worry about in terms of the sort of current generation of probiotics is they’re always a few strains.  I mean, that’s how companies that create these microbes work.  You patent a strain and then you sell it, right?

Chris Kresser:  Right.

Moises Velasquez-Manoff:  How it that going to address this question of diversity?  It doesn’t seem to, and honestly I have to say that in terms of the science with existing probiotic strains, it’s really underwhelming in humans.

Chris Kresser:  Yeah, we’re talking about how a broad-spectrum product might have 13 or 14 species, but we know that there are at least 500 species, and I’ve seen some studies suggesting that there may be even more in the gut.

Moises Velasquez-Manoff:  Sure.

Chris Kresser:  And I imagine that’s why fecal transplants are so much more effective than probiotics because you’re getting the actual wide, broad range of microbiota that exists in a theoretically healthy human host rather than just a few select strains of lactobacilli, for example.

Moises Velasquez-Manoff:  Yeah, I think that’s exactly right.  And they’re native.  Probiotic strains aren’t always native to the human gut.  It doesn’t mean they don’t interface, but they don’t necessarily take up residence.

Why the Genes That Predispose Us to Disease Are Selected For?

Chris Kresser:  Right.  So you may have seen this study, Moises, that was recently published.  I think it was The American Journal of Human Genetics, and it was a paper by Raj and colleagues, and they were basically speculating that genes that predispose for inflammatory bowel disease, Crohn’s and ulcerative colitis, have been targets of recent positive selection, which of course suggests that these alleles had, at some point, some benefit to humans.  Otherwise they wouldn’t have been selected for and they wouldn’t have been as common as they are now.  With that in mind, why would genes that predispose us for something like inflammatory bowel disease have been selected for?

Moises Velasquez-Manoff:  Well, because they amp up certain aspects of the immune defending response that are probably important.  What’s interesting about those studies that look at positive selection for these alleles is that the timeframe for that selection is almost invariably mostly since the Neolithic Revolution, the last 10,000 or 12,000 years, when we’re living in increasingly crowded conditions with other humans, other animals that basically enhance pestilence.  Hunter-gatherers were in small groups of 50 to 70 people.  The network as a whole would be a few hundred people.  Once we start settling down, we’re talking thousands and thousands of people living in a smaller space with all these animals.  You’re not moving.  Sewer becomes a problem.  Suddenly we’re starting to encounter infections that we didn’t encounter before in the same quantity, so certain aspects of our immunity get amped up.  Now, what’s interesting about thinking on this is that during that same period of our evolution, all the evidence suggests that parasite infections also increased because you’re stewing in your own feces for most the Neolithic.

Chris Kresser:  Yeah.

Moises Velasquez-Manoff:  And that’s how these things — they’re transmitted orofecally.  The parasites suppress your immune systems, including the very kinds of response that defend you against worse pathogens.  So if you have a parasite, you’re much more susceptible to other types of infections that would just kill you in a day.  But the parasite won’t kill you directly; it just makes you more vulnerable.  So in the context of these chronic, relatively heavy parasite loads, it’s not surprising, in some respects, to see a selection for the amping up of aspects of immunity that protect against acute infections.  But then if you imagine the human superorganism, the body with all its flora and fauna, including parasites, those alleles, which are the same ones that predispose to autoimmune disorders these days, probably just protected us and didn’t cause autoimmune disease because there was this constant drag or sort of cooling effect of the parasite infection.  And that’s in fact what analysis by Italian scientist Matteo Fumagalli, they sort of show this in a very 10,000-foot kind of way that those alleles are enriched in populations that also had a lot of parasite infections in the recent evolutionary past.

Chris Kresser:  Um-hum.  So let’s talk a little bit more about that, going to back to Weinstock when he initially developed the theory on Trichuris suis, or pig whipworm.  At that time, I think the paradigm of understanding autoimmunity was this idea that there were two sides of the immune system:  the Th1 side that would deal with a certain type of problem, and then the Th2 side would deal with a different type of problem, like parasitic infections, and that inflammatory bowel disease, ulcerative colitis and Crohn’s disease, often involved an overactive Th1 response, and then introducing the whipworm would ramp up the Th2 side and kind of balance things out.  But that’s really not the prevailing understanding at this point, is it?

Moises Velasquez-Manoff:  No, it’s not.  What’s interesting is that Weinstock’s original hypothesis was completely at odds with the parallel development of the so-called hygiene hypothesis.  He was saying that we’re skewing the immune response to Th2, thus preventing diseases that are autoimmune or inflammatory characterized by Th1.  Meanwhile, the hygiene hypothesis guys are saying:  Well, we need more Th1 stimulation to avoid this excess Th2, which is what creates allergic disease.  So clearly something was going on, and in fact, if you look, there are a few mouse studies where they tried to actually test this idea, and they took Th1 cells and transplanted them to see if they could skew it, and of course, it didn’t work because then you just end up with double the inflammation of two different kinds.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  What’s important is this other arm of the immune system that suppresses all immune responses, the regulatory arm.  It’s sort of epitomized in these regulatory T cells that parasites induce but also microbes induce.  And in fact, it seems that even some certain types of omega-3’s may induce.  It’s interesting that a lot of foods, it turns out, actually directly stimulate the immune system — in good and bad ways, depending on what they are.

