On Wednesday the 19th I’ll be on the excellent new Balanced Bites podcast with Diane Sanfilippo of Balanced Bites and Liz Wolfe of Cave Girl Eats to discuss digestive health. Topics covered will include:

• FODMAPs
• Small intestinal bacterial overgrowth (SIBO)
• Gut pathogens
• Maintaining healthy gut flora
• The best nutritional approaches for gut healing

Leave your questions in the comments section before the end of the day on Thursday (the 13th).

Diane and Liz have a great show. If your eyes start to glaze over when people (like me) start rambling about the finer points of scientific studies and physiological mechanisms, but you love practical, down-to-earth discussion about Paleo food and nutrition, their podcast is for you. Check it out!

In this episode I answer frequently asked questions about digestion, covering topics like parasites, stomach acid, the GAPS diet, SIBO and more.

Questions include:

• How to differentiate between a gut infection and food sensitivities?
• How to boost your HCL production
• Can strengthening the immune system take care of parasites?
• When to call it quits on the GAPS diet
• Is FODMAP sensitivity permanent, or can it be treated?
• What causes digestive reactions to carbohydrates?

The next podcast will be our last with Danny. We’ll make it a good one!

Full Text Transcript

Danny Roddy:  Hello everyone, and welcome to the Healthy Skeptic Podcast.  My name is Danny Roddy of DannyRoddy.com, and with me is Chris Kresser, health detective and creator of ChrisKresser.com.  Chris, how are you doing, my friend?

Chris Kresser:  I’m good.  A little sleep deprived, and I can’t blame Sylvie this time.

Danny Roddy:  Well, you just showed me why.  Why don’t you tell everybody listening why.

Chris Kresser:  Yeah, so I’m super excited about this program that I’ve been slaving away on.  You know, I’ve been working with people on health-related issues for a long time now, probably, I don’t know, over 10 years, and there’s absolutely no doubt that the biggest issue that I see in my practice and I hear about from people on my blog and who listen to the podcast is confusion about what to eat.  I’m sure you see this a lot, Danny, too.  I mean, people are basically paralyzed because they don’t know what to eat.  And I have patients that tell me they feel like they’ve got this voice in their head like everything they could put in their mouth is wrong or bad from one perspective or another.

Danny Roddy:  I can find a reason not to eat anything.

Chris Kresser:  Right, except air, right?  You could be a breatharian, but actually you can find a reason not to do that because you’ll starve to death.  So, I created this new online program called the Personal Paleo Code, and it was born of my experience working with hundreds of patients and hearing from thousands of blog readers and podcast listeners around the world, and it includes a 3-step process to help you figure out exactly what works and doesn’t work for your body.  So, rather than following a canned approach, however good of a starting point that canned approach is, it will never be totally customized for your particular body.  So, I have a process that I use in my practice for helping patients to figure out what that is, and the feedback has been so good, and it seems to be so effective that I just wanted to share that with a wider audience.  So, the core of the program is that 3-step process for determining what your own optimal diet is instead of following some guru’s advice, including mine!

And then the second part, which I’m really, really excited about, is we’ve built this meal plan generator.  It’s a web application, and it allows you to create a completely customized meal plan using only the ingredients you want to include.  So, you open it up, and let’s say you’re on an autoimmune Paleo diet, and you want to keep it under 50 grams of carbohydrates.  All you do is select remove nightshades, remove dairy, and then there’s a little button that says keep it under 50 grams of carbs, and then you can generate a single meal, you can generate a one-day meal plan, or you can generate a one-week meal plan.  And then all of those meals pop up on a grid, and they’re hyperlinked so you can click on the recipe and it goes to the single recipe page, picture, instructions, everything.  You can print that out.  You can print out the whole meal plan.  And you can save recipes to favorites.  You can search; it has a full search function.  It has an index so you can look up recipes by category, like if you only want to look at breakfast or you want to only look at snacks.  So, this is just incredible.  My wife, Elanne, is more excited about it than, I think, anybody else, because it’s pulling recipes from all of the, in my opinion, best Paleo recipe sites, like Health-Bent and Nom Nom Paleo and Paleo Diet Lifestyle.  And we’re gonna launch with over 300 recipes, but we are just gonna keep adding recipes as we go each month, so that’s awesome.

And then we’ve got all kinds of extra stuff.  Like, we’ve got guides on fermented foods; on fats and oils, you know, which ones to cook with, which to use cold, which to avoid completely; nuts and seeds, you know, how to properly prepare them, which I’ve written about recently; how to make bone broth, because that’s something I think that’s often overlooked as part of a healthy diet.  We’ve got even a guide on kitchen equipment, like my picks on particular kitchen stuff that’s good to have around.  We’ve got special tweaks for blood sugar and thyroid issues, weight loss, autoimmune disease, and other health conditions, so it’s kinda like being a patient in my practice without actually being a patient, but even a lot more beyond that with the meal plan generator.  And then we’ve got another web app called the progress tracking app, where you can go in there and fill out a questionnaire each week, and then you get to see your progress charted on a graph as you move through the stages of the program.  So, yeah, I’ve been a little busy!

Danny Roddy:  I don’t understand how you have a new child and you put all this together.  It consumed my whole life writing, like, 40 pages, and you get all this done.  Unbelieveable.

Chris Kresser:  I don’t know.  I’ve definitely brought on more help this time around, so that makes a big difference, but I have to say the last several weeks have been probably the most productive period of my life somehow.  I don’t really understand it either.  So, the other thing I want to mention is we’ve finally figured out a name.  You know, we’ve been talking about changing the name of the show, and we’re gonna do that.  It’s gonna be called Revolution Health Radio.  Probably the logo will have some kind of wordplay with revolution, evolution, evolutionary health.  And radio over podcast because I’ve just never really liked the term “podcast,” and this is my show, so I get to choose!  I’d rather have a radio show than a podcast, so it’s Revolution Health Radio.  We’ll have a new graphic, new show title in iTunes.  You don’t have to do anything, dear listener.  You’ll just notice that next week Danny will say, “Welcome to Revolution Health Radio,” and that’s it.

Danny Roddy:  I might screw that up, though, Chris.

Chris Kresser:  That’s all right.  You’re allowed.  You get a couple times before you’re fired!

Danny Roddy:  Good thing I edit this show.

Chris Kresser:  Right!  So, what’s happening with you, Danny?

Danny Roddy:  Nothing much.  Just wrapping up, kinda sitting on the book, tweaking a few things because I’ve actually had an amazing chance to work with a couple people, so it’s really putting a lot of my ideas to the test, and I’m getting a lot of feedback from them.  Like, they fell in my lap, so I’m really thankful.

Chris Kresser:  That’s where the rubber hits the road, huh?

Danny Roddy:  Exactly, like, you get to kinda test out your ideas every day, where I meet with a lot fewer people, or I only really correspond with people over Facebook or email.  So, it’s exciting.

Chris Kresser:  Yeah.  I keep waiting for you to send me the damn book!

Danny Roddy:  I will as soon as it’s finished.

Chris Kresser:  Are you making me pay for it?  Is that what it is?

Danny Roddy:  No!

Chris Kresser:  I’m happy to pay for it!

Danny Roddy:  With that said, do you want to get to our first question, Chris?

Chris Kresser:  Yeah.  We’re gonna do an episode about digestion.  So, I was on the awesome Balanced Bites Podcast.  I hope you guys all go listen to it.  It’s Diane Sanfilippo and Liz — Do you know Liz’s last name?  I feel bad.

Danny Roddy:  I don’t.  I’ve just met Diane at AHS.

Chris Kresser:  Cave Girl Eats, right?  But they have a great podcast, and Diane totally gets the science, but she’s really into breaking it down into an easy-to-understand format and really focusing on the nutritional angle.  It’s an awesome show.  You should check it out if you haven’t already.  And she wanted to have me on to talk about digestion, and I did a blog post soliciting questions about digestion, and we got, like, 60.  So, obviously we didn’t have time to answer them, and I thought it would be a good idea to try to get to some of them, just to do a whole show on digestion, so here we are.

How to differentiate between a gut infection and food sensitivities

Danny Roddy:  Let’s do it.  This first question is from Emm.  She asks:  “I’ve been trying to follow a Paleo diet since I got a bad GI virus in July.”  She puts in parentheses:  “(I didn’t take any antibiotics, just waited it out), and now my stomach is not the same. I get cramping/pain/bloating after eating any food.  That includes meat, veggies, fruits, white or whole grains, fats, both together or alone.”  She continues and says:  “I followed a Paleo diet with just veggies and meat for two weeks, and I felt like I had knives in my intestines.  The only thing I can digest without incident is freshly made veggie juice.  I take a probiotic two times a day with meals.  Note: Drinking red wine with any food relieves all of my symptoms!  Please help.  I’m slowly losing my daily life, and I need to go back to digesting at least some food again!”

Chris Kresser:  Yeah, that’s bizarre.  Drinking red wine relieves all symptoms.  I thought I had it all figured out up until that line.

Danny Roddy:  I could guess why that was happening.  I think red wine might increase gastrin?

Chris Kresser:  Yeah, I mean, there’s a few possibilities there.  One is just the increase in HCl production from the wine.  Another is that alcohol can be mildly bactericidal.

Danny Roddy:  Oh, yeah.

Chris Kresser:  Although, I mean, you hear about people drinking, like, a fifth of tequila or something in Mexico if they get sick with a gut infection.  I don’t know that the same principle applies here.  But let’s back up a little bit and talk about her exposure to the GI virus.  So, I’m not so sure that that was a virus.  It’s possible it was a parasite or something else.  I mean, the symptoms can be really similar, and if she continues to have symptoms after a while, one possibility is that it was a virus that just really altered the gut flora and caused some gut-brain axis issue.  But another possibility is that it wasn’t a virus and it was a parasite or an opportunistic or pathogenic bacteria and that she still has it and that’s why she continues to have the symptoms she has.  That’s actually fairly common in my practice, and when I see somebody who has made all of the dietary changes, you know, they’re eating a clean diet, and they’ve been doing that for a while, and they’re still having crazy symptoms no matter what they eat, that’s a big red flag for me to start going looking for an infection.  And I would do a stool test.  I use Metametrix.  I prefer them over other labs.  And I would try to at least rule that out, if there is something present that’s causing this continuation of symptoms, because that’s definitely my guess.

Danny Roddy:  I’m actually trying to reference it.  Paul Jaminet.  He was saying there was some way, like, depending on if you had really bad gas you could find out what kind of infection you had, but you were saying if it’s persistent, then it’s more likely a parasite.

Chris Kresser:  Yeah, I think it’s more likely a parasite or bacteria than a virus that was just passing through.  Like, stomach viruses tend to be transient, you know, just in the same way that you get a cold.  But parasites tend to stick around unless you treat them.  That’s what they do.  I think what you might be thinking of is Paul, when he was on the show, was talking about how ketones can feed yeast, and a ketogenic diet can actually be harmful when someone has a yeast infection, and I think that’s one of the perils of the GAPS diet, and we’re gonna talk about that later in another question.  But for now, I would say to Emm the first thing to do would be to get a Metametrix stool test.  Usually you have to work with a practitioner for that because they don’t deal with the public directly, and at least rule out some type of pathogenic infection that’s still present, because that would be my guess, hearing those symptoms.

Danny Roddy:  Cool.  Good stuff.  I’m looking at Paul’s thing.  It was the difference between bacteria.  He says bacteria tends to produce more acute transient postprandial symptoms like gas and bloating.  OK, I’m thinking of fungi.  And he says fungi tend to produce more chronic, slowly varying symptoms, like from circulating toxins.

Chris Kresser:  Systemic, yeah.  I would agree with that for the most part.  There are certainly chronic bacterial infections that can produce chronic and slowly changing systemic symptoms, but in general, that’s a fair characterization, I think.

Danny Roddy:  Would there be a way of telling if it was a parasite or a fungus, or is that where testing would be really helpful?

Chris Kresser:  Yeah, that’s where testing would be helpful, but some of the cardinal symptoms of parasitic infections are cyclical symptoms because parasites have specific life cycles.  So, if I have a patient that is basically fine or does pretty well for 10 days and then has an intense flare-up of symptoms for a few days and then does well for 10 days and then has an intense flare-up and it’s pretty regular like that, that can be a real sign of parasitosis.  Extreme hunger even after eating is another typical sign of parasitosis.  Skin stuff can be either fungal or a parasite.  A strange test in the mouth, like a bitter or metallic taste, can be parasitic.  So, there are some things that make me think in that direction, but it’s difficult to do without a test.  And let me just say that you don’t need to go to a third world country to get a parasite infection.  In fact, most of my patients that have parasite infections have not done third world travel, so they’re all around us in the environment, even here in the highly sterilized first world country we live in.

How to boost your HCl production

Danny Roddy:  OK, this is the next question.  This is from Daisy, and this is a related question:  “How can I boost my HCl production?  From what I understand, we all lose the ability to make enough as we age and lack of it is the root of all sorts of issues.”  And she notes:  “Excess gas, bloating, general belly discomfort after eating, candida overgrowth, recurrent UTIs.  Have I understood right, and if so, is there an alternative to lifelong supplementation?”  She she adds:  “I know it’s a good idea not to drink loads of water while eating because I might choke , but could low level, chronic dehydration have an effect on stomach acid production?”  What do you think, Chris?

Chris Kresser:  OK, so in order to answer the question how can I boost my HCl production, we, of course, always want to ask the other question, which is what’s causing the decline in stomach acid production?  There are some common causes of that.  The most common ones would be obviously drugs that decrease stomach acid production.  So, those would include the obvious PPIs and over-the-counter acid-suppressing drugs, but they also include drugs like antibiotics and birth control pills.  And the second thing would be H. pylori infection.  So, H. pylori, Helicobacter pylori, is the bacterium that has been shown to contribute to ulcer formation, and this was a pretty interesting story. . . thinking if I want to go there. . . no, I don’t.  We probably don’t have time.  I like to ramble off on those tangents sometimes, but basically I’ll give you the short version because it is pretty cool.  It used to be thought that ulcers were caused just by stress, and there was a guy in Australia, a doctor who came to believe that they were actually caused by a bacterium called H. pylori.  Nobody believed him.  He presented this data at medical conferences.  He was basically laughed off the stage, and growing increasingly desperate over the years, he finally decided to swallow a vial full of H. pylori.

Danny Roddy:  Shut up.  Really?

Chris Kresser:  I’m not joking.  This is 100% true.

Danny Roddy:  I didn’t know that’s how –

Chris Kresser:  This is commitment to science, OK?  Or being right!  I don’t know what was driving him, but his name is Dr. Marshall, I think.  And he swallowed the H. pylori, and lo and behold, he developed an ulcer, which he did not have before.  And then the coup d’etat was that he treated himself with an antibiotic and cured his ulcer.  So, even after that, believe it or not, people were still skeptical for a while, I mean, which is just crazy.  Shows you how hard it is to change the dominant paradigm.  So, he ended up winning the Nobel Prize for Medicine, so he got the last laugh, right?  Anyways, we know now that H. pylori does contribute to ulcers.  It’s a very common infection.  By the time we’re 55 years old, one in two people have H. pylori.  Some people believe it’s a normal resident of the digestive tract, and the evidence that supports that is that H. pylori has been shown to have some pretty positive immunoregulatory effects.  So, we evolved over millions of years with pathogens, and some of those pathogens actually exist in a symbiotic relationship with us, so they tune our immune system, they affect our genetic expression.  Actually a lot of what used to be called junk DNA, which is now called noncoding DNA, is thought to have been originally derived from retroviruses.  So, essentially a lot of our genetic code is from viruses that we evolved with over time that came to play an important role in our genetic evolution.  H. pylori, however, when it becomes overgrown, that’s when it is an issue.  So, for a lot of people who carry H. pylori it’s probably not an issue if they have a good balance of gut flora and a healthy gut environment, but when it becomes overgrown, just like when anything becomes overgrown in an ecosystem, that’s when all hell breaks loose.

In the case of H. pylori, one of its survival strategies is to suppress stomach acid production because one of the purposes of stomach acid is to protect us from pathogens.  Pathogens can’t live in a highly acidic environment.  Most of them can’t, anyways.  So, H. pylori is pretty clever.  It goes in the stomach and suppresses stomach acid production so it can survive.  So, I think for people, especially people over 50, one of major causes of declining stomach acid production is H. pylori.  And so, in that case, I would want to treat the H. pylori, but the way I do it is a little bit different than the conventional approach, which is to eradicate it completely.  The more I work with people, the more I think it doesn’t need to be eradicated completely for the reasons that I just said, you know, if it’s a normal resident of the digestive tract and it’s a question of optimizing and normalizing the environment or the ecosystem instead of total eradication, which can actually cause a lot of other problems.  The number of antibiotics you have to take and the intensity of that course of antibiotics you have to take to fully eradicate H. pylori is gonna eradicate a lot of other stuff too, good stuff, good bacteria that we need to perform all of the functions that good bacteria does, like digesting food and regulating the immune system.

So, I would say, obviously don’t take any drugs that suppress stomach acid production.  I would say treat H. pylori.  I would say another cause is stress.  So, acute stress can actually increase stomach acid production, and most people probably experience that, but chronic stress has the opposite effect; it decreases stomach acid production over time.  So, taking steps to manage stress is important.  And then, eating fermented foods, using apple cider vinegar and, to some extent, alcohol, as we talked about in the last question, can promote stomach acid production.  So, those are some ideas.

Danny Roddy:  What percentage of your patients do you think have H. pylori?  I remember Stephan’s article, and he pointed to some article on PubMed that said, like, 80% of Americans or some ridiculously high number.

Chris Kresser:  Yeah, I’ve seen different estimates.  I’ve seen everything from 1 in 2 to up to 80% to 90%.  I think the better question is what percentage have a pathogenic load of H. pylori.  And that’s fairly high, because I have a questionnaire that’s designed to identify low stomach acid production, and like I said, there are other possible causes of that, but I think in a lot of cases it’s H. pylori.  And I would say about 60% to 70% of my patients have low stomach acid.  So, it is definitely a big deal.  The last part of her question, the reason it’s not a good idea to drink a lot of water while eating is that it can dilute the stomach acid, right?  So, if you fill up your stomach with water, then the stomach acid is not gonna be as effective as it would be if you’re just eating the food.  Chronic dehydration effect on stomach acid production — I’m not aware of any particular link, but dehydration can cause so many problems that I wouldn’t be surprised.

Can strengthening the immune system take care of parasites?

Danny Roddy:  Good stuff.  This next question is from Brianna, and she asks:  “Can strengthening my immune system alone take care of a parasite issue?”

Chris Kresser:  It’s possible, but I rarely see that.  Parasites need to be treated, in my experience.  And I might surprise some people here when I say this, but I think in a lot of cases drug treatment for parasites is actually a better choice than natural treatment.

Danny Roddy:  Bite your tongue!

Chris Kresser:  Yeah, exactly!  You know, my philosophy on medicine has always been whatever works and causes the least harm.  I’m really not that dogmatic.  Of course, I prefer natural approaches because I think they satisfy that criteria more often.  They work well, and they’re less likely to cause harm, so I prefer them.  But if a drug satisfies that criteria and I think it’s a better choice than a natural alternative in that it causes less harm and it’s more effective, I’m gonna recommend that, and that’s true, like in cases of people with Hashimoto’s, I think taking thyroid hormone is a good idea for most people.  Low-dose naltrexone we’ve talked about a lot on the show, and I think that’s one of the classic examples.  I mean, if you can take a very safe low dose of a drug like that and avoid life-altering drugs that are common in conditions that people take LDN for or the intense suffering and increased risk of complication for other diseases, then I’m all for it 100%.  And with parasites, it’s not a hard-and-fast rule, and it’s a case-by-case decision in my practice, but in some cases with certain parasites, particularly the ones that are really difficult to treat, like Blastocystis hominis and Dientamoeba fragilis, I will often refer a patient out to a doctor to do a particular antibiotic protocol that I’ve learned about from the clinic in Australia that is more experienced treating parasites than just about any other place I know about, because what I’ve seen is that those drugs work and they work pretty quickly, and so, yes, there is some damage to the gut flora, but often with herbs for parasites, you have to take them for a really long time for them to completely get rid of the parasites, and even then they don’t necessarily always work for the more virulent ones.  And that means that over that entire time, you’re taking pretty intense antimicrobial substances that are gonna have an effect on the gut flora and that are gonna be really depleting.  So, in my experience personally, a lot of people know that I got into this whole thing, medicine and my blog, because I was infected with several parasites when I was traveling in Indonesia back in 1998.  And it was a long, multi-year process of figuring out how to deal with it, and I took a lot of herbs during that time because that was my inclination and I was studying Chinese medicine, and the herbal formulas that I took kind of wrecked me more than the drug treatments that I ended up doing, and they didn’t work as well.  So, once again, it’s never black or white.  That’s why I try not to be dogmatic about things.  Whenever I think I have an approach that works, there’s always an exception that comes up.

Danny Roddy:  Well said.  At least in the case of thyroid, is it true that traditional diets used to contain a fair amount of thyroid, so in a sense, taking something like Armour or desiccated thyroid you are kind of getting back to the roots of a traditional diet that would have contained — I think I read something that almost 1/2 grain of thyroid would have been consumed daily?

Chris Kresser:  I haven’t read that.  I haven’t thought about it that way, but that’s interesting.  I think yes and no.  I know a lot of people are supplementing with or taking thyroid hormone, and I’m a big fan of that when it’s necessary.  I’m not such a big fan of just kind of the idea that everybody should take thyroid hormone, and there is that idea out there in natural medicine.  A lot of patients come to me and they’re taking Armour or something, and I say:  Oh, so you have hypothyroidism?  And they’re like:  No, I was just seeing a naturopath and they thought, you know, since I was having some trouble with weight loss that I should take Armour.  And I’m not really a fan of it in that respect, because taking thyroid hormone when you don’t need it can really trash your adrenals, and I have a lot of patients in that category who have been on thyroid medication for a long time, they didn’t need it, and that really kind of worked over their adrenals because it up-regulates your metabolic rate, and it’s kinda like having the idle of your engine of your car turned up too high for too long, and that’s gonna shorten the lifespan of the engine and cause other mechanical problems.  So, I think eating actual thyroid gland and even maybe taking some glandulars for people who might have a subclinical hypothyroid condition, there’s something to be said for that, but — and I’m not saying you were suggesting this, Danny — but just I see a lot of people in my practice who are taking thyroid medication that don’t need to be.

Danny Roddy:  Totally.  I wouldn’t suggest it either.  And also taking thyroid can increase the need for almost every nutrient, so if your diet isn’t in place, it’s really –

Chris Kresser:  Bad news.

When to call it quits on the GAPS Diet

Danny Roddy:  Playing with fire, yeah.  All right, this next question is from Kaitlyn:  “I’ve been following your recommended diet for about 1-1/2 years now.”  I didn’t know you had a recommended diet!  “Started GAPS Intro four months ago but can’t comfortably move on to Full GAPS.  I feel like I have more constipation and more bloating problems as I’m purposefully trying to heal my gut flora than I ever did before starting GAPS.  How is that possible?”  So, she’s having more issues since going GAPS.  She goes on to say:  “Pretty frustrating.  My husband has been eating the same as me and also can’t move on to Full GAPS.  He now has persistent bloating and diarrhea but never had either before GAPS.  We both consume plenty of fermented foods, Bio-Kult, and fermented cod liver oil.  I take magnesium supplements each day to try to prevent the constipation, but my husband does not use magnesium since his digestion tips the other way.”  I don’t know what. . . oh, OK.

Chris Kresser:  Because they were using magnesium for constipation, but if he’s having diarrhea, he obviously doesn’t want to do that anymore.

Danny Roddy:  Got it, and she asks:  “Are all of these symptoms just part of the long healing process, or is something else going on altogether?”

Chris Kresser:  OK, this is a great question.  I’m so glad it came in, because we can cover a lot of important practical and philosophical issues.  So, let’s start with the philosophical.  You know, it’s already a theme in this episode, and I think people know this about me just from listening to my podcast and reading my blog, is that there is no one-size-fits-all approach.  And of course, that’s the whole purpose behind the Personal Paleo Code program that I just created, because I think a lot of the confusion about diet, like people saying:  Well, is white rice OK, or is dairy OK?  The answer is always it depends, and any prescription that claims to be appropriate for the 6-1/2 billion people on Earth is always gonna fall short.  [baby crying in background]  It sounds like Sylvie’s having a little meltdown out there!  So, yeah, I mean, I just can’t emphasize that enough.  And I think that my, sort of, mission is to try to alleviate some of the suffering and confusion out there about diet by getting the message across that the only diet that is the right diet is the one that works for you.  And so, with GAPS, I think the GAPS diet is great.  I use it in my practice.  It’s really helpful for certain people, but it doesn’t work for everyone, and it doesn’t work forever even for somebody that it does work for.

So myself, I was on the GAPS diet for about eight months, and then at the end of that eight-month period, things started to shift back in the other direction.  I just started to have some digestive symptoms again, and I started to feel lower energy.  I just wasn’t feeling as good overall, so that was my trigger to start adding things back in.  The first thing I added back in was starch, and I had absolutely no problem with it at all, and I felt great.  It was awesome to start eating sweet potatoes and potatoes and yuca and taro and all of that stuff, and it increased my energy levels, and it made my digestion better.  So, I could have at that point, if I would’ve gone on the Yahoo group for the GAPS diet and said:  Geez, guys, I’m having all these problems.  What should I do?  I guarantee they wouldn’t have told me to start eating starch.  They would’ve said:  Oh, maybe you should be doing more enemas or maybe you should cut back more on the fruit.  Or whatever it is, it would all be in the context of, like, you’re not doing the GAPS diet right and you should try harder, because when people adopt a certain approach, I mean, this seems to be some kind of human tendency, right?  Like being part of a club.  It’s ubiquitous across human culture, and people get really wedded to a particular perspective or approach, and then it’s like that old saying when you have a hammer, everything starts to look like a nail.  And so, if an approach stops working, then rather than saying:  Hmm, maybe this approach isn’t the right one for me, it’s like maybe I’m doing it wrong or maybe I should do it more or harder or better, and I see that a lot on the Internet and within all of these communities around dietary approaches.

So, the tricky thing, as Kaitlyn is asking about, is when to know whether it’s just a temporary kind of road bump, a die-off reaction, where maybe you’ve reached another level of healing and there’s another level of bacteria or yeast that are dying and that’s causing the symptoms and you should just push through it or whether it’s actually an indication that this is not the right approach anymore and it’s time to move on.  Unfortunately there’s no easy way to answer that question, and it’s really a case-by-case thing, but I would say in general, if you’ve gone for two, three, four weeks and the situation is just deteriorating, you’re not having any windows of time in that period where you’re actually feeling better, because die-off shouldn’t be just persistently bad without any let-up.  Usually die-off looks like a period of worsening symptoms, followed by a period of improving symptoms, followed by an improving of worsening, like that.  Whereas, something that’s not working, you would just expect things to get worse and worse over time.  So, that’s one possibility in terms of determining when to make the change.

Danny Roddy:  Also, let your body guide you, like your skin and your nails, measuring progress in other ways besides just digestion.  What do you think about that?

Chris Kresser:  Oh, yeah, absolutely.  I mean, all of the symptoms — fatigue, skin, hair.  Mood is a big one.

Danny Roddy:  Totally.

Chris Kresser:  Those should all be considered, and I think she probably is, but it’s a little bit of an art, but I would say that after a few weeks and things are just deteriorating and there is no improvement at all, I would actually start to question whether that approach is going to be valuable over a longer period of time.  Now, more specifically about GAPS, there are a few issues with it and that can make it not helpful or appropriate for certain people.  Number one is that, as we talked about earlier and talked about in more length with Paul when he came on the show, is that yeast can thrive on ketones, and GAPS, especially the Intro GAPS diet, is by definition a very low-carbohydrate diet and will probably be ketogenic.  So, for some people who have a systemic yeast infection, doing a ketogenic diet can actually make things worse, and I’ve seen this in my practice.  What’s a little confusing to me is that it doesn’t seem to always be the case.  Some people tend to improve, so I don’t know how to explain that.  Maybe some species of yeast are more able to utilize ketones than others, I’m not sure.  But I sometimes even use that as a diagnostic protocol.  If you put somebody on a ketogenic diet for a short period of time and they get a lot worse, then that could be an indicator of a yeast infection.  So, that’s one issue.  Another issue is that because it’s a low-carb diet and someone’s on GAPS for a long time, that could affect thyroid function, which we’ve talked about before.  Glucose is required for the conversion of T4 to T3.  There are studies showing that fasting and very low carb diets over a prolonged period can cause a decline in thyroid hormone and conversion of T4 to T3, and T3 is five times more metabolically active than T4, so that’s significant.

A third problem is people who have issues with fat digestion.  Some people when they eat a diet that’s extremely high in fat and low in carbs like GAPS, if they have any kind of gallbladder insufficiency, it can be really, really hard on them.  It causes a lot of bloating and pain, sometimes even vomiting and really difficult digestive symptoms.  So, in that case, it doesn’t necessarily mean that the GAPS approach won’t work for them or isn’t a good idea, but they may need some additional gallbladder support to make it work.  And then the other thing I would say is that my diet, actually you could call it Paleo plus GAPS, or you could call it GAPS plus starch, so I’m not that far from the GAPS diet now in the sense that I eat a lot of bone broth, I eat a lot of fermented foods, which are two characteristics of the GAPS diet, but I do eat starch and starch really works well for me.  And what I’ve seen in my practice is that of all the things that are removed from the GAPS diet, starch is usually the thing that causes the least problems for people.  So, if somebody has been on the GAPS diet for a long time and they are starting to have issues, I would suggest adding more starch back in, you know, if it’s been a while since they’ve had the issues, not two days, but if it’s been weeks, like with Kaitlyn and her husband.

Danny Roddy:  It’s been a while.  Natasha Campbell doesn’t like starch because it passes through the gut lining easier?

Chris Kresser:  Well, the whole principle of the GAPS diet — We probably should have done this before.  I realize not everybody listening to this even knows what the GAPS diet is.  So, the GAPS diet is very similar to the Paleo diet actually, but it goes a step further.  I removes disaccharide and polysaccharide molecules.  Carbohydrates are broken down into sugar molecules, ultimately into monosaccharides like glucose and fructose.  So, monosaccharide is a single molecule of a sugar, and a single molecule of sugar can be directly absorbed from the gut across the lumen of the intestine into the bloodstream without any additional breaking down.  So, when you eat a carbohydrate, it has to be broken down into those single molecules, monosaccharides, to be absorbed into the bloodstream.  Disaccharides are molecules with two sugars, so lactose is a disaccharide.  And then you have polysaccharides, which have multiple sugar molecules chained together, and that would be a starch.  So, when you eat a polysaccharide or a disaccharide, there’s some digestive action that needs to take place to break those longer-chain sugars into the monosaccharides, the single molecules of sugar, so that they can be absorbed, and that involves the brush border enzymes, which are enzymes on the villi, these hair-like projections on the lining of the intestine, and they need to act on those longer-chain sugar molecules to break them into those smaller molecules, right?  So, what happens with people with gut problems is those brush border enzymes don’t work as well, and they don’t break those longer-chain sugars into the monosaccharides, and as a result, they end up floating around in the gut for longer than they should, and in doing that, they become food for pathogenic gut bacteria and yeast.  That’s the whole theory of the GAPS diet.  So, the GAPS diet removes disaccharides and polysaccharides and only allows the simpler sugars like glucose and fructose and fruit.  So, not only does the GAPS diet eliminate grains, which the Paleo diet does too, it also eliminates all starch, so no sweet potatoes, no potatoes, none of the starchy tubers that the Paleo diet does allow.

So, what I’m saying is that what I’ve seen is that if somebody goes on the GAPS diet for a while and they reach a point where Kaitlyn’s reached or I’ve reached and they start adding starch back in, that can sometimes be helpful, and I think one of the reasons behind that is that when you only eat the single-molecule sugars, the monosaccharides, then in addition to starving the bad gut flora, you can also end up starving the good gut flora.  And when you’re eating a lot of fermented food, that may not be a problem, but for some people even who are eating a lot of fermented food, it does seem like it is a problem.  And then adding the starches back in, starches have a prebiotic effect, meaning they stimulate the growth of certain species of bacteria in the gut, and then people’s stools might tend to normalize and their digestive system just starts to work better.  So, yeah, it’s a really individual issue, but those are some of the variables to consider.

Is FODMAP sensitivity permanent, or can it be treated?

Danny Roddy:  Great stuff.  OK, this next question:  “I’m curious why and how a person develops a sensitivity to FODMAP foods, and is there any way you can heal it or if one just has to avoid these problem-causing foods forever.  For me, apples and onions cause a lot of digestion pain.  These are foods I’ve been eating since I was a baby.”  What do you think about FODMAPs?

Chris Kresser:  Yeah, I talked about this a little bit on Diane’s show, but I think FODMAP intolerance is a symptom of a deeper problem usually.  I don’t think anyone is born with FODMAP intolerance, for example.  But I think it’s probably a consequence of small bowel bacterial overgrowth or any other kind of dysregulation of the gut flora, which could also include a pathogen like a parasite or yeast or pathogenic bacteria.  So, my approach, I do use the FODMAP diet in my practice.  I talk about it in the Personal Paleo Code as one possible adaptation to digestive issues, but it’s more of a temporary thing to provide some symptom relief while we figure out what those underlying issues are, and then oftentimes people will be able to add back in at least some of the FODMAPs once those issues are resolved.  It probably bears noting that a lot of the FODMAPs are things we shouldn’t be eating anyways, like wheat flour.  And for those of you who don’t know, who are just swimming in acronym soup right now and have no idea, with GAPS and FODMAPs and all that stuff, FODMAP stands for fructo-, oligo-, disaccharide — What’s the M, Danny?  I always forget the M.

Danny Roddy:  I have no idea.

Chris Kresser:  P is polyols, sugar alcohols like sorbitol and stuff like that.  Anyways, it’s similar actually to GAPS in the sense that there are these certain foods that this theory holds are more likely to be undigested and unabsorbed, and then they become food for pathogenic gut bacteria, and that’s what causes the symptoms.

Danny Roddy:  Here we go:  fermentable oligo-, di-, and monosaccharides, and polyols.

Chris Kresser:  Right.  So, catchy name.  You can see why they’re going with FODMAP!  Yeah, this is, like, fructans and then fructose, not all fructose, just any excess fructose.  Fructose can be well absorbed by the body when there is a sufficient amount of glucose that’s eaten with it.  So, if somebody eats a food like a banana that has equal or greater amounts of glucose than fructose, then they shouldn’t have any problem digesting the fructose, but if someone with FODMAP intolerance eats a fruit like a pineapple that has a lot more fructose than glucose, than that excess fructose is what causes the issue.  Yeah, these are foods that are all aggressively fermented by the bacteria in the gut when they’re undigested, and again, I think it’s a result of already dysregulated gut flora and that if you deal with that, you usually can reintegrate some of the foods, not always, but in most cases in my practice.  And dealing with the pathogen is one step, but also restoring healthy gut flora using probiotics is another.  Let’s go on to the next one.  Got one more, maybe?  We have time for one more.

What causes digestive reactions to carbohydrates?

Danny Roddy:  Time for one more.  OK, let’s get to Niklax’s problem.  He or she says:  “My problem is bloating from carbs.  It doesn’t really make much sound, but it looks like a beer belly although my BMI is OK.  Switching to a VLC diet solves the problem, but I am fed up with eating so much fat all the time.  Also quite fond of rice noodles and potatoes.  Is there a solution?”

Chris Kresser:  So, yeah, I think this is closely related to the last question and the earlier question.  Carbohydrate intolerance is almost always a sign of messed-up gut flora because, as I was just explaining, when carbohydrates remain undigested in the small intestine, they provide food for pathogenic gut bacteria, and then when those pathogenic gut bacteria are killed by the immune system, they release toxins.  Those toxins can cause all kinds of symptoms ranging from brain fog and depression to leaky gut, skin conditions like psoriasis and eczema, etc.  Also the process of the bacteria fermenting the carbohydrate produces gas, and that gas is what produces that beer belly type of bloating that he or she is talking about.  So, one possibility is to get some testing done to see if there is a pathogen present.  There’s a small bowel bacterial overgrowth breath test that you can do to test that out, and then dealing with those issues and restoring healthy gut flora would be the thing that you would need to do to increase the carbohydrate tolerance so you can expand your diet and eat a broader mix of macronutrients.  I think that’s it.

Danny Roddy:  Killer, Chris.  That’s gonna bring us to the end of this week’s episode.  Chris, where can we find more of your work on the Internet this week?  What are you working on?

Chris Kresser:  OK, so we talked about the Personal Paleo Code in the beginning of the show.  This show is gonna be released on November 1, so the actual program itself is gonna be ready is about a week from today, you know, today if you’re listening to this on November 1.  But right now, I’m doing a promotion where I’m given away a free iPad 2.

Danny Roddy:  Oh, my god.

Chris Kresser:  Yes.  I hope I win!  No, I’m just kidding.  I’m not gonna win.  So, if you can help me get the word out, I’m really excited about this program, I want to get the word out far and wide, and so I’ve created this page, a landing page that describes the product.  I have a little video of me talking about it and just a couple short bullet points, gives the basic idea.  And if you go there, it’s iPad.PersonalPaleoCode.com, and if you pull that up and you share that page on Facebook or Twitter — you can use either one, and you can change the text.  I mean, there’s some text that’s prepopulated in there, but you can change it if you want.  You share it on your Facebook or Twitter account, help me get the word out, you’ll be entered into this drawing to win the free iPad.  It’s a 16GB black one with Wi-Fi, and the contest is over on November 20.  And then by entering that contest, you’ll also be put on the email list where I’ll send you an email once the product is ready.  We’re gonna be offering a discount for my podcast listeners and blog readers and faithful fans, and that’ll be available for only a couple of weeks after the product launches.  So, yeah, if you’re interested in an iPad, which is actually a perfect way to access this content so you can be in the kitchen and pull up a meal plan on the iPad and check it out before you make some food for the day, I’d appreciate you helping me get the word out, and I wish you luck in winning the iPad!  I’ll be jealous.  Let’s see.  What else?  I think that’s it.  I mean, we’re changing the name of the show next week, like I said, and yeah, that’s it.  I think I’m gonna take a rest for a little while.

