Here is The Roundup, Edition 14, bringing you the best from around the web from the past two weeks!

Blast from the Past

A great study was just published illustrating the gut-skin-immune connection and the ability of probiotics to influence that axis. The authors discuss the vicious cycle of inflammatory gut disease, where inflammation leads to leaky gut, which leads to more inflammation, and so on. The inflammatory cytokines produced by this inflammation in the gut can trigger a whole host of different skin conditions, including eczema and other allergic skin diseases.

As many of you know, the gut-skin-axis is a special interest of mine. I recorded a podcast back in December of 2011 describing how the gut-skin axis contributes to skin conditions like acne (vulgaris and rosacea), psoriasis, eczema, dermatitis and others. In November of 2012, I gave a presentation at the Weston A. Price Foundation annual conference on the gut-skin connection, and even wrote an accompanying article describing the most recent research on the topic. In my series on Nutrition for Healthy Skin, I explained how probiotics can be an important tool in treating skin conditions, provided the appropriate precautions are taken when choosing a probiotic product.

I’ve had many patients who struggle with skin problems such as acne, rosacea, and eczema, and I’ve been pleased to see how many of them have been able to significantly improve the health of their skin by changing their diet to a more gut-supportive approach. While most conventional health professionals treat problem skin with antibiotics and medication, I believe the future of skin care will pay far more attention to the patient’s gut health and to encouraging a diet that supports a healthy gut barrier and microbiome.

Research Report

• This study explains why I’ve been encouraging people to think of probiotics as immune regulators as much as gut support.
• New research suggests that Gymnema (an herb used for blood sugar control) kills Candida & disrupts biofilms.
• An interesting comment on recent low-dose naltrexone study speculates that autism and M.S. may share a common cause: high levels of inducible nitric oxide synthase (iNOS) in the brain.
• Research demonstrates that H. pylori suppresses natural immunity and increases the risk of other infections and cancer.
• A new study elaborates on how antibiotics increase the risk the risk of gut infections.

Worth A Look

• Free the Animal explores how resistant starch improves insulin sensitivity.
• The Wall Street Journal examines how stress and anxiety propel us to eat more.
• The New York Times discusses research that suggests that intense exercise leads to a short-term suppression of food intake and reduction in appetite.
• Jill Carnahan, MD explains how gut permeability impacts a wide range of health conditions, including cancer, autoimmune disease, inflammation, and food sensitivities.

For the Foodies

• PaleOMG: Spaghetti Squash Crusted Quiche
• Paleo Parents: Chicken Liver Mousse
• NomNomPaleo: Fig & Watermelon Salad with Honey Vanilla Cashews
• Everyday Paleo: Spinach and Salmon Salad with Arugula Pesto
• Paleo Spirit: Roasted Tomatillo Peach Salsa with Pan-Fried Halibut
• The Healthy Foodie: Avocado Stuffed Meatballs
• Against All Grain: Caramel Apple Spice Waffles

We’re back (after a brief hiatus) with an update on Fukushima radiation and seafood, and answers to several of your questions.

In this episode, we cover:

2:41 Is There Really Fukushima Radiation in My Fish?
14:16 The truth about “eating too much meat”
18:50 Naturally healing cavities
23:50 Hepatitis C and Liver Disease
30:03 What to do about esophagitis and GERD
33:27 Is resistant starch useful?
37:18 Treating skin conditions with FMT

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, and I’m your host, Steve Wright from SCDLifestyle.com.  With me is integrative medical practitioner and healthy skeptic Chris Kresser.  So, Chris, how’s your day going?

Chris Kresser:  It’s pretty good, Steve.  How are you?

Steve Wright:  Mine is going very well as well.

Chris Kresser:  Great.

Steve Wright:  It’s just been a busy day.

Chris Kresser:  Yeah.  So, I’m sure folks have noticed that it’s been a while since we did a podcast.  We’ve been pretty regular about it the past few years, but life intervened and I’ve been so overwhelmingly busy with the book and putting the final touches on that, finishing the manuscript, responding to the copyedits and getting that ready, and then doing some media stuff related to it that I just couldn’t find the time to do a podcast, so here we are!  Know that I can’t guarantee an every-other-week, regular show between now and maybe February or March because of all the book activities, but I’ll do my absolute best to keep the show going during that time.  And we’re going to have lots of other great stuff for you, too, in the next few months related to the book, so hopefully you won’t miss it too much if we miss a week or two here and there.

Steve Wright:  Yeah, we appreciate everyone’s patience with Chris’ schedule and know that Chris puts a lot of time and effort into these podcasts.  I just talk, so it’s not a huge burden for me, but Chris works his butt off to get ready for these types of podcasts.  So, Chris, we’re going to start with a little talk of Fukushima, and then we’re going to transition over to some long-awaited Q&A.

Chris Kresser:  Sounds great.

Steve Wright:  All right.  Well, before we get into radioactive substances in seafood, let me tell you all about Beyond Paleo.  If you haven’t heard yet, Chris put together his best tips and tricks into a free 13-part email series that well over 30,000 people have already downloaded and basically subscribed to.  It’s an email series.  It’s going to blast you an email every so often, again, with Chris’ best tips and tricks on burning fat, boosting energy, and preventing and reversing disease without drugs.  So, it’s pretty simple.  If you’d like this and you don’t have this info yet, you just go over to ChrisKresser.com, look for the big red box, and go ahead and put your name and email in that box, and Chris will start sending you those free emails.

Is There Really Fukushima Radiation in My Fish?

So, Chris, there’s been a lot of talk about radioactive substances in the water and seafood.  What’s going on here?

Chris Kresser:  Yeah, so I’ve heard from a lot of people, both in my personal life, family members, friends, and then also on the blog, podcast questions, just people I meet here and there – everyone wants to know if they should be wary of eating seafood because of the Fukushima radiation.  And there has been a lot of fear-mongering type of articles on the Internet, sites like Natural Health News and other similar types of sites that claim that the levels of radiation in fish are harmful and we should be taking all kinds of detox supplements to try to get rid of this excess radiation and we should be avoiding any fish that’s caught in the Pacific Ocean.  As usual, we always want to look at all these kinds of claims with a grain of skepticism and look to the scientific literature to see if these claims can actually be substantiated by peer-reviewed evidence, and this is especially true when you’re talking about stopping consumption of a type of food that most people don’t get enough of and that’s extremely nutrient dense, that contains long-chain omega-3 fats that are really impossible to get anywhere else in the diet in their preformed state and one of the sole sources of vitamin D in the diet as well.  And if there’s anything most people need to be concerned with, it’s not eating enough fish rather than eating too much of it.  So, whenever there’s some kind of claim that we shouldn’t be eating fish, it has to, of course, be evaluated very seriously because there are actual health repercussions for not eating fish.  I mean, if there was a claim that we shouldn’t eat industrial seed oil or… I don’t know… eggplants?  If something happened to them where they became toxic and we couldn’t eat eggplants anymore, I think we could get by.  We’d still want to evaluate that claim because there’s no sense in removing a food like that from our diet if we don’t have to, but the seriousness of it isn’t at the level of telling someone to remove fish because we’ve spent so much time studying the health benefits of the nutrients that fish contain, and I think that it’s really, like I said, important that people continue to eat it if that makes sense.

It’s completely natural and appropriate to be concerned about radiation, and I think there’s also a little bit of hysteria around radiation that makes sense on a certain level as well.  It’s kind of a scary thing.  You can’t see it.  It’s potentially fatal, life threatening, it’s a way of getting sick and then perhaps dying that seems particularly egregious.  And for whatever reason, there’s just a very heightened level of concern about radiation for better or for worse.  And there is obviously a real issue here with Fukushima radiation.  In fact, some recent news reports suggest that the radiation is not only still occurring, but it’s actually possibly occurring at a greater rate than ever.  Steve actually just sent me a couple articles today about that.  So, this is a significant concern.  But the question that we’re talking about today is whether eating seafood that has been contaminated with radioactive isotopes from the Fukushima fallout will cause health problems.  That’s the only question that we’re talking about today.  And hopefully you’ll be relieved to know that all the peer-reviewed studies that have looked at this question have found that there’s not even a miniscule risk of getting sick from eating fish caught in the Pacific.

There was one large review in the Proceedings of the National Academy of Sciences, PNAS, the journal, and it evaluated the health risk of consuming Pacific Bluefin tuna that was caught in the Pacific after the Fukushima event around San Diego, I believe is where the fish were caught were for this study.  And the study was done by some researchers from the Woods Hole Oceanographic Institution and a couple other organizations around the world, and they’re all independent researchers.  There were no conflicts of interest, nobody that was working for the fish lobby!  And let me just highlight a few of the findings for you.  They estimated that a typical restaurant-sized portion of Pacific Bluefin tuna that was contaminated with radioactive isotopes cesium-134 and cesium-137 contains about 5% of the radiation you’d get from eating one uncontaminated banana and absorbing its naturally occurring radiation.

The really important thing to remember here is that all foods contain radiation because there’s radiation that’s just naturally a part of our planet.  Bananas contain much more radiation in them, despite not being contaminated by Fukushima fallout, than a restaurant-sized portion, a 7-ounce portion, of fish.  So, the issue is not whether we’re exposed to radiation, because we are, all of us, on a daily basis exposed to radiation in food, just walking around.  If we go on a cross-country flight, we’re exposed to radiation.  Like every other toxin, the question is what’s the dose?  A small amount of toxin we can handle.  A large amount of toxin causes problems.  That’s really important to keep in mind with this.  It is true that cesium-134 and cesium-137, which are these radioactive isotopes, have been found in fish because of Fukushima, but the levels are so low that they’re not going to cause any health problems, even in people who are eating fish at extremely high levels.  For example, if you ate three-quarters of a pound a day of this contaminated Bluefin tuna for an entire year, you’d still receive only 12% of the dose of radiation you’re exposed to during a single cross-country flight from LA to New York.  That should put it into perspective a little bit.  Also, at that same level of consumption, the excess relative risk of fatal cancers would only be two additional cases per 10 million similarly exposed people, and that’s such a low number that in statistics and health there’s really reason to believe that’s no more than chance.  And, in fact, statistically significant elevations in cancer risk are only observed typically at doses of radiation that are 25,000 times higher than what you’d expect to be exposed to by eating the three-quarters of a pound a day of Bluefin tuna.

The other thing – and I mentioned this before with the banana example – is that levels of naturally occurring radioactive isotopes, like polonium-210 and potassium-40, in Bluefin tuna are greater by several orders of magnitude than the radioactive isotopes from the Fukushima contamination in the fish, which is cesium-134 and cesium-137.  In fact, levels of polonium-210 in fish prior to the Fukushima event were 600 times higher than the levels of cesium from Fukushima that were found.  This suggests that the additional radiation in the form of cesium from Fukushima is completely insignificant from a health perspective.

Another thing I want to mention is that there are some bottom-feeding fish that are right off of where the reactor is in Japan, right off the coast, that contain extremely high levels of radiation, like 250 times more cesium in those fish or more than what are found in Pacific Bluefin tuna, and even if you consumed a third of a pound per day of this really highly contaminated fish, you’d still be below the international dose limit for radiation exposure from seafood.

And then the last thing that I want to point out is that Dr. Robert Emery at the University of Texas Health Center in one article said that you’d need to eat 2-1/2 to 4 tons of tuna in a year to get a dose of cesium-137 that exceeds the recommended health limit.  So, to put that in perspective, that’s 14 to 22 pounds of tuna a day that you would have to eat to have a problem from this radiation in fish.  All of that to say at least right now I have not seen any peer-reviewed, reliable evidence to suggest that there’s any problem eating seafood caught in the Pacific.  Of course, I’ll continue to evaluate this, and if anyone has seen any studies published in a reputable journal that contradict this, I would be happy to look at them, and I’ll be the first person to change my mind if I see such evidence.  But like I said before, articles on Internet sites that aren’t substantiated and don’t contain references to peer-reviewed research, you really can’t rely on those.  I don’t see any evidence of a conspiracy within the scientific community to cover this up.  Scientists that work at oceanographic institutes and other independent organizations don’t really have any reason to cover this up.  There’s no plausible motivation for it.  So, that’s my current take on it.

Steve Wright:  Yeah, thanks, everyone, for listening to this episode of myth-busters with Chris Kresser!

Chris Kresser:  Yeah, so keep eating that fish.  It’s good for you, and it’s going to improve your health, not harm it.

Steve Wright:  It’s always about the scale, isn’t it?  It’s always about in relation to other things.

Chris Kresser:  That’s right.  Even water can be a toxin at a high enough dose.

Steve Wright:  So, stop drinking water, everyone.  Just kidding.  OK, Chris, we really appreciate that AP bulletin you put out there.  It was very well done.  I had seen a lot of the fear mongering as well.  Hopefully they do get those reactors under control out there and can hopefully avert any more problems.

The truth about “eating too much meat”

Let’s roll on to some Q&A.  This first question, I think, a lot of listeners are going to identify with, and I thought it was really well put.  This comes from Lauren, and, Chris, she wants to know:  “Are there any concerns about excess meat consumption for those of us on an autoimmune diet or a similar plan who can’t have eggs or nuts for protein?  My main protein sources are grass-fed beef, salmon, and sardines with chicken occasionally.  I’m not sure what percentage of my diet comes from meat.  Are there potentially detrimental effects from this long-term high consumption of meat, and if so, is there anything I can do to mitigate these effects?”

Chris Kresser:  I’ve never seen any evidence that suggests that there would be any detrimental effect.  All of the concern about eating too much meat was primarily based on fear of saturated fat, and we now know that saturated fat isn’t a major contributor to cardiovascular disease or metabolic disease, and I haven’t really seen any evidence that it’s a major contributor to any disease.  And you’re eating beef, but you’re also eating sardines and chicken, other types of meat, so you’re getting different types of fatty acids there.  Meat is very nutrient dense.  It is, in fact, more nutrient dense than a lot of vegetables and fruits, especially when you’re considering the nutrients that are known to be essential for human health and not phytonutrients and antioxidants and things that are certainly beneficial, but not necessarily essential.  So, no, I don’t really see any problem with that.  The only thing that comes to mind is that some people have a genetic predisposition to accumulate excess iron, and if that’s the case, eating a lot of red meat could be problematic because it could increase iron levels, but that’s easily tested for just by getting your iron levels tests once a year or something like that, an iron panel and ferritin.  And that doesn’t affect everybody.  Most people just excrete any excess iron that they take in from food, so it’s not a concern that everybody needs to pay attention to.  It’s only for a small segment of the population.

Steve Wright:  Chris, I’m concerned Lauren didn’t mention bacon.

Chris Kresser:  She didn’t mention bacon, yeah.  You know, it’s not for everyone.  Amazing, huh?

Steve Wright:  I think there might be an underlying question here, Chris.  When you’re eating a high-meat diet like this, could there be a protein consumption problem?

Chris Kresser:  It’s really unusual for anyone to eat more protein than is healthy for them without trying hard.  Humans can generally deal with up to 30% to 35% of total calories from protein without experiencing any chronic long-term health problems.  Once you exceed 35% of total calories, you start to develop the possibility of ammonia toxicity or ammonia overload, urea ammonia issues, but that’s really, really rare and it usually happens with bodybuilders or people who are taking lots of lots of protein powder and eating super-high protein diets to try to put on muscle mass or something like that.  We have a system in our brain that kind of regulates protein intake, and when we need more, we crave more protein, and when we need less, we’re averse to it.  If you yourself have ever been pregnant, women listening to this show, or you know someone that has, you probably either yourself or know someone who experienced extreme protein aversion during some point during pregnancy.  That’s not an unusual symptom, and there’s some evolutionary reasoning behind that, and women generally crave less protein during pregnancy and can sometimes even feel nauseous when they think about protein or high protein foods during pregnancy.  That’s not always the case, but it does happen.  So, generally the brain will regulate it well, and even if you’re eating meat at every meal, it’s unlikely that you’re going to exceed 35% of total calories from protein.

Naturally healing cavities

Steve Wright:  Awesome.  Let’s move on to the next question, Chris.  This one comes from Josie.  She’s seen several claims that eating a diet similar to yours, Chris, plus taking grass-fed butter oil and fermented cod liver oil heals cavities.  Is this a fact or fiction?  And this continues our myth-busters episode.

Chris Kresser:  I haven’t looked into the evidence on this, like in the scientific literature, but certainly anecdotal evidence supports the idea that proper diet can help remineralize teeth.  There’s a book called Cure Tooth Decay by Ramiel Nagel, and he talks about using a nutrient-dense diet and superfoods like cod liver oil, raw milk or cheese, raw dairy, bone broth, and maybe grass-fed bone marrow, either raw or cooked, to remineralize teeth and prevent the progression of and, in some cases, even reverse cavities.  I know a lot of people and patients who’ve had issues with dental health and switched to a nutrient-dense diet and seen really big changes, so I think it’s possible, based on anecdotal experience.

There are also special probiotics that you can use for dental health.  Streptococcus salivarius K12 and M18 are two special species that have been shown in clinical studies to have benefits for dental health, and they work by attacking some of the bacteria and plaque, and also they break up the biofilm which plaque is formed from, and that can be really difficult to do otherwise.  Generally these probiotics, you get them and you put them in water, and then you swish them around in your mouth on a daily basis, and that can lead to significant benefits as well.

And then some people use xylitol chewing gum for reducing biofilm and cavities, but I’ve read a couple reviews that suggest that while it’s true that sugarless chewing gum has been shown to reduce cavities, it’s not the xylitol in the gum that’s doing it.  They did a study where they gave people xylitol lozenges rather than chewing gum and there was no reaction, no reduction in cavities.  The author speculated that it was maybe active chewing which increased the salivary flow that led to the benefit of reduced cavities rather than the xylitol itself, but nevertheless, some sugarless gum has been shown to help in that way.  You have to be careful with the sugarless gums, though, because, of course, a lot of them contain artificial sweeteners, and xylitol is a FODMAP and can be difficult for people with digestive issues.  And then some of the other artificial sweeteners have been shown potentially to have adverse health effects.  The research is a little mixed on that, and I’m not ready to make a definitive statement, but there are some studies that suggest that they may be harmful, so I think the better choice is to do the oral/dental probiotics and then the nutrient-dense superfoods, the fermented cod liver oil/butter oil blend has vitamin A, vitamin D, vitamin K2.  All the fat-soluble vitamins are especially helpful for dental health.  Then you have the grass-fed dairy, also a great source of K2 and vitamin A.  You have bone broth soup, which will have minerals, calcium, glycine, which is helpful for tissue rebuilding, and then the bone marrow and organ meats are also incredibly nutrient dense as well.  So, if you do all that and the dental probiotics, I think that’s a great place to start.

Steve Wright:  Yeah, and I think we couldn’t mention this without saying that if you haven’t read Weston A. Price’s book, you should probably just read that if you’re interested in this topic.

Chris Kresser:  Absolutely.  And that’s what Ramiel Nagel’s book is based on.  He’s a member or has been involved in the Weston A. Price Foundation, and he’s known in that community, and that’s what his approach is based on, although I think he’s more along the lines of paleo plus raw dairy because he’s not a fan of grains for people who have dental issues, grains or legumes.

Steve Wright:  Hmm, interesting.  I’m going to have to get that book.

Hepatitis C and Liver Disease

OK, let’s roll on to the next question, Chris.  This comes from Anonymous.  First off, they have hepatitis C, and they’re mostly asymptomatic with the exception of debilitating fatigue.  They follow a super-strict paleo diet and have never drank alcohol… well, at least lately.  The last drink that this person had was on December 31, 1999.  They’re now 46 years old and have had the virus for around 25 years.  Getting to the question, they would like to know, should they get a liver biopsy to determine if they have cirrhosis, so liver cirrhosis?  Their mom is adamant that sticking a needle into the liver is a bad idea and that once you start cutting and poking and doing these types of invasive things that it might lead to cancer.  It’s a wacky theory, but she’s adamant about this.  So, what this woman is looking into is a doctor named Dr. Sylvestre in Oakland who treats hepatitis C with ribavirin and interferon.  She treats everyone regardless of whether they have healthcare.  She has a remarkable cure rate unless cirrhosis is present, but even then, she still will recommend treatment.  She is somewhat of a hepatitis C guru.  But this person has a question, Chris.  She’s terrified of what these drugs will do to her gut, brain, and bones.  She would like to know what you would do if you were her.

Chris Kresser:  OK, so let’s break this up a little bit.  The first question was about liver biopsy and whether that’s a useful test.  It is useful in the sense that it can provide useful information, but her mom is correct in that it’s invasive and potentially dangerous.  There were adverse effects that can happen with liver biopsy, and actually many doctors are even hesitant to recommend it at this point because of that.  Sticking a large needle into your liver is definitely not risk free.  Luckily, there is a test called FibroSURE, which is a combination of six serum tests, six blood tests, and it generates a score that is correlated with the degree of liver damage in people with a variety of liver diseases, and it actually has been clinically validated to have the same prognostic value as a liver biopsy with a tiny fraction of the risk, and the risk is only the risk that you would be exposed to by getting blood drawn, which is very, very small now.  The six tests are A2-macroglobulin, haptoglobin, apolipoprotein A1, bilirubin, GGT, and ALT, and with the exception of A2-macroglobulin and apolipoprotein A1, they’re fairly commonly available tests, but when they put that together into a certain algorithm or score, that score is as good of a marker for liver issues as the liver biopsy.  And there’s a hep C FibroSURE that you can take that I would definitely recommend instead of a biopsy.

The other test that’s useful for tracking hep C over time is the reverse transcription polymerase chain reaction test, or HCV RT-PCR, and that’s used to monitor the status of hep C over time.  It basically tells you the viral load and the amount of disease activity that you’re experiencing, and you can use it as a barometer for how treatment is progressing, and that should go down over time if the treatment is working, so you could run it, like, every six months as a way of gauging the success of the treatment.  So, those are things to definitely talk to your doctor about.

In terms of treating hep C, it’s, of course, a virus, and like all viral infections, often the best approach is to strengthen your own innate immunity as much as possible and then to use additional things that are specifically antiviral on top of that.  We’ve on several shows, I think, talked about basic nutrients for immune support.  That would be vitamin C, glutathione – I like the liposomal forms of both of those.  Selenium and zinc.  There are some botanicals that have very impressive immune-boosting ability.  One combination that I like is equal parts of astragalus, Cordyceps, and rhodiola.  You just take 30 or 40 drops of that or maybe twice that dose three times a day.  And then you have antiviral nutrients, like Lauricidin, which is an extract of lauric acid, monolaurin.  That’s antiviral and also has activity against biofilm and gram-negative bacteria and fungi.  Apolactoferrin is antiviral.  EDTA, which is in InterFase Plus; it has activity against biofilm, but also it’s antiviral.  And then you have some antiviral herbs, like Chinese skullcap, elder, ginger.  Licorice, a lot of people don’t know, is strongly antiviral.  Lomatium, which is biscuitroot, another name for it, and rhodiola also has antiviral activity.

So, there are a lot of different alternative approaches to treating viral infections, including hep C.  I’m not familiar with that particular physician and her work, so I can’t really comment on that, but there are a lot of people around the Bay Area, if that’s where you are, herbalists and alternative practitioners that specialize in these kinds of treatments if you don’t want to go the drug route, but that’s, of course, something you’d need to discuss with your doctor.

What to do about esophagitis and GERD

Steve Wright:  OK, let’s roll on to the next question.  This one comes from Heather, Chris.  She’d like to thank you for all the wonderful articles that you’ve written on heartburn and GERD.  However, she did not see any mention of how to heal existing esophagitis.  She has a “15-year-old son who just recently had an endoscopy, and his GI doctor showed me the photos of his very inflamed tissue.  Apparently the biopsy came back negative for H. pylori, and the GI doc wants to put him on Prilosec.  I’m planning on finding someone to do a Heidelberg capsule test for him just so we can figure out what we’re truly dealing with, but I’m concerned about getting his existing damage healed.  Could you comment and provide any suggestions about this?”

Chris Kresser:  Yeah.  I mean, the best way to stop the tissue damage and reverse it is to stop the GERD from happening, and the body actually has a remarkable ability to heal tissue in many cases, so if you stop the insult from continuing to occur, then especially for a 15-year-old, their regenerative capacity is often quite a bit stronger than someone who’s a lot older, and it will often heal on its own.  But there are a few things you can do to help things along.  Marshmallow, slippery elm, and deglycyrrhizinated licorice – that’s DGL – they’re all botanical plant substances that are mucilaginous.  They have a really soothing and healing effect on tissue, mucosal tissue in particular.  Manuka honey – or any honey, actually – is one of the best wound-healing substances there is.  It’s even used in a lot of hospitals now.  There’s a lot of scientific literature on this.  A lot of people are surprised and they kind of consider it a folk remedy, but if you go on PubMed and do some research, you’ll see there’s a lot of studies on it, and there’s also an extremely long tradition in all different kinds of cultural traditional medicines of using honey for wound healing.  Manuka honey from New Zealand, I think, seems to work best, but other raw forms of honey will do it.  Zinc carnosine and MSM are both mucosal protective and anti-ulcerative.  And then glycine, which is an amino acid found in cartilaginous types of meat, tougher cuts like oxtail, shanks, brisket, chuck roast, and then drinking one to two cups of bone broth a day made from chicken – make sure to include the heads and feet – and femur bones and marrow bones from beef.  These are all things that can really help with rebuilding the tissue layer in the esophagus.  And one product that has a number of these things in it is GastroMend from Designs for Health.  That’s something I use.  So, you could do the GastroMend plus some honey plus glycine-rich foods, and I think that would be a great start.

Is resistant starch useful?

Steve Wright:  Yeah, sounds like a great protocol.  OK, let’s roll on to the next question.  This question comes from Joss.  “Chris, what’s your take on resistant starch?  Do you think it can be useful as a prebiotic?  How about other uses such as hunger control, etc.?”

Chris Kresser:  Yeah, I am pretty interested in resistant starch.  I’ve been studying it quite a bit lately and using it in my practice.  It’s a type of insoluble fiber that’s fermentable by gut bacteria.  There are several different types of fiber.  The two main categorizations are soluble and insoluble.  Soluble fiber is fermentable by gut bacteria, and I consider it to be more beneficial for that reason.  Insoluble generally isn’t, but resistant starch is a type of insoluble fiber that is fermentable, so it can be used as a prebiotic to increase the levels of beneficial bacteria in the gut, but it’s also – and I would say primarily – being used now for blood sugar management and metabolic issues.  It seems to have a pretty significant impact on especially fasting blood sugar.  I’ve seen 10-or-15-point drops and heard of even greater reductions in fasting blood sugar just by using resistant starch.

It’s difficult to obtain in food.  One way to get it is in potatoes that have been cooked and then cooled for 24 hours.  It’s the cooling that actually transforms the starch in potatoes to resistant starch, so cooked potatoes that haven’t been cooled don’t really have any resistant starch or very little, but potatoes that have been cooled for 24 hours do have a significant amount.  Another way is eating green plantains.  The only way to make green plantains edible without cooking them is dehydrating them into chips.  Green bananas have some resistant starch, but I don’t find them to be very appetizing myself, so the way that most people are using resistant starch is by taking potato starch and mixing it with water.  The Bob’s Red Mill variety is gluten free, and you can do 2 to 4 tablespoons a day.  If you have a really high fasting blood sugar, doing maybe 3 to 4 tablespoons at night before you go to bed mixed with water is one way you can get the benefits of it.

So, yeah, I think it’s promising and it’s cheap.  Potato starch is pretty darn cheap.  There’s no risk to it really, and I’ve been hearing about some other interesting metabolic effects, like increases in body temperature with people who have thyroid or adrenal issues.  Richard over at Free The Animal has been writing a lot about resistant starch, so if you want to learn more about it, you can go check out his blog, FreeTheAnimal.com.  It’s not for kids, let’s just say!  There is language.  Yeah, but if you’re a consenting adult, you can head over there, and there’s some great information on resistant starch.

And be careful with resistant starch if you have SIBO or other gut issues, like IBS, because as a prebiotic, it can cause some pretty profound changes in the gut flora pretty quickly, and that can, in some cases, increase gas and bloating and lead to some digestive difficulty.  The best way to mitigate that is just to go slowly.  So, instead of starting with 3 tablespoons, start with a teaspoon and see how you tolerate that and go from there.

Treating skin conditions with FMT

Steve Wright:  Awesome.  Great advice.  Let’s roll on to another digestion-related question, Chris.  This one comes from Simon.  He wants to know about fecal microbiota transplantation, FMT.  “This has been gaining a lot of attention lately, and most of it is regarding treating ulcerative colitis or IBS” – and I’ll add in C. difficile.  He wants to know specifically is it possible for FMT to be used for treating skin disorders, such as psoriasis?

Chris Kresser:  Yeah, so we’ve talked about fecal transplants on the show before, and I’ve written about them on my blog.  It’s a very exciting new treatment, and I think it could potentially benefit many different conditions, including skin conditions because of the gut-skin axis, but also depression and other kinds of cognitive behavioral issues, possibly even autism.  The gut-brain axis we’ve talked about a lot.  The fact is there isn’t really much in the body that’s not affected by gut and gut health, and every month there is an increasing number of studies published that directly link gut health to things that aren’t apparently related to the gut, like Parkinson’s disease, Alzheimer’s, like I said, depression and autism, all different types of autoimmune diseases, skin diseases.  It’s really difficult to find conditions that aren’t in some way affected by the gut microbiota now, and I think our awareness of that is only going to increase.  So, potentially FMT could affect a very broad range of medical conditions.

The problem is it’s inaccessible to most people.  In fact, it looked like it was going to become more accessible and that people were starting to use it and study it for a lot of other conditions, and it is still being studied for other conditions in research setting, but the FDA just come out with some rules that suggest that it can only legally be used for antibiotic-resistant C. difficile, which is a gut infection that can be lethal, especially if it’s antibiotic resistant.  So, the only case in which a doctor is legally allowed to perform it is with someone who has antibiotic-resistant C. diff, and in that case, it can certainly be a life-saving treatment almost overnight.  This means that we’re starting to see an underground where people are performing these procedures at home because they read about it and they’re really interested and they want to do it themselves and try to get some of the benefits.  And I completely understand that, and in some way, I’m in support of the idea behind it and the treatment itself, but I do want to caution people that it is not a risk-free treatment, and it is potentially dangerous if it’s not done correctly, and it’s potentially dangerous if the donor isn’t screened adequately, which, I think, almost always is the case when people are doing it at home.

A lot of diseases can be transmitted via the stool, and there are certain bacteria, parasites, etc., that might be in your donor that aren’t causing problems for your donor because their overall microbiota is strong enough that they keep those things in check, but when it’s transferred into someone who is immunocompromised and has a different baseline microbiota, then those organisms could become problematic.  And I’ve also heard and read about some reports of changes in mood and personality after receiving gut microbiota transplant, and if you think about it and we’ve talked a lot about how the gut microbiota affect behavior and the brain, getting someone else’s gut microbiota in your gut could potentially affect your behavior and your brain and your cognition.

So, there’s a lot more to it, I think, than some people realize in terms of what can go wrong, and while I’m extremely enthusiastic about its potential and I’ve seen it really work miracles in people, I’m a little bit more cautious than maybe some of my colleagues and a lot of people in the general public because I’m just a little bit more circumspect about it because of what can possibly go wrong.  And I know myself as a clinician, back before these FDA regulations when I was looking into it when people would be curious about it and wanted to find a donor and were going to be working with another doctor, perhaps, to find a donor, I would help them to screen their donors, and I’m telling you that probably 8 out of 10 times the donor would fail some aspect of the screening process.  I was using labs for screening stool that are more sensitive and specific than the typical stool tests that you get at, like, Quest or LabCorp, and so I probably was picking up on more stuff than someone who went through a more general screening process.  And then I was also excluding people if they had autoimmune disease, which I think should absolutely be done because we know that a lot of people with autoimmune disease have gut issues and vice versa.  So, my criteria were strict, but they weren’t any more strict than the new – You know, I just read a paper about the new criteria for donors, and my criteria was right in line with that, and it was really hard to find qualified donors.

So, my fear is that people will do this at home, they won’t adequately test the donor, they’re just kind of desperate to get well, which I completely understand, but then they transfer stool from a donor who’s not suitable for whatever reason, and even though that person’s not sick, the recipient gets sick or more sick because their own microbiota is not compatible with something that came into them from the donor.  As I’ve said before, I’m excited about it, I think it has great potential, but I think it also deserves caution, and if you’re thinking about doing it at home, please get proper supervision and do it with someone who knows how to screen a donor properly, etc.  That person will be doing it illegally, so I’m not advocating this, but I’m saying if you’re the kind of person who’s just going to do it anyway, really, please do it with supervision.

Steve Wright:  Yeah, I think that’s beautifully put, Chris, and I think everyone should definitely remember that the ways in which your gut microbiota, everywhere from your mouth all the way to the anus, how it works within your body is still misunderstood.  I mean, we don’t know how many ways it affects you, and so these changes in behavior and even what can happen from just wiping out that gut bacteria from a colonoscopy prep and/or an antibiotic route changes that forever, so when you’re thinking about overhauling everything with some sort of treatment like this, as Chris said, follow his idea.

Chris Kresser:  Yeah, you alluded to this, Steve, but the Human Microbiome Project has told us that every person’s gut flora is unique, like a snowflake or a fingerprint.  And so, the consequences of transferring someone else’s microbiome into you are unknown.  I mean, certainly there’s a lot of evidence that suggests it can be extremely beneficial, so I’m not diminishing that evidence.  And if it’s a life-threatening situation where someone has C. diff and they’re at death’s door, then the risk is deemed to be less than the potential benefit, which is staying alive, right?  I mean, there’s no question in that situation.  In fact, the paper that I read was suggesting that in those cases you don’t even need to screen the donor because if you have a healthy donor that’s available, the benefit of keeping that person alive is far greater than the potential risk of something else being introduced in that circumstance, especially if it’s a close family member.  So, yes, very promising, and I completely understand.  I mean, the people who are considering this procedure are generally people who have tried a lot of other stuff and haven’t had success, and it’s so alluring to think that you could do this one procedure and then literally overnight have a pretty profound change in your health, and that sometimes does happen, so it’s extremely appealing from that perspective, but I just want people to consider some of the potential risks that haven’t been articulated or talked about much in the alternative medical community regarding this procedure.

Steve Wright:  Yeah, and I don’t want people to get me wrong.  I think it’s an amazing procedure.  I’ve talked with many people who have had it and seen the same kind of benefits that Chris just talked about, but as Chris said, I think not enough people actually talk about the full range and scale of effects that treatments can have, whether they be alternative or conventional, so it was a great discussion.

Chris Kresser:  Exactly.  All right, well, I hope you enjoyed the show.  I hope it was worth the wait, and we’ll have another one for you soon.  Thanks, everyone, for your continued support.  I’m really excited about the book.  It’s now been copyedited and I’m about to get the final pages proofed – I think they call them pages, where I make any small, last-minute changes.  And then in mid-October, that’s it.  It goes into the print production process, and we’ll start doing a lot of cool stuff.

Steve Wright:  That’s when you go to the Bahamas, right?

Chris Kresser:  Yeah!  Not exactly!  That’s when a lot of other work starts related to the book, but you’ll be hearing more about it in the months to come.  I’m really excited about it.  I actually was in New York last week doing a media lunch that my publisher put together with some people from the media, and I got a chance to see the book bound in pre-pre-production form in a softcover form, but it was pretty exciting to see it in its bound form for the first time.

Steve Wright:  Well, I’m pretty excited to see it.  I know you’re working hard, Chris, and we’re going to continue to try to get these podcasts out as you have time.  So, thanks, Chris, for taking time today.  Thanks, everyone, for listening to this podcast.  Just so you know, you can always submit your questions for these Q&A episodes at ChrisKresser.com using the podcast submission link.  And Chris and I would really appreciate it if you enjoy these episodes to go over to iTunes, leave us a review, and let us know what we’re doing well and what we could do better.

Chris Kresser:  Thank you, Steve, and see you all next time.

Here is The Roundup, Edition 18, bringing you the best from around the web from the past two weeks!

Blast from the Past

A recent article in the New York Times (by one of my favorite researchers, Moises Velasquez-Manoff) suggests that exposure to beneficial microbes through spending time on farms and drinking raw milk may actually be a way to “cure” allergies. Velasquez-Manoff writes that “innocuous cowshed microbes, plant material and raw milk protect farming children by favorably stimulating their immune systems throughout life, particularly early on.” This article is a fantastic read for anyone interested in the Old Friends Hypothesis, as Velasquez-Manoff skillfully describes how his visit to “a manure-spattered cowshed in Indiana’s Amish country” provided hands-on evidence for the theory that inadequate exposure to a variety of naturally occurring microbes may be the reason behind the significant increase in allergic disease in the past few decades.