This new paradigm you can imagine as a triplicate.  There’s Th1, there’s Th2, and then regulating either one of those is the regulatory response.  And of course, it’s not just your T cells.  It’s turning out there are regulatory B cells, which produce antibodies normally, but these regulatory B cells control other B cells.  It seems like every immune cell, every white blood cell you have, has a version that attacks and a version that holds back.  So there are macrophages that hold back, alternatively activated macrophages.  There are dendritic cells that hold back.  This seems to be the emerging paradigm.  And so the question is, why is that entire repertoire of cells not coming on line these days the way it should?

Does Raw Milk Protect against Asthma?

Chris Kresser:  Um-hum.  And the hypothesis here we’re talking about is because these old friends are missing in our environment.  Let’s talk about some examples.  You had several fascinating examples in your book.  One of the ones that I’ve talked about before in the context of city versus rural, the contribution of raw milk.  There are few studies that suggested that raw milk might confer some protection against asthma, and you wrote not specifically about raw milk, per se, but the difference between rates of asthma in rural and city kids.  Can you talk a little bit about that?

Moises Velasquez-Manoff:  Yeah, so those studies emerged from rural areas of Switzerland and Bavaria originally, and they were comparing farm kids with other rural-dwelling people who were not farmers.  And it’s usually misconstrued as farm kids with urban kids, but in fact they were all rural kids, and the farming kids just were dramatically less allergic, like one-third as allergic.  So they, of course, are exposed to this microbially enriched environment of the cowshed, which is manure and mud, and feed is fermented.  I don’t know if you’ve ever been on a farm.  I hadn’t until I actually visited an Amish farm last year, and it’s like once you’re there, you realize that there is no way that you are not encountering this!

Chris Kresser:  Haha, right.

Moises Velasquez-Manoff:  Like, you’re eating stuff just by breathing that you just don’t encounter elsewhere.

Chris Kresser:  Just in the air, yeah.

Moises Velasquez-Manoff:  And in fact, I shoveled some — The feed is fermented, and of course, that’s all lactobacilli.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  And the particles are all just floating in the air.  You inhale that stuff, but that stuff ultimately comes out of your lungs and goes down into your stomach, so it got me thinking about prebiotics, which is sort of tangential.

Chris Kresser:  Haha, right.

Moises Velasquez-Manoff:  I mean, you’re eating fermented hay, is what it comes down to, without realizing it, right?

Chris Kresser:  Right.  So even the rural kids who were presumably exposed to something but not nearly to the same degree as the kids that were actually living on farms, and there was that big of a difference?

Moises Velasquez-Manoff:  Yeah, well, that sort of recasts this rural-urban gradient that people had noticed for a long time, and it was really just a farm-nonfarm gradient, it seemed.

Chris Kresser:  Um-hum, but it’s not just microbes, necessarily, that protect against asthma, because you talk about the Tsimane that Gurven worked with, and in their case it was something different, right?

Moises Velasquez-Manoff:  Well, no one really knows what it is in their case, but it’s very extreme.  They live in kind of this transition phase between hunter-gathering and farming.  They’re called horticulturalists.  But they live outside, essentially.  Everything is made from the jungle.  They live the way we all used to live, really.

Chris Kresser:  And they’re where, Moises?

Moises Velasquez-Manoff:  They’re in Bolivia.  There’s a part of Bolivia, which he usually think of as a mountain country in the Andes that’s actually rainforest.  It’s sort of the eastern slope of the Andes.  So they live in the foothills to the Andes, and they’ve somehow resisted Westernization throughout the centuries, and they have a little protected area now.  They live off jungle meat, they live off fruits, but they also live off rice and whatever else was given to them by the Spanish, which they grow in the jungle.  And they have no asthma, no allergic disease, like startlingly low.  It could be genetic.  This phenomenon, though, has been observed in other people who live in those kinds of circumstances, and they have almost universal hookworm infection.

Chris Kresser:  That’s what I was going to say.  Yeah, very high rates of hookworm.  Let’s talk a little bit about Sardinia and rates of autoimmune diseases.  I found that to be really interesting.  And you mentioned the Italian study that found that people who had higher rates of parasite infection previously were more likely to have genes that predisposed them to autoimmune disease.  Is that what was going on in Sardinia?

Moises Velasquez-Manoff:  Yeah, that’s the theory.  Sardinians are very genetically unique in the European family, almost like they’re not really European in some respects.  The Iranians are more related to mainland Europeans than Sardinians are.  It’s interesting, actually.  I saw a study about the Iceman, that guy Otzi who showed up in the glacier.  He’s 5300 years old.

Chris Kresser:  Sure.

Moises Velasquez-Manoff:  He’s like an archaic European population.  He actually had polymorphisms that are related to current-day Sardinians.  He’s more related to them.

Chris Kresser:  Wow.