Danny Roddy:  You can find all of my work on DannyRoddy.com.  Hopefully, I’ll be releasing my new book, Hair Like a Fox, sometime next month.  The ETA is unknown at this time.

Chris Kresser:  C’mon, Danny, get with the program.  We’ll all waiting with bated breath!

Danny Roddy:  But keep sending us your questions at ChrisKresser.com using the podcast submission link.  If you enjoyed listening to this podcast, head over to iTunes and leave us a review.  Thank you for listening, and thank you for your support.

Chris Kresser:  Thanks everybody.  Good digestion to all of you!

Another Q&A episode, folks! Remember to tune in next week for our interview with Dr. Alessio Fasano, a pioneer in the fields of gluten intolerance, leaky gut and autoimmunity.

In this episode, we cover:

12:39 How to tell if digestive problems are caused by leaky gut, SIBO, or food intolerance
26:25 What to do about Epstein-Barr Virus
32:43 Does a furry tongue mean anything?
35:43 How baby is telling you it’s time for different foods
37:50 The specific Graves Disease Protocol to keep it in check… for good
48:52 Everything you need to know about Anemia (and more)

Links We Discuss:

• Betaine HCL Protocol
• Real Food Summit

Full Text Transcript:

Steve Wright:  Hi, and welcome to another episode of the Revolution Health Radio Show.  I’m Steve Wright from SCDlifestyle.com, and with me is Chris Kresser, health detective and creator of ChrisKresser.com.  Chris, how are you doing today, man?

Chris Kresser:  Oh, I’m pretty good, Steve.  How are you?

Steve Wright:  I’m good, man.  I’m pumped up.  We’ve got a lot of questions to cover today.

Chris Kresser:  Yeah.  A Q&A episode.  We’re doing it again.

Steve Wright:  Going rapid fire this time.

Chris Kresser:  So, before we get into that, I want to make a couple announcements.  One is just a reminder that the next show we’re gonna be interviewing Dr. Alessio Fasano, which I’m really excited about.  He’s a pioneer in the field of gluten intolerance and celiac disease research and also in establishing the connection between intestinal permeability, or leaky gut, and autoimmune disease.  He’s a real research hero of mine, and we’re honored that he’s gonna be joining us on the show, so make sure to tune into that one.  Don’t miss it.  It’s gonna be a great episode.

And then, as I’m sure all you know, the Ancestral Health Symposium is coming up, and I’ve been busy preparing my talk for that.  The topic is on iron overload.  That’s something I’ve talked about on the show quite a bit, and specifically I’m gonna be discussing how even mild iron overload, you know, nonhereditary hemochromatosis iron overload, can contribute to a number of different diseases and even increase the risk of death, and of course, how to test for it and what to do about it.  So if you’re at AHS, I look forward to seeing you at my talk and meeting you.  And I think, if last year was any indication, the talks will be available online after the event.  So if you’re not able to make it there in person, I think you’ll still be able to watch the talk.  I’m not sure about that, but that’s at least what happened last year in most cases.

And then the last thing I want to do is talk a little bit about something that I’m also really excited about, which is a new program that I’ve been working on over the past few months.  Actually really I’ve been working on it over the past several years because it’s a topic that I’ve, of course, been interested in for a long time, as you’ll know if you’ve been following my blog, and it’s really how my blog started.  The very first articles I ever wrote for my blog back when it was The Healthy Skeptic were about the relationship between cholesterol and heart disease.  And this program is gonna be called The High Cholesterol Action Plan, and the reason I’m doing it is that there’s still a lot of confusion out there about the relationship between cholesterol and heart disease, and that’s understandable because it’s an extremely complex topic.  In fact, the more I learn about it, the more intricacies I discover and subtle distinctions that become apparent and the more that I realize that the two extremes that we typically see out there, like, the one extreme, as Chris Masterjohn said, the cholesterol warriors, the people who say that high cholesterol is the cause of heart disease and that, you know, eating saturated fat and cholesterol in the diet raise cholesterol levels and so we should eat a low-fat diet and take statin drugs and do everything possible to lower our cholesterol to reduce our risk of heart disease.  We have that.  That’s one extreme, the cholesterol warriors.  And then on the other side of the extreme you’ve got the cholesterol skeptics who say cholesterol has nothing to do with heart disease, we shouldn’t worry about our cholesterol levels at all, and if you get your cholesterol tested and it’s 350, you know, go out and celebrate with a low-carb, high-fat meal!  So those are two extremes, and it turns out that I think the truth is somewhere in the middle.

And over even the last year, I’ve learned a tremendous amount about this issue, and because I’ve just been so busy with my practice and the show and my writing and everything else I’m doing, I haven’t unfortunately had the chance to update a lot of the articles on my site, and I haven’t had the chance to write new articles sharing all of my new research and what that means to you or anybody that you know that has been diagnosed with “high cholesterol” and usually then prescribed a statin.  And I have so many patients and so many readers and listeners and people in my life who write me and say:  Hey, I got diagnosed with high cholesterol, and my doctor wants me to take a statin.  I’m really confused about this.  Should I get my particle size tested?  Should I get CRP tested?  What other tests should I get to really figure out what my risk is?  Or maybe my dad or my mom was diagnosed with high cholesterol, and they’re already on a statin, and I’m concerned about them.  And you know, it’s a big issue, and it affects a lot of people, and there’s probably not a single one of us listening to this show right now that doesn’t know somebody that’s on a statin or that’s been prescribed a statin.  So I wanted to just put all of the information in one place, like, to just talk about the most current research, all of the cutting-edge staff about how to really truly determine your heart disease risk, which tests are best, which tests are bunk and a waste of time and money.  And then once you establish what your risk is, how you decide what to do about it.  What’s the best dietary approach?  You know, is a low-carb, paleo type of diet best for everybody, or is there a situation where that’s not a good choice?  And statins, should they always be avoided, or are there some people that may actually be good candidates for statins?  And for those who statins aren’t a good choice for, what are the natural alternatives to statins?

So it’s a huge topic, and I started out thinking that I’d be able to do it in a pretty succinct way, and it still will be very practical and focused, but it’s gonna cover, you know, it’s gonna be like a soup-to-nuts thing, from beginning to end, and it’ll have a really practical framework, like a decision tree for going through the process step by step of determining what your risk is and then how to respond appropriately.  It’s probably about six weeks away, and I’ve been working a little bit too much on it.  I get into these modes where I just completely dork out and get really lost in what I’m doing, and yeah, that’s how I’ve been spending my time lately, but I’m excited about it and I can’t wait to get it out there because I think it’s gonna help a lot of people.

Steve Wright:  Sounds like an awesome project.  I am excited to get my hands on it.  So you’re talking the end of August-ish right now tentatively?

Chris Kresser:  That’s what I’m hoping for.  This thing, you know, sleep is getting in the way.

Steve Wright:  I hate sleep.  God.

Chris Kresser:  The need to sleep at least a little bit and take care of my body and stuff, but yeah, I’m shooting for the end of August, and it’s gonna be a combination of video screencasts, me going through presentation slides, audio versions of that, PDF transcripts, and then an action guide, as I described, takes you through step by step, and you know, specific recommendations for supplements and diet and exercise and other ways of treating and preventing heart disease naturally.  So yeah, we’ll talk about it again when the time comes and go into a little bit more detail on it, but it’s on my mind and I’m excited about it, so I just wanted to share a little bit.

Steve Wright:  Well, it sounds great.  And if anybody caught my Real Food Summit talk, you know I love step-by-step, so I’m excited right now, to say the least.

So you had an awesome Real Food Summit talk, Chris, I think probably one of the most popular, seeing how you got the encore day and everything.

Chris Kresser:  Thanks, Steve.  Yeah, I mean, it was a good experience.  I, as many of you know, did the Paleo Summit with Sean a while back, and this was similar.  It was an online conference with a number of experts and authorities in the real food genre, so not paleo, per se, but nutrient-dense approaches to diet, which would include, like, the diet that the Weston A. Price Foundation advocates.  And it was a great conference.  I think it was even better attended than the Paleo Summit.  And my talk was on the importance of eating fish and seafood in the context of a real food diet and why it’s important to do that, how much and which types and fish are best to eat.  You know, I talk a little bit about some of the concerns surrounding fish consumption like mercury and PCBs and dioxins and why for much people and much types of fish that’s not really a concern.  So yeah, if you missed it, you can buy the whole set of talks.  I think there are about 27 presentations.  Is that right, Steve?

Steve Wright:  Yeah, I think there were 27 that were live, and then there were six or seven bonus.

Chris Kresser:  Oh, right.  Yeah, so there are like 33 presentations, all like an hour or an hour and a half, and then there are audio recordings, PDF transcripts.  I think you get a free subscription to Organic Gardening.  There are some other bonuses thrown in there.  You can go to my website and look at the homepage.  I think one or two pages back there’s an article there that I wrote about the Summit, and you can check it out and then click through there if you’re interested in getting the talks.

Steve Wright:  Yeah, I thought it was a great summit.  There was a ton of top-notch presenters who shared some really awesome concepts.  It took me, like, three days to download it.  There was so much info, so you definitely get your money’s worth.

Chris Kresser:  Actually, I guess, we could put a link to it in the show notes for this show, so rather than going and digging around my website, you can just check out the show notes and we’ll put a link in there where you can get the recordings.

Steve Wright:  OK, great.  Well, this was a heck of an intro, Chris.  Take a water break, and I’m gonna tell everyone about Beyond Paleo.  Now, if you’re listening to the show, we’re assuming that you’re into your health, you’re into optimizing your health, and you’re probably gonna want to check out what over 10,000 other people have already signed up for, and that’s what I talked about before called Beyond Paleo.  Beyond Paleo is Chris’ brainchild.  It’s 13 emails.  It covers everything from food to being happy, and all of these things together are gonna help you burn fat, boost energy, and prevent and reverse disease without drugs.  So you’re gonna want to get your hands on it if you haven’t yet.  Go over to ChrisKresser.com, and look for the big red box.

Chris, are you hydrated?

Chris Kresser:  I’m ready to go.

How to tell if digestive problems are caused by leaky gut, SIBO, or food intolerance

Steve Wright:  OK, let’s do this.  Our first question comes from Megan:  “Is there an easy way to tell if your GI problems are due to leaky gut versus SIBO versus general food intolerances, for example, FODMAPs?  Or is it more likely that these issues all overlap in someone with an unhealthy gut?”

Chris Kresser:  Yeah, it’s a great question.  I guess it depends on what you mean by ‘easy’ for the first part of your question, because there are tests that can be done for SIBO.  There are a couple tests that I’ll mention in a second.  And then there are also stool tests that can be done to identify gut pathogens like opportunistic or pathogenic bacteria and fungal infections and parasites.  And there are tests that can be done for fructose intolerance.  And then there are also tests for food intolerance and tests for leaky gut, though I think those are less useful, and I’ll come back to that in a second.  So let’s talk first about the tests for SIBO.  There are two main ways of testing for small intestine bacterial overgrowth.  And for those of you who aren’t aware of this is, normally the small intestine should be relatively sterile, meaning there shouldn’t be a lot of bacteria in it.  Most of the bacteria that resides in our gut is in the colon and, to a lesser extent, the very end of the terminal ileum, which is the end of the small intestine.  But in some cases, the bacteria can translocate from the colon into the small intestine where it doesn’t belong, and then that causes gas and bloating and pain and changes in stool frequency and consistency.

So there are two ways of testing for small intestine bacterial overgrowth.  One, and the most common one is a breath test, where you drink a solution that contains some simple sugars, which can be fermented by small intestine bacteria.  And then you blow into a little tube that’s attached to a balloon or a bag, and then you send that bag to the lab, and the lab tests it for certain gases that are produced by certain kinds of bacteria.  And if the levels of the gases are high, then that indicates you have an overgrowth of bacteria in the small intestine.  So that’s one way of testing for it.  Another way of testing for it is a urine organic acids test, and these are offered by labs like Metametrix and Genova Diagnostics, who just bought Metametrix actually last week, so they’re gonna be merging together.  And organic acids are byproducts of bacterial metabolism.  So certain types of organic acids, if they’re elevated in the urine, can indicate an overgrowth of bacteria in the gut and also an overgrowth of fungi.  So D-arabinitol is an organic acid that’s produced in fungal metabolism, and so if you have an overgrowth of D-arabinitol in the urine, then that can indicate a yeast overgrowth.

So those are the two main tests.  I tend to use the organic acids test more, and that’s partly because it has a number of markers that I find to be useful, and so I just can kill several birds with one stone, and I tend to order that more, but the breath test is also good.  One lab that’s pretty well known for the breath test is Metabolic Solutions, and it’s pretty affordable.  It’s like a hundred bucks, maybe 95 bucks or something.  At least, that’s what it costs me to order it.  I don’t know if they have different prices for clinicians and patients.  I think that same lab, Metabolic Solutions, they also offer a fructose intolerance test, which is very similar to the SIBO test, and that is one that you could do to identify any potential problem with FODMAPs.  If you test positive for fructose intolerance, then you’re almost certainly gonna benefit from doing the FODMAP approach since the FODMAP approach is based on reducing foods that have excess fructose or fructans or polyols, sugar alcohols.  So if you have access to that kind of testing and you have the resources to do it, they’re all pretty easy to do, and they can help you identify what the underlying cause of your problem is, and then maybe that can help determine what kind of action to take, both which diet would be most effective for you and then what other interventions might be effective.  For example, if you have SIBO, you’re probably gonna want to do some antimicrobial protocol in order to treat that.

As far as food intolerance testing goes, we’ve either talked about it on the show or I’ve written about it or both, but I don’t consider food intolerance testing to be very useful for a couple different reasons.  Number one, and I’m pretty sure I’ve mentioned this on the show, there have been some kind of blinded trials done anecdotally by clinicians, where they’ve drawn their own blood and put it two vials, you know, on the same day, same blood draw, and labeled the two vials with different names and sent them into the same lab and come back with completely different results for the two different vials of blood that came from the same person on the same day.  So that’s a little suspect.  And then number two, even if the test was completely reliable, the question is still what’s causing those food intolerances?  I mean, food intolerance is a symptom; it’s not a disease.  There’s an underlying disease or pathology that’s causing those food intolerances, and that would usually be SIBO or intestinal permeability or a parasite or a fungal infection or some other gut problem, maybe a gut-brain axis issue or maybe gluten exposure, undiagnosed gluten intolerance.  Those are mechanisms.  Those are problems that lead to symptoms.  So if you just remove the foods that the food intolerance testing shows that you’re sensitive to, certainly that will help with the symptoms, and there’s nothing wrong with that, but assuming you want to be able to eat some of those foods again, addressing the underlying problem is a much better approach.  So I don’t put a lot of stock into food intolerance testing for those reasons.

And then intestinal permeability, well, there are a couple of different ways to test for leaky gut.  And I actually want to talk to Dr. Fasano about this a little bit.  I’ll be curious to see what he has to say about it.  But there’s the lactulose/mannitol test, and that’s the one that’s best known.  And again, you drink a solution of lactulose and mannitol sugars.  They’re rather large molecules, and they shouldn’t pass through the gut when the gut barrier is intact.  And if they are detected in the blood, that means they’ve passed through the gut, and that means, then, that you have a leaky gut.  So that’s one way of testing.  A newer way of testing was developed by Dr. Aristo Vojdani.  I hope I’m pronouncing his name right.  But he’s the clinical advisor at Cyrex Labs, and they developed a test that screens for antibodies that are involved in the immune response that destroys the gut barrier.  So I think there are actomyosin antibodies, zonulin antibodies, and one more, which I can’t remember off the top of my head.  And that’s a completely different way of testing for leaky gut, but if we take Dr. Vojdani’s research at face value, it’s apparently much more effective and accurate than testing the lactulose/mannitol route, which some doubt has been cast upon in recent research.

The reason I don’t find myself testing for leaky gut very often is my benchmark for determining whether to run a test is whether it will change the outcome of the treatment, and usually with leaky gut it doesn’t, because if I get the test results back — Let’s say someone comes to me and they have a gut problem.  If we were to run a test for leaky gut and it came back and it said they didn’t have a leaky gut, well, I still have a person with a gut problem.  You know, I still need to figure out what’s causing their gut problem and what to do about it.  And if someone comes back with a leaky gut, I still need to figure out what’s causing that leaky gut.  So again, I look at leaky gut kind of more like food intolerance in a sense because even though it is an underlying mechanism to some extent, meaning it can contribute to and cause a lot of other problems, there’s still usually something causing leaky gut itself.  It doesn’t just come out of nowhere, you know, and that could be, again, like, gluten intolerance or a pathogen, some kind of inflammatory process, small intestine bacterial overgrowth, stress, gut-brain axis problem.  So there’s usually still more work to be done to determine what the underlying cause is, and I just think often it pays to just do that.  But the one area where I think the testing can be helpful is gauging the success of the treatment.  So if we do a bunch of treatment and the person is improving, then we might do the leaky gut test and see, OK, let’s see what’s happening to your gut barrier.  Is it still permeable or has it improved based on the treatment we’re doing?  And if it hasn’t, then we can adjust the treatment and make different choices.

So, yeah, I mean, there’s obviously a lot to talk about here too, and maybe as another announcement, for some time, you know, I’ve always known that I would write a book and probably several books, but I’ve really been struggling a lot over the past several months deciding what book I want to write and, you know, what my first book would be.  And I finally have decided, and it’s gonna be a book on gut health.  And specifically it’s gonna be a book that examines what the real causes of digestive problems are, because most of the diagnoses that we have for digestive problems just name the symptoms that people experience.  So think about it:  Irritable bowel syndrome, IBS.  Somebody goes in to the doctor.  They say:  Oh, my stomach hurts.  I have pain.  I have gas and bloating, and I have diarrhea or constipation.  And the doctor goes:  OK, well, you’ve got IBS.  And you know, it’s basically like the patient is like:  Well, isn’t that what I just told you?  My gut is irritable?  And you know, the same is true for heartburn and a lot of other “gut diseases.”  They don’t actually describe what’s wrong; they just describe the symptoms that people are experiencing.  So my book is gonna focus on the underlying causes of gut problems like SIBO, like parasites and other gut pathogens, like gut-brain axis problems.  And then, of course, talk about how to address those problems with natural remedies.  So we’re gonna be talking about this subject in a lot more detail in the next year because I’m gonna be up to my ears in it as I start writing the book, which I haven’t started.  I’ve outlined it.  I’m gonna start writing probably, I don’t know, in the fall once I get through these other projects I’m working on.

Steve Wright:  You’re signing yourself up for a lot of projects, man.

Chris Kresser:  I know!

Steve Wright:  We’re expecting this from you.

Chris Kresser:  Yeah.  You guys gotta remind me to take my own medicine and remember to, you know, take care of myself and lay down and take a nap every now and then.

Steve Wright:  Yeah.  You need to be sleeping.  I know you like to laugh when you say IBS, but you know, you need to be laughing outside of the podcast too.  We can’t forget the happiness piece.

Chris Kresser:  Not at all.  It’s a crucial part of my well-being.  That’s for sure.

Steve Wright:  Well, I’ll just throw a little plug in there for our Real Food Summit talk because Megan’s question was really the topic of Jordan’s and my presentation:  what to do when you go paleo or you go Weston A. Price and your gut problems don’t necessarily go away.  And so we tried to give some really practical tips that we’ve learned over the years.  So that might be a place to go, Megan, for more information until the thesis that is in Chris’ head is in our hands.

Chris Kresser:  All right, let’s do the next one.

What to do about Epstein-Barr Virus

Steve Wright:  OK.  This question comes from Teresa:  “Hi, Chris.  Thanks for the high-level discourse actually based on science.  Any suggestions for chronic acute Epstein-Barr?  Besides the obvious tenets of good health, sleep, good nutrition, smart exercise, good vitamin D levels, omegas, and the normal antiinflammatory steps, I tried a run of cat’s claw with no obvious results.  There’s nothing in the literature of help.  Can you help me?”

Chris Kresser:  Yeah.  So by chronic acute Epstein-Barr, I’m assuming she means a latent Epstein-Barr infection that was reactivated.  For those of you that don’t know, Epstein-Barr virus is extremely common in the sense that over 90% of North Americans have been exposed to it and then have IgG antibodies, which means we were exposed to it.  And once we are exposed to a virus like that, it usually doesn’t leave our bodies completely.  It can stay latent in our cells, and it can get reactivated when our immune defenses are down, often when we’re under great stress or possibly when we get another infection of a different type or if we’re eating an inflammatory diet or, you know, anything that can throw our immune defenses off.  To determine if you have this, by the way, it’s very important not only to get IgG antibodies tested since most people will turn out being positive for IgG Epstein-Barr, but to get IgM antibodies, which would be indicative of an active infection or chronic acute, which I assume is what she means.

So yeah, I do have some suggestions for working with this.  I have quite a few patients that are dealing with reactivated infections like Epstein-Barr or cytomegalovirus or herpes, HPV, or HHV, human herpesvirus.  The key thing in a general sense to realize when working with viruses, unlike bacterial infections or yeast infections, is that the number one thing you want to do is strengthen your own immune system’s defenses because while there are antiviral treatments, both drug and nondrug antiviral treatments, they’re generally not as effective as antibiotic treatments or antifungal treatments, and therefore the goal is to really boost our own innate immune defenses so that our immune system can do what it does best, which is eradicate these infections.  So the basics there, I think, she’s already doing, but would be antiinflammatory diet, high doses of vitamin C, so we’re talking about gram-level doses, several grams a day to bowel tolerance, maybe like 1 g three to four times a day.  You could even go that high.  Selenium and iodine are both important for the immune system.  Glutathione precursors like N-acetyl cysteine, lipoic acid, and then things that help with intracellular glutathione recycling like milk thistle.  Those are all really solid basic choices for supporting immune function.

But in terms of a natural antiviral that you might try, I like monolaurin, and monolaurin is an extract of lauric acid, which is a fatty acid that’s found in coconut products and in breast milk.  And when lauric acid is attached to glycerin, it forms a monoglyceride known as monolaurin.  And monolaurin works directly on the envelope coat of the virus by disrupting the conformation of the lipid bilayer, which in turn prevents its attachment or absorption to host cells.  So there actually is some research on monolaurin and its antiviral activity.  It’s also antifungal, and it has efficacy against gram-negative bacteria too.  The cool thing about monolaurin is that it’s pretty well tolerated and safe.  It doesn’t seem to have a negative impact on the beneficial gut flora.  And when compared with some other options in terms of natural antimicrobials, I’ve found it to be pretty easy to work with and not cause a lot of side effects.  So the sort of typical starting dose would be 1200 mg two times a day for an adult.  So I would definitely try that.

In my practice, I use some custom botanical formulas to treat viral infections, and I’ll customize them based on the specific presentation of the patient, based on the type of virus that they have, and you know, their own constitution and symptom profile.  But some of the medicinals that I will use are familiar, I’m sure, to a lot of you.  Echinacea is one; laurea; usnea, or old man’s beard — I love that name; dandelion; pau d’arco; astragalus; lemon balm.  It’s generally better rather than, you know, just going down to the store and getting a bunch of these and brewing them up, to work with an experienced herbalist if you can.  But some of these herbs, particularly echinacea and dandelion and lemon balm, are pretty safe and can be used at home.  You can just make teas or even buy teas with echinacea and some of these herbs in them.  So give that a shot, and let us know how it works out.

Does a furry tongue mean anything?

Steve Wright:  OK.  Let’s roll on.  This next one is from Anonymous:  “Hi.  I started the paleo/Perfect Health Diet at the start of this year.  All is generally going great.  I’ve lost weight and feel a lot better.  The only problem I’m having is a furry tongue.  It gives me horrible breath in the morning.  Throughout the day after eating sometimes it goes green.  I’ve been to the doctor, who gave me some antifungal lozenges to use for candida, but two of these lots have not worked yet.  The doctor said it was unusual to get unless you have a low immune system.  I haven’t been sick since going paleo, nor have I taken antibiotics.  Do you have any ideas what’s going on with my tongue?”

Chris Kresser:  My guess would be low stomach acid.  And I see this a lot on people who start a paleo diet coming from a diet with less animal protein.  We’ve talked about tons of times on the show.  Stomach acid, as you all know by now, is crucial to breaking down protein, particularly animal protein, and if you don’t have enough stomach acid, the protein can putrefy in the stomach.  And I haven’t seen any research on this from a conventional medical perspective, but certainly anyone who is familiar with Chinese medicine will know that they put a lot of stock into the appearance of the tongue, and a thick coating on the tongue is definitely an indicator of digestive disharmony.  And I don’t really know how to explain that with precision from a Western medical paradigm perspective, but I certainly have seen it to be, you know — In nearly everyone who has a digestive issue, there tends to be a coat on the tongue.  So that’s my guess:  low stomach acid.  It could also be small bowel bacterial overgrowth, and we talked earlier about how to get tested for that.  The easiest thing to do to test out the stomach acid hypothesis would be to just take some hydrochloric acid, that betaine HCl protocol.  We’ll put a link in the show notes to the post on my website where I discuss the protocol in detail and go through it step by step.  And if that doesn’t work, I would probably get tested for SIBO.  Or if you do the organic acids test, that will test for both SIBO and a fungal overgrowth, which would probably be an even better idea.

Steve Wright:  OK, well, that should get them started, and I’ll just add that back before I started my health reversal, I did have a white-coated tongue, and I did and still am getting over low stomach acid, so just my two cents that might help you do what Chris said.

How baby is telling you it’s time for different foods

OK, let’s move on to the next question from Thomas:  “Hi.  I purchased the Healthy Baby Code after the birth of my son.  He is now 6-1/2 months old.  We are trying to feed him egg yolks as his first food as you recommend, but he doesn’t seem to like them.  We’ve mixed it with breast milk, but it doesn’t seem to help.  Should we continue trying to feed him this or move on to other foods?”

Chris Kresser:  Definitely move on to other foods.  The guidelines for introducing first foods are general and will apply to many babies, but as any parent who has had more than one child will tell you, just like adults, babies have preferences and likes and dislikes.  So if your baby doesn’t like eggs, then yeah, just skip it and move on to the next thing and try something else and then maybe come back to it later.  It seems that some percentage of babies also can’t really tolerate egg yolks very well at that age, and I’ve had some reports of vomiting and just some bad digestive reactions.  I don’t think they’re mediated by allergy.   I just think that for whatever reason it’s maybe a little bit too soon to introduce that particular food.  So use the guidelines as a rough blueprint, so to speak, but feel free to improvise a little bit based on your child’s preferences and what’s available to you.  Some of the things that are — I mean, you wouldn’t want to skip too far ahead because the guidelines are laid out with particular stages of development of the digestive tract in mind, but certainly just going forward a little bit and expanding the options that way is completely fine and would definitely be recommended in this situation.

Steve Wright:  OK, well, I have nothing to add there, so glad you covered that.

The specific Graves Disease Protocol to keep it in check… for good

Chris Kresser:  Steve, did we miss the Graves’ disease question or did I not put that in there?

Steve Wright:  I don’t see a Graves’ disease…

Chris Kresser:  Scroll down a little bit.  It’s in there somewhere.  If you can’t see it, we’ll come back to it in a different episode.

Steve Wright:  I copied down to the intermittent fasting one.  I don’t see it in there.

Chris Kresser:  Well, let me just kind of paraphrase it.  The question, I think, was essentially we’ve talked a lot about hypothyroidism and Hashimoto’s but haven’t talked much about Graves’ disease and how would I recommend approaching Graves’ disease.  Graves’ disease is certainly more rare than Hashimoto’s and hypothyroidism.  That’s one of the reasons I haven’t talked about it as much, but I do know quite a bit about it because my wife was diagnosed with Graves’ disease, and this was back when we were still trying to get pregnant with Sylvie and we were having some difficulty, and I was doing some investigation figuring out what was going on, and we discovered that she had Graves’.  And shortly after discovering that and treating her for that, she got pregnant with Sylvie.  So it’s something that I’ve done quite a bit of research into and I have obviously a personal motivation to stay up with it.

So for us, for my wife, the number one thing by far in terms of turning her health around was low-dose naltrexone, which we’ve discussed a few different times.  Low-dose naltrexone is a low dose of a medication called naltrexone, of course.  Naltrexone, if you look it up, you’ll find that it’s used for some things that have nothing to do with autoimmune disease and Graves’ disease.  Naltrexone at 50 mg is used for opiate and alcohol withdrawal.  You know, so basically it blocks the endogenous opiate receptors at that dose, which are our natural feel-good chemicals, so that if a heroin addict that was on 50 mg of naltrexone shot heroin, they wouldn’t feel a thing.  The problem at that dose was that not only did they not feel any pleasure from shooting heroin, they felt no pleasure at all at any other time in their life because their pleasure-producing chemicals were completely blocked.  So naltrexone was not very successful from that perspective, but a doctor in the ‘80s named Dr. Bihari found that if you used a lower dose of naltrexone and created a temporary blockade of the opiate receptors overnight, you could basically trick the body into producing more endogenous opiates.

And if you’re wondering how this relates to autoimmune disease, we know now that white blood cells have receptors for these endogenous endorphins, and that suggests that the endorphins have an immunoregulatory effect.  And sure enough, later research showed that low-dose naltrexone stimulates T regulatory cell function.  The T regulatory cells balance the immune system, and they turn off the inflammatory response once it’s turned on, and that’s a characteristic of autoimmune disease, is they’re often runaway inflammatory responses.  They’re basically inflammatory conditions run amok, where you get an inflammatory process and it just goes on and on and doesn’t get turned off.  So low-dose naltrexone, there are studies examining it in multiple sclerosis, in fibromyalgia, Crohn’s disease, probably the most well-known and best-designed trials, and it was remarkably effective for Crohn’s disease.  There was something like a 77% remission rate, which is just unheard of for a Crohn’s disease treatment, and with no side effects compared to placebo, which again, is unheard of because most of the drugs that are used to treat Crohn’s are pretty potent and can cause some pretty nasty side effects, like prednisone and Imuran and Remicade and some immunosuppressive drugs.

So low-dose naltrexone has not been clinically studied specifically for autoimmune thyroid disease, but many autoimmune diseases share common mechanisms, so it’s not that much of a stretch to think that if it works for MS and IBD and fibromyalgia that it could work for Hashimoto’s and Graves’, and sure enough, it does work very well for those conditions in my anecdotal experience and then the experience of a lot of other practitioners that use it and have hundreds of patients that are taking it for autoimmune thyroid disease.  So that would be absolutely my number one priority if I had Graves’ disease, is trying low-dose naltrexone.  There’s little risk to doing it.  There are no known long-term complications or risk associated with it at such a low dose, and especially when you compare it to the other treatment options in Graves’, which are basically having your thyroid radioactively ablated, or nuked, in layperson’s terms, or taking radioactive drugs like PTU or methimazole that have pretty nasty side effects including liver failure and death, I think low-dose naltrexone is a pretty attractive alternative.  I actually have a friend or a friend, or a friend’s mom, who had had Graves’ for 30, 40 years and had been taking medication, I think, PTU for that length of time, was extremely skeptical that LDN could help her because she had been on medication for so long.  But she heard about Elanne’s experience, and she decided to give it a shot, and now she’s off of those toxic drugs and she’s just taking LDN.  So it works even after that length of time in some people.

The next thing is that there are some studies, a couple studies, that suggest that L-tyrosine at pretty high doses can suppress the conversion of T4 to T3.  Graves’ disease is a hyperthyroid condition, and reducing the conversion of T4 to T3 can be helpful in those situations.  So the dosage that was observed in those studies to do that was around 1000 mg two to three times a day.

There’s some research that suggests that lithium orotate can help because it blocks the release of iodine and thyroid hormones, and in fact, it’s often used after radioactive ablation of the thyroid gland in Graves’ disease, when patients can experience a transitory increase in thyroid hormone after that ablation, and lithium is used to bring the levels down to prevent a thyroid storm or thyrotoxicosis.  So the dose, though, for that with lithium orotate is very low.  Some of you might be familiar with lithium as a treatment for bipolar disorder.  In the case of bipolar disorder, it’s used at a dose of, like, 800 to 2400 mg, but the way it’s used to bring levels down of thyroid hormone is a lot lower.  It’s about 120 mg.  I would not do this without supervision of a clinician who knows what they’re doing because lithium, if it’s not dosed properly, can have probably some undesirable effects, so it’s good to get some support there.

Those are the main ones.  Again, for us, I did some other things, like a custom herbal formula for my wife, but it’s difficult to give general recommendations for that because it’s really tailored to each person’s particular presentation.  But what happened is after she went on LDN, within two months she was pregnant, and then we had a very healthy baby girl who’s actually turning 1 in two days, three days.  This weekend we’re having her 1-year birthday party, which is gonna be fun.  So it can be quite remarkable, and really she’s been euthyroid the entire time since she’s been on LDN.  She’s never had to take any other drug.  And she’s healthy and doing great, so it’s definitely an exciting treatment for people who have that condition.

Steve Wright:  That’s a great story.  Are you inviting everybody to the birthday party?

Chris Kresser:  Yeah, c’mon over!

Steve Wright:  Hey, now, just to clarify, I’m assuming that you would also want to be gluten-free at least, if not paleo?

Chris Kresser:  Yes, definitely.  I mean, sometimes I think that that goes without saying, but of course, it doesn’t, so thanks for reminding me.  You want to eat a generally antiinflammatory diet, which means avoiding gluten because it can aggravate the immune system, and any other foods that can aggravate the immune system.  And another thing you want to be careful of is iodine.  I think iodine actually can be helpful in some cases of Graves’ disease, but you need to make sure that you have enough selenium if you’re taking iodine, and you need to make sure that you’re taking a very low dose of iodine to begin with and building up slowly.  And it’s probably a good idea to just get your iodine levels tested to see if you even need to take it, because if you take a higher dose of iodine right off the bat and you’re selenium-deficient, then iodine can, in that situation, exacerbate the autoimmune reaction.

Steve Wright:  OK, great.  Do you want to do one more?

Chris Kresser:  Let’s do the anemia question.

Everything you need to know about Anemia (and more)

Steve Wright:  OK.  It’s a bit long, so hang with me here.  This comes from Chris:  “About anemia, I heard you briefly mention during a podcast that something like 30% of your patients are anemic, and I was hoping that you would offer me some avenues for research into this problem.  I’ve been anemic for 15 years now, probably about the same amount of time that I’ve had intestinal/digestive issues.  Only in the last six months have I discovered paleo, Weston A. Price, and GAPS.  So I’ve finally gotten control of my depression/anxiety/psoriasis/gas/allergies/ asthma/fatigue/general immunity” — he’s got some things going on — “But the anemia persists.”  He lists some specific counts here.  We’ll skip over those, but basically it comes down to he’s borderline anemic, and it’s continuing to persist.  Chris, can you offer him some help?

Chris Kresser:  Yeah, I mean, if you want some avenues for research, I can keep you busy for the next five to ten years probably because anemia — There are few topics actually in medicine that are more poorly understood and more complex.  Anemia is one of those topics that, I think, is not taught well in any medical school, whether we’re talking about conventional medical school or the more alternative kind of medical schools.  A lot of clinicians just don’t really understand it very well, and I know this because I frequently see patients coming from all different types of clinicians, doctors, naturopaths, acupuncturists, whatever, and they tell me their history, and they show me their labs, and they show me what their clinicians did, and I’m often pretty shocked.  And you know, it is complex, as you’ll see.  I’ll go through some of the basics of anemia and the things that can cause it, and you’ll get a sense of why there is so much misunderstanding.  But on the other hand, it’s really frustrating because there are some things that are pretty easy to grasp that I think all clinicians should know, but I guess we just have to blame the schools because they’re not teaching it very well.

A lot of people can’t even agree on a definition of anemia.  That’s where the complexity and the problems start, is if you look up what is anemia, you’ll get all different kinds of responses.  One is a condition where the number of red blood cells in the blood is below normal.  Well, then, of course, there are different opinions on what’s normal.  And then another might be more specific, like hemoglobin level of below 12 in women or below 13 in men.  But my preferred definition is compromised ability of red blood cells to deliver adequate oxygen to body tissues, because that’s, in the end, what we’re really concerned about, is the capacity of hemoglobin to deliver oxygen to the cells, and all the cells in the body need oxygen to function properly.

So the causes of anemia can be basically split into four categories.  One would be insufficient production of red blood cells, hemoglobin.  Number two would be excessive breakdown of red blood cells.  Number three would be loss of blood.  And number four would be fluid overload.  So when we talk about insufficient production, that can be further broken down into stem cell problems like aplastic anemia or insufficient erythropoietin production; inadequate maturation of the red blood cells, which is usually in turn caused by nutrient deficiencies, specifically iron, folate, B12, or B6; myelodysplastic syndrome, or MDS, which was previously known as preleukemia; and then anemia of chronic disease, also known as anemia of chronic inflammation.  Now, when we talk about excessive breakdown, the second major group of causes, we’re talking mostly about the hemolytic anemias.  This generally will feature jaundice clinically.  You’ll see some yellowing and orange-bronzing of the skin and increased levels of an enzyme called lactate dehydrogenase on a lab test.  And these are often due to genetic mutations like sickle cell anemia and also enzymopathies like glucose-6-phosphate dehydrogenase deficiency, or G6PD.  The third category is blood loss, and short of trauma, you know, if you get in an accident and lose a lot of blood, we’re mostly talking in women about menstrual disorders like heavy periods or endometriosis or something like that, and in both men and women, gastrointestinal bleeding, so inflammatory bowel disease or ulcers, something like that where there’s significant ongoing blood loss.