The Old Friends Hypothesis is one of my favorite geek-out research topics. I recently had a Moises Velasquez-Manoff as a guest on my podcast, and I’ve also presented the topic recently at the Ancestral Health Symposium (check out my summary here.) I’ve also written an article about how dirt may be a “Paleo Superfood”, and how controlled exposure to everyday germs may play a significant role in the health of our immune system. I also believe that responsibly produced raw milk can be a wonderfully healthy food for the right people, and raw milk has been anecdotally reported by many to have been the cure for their own or their children’s allergies.

For those who do not want to take the [slight] risk that drinking raw milk entails, I recommend supplementing with a soil-based probiotic that can help introduce these beneficial bacteria to the gut in a controlled way. My personal preference for a product containing these bacteria is Prescript-Assist, which provides a great mix of soil-based organisms along with prebiotics to help populate the gut with beneficial microbes. And getting outside to play in the dirt doesn’t hurt either!

Research Report

• An article in the journal Science suggests that civilizations have fallen because they failed to prevent the degradation of the soils on which they were founded.
• An analysis in Canadian medical journal finds ‘healthy’ vegetable oils may actually increase risk of heart disease.
• New research indicates that a disruption of brain signals for reward and punishment contributes to increased pain sensitivity, known as hyperalgesia, in fibromyalgia patients. This explains why low-dose naltrexone works for these patients.
• A recent study suggests that non-celiac wheat sensitivity is a non-IgE-mediated food allergy.
• Yet another study shows that full-fat dairy (cheese in this case) inversely associated with obesity.

Worth A Look

• Some interesting discussion and a critique on the recent study about herbal supplements.
• A new Gallup poll suggests that the US obesity rate may have increased in 2013.
• An article in Nature by Tim Radford contemplates three fascinating studies on what it means to be human.
• An article in The New York Times suggests that transcranial direct-current stimulation improves cognition, mood and more. Could this be like jumper cables for your brain?
• You can help launch a Boulder Paleo Restaurant: Blooming Beets Kitchen.

For the Foodies

• NomNomPaleo: Saag Gosht (Lamb with Spinach Sauce)
• The Domestic Man: Brudet (Croatian Seafood Stew)
• Everyday Maven: Shredded Brussels Spouts with Crispy Shallots
• The Healthy Foodie: Creamy Plantain and Squash Ground Beef Mash
• The Clothes Make The Girl: Crispy, Oven-Baked Sweet Potato Fries
• Jan’s Sushi Bar: French Onion Oxtail Stew
• The Paleo Mom: Chocolate Frozen Yogurt
• Gutsy By Nature: Apple Cardamom Cupcakes

Join Kelsey Marksteiner, MS, RD and Laura Schoenfeld, MPH, RD, staff nutritionists at ChrisKresser.com, as they answer your questions about ancestral and Paleo nutrition. A must-listen for anyone new to the Paleo diet or looking to improve their current Paleo diet based on their personal needs and health goals.

The content on this show reflects the opinion of Kelsey and Laura and does not represent the opinions of Chris Kresser, who has not reviewed the content of this podcast.

Have a question for our nutritionists? Submit it here.

This week in our Ask the RD podcast, we’re answering not one but two separate questions! We sincerely appreciate everyone submitting their great questions and we encourage you to continue asking nutrition related questions by clicking the link above. Laura and Kelsey will be addressing the following topics in this podcast:

1. Should I take probiotics on an empty stomach or with a meal?
2. What do you think about the “eating for your blood type” diet?

Links discussed:

• The impact of meals on a probiotic during transit through a model of the human upper gastrointestinal tract.
• Blood type diets lack supporting evidence: a systematic review.
• Probiotic chart ($15 for purchase, but lots of free resources too!)
• ABO Genotype, ‘Blood-Type’ Diet and Cardiometabolic Risk Factors (Published in 2014)

About Laura: Laura is a Registered Dietitian with a Master’s degree in Public Health from UNC Chapel Hill. She has been a content manager for ChrisKresser.com since 2011. She is passionate about making traditional diets healthful and accessible for all her clients. You can learn more about Laura by checking out her blog or visiting her on Facebook.

About Kelsey: Kelsey is a Registered Dietitian with a Master’s degree in human nutrition and functional medicine. She works in private practice and recommends individualized dietary therapy focusing on biologically appropriate diet principles to aid her clients in losing weight, gaining energy, and pursuing continued health.  You can learn more about Kelsey on her staff bio page, or by visiting her website. Join her newsletter here!

 

TRANSCRIPT

Thanks to Noelle Kahne for volunteering to transcribe this week’s podcast.

LAURA: Hi everyone, welcome to this week’s episode of Ask the RD. I’m Laura; I’m a graduate student at UNC Chapel Hill studying public health and nutrition and I’ll have my RD at the end of 2013.

KELSEY: And I’m Kelsey, a registered dietitian specializing in whole food, ancestral diets, and I’m working on my master’s in nutrition and functional medicine.

LAURA: Thanks for joining us for this week’s Ask the RD podcast. We’re excited to be here and we hope that you’ll enjoy learning about nutrition-related topics. Remember to submit your nutrition-related questions through the online submission form, which we’ve linked to on Chris’s site. We’ll be answering your questions on the show, so feel free to submit as many as you want. As a reminder to everyone this is just general advice and should NOT be used in place of medical advice from a licensed professional. So let’s get started with our podcast. Kelsey, I think the first question that we have is for you.

KELSEY: All right.

LAURA: Should I take probiotics on an empty stomach, or with food?

KELSEY: Excellent question. So first, I just want to talk a little bit about probiotic supplements in general and then move on to the crux of the question because I think a little bit of background information is useful here.

First, it’s really important to think about probiotics in terms of what strains you’re introducing. And when I say strain I don’t just mean Lactobacillus acidophilus, I mean Lactobacillus acidophilus LA-5. That third letter number or name is really important. Just saying Lactobacillus acidophilus is just like saying ‘dog’, but what we’re looking for is the particular breed of dog, which would be equivalent to that strain of bacteria. And, the point being that we’re looking for something more specific. So once you know the actual strain of bacteria, you can look at research on it to see it’s survival in the gut, and it’s specific effects on body systems.

The reason I bring this up is because if you buy a supplement that doesn’t specify that strain of bacteria, you really have no idea what the supplement is going to do because different strains have completely different effects on the body and completely different survival through the gastro-intestinal tract. So I really only recommend supplement companies that are willing to disclose which strains their products contain, because that means that they did the research, saw that those are really good strains to be using, that they’ve survived through the GI tract, and they’re being used for a particular purpose, and put them in a product. So if a supplement company doesn’t disclose that information, to me that means that either they don’t know that strain is important, or they know it’s important and they don’t put the best strain in or most researched strain in order to keep the price down. So they’ll use just a general lactobacillus acidophilus strain that they don’t even know what it is because it’s cheaper than lactobacillus acidophilus LA-5 or some well-researched strain. Either way, you know, whether they don’t know it’s important or they know it’s important and choose not to put it in there, it’s not a company I want to buy from.

So I just want to preface this conversation with that information, because usually the strains they’ll put in a supplement are going to be the ones we know survive well in the GI-tract and actually get where they’re supposed to go, which is important when we’re talking about when to take these supplements. If it’s a good strain and it’s known to be acid-resistant and bile-resistant, then it shouldn’t matter too too much when you take it, but we’ll talk about what can kind of give you an edge when you’re talking about when to take a particular probiotic supplement.

So, another thing to just keep in mind too is some of these companies will use general strains where they don’t tell you the strain and they might try to convince you that their enteric coating will help them to survive through the GI-tract, but it’s usually just because they’ll do something like that which is an expensive process to not only drive up the price but also to go around the fact that they’re not using a well-researched strain that’s known to be able to survive stomach acid and bile very well. So I want you to keep that all in mind as we’re talking about this. And you definitely want to know that the probiotics you’re taking have been studied and been shown to survive the long journey through the GI-tract very well.

So, moving on to whether or not we should take probiotics with food or without – it’s important to think about our ancestors here, because if you think about them, our ancestors would have always had their probiotics with food, because that’s where the probiotics came from. They didn’t have these nice supplement companies to isolate probiotics and put them in a little pill for us to take every day, it’s just not how it works in nature. So I want to point that out first because there’s not a ton of research on this topic, so you’ve got to kind of think about the context behind this and another thing to consider with our ancestors is things like sauerkraut or kim chi they were usually used as condiments, so they were eaten with a meal, usually. It’s not like you would just eat kim chi on it’s own, it was part of a meal. So, think about that context as we start to talk about some of the research behind this as well.

So, what you’ll hear very often, in blogs and you know if you just Googled ‘should I take probiotics on an empty stomach or not’, people will tell you to take probiotics on an empty stomach, which is not something that I necessarily agree with. I think there might be some strains that survive just fine without a meal, but for the most part research has shown that probiotics are better absorbed, either about 30 minutes before a meal, or with meals. So ones that I looked at used a multi-strain product and used an in-vitro model of the digestive system and compared different timings of meals and different meal types to the survival of the probiotics through the GI-tract. And what they found, was that the survival of the probiotics, like I said, was best about 30 minutes before or with the meal. And there were less bacteria that survived if the probiotics were given 30 minutes after the meal. They also compared the probiotic survival to which meal the digestive simulator was given, and the options were apple juice, water, or oatmeal with 1% milk. And what they found was that the survival was significantly better with the oatmeal and the authors actually related that to the fat content, but I think that it’s also important to note that oatmeal has some fiber and resistant starch, which would have helped survival as well. So, I think that’s important to think about when we’re deciding when to take our probiotics.

Like I said, if you have a really well-researched strain that’s been known to survive really well with stomach acid and bile, which are the two main killers of probiotic bacteria, then usually it can survive even if you do take it on an empty stomach, you might get a little bit less than you would if you took it with a meal, but overall it should be OK. What you want to think about here is that also, when you’re eating with a meal, you’re usually getting some kind of prebiotic with your meal, so if you had something with you know a starch, like we said, that study showed the oatmeal was particularly helpful, and of course oatmeal is not part of our usual diet on a Paleo diet but if you had something like a sweet potato or a potato, that would give you some of those prebiotic components with your probiotics to enhance survival.

In a study on rats they tested a few different strains of probiotics and the effect of different prebiotics on their survival and found that the different prebiotics actually helped different strains survive better, so some particular strains of probiotics did better with FOS, which is fructo-oligo-saccharide, some did better with inulin, etc.

LAURA: Are some probiotic supplements, are they packaged with the prebiotics as well?

KELSEY: Right, yes that’s called a symbiotic when they have some prebiotic component in there. So I think that can be a good idea. I don’t know how much more significantly it gives you an edge because with prebiotics usually the biggest difference is shown in the gram levels of taking probiotics. So for example FOS – that has been shown to be the most significant, getting the most significant benefits at about 10grams. So that’s not what you’re going to get in a supplement that’s also packaged with probiotics. You’re not going to get anywhere near there.

But that’s not to say that it won’t help to get those probiotic that are in there to where they’re supposed to go and survive better. So I definitely don’t think it’s a bad idea, for sure. And I would probably suggest that, over something that’s just plain probiotics. But the issue with that is that sometimes a lot of the really good companies that are using really well-researched strains, I find that they don’t tend to package them together because some people are really sensitive to prebiotics, so if you’re FODMAP intolerant you won’t usually do well with FOS, though the amount they would normally put in a symbiotic you might be able to tolerate just fine. So I think they usually will sell them separately, in some cases just because of that. But if you’re someone who’s taking a prebiotic as well as your probiotics, it’s just a good idea to take them together, because it will help the probiotics to survive, certainly. And if you can tolerate prebiotics than definitely, you know, consider a symbiotic product as long as you know that the probiotic strains are well researched. Does that make sense?

LAURA: Yeah, I guess at that point it might just be easier to get the probiotic strain that you know is good and then just add your own prebiotic to the mix.

KELSEY: Right, right. Exactly. So if your probiotic mixture that you have already, as long as it’s telling you the strains, of course, if it has some prebiotic in there – go for it. I think that’s an excellent idea. It might not do a ton to help, but it’s certainly not going to hurt anything. And then the other thing to think about in terms of prebiotics and starch and everything is just to eat something, I would say it’s a good idea if you eat starch on a regular basis, to just take your probiotic when you’re eating something starchy. So if that tends to be breakfast for you, or after working out, I would say that’s a good time to take your probiotic supplement because it will help that survival.

All said, I don’t think it’s the end of the world, if for some reason you can’t take your probiotics near when you eat food. Like I said as long as it’s a type, a strain, of probiotics that’s been shown to be bile- and acid-resistant, you should still get most of that probiotic benefit all the way into the intestine. but, most of us have the ability to eat or take our probiotics when we’re going to eat. I think that if we can do that then it’s beneficial to do so and especially if it’s a starchy meal. again, you should take your probiotics sometime within that half hour before you eat because that’s been shown to have the best survival of probiotics to where we want them to get. and of course, if you’re taking a prebiotic, that’s an excellent time to take it as well because it will help all those nice probiotics to survive. So does that all make sense? I know it’s a little bit, kind of complicated.

LAURA: I think it’s pretty simple in my opinion, whether you take it on an empty stomach or not. I think you’ve explained to our listeners that whoever is telling them to take it on an empty stomach is probably not accurate.

I’m actually not even sure what the idea behind taking it on an empty stomach is, because it almost sounds like the food combination discussion we had, where it’s like ‘oh if you take it on an empty stomach there’s not going to be acid or bile’ and, well that stuff ‘s still going to be there, it just won’t you know, be buffered by any food.

KELSEY: Right and that’s actually exactly the point. You want it be buffered by food, so that the bacteria survive better. You know, if they’re just exposed to plain stomach acid that’s going to do a lot to kill them. So you want it to be buffered by food, which is part of why this makes sense.

LAURA: Yeah and like you said before, just looking at it from an ancestral perspective, people were not eating probiotic like anything on it’s own, they were eating food that had been fermented or you know even if you go back farther it’s probably that they were eating food that had dirt on it or something. But they weren’t just eating the dirt you know,

So there’s really no natural situation where somebody would be taking in a lot of probiotics without there being some kind of food.

KELSEY: Yeah

LAURA: I just think it’s a little strange that people would recommend it if there’s really no instance where that would be happening in nature.

KELSEY: Yeah, and I tried to find why people say that. And what I found on most sites was that they say to take it with a glass of water because it gets to the intestines more quickly, which maybe that’s true, but the fact that it’s then exposed to plain stomach acid, you know, that’s not helpful either. You want it to be buffered by the food. So a lot of the sites were just like… ‘it helps it to survive better’ which clearly is not the case, so I think the reasoning is a little bit vague, even to the people who are recommending to take them that way, which is definitely problematic. So you should know always, why you’re recommending someone take something a certain way and it sounds like for a lot of people they are either just you know taking the word of someone else and maybe don’t really understand the reasoning behind it, or they think that because it goes through quicker, it’s better, which is not the case because then it’s just, it’s not buffered by food, like we’ve talked about.

LAURA: Right, and  it could also be that people … you know how you’re supposed to take antibiotics on an empty stomach, well some people might say ‘well if you need antibiotics on an empty stomach then maybe probiotics need to be on an empty stomach too’ and they’re such different actions that they can’t be compared. So …

KELSEY: Right. Yeah, so I think what I wanted to mention with this is really just that you should be making sure you’re getting good probiotic strains to begin with, because if it’s not a good probiotic strain, you have no idea whether it’s going to survive well at all because there’s been very little research on it. And the types of strains that good supplement companies will put in their products, they’ve been shown to be able to survive well the stomach acid and the bile. So in that case, it shouldn’t make too much of a difference whether you take it with food or without food, but you probably even then still get a little bit of benefit from taking it with your food.

LAURA: Yeah and unfortunately the ones that are research-supported are typically more expensive. and I’ve had patients before that don’t want to spend the extra money on their probiotics so they’ll end up just getting one of those little Culturelle or whatever, and…

KELSEY: Culturelle actually is a researched strain, I will tell you that.

LAURA: Well, anyway. So, you know, as opposed to the VSL-3 or something like that …

KELSEY: Right.

LAURA: … that has shown benefits for specific conditions, or they just go out and buy Activia yogurt or something and think that that’s going to do the trick, but, I do think that it’s worth spending a little more money on the ones that are more researched and also… I think Culturelle’s what, one type of bacteria?

KELSEY: Yeah I think it’s Lactobacillus Rhamnosus GG if I remember correctly.

LAURA: I wouldn’t know, I’m not a probiotic expert the way you are, but I think that one of the things about probiotics that is helpful is to have a variety of strains. So you know, if you’re only taking the Culturelle, and that’s it, then you’re not going to be getting the different types of strains that have different purposes, so I think that if you’re going to go the route of taking a probiotic, then it’s worth spending maybe a little more money than just getting even like a Brand X at Walmart or something.

KELSEY: Mh, hmm. Yeah, I will say that, in general for healthy people who are just trying to keep up the good bacteria in their gut, yes a broad-spectrum product is probably a good idea that has a few different strains, but the reason some of the products have only one strain is because they’re used for particular things. So Florastor for example, that’s…

LAURA: Saccharomyces boulardii.

KELSEY: … that’s uh, yes and boulardi lyo is the strain. So Saccharomyces boulardii lyo is the full name. And that’s a particular strain that’s been shown to, you know, help get rid of other bad guys in the gut. So it’s used particularly for that. And also for c-diff and other infections like that.

LAURA: So S. boulardii’s actually, I’m sure you know, but for our listeners, it’s a yeast and not a bacteria, so, you know, in that case, that’s completely different than a single-strain bacteria.

KELSEY: Right, so even things like the Culturelle product with the Lactobacillus rhamnosus GG, or Align, which I’m forgetting the actual bacteria in there, but it’s again a one-strain product, they’re used for different, they’re used for different things. So, they’re better for particular conditions than other strains are. So, that’s the reason for sometimes having a single-strain product. They can certainly put it in with other strains, but for whatever reason they tend not to, so you kind of have to take it separately, unless you can find a product with that particular strain, that’s packaged with a few other strains. But, at least for the one in Culturelle, GG, I don’t know if they make a product that has more than just that strain. But I’ll have to look into that. But, that’s the reason why. Sometimes you just want one particular strain for particular purpose. And that’s when it’s useful to use one of those because you’re looking for that particular strain and a lot of other commercial products maybe won’t have it.

LAURA: So, for when you’re recommending probiotics to your patients… Do you normally do the one strain or do you normally do one that’s multi-strain?

KELSEY: It depends. For someone who maybe just has dysbiosis and we’re just trying to fix that I’ll usually do one with a few different strains. But if we’re doing something in particular like trying to deal with a particular condition, I have a whole chart of what strains are useful for what conditions …

LAURA: Oh wow.

KELSEY: … so then, yeah, I’ll use that determine a particular probiotic if I think it will be useful in that particular case.

LAURA: Interesting. I might need you to send me that.

KELSEY: Yeah, it’s a good little chart. I got it from school, actually.

LAURA: Unfortunately this is one of those things we don’t talk about in normal dietetic programs, which is a shame because it’s obviously something that could be very helpful for people. I was always under the impression that the more variety, the better, just because you’re getting, you know, the different strains that would normally be found in a probiotic food, but I’ll need to …

KELSEY: Right, and in general for healthy people that does make more sense. but when you’re trying to deal with a specific condition, just to get extra benefit you want to use particular strains that have been researched to be useful against those conditions.

LAURA: Interesting. Well now I’m glad we talked about it because I actually wasn’t aware of that.

KELSEY: Yeah, it’s an interesting topic.

LAURA: I knew Florastor was effective against c-diff. and you know, I actually have recommended that multiple times in the hospital I worked at, but you know we don’t usually get to even recommend specific types of probiotics, so you know it’s very limited in the hospital environment or even in a typical medical environment that you can actually get that level of detail about what strains you’re using.

KELSEY: And I think that’s part of the issue is because most people just don’t realize that probiotics and their effects are absolutely strain-specific. And that’s just such an important thing to remember when you’re deciding what strains to take because one strain might be totally useless for you, while another one could be really, really beneficial.

LAURA: I was always under the impression that it was just more about amount of CFUs, so colony forming units, and then a greater variety, so…

KELSEY: Right. And the colony forming units, those are important too. There’s a certain number you need to take in order for it to be beneficial. So if you’re taking a low amount, then, yeah, it’s not, even if it’s been shown to be useful for a certain condition, if you’re not taking the required dose, then it’s not going to be useful for you, either. So that is important to consider. And when you’re healthy, that’s why, you know things like yogurt or other fermented foods, there’s tons of different bacteria in there, and that’s useful for healthy people just to continue getting probiotics on a regular basis because as you know, they don’t really colonize for a long time in the gut, they’re very transient, but still very useful. So, in that case for healthy people, yeah, a big amount of bacteria is a good idea, different types of strains.

LAURA: Cool. Well, maybe we’ll have to do a whole show on the different strains of probiotics you recommend for different conditions. I feel like that would be really helpful for some people, including me, who I feel a little silly that I didn’t know that there was information about specific bacterial types for specific conditions.

KELSEY: I think people don’t talk about it enough, honestly. That’s why a lot of people don’t know that, because we just think that ‘OK as long as I’m getting a bunch of bacteria, a bunch of different strains then I should be OK’. Which is correct for most healthy people, but when you’re dealing with sick people with particular conditions that you want to be working with, then yeah that’s when the strains become important.

LAURA: All right, well, I don’t want to run this too long, we’ll definitely have to do a show on bacterial strains as I’m sure there’ll be a lot of interest after this show. But I guess we should move on to the next question so that we have enough time to get through both of them.

KELSEY: Yes, all right. And this is for you, LAURA.

LAURA: Okay.

KELSEY: What do you think about the eating for your blood type diet?

LAURA: Okay, so before I share my opinion on the blood type diet, I’m going to describe what the diet is, since I’m sure some of our listeners may not actually be familiar with the diet. The blood type diet is based on the premise that we all have different ABO blood types that effect what our bodies recognize as self vs other through the presentation of antigens to the to the immune system. So we generally all know our own blood type or at least we should know our own blood type, and our blood type mainly determines the type of blood we can accept from transfusions, based on the antigens present on our blood cells. So there are two types of antigens; A and B. Our bodies produce antibodies against any of the antigens that are not present on our blood cells. So if you have type A blood that means you have type A antigens and anti-B antibodies. If you have type O blood that means you have no antigens and you have both anti-A and anti-B antibodies. But if you have type AB like I do, you have both types of antigens and no antibodies in your blood. So the reason why this is important during blood transfusions is because you can only accept blood types that do not have the antigen for which you have an antibody. So A types can only take type A and type O; AB types can take any of the blood, so A, B, AB, and O; and type O can actually only take O blood.

And the positive and negative refer to the RH protein which effects whether you can take the blood as well. So if you get the wrong type of blood, your immune system attacks the new blood cells and lyses them, which causes rapid destruction of the donor red blood cells and can either lead to acute renal failure or even death in some conditions.

So this is why type AB+ blood is known as the universal acceptor and type O- is the universal donor since AB+ can take any type of blood and O- can be used as blood for anyone.

So you inherit your blood type from your parents. Each parent has two copies of the gene and give one each to you. So in my case, I believe my mom is type A and my dad is type B, so they each gave me one of their A and B genes, and that’s how I ended up being an AB.

So the theory behind this diet is that each blood type can be traced back to a certain type of ancestral background. The guy who came up with this diet is named Dr. Peter d’Adamo. I’m actually not sure how to pronounce his last name, but we’ll go with D’Adamo. And he groups each blood type into a common ancestry with a specific diet recommendation. So the book that he has written is called Eat Right 4 Your Type and the four is a number four, and the claim here is that each ABO blood type processes food differently, and following a diet specific to you’re A, B, or O blood type may improve your health, general well-being, energy levels, and reduce your risk of developing chronic diseases like cancer and cardiovascular disease.

So the book is based on a theory that each blood type contains the genetic message of the diets and behaviors of our ancestors and that these traits still have an impact on us today. And blood type O is described by D’Adamo as a Hunter. He recommends that those of this blood type eat a higher protein diet. Blood type A is called the Agrarian or Cultivator, and is recommended to eat a diet which emphasizes vegetables and is actually free of red meat, which is a diet that’s more closely vegetarian. Blood type B is called the Nomad and Dr. D’Adamo said that this type is associated with a strong immune system and a flexible digestive system and that people of blood type B are the only people that can thrive on dairy products. And he calls blood type AB The Enigma, which is, you know, apparently I’m an enigma so that’s interesting, but this group’s diet is actually a mix between type A and type B.

So now that I’ve described the basics of this diet theory, we can actually talk about the evidence for the diet or the lack thereof. There’s some evidence to suggest that different blood types have different susceptibility to certain diseases like heart attacks, pancreatic cancer, and stroke. But as far as the diet goes, there’s really no concrete evidence that the diet works the way D’Adamo says it does. And there was actually a really good study that came out in May that searched for blood type diet studies that fit a list of criteria for legitimacy, such as only using in-vivo human studies, which means you know actually experimenting with human subjects. And they actually didn’t find one single study that met their criteria and showed an association between ABO blood type diets and health-related outcomes. There’s really only one study that even met all the criteria and it didn’t show any health benefits. Yeah, so I’ll link to this study in the show notes so that people can read it for themselves, but unfortunately it shows that there is really no evidence to support this diet theory.

Now I know lack of evidence isn’t evidence against, but I really think this concept is silly if you think about it. Blood types are distributed amongst the different countries of the world and are not really associated with one type of eating pattern. So to suggest that a person would benefit in any way from eating in a way that has been somewhat arbitrarily assigned to their blood type, it doesn’t really make any sense to me from a scientific standpoint.

KELSEY: Yeah plus if you think about families in general, wouldn’t you all have to be eating different types of diets.

LAURA: Well yeah that’s a really good point because as I mentioned before my mom is a type A and my dad is a type B and I’m type AB. So in Dr. D’Adamo’s perspective we all three should be eating different diets.

KELSEY: Like completely different diets.

LAURA: Yeah. Well at least my parents should be eating completely different diets, and mine, being the enigma and all, I could eat a combination of what my parents eat.

KELSEY: Interesting.

LAURA: As far as like ethnicity goes, my parents’ ethnicity is similar. My whole family’s from like the German or Germany, Austria, Hungry, and Ireland areas of Europe so it’s not like one of my parents is Chinese and one of them is like, you know, English.

KELSEY: Right.

LAURA: You know, they’re very similar in ethnicity and they have different blood types, so I just feel it doesn’t really make sense that we would be eating differently in any normal situation in life.

KELSEY: Right.

LAURA: And this book came out, in I think 1996, so I feel like at this point if it was a valid diet that there should be some amount of research conducted to back it up. Really at the end of the day I feel like personal experience is going to tell you way more about a diet’s appropriateness for you than something like a blood type assignment. And for me, it’s really hard for me to know if any of these blood type diets would be helpful because being an AB, it really doesn’t even give me any explanation as to what I should be eating.

KELSEY: Right, you can kind of eat whatever you want.

LAURA: Right, except for I guess with AB, lacto-vegetarian would be ideal, but I don’t necessarily think that’s right.

KELSEY: I’m B, so which type would that be.

LAURA: The Nomad. So you have a flexible digestive system and you would thrive on dairy products.

KELSEY: Hm, well OK that’s interesting because I don’t do well on dairy products. I can eat some but like fluid milk, or even yogurt gives me issues. So, interesting.

LAURA: So there you go, just based on your experience, it’s not necessarily an accurate description.

It’s ironic because I think type O tends to be a more rare blood type and this one is the one that more closely resembles a Paleo diet. (CORRECTION: Type O is actually the most common blood type world wide, with type A being a close second.) So I don’t know, I just feel like the fact that most people that go Paleo tend to do better than they were doing on say, vegetarian diet; I doubt that these are all people that are type O blood types. Maybe I’m wrong, I don’t know; we could take a poll.

KELSEY: Yeah, we need to do a poll apparently.

LAURA: Yeah, and see like what people’s blood types are.

(This section of the transcript has been deleted due to speaker error. Sorry about that folks! )

KELSEY: hm.

LAURA: So anyway I’m open to hearing if anyone has evidence to support this diet. I didn’t find any and this one study that was conducted just in the last six months didn’t find any. So yeah I think that most of the evidence is coming from D’Adamo having clinical evidence or anecdotal evidence that his patients do well. But honestly a lot of this could just be that they’re paying attention to their diet when they might not have been doing so before.

KELSEY: Right. If you’re come from a Standard American Diet and going to vegetarian or lacto-vegetarian, you’re probably going to be doing a lot better than you were before.

LAURA: Yeah, and that’s usually the reason why vegetarianism is associated with things like lower BMI and just healthier outcomes is because people who are vegetarian, compared to the average omnivore, they’re focusing on eating a certain way.

So there’s evidence that just paying attention to your diet for any reason is enough to make you healthier than someone who doesn’t care what they’re eating.

KELSEY: Exactly, that’s a really good point.

LAURA: So, I feel like this blood type thing, I would think, and this is just my theory, but I would think that a big part of it is just that people go from eating whatever they want to eating a way that they think is healthier for them.

KELSEY: There’s something to be said for the placebo effect. If you’re eating a diet that you think is better for you, you’re probably going to feel better than if you’re eating a way that you think is bad.

LAURA: Right.

KELSEY: And usually when people are changing their diet they’re changing other lifestyle factors as well to make themselves healthier. Maybe they’re getting more sleep, they’re exercising more, so there’s a lot of other healthy behaviors that go along with changing your diet to ‘be healthier’ in whatever way you’re choosing.

LAURA: Right, so Kelsey and I would always agree with Chris, in that people need to figure out what diet works for them. And there’s really no better way to do it than self-experimentation. Fortunately Chris’s book which is coming out in December is going to focus very closely on this strategy. So figuring out how to eat in a way which makes you feel the best. Really you need to be doing personal experimentation and not just arbitrarily saying ‘Oh I’m a type B, so that means I should eat a lot of dairy products’. Like you said, you don’t do so well on tons of dairy, so if you were just following this blood type diet you might actually do worse.

KELSEY: Right. I would imagine I would do a lot worse.

LAURA: So that’s my opinion on the blood type diet, I think Kelsey you would agree with me?

KELSEY: Yeah, first of all like you said there’s not a lot of research to back it up. And like you said, doesn’t mean it doesn’t work, but I think there are some other factors that we discussed like just paying attention to what you’re eating and other lifestyle factors – coming from a Standard American Diet you’re certainly going to feel better. So that’s probably where that anecdotal clinical experience is coming from for this doctor that wrote the book.

LAURA: And if you just look at the recommendations… So if you’re type O and they say ‘Oh eat more protein’ well you’re probably going to do better anyway because we know that most people do better on a somewhat higher protein diet, just because, you know, of the way that most people are eating normally. They’re not necessarily eating a good amount of protein, and protein enhances satiety and helps build lean muscle, and all that. So people that switch to the O diet are probably going to do better than they were doing before. And then even looking at blood type A, which is the sort of vegetarian and red meat-avoidance diet, that one is recommending more vegetables. So eating more vegetables is probably going to be an improvement in diet compared to the way a lot of normal people eat. And then, the dairy thing. You know, some people do actually thrive on dairy products so …

KELSEY: Yeah Chris is an example, he always talks about that.

LAURA: Right, so I think some of these diets might just be general improvements over what people are normally eating. You know eating more protein or eating more vegetables or eating good quality dairy products. Like I don’t think anyone would argue that this is not a good way to improve your diet. The fact that it’s blood group based I think is a little hokey.

KELSEY: Right, and maybe just a little arbitrary. It doesn’t really matter as long as you’re paying attention and eating more vegetables or more dairy if that’s great for you, or more protein. You’re probably going to be eating a lot better than you were before.

LAURA: Like I said, if anyone knows of research to support this diet, then please feel free to share it in the comments.

KELSEY: Yeah we’re all ears.

LAURA: But as far as what I could find, and apparently what these researchers could find on any actual evidence to support this diet, there really isn’t any. So, yeah that’s pretty much what I would like to say about the blood type diet. Who knows, maybe in five years we’ll have some really great study that’s actually tested it and shows that it’s got a benefit to it. But as of right now I can’t find any reason to follow it in a way that’s, you know, too strict or anything like that.

KELSEY: Again, personal experience is going to trump any of that, these just blanket diets even if it is somewhat based on different factors like blood type or any other kind of diet that’s for a particular kind of person. Personal experience is always going to be best because it’s based on you.

LAURA: And this even goes for just like strict Paleo. I don’t think a lot of people necessarily feel great doing what they would consider to be “strict” Paleo.

KELSEY: For a long period of time.

LAURA: Right. I don’t know, I really feel like personal experimentation at this point is the only way to know for sure whether a diet is good for you.

KELSEY: Absolutely.

LAURA: Maybe in like twenty years we’ll have some kind of blood test that you can get done that will tell you exactly what you should eat. But, as of right now, we don’t.

KELSEY: Right, got to just experiment.

LAURA: And I know it’s not usually what people want to hear, but unfortunately that’s the way things are. If somebody wants to invent that blood test, they’ll probably be a millionaire, but as of right now we don’t have it. Anyway, that’s all I wanted to talk about with the blood type diet. Did you want to add anything?

KELSEY: No. I think you brought up all the important points there, and at the end of the day, it’s about experimentation.

LAURA: Right. Okay, well that’s all the questions we have for this week everyone. So thanks again for joining us on this episode of Ask the RD. We hope you enjoyed the show and we’d love any feedback you have on how we can make our podcasts even better. And as a reminder you can submit your nutrition- related questions through the link that we’ve provided on Chris’s website. And who knows, we might answer your question on the next show. So have a great week everyone and we’ll see you next time.

KELSEY: All right, take care Laura.

LAURA: You too, Kelsey.

In this show we have Glenn Taylor of the Taymount Clinic, one of the few places doing fecal microbiota transplants, otherwise known as FMTs. He’s doing some great work, and I know a lot of people are interested in this. It’s a revolutionary treatment, and so I’m looking forward to getting the lowdown.

In this episode, we cover:

3:10 The history of Fecal Transplants
10:50 How the Taymount Clinic approaches FMT
16:40 How to screen for the right donor
24:15 What conditions can FMT treat?
30:50 The future of FMT technology
32:45 The side effects of Fecal Transplants
39:50 Why FMT is approved in the UK

Full Text Transcript:

Steve Wright:  Hi, everyone.  Welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com, and I’m your host, Steve Wright from SCDlifestyle.com.  With me is integrative medical practitioner, New York Times bestseller, and healthy skeptic Chris Kresser.  Chris, are you ready for today’s show?

Chris Kresser:  I’m ready, Steve.  I’m really looking forward to it.

Steve Wright:  It’s my favorite topic, man.

Chris Kresser:  I know it.  Who doesn’t like to talk about poop?

Steve Wright:  It just puts a smile on your face.  You can’t say it without smiling.

Chris Kresser:  Yeah, we have Glenn Taylor of the Taymount Clinic in the UK, one of the few places doing fecal microbiota transplants, otherwise known as FMTs, and we’re really excited to have him come on the show.  He’s doing some great work, and I know a lot of people are interested in this.  It’s a pretty revolutionary treatment, and so I’m looking forward to getting the lowdown.

Steve Wright:  All right, so before we bring him on, I just want to let the listeners know that as of today over 76,511 people have already signed up for Chris’ free membership.  Yes, I just looked that number up.  It is true.  Chris has just recently redone his site at ChrisKresser.com, and what he’s done is he has reorganized his content and created a lot of in-depth eBooks on weight loss, gut health, and thyroid health that you get access to when you sign up for his free membership, not to mention you’ll get some in-depth audio seminars that have never been released to the public before as well as a free 30-part email series on Chris’ most essential topics for anyone serious about feeling great.  If this isn’t something that you have access to yet, you’re going to want to take advantage of it.  Go over to ChrisKresser.com and sign up for the free membership.

OK, Chris, our guest today is Glenn Taylor from the Taymount Clinic, and as you were saying before, he specializes in fecal microbiota transplants.  Glenn is not conventionally medically trained.  He’s a qualified engineer and a microbiologist, so we kind of have something going on there.  For some years, he was running a training center for health professionals, but he was unhappy with the colon lavage not appearing to bring about any long-term improvements.  He took a phone call one day, and a young man was asking about fecal transplants.  That got him thinking.  After two years’ worth of research and experimentation, that gave rise to the new FMT clinic.  He has been doing FMT treatments now for nearly two years, and he has carried out over 800 of them to date.  Over the last few months, he has been invited to give talks at several top London hospitals and primary care trust hospitals.  In other words, this guy knows poop.  I’m excited.

Chris Kresser:  Let’s bring him on.

Glenn, welcome to the show.  Pleasure to have you on.  Pleasure to speak with you again.

Glenn Taylor:  Well, thank you very much for inviting me on.  It’s good to talk to you again.  It’s good to get to talk to everybody out there.