Moises Velasquez-Manoff:  So maybe it was more widespread in the past before whatever happened, happened.  In any case, they’ve been isolated for a long time.  They didn’t really mix in, although the island has been ruled by everyone from the Phoenicians to the Spanish most recently.  And they’ve been plagued by malaria, the nasty one, Plasmodium falciparum.  So they, the theory goes, evolved defenses against it.  The classic defense is the sickle cell trait, where if you have one copy of the gene you’re protected from cerebral malaria.  You’re not protected from infection; you’re protected from dying from infection.  So it’s likely that there are other adaptations, and in fact, there are.  Thalassemia is another one.  It’s another kind of anemia which is very common in Sardinia and actually correlates with altitude in Sardinia.  So at the higher altitudes where there are fewer mosquitos, they have this trait less often.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  But the whole island, everyone was constantly sort of attacked by this parasite, and then in the post-World War II 1950s they moved to eradicate it, and they did eradicate it in the manner of, like, a few years, funded by the Rockefeller Foundation.  And immediately autoimmune disease started increasing, type 1 diabetes and multiple sclerosis, such that these days they’re probably maybe number one for multiple sclerosis even though some areas of Canada might be higher, and Scotland maybe as well.  But they’re number two for type 1 diabetes, which is an autoimmune diabetes.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  And it began immediately after the eradication of malaria.  Now, malaria is a kind of chronic infection.  And there’s a theme here that chronic infections if you get them early enough in life prevent the onset of autoimmune disease, because any chronic infection, it means that some animal or some microbe, in this case, these plasmodia, are manipulating your immune system such that your immune system doesn’t destroy them and expel them, right?

Chris Kresser:  Right.

Moises Velasquez-Manoff:  Part of how they do that is by inducing those regulatory cells, and chronic malaria infection does indeed have a very strong component of regulatory T cells so that in Africa these days if you go to the countryside where everyone has the parasite, people have more regulatory T cells circulating than they do in the cities where fewer people have the parasite.

Chris Kresser:  Um-hum.  And they even have more things like rheumatoid factor.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  Where it’s not problematic in them, whereas high levels of rheumatoid factor here can mean something like rheumatoid arthritis.

Moises Velasquez-Manoff:  Yeah, that’s right.  So the meta-picture is that the activation of the immune system that we now associate with autoimmune disease in its proper context, which is usually some kind of chronic infection, it’s actually part of a defense mechanism.  And the question is, what’s missing?  You know, you get the elevated rheumatoid factor, say.  What’s missing is usually that activated regulatory aspect that’s also elevated.  So you’ll get rheumatoid factor and then some regulatory aspect elevated.  That’s how it looked throughout our evolution.  That’s how it was activated.  These days just the proinflammatory part of it gets activated, and then it produces disease.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  We need to sort of figure out ways to reactivate that regulatory part as well to protect ourselves from disease.

Could H. Pylori Actually Benefit Humans?

Chris Kresser:  Um-hum.  Let’s talk about that, but before we do, I want to talk about another specific example.  You mentioned earlier this spectrum of organisms and that maybe on the one end you have mutualists that are just beneficial and they don’t really cause any harm at all.  On the other end you have pure pathogens that basically provide no benefit to us and just kill us.  And then in the middle you have organisms that perhaps are capable of causing harm in certain situations or maybe at certain concentrations or at certain times of life and that are capable of benefitting us in other circumstances.  So I thought H. pylori is probably the best example of the middle ground there because, of course, we know it’s associated with gastric cancer and a lot of other problems, but you also mention in your book that there’s some evidence that it could be an old friend in certain circumstances.

Moises Velasquez-Manoff:  Yeah, I mean, let me preface this whole story by saying that I don’t think anyone who’s an adult should go out and try to get an H. pylori infection.

Chris Kresser:  Haha, yeah.  We spend a lot of time trying to get rid of it, that’s for sure.

Moises Velasquez-Manoff:  But it’s also because that interpretation of these findings totally ignores the aspect of timing of when these things arrive, right?

Chris Kresser:  That’s right.

Moises Velasquez-Manoff:  And that’s really important.  So in the animal studies on H. pylori where it’s protective against asthma, it has to arrive early.  And the earlier it arrives, the more protective it is.  The later it arrives, the more inflammation it causes and the more it predisposes to gastric cancer.  So that speaks to this thing called the African enigma, which is this observation that why don’t Africans get stomach cancer when everyone has H. pylori?  One answer to that is they get it so early that it actually doesn’t cause as much inflammation as it does cause in populations that are in transition or in Western populations.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  I mean, it’s also probably because they have different strains of it which are less carcinogenic.  But another possibility is that other infections or other just residents of the microbiome modulate the impact.  There was a recent study, actually, on lactobacilli that if you had these bacteria it protected against the carcinogenic effects of H. pylori.

Chris Kresser:  Interesting.

Moises Velasquez-Manoff:  Another one is parasites or worm infections.  They also both observationally and experimentally seem to protect against the carcinogenic aspect of this bug.