And then the fourth category there is hypervolemia from excessive sodium or fluid intake, also sodium or water retention.  And it’s kind of a tangent, but it’s really important to point this out:  This hypervolemia happens naturally in pregnancy during the second and third trimesters as the blood volume expands to accommodate the growing fetus, and I see this a lot in my practice because I do a lot of fertility/pregnancy work.  A lot of women are misdiagnosed with anemia by their physicians or other health care providers during this period because a lot of clinicians, surprisingly, aren’t aware of this phenomenon, that the normal range for hemoglobin during pregnancy drops quite significantly.  So for example, the normal level for hemoglobin in nonpregnant women is between 12 and 16 g/dL, but the normal levels in pregnant women at 28 weeks are between 10 and 14 g/dL, and some research actually suggests that the lower end of that scale leads to better outcomes in pregnancy.  So if you’re pregnant and your hemoglobin is at 10.5, that actually pretty ideal and it doesn’t mean that you’re anemic.

OK, back to regular programming.  So I think you’re getting a sense now of how complex this is.  The typical thing is, like, you go in to the doctor and your hemoglobin is below the average level.  They’re just gonna give you an iron supplement, but iron deficiency is just one subtopic in one of those four categories of potential things that can cause anemia.  And certainly statistically speaking worldwide, iron deficiency is the major cause of anemia.  It affects about 2 billion people around the world, but it tends to affect more people in developing countries where iron-rich foods, particularly animal protein, is not available or not as readily available and in disadvantaged socioeconomic communities in the US for the same reason.  But iron deficiency anemia is more rare — I mean, I’m hard pressed to think of — I think I can recall maybe two or three patients that I’ve ever seen that have had iron deficiency anemia.  But as the questioner pointed out, I have a lot of patients with anemia.  Almost always the anemia is caused by something other than iron deficiency in my patient population.  And that might be unusual, but I frequently will get people come to me that have had low hemoglobin and their doctor just prescribed iron pills.  And the problem with that is that sometimes these patients are iron loaded, or sometimes they have something called anemia of chronic disease, which I’ll mention in a second, and giving someone who has anemia of chronic disease iron can really be problematic because anemia of chronic disease is caused often by an infection, and all pathogens utilize iron to proliferate and grow, just like most life on Earth.  And so if you give someone with an infection and anemia of chronic disease that’s caused by that infection iron supplements, you’re gonna make them much worse, and this actually happened to one of my patients.  It was quite sad.  Someone that I was consulting with in Texas, an older woman in her early 80s, and she sent me her blood work, and she did have anemia.  Her hemoglobin was low and her iron saturation was low, but — and this is really important — her ferritin levels were high, and that’s what distinguishes iron deficiency anemia from anemia of chronic disease, is the ferritin is elevated because ferritin is an acute phase reactant that’s elevated in the inflammatory response, and so that indicates that there’s some infection or inflammation, and also the body is trying to sequester iron and ferritin to keep it away from the pathogen.  So she sent me that, and then she ended up going to the hospital or to her doctor for some other reason, and the doctor saw that she had low hemoglobin, either didn’t test for or pay attention to ferritin, gave her iron pills, and she ended up spending a day or two in the hospital and nearly died.  It was really scary.  So this is a serious issue, and I think it’s important to grasp the complexity of it and to investigate these possible mechanisms because it’s often not simple.

So, let’s see.  We got a little lost there.  I guess what I would say is assuming some of those medical causes have been ruled out, like you don’t have stem cell problems, you don’t have myelodysplastic syndrome, you don’t have a hemolytic anemia, you’re not experiencing any blood loss, and you’re not hypervolemic, you don’t have excessive sodium or fluid intake, in that case then it usually does come down to a nutrient deficiency, and then we’d be looking at either iron deficiency on the one hand or folate, B12, or B6 deficiency on the other hand.  Luckily, it’s pretty easy to distinguish between those two, and the way you do that is you look at other markers that are included in a complete blood count, which he’s obviously had.  Usually when you test hemoglobin and red blood cells, that’s part of a panel called a complete blood count that measures some other markers.  So what you need to do is you look at MCV, mean corpuscular volume, and then MCH and MCHC, and if MCV is low, below the lab range, and hemoglobin and red blood cells are low, that’s usually indicative of iron deficiency anemia.  If MCV is high or high normal, then that’s a macrocytic anemia, and that’s indicative of B12, folate, or B6 deficiency.  So it’s fairly straightforward to do that, and of course, you can test your iron levels, doing an iron panel and ferritin to determine if you’re iron deficient.  And you can test your B12 levels using a standard serum B12 test and also urinary methylmalonic acid to see if you’re B12 deficient.  You can also test folate levels in the serum, but that’s a little less accurate.  The best way to test folate status is formiminoglutamic acid, which is one of the organic acids on the urine panel that I mentioned earlier.

So if your eyes have rolled back in your head and you’re just completely lost, don’t worry about it.  This is a complex topic.  I hope this was helpful for the questioner.  I would definitely get an iron panel and ferritin and then test for your B12, B6, and folate status.  Those are the most likely causes of ongoing anemia even after all of the kind of changes that you’ve made.  And if those are all normal, I would definitely seek out a practitioner who knows this stuff and can help you out.

Steve Wright:  That was a wealth of information that blew my mind.

Chris Kresser:  All right, we did it.  I think we made it through quite a few this time, huh?

Steve Wright:  Yeah, that was a good rapid-fire session right there.  OK, great.  Do you have anything to close with?

Chris Kresser:  No, just make sure to tune in next time for Dr. Fasano and then hopefully the time after that maybe — We’ll be AHS.  So we’ll either be taking a week off, one show off for a little summer break, or I’ve been talking with Jordan and Steve about the possibility of doing a kind of on-location, informal episode there if we can find the time and we can work it out technologically.

Steve Wright:  Yeah, we’re gonna do our best to see what we can come up with, and you definitely don’t want to miss the next show.  That’s for sure.

OK, great, so if you liked what you heard today, please head over to iTunes and leave us a review.  Leaving reviews really helps the popularity of the show, helps get the word out so other people can listen to it.  Please keep sending us your questions at ChrisKresser.com, and we’ll talk to you next time.

It’s no secret that obesity, diabetes, and metabolic disease are afflicting an incredible number of Americans; in fact, the prevalence of the metabolic syndrome in our country has reached an astonishing 34% and is continuing to rise. (1) This disease, characterized by long term low-grade inflammation, causes metabolic disturbances that lead to the development of complications such as nonalcoholic fatty liver disease, cardiovascular disease, and type 2 diabetes. This is a serious health problem for many Americans – one that isn’t going away any time soon – and determining the cause of these metabolic conditions is a top priority for obesity researchers across the country.

I’ve been writing about the connection between gut health and “diabesity” for quite some time now; I have an entire series on my website dedicated to the relationships between obesity, insulin resistance, metabolic syndrome and type 2 diabetes, and I believe that inflammation and leaky gut caused by gut dysbiosis are the key players in this metabolic epidemic. While the existence of leaky gut syndrome is still debated among doctors and scientists, it is clear to me that having healthy gut bacteria is crucial to maintaining a normal weight and functional metabolism.

Is healing your gut the hidden key to weight loss? 

Recently, a group of researchers in Brazil published a new review exploring the idea that intestinal permeability is a contributing factor to obesity. They identified three separate but related mechanisms: gut dysbiosis, an unhealthy dietary pattern, and specific nutrient deficiencies. These three risk factors likely interact to cause intestinal permeability and promote the development of the metabolic syndrome and obesity.

Gut dysbiosis and leaky gut

It is well documented that those with obesity have significantly impaired gut function compared to the general population. Obese individuals are shown to have problems with effective digestion and absorption of food, gastrointestinal illness, unstable or pathological intestinal microbiota, poor immune status, and overall lower wellbeing, suggestion a lack of gut health. (2) This gut dysbiosis is thought to cause increased permeability in the small intestine, allowing the entry of toxins called lipopolysaccharides (LPS) into the blood and triggering systemic inflammation.

While it is uncertain whether the alterations in gut health are the cause or consequence of obesity, the association between dysbiosis and obesity is strong. One theory is that the metabolic activity of gut microbiota contributes to weight gain by causing more calories to be extracted from the food passing through the gut. Small intestinal bacterial overgrowth (SIBO) may also play a role in intestinal permeability by increasing constipation, reducing pancreatic enzyme and gastric acid activity, and disturbing the microbiota and host immune system relationship.

Probiotic supplementation can help strengthen the tight junctions of the intestine, reducing overall permeability. Probiotics can have anti-inflammatory effects in the gut, regulating the production of inflammatory cytokines and reducing intestinal permeability. This demonstrates the benefits of a balanced microbiota in the gut to maintain the function of the intestinal barrier, particularly in obesity.

Dietary effects on leaky gut

Besides just the composition of gut bacteria, nutritional factors play an important role in permeability as well. The authors of this study suggest that there are two major components of the diet that can affect intestinal permeability: fructose and fat. Fructose is thought to damage the liver directly by increasing blood levels of LPS toxins, causing fatty liver, inflammation, and hepatic insulin resistance. These effects explain why high fructose consumption has been implicated in the development of metabolic syndrome.

As far as fat goes, the authors of this study suggest that fat is more efficient than carbohydrates at transporting LPS toxins to the liver through the formation of chylomicrons, molecules that deliver dietary fats from digestion to the liver. An increase in liver toxins was demonstrated to induce obesity, diabetes, and insulin resistance in rats, demonstrating why a high fat diet could exacerbate metabolic disease. The type of fat matters though; oleate, a monounsaturated fat, promotes the delivery of toxins to the liver, while butyrate, a short chain saturated fat, does not form chylomicrons or increase LPS toxins in the liver. It has also been found that changes in bile secretion are associated with altered intestinal permeability, and a decrease in bile allows for greater bacterial growth in the small intestine and more LPS being produced.

It is important that future research determine the type of fatty acids that increase intestinal permeability of endotoxins, and whether or not there is an interaction with the type and amount of bacteria in the gut.  The authors of this review do suggest, however, that a combination of a high fructose and high fat diet can lead to an increase in toxin-related liver inflammation and weight gain, which is likely true. (Did someone say McDonald’s Value Meal?)

Nutritional deficiencies and leaky gut

There are several micronutrient deficiencies that the authors found to be associated with gut barrier function, specifically vitamin A, magnesium, zinc, vitamin D, and calcium. Vitamin A, zinc, and magnesium all help maintain tight junctions in the intestine and regulate endothelial differentiation in the gut, while vitamin D stimulates intestinal lining renewal and resistance to damage by modulating the immune system. Vitamin D and calcium play a joint role in maintaining the intestinal barrier by supporting the ATP-dependent pumps in the intestinal cells. In obesity, intake of these micronutrients is typically low, so deficiencies could play a significant role in exacerbating leaky gut conditions, especially when combined with intestinal dysbiosis and poor dietary choices. Therefore, having good intake of these micronutrients could be protective against the development of leaky gut and the inflammation and eventual obesity it can cause.

Obesity caused by a leaky brain?

One more potential issue (not discussed by this particular review paper) is the possibility that systemic inflammation can actually cause leakiness in the blood-brain barrier as well. (3) C-reactive protein (CRP), an inflammatory protein that is elevated in obesity, has been found to increase permeability of the blood-brain barrier, possibly leading to inflammation in the hypothalamus. This neuroinflammation can cause impairment of central nervous system (CNS) function, which has been associated with poor control of food intake, leptin resistance, and obesity.

Furthermore, LPS toxins, released into the blood by a leaky gut, can rapidly increase blood leptin concentrations; this increase is enhanced by the presence of CRP, which could explain why chronic inflammation is associated with a rise in both CRP and leptin in humans. In this way, a leaky gut and a leaky brain, both caused by systemic inflammation and exacerbated by gut dysbiosis, can increase the risk of developing obesity due to the disruption in CNS and leptin function.

Gaining weight? Check your gut health!

The take home message of this study is that the interplay of gut health and diet has a significant role in weight gain and risk of obesity and metabolic disease. If you are struggling to lose weight, you may be dealing with inflammation caused by leaky gut and dysbiosis. And remember, you don’t have to have gut symptoms to have a leaky gut! Weight gain alone could be your only symptom, but it’s an important one to consider.

There are many steps you can take to ensure a healthy gut. Using probiotics and prebiotics can change the quality of the microbiome in the gut, and there are certain dietary strategies that can help improve the strength of the tight junctions between intestinal cells. Other issues such as stress, antibiotic and other medication use, autoimmune disease, and dietary toxins can increase intestinal permeability, so these are gut health factors that must be addressed as well.

Just be sure that you take the necessary steps heal your gut if you’re struggling with weight loss despite making changes in your diet and lifestyle. It may be the last piece in the weight loss puzzle that you’re missing!

In this episode, we answer more reader questions on SIBO, probiotics, Hashimoto’s, and Cold Thermogenesis.

In this episode, we cover:

4:12 It’s back – what Chris ate for breakfast
7:50 The most effective treatment for SIBO
18:42 Does Cold Thermogenesis really work?
22:05 What to do when the autoimmune paleo protocol doesn’t work
33:42 Why is my antibody count going up on natural thyroid hormone?
36:40 Proper carb consumption for Hashimoto’s patients
47:10 What does Chris’s daughter eat on a daily basis?
51:48 When to take probiotics

Links We Discuss:

• Lauricidin
• Life Extension Lactoferrin (Apolactoferrin)
• Klaire Labs InterFase Plus
• An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases
• The Chris Kresser Recommended Products Store

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, and you can find my work at SCDLifestyle.com, but we’re both here for the star of the show, integrative medical practitioner and healthy skeptic Chris Kresser, so welcome to the show, Chris.  How’s it going

Chris Kresser:  I’m doing pretty well, Steve.  How are you?

Steve Wright:  I’m doing well as well.  What’s this big news I hear about The Huffington Post?

Chris Kresser:  Well, I got a gig as a columnist or regular blogger there, which should be pretty interesting, I think.

Steve Wright:  Yeah, no big deal.  That’s a pretty major media outlet.

Chris Kresser:  Well, what I meant by ‘interesting’ is that some of you may know that Dr. Dean Ornish is the health editor at The Huffington Post, and Mark Hyman is a pretty prominent health blogger there too, and they’re both strong advocates of a plant-based diet — and I am too.  It’s just that my plant-based diet includes meat and fat in pretty substantial amounts, whereas their plant-based diet doesn’t.  And a lot of the really active commenters there and just from my — I don’t actually read The Huffington Post very much or any other health or news blog for that matter, but the few health articles I have seen there — and I’ve just scanned through the comments — they’re really heavily oriented towards a kind of vegan/vegetarian perspective.  My first article is going to be on debunking the myth that cholesterol and saturated fat cause heart disease, so I’m really curious to see what the response to that is going to be like and if I end up having the shortest tenure of any health columnist at The Huffington Post!

Steve Wright:  Well, first, Chris, I am totally shocked and just appalled that you’re not a regular reader of my blog, but I understand you’re pretty busy.

Chris Kresser:  Haha!

Steve Wright:  So, what we need to have happen here is we need to have everyone that listens to the show pay very close attention to your Twitter, your Facebook, and when this goes live, we all need to chime in with greens are the greatest delivery vehicle for butter ever.

Chris Kresser:  That’s right, butter carriers.  Yeah, I hope you guys can all come over and make your voices heard and share your experience with a paleo, higher-fat type of diet, because we’re going to be fighting an uphill battle, so to speak.

Steve Wright:  Well, there should prove to be some hilarious comments, anyway.

Chris Kresser:  Yeah.  I’m excited about it.  I mean, I do want to get this message out to a wider audience, and whatever you think about The Huffington Post, whatever your politics are, whatever you think of it as a blog, it certainly has a big audience and a wide readership, so I’m excited about that part of it for sure.

Steve Wright:  Yeah, I think it’s a great honor, and I’m excited for the first post.

Chris Kresser:  All right.  I’m not sure when it’s going to be, but I will definitely post a link to it on Facebook and Twitter and maybe even on my blog as well, at least for the first post.  I still haven’t even gotten the guidelines.  I’m not sure how often I’ll be posting there, but whenever I do, I’ll definitely post a link to it on Facebook or Twitter, so that’s the best way to stay current.  There may even be a way to follow particular bloggers on The Huffington Post — I don’t even know!  But if there is, maybe that’s worth looking into also.

Steve Wright:  And if you’re not following Chris on Facebook, you can go to Facebook.com/ChrisKresserLAc, and you can also find him at Twitter.com/ChrisKresser.

It’s back – what Chris ate for breakfast

So, Chris, we’ve been receiving some feedback, and people are a little angry that I didn’t ask you a specific question on our last episode.  Listeners, it was totally my fault.  It was my bad.  Chris, what did you have for breakfast today?

Chris Kresser:  Well, I’ll have to call it brunch because I’ve still lately been on my kind of spontaneous intermittent fasting kick.  I’ve been eating around 10:30 or 11 for the first meal of the day and having a couple big meals a day and maybe a snack in between.  Today I had a couple scrambled eggs and a little bit of leftover ground beef from a dish that we made the other night and some collard greens, and here’s how I cooked the collard greens this time, and it came out really well.  I stir-fried them in a little bit of bacon grease, and then I added some chicken broth, but I also added just a little bit of this brine.  My wife and I made some pickled vegetables recently, and so we saved the brine for this kind of thing, and I added just a little bit of brine to the greens and then covered them and kind of cooked them in the broth and the brine for a while and then uncovered them and turned up the heat and kind of cooked off all the extra liquid.  They were really good.  And then I had some sort of almost-ripe plantains cooked in a blend of coconut oil and ghee that I get from Green Pasture, which is really great.  It’s not as sweet as coconut oil alone.  It’s one of my favorite cooking fats.  And then I had some homemade sauerkraut that was actually a blend of cabbage, beets, and carrots and a little bit of ginger that we make that I really like a lot.  And then I had coffee and cream when I woke up, so that was actually the first thing I had not right when I woke up but maybe an hour and a half after I woke up.  So, there it is.

Steve Wright:  That’s a diverse breakfast, er, lunch, brunch.

Chris Kresser:  Yeah, it was a fairly big meal, and I haven’t eaten since then and probably won’t eat until dinner again today.

Steve Wright:  Awesome.  Well, I think today we’re today we’re doing a Q&A episode, correct?

Chris Kresser:  We are.  Let’s do it.

Steve Wright:  OK.  Well, we have a lot of questions here.  Thanks again, everyone, for sending in your questions.  Chris, I’d like to make sure that you have your treadmill set at the right speed and the right height, and while you’re doing that, I am going to go ahead and tell everyone about Beyond Paleo.  If you’re new to the Revolution Health Radio Show, the paleo diet, if you’re coming over from The Huffington Post or you’re just interested in optimizing your health, you’re going to want to go over and check out what over 30,000 other people have already signed up for.  It’s a free 13-part email series that Chris has put together called Beyond Paleo.  Now, in these free 13 emails you’re going to learn about burning fat, boosting energy, and preventing and reversing disease without drugs.  To get this, go over to ChrisKresser.com and look for the big red box.  Go ahead and put your name and email in that box, and Chris will start sending them your way.

So, Chris, you all set?

Chris Kresser:  I’m ready.

The most effective treatment for SIBO

Steve Wright:  OK, so for the first question, it comes from Sheilaa.  She wants to know what is the most effective antimicrobial treatment for SIBO, which is small intestinal bacterial overgrowth, that doesn’t create dysbiosis?

Chris Kresser:  I guess the first thing I would say is if at all possible, it’s a good idea to do this under the supervision of someone who’s experienced with these kind of treatments, because even though what I’m about to describe is relatively benign compared to, let’s say, antibiotic treatment or using prescription drugs, there still are potential issues, and SIBO can be a recalcitrant, relatively difficult condition to treat, so if you do have access to someone that can guide you through this, I do recommend that.  It’s a good idea, in general, for this kind of thing.

Having said that, there are some natural antimicrobials that you can get over the counter that I’ve found to be pretty effective for SIBO and don’t contribute to dysbiosis.  In some cases, the treatment, depending on how long you have to be on it, may moderately or mildly decrease levels of beneficial bacteria in the gut, but we wouldn’t expect that effect to be anywhere near as significant as it would be if you took antibiotics, although the antibiotic that’s typically used for SIBO now, which is rifaximin, is a fairly narrow-spectrum antibiotic that doesn’t completely wipe out the gut flora like some of the broader-spectrum ones that are more systemically absorbed do.  But I always recommend starting with this more natural approach, and as I said, I’ve had really good success with it both in terms of symptom improvement and then confirming the results using follow-up lab testing.

So, one thing that can be helpful that we’ve talked about on a few different shows is Lauricidin or monolaurin.  It’s an extract of lauric acid, which has antimicrobial effects, and it’s pretty well tolerated by most people and, I think, doesn’t really tend to have a negative impact on the gut flora.  It’s pretty safe to take and even safe to take for several weeks at a time.

Another thing you want to consider in a SIBO protocol is biofilm disruption because a lot of bacteria can form biofilm, which is an extracellular matrix where they share nutrients and even DNA, and the biofilm protects the bacteria inside it from our innate immune defenses.  It’s much more difficult for us to get rid of biofilm than it is bacteria in other states.  And there are a number of different nutrients that disrupt biofilm formation.  One is lactoferrin, apolactoferrin.  I think we’ve talked about that in the context of iron chelation in the past.  Life Extension Foundation has a lactoferrin supplement.  N-acetyl-cysteine or NAC is another biofilm disruptor, and then there are certain blends out there for biofilm, like Klaire Labs has one called InterFase Plus that I use and Kirkman, which I think is a Costco brand, has Biofilm Defense, and they’re a combination of things that disrupt biofilm.  Lumbrokinase and nattokinase, which are enzymes, also have an effect on biofilm.  So, those are some options for disrupting biofilm, and that’s something that’s often left out of antimicrobial treatments, but it can really make them a lot stronger, and it tends to be one of the things that causes the greatest die-off reaction, so that’s something to be aware of.

There are many different botanicals that are antimicrobial that can be used, including cat’s claw, which also has some other beneficial effects for intestinal health.  It’s a South American medicinal that’s used traditionally for a lot of different gut issues down there.  Wormwood, goldenseal, pau d’arco, olive leaf extract, garlic, barberry, and Oregon grape.  There are many more, but those are some of the more common and readily available ones.  They can be taken individually, or they can be taken in formulas in combination.  Some of those can be fairly strong, and then there are others, like oregano oil extract, that can be so strong that I generally recommend that people only take that under the supervision of a health care practitioner because oregano oil and some of the other wild spice oils are used by the food industry as antimicrobials, and that’s how potent they are.  I mean, they could use anything they want, and they choose to use those because they’re that strong.  I’ve seen actually quite a few people who have gotten on those, you know, they were either self-medicating or prescribed them by a practitioner, and unknowingly continued to take them for an extended period of time and really had an adverse effect on their gut flora.  So, that’s something to be careful about.

Probiotics are actually a mixed bag with SIBO because SIBO often involves an overgrowth of D-lactate-producing probiotic species, and that causes a buildup of D-lactate in the gut, and a lot of the symptoms associated with SIBO are caused by that.  So, you want to avoid in many cases taking any probiotics that have D-lactate-forming species like Lactobacillus acidophilus, which is, of course, one of the most common probiotics that people take.  There’s a D-lactate-free product sold by Custom Probiotics that’s helpful.

I’ve also found soil-based organisms to be helpful when SIBO is present, and the one that I like the most right now is called Prescript-Assist, and I just added it to my store if you go to ChrisKresser.com and you click on the store link in the upper right, I’m now selling it because I’ve actually had a lot of success with it myself and with my patients in my practice.  I recently learned about it.  A few months ago, I started doing some research about it.  There’s one study that was double-blind, placebo-controlled that lasted for quite a long time, especially for probiotics.  A lot of the studies are pretty short in duration.  And essentially the theory behind it is that we evolved in an environment where we were continually exposed to these soil-based organisms.  Our ancestors were not scrubbing their vegetables and fruits before they ate them.  They were taking them out of the ground and maybe wiping them off a little bit and eating them.  They weren’t buying them in the store after they had been scrubbed, and they weren’t scrubbing them themselves.  And the other thing is that the soil diversity and quality has changed a lot since the industrialization of agriculture, and so we’re just not exposed to the same number and types of soil-based organisms to the same extent that we probably were for most of our evolutionary history.  And as we’re going to discuss in a lot more detail in a later question, there’s a lot of evidence that these soil-based organisms have profound immunoregulatory effects.  In other words, we evolved with them over a long period of time, and our immune systems have a symbiotic relationship with them and function much better in their presence.  And so the soil-based organisms are a different approach than the lactic acid-forming types of probiotics, and I’ve found that they’re better tolerated in people with SIBO.  As a fairly unrelated side note, they tend to work better for constipation than a lot of other probiotics.  Oftentimes, probiotics can make constipation worse, so the soil-based organisms and Prescript-Assist, I think, is a really good choice for people with SIBO.

And then another probiotic that can be helpful with SIBO is Saccharomyces boulardii, which is a beneficial strain of yeast, and I’ve had some success with that as well.

So, there’s more to it, but that’s a really good place to start, all of those things that I just mentioned:  Lauricidin, the biofilm disruption, some of the botanicals, soil-based organisms, and Saccharomyces boulardii.

Steve Wright:  Is there anyone that should worry about taking soil-based organisms?  Is there any certain class of patients that you’ve seen that don’t seem to do well with them?

Chris Kresser:  Not yet.  There are certain people who are just very sensitive to probiotics of any type, and I suspect that that has more to do with immune dysregulation than anything else because of the way that I think probiotics are exerting their effect, which we’re going to talk about in a couple questions, but so far, the soil-based organisms are much better tolerated than the lactobacilli in most cases.

Does Cold Thermogenesis really work?

Steve Wright:  Interesting.  Cool stuff.  Well, let’s move on to question #2.  This one comes from Andrew.  He wants to know, Chris, what’s your take on cold thermogenesis?

Chris Kresser:  Right, so there was a big brouhaha about this a while back when Jack Kruse was recommending that people get in ice baths and submerge themselves and stay in there for a really long time.  I think that’s a really bad idea, but there is absolutely something to cold thermogenesis, and that’s been known for a long time.  For decades, it’s been something that’s used and talked about in fitness communities, and I’m sure a lot of you have a personal experience with it whether you know it or not.  For me, for example, I’m a surfer.  I grew up surfing, and I’ve been aware for a long time that spending some time in water that’s colder than what the ambient temperature is outside, I’ll feel really good after I do that, after I’ve spent an hour or two in the water.

There was a great follow-up post.  I can’t remember where I read it.  I might have been on Richard Nikoley’s site, but he linked to it and it was a really kind of evenhanded, well-referenced article about thermogenesis, and essentially the gist of it was that you don’t need to go to extreme lengths to get the benefits.  Even water temperature that’s is like 72 or 74 degrees, which most of us would say is pretty warm water, it’s lower enough than our body temperature that it’s going to have a thermogenic effect.  So, even going swimming in Hawaii, for example, could have that effect, or just turning the temperature down a little bit in your house can have that effect, or taking a walk and maybe wearing a little bit lighter clothing than you would normally wear.  So, I think there is something to it, and it is one of many tools that can be useful for weight regulation, but I don’t think you need to be really extreme about it, and I think there are definitely some downsides to being extreme about it.

Steve Wright:  Well, I know that instead of coffee I can definitely use a cold shower in the morning and I will be pretty much ready to go after that.

Chris Kresser:  Um-hum, yeah.

Steve Wright:  There’s something to the — what is it, the endorphin release?

Chris Kresser:  Is that the way it feels for you?

Steve Wright:  That’s what it feels like to me.

Chris Kresser:  Yeah, there are a lot of different physiological effects of it, and so it’s a little hard to answer the question.  It depends somewhat on why you’re asking.  I mean, a lot of times when people ask about it, they’re talking about weight regulation.

Steve Wright:  Right, right, and I was just commenting on cold showers.

Chris Kresser:  Haha, right.

Steve Wright:  And we’ll leave it at that, Chris.

Chris Kresser:  No comment.

What to do when the autoimmune paleo protocol doesn’t work

Steve Wright:  We’ll leave it at that.  We’re going to move on to question #3 from Bobbi:  “What to do next when after six months of autoimmune paleo eating doesn’t work for chronic fatigue and fibromyalgia?”

Chris Kresser:  Yeah, that’s a good question.  Diet is always a great starting place, of course, but as I’ve said many times, it’s not necessarily magic.  I mean, it can’t solve all problems.  With autoimmune disease, it’s just a really fascinating topic, and it’s a really active area of research, and believe it or not, there’s really no consensus on what causes autoimmune disease, and identifying the underlying cause of a problem is always the most important step in figuring out how to treat it.  My take on autoimmunity is that it’s multifactorial and there’s more than one cause, as is the case with most diseases.  But I think infection is probably one of the main causes of autoimmunity, and it could be an infection that comes and goes and it’s sufficient to dysregulate the immune system and throw it out of balance and create an autoimmune condition, or it could be an ongoing infection that has been misdiagnosed as an autoimmune disease.  There is plenty of evidence behind both of those theories and a lot of attention there.  We had Dr. Fasano on the show a while back, and he has written and spoken about a theory of autoimmune disease which holds that you have to have leaky gut to develop autoimmune disease, that it’s a precondition to developing autoimmune disease.  You need a genetic predisposition, but you also need intestinal permeability, and the inflammatory cytokines that get produced in that intestinal permeability and the immune attack against substances that make their way through the intestinal barrier is part of what initiates the whole process of autoimmune disease, so focusing on gut health is another key thing to do when you have autoimmune disease.

I think those two things would be where I would put my attention.  If you came to see me in the clinic, I would be looking for any evidence of infection, like a chronic viral infection — viral infections seem to be particularly associated with autoimmune disease — or bacterial infections, particularly intracellular bacterial infections like Chlamydia pneumoniae, and then I would be paying a lot of attention to gut, so are there any gut pathogens like parasites or fungal infections or opportunistic or pathogenic bacteria?  Is SIBO present, which we were just talking about?  Is the gut permeable?  In that case, I might even do a test for gut permeability.  So, doing all of those things, trying to figure out if there is some underlying cause that hasn’t been identified, that’s definitely step one.

But let’s say you that and nothing is there.  Your gut is perfectly fine, and you can’t find any evidence of infection.  With fibromyalgia in particular, I’ve read some pretty interesting research recently on the use of low-dose naltrexone in fibromyalgia, which we’ve talked about before, and the theory is really interesting.  Endorphins, which you just mentioned, Steve, in your cold shower story, they play a significant role in pain perception, and studies have shown that beta-endorphin levels are lower in patients with fibromyalgia, and then other studies have shown that met-enkephalin and dynorphin, which are two other endorphins, are elevated, which suggests that there’s some kind of abnormality in the endogenous opioid system.  And this could actually lead to a desensitization of opioid receptors, in other words, opioid resistance.  So just like in insulin resistance and even cortisol resistance, which we talked about before, there is plenty or hormone — or in this case, opioids — but the receptors are not being stimulated by them.  They’re not listening, so to speak, and so what you get then are symptoms of opioid deficiency and a decreased inhibition of substance P, which is an important neuropeptide or neurotransmitter in pain perception, so if you have increased substance P levels, you’ll have increased perception of pain.  And so, what low-dose naltrexone does is it temporarily blockades the opioid receptors, and that causes an increase in production of opioids, and it also causes an increase in the expression of opioid receptors.  So, the net effect of all of that is an increase in opiate activity, and that then, in theory, because of the changes that have been observed in opioid levels in fibromyalgia patients, that’s why low-dose naltrexone can be helpful in those situations.

So far, there haven’t been any big studies.  There have been some smaller pilot trials.  One trial, I remember, was 10 patients and there was a 30% reduction in symptoms.  And then there are a few case reports where the results were even more dramatic, like total remission after a month of taking low-dose naltrexone.  So, more research definitely needs to be done there, but LDN, which is the acronym we use for that, is a very safe medication because it’s such a low dose, it’s really well tolerated, it’s cheap, it’s off patent, and you know, my philosophy in terms of treatment is whatever works and causes the least harm.  Usually that’s not a drug, but there are times where a drug does fit that criteria or a drug is the best choice according to that guideline, and I don’t know that that’s the case for LDN in fibromyalgia yet, but it’s something that I would consider if all of these other things have been ruled out, like gut dysfunction, chronic infection.  Of course, addressing diet comes first, which the questioner has already done here.  Adrenal function is something else you’d want to pay a lot of attention to because low cortisol levels or dysregulated cortisol levels can cause muscle fatigue and a lot of symptoms that are reminiscent of fibromyalgia.  I’d want to make sure that micronutrient status was adequate and there weren’t any significant deficiencies, so there’s a lot of work to be done before I would even get to the point of considering low-dose naltrexone, but I think it is worth consideration if all that work has been done.

And then there are some other things to consider that are kind of out there too and are maybe a few years away in terms of their availability, but one would be fecal bacteriotherapy, because if there is a strong connection between the gut microbiome and immune system, which the research certainly suggests, then fecal bacteriotherapy could be a really powerful way of modulating the immune response, and I think there is almost certainly some kind of immune dysregulation going on in both chronic fatigue syndrome and fibromyalgia.  I think in the next 10 years we’re going to start seeing fecal bacteriotherapy becoming available for conditions other than C. difficile, which is what it’s primarily used for right now.  Already some doctors are more progressive in how they use it.  They’re starting to use it more for inflammatory bowel disease and even IBS, but I haven’t yet seen it used for autoimmune conditions other than inflammatory bowel disease, but I think it will be at some point.

And another promising treatment along those same lines is helminthic therapy, and I won’t say too much about this now because we’re going to talk about it in detail on one of the next questions, but this will sound totally bizarre to some of you who haven’t heard of this yet, but this is actually introducing worms, either whipworms or hookworms, into the gut in order to get an immune-regulating benefit from these organisms.  And if you’re scratching your head and wondering how that works, we’re going to talk about it in a lot more detail, but this therapy is available in Europe. There have been a lot of interesting studies done on it.  It has been used for ulcerative colitis and Crohn’s disease.  They actually give patients pig whipworm, Trichuris suis, and it’s remarkably effective in some cases.  I think the remission rate in one of the studies for Crohn’s disease was about 70%.  I may be wrong.  I’m just going from memory there, but pretty incredibly effective.  So I think that’s a therapy that we’re going to see a lot more of in the future, and in fact, it’s not preposterous to imagine that at some point people might go to the doctor and get inoculated with hookworm or a similar organism in the same way that people get vaccination now.

Steve Wright:  We’ll obviously hear more about that in a little bit, but I wanted to circle back to a few ideas that you hit on in that answer.  One would be that — just throwing in my two cents here — but something that they could do on the cheap and easy right now would be to definitely do a 24-hour cortisol panel and definitely check what’s going on with the hormones and the adrenal system because they might be able to get to some short-term relief there on the energy front.  And then the other thing is that actually I have a PR Newswire article here from January 8, 2013, where TNI BioTech has exclusively picked up the rights to LDN, so hopefully as we go forward, they don’t try to take over the market and jack prices up on us.

Chris Kresser:  Yeah.  Can you send that to me?  I don’t even understand how that’s possible.  I mean, it’s a low dose of a medication called naltrexone, so how could they — That sounds strange to me.  Definitely send that to me, Steve.  I’d love to see it.

Steve Wright:  Yeah, I’ll send that over, so just a couple newsworthy pieces there.

Chris Kresser:  Yeah.  Let’s see.  What’s next here?

Why is my antibody count going up on natural thyroid hormone?

Steve Wright:  All right, this next question comes from Alicia.  She asks:  “I have Hashimoto’s.  Why is my immune system now attacking itself even more despite being on natural thyroid and following a gluten-free, soy-free, dairy-free diet?  My antibodies were 272 at diagnosis, and it’s three months later, and I’m trying two NTH replacements and they went up to approximately 1300.”

Chris Kresser:  NTH being natural thyroid hormone, for anyone who got lost in the acronym soup.  So here’s one possibility:  There are different arms of the immune system.  There’s the Th1 side and the Th2 side, and the Th2 side is the one that’s responsible for antibody production.  Some autoimmune diseases can be Th1 dominant, and others are Th2 dominant.  If an autoimmune disease is Th1 dominant and the Th2 side of the immune system is suppressed, it’s conceivable that antibody production would be reduced, and if the immune system improves and things kind of balance out and the Th2 suppression decreases, then it’s possible that antibody production would actually increase in those circumstances, and that wouldn’t necessarily reflect a problem.  It would actually reflect an improvement that was happening in the immune system.

So, I guess I would ask what the other symptoms are.  If she’s feeling better and doing better in every other way and the only thing that’s happening is the antibodies are going up, I wouldn’t worry too much about that necessarily, and it’s possible that they’ll go back down as time progresses.  But if the whole picture is getting worse, you know, like the antibodies are going up and your symptoms are getting worse, then I would actually think that the autoimmune condition is getting worse, so it really depends on that distinction there.  And if the whole condition is worsening, then I would suspect there’s something else going on that’s aggravating things that’s not related to diet, and some of the same things we talked about in the last question would apply here.

Steve Wright:  So how long do you think she should wait before getting those retested?

Chris Kresser:  If she’s feeling better in general and the symptoms are getting more and more under control, maybe wait another three months or something.  If she’s getting worse, then I think the testing should be more focused on what’s causing further immune dysregulation in spite of a healthy diet.