The history of Fecal Transplants

Chris Kresser:  Great.  Let’s take a step back a little bit for those who aren’t that familiar with fecal microbiota transplants, and maybe you could just tell everyone what they are and a little bit of the history, how they were discovered and initially used therapeutically.

Glenn Taylor:  OK, well, it’s a process of basically bringing the human gut back to as close as normal as we can hope to get it in the attempt to bring all the other processes that it impinges upon back to normal as well.  The first cases of manipulation of gut flora were, I guess, back in about 1908.  A Russian physician, Ilya Mechnikov, working in Paris had noticed the changes in human health and behavior when people were exposed to different types of bacteria in terms of probiotics.  He wrote a few papers on it that disappeared from view but ended up in just a couple of hospitals.

Then in 1958 in a fit of desperation, one of your countrymen, Ben Eiseman, a doctor working out of Denver, was faced with four patients with a really advanced case of toxic megacolon, which is an infection of Clostridium difficile, and the four patients were completely refractory to all kinds of treatments and their prospects were very grim.  Eiseman went to the hospital library and looked up some papers that might help him and came across the original Mechnikov papers, and he thought, well, we have some evidence here that borrowed microflora from another human being may be the answer to the problem.  Back in ’58, this was very radical.  I mean, the idea of swapping poop really wasn’t taken quite as easily as it is now, but he went to the four families and told them what he had found.  Obviously faced with the prospect of losing their loved ones, they just said, please, go ahead.

The astonishing thing was that all four patients made a very rapid recovery.  He wrote his own paper, and this was all before the Internet, so it meant people had to keep this stuff in a library.  And I guess most people now are aware that those papers ended up in Sydney, Australia, where a young professor of gastroenterology, Tom Borody, read them when he was faced with a similar situation, and I think from then on people have become more and more aware of its potential.

The astonishing thing is that farmers have been passing this down by word of mouth from generation to generation, that the beasts on their farm can benefit from getting the bacteria from healthy beasts and cattle and birds transferring them to sick creatures, and they’ve been doing this for literally hundreds of years.  I have a couple of veterinarian friends who swap stories like this and then throw their hands up in horror and say, well, surely you’re not now talking about doing this in humans!  And I’m always tempted to say, what [indiscernible]!

Chris Kresser:  Right!  Well, it’s amazing how much more open minded we become if our life is threatened, and certainly as you pointed out with C. diff, it’s a potentially life-threatening infection.  There are antibiotic-resistant forms that don’t respond well even to some of the most potent broad-spectrum antibiotics, and people in the year 2014 are still dying from it.  In a way, it’s sort of a blessing in disguise that we’ve had this testing ground for this remarkable new treatment because I don’t think it would have achieved such rapid acceptance in the scientific community if it hadn’t demonstrated such an incredible ability to be effective in a situation where nothing else is.  I think that really opened the door for people to be amenable to it in a way that they wouldn’t have been otherwise.

Glenn Taylor:  Yeah, I partially agree with you, but don’t you find it actually extraordinary that despite the amount of coverage, I mean, scientific papers, academic papers being available now that discuss this in fine detail, so many papers saying that this is an effective treatment for, in particular, Clostridium difficile, and articles being written in all the world’s top gastroenterological journals and mouthpieces, and yet when you talk to the average gastroenterologist, they’re still wide mouthed and amazed about it?  It makes you wonder, don’t they read their own professional journals?

Chris Kresser:  Well, Glenn, I wish that did surprise me.  Unfortunately it doesn’t surprise me in the least because I come across that every day in my practice, where I refer a patient to a specialist, like a gastroenterologist.  Or another case where this often happens for me is I discover that someone has iron overload and I refer them to a hematologist only for them to be told that there’s nothing to be concerned about, and I just want to pull my hair out because I’ve read numerous papers published in the scientific literature about the risks of even somewhat mildly elevated iron levels, but seemingly these hematologists who are the top specialists in the field are not staying current with the literature in their very field.  Unfortunately I was prepared for that to some extent, but there’s this frustrating gap between what’s in the scientific literature and then what even specialists in that field, much less primary care physicians and the general public, have accepted, but it seems to me – and maybe you disagree – but it seems to me that the acceptance of this procedure sort of skipped over the gastroenterologists and the medical community and we’ve seen a lot of articles about it in the public media that are more friendly to it than you find just talking to the average gastroenterologist.

Glenn Taylor:  Oh, yeah.  I had a phone call from New Scientist.  They really just wanted to know the background and to talk about it and see if they could have access to one of my patients.  Scientists are now beginning to really want to know more about the biological value, and that’s why I say it is good old fashioned biology, which if you’ve been brought up on an entire menu of pharmacology and chemistry, it’s perhaps a step too far.  It depends on how you’re trained, I guess, Chris.  If your professor at college fed you pure pharmacology, then you’re going to carry that [indiscernible].

Chris Kresser:  Yeah.

Glenn Taylor:  I think we have to look further back to why people have these ideas that only one type of medicine is effective and when you run out of pharmacological solutions, you should then actually deem something to be incurable.  I think it’s a little unfair.  The term ‘incurable’ means you haven’t found a cure.

Chris Kresser:  Exactly!

Glenn Taylor:  It’s doesn’t mean to say that it doesn’t exist.

How the Taymount Clinic approaches FMT

Chris Kresser:  Yes.  I think also that the increase in interest – and this, of course, is not coincidental – but there is a lot of attention being paid now to the microbiome.  We’ve had front page stories on The New York Times Magazine, Michael Pollan, and I know that there are some books in the pipeline that are coming out about the microbiome and its connection between health and disease.  That’s, of course, the theoretical underpinnings of why a fecal microbiota transplant would work in the first place and why it’s something we might want to investigate, and then we have these research projects, like, we had Jeff Leach on to talk about the American Gut Project and all of these ongoing research projects looking at the microbiome.  So, I’m cautiously optimistic.  I think there are definitely some hurdles, especially regulatory hurdles in the US, and I’ll be curious to hear what’s happening in the UK with that, but before we get into that, why don’t you tell us a little bit about how you and your team over at Taymount approach FMT, because I think what you’re doing, from our previous conversations, is somewhat unique in the world, really.

Glenn Taylor:  OK, so maybe I’m a little bit too much of a scientist, in that I really wanted to know how to make the very best of the procedure.  And that led me to many, many long hours in the lab, a lot of research along with some of the leading people in the world, particularly some of the best food microbiologists in the world – and I take my hat off to the amazing team at Reading University in the UK who are trying very, very hard to understand all gut functions in relation to the microbiome – but what I needed to do was to understand why the process did and didn’t work in certain cases and why was it that home treatments – and I can understand why people do it; it’s out of complete desperation because it’s not available to them or the cost is prohibitive – why home treatments had relatively poor outcomes.  I guess the answer lies in a very simple feature.  It’s a simple biological fact that 90% of the gut microbiome is of a group called obligate anaerobes.  Now, that quite simply means that they cannot survive in oxygen.  If you expose them to an oxygen-rich environment, they die.

So, all these poor people who don’t really quite understand that particular aspect are taking stool from a friend or a loved one, putting it into an ordinary kitchen blender, blending it up in the presence of oxygen and perhaps not quite the right liquid medium, and almost instantly they’re killing 90% of the bacteria that would have been available.  When you don’t know precisely which one you’re missing, I cannot understand why you’d take the risk of killing 90% and hoping that the one you need is in the remainder.  Then subsequent mishandling of the rest of the process means that people are getting exposed to a very, very small amount of what they need.

What we did at the clinic was we addressed that fact, and we work in an almost completely anaerobic environment.  The collection process is anaerobic, without oxygen.  The homogenization, breaking up, the separation, filtration – everything is done in an anaerobic environment, which means that when we collect bacteria, at the end of the two-hour process, we have a pellet of bacteria that’s pretty much intact.  Now, that’s what everybody’s after.  When you’re trying to take a microbiome out of one human being to put it another, what you’re hoping for is to get as close to 100% of that bacteria as you possibly can because at this moment we don’t know exactly which of the, oh, it could be a thousand, it could be 1150 species at this moment.  There are new methods of assay, new methods of measuring which are kind of suggesting at this moment that there may be many more thousands of species in the gut than we actually realize, and because of the way the morphology goes on, it could be literally a never-ending number of species because they’re constantly mutating.  And there’s no catalog for this.  We just don’t know where we’re going to end up, so we try and gather safely together as many as we possibly can and store them in the correct way.  That’s the process.

Also we want them to go back in and be effective, so we’ve spent some time working on the implant method, and we’re feeling quite comfortable that we’ve found the most benign and most comfortable, in itself with the patient, the most comfortable method, the most effective method of complete dissemination around the whole of the colon, and we had to work hard on this to come up with a gentle, effective method of delivery.  I also have a method I’m working on in the background, and I’ll probably bring it to a much wider audience and make it much more acceptable to the public at large, but I have some pegs to put in place before I can talk about it.

How to screen for the right donor

Chris Kresser:  All right, that’s exciting.  We’ll have you back on the show when you’re ready to release the goods, so to speak!

Glenn, another potential concern that I have in terms of DIY, at-home FMTs is improper screening of donors.  I know when people really get desperate because I’ve been there myself in my past and with my pretty severe chronic illness that judgment can be impaired, let’s just say.  And when there’s a treatment that promises some potentially miraculous benefits, it can be relatively easy to minimize the risk, at least in our own mind.  Why don’t you talk a little bit about how you’re screening donors and making sure that the donations are of the highest quality, which, of course, will lead to the best results?

Glenn Taylor:  Well, first of all, I have huge sympathy for all those people who because of the lack of interest of their own physician or the lack of a facility wherever they live they’re being driven to do this themselves.  And on top of that, they simply don’t have the finances in many instances to be able to take all the precautions they should, but we really have to urge people that if they’re already immunocompromised with a condition, they could make things very, very much worse for themselves.  The donor they choose may not display the symptoms of a severe disease, but they could simply be a carrier, and you never know what you’re going to get, so you owe it to yourself and your loved ones around you to be absolutely sure that your donor is safe.  You have to do your best to make sure there are no communicable diseases.  I know it means having to go through some medical professional to see if you can get the testing done, but when the alternative is so horrendous, you really should just take that extra bit of effort to make sure that your donor is good.

Also this idea that the donor should be somebody from the family and who shares the same environment in biological terms is actually erroneous because people living together over a period of time gradually share their bacteria.  This is a simple biological fact.  They share their bacteria, and their microbiomes become very similar.  There will be some minor changes in them, but despite the fact that everybody has this unique microbiome, almost a fingerprint style, it’s quite unique to them, in general terms, we all have little wavy lines on our fingers, same thing as we all have x number of bacteria.  People living in the same environment generally have the same type of bacteria.  Now, if your condition has been brought about because you’re missing certain bacteria, what on earth makes you think that your partner, spouse, friend, or cousin is going to have that bacteria if they share the same environment, share the same food, etc.?  It doesn’t actually make good biological sense.  What you actually really need is somebody outside your environment who has a completely different profile of gut flora.  That’s the person you’re after.  And then if you get them tested and they’re good, that’s the person you should go for.

But equally, I’ve heard talk saying, I want the microbiome from somebody’s who has never had antibiotics, so let’s go for an infant, a child.  Please, don’t forget for a second that a child only gets the microbiome that it got from its mother during the birth.  If the mother didn’t have a good microbiome, the child’s not going to have a very good one.  And then it takes up to two years for a child to develop an adult-like microbiome.  Despite the fact the child may not have been exposed to antibiotics, they’ll have an immature microbiome as well, and that might not suit your purpose.

Chris Kresser:  Mm-hmm.  So, give us an idea a little more specifically of what kind of tests that you’re doing to screen donors just so people have a sense of what the spectrum of these tests are that need to be done.

Glenn Taylor:  Obviously, all the sexually transmitted diseases and HIV.  I think most of it’s sitting on our website where you can see precisely what we’re doing, but in essence, we really are trying to protect people from the serious life-taking diseases and the other diseases that would affect you if you’re immunocompromised, even down to sort of rheumatoid factor, arthritic – there’s a whole group of things that you really don’t want to pick up just because you want a good microbiome.

Chris Kresser:  Right.

Glenn Taylor:  You just have to use common sense, and actually what I noticed this afternoon when I was just cruising through some websites is that there’s a lot of information out there that people can go and look for when looking for the testing.  Tom Borody did a paper that has a home protocol that’s pretty comprehensive.  Alex Khoruts has, as well, so there’s stuff out there from people who have been doing this for a very long time that’s very valuable information to make sure that you can protect yourself.

Chris Kresser:  Yeah, and it’s worth saying that as our understanding of the microbiome expands, the kinds of testing that we’re doing to screen donors expands as well.  I was in contact with the Center for Digestive Diseases and Dr. Borody’s clinic probably 10 years ago, and I’m pretty sure – and they may still not be doing this, I’m not sure – but they weren’t at that time doing tests for autoimmunity because it wasn’t as clearly understood as it is today that autoimmunity is linked to the microbiome, so it’s really great to know that you’re thinking more broadly in terms of what an optimal donor might be and which markers that we can currently test for might exclude them from being donors based on that connection between the gut microbiome and not just digestive conditions, of course, but now many other conditions including immune dysregulation and mental and behavioral problems, the whole gamut.  It’s really actually difficult to find a modern chronic inflammatory disease that the gut microbiome is not linked to at this point.

Glenn Taylor:  Isn’t it astonishing?  I get inquiries all the time with obscure diseases, saying, what do you think?  And my only response can be, well, we haven’t found anybody or we haven’t treated anybody with that particular condition, but hey, I’ve learned enough by now not to discount it, and do you want to be the first?

Chris Kresser:  Yeah, worth a try.

Glenn Taylor:  Shall we give it a try?  I’m not discounting anything, really.  The likelihood is that we could be going on for years and years, bumping in more and more conditions that respond favorably once we’ve normalized the gut microbiome.

What conditions can FMT treat?

Chris Kresser:  Mm-hmm.  I don’t doubt it at all.  Along those lines, though, tell us some of the conditions that you’ve seen respond particularly well.  Now you’ve done about 800 of these, it sounds like, so you’ve had a broad spectrum of patients or people that have come and have had experiences.  Tell us a little bit about what you’ve learned.

Glenn Taylor:  Everybody knows that the whole thing started off with Clostridium difficile, so we’ve done our fair share of C. diff.  We’re actually really, really lucky at this moment in that in every case of C. diff we’ve managed to get full remission.  It’s completely clear.  We’re doing testing before and after, and everybody so far is absolutely clear.  I have a young lady who started this week, who I can’t name, but she is a midwife and she picked it up at her place of work.  And after two years of them trying to get rid of the Clostridium difficile recurring every three months, they’d given up, and basically they were trying to railroad her out of a job.  They gave her the thing in the first place, and now they’re trying to get her out of a job.  She came to me, and on day one I just completed the implant, and I sat her up and said, right, in about a half an hour’s time, that’s it.  It’s over and done with.  You’re back to work.  And she just broke down.  She couldn’t quite take it all in.

Chris Kresser:  Yeah.

Glenn Taylor:  On the second morning, she came back.  I had her come into the clinic.  She was taking the stairs five at a time, and she just threw herself through the door and said, I feel just extraordinary, absolutely amazing!  She got her life back again.  C. diff is easy.  What I’m finding really, really interesting is I’m working quite a bit with that very, very nebulous of conditions that’s called IBS.

Chris Kresser:  Yes.

Glenn Taylor:  You can probably hear in my voice that I’m smiling at the moment.

Chris Kresser:  Mm-hmm.

Glenn Taylor:  The lengthy protocol, you get a list of 10 symptoms, and if you sit with your physician and he can tick three of them, then great.  He’s happy because he has a diagnosis and he has a stamp that he can put on your forehead and say, you have IBS.  There’s probably not much we can do about it.  You’ll have to just get used to living with it.

Chris Kresser:  And more importantly, drugs they can prescribe that have been created for that condition that was created for the purpose of making drugs for it!

Glenn Taylor:  Chris, you are turning into an old cynic, you are.

Chris Kresser:  I can’t help it.  I can’t help it.

Glenn Taylor:  So, I look down the list of their own three of I think, yes, dysbiosis.  Yeah, that’s bacteria.  Yeah, that’s bacteria.  That’s bacteria.  Basically change the gut flora with people with IBS.  Stop.  Take a step back.  Watch their symptoms.  Send them back to their physician again who did the diagnosis, and say, now what do you think they have?  It’s a real eye opener.  We’re having a great time with IBS at the moment.  Really, a good time.  People are coming in for post-antibiotic, post-infectious IBS, for a combination of constipation and diarrhea or one or the other, and we have some very, very happy [indiscernible] walking home at the moment.  And I think it’s perhaps it won’t take too long before FMT becomes the treatment of choice, the first treatment of choice for all IBS.

I was talking to two major gastroenterologists in London a couple months ago.  These guys are professors of gastroenterology at the top of their field, and they were saying, we really are looking forward to the day when it’s available as a first choice, not a last resort, because patients come to us with this whole mass of white noise that’s going on with the various symptoms they’ve got.

Chris Kresser:  Yeah.

Glenn Taylor:  And it’s so very confusing trying to work your way through all these various symptoms to work out precisely what the problem is.  If only we had a method where we could normalize them and get rid of this effective white noise, and we believe that FMT might be the answer because normalization of the gut normalizes other processes.  Then we send the patients back to their doctor much quieter, and the doctors go, oh, crikey, yeah.  Now I can see what you’ve got.  Oh, that’s really much clearer.  It was cloudy before.  I couldn’t quite work it out, but yeah, I can diagnose, and here’s the remedy for it.

Chris Kresser:  Glenn, this is so similar to a paleo challenge or intervention, which you’ve probably heard of.  When I see a patient who comes in to me with all of these varying symptoms that are seemingly disconnected and all over the place and they’re on a kind of Standard American Diet, the first thing I do is put them on a paleo type of diet for 30 days, and I use the exact same language that you just used.  It’s like a cloud settling or silt in a pond going to the bottom, and at the end of that 30 days, it doesn’t mean that they won’t have any issues, but it’ll be much clearer what those issues are because all of the triggers that were causing all that chaos in their body have been removed and the dust has settled and the things that are remaining are much more easier to go after, after that.  Imagine if we combine a nutrient-dense, whole-foods dietary intervention like paleo for 30 days with an FMT.  The potential for that is just mind blowing.

Glenn Taylor:  Exactly.  As anybody that works in a hospital will tell you, patients turn up with a whole range of comorbid conditions, and it makes it very difficult for them to be quite precise.  And if there was a standardized procedure that they could employ that would help them sort the wheat from the chaff, it would be hugely helpful.  Now, you know that doctors of functional medicine have this fixation on the gut, if you can fix the gut first and then look at the rest of the patient.  They only know that it’s a good idea, but perhaps they don’t quite understand the microbiology of why.  But when you say to them, yeah, the reason why you’re going to sort the gut is to normalize the gut flora because of all the other things that impinge upon it.  Then you stand more of a chance of actually highlighting precisely what the problem is.  Yeah, it will be a treatment of the future, I’m sure, but it’s all come down to the method of delivery, and that’s the bit.

Chris Kresser:  Yeah.

Glenn Taylor:  I think Tom and I are on a bit of a race at this moment to come up with that.

The future of FMT technology

Chris Kresser:  Well, I’m rooting for everyone in this race because we’re all going to be the beneficiaries of your passion and investigation, so I’m excited.  I was going to ask you a question about the oral form of delivery, which has gotten some press recently.  I believe it was a Canadian physician who was written up about that.  I’m not sure if you want to go into that or leave that for the next time when you come on the show.

Glenn Taylor:  No, that’s OK.  You’re talking about Robogut, are you now?

Chris Kresser:  Yeah.

Glenn Taylor:  Or you’re talking about Hamilton’s project.  On Robogut, yeah.  It’s a good attempt.  At the moment, the best that they’re coming up with is about 10% of the microflora, but it’s a controlled, standardized system, and it’s quite effective, yet it’s 10% of what’s actually needed.  But it might to the 10% that works, Chris.  It may be, but we’ve still got to see how that goes.

Chris Kresser:  Sure.

Glenn Taylor:  The oral route – you see, now you’re trying to get me to tell you what I’m doing!

Chris Kresser:  No, no, no, I’m really not!  I shared an article a while back about the Hamilton, the oral delivery system for this, and of course, it generated a lot of attention and interest.  I’m not going to force you to talk about it at all.  You can just say whatever you want to say, and as long as you promise to come back on the show when you’re ready to say more, we’ll leave it at that.  We’ve got plenty more to talk about.

Glenn Taylor:  OK, well, how about this?  If I’m right about the method of delivery and if I get it right and if I can put all the factors together to make it effective and it becomes scalable and deliverable, we hope to be able to slash the price of the treatment by 10.

Chris Kresser:  That’s tremendously exciting, and I’m sure that a lot of my listeners are jubilant hearing that!

The side effects of Fecal Transplants

Let’s get back to some of the nittier, grittier details.  We were talking about the importance of screening donors, we’ve talked about how – really, there’s no other word – miraculous some of the transformations can be with this procedure.  I’m sure a lot of people are wondering, well, is there is a downside?  What are the side effects of FMT, and what are the risks when it’s done properly?  Since we’ve already discussed the importance of doing it properly, let’s just assume that it’s done properly.  Are there side effects and are there risks?

Glenn Taylor:  OK, in the clinical environment, side effects.  Well, in terms of the biology, you ask the question, if you take perfectly functioning bacteria out of a healthy person and you put them into a person who has dysbiosis, what reason would there be to be a side effect or a negative effect?  And the reality is, no, there isn’t.  However, that’s not totally true because we have had a couple of occasions where people have been teetering on the very edge of an IBD flare and just interfering with their microbiome sets them off, so we’ve had to stop treatment, send them home, and get their physicians to bring their flare back under control before they can come back in.  So, it has happened where a flare tips over simply because we’re working in that area.  It may well be that they were scheduled to have a flare and it was the last straw that broke that particular camel’s back.  But in all other cases, I don’t believe there are any recorded cases of a clinic application that have had any kind of negative side effects.

Chris Kresser:  Which makes this, of course, all the more remarkable.  I want to actually move backwards because there’s a question I forgot to ask you that I wanted to.  Have you had any people coming over with chronic infections that have had any success?  I’m thinking of things, you know, intracellular infections, Chlamydia pneumoniae, some of the stealth infections, like Lyme and Bartonella, Mycoplasma, stuff like that.

Glenn Taylor:  No, I haven’t.  Please, where are these people?

Chris Kresser:  Careful what you ask for because I’m sure a lot of them are listening right now!

Glenn Taylor:  Well, that’s the kind of stuff that we need to be able to do sufficient numbers of.  I know the medical community wants big n numbers, big numbers in a sample, a large sample, before they’ll even listen to the result.

Chris Kresser:  Yeah.

Glenn Taylor:  But remember the world’s first medical trials took place on a British warship in the 1700s when the surgeon on board the vessel chose six crewmen, all suffering with scurvy, and gave three of them lemons and three a placebo effect, and the n number, the total sample, was 6.  Now, the first trial went down as a huge, huge success with such a low number and we applaud what went on.  You try and do a trial today with 6, and they’ll laugh you out of the room.

Chris Kresser:  Yeah.

Glenn Taylor:  They only want hundreds or thousands.  But if it works and it works again and again and again, don’t we owe it to take it seriously and see if we can try and get more interest, get people to listen to us?  There’s such a fixation on high n numbers as being the only credibility in terms of treatments.

Chris Kresser:  Yeah.  It’s a real obstacle.  There are even n=1 experiments in the history of science, like, was it Warren and Marshall and the discovery of H. pylori?

Glenn Taylor:  Yeah.  Tom, by the way, Borody was involved in that.

Chris Kresser:  Yeah.  He was a grad student for them or something?  Yeah.  For people who don’t know that story – and correct me if I’m wrong; I’m a little hazy on it.  At that time, everyone thought ulcers were caused by stress, and they presented the idea that they were actually caused by a bacterium called H. pylori, and they were literally laughed off the stage at the conference that they presented at and then proceeded to labor in obscurity for several years and be completely ignored by their professional colleagues.  And it wasn’t until he infected himself with H. pylori, developed an ulcer, and then cured it with antibiotics that he was taken seriously.

Glenn Taylor:  Absolutely.  I remember watching Barry and Robin sitting together. – That’s not the Gibb brothers, by the way! – They were sitting at a restaurant, and this was 10 years after their first discovery.  And I remember looking at Barry’s face, and he was so jaded about his.  He said, look, it’s been 10 years since we discovered Helicobacter pylori and we’ve now got 10% of the doctors accepting and treating for it.  Maybe in a hundred years’ time we’ll have everybody doing it.

Chris Kresser:  Wow.

Glenn Taylor:  Yeah, he wasn’t impressed with his peers.  That was a typical case.  They had to peddle that all over the world for people to listen, and the established structure, the old guard, were really not ready for this young upstart to stand there and tell them how things worked.  And yes, Marshall had to infect himself and then cure himself in an effort to make people sit up and take notice.  You know, that’s not uncommon in history, where the only chance you get to do the research is on yourself!

Chris Kresser:  That’s right!  And it’s ludicrous to discard that result, in particular, simply because it was only one person.  That’s a rather compelling result, which actually in one experiment shows a causal relationship and not just an association and makes it certainly worthy for further exploration, so I completely agree with you on the recent trend of the over-focus on sample size and even on RCTs as if we can’t still use our common sense to reach conclusions, as if common sense is not part of the scientific process or even the basis of it.

Glenn Taylor:  I agree.  What I’m seeing is a lot of physicians being interviewed and dismissing the procedure on the basis that they’ve yet to see large-scale trials.

Chris Kresser:  Right.

Glenn Taylor:  And I think we’ve worked that one to death.

Why FMT is approved in the UK

Chris Kresser:  Yeah, exactly!  Tell us a little bit about the regulatory system in the UK.  I’ve posted several articles on what has happened in the US.  The FDA has only approved the use of FMT for antibiotic-resistant C. diff.  That means it’s not technically approved to do for any other uses, and I know there was a clinic in Portland that was doing some FMTs that was doing them for other conditions but is now only doing them for antibiotic-resistant C. diff.  I imagine the environment must be a little bit different in the UK, given your presence and operation, so tell us about that.

Glenn Taylor:  OK, yeah, that’s because of Europe and the UK having a completely different medical structure than the United States.  Our structure is based on a state system, a state kind of insurance system.  It’s very different from the health industry.  Oops.  Did I say ‘industry’ instead of ‘profession’?  Very, very different from the way that it’s financially structured over in the United States, this triangle of insurance company, physician, and drug company that you guys have yourselves stuck in and don’t seem to be able to extricate yourselves from, which has allowed – boy, I’m going to have to choose my words carefully here!  I am not making any accusations, not making any suggestions, but I would really like to see the structure of the ethics committee that came up with the decision that FMT or human feces should be regarded as an investigational new drug.  I’d like, honestly, to see the structure of that committee and see who is a genuine physician and who is in medicine and who is in pharmacology.

Chris Kresser:  Yeah.

Glenn Taylor:  But then you never forget there’s a big issue of safety, and I think also – and this is genuine – that they needed to see a standardized system of reporting in this particular respect.  Clearly it was a health thing, and it appeared to be effective, and no health authority in the world can afford to let this just run amok, so some form of regulation was needed, as will be needed in the UK, and I look forward to it.  I’m sure that at some point the lack of regulation could equally lead to many, many problems, but in the UK at the moment, this is research work, and scientists are permitted to go on with research without being over-encumbered with too many restrictions by medicine itself.  Medicine in Europe tends to respond to what scientists discover.

Chris Kresser:  Imagine that!

Glenn Taylor:  And then what we find out we hand over to physicians who then make use of it.  I think that we’re getting a lot of interest.  There are journals, there’s the media, there are doctors and hospitals who are sitting on the sidelines watching with great eagerness as to what we’re going to be able to do with this, and I’m regularly asked, what kind of response are you getting with this condition or with that condition?  They’re all hopping from one foot to the other, hoping that something will happen soon, and I think we really are – actually, Chris, would you say that we’re reaching tipping point?  I think the exposure of this is such that we’re getting to the point where no matter what interested parties might be out there that wouldn’t want to see this progress, when the public know enough about it, you can’t put this back in the tube.

Chris Kresser:  Yeah.

Glenn Taylor:  We’re going to reach a point where everybody will want to know.

Chris Kresser:  I would definitely agree with that, and I do think we’re nearing that point, if not right on the cusp of it, so it’s an exciting time to be involved in this, to be, I imagine, in your shoes, to be a functional medicine practitioner, someone who works with patients and may be able to administer this kind of treatment or at least refer them to it, so I’m really looking forward to seeing what unfolds, and I really appreciate you taking the time to come on the show.  Stay in touch, and we’ll definitely have you back when you’re ready to talk about the new delivery system.

Glenn Taylor:  Absolutely, I’d love to.  No problem at all, Chris.  Big thanks to you guys.

Chris Kresser:  Take care.

Glenn Taylor:  Thank you.  Bye-bye.

Chris Kresser:  Bye-bye.

We received a question about how to restore gut flora and function when unable to tolerate probiotics and fermented foods not likely due to histamine allergy. This is a great question, it’s one that I get a lot, and it turns out there are several potential reasons why somebody may not be able to tolerate fermented foods or probiotics, and one of them is histamine intolerance.

In this episode, we cover:

4:58 4 reasons why you may not be able to tolerate fermented foods or probiotics
12:32 How to improve your tolerance for fermentable fiber and prebiotics
22:38 Is it better to eat fermentable fibers in whole food, or is it better to use supplements?

Full Text Transcript:

Steve Wright: Hey, everyone. Welcome to another episode of the Revolution Health Radio Show brought to you by ChrisKresser.com. I’m your host, Steve Wright from SCDlifestyle.com, and with me is integrative medical practitioner, New York Times bestseller, and healthy skeptic, Chris Kresser. Chris, how’s the weather in California?

Chris Kresser: Well, it’s schizophrenic, actually. A couple days ago it was 95 or something and so hot we could hardly even sleep. None of the houses here really have air conditioning because you don’t need it most of the year, but there are a few days where I wish we did have it, and that was one of them. And then yesterday and today it’s been in the 50s. This is kind of how it can be in June in the Bay Area.

Steve Wright: Mother Nature’s playing tricks on you.

Chris Kresser: How about Colorado? Beautiful Boulder?

Steve Wright: Well, it’s been pretty steady here, 75 or 80s, sunny, and we’ve had a few rainy days, but we are getting into what I hear is the best part of Colorado.

Chris Kresser: Nice.

Steve Wright: This will be my first Colorado summer. I don’t really know what to expect.

Chris Kresser: Nice. Well, I’m headed to Tucson tomorrow to participate in this event called Revitalize that MindBodyGreen is putting together. They actually rented out the entire Miraval Resort, which is this super chichi eco-resort kind of place, and I’m really looking forward to it because there are going to be a lot of great folks there. I’m speaking on Saturday morning, and it’s going to be live streamed. By the time this podcast comes out, I think it will have already happened, but there will probably be a recording of some type. They invited a hundred thought leaders, both health experts and authors, but also actors, musicians, CEOs, and people of all different backgrounds who share an interest in health, so it’s kind of like a horizontal focus on health from people in a lot of different industries. We’re going to be there for three days hiking, hanging out, and doing these talks, which will be live streamed, so I’m looking forward to that except when it comes to weather, being in Tucson in June is probably not my first choice. They’re like, you can expect it to be 80 or 85 to 105, and I’m thinking, yeah, 85 is probably at 4 in the morning, right?

Steve Wright: But they probably have air conditioning.

Chris Kresser: Yeah, you’re right. They definitely have air conditioning. They have infinity pools and massage therapists and all kinds of stuff set up for us, so I’m not complaining. I’m really excited to go. It’s going to be great.

Steve Wright: Well, it sounds awesome. I’m definitely not going to shed a tear for you if it gets up to 100.

Chris Kresser: All right.

Steve Wright: Before we roll into today’s awesome topic, what did you have for breakfast, Chris?

Chris Kresser: I had some chorizo. We just got another half pig from a local farmer, Freestone Ranch, who is awesome. We had some chorizo from that and then also some plantains and then some sauerkraut and a little bit of beet kvass. I made that for Sylvie before we took her to preschool, and that’s what I had, too.

Steve Wright: Well, that sounds a lot more delicious than my black coffee.

Chris Kresser: Well, I do that sometimes as well, as you know.

Steve Wright: Yeah.

Chris Kresser: We’re going to answer a question I think a lot of people are interested in today, so let’s do that.

Steve Wright: OK, well, before we get into that, I just want to let the listeners know if this is the first time you’re listening to this awesome podcast or you’re a longtime listener, we thank you, and we want to let you know that Chris has created a membership area on his site at ChrisKresser.com where he’s categorized and he’s made it really easy for you to digest – pun intended – all of his awesome info on paleo weight loss, thyroid health, gut health, everything that Chris has been doing over the last many years he has created inside of his membership site. So you can go over to ChrisKresser.com and join. As of today, there are over 103,000 people who have already signed up for the membership site, who are in there, who have access to these expert interviews with people around the world with the eBooks that Chris has put out for free. So if you haven’t checked that out, definitely head over there and get signed up.

Today, Chris, the pun intended was because we’re talking about digestion.

4 reasons somebody may not be able to tolerate fermented foods or probiotics

Chris Kresser: Yeah, absolutely. We got a question from – I can’t remember where it was from, maybe Facebook or sent in through the contact form, and it was how to restore gut flora and function when unable to tolerate probiotics and fermented foods not likely due to histamine allergy. This is a great question, it’s one that I get a lot, and it turns out there are several potential reasons why somebody may not be able to tolerate fermented foods or probiotics, and one of them is histamine intolerance, which the questioner mentioned in the question. Fermented foods tend to be very high in histamine, and some people have either a genetic mutation that impairs their production of the enzyme that breaks down histamine. Other people have disruptions in the gut flora, which makes them less able to tolerate histamine, and so when they eat fermented foods like cheese or yogurt or sauerkraut or wine or vinegar, they experience all kinds of different symptoms ranging from headaches to hives, skin issues, fatigue, bloodshot eyes, nausea, all of which are mediated by histamine, which is what is involved in the kind of allergic response, like if you get stung by a bee. So that’s one possible reason that people don’t tolerate fermented foods, although that wouldn’t necessarily cause an intolerance of probiotics.

Another potential reason is SIBO, small intestinal bacterial overgrowth, because SIBO sometimes involves an overgrowth of certain types of bacteria that produce lactic acid, and Lactobacillus acidophilus is one of those kinds of bacteria, and that’s frequently included in probiotics, and it’s also in fermented foods. So if you have SIBO, you have an overgrowth of this kind of bacteria, and then you take probiotics or fermented foods, you could actually end up making yourself worse. I’ve seen that a lot, and actually sometimes intolerance of probiotics is one red flag for me that makes me want to look for SIBO and other gut issues.

Have you seen that as well, Steve?

Steve Wright: Yeah, it’s been in a lot smaller population from the case studies and what we’ve seen. It seems like maybe – I don’t know what it is, but it definitely seems like a minority of people who can’t tolerate the lactobacillus strains who have SIBO. Before you were kind of talking about this, sort of our go-to had been a lactobacillus strain that was very pure, and we had seen a lot of good results, but we had seen some reactions to it. As far as my digging goes, there seems to be an issue with the clearance of D-lactate, like a genetic potentially or an environmental trigger that happens. I think it’s interesting. It’s definitely developing. I think, like you said, if you’re having a probiotic intolerance, there is digging to be done there, and there is definitely something going on.

Chris Kresser: Yeah. From what I’ve seen, it depends on the type of bacteria that’s overgrown in SIBO. It also depends on the specific nature of the dysbiosis. You could have not enough good bacteria and too much bad bacteria, and that can cause probiotic intolerance. I’ve seen gut infections cause probiotic intolerance, like parasite infections, particularly. Inflammatory bowel disease can cause probiotic intolerance because in some cases in IBD people react negatively to their own commensal gut bacteria, the bacteria that’s normally in their gut, and if you introduce new bacteria to a really inflamed gut, that can also be problematic even if those bacteria are beneficial.

Steve Wright: Especially if you’re somebody who’s really messed up with a really bad leaky gut where you’re reacting to most all the foods out there when you introduce a probiotic strain sometimes. Jordan, for instance, actually had to start with, like, one strand of sauerkraut.

Chris Kresser: Yeah, exactly, and we’re going to get to that. I have my own story about that, too.

The last thing is FODMAP intolerance. People who are sensitive to FODMAPs, I’ve found, can sometimes be more sensitive to probiotics and fermented foods.

Now, here’s the really tricky thing or the catch-22 about this, which is generally the extent to which you react adversely to probiotics and fermented foods and prebiotics, which we’re going to talk about in a second, is roughly proportionate to how screwed up your gut is. In other words, the more strongly you react to these things, the more likely it is that you need them over the long term, and that’s the tricky thing about working with these situations because it’s always a dance between addressing the short-term issue, like symptom alleviation, making somebody feel better and comfortable, and then making sure that you’re progressing and dealing with the long-term problem, and that always involves restoring healthy gut flora.