Chris Kresser:  And then what about lifespan?  I think I recall from your book the rates of gastric cancer, which is certainly a disease that tends to develop later in life, and if the average lifespan of our ancestors was lower, than perhaps it wasn’t as much of a problem and so we didn’t evolve a defense to it like we would have otherwise.

Moises Velasquez-Manoff:  Right.  It’s interesting.  If you talk to Martin Blaser, who’s the proponent of the “H. pylori is actually a resident of your stomach” idea and sort of spearheaded this whole line of inquiry, he’ll say that actually part of the good that it does to you is it kills you off when you’re old.

Chris Kresser:  Haha.

Moises Velasquez-Manoff:  Because having old people around would just drain resources if they don’t actively contribute.  Actually if you look at the sort of group selection theory idea of a group of humans who are selected, it’s a major drag.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  A lot of anthropologists would disagree with him.

Chris Kresser:  Yeah, that might not go over so well in some circles!

Moises Velasquez-Manoff:  Right, and you know, he would say:  Well, I didn’t make this up.  These are just the rules of life in the old days.

Chris Kresser:  Yeah.

Moises Velasquez-Manoff:  But there’s some great work by the epidemiologist Amnon Sonnenberg looking at, like the African enigma, it turns out there was a European enigma.  It’s just that it’s buried in the past.  So he did this work where he looked at death certificates and was able to sort of put together the rates of gastric cancer and gastric ulcers.  And what he sees, basically, is that in Europe with the Industrial Revolution, suddenly everything starts going up.  Gastric cancer starts going up, and then about a few decades later, gastric ulcers start going up while gastric cancer starts declining.  So the idea is that there’s this baseline where it’s not causing as much disease.  And he’s comparing like age groups with like age groups, so he’s not seeing the effect of just shorter lifespan.  It’s just that 60-year-olds didn’t use to get as much gastric cancer, say.  That’s basically what we’re seeing.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  And so this speaks to sort of the things we were talking about at the beginning, which is that there are possibly other individual microbes that protect you against the carcinogenesis of H. pylori where infections might protect you even in old age.  So it may have nothing to do with what Martin Blaser argues with this idea that killing off makes it not be deselected for because if you die in old age it doesn’t really matter.

Chris Kresser:  Right.  Let’s move on now and talk about some emerging therapies that have come out of this hypothesis and then maybe finish up with a discussion of what — It sounds like you’re a new parent.  Is that right, Moises?

Moises Velasquez-Manoff:  Yeah, that’s right.

Will Fecal Transplants Become a Common Therapy in the Future?

Chris Kresser:  Yeah, so I’m fairly new, too.  We have a 20-month-old daughter.  And maybe we can talk a little bit about what either parents with young kids or people who might have kids in the future might be able to do with this in mind, some ways that we could maybe change the environment and precautions that we could take to help our kids develop a healthy immune system.

Most of my readers and listeners are familiar, I think, now with fecal transplants.  I’ve written about them and linked to them, and we’ve talked about them on the show.  And you have, I think, a chapter or at least part of a chapter in your book when you talk a little bit about that.  Are you following the research on this now, and what do you think their potential is for the future?

Moises Velasquez-Manoff:  Of fecal transplants?

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  I think in terms of C. diff it’s like a wonder drug.  C. diff is pretty horrific.  That’s Clostridium difficile, which is antibiotic-resistant often these days, and it’s like 95% effective.  And you know, they haven’t done huge, huge studies yet, but it’s like so far the downsides have yet to emerge, and the upsides are almost miraculous, right?

Chris Kresser:  Yeah.

Moises Velasquez-Manoff:  For C. diff, in particular.

Chris Kresser:  Yeah, I have a doctor here in the East Bay, actually, who has saved a few lives with fecal transplants.  And it’s just pretty remarkable what can happen when someone has taken multiple courses of the most powerful antibiotics and they’re still dying, and it can be almost overnight or within a couple of days that they experience a turnaround.

Moises Velasquez-Manoff:  Yeah.  You know, it’s funny, as an aside, I don’t think that the lesson of why this works and why C. diff is becoming so dangerous has really sunk in.  C. diff is related to a bunch of bacteria that are actually quite good, these clostridial clusters —

Chris Kresser:  Sure.

Moises Velasquez-Manoff:  — that include a bunch of anti-inflammatory bacteria, and it’s plausible that the retreat of those bacteria from our guts because of diet, because of antibiotics, has opened up a niche for a related bacteria to sort of expand.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  So the implications being that C. diff is not necessarily — The antibiotic resistance is clearly new, but the existence is not.  It’s been around for a long time.  It colonizes a huge number of infant stomachs without causing problems.  A good number of us carry it all the time, so why is it causing disease all of a sudden?  And it’s probably because of sort of extinctions that are happening within.

Chris Kresser:  Right.  Makes sense.

Moises Velasquez-Manoff:  I mean that’s a little bit tangential, but in terms of addressing these other diseases, like autoimmune diseases, maybe metabolic diseases.  You know, if it’s true that the microbes are unique to you and that your community is unique to you, it’s probably worthwhile to inject a note of caution because it could be that you end up causing worse things, like sort of messing things up in these much more complicated disorders that don’t relate to one bug wreaking havoc.  And everybody I talk to usually says some version of that to me, and so they’re much more interested in synbiotics or prebiotics, like figuring out how to modulate bugs that are good that you already have.