Proper carb consumption for Hashimoto’s patients

Steve Wright:  Gotcha.  OK.  Well, this next one is sort of a follow-up question to this first question, and it comes from Jill.  She asks:  “Also on Hashimoto’s, can one ever get off thyroid meds?  There are differing opinions on carb consumption and Hashimoto’s (some like moderate, some like low, some like high).  What’s your opinion?”

Chris Kresser:  My opinion is that it’s completely dependent on the individual.  I mean, I think we’ve talked and I’ve written about the potential issues with a very low-carbohydrate diet and thyroid conditions because some insulin is required to convert T4 into T3, which is the active form of thyroid hormone.  If you’re on a really low-carbohydrate diet, then your insulin levels will be chronically low, which is not necessarily a bad thing in the context of blood sugar regulation and things like that, but insulin actually has plenty of beneficial effects.  It has kind of been labeled as a bad hormone in a similar way that cholesterol has been labeled as bad, but the truth is that insulin plays a lot of important roles in the body, and of course, all you have to do is look at type 1 diabetes to see what kind of problems can happen when you don’t have enough insulin.  There are a lot of studies that show that people who are fasting or people who are on very low-carbohydrate diets have lower levels of T3, and there’s some controversy about the significance of that, but in my practice I would say in general, people with thyroid issues do better on a moderate-carbohydrate diet than a low-carb diet.  However, there are always exceptions to these kinds of rules, and I do have some patients that do just fine on a low-carb diet and don’t seem to experience any decline in thyroid function.  And then I have patients on the other end of the spectrum who need actually quite a high-carbohydrate diet to feel like they function well with thyroid issues.

Steve Wright:  Chris, just because I hate low-carb and high-carb because they’re really totally contextual, what are you saying?  Is low-carb to you anything under 150 g roughly a day?  What are kind of your markers?

Chris Kresser:  I would call low-carb under 100 g, and I would call very low-carb under 50 g.  And when I speak about carbohydrates, I’m only talking about carbohydrates from starch and fruit.  I kind of agree with Paul Jaminet on that.  I just don’t think that carbohydrates from non-starchy vegetables really contribute much to carbohydrate load because you have to expend some glucose to digest them, and so the net intake of glucose is probably very low with something like broccoli.  So yeah, when I say very low-carb, it’s below 50 g, and when we’re talking about the effects of very low-carb diets on thyroid, that’s primarily what I’m talking about.  There are studies, though, that show that increasing carbs above 100 g or even 200 g continues to increase the production of T3 and reduce the production of reverse T3, which is the kind of dead-end, decoy form of T3 that blocks the thyroid receptors and doesn’t perform all of the beneficial functions of T3.

So I guess I could sum this up by saying the only way to really find out is to experiment.  You have to try different macronutrient ratios, try a period of time where you’re eating a higher-carbohydrate diet, try a period of time where you’re eating a lower-carbohydrate diet.  Be aware, though, that low carb might work for a period of time, but then after a while and after the effects become prolonged, then you can start to experience some symptoms, and that’s often what happens with people.  It’s pretty common for me to see someone who comes to my practice and they have some variation of this story.  They say:  I switched to paleo.  It was amazing.  I lost all this weight.  I had more energy than I’ve had in a long time, just felt so much better.  And then I say:  OK, so when you say “paleo,” tell me more about how much carbohydrate you’re eating.  Then they go into detail and it becomes clear that they’ve been doing a very low-carb paleo.  You know, the full extent of their carbohydrate intake is maybe a quarter cup of blueberries a day or something, so that I would consider to be a really very low-carb diet.  And then after a while, their energy starts to drop, they start to develop insomnia, their hair starts to fall out, they get cold hands and feet, they start to develop a number of symptoms, and then they call me.  That’s a very typical kind of presentation that I see a lot.  So, I do think it’s an issue, but I think that it’s very individual, and the only way to really find out is to experiment.

Steve Wright:  OK, Chris, let’s not gloss over the first question there.  Have you ever seen any of your patients or do you know of people who actually get off their thyroid meds while they have Hashimoto’s?

Chris Kresser:  It depends, again.  I know people are probably tired of hearing me say that, but that is really how it is.  Some people might not know what actually happens with Hashimoto’s, so let me explain that because it’s relevant to this question.  Hashimoto’s is an autoimmune disease where the body attacks the thyroid gland and destroys tissue progressively over time if it’s not treated.  And this is actually one of the problems with conventional treatment of hypothyroidism.  If someone goes in to the doctor and their TSH is high and their T4 or T3 is low, usually the doctor is just going to put them on thyroid hormone replacement medication without doing any testing to determine if they have Hashimoto’s.  And the fact that they get put on thyroid replacement medication isn’t necessarily the problem, because sometimes that is necessary, but the issue is that the underlying cause is not being addressed, which in this case is the immune system attacking the thyroid.  So, the person will likely need to take a higher and higher dose of thyroid hormone and even switch to different kinds of thyroid hormone as they progress because the immune attack is just going without being addressed and more and more thyroid tissue is being destroyed, and thyroid tissue is where thyroid hormone is produced.

This is also a common story, and I’m sure many of you listening to this might be able to relate, where first you start out with a certain dose of Synthroid, and then you have to take more Synthroid, and then Synthroid stops working altogether, and so you switch over to Armour and you feel a little bit better on Armour at first, but then you have to take more Armour, and then the dose of Armour that you have to take to maintain your thyroid function starts causing other side effects like insomnia and anxiety.  The problem there in many cases is that the immune dysfunction has never been even identified, much less addressed.

If you catch Hashimoto’s early before much tissue has been destroyed and you’re able to intervene and stop or mitigate the tissue destruction by regulating the immune system, then I do think it’s possible to not take thyroid hormone.  But if you catch Hashimoto’s after it’s been going for several years and after a significant amount of tissue has been destroyed, then the capacity to produce thyroid hormone in that situation might be permanently impaired.  And even if you, at that point, regulate the immune system and bring things back into balance, you just might have not enough tissue or capacity to produce the amount of thyroid hormone that you need to function well.  So, in those cases, I think thyroid hormone probably is necessary and that the goal should just to be to continue to regulate the immune system and minimize the dose that you need.  I often will have patients come to me, and they’ll be on a particular dose of thyroid medication, and when we start regulating their immune system, I’ll always warn them and say:  Look, you might start to feel hyperthyroid.  As we adjust your immune system, the dose that you’ve needed up until now will be too much, and you’ll have to talk to your doctor about decreasing the dose.  So, in those cases, just minimizing the dose of medication that’s required is the goal, not necessarily getting off of it.

Steve Wright:  OK, great.

Chris Kresser:  One more thing about that.  I mentioned before whatever works and causes the least harm.  In this case, when you’ve lost the capacity to produce thyroid hormone, thyroid hormone is so important, you know, every single cell in the body basically is affected by thyroid hormone, so it’s really, really crucial, and going without enough thyroid hormone, I would argue, is more problematic and dangerous than any potential side effects of thyroid hormone replacement over the long term.

What does Chris’s daughter eat on a daily basis?

Steve Wright:  That’s great news to know.  This next question comes from Davidrei:  “In the spirit of The Healthy Baby Code, what is your daughter’s day of eating like?”

Chris Kresser:  Well, it varies quite a bit, but she basically eats what we eat, what we have around.  One thing that really just makes me scratch my head is this concept of “baby food.”

Steve Wright:  How old is Sylvie?

Chris Kresser:  Sylvie is 19 months now, so yeah, obviously it does depend on what stage they’re at, but pretty much from the beginning she has eaten what we’ve eaten.  And early on, we had to maybe chew up some of the stuff before we fed it to her because she just wasn’t able to process it in the same way.  Let me think about today.  So, today we woke up, went on a walk together, which we often do, and came back, and she was hungry so I gave her some of the same ground beef that I had from my lunch that was left over.  It has some broth and some carrots and a little bit of tomato in it and some chopped-up liver in there.  And with that, she had some sauerkraut, which she absolutely loves, and some blueberries, so that was her breakfast.  Then when I ate, she was hungry again.  She’s eating a lot right now, so she had basically a little bit of everything that I had.  So, she had some eggs, which she loves, and she eats greens if there’s enough fat on them.

Steve Wright:  Haha.

Chris Kresser:  She had some of the greens, and she likes plantains now.  She didn’t at first.  In fact, she really didn’t like any starch or much carbohydrate other than berries, but now she’s enjoying some starches more.  Plantain is one that she likes.  And I’m not sure what else she’s had because I haven’t seen her since 10:30 or 11 and it’s like 2:30 right now.  But she has probably eaten again, and then she’ll have dinner probably around 5:30 this evening, and we’ll just give her either something that we’re cooking for ourselves tonight, or another common meal that we feed her is salmon.  She loves salmon.  We’ll either give her salmon that we’ve cooked recently and left over, or we give her Vital Choice canned salmon, which is really yummy and one of my favorites.  And maybe some broccoli with butter on it and some bone broth with some vegetables in it, or if she’s not having salmon, we might give her some bone broth with chicken or something like that.  So it’s mostly meat, fish, fruit, vegetables, some starch, although she’s just really not that crazy about it yet.  Like for example, she’ll eat some potatoes if they’re in broth.  And she likes taro chips when we make taro chips.  Sometimes she’ll eat a little bit of yuca, but not really crazy about starch right now.

Steve Wright:  All right.  It sounds like she eats pretty well.

Chris Kresser:  I think so, and she loves the food she eats.  It’s kind of crazy when her friends come over and they have all kinds of crackers and cookies and things like that.  And I imagine Sylvie will show interest in those things at some point, and I’m not too worried about it because she eats so well.  I just don’t think it’s going to be an issue for her.  But really she loves the food she eats and is satisfied, and she’s at the 80th to 90th percentile for height for her age, and I think the 75th percentile for weight.  She’s super healthy.  When you provide the right raw material, the body does the rest.

Steve Wright:  That’s pretty powerful right there.  Do we have time for one more?

Chris Kresser:  Yeah, is this the probiotics question?

Steve Wright:  It is.

Chris Kresser:  Yeah, this will be a longer answer, so we might go a little over than normal time, but we have to answer this because I referred to it about four times in an earlier question.

Steve Wright:  Foreshadowing.  Dang it.

Chris Kresser:  Let’s do it.

When to take probiotics

Steve Wright:  All right.  This comes in from Jessica.  She wants to know more on probiotics, Chris.  “When are they a good idea?  Do they facilitate healthy endemic microbiota populations or compete?  How effective are they for dysbiosis or recolonization after loss of microbes?”

Chris Kresser:  All right.  Well, this is a fascinating question.  In fact, to some extent, this will be the topic of my presentation at the Ancestral Health Symposium this year.  I’m going to answer this in a way that’s maybe not obviously or directly related to the initial question to start with, but you’ll see how it all ties together.  I think at this point that probiotic bacteria should really be mostly considered as old friends.  And I’ll say more about that.  We coevolved with certain organisms like worms, which I mentioned previously, cowshed microbes like saprophytes and soil-based organisms and microbes that you would tend to encounter amongst animals on the farm more recently, and then lactobacilli and fecal bacteria.  And they helped shape our immune system and the development of our immune system, and we have a symbiotic relationship with all of these microorganisms.

There’s a great quote from a book called An Epidemic of Absence, which I highly recommend if you’re interested in this subject, and the quote is that:  “It is now widely appreciated that humans did not evolve as a single species, but rather that humans and the microbiomes associated with us have co-evolved as a ‘super-organism,’ and that our evolution as a species and the evolution of our associated microbiomes have always been intertwined,” and that’s from the beginning of one of the chapters in the book.  It’s from a physician or researcher named William Parker from Duke University.  So, what this means is that our immune system probably evolved in part as an adaptation to the microorganisms that we were hosting for millions of years and more importantly that our immune system may not be able to function optimally without the presence of these microorganisms.  That’s the weirdest thing to get your head around because in the modern kind of sanitary conditions we’ve done everything we possibly can to eradicate these organisms from our systems, and now we’re learning that eradicating these organisms might have profound impacts that we didn’t really foresee.

The old friends hypothesis is the idea that the increase in inflammatory disorders and autoimmune disease that we’ve witnessed over the past several decades is caused by a lack of exposure to these microorganisms that we evolved with.  And when the normal background levels of immunoregulation that these organisms provide is taken away, our immune system goes haywire and starts to attack itself.  One analogy or way of understanding this would be if you’re standing and facing someone, let’s say, standing up, two people facing each other, and you put your hands up and you press against each other’s hands and you lean into each other, if you’re using the same amount of pressure, you’re going to both be kind of standing in a balanced way.  But what happens if the person you’re doing this with all of a sudden steps away?  You’re going to fall down on your face.  It’s kind of a crude analogy, but these microorganisms provide a background level of immunoregulation or something that our immune system is kind of continually in a state of dynamic tension with.  Our immune system has been tuned for millions of years to work in that dynamic tension against those organisms, and if you take them away, then that energy that the immune system uses to fight those organisms will be directed at self-tissue in some cases if there’s a genetic predisposition to that. So, this is actually one of the most exciting and popular and well-supported theories on what causes autoimmune disease at this point, and it explains a lot of the apparently contradictory observations that have been made epidemiologically with autoimmune disease.  For example, we’ve known for a long time that people in developing countries have far lower rates of autoimmune disease than people in developed countries.  Early on, one theory was that that was more related to latitude and vitamin D and since more developed countries are in northern latitudes with lower exposure to vitamin D, but then they found some groups of people — For example, there’s a group of, I think, Finnish people.  There’s a town or an area where on one side is a highly developed industrialized culture, modern culture with really sanitary conditions in Finland, and on the other side of the border, just a few miles away, is a group of people in Russia, and it’s far less developed and far less sanitary so that they have the same genes but the incidence of asthma and allergies is way, way less on the Russian side that’s poorly developed and has the less sanitary conditions, and the kids there are more likely to have hookworm or whipworm and other parasites, and they’re also more likely to be exposed to saprophytes and other mycobacteria.  So, that kind of threw out the latitude theory because there was a difference even at the same latitude in people with the same genetics.  But when you see a country developing better sanitation, then you see the rates of autoimmune disease start to go up.

In fact, even in the US up until about 100 or 150 years ago, most people still had hookworm and were carrying some of these other organisms, and incidentally, H. pylori is one that might have some of these beneficial immunoregulatory effects, and that’s one of the reasons that I’ve mentioned before that it’s not so black or white with H. pylori as we learn more about the old friends hypothesis and the beneficial impact that some of these microbes can have.  It becomes a little bit more of a gray area in terms of knowing what to do when these organisms are present.  And this theory also explains why asthma rates, I think, are lower in kids who live on farms, for example, and why kids who drink raw milk have lower rates of asthma and allergies than kids who drink pasteurized milk because some of the microorganisms in raw milk can have this immunoregulatory effect.

So, I think that there is probably more than one mechanism for how probiotics work, but I think that perhaps the main way that they work is through this kind of “old friends” effect, by stimulating immunoregulatory mechanisms and activating these ancient pathways that have been part of our physiology long before we were human, that probably originated with the emergence of mammals, which was a really long time ago.  The idea that taking probiotics is simply about replenishing gut flora and just kind of adding bacteria to the tank, so to speak, is probably overly simplistic.  There may be some truth to that, I think there is some truth to that, but it may be a smaller contribution than the immune-tuning effects that the bacteria have.

I hope that answered the question to some degree.  In terms of recolonization, I think prebiotics actually may be more effective because they’re selectively stimulating the growth of the flora that are present, and particularly growth of flora in the large intestine, which is where most of the flora is.  So, prebiotics and soluble fibers and fermentable fibers may be more effective at actually increasing the number of beneficial bacteria in the gut, whereas probiotics may have a more potent immunoregulatory effect.  And I’ve also seen some studies that suggest that probiotics, because of their immunoregulatory effect, they cause changes that predispose us to having a better balance of bacteria in the gut, so kind of indirectly they do lead to recolonization.

Steve Wright:  Do you consider probiotics just coming out of pills, or do you consider them coming from all fermented foods?

Chris Kresser:  Yeah, anything that has bacteria in it would have this effect.

Steve Wright:  OK.  So, then when she asked when would it be a good idea, would you be arguing that every day for everyone getting some of this in your life is probably generally a good rule at this point in time in the research?

Chris Kresser:  Yeah, I think that’s probably wise, and I think that we were exposed to that for most of our evolutionary history.  Refrigeration is ubiquitous now.  Most of us, at least, have the capacity to store foods in the refrigerator, but that’s a relatively recent development, and most of our ancestors didn’t have that opportunity, so they would probably ferment foods to store them, and they probably ate foods even sometimes that were spoiled.  So yeah, I think our exposure to these “old friends” is much less than it used to be, and I think increasing our exposure to them is probably a really good thing we can do for health.  And just like I was talking about with probiotics, the reason that fermented foods are beneficial may be more related to this than just the kind of mechanical replacement of bacteria.

Steve Wright:  It’s fascinating.  I’m going to have to check out that book that you mentioned.  Great question.  I’m looking forward to seeing that presentation at PaleoFX.

Chris Kresser:  I’m looking forward to doing it.  It’ll be a lot of fun to put together.

Steve Wright:  All right.  Well, that wraps up this episode, Chris.

Chris Kresser:  Yeah, it was a lot of fun.  I enjoyed it.

Steve Wright:  We got a lot of questions from the listeners.  Thanks again for sending those in.  Please keep sending us your questions at ChrisKresser.com using the podcast submission link, and if you enjoyed the show, please head over to iTunes and you can leave us a review there.  I think that’s all for now.  Right, Chris?

Chris Kresser:  I think that’s it.  Just a heads-up, I may be away and unable to record the next show.  I’m not sure yet.  I’m still working that out.  So, if we miss a week, that’s what’s happening, and we’ll be back with the regularly scheduled programming the next week.

Steve Wright:  All right, thanks.  Thanks everyone for listening.

Note: I earn a small commission if you use the links in this article to purchase the products I mentioned. I only recommend products I would use myself or that I use with patients in my practice. Your purchase helps support this site and my ongoing research.

Here is The Roundup, Edition 15, bringing you the best from around the web from the past two weeks!

Blast from the Past

Dr. Arya Sharma, founder and Scientific Director of the Canadian Obesity Network, recently wrote a post on the evidence in favor of universal sodium reduction, and described it as “less than conclusive”. Dr. Sharma spent the first 10 years of his research career studying the effects of sodium on blood pressure, and he has found that the evidence is mixed at best, and that there is evidence for potential harm as well. As Dr. Sharma writes, “in some cases we even reported adverse consequences of sodium restriction resulting both in significant elevations in plasma lipids and insulin resistance (perhaps not surprising given that reducing sodium intake markedly stimulates both the sympathetic and renin-angiotensin systems – the very systems we seek to block to reduce cardiovascular risk).”

This shouldn’t be surprising to anyone who has read my series on salt, which touches on those same concerns that Dr. Sharma has brought to light. In particular, my article on the dangers of salt restriction notes that a low-salt diet may cause serious health consequences and higher overall mortality, especially in the presence of certain chronic health conditions and lifestyle factors, such as cardiovascular disease and diabetes. Ironically, it is these two populations that are frequently told to reduce sodium intake to less than 2,300 milligrams, or about one teaspoon per day.

While I don’t promote the consumption of high-sodium packaged and processed foods, I’ve said many times before that most healthy people can happily add 1.5 to 3.5 teaspoons of unrefined salt to their whole foods diet. There are a few exceptions to this, such as people with kidney disease, but in general I believe that salt restriction for the general population is not only unnecessary, but potentially dangerous. It would appear that Dr. Sharma might agree with me.

Research Report

• Could this research suggest another reason to avoid grains? It’s a mechanistic study, but it’s interesting.
• A fascinating study shows higher prevalence of SIBO in Parkinson’s patients, and eradication improves symptoms.
• Research suggests that classroom naps support learning in preschool children by enhancing memory.
• A study demonstrates that the heritability of sleep duration is between 31%-55%, which suggests a substantial amount of sleep need is genetically determined.
• Another study shows that shorter sleep duration increases expression of genetic risks for high body weight.

Worth A Look

• Louis C.K. opines on smartphones for kids: I couldn’t agree more.
• The New York Times explains how most women aren’t getting support for breastfeeding by their insurance companies.
• Diane Sanfilippo shares her view on flax and chia seeds, juice cleanses, and green drinks.
• Ancestralize Me has compiled a list of the ten most nutrient-dense foods you can eat, and all of her suggestions are budget-friendly.

For the Foodies

• Edible Harmony: Blueberry Banana Frittata
• The Paleo Mama: No Bean Paleo Pumpkin Hummus
• Rubies and Radishes: Slow Cooker Beef & Butternut Squash Stew
• Stupid Easy Paleo: Kickin’ BBQ Shredded Chicken
• Civilized Caveman: Beef Noodle Soup with Shitake Mushrooms and Baby Bok Choy
• The Domestic Man: Karniyarik (Turkish Stuffed Eggplant)
• PaleOMG: Pumpkin Chocolate Chip Muffins

Another Q&A episode, folks! Remember to tune in next week for our interview with Dr. Alessio Fasano, a pioneer in the fields of gluten intolerance, leaky gut and autoimmunity.

In this episode, we cover:

12:39 How to tell if digestive problems are caused by leaky gut, SIBO, or food intolerance
26:25 What to do about Epstein-Barr Virus
32:43 Does a furry tongue mean anything?
35:43 How baby is telling you it’s time for different foods
37:50 The specific Graves Disease Protocol to keep it in check… for good
48:52 Everything you need to know about Anemia (and more)

Links We Discuss:

• Betaine HCL Protocol
• Real Food Summit

Full Text Transcript:

Steve Wright:  Hi, and welcome to another episode of the Revolution Health Radio Show.  I’m Steve Wright from SCDlifestyle.com, and with me is Chris Kresser, health detective and creator of ChrisKresser.com.  Chris, how are you doing today, man?

Chris Kresser:  Oh, I’m pretty good, Steve.  How are you?

Steve Wright:  I’m good, man.  I’m pumped up.  We’ve got a lot of questions to cover today.

Chris Kresser:  Yeah.  A Q&A episode.  We’re doing it again.

Steve Wright:  Going rapid fire this time.

Chris Kresser:  So, before we get into that, I want to make a couple announcements.  One is just a reminder that the next show we’re gonna be interviewing Dr. Alessio Fasano, which I’m really excited about.  He’s a pioneer in the field of gluten intolerance and celiac disease research and also in establishing the connection between intestinal permeability, or leaky gut, and autoimmune disease.  He’s a real research hero of mine, and we’re honored that he’s gonna be joining us on the show, so make sure to tune into that one.  Don’t miss it.  It’s gonna be a great episode.

And then, as I’m sure all you know, the Ancestral Health Symposium is coming up, and I’ve been busy preparing my talk for that.  The topic is on iron overload.  That’s something I’ve talked about on the show quite a bit, and specifically I’m gonna be discussing how even mild iron overload, you know, nonhereditary hemochromatosis iron overload, can contribute to a number of different diseases and even increase the risk of death, and of course, how to test for it and what to do about it.  So if you’re at AHS, I look forward to seeing you at my talk and meeting you.  And I think, if last year was any indication, the talks will be available online after the event.  So if you’re not able to make it there in person, I think you’ll still be able to watch the talk.  I’m not sure about that, but that’s at least what happened last year in most cases.

And then the last thing I want to do is talk a little bit about something that I’m also really excited about, which is a new program that I’ve been working on over the past few months.  Actually really I’ve been working on it over the past several years because it’s a topic that I’ve, of course, been interested in for a long time, as you’ll know if you’ve been following my blog, and it’s really how my blog started.  The very first articles I ever wrote for my blog back when it was The Healthy Skeptic were about the relationship between cholesterol and heart disease.  And this program is gonna be called The High Cholesterol Action Plan, and the reason I’m doing it is that there’s still a lot of confusion out there about the relationship between cholesterol and heart disease, and that’s understandable because it’s an extremely complex topic.  In fact, the more I learn about it, the more intricacies I discover and subtle distinctions that become apparent and the more that I realize that the two extremes that we typically see out there, like, the one extreme, as Chris Masterjohn said, the cholesterol warriors, the people who say that high cholesterol is the cause of heart disease and that, you know, eating saturated fat and cholesterol in the diet raise cholesterol levels and so we should eat a low-fat diet and take statin drugs and do everything possible to lower our cholesterol to reduce our risk of heart disease.  We have that.  That’s one extreme, the cholesterol warriors.  And then on the other side of the extreme you’ve got the cholesterol skeptics who say cholesterol has nothing to do with heart disease, we shouldn’t worry about our cholesterol levels at all, and if you get your cholesterol tested and it’s 350, you know, go out and celebrate with a low-carb, high-fat meal!  So those are two extremes, and it turns out that I think the truth is somewhere in the middle.

And over even the last year, I’ve learned a tremendous amount about this issue, and because I’ve just been so busy with my practice and the show and my writing and everything else I’m doing, I haven’t unfortunately had the chance to update a lot of the articles on my site, and I haven’t had the chance to write new articles sharing all of my new research and what that means to you or anybody that you know that has been diagnosed with “high cholesterol” and usually then prescribed a statin.  And I have so many patients and so many readers and listeners and people in my life who write me and say:  Hey, I got diagnosed with high cholesterol, and my doctor wants me to take a statin.  I’m really confused about this.  Should I get my particle size tested?  Should I get CRP tested?  What other tests should I get to really figure out what my risk is?  Or maybe my dad or my mom was diagnosed with high cholesterol, and they’re already on a statin, and I’m concerned about them.  And you know, it’s a big issue, and it affects a lot of people, and there’s probably not a single one of us listening to this show right now that doesn’t know somebody that’s on a statin or that’s been prescribed a statin.  So I wanted to just put all of the information in one place, like, to just talk about the most current research, all of the cutting-edge staff about how to really truly determine your heart disease risk, which tests are best, which tests are bunk and a waste of time and money.  And then once you establish what your risk is, how you decide what to do about it.  What’s the best dietary approach?  You know, is a low-carb, paleo type of diet best for everybody, or is there a situation where that’s not a good choice?  And statins, should they always be avoided, or are there some people that may actually be good candidates for statins?  And for those who statins aren’t a good choice for, what are the natural alternatives to statins?

So it’s a huge topic, and I started out thinking that I’d be able to do it in a pretty succinct way, and it still will be very practical and focused, but it’s gonna cover, you know, it’s gonna be like a soup-to-nuts thing, from beginning to end, and it’ll have a really practical framework, like a decision tree for going through the process step by step of determining what your risk is and then how to respond appropriately.  It’s probably about six weeks away, and I’ve been working a little bit too much on it.  I get into these modes where I just completely dork out and get really lost in what I’m doing, and yeah, that’s how I’ve been spending my time lately, but I’m excited about it and I can’t wait to get it out there because I think it’s gonna help a lot of people.

Steve Wright:  Sounds like an awesome project.  I am excited to get my hands on it.  So you’re talking the end of August-ish right now tentatively?

Chris Kresser:  That’s what I’m hoping for.  This thing, you know, sleep is getting in the way.

Steve Wright:  I hate sleep.  God.

Chris Kresser:  The need to sleep at least a little bit and take care of my body and stuff, but yeah, I’m shooting for the end of August, and it’s gonna be a combination of video screencasts, me going through presentation slides, audio versions of that, PDF transcripts, and then an action guide, as I described, takes you through step by step, and you know, specific recommendations for supplements and diet and exercise and other ways of treating and preventing heart disease naturally.  So yeah, we’ll talk about it again when the time comes and go into a little bit more detail on it, but it’s on my mind and I’m excited about it, so I just wanted to share a little bit.

Steve Wright:  Well, it sounds great.  And if anybody caught my Real Food Summit talk, you know I love step-by-step, so I’m excited right now, to say the least.

So you had an awesome Real Food Summit talk, Chris, I think probably one of the most popular, seeing how you got the encore day and everything.

Chris Kresser:  Thanks, Steve.  Yeah, I mean, it was a good experience.  I, as many of you know, did the Paleo Summit with Sean a while back, and this was similar.  It was an online conference with a number of experts and authorities in the real food genre, so not paleo, per se, but nutrient-dense approaches to diet, which would include, like, the diet that the Weston A. Price Foundation advocates.  And it was a great conference.  I think it was even better attended than the Paleo Summit.  And my talk was on the importance of eating fish and seafood in the context of a real food diet and why it’s important to do that, how much and which types and fish are best to eat.  You know, I talk a little bit about some of the concerns surrounding fish consumption like mercury and PCBs and dioxins and why for much people and much types of fish that’s not really a concern.  So yeah, if you missed it, you can buy the whole set of talks.  I think there are about 27 presentations.  Is that right, Steve?

Steve Wright:  Yeah, I think there were 27 that were live, and then there were six or seven bonus.

Chris Kresser:  Oh, right.  Yeah, so there are like 33 presentations, all like an hour or an hour and a half, and then there are audio recordings, PDF transcripts.  I think you get a free subscription to Organic Gardening.  There are some other bonuses thrown in there.  You can go to my website and look at the homepage.  I think one or two pages back there’s an article there that I wrote about the Summit, and you can check it out and then click through there if you’re interested in getting the talks.

Steve Wright:  Yeah, I thought it was a great summit.  There was a ton of top-notch presenters who shared some really awesome concepts.  It took me, like, three days to download it.  There was so much info, so you definitely get your money’s worth.

Chris Kresser:  Actually, I guess, we could put a link to it in the show notes for this show, so rather than going and digging around my website, you can just check out the show notes and we’ll put a link in there where you can get the recordings.

Steve Wright:  OK, great.  Well, this was a heck of an intro, Chris.  Take a water break, and I’m gonna tell everyone about Beyond Paleo.  Now, if you’re listening to the show, we’re assuming that you’re into your health, you’re into optimizing your health, and you’re probably gonna want to check out what over 10,000 other people have already signed up for, and that’s what I talked about before called Beyond Paleo.  Beyond Paleo is Chris’ brainchild.  It’s 13 emails.  It covers everything from food to being happy, and all of these things together are gonna help you burn fat, boost energy, and prevent and reverse disease without drugs.  So you’re gonna want to get your hands on it if you haven’t yet.  Go over to ChrisKresser.com, and look for the big red box.

Chris, are you hydrated?

Chris Kresser:  I’m ready to go.

How to tell if digestive problems are caused by leaky gut, SIBO, or food intolerance

Steve Wright:  OK, let’s do this.  Our first question comes from Megan:  “Is there an easy way to tell if your GI problems are due to leaky gut versus SIBO versus general food intolerances, for example, FODMAPs?  Or is it more likely that these issues all overlap in someone with an unhealthy gut?”

Chris Kresser:  Yeah, it’s a great question.  I guess it depends on what you mean by ‘easy’ for the first part of your question, because there are tests that can be done for SIBO.  There are a couple tests that I’ll mention in a second.  And then there are also stool tests that can be done to identify gut pathogens like opportunistic or pathogenic bacteria and fungal infections and parasites.  And there are tests that can be done for fructose intolerance.  And then there are also tests for food intolerance and tests for leaky gut, though I think those are less useful, and I’ll come back to that in a second.  So let’s talk first about the tests for SIBO.  There are two main ways of testing for small intestine bacterial overgrowth.  And for those of you who aren’t aware of this is, normally the small intestine should be relatively sterile, meaning there shouldn’t be a lot of bacteria in it.  Most of the bacteria that resides in our gut is in the colon and, to a lesser extent, the very end of the terminal ileum, which is the end of the small intestine.  But in some cases, the bacteria can translocate from the colon into the small intestine where it doesn’t belong, and then that causes gas and bloating and pain and changes in stool frequency and consistency.

So there are two ways of testing for small intestine bacterial overgrowth.  One, and the most common one is a breath test, where you drink a solution that contains some simple sugars, which can be fermented by small intestine bacteria.  And then you blow into a little tube that’s attached to a balloon or a bag, and then you send that bag to the lab, and the lab tests it for certain gases that are produced by certain kinds of bacteria.  And if the levels of the gases are high, then that indicates you have an overgrowth of bacteria in the small intestine.  So that’s one way of testing for it.  Another way of testing for it is a urine organic acids test, and these are offered by labs like Metametrix and Genova Diagnostics, who just bought Metametrix actually last week, so they’re gonna be merging together.  And organic acids are byproducts of bacterial metabolism.  So certain types of organic acids, if they’re elevated in the urine, can indicate an overgrowth of bacteria in the gut and also an overgrowth of fungi.  So D-arabinitol is an organic acid that’s produced in fungal metabolism, and so if you have an overgrowth of D-arabinitol in the urine, then that can indicate a yeast overgrowth.

So those are the two main tests.  I tend to use the organic acids test more, and that’s partly because it has a number of markers that I find to be useful, and so I just can kill several birds with one stone, and I tend to order that more, but the breath test is also good.  One lab that’s pretty well known for the breath test is Metabolic Solutions, and it’s pretty affordable.  It’s like a hundred bucks, maybe 95 bucks or something.  At least, that’s what it costs me to order it.  I don’t know if they have different prices for clinicians and patients.  I think that same lab, Metabolic Solutions, they also offer a fructose intolerance test, which is very similar to the SIBO test, and that is one that you could do to identify any potential problem with FODMAPs.  If you test positive for fructose intolerance, then you’re almost certainly gonna benefit from doing the FODMAP approach since the FODMAP approach is based on reducing foods that have excess fructose or fructans or polyols, sugar alcohols.  So if you have access to that kind of testing and you have the resources to do it, they’re all pretty easy to do, and they can help you identify what the underlying cause of your problem is, and then maybe that can help determine what kind of action to take, both which diet would be most effective for you and then what other interventions might be effective.  For example, if you have SIBO, you’re probably gonna want to do some antimicrobial protocol in order to treat that.

As far as food intolerance testing goes, we’ve either talked about it on the show or I’ve written about it or both, but I don’t consider food intolerance testing to be very useful for a couple different reasons.  Number one, and I’m pretty sure I’ve mentioned this on the show, there have been some kind of blinded trials done anecdotally by clinicians, where they’ve drawn their own blood and put it two vials, you know, on the same day, same blood draw, and labeled the two vials with different names and sent them into the same lab and come back with completely different results for the two different vials of blood that came from the same person on the same day.  So that’s a little suspect.  And then number two, even if the test was completely reliable, the question is still what’s causing those food intolerances?  I mean, food intolerance is a symptom; it’s not a disease.  There’s an underlying disease or pathology that’s causing those food intolerances, and that would usually be SIBO or intestinal permeability or a parasite or a fungal infection or some other gut problem, maybe a gut-brain axis issue or maybe gluten exposure, undiagnosed gluten intolerance.  Those are mechanisms.  Those are problems that lead to symptoms.  So if you just remove the foods that the food intolerance testing shows that you’re sensitive to, certainly that will help with the symptoms, and there’s nothing wrong with that, but assuming you want to be able to eat some of those foods again, addressing the underlying problem is a much better approach.  So I don’t put a lot of stock into food intolerance testing for those reasons.

And then intestinal permeability, well, there are a couple of different ways to test for leaky gut.  And I actually want to talk to Dr. Fasano about this a little bit.  I’ll be curious to see what he has to say about it.  But there’s the lactulose/mannitol test, and that’s the one that’s best known.  And again, you drink a solution of lactulose and mannitol sugars.  They’re rather large molecules, and they shouldn’t pass through the gut when the gut barrier is intact.  And if they are detected in the blood, that means they’ve passed through the gut, and that means, then, that you have a leaky gut.  So that’s one way of testing.  A newer way of testing was developed by Dr. Aristo Vojdani.  I hope I’m pronouncing his name right.  But he’s the clinical advisor at Cyrex Labs, and they developed a test that screens for antibodies that are involved in the immune response that destroys the gut barrier.  So I think there are actomyosin antibodies, zonulin antibodies, and one more, which I can’t remember off the top of my head.  And that’s a completely different way of testing for leaky gut, but if we take Dr. Vojdani’s research at face value, it’s apparently much more effective and accurate than testing the lactulose/mannitol route, which some doubt has been cast upon in recent research.

The reason I don’t find myself testing for leaky gut very often is my benchmark for determining whether to run a test is whether it will change the outcome of the treatment, and usually with leaky gut it doesn’t, because if I get the test results back — Let’s say someone comes to me and they have a gut problem.  If we were to run a test for leaky gut and it came back and it said they didn’t have a leaky gut, well, I still have a person with a gut problem.  You know, I still need to figure out what’s causing their gut problem and what to do about it.  And if someone comes back with a leaky gut, I still need to figure out what’s causing that leaky gut.  So again, I look at leaky gut kind of more like food intolerance in a sense because even though it is an underlying mechanism to some extent, meaning it can contribute to and cause a lot of other problems, there’s still usually something causing leaky gut itself.  It doesn’t just come out of nowhere, you know, and that could be, again, like, gluten intolerance or a pathogen, some kind of inflammatory process, small intestine bacterial overgrowth, stress, gut-brain axis problem.  So there’s usually still more work to be done to determine what the underlying cause is, and I just think often it pays to just do that.  But the one area where I think the testing can be helpful is gauging the success of the treatment.  So if we do a bunch of treatment and the person is improving, then we might do the leaky gut test and see, OK, let’s see what’s happening to your gut barrier.  Is it still permeable or has it improved based on the treatment we’re doing?  And if it hasn’t, then we can adjust the treatment and make different choices.