Steve Wright: Have you seen that with FODMAPs, Chris? That’s an experience that I’ve seen, is that the more intolerant you are to FODMAPs, typically the more messed up you are and that that intolerance alleviates over time as everything improves.

Chris Kresser: Absolutely. That’s absolutely true, and the same principle applies there with FODMAPs and prebiotics. Most people who have a screwed-up gut are really sensitive to prebiotics and FODMAPs, but fermentable fibers, which is what FODMAPs are and prebiotics are, are absolutely crucial to restoring healthy gut flora over the long term. In fact, I’ve mentioned this before, but the most recent research has shown that probiotics do not quantitatively affect levels of beneficial bacteria in the gut. So you could take probiotics all day long, and it’s not going to increase the levels of certain bacteria like bifidobacteria and lactobacilli over the long term. Probiotics seem to have more of an immunoregulatory effect, so you take probiotics, they have a tuning and regulating effect on the immune system and the gut immune system, which is incredibly beneficial and important, but they don’t necessarily fill up the tank, so to speak, in terms of the beneficial bacteria you have in your gut. That’s what prebiotics, fermentable fibers, do, things like resistant starch, non-starch polysaccharides like inulin and fructooligosaccharides and galactooligosaccharides, those kinds of things. They provide food for the beneficial bacteria in your gut and can increase their levels by orders of magnitude. So it’s another catch-22 where you have someone with FODMAP intolerance who can’t handle any kind of fermentable fiber or prebiotics, where in my work with them I will very, very gradually introduce those things over time so that eventually they become less intolerant of FODMAPs and fermentable fiber because their gut flora is in a better situation.

How to improve your tolerance for fermentable fiber and probiotics

Here are the basic steps that I would use in this situation: The first thing would be, if possible – and I know this isn’t always possible – hook up with a functional medicine provider and get some testing done to see if you have SIBO, dysbiosis, gut infections, FODMAP intolerance, etc., because knowing what you’re dealing with can really accelerate things in terms of what kind of treatment you want to do. But even if you can’t do that and if you do, do that and you find you have some SIBO or overgrowth of bacteria in your gut, you can do a herbal, botanical antimicrobial protocol for SIBO. I’m going to be writing a post on this soon, but I just came across a study which I was really excited about that showed that botanical protocols are more effective than Rifaximin, which is the drug of choice for SIBO, and not only are they more effective, they’re, of course, much safer, they don’t tend to produce as many side effects, nor do they have as negative of an impact on the gut flora, and they’re even effective in people who have done Rifaximin and haven’t had success with it. This is exciting, and it means that a lot of the herbal preparations out there – there are many different varieties. There’s GI-Synergy or H-PLR from Apex, which I use a lot in my practice. Pretty much every major brand name like Thorne or Pure Encapsulations or Apex or Innate Response – all of these companies that are high quality supplement manufacturers have an antimicrobial protocol with many of the same botanicals in them, and these can be effectively used in many cases to deal with SIBO.

That’s the first step. You find out what’s going on. The second step is you can use a protocol to knock back some of the bacteria in the small intestine that may be making you intolerant of these probiotics.

Steve Wright: Chris, I have to jump in really quick.

Chris Kresser: Yeah.

Steve Wright: I just want to add in that there’s a really sexy – just coming from my own experience, and maybe you can relate to this – but there’s a sexy idea here that somebody’s going to be able to just execute these protocols with skipping step one and just going to step two and treating. And while I guess I’m saying that’s not the worst case in the world, I would caution and say that in my own health history as well as a lot of the people that I’ve worked with, SIBO doesn’t just grow by itself. When you have a really messed-up gut and therefore the more intolerant you are to a lot of these things that we’re talking about here today, the higher the likelihood that you have a deeper infection that maybe a general SIBO protocol is not going to take away. Especially those of you who are super sensitive, don’t skip over step one, which is getting testing and working with somebody who gets this stuff.

Chris Kresser: Yeah, I wish it was easier for people to find someone to work with because I often hear from people when I go speak elsewhere – you know, I just did a one-day seminar with Robb in New Jersey, and so many people came up and said, how can I find someone who has this kind of perspective to work with? It’s really difficult. I’ve been trying for a long time, and it just seems impossible. So I totally agree, Steve. For sure, the ideal would be to find a practitioner like that, and I also know that that’s not possible for a lot of people.

Steve Wright: Yeah.

Chris Kresser: And I think that many of the botanical protocols are generally safe, and even if you don’t necessarily get to the full root of the problem with it, you might get some improvement.

Steve Wright: Totally.

Chris Kresser: I’ve also talked about Lauricidin, which I like, on the show before, and then there are some prebiotics and probiotics, and we’ll talk about that in a second.

From a dietary perspective, a low FODMAP diet can be really helpful. If you’re not tolerating probiotics or fermented foods, it’s likely you have FODMAP intolerance or dysbiosis of some kind, and a paleo version of a low FODMAP diet can be really helpful.

Now, in terms of probiotics and prebiotics, as I said, even though taking them in normal doses might cause problems initially, that doesn’t mean that you don’t want to take them at all and that you should just write them off forever. What I suggest instead is starting at an extremely low dose and building up very, very slowly over time. Steve just mentioned that Jordan had to start with, like, a single strand of sauerkraut. Some people even just start with a tiny bit of the juice from the sauerkraut, like maybe a half a teaspoon of the juice once a day. When I was really restoring my gut, I started with a half of a teaspoon of kefir, and it took my nine months to build up to the point where I could have a full cup of kefir a day. Now I could drink, you know, three glasses of kefir in a day and feel great, but it was rough initially. I had a lot of reactions, there was a lot of starting and stopping, two steps forward, one step back, and unfortunately that’s just how it often has to be to begin with when you’re dealing with a situation like this because you’re really dramatically changing the composition of your gut flora, and because the gut flora affects virtually everything, that can produce a lot of different symptoms. So I suggest starting with very low doses, being methodical about it. One of the mistakes I often see in my practice is people will get excited, understandably, about being able to tolerate more and they’ll go too quickly, so just be very slow and methodical about it.

Steve Wright: Just to kind of differentiate here because we’re speaking on Jordan’s story with sauerkraut, your story on kefir, and we’ve also mentioned probiotics and prebiotics, is there a pattern that we should look for, because for instance, kefir might be a worse choice due to potentially the milk casein issue. Sauerkraut, you’re dealing with a FODMAP for sure, so the source of the fermented food has a role here, and then, of course, there’s also choosing a standardized commercialized product.

Chris Kresser: Yeah.

Steve Wright: Do you have sort of any thoughts on differentiating which one to start with?

Chris Kresser: I don’t think there’s really much of a FODMAP issue with sauerkraut because the sugar in cabbage is what is the FODMAP component, and when sauerkraut is made that sugar is consumed mostly by the bacteria, so there shouldn’t be much sugar left in cabbage, which means that it wouldn’t really be a FODMAP anymore, so I do think sauerkraut is a good starting place for a lot of people for that reason. Dairy kefir, as you pointed out, can be problematic if people are intolerant of the proteins; however, if you have lactose intolerance, dairy kefir is not an issue if you make it at home and you ferment it for at least 24 hours because all of the lactose will be gone, and in fact, there are some studies which suggest that you can cure lactose intolerance or at least significantly improve it by consuming fermented dairy products like yogurt and kefir. So if you know that the dairy proteins aren’t a problem for you, as I did, then dairy kefir can actually be very healing. Another option is water kefir. You can get water kefir grains from someone like CulturesForHealth.com, and you just make it with sugar and water. The cultures consume all of the sugar, and then you can flavor it with a little bit of fruit, and that has a very therapeutic effect as well. Beet kvass is another great fermented beverage that I’ve found to be pretty therapeutic, and then, yes, you get into the commercial probiotics.

My experience, especially over the last year, is that a lot of people who don’t tolerate lactic acid-based probiotics do tolerate soil-based organisms and often very well, and I know you guys have had the same experience. I’ve talked to a lot of colleagues who have had the same experience. Prescript-Assist, which is the product that I sell in my store, is by far my favorite right now as a general use product, and I think it’s safe to use in SIBO. It works well for people with constipation, and those people often tend to be the ones who don’t respond well to probiotics. It also works well for people with loose stools or diarrhea, too, but it’s really versatile and really safe and well tolerated and really effective, which is why I find myself using it a lot. If you’ve tried other kinds of probiotics and fermented foods and you don’t react well to those, you could start with Prescript-Assist, but instead of taking two capsules a day, which they recommend on the bottle to start with, you would take maybe a third of a capsule. You actually open the capsule, pour a third of it in a little bit of water or just directly into your mouth – it tastes fine – and take it that way and then just gradually build up to one capsule, then gradually build up to two capsules and stay on that dose for maybe two to three months therapeutically, and then you can go back down to one capsule as a maintenance dose. You can, of course, do that same approach with any kind of probiotic, but if you’re having trouble tolerating them, I definitely would recommend starting with something like Prescript-Assist.

Is it better to eat fermentable fibers in whole food, or is it better to use supplements?

This brings us to the same question that you asked, Steve, about prebiotics: Is it better to eat fermentable fibers in whole food, or is it better to use supplements? Well, over the long term, I think, you’ll probably guess what my answer is. I think it’s better to get it from food. But in the short term, I actually find that it’s easier to use supplements to start, and the reason for that is that prebiotics tend to really cause problems for people who have a screwed-up gut, and I’ve found that it’s easier to adjust the dose and build up really slowly and cautiously over time with a prebiotic powder than it is to do with food. It’s just harder to control the exact amount of prebiotic fibers you’re getting when you’re eating whole foods than it is using a powder. We’ve talked about resistant starch as one potential prebiotic that you could use to do this, and potato starch is the version that’s most often used, and then there are things like Prebiogen, which I also sell in my store, which is a blend of non-starch polysaccharides, and I actually recommend that people use both because they stimulate the growth of different kinds of bacteria in the gut. Resistant starch will stimulate growth of a certain type of groups of bacteria, and then the non-starch polysaccharides will have an effect on other types of bacteria.

But let me remind you again that starting at the full dose which is often recommended, like one or two tablespoons twice a day, is absolutely not advised for people with gut issues! I just talked to another patient last week who ended up in the hospital because she was so certain that she was having appendicitis or some major issue in her gut, and what had happened is she had started taking one tablespoon twice a day of resistant starch, and on the second or third day, she was curled up in a ball on the floor for hours until she went to the hospital. It turned out it was just gas pains that were causing that pain. They can be super, super intense, and some people who are listening might have experienced this. That really triggered a flare for her that lasted about two and a half or three weeks. That’s not a typical response, but I just tell you that story to emphasize the importance of starting slowly with any prebiotics. I would say, like, a half of an eighth of a teaspoon, like, a sixteenth of a teaspoon, an eighth of a teaspoon, and then just really, really slowly build up over time. That way, I think, you’ll eventually get to reach the goal, but it could take months or even years to finally get to where you’re going, but you’ll see improvement all along the way, so that’s the bright side.

Steve Wright: Yeah, in case people are wondering, I think Chris and I just giggle a little bit about doing these experiments on yourself and the negative consequences that can happen, so we won’t say anything about the woman that Chris was talking about, and hopefully trying to let you know that, in general, you definitely want to ramp up all the time, whether it’s prebiotics or something else. As we’ve talked about on the show numerous times, essentially you’re changing your gut flora with every bite that you take. Resistant starch is kind of like rocket fuel for your gut flora. If you dump a bunch of rocket fuel down there and you haven’t been running that kind of octane in the engine for a while, there can be some serious consequences.

Chris Kresser: Absolutely. All right, so that’s today. I hope that answers your question about how to restore healthy gut flora when you don’t tolerate probiotics or fermented foods well, and we’ll be back next week with another question.

Steve Wright: Yeah. Thanks, everyone, for listening. If you want more information from Chris in between episodes, definitely check out ChrisKresser.com, but you can also get more tidbits on Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser.

If you have a kid and your kid gets an ear infection and you take him or her to the doctor, chances are you’re going to walk out of there with a prescription for an antibiotic. For many years, researchers and doctors thought that ear infections were primarily bacterial, which is why they prescribed antibiotics, but we now know that 80% of ear infections are viral in origin, not bacterial, and they’ll actually resolve within four to seven days without any antibiotic treatment at all. This is clear in the research. Unfortunately, the memo hasn’t really gotten out because most doctors are still prescribing antibiotics and most parents are still asking for them.

In this episode, we cover:

8:00  Why ear infections are a big deal
11:56  Four common causes of ear infections
16:51  How to treat chronic and recurring ear infections

Links we discuss

• Martin Blaser’s new book, Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues

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 host, Steve Wright from SCDlifestyle.com, and with me is integrative medical practitioner and New York Times bestseller and gorgeous man right there, Chris Kresser! What’s up, video?

Chris Kresser: Hey, Steve, how are you doing? Pretty exciting, huh? Do you like my high-tech background here?

Steve Wright: Yeah, I think you should get some pictures or something put up.

Chris Kresser: Yeah, in my phone cave? This is what makes the audio so good. We finally figured it out, but it’s not esthetically that pleasing, so you’re just going to have to deal for now with this rather utilitarian-looking background, but it’s all in the name of production quality.

Steve Wright: It’s all for the listeners.

Chris Kresser: Yeah, your background is much nicer, Steve.

Steve Wright: Yeah, I’m blessed with this room right here that mostly just contains a bookshelf and window.

Chris Kresser: That’s perfect, built for video.

Steve Wright: It is.

Chris Kresser: Yeah, we’ve been transitioning to this new format, as I’m sure people have noticed, so we’re going to start doing video for you YouTube watchers out there, and we’re doing somewhat shorter episodes typically that are focused on a single topic, and these are going to be really driven by your questions. We have a new format for submitting those questions. If you go to ChrisKresser.com/PodcastQuestion, there’s a little button you can hit to record a voice question, and then we’re going to shift through those and I’ll pick a question to answer each week and we’ll play back your voice question at the beginning of the episode. I like that because your voices will be included and heard in the show, and I think it’ll be great to do it that way. Most episodes will be maybe 20, 25, or 30 minutes. Of course, if we do an interview, we’ll probably do longer episodes, but we’re going to try this out and see how it works. Let us know what you think of the new format.

Steve Wright: Awesome. Well, I’m excited about the new format, and before we get to this week’s listener SpeakPipe question, I just want to let everybody know that if you didn’t see yet, Chris just invested a whole lot more time and energy into his website and made it even easier now to navigate around. Personally, Chris, I like the new design for sure, and if you go to ChrisKresser.com, you’ll see a big Chris Kresser picture and then right to the right of that is an opt-in box for Chris’ 9 Steps to Perfect Health eBook. It’s a 63-page eBook that has nine different steps that if you haven’t started to think about or implement in your life, I would definitely recommend that you get it and start to think about these things. Don’t probably try all nine at once, but definitely get started one at a time. I think as of now, Chris, there are over 106,000 people that have already opted in for this type of eBook, so it’s a pretty powerful eBook.

Chris Kresser: Yeah, it’s kind of my top tips for optimizing your health, especially for people who are pretty new to it. I cover the basics on diet and nutrition, exercise, sleep, stress management, supplementing wisely, and some of the other lifestyle stuff that we’ve talked about a lot on the show and that I’ve written about on the blog, so it’s a really excellent primer for yourself or for anybody that you know that’s getting started with this stuff.

Steve Wright: Yeah, check it out if you haven’t, and now we’ll play this week’s question. YouTubers, you won’t hear the question. That’s an interesting thing we didn’t think about.

Chris Kresser: Mm-hmm. We’ll have to figure that out.

Steve Wright: So, Chris, what’s question?

Chris Kresser: The question was from a woman from Australia, I think, judging by her accent, and she has a 12-month-old breastfed baby that is getting recurrent ear infections, and she’s wondering what to do about that, and then she specifically asked about grommets as a potential remedy. These are ear tubes, tiny tubes that are put into the eardrum when kids are having chronic ear infections. This is a great question, and it actually leads to several other questions and an interesting discussion, so I thought it would be a good topic to cover on this show.

If you have a kid and your kid gets an ear infection and you take him or her to the doctor, chances are you’re going to walk out of there with a prescription for an antibiotic. For many years, researchers and doctors thought that ear infections were primarily bacterial, which is why they prescribed antibiotics, but we now know that 80% of ear infections are viral in origin, not bacterial, and they’ll actually resolve within four to seven days without any antibiotic treatment at all. This is clear in the research. Unfortunately, the memo hasn’t really gotten out because most doctors are still prescribing antibiotics and most parents are still asking for them. I know of some doctors who are aware of this, but it’s very difficult for them not to prescribe antibiotics because the parents are really distressed. If you’ve ever been around a small child with an ear infection, you know that they’re really painful and difficult. It’s hard as a parent to witness that and not know what to do and feel like you’re powerless, so I certainly don’t blame parents for wanting to alleviate the suffering of their children. The problem is, as I just mentioned, the antibiotic won’t be helpful 80% of the time, and it only works 20% of the time, and that’s a pretty big risk you’re taking, to take an antibiotic when there’s only a 2-in-10 chance that it will work. If antibiotics were harmless, as we originally thought they were, it wouldn’t be a big deal, right? But we know that they’re not harmless, and ironically, taking antibiotics is actually going to increase the risk of getting future ear infections because it disrupts the microbiome, which then makes the child more susceptible to future ear infections, so it becomes almost like a self-fulfilling prophecy – antibiotic for ear infection, more ear infections, more antibiotics, and kids really just get stuck in this loop.

Steve Wright: What about those other two times, though, Chris? Just playing the other side of the coin here, is there a risk to the two times when it would’ve worked?

Chris Kresser: There is a risk, and that’s why this is such a difficult problem because there can be complications from middle ear infections that can go deeper and they can cause all kinds of problems. Up until recently, I think the thinking even for doctors who knew that most of them are viral is, hey, there is a chance of complications if it isn’t treated, so we’ll just prescribe the antibiotic and deal with that in case it is bacterial, and if it’s not, no big deal. But again, the problem is it is a big deal. It’s a much bigger deal than we ever thought it was, and we’re only now beginning to understand the extent to which it’s a big deal.

Why ear infections are a big deal

In an ideal world, we’d have, like, a rapid culture where the doctor could just take an immediate culture to figure out right there in the office if it’s viral or bacterial, and even if it’s bacteria, what kind of bacteria it is so that they can prescribe a narrow-spectrum antibiotic that just deals with that particular form of bacteria instead of a broad-spectrum antibiotic that’s going to wipe everything out because typically the antibiotics they prescribe for these things are broad spectrum because they don’t know what bacteria is causing it. That’s ideal but we’re not there yet, and the development of that kind of culture method has been slow. I think it’s possible, but it’s really expensive and it’s going to be a while before we get to that point.

The recommendation that I think makes the most sense to me is to monitor closely, to try some of the things we’re going to talk about that are alternative treatments for ear infections that get more at the viral cause and just monitor closely. If you see your child getting worse and not responding to any of these treatments, then you go back to the doctor and then you could consider an antibiotic to prevent complications. That would lead to far, far fewer antibiotic prescriptions because, as I said, most of these resolve within four to seven days without antibiotics and they don’t get progressively worse.

It’s a huge problem. The average American child has received three courses of antibiotics in their first two years of life, and then they go on to receive another eight courses of antibiotics over the next eight years, 17 courses of antibiotics before the age of 20, and 30 courses of antibiotics before the age of 40.

Steve Wright: That’s average?!

Chris Kresser: This is average, so, of course, some people are much higher than that, and other people are lower. But to have an average of 30 courses of antibiotics before 40 is totally catastrophic.

Steve Wright: Oh, yeah.

Chris Kresser: I think I mentioned Martin Blaser’s new book. Dr. Blaser is a real pioneer in the field of microbiome research. His book is called Missing Microbes, and it details the consequences of overuse of antibiotics. It’s a fantastic book. It scared the hell out of me! There were things I had been aware of for a long time, but to see it all in one place and to see all the statistics and to really consider the possibly permanent changes to the human race…

Steve Wright: Wow.

Chris Kresser: We’re talking about that level of significance because we’re changing our microbiome in such a way and we know now that we pass our microbiomes down to our children, so if we change or eliminate certain species of gut flora that have been living in our guts for millions of years or hundreds of thousands of generations and we wipe them out, we’ve permanently changed essentially what it means to be human because we have 10 times more bacterial cells than we do human cells, so it’s a big deal. It doesn’t mean that antibiotics aren’t necessary. They’re lifesaving. They have to be used in certain cases, and we should continue to use them for those cases, but what we should not do is prescribe them indiscriminately in situations where they’re not likely to be effective. If we just change that alone, it would have a huge difference on the number of prescriptions, and in fact, there are other industrial countries that have much better health care than us in terms of rankings and when you look at infant mortality and all the objective measures, like Sweden, for example, and Denmark, and their prescription of antibiotics is way, way lower than ours, so it’s definitely possible to have really high quality health care without a lot of antibiotic use.

Four common causes of ear infections

I think actually one of the causes of chronic viral ear infections in kids can be antibiotic use. If a child received antibiotics when they were young, maybe a C-section birth or an initial infection or something like that, that can disrupt the gut flora and predispose them to becoming more susceptible to ear infections as they get older.

Food allergies – this is really interesting. I did some research on this recently, and studies show between 45% and 80% of kids with recurring ear infections have food allergies. In other words, it’s more likely than not that a food allergy is at the root of the chronic ear infections. The most typical would be to gluten, dairy products, soy, peanuts, and some of the non-gluten grains, and we’ll talk a little bit about what to do about that when we get to the section.

Steve Wright: That’s fascinating. I mean, we know from the research also that antibiotic usage predisposes to leaky gut, so that’s obviously the connection – one of the connections, anyway.

Chris Kresser: Yeah.

Steve Wright: Just changing our diets that we give to the kids potentially could stop these cycles. I have several friends whose babies are stuck in these cycles, and I wish they listened to this show.

Chris Kresser: Yeah, and unfortunately in the mainstream there’s still this idea that food doesn’t matter that much for things like this, which is kind of preposterous. The food allergies, I think, contribute via leaky gut, like you said, Steve, and then they activate the immune system and cause this immune dysregulation, which then makes us more susceptible to viral infections, which are the cause of most ear infections.

Another related cause of ear infections would be disrupted gut microbiome. I talked about that in the context of antibiotics, so lack of beneficial bacteria because the breast milk isn’t sufficient in that regard or because the baby is consuming formula, which is not the case for the questioner but is definitely a potential issue. If the baby was born via C-section rather than vaginally, we know now that the initial exposure to bacteria happens in the birth canal, whereas if you have a C-section birth, the initial exposure for the baby to bacteria is actually just to the hospital bacteria, which is obviously not as desirable as the mother’s bacteria in the birth canal. One in 3 births now in the US are C-section births.

Steve Wright: Wow. That’s crazy, but also what I just thought of is I’m picturing this idea that we’re changing the gut flora forever and I’m thinking about the different Third World countries and the hunter-gatherer tribes that are still alive and the fact that I don’t have any kids yet, but all of the babies that I’ve ever seen are, like, wrapped in the most non-microbial environment ever.

Chris Kresser: Yeah.

Steve Wright: Like, if some dirt or something ever got on a newborn, I think everyone would freak out, including myself. I’d be like, Oh, that’s weird!

Chris Kresser: Yeah.

Steve Wright: But in a different time and age, these babies would have been exposed to soil-based organisms right away.

Chris Kresser: Absolutely, right away, and they were certainly born vaginally and they were breastfed 100% of the time, so yeah, a much different environment. So that’s another possibility, and we know that 75% to 80% of the immune cells in the body are in the gut, so if you have changes to your gut microbiome, that’s absolutely going to affect immunity and your ability to fight off these ear infections.

Another problem that can predispose to ear infections is low vitamin D levels, and there was one study I found that showed that of 116 kids, on average, they had low vitamin D levels. The norm in the study was that kids’ vitamin D level was 27 or something, which is below the commonly recognized range of 30. Now, that range is somewhat controversial, and I think that you can make an argument that 27 may not be a problem, especially in kids that young, but we know if that’s the average that a lot of kids had levels of 15, 18, 20, and that’s definitely an issue because vitamin D plays such an important role in regulating immune function.

How to treat ear infections

Those are a few of the causes and things that can increase the susceptibility to chronic and recurring ear infections. Now we’re going to start talking about treatment, and of course, we’re going to be thinking about it in terms of all of these causes. So the goals are we want to eliminate any food triggers that could be contributing to these recurring infections since the food allergies are a factor in many, if not most, cases of recurring ear infections. We want to fix the gut, you know, improve levels of beneficial bacteria, and we want to strengthen the immune system and then also even consider what some botanical or herbal alternatives to antibiotics might be that can be used either internally or topically.

Steve Wright: And you would do this with a newborn that has been having multiple infections and may or may not already have tubes in their ears.

Chris Kresser: That’s right. The first step would be an elimination diet. At 12 months old, baby is probably eating some solid food now, probably not too much, depending on how you’ve done it, but if baby is eating solid food, then you definitely would want to remove gluten, dairy, soy, peanuts, and probably all grains from baby’s diet for a period of time and see how they respond and if this makes a difference. If breastfeeding is still happening a lot, which it sounds like it was, then it probably makes sense for mom to remove those foods from her diet for a period of time. We don’t have a lot of research on how much of these proteins get through the breast milk and into the child’s belly, but I know anecdotally and from working with a lot of moms that changes in mom’s diet absolutely do affect baby when they’re breastfeeding, so I think it definitely makes sense to do that.

The second thing is a nasal spray called Xlear, and this is a xylitol-based nasal spray. Xylitol is a sugar alcohol that breaks down biofilm, and in a lot of cases of any kind of chronic viral infections or chronic infections in general, what happens is biofilm forms and it makes it really hard for the immune system to get rid of whatever’s in that biofilm. Xylitol actually breaks up the biofilm and makes it easier for our immune system to deal with those pathogens. You can use the Xlear nasal spray. If you go to the website, there are some directions on how to do that.

In terms of alternatives to antibiotic eardrops and internal antibiotics, there’s a garlic and mullein oil. It’s sold in a small bottle. I think it’s mixed in a base of olive oil, and there’s garlic and mullein, which are both antimicrobial, and mullein, in particular, has a soothing effect on the ear. So you warm it up slightly, put it is a pan with some hot water so it warms up, and you can put some drops of oil in the ear, and that can be really effective. I actually have used that myself sometimes. I have a condition called surfer’s ear where the bones in my ear have grown closer together because of too much exposure to cold water. It means that sometimes if I’m surfing and I forget my earplugs then my ear will tend to fill up with water, and it doesn’t drain properly and then I can get an infection, and when I do I use the garlic and mullein oil, and it works pretty well.

Steve Wright: Nice. Is there a brand for that that you would trust?

Chris Kresser: I think Herb Pharm makes one, but there should be a few different options, and I don’t think the brand matters quite as much in this case.

Then we have things that are immune stimulants that can help strengthen immunity and that are safe to take even for relatively young kids as long as you’re using the kids’ dosages. There’s elderberry and echinacea. Typically most recommendations are not to give these to kids under 2 years old, but if you have an herbalist or a functional medicine practitioner that’s experienced with treating kids, I think it’s probably fine to do that under supervision. We’ve done that with Sylvie at times if people around her, like her friends, were sick just to help her fight off colds. It’s, I think, safe if you use a low enough dose.

So we have the Xlear, the garlic and mullein oil, and then the echinacea and elderberry. Then we have, of course, vitamin C, which you can use up to 400 mg in a 1 to 3-year-old child. I wouldn’t exceed 400 mg. You have foods like bell peppers, papaya, guava, strawberries, kiwi, broccoli, kale, and other leafy greens that are high in vitamin C, and you can also supplement with vitamin C and that can really strengthen the immune system.

Fermented cod liver, our old friend, which always seems to come up in these discussions, the reason it’s so potent for immunity is it has high levels of vitamin A, retinol, which is the active form of vitamin A, which is very important for the immune system. It has vitamin D, which we just talked about. A lot of kids are low in it. It has EPA and DHA, which are also helpful for the immune system. It has some vitamin K2, which, now we are understanding, plays a role in immune function, and vitamin E and the various quinones, so it’s a really kind of potent immune booster. Cod liver oil was actually Sylvie’s first real food other than breast milk. You can start with that at 9 months if not earlier, and certainly for a 1-year-old you could be using 1 mL or even 1.5 mL or 2 mL during an active infection. A lot of adults that I work with and kids, I hear from their parents, just adding cod liver oil to their routine sometimes dramatically reduces the frequency and severity of colds and flus and other kinds of infections.

Then we have probiotics and prebiotics. Regarding probiotics, for kids under 2, it’s important to use different products than you use with adults. What you want to do is look for strains that are naturally in the gut of infants at that time, and Bifidobacterium infantis is the main one. There’s a product in the US called Ther-Biotic Infant that I like to prescribe for kids under 2 years of age, which is really effective. I’m not sure if there’s an Australian equivalent, but look for Bifidobacterium infantis as the most important strain. Of course, there are fermented foods, too, if your child is old enough to eat them and will eat them. Sauerkraut was actually Sylvie’s favorite food for a number of months early on. She absolutely loved it. I think that was the wisdom of her body speaking. If dairy turns out to not be a problem, there’s dairy kefir. Water kefir is really great, beet kvass. Kombucha I don’t find to be as therapeutic, and it’s a little bit sweeter, so that might not be the greatest idea. And then you can ferment just about any kinds of vegetables and even fruit, so there’s a lot of leeway there to get more fermented foods into the diet.

Prebiotics, though, have a greater impact over the long term in terms of increasing the levels of beneficial bacteria. Probiotics are immune regulators, and that’s important, of course, when you’re trying to address the immune system, but they don’t quantitatively increase levels of beneficial bacteria over time. That’s what prebiotics so. You could use something like I have in my store. It’s Prebiogen, so it’s inulin, larch arabinogalactan, and some other non-starch polysaccharides that selectively stimulate the growth of good bacteria. You could try a little bit of potato starch mixed with something, either yogurt if they tolerate dairy or coconut milk or something like that. Go very slowly and give your child a lot less than the adult dose. For Prebiogen, that would be maybe one-sixteenth of a teaspoon. They say start with a scoop on the jar, and that’s a terrible idea! And the same for resistant starch, any potato starch. Start at a much lower dose and build up slowly over time.

Steve Wright: It seems like if they start playing around with these prebiotics that they should really monitor for increased gas just in case they’ve already developed a SIBO infection or something.

Chris Kresser: Yeah, absolutely, and if your child is 1 year old, they’re not going to be able to tell you, so you’re going to have to watch for pain and listen for changes in their digestion and observe for changes in their stools.

Going back to probiotics, if your child is over 2 years old, I think soil-based organisms make a lot of sense for prevention because some of the bacillus species of bacteria which are in soil-based organisms, their particular claim to fame is their potency as immune regulators and stimulators. Bacillus species and soil-based organisms in general have a particular effect on immune function compared to other probiotic strains, so I think the soil-based organisms are important.

That’s the program. That’s a lot of stuff to focus on. I imagine there will be something there that helps, and I sure hope so because I know it can be really challenging to have these recurring infections.

I want to address the question about grommets, AKA ear tubes, quickly. These are tiny tubes that are inserted into the eardrum under general anesthesia, and they usually stay in place for six months or a year or maybe longer. The reason they do it is the tubes help drain chronic ear fluid that builds up in these recurring ear infections, which is often referred to as glue ear, and that helps an ear infection from occurring again because that glue, the fluid that builds up there, makes the kids more susceptible to recurrent infections. The other idea behind the tubes is if the child is having recurrent infections and they’re not resolving, there’s a potential – even though it’s very rare – for chronic hearing loss to happen, and so the tubes are used to prevent that from happening.

There are some risks, though. As with any surgery, there’s always risk, especially under general anesthesia. A fairly non-significant percentage of people have bad reactions to general anesthesia, and the ears are very delicate structures, so getting in there is potentially problematic. The tubes often leave a little scar that covers about one-sixth of the eardrum, and most doctors and researchers seem to think this isn’t a problem, but the jury is still out. We don’t really know, so there’s a question mark there. And then some studies show that the ear tubes don’t actually work to prevent recurring ear infections, and some kids get just as many ear infections as they did when they didn’t have the tubes. This, I think, gets back to the importance of addressing the underlying problem. If you have a food allergy, if a kid is gluten intolerant, and that’s what’s causing the immune activation, which is then predisposing to ear infections, then using ear tubes is possibly going to help, but if the gluten is not taken out of the diet, then the underlying problem hasn’t been addressed and they’ll just keep getting worse. So I would say ear tubes would be a last resort and that trying all the things that we’ve talked about here would be the starting place.

Steve Wright: Well, I think that’s a lot of information. That’s a lot of different steps to take.

Chris Kresser: Yeah. I hope that was helpful, and I hope everyone is enjoying the new format. Please do let us know in the comments section, and remember to submit your voice questions because that’s what we’re going to be doing now. You can do that at ChrisKresser.com/PodcastQuestion. Please do keep the questions short because you know we’re going to be playing them back during the show and it’s not really possible for me to address individual health concerns, anyway, during the podcast, so keep it short and somewhat general so it can benefit everybody, and we’ll do our best to answer them.

Steve Wright: Awesome. And obviously you can always check us out and leave us a rating on iTunes, the Revolution Health Radio page there, and in between these episodes, Chris always is sharing the studies and the books that he’s consuming on Facebook and Twitter, so you can go to Facebook.com/ChrisKresserLAc and then Twitter.com/ChrisKresser.

Chris Kresser: And Pinterest now. We’re starting to beef up our Pinterest presence.

Steve Wright: I think we’re going to put this on Pinterest right here.

Chris Kresser: Yeah, this beautiful background! Maybe we can Photoshop it, me in a jungle or something or on the beach with my microphone. It is white, right? Someone could cut it out.

Steve Wright: True.

Chris Kresser: All right, everybody, thanks again. Good to see you and talk to you, and we’ll see you next week.

I asked Dr. Amy Nett, MD, to contribute this guest post. She recently joined my private practice and will be working with me in the clinic.  Amy initially completed her medical training in radiology at Stanford University Hospital, but wanted to work more directly with patients, helping them to prevent and reverse chronic disease and truly transform their health.  Combined with her passion for nutrition she decided to pursue a career in functional medicine, and is excited to have the opportunity to work more closely with patients in achieving their goals and realizing their best potential.  You’ll be hearing more from Amy in the future!

Over the past several years there has been an exponential increase in the number of studies linking imbalances or disturbances of the gut microbiota to a wide range of diseases including obesity, inflammatory bowel diseases, depression and anxiety (1,2,3,4,5).  One of the best ways to establish and support a healthy gut microbiome is by providing the right “foods” for your gut bacteria.  These “foods” are called prebiotics.

Why you should add resistant starch to your diet.

Prebiotics are indigestible carbohydrates, or at least indigestible to us, that reach the colon intact and selectively feed many strains of beneficial bacteria.  Prebiotics are generally classified into three different types: non-starch polysaccharides (such as inulin and fructooligosaccharide), soluble fiber (including psyllium husk and acacia fibers), and resistant starch (RS).  Each of these types of prebiotics feeds different species of gut bacteria, but among these, RS is emerging as uniquely beneficial.

The distinctive benefits of RS seem to be unequivocally recognized, even amongst advocates of a low carbohydrate diet. 

What is resistant starch?

Resistant starch is a type of starch that is not digested in the stomach or small intestine, reaching the colon intact.  Thus, it “resists” digestion.  This explains why we do not see spikes in either blood glucose or insulin after eating RS, and why we do not obtain significant calories from RS.  

There are four types of resistant starch:

RS Type 1: Starch is physically inaccessible, bound within the fibrous cell walls of plants.  This is found in grains, seeds, and legumes.

RS Type 2: Starch with a high amylose content, which is indigestible in the raw state.  This is found in potatoes, green (unripe) bananas, and plantains.  Cooking these foods causes changes in the starch making it digestible to us, and removing the resistant starch.

RS Type 3: Also called retrograde RS since this type of RS forms after Type 1 or Type 2 RS is cooked and then cooled.  These cooked and cooled foods can be reheated at low temperatures, less than 130 degrees and maintain the benefits of RS (6).  Heating at higher temperatures will again convert the starch into a form that is digestible to us rather than “feeding” our gut bacteria.  Examples include cooked and cooled parboiled rice, cooked and cooled potatoes, and cooked and cooled properly prepared (soaked or sprouted) legumes.

RS Type 4: This is a synthetic form of RS that I’m including for completeness, but would not recommend.  A common example is “hi-maize resistant starch.”

Once RS reaches the large intestine, bacteria attach to and digest, or ferment, the starch.  This is when we receive the benefits of RS.