Chris Kresser:  Boost the innate population, yeah.  It’s a way of amplifying your own existing pattern without amplifying the parts that have gone awry.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  I guess that’s the trick, is finding prebiotics that selectively stimulate the growth of the beneficial bacteria rather than the parts that have gone out of whack.  I think it is interesting.  Again, I can’t recall if this is from your book or if I came across it elsewhere, that Dr. Borody from the Centre for Digestive Diseases in Australia that started using this procedure has done at least one study of fecal transplants for chronic fatigue syndrome.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  I think it was a pretty small study.  You might recall the details better than I, but it is interesting because as you said before, 70% to 80% of the immune system resides in the gut-associated lymphoid tissue, and so it’s not hard to imagine how a fecal transplant could benefit several other conditions beyond something like C. diff, but the note of caution is definitely warranted because we don’t yet understand how the gut microbiota — I mean, it feels like we’re just scratching the surface here in terms of understanding.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  I will say, though, that I was at a conference recently, and I ran into somebody there who had done a fecal transplant.  I’m not sure how they did it or where they got it.  Gut symptoms were one of main symptoms that this person experienced, but they had also struggled for a long time with weight and extreme fatigue, and she had lost 10 or 15 pounds relatively immediately, her energy level just turned around almost overnight, and her longstanding gut symptoms disappeared relatively quickly.  So it seems to have a lot of promise, but I think another problem is finding donors that are qualified.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  And I’m always urging my patients and listeners and readers not to just try this at home!  It can be really dangerous.  Someone else could have a pathogen or an organism that doesn’t cause problems for them because their system is used to that, like we’ve been saying, or their gut flora is healthier, and if you introduce that into a system that’s immunocompromised or the gut flora is really poor, then it could certainly cause a lot of problems.  So please, don’t take this into your own hands at this point.

Moises Velasquez-Manoff:  Yeah.  And if you must, do it with somebody you live with because you already have been exposed to their microbiota anyway.

What Are the Risks Associated with Helminthic and Hookworm Therapy?

Chris Kresser:  That’s right.  So what about helminthic therapy?  We’ve kind of touched on Trichuris suis, pig whipworm, and Weinstock developed this, and I think it may be worth pointing out that pig whipworm is, at least for the most part, thought to not colonize human hosts, and that’s one of the reasons it was chosen, but it seems like there have been some recent studies that suggest that there are maybe some risks to using whipworm.

Moises Velasquez-Manoff:  Yeah, well, there was one study of a teenage boy who took it for his Crohn’s, and his status worsened.  And then they did an endoscopy, and there was, in their eyes, what qualified as a sexually mature worm hanging on in there.  And one thing that I’ve never understood about Trichuris suis — I mean, the science so far is very compelling — is that generally speaking zoonotic parasite infections are very, very damaging to the hosts.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  Because the parasites are very host-specific and everybody’s immune system works a little bit differently.  Now it may turn out that pigs — and they do have a very similar digestive system to ours, and they’re omnivores just like we have — have a similar-enough immune system that it doesn’t matter.  But if you get, like, a dog hookworm, that’ll cause horrible, almost inflammatory-bowel-disease-like symptoms in humans.  Or the worm that you get from eating fish that are undercooked that’s native to seals, that can even lead to convulsions, you know?

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  But that said, the reason Joel Weinstock chose this worm is that he surmised in Iowa, where he was at the time, that so many pig farmers — it’s the number one pig-producing state in the country — encountered this worm and they had no problems with it that it must be safe.  And I think he was probably mostly right.

Chris Kresser:  Yeah, it seems like the reports have been pretty rare of any significant issue.  And at least some of the studies — I haven’t looked into any more recent research, but back when I was looking into this, which was several years ago, I think I remember seeing some remission rates for Crohn’s disease up around 70%, which is pretty remarkable.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  I mean if you look at any other treatment for Crohn’s, it’s not 70% and the side effects of some of the treatments like the immunosuppressant drugs, like Imuran and Remicade and Prednisone, certainly are pretty rough.  Is it just Ovamed in Germany that’s still doing this?  Or is anybody doing this in the US?  They weren’t last time I had checked.

Moises Velasquez-Manoff:  Well, Ovamed is the producer of these eggs.  They have the good manufacturing process approval from the FDA.  But the company that’s now taking it forward for FDA approval is Coronado Biosciences out of Boston, and they signed some deal with Ovamed to now produce them stateside, so they’re going to be produced here in these miniature Danish pigs kept in very hygienic conditions, I think.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  And they have trials in the works for MS, for inflammatory bowel disease, for type 1 diabetes, which is very interesting because they’re aiming to prevent the onset of type 1 diabetes in people at risk, which is really the best application of any of this stuff, would be to prevent disease.

Chris Kresser:  Right.  So if someone had a strong risk profile, when are they talking about introducing it?  Early in childhood?