So, yeah, I mean, there’s obviously a lot to talk about here too, and maybe as another announcement, for some time, you know, I’ve always known that I would write a book and probably several books, but I’ve really been struggling a lot over the past several months deciding what book I want to write and, you know, what my first book would be.  And I finally have decided, and it’s gonna be a book on gut health.  And specifically it’s gonna be a book that examines what the real causes of digestive problems are, because most of the diagnoses that we have for digestive problems just name the symptoms that people experience.  So think about it:  Irritable bowel syndrome, IBS.  Somebody goes in to the doctor.  They say:  Oh, my stomach hurts.  I have pain.  I have gas and bloating, and I have diarrhea or constipation.  And the doctor goes:  OK, well, you’ve got IBS.  And you know, it’s basically like the patient is like:  Well, isn’t that what I just told you?  My gut is irritable?  And you know, the same is true for heartburn and a lot of other “gut diseases.”  They don’t actually describe what’s wrong; they just describe the symptoms that people are experiencing.  So my book is gonna focus on the underlying causes of gut problems like SIBO, like parasites and other gut pathogens, like gut-brain axis problems.  And then, of course, talk about how to address those problems with natural remedies.  So we’re gonna be talking about this subject in a lot more detail in the next year because I’m gonna be up to my ears in it as I start writing the book, which I haven’t started.  I’ve outlined it.  I’m gonna start writing probably, I don’t know, in the fall once I get through these other projects I’m working on.

Steve Wright:  You’re signing yourself up for a lot of projects, man.

Chris Kresser:  I know!

Steve Wright:  We’re expecting this from you.

Chris Kresser:  Yeah.  You guys gotta remind me to take my own medicine and remember to, you know, take care of myself and lay down and take a nap every now and then.

Steve Wright:  Yeah.  You need to be sleeping.  I know you like to laugh when you say IBS, but you know, you need to be laughing outside of the podcast too.  We can’t forget the happiness piece.

Chris Kresser:  Not at all.  It’s a crucial part of my well-being.  That’s for sure.

Steve Wright:  Well, I’ll just throw a little plug in there for our Real Food Summit talk because Megan’s question was really the topic of Jordan’s and my presentation:  what to do when you go paleo or you go Weston A. Price and your gut problems don’t necessarily go away.  And so we tried to give some really practical tips that we’ve learned over the years.  So that might be a place to go, Megan, for more information until the thesis that is in Chris’ head is in our hands.

Chris Kresser:  All right, let’s do the next one.

What to do about Epstein-Barr Virus

Steve Wright:  OK.  This question comes from Teresa:  “Hi, Chris.  Thanks for the high-level discourse actually based on science.  Any suggestions for chronic acute Epstein-Barr?  Besides the obvious tenets of good health, sleep, good nutrition, smart exercise, good vitamin D levels, omegas, and the normal antiinflammatory steps, I tried a run of cat’s claw with no obvious results.  There’s nothing in the literature of help.  Can you help me?”

Chris Kresser:  Yeah.  So by chronic acute Epstein-Barr, I’m assuming she means a latent Epstein-Barr infection that was reactivated.  For those of you that don’t know, Epstein-Barr virus is extremely common in the sense that over 90% of North Americans have been exposed to it and then have IgG antibodies, which means we were exposed to it.  And once we are exposed to a virus like that, it usually doesn’t leave our bodies completely.  It can stay latent in our cells, and it can get reactivated when our immune defenses are down, often when we’re under great stress or possibly when we get another infection of a different type or if we’re eating an inflammatory diet or, you know, anything that can throw our immune defenses off.  To determine if you have this, by the way, it’s very important not only to get IgG antibodies tested since most people will turn out being positive for IgG Epstein-Barr, but to get IgM antibodies, which would be indicative of an active infection or chronic acute, which I assume is what she means.

So yeah, I do have some suggestions for working with this.  I have quite a few patients that are dealing with reactivated infections like Epstein-Barr or cytomegalovirus or herpes, HPV, or HHV, human herpesvirus.  The key thing in a general sense to realize when working with viruses, unlike bacterial infections or yeast infections, is that the number one thing you want to do is strengthen your own immune system’s defenses because while there are antiviral treatments, both drug and nondrug antiviral treatments, they’re generally not as effective as antibiotic treatments or antifungal treatments, and therefore the goal is to really boost our own innate immune defenses so that our immune system can do what it does best, which is eradicate these infections.  So the basics there, I think, she’s already doing, but would be antiinflammatory diet, high doses of vitamin C, so we’re talking about gram-level doses, several grams a day to bowel tolerance, maybe like 1 g three to four times a day.  You could even go that high.  Selenium and iodine are both important for the immune system.  Glutathione precursors like N-acetyl cysteine, lipoic acid, and then things that help with intracellular glutathione recycling like milk thistle.  Those are all really solid basic choices for supporting immune function.

But in terms of a natural antiviral that you might try, I like monolaurin, and monolaurin is an extract of lauric acid, which is a fatty acid that’s found in coconut products and in breast milk.  And when lauric acid is attached to glycerin, it forms a monoglyceride known as monolaurin.  And monolaurin works directly on the envelope coat of the virus by disrupting the conformation of the lipid bilayer, which in turn prevents its attachment or absorption to host cells.  So there actually is some research on monolaurin and its antiviral activity.  It’s also antifungal, and it has efficacy against gram-negative bacteria too.  The cool thing about monolaurin is that it’s pretty well tolerated and safe.  It doesn’t seem to have a negative impact on the beneficial gut flora.  And when compared with some other options in terms of natural antimicrobials, I’ve found it to be pretty easy to work with and not cause a lot of side effects.  So the sort of typical starting dose would be 1200 mg two times a day for an adult.  So I would definitely try that.

In my practice, I use some custom botanical formulas to treat viral infections, and I’ll customize them based on the specific presentation of the patient, based on the type of virus that they have, and you know, their own constitution and symptom profile.  But some of the medicinals that I will use are familiar, I’m sure, to a lot of you.  Echinacea is one; laurea; usnea, or old man’s beard — I love that name; dandelion; pau d’arco; astragalus; lemon balm.  It’s generally better rather than, you know, just going down to the store and getting a bunch of these and brewing them up, to work with an experienced herbalist if you can.  But some of these herbs, particularly echinacea and dandelion and lemon balm, are pretty safe and can be used at home.  You can just make teas or even buy teas with echinacea and some of these herbs in them.  So give that a shot, and let us know how it works out.

Does a furry tongue mean anything?

Steve Wright:  OK.  Let’s roll on.  This next one is from Anonymous:  “Hi.  I started the paleo/Perfect Health Diet at the start of this year.  All is generally going great.  I’ve lost weight and feel a lot better.  The only problem I’m having is a furry tongue.  It gives me horrible breath in the morning.  Throughout the day after eating sometimes it goes green.  I’ve been to the doctor, who gave me some antifungal lozenges to use for candida, but two of these lots have not worked yet.  The doctor said it was unusual to get unless you have a low immune system.  I haven’t been sick since going paleo, nor have I taken antibiotics.  Do you have any ideas what’s going on with my tongue?”

Chris Kresser:  My guess would be low stomach acid.  And I see this a lot on people who start a paleo diet coming from a diet with less animal protein.  We’ve talked about tons of times on the show.  Stomach acid, as you all know by now, is crucial to breaking down protein, particularly animal protein, and if you don’t have enough stomach acid, the protein can putrefy in the stomach.  And I haven’t seen any research on this from a conventional medical perspective, but certainly anyone who is familiar with Chinese medicine will know that they put a lot of stock into the appearance of the tongue, and a thick coating on the tongue is definitely an indicator of digestive disharmony.  And I don’t really know how to explain that with precision from a Western medical paradigm perspective, but I certainly have seen it to be, you know — In nearly everyone who has a digestive issue, there tends to be a coat on the tongue.  So that’s my guess:  low stomach acid.  It could also be small bowel bacterial overgrowth, and we talked earlier about how to get tested for that.  The easiest thing to do to test out the stomach acid hypothesis would be to just take some hydrochloric acid, that betaine HCl protocol.  We’ll put a link in the show notes to the post on my website where I discuss the protocol in detail and go through it step by step.  And if that doesn’t work, I would probably get tested for SIBO.  Or if you do the organic acids test, that will test for both SIBO and a fungal overgrowth, which would probably be an even better idea.

Steve Wright:  OK, well, that should get them started, and I’ll just add that back before I started my health reversal, I did have a white-coated tongue, and I did and still am getting over low stomach acid, so just my two cents that might help you do what Chris said.

How baby is telling you it’s time for different foods

OK, let’s move on to the next question from Thomas:  “Hi.  I purchased the Healthy Baby Code after the birth of my son.  He is now 6-1/2 months old.  We are trying to feed him egg yolks as his first food as you recommend, but he doesn’t seem to like them.  We’ve mixed it with breast milk, but it doesn’t seem to help.  Should we continue trying to feed him this or move on to other foods?”

Chris Kresser:  Definitely move on to other foods.  The guidelines for introducing first foods are general and will apply to many babies, but as any parent who has had more than one child will tell you, just like adults, babies have preferences and likes and dislikes.  So if your baby doesn’t like eggs, then yeah, just skip it and move on to the next thing and try something else and then maybe come back to it later.  It seems that some percentage of babies also can’t really tolerate egg yolks very well at that age, and I’ve had some reports of vomiting and just some bad digestive reactions.  I don’t think they’re mediated by allergy.   I just think that for whatever reason it’s maybe a little bit too soon to introduce that particular food.  So use the guidelines as a rough blueprint, so to speak, but feel free to improvise a little bit based on your child’s preferences and what’s available to you.  Some of the things that are — I mean, you wouldn’t want to skip too far ahead because the guidelines are laid out with particular stages of development of the digestive tract in mind, but certainly just going forward a little bit and expanding the options that way is completely fine and would definitely be recommended in this situation.

Steve Wright:  OK, well, I have nothing to add there, so glad you covered that.

The specific Graves Disease Protocol to keep it in check… for good

Chris Kresser:  Steve, did we miss the Graves’ disease question or did I not put that in there?

Steve Wright:  I don’t see a Graves’ disease…

Chris Kresser:  Scroll down a little bit.  It’s in there somewhere.  If you can’t see it, we’ll come back to it in a different episode.

Steve Wright:  I copied down to the intermittent fasting one.  I don’t see it in there.

Chris Kresser:  Well, let me just kind of paraphrase it.  The question, I think, was essentially we’ve talked a lot about hypothyroidism and Hashimoto’s but haven’t talked much about Graves’ disease and how would I recommend approaching Graves’ disease.  Graves’ disease is certainly more rare than Hashimoto’s and hypothyroidism.  That’s one of the reasons I haven’t talked about it as much, but I do know quite a bit about it because my wife was diagnosed with Graves’ disease, and this was back when we were still trying to get pregnant with Sylvie and we were having some difficulty, and I was doing some investigation figuring out what was going on, and we discovered that she had Graves’.  And shortly after discovering that and treating her for that, she got pregnant with Sylvie.  So it’s something that I’ve done quite a bit of research into and I have obviously a personal motivation to stay up with it.

So for us, for my wife, the number one thing by far in terms of turning her health around was low-dose naltrexone, which we’ve discussed a few different times.  Low-dose naltrexone is a low dose of a medication called naltrexone, of course.  Naltrexone, if you look it up, you’ll find that it’s used for some things that have nothing to do with autoimmune disease and Graves’ disease.  Naltrexone at 50 mg is used for opiate and alcohol withdrawal.  You know, so basically it blocks the endogenous opiate receptors at that dose, which are our natural feel-good chemicals, so that if a heroin addict that was on 50 mg of naltrexone shot heroin, they wouldn’t feel a thing.  The problem at that dose was that not only did they not feel any pleasure from shooting heroin, they felt no pleasure at all at any other time in their life because their pleasure-producing chemicals were completely blocked.  So naltrexone was not very successful from that perspective, but a doctor in the ‘80s named Dr. Bihari found that if you used a lower dose of naltrexone and created a temporary blockade of the opiate receptors overnight, you could basically trick the body into producing more endogenous opiates.

And if you’re wondering how this relates to autoimmune disease, we know now that white blood cells have receptors for these endogenous endorphins, and that suggests that the endorphins have an immunoregulatory effect.  And sure enough, later research showed that low-dose naltrexone stimulates T regulatory cell function.  The T regulatory cells balance the immune system, and they turn off the inflammatory response once it’s turned on, and that’s a characteristic of autoimmune disease, is they’re often runaway inflammatory responses.  They’re basically inflammatory conditions run amok, where you get an inflammatory process and it just goes on and on and doesn’t get turned off.  So low-dose naltrexone, there are studies examining it in multiple sclerosis, in fibromyalgia, Crohn’s disease, probably the most well-known and best-designed trials, and it was remarkably effective for Crohn’s disease.  There was something like a 77% remission rate, which is just unheard of for a Crohn’s disease treatment, and with no side effects compared to placebo, which again, is unheard of because most of the drugs that are used to treat Crohn’s are pretty potent and can cause some pretty nasty side effects, like prednisone and Imuran and Remicade and some immunosuppressive drugs.

So low-dose naltrexone has not been clinically studied specifically for autoimmune thyroid disease, but many autoimmune diseases share common mechanisms, so it’s not that much of a stretch to think that if it works for MS and IBD and fibromyalgia that it could work for Hashimoto’s and Graves’, and sure enough, it does work very well for those conditions in my anecdotal experience and then the experience of a lot of other practitioners that use it and have hundreds of patients that are taking it for autoimmune thyroid disease.  So that would be absolutely my number one priority if I had Graves’ disease, is trying low-dose naltrexone.  There’s little risk to doing it.  There are no known long-term complications or risk associated with it at such a low dose, and especially when you compare it to the other treatment options in Graves’, which are basically having your thyroid radioactively ablated, or nuked, in layperson’s terms, or taking radioactive drugs like PTU or methimazole that have pretty nasty side effects including liver failure and death, I think low-dose naltrexone is a pretty attractive alternative.  I actually have a friend or a friend, or a friend’s mom, who had had Graves’ for 30, 40 years and had been taking medication, I think, PTU for that length of time, was extremely skeptical that LDN could help her because she had been on medication for so long.  But she heard about Elanne’s experience, and she decided to give it a shot, and now she’s off of those toxic drugs and she’s just taking LDN.  So it works even after that length of time in some people.

The next thing is that there are some studies, a couple studies, that suggest that L-tyrosine at pretty high doses can suppress the conversion of T4 to T3.  Graves’ disease is a hyperthyroid condition, and reducing the conversion of T4 to T3 can be helpful in those situations.  So the dosage that was observed in those studies to do that was around 1000 mg two to three times a day.

There’s some research that suggests that lithium orotate can help because it blocks the release of iodine and thyroid hormones, and in fact, it’s often used after radioactive ablation of the thyroid gland in Graves’ disease, when patients can experience a transitory increase in thyroid hormone after that ablation, and lithium is used to bring the levels down to prevent a thyroid storm or thyrotoxicosis.  So the dose, though, for that with lithium orotate is very low.  Some of you might be familiar with lithium as a treatment for bipolar disorder.  In the case of bipolar disorder, it’s used at a dose of, like, 800 to 2400 mg, but the way it’s used to bring levels down of thyroid hormone is a lot lower.  It’s about 120 mg.  I would not do this without supervision of a clinician who knows what they’re doing because lithium, if it’s not dosed properly, can have probably some undesirable effects, so it’s good to get some support there.

Those are the main ones.  Again, for us, I did some other things, like a custom herbal formula for my wife, but it’s difficult to give general recommendations for that because it’s really tailored to each person’s particular presentation.  But what happened is after she went on LDN, within two months she was pregnant, and then we had a very healthy baby girl who’s actually turning 1 in two days, three days.  This weekend we’re having her 1-year birthday party, which is gonna be fun.  So it can be quite remarkable, and really she’s been euthyroid the entire time since she’s been on LDN.  She’s never had to take any other drug.  And she’s healthy and doing great, so it’s definitely an exciting treatment for people who have that condition.

Steve Wright:  That’s a great story.  Are you inviting everybody to the birthday party?

Chris Kresser:  Yeah, c’mon over!

Steve Wright:  Hey, now, just to clarify, I’m assuming that you would also want to be gluten-free at least, if not paleo?

Chris Kresser:  Yes, definitely.  I mean, sometimes I think that that goes without saying, but of course, it doesn’t, so thanks for reminding me.  You want to eat a generally antiinflammatory diet, which means avoiding gluten because it can aggravate the immune system, and any other foods that can aggravate the immune system.  And another thing you want to be careful of is iodine.  I think iodine actually can be helpful in some cases of Graves’ disease, but you need to make sure that you have enough selenium if you’re taking iodine, and you need to make sure that you’re taking a very low dose of iodine to begin with and building up slowly.  And it’s probably a good idea to just get your iodine levels tested to see if you even need to take it, because if you take a higher dose of iodine right off the bat and you’re selenium-deficient, then iodine can, in that situation, exacerbate the autoimmune reaction.

Steve Wright:  OK, great.  Do you want to do one more?

Chris Kresser:  Let’s do the anemia question.

Everything you need to know about Anemia (and more)

Steve Wright:  OK.  It’s a bit long, so hang with me here.  This comes from Chris:  “About anemia, I heard you briefly mention during a podcast that something like 30% of your patients are anemic, and I was hoping that you would offer me some avenues for research into this problem.  I’ve been anemic for 15 years now, probably about the same amount of time that I’ve had intestinal/digestive issues.  Only in the last six months have I discovered paleo, Weston A. Price, and GAPS.  So I’ve finally gotten control of my depression/anxiety/psoriasis/gas/allergies/ asthma/fatigue/general immunity” — he’s got some things going on — “But the anemia persists.”  He lists some specific counts here.  We’ll skip over those, but basically it comes down to he’s borderline anemic, and it’s continuing to persist.  Chris, can you offer him some help?

Chris Kresser:  Yeah, I mean, if you want some avenues for research, I can keep you busy for the next five to ten years probably because anemia — There are few topics actually in medicine that are more poorly understood and more complex.  Anemia is one of those topics that, I think, is not taught well in any medical school, whether we’re talking about conventional medical school or the more alternative kind of medical schools.  A lot of clinicians just don’t really understand it very well, and I know this because I frequently see patients coming from all different types of clinicians, doctors, naturopaths, acupuncturists, whatever, and they tell me their history, and they show me their labs, and they show me what their clinicians did, and I’m often pretty shocked.  And you know, it is complex, as you’ll see.  I’ll go through some of the basics of anemia and the things that can cause it, and you’ll get a sense of why there is so much misunderstanding.  But on the other hand, it’s really frustrating because there are some things that are pretty easy to grasp that I think all clinicians should know, but I guess we just have to blame the schools because they’re not teaching it very well.

A lot of people can’t even agree on a definition of anemia.  That’s where the complexity and the problems start, is if you look up what is anemia, you’ll get all different kinds of responses.  One is a condition where the number of red blood cells in the blood is below normal.  Well, then, of course, there are different opinions on what’s normal.  And then another might be more specific, like hemoglobin level of below 12 in women or below 13 in men.  But my preferred definition is compromised ability of red blood cells to deliver adequate oxygen to body tissues, because that’s, in the end, what we’re really concerned about, is the capacity of hemoglobin to deliver oxygen to the cells, and all the cells in the body need oxygen to function properly.

So the causes of anemia can be basically split into four categories.  One would be insufficient production of red blood cells, hemoglobin.  Number two would be excessive breakdown of red blood cells.  Number three would be loss of blood.  And number four would be fluid overload.  So when we talk about insufficient production, that can be further broken down into stem cell problems like aplastic anemia or insufficient erythropoietin production; inadequate maturation of the red blood cells, which is usually in turn caused by nutrient deficiencies, specifically iron, folate, B12, or B6; myelodysplastic syndrome, or MDS, which was previously known as preleukemia; and then anemia of chronic disease, also known as anemia of chronic inflammation.  Now, when we talk about excessive breakdown, the second major group of causes, we’re talking mostly about the hemolytic anemias.  This generally will feature jaundice clinically.  You’ll see some yellowing and orange-bronzing of the skin and increased levels of an enzyme called lactate dehydrogenase on a lab test.  And these are often due to genetic mutations like sickle cell anemia and also enzymopathies like glucose-6-phosphate dehydrogenase deficiency, or G6PD.  The third category is blood loss, and short of trauma, you know, if you get in an accident and lose a lot of blood, we’re mostly talking in women about menstrual disorders like heavy periods or endometriosis or something like that, and in both men and women, gastrointestinal bleeding, so inflammatory bowel disease or ulcers, something like that where there’s significant ongoing blood loss.

And then the fourth category there is hypervolemia from excessive sodium or fluid intake, also sodium or water retention.  And it’s kind of a tangent, but it’s really important to point this out:  This hypervolemia happens naturally in pregnancy during the second and third trimesters as the blood volume expands to accommodate the growing fetus, and I see this a lot in my practice because I do a lot of fertility/pregnancy work.  A lot of women are misdiagnosed with anemia by their physicians or other health care providers during this period because a lot of clinicians, surprisingly, aren’t aware of this phenomenon, that the normal range for hemoglobin during pregnancy drops quite significantly.  So for example, the normal level for hemoglobin in nonpregnant women is between 12 and 16 g/dL, but the normal levels in pregnant women at 28 weeks are between 10 and 14 g/dL, and some research actually suggests that the lower end of that scale leads to better outcomes in pregnancy.  So if you’re pregnant and your hemoglobin is at 10.5, that actually pretty ideal and it doesn’t mean that you’re anemic.

OK, back to regular programming.  So I think you’re getting a sense now of how complex this is.  The typical thing is, like, you go in to the doctor and your hemoglobin is below the average level.  They’re just gonna give you an iron supplement, but iron deficiency is just one subtopic in one of those four categories of potential things that can cause anemia.  And certainly statistically speaking worldwide, iron deficiency is the major cause of anemia.  It affects about 2 billion people around the world, but it tends to affect more people in developing countries where iron-rich foods, particularly animal protein, is not available or not as readily available and in disadvantaged socioeconomic communities in the US for the same reason.  But iron deficiency anemia is more rare — I mean, I’m hard pressed to think of — I think I can recall maybe two or three patients that I’ve ever seen that have had iron deficiency anemia.  But as the questioner pointed out, I have a lot of patients with anemia.  Almost always the anemia is caused by something other than iron deficiency in my patient population.  And that might be unusual, but I frequently will get people come to me that have had low hemoglobin and their doctor just prescribed iron pills.  And the problem with that is that sometimes these patients are iron loaded, or sometimes they have something called anemia of chronic disease, which I’ll mention in a second, and giving someone who has anemia of chronic disease iron can really be problematic because anemia of chronic disease is caused often by an infection, and all pathogens utilize iron to proliferate and grow, just like most life on Earth.  And so if you give someone with an infection and anemia of chronic disease that’s caused by that infection iron supplements, you’re gonna make them much worse, and this actually happened to one of my patients.  It was quite sad.  Someone that I was consulting with in Texas, an older woman in her early 80s, and she sent me her blood work, and she did have anemia.  Her hemoglobin was low and her iron saturation was low, but — and this is really important — her ferritin levels were high, and that’s what distinguishes iron deficiency anemia from anemia of chronic disease, is the ferritin is elevated because ferritin is an acute phase reactant that’s elevated in the inflammatory response, and so that indicates that there’s some infection or inflammation, and also the body is trying to sequester iron and ferritin to keep it away from the pathogen.  So she sent me that, and then she ended up going to the hospital or to her doctor for some other reason, and the doctor saw that she had low hemoglobin, either didn’t test for or pay attention to ferritin, gave her iron pills, and she ended up spending a day or two in the hospital and nearly died.  It was really scary.  So this is a serious issue, and I think it’s important to grasp the complexity of it and to investigate these possible mechanisms because it’s often not simple.

So, let’s see.  We got a little lost there.  I guess what I would say is assuming some of those medical causes have been ruled out, like you don’t have stem cell problems, you don’t have myelodysplastic syndrome, you don’t have a hemolytic anemia, you’re not experiencing any blood loss, and you’re not hypervolemic, you don’t have excessive sodium or fluid intake, in that case then it usually does come down to a nutrient deficiency, and then we’d be looking at either iron deficiency on the one hand or folate, B12, or B6 deficiency on the other hand.  Luckily, it’s pretty easy to distinguish between those two, and the way you do that is you look at other markers that are included in a complete blood count, which he’s obviously had.  Usually when you test hemoglobin and red blood cells, that’s part of a panel called a complete blood count that measures some other markers.  So what you need to do is you look at MCV, mean corpuscular volume, and then MCH and MCHC, and if MCV is low, below the lab range, and hemoglobin and red blood cells are low, that’s usually indicative of iron deficiency anemia.  If MCV is high or high normal, then that’s a macrocytic anemia, and that’s indicative of B12, folate, or B6 deficiency.  So it’s fairly straightforward to do that, and of course, you can test your iron levels, doing an iron panel and ferritin to determine if you’re iron deficient.  And you can test your B12 levels using a standard serum B12 test and also urinary methylmalonic acid to see if you’re B12 deficient.  You can also test folate levels in the serum, but that’s a little less accurate.  The best way to test folate status is formiminoglutamic acid, which is one of the organic acids on the urine panel that I mentioned earlier.

So if your eyes have rolled back in your head and you’re just completely lost, don’t worry about it.  This is a complex topic.  I hope this was helpful for the questioner.  I would definitely get an iron panel and ferritin and then test for your B12, B6, and folate status.  Those are the most likely causes of ongoing anemia even after all of the kind of changes that you’ve made.  And if those are all normal, I would definitely seek out a practitioner who knows this stuff and can help you out.

Steve Wright:  That was a wealth of information that blew my mind.

Chris Kresser:  All right, we did it.  I think we made it through quite a few this time, huh?

Steve Wright:  Yeah, that was a good rapid-fire session right there.  OK, great.  Do you have anything to close with?

Chris Kresser:  No, just make sure to tune in next time for Dr. Fasano and then hopefully the time after that maybe — We’ll be AHS.  So we’ll either be taking a week off, one show off for a little summer break, or I’ve been talking with Jordan and Steve about the possibility of doing a kind of on-location, informal episode there if we can find the time and we can work it out technologically.

Steve Wright:  Yeah, we’re gonna do our best to see what we can come up with, and you definitely don’t want to miss the next show.  That’s for sure.

OK, great, so if you liked what you heard today, please head over to iTunes and leave us a review.  Leaving reviews really helps the popularity of the show, helps get the word out so other people can listen to it.  Please keep sending us your questions at ChrisKresser.com, and we’ll talk to you next time.

Fibromyalgia is a disorder that causes muscle pain and fatigue. People with fibromyalgia often experience tenderness at certain points on their body when pressure is applied.

Fibromyalgia sufferers also experience other symptoms, including:

• Insomnia or difficulty sleeping
• Morning stiffness
• Headaches
• Numbness or tingling in the hands and feet
• Menstrual irregularities and pain
• Difficulty concentrating (i.e. “brain fog”)

According to the most recent statistics, about five million Americans (roughly 1 in 50) suffer from fibromyalgia. It’s the second most common musculoskeletal ailment behind arthritis, and it affects females far more often than males (it is seven times more common in women).

As anyone with fibromyalgia will tell you, it’s a debilitating condition that affects every aspect of life. For example:

• People with fibromyalgia are three to four times more likely to suffer from depression.
• 50% of fibromyalgia sufferers have difficulty performing daily activities.
• 30–40% of people with fibromyalgia have to quit work or change jobs.
• People with fibromyalgia are hospitalized once every three years on average.
• The average fibromyalgia patient uses three or four drugs daily to control symptoms.

What is the conventional approach to fibromyalgia?

There is no laboratory test to diagnose fibromyalgia. Instead, patients are diagnosed based on their symptoms and history, and after excluding other diseases that may present with similar symptoms, such as rheumatoid arthritis, major depressive disorder, multiple sclerosis, and other autoimmune diseases.

There is no consensus in the medical community on what causes fibromyalgia. However, the current theory is that it may involve a variety of factors, including:

• Genetics. Fibromyalgia runs in families, so there may be genetic mutations that make people more susceptible to it.
• Infections. Some viral or bacterial infections appear to trigger or aggravate fibromyalgia.
• Physical or emotional trauma. Post-traumatic stress disorder has been linked to fibromyalgia.

Because the cause of fibromyalgia is unknown, conventional treatment is focused on managing symptoms. Common medications prescribed include analgesics (OTC pain relievers like ibuprofen, or prescription drugs like tramadol), antidepressants, and anti-seizure drugs (which are sometimes helpful in reducing certain types of pain).

An alternative theory on what causes fibromyalgia

For many years I’ve suspected that fibromyalgia is caused by gut dysfunction. I noticed that the vast majority of my patients with fibromyalgia also had digestive problems, and when I started to run tests on them, I discovered that many of them had gut infections, dysbiosis, small intestinal bacterial overgrowth (SIBO), and leaky gut.

Could an unhealthy gut be the cause of fibromyalgia?

Then I decided to look into whether this connection had been explored in the scientific literature. Sure enough, there were several studies connecting fibromyalgia with problems in the gut. For example:

• 73% of patients with fibromyalgia reported GI symptoms, compared with 37% of those with osteoarthritis. (1)
• Irritable Bowel Syndrome (IBS) is present in 30–70% of fibromyalgia patients. (2)
• 33% of IBS patients meet the diagnostic criteria for fibromyalgia, compared to just 4% of control subjects. (3)
• Up to 50% of patients with fibromyalgia have functional dyspepsia, which is a fancy term for “indigestion” with no known cause. (4)

While I was intrigued by these correlations, they are just that—correlations. What’s more, like fibromyalgia, IBS and functional dyspepsia are simply diagnoses based on symptoms, so these papers didn’t shed much light on what actually might be causing both the fibromyalgia and the IBS/indigestion.

In functional medicine, we’re always concerned with finding the underlying mechanism or cause, because addressing that is what will lead to the most effective and long-lasting treatment.

So I kept digging through the research, and I hit the jackpot. I found several papers associating fibromyalgia with specific mechanisms of gut dysfunction. For example:

• A study in 2008 found a relationship between alterations of the intestinal microbiota (i.e. “gut flora”) and fibromyalgia. (5)
• Researchers at Cedars-Sinai Medical Center in Los Angeles found that 100% (42/42) of fibromyalgia patients they studied had small intestinal bacterial overgrowth (SIBO). This is astounding. (6)
• A study of 40 patients with fibromyalgia, 28 (70%) had intestinal permeability (i.e. leaky gut). Importantly, 12 of the 28 patients with leaky gut had no gut symptoms. I believe this is one reason the gut is often overlooked as a potential underlying cause of fibromyalgia. (7)

Are gut problems the cause—or effect—of fibromyalgia?

Of course, one might ask “Are these gut problems causing fibromyalgia, or is it the other way around?”

At least one study has directly addressed this question. A group of patients with fibromyalgia that were positive for SIBO were split into two groups. One group received antibiotics to treat the SIBO, and the other group received a placebo. Significant improvement of fibromyalgia symptoms was observed in the patients that achieved eradication of SIBO with antibiotics, whereas no improvement was seen in patients who took placebo or who still tested positive for SIBO after the antibiotics. (8) This suggests that SIBO plays a causal role in fibromyalgia for at least some patients.

A new approach to treating fibromyalgia

If GI problems such as SIBO, dysbiosis, infections, and leaky gut are the underlying cause of fibromyalgia, it follows that healing the gut is the key to long-term improvement for fibromyalgia sufferers.

I’ve written extensively about how to do that elsewhere on my blog (this free eBook on gut health is a great place to start), but here’s a brief summary of the most important steps:

• Avoid foods, medications (e.g. antibiotics), and chemicals (e.g. BPA) that irritate the gut.
• Eat plenty of fermentable fibers (starches like sweet potato, yam, yucca, etc.).
• Eat fermented foods like kefir, yogurt, sauerkraut, kim chi, etc..
• Consume bone broth and glycine-rich foods (e.g. tougher cuts of meat like beef shanks, oxtail, brisket, and chuck roast).
• Consider taking a probiotic (I prefer soil-based organisms like Prescript Assist) and/or a prebiotic supplement (like PreBiogen).
• Treat any intestinal pathogens (such as parasites) that may be present.
• Manage your stress (with mediation, mindfulness practice, biofeedback, etc.).
• Get at least 7–8 hours of sleep each night.

Now I’d like to hear from you. Have you been diagnosed with fibromyalgia? If so, do you also have digestive problems? Have you noticed any improvement in your fibromyalgia symptoms after taking steps to heal your gut? Please share your experience in the comments section.

A lot of people might not be familiar with the term methanogen, but it is something that people should be aware of, especially if you have SIBO or suspect you may have SIBO.  We’ve talked about SIBO a lot.  For people new to the show or new to this work, this stands for small intestinal bacterial overgrowth.  It’s defined as a pathological increase in bacteria in the small bowel.  As a reminder, we have a lot of bacteria in our gut.  In fact, the bacteria and other organisms in our gut outnumber human cells by 10 to 1, but the location of that bacteria is really important.  In this episode, we cover: 1:29 What Chris had for breakfast 4:44 The role archaea play in gut health 7:50 What's the big deal about methane? 14:38 How to address SIBO in methane-producing patients 23:56 Gut healthy treatment recommendations [powerpress] Jordan Reasoner:  Hi.  Welcome to another episode of the Revolution Health Radio show.  The show is brought to you by ChrisKresser.com.  Steve is off today on a meditation retreat.  I’m your guest host Jordan Reasoner, from SCDlifestyle.com.  With me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser.  Chris, welcome. Chris Kresser:  Jordan, I’m happy you’re here.  And I’m happy Steve’s off walking the talk.  It will be interesting to hear about his experience when he gets back. Jordan Reasoner:  I’m excited.  He’ll be back tomorrow, so I’m looking forward to it. Chris Kresser:  This was his first 10-day Vipassana, is that right? Jordan Reasoner:  Yeah, it’s his first one. Chris Kresser:  It should be really interesting to hear about. Jordan Reasoner:  All of our friends are just coming back from Burning Man, and Steve’s coming back from a meditation retreat. Chris Kresser:  Yeah, other side of the spectrum.  Hopefully, you haven’t been getting any text messages from him in the last 10 days. Jordan Reasoner:  No.  It’s been radio silence. Chris Kresser:  Good, good. Jordan Reasoner:  So he’s been a good boy. Chris Kresser:  All right.  Cool. Jordan Reasoner:  Before we dive in, let’s talk about your breakfast, because I know we always get a lot of flak from the listeners if you don’t tell us about your breakfast, right?

What Chris ate for breakfast

Chris Kresser:  Okay.  So let’s see, I had some chorizo. We buy half a pig from a local rancher a couple of times a year, and then a butcher in Santa Rosa, Willowside Meats, butchers it and gives us a whole bunch of different cuts.  One of the things they do is make this really amazing chorizo.  So we had some of that, some scrambled eggs, some sauerkraut, beet kvass, and some plantains fried in expeller-pressed coconut oil.  That’s pretty standard breakfast around here.  It’s a good one.  Sylvie loves it.  We all like it.  It’s pretty easy to make. Jordan Reasoner:  I love your breakfast because it always has like five to seven parts to it. Chris Kresser:  It’s all about the diversity, right? Jordan Reasoner:  Yeah, exactly. Chris Kresser:  Feed those gut bugs. Jordan Reasoner:  You grew up on Lucky Charms.  It’s a nice transition, right? Chris Kresser:  Thankfully, I didn’t grow up on Lucky Charms.  As I get older, I have more and more appreciation for my parents, and the way that my mom fed us when we were young.  I mean, certainly, she wasn’t feeding us Paleo.  That wasn’t really part of the understanding at that point.  But she fed us, really, a pretty healthy diet overall, so I’m happy about that.  We have a good question today from Simas I think it is.  I’m not sure how to pronounce it, but I think that’s the right way.  Let’s give it a listen. Simas:  Hi, Chris.  I just wanted to ask, what would be the best way to deal with methanogens in people with SIBO?  I know Dr. Siebecker says that it’s best to use allicin, but it seems that I have a negative response, extreme fatigue and things like that, after taking it.  Thanks. Chris Kresser:  All right.  So let’s jump in here.  That’s a great question.  A lot of people might not be familiar with the term methanogen, but it is something that people should be aware of, especially if you have SIBO or suspect you may have SIBO.  We’ve talked about SIBO a lot.  For people new to the show or new to this work, this stands for small intestinal bacterial overgrowth.  It’s defined as a pathological increase in bacteria in the small bowel.  As a reminder, we have a lot of bacteria in our gut.  In fact, the bacteria and other organisms in our gut outnumber human cells by 10 to 1, but the location of that bacteria is really important.  They should mostly be in the colon, the large intestine.  We do have small amounts of bacteria all the way through the digestive tract, from the mouth to the anus, but the majority of the bacteria should be in the colon.  Very little should be in the small intestine, because the small intestine is where we digest and absorb food.  If you have a lot of bacteria growing in the small intestine, that’s going to interfere with the assimilation of nutrients from food, which is one of the major adverse effects of SIBO.

The role archaea play in gut health

So most of the research that you’ve probably heard about has focused on the role of bacteria in the gut, but recent evidence suggests that archaea also play a role.  That’s A-R-C-H-A-E-A.  Archaea are actually a completely different class of organism than bacteria.  They’re pretty ancient, single-celled organisms with no cell nucleus and no membrane-bound organelles.  They were originally classified as bacteria, but they’re now classified as prokaryotes, which again are a completely different class.  They’re considered totally unique from the other two major domains of life, which are bacteria and eukaryotes.  Some of the archaea that you might have heard of in the news, in the mainstream media are halophiles and thermophiles.  So these are archaea that live in extreme environments like salt lakes or hot springs.  But we now know that archaea are present in pretty much every habitat where you see biodegradation of organic compounds occurring, and that includes animal guts and human guts. When you go to get a breath test for SIBO—which is one of the major ways of testing for SIBO that we talked about—they’re going to measure the presence of, and the production of, methane and hydrogen gases at baseline.  Then they’re also going to measure the increase in hydrogen and methane production that occurs after you drink a sugary solution that they give you as part of the test procedure.  So typically, if you have a significant increase in hydrogen or methane after drinking the sugary solution, it means you have an overgrowth of bacteria in your gut.  To be more specific, when you have an increase in methane after drinking this solution, or if you just have high levels of methane at baseline, that indicates an overgrowth not of bacteria, but of these methane-producing archaea.  Unlike bacteria, which primarily produce hydrogen, the archaea are what produce this methane, and they do this actually not by fermenting carbohydrates.  So bacteria produce hydrogen and the way they do that is by fermenting fibers.  The methane production works differently.  The archaea consume the hydrogen that’s produced by the hydrogen-producing bacteria, and then they produce methane as a by-product of that process.  So this is actually one of the ways that excess hydrogen in the gut gets metabolized, is by these methanogenic archaea converting that hydrogen into methane.  And another way that hydrogen gets dealt with is by bacteria that convert hydrogen into sulfites.  That’s probably a little more detail than you needed, but it’s kind of interesting to see how this all works.