How resistant starch impacts our health

The normal human gut has hundreds of bacterial species, some good and some not so good.  The overall number and relative quantity of each type has a profound effect on our health and well being.  Resistant starch selectively stimulates the good bacteria in our intestines, helping to maintain a healthy balance of bacteria (7).

These good bacteria “feed” on RS and produce short chain fatty acids (through fermentation), the most significant of which are acetate, butyrate, and propionate.  Of these three short chain fatty acids (SCFA), butyrate is of particular importance due to its beneficial effects on the colon and overall health, and RS appears to increase butyrate production more when compared with other soluble fibers (8).

Butyrate is the preferred energy source of the cells lining the colon, and it also plays a number of roles in increasing metabolism, decreasing inflammation and improving stress resistance, as described in more detail below and previously in this great article by Stephan Guyenet.

Resistant starch helps to lower blood glucose levels and improve insulin sensitivity

Insulin resistance and chronically elevated blood glucose are associated with a host of chronic diseases, including metabolic syndrome.  Several studies have shown that RS may improve insulin sensitivity (9), and decrease blood glucose levels in response to meals (10, 11, 12).  In one study, consumption of 15 and 30 grams per day of resistant starch showed improved insulin sensitivity in overweight and obese men, equivalent to the improvement that would be expected with weight loss equal to approximately 10% of body weight (13).

Further, RS has been shown to exert a “second meal effect.”  This means that not only does RS beneficially decrease the blood glucose response at the time it’s consumed, but, somewhat surprisingly, blood glucose and insulin levels also rise less than would otherwise be expected with the subsequent meal (14).

Why the popular press has touted resistant starch as a “weight loss wonder food”

RS appears to have several beneficial effects that may contribute to weight loss, including decreased blood insulin spikes after meals (as discussed above), decreased appetite, and decreased fat storage in fat cells.  There may also be preservation of lean body mass, though further studies in humans are needed to confirm if there is a significant impact in overall body weight (15).

Further, several studies have shown alterations in the gut microbiome in association with obesity, which subsequently change towards that seen in lean individuals with weight loss (16, 17).  For example, one study demonstrated that the relative composition of the gut microbiota of two predominate beneficial bacteria, Bacteroidetes and Firmicutes, varied considerably in association with body composition.  Specifically, obese individuals often have a higher proportion of Firmicutes to Bacteroidetes, which may be reversed with weight loss, gastric bypass surgery, or treatment with prebiotics (3).  However, not all studies confirm a significant or measurable change in the composition of the microbiome in obese compared to lean individuals, and further studies are needed (18, 19).

Butyrate plays an important role in gut health and decreasing inflammation in the gut and other tissues

As mentioned above, RS intake allows for increased production of butyrate by our gut microbes.  Butyrate acts as a powerful anti-inflammatory agent for the colonic cells, and functions to improve the integrity of our gut by decreasing intestinal permeability and therefore keeping toxins in the gut and out of the bloodstream. (20, 21).  

The SCFAs that aren’t utilized by the colonic cells enter the bloodstream, travel to the liver, and spread throughout the body where they exert additional anti-inflammatory effects.

Resistant starch is also associated with decreased risk of colorectal cancer, thought to occur through several different mechanisms including: protection from DNA damage, favorable changes in gene expression, and increased apoptosis (programmed cell death) of cancerous or pre-cancerous cells (22, 23).

Adding resistant starch to your diet

Some common food sources of RS include green (unripe) bananas, plantains, properly prepared cooked and cooled parboiled rice or legumes, and cooked and cooled potatoes.  See this link for a more complete list of RS quantities in food.

However, if you are on a low carbohydrate diet or don’t tolerate those foods well, you can add RS to your diet without adding digestible carbohydrates.

Bob’s Red Mill Unmodified Potato Starch (NOT potato flour) is one of the best sources of RS with approximately eight grams of RS in one tablespoon.  Potato starch is generally well tolerated even by those who react adversely to nightshades.

Plantain flour and green banana flour are also excellent sources of RS, and there may be benefit to including all three of these sources (specifically alternating your source of RS rather than relying on a single one).

These are relatively bland in flavor and can be added to cold or room temperature water, almond milk, or mixed into smoothies.  But to maintain the benefits of RS, these should not be heated above 130 degrees.

Tim Steele (Tatertot) has written about some of the research on RS supplementation, and in particular the potential further benefit of combining potato starch with psyllium husk fiber to even further increase butyrate production in the colon.

Take it slow

If you choose to try supplementing with RS, start with small doses of about ¼ teaspoon once daily, and very gradually increase the amount as tolerated.  Some increased gas and bloating is expected as your gut flora changes and adapts, but you do not want to feel uncomfortable.  If you experience marked discomfort, then decrease the amount you’re taking for a few days until your symptoms resolve, and then try increasing again gradually.

Studies indicate that the benefits of resistant starch may be seen when consuming around 15 to 30 grams daily (equivalent to two to four tablespoons of potato starch).  This may be too much for some people to tolerate, particularly in the setting of gut dysbiosis, and going above this amount is not necessarily beneficial.

If you experience marked GI distress with even small amounts of RS, this may be an indication of SIBO (small intestinal bacterial overgrowth) or microbial dysbiosis, and you may need to consider working with a healthcare practitioner to establish a more balanced gut microbiome through the use of herbal antimicrobials and probiotics before adding RS or other prebiotics.

Blast from the Past

Probiotics have been a hot research topic over the past few years, and it seems like every week a new study is published that demonstrates the powerful effects of probiotics that extend far beyond simple improvements in digestion.

For example, a study of certain probiotic strains has shown promise for treating the symptoms of celiac disease, and a second study explores the evidence that gut microbes may play a role in the development of celiac disease. And another new study suggests a treatment for autism may one day come in the form of live, friendly probiotic bacteria. These are just a few of the most recent papers to be published on the topic of probiotics and their potential therapeutic benefits.

Last year I wrote an article explaining five other uses for probiotics that go beyond gut health. Specific strains of probiotics have been shown to have a beneficial impact on issues such as depression, nasal congestion, oral health, and acne, just to name a few. As time goes on I believe we’ll discover even more therapeutic uses for beneficial bacteria that can be used in the clinical treatment of a wide variety of diseases.

Research Report

• Saturated fat intake is not associated with an increased risk for heart attack even in those with established heart disease.
• This article reviews the state of the literature on vegetarian diets and athletic performance and more.
• One 30-minute session of vigorous exercise leads to changes in the brain making it more “plastic."
• A new study reveals saturated fats aren't the cause of increased fatty acid in the blood.
• A new study's findings indicate that host genetics influence the composition of the human gut microbiome.
• NIH researchers uncovered links between poor sleep and health issues from obesity to cardiovascular disease.
• Preteens who spent five days camping with no screen time became better at recognizing emotions in other faces.
• Scientists have identified an important factor for how stress processes work in the brain.
• Fruit juice may be a gateway drink for infants who later become obese.

Worth A Look

• How do you spend your energy? If you don’t prioritize your life, someone else will.
• Sometimes we experience moments of intense stress. Learn three do's and don'ts for handling stress in those tough situations.
• The search is on for alternatives to antibiotics. Learn why.
• Mark Sisson was a guest on Dr. Oz, where he discussed how diet can affect chronic pain.
• Turns out a nightcap may not really aid sleep at all—it could be reducing sleep quality.
• When health-related headlines are sensationalized or alarmist, who’s to blame? The answer may surprise you.
• Having positive experiences and a fulfilling life may help prevent mental illness. This article shares tips to help build mental wellbeing.
• Are you walking enough during the day? Find seven tips to add more movement to your work day.

For the Foodies

• Bare Root Girl: Bacon-Wrapped Dates Stuffed with Almonds and Rosemary
• Healing and Eating: Roasted Red Pepper and Tomato Soup
• Phoenix Helix: Rosemary & Shallot Roasted Butternut Squash
• Stinky Kitchen: Gluten-Free Green Bean Casserole
• Gourmande in the Kitchen: Roasted Chestnuts with Sage Browned Butter
• I Breathe I’m Hungry: Zucchini and Sweet potato latkes
• Plaid & Paleo: Pomegranate Balsamic Brussels Sprouts
• VA Is For Hunter Gatherers: Cider-Stewed Mashed Sweet Potatoes
• Everyday Maven: Spiced Maple glazed ham
• The Domestic Man: Seasoned London Broil
• Fermented Food Lab: Probiotic Holiday Relish
• Healthy Nibbles And Bits: Slow cooker applesauce
• Against All Grain: Cranberry Chocolate Gingerbread Cake
• On Sable Hill: Soft and Spicy Ginger Cookies
• Great Food Lifestyle: Cran-Orange Paleo Macaroons
• Cook Eat Paleo: Peppermint Hot Chocolate
• The Healthy Foodie: Quick and Easy Dairy Free Eggnog

This is a guest post written by staff clinician Amy Nett, MD.

Meet your microbiome

If you commonly read this blog, or listen to Chris’s podcast, you have undoubtedly developed an appreciation for the trillions of microbial organisms that normally inhabit a healthy small and large intestine. Most of these microbes are bacteria that have co-evolved with humans, depending on us for their survival just as we depend on them for our health and well-being. For example, we provide nutrients for bacteria which then keep our immune system in check, digest certain carbohydrates that would be indigestible to us, and make vitamins and other important compounds that we would otherwise be unable to produce. This wonderful, symbiotic relationship is what makes up your microbiome. A (hopefully) harmonious collection of microorganisms in our guts that aid in so many of our body’s vital functions.

The microbiome changes with disease

Our microbiome can affect us in multiple, profound ways ranging from how we store fat (1, 2, 3) to whether we feel happy, anxious or depressed (4, 5, 6). When the normal gut microbial communities are disturbed, whether you've used antibiotics or are suffering from a bacterial infection, it can lead to dysbiosis or small intestinal bacterial overgrowth.

Antibiotics, C-sections, poor diet, and autoimmune disease; what’s the connection?

Dysbiosis is associated with a growing number of diseases such as Crohn’s disease (7), ulcerative colitis (8, 9), irritable bowel syndrome (10), and both type 1 and type 2 diabetes (11, 12). You'll find that the variety and balance of gut bacteria is often different in patients with chronic inflammatory conditions as compared with healthy individuals. Research now suggests that these diseases are not due to any single bacterium, but from changes to the entire microbiome. And since a large part of our immune system is found within the gut, several diseases resulting from dysbiosis are autoimmune diseases.

What is autoimmune disease?

Autoimmune disease can be thought of as a case of mistaken identity: the immune system targets normal proteins as if they were harmful foreign invaders and becomes overactive. Normally, the immune system responds to a specific pathogen, like a cold virus, and once that pathogen is cleared, the immune system can settle down to its normal state. In the case of autoimmune disease, the immune system often stays on high alert, resulting in chronic inflammation.

With more than 80 different types of autoimmune disease, this class of disease has been particularly difficult to understand: what exactly causes the immune system to attack otherwise normal healthy human cells?

The three legged stool of autoimmune disease.

Dr. Alessio Fasano, a world-renowned gastroenterologist, expert in autoimmune disease, and pioneer in understanding celiac disease, describes autoimmunity as a three-legged stool, meaning that three essential components must be present in order for someone to develop an autoimmune disease:

1. Genetic predisposition: certain genes make individuals more likely to develop certain diseases.
2. A trigger: specific antigen, or protein, that the immune system recognizes as a threat (real or not), that sets off the cascade of over-activation. In the case of celiac disease, the trigger is gluten. However, in the vast majority of autoimmune diseases the trigger remains unknown.
3. Intestinal permeability (also referred to as “leaky gut”): this increased permeability means that the normally tightly knit cells of the intestines are weakened and "leaky". This allows large compounds, such as proteins from food or bacteria, entry into our bloodstream. Leaky gut can occur due to any number of reasons such a food sensitivities, gut infections, or chronic stress.

Does the microbiome play a role in autoimmune disease?

Increasing attention is being paid to the importance of the microbiome in health and disease—even slight imbalances have far reaching consequences. It has become clear that the microbiome profoundly affects our immune system, and new research provides insights into how changes in the microbiome can act as the trigger in developing autoimmune disease.

A recent paper reviewed some of the most recent research that the health of our microbiome may be the key factor in whether or not we develop an autoimmune disease (13). Below are a few of the key points:

Two of the most significant autoimmune diseases in terms of global morbidity and mortality are Type 1 diabetes mellitus, and rheumatoid arthritis (RA).

Type 1 Diabetes Mellitus

Type 1 diabetes (T1D) is an autoimmune disease with antibodies that destroy the insulin-producing cells of the pancreas, leading to insulin deficiency and blood sugar irregularities. Most often patients are diagnosed in childhood or adolescence, and there is a known genetic association. However, in studies with twins (who share the same genes), only about 50% of twins both go on to develop the disease. This further supports the idea that the development of disease depends on more than genes alone. For instance, immigrants have a risk of developing T1D that is dependent on their place of residence, not their country of origin.

Studies looking at differences in the gut microbiome between people with T1D and healthy individuals have found the following differences:

• Children with T1D have a smaller amount of beneficial bacteria.
• Children with T1D have less stability and diversity of bacteria in their gut.
• There are significant differences in both bacterial composition and metabolic capabilities between those with T1D and without.
• After treatments to normalize blood sugar in T1D patients, there was also a return to microbial diversity in those individuals.

Overall, the research is convincing that T1D is associated with a disruption in the normal microbiome. At this time, no single organism is responsible for the onset of this disease. However, in genetically predisposed individuals a disruption of the normal microbial communities provides an environment in which the disease may develop.

Rheumatoid Arthritis

Rheumatoid arthritis affects about 1.5 million people in the United States, and up to 1% of adults worldwide. It is an autoimmune disease that affects many of the joints throughout the body, most commonly the joints of the wrists and hands.

As with T1D, there is a known genetic association.  However, studies with twins again prove that genes play even less of a role in the development of RA when compared with T1D. Research again supports a relationship between the microbiome and the development and progression of RA. Of particular interest is the role of the bacteria living in ones mouth.

Periodontal disease and RA

• Patients with newly diagnosed RA have higher rates of severe periodontitis and more tooth loss despite normal oral hygiene compared to healthy individuals.
• The severity of a patients periodontal disease can be correlated with the severity of their RA disease activity.
• Specific bacteria that live in the mouth have been shown in animal models to increase the severity of joint disease.
• Specific bacteria are present in both dental plaque of patients with RA, and in joint fluid.

Many other autoimmune diseases are being studied to look for related dysbiosis, providing increasing evidence that disruption of the microbiome is associated with the development of some autoimmune diseases. Though there is clear correlation between changes in the microbiome and autoimmune disease, causation is not yet clear. This means we cannot say if it is the dysbiosis that leads to autoimmune disease, or if dysbiosis is the result of an overactive and misdirected immune system.

One more reason to take care of your gut?

As if we didn’t already have enough reasons to take care of our gut and help our beneficial bacteria thrive, it may be that decreasing our risk of developing an autoimmune disease is one more important reason to be good to your microbiome.

Now I’d like to hear from you: Have you made changes in your diet or gut health that have affected your autoimmune disease? Do you notice flares or exacerbations of your autoimmune disease when you eat certain foods?

About Amy:  Amy Nett, MD, graduated from Georgetown University School of Medicine in 2007.  She subsequently completed a year of internal medicine training at Santa Barbara Cottage Hospital, followed by five years of specialty training in radiology at Stanford University Hospital, with additional subspecialty training in pediatric radiology.

Along the course of her medical training and working through her own personal health issues, she found her passion for functional medicine, and began training with Chris in June of 2014.  She has recently joined his clinical practice to work with patients through a functional medicine approach, working to identify and treat the root causes of illness.  Similar to Chris, she uses nutritional therapy, herbal medicine, supplements, stress management, detoxification and lifestyle changes to restore proper function and improve health.

A lot of my patients are curious about this. I’m not going to say that we’re seeing more of it, because I’m not sure if that’s actually true. I think the awareness of it is higher, so we’re paying more attention to it. It may also be true that we’re seeing more of it, and there are some reasons why that might be the case, which will be revealed as we go through this answer. We’ll go into the basics of what histamine is and then we’ll talk about why histamine might be a problem for some people. Then I’ll finally get around to discussing diet for histamine intolerance. In this episode, we cover: 4:03  What Chris ate for breakfast 6:20  What is histamine? 11:49  Why histamine might be a problem for some people 17:36  Recommended diet for histamine intolerance [powerpress] Steve Wright: Good morning, good afternoon, and good evening. You are listening to the Revolution Health Radio show. This show is brought to you by 14Four.me, the 14-day healthy lifestyle reset program. If you’re someone who’s trying to put all the pieces of great health together that Chris talks about—such as diet, sleep, movement, and stress—but can’t seem to make them fit in your lifestyle, well, number one, I totally understand; and number two, this program is for you. So go check out 14Four.me, Chris’ new lifestyle reset program. You’re listening to the Revolution Health Radio show. I’m your co-host, Steve Wright from SCDlifestyle.com. With me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, how you doing? Chris Kresser: Hey, Steve. I’m good. How are you? Steve Wright: I’m tuned up, man. Chris Kresser: I hear that. Steve Wright: I got a big old workout in today, and I just got energy. Chris Kresser: All right. I’d like to see that. Yeah, I’m not there yet. I’m going to the gym after this. So hopefully, I’ll catch up with you. Steve Wright: Are you guys getting hit by the polar vortex right now? Chris Kresser: It definitely feels colder than normal here. There’s no doubt about that. I feel the fall setting in, which is cool. I like the fall. It’s my favorite season. But yeah, I’m having to make a little adjustment. Because up until I left last week—I spoke at the Weston A. Price conference this weekend on the acid-alkaline hypothesis. When I got on the plane, it was like 75 degrees. When I got off the plane in Indianapolis, it was not 75 degrees, definitely. I was like, “Oh yeah, I live in a little bubble called California, where the weather is really different than other places.” Then when I came back, it was actually fairly chilly as well. Steve Wright: You said fall. And I just looked out on my deck, and there’s six inches of snow out there. Chris Kresser: You’re like, “Hey buddy, that’s winter.” Steve Wright: Yeah. Chris Kresser: Well, it’s all good. I mean, it’s sunny and nice out, but it’s just a little chilly. I’m not complaining. Of course, I have nothing to complain about. It’s all good. Steve Wright: So how was the talk? Chris Kresser: The talk went well. It was fun. It was well-received. You know, it’s another one of those myths that just keep sticking around despite a lack of evidence that really supports it. If this is new to anyone listening, you can Google “Chris Kresser acid-alkaline.” There are a couple of blog posts that we wrote about that a while back. I’ll probably eventually record the talk as a screencast and make it available for free, because there’s more updated and a deeper level of information in the talk, because it was a 1-hour-and-15-minute presentation. Steve Wright: Wow. So are you saying that your myth-busting power got even stronger? Chris Kresser: Took it up to a new level. The live talks, I like to do that. Also, I make an effort to make it accessible and fun, so that people aren’t bored out of their mind listening to me talk for 1 hour and 15 minutes. It was good. And it was good that I saw Chris Masterjohn. I watched him and he did a whole day on fat-soluble vitamins, which was pretty cool. I caught a fair amount of that. Then we had a couple of meals together. It’s always good to catch up with him. So it was a nice time. Steve Wright: Were you referring to him by his new nickname, Professor J? Chris Kresser: The Professor? Steve Wright: The Professor, okay. Chris Kresser: Yeah, I was. And he’s settling into his new position. He likes it a lot. He’s super busy. You know, he had to prepare last-minute for a couple of classes he’s teaching. But it’s great. Great to see him getting that kind of position and recognition.

What Chris ate for breakfast

Steve Wright: Awesome. Before we dive into this week’s question, Chris, did you have anything for breakfast today? Chris Kresser: It was pretty standard today, Steve. Nothing exciting. I had scrambled eggs, sauerkraut, and some bacon. Then I had some coffee with cream. What can I say? Steve Wright: Gosh, Chris, I’m let down. I’m so sad. Chris Kresser: I’ll try to do better next time. All right. We have a great question from Genevieve today. It’s about histamine, which I know is a hot topic. A lot of people want to know more about it. I think this is going to be a really helpful show for a lot of folks. Let’s give it a listen. Genevieve: Hi. Just wondering what kind of diet you recommend most for histamine intolerance, because I know there’s a few out there. The typical low-histamine diet includes grains. I think The Low Histamine Chef limits animal protein. Then, of course, you have GAPS, which is full of nourishing foods, but many are high histamine. And that’s what kind of caused my problem to begin with, was the high-histamine foods on the GAPS diet. So I’m just wondering what you would recommend most to follow to try and heal it, if it can be healed, although I know sometimes it might be related to methylation. Thanks. Chris Kresser: Thanks, Genevieve, for sending that in. As I said, this is definitely a hot topic. We receive a lot of questions about it. A lot of my patients are curious about it. I’m not going to say necessarily that we’re seeing more of it, because I’m not sure if that’s actually true. I think just the awareness of it is higher, so we’re paying more attention to it. It may also be true that we’re seeing more of it, and there are some reasons why that might be the case, which will be revealed as we go through this answer. But let’s talk a little bit about basics, and then we’ll go into—basics of what histamine is, and then we’ll talk about why histamine might be a problem for some people. Then I’ll finally get around to answering her actual question about the diet for histamine intolerance. But I think it’s important to kind of maybe correct some misconceptions and go over some of the basics before we do that. Steve Wright: That sounds like a plan, man. What is histamine?

What is histamine?

Chris Kresser: Histamine is an organic nitrogen compound that’s involved in local immune response and systemic inflammatory responses. It regulates physiological function in the gut and it acts as a neurotransmitter. It’s produced by immune cells called basophils and eosinophils and also mast cells, all of which are typically involved in allergic responses, among other things. To bring this home, if you’ve ever been stung by a bee or bitten by a mosquito and you see the redness and swelling there, that’s histamine-mediated. So everyone’s had experience with histamine. What it does in the inflammatory response is increases the permeability of capillaries—which are the small blood vessels—to white blood cells and some proteins, so that those white blood cells can engage the pathogens or the toxin in the tissue. From a dietary perspective, histamine is derived from the amino acid histidine, which is found in many different foods, especially fermented foods. We’re going to talk more about that later. But it’s also produced by some of the species of bacteria found in our gut. That is actually one reason why it’s possible that histamine intolerance is on the rise, because of this profound shift that we’ve seen in our gut microbiota over the past several decades. So just as celiac disease and gluten intolerance is probably on the rise because of that, I think it’s at least plausible that other conditions, like histamine intolerance, might be on the rise because of that as well. Steve Wright: When I think histamine, the first thing that comes to my mind is allergies. Is that a good association or are there a lot of other things going on? Because I know you used the bee analogy there. Chris Kresser: It is a good association. Like I said, basophils, eosinophils, and mast cells are all very much involved in the allergic response, and histamine mediates that allergic response. The itchy eyes, watery eyes, itchy skin, all the things that you associate with allergy and atopy, those are definitely mediated by histamine. So if someone has a lot of allergies or they’re having kind of allergic responses that they don’t necessarily associate with any particular trigger, that could be an issue with histamine. Steve Wright: When you say mediated, what does that mean? Chris Kresser: It means that histamine is probably causing the symptom. The excess production or the inability to break down histamine is causing those symptoms. And it’s not just doing it to irritate you. Histamine actually, like I said, plays an important role. It increases the permeability of capillaries to white bloods cells, so that the white blood cells can do what they’re supposed to do and they can get there. So we need histamine. The problem isn’t histamine itself; it’s when people have problems breaking it down or they’re overproducing it. I do want to point out that this phrase we’re using of histamine intolerance, if you look it up in the scientific literature, you’ll find a couple of papers that talk about it, but it’s not a legitimate medical condition, like diabetes or something, that has a clear etiology and pathology, and a clear treatment. A lot of people will argue that histamine intolerance doesn’t exist and it’s imaginary. I think just like adrenal fatigue and some of the other things that we talk about, it’s true that it doesn’t exist as a distinct disease entity. But it’s also true, and there’s plenty of research to support this, that there can be problems with histamine breakdown. And if that’s the case, excess histamine can certainly cause symptoms, and that’s well-established. So we use the phrase “histamine intolerance” just as a colloquial way to talk about it. But just understand that if you go to doctor and start talking about histamine intolerance, they’re probably going to look at you strangely. There’s actually a new term that’s been proposed for this syndrome. It’s mast cell activation syndrome (MCAS), which we’re going to talk about in a second. There are a few papers that have been published about that. So if you want to impress your doctor with a fancy term and show him/her some scientific papers that support this, you can bust out the MCAS term. All right. Steve Wright: Just dropping it! Chris Kresser: So I’ve mentioned that the real issue with histamine is—well, let’s go back to the background. Once histamine is produced, it’s broken down by two primary enzymes. One is histamine N-methyltransferase, and the second is diamine oxidase. For a long time, it was thought that diamine oxidase played the major role in breaking down histamine. And it probably does. But lately, there’s been a little bit more focus on histamine N-methyltransferase. If you recognize that term methyl, you know, we’ve been talking about methylation and methyl donors lately on the show. That’s another hot topic. They’re definitely related, which we’re going to discuss. So the key thing to understand here is that for most people, histamine is not a problem. Histamine is a normal part of the physiological response. If you get exposed to something, histamine can help the inflammatory reaction, and then the diamine oxidase or methyltransferase breaks it down. That’s the end of the story. You never need to think about histamine, it’s not an issue. That’s what’s true for most people. But there are potential issues that can make histamine a problem for some people.

Why histamine might be a problem for some people

The issues are broken into two categories. One would be overproduction, so making too much histamine. The second would be inability to break it down properly. Let’s look at each of these in turn. Overproduction typically would have two main causes. The first could be gut dysbiosis, because we know that certain types of bacteria produce histamine and certain types of bacteria degrade it. So if we have an overrepresentation of the kinds of bacteria that produce histamine, then you could theoretically have excess histamine production. That could cause some of these histamine intolerance issues that we’re talking about. The second cause is something called mast cell activation syndrome, which I just mentioned. This is still a relatively poorly understood entity. There was a paper. I think the first papers were published on it just a couple of years ago. There’s one kind of review paper in 2013. Basically, it involves an overactivation of mast cells, which are the cells that primarily produce histamine. We don’t really know what causes this. Certainly, genetics play a role. There are a lot of mutations that can affect mast cells and the production of histamine. But there are likely other causes that haven’t been well-defined at this point. Steve Wright: Chris, how many mast cells do we have in our gut? Chris Kresser: I don’t know the specific number, but there are lots of mast cells all throughout the body. The production and breakdown of histamine is particularly notable in the gut. This is why histamine intolerance can lead to gut issues, and disturbance in the microbiota can lead to excess production of histamine or inability to break it down. So speaking of inability to break it down, that’s the second major problem. That can be broken into three subcauses. One would be impaired methylation, because histamine N-methyltransferase requires methylation to function properly, that enzyme. So if you’re not methylating properly, you won’t break it down. Second, not enough histamine-degrading bacteria. So dysbiosis, again. The third reason would be a genetic issue with diamine oxidase production. Some people just genetically don’t make enough diamine oxidase to break down histamine. So those are the main problems with histamine and the causes of those problems. I just want to point out, before I go to the symptoms, that there are other mutations and genes related to the methylation pathways that can cause histamine issues. One is monoamine oxidase (MAO). If you’ve done a 23andMe gene profile and then you’ve run it through Genetic Genie or MTHFR Support or something like that, if you look on there and you’re homozygous for MAO, then there’s a decent chance that you may be sensitive to histamine. So that’s something to be aware of. The symptoms of histamine intolerance are very similar to some of the symptoms of allergies. You have itching of the skin, eyes, ears, and nose; hives; tissue swelling, especially facial and oral tissues; a feeling of throat constriction or tightness; hypotension, like a drop in blood pressure, especially you get dizzy when you stand up quickly; tachycardia, so rapid heartbeat, increased pulse rate; palpitations; symptoms that kind of resemble anxiety or panic attack; chest pain; nasal congestion; runny nose; seasonal allergies; conjunctivitis, which is irritated, watery, reddened eyes; some types of headache, like migraine can be related to histamine; fatigue; confusion; irritability; digestive upset, especially heartburn and reflux; and much more rarely, occasional loss of consciousness, blacking out just for a few seconds that’s unexplained by other causes. Steve Wright: So Chris, that’s like a list of symptoms that if we stack them on like a severity scale, goes from annoying to life-threatening. Chris Kresser: Yes. Steve Wright: Would it be safe to assume that the lower you are maybe on your health ladder, the more this could be an issue for you? And as you sort of have more things in balance as far as health-wise, maybe histamine issues are going to be more on that annoyance scale? Chris Kresser: I think the health status is one factor that determines sensitivity. But there are other factors that don’t necessarily relate to current health status, which are genetic. So if somebody has homozygous MAO mutation and they’re also homozygous for MTHFR mutation and they have very poor methylation because of that, and then they also have a defect in diamine oxidase, an inability to break down histamine once it’s produced, and then maybe they even have defects that lead to overactivation of mast cells and production of histamine, that person’s probably going to be pretty sensitive to histamine even if they’ve got everything dialed in. I don’t know how many of those people there are that have that unique constellation of things together; probably not that many. But they may always need to be careful, for example, with fermented foods, and some of the foods that we’re going to talk about that are high in histidine, and therefore, histamine. And/or they may need to use some natural antihistamine support or take some diamine oxidase as a treatment.

Recommended diet for histamine intolerance

Now, let’s talk about the low-histamine diet, because this is something that can be really helpful symptomatically. Of course, for longer-term healing, you want to address the underlying cause and things like that, dysbiosis or methylation problems, but the diet is an important part of the treatment always and getting some symptom relief. Fermented food, as I mentioned, is the biggest offender. That’s because the bacteria during the fermentation process produce histamine. So things like wine, cheese, yogurt, kefir, vinegar, all of which are healthy foods otherwise, are like kryptonite for people who have serious histamine intolerance. I’ve often had patients come and say, “God…” They’ll fill out the diet survey and they’ll mention something about how they’re intolerant of these things. It’s kind of a revelation for them to learn about histamine, because they’d never been able to figure out what the common thread is between all of these foods that they’re reacting to. Seafood, unfortunately—I say unfortunately because it’s such a healthy food, and it’s underrepresented already in many people’s diets—but seafood, shellfish, finfish, fresh, particularly smoked or canned seafood, is also really problematic from a histamine perspective. Eggs; processed, cured, smoked, and fermented meats like bacon, sausage, salami, pepperoni; leftover meat, because after meat is cooked, the histamine levels increase due to microbial action as the meat sits; all fermented milk products, of course; citrus fruits; berries; dried fruit; spinach; tomatoes; artificial food colors and preservatives; certain spices like cinnamon, chili powder, cloves; herbal teas; alcohol; chocolate; cocoa; and then vinegar and foods containing vinegar, such as pickles, relishes, ketchup, and prepared mustard. Steve Wright: No wine, no pickles, and no chocolate. We have to help these people. Chris Kresser: Sorry, I just removed all of your favorite foods. Don’t hate me. It’s not my fault. I didn’t make this stuff up. If you didn’t get that down and you’re listening to this in your car, don’t worry about it. If you Google “Chris Kresser histamine,” you’ll see a blog post that has this list. Also, don’t freak out if you have to remove these foods for a period of time to feel better. Because in most cases, when you do address the underlying causes—like the gut dysbiosis and methylation—then most people are able to add some of these foods back in without any ill effects. Now I do want to point out that there’s a huge spectrum in terms of histamine intolerance. You were probably hinting at this, Steve. But there are some people who, red wine, they can’t tolerate. But almost everything else on this list, they do okay with. Then there are people on the far end of the other spectrum—and there are a lot fewer of these, but I’ve had some patients who fit this profile—who, the only meat they can tolerate is meat that’s literally been slaughtered. Like, they have to go to the farm right after it’s been slaughtered and get it, because if the meat even sits for a little bit, the time that it takes to get to the store and sit in the meat case at the store, it’s already got more histamine that they can tolerate. A couple of my patients have had to go on almost like a completely plant-based diet, because all of the animal products, they haven’t been able to tolerate. Over time, fortunately, that changed a little bit for them. And they were among the sicker patients that I had. So again, like I said, it’s not very common. But just know that there’s a big spectrum, and you need to really experiment a lot with this stuff to figure out what works for you and what doesn’t work for you. Steve Wright: I think Chris points this out in the article, but if we have anything that can help you with that, just remove it all at once. Just remove it all at once. Just take the pain. If you think of it as painful to get rid of some of these foods, which I’m sure some people do, just do it all at once. Don’t just mess around and say, “Okay, I won’t do wine for a little while or chocolate for a little while,” because you’re not going to figure it out. Chris Kresser: That’s never going to get you anywhere. That’s a great point. You have to just suck it up, take it all out, and then start adding stuff back in one by one. That’s the only way to do it. It’s really laborious, but it works. And both Steve and I know this from experience, working with a lot of people. You can get your diamine oxidase levels tested actually. It’s a serum test. So you can get diamine oxidase. You can get serum histamine tested. Serum tryptase, T-R-Y-P-T-A-S-E, is considered one of the most sensitive markers for mast cell activation syndrome. So you can run some tests, and that might be helpful in seeing where the problem lies. For example, if you run the test and your diamine oxidase levels are normal but your histamine is very high, that means that you may not have an issue with breaking down histamine. It may be more of an issue of overproduction of histamine due to gut dysbiosis, for example. In that case, fixing the gut and doing a low-histamine diet would probably be enough, without any additional intervention. However, if you get tested and your histamine levels are normal, but your diamine oxidase is really low, then that suggests you have possibly a genetic deficiency of diamine oxidase. And what’s probably going to help you more is to take diamine oxidase, which you can take as a supplement. Seeking Health sells it as Histamine Block. There’s also DAOSin, D-A-O-S-I-N, from Swanson. There’s Histame. They’re all basically the same thing. It’s actually taking diamine oxidase, the enzyme that breaks down histamine. You take it with meals. That can help a lot. Then there are some natural antihistamines that are probably a better idea for excess histamine production. Those include quercetin; bromelain, which is an enzyme; pine bark extract, which is also known as Pycnogenol. That’s pretty expensive, but it can be effective. Then there are, as I said, certain species of bacteria that break down histamine and certain species of bacteria that produce histamine. So Lactobacillus casei, Lactobacillus delbrueckii, and Lactobacillus bulgaricus, which are typically in yogurt and fermented dairy products, those are notorious histamine producers, which is why fermented dairy can be like kryptonite. Lactobacillus plantarum and Bifidobacterium infantis are two histamine degraders. It’s quite difficult though to get Bifidobacterium infantis separately as an individual strain, without other strains that are also in it. But it is possible to get Lactobacillus plantarum that way, just as a single strain, pretty easily. So that can be a good one to take. Then soil-based organisms like Prescript-Assist, which I like for many other reasons. This is another reason that I like it. There’s not a lot of research on this, but my experience is that soil-based organisms tend to be neutral or even histamine-degrading. They tend to be tolerated pretty well by people with histamine issues. That’s it, Steve. I hope that was helpful, Genevieve, and that we answered your question. Steve Wright: Nuh-uh. I’m not letting you off the hook just yet, Chris. Chris Kresser: All right. Steve Wright: I have one question here to follow that up. So that was all, like, at the mast cell level. But the mast cells and everything we’re talking about here is part of—the inflammation pathway is part of the immune system. And I feel like this podcast would not be complete with at least a couple minutes about me asking, is there some play here with maybe improving your hormone levels, maybe your anti-inflammatory hormones—cortisol, for instance, if you’re having adrenal issues—something like that, that would be part of this whole equation as well, that people with histamine intolerance could get lost in the forest? Chris Kresser: Yeah. No doubt, Steve. The reality is, we do these 25-minute shows—or 30 minutes—and we focus on a single topic. But that’s never really how it works in practice, right? There’s always a person that’s attached to one of these topics, and they don’t just have histamine intolerance. They have several other issues: adrenal fatigue, autoimmune disease, and whatnot. Certainly, all of those things have to be addressed for a successful outcome. It’s a great question. It’s true that mast cells, basophils, and eosinophils are part of the immune system. And if you have a hyperactive or underactive or swinging between hyperactive and underactive immune system, then that is going to exacerbate the problem. If you have high cortisol, low cortisol or inappropriate production of cortisol throughout the day, that’s going to cause an inflammatory response and affect probably histamine production in different ways. Certainly, imbalances of sex hormones can affect that. And as we mentioned, dysbiosis, but also several other gut issues. So SIBO and parasites and intestinal permeability and all of the potential things that can go wrong can affect it. There are probably the things that we’re not even thinking about at this point that can affect it as well. So certainly, you need to always consider the entire picture. But I can say with some confidence that the things that we’ve talked about in this show are probably the most important from the histamine perspective, and will give at least some relief while you’re working on those other bigger picture concerns. Steve Wright: Awesome. Thanks for wrapping that up and bringing it back up to the top. Chris Kresser: Sure. Good question. A couple of announcements. The paperback version of my book is coming out on December 30^th at the end of this year. It’s been renamed as The Paleo Cure instead of Your Personal Paleo Code, which is the hardcover title. There are a number of reasons behind that, which I’ll talk about on a later show. But it’s the same book, just a different cover, different name. We’re going to be doing some cool stuff around the book launch in December, so keep an eye out for that. We’ll be back with some more details. 14Four has been just a blast to see how many people have signed up. I think almost 2,000 people have signed up. Lots of folks are well into their 14-day reboot now. They’ve been through the preparation phase, and they’re starting. They’re having a great experience with it. We’re getting incredible feedback. There’s just a ton of activity in the Facebook group and community building around it. It’s just really exciting for me to see that this is really hitting in the way that I wanted it to hit. I know, from my own experience and from working with so many people, that it’s not really about information. Like, a lot of people know what to do at this point. It’s just about implementing it in your life. That’s the hard part. And that’s really what 14Four is about. So it’s just really—I’m excited to see the success that people are having and putting all these things together. If you haven’t checked it out yet, it’s 14Four.me. Keep the questions coming. We’ll talk to you. We’ll be back next week. Steve Wright: Thanks, everyone, for listening. In-between episodes, if you’re wondering what Chris is researching—when he’s preparing for these episodes and his blog posts, a lot of times, he’s posting new things that he’s discovering on Facebook and Twitter. So if you’re not, I would encourage you to go over to Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser to get updated ideas and things that he’s working on and things that he’s found. Thanks for listening. We’ll see you on the next show. Chris Kresser: Thanks, everyone. Bye-bye.