Moises Velasquez-Manoff:  Yeah, well, the population already exists that’s being followed that’s at risk, by another group.  Usually it’s like familial prevalence in the family, you know, someone has it.  Plus it’s associated with certain HLA receptors, which are genetic.  And then on top of that, before you have full-blown type 1 diabetes, certain self-directed antibodies show up.  And it’s like you have to have, I think, two or three of them before you actually have diabetes.  So they can catch it when you just have one.  That’s when they can introduce it.

Chris Kresser:  Wow, that’s really exciting, and I agree that doing it then, before the onset certainly makes a lot more sense, and this, of course, is probably how it happened for hundreds of thousands of generations.

Moises Velasquez-Manoff:  Yeah.

Chris Kresser:  Before we go on to prevention, let’s talk a little bit about Necator americanus and human hookworm.  You talked about this a little bit in your book, and I’m not sure about the legality, but it’s not an approved treatment right now.  Nevertheless, there are people who are out there doing it and trying it, and there are some pretty interesting studies on it.  So tell us a little bit about that and what you see as the potential future for human hookworm as a therapeutic agent.

Moises Velasquez-Manoff:  Well, hookworm as a possible treatment was pioneered by scientists at the University of Nottingham.  And they, of course, were aware of Joel Weinstock’s work, and their argument was basically along the lines of what I said earlier, like if we want a parasite, it should be a human-adapted parasite.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  Now, those are the very qualities that Joel Weinstock was trying to avoid because he didn’t want to risk spreading it from person to person.  I mean, we spend a lot of money in this country trying to get rid of hookworm, specifically.

Chris Kresser:  Right, yeah.

Moises Velasquez-Manoff:  Maybe in Britain because they never had a hookworm problem they were a little bit more nonchalant about it.  But in any case, they tried it on humans.  They did it at a very low dose after these dose-ranging trials on themselves.  The scientists tested it on themselves first, between 10 and 100 worms.  And the people at 100 were deathly ill, and the people at 50 were pretty deathly ill, 25 hurt a little bit, so they went with 10, and then nothing happened in the trial, so it was too low.  So then there were some people in the world who read the science, found it very compelling, went in and got their own hookworms, came up with these stories about how they sent their own diseases into remission, and now sell the hookworms on the black market.  Now, I interviewed people who used it.  I joined this so-called hookworm underground.  I went to a clinic in Tijuana and self-infected.  It’s not something I would recommend.  I interviewed people for whom it was miraculous.  It was able to confirm as well with their doctors that it helped.  I also interviewed people for whom it made things worse, so it’s hard to say how much it works.  You know, you don’t know anything until you put it in a real trial.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  From my own experience, yes, it does modulate your immune system.  It’s kind of amazing.  I had eczema that went away.  I have an autoimmune disorder called alopecia areata.  I basically am totally hairless.  I had, like, fuzz starting to grow, peach fuzz starting to grow.  And the best part actually was for about half of allergy season that spring after I self-infected, my hay fever was totally gone.  It was just amazing.  But then it was all very variable.  It was like the effect would come and go and blah, blah, blah.  So I don’t recommend it.  It doesn’t mean that it might not work, and honestly there are hundreds, possibly thousands of people out there right now who are carrying hookworm.  They walk among us.  And it was interesting that Joel Weinstock wrote an essay for the journal Nature recently, actually late last year, and then someone wrote in and said:  Well, look.  You’re developing this therapy that has to be approved and yada-yada, but people meanwhile are already taking matters into their hand and seeking and treating themselves with hookworm.  And these were some professors who study user-driven innovation in the UK.  It was just interesting to see that this hookworm underground movement had made it to the pages of one of the most prestigious science journals in the world, right?

Chris Kresser:  Right.

Moises Velasquez-Manoff:  And the idea being, will this movement of users accelerate the science?  Because the few doctors who are willing to chaperone patients and who see these miraculous improvements in these impossible-to-treat diseases — and there are a few — they’re inevitably going to go to conferences and say:  Look, so-and-so fixed his intractable Crohn’s disease.  We’d already resected, you know, two feet of his bowel, and now he’s been in remission for three years.  Like, maybe we should figure out how to study this more closely or whatever the case may be.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  And in fact, I’ve argued with scientists.  I’ve tried to urge them to do case studies on these people who’ve self-infected, of course, the problem being that in the US, anyway, no internal review board is going to give ethics approval for this type of thing.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  But if someone shows up with an infection already, it’s a different story.

Chris Kresser:  Um-hum, that you had no prior knowledge of.