What's the big deal about methane?

Methane production begins at about three years of age.  You don’t see any methane production in infants, for example.  This suggests that methane production has everything to do with how the gut is colonized initially, because there are no archaea initially in the gut.  And it peaks at about 10 years of age, when adult levels are reached.  So by the time a child is 10, they’re typically producing the adult amounts of methane that they would produce for their whole life.  But here’s the thing—not everybody produces methane.  Depending on the studies that you look at, the numbers I’ve seen range from 30 percent to 50 percent of adults being methane producers.  So anywhere from a third to half of people have significant amounts of archaea that produce detectible amounts of methane.  That’s something important to understand—this is not an issue that affects everybody. So what’s the big deal about methane?  Simas’s question, “Is the presence of methane different?  Does it require a different approach?”  I think the answer is yes.  For what we see in the research and then what I’ve seen in my clinical experience working with patients.  Methane is a colorless, odorless, inert gas.  For a long time, it was thought that it didn’t really have any impact on human health, except for maybe causing a little bit of bloating and distention, if you had high levels of it.  But more recent evidence actually has linked methane production to various disease states.  And it’s still somewhat unclear whether that’s because of the level of methane itself, or whether it’s because of the removal of hydrogen from the bowel that happens when that hydrogen is converted to methane by archaea.  But we do know from studies that methane-producing archaea are present in 45 percent of people with SIBO.  In other words, a substantial percentage of people with SIBO have methane-producing archaea.  And the amount of methane that’s produced is significantly higher in patients with SIBO, compared with patients with fructose and lactose malabsorption, which are other gut issues.  So if you’re looking at a breath test, the presence of methane, to consider yourself a methane producer, you would have baseline methane levels of over 3 parts per million.  And I can tell you, from running a lot of these tests, that that’s quite common.  It’s more than 50 percent, I would say, in my patient population.  Then again, I’m testing people that mostly have SIBO and other gut issues, so it’s not necessarily a representative sample. Jordan Reasoner:  Now Chris, if I’m a patient and I’m experiencing problems, I think it’s SIBO and I’m not looking at a test, are there symptoms that are different in somebody who is predominantly going to have methane-producing bacteria versus non-methane-producing? Chris Kresser:  Yeah.  That’s a good question.  And it takes us right into the next section, which is, the answer to that is constipation.  Constipation, of course, can be caused by many things.  So it’s not to say that methane-producing archaea are the only cause of constipation.  But methanogenic flora, or archaea that produce methane, are significantly associated with chronic constipation in the scientific literature.  The amount of methane produced is correlated with colonic transit time.  So the more methane you have, the slower your transit time is.  In one study, if a breath test was positive for methane, they saw a 100 percent association with constipation-predominant IBS. Jordan Reasoner: Wow. Chris Kresser:  So yeah, it’s pretty strong in terms of association.  In other words, to put it in plain language, everyone who is positive for methane had constipation-predominant IBS in that study.  In contrast, the prevalence of methane was very low among patients with inflammatory bowel diseases like Crohn’s and ulcerative colitis, which typically present with diarrhea.  So you see that it’s much more common in people with constipation than it is in people with diarrhea.  I’ve also seen this correlation in my work with patients, people who have the really chronic, intractable constipation that doesn’t tend to respond well to a lot of different interventions.  I will often see really high baseline levels of methane and/or an increase in methane production after the challenge test.  A few other things you’ll see clinically are methane producers can have a higher prevalence of rectal hypersensitivity compared to non-methane-producing patients.  So sometimes, pain in that area or just a feeling of urgency can signal methane production.  This is not something that patients will be aware of, but if you’re looking at test results in constipated patients, the average pH of the colon will be significantly lower in patients with methane-producing flora.  So if you see a low pH on a stool test, it might be one potential sign of methane production.  Also, I think the other thing that’s important to know is that methane production seems to be much more common in women than it is in men.  That’s the only real demographic characteristic I’ve been able to find.  It seems there’s no age-specific distribution, other than the fact that you don’t get methane production until three years of age, as I mentioned before, and it will be lower in kids up to 10 years of age typically.  But other than that, the only significant association I found is that it’s more common in women than it is in men. Jordan Reasoner:  In your research, have you seen any associations between being breastfed or vaginal birth versus C-section?  Have you seen any associations around that? Chris Kresser:  No, I haven’t.  I don’t think that that means there aren’t any, but there are only a handful of studies on this topic.  Most of them are pretty recent; most of them were done by Dr. Mark Pimentel’s group.  He, as many people know, has been a pioneer in research on SIBO and has a research clinic at Cedars-Sinai down in LA.  It does a lot of great work.  So I think there’s still a lot to be learned about this.  My guess is there is possibly an association, Jordan, but we don’t really know for sure about that.

How to address SIBO in methane-producing patients

Jordan Reasoner:  Chris, before we move on, what do I do about this in general?  If I’m somebody who, I find with a practitioner that I have more of these methane gases in my body, and I’m that type of a person with small intestinal bacterial overgrowth, how does that change your approach as a practitioner?  And how does that change what I do, as somebody who’s trying to recover from this? Chris Kresser:  So it could change the medications that you take for SIBO, if you are going to take medications, and may change the way you treat it overall.  The first thing, taking even a step back before we get into that, is to determine—so far, we’ve been talking about associations between methane and constipation, but that doesn’t necessarily tell us that methane is causing the constipation.  It could be that constipation is causing the high methane levels.  There is actually some research that suggests that might be true.  There are studies showing that treatment with laxatives and bowel cleansing, like a colonic, can reduce or eliminate methane production in some patients.  So that would suggest that constipation, at least to some extent, may increase—methanogens may favor a slow transit type of environment, and when you’re constipated, you might get an increase in methane-producing species. However, there are also a lot of other studies that suggests that methane directly causes the constipation in the first place.  For example, in animal models, they directly infuse methane into the small intestine.  You’ll see a reduction in transit time of 60 percent, compared to just infusing normal room air.  They suspect, right now, that this effect may be mediated by serotonin, which is a neurotransmitter—as I’m sure most people know—that is present in the gut in about 400-fold higher concentrations than is present in the brain.  So serotonin really, more than anything else, is a gut neurotransmitter, and it’s thought to affect intestinal motility.  Studies have found that methane producers have lower post-meal serotonin levels than people who produce primarily hydrogen.  So I think it is pretty reasonable to assume that methane does play a causative role in constipation.  Then there are also studies that show that the elimination of methane in treatment correlates very closely with symptom improvement.  That’s where your question comes in, Jordan.  So if you treat SIBO and you don’t address the methane production, even if you get rid of the hydrogen, the patient is probably not going to improve to the extent that they should, because you’re not getting rid of the methane. So here’s the tricky thing—rifaximin, which is the drug that is typically used to treat SIBO, is not very effective against methane-producing species on its own.  For example, in a study with patients who all had baseline levels of methane above 3 parts per million—which established them as methane producers—10 days of rifaximin alone led to a clinical response about 56 percent of the time, so roughly half the time.  But it only led to a negative result on the breath test 28 percent of the time.  So about 70 perecent of the time, rifaximin was not clearing the methane from the breath test, and about half the time, it wasn’t leading to any clinical improvement at all.  Now, 10 days of another drug that’s often used to treat SIBO on its own, called neomycin, led to a clinical improvement in 63 percent of cases, which is a little bit better than rifaximin on its own.  And it led to a negative breath test result 33 percent of the time, which is again, a little bit better than 28 percent for rifaximin.  But it’s not great, right?  We’re still talking about two-thirds of the time that it’s not working.  But if you combine rifaximin with neomycin together and take them for 10 days, that led to a clinical improvement 85 percent of the time, and a negative breath test result 87 percent of the time.  So now we’re talking about some real treatment efficacy numbers here.  Actually, they don’t really understand why the combo of rifaximin and neomycin works better than either of these two drugs alone, but there are other examples where this happens.  For example, the H. pylori treatment, right?  That requires two different antibiotics, and if you use one alone, or the other alone, you don’t get the same efficacy than if you use the two antibiotics together.  So there is a precedent for this kind of thing happening. The other thing to be aware of is that outside of rifaximin and neomycin, most methanogenic archaea are resistant to the majority of the antibiotics that are typically used against gram-positive and gram-negative bacteria.  So your ciprofloxacins and Flagyls and things like that that a lot of practitioners would use to clear out bacterial infection are probably not going to work for these types of archaea.  And in my mind, this is another reason why botanical treatments can really make a lot of sense.  We talked on a previous show about a study that showed that botanical treatments were as effective, or more effective, than antibiotics for SIBO, and had far fewer side effects.  One of the reasons for this is that botanicals, herbs, plant substances, have a really broad spectrum of activity.  And it’s far less likely that organisms will be able to develop resistance against a botanical, because within each single herb, there are many different active compounds, instead of just one active compound that’s in an antibiotic.  So it’s much harder for the organism to adapt to that.  And typically, herbs or botanicals are used in formulas, where you have many different herbs together.  You’ve got many different herbs, each with multiple compounds, and then they form together to create synergistic compounds.  It starts to become exponentially more diverse, complex, and more difficult for organisms to develop resistance to.  I think given some of the research we have on the efficacy of botanical treatments, given the increasing problem of antibiotic resistance, and possibly these archaea developing resistance to rifaximin and neomycin eventually, given the fact that studies show that about one out of two people who have SIBO and are treated successfully for it will relapse in the future, which is kind of a depressing statistic. Jordan Reasoner:  Yeah. Chris Kresser:  I mean, not to get too far off on a tangent, but I bet a lot of people in those studies aren’t doing low-FODMAP, Paleo type of diets or SCD type of diets.  They’re only just taking the drugs, and then they’re going back to eating the same crappy diet that led to the problem in the first place.  In my population, the relapse rates are not that high.  But given all that stuff, it’s possible that people will have to get treated more than once.  That’s what I’m getting at.  And I’m much more comfortable with the idea of someone doing multiple botanical protocols and using probiotics that secrete antimicrobial peptides—which probably may work against methanogens—and food-based treatments, like removing FODMAPs, which are the certain class of carbohydrates that feed the bacteria which produce hydrogen, which feed the archaea.  So if you starve the bacteria, you’re reducing the hydrogen levels.  That, in theory, would reduce the levels of substrate that are available to the archaea for producing the methane.  So the food-based treatments still work there.  I did mention, when we talked about the causal relationship with methane, that some studies show that a bowel lavage, a colonic, or a laxative kind of thing, can lower or even eliminate methane production.  But I would be careful with that, because colonics, while they do wash out some of the bad gut flora, they also wash out a lot of the good gut flora.  They’re also pretty invasive.  I think it’s probably best to try to treat with herbs, diet, and other antimicrobial nutrients than it is to use laxatives or colonics. Jordan Reasoner:  One of the common objections that I always hear with somebody that follows Dr. Pimentel’s work, they’re very familiar with this type of thing, and they’re going to end up on this combo of neomycin or rifaximin, people freeze.  That’s because we’re all really afraid to use antibiotics now almost in this health community, right? Chris Kresser:  Mm-hmm. Jordan Reasoner:  One of the most common things I get asked is, “What can I do before, during, and after this protocol to not totally set me back and destroy all my good gut flora?”

Gut healthy treatment recommendations

Chris Kresser:  That’s a valid question.  The good news is that rifaximin and neomycin are narrower in spectrum than ciprofloxacin or some of the really broad-spectrum antibiotics, and they’re not going to wipe out your gut flora to the extent that some of those other antibiotics will.  They’re also not absorbed systemically, that’s another advantage to those drugs.  I think rifaximin, 99.8 percent stays in your gut and doesn’t get absorbed, so it’s not going to affect flora in other parts of your body as much.  So they are safer than a lot of other antibiotics. My strategy is to start with the botanical protocols, and use antimicrobial botanicals like olive leaf extract, uva ursi, cat’s claw, yerba mansa, coptis, artemesia, sida, et cetera.  Then use soil-based organisms that secrete antimicrobial peptides—Prescript-Assist, which I sell in my store.  It’s available in my store, because I’ve just had such great success with it in just about everybody, which is rare with probiotics.  You know, a lot of people don’t respond to probiotics very well.  Then we have nutrients like Lauricidin or lauric acid, which are antimicrobial, which may be helpful in this kind of situation.  So I like to start a protocol with a whole bunch of natural things like that, and see how they do.  I only really recommend the rifaximin and neomycin combo if a couple of rounds of this initial protocol aren’t successful.  Then I would definitely suggest patients take things like Saccharomyces boulardii or other probiotics while they’re doing the protocol and after the protocol.  Then ironically, prebiotics often are a big part of the healing process.  This is where it gets tricky, because prebiotics are the fiber that feed the bacteria, which then produce hydrogen, which feed the archaea.  You have to make sure you reduce the levels of those bacteria and archaea first, and then come in with the prebiotics to rebuild a healthy gut flora that will make it less likely that you’ll develop this problem again in the future.  So it’s a pretty involved process, there’s a lot to it, and it has to be timed right.  But it’s definitely possible, and it works.  It just takes more time, in some cases, than people expect.  Generally, with SIBO, and especially if it’s a recalcitrant case and the levels of methane are really high, I tend to tell patients that this is going to be a 6- to 12-month process to fully deal with it, and that’s what we’re seeing in the clinic. Jordan Reasoner:  Well, Chris, I think we answered Simas’s question pretty in-depth today. Chris Kresser:  All right.  Great question.  Keep them coming, everyone.  It’s really fun to hear your questions.  Of course, we don’t have the chance to answer them all.  We try to choose ones that we think will be of greatest interest to the greatest number of people, and kind of spread out the topics.  Keep them coming and we’ll see you next week. Jordan Reasoner:  If you want to get more info about what Chris is researching in-between all these show recordings and all the studies that he’s sharing, head over to Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser.  Thanks, everyone.

This is a guest post by Laura Schoenfeld, a Registered Dietitian with a Master’s degree in Public Health, and staff nutritionist for ChrisKresser.com. You can learn more about Laura by checking out her popular blog or visiting her on Facebook. And if you need one-on-one help with your diet, click here to learn more about her nutrition consulting services. Recently, I wrote an article about the potential pitfalls of following an excessively low carb diet, and the symptoms to watch out for to know if you’d benefit from adding carbs back into your diet. While I repeatedly pointed out that there are many people who thrive on a very low carb or ketogenic approach, there were commenters who staunchly disagreed with my recommendations. While I stand by my original article (as well as Chris’s subsequent supporting articles here and here), I wanted to make sure that those who would benefit from a very low carbohydrate or ketogenic diet were aware of the positive impact this nutritional approach can have when implemented correctly. Yes, you read that correctly: there are many people who can do incredibly well on a properly designed, nutritionally adequate ketogenic diet.

Some people find that they thrive on a very low carb or ketogenic diet. Could you be one of them?

In this article, I’ll describe seven different classes of people who could experience improved health and wellbeing by following a ketogenic diet, as well as briefly explain the precautions you’ll need to take if choosing to experiment with this therapeutic diet strategy.

Overweight and Obesity

One of the biggest draws of a low carbohydrate diet is that it can be a highly effective tool for rapid weight loss, especially in those who are significantly overweight and/or obese. When compared to low fat diets, dozens of studies show that a very low carb approach can be help those who are overweight lose weight, maintain lean muscle mass, and improve many of the metabolic risk factors for diabetes and heart disease, including elevated triglycerides, low HDL, and chronically elevated blood sugar. There’s no denying that a low carb diet can be a highly effective obesity treatment. Most people believe low carb diets cause weight loss so rapidly by lowering circulating insulin, but another reason why low carb dieting may promote weight loss is because these diets frequently lead to a spontaneous reduction in overall food intake. Combining that with low insulin and high glucagon levels is generally a recipe for immediate weight loss, though this is not always sustainable for a variety of reasons. The longer a person stays on a low carb diet, the more they may start to find ways to make their diet more palatable, and thus increase their overall calorie intake. Also, as weight loss occurs, a person’s overall calorie expenditure will drop, meaning that the same amount of food that made them lose weight in the first place will eventually cause them to maintain their weight - the dreaded “plateau”. If you’re eating more calories than you’re expending, even on a low carb diet, you won’t lose weight. If you’re using low carb as a weight loss diet, this doesn’t give you license to eat high fat foods in unlimited quantities. Eat good quality protein, plenty of non-starchy vegetables, and enough fat to meet your daily needs without going overboard and you may find that a nutrient-dense low carb diet is the perfect strategy for sustainable weight loss and reversal of metabolic syndrome. And remember - obesity is a far different health situation than trying to “lose the last 10 pounds”, so many of the same weight loss principles that work well for people who are significantly overweight may not work so well for those trying to reach their ideal “look good naked” weight. Keep that in mind when considering how much weight you want to lose and whether or not it’s truly necessary for health purposes. Those who don’t really have much excess weight to lose may be more prone to the potential problems with a long term low-carb diet.

Blood Sugar Imbalances

Blood sugar control plays an important part in weight management as well as the prevention of chronic disease, including diabetes, heart disease, cancer, and possibly even Alzheimer’s disease, among others. If your blood sugar is always elevated, you’re at an exponentially higher risk for dozens of diseases, and you’re more likely to die earlier from these diseases as well. So if you have consistently high blood sugar, you’ll likely find that reducing your carbohydrate intake significantly can bring that number down quickly, particularly if you’re relatively sedentary. Low carb diets can also be helpful in reactive hypoglycemia, a condition where blood sugar drops too low following a meal, causing symptoms such as dizziness, anxiety, shakiness, hunger, and confusion. This issue can be made worse by caffeine and stress, and I find it more commonly in my clients with adrenal issues. A common cause of this reaction is when a meal too high in easily absorbed carbohydrates is consumed, and blood sugar rises rapidly, leading to a release of insulin. The insulin causes a subsequent drop in blood sugar, and this drop can sometimes go too low or happen too quickly, leading to the hypoglycemic symptoms. If you’re someone who eats a lot of sugar-laden foods, or generally is eating a high carb, low fat diet, you may be more prone to these blood sugar swings that can lead to hypoglycemia symptoms. In this case, a reduction in carbs and an increase in fat at meals will help keep your blood sugar levels steady, and get you off the blood sugar roller coaster. But if you’re already eating a very low carbohydrate diet, a bit of healthy carbs at each meal may actually help normalize your blood sugar too, so it’s important to consider your current dietary habits before dropping your carbs any lower. And if you’re completely unsure where you stand on this issue, it might be worthwhile getting some help with your diet!

Neurological Disorders

One of the oldest uses of a ketogenic diet has been the treatment of seizure disorders  - even the Bible refers to fasting as a treatment for “fits”, and the ketogenic diet has been used by doctors as a treatment for epilepsy since the early 1900s. Though the creation of anti-seizure medication significantly reduced the reliance on this treatment, there has been a surge in the demand for this therapeutic diet over the past 20 years. These days, there are even dietitians who specialize in the ketogenic diet who work with patients, mostly children, suffering from frequent seizures. Other neurological conditions that have been shown to respond well to a ketogenic diet are Parkinson’s disease, Alzheimer’s disease, ALS, stroke, and dementia. (1, 2, 3, 4, 5, 6) In fact, Alzheimer’s disease is now being referred to as Type 3 Diabetes, highlighting the importance of blood sugar control in managing this often devastating condition. Ketogenic diets may also be therapeutic in the treatment of traumatic brain injury, a major cause of mortality and morbidity in young adults. (6a) One of the most comprehensive books covering the role of a low carb and/or ketogenic diet in the treatment of neurological conditions is Grain Brain by Dr. David Perlmutter, a well known neurologist. Dr. Perlmutter has had a great deal of success using low carb, grain-free, and ketogenic diets in the treatment of thousands of patients with neurological disorders. However, it’s important to remember that while these very low carb diets are helpful in treating these conditions, it’s unknown whether or not these restrictive diets would be necessary to prevent these conditions. Ultimately, I’d personally reserve the use of a ketogenic diet as a treatment for neurological disorders rather than a long term preventative diet.

Mood Disturbances

Similar to the neurological conditions already discussed, low carb and/or ketogenic diets may be helpful in reducing or eliminating symptoms of mood disorders like anxiety or depression. Some preliminary evidence suggests that these diets can have similar effects as antidepressant drugs. (7) Most of the research has been conducted in animals, but there have been studies showing benefits in improving aggression, fear behavior, and overall mood and quality of life. (8, 9, 10, 11) On the contrary, one study demonstrated a decline in overall mood in subjects on a low carb diet, energy-restricted diet compared to a low fat diet, while another showed a decline in mood in female cyclists following a low carb compared to moderate and high carb diets. (12, 13) There hasn’t been a ton of research on this issue, so ultimately you’ll have to determine for yourself what the appropriate level of carb intake will be for your particular mood issues. I’ve seen plenty of clients (myself included) who find that their levels of anxiety skyrocket on an excessively low carb diet, so what works for one person (or a rat!) may not work for you. Whether or not carbs are at play in your anxiety or depression, there’s a major role for a healthy diet and ancestrally appropriate lifestyle. I do believe food is medicine when it comes to mood issues, and I’ve seen multiple clients get off their antidepressants after making targeted, individualized changes to their diets, even if they were already eating “Paleo”. And none of these improvements required strict carbohydrate restriction, so a moderate intake on a nutrient-dense diet may be enough to see positive changes.

Polycystic Ovarian Syndrome (PCOS)

PCOS is an incredibly common endocrine issue in young women, with a prevalence as high as 15%-20% of women. Typically, PCOS affects ovulation and menstrual function in women, and can also cause an androgen excess. These changes are the root cause of many of the most frustrating symptoms, including amenorrhea, acne, hirsutism (male-pattern body hair), weight gain, dandruff, thinning hair, and mood issues. One of the primary dietary recommendations for women with PCOS is to limit refined carbohydrates and sugars, and to generally follow a lower carb diet. (14, 15) Reduced carbohydrate diets can help improve body composition, increase fat loss, repair insulin sensitivity, and promote menstrual regularity in these women (16, 17, 18) One pilot study found that overweight women following a low-carbohydrate ketogenic diet lost weight, reduced their testosterone levels, and decreased their fasting insulin. (19) These women also experienced non-significant decreases in insulin, glucose, testosterone, HgbA1c, triglyceride, and perceived body hair. Two women even became pregnant during the study, when they had previously been experiencing infertility. But before those of you with PCOS jump straight on a ketogenic diet, it’s crucial to note that there was no control group in this study. So it’s hard to know if the ketogenic diet was really necessary to get these results, or if a significant reduction in sugar, processed carbs, and grains might have been adequate, while still allowing these women to get a substantial amount of carbs from Paleo-friendly fruit and starchy vegetables. You may find that the right diet for you allows for plenty of healthy variety, and that a reduced carbohydrate, whole foods diet is enough to get you on the right path towards healing from your PCOS.

Small Intestine Bacterial Overgrowth (SIBO) and Reflux (GERD)

SIBO and GERD seem to be increasingly common these days, likely stemming from our overuse of antibiotics, inadequate exposure to healthy bacteria, poor dietary choices, and high levels of stress. In my work with clients, I’ve also noticed an uncanny connection between SIBO or reflux and a history of binge eating or bulimia disorder, so I’d guess that overeating in general can put someone at higher risk for low stomach acid and an overgrowth of bacteria in their small intestine. You can get great information about reflux from Chris’s free eBook on the topic. And if you’ve never heard of SIBO and you don’t know what the primary treatment for this condition is, I’d suggest listening to this podcast that Kelsey Marksteiner and I recorded for a great primer on the subject. But I’m sure some of you reading this either know what SIBO is, or actually have SIBO yourself. SIBO and reflux are often found simultaneously, so that’s why I’m lumping these two conditions together. One of the primary dietary treatments for SIBO and reflux is the restriction of fermentable carbohydrates, often referred to as FODMAPs. But some practitioners even recommend using a completely low carbohdyrate or ketogenic diet, as some bacteria can feed off of low FODMAP carbs and starches. It may depend on the severity of your SIBO case, and some SIBO patients do just fine restricting FODMAPs and simple sugars. And if you’re eating too many high FODMAP veggies on a low-carb diet, you may actually make the problem worse! Generally for reflux and/or SIBO, I tend to recommend a lower carbohydrate diet which restricts fermentable carbohydrates and sugar, but allows for a moderate amount of starches such as white rice or potatoes, which are often well tolerated. So while a strict low carb or ketogenic diet may be useful in dealing with these digestive disorders, I don’t think that it’s necessary to stay on these diets indefinitely to get the results you’re looking for.

Cancer...?

At the risk of opening a giant can of worms, I’ll briefly mention that there are many scientists, doctors and clinicians who promote the use of a low carb ketogenic diet for cancer. The major argument is that unlike the majority of our body cells, cancer cells lack the ability to metabolize ketones, and require a significant amount of glucose to survive and replicate. Since a ketogenic diet can keep blood sugar low, the theory (in a nutshell) is that cancer cells won’t be able to survive and thus the cancer will not grow and metastasize. Some doctors have reported amazing results in the use of these diets in helping their patients go into remission. There are a few studies that show potential benefits for some (but not all) cancer patients, especially brain cancer. (20, 21, 22, 23, 24) But another study showed that in 16 patients with advanced metastatic cancer, only 5 of the 16 patients recruited could even stick to the diet, and none showed any remission of the cancer, so it likely depends on the type and severity of the cancer whether or not a ketogenic diet will make any difference to the outcome. (25) And none of these studies show any data that suggests a ketogenic diet would be necessary or helpful to prevent cancer. When it comes to dietary recommendations and carbohydrate restriction for cancer patients, I don’t know if there’s enough data on the subject to make a strong recommendation either way. Ultimately, we’ll always have some level of sugar circulating in our bloodstream, and while I agree that good blood sugar control is likely helpful in preventing cancer in the first place, I’m not entirely convinced that a ketogenic diet is the best diet in all cancer patients, especially for those who are in more advanced stages. And having had relatives die from advanced stage cancer, I can also understand the fear that would come from feeding a cachexic cancer patient a hypocaloric ketogenic diet if they’re already wasting away. For now, I’ll “plead the fifth” on this topic, and wait and see if more studies come out in the future supporting this particular therapeutic use of the ketogenic diet.

Important Considerations When Starting A Low Carb Diet

As you can see, a low carb diet can be a good choice for certain people, as long as they pay attention to several important factors that can ensure their nutritional status isn’t negatively impacted by this somewhat restrictive diet. The biggest issue I see with many people who first switch to a low carb diet is that they’re unintentionally undereating, largely due to their discomfort with eating enough fat to make up for the carbs they’re not consuming. While this can be okay in the short term, especially for weight loss, over time this can lead to malnutrition and unhealthy stress on various organs, and may even cause weight gain as the body tries to conserve energy. If you’re on a low carb diet, make sure you’re eating enough to support your daily activity and to get a wide range of nutrients. Also, even though some of your favorite foods might be low carb - like bacon, cheese, steak, and butter - make sure you’re still eating plenty of nonstarchy vegetables. These will help keep your gut bacteria healthy, as well as providing a variety of important minerals that can get deficient on a low carb diet. Potassium is a particular mineral that is prone to deficiency on a low carb diet, so eating a wide variety of vegetables and low carb plant foods at every meal (in addition to nutrient-dense animal foods) will help keep you nourished. Avoid low carb products sold in the grocery store. These products often have artificial sweeteners and other additives that make them taste similar to their high carb counterparts, and sometimes can cause digestive distress in larger quantities. If you’re going to do a low carb diet, make sure you’re still eating real food and not buying a ton of low carb packaged food to replace the junk food you used to eat. It’s important to keep an eye on your blood work as well, since not everyone experiences positive results on a low carb diet. Franziska Spritzler is a low carb dietitian who explained the adverse effects she experienced on a low carb ketogenic diet, with her LDL cholesterol and particle number shooting up to a potentially dangerous level. While this won’t happen to everyone, if it does happen to you it may be a sign that the diet isn’t a great choice for your long term health. Finally, pay close attention to how you look, feel, and perform while on a low carb diet. While you’ll need to give it some time to truly determine if the diet can support your activity, energy, and daily lifestyle, it’s hard to know who will thrive and who will crash and burn on a long term low carb diet. If you’re experiencing negative health effects like excess weight gain, sluggishness, mood issues, or poor athletic performance after trying the diet for several weeks, it may be a sign that you’d do better on a more moderate carb approach. Don’t let someone else’s experience with the diet dictate how you should expect to feel. You’ll be your own judge when it comes to figuring out the most appropriate diet for you. And if you need help figuring out how to optimize your carbohydrate intake, don’t hesitate to get in touch with me - I’ve worked with dozens of clients in this situation and can help you figure out if a low carb diet is right for you. You can sign up for a free 15 minute consult and we’ll discuss your nutrition and health concerns and determine if you’d benefit from professional and personalized guidance. Now I’d like to hear from you - what side of the carbohydrate “fence” are you on? Low carb? Moderate carb? High carb? How did you figure out the right diet for you? Share your story in the comments below! About Laura: Laura uses her knowledge of traditional and biologically appropriate diets to improve her clients’ health. Growing up with a family that practices Weston A. Price principles of nutrition, she understands the foods and cooking practices that make up a nutrient dense diet. With her strong educational background in biochemistry, clinical nutrition, and research translation, she blends current scientific evidence with traditional food practices to help her clients determine their ideal diet. You can find her at AncestralizeMe.com, on Facebook, and Twitter!

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

The normal small bowel, which connects the stomach to the large bowel, is approximately 20 feet long. Bacteria are normally present throughout the entire gastrointestinal tract, but in varied amounts. Relatively few bacteria normally live in the small bowel (less than 10,000 bacteria per milliliter of fluid) when compared with the large bowel, or colon (at least 1,000,000,000 bacteria per milliliter of fluid). And, the types of bacteria normally present in the small bowel are different from those in the colon.

Why you should thank your small bowel and the beneficial bacteria that live there

The small bowel plays an important role in digesting food and absorbing nutrients. It is also an important part of the immune system, containing an impressive network of lymphoid cells (cells of the immune system that help fight infections and regulate the immune system).

Are you at risk for small intestinal bacterial overgrowth? Find out what the most common risk factors and symptoms are.

The normal (beneficial) bacteria that are an essential part of the healthy small bowel also perform important functions. These beneficial microorganisms help protect against bad (i.e. pathogenic) bacteria and yeast that are ingested. They help the body absorb nutrients, and also produce several nutrients (such as short chain fatty acids) and vitamins like folate and vitamin K. These bacteria help maintain the normal muscular activity of the small bowel, which creates waves that move the intestinal contents, like food, through the gut.    

What is SIBO?

SIBO, small intestinal bacterial overgrowth, is defined as an increase in the number of bacteria, and/or changes in the types of bacteria present in the small bowel. In most patients, SIBO is not caused by a single type of bacteria, but is an overgrowth of the various types of bacteria that should normally be found in the colon (1). Less commonly, SIBO results from an increase in the otherwise normal bacteria of the small bowel. 

SIBO has been shown to negatively affect both the structure and function of the small bowel. It may significantly interfere with digestion of food and absorption of nutrients, primarily by damaging the cells lining the small bowel (the mucosa). Additionally, this damage to the small bowel mucosa can lead to leaky gut (when the intestinal barrier becomes permeable, allowing large protein molecules to escape into the bloodstream), which is known to have a number of potential complications including immune reactions that cause food allergies or sensitivities, generalized inflammation, and autoimmune diseases (2).

These pathogenic bacteria, whether too many or the wrong types, can lead to nutritional deficiencies on top of those due to poor digestion or absorption. In particular, the bacteria will take up certain B vitamins, such as vitamin B12, before our own cells have a chance to absorb these important nutrients. They may also consume some of the amino acids, or protein, that we’ve ingested, which can lead to both mild protein deficiency and an increase in ammonia production by certain bacteria. (We normally produce some ammonia daily from normal metabolism, but ammonia requires detoxification, so this may add to an already burdened detoxification system.) The bacteria may also decrease fat absorption through their effect on bile acids, leading to deficiencies in fat soluble vitamins like A and D.

What causes SIBO?

The body has several different ways of preventing SIBO. These include gastric acid secretion (maintaining an acidic environment), waves of bowel wall muscular activity, immunoglobulins in the intestinal fluid, and a valve that normally allows the flow of contents into the large bowel but prevents them from refluxing back into the small bowel. (This is called the ileocecal valve because it’s located between the ileum, or terminal end of the small intestine, and the cecum, a pouch forming the first part of the large bowel.)

The cause of SIBO is usually complex, and likely affects more than one of the protective mechanisms listed above.  A number of risk factors for SIBO have been identified, with some of the more common risk factors listed below.  For a more complete discussion of associated diseases and risk factors check out this study and this study.

Risk factors for SIBO

• Low stomach acid
• Irritable bowel syndrome
• Celiac disease (long-standing)
• Crohn’s disease
• Prior bowel surgery
• Diabetes mellitus (type I and type II)
• Multiple courses of antibiotics
• Organ system dysfunction, such as liver cirrhosis, chronic pancreatitis, or renal failure

Moderate alcohol consumption and oral contraceptive pills (OCPs) also increase the risk for SIBO

Heavy alcohol use has long been recognized in association with SIBO (3). This study also found an association between SIBO and moderate alcohol consumption, defined as up to one drink per day for women and two drinks per day for men. Alcohol appears to have effects on several of the normal protective mechanisms, including causing injury to the small bowel mucosal cells, contributing to leaky gut, and decreasing the muscular contractions. Additionally, alcohol may “feed” a few specific types of bacteria contributing to overgrowth (4).

Overall there appears to be a moderate association between OCPs and inflammatory bowel disease (IBD) such as Crohn’s disease (5). Though no studies to date specifically correlate the use of OCPs with SIBO, given the known relationship between IBD and SIBO, it is likely that this association holds true for SIBO as well. However, once patients stop taking OCPs, this risk appears to reverse.

How do you know if you have SIBO?

The number of people with SIBO in the general population remains unknown. Some studies suggest that between 6 to 15% of healthy, asymptomatic people have SIBO, while up to 80% of people with irritable bowel syndrome (IBS) have SIBO (6). 

SIBO is largely under-diagnosed. This is because many people don’t seek medical care for their SIBO symptoms, and because many doctors aren’t aware of how common SIBO is. Complicating this, the most commonly used tests (breath tests measuring levels of hydrogen and methane gas) still have fairly high rates of false negatives (meaning the test results come back as negative but you actually do have the disease) (7).

The most common symptoms of SIBO include:

• Abdominal pain/discomfort
• Bloating and abdominal distention
• Diarrhea
• Constipation (generally associated with methanogens as Chris discussed in his recent podcast)
• Gas and belching
• In more severe cases, there may be weight loss and symptoms related to vitamin deficiencies.

Is SIBO contagious?

Unlike many other bacterial infections of the gastrointestinal tract, SIBO is not contagious, and there is no evidence that exposure to any single microorganism increases the risk for developing SIBO. SIBO occurs due to a complex interplay of many different factors and is not passed on between individuals.

Why SIBO can be difficult to treat

Antibiotics are often used to treat SIBO. However, studies show that despite treatment with antibiotics, recurrence develops in almost half of all patients within one year. One study comparing treatment with rifaximin (the most commonly used antibiotic for SIBO) and botanical antimicrobials showed slightly better outcomes with the botanical protocol, but still with successful treatment in close to only half of all patients after one course of treatment.

These finding suggests that treatment of the overgrowth alone is not enough for most people. An additional piece of successful treatment must include addressing the underlying cause, or predisposing factor.

Though there are many identified associations between SIBO and other diseases as described above, abnormalities in gut motility are recognized as one of the most common associations. One study published this month demonstrated that patients with SIBO do have significant delays in small bowel transit time (the amount of time it takes something to move through the small bowel). This finding suggests that patients with SIBO, who do not recover after a standard course of antibiotics, or botanical antimicrobial protocol (which we prefer), may benefit from the addition of a prokinetic agent, which increases the muscular contractions of the small bowel. Octreotide and low dose naltrexone are two such options that are being investigated, and may help treat some cases of SIBO that don’t respond to antimicrobials alone.

As research into SIBO continues, we are increasingly understanding the complexity of this disease, and how treatment must be tailored to each individual to maximize success.

Now we’d like to hear from you. Have you had SIBO requiring more than one round of antimicrobial therapy? What helped you recover from SIBO?

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.