There's no denying that celiac disease (CD) is more prevalent now than ever. In the US, rates of CD have increased at least 5-fold over the past few decades, and prevalence in Finland has doubled. (1, 2, 3) The incidence of CD has also increased four-fold in the UK and three-fold in the Netherlands in the past 20 years, and the incidence of pediatric CD in Scotland has increased 6.4-fold. (4, 5, 6)

So naturally, everyone is wondering - why? We know that there’s a strong genetic component to celiac disease (and our ability to detect the disease has vastly improved), but the rising rates have occurred too quickly to be explained by a genetic shift in the population.

Besides, the genes that predispose an individual to CD are actually relatively common in the population, but only a very small percentage of those people actually develop the disease. In other words, genetics appear to be necessary - but not sufficient - for someone to develop CD.

Can the overuse of #antibiotics trigger celiac disease?

Antibiotics can cause intestinal dysbiosis and infection

Clearly, something has changed in the environment to trigger celiac disease in a higher proportion of genetically susceptible people. Multiple factors probably play a role, but evidence indicates that one big factor is the intestinal microbiota. And a major contributor to disordered intestinal microbiota is antibiotic overuse.

In my previous article on the effects of antibiotics, I reviewed several studies that demonstrate how drastically antibiotics can alter the gut microbiome. Just a single course of antibiotics can reduce the richness and diversity of the intestinal microbiota, and in many cases, people never completely regain the diversity they lost.

Even if a person doesn’t develop an overt, clinically-diagnosable infection such as C. difficile, imbalances in the types of bacteria that colonize the gut can still cause serious problems. But to understand how antibiotic-induced gut dysbiosis could trigger celiac disease in genetically-susceptible individuals, it helps to first understand some of the basic mechanisms behind celiac disease.

Celiac disease involves an immune reaction to both gliadin and tissue transglutaminase

The biological mechanisms behind celiac disease are complicated and still not fully understood, but the general idea is that gluten - a group of proteins found in wheat, rye, and barley - triggers an autoimmune response that results in severe damage to the epithelial lining of the intestine.

Gliadins and glutenins are the two main components of gluten, with gliadins being the primary trigger for celiac disease. These proteins are very difficult for the body to digest fully, but in most people, this isn’t a problem. However, in people with celiac disease, certain cells (known as “antigen-presenting cells”) get a hold of these large, undigested fragments of protein and present them to T-cells, triggering an immune response. (7, 8)

An enzyme called tissue transglutaminase (TG2) is also important in the development of CD. This is because antigen-presenting cells only bind certain types of proteins, and they don’t usually bind normal gliadin fragments. (9) On the other hand, TG2 readily binds gliadin, and actually modifies it to make the gliadin much more attractive to antigen-presenting cells. This vastly increases the likelihood of an immune response.

Once this happens, the body starts creating antibodies against gliadin. But because the gliadin is usually bound to TG2, the body also creates antibodies against TG2, its own enzyme. This attack of “self” is what earns CD the classification of “autoimmune.”

Intestinal dysbiosis and infection can lead to up-regulation of tissue transglutaminase

In healthy individuals, TG2 plays a role in tissue repair, as well as in other processes such as regulation of cell death; it’s not an enzyme that’s “supposed” to interact with gluten. (Interestingly, TG2 also plays a role in other diseases, such as Parkinson’s and Huntington’s, by modifying proteins that it isn’t supposed to modify.) (10)

Most TG2 appears to be either stored safely inside cells or inactive under normal conditions, and is only activated in the event of tissue injury, bacterial or viral infection, or another source of inflammation. (11, 12) This indicates that tissue damage or inflammation in the intestine (and subsequent TG2 up-regulation) might actually be necessary for the development of CD.

Without substantial TG2 activity, it’s unlikely that the antigen-presenting cells would bind and present enough gluten fragments to provoke a major immune response. But a bacterial or viral infection could create inflammation and tissue damage that would activate TG2, and thus trigger the cascade of events eventually leading to celiac disease.

Intestinal dysbiosis and infection can contribute to leaky gut

Another factor to consider is the location of tissue transglutaminase. Nearly all TG2 is found in the sub-epithelial region of the intestine, a place that gluten shouldn’t have access to. This means the intestinal barrier would need to be compromised in some way for gluten proteins to significantly interact with TG2. (13)

This fits with previous work done by researchers such as Alessio Fasano, who have hypothesized that a person cannot develop an autoimmune condition such as CD if they don’t have leaky gut. If the intestinal barrier is intact, the immune system will never “see” the antigens, so it won’t mount an immune response.

But one big risk factor for developing leaky gut is intestinal dysbiosis or infection. Bacterial components such as lipopolysaccharides can induce inflammation and increase intestinal permeability, which would allow gluten into the sub-epithelial region of the intestine where it could be modified by TG2 and trigger CD. (14)

Candida infection may trigger celiac disease through cross-reactivity

So far, we’ve been talking about dysbiosis in a general sense, but there’s evidence that specific microbes could trigger celiac disease as well. A recent study (hat tip to Questioning Answers for the find) found that an overabundance of the yeast Candida albicans could contribute to the development of CD, and unfortunately, antibiotic use is a big risk factor for developing a candida infection. (15)

Candida is a normal part of the intestinal microbiome of healthy individuals, but problems can arise when it overgrows relative to other inhabitants of the intestine. Remember how tissue transglutaminase (TG2) readily binds gliadin? Well, it turns out that candida expresses a protein named Hwp1 that also binds TG2, potentially leading to immune activation and cross-reactivity with gluten.

The study found that people without CD who had candida infections produced anti-gliadin antibodies, as well as the expected anti-Hwp1 antibodies. People with CD produced antibodies to both proteins as well. This means that in theory, a person who is genetically susceptible to CD but who doesn’t have the disease could develop the disease in response to a candida infection.

So, what does this mean for you?

As you can see, there are several ways in which antibiotic overuse and subsequent intestinal dysbiosis or infection could lead to the development of celiac disease. As I’ve said before, antibiotics can be lifesaving and are necessary in some situations, but that doesn’t mean they’re free of consequences.

It’s becoming more and more clear how vitally important it is to use antibiotics responsibly, whether that’s not using them at all, or properly rehabilitating the gut during and after a course when they’re deemed necessary.

Now I’d like to hear from you. If you have Celiac disease, do you have a history of antibiotic use prior to the expression of the disease? What do you think about this theory? Share your opinion in the comments below.

Chronic sinusitis (also known as chronic rhinosinusitis, or CRS) is one of the most common human diseases, affecting 1 in 7 American adults. And like many other modern, chronic conditions, its prevalence appears to be increasing. CRS is a debilitating and often intractable disease. Over 20 percent of patients are unresponsive to drug therapy, and up to 40 percent of patients do not respond to surgery. The conventional viewpoint is that CRS is caused by the presence of certain harmful species of bacteria, such as Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. (1) In other cases, CRS may result from an immunologic reaction to fungi that colonize the sinuses. (2) Fungal species associated with this syndrome include Bipolaris specifera and Aspergillus, Curvularia, and Fusarium. However, in a recent paper out of the University of California, San Francisco, Dr. Susan Lynch demonstrated that the primary difference between patients with CRS and control subjects was not the presence of any particular pathogenic species (which both groups had in similar amounts), but the overall diversity of the sinus microbiome. (3) This discovery has important implications for how we can successfully treat CRS, and I will come back to it later in the article. But first, let’s take a step back and discuss the sinus microbiome—since this may be the first time you’ve heard about it.

The microbiome: it’s not just about the gut!

If you’ve been following this blog, listening to my podcast, or have read my book, you’ll know that the gut microbiome is one of my favorite topics. But I’m not alone. Even mainstream media outlets like The New York Times, Time, The Wall Street Journal, and FOX News have done major stories on the gut microbiome and its importance in health and disease. It’s no longer an exotic concept that only scientists and health care professionals discuss; it’s now a household term.

Could probiotics be the answer to chronic sinusitis and nasal congestion?

Yet while it’s true that the majority of microbes that comprise our microbiome live in the gut, it’s also true that we have microbes in other areas of our bodies that play similarly important roles in maintaining health and preventing disease. These areas include the skin, vagina, penis, mouth, respiratory tract, and—you guessed it—the sinus cavity. Prior to the development of DNA/PCR technology, our ability to determine the composition of microorganisms in these various areas was extremely limited. But thanks to recent advances in technology, we now have a much better idea of what “normal” and “abnormal” microbiomes look like—not only in the gut, but also on the skin and the penis and in the mouth, respiratory tract, and sinuses. This understanding has profound implications for how we view the pathogenesis of diseases like CRS, and in turn, what treatment options might be available to patients in the future.

It’s the forest that’s important, not the trees

As I was reading Dr. Lynch’s seminal paper, I came across the following quote, which summarizes the importance of these recent discoveries and how they will change our approach to treating conditions that are microbial in their origin:

Because of extensive use of conventional laboratory culture approaches to detect microbial species, we have been conditioned to view chronic or acute infections as exclusively due to a single pathogenic species. However, recent studies have demonstrated that the composition of the resident microbiota in a given niche can strongly influence the behavior of specific species, particularly pathogens, and, as such, represents an important contributory factor to disease etiology.

The idea here is that it isn't the presence of a particular pathogen that matters most, but rather the environment in which the pathogen is present. If you extend this idea to thinking about treatment approaches, it follows that focusing on eradicating a particular pathogen or species may be misguided, and that a better approach is restoring microbial diversity. This has already become evident with the gut microbiome. Clostridium difficile is a virulent infection that still kills almost 30,000 people in the U.S. each year. We’ve thrown every antibiotic we have at it, but they are often ineffective in the most severe cases. Yet fecal microbiota transplants—which are essentially massive infusions of human probiotics—are over 90 percent effective, even in cases where patients have failed multiple courses of antibiotics. (4) If we apply this same reasoning to the treatment of CRS, it suggests that probiotics—rather than antibiotics—may be a better solution. Antibiotics may kill harmful species of bacteria, but they are likely to further reduce microbial diversity, which would be expected to worsen CRS over time if Dr. Lynch’s theory is correct. With this in mind, let’s see what the research has to say about probiotics and sinus problems.

Probiotics for chronic sinus problems

As it turns out, there are several published studies suggesting that probiotics may be an effective treatment for chronic sinus problems. One review in the Journal of Allergy found that “an emerging number of publications demonstrate beneficial effects using probiotics in clinical double-blind placebo-controlled trials in allergic rhinitis (AR).” (5) Although data on probiotics and non-allergic CRS are lacking, there are several lines of evidence to suggest that probiotics may be effective in these cases. First, probiotics have been shown to disrupt biofilms, which are present in CRS and difficult to eradicate through other means. (6) Second, both human and animal studies have shown that oral probiotics reduce colonization of the nose and upper respiratory tract by pathogenic bacteria (e.g., Staphylococcus aureus, Streptococcus pneumoniae, and β-hemolytic streptococci). (7, 8) Third, upper respiratory tract infections often precede the development of CRS, and probiotics have been shown to be effective in preventing them. (9) Finally, although this is certainly not peer-reviewed evidence, I can tell you anecdotally from my work with patients that many CRS sufferers do seem to improve with strategies aimed at restoring the microbiome—such as eating more fermentable fiber and fermented foods, and/or taking prebiotics and probiotics.

Future directions: nasal probiotic sprays for repopulating the sinus microbiome?

So far we’ve been talking about the role of oral probiotics in treating CRS. But if a disruption of the sinus microbiome is the true underlying cause of CRS, wouldn’t it make more sense to address that more directly? Dr. Lynch found that most patients with CRS are lacking in a particular species of bacteria called Lactobacillus sakei. This bacteria is a natural, protective species in our nose, but (as the name implies) it is also used to make certain fermented beverages and foods like sake and kimchi. One might suspect that Dr. Lynch and her peers are developing a nasal spray that contains Lactobacillus sakei to be used in the treatment of CRS. Of course such a treatment will have to be developed and tested for safety and effectiveness in human clinical trials. Given that this may take several years, some folks have decided to take matters into their own hands, er, noses. A blog called Lacto Bacto, which is written by CRS sufferer Mara Silgailis, describes a DIY approach that appears to have helped many people with CRS. It involves putting small amounts of kimchi juice directly into the nostrils. According to Mara, she has essentially cured herself and her family of their long-term CRS, and they have been antibiotic-free for more than two years. Along the same lines, I’ve heard anecdotal reports from patients and people online who have created DIY nasal probiotic sprays and even crushed up probiotic tablets and sniffed them, achieving somewhat miraculous results. Of course I can’t recommend or endorse these procedures, because they haven’t been tested for safety or efficacy. It would seem that the risk is relatively low, but it’s at least possible that some of the other microbes in kimchi or other oral probiotics may not be beneficial for the sinus microbiome. We’re really just starting to scratch the surface in this area of research, and there’s still a lot that we don’t understand. So if you decide to perform these experiments at home, proceed at your own risk! Okay, now I’d like to hear from you. Do you suffer from CRS? Have you tried oral probiotics? If so, with what result? What other treatments have you found to be effective? Please let us know in the comments section.

Irritable Bowel Syndrome (IBS) is the most common functional gastrointestinal disorder worldwide, with prevalence rates ranging from 9 to 23 percent depending on location. IBS affects approximately 15 percent of Americans and is the second leading cause of missed work (behind only the common cold). It accounts for 12 percent of visits to primary care providers and an estimated $21 billion annually in direct medical expenses and indirect costs associated with decreased productivity and absenteeism. The symptoms of IBS include gas, bloating, constipation, diarrhea, alternating constipation and diarrhea, and abdominal pain. They can range from mildly annoying to completely debilitating. But what is IBS? In medical terms, it’s a “diagnosis of exclusion.” This means that it’s a label applied when other disease conditions are ruled out. If you go to your doctor complaining of gas, bloating, and pain, she may run a number of tests to determine if you have inflammatory bowel disease (IBD), GERD, diverticulitis, and other problems that affect the structure of the intestines. If these structural conditions are ruled out, the doctor will evaluate your symptoms based on the Rome Criteria, a set of guidelines developed by consensus to diagnose IBS. These include: Recurrent abdominal pain or discomfort at least three days per month in the last three months associated with two or more of the following:

• Improvement with defecation
• Onset associated with a change in stool frequency
• Onset associated with a change in stool consistency

If you meet these criteria, you will be diagnosed with IBS. Your doctor will then likely prescribe any of the following medications, as dictated by your symptoms:

• Anti-diarrheal medications. These include OTC drugs like loperamide or bile acid binders like cholestyramine or colesevelam. (Ironically, many of these medications cause bloating as a side effect!)
• Anticholinergic or antispasmodic medications. These include hyoscyamine and dicyclomine and are used to reduce bowel spasms and pain. (Unfortunately, they worsen constipation and can lead to other symptoms like difficult urination. They also increase the risk of SIBO, which is an underlying cause of IBS—see below.)
• Doctors will often prescribe SSRIs to people with IBS because they help relieve depression (associated with IBS) as well as inhibit the activity of neurons that control the intestines.
• Specific medications for IBS. These include alosetron, which is designed to slow intestinal motility and reduce diarrhea, and lubiprostone, which increases fluid secretion in the intestine and speeds up motility. These drugs are typically used as a last resort, and alosetron can only be prescribed by doctors enrolled in a special program because it has previously been removed from the market due to side effects and risks.

What’s wrong with the conventional treatment for IBS?

The fundamental problem with the conventional approach to IBS is that it merely suppresses symptoms and doesn’t address the underlying causes. Look at the list of medications above. They are aimed primarily at slowing or increasing intestinal motility (to reduce diarrhea or constipation) and relieving pain.

Tired of struggling with IBS? Treat the underlying cause and heal from the inside out.

Even if these medications are effective for those purposes (which they often aren’t, according to many IBS sufferers), they often have side effects that are identical to symptoms that people with IBS already experience—such as gas and bloating. And in some cases, the drugs have more serious complications and risks. Alosetron, a medication used to treat severe diarrhea-predominant IBS, was temporarily withdrawn from the market by GlaxoWellcome after the occurrence of serious life-threatening adverse effects, including five deaths and additional bowel surgeries.

A better approach to IBS: treat the underlying cause!

Given the failure of the conventional approach to successfully treat IBS, and the side effects and risks associated with drug treatment, patients deserve another alternative. Fortunately, IBS can be successfully treated—and even cured—using functional medicine. In functional medicine, we focus on addressing the underlying cause of health problems rather than just suppressing symptoms. This leads to lasting improvement and genuine healing. But what are the underlying causes of IBS? The answer depends on the individual patient. IBS is not a single disease with a single cause. Rather, it’s a syndrome—a collection of signs and symptoms—that has multiple possible causes. That said, both the scientific research and my clinical experience suggest that the following five pathologies are the underlying cause of IBS in most cases. Traditionally, IBS has been considered a “functional” gastrointestinal disorder. This means that it is caused by abnormal function of the GI tract, rather than structural or biochemical abnormalities. As you’ll see below, that may be true in some cases, but in others there is very likely a biochemical abnormality present (such as bacterial overgrowth). This is crucial to understand, because for many years patients with IBS were told that it was “all in their head.” The implication was that IBS is a psychosomatic disorder caused by anxiety, depression, or some unknown psychological problem. While IBS may involve a dysfunction in the gut–brain axis, we now know that it is primarily caused by distinct biochemical and even structural changes in the GI tract. This important discovery has removed the painful (and unwarranted) stigma from the IBS diagnoses and offers hope to the hundreds of millions of IBS sufferers around the world.

#1: Small intestine bacterial overgrowth (SIBO)

SIBO is a condition characterized by abnormal overgrowth of bacteria in the small intestine. One study reported that up to 84 percent of IBS patients have SIBO and that patients with IBS were 26 times more likely to have SIBO than controls. (1) Results from subsequent studies examining the association between SIBO and IBS were mixed. This is in part because there is currently no consistently accepted, gold-standard method of testing for SIBO, and the techniques varied from study to study. However, there is other evidence to support the idea that SIBO plays a causal role in IBS for at least some patients. Antibiotics that are used to treat SIBO—such as rifaximin and neomycin—have been shown to be effective for treating IBS. For example, in one randomized controlled trial (RCT), treatment with rifaximin for 10 days resulted in symptom improvement that lasted for up to 10 weeks in IBS patients. (2) A recent meta-analysis of five studies found rifaximin to be effective for global IBS symptom improvement and more likely to reduce bloating than a placebo. (3)

#2: Disrupted gut microbiota (aka “dysbiosis”)

The human gut microbiota is a complex community of over 100 trillion microorganisms that influence physiology, metabolism, nutrition, and immune function. Disruption of the gut microbiota has been linked with GI conditions like inflammatory bowel disease as well as a wide range of extra-intestinal inflammatory conditions like diabetes and obesity. Studies have shown that up to 83 percent of patients with IBS have abnormal fecal biomarkers, and 73 percent have intestinal dysbiosis (i.e., a disrupted gut microbiome). (4) Numerous studies have also found that both prebiotics and probiotics, which modulate the gut microbiota, can be effective for treating IBS. (5) In addition, the low FODMAP diet, which restricts certain carbohydrates that feed intestinal bacteria, has been shown to benefit IBS patients. (6)

#3: Increased intestinal barrier permeability (aka “leaky gut”)

One of the primary roles of the gastrointestinal tract is to serve as a barrier system that prevents pathogens, undigested food particles, and other undesirable substances from entering the body. IBS has been associated with increased permeability of the intestinal barrier in several studies, which may be modulated by a cytokine called interleukin-22 (IL-22) that is known to play a role in regulating gut permeability. (7, 8) Note that this is a structural change to the gut, which would suggest that IBS is not always a functional disorder.

#4: Gut infections

The human gut is naturally resistant to infection by pathogenic bacteria, thanks to acid produced in the stomach that is designed to kill potential invaders. However, many aspects of the modern diet lifestyle—such as chronic stress, poor diet, and use of acid-suppressing drugs—have compromised this defense system. A number of gut infections have been linked to IBS. For example, food poisoning caused by Campylobacter bacteria leads to chronic, persistent IBS in as many as 10 percent of cases. (9) Intestinal parasites like Blastocystis hominis, Dientamoeba fragilis, and Giardia lamblia may be relatively common—yet often undiagnosed—causes of IBS, even in the developed world. (10)

#5: Non-Celiac Gluten Sensitivity and other food intolerances

Non-Celiac Gluten Sensitivity (NCGS) is a reaction to gluten that is not autoimmune (celiac disease) or allergic (wheat allergy). Despite claims to the contrary in the popular media, NCGS is a legitimate and potentially serious condition. In fact, I recently argued that it may be a greater public health challenge than celiac disease itself. NCGS patients usually present with symptoms such as gas, bloating, abdominal pain, and changes in stool frequency and consistency that are indistinguishable from IBS. They also often present with extra-intestinal symptoms like “brain fog” and fatigue, which are common among IBS sufferers. Intolerances to other foods like dairy products, eggs, peanuts, and seafood are also common among IBS sufferers. These may be true food allergies (IgE-mediated) or more mild intolerances (IgG- or IgA-mediated). One recent, large review of 73 individual studies concluded that food allergy and intolerance—including reactions to wheat and gluten—should be considered as a potential underlying pathology for IBS. (11) In my own clinical experience, I’ve found that both gluten/wheat sensitivity and other food intolerances are extremely common contributing factors to IBS. It’s worth pointing out that, in many cases, food intolerances are themselves caused by some of the other pathologies we’ve already discussed in this article. Put another way, both IBS and food intolerances are symptoms of deeper causes like SIBO and gut infections.

Summary and recommendations

As I’ve demonstrated in this article, the conventional approach to IBS is ineffective at best, and potentially dangerous at worst. Simply suppressing the symptoms of IBS with drugs, without addressing its underlying causes, dooms the patient to a lifetime of unnecessary medication, suffering, and frustration. The good news is that we now have a much better idea of what causes IBS. When those causes are addressed, excellent outcomes are possible. In my practice, I’ve seen people with chronic, intractable IBS for more than 20 years almost entirely recover after we treat their underlying gut problems and fix their diet. If you’ve been diagnosed with IBS, I recommend finding a functional medicine practitioner to work with that can identify and treat the causal factors in your case. You don’t have to accept a diagnosis of IBS, or spend your life fighting against it. Now I’d like to hear from you. Have you been diagnosed with IBS? If so, what did your doctor recommend? Have those treatments been effective? Have you explored any of the potential causes I mentioned in this article? What did you discover? Please share your experience in the comments section.

Are you dealing with SIBO? If so, you’ve probably tried a low-FODMAP diet and noticed significant improvements in your symptoms. Once you’ve noticed such an improvement, it’s easy to think that this must be the answer—a low-FODMAP (or low-carb) diet has cured you! Unfortunately, this is not the case. A low-FODMAP (or low-carbohydrate) diet will keep symptoms under control simply by starving the bacteria in your small intestine. When these bacteria don’t have food to eat, they aren’t able to metabolize that food and produce gas as a result. This gas is what causes the common symptoms of SIBO—bloating, abdominal pain, diarrhea (in the case of hydrogen gas), and constipation (in the case of methane gas) (1).   But starving the bacteria over the short term does not eradicate the bacteria, which is what we’re trying to accomplish, as the small intestine is not supposed to contain much bacteria. If you continue this restriction for a long period of time in an effort to kill the bacteria, you’re also starving the bacteria in your large intestine that should be there and that play a vital role in your health. Simply put, a low-FODMAP or low-carb diet does not eradicate an overgrowth in the small intestine in a short period of time, and continuing on a long-term low-FODMAP/carbohydrate diet in an effort to starve the bacteria to death has potential detrimental effects on the bacteria in the large intestine. I have had clients who have been on long-term low-FODMAP diets prior to working with me who still have positive breath tests for SIBO despite their restricted diet. There is a difference between controlling symptoms and actually clearing the bacteria. We want to do the latter, which has the added benefit of improving symptoms as well.

The Negative Impact of a Long-Term Low-FODMAP Diet

There have been limited studies on the long-term impact of low-FODMAP diets on microbial balance in the large intestine. The studies we have showing the impact of short-term FODMAP restriction on the microbiome, however, do not bode well for the long-term implications. FODMAPs are fermentable carbohydrates that help to feed the beneficial bacteria in the large intestine. When you begin to think about them this way, it becomes a lot easier to understand why adhering to a diet low in the substrates that our healthy gut bacteria thrive on may not be a great idea.

Is your SIBO diet controlling your symptoms or actually clearing the bacteria? #sibo

Indeed, the studies to date on the effects of FODMAP restriction show exactly what we would imagine would happen when restricting these beneficial substrates: the overall amount of bacteria was decreased (by 47% in this study), along with a decline in bacteria that produce butyrate (a beneficial substance made when probiotics feed on fermentable fibers) (2). While this particular study did not show a decrease in the probiotic strain bifidobacteria, another study has (3). In my clinical experience, it is very common to see low levels of both the bifidobacteria and lactobacillus strains in my client’s stool tests if they’ve been on long-term low-FODMAP diets. While these bacteria would likely thrive once again with the addition of prebiotic substances, staying in a chronically diet-induced altered microbiological state is likely not a healthy choice when you start to think about the importance of our microbiome and its effect on our health. Clearly, more research needs to be done in this area if patients are going to be on long-term low-FODMAP diets. However, after reading this article, it is my hope that you won’t need to be on a long-term low-FODMAP diet to keep your symptoms under control.

Treating SIBO

So if you’re not treating your SIBO with diet, what is used to treat it? Rifaximin is the most commonly used antibiotic for treatment of SIBO and has been shown to be safe and well-tolerated (4). Figures vary on its efficacy (with rates as high as 87% in one study), but on average it is about 50% effective (5). However, this may not take into account the necessary difference in treatment for those with methane-positive SIBO. A study on those with methane-positive SIBO shows that when rifaximin is combined with another antibiotic, neomycin, it is about 85% effective (6). If you’re getting tested for SIBO, make sure you’re getting tested for both methane and hydrogen. These tests will guide your practitioner in treating you more effectively. Herbal antimicrobials have been shown to be at least as effective as rifaximin, and about 57% of those who fail on rifaximin will succeed on herbal antimicrobials (7). I have personally seen this the other way around as well; those who fail on herbal antimicrobials usually do well with rifaximin. Others may need to do multiple rounds of either herbal or pharmaceutical antibiotics to clear the overgrowth. Whether you choose herbal or pharmaceutical antibiotics, the important thing is that you are using something that will eradicate the bacteria instead of covering up the symptoms with diet change. You’re getting to the root cause of your symptoms!

Diet during SIBO treatment

Now that you’re being treated with herbal or pharmaceutical antibiotics, what should you eat? If you listened to Chris’ recent podcast with Dr. Pimentel, you’ll know that having happy and fed bacteria is a good thing when treating SIBO—this is not the time to be starving them, as they will “hide” and become more difficult to eradicate. Eating FODMAPs and carbohydrates is exactly what you want to be doing! In my own practice, I recommend that clients undergoing treatment eat as many FODMAP foods as they can tolerate and that they do not go on a low-carb diet. (I like to see a minimum of 100 grams of carbohydrates daily, and more, if tolerated.) I also will typically add some kind of prebiotic if the client can tolerate it. A study that compared rifaximin alone versus rifaximin treatment plus partially hydrolyzed guar gum supplementation showed that providing fermentable carbohydrate along with the antibiotic improved success rates from about 62% (rifaximin alone) to 87% (rifaximin plus guar gum) (8). Of course, I don’t want my clients to be miserable with digestive symptoms during this time, so treatment is always personalized to each client. Some may have no problems whatsoever eating FODMAPs or high-carbohydrate foods, while others may be very sensitive. I encourage clients to eat the maximum amount that they are comfortable with and remind them that in the end, feeding these bacteria is a good thing. They may experience some uncomfortable symptoms like bloating or gas during this time, but as long as it is not interrupting their life or causing pain, the more FODMAPs or carbohydrates they can eat, the better.

Diet After SIBO Treatment

As many SIBO sufferers know, SIBO has a high rate of recurrence, which begs the question: what should you be eating after treatment to prevent another overgrowth? In my eyes, that’s the million dollar question right now, and it’s a question we don’t have the answer to quite yet. For now, I have my clients eat whatever they can tolerate on a healthy, real-food, ancestral diet. If they need to restrict FODMAPs slightly or eat rapidly digested carbohydrates to keep symptoms under control, that’s okay. (However, if you can’t tolerate FODMAPs or complex carbohydrates after your treatment, you’ll definitely want to retest to make sure that you’ve completely eradicated the overgrowth in the first place.) We’ll also investigate any potential underlying causes of their SIBO, such as low stomach acid, pancreatic enzyme insufficiency, intestinal motility disorders, and so on. I know from speaking with Chris that he has come to believe that SIBO—and especially recurring SIBO—is often a symptom of a deeper problem. The solution in that case isn’t just to keep treating the SIBO, but to address that root cause. There’s a lot we still don’t know about SIBO. As we learn more, some of these protocols may change, but I hope this article has given you a better idea of what you should be doing to heal from SIBO with the knowledge we have now. Now I want to hear from you: What has been your experience with SIBO? This is a guest post written by Kelsey Marksteiner, RD. Kelsey is a Registered Dietitian with a Bachelors degree in Nutrition from NYU and a Master’s in Human Nutrition and Functional Medicine. She works in private practice and recommends individualized dietary therapy focusing on biologically appropriate diet principles to aid her clients in losing weight, gaining energy, and pursuing continued health. She is a firm believer that everyone is different, and she tailors her plan for each and every individual. Through her work, she aims to meld the dietary wisdom of traditional cultures with the latest science in integrative and functional medicine to create plans for her clients that work in the modern world. You can learn more about Kelsey on her staff bio page, or by visiting her private practice website. Join her newsletter here!

The trillions of bacteria that inhabit our gastrointestinal tract play an intricate and increasingly appreciated role in human health. Deemed by some as the “forgotten organ” (1), new connections between these microorganisms and our physiology are being discovered all the time. In recent months, I’ve written extensively about these connections. Check out my other blog articles to learn more about the influence of microbes on your health:

• Skin microbiota and your health
• Got allergies? Your microbes could be responsible.
• Your gut microbes and your thyroid: What’s the connection?
• Does the gut microbiome play a role in autoimmune disease?
• Heal your gut, heal your brain
• Do gut microbes control your food cravings?

Next up in the series, and yet another reason to protect your gut microbes: bone health! Before we dive in, let’s review a few fundamentals of bone physiology and how we determine bone health.

Bone health: The basics

Bone is not a static structure and is constantly being remodeled. Mature bone tissue is regularly removed from the skeleton by cells called osteoclasts (a process called resorption), and new bone tissue is formed by cells called osteoblasts (a process called ossification). Remodeling helps to reshape bone following fractures and also responds to mechanical loads like exercise (2). An imbalance in bone resorption and formation can result in bone diseases like osteoporosis and arthritis (3). There are numerous measures of bone health. In humans, researchers often use a DEXA scan to determine bone mineral density. In rodent models, scientists can also measure bone mass, length, volume, and mineral composition to get a more complete assessment of bone structure. In general, higher bone mineral density is associated with reduced risk of fracture and bone disease. However, increased bone mineral density, bone mass, and bone length do not always suggest better bone health (4).

Three ways your gut microbes can support healthy bones.

The association between gut microbes and bone

One of the key ways that researchers study the effects of the microbiota on an organ system is using mice that don’t have one at all. Called “germ-free” (GF), these mice are born and raised in sterile incubators. Studies of skeletal health in GF mice have found mixed results. In one type of mice, GF mice had reduced bone mass compared with conventionally raised animals, which have a full consortium of microbes (5). In another type of mouse, the GF environment resulted in increased bone mass, while the conventional environment increased measures of bone turnover (6). Although it is difficult to reconcile these contradictory findings, the key feature of both studies was that the mere presence or absence of a microbiota significantly changed the structure of the bone. Antibiotic models provide further evidence for an association between gut microbes and bone, and the results are much more translational to humans. One study found that exposing mice to subtherapeutic doses of antibiotics at weaning resulted in a significant increase in bone mineral density after three weeks (7). Another study found that animals treated with tylosin, amoxicillin, or a mixture of both had larger bones and a higher bone mineral content than control mice (8). Low-dose antibiotics have long been used in the agricultural industry in animal feed for this very reason; they influence skeletal growth and make for larger, more profitable livestock.

Bone disease is partly heritable and associated with GI disorders

All that nitty-gritty science in animal models is great, but what about humans? Is there evidence of a gut–bone connection in humans? Epidemiological evidence and observational studies suggest that there is. In adult humans, bone mineral density is 50 to 80 percent heritable (9). For quite some time, heritable traits were thought to be only passed on from parent to offspring through DNA. We now know that vertical transmission of microbes occurs at birth—as a baby passes through the mother’s birth canal, he or she acquires crucial microbes that shape the composition of their gut microbiota (5). It’s possible that in addition to the heritable traits encoded by our own genetics, additional determinants of our bone health are acquired based on our microbial inheritance. Bone complications are often seen in individuals with GI disorders. Patients with inflammatory bowel disease (IBD) have an increased risk of osteopenia, osteoporosis, and bone fracture. This has been attributed to malabsorption of calcium, reduced blood levels of vitamin D and K, or bone loss after glucocorticoid treatment (10). Gut and systemic inflammation are also associated with increased production of cytokines that are key contributors to bone loss (11). We’ll discuss this in detail in the next two sections.

Leaky gut and bone health

If you’re an avid reader of my blog, you might be thinking: leaky gut, again? Yep. When the intestinal barrier becomes compromised, microbes or parts of microbes can translocate from the gut lumen to the bloodstream. Your immune system recognizes these bacterial components in the bloodstream and launches a systemic immune response. Indeed, studies have found a strong association between microbial translocation and joint pathologies like rheumatoid arthritis (12, 13). The most common of the bacterial components include peptidoglycan, lipopolysaccharide, and flagellin. These stimulate various “toll-like” receptors (TLRs) on innate immune cells: peptidoglycan is the primary component of bacterial cell walls and stimulates TLR2; lipopolysaccharide is located in the outer membrane of gram-negative bacteria and stimulates TLR4; and flagellin is the main protein that makes up the filamentous “tail” of bacteria and stimulates TLR5 (14, 15, 16). Stimulation of innate immune receptors has effects throughout the body, which is why a leaky gut can manifest as a number of different chronic health conditions. In regard to bone health, stimulation of innate immune cells has a direct effect on bone remodeling.

Microbes shape the systemic and mucosal immune system to influence bone remodeling

The microbiota plays a key role in the initial development of the immune system as a child and the maintenance of proper immune responses later in life. This represents yet another pathway by which microbes are connected to bone health, as the immune system is intricately involved in the regulation of bone metabolism and physiology. Immune cells that are activated by microbes in the gut can migrate to bone and directly regulate bone remodeling via osteoclast-inducing factor, RANKL, and other bone-active molecules (17). Increased levels of activated innate immune cells have been shown to increase expression of the signaling molecule TNFα in bone marrow. TNFα stimulates stems cells in the bone marrow to differentiate into osteoclasts. This tips the normal balance of bone resorption and formation, resulting in higher levels of bone breakdown and lower bone density (18, 19)

Gut microbes regulate the availability of nutrients important for bone health

Healthy bones require a multitude of nutrients, including calcium, phosphorus, vitamin D, vitamin K2, vitamin A, and magnesium. Recent research has also suggested a role of several B vitamins and even vitamins C and E in bone health (20). Animals raised on a nutrient-depleted diet have reduced bone length (21). Disruption of the microbiota can significantly alter nutrient absorption. Gut dysbiosis has been shown to increase the number of calories absorbed from food (22, 23). Yet it can also result in inflammation of the gut epithelium, the location of nutrient transporters that allow for the absorption of vitamins and minerals. This paradoxically results in individuals that are both overweight and malnourished (24). In addition to influencing absorption and metabolism, microbes themselves also synthesize some of our vitamins. These include thiamin (B1), niacin (B3), pantothenic acid (B5), biotin (B7), folate, tetrahydrofolate, pyridoxal phosphate, and vitamin K2 (25, 26).