Moises Velasquez-Manoff:  Yeah, that you didn’t participate in.  And one of the new major hypotheses concerning inflammatory bowel disease emerged from just such a case study where a guy acquired a whipworm infection in Thailand and sent his ulcerative colitis into remission — this was human whipworm, not pig whipworm — and then had a scientist named P’ng Loke study him and the hypothesis being that somehow parasite infections restore the mucus barrier.  No one was talking about this before he did this case study, and now everybody’s looking at mucus, like how important is it?  And it turns out mucus selects for the right microbes.  You secrete things in your mucus that only certain microbes can degrade, so it’s like you’re feeding the right ones.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  So what happens when you stop producing mucus for whatever reason?  First of all, the microbes come up right against you, so you get inflamed.  Inflammation itself selects for nasty bugs possibly, so you end up in this feedback cycle where everything’s going wrong, and then meanwhile it’s literally killing you possibly.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  So anyway, I am not averse — I mean, I think that scientists should take more advantage of this underground movement.  On the other hand, don’t believe everything you hear out there because there are a lot of vested interests in this working in the underground because basically the people who are telling the stories are (A) people who are selling the parasites or (B) people who have paid thousands of dollars for the parasites, which I’m sorry to say, skews your assessment of the results.

Chris Kresser:  Sure.  You want it to work when you spend that kind of money.

Moises Velasquez-Manoff:  You’re darn right!

How Can We Put These Theories into Practice with Our Children?

Chris Kresser:  Haha, absolutely.  Well, I’m personally fascinated by these therapies, and actually my story is that I went traveling in my 20s, spent a lot of time in places like Indonesia, and acquired something that I later found out was multiple parasitic infections.  At the time, I didn’t know.  And while I was trying to figure out what was going on, one of the diagnoses I received because I had a colonoscopy was that the terminal ileum of my small intestine was inflamed.  And the guy who scoped me said:  Well, your intestine is inflamed.  It looks kind of like Crohn’s disease, but it might not be.  And at that time, I was still kind of trying to determine what was happening, and so I pursued the autoimmune hypothesis and was somewhat averse to the medication that was available, and so I did some research and ended up trying the whipworm therapy.  And I did a full course, maybe even a little longer than a full course, and it didn’t work for me, and none of the sort of autoimmune stuff did.  And I actually later found out that I had Entameba histolytica and some other not-so-nice parasites, and as soon as I got rid of those, I got better, but I’ve always been personally interested in these things and even willing to experiment on myself with them.  But I think it seems pretty clear that the most effective way of putting this stuff into practice may not be for ourselves as adults, but for our children and creating changes in the environment that might keep them from ever getting these conditions in the first place.  So let’s talk a little bit about what those changes might be and maybe anything you’re personally thinking of as a father now.

Moises Velasquez-Manoff:  Right.  You know, if you spent the time to read the whole book — and it’s kind of a long work!

Chris Kresser:  I did!  It was one of the best science books I’ve ever read, Moises.  It was incredible, and I highly recommend that everyone who’s listening to this read it.  It read like a cross between a detective novel and a really fascinating scientific study.

Moises Velasquez-Manoff:  Well, thanks for the kudos!  I mean, what I was going to say is that I make the reader wade through all the science, and in the end, there’s not really much to say!

Chris Kresser:  Oh, I don’t know.  I think there is.  I mean, just even something as simple as the mother during pregnancy spending time if they have access to a farm or getting a pet if they don’t already have a pet.

Moises Velasquez-Manoff:  Yeah, yeah.

Chris Kresser:  I mean, a lot of this stuff is not proven beyond a shadow of a doubt, but I think some of things you mention are worth at least talking about a little bit.

Moises Velasquez-Manoff:  Right.  So the farm thing:  What I usually do is I tell people what I would like to say and then what I can say.

Chris Kresser:  Haha.

Moises Velasquez-Manoff:  So what I would like to say is exactly that.  I would like to say go to a farm as quick as possible while you’re pregnant and possibly take this multicellular probiotic, aka, a worm.  The reality is that there are some studies actually that I’ve come across since writing the book that show that pregnant mothers who spend time around animals actually give birth to kids who have worse allergies.

Chris Kresser:  Interesting.

Moises Velasquez-Manoff:  Yeah, so these are not the same studies that are done in Central Europe, they’re done in other countries, so it’s hard to know what’s happening.  What seems to be true is that the environment that characterizes a barn in Germany or Bavaria — I mean, Bavaria is clearly in Germany — but in that sort of temperate zone where things are moldy and cool and moist, that environment protects.

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  Other environments maybe do not.  And one of the possibilities is that you’re actually getting zoonotic helminth infections if you spend a lot of time around animals, you know, when you’re pregnant in Africa, say.  Actually these weren’t Africa, but in other parts.  So I guess the point is these are important switches in the body, and since we don’t entirely understand how they work, it’s entirely possible that we end up switching them the wrong way, right?

Chris Kresser:  Um-hum.

Moises Velasquez-Manoff:  That said, the things that I think you can do for real are, like, don’t worry about daycare.  Daycare is pretty consistently protective for people with the right genotype.  Of course, this is gene-environment interaction, but kids who go to daycare later on end up with fewer allergies pretty consistently.  Even more easy and more important is just eat a good diet when you’re pregnant.  Don’t eat a lot of junk food, which is proinflammatory.  Eat more of a Mediterranean-type diet or things that are full of omega-3’s and whole grains and fruits and vegetables if possible.  Try to not develop inflammatory conditions like gestational diabetes, or try not to be overweight.  I mean, that’s actually probably asking a lot since you might not be hearing this until you’re already pregnant, but the point is to take care of yourself while this kid is forming inside you, in its most plastic, vulnerable phases, really.  And then early in life, don’t be worried about other kids.  Pets, yes, they seem to be pretty universally good, especially around the pregnant mother.