This is an important topic and something that’s fairly commonly experienced. There’s not a lot of great information out there in the conventional medical world on how to troubleshoot neuropathy if you’re experiencing it. In this episode, we cover: 2:28 Potential Causes of Neuropathy 5:44 Testing for B12 Deficiency 10:10 Four stages of B12 Deficiency 14:40 Five Potential Causes of B12 Deficiency 17:36 Treating B12 Deficiency  [powerpress] Chris Kresser:  Hey, everyone. It’s Chris here. Steve is away. Unfortunately, he had a death in the family and Jordan is not available. So you’re stuck just listening to me go on and on for this episode. We’ll keep it relatively short, since listening to a monologue is never as interesting as a conversation. But this is an important topic and I figured I would just go ahead and do it, because it’s something that’s fairly commonly experienced, and there’s not a lot of great information out there in the conventional medical world on how to troubleshoot this if you’re experiencing it. Let’s go ahead and listen to the question, and then we’ll get started. Matt:  Hi, Chris. My question is, what sort of dietary changes, lifestyle changes, and possible supplementation would you recommend for neuropathy? As neuropathy can be associated with diabetes, B12 deficiency, toxin exposure, among other things, what tweaks would you make to your approach of those conditions, if neuropathy is also an issue? Similarly, if one just has idiopathic neuropathy, what recommendations would you suggest? Thanks. Chris Kresser:  Again, great question. As is often the case, diagnosis is really key. In functional medicine, we always want to address the underlying cause of a problem. That’s what’s going to lead to the most effective and longest-lasting change and solution. That’s the difference with the conventional model, which is often oriented more around symptoms suppression and disease management, irrespective of the underlying cause. For example, if you have high blood pressure, you take a medication to lower it. If you have high cholesterol, you take a medication to lower it. There’s oftentimes very little investigation into what the underlying causes of those symptoms or conditions may be.

Potential causes of neuropathy

With neuropathy, there are a number of potential causes, too many to cover in detail here. We’re going to focus on the ones that I think are the most common and most likely for listeners to be experiencing. Just to give you an idea of the many different things that can lead to neuropathy: we’ve got B12 deficiency; diabetes; toxic exposure, heavy metals; mold toxicity or something called chronic inflammatory response syndrome (CIRS), which I’m going to be talking more about in the future; liver-kidney disease; infections like Lyme disease; obstructive sleep apnea can worsen neuropathy. Then you have some drugs that have neuropathy as a side effect. Cardiac drugs for arrhythmias, certain antibiotics and antivirals that are used to treat HIV, some blood pressure medications, psychiatric drugs that are used to treat bipolar disorders, and anti-seizure medications. To use a really simple example, if you’re taking one of these drugs and you have neuropathy, the simplest solution would be to talk to your doctor about finding another alternative treatment that’s not going to cause that kind of side effect. But for most people who are listening to this, I imagine that the cause of their neuropathy is something else. B12 deficiency is, in my experience, by far the most common, and definitely the most common in my patient population. Statistically speaking, in the US, probably diabetes is the most common cause of neuropathy, because diabetes is just epidemic at this point. Then things like toxic exposure, mold toxicity, liver-kidney disease, and infections are probably less common causes. Again, the most effective treatment here will depend on the cause. If blood sugar is the issue, diabetic neuropathy, then there is some evidence that a ketogenic diet may be helpful. There’s one account in the scientific literature of a complete reversal of diabetic neuropathy after two months of a ketogenic diet. The caveat is that the study was done in mice, not humans, so we can’t say for sure that that’s going to apply to humans. But we have enough research behind the effects of ketogenic diets in many other conditions with humans that I think it’s at least plausible. And of course, all of the other things that we’ve talked about on the show and on my website and in my book about managing blood sugar, making sure you’re eating enough protein, making sure you’re getting enough exercise, particularly high-intensity exercise and strength training, can be helpful for improving metabolic health.  You want to make sure you’re getting enough sleep. We have tons of research now that shows how poor sleep contributes to diabetes and obesity. You want to make sure you’re managing your stress, reducing your intake of all of the highly-processed and refined foods that contribute to obesity and diabetes, and really focusing on real nutrient-dense, whole foods. We have all those basics. On top of that, doing a ketogenic approach for a period of time might be helpful, as the study I mentioned suggests.

Testing for B12 deficiency

The next cause is B12 deficiency. We’re going to spend a little bit more time on this, because it’s much more poorly understood in general, even in the sort of functional, alternative medicine community I think. I’ve written a couple of articles on B12 deficiency that you should definitely check out, if you haven’t already. If you just Google “Chris Kresser B12,” they’ll pop right up at the top. I go into some detail about the prevalence of B12 deficiency in various populations: omnivores, vegans, vegetarians. We talked about some really important information, not very well-known information about testing and diagnosis of B12 deficiency, which I’m going to kind of review here. Then we talked a little bit about treatment. One of the most important things to understand about B12 deficiency is that the serum B12 is not a very reliable marker for diagnosing B12 deficiency. When you measure B12 in the serum, you’re measuring all of the different cobalamins. Cobalamins are all the different B12 compounds. That ranges from the most inactive forms of cobalamin, like cyanocobalamin, to the more active forms of cobalamin, like methylcobalamin and adenosylcobalamin, which are referred to as active B12. That’s the type of B12 that can actually be delivered, get in the cells, and do what it’s supposed to do. Then there are intermediate forms of cobalamins, like hydroxocobalamin, which are not super active, but more active than something like cyanocobalamin. When you measure serum B12, you’re measuring all of those different B12s. So it would be possible to have a normal or even high level of serum B12, and have most of that be inactive, and still be suffering from B12 deficiency, because you don’t really have enough of the active B12 that gets in the cells. I’ve definitely seen that in my practice when I run B12 tests. Every patient that comes to my practice gets a blood test that includes B12. In many cases, we’ll also go on to do more advanced testing for B12 deficiency, which I’m about to tell you about. And I see many patients who have normal B12 levels in the serum, but have evidence of B12 deficiency using the more sensitive markers. So this is something that’s really important to understand. What are those sensitive markers? Well, the most practical and most available at this time is methylmalonic acid, or MMA for short. You can test methylmalonic acid in the urine or the serum. Methylmalonic acid is an organic acid. It’s a by-product of normal cellular metabolism. It’s converted into succinic acid via a B12-dependent enzyme. That enzyme only can use active B12. So if methylmalonic acid (MMA) is elevated, it suggests there’s not enough active B12 to make that conversion. Therefore, it’s a sensitive indicator for active B12 deficiency. Urine methylmalonic acid is thought to be more sensitive than serum methylmalonic acid as a marker, because MMA is more concentrated in the urine than it is in the serum. But there are a couple of caveats. Urine methylmalonic acid is not accurate in the case of kidney disease. So if you have kidney issues, it’s not a good marker for B12 deficiency. And serum methylmalonic acid is not accurate in cases of intestinal bacterial overgrowth, which we know is very common. In my patient population, intestinal bacterial overgrowth is far, far more common than kidney disease. In fact, in all the years that I’ve been doing this, I think I’ve only had a few patients with full-blown kidney disease. So I run urine methylmalonic acid as a result, because it’s much more reliable in my patient population. There is another marker that’s even more sensitive for detecting B12 deficiency. That’s called holotranscobalamin (holoTC). HoloTC is composed of B12 attached to transcobalamin. This represents the biologically active part of B12 that can be delivered into the cells.

Four stages of B12 deficiency

There are actually four stages of B12 deficiency. I want to go over them with you, because it really highlights the importance of using this more sensitive testing and the limitations of using serum B12, and then also markers like hemoglobin and red blood cells—the markers of anemia—to detect B12 deficiency. Stage I and II of B12 deficiency is when the plasma and cell stores of B12 become depleted, and transcobalamin is reduced. That’s all that happens in stage I and II. Typically, there are no other noticeable signs or symptoms. That is what holotranscobalamin (holoTC) will pick up. So there’s no other way that we know of right now to detect B12 deficiency in stage I and II, other than holotranscobalamin. Stage III characterizes functional B12 imbalance, which involves elevated homocysteine and blood methylmalonic acid. That’s where you can detect B12 deficiency using methylmalonic acid as a marker, in that stage III. That may manifest in some symptoms, but it’s often not obvious to either the patient or the doctor, that those symptoms are B12-related. I mentioned homocysteine. This is another marker that can be used to detect B12 deficiency at an earlier stage than serum B12. Homocysteine requires B12 and folate to be converted back into methionine. So if you see elevated homocysteine, you can suspect either B12 or folate deficiency. It’s important to understand that homocysteine is not specific to B12. The elevated homocysteine could be more related to folate deficiency than B12, so you can’t use it as an exclusive marker for B12 deficiency. But used in combination with methylmalonic acid, it can be really helpful for detecting B12 deficiency at that earlier stage. Stage IV of B12 deficiency is when the clinical signs and symptoms of it become evident. That’s when you start to see things like neuropathy, anemia, severe fatigue, and other symptoms that develop with B12 deficiency. If you think about this, in the conventional model, most people won’t even end up at the doctor until stage III or IV, because that’s when the symptoms start to become evident. By then, B12 deficiency has already progressed to the later stages. If it’s stage III, the doctor runs a serum B12 test, it’s in the normal range, they’ll say, “Oh, this isn’t a problem. Nothing to worry about.” But if you run homocysteine or methylmalonic acid in that stage, you’ll actually be able to detect it before it progresses into that stage IV, where in some cases, the effects of B12 deficiency, neurological damage, can be irreversible. So it’s really, really important to intervene at an early point here. So why not test holoTC, since it can detect stage I and stage II B12 deficiency? I would love to be able to test that. Unfortunately, it’s not a readily available marker right now. When I wrote the article that I mentioned earlier, Quest Diagnostics had listed it on their website. It’s listed as a test that’s available. But at least here in the Bay Area, it’s not yet available at any Quest lab location. I have yet to hear anyone that’s been able to reliably order it. Hopefully, that will change in the near future. For now, we can use methylmalonic acid and homocysteine to at least detect B12 deficiency that’s progressed to stage III. Fortunately, if you intervene at that point, it’s usually, in my experience, the symptoms of B12 deficiency, including neuropathy, are reversible at that point.

Potential causes of B12 deficiency

Let’s talk a little bit about what the potential causes of B12 deficiency are, because it is, as I mentioned, at least in my patient population, the most common cause of neuropathy. One would be pernicious anemia. This is often missed, I find. I’ve diagnosed several patients with pernicious anemia that didn’t know that they had it. This is an autoimmune disease that involves destruction of the parietal cells in the stomach. The parietal cells are where intrinsic factor is produced. Intrinsic factor binds to B12. The complex of intrinsic factor in B12 is absorbed in the small intestine. If you can’t produce intrinsic factor because your parietal cells are being attacked by your immune system, then essentially, you can’t absorb B12 orally. So people could be eating meat and all kinds of B12-rich foods like liver and shellfish, and they can still be B12 deficient. That’s important to understand, because it’s definitely true that B12 deficiency is way more common in vegans and vegetarians. According to recent tests that have used these more sensitive markers like methylmalonic acid, about 83% of vegans are deficient in B12 and 68% of vegetarians are deficient in B12, versus 5% of omnivores. But an omnivore who has pernicious anemia, for example, could still have B12 deficiency. Small intestinal bacterial overgrowth (SIBO) and low stomach acid can both impair the absorption of B vitamins, including B12. So I see B12 deficiency in people with SIBO. Glutathione deficiency can lower B12 levels, because one of glutathione’s roles is to protect B12 in the circulation. If it can’t protect it, then B12 gets damaged, and it can’t activate the cells as it should. So you could be glutathione-deficient if you have any kind of autoimmune disease, if you’re suffering from oxidative stress, if you’re not sleeping enough, if you’re not getting enough exercise or getting too much. Basically, anything that causes oxidative stress can deplete glutathione levels. Then impaired methylation can cause B12 deficiency or interfere with B12 metabolism. We talked a lot about methylation on a recent episode, so I’ll just refer you to that. Of course, inadequate dietary intake can cause B12 deficiency, which is why vegans and vegetarians have such high levels of B12 deficiency. There are really no adequate sources of B12 in the vegan and vegetarian diet. So if they’re not supplementing with B12 and preferably active forms of B12, then they could definitely have this problem.

Addressing B12 deficiency

In terms of addressing this, if it is B12 deficiency and it is dietary intake, of course, adding animal foods that contain B12 to your diet is a good idea, if you’re open to that. I list what the highest sources of B12 are in the articles that I mentioned, so check that out. Shellfish, organ meats, and meats, red meat in general, are among the higher sources of B12. If you’re going to supplement with B12, it’s best to take an active form. So methylcobalamin and/or adenosylcobalamin, which is sometimes referred to as dibencozide, are the best forms of B12. If you’re dealing with pernicious anemia, SIBO, or low stomach acid, you’re going to have problems digesting capsules or tablets of B12. The best thing to do would be to use a sublingual form, so that the B12 gets absorbed that way and bypasses the digestive route. I think I carry a form of B12 in my store that I recommend, which is Jarrow Formulas sublingual lozenge of methylcobalamin. There are studies that show that higher dose sublingual administration of B12 is as effective as injections in some cases. But what I’ve seen is that while most patients do well with B12 lozenges, sublingual form, some actually do better with injections, and they’re not comparable. So if you’re really dealing with pretty serious neuropathy, you’ve got B12 deficiency and have had it for a while, you’ve tried the sublingual lozenges and they’re not working for you, you may want to talk to your doctor about injections. You can get the active forms of vitamin B12 in injection. The typical injection that a doctor will prescribe will be the inactive form, cyanocobalamin. But you can get methylcobalamin injections. Those will generally be more effective. There are some other supportive nutrients for B12 deficiency. Those include folate; trimethylglycine; vitamin B6, or the active form, which is pyridoxal-5-phosphate (P5P); and vitamin B2, or the active form, which is riboflavin 5’-phosphate (R5P). If you’re dealing with a lot of oxidative stress and glutathione deficiency, then the antioxidants like vitamin A, E, and C, CoQ10, glutathione itself, selenium, which is important for immune regulation and glutathione production, N-acetylcysteine (NAC), and alpha lipoic acid (ALA) can all be really helpful in putting the brakes on oxidative stress. I think we’ll stop there. I know that was a ton of information. I didn’t have Steve to interrupt me and help you to absorb everything. Hopefully, that helps those of you who are dealing with neuropathy, especially if it’s related to B12 deficiency. We’ll talk to you next week. Steve will be back. Keep sending us your questions. We continue to get some really great questions and SI want this show to be all about you and what you want to know, so keep the questions coming in. We’ll talk to you next week.

On Wednesday the 19th I'll be on the excellent new Balanced Bites podcast with Diane Sanfilippo of Balanced Bites and Liz Wolfe of Cave Girl Eats to discuss digestive health. Topics covered will include:

• FODMAPs
• Small intestinal bacterial overgrowth (SIBO)
• Gut pathogens
• Maintaining healthy gut flora
• The best nutritional approaches for gut healing

Leave your questions in the comments section before the end of the day on Thursday (the 13th). Diane and Liz have a great show. If your eyes start to glaze over when people (like me) start rambling about the finer points of scientific studies and physiological mechanisms, but you love practical, down-to-earth discussion about Paleo food and nutrition, their podcast is for you. Check it out!

In this episode I answer frequently asked questions about digestion, covering topics like parasites, stomach acid, the GAPS diet, SIBO and more. Questions include:

• How to differentiate between a gut infection and food sensitivities?
• How to boost your HCL production
• Can strengthening the immune system take care of parasites?
• When to call it quits on the GAPS diet
• Is FODMAP sensitivity permanent, or can it be treated?
• What causes digestive reactions to carbohydrates?

The next podcast will be our last with Danny. We'll make it a good one! [powerpress]

Full Text Transcript

Danny Roddy:  Hello everyone, and welcome to the Healthy Skeptic Podcast.  My name is Danny Roddy of DannyRoddy.com, and with me is Chris Kresser, health detective and creator of ChrisKresser.com.  Chris, how are you doing, my friend? Chris Kresser:  I’m good.  A little sleep deprived, and I can’t blame Sylvie this time. Danny Roddy:  Well, you just showed me why.  Why don’t you tell everybody listening why. Chris Kresser:  Yeah, so I’m super excited about this program that I’ve been slaving away on.  You know, I’ve been working with people on health-related issues for a long time now, probably, I don’t know, over 10 years, and there’s absolutely no doubt that the biggest issue that I see in my practice and I hear about from people on my blog and who listen to the podcast is confusion about what to eat.  I’m sure you see this a lot, Danny, too.  I mean, people are basically paralyzed because they don’t know what to eat.  And I have patients that tell me they feel like they’ve got this voice in their head like everything they could put in their mouth is wrong or bad from one perspective or another. Danny Roddy:  I can find a reason not to eat anything. Chris Kresser:  Right, except air, right?  You could be a breatharian, but actually you can find a reason not to do that because you’ll starve to death.  So, I created this new online program called the Personal Paleo Code, and it was born of my experience working with hundreds of patients and hearing from thousands of blog readers and podcast listeners around the world, and it includes a 3-step process to help you figure out exactly what works and doesn’t work for your body.  So, rather than following a canned approach, however good of a starting point that canned approach is, it will never be totally customized for your particular body.  So, I have a process that I use in my practice for helping patients to figure out what that is, and the feedback has been so good, and it seems to be so effective that I just wanted to share that with a wider audience.  So, the core of the program is that 3-step process for determining what your own optimal diet is instead of following some guru’s advice, including mine! And then the second part, which I’m really, really excited about, is we’ve built this meal plan generator.  It’s a web application, and it allows you to create a completely customized meal plan using only the ingredients you want to include.  So, you open it up, and let’s say you’re on an autoimmune Paleo diet, and you want to keep it under 50 grams of carbohydrates.  All you do is select remove nightshades, remove dairy, and then there’s a little button that says keep it under 50 grams of carbs, and then you can generate a single meal, you can generate a one-day meal plan, or you can generate a one-week meal plan.  And then all of those meals pop up on a grid, and they’re hyperlinked so you can click on the recipe and it goes to the single recipe page, picture, instructions, everything.  You can print that out.  You can print out the whole meal plan.  And you can save recipes to favorites.  You can search; it has a full search function.  It has an index so you can look up recipes by category, like if you only want to look at breakfast or you want to only look at snacks.  So, this is just incredible.  My wife, Elanne, is more excited about it than, I think, anybody else, because it’s pulling recipes from all of the, in my opinion, best Paleo recipe sites, like Health-Bent and Nom Nom Paleo and Paleo Diet Lifestyle.  And we’re gonna launch with over 300 recipes, but we are just gonna keep adding recipes as we go each month, so that’s awesome. And then we’ve got all kinds of extra stuff.  Like, we’ve got guides on fermented foods; on fats and oils, you know, which ones to cook with, which to use cold, which to avoid completely; nuts and seeds, you know, how to properly prepare them, which I’ve written about recently; how to make bone broth, because that’s something I think that’s often overlooked as part of a healthy diet.  We’ve got even a guide on kitchen equipment, like my picks on particular kitchen stuff that’s good to have around.  We’ve got special tweaks for blood sugar and thyroid issues, weight loss, autoimmune disease, and other health conditions, so it’s kinda like being a patient in my practice without actually being a patient, but even a lot more beyond that with the meal plan generator.  And then we’ve got another web app called the progress tracking app, where you can go in there and fill out a questionnaire each week, and then you get to see your progress charted on a graph as you move through the stages of the program.  So, yeah, I’ve been a little busy! Danny Roddy:  I don’t understand how you have a new child and you put all this together.  It consumed my whole life writing, like, 40 pages, and you get all this done.  Unbelieveable. Chris Kresser:  I don’t know.  I’ve definitely brought on more help this time around, so that makes a big difference, but I have to say the last several weeks have been probably the most productive period of my life somehow.  I don’t really understand it either.  So, the other thing I want to mention is we’ve finally figured out a name.  You know, we’ve been talking about changing the name of the show, and we’re gonna do that.  It’s gonna be called Revolution Health Radio.  Probably the logo will have some kind of wordplay with revolution, evolution, evolutionary health.  And radio over podcast because I’ve just never really liked the term “podcast,” and this is my show, so I get to choose!  I’d rather have a radio show than a podcast, so it’s Revolution Health Radio.  We’ll have a new graphic, new show title in iTunes.  You don’t have to do anything, dear listener.  You’ll just notice that next week Danny will say, “Welcome to Revolution Health Radio,” and that’s it. Danny Roddy:  I might screw that up, though, Chris. Chris Kresser:  That’s all right.  You’re allowed.  You get a couple times before you’re fired! Danny Roddy:  Good thing I edit this show. Chris Kresser:  Right!  So, what’s happening with you, Danny? Danny Roddy:  Nothing much.  Just wrapping up, kinda sitting on the book, tweaking a few things because I’ve actually had an amazing chance to work with a couple people, so it’s really putting a lot of my ideas to the test, and I’m getting a lot of feedback from them.  Like, they fell in my lap, so I’m really thankful. Chris Kresser:  That’s where the rubber hits the road, huh? Danny Roddy:  Exactly, like, you get to kinda test out your ideas every day, where I meet with a lot fewer people, or I only really correspond with people over Facebook or email.  So, it’s exciting. Chris Kresser:  Yeah.  I keep waiting for you to send me the damn book! Danny Roddy:  I will as soon as it’s finished. Chris Kresser:  Are you making me pay for it?  Is that what it is? Danny Roddy:  No! Chris Kresser:  I’m happy to pay for it! Danny Roddy:  With that said, do you want to get to our first question, Chris? Chris Kresser:  Yeah.  We’re gonna do an episode about digestion.  So, I was on the awesome Balanced Bites Podcast.  I hope you guys all go listen to it.  It’s Diane Sanfilippo and Liz -- Do you know Liz’s last name?  I feel bad. Danny Roddy:  I don’t.  I’ve just met Diane at AHS. Chris Kresser:  Cave Girl Eats, right?  But they have a great podcast, and Diane totally gets the science, but she’s really into breaking it down into an easy-to-understand format and really focusing on the nutritional angle.  It’s an awesome show.  You should check it out if you haven’t already.  And she wanted to have me on to talk about digestion, and I did a blog post soliciting questions about digestion, and we got, like, 60.  So, obviously we didn’t have time to answer them, and I thought it would be a good idea to try to get to some of them, just to do a whole show on digestion, so here we are.

How to differentiate between a gut infection and food sensitivities

Danny Roddy:  Let’s do it.  This first question is from Emm.  She asks:  “I’ve been trying to follow a Paleo diet since I got a bad GI virus in July.”  She puts in parentheses:  “(I didn’t take any antibiotics, just waited it out), and now my stomach is not the same. I get cramping/pain/bloating after eating any food.  That includes meat, veggies, fruits, white or whole grains, fats, both together or alone.”  She continues and says:  “I followed a Paleo diet with just veggies and meat for two weeks, and I felt like I had knives in my intestines.  The only thing I can digest without incident is freshly made veggie juice.  I take a probiotic two times a day with meals.  Note: Drinking red wine with any food relieves all of my symptoms!  Please help.  I’m slowly losing my daily life, and I need to go back to digesting at least some food again!” Chris Kresser:  Yeah, that’s bizarre.  Drinking red wine relieves all symptoms.  I thought I had it all figured out up until that line. Danny Roddy:  I could guess why that was happening.  I think red wine might increase gastrin? Chris Kresser:  Yeah, I mean, there’s a few possibilities there.  One is just the increase in HCl production from the wine.  Another is that alcohol can be mildly bactericidal. Danny Roddy:  Oh, yeah. Chris Kresser:  Although, I mean, you hear about people drinking, like, a fifth of tequila or something in Mexico if they get sick with a gut infection.  I don’t know that the same principle applies here.  But let’s back up a little bit and talk about her exposure to the GI virus.  So, I’m not so sure that that was a virus.  It’s possible it was a parasite or something else.  I mean, the symptoms can be really similar, and if she continues to have symptoms after a while, one possibility is that it was a virus that just really altered the gut flora and caused some gut-brain axis issue.  But another possibility is that it wasn’t a virus and it was a parasite or an opportunistic or pathogenic bacteria and that she still has it and that’s why she continues to have the symptoms she has.  That’s actually fairly common in my practice, and when I see somebody who has made all of the dietary changes, you know, they’re eating a clean diet, and they’ve been doing that for a while, and they’re still having crazy symptoms no matter what they eat, that’s a big red flag for me to start going looking for an infection.  And I would do a stool test.  I use Metametrix.  I prefer them over other labs.  And I would try to at least rule that out, if there is something present that’s causing this continuation of symptoms, because that’s definitely my guess. Danny Roddy:  I’m actually trying to reference it.  Paul Jaminet.  He was saying there was some way, like, depending on if you had really bad gas you could find out what kind of infection you had, but you were saying if it’s persistent, then it’s more likely a parasite. Chris Kresser:  Yeah, I think it’s more likely a parasite or bacteria than a virus that was just passing through.  Like, stomach viruses tend to be transient, you know, just in the same way that you get a cold.  But parasites tend to stick around unless you treat them.  That’s what they do.  I think what you might be thinking of is Paul, when he was on the show, was talking about how ketones can feed yeast, and a ketogenic diet can actually be harmful when someone has a yeast infection, and I think that’s one of the perils of the GAPS diet, and we’re gonna talk about that later in another question.  But for now, I would say to Emm the first thing to do would be to get a Metametrix stool test.  Usually you have to work with a practitioner for that because they don’t deal with the public directly, and at least rule out some type of pathogenic infection that’s still present, because that would be my guess, hearing those symptoms. Danny Roddy:  Cool.  Good stuff.  I’m looking at Paul’s thing.  It was the difference between bacteria.  He says bacteria tends to produce more acute transient postprandial symptoms like gas and bloating.  OK, I’m thinking of fungi.  And he says fungi tend to produce more chronic, slowly varying symptoms, like from circulating toxins. Chris Kresser:  Systemic, yeah.  I would agree with that for the most part.  There are certainly chronic bacterial infections that can produce chronic and slowly changing systemic symptoms, but in general, that’s a fair characterization, I think. Danny Roddy:  Would there be a way of telling if it was a parasite or a fungus, or is that where testing would be really helpful? Chris Kresser:  Yeah, that’s where testing would be helpful, but some of the cardinal symptoms of parasitic infections are cyclical symptoms because parasites have specific life cycles.  So, if I have a patient that is basically fine or does pretty well for 10 days and then has an intense flare-up of symptoms for a few days and then does well for 10 days and then has an intense flare-up and it’s pretty regular like that, that can be a real sign of parasitosis.  Extreme hunger even after eating is another typical sign of parasitosis.  Skin stuff can be either fungal or a parasite.  A strange test in the mouth, like a bitter or metallic taste, can be parasitic.  So, there are some things that make me think in that direction, but it’s difficult to do without a test.  And let me just say that you don’t need to go to a third world country to get a parasite infection.  In fact, most of my patients that have parasite infections have not done third world travel, so they’re all around us in the environment, even here in the highly sterilized first world country we live in.

How to boost your HCl production

Danny Roddy:  OK, this is the next question.  This is from Daisy, and this is a related question:  “How can I boost my HCl production?  From what I understand, we all lose the ability to make enough as we age and lack of it is the root of all sorts of issues.”  And she notes:  “Excess gas, bloating, general belly discomfort after eating, candida overgrowth, recurrent UTIs.  Have I understood right, and if so, is there an alternative to lifelong supplementation?”  She she adds:  “I know it’s a good idea not to drink loads of water while eating because I might choke :), but could low level, chronic dehydration have an effect on stomach acid production?”  What do you think, Chris? Chris Kresser:  OK, so in order to answer the question how can I boost my HCl production, we, of course, always want to ask the other question, which is what’s causing the decline in stomach acid production?  There are some common causes of that.  The most common ones would be obviously drugs that decrease stomach acid production.  So, those would include the obvious PPIs and over-the-counter acid-suppressing drugs, but they also include drugs like antibiotics and birth control pills.  And the second thing would be H. pylori infection.  So, H. pylori, Helicobacter pylori, is the bacterium that has been shown to contribute to ulcer formation, and this was a pretty interesting story. . . thinking if I want to go there. . . no, I don’t.  We probably don’t have time.  I like to ramble off on those tangents sometimes, but basically I’ll give you the short version because it is pretty cool.  It used to be thought that ulcers were caused just by stress, and there was a guy in Australia, a doctor who came to believe that they were actually caused by a bacterium called H. pylori.  Nobody believed him.  He presented this data at medical conferences.  He was basically laughed off the stage, and growing increasingly desperate over the years, he finally decided to swallow a vial full of H. pylori. Danny Roddy:  Shut up.  Really? Chris Kresser:  I’m not joking.  This is 100% true. Danny Roddy:  I didn’t know that’s how -- Chris Kresser:  This is commitment to science, OK?  Or being right!  I don’t know what was driving him, but his name is Dr. Marshall, I think.  And he swallowed the H. pylori, and lo and behold, he developed an ulcer, which he did not have before.  And then the coup d'etat was that he treated himself with an antibiotic and cured his ulcer.  So, even after that, believe it or not, people were still skeptical for a while, I mean, which is just crazy.  Shows you how hard it is to change the dominant paradigm.  So, he ended up winning the Nobel Prize for Medicine, so he got the last laugh, right?  Anyways, we know now that H. pylori does contribute to ulcers.  It’s a very common infection.  By the time we’re 55 years old, one in two people have H. pylori.  Some people believe it’s a normal resident of the digestive tract, and the evidence that supports that is that H. pylori has been shown to have some pretty positive immunoregulatory effects.  So, we evolved over millions of years with pathogens, and some of those pathogens actually exist in a symbiotic relationship with us, so they tune our immune system, they affect our genetic expression.  Actually a lot of what used to be called junk DNA, which is now called noncoding DNA, is thought to have been originally derived from retroviruses.  So, essentially a lot of our genetic code is from viruses that we evolved with over time that came to play an important role in our genetic evolution.  H. pylori, however, when it becomes overgrown, that’s when it is an issue.  So, for a lot of people who carry H. pylori it’s probably not an issue if they have a good balance of gut flora and a healthy gut environment, but when it becomes overgrown, just like when anything becomes overgrown in an ecosystem, that’s when all hell breaks loose. In the case of H. pylori, one of its survival strategies is to suppress stomach acid production because one of the purposes of stomach acid is to protect us from pathogens.  Pathogens can’t live in a highly acidic environment.  Most of them can’t, anyways.  So, H. pylori is pretty clever.  It goes in the stomach and suppresses stomach acid production so it can survive.  So, I think for people, especially people over 50, one of major causes of declining stomach acid production is H. pylori.  And so, in that case, I would want to treat the H. pylori, but the way I do it is a little bit different than the conventional approach, which is to eradicate it completely.  The more I work with people, the more I think it doesn’t need to be eradicated completely for the reasons that I just said, you know, if it’s a normal resident of the digestive tract and it’s a question of optimizing and normalizing the environment or the ecosystem instead of total eradication, which can actually cause a lot of other problems.  The number of antibiotics you have to take and the intensity of that course of antibiotics you have to take to fully eradicate H. pylori is gonna eradicate a lot of other stuff too, good stuff, good bacteria that we need to perform all of the functions that good bacteria does, like digesting food and regulating the immune system. So, I would say, obviously don’t take any drugs that suppress stomach acid production.  I would say treat H. pylori.  I would say another cause is stress.  So, acute stress can actually increase stomach acid production, and most people probably experience that, but chronic stress has the opposite effect; it decreases stomach acid production over time.  So, taking steps to manage stress is important.  And then, eating fermented foods, using apple cider vinegar and, to some extent, alcohol, as we talked about in the last question, can promote stomach acid production.  So, those are some ideas. Danny Roddy:  What percentage of your patients do you think have H. pylori?  I remember Stephan’s article, and he pointed to some article on PubMed that said, like, 80% of Americans or some ridiculously high number. Chris Kresser:  Yeah, I’ve seen different estimates.  I’ve seen everything from 1 in 2 to up to 80% to 90%.  I think the better question is what percentage have a pathogenic load of H. pylori.  And that’s fairly high, because I have a questionnaire that’s designed to identify low stomach acid production, and like I said, there are other possible causes of that, but I think in a lot of cases it’s H. pylori.  And I would say about 60% to 70% of my patients have low stomach acid.  So, it is definitely a big deal.  The last part of her question, the reason it’s not a good idea to drink a lot of water while eating is that it can dilute the stomach acid, right?  So, if you fill up your stomach with water, then the stomach acid is not gonna be as effective as it would be if you’re just eating the food.  Chronic dehydration effect on stomach acid production -- I’m not aware of any particular link, but dehydration can cause so many problems that I wouldn’t be surprised.

Can strengthening the immune system take care of parasites?

Danny Roddy:  Good stuff.  This next question is from Brianna, and she asks:  “Can strengthening my immune system alone take care of a parasite issue?” Chris Kresser:  It’s possible, but I rarely see that.  Parasites need to be treated, in my experience.  And I might surprise some people here when I say this, but I think in a lot of cases drug treatment for parasites is actually a better choice than natural treatment. Danny Roddy:  Bite your tongue! Chris Kresser:  Yeah, exactly!  You know, my philosophy on medicine has always been whatever works and causes the least harm.  I’m really not that dogmatic.  Of course, I prefer natural approaches because I think they satisfy that criteria more often.  They work well, and they’re less likely to cause harm, so I prefer them.  But if a drug satisfies that criteria and I think it’s a better choice than a natural alternative in that it causes less harm and it’s more effective, I’m gonna recommend that, and that’s true, like in cases of people with Hashimoto’s, I think taking thyroid hormone is a good idea for most people.  Low-dose naltrexone we’ve talked about a lot on the show, and I think that’s one of the classic examples.  I mean, if you can take a very safe low dose of a drug like that and avoid life-altering drugs that are common in conditions that people take LDN for or the intense suffering and increased risk of complication for other diseases, then I’m all for it 100%.  And with parasites, it’s not a hard-and-fast rule, and it’s a case-by-case decision in my practice, but in some cases with certain parasites, particularly the ones that are really difficult to treat, like Blastocystis hominis and Dientamoeba fragilis, I will often refer a patient out to a doctor to do a particular antibiotic protocol that I’ve learned about from the clinic in Australia that is more experienced treating parasites than just about any other place I know about, because what I’ve seen is that those drugs work and they work pretty quickly, and so, yes, there is some damage to the gut flora, but often with herbs for parasites, you have to take them for a really long time for them to completely get rid of the parasites, and even then they don’t necessarily always work for the more virulent ones.  And that means that over that entire time, you’re taking pretty intense antimicrobial substances that are gonna have an effect on the gut flora and that are gonna be really depleting.  So, in my experience personally, a lot of people know that I got into this whole thing, medicine and my blog, because I was infected with several parasites when I was traveling in Indonesia back in 1998.  And it was a long, multi-year process of figuring out how to deal with it, and I took a lot of herbs during that time because that was my inclination and I was studying Chinese medicine, and the herbal formulas that I took kind of wrecked me more than the drug treatments that I ended up doing, and they didn’t work as well.  So, once again, it’s never black or white.  That’s why I try not to be dogmatic about things.  Whenever I think I have an approach that works, there’s always an exception that comes up. Danny Roddy:  Well said.  At least in the case of thyroid, is it true that traditional diets used to contain a fair amount of thyroid, so in a sense, taking something like Armour or desiccated thyroid you are kind of getting back to the roots of a traditional diet that would have contained -- I think I read something that almost 1/2 grain of thyroid would have been consumed daily? Chris Kresser:  I haven’t read that.  I haven’t thought about it that way, but that’s interesting.  I think yes and no.  I know a lot of people are supplementing with or taking thyroid hormone, and I’m a big fan of that when it’s necessary.  I’m not such a big fan of just kind of the idea that everybody should take thyroid hormone, and there is that idea out there in natural medicine.  A lot of patients come to me and they’re taking Armour or something, and I say:  Oh, so you have hypothyroidism?  And they’re like:  No, I was just seeing a naturopath and they thought, you know, since I was having some trouble with weight loss that I should take Armour.  And I’m not really a fan of it in that respect, because taking thyroid hormone when you don’t need it can really trash your adrenals, and I have a lot of patients in that category who have been on thyroid medication for a long time, they didn’t need it, and that really kind of worked over their adrenals because it up-regulates your metabolic rate, and it’s kinda like having the idle of your engine of your car turned up too high for too long, and that’s gonna shorten the lifespan of the engine and cause other mechanical problems.  So, I think eating actual thyroid gland and even maybe taking some glandulars for people who might have a subclinical hypothyroid condition, there’s something to be said for that, but -- and I’m not saying you were suggesting this, Danny -- but just I see a lot of people in my practice who are taking thyroid medication that don’t need to be. Danny Roddy:  Totally.  I wouldn’t suggest it either.  And also taking thyroid can increase the need for almost every nutrient, so if your diet isn’t in place, it’s really -- Chris Kresser:  Bad news.