Protect your microbes to support healthy bones

While there are certainly many factors that influence bone health, including genetics, diet, mechanical loading, and other environmental factors, gut health seems to play a crucial role. Below I have compiled a list of ways to support a healthy gut flora and how each might improve bone health.

• Probiotics. Eat your fermented foods! Adult male mice treated with Lactobacilli for four weeks showed increased femoral bone volume, increased bone formation, and a reduction in circulating pro-inflammatory cytokine expression (27). Lactobacilli were also shown to prevent bone loss in a model of type 1 diabetes (28). You can find Lactobacilli in sauerkraut, kimchi, and other fermented vegetables.

• Prebiotics. Prebiotic fibers in dandelion greens, plantains, and other foods promote the growth of beneficial bacteria. Prebiotics have been shown to have a beneficial role in mineral metabolism, enhancing calcium absorption in both rodents and humans (29, 30). This enhanced absorption translates to increased bone density (31). While different fibers have different effects, a study testing eight different prebiotic fibers in young rats showed that most prebiotic fibers had significant effects on bone density measures (32).

• Bone broth. Bone broth supports a healthy gut lining and a healthy microbial community.  Homemade broth also provides all of the necessary vitamins and minerals for building bone, as well as the proteins collagen and glucosamine for healthy joints and cartilage.

Now I’d love to hear your thoughts. Did you know about the gut–bone connection? Do you or someone you know suffer from osteoarthritis, osteoporosis, or another bone disorder? Let us know in the comments!

A little over two years ago, I wrote a post titled “The Unbiased Truth about Artificial Sweeteners.” At the time of writing, the scientific literature did not really suggest any significant negative effects of artificial sweeteners. A few studies had found negative effects, but many others showed no correlation at all. While I urged caution in the consumption of these sugar substitutes, there was really no solid evidence at the time to recommend their strict avoidance. Fast forward to today, and enter the gut microbiota. The trillions of bacteria that inhabit your gastrointestinal tract have received a tremendous amount of attention in recent years. A comprehensive research study has now shown (almost unequivocally) that artificial sweeteners can in fact impact health via altering gut microbes. (1).

Non-caloric artificial sweeteners

A sugar substitute is any food additive that provides a sugary taste but has significantly less associated calories, or food energy. Some sugar substitutes are natural, like stevia, while others are synthetic, termed “artificial sweeteners.” In the United States, six artificial sweeteners have been approved for use: aspartame, sucralose, neotame, acesulfame potassium (Ace-K), saccharin, and advantame. All have been deemed Generally Recognized as Safe (GRAS) by the FDA (2). As high-fructose corn syrup continues to receive opposition from consumers and health organizations alike, the food and beverage industry is increasingly turning to artificial sweeteners instead. According to BCC Research, the global market for high-intensity sweeteners is expected to reach almost $1.9 billion in 2017, with the non-nutritive category growing particularly rapidly (3). The most commonly used non-caloric artificial sweeteners (NASs) are saccharin (Sweet’n Low), aspartame (Equal, NutraSweet and Canderel), and sucralose (Splenda).

Did you know artificial sweeteners can cause glucose intolerance?

Most NASs pass through the human GI tract without being digested by the human host. They therefore come in direct contact with microbes in the colon. As we’ll see from the results of this study, this has dramatic implications for the health of the host.

Prolonged consumption of non-caloric artificial sweeteners makes mice glucose intolerant

In the first part of the study, described in Nature, researchers from the Weizmann Institute of Science in Israel added saccharin, sucralose, or aspartame to the drinking water of three different groups of lean 10-week-old mice. They also had several control groups, including mice drinking only water or mice drinking water supplemented with glucose or sucrose, to see how the artificial sweeteners compared to normal sugars. The researchers then performed a glucose tolerance test. As this is a crucial aspect of the study, I’m going to briefly describe how this is done. All of the mice are given only water for six hours prior to the test so that they are in a fasted state (and the NAS, glucose, and sucrose mice do not continue to eat sweeteners). They are then given 40 mg of glucose orally. Blood from the tail vein is used to measure glucose immediately before and at 15, 30, 60, 90, and 120 minutes after the glucose is given. From these data, the researchers can create a glucose tolerance curve to determine (a) fasting glucose levels, (b) how high the blood glucose spikes, and (c) how quickly glucose is cleared from the bloodstream. So what did they find? At week 11 of feeding, the three control groups (water, water+glucose, water+sucrose) had comparable glucose tolerance curves, whereas all three NAS groups (water+saccharin, water+sucralose, water+aspartame) had developed significant glucose intolerance. Saccharin had the largest effect. They duplicated the experiment, this time in mice with diet-induced obesity, and observed the same result: NAS made the obese mice more glucose intolerant.

Treating mice with antibiotics abolished glucose intolerance

The researchers next wanted to see if the microbiota was responsible for the glucose intolerance. One of the simplest methods for determining if the microbiota plays a role in a particular trait or condition is to administer antibiotics and observe any changes. They did exactly this: the researchers treated mice with a combination of ciprofloxacin and metronidazole or vancomycin alone for four weeks and found that antibiotic treatment abolished glucose intolerance in both the lean and obese models. This suggests that NAS induction of glucose intolerance is very likely mediated by the gut microbiota. However, there is always the slight possibility that off-target effects of the antibiotics on the host abolished the glucose intolerance, rather than the changes in microbiota composition. To rule this out and confirm the causality of the relationship, the researchers turned to germ-free mice.

Transferring NAS microbiota to germ-free mice transfers the glucose-intolerant phenotype

I’ve written about germ-free (GF) mice before in several of my blog articles on the microbiota (4, 5, 6, 7). Raised in sterile conditions, GF mice lack any microbes at all but can be selectively recolonized for experiments. Researchers can therefore perform an intervention in normal mice, take their fecal material, and transplant it into GF mice to determine if a particular effect of the intervention is mediated by the microbiota. If it is, the simple act of transferring the fecal material will elicit the effect in the recipient mice. In this case, the researchers had two groups of mice that would serve as their fecal donors for the experiment, both of which were kept in normal (non-sterile) housing. One group was fed normal mouse chow + saccharin, and the other was fed normal mouse chow + glucose as a control. The amount of saccharin given was the mouse equivalent of the acceptable daily intake (ADI) of saccharin in humans (5 mg/kg, suggested by the FDA). Fecal pellets from these two groups of mice were then transplanted into two groups of naïve GF mice. The GF recipient mice were therefore colonized by microbes from saccharin-fed or glucose-fed donors but were maintained on normal chow themselves. Six days after the transfer, the researchers performed a glucose tolerance test on the recipients. They found that those mice that received the saccharin-fed microbiota had developed significant glucose intolerance compared to those that received the glucose-fed (control) microbiota. This confirmed the findings in the antibiotic model, suggesting that alterations in the microbiota were in fact responsible for the differential glucose tolerance.

NAS alters microbiota composition and function

The most pressing research question then was, how had the microbiota been altered? Using 16S sequencing technology, they characterized the microbiota of each group. They found that mice consuming saccharin had a distinct microbiota composition from all three control groups. The authors reported over 40 operational taxonomic units (groups of bacteria) that were significantly altered in abundance, an indication of considerable dysbiosis. Which bacteria changed? In the saccharin group, the Bacteroides genus increased, while Lactobacillus reuteri and Akkermansia muciniphila (two microbes generally considered to be beneficial) decreased. Several members of the Clostridiales order increased, while other Clostridiales decreased. They next wanted to look at microbial function, and this is where the technology gets really cool.  The researchers performed shotgun metagenomic sequencing, which allows for mass sequencing the genome of virtually every microbe in the gut. They did this sequencing on fecal samples collected before and after the 11 weeks for all of the groups of mice. The results showed that saccharin-fed mice had a strong increase in genes associated with glycan degradation pathways, which have been linked to enhanced energy harvest and metabolic disease (8, 9). As if their prior findings in mice weren’t robust already, the researchers also cultured naïve mouse fecal material with NAS. They then transferred the NAS-exposed fecal material, or control fecal material, into GF mice. Recipients of the NAS-exposed fecal material showed increased glucose intolerance compared to GF mice given the control culture and similar alterations in microbial composition to the previous experiment.

What about humans? NAS consumption in humans is associated with impaired glucose intolerance

I discussed many of the human studies looking at NAS consumption in my previous article. When that was published, most human studies had shown mixed results with NAS. After finding such robust effects on the microbiota and glucose intolerance in mice, Suez and colleagues decided to see if the findings would translate to humans in their hands. They first performed a cross-sectional study, using a food frequency questionnaire to determine approximate NAS consumption, and also looked at several measures of metabolic disease. Contrary to previous studies, they found significant positive correlation between NAS consumption and a number of clinical parameters related to metabolic syndrome: weight, waist-to-hip ratio, fasting blood glucose, hemoglobin A1c, glucose tolerance test, and ALT. You might be thinking: well, sure, it’s correlated because people with excess weight and metabolic syndrome are the most likely to use NAS in place of sugar as a means of losing weight. Luckily, the researchers took this into account and the effect still remained after correcting for BMI.

More human evidence

Correlations are great and all, but that’s all they are: correlations. We can’t infer causation from simple associations between consumption of a substance and outcomes. Fortunately, Suez et al. took it to the next level and performed a longitudinal study. Seven healthy volunteers who do not normally consume NAS or NAS-containing foods were followed for one week. On days two through seven, participants consumed the FDA’s maximal acceptable daily intake of saccharin (5 mg/kg body weight) as three divided daily doses. They were monitored by continuous glucose measurements and daily glucose tolerance tests. Astoundingly, in just this short week-long period, four out of seven individuals had already developed significantly poorer glycemic responses (NAS responders) and pronounced changes in microbiota composition. The remaining three individuals had no change (NAS non-responders). Transfer of NAS-responders’ day seven stool into GF mice resulted in glucose intolerance (compared to day 1 stool transfer), while transfer of NAS-non-responder day 7 stool did not.

Takeaways from this study

Phew. Hopefully you stayed with me through all that! This was an extremely robust study with lots of different components, but it provides an incredible wealth of evidence against the use of NAS. If you glazed over some of the details, here are the main takeaways:

1. NAS consumption in both mice and humans increases the risk of developing glucose intolerance and metabolic disease.
2. The adverse metabolic effects are mediated by alterations in the composition and function of the microbiota.
3. This study calls for a serious need to reassess the ubiquitous and ever-increasing use of NAS in the food and beverage industry.

Now I’d like to hear from you. Had you seen this study? Will this change your approach to sweeteners? Share your thoughts in the comments!

In this episode we discuss:

• Questions to ask about these findings
• High fiber and its impact on high-fat diets
• Low-carb, low-fiber diets can be detrimental
• Each person responds to high-fat diets differently

[smart_track_player url="http://traffic.libsyn.com/thehealthyskeptic/RHR_Are_High-fat_Diets_Bad_for_the_Microbiome.mp3" title="RHR: Are High-Fat Diets Bad for the Microbiome?" artist="Chris Kresser" ] Chris Kresser: Hey, everybody, Chris Kresser here. Welcome to another episode of Revolution Health Radio. This week we have a question from Carrie. Let's give it a listen. Carrie: Hi, Chris. Carrie Bennett from Carrie B Wellness. I have a question when it comes to a high-fat diet and the health of the gut microbiome when I'm coaching my nutrition clients. After reading the Sonnenburgs’ book about gut health and the gut microbiome, it seems to be that their recommendation is that fat can change the gut microbiota in a negative way. I'm just wondering how you view this in light of a Paleolithic, primal-style diet. I'm wondering if the studies that they're referencing are utilizing poor fat sources as opposed to high-quality pastured or grass-fed animal fats, and just your take on, is high-fat healthy for the gut microbiota? Thanks. Chris: Thanks so much for sending your question in, Carrie. This is a really good example of the complexity of modern research and where it often goes awry. Some studies do show an adverse effect of a high-fat diet on a microbiome, but there are many important questions that we have to ask about these findings.

Questions to ask about these findings

1. The first question is whether these studies are in mice or in humans. They're often in mice, rats, or other animals, and it's just not clear how applicable those findings are to humans. Certainly some animals share common physiological mechanisms with humans, and we've learned a lot from animal research, but there are some important differences as well, and the microbiome and the gastrointestinal system is definitely one of those.
2. Second, what is the quality of fats that's being used in the study? Carrie alluded to this in the question. The assumption in much of the research out there is that fat is fat, so it doesn't really matter what kind of fat you use. They often will use corn oil or soybean oil in these studies, particularly with the animal studies, and I don't think that that's actually a safe assumption that all fat affects us in the same way. We know there are already some studies that suggest that industrialized seed oils like soybean oil and corn oil have different effects on the microbiome than traditional fats do. I think if people embrace this question and there were more studies separating the different effects of different types of fats, we'd see even more support for that.
3. Third question is: what is the context of the overall diet that the high-fat intake is occurring in? This is probably the most important question, in my opinion. It should be obvious that the effects of a high-fat diet that is occurring in the context of a Standard American Diet would be very different than a high-fat intake in the context of a nutrient-dense, whole-foods diet, but this is rarely acknowledged in any of these studies. Our hunter–gatherer ancestors, as you know, ate primarily meat and fish, wild fruits and vegetables, nuts and seeds, and some starchy plants. Those are the top sources of their calories, whereas the top six sources of calories today in the industrialized diet are bread, grain-based desserts, pizza, sugar-sweetened beverages, alcohol, and fried chicken dishes. Are we really supposed to believe that a high-fat diet for hunter–gatherers eating all real whole foods affects the microbiome in the same way as a high-fat diet in the context of an overall diet that's rich in processed and refined foods? I think that there's plenty of evidence to suggest that the answer to that question is no.

High fiber and its impact on high-fat diets

We have studies that have shown that high fiber intake blunts the possible adverse effects of a high fat intake, and I'm just going to read some titles from studies on the subject and then we'll put the links in the show notes, but one is “Insoluble dietary fiber from pear pomace can prevent high-fat diet-induced obesity in rats mainly by improving the structure of the gut microbiota.” Essentially, they found that insoluble dietary fiber from pear protects against the effects of high-fat diet that could otherwise adversely affect the gut microbiota. Here's another one. “Long-term intake of a high prebiotic fiber diet but not high protein reduces metabolic risk after a high fat challenge and uniquely alters gut microbiota and hepatic gene expression.” They found that consuming probiotics, which of course are fermentable fibers, reduces any metabolic risk that would be confirmed by a high-fat diet and its effects on the gut microbiota and gene expression. Here's another one. “Effects of cereal fiber on leptin resistance and sensitivity in C57BL/6J mice fed a high-fat/cholesterol diet.” Cereal fibers probably wouldn't be my preferred way of increasing the fiber intake, but it's still fiber that would be expected to affect the gut microbiota, and in this occasion, mice that were fed a high-fat, high-cholesterol diet, the higher fiber intake protected against leptin resistance and improved overall metabolic health. The last one is kind of a mouthful, but it's “Dietary fiber prevents obesity-related liver lipotoxicity by modulating sterol-regulatory element binding protein pathway in C57BL/6J mice fed a high-fat/cholesterol diet.” So that's pretty similar to the previous one that I just mentioned. Except that they were looking at dietary fiber in general and they were looking at its ability to protect against lipotoxicity that is obesity related. Don't worry if you didn't get all that. There's a lot of jargon there and in some of those study titles, but the gist of it is that fiber protects against the potential adverse effects of a high-fat diet on the gut microbiota. Given all this, I think we can conclusively say that the effects of a high-fat diet will vary considerably depending on the overall quality of the diet. Context is king. That's a good saying in this particular instance, and this is one of the huge problems with the way that modern nutritional research is done today because the goal is often to isolate a single variable, especially in a randomized controlled trial, and then to determine the effects of changing just that one variable. But that approach, while it can be helpful if you're studying the effects of a drug versus placebo, is not really realistic or the way to go about studying the effects of nutritional changes because we don't live in a metabolic ward where you can control every other aspect of the diet and then only change one variable.

Low-carb, low-fiber diets can be detrimental

Now, all of this said, I do think there are some important caveats that I like to point out here. I have argued previously that one of the risks of a very-low-carb, high-fat diet is a potentially negative effect on the gut flora. This might seem to contradict what I've said so far, but it really doesn't. If you think about it, it supports it. Imagine somebody goes on an Atkins type of diet and is eating very high intake fat and very low carb, but they're still on a kind of Standard American Diet. They're not eating a lot of high-fiber whole foods like non-starchy veggies. They're probably not eating any fruits or very little and maybe not eating any starchy fiber-rich plants, not a lot of onions, garlic, juice, artichoke, or specific vegetables that are known to be high in fermentable fiber. They may be eating a lot of low-carb junk foods like low-carb tortillas and packaged and processed foods that Atkins sells. Maybe they're eating a lot of cheese and dairy products, which I don't necessarily have a problem with if the individual tolerates them well, but in this context where we're talking about from fermentable fiber, dairy does not have any. This person on this sort of Atkins diet could definitely suffer some negative effects of a low-carb, high-fat diet, but that's not due to the high fat intake per se; it's due to the lack of fermentable fiber in this type of diet.

Following a high-fat diet? Use these tips to keep your microbiome happy.

Jeff Leach, who is involved in the American Gut Project, an expert on the human microbiome, wrote an interesting article that alluded to this a while back called “Sorry low carbers, your microbiome is just not that into you.” In this article, which we’ll also provide a link to in the show notes, he talks about just some really informal research that they did at American Gut. I don't believe it was ever published but they just looked at ... American Gut Project is a microbiome sequencing project where people send in a stool sample and they sequence them with their gut microbiome. They have a lot of data from people following a lot of different kinds of diets because when you send in the sample to them, you have to indicate what kind of diet you're eating; not everybody does that, but a lot of people did. What Jeff found was that people who were eating a very-low-carb diet did actually have a different microbiome profile than people that were eating more carbohydrates. But as he pointed out in the article, it mattered what type of low-carb diet they were eating. For example, if someone who was on a low-carb diet or even a ketogenic diet, but they were maximizing their intake of veggies that were in fermentable fiber and possibly even supplementing with resistant starch and other fibers, then their microbiome looked really different than somebody who was on that kind of Atkins low-carb diet that I mentioned that was really low in fermentable fiber. Certainly if someone is on a very-low-carb diet and they're not paying attention to fiber intake, then just by reducing or eliminating things like grains and legumes, which are very rich in fiber, and also starchy tubers, which are rich in fiber, it certainly is a concern. It’s something that somebody on a very-low-carb diet long term should be paying a lot of attention to. I have even argued that a lot of people who are on keto or low-carb diets should consider supplementing with prebiotic fibers that are non-caloric, so they don't contribute to carb intake and won't kick someone out of ketosis, but that could really help just shore up the fiber intake (which for us in the modern world is much lower than our Paleolithic ancestors and even contemporary hunter–gatherers). That's probably one of the biggest differences, in fact, between our modern diet, even our modern kind of Paleo, ketogenic-type of diet versus our ancestral diet, is the fiber intake. Americans on average get 15 or 20 grams of fiber. In some traditional cultures it was as high as 100. I don't think all traditional cultures ate that much, but it was certainly anywhere from 40 to 60, I think, on average, which is three or four times higher than in the industrialized diet. Given what we know about how fiber feeds and supports the gut microbiome and the importance of the gut microbiome to overall health, I think that we could say that that's a really, really significant difference that often is probably underemphasized in the discussion of these different types of diets. This is, incidentally, one of the reasons I don't just recommend a ketogenic or low-carb diet for the average person unless there is a specific therapeutic goal that they're trying to achieve. And even then, with patients, I would work to try to get them to be able to start increasing whole-food carbohydrates in their diet if they can once they've achieved that therapeutic goal, unless that's not possible. Because overall I think it's easier to maintain a healthy gut microbiota and adequate levels of fiber intake when you're not on a super-low-carb diet. It still is possible, as I mentioned, if you're sticking with keto or low carb by adding fermentable fiber supplements or even just focusing on certain very fiber-rich foods like some artichokes, onions and garlic, and things like that, but it does require more attention and focus, and not everyone, unfortunately, is paying that attention.

Each person responds to high-fat diets differently

Another caveat here of course is that not everybody will respond to a high-fat diet in the same way. I say “of course” because I think that's obvious to most of you at this point, but in the conventional world they've tended to approach these dietary questions as if humans are robots and all the same and all respond to foods and other environmental inputs in the same way. We know now that that's just completely false. We not only have differences in our human genes and gene expression, for example, but we also have profound differences in our microbiome, and our microbiome has different genes and different gene expression, which we’re only beginning to understand. If you look at somebody who is from East Africa, for example, and compare them to our traditional Inuits, those two people could be expected to respond quite differently to the effects of dietary fat and carbohydrates. I think we're moving toward a place where we're going to have a lot more sophistication in being able to answer these questions. We're going to have all of the “omics” like transcriptomics, metabolomics, proteomics, kind of next-generation level of microbiome sequencing that's beyond the 16S DNA sequencing that companies like uBiome and American Gut are offering that’s going to give us a more finely resolved view on the microbiome and even the expression of genes, proteins, and metabolic factors that will help us to answer perhaps a little bit more objectively than just experimenting what macronutrient ratios are right for each person. I don't think we're there yet, but I think we're going to definitely get there and in the lifetime of everybody listening to this podcast and very possibly in the next five to 10 years. The good news is that we don't necessarily need that data to answer these questions. We can, I think, empirically answer many of them just by experimenting with different macronutrient ratios and watching how our digestion, elimination, and all of these things are influenced by the health of our microbiome respond. Finally, I hope you'll see that there are parallels here with a lot of similar questions. For example, you’ll often see this question: “Does a high-saturated-fat intake increase the risk of cardiovascular disease?” We've been trying to answer that question with a sort of blanket yes or no, but again we're getting a lot more sophisticated in our approach here, and we now understand that the answer to that question depends on many factors including the overall context of the diet, which we just mentioned. Is high-saturated-fat intake occurring in a context of a Standard American Diet with a lot of processed refined foods? Or is it occurring in a context of a Paleo type of diet? That will affect the answer to the question but also the individual genes. Is the person’s APOE 34 or 44? Do they have an LDL receptor, a mutation that affects their ability to clear LDL particles? Now, those people might have a different response to saturated fat, and they may need to limit their saturated fat intake compared to someone who doesn't have that genotype. We're moving toward a more nuanced approach. We've got a lot more to learn, but in the meantime we can look to traditional cultures to help resolve these questions because when we look at contemporary hunter–gatherers like the Tsimane, whom I have written about recently, in Bolivia, who have maintained their traditional diet and lifestyle; the Maasai in Africa; traditional Inuit; or other cultures around the world that have largely maintained their traditional ways. And some cases, like the Maasai, have a relatively high-fat intake, but no evidence of cardiovascular disease or other chronic diseases that plague us like diabetes and obesity. Then that tells us that higher fat intake within the context of a traditional diet and lifestyle does not necessarily have the same effects of higher fat intake in the context of our modern diet and lifestyle. This, of course, is the core argument following a genetically aligned diet and lifestyle—a Paleo type of diet and lifestyle. It really tells us what we need to know, which is that context is king. We can't extrapolate findings—isolated findings—about macronutrients like fat or carbohydrate in the context of an industrialized diet to a Paleo type of diet. If you see a study about high-saturated-fat intake and how it affects people, you have to assume that that study is being done on people who are following a Standard American Diet, and therefore those findings are not necessarily relevant to you if you're following a Paleo type of diet. Again this is a nuance that often gets left out of not only the study itself, but also any kind of media discussion about that study. Okay, so thanks, Carrie, for sending in your great question. Everybody else, please keep sending your questions in to chriskresser.com/podcastquestion, and I'll talk to you next time.

In this show we have Glenn Taylor of the Taymount Clinic, one of the few places doing fecal microbiota transplants, otherwise known as FMTs. He's doing some great work, and I know a lot of people are interested in this. It's a revolutionary treatment, and so I'm looking forward to getting the lowdown.

In this episode, we cover:

3:10 The history of Fecal Transplants
10:50 How the Taymount Clinic approaches FMT
16:40 How to screen for the right donor
24:15 What conditions can FMT treat?
30:50 The future of FMT technology
32:45 The side effects of Fecal Transplants
39:50 Why FMT is approved in the UK

[powerpress]

Full Text Transcript:

Steve Wright:  Hi, everyone.  Welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com, and I'm your host, Steve Wright from SCDlifestyle.com.  With me is integrative medical practitioner, New York Times bestseller, and healthy skeptic Chris Kresser.  Chris, are you ready for today's show?

Chris Kresser:  I'm ready, Steve.  I'm really looking forward to it.

Steve Wright:  It's my favorite topic, man.

Chris Kresser:  I know it.  Who doesn't like to talk about poop?

Steve Wright:  It just puts a smile on your face.  You can't say it without smiling.

Chris Kresser:  Yeah, we have Glenn Taylor of the Taymount Clinic in the UK, one of the few places doing fecal microbiota transplants, otherwise known as FMTs, and we're really excited to have him come on the show.  He's doing some great work, and I know a lot of people are interested in this.  It's a pretty revolutionary treatment, and so I'm looking forward to getting the lowdown.

Steve Wright:  All right, so before we bring him on, I just want to let the listeners know that as of today over 76,511 people have already signed up for Chris' free membership.  Yes, I just looked that number up.  It is true.  Chris has just recently redone his site at ChrisKresser.com, and what he's done is he has reorganized his content and created a lot of in-depth eBooks on weight loss, gut health, and thyroid health that you get access to when you sign up for his free membership, not to mention you'll get some in-depth audio seminars that have never been released to the public before as well as a free 30-part email series on Chris' most essential topics for anyone serious about feeling great.  If this isn't something that you have access to yet, you're going to want to take advantage of it.  Go over to ChrisKresser.com and sign up for the free membership.

OK, Chris, our guest today is Glenn Taylor from the Taymount Clinic, and as you were saying before, he specializes in fecal microbiota transplants.  Glenn is not conventionally medically trained.  He's a qualified engineer and a microbiologist, so we kind of have something going on there.  For some years, he was running a training center for health professionals, but he was unhappy with the colon lavage not appearing to bring about any long-term improvements.  He took a phone call one day, and a young man was asking about fecal transplants.  That got him thinking.  After two years' worth of research and experimentation, that gave rise to the new FMT clinic.  He has been doing FMT treatments now for nearly two years, and he has carried out over 800 of them to date.  Over the last few months, he has been invited to give talks at several top London hospitals and primary care trust hospitals.  In other words, this guy knows poop.  I'm excited.

Chris Kresser:  Let's bring him on.

Glenn, welcome to the show.  Pleasure to have you on.  Pleasure to speak with you again.

Glenn Taylor:  Well, thank you very much for inviting me on.  It's good to talk to you again.  It's good to get to talk to everybody out there.

The history of Fecal Transplants

Chris Kresser:  Great.  Let's take a step back a little bit for those who aren't that familiar with fecal microbiota transplants, and maybe you could just tell everyone what they are and a little bit of the history, how they were discovered and initially used therapeutically.

Glenn Taylor:  OK, well, it's a process of basically bringing the human gut back to as close as normal as we can hope to get it in the attempt to bring all the other processes that it impinges upon back to normal as well.  The first cases of manipulation of gut flora were, I guess, back in about 1908.  A Russian physician, Ilya Mechnikov, working in Paris had noticed the changes in human health and behavior when people were exposed to different types of bacteria in terms of probiotics.  He wrote a few papers on it that disappeared from view but ended up in just a couple of hospitals.

Then in 1958 in a fit of desperation, one of your countrymen, Ben Eiseman, a doctor working out of Denver, was faced with four patients with a really advanced case of toxic megacolon, which is an infection of Clostridium difficile, and the four patients were completely refractory to all kinds of treatments and their prospects were very grim.  Eiseman went to the hospital library and looked up some papers that might help him and came across the original Mechnikov papers, and he thought, well, we have some evidence here that borrowed microflora from another human being may be the answer to the problem.  Back in '58, this was very radical.  I mean, the idea of swapping poop really wasn't taken quite as easily as it is now, but he went to the four families and told them what he had found.  Obviously faced with the prospect of losing their loved ones, they just said, please, go ahead.

The astonishing thing was that all four patients made a very rapid recovery.  He wrote his own paper, and this was all before the Internet, so it meant people had to keep this stuff in a library.  And I guess most people now are aware that those papers ended up in Sydney, Australia, where a young professor of gastroenterology, Tom Borody, read them when he was faced with a similar situation, and I think from then on people have become more and more aware of its potential.

The astonishing thing is that farmers have been passing this down by word of mouth from generation to generation, that the beasts on their farm can benefit from getting the bacteria from healthy beasts and cattle and birds transferring them to sick creatures, and they've been doing this for literally hundreds of years.  I have a couple of veterinarian friends who swap stories like this and then throw their hands up in horror and say, well, surely you're not now talking about doing this in humans!  And I'm always tempted to say, what [indiscernible]!

Chris Kresser:  Right!  Well, it's amazing how much more open minded we become if our life is threatened, and certainly as you pointed out with C. diff, it's a potentially life-threatening infection.  There are antibiotic-resistant forms that don't respond well even to some of the most potent broad-spectrum antibiotics, and people in the year 2014 are still dying from it.  In a way, it's sort of a blessing in disguise that we've had this testing ground for this remarkable new treatment because I don't think it would have achieved such rapid acceptance in the scientific community if it hadn't demonstrated such an incredible ability to be effective in a situation where nothing else is.  I think that really opened the door for people to be amenable to it in a way that they wouldn't have been otherwise.

Glenn Taylor:  Yeah, I partially agree with you, but don't you find it actually extraordinary that despite the amount of coverage, I mean, scientific papers, academic papers being available now that discuss this in fine detail, so many papers saying that this is an effective treatment for, in particular, Clostridium difficile, and articles being written in all the world's top gastroenterological journals and mouthpieces, and yet when you talk to the average gastroenterologist, they're still wide mouthed and amazed about it?  It makes you wonder, don't they read their own professional journals?

Chris Kresser:  Well, Glenn, I wish that did surprise me.  Unfortunately it doesn't surprise me in the least because I come across that every day in my practice, where I refer a patient to a specialist, like a gastroenterologist.  Or another case where this often happens for me is I discover that someone has iron overload and I refer them to a hematologist only for them to be told that there's nothing to be concerned about, and I just want to pull my hair out because I've read numerous papers published in the scientific literature about the risks of even somewhat mildly elevated iron levels, but seemingly these hematologists who are the top specialists in the field are not staying current with the literature in their very field.  Unfortunately I was prepared for that to some extent, but there's this frustrating gap between what's in the scientific literature and then what even specialists in that field, much less primary care physicians and the general public, have accepted, but it seems to me – and maybe you disagree – but it seems to me that the acceptance of this procedure sort of skipped over the gastroenterologists and the medical community and we've seen a lot of articles about it in the public media that are more friendly to it than you find just talking to the average gastroenterologist.

Glenn Taylor:  Oh, yeah.  I had a phone call from New Scientist.  They really just wanted to know the background and to talk about it and see if they could have access to one of my patients.  Scientists are now beginning to really want to know more about the biological value, and that's why I say it is good old fashioned biology, which if you've been brought up on an entire menu of pharmacology and chemistry, it's perhaps a step too far.  It depends on how you're trained, I guess, Chris.  If your professor at college fed you pure pharmacology, then you're going to carry that [indiscernible].

Chris Kresser:  Yeah.

Glenn Taylor:  I think we have to look further back to why people have these ideas that only one type of medicine is effective and when you run out of pharmacological solutions, you should then actually deem something to be incurable.  I think it's a little unfair.  The term 'incurable' means you haven't found a cure.

Chris Kresser:  Exactly!

Glenn Taylor:  It's doesn't mean to say that it doesn't exist.

How the Taymount Clinic approaches FMT

Chris Kresser:  Yes.  I think also that the increase in interest – and this, of course, is not coincidental – but there is a lot of attention being paid now to the microbiome.  We've had front page stories on The New York Times Magazine, Michael Pollan, and I know that there are some books in the pipeline that are coming out about the microbiome and its connection between health and disease.  That's, of course, the theoretical underpinnings of why a fecal microbiota transplant would work in the first place and why it's something we might want to investigate, and then we have these research projects, like, we had Jeff Leach on to talk about the American Gut Project and all of these ongoing research projects looking at the microbiome.  So, I'm cautiously optimistic.  I think there are definitely some hurdles, especially regulatory hurdles in the US, and I'll be curious to hear what's happening in the UK with that, but before we get into that, why don't you tell us a little bit about how you and your team over at Taymount approach FMT, because I think what you're doing, from our previous conversations, is somewhat unique in the world, really.

Glenn Taylor:  OK, so maybe I'm a little bit too much of a scientist, in that I really wanted to know how to make the very best of the procedure.  And that led me to many, many long hours in the lab, a lot of research along with some of the leading people in the world, particularly some of the best food microbiologists in the world – and I take my hat off to the amazing team at Reading University in the UK who are trying very, very hard to understand all gut functions in relation to the microbiome – but what I needed to do was to understand why the process did and didn't work in certain cases and why was it that home treatments – and I can understand why people do it; it's out of complete desperation because it's not available to them or the cost is prohibitive – why home treatments had relatively poor outcomes.  I guess the answer lies in a very simple feature.  It's a simple biological fact that 90% of the gut microbiome is of a group called obligate anaerobes.  Now, that quite simply means that they cannot survive in oxygen.  If you expose them to an oxygen-rich environment, they die.

So, all these poor people who don't really quite understand that particular aspect are taking stool from a friend or a loved one, putting it into an ordinary kitchen blender, blending it up in the presence of oxygen and perhaps not quite the right liquid medium, and almost instantly they're killing 90% of the bacteria that would have been available.  When you don't know precisely which one you're missing, I cannot understand why you'd take the risk of killing 90% and hoping that the one you need is in the remainder.  Then subsequent mishandling of the rest of the process means that people are getting exposed to a very, very small amount of what they need.

What we did at the clinic was we addressed that fact, and we work in an almost completely anaerobic environment.  The collection process is anaerobic, without oxygen.  The homogenization, breaking up, the separation, filtration – everything is done in an anaerobic environment, which means that when we collect bacteria, at the end of the two-hour process, we have a pellet of bacteria that's pretty much intact.  Now, that's what everybody's after.  When you're trying to take a microbiome out of one human being to put it another, what you're hoping for is to get as close to 100% of that bacteria as you possibly can because at this moment we don't know exactly which of the, oh, it could be a thousand, it could be 1150 species at this moment.  There are new methods of assay, new methods of measuring which are kind of suggesting at this moment that there may be many more thousands of species in the gut than we actually realize, and because of the way the morphology goes on, it could be literally a never-ending number of species because they're constantly mutating.  And there's no catalog for this.  We just don't know where we're going to end up, so we try and gather safely together as many as we possibly can and store them in the correct way.  That's the process.

Also we want them to go back in and be effective, so we’ve spent some time working on the implant method, and we're feeling quite comfortable that we've found the most benign and most comfortable, in itself with the patient, the most comfortable method, the most effective method of complete dissemination around the whole of the colon, and we had to work hard on this to come up with a gentle, effective method of delivery.  I also have a method I'm working on in the background, and I'll probably bring it to a much wider audience and make it much more acceptable to the public at large, but I have some pegs to put in place before I can talk about it.

How to screen for the right donor

Chris Kresser:  All right, that's exciting.  We'll have you back on the show when you're ready to release the goods, so to speak!

Glenn, another potential concern that I have in terms of DIY, at-home FMTs is improper screening of donors.  I know when people really get desperate because I've been there myself in my past and with my pretty severe chronic illness that judgment can be impaired, let's just say.  And when there's a treatment that promises some potentially miraculous benefits, it can be relatively easy to minimize the risk, at least in our own mind.  Why don't you talk a little bit about how you're screening donors and making sure that the donations are of the highest quality, which, of course, will lead to the best results?