Chris Kresser:  Um-hum.  Breastfeeding?

Moises Velasquez-Manoff:  Breastfeeding, yes, but again there are nuances here.  Like that celiac article.  In overweight mothers, the colostrum, for example, has excess — according to one study, anyway — excess proinflammatory factors.  I mean, your whole immune system travels out in your breast milk, so however your immune system is working, it’s going to come out in your breast milk, and the signature of cytokines and antibodies and so on.  So if you’re overweight, it means probably that you’re a little bit inflamed.  You know, that’s one of the features of metabolic syndrome.  That’s going to come out.  And indeed, kids of mothers who are overweight are more likely to develop asthma, one inflammatory disease among many other things which are highly unpleasant.  But what I would like to say at this point about breastfeeding is you, the mom, take some magical probiotic, eat a lot of prebiotics, eat a lot of omega-3’s.  All that stuff is going to come out in your breast milk.  And breastfeed at the same time as you introduce the kid to foods because then they’re getting this hopefully cooling and peace-inducing effect through your breast milk while they’re encountering food proteins for the first time.

Chris Kresser:  Um-hum.  So what about this idea, and we actually didn’t cover this in terms of viruses, but you mention in the book that just like there’s some evidence that supports the idea that early exposure to H. pylori is protective, there’s also some evidence that early exposure to viruses may be effective.  And the way that that might have happened in traditional societies is mothers chewing food.  A large percentage of people have antibodies to Epstein-Barr, for example.  So what about that idea?  Are you going to be chewing any food for your daughter?

Moises Velasquez-Manoff:  Well, it’s more like I end up eating her chewed food that she drops on the floor!

Chris Kresser:  Haha.

Moises Velasquez-Manoff:  But you know, that is an interesting idea, and I wish we would investigate it more because when you chew food, not only do you pass on these potential antibionts, which could be either good or bad, in your saliva there are all these antibodies, and there are good antibodies and bad antibodies, and if you have IgA, that’s a peaceful antibody.  It’s basically signaling:  Don’t worry about whatever this is.  There’s a ton of that in your saliva.  So by chewing food, you possible train the immune system to not respond to the food antigens or whatever else.  I haven’t put that into practice, honestly.  I think it speaks to a much larger issue, though, of the timing again of when you get these viral infections or when you get a lot of these infections.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  And one of the most interesting historical examples of that were the polio epidemics that emerged in the later 19th century in Northern Europe and then sort of spread.  The polio virus has been around with us forever.  Why did it start causing disease?  It’s because it was apparently getting introduced later and later as the cities cleaned up and sewage control went into effect.  Early infection, babies don’t have a problem because they’re still being breastfed.  They’re still protected with those antibodies.  Late infection, you become paralyzed and possibly die.  But there’s no new bug.  There’s just a change in the timing of its arrival.  And that is so unexplored in terms of all of these.  Again, in terms of generally thinking of the microbiota, people don’t use timing.  Timing is going to be very important.  The microbiota that you get in the first two years of age is going to be much more important than any probiotics you can take later.

Chris Kresser:  As an adult.

Moises Velasquez-Manoff:  It’s just not going to be the same.  And that speaks to another issue, which is early-life antibiotic usage, which over and over keeps showing up as a predictor of asthma and inflammatory bowel disease now.  So you think that maybe people who are sickly are more likely to take antibiotics.  The problem is in animal studies they can basically knock out the anti-inflammatory bacteria with broad-spectrum antibiotics, and then the mice become more prone to these diseases.

Chris Kresser:  Right.

Moises Velasquez-Manoff:  I mean, obviously these life-threatening infections you have to treat with antibiotics for your kid, but for myself — Listen to what your doctor says, number one, but ask your doctor:  Do we have to use antibiotics?  Is this maybe a viral infection?  Is it not going to do anything?  Otitis media, which they used to throw antibiotics at left and right without thinking, it turns out to be viral and it clears up most of the time by itself.  So do we really need antibiotics for it?

Chris Kresser:  Yeah, I think there’s a lot more awareness about that, but I think we also have a ways to go.  It seems to me they’re still overprescribed, especially in young kids.  So I’m in agreement with you on that.  There’s certainly a time and a place for them, and they can save lives, but for me personally, I definitely consider them as something I would try only when there aren’t other viable options.

Moises, I want to thank you for coming on the show.  Again, it’s one of the best books I’ve ever read, and I’ve read a lot of science books because I’m a science geek!  So I really enjoyed it.  It’s a fascinating topic, and I highly recommend checking it out if you haven’t.  I know I’ve mentioned it on the show a few times.  It’s called An Epidemic of Absence, and yeah, thanks again, Moises, and hopefully we can meet up now that we’re neighbors.

Moises Velasquez-Manoff:  Yeah, thanks a lot.  That would be terrific.

Chris Kresser:  Thanks again, and I look forward to meeting you in person.

Moises Velasquez-Manoff:  Likewise.