Glenn Taylor:  Well, first of all, I have huge sympathy for all those people who because of the lack of interest of their own physician or the lack of a facility wherever they live they're being driven to do this themselves.  And on top of that, they simply don't have the finances in many instances to be able to take all the precautions they should, but we really have to urge people that if they're already immunocompromised with a condition, they could make things very, very much worse for themselves.  The donor they choose may not display the symptoms of a severe disease, but they could simply be a carrier, and you never know what you're going to get, so you owe it to yourself and your loved ones around you to be absolutely sure that your donor is safe.  You have to do your best to make sure there are no communicable diseases.  I know it means having to go through some medical professional to see if you can get the testing done, but when the alternative is so horrendous, you really should just take that extra bit of effort to make sure that your donor is good.

Also this idea that the donor should be somebody from the family and who shares the same environment in biological terms is actually erroneous because people living together over a period of time gradually share their bacteria.  This is a simple biological fact.  They share their bacteria, and their microbiomes become very similar.  There will be some minor changes in them, but despite the fact that everybody has this unique microbiome, almost a fingerprint style, it's quite unique to them, in general terms, we all have little wavy lines on our fingers, same thing as we all have x number of bacteria.  People living in the same environment generally have the same type of bacteria.  Now, if your condition has been brought about because you're missing certain bacteria, what on earth makes you think that your partner, spouse, friend, or cousin is going to have that bacteria if they share the same environment, share the same food, etc.?  It doesn't actually make good biological sense.  What you actually really need is somebody outside your environment who has a completely different profile of gut flora.  That's the person you're after.  And then if you get them tested and they're good, that's the person you should go for.

But equally, I’ve heard talk saying, I want the microbiome from somebody's who has never had antibiotics, so let's go for an infant, a child.  Please, don't forget for a second that a child only gets the microbiome that it got from its mother during the birth.  If the mother didn't have a good microbiome, the child's not going to have a very good one.  And then it takes up to two years for a child to develop an adult-like microbiome.  Despite the fact the child may not have been exposed to antibiotics, they'll have an immature microbiome as well, and that might not suit your purpose.

Chris Kresser:  Mm-hmm.  So, give us an idea a little more specifically of what kind of tests that you're doing to screen donors just so people have a sense of what the spectrum of these tests are that need to be done.

Glenn Taylor:  Obviously, all the sexually transmitted diseases and HIV.  I think most of it's sitting on our website where you can see precisely what we're doing, but in essence, we really are trying to protect people from the serious life-taking diseases and the other diseases that would affect you if you're immunocompromised, even down to sort of rheumatoid factor, arthritic – there's a whole group of things that you really don't want to pick up just because you want a good microbiome.

Chris Kresser:  Right.

Glenn Taylor:  You just have to use common sense, and actually what I noticed this afternoon when I was just cruising through some websites is that there's a lot of information out there that people can go and look for when looking for the testing.  Tom Borody did a paper that has a home protocol that's pretty comprehensive.  Alex Khoruts has, as well, so there's stuff out there from people who have been doing this for a very long time that's very valuable information to make sure that you can protect yourself.

Chris Kresser:  Yeah, and it's worth saying that as our understanding of the microbiome expands, the kinds of testing that we're doing to screen donors expands as well.  I was in contact with the Center for Digestive Diseases and Dr. Borody's clinic probably 10 years ago, and I'm pretty sure – and they may still not be doing this, I'm not sure – but they weren't at that time doing tests for autoimmunity because it wasn't as clearly understood as it is today that autoimmunity is linked to the microbiome, so it's really great to know that you're thinking more broadly in terms of what an optimal donor might be and which markers that we can currently test for might exclude them from being donors based on that connection between the gut microbiome and not just digestive conditions, of course, but now many other conditions including immune dysregulation and mental and behavioral problems, the whole gamut.  It's really actually difficult to find a modern chronic inflammatory disease that the gut microbiome is not linked to at this point.

Glenn Taylor:  Isn't it astonishing?  I get inquiries all the time with obscure diseases, saying, what do you think?  And my only response can be, well, we haven't found anybody or we haven't treated anybody with that particular condition, but hey, I've learned enough by now not to discount it, and do you want to be the first?

Chris Kresser:  Yeah, worth a try.

Glenn Taylor:  Shall we give it a try?  I'm not discounting anything, really.  The likelihood is that we could be going on for years and years, bumping in more and more conditions that respond favorably once we've normalized the gut microbiome.

What conditions can FMT treat?

Chris Kresser:  Mm-hmm.  I don't doubt it at all.  Along those lines, though, tell us some of the conditions that you've seen respond particularly well.  Now you've done about 800 of these, it sounds like, so you've had a broad spectrum of patients or people that have come and have had experiences.  Tell us a little bit about what you've learned.

Glenn Taylor:  Everybody knows that the whole thing started off with Clostridium difficile, so we've done our fair share of C. diff.  We're actually really, really lucky at this moment in that in every case of C. diff we've managed to get full remission.  It's completely clear.  We're doing testing before and after, and everybody so far is absolutely clear.  I have a young lady who started this week, who I can't name, but she is a midwife and she picked it up at her place of work.  And after two years of them trying to get rid of the Clostridium difficile recurring every three months, they'd given up, and basically they were trying to railroad her out of a job.  They gave her the thing in the first place, and now they're trying to get her out of a job.  She came to me, and on day one I just completed the implant, and I sat her up and said, right, in about a half an hour's time, that's it.  It's over and done with.  You're back to work.  And she just broke down.  She couldn't quite take it all in.

Chris Kresser:  Yeah.

Glenn Taylor:  On the second morning, she came back.  I had her come into the clinic.  She was taking the stairs five at a time, and she just threw herself through the door and said, I feel just extraordinary, absolutely amazing!  She got her life back again.  C. diff is easy.  What I'm finding really, really interesting is I'm working quite a bit with that very, very nebulous of conditions that's called IBS.

Chris Kresser:  Yes.

Glenn Taylor:  You can probably hear in my voice that I'm smiling at the moment.

Chris Kresser:  Mm-hmm.

Glenn Taylor:  The lengthy protocol, you get a list of 10 symptoms, and if you sit with your physician and he can tick three of them, then great.  He's happy because he has a diagnosis and he has a stamp that he can put on your forehead and say, you have IBS.  There's probably not much we can do about it.  You'll have to just get used to living with it.

Chris Kresser:  And more importantly, drugs they can prescribe that have been created for that condition that was created for the purpose of making drugs for it!

Glenn Taylor:  Chris, you are turning into an old cynic, you are.

Chris Kresser:  I can't help it.  I can't help it.

Glenn Taylor:  So, I look down the list of their own three of I think, yes, dysbiosis.  Yeah, that's bacteria.  Yeah, that's bacteria.  That's bacteria.  Basically change the gut flora with people with IBS.  Stop.  Take a step back.  Watch their symptoms.  Send them back to their physician again who did the diagnosis, and say, now what do you think they have?  It's a real eye opener.  We're having a great time with IBS at the moment.  Really, a good time.  People are coming in for post-antibiotic, post-infectious IBS, for a combination of constipation and diarrhea or one or the other, and we have some very, very happy [indiscernible] walking home at the moment.  And I think it's perhaps it won't take too long before FMT becomes the treatment of choice, the first treatment of choice for all IBS.

I was talking to two major gastroenterologists in London a couple months ago.  These guys are professors of gastroenterology at the top of their field, and they were saying, we really are looking forward to the day when it's available as a first choice, not a last resort, because patients come to us with this whole mass of white noise that's going on with the various symptoms they've got.

Chris Kresser:  Yeah.

Glenn Taylor:  And it's so very confusing trying to work your way through all these various symptoms to work out precisely what the problem is.  If only we had a method where we could normalize them and get rid of this effective white noise, and we believe that FMT might be the answer because normalization of the gut normalizes other processes.  Then we send the patients back to their doctor much quieter, and the doctors go, oh, crikey, yeah.  Now I can see what you've got.  Oh, that's really much clearer.  It was cloudy before.  I couldn't quite work it out, but yeah, I can diagnose, and here's the remedy for it.

Chris Kresser:  Glenn, this is so similar to a paleo challenge or intervention, which you've probably heard of.  When I see a patient who comes in to me with all of these varying symptoms that are seemingly disconnected and all over the place and they're on a kind of Standard American Diet, the first thing I do is put them on a paleo type of diet for 30 days, and I use the exact same language that you just used.  It's like a cloud settling or silt in a pond going to the bottom, and at the end of that 30 days, it doesn't mean that they won't have any issues, but it'll be much clearer what those issues are because all of the triggers that were causing all that chaos in their body have been removed and the dust has settled and the things that are remaining are much more easier to go after, after that.  Imagine if we combine a nutrient-dense, whole-foods dietary intervention like paleo for 30 days with an FMT.  The potential for that is just mind blowing.

Glenn Taylor:  Exactly.  As anybody that works in a hospital will tell you, patients turn up with a whole range of comorbid conditions, and it makes it very difficult for them to be quite precise.  And if there was a standardized procedure that they could employ that would help them sort the wheat from the chaff, it would be hugely helpful.  Now, you know that doctors of functional medicine have this fixation on the gut, if you can fix the gut first and then look at the rest of the patient.  They only know that it's a good idea, but perhaps they don't quite understand the microbiology of why.  But when you say to them, yeah, the reason why you're going to sort the gut is to normalize the gut flora because of all the other things that impinge upon it.  Then you stand more of a chance of actually highlighting precisely what the problem is.  Yeah, it will be a treatment of the future, I'm sure, but it's all come down to the method of delivery, and that's the bit.

Chris Kresser:  Yeah.

Glenn Taylor:  I think Tom and I are on a bit of a race at this moment to come up with that.

The future of FMT technology

Chris Kresser:  Well, I'm rooting for everyone in this race because we're all going to be the beneficiaries of your passion and investigation, so I'm excited.  I was going to ask you a question about the oral form of delivery, which has gotten some press recently.  I believe it was a Canadian physician who was written up about that.  I'm not sure if you want to go into that or leave that for the next time when you come on the show.

Glenn Taylor:  No, that's OK.  You're talking about Robogut, are you now?

Chris Kresser:  Yeah.

Glenn Taylor:  Or you're talking about Hamilton's project.  On Robogut, yeah.  It's a good attempt.  At the moment, the best that they're coming up with is about 10% of the microflora, but it's a controlled, standardized system, and it's quite effective, yet it's 10% of what's actually needed.  But it might to the 10% that works, Chris.  It may be, but we've still got to see how that goes.

Chris Kresser:  Sure.

Glenn Taylor:  The oral route – you see, now you're trying to get me to tell you what I'm doing!

Chris Kresser:  No, no, no, I'm really not!  I shared an article a while back about the Hamilton, the oral delivery system for this, and of course, it generated a lot of attention and interest.  I'm not going to force you to talk about it at all.  You can just say whatever you want to say, and as long as you promise to come back on the show when you're ready to say more, we'll leave it at that.  We've got plenty more to talk about.

Glenn Taylor:  OK, well, how about this?  If I'm right about the method of delivery and if I get it right and if I can put all the factors together to make it effective and it becomes scalable and deliverable, we hope to be able to slash the price of the treatment by 10.

Chris Kresser:  That's tremendously exciting, and I'm sure that a lot of my listeners are jubilant hearing that!

The side effects of Fecal Transplants

Let's get back to some of the nittier, grittier details.  We were talking about the importance of screening donors, we've talked about how – really, there's no other word – miraculous some of the transformations can be with this procedure.  I'm sure a lot of people are wondering, well, is there is a downside?  What are the side effects of FMT, and what are the risks when it's done properly?  Since we've already discussed the importance of doing it properly, let's just assume that it's done properly.  Are there side effects and are there risks?

Glenn Taylor:  OK, in the clinical environment, side effects.  Well, in terms of the biology, you ask the question, if you take perfectly functioning bacteria out of a healthy person and you put them into a person who has dysbiosis, what reason would there be to be a side effect or a negative effect?  And the reality is, no, there isn't.  However, that's not totally true because we have had a couple of occasions where people have been teetering on the very edge of an IBD flare and just interfering with their microbiome sets them off, so we've had to stop treatment, send them home, and get their physicians to bring their flare back under control before they can come back in.  So, it has happened where a flare tips over simply because we're working in that area.  It may well be that they were scheduled to have a flare and it was the last straw that broke that particular camel's back.  But in all other cases, I don't believe there are any recorded cases of a clinic application that have had any kind of negative side effects.

Chris Kresser:  Which makes this, of course, all the more remarkable.  I want to actually move backwards because there's a question I forgot to ask you that I wanted to.  Have you had any people coming over with chronic infections that have had any success?  I'm thinking of things, you know, intracellular infections, Chlamydia pneumoniae, some of the stealth infections, like Lyme and Bartonella, Mycoplasma, stuff like that.

Glenn Taylor:  No, I haven't.  Please, where are these people?

Chris Kresser:  Careful what you ask for because I'm sure a lot of them are listening right now!

Glenn Taylor:  Well, that's the kind of stuff that we need to be able to do sufficient numbers of.  I know the medical community wants big n numbers, big numbers in a sample, a large sample, before they'll even listen to the result.

Chris Kresser:  Yeah.

Glenn Taylor:  But remember the world's first medical trials took place on a British warship in the 1700s when the surgeon on board the vessel chose six crewmen, all suffering with scurvy, and gave three of them lemons and three a placebo effect, and the n number, the total sample, was 6.  Now, the first trial went down as a huge, huge success with such a low number and we applaud what went on.  You try and do a trial today with 6, and they'll laugh you out of the room.

Chris Kresser:  Yeah.

Glenn Taylor:  They only want hundreds or thousands.  But if it works and it works again and again and again, don't we owe it to take it seriously and see if we can try and get more interest, get people to listen to us?  There's such a fixation on high n numbers as being the only credibility in terms of treatments.

Chris Kresser:  Yeah.  It's a real obstacle.  There are even n=1 experiments in the history of science, like, was it Warren and Marshall and the discovery of H. pylori?

Glenn Taylor:  Yeah.  Tom, by the way, Borody was involved in that.

Chris Kresser:  Yeah.  He was a grad student for them or something?  Yeah.  For people who don't know that story – and correct me if I'm wrong; I'm a little hazy on it.  At that time, everyone thought ulcers were caused by stress, and they presented the idea that they were actually caused by a bacterium called H. pylori, and they were literally laughed off the stage at the conference that they presented at and then proceeded to labor in obscurity for several years and be completely ignored by their professional colleagues.  And it wasn't until he infected himself with H. pylori, developed an ulcer, and then cured it with antibiotics that he was taken seriously.

Glenn Taylor:  Absolutely.  I remember watching Barry and Robin sitting together. – That's not the Gibb brothers, by the way! – They were sitting at a restaurant, and this was 10 years after their first discovery.  And I remember looking at Barry's face, and he was so jaded about his.  He said, look, it's been 10 years since we discovered Helicobacter pylori and we've now got 10% of the doctors accepting and treating for it.  Maybe in a hundred years' time we'll have everybody doing it.

Chris Kresser:  Wow.

Glenn Taylor:  Yeah, he wasn't impressed with his peers.  That was a typical case.  They had to peddle that all over the world for people to listen, and the established structure, the old guard, were really not ready for this young upstart to stand there and tell them how things worked.  And yes, Marshall had to infect himself and then cure himself in an effort to make people sit up and take notice.  You know, that's not uncommon in history, where the only chance you get to do the research is on yourself!

Chris Kresser:  That's right!  And it's ludicrous to discard that result, in particular, simply because it was only one person.  That's a rather compelling result, which actually in one experiment shows a causal relationship and not just an association and makes it certainly worthy for further exploration, so I completely agree with you on the recent trend of the over-focus on sample size and even on RCTs as if we can't still use our common sense to reach conclusions, as if common sense is not part of the scientific process or even the basis of it.

Glenn Taylor:  I agree.  What I'm seeing is a lot of physicians being interviewed and dismissing the procedure on the basis that they've yet to see large-scale trials.

Chris Kresser:  Right.

Glenn Taylor:  And I think we've worked that one to death.

Why FMT is approved in the UK

Chris Kresser:  Yeah, exactly!  Tell us a little bit about the regulatory system in the UK.  I've posted several articles on what has happened in the US.  The FDA has only approved the use of FMT for antibiotic-resistant C. diff.  That means it's not technically approved to do for any other uses, and I know there was a clinic in Portland that was doing some FMTs that was doing them for other conditions but is now only doing them for antibiotic-resistant C. diff.  I imagine the environment must be a little bit different in the UK, given your presence and operation, so tell us about that.

Glenn Taylor:  OK, yeah, that's because of Europe and the UK having a completely different medical structure than the United States.  Our structure is based on a state system, a state kind of insurance system.  It's very different from the health industry.  Oops.  Did I say 'industry' instead of 'profession'?  Very, very different from the way that it's financially structured over in the United States, this triangle of insurance company, physician, and drug company that you guys have yourselves stuck in and don't seem to be able to extricate yourselves from, which has allowed – boy, I'm going to have to choose my words carefully here!  I am not making any accusations, not making any suggestions, but I would really like to see the structure of the ethics committee that came up with the decision that FMT or human feces should be regarded as an investigational new drug.  I'd like, honestly, to see the structure of that committee and see who is a genuine physician and who is in medicine and who is in pharmacology.

Chris Kresser:  Yeah.

Glenn Taylor:  But then you never forget there's a big issue of safety, and I think also – and this is genuine – that they needed to see a standardized system of reporting in this particular respect.  Clearly it was a health thing, and it appeared to be effective, and no health authority in the world can afford to let this just run amok, so some form of regulation was needed, as will be needed in the UK, and I look forward to it.  I'm sure that at some point the lack of regulation could equally lead to many, many problems, but in the UK at the moment, this is research work, and scientists are permitted to go on with research without being over-encumbered with too many restrictions by medicine itself.  Medicine in Europe tends to respond to what scientists discover.

Chris Kresser:  Imagine that!

Glenn Taylor:  And then what we find out we hand over to physicians who then make use of it.  I think that we're getting a lot of interest.  There are journals, there's the media, there are doctors and hospitals who are sitting on the sidelines watching with great eagerness as to what we're going to be able to do with this, and I'm regularly asked, what kind of response are you getting with this condition or with that condition?  They're all hopping from one foot to the other, hoping that something will happen soon, and I think we really are – actually, Chris, would you say that we're reaching tipping point?  I think the exposure of this is such that we're getting to the point where no matter what interested parties might be out there that wouldn't want to see this progress, when the public know enough about it, you can't put this back in the tube.

Chris Kresser:  Yeah.

Glenn Taylor:  We're going to reach a point where everybody will want to know.

Chris Kresser:  I would definitely agree with that, and I do think we're nearing that point, if not right on the cusp of it, so it's an exciting time to be involved in this, to be, I imagine, in your shoes, to be a functional medicine practitioner, someone who works with patients and may be able to administer this kind of treatment or at least refer them to it, so I'm really looking forward to seeing what unfolds, and I really appreciate you taking the time to come on the show.  Stay in touch, and we'll definitely have you back when you're ready to talk about the new delivery system.

Glenn Taylor:  Absolutely, I'd love to.  No problem at all, Chris.  Big thanks to you guys.

Chris Kresser:  Take care.

Glenn Taylor:  Thank you.  Bye-bye.

Chris Kresser:  Bye-bye.

The post RHR: All About Fecal Microbiota Transplants appeared first on Chris Kresser.

An altered gut microbiome is associated with a number of different chronic diseases, including obesity, diabetes, metabolic syndrome, inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), skin conditions, anxiety, depression, and multiple sclerosis, to name a few. (1) Animal studies have confirmed that many of these relationships are causal—in other words, gut dysbiosis in and of itself is sufficient to cause disease. (2)

Recent media coverage is painting probiotics as anything from completely purposeless to potentially harmful. So, are probiotics useless? Check out this article to find out what the research really says.

With all of this emerging research, it’s no surprise that there is increasing interest in ways to alter the gut microbiota to improve our health.

According to a 2012 survey, 3.9 million Americans regularly take probiotics or consume them in yogurts, smoothies, or other foods, and 61 percent of physicians regularly prescribe probiotics to their patients. (3)

While probiotics are largely unregulated and their use has always been controversial, there are now hundreds of peer-reviewed, randomized, placebo-controlled trials that have demonstrated the safety and efficacy of a variety of probiotic strains. (4)

So yesterday, I was surprised to find that my inbox was inundated with emails asking for my opinion on the latest media headlines:

• “Probiotics are mostly useless and can actually hurt you”
• “Probiotics: don’t believe the hype?”
• “There’s really not much proof probiotics work”

These media articles appeared in the wake of two new papers published in the prestigious journal Cell, authored by scientists at the Weizmann Institute of Science in Tel Aviv, Israel:

• Study #1: Personalized Gut Mucosal Colonization Resistance to Empiric Probiotics Is Associated with Unique Host and Microbiome Features
• Study #2: Post-Antibiotic Gut Mucosal Microbiome Reconstitution Is Impaired by Probiotics and Improved by Autologous FMT

As I scanned through the full text of the studies, it didn’t take long to realize that the media had shrouded any real discussion of the study findings in favor of scare tactics and click-bait titles.

If you want the real evidence, I’ll break it down here, including a nuanced discussion of the fecal vs. gut microbiome and the evidence for and against probiotics. If you want to skip the scientific details and just hear my take on this research, feel free to skip to the “Takeaways and Implications” section at the end.

Finding #1: The Fecal Microbiome Isn’t Really the Gut Microbiome (But We’ve Actually Known That for a While)

Many clinicians, researchers, and citizen scientists alike use stool samples as a relatively inexpensive and noninvasive way to sample the gut microbiome. I use them regularly in my own research. Unfortunately, stool samples may not be reflective of the microbes that are actually present in the gut.

The gut can be divided into the upper GI tract (small intestine) and the lower GI tract (large intestine, or colon). It can also be divided cross-sectionally into the gut lumen and the gut mucosa. If you think of the gut as a hollow tube, the lumen is the innermost (center) part of the tube, while the mucosa is like a sticky gel-like substance coating the wall of the tube.

In the first study, researchers took samples from the feces, gut lumen, and gut mucosa of mice and humans. They found that each sample type harbored a distinct community of microbes and that fecal samples were a far cry from accurately predicting abundance of bacteria from even the most distal part of the GI tract. In humans, more than 10 bacterial taxa were significantly over- or underrepresented in stool samples compared to the lower GI tract lumen and mucosa.

Finding #2: Probiotic Colonization Is Largely Transient in Mice (But We’ve Known That for a While, Too)

Next, the researchers investigated whether probiotic supplementation would result in effective colonization of the mouse gut. For four weeks, they gave mice a cellulose placebo or a probiotic supplement containing a total of 5 billion colony-forming units (CFU) from 11 different human-associated strains, including:

• Lactobacillus acidophilus
• Lactobacillus casei
• Lactobacillus casei subsp. paracasei
• Lactobacillus plantarum
• Lactobacillus rhamnosus
• Bifidobacterium longum
• Bifidobacterium bifidum
• Bifidobacterium breve
• Bifidobacterium longum subsp. infantis
• Lactococcus lactis
• Streptococcus thermophilus

Analysis of the upper and lower GI tract lumen and mucosa found no evidence of probiotic colonization. However, probiotics did significantly alter the the lower GI tract microbiome. Altogether, 21 bacterial taxa differed between the probiotic and control groups in the lower GI mucosa.

Finding #3: The Normal Microbiome Inhibits Probiotic Colonization

The authors hypothesized that the mice were not colonized by the probiotics because their normal, commensal microbiome was resistant to the supplemented strains.

To test this, they used germ-free mice, which are raised in sterile incubators with no exposure to microbes. These previously sterile mice were given the same 11-strain probiotic supplement for 14 days.

In the absence of a normal microbiome, the mice had massive colonization of the probiotic strains. This confirmed that commensal microbes were inhibiting the colonization of the probiotic strains.

The authors summarized their findings:

Taken together, these findings suggest that despite daily administration, human-targeted probiotics feature low-level murine mucosal colonization, mediated by resistance exerted by the indigenous murine gut microbiome.

Finding #4: Probiotic Colonization in Humans Is Individualized

While inbred lab mice allow for reduced variability microbiome research, they are not necessarily indicative of what happens in genetically diverse human populations. Thus, the researchers next recruited 15 healthy volunteers to receive the 11-strain probiotic or a cellulose placebo twice daily for four weeks.

Unlike in mice, they found that nine out of 11 probiotic species were significantly enriched in the mucosa of the probiotic-supplemented group after four weeks. The effect was most pronounced in the ascending and descending colon of the lower GI tract.

Interestingly, there was significant variability between participants in terms of how receptive they were to probiotic colonization:

• Six of the 15 volunteers had significant elevation in the absolute abundance of probiotic strains in the gut mucosa and were deemed “permissive” probiotic colonizers.
• Nine of the 15 volunteers did not have significant enrichment of these strains and were termed “resistant” to probiotic colonization.

Despite clear evidence of colonization, the researchers found no alterations in the gut microbiome in any region of the lower or upper GI tract when all 15 individuals were considered. Only when “permissive” probiotic colonizers were analyzed separately did they find significant shifts in the gut microbiome.

This doesn’t mean that the probiotics had no effect, though. The authors write:

Nonetheless, when all probiotic-consumers were considered together, probiotics consumption led to transcriptional changes in the ileum, with 19 downregulated and 194 upregulated genes noted, many of which related to the immune system including B cells.

Finding #5: Probiotics Slow Recovery of the Normal Microbiome after Antibiotics

As though the first four findings weren’t enough, the researchers then sought to determine how probiotic colonization might differ after broad-spectrum antibiotic treatment. (This begins the second paper.)

It’s well known that the human microbiome can take many months to recover from a single course of broad-spectrum antibiotics, and even then, recovery may be incomplete. (10, 11)

Moreover, antibiotic exposure, especially during the early years of life, is associated with an increased risk of developing allergies, asthma, autoimmunity, obesity, IBD, and skin conditions. (12, 13)

Thus, probiotics are widely used and prescribed during or after antibiotics, with the idea that flooding the system with good bacteria can help prevent the adverse effects of antibiotic-induced gut dysbiosis. Indeed, several short-term studies have suggested that probiotics might be helpful in preventing antibiotic-associated diarrhea. (14)

However, the impact of probiotics on the long-term restoration of the gut microbiota after antibiotics had not been studied—until now.

The Israeli researchers first treated both mice and a cohort of 21 healthy human volunteers with a single course of the broad-spectrum antibiotics ciprofloxacin and metronidazole (14 days in mice, seven days in humans). They then split the mice and humans into three groups:

• Group 1 was allowed to spontaneously recover over time.
• Group 2 was supplemented with an 11-strain probiotic (in the same formulation as above) for four weeks following antibiotics.
• Group 3 underwent autologous fecal microbiota transplant (aFMT), where their own fecal samples before antibiotics were frozen and used to re-inoculate their gut a day after the antibiotics finished.

So, what did they find? Antibiotic perturbation of the gut microbiome only mildly improved probiotic colonization in mice, but it significantly enhanced probiotic colonization in the human gut mucosa, particularly in the distal small intestine and lower GI tract.

More importantly, they found that treating the gut with probiotics actually delayed the normal recovery process of the gut microbiome.

To be honest, I wasn’t sure what to make of this at first. I first read the mouse data, which suggested that probiotic supplementation significantly delayed the return to baseline microbiome richness, even compared to spontaneous recovery, and that several taxa were slower to return to baseline.

My initial reaction was, “Okay, does species richness matter, though?” What if the interim microbiota has less richness but is in some way protecting the host? Perhaps the gut mucosa is selecting for certain microbes to take up some extra space within the gut environment, providing protection until the ecosystem can recover?

But then I reviewed the human data. The authors write:

“…probiotics-consuming individuals did not return to their baseline stool microbiome configuration by the end of the intervention period (day 28), and dysbiosis was maintained even 5 months after probiotics cessation, with all stool samples collected through day 180 remaining significantly different from baseline. [emphasis added]

The lower GI mucosa of the probiotics group experienced a significant bloom of Blautia, Akkermansia, Enterococcus, and Bifidobacterium spp. and maintained low alpha diversity for several months. Meanwhile, in the spontaneous recovery group, significant differences in stool composition from baseline had vanished within 21 days after antibiotics.

The authors did note a few limitations:

• No clinical symptoms were measured during or after antibiotic treatment.
• They tested a single combination of broad-spectrum antibiotics and a single oral probiotic supplement mixture: “Other combinations of antibiotics, probiotics, and treatment routes and timings merit further studies.”
• The study was also conducted in healthy adults, so these results can’t necessarily be extrapolated to children, the elderly, or those with gut pathologies.

One experiment I wish they had performed: I would have LOVED to see them “challenge” the mice with Salmonella or some other enteropathogen in the aftermath of the antibiotics. This would help determine if there is any potential trade-off; for instance, perhaps normal restoration of the gut microbiome is delayed, but the probiotic-colonized gut confers greater protection against pathogens until the ecosystem recovers. I’ll discuss what data we do have in this regard in the “Takeaways and Implications” section at the end.

Finding #6: Lactobacillus in Particular Prevented Microbiota Recovery

Perhaps the coolest part of this study was the culture-based experiments that the researchers performed last. They took the probiotic pill and cultured it in five different growth conditions that differentially supported the growth of each of the four genera (Lactobacillus, Bifidobacterium, Lactococcus, Streptococcus).

After 24 hours of culture, they collected the biochemical “soups” surrounding the probiotics on the dish and added each to an anaerobic culture of fresh human fecal microbiota. They found that the “soups” that had come from the plate with lots of Lactobacillus showed the strongest inhibition of the native human fecal microbiome.

Specifically, Lactobacillus significantly reduced the diversity and altered the gut community structure. Abundance of Prevotella and Clostridiales were particularly affected, in line with what the researchers saw in the live mice and human experiments.

Finding #7: A Personal Poop Transplant Results in Rapid Recovery After Antibiotics

By this point you should be asking: what about Group 3, the ones that received their own fecal samples to reinoculate their gut?

In stark contrast to the probiotic-supplemented group, both mice and humans in the aFMT group “achieved a rapid and near-complete gut mucosal microbiome recolonization.” In mice, fecal microbial diversity was back to normal within eight days after aFMT, and fecal microbiota composition was indistinguishable from baseline at four weeks post-antibiotics. Similar results were seen in the lower GI tract and upper GI tract.

In humans, the fecal microbiota had recovered to baseline composition as early as one day after aFMT! Unlike the probiotic-supplemented and spontaneous recovery groups, aFMT was also capable of restoring several key species, including Alistipes shahii, Roseburia intestinalis, and Coprococcus spp. Notably, these are all microbes that produce butyrate, an essential metabolite for the health of the gut barrier.

Importantly, aFMT also restored native host gene expression profiles along the GI tract.

Takeaways and Implications

That was quite a lot of information for just two studies! If you got bogged down in the details, here are the major takeaways and implications of this research and how it will affect my thinking about the gut microbiome going forward.

The Fecal Microbiome Is Not the Same as the Gut Microbiome

Study #1 is aligned with prior findings that suggest fecal samples are a poor indicator of gut microbial composition. This is why I don’t put too much stock in uBiome results, as much as I find them fascinating. I still believe comprehensive stool analysis is useful, as it can help screen for potential pathogens, parasites, and yeast, among other important markers.

However, I take any bacterial abundance information with a grain of salt and recognize that it is not directly representative of community dynamics in the gut environment. I am increasingly using a combination of comprehensive stool analysis, PCR-based stool testing, organic acids testing, and SIBO breath testing with my clients to provide a better overall picture of what’s going on in the gut.

Probiotics May Not Always Colonize the Gut, but They Are NOT Useless

Study #1 showed that probiotic colonization is very individualized and likely depends on the state of your gut and the probiotic strains used. In mice, the normal commensal gut microbiome inhibited colonization of probiotic strains.

Still, hundreds of randomized, placebo-controlled human clinical trials have shown that probiotics have efficacy for IBS, IBD, skin conditions, anxiety, depression, and more. (15, 16, 17)

Even when probiotics do not colonize the gut, they may impact host gene expression and the host immune system.

Not All Probiotics Are Created Equal, and It IS Possible That They Could Cause Harm

Probiotics are largely unregulated, and some studies have reported probiotic-associated deaths. (18, 19) Several meta-analyses also suggest that probiotic-associated adverse events may be underreported in clinical trials. (20)

There is likely a huge difference between the probiotic strains tested and validated in human clinical trials and the ones found on the average grocery store shelf.

This is part of the reason I’ve spent over 50 hours putting together an extensive analysis of the most popular soil-based probiotics on the market, to determine which strains have shown clinical efficacy and have been shown to be safe in clinical trials. (You can subscribe to my newsletter to be notified when it is released next week.) I also plan to do a similar analysis of Lactobacillus- and Bifidobacterium-based probiotics in the near future.

Probiotic Use Delays Restoration of the Gut Microbiota, Which May Represent a Trade-Off for Protection against Infection

Study #2 clearly showed that probiotic use after antibiotics can delay restoration of the normal gut microbiota for at least five months. Lactobacillus strains, in particular, appeared to inhibit the “normal” commensal microbiota. However, several studies suggest that probiotic use during antibiotics does confer protection to the host.

A 2012 meta-analysis of RCTs published in the Journal of the American Medical Association found that probiotic use was associated with a significantly lower risk of developing antibiotic-associated diarrhea. (21) However, the reduction in absolute risk was only 0.07. This means that 13 people would need to be treated and potentially delay normal restoration of their gut microbiome for one person to avoid diarrhea.

Subgroup analyses revealed a trend for an increased relative risk of antibiotic-associated diarrhea in those receiving Lactobacillus- (p=0.09) and Bifidobacterium- (p=0.16) containing probiotics. Saccharomyces and Bacillus spp., on the other hand, showed a numerical (non-significant) reduction in absolute risk.

A 2017 meta-analysis of RCTs published in Gastroenterology found that probiotic use reduced the risk of Clostridium difficile (since renamed Clostridioides difficile) infection in hospitalized adults taking antibiotics. (22, 23)

Probiotics given within two days of antibiotic initiation were the most effective in preventing C. diff infection.

Again, the reduction in absolute risk was small. This time, 43 people would need to be treated with probiotics and potentially delay normal restoration of their gut microbiome for one person to avoid C. diff. This was also performed in hospitalized patients, who are at much higher risk of C. diff. infection than individuals taking antibiotics in an outpatient setting.

Based on the current human data that we have, I do not think the benefits of probiotic use during or after antibiotics outweigh the long-term delay in native microbiome restoration (in most cases). However, I certainly encourage everyone to weigh the potential costs and benefits for themselves and with their physician and make an educated decision about whether to take probiotics based on their individual circumstances.

I eagerly await future studies that may help determine whether other types of probiotics (such as Bacillus spp. or S. boulardii) can confer protection to the host without delaying restoration of the gut ecosystem, and when they should be initiated in relation to the course of antibiotics.

Diet and Lifestyle Are Still the Most Potent Modulators of Gut Microbial Composition

Probiotics are NOT a replacement for a nutrient-dense diet, and diet is still the primary determinant of microbiota composition. Data from my lab shows that exercise may help promote a healthy gut microbiota as well.

aFMT Is the Best Solution for Rapid Recovery after Antibiotics (And Maybe We Should All Be Banking Poo for Later!)

Study #2 showed that aFMT, or infusing the gut with your individual stored, frozen pre-antibiotic fecal material, leads to the most rapid reconstitution of the normal microbiome after taking antibiotics.

You can imagine doctor’s offices in the future having large bio-banks of stool, ready to reinoculate a patient with their own personal fecal microbiota should they ever acquire a harmful pathogen or have to take antibiotics. I certainly know that I’m planning to create my own personal bio-bank after seeing this research!

Which brings me to another somewhat crazy, but related, thought: could we save stool samples from when we’re young, and reinoculate ourselves later in life with a younger microbiome? In controlled studies, FMTs from younger animals have been shown to reduce aging-associated chronic inflammation and increase lifespan in mice and fish, after all, and frozen stool can be stored for many years without major changes in microbial composition. (24, 25, 26)

If you have to take antibiotics and don’t have the ability to do aFMT (i.e., have a pathogenic infection or have no stored healthy fecal samples), allowing the gut to recover on its own and supporting it with a nutrient-dense diet may be the best course of action.

Hope you enjoyed this article! Be sure to let me know what you thought in the comments below. You can also subscribe to my weekly newsletter for more great content and get exclusive access to my definitive gut–skin axis guide.

About Lucy: Lucy is a fourth-year MD-PhD student in Nutritional Sciences at the University of Illinois. Her research focuses on understanding how diet and exercise can beneficially modulate the gut microbiota and gut barrier function in states of health and disease.

Lucy is also a staff research associate for Kresser Institute and writes weekly on her blog at NGmedicine.com. She strives to be a resource for unbiased, non-sensationalist information and hopes to use her degrees to create a world where functional, integrative, and preventive medicine is not only accepted by conventional doctors, but is the norm.

Lucy consults regularly with clients that have gut, skin, and autoimmune conditions. You can find out more about her at NGmedicine.com or subscribe to her weekly newsletter here!

The post Are Probiotics Useless? A Microbiome Researcher’s Perspective appeared first on Chris Kresser.