When to call it quits on the GAPS Diet

Danny Roddy:  Playing with fire, yeah.  All right, this next question is from Kaitlyn:  “I’ve been following your recommended diet for about 1-1/2 years now.”  I didn’t know you had a recommended diet!  “Started GAPS Intro four months ago but can’t comfortably move on to Full GAPS.  I feel like I have more constipation and more bloating problems as I’m purposefully trying to heal my gut flora than I ever did before starting GAPS.  How is that possible?”  So, she’s having more issues since going GAPS.  She goes on to say:  “Pretty frustrating.  My husband has been eating the same as me and also can’t move on to Full GAPS.  He now has persistent bloating and diarrhea but never had either before GAPS.  We both consume plenty of fermented foods, Bio-Kult, and fermented cod liver oil.  I take magnesium supplements each day to try to prevent the constipation, but my husband does not use magnesium since his digestion tips the other way.”  I don’t know what. . . oh, OK. Chris Kresser:  Because they were using magnesium for constipation, but if he’s having diarrhea, he obviously doesn’t want to do that anymore. Danny Roddy:  Got it, and she asks:  “Are all of these symptoms just part of the long healing process, or is something else going on altogether?” Chris Kresser:  OK, this is a great question.  I’m so glad it came in, because we can cover a lot of important practical and philosophical issues.  So, let’s start with the philosophical.  You know, it’s already a theme in this episode, and I think people know this about me just from listening to my podcast and reading my blog, is that there is no one-size-fits-all approach.  And of course, that’s the whole purpose behind the Personal Paleo Code program that I just created, because I think a lot of the confusion about diet, like people saying:  Well, is white rice OK, or is dairy OK?  The answer is always it depends, and any prescription that claims to be appropriate for the 6-1/2 billion people on Earth is always gonna fall short.  [baby crying in background]  It sounds like Sylvie’s having a little meltdown out there!  So, yeah, I mean, I just can’t emphasize that enough.  And I think that my, sort of, mission is to try to alleviate some of the suffering and confusion out there about diet by getting the message across that the only diet that is the right diet is the one that works for you.  And so, with GAPS, I think the GAPS diet is great.  I use it in my practice.  It’s really helpful for certain people, but it doesn’t work for everyone, and it doesn’t work forever even for somebody that it does work for. So myself, I was on the GAPS diet for about eight months, and then at the end of that eight-month period, things started to shift back in the other direction.  I just started to have some digestive symptoms again, and I started to feel lower energy.  I just wasn’t feeling as good overall, so that was my trigger to start adding things back in.  The first thing I added back in was starch, and I had absolutely no problem with it at all, and I felt great.  It was awesome to start eating sweet potatoes and potatoes and yuca and taro and all of that stuff, and it increased my energy levels, and it made my digestion better.  So, I could have at that point, if I would’ve gone on the Yahoo group for the GAPS diet and said:  Geez, guys, I’m having all these problems.  What should I do?  I guarantee they wouldn’t have told me to start eating starch.  They would’ve said:  Oh, maybe you should be doing more enemas or maybe you should cut back more on the fruit.  Or whatever it is, it would all be in the context of, like, you’re not doing the GAPS diet right and you should try harder, because when people adopt a certain approach, I mean, this seems to be some kind of human tendency, right?  Like being part of a club.  It’s ubiquitous across human culture, and people get really wedded to a particular perspective or approach, and then it’s like that old saying when you have a hammer, everything starts to look like a nail.  And so, if an approach stops working, then rather than saying:  Hmm, maybe this approach isn’t the right one for me, it’s like maybe I’m doing it wrong or maybe I should do it more or harder or better, and I see that a lot on the Internet and within all of these communities around dietary approaches. So, the tricky thing, as Kaitlyn is asking about, is when to know whether it’s just a temporary kind of road bump, a die-off reaction, where maybe you’ve reached another level of healing and there’s another level of bacteria or yeast that are dying and that’s causing the symptoms and you should just push through it or whether it’s actually an indication that this is not the right approach anymore and it’s time to move on.  Unfortunately there’s no easy way to answer that question, and it’s really a case-by-case thing, but I would say in general, if you’ve gone for two, three, four weeks and the situation is just deteriorating, you’re not having any windows of time in that period where you’re actually feeling better, because die-off shouldn’t be just persistently bad without any let-up.  Usually die-off looks like a period of worsening symptoms, followed by a period of improving symptoms, followed by an improving of worsening, like that.  Whereas, something that’s not working, you would just expect things to get worse and worse over time.  So, that’s one possibility in terms of determining when to make the change. Danny Roddy:  Also, let your body guide you, like your skin and your nails, measuring progress in other ways besides just digestion.  What do you think about that? Chris Kresser:  Oh, yeah, absolutely.  I mean, all of the symptoms -- fatigue, skin, hair.  Mood is a big one. Danny Roddy:  Totally. Chris Kresser:  Those should all be considered, and I think she probably is, but it’s a little bit of an art, but I would say that after a few weeks and things are just deteriorating and there is no improvement at all, I would actually start to question whether that approach is going to be valuable over a longer period of time.  Now, more specifically about GAPS, there are a few issues with it and that can make it not helpful or appropriate for certain people.  Number one is that, as we talked about earlier and talked about in more length with Paul when he came on the show, is that yeast can thrive on ketones, and GAPS, especially the Intro GAPS diet, is by definition a very low-carbohydrate diet and will probably be ketogenic.  So, for some people who have a systemic yeast infection, doing a ketogenic diet can actually make things worse, and I’ve seen this in my practice.  What’s a little confusing to me is that it doesn’t seem to always be the case.  Some people tend to improve, so I don’t know how to explain that.  Maybe some species of yeast are more able to utilize ketones than others, I’m not sure.  But I sometimes even use that as a diagnostic protocol.  If you put somebody on a ketogenic diet for a short period of time and they get a lot worse, then that could be an indicator of a yeast infection.  So, that’s one issue.  Another issue is that because it’s a low-carb diet and someone’s on GAPS for a long time, that could affect thyroid function, which we’ve talked about before.  Glucose is required for the conversion of T4 to T3.  There are studies showing that fasting and very low carb diets over a prolonged period can cause a decline in thyroid hormone and conversion of T4 to T3, and T3 is five times more metabolically active than T4, so that’s significant. A third problem is people who have issues with fat digestion.  Some people when they eat a diet that’s extremely high in fat and low in carbs like GAPS, if they have any kind of gallbladder insufficiency, it can be really, really hard on them.  It causes a lot of bloating and pain, sometimes even vomiting and really difficult digestive symptoms.  So, in that case, it doesn’t necessarily mean that the GAPS approach won’t work for them or isn’t a good idea, but they may need some additional gallbladder support to make it work.  And then the other thing I would say is that my diet, actually you could call it Paleo plus GAPS, or you could call it GAPS plus starch, so I’m not that far from the GAPS diet now in the sense that I eat a lot of bone broth, I eat a lot of fermented foods, which are two characteristics of the GAPS diet, but I do eat starch and starch really works well for me.  And what I’ve seen in my practice is that of all the things that are removed from the GAPS diet, starch is usually the thing that causes the least problems for people.  So, if somebody has been on the GAPS diet for a long time and they are starting to have issues, I would suggest adding more starch back in, you know, if it’s been a while since they’ve had the issues, not two days, but if it’s been weeks, like with Kaitlyn and her husband. Danny Roddy:  It’s been a while.  Natasha Campbell doesn’t like starch because it passes through the gut lining easier? Chris Kresser:  Well, the whole principle of the GAPS diet -- We probably should have done this before.  I realize not everybody listening to this even knows what the GAPS diet is.  So, the GAPS diet is very similar to the Paleo diet actually, but it goes a step further.  I removes disaccharide and polysaccharide molecules.  Carbohydrates are broken down into sugar molecules, ultimately into monosaccharides like glucose and fructose.  So, monosaccharide is a single molecule of a sugar, and a single molecule of sugar can be directly absorbed from the gut across the lumen of the intestine into the bloodstream without any additional breaking down.  So, when you eat a carbohydrate, it has to be broken down into those single molecules, monosaccharides, to be absorbed into the bloodstream.  Disaccharides are molecules with two sugars, so lactose is a disaccharide.  And then you have polysaccharides, which have multiple sugar molecules chained together, and that would be a starch.  So, when you eat a polysaccharide or a disaccharide, there’s some digestive action that needs to take place to break those longer-chain sugars into the monosaccharides, the single molecules of sugar, so that they can be absorbed, and that involves the brush border enzymes, which are enzymes on the villi, these hair-like projections on the lining of the intestine, and they need to act on those longer-chain sugar molecules to break them into those smaller molecules, right?  So, what happens with people with gut problems is those brush border enzymes don’t work as well, and they don’t break those longer-chain sugars into the monosaccharides, and as a result, they end up floating around in the gut for longer than they should, and in doing that, they become food for pathogenic gut bacteria and yeast.  That’s the whole theory of the GAPS diet.  So, the GAPS diet removes disaccharides and polysaccharides and only allows the simpler sugars like glucose and fructose and fruit.  So, not only does the GAPS diet eliminate grains, which the Paleo diet does too, it also eliminates all starch, so no sweet potatoes, no potatoes, none of the starchy tubers that the Paleo diet does allow. So, what I’m saying is that what I’ve seen is that if somebody goes on the GAPS diet for a while and they reach a point where Kaitlyn’s reached or I’ve reached and they start adding starch back in, that can sometimes be helpful, and I think one of the reasons behind that is that when you only eat the single-molecule sugars, the monosaccharides, then in addition to starving the bad gut flora, you can also end up starving the good gut flora.  And when you’re eating a lot of fermented food, that may not be a problem, but for some people even who are eating a lot of fermented food, it does seem like it is a problem.  And then adding the starches back in, starches have a prebiotic effect, meaning they stimulate the growth of certain species of bacteria in the gut, and then people’s stools might tend to normalize and their digestive system just starts to work better.  So, yeah, it’s a really individual issue, but those are some of the variables to consider.

Is FODMAP sensitivity permanent, or can it be treated?

Danny Roddy:  Great stuff.  OK, this next question:  “I’m curious why and how a person develops a sensitivity to FODMAP foods, and is there any way you can heal it or if one just has to avoid these problem-causing foods forever.  For me, apples and onions cause a lot of digestion pain.  These are foods I’ve been eating since I was a baby.”  What do you think about FODMAPs? Chris Kresser:  Yeah, I talked about this a little bit on Diane’s show, but I think FODMAP intolerance is a symptom of a deeper problem usually.  I don’t think anyone is born with FODMAP intolerance, for example.  But I think it’s probably a consequence of small bowel bacterial overgrowth or any other kind of dysregulation of the gut flora, which could also include a pathogen like a parasite or yeast or pathogenic bacteria.  So, my approach, I do use the FODMAP diet in my practice.  I talk about it in the Personal Paleo Code as one possible adaptation to digestive issues, but it’s more of a temporary thing to provide some symptom relief while we figure out what those underlying issues are, and then oftentimes people will be able to add back in at least some of the FODMAPs once those issues are resolved.  It probably bears noting that a lot of the FODMAPs are things we shouldn’t be eating anyways, like wheat flour.  And for those of you who don’t know, who are just swimming in acronym soup right now and have no idea, with GAPS and FODMAPs and all that stuff, FODMAP stands for fructo-, oligo-, disaccharide -- What’s the M, Danny?  I always forget the M. Danny Roddy:  I have no idea. Chris Kresser:  P is polyols, sugar alcohols like sorbitol and stuff like that.  Anyways, it’s similar actually to GAPS in the sense that there are these certain foods that this theory holds are more likely to be undigested and unabsorbed, and then they become food for pathogenic gut bacteria, and that’s what causes the symptoms. Danny Roddy:  Here we go:  fermentable oligo-, di-, and monosaccharides, and polyols. Chris Kresser:  Right.  So, catchy name.  You can see why they’re going with FODMAP!  Yeah, this is, like, fructans and then fructose, not all fructose, just any excess fructose.  Fructose can be well absorbed by the body when there is a sufficient amount of glucose that’s eaten with it.  So, if somebody eats a food like a banana that has equal or greater amounts of glucose than fructose, then they shouldn’t have any problem digesting the fructose, but if someone with FODMAP intolerance eats a fruit like a pineapple that has a lot more fructose than glucose, than that excess fructose is what causes the issue.  Yeah, these are foods that are all aggressively fermented by the bacteria in the gut when they’re undigested, and again, I think it’s a result of already dysregulated gut flora and that if you deal with that, you usually can reintegrate some of the foods, not always, but in most cases in my practice.  And dealing with the pathogen is one step, but also restoring healthy gut flora using probiotics is another.  Let’s go on to the next one.  Got one more, maybe?  We have time for one more.

What causes digestive reactions to carbohydrates?

Danny Roddy:  Time for one more.  OK, let’s get to Niklax’s problem.  He or she says:  “My problem is bloating from carbs.  It doesn’t really make much sound, but it looks like a beer belly although my BMI is OK.  Switching to a VLC diet solves the problem, but I am fed up with eating so much fat all the time.  Also quite fond of rice noodles and potatoes.  Is there a solution?” Chris Kresser:  So, yeah, I think this is closely related to the last question and the earlier question.  Carbohydrate intolerance is almost always a sign of messed-up gut flora because, as I was just explaining, when carbohydrates remain undigested in the small intestine, they provide food for pathogenic gut bacteria, and then when those pathogenic gut bacteria are killed by the immune system, they release toxins.  Those toxins can cause all kinds of symptoms ranging from brain fog and depression to leaky gut, skin conditions like psoriasis and eczema, etc.  Also the process of the bacteria fermenting the carbohydrate produces gas, and that gas is what produces that beer belly type of bloating that he or she is talking about.  So, one possibility is to get some testing done to see if there is a pathogen present.  There’s a small bowel bacterial overgrowth breath test that you can do to test that out, and then dealing with those issues and restoring healthy gut flora would be the thing that you would need to do to increase the carbohydrate tolerance so you can expand your diet and eat a broader mix of macronutrients.  I think that’s it. Danny Roddy:  Killer, Chris.  That’s gonna bring us to the end of this week’s episode.  Chris, where can we find more of your work on the Internet this week?  What are you working on? Chris Kresser:  OK, so we talked about the Personal Paleo Code in the beginning of the show.  This show is gonna be released on November 1, so the actual program itself is gonna be ready is about a week from today, you know, today if you’re listening to this on November 1.  But right now, I’m doing a promotion where I’m given away a free iPad 2. Danny Roddy:  Oh, my god. Chris Kresser:  Yes.  I hope I win!  No, I’m just kidding.  I’m not gonna win.  So, if you can help me get the word out, I’m really excited about this program, I want to get the word out far and wide, and so I’ve created this page, a landing page that describes the product.  I have a little video of me talking about it and just a couple short bullet points, gives the basic idea.  And if you go there, it’s iPad.PersonalPaleoCode.com, and if you pull that up and you share that page on Facebook or Twitter -- you can use either one, and you can change the text.  I mean, there’s some text that’s prepopulated in there, but you can change it if you want.  You share it on your Facebook or Twitter account, help me get the word out, you’ll be entered into this drawing to win the free iPad.  It’s a 16GB black one with Wi-Fi, and the contest is over on November 20.  And then by entering that contest, you’ll also be put on the email list where I’ll send you an email once the product is ready.  We’re gonna be offering a discount for my podcast listeners and blog readers and faithful fans, and that’ll be available for only a couple of weeks after the product launches.  So, yeah, if you’re interested in an iPad, which is actually a perfect way to access this content so you can be in the kitchen and pull up a meal plan on the iPad and check it out before you make some food for the day, I’d appreciate you helping me get the word out, and I wish you luck in winning the iPad!  I’ll be jealous.  Let’s see.  What else?  I think that’s it.  I mean, we’re changing the name of the show next week, like I said, and yeah, that’s it.  I think I’m gonna take a rest for a little while. Danny Roddy:  You can find all of my work on DannyRoddy.com.  Hopefully, I’ll be releasing my new book, Hair Like a Fox, sometime next month.  The ETA is unknown at this time. Chris Kresser:  C’mon, Danny, get with the program.  We’ll all waiting with bated breath! Danny Roddy:  But keep sending us your questions at ChrisKresser.com using the podcast submission link.  If you enjoyed listening to this podcast, head over to iTunes and leave us a review.  Thank you for listening, and thank you for your support. Chris Kresser:  Thanks everybody.  Good digestion to all of you!

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.

“Test. Don’t guess.” One of the tenets of functional medicine is you have to address the underlying cause of a problem in order to get the best result long term. You can’t address the underlying cause if you don’t know what it is. If you just assume that it’s yeast overgrowth based on some symptoms, that’s not really adequate in terms of making a diagnosis because the symptoms of fungal overgrowth are extremely nonspecific. Find out what you’re dealing with because the treatments will differ.

In this episode, we cover:

2:06  What Chris ate for breakfast 5:20  Is it really yeast overgrowth? 10:28  Diet for treating yeast overgrowth 21:51  When to use antimicrobials 24:15  Restoring and rebuilding the gut

[powerpress] Steve Wright:  Good morning, good afternoon, and good evening. You are listening to the Revolution Health Radio show. I’m your host, Steve Wright, co-author at SCDlifestyle.com. Revolution Health Radio is created for you and by you. It’s also brought to you by 14Four.me. 14Four.me is a 14-day healthy lifestyle reset program Chris has put together. Based on just working with hundreds of people and interacting with thousands of people on his blog, he has really realized, much like I have, that it’s just really hard to implement things that we talk about when it comes to healthy habits. Sleep, diet, exercise, and stress are all major components that we talk about on the show all the time. But to do them all at one time is pretty much guaranteed in the research literature, unless you have someone holding your hand, you’re going to fail. So 14Four.me does that in 14 days, where step by step, day by day, Chris actually walks you through how to do all of these healthy habits at the same time, so that you can do 14 days of really resetting, getting back to zero, and hopefully starting your new year off or whatever month it is right. If you haven’t checked it out yet, go over to 14Four.me and do that now. As always, with me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, how are you doing today? Chris Kresser:  Good, Steve. How are you? Steve Wright:  I’m pretty pumped, man. Chris Kresser:  All right. Steve Wright:  It’s a good day. Chris Kresser:  Good day. Yeah, it’s a beautiful day here as well. We have a good question. It’s one we get a lot and one that I think a lot of people are going to be interested in, and one that there are quite a few amiss and maybe misconceptions about.

What Chris ate for breakfast

Steve Wright:  Before we get into that though, Chris, we can’t go too many episodes without finding out what you were eating before the episode started. Chris Kresser:  Right. Not much to report today: coffee and cream. You know, we record the episodes a few weeks before they’re published, so this is actually right before Christmas. Lots going on. I’m getting on a plane soon to go visit family. There’s a lot happening. It’s a perfect opportunity to do some intermittent fasting. So that’s what I did today. Steve Wright:  Awesome. Yes, and that’s why my background is slightly different than the white walls. I’m at my parents’ house here in Michigan. Chris Kresser:  Nice. You don’t have the impressive phone cave that I have and that you normally have on. Steve Wright:  No, no. The audio quality is not going to be quite as well, but the background is a little bit more interesting. Chris Kresser:  Better scenery. Steve Wright:  Exactly. Chris Kresser:  Cool. Let’s give this question from Nada a listen. Nada:  I have a question for you about yeast overgrowth. I’ve been on the GAPS diet for about six months now. I’ve gotten better, but still having some symptoms, so I went to a holistic practitioner. She did the Metametrix test, the TRIAD test. It confirmed I had a yeast overgrowth. She wants me to start adding potatoes and things like that back into my diet, but I’m really scared to because I know that disaccharides are hard to digest. So I wanted to know what your recommendations are about yeast overgrowth, treating Candida, and sealing the gut barrier. Chris Kresser:  All right. Again, this is something that so many people are interested in. If you do some searching for Candida or yeast overgrowth on the Internet, you’re bound to just get bludgeoned with a crazy level of information. And a lot of it’s pretty kooky and quacky and unreliable. So I’m glad to have a chance to address this. I mean, we’ve talked about it here and there in the past, but it’s good to just do a really focused episode on it. Steve Wright:  Before you dive in, Chris, I just want to let everybody listening know that if you’d like to have your question answered, go to ChrisKresser.com/podcastquestion. Go there. Chris Kresser:  Hijack the show. Steve Wright:  Yeah, hijack the show. You want to talk to us? You have to go there. Chris Kresser:  Thanks for reminding me. It’s so great, as Steve said, to be able to make this show super relevant to you and your needs, and what you want to hear about. That’s really how it works. Definitely head over there and record a question. We want to hear your voice.

Is it really yeast overgrowth?

All right. I’m going to break this down into a few different categories. The first is not necessary based on what Nada said in her case. Or I’m assuming it’s a her. Sorry if it’s a he. But I want to point this out because it is something that often gets overlooked. It’s important for the general population that’s thinking about this. That is the question—is it really yeast overgrowth? One of my pet peeves is when I hear people say, “Oh, I’ve got yeast overgrowth,” or, “I’ve got Candida,” or, “I’m on a Candida diet.” I ask them, “How do you know that you have Candida?” And they say, “Well, because my tongue is white and I spit into a glass of water, and the saliva…” You know, all of these sorts of tests or even just symptoms that are not reliable as a means of diagnosing yeast overgrowth. There’s always an assumption made that it’s Candida, which may be, but it could be any number of other fungal species. It’s really important to test. I’ve always said on this show that we’re a big believer in the saying, “Test. Don’t guess.” Because one of the tenets of functional medicine is you have to address the underlying cause of a problem in order to get the best result long term. And you can’t address the underlying cause if you don’t know what it is. If you just assume that it’s yeast overgrowth based on some symptoms, that’s not really adequate in terms of making a diagnosis. That’s because the symptoms of fungal overgrowth are extremely nonspecific. What that means is there are things that could be caused by any number of other conditions that aren’t yeast overgrowth: fatigue, digestive discomfort, muscle aches, brain fog, low libido, hormone imbalance, skin rashes. These are all symptoms that could be attributed to Candida or fungal overgrowth, but they could also be caused by a parasite, SIBO, general dysbiosis. Or it could be something entirely different, like chronic infections such as Lyme disease, coinfection or a biotoxin-related illness, like a mold problem, exposure to a water-damaged building, or even potentially an autoimmune condition or a thyroid condition. And those are not all mutually exclusive. You can have fungal overgrowth and those conditions, and they often do go together. But the point is, you need to find out what you’re dealing with because the treatments will differ. I treat fungal overgrowth slightly differently than I treat SIBO, for example, or general dysbiosis or a parasite. Certainly, I would approach autoimmune disease differently than I would approach fungal overgrowth. There are pretty good tests for fungal overgrowth at this point. The best ones are stool tests through Genova (formerly Metametrix) or Doctor’s Data that can detect fungal overgrowth in the stool. You can get a urine organic acids test from Great Plains Laboratory. It’s a good one. Then the Genova Organix Profile is also a good one. They will detect organic acids, which are by-products of fungal metabolism in the urine. If they’re elevated, it’s a sign that there may be a fungal overgrowth. You can also test antibodies to Candida in the blood. So there’s a range of ways that you can get some objective data on whether you have Candida. In this case, as I mentioned, Nada already had the Metametrix test. I’m assuming she means stool, but she could mean the organic acids test as well, I’m not sure, and confirmed that there was a fungal overgrowth. It seems like she’s covered that base. Steve Wright:  Yeah. I think it’s really important, just to kind of reiterate what you were saying there, that a lot of the general symptoms or things that we notice in our lives when we’re sick could be attributed to yeast overgrowth, but they could be attributed to lots of other things. I don’t know what your experience has been, but my personal health history, as well as the people that I’ve worked with and the thousands I’ve talked to, typically, it’s not just yeast. Chris Kresser:  Yeah. Steve Wright:  So this idea of not testing and sort of just—or going off just one test and assuming, “Hey, I found something. That’s it. That’s the one singular root cause.” I think it’s really important to make sure people understand that that could set you back. That sort of belief could set you back quite a bit and have you wasting a lot of time and money. Chris Kresser:  Great point. I agree. I would say maybe 15% of the time or 20% max, it’s just fungal overgrowth without SIBO, parasites or some other issue. 80% or 85% of the time, it’s something else in addition to fungal overgrowth. Great point, Steve.

Diet for treating yeast overgrowth

Moving on to the second point, which is the appropriate diet for treating yeast overgrowth. Nada mentioned she’s been on GAPS for six months. This is certainly a good choice, with some caveats, for yeast overgrowth. Now, if you’re not familiar with GAPS, it’s based on a specific carbohydrate diet. Both of those approaches remove complex carbohydrates—polysaccharides and disaccharides—from the diet. So when we talk about carbohydrates, we’re talking about different arrangements of glucose molecules. We have monosaccharides, which are single sugars like glucose, which are very rapidly absorbed in the upper part of the small intestine. They just don’t require a lot of absorption, because single molecules can pass directly across the lumen of the gut into the bloodstream. Then you have things like disaccharides, which would be lactose, as an example, which have to be split. They’re double sugar molecules. They have to be split into single sugar molecules before they can be absorbed. In people with poor digestion and absorption, fungal overgrowth, SIBO, and these conditions, those disaccharides don’t get properly broken down. They linger around in the gut, and they can become food for pathogenic yeast, bacteria, and other critters in the gut that we don’t necessarily want to be feeding. Then polysaccharides would be starches or any carbohydrates that have longer chains of glucose molecules linked together. They’re even more difficult to break down. That’s the theory with Gut and Psychology Syndrome (GAPS) and Specific Carbohydrate Diet (SCD). So the idea is if you have a fungal overgrowth, you should avoid disaccharides and polysaccharides, because they’re difficult to break down and they may potentially feed these overgrowths or infections. Now I want to point out that overgrowth is probably the best term, because Candida is a normal resident of the digestive tract, as are many other species of bacteria that become overgrown in SIBO. It’s not like you have an infection with a parasite or something that shouldn’t be in the gut but is there. What’s generally happening in these situations is if something that is normally in the gut has become overgrown and overrepresented in relation to some of the other beneficial species of gut bacteria. So the reason I mention that is because it hints at a different approach. The idea is not to just completely wipe out these species, because that’s not even necessarily desirable. The idea is to get things back into balance. That’s really the focus of any kind of treatment for fungal overgrowth. Steve Wright:  That’s such a great point, Chris, that I think has taken a long time to sort of begin to get out in the world. So a lot of the articles people are going to be reading when they have yeast overgrowth are not pointing that out. I think that’s one of those other fundamental beliefs, that if you have the belief that all yeast is bad or something like that, then you’re probably going to adopt a different treatment strategy that I think you and I have both seen to be very ineffective. Chris Kresser:  Yeah. Well, the systemic antifungal drugs are a good example of that. They can just really wipe out fungal species in the body. That can have a pretty dramatic effect. When you move from yeast overgrowth and you start using those drugs, you can have a big improvement in symptoms. But if you take them for too long, you start wiping out the beneficial yeast in the body. Beneficial yeast actually protect against bacterial overgrowth. So ironically, what happens with long-term use of those systemic antifungals is you can have a higher risk of SIBO, bacterial overgrowth, and dysbiosis that’s caused by a lack of beneficial yeast. You know, we need to get away from this warlike mentality that we have with—I mean, I think this came out of the whole age of antibiotics and the discovery that pathogens cause disease. That was an important discovery. But it led to this sort of warlike mentality where we’re going to use these powerful drugs to absolutely obliterate and destroy bacteria and other pathogens. But of course, now we have a much different understanding, where we know that these bacteria are—we live in symbiosis with them. We absolutely depend on them for not only our survival, but for several different aspects of health. So we’ve gotten a little bit overzealous in our killing mentality.  I think in the next—it’s already shifting, as you said, Steve. Within the next 10 to 20 years, there’s going to be much more of an appreciation of balance and regulation of the ecosystem, rather than the carpet bombing type of approach we’ve been doing so far. Back to the diet. The trouble with GAPS and SCD, depending on how they’re done, is that they can be extremely low-carb diets. If they’re extremely low-carb, they can become ketogenic, which means you start producing ketones. Paul Jaminet was one of the first people to start talking about this a few years ago. But there are several studies that suggest that Candida and other yeast can actually thrive on ketones. So this is one of my biggest problems with a very low-carbohydrate diet—GAPS, SCD or even sort of typical Candida diet—that removes every possible source of glucose or sugar in the diet. That can lead to ketone production. Then there are studies, for example, that show that neutrophils, which are white blood cells, are less able to kill Candida when ketones are present. There are studies of diabetic patients with ketoacidosis—you know, a lot of ketone production—developing Candida overgrowth. There are studies of obese people developing Candida infections when fasting causes ketosis. There are studies showing that serum drawn from fasting patients is less protected against Candida than serum drawn after meals, and that antifungal drugs, and I would assume botanicals, tend to work better in a fed state than a fasted state, where ketone production would be occurring. So there’s this whole kind of constellation of evidence that’s pointing to the idea that ketone production is not a good idea. I guess what I would say is if you do do a GAPS or especially like a GAPS intro or an SCD intro, that should probably be temporary. Even then, you might not want to do it so that it’s so low carb. You can test your urine with Ketostix to make sure that you’re not in ketosis and you can eat more of the non-disaccharides—you know, the safe fruits, for example, that are permitted on the GAPS or the SCD diet, if you’re continuing to avoid the disaccharides and polysaccharides, like the starches and the more complex sugar molecules. Steve Wright:  I think it’s important to sort of point out what I think you’re hinting at, which is that these diets—GAPS and SCD, which I’m a big fan of and have done a lot of work around—are not the solution. Chris Kresser:  Yeah. Steve Wright:  It’s another form of sort of starving and destroying. A lot of people, including myself, have gotten a lot of benefit from being on a diet like this. But the idea that any one of these diets is going to starve or kill yeast infection or a SIBO infection is, in my opinion, thoroughly false now. Chris Kresser:  You’re a step ahead of me. That’s point number three that we’re about to make. Steve Wright:  Okay, cool. Chris Kresser:  Awesome. We’re on the same page. Before I go on, I do want to say that generally, in my practice, I don’t start people with GAPS or SCD for fungal overgrowth or SIBO. We use a low-FODMAP diet for those conditions. I find that that typically works very well. FODMAPs are a slightly different take. It’s a similar theory. The idea is FODMAPs are fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. So there are certain types of carbohydrates that are poorly broken down. They become food for the fungal overgrowth or bacterial overgrowth. However, with a low-FODMAP diet, I think it’s easier. There are more carbohydrates that are permitted, including some starches, which might seem contradictory to the GAPS approach. And it is. It’s a different approach. But I found that many people can tolerate some starches on the FODMAP diet if they have fungal overgrowth and bacterial overgrowth. They do well and we see success. You know, we test people and then we retest people after they’re treated. We see the fungal markers and the bacterial markers changing and going away. If they don’t, we might then switch to like a GAPS or SCD intro, as long as there are enough carbohydrates so that it’s not ketogenic. I think either of those will work. Low-FODMAP diet is a starting place. GAPS or SCD, as long as you’re eating enough fruit and carbohydrates, so that you’re not going into ketosis. And again, you can test that with the Ketostix, which are these urine strips. Those are both good choices. Steve Wright:  One thing that neither one of us have mentioned—probably because we don’t like it or don’t like to mention it—is the anti-Candida diet, which anybody who’s Googling this issue is going to run into a thousand websites that talk about this. Chris Kresser:  Yeah. I’m right there with you. I was just about to mention that I’m not a big fan of the anti-Candida diet. I think it’s both unnecessarily restrictive and not restrictive enough. In the unnecessarily restrictive category, it removes literally every source of glucose. I mean, on the extreme versions, you see even carrots and things like that prohibited because they have too much sugar. However, as I mentioned, if you do that, you’re going to probably end up in ketosis, which can actually make things worse. And I’ve just never seen any peer-reviewed evidence that suggests that that’s necessary. In terms of the not restrictive enough, many Candida diets actually permit grains, which is strange when they’re trying to get rid of every source of sugar. Grains are ultimately carbohydrate, for the most part. They’re also poorly broken down for many people because they’re complex carbohydrates. So you’ll see the anti-Candida diet permitting grains, particularly the alternative grains like quinoa, millet, and things like that. I just don’t see those things working well for most people who have gut issues. That’s something to keep in mind. I don’t think the anti-Candida diet is very effective. If it was, you wouldn’t see people on it for years and years having the experience that they have. So that’s something to be avoided.

When to use antimicrobials

Point number three is what you just mentioned a little while back, Steve. That’s this—diet is not typically enough to treat fungal overgrowth and SIBO, in my opinion. It’s definitely a big part of strategy and it’s important. But when we have a patient that has fungal overgrowth or SIBO, we absolutely, without exception, will use antimicrobials. We start with botanicals. 90% of the time, that’s what we use. In some cases where the patient has just recurring, recalcitrant infections, we might start to use some prokinetics like low-dose naltrexone and possibly rifaximin and neomycin, if they have a methane overgrowth, which are medications. But almost exclusively, we’re using botanical, nutrient-based protocols. Some of the ones that we use, that have research behind them, and tend to work well would be undecylenic acid; uva ursi; cat’s claw; pau d’arco; lauric acid, which is monolaurin (Lauricidin); high-dose biotin actually is antifungal, like 5 mg per day; Gymnema sylvestre, which is an herb that has been used historically in India for blood sugar issues because it reduces sugar cravings and helps balance blood sugar, has recently been shown to be very effective in terms of inhibiting Candida growth; Saccharomyces boulardii, which is a beneficial strain of yeast, has been shown to inhibit the growth of Candida and also reduce inflammatory cytokine production that is associated with cells that are infected with Candida; soil-based probiotics like Prescript-Assist are I think effective in terms of outcompeting Candida for adhesion sites in the gut. So all of these things, many of which we’ve talked about before, can be really effective in an overall antifungal strategy. I think they’re very important. And if you’ve been doing a GAPS approach, for example, for six months, and you still have symptoms and you’re not doing these other things, then that’s absolutely something to look into.

Restoring and rebuilding the gut

The last point would be—remember the kind of two-phase approach, which is when there’s any kind of infection, the first phase is clearing out the infection and the pathogens or the overgrowth, if it’s not an infection but it’s an overgrowth. But the second phase is really important as well. That’s restoring and rebuilding. The reason you can’t necessarily do both at the same time is some of the things that you use to restore and rebuild, like prebiotics, for example, can actually make the overgrowth worse. So resistant starch and non-starch polysaccharides, which are FODMAPs, of course, and also prohibited on a GAPS type of approach, they’re really helpful over the long term for restoring, growing beneficial bacteria in the colon. The reason you want to do that is because that’s what’s going to prevent a recurrence of fungal overgrowth in the future. What I often see happening is patients will focus too much on the killing part and the eradication. They’ll stay on that diet or that approach kind of perpetually. They’re essentially continuing to starve their good gut bacteria. It’s interesting to see that there have even been studies about this now. I recently saw a paper that essentially was saying, something that we could have talked about, Steve, on the show. But the paper was saying, “Yeah, the low-FODMAP diet is undoubtedly effective for IBS, but maybe we don’t want to be prescribing this to patients long term because it’s really low on microbiota-accessible carbohydrates, which are the types of carbohydrates that feed the beneficial gut bacteria.” Now, of course, we know how important that is over the long term. I thought it was a great paper, because the researchers were basically backing up what we’ve said numerous times on this program, which is you have to distinguish between a therapy, something that has a therapeutic effect and that you use for a short period of time until you don’t need it anymore, with something that you might do over the long term. To use an analogy, if you need a raft to cross the river, when you get to the other side of the river, you just leave the raft behind. You don’t carry it on your head—well, unless you’re doing some portage and you’re expecting another river pretty soon. But the basic idea is you use it when you need it, and then you leave it behind. For whatever reason, people have a really hard time grasping that.  You see that in the low-carb world I think, where I think it can be a super effective therapy and a shorter-term approach for a lot of conditions and people, but doesn’t necessarily need to be the lifetime approach. Or the fact that it tends to work really well as a therapeutic intervention, that doesn’t necessarily translate into meaning that eating carbohydrates led to the condition in the first place. It all tends to get kind of convoluted. The point here that I really want to stress is that once you get the Candida or fungal overgrowth back into balance, that’s not the stopping place. The next step from there is to rebuild then your beneficial gut bacteria, which is what will prevent the Candida from getting overgrown again. I can tell you, and I’m sure you’ve had this experience, Steve, that people who get Candida, they don’t often just deal with it once; it tends to recur and be an issue. I think one of the reasons for that is they don’t stress the rebuilding part as much as they should. Steve Wright:  All right. So I’m just going to recap this. Correct me if I’m missing any here, Chris. But working backwards, one that you just mentioned was people tend to stay in the killing phase too long and don’t think about actually rebalancing the microflora and actually feeding it. Some people assume that diet is the solution to yeast and fungal overgrowth, when many times, it’s not; there needs to be other interventions. When people do do diets to try to help with yeast overgrowth and Candida, they typically will end up on a ketogenic diet, which can actually inhibit sort of the short-term treatments that will actually get rid of the Candida. Then I think another big one that we mentioned was the idea that—I think you put around 80% to 85% of the time, it’s not just a yeast overgrowth issue. I think this is one of the reasons why people keep getting yeast overgrowth as well. It’s because they don’t ever get off the killing protocol. They don’t realize that there’s an 80% chance or more that they have maybe another infection, they have a hormone issue or they have an autoimmune issue that they’re not looking at. Chris Kresser:  Yeah. Great recap, Steve. Perfect. Maybe we’ll call this episode, “Four Biggest Mistakes People Make When Treating Yeast Overgrowth.” Steve Wright:  Awesome. Chris Kresser:  I like it. All right, everybody. Thanks for listening again. Remember to submit your questions so your voice can be heard. Thanks, as always, for listening. Steve Wright:  In-between episodes, if you want to get Chris’s latest studies or the latest recipes he’s posting, things like that, make sure you’re following him on social media. If you’re a Facebook user, go to Facebook.com/ChrisKresserLAc. If you’re a Twitter user, go to Twitter.com/ChrisKresser. Thank you for listening. We’ll talk to you on the next show. Chris Kresser:  Thanks, everyone.

We have a great question today. It revolves around the gut, one of our favorite topics, and in particular the connection between the gut and the heart, which is something we haven't talked about a lot. We know there are connections between the gut and just about everything, but this is one area we haven't explored in a lot of detail.

In this episode, we cover:

2:21 What Chris ate today 5:13 TMAO and heart disease 11:15 Four gut-heart connections

Links we discuss

• Choline and TMAO: Eggs Still Don’t Cause Heart Disease
• Red Meat and TMAO: Cause for Concern, or Another Red Herring?
• SIBO is associated with cardiovascular autonomic neuropathy.
• H. pylori has been detected within plaque in coronary and carotid artery walls using polymerase chain reaction (PCR)—a way of testing for the DNA of microorganisms.
• Intestinal permeability may contribute to coronary heart disease via increasing production of inflammatory cytokines and weakening the stability of plaque.
• Intestinal permeability has been associated with an increase in visceral fat.
• Patients with coronary disease, characterized by increased intestinal permeability, have been shown to have increased intima media thickness of carotid arteries.
• Studies link changes in gut microbiome with intestinal permeability, inflammation, insulin & leptin resistance, and metabolic problems: all major risk factors for coronary heart disease.

[powerpress] Steve Wright: Good morning, good afternoon, and good evening. You are listening to the Revolution Health Radio Show. I'm your host, Steve Wright, co-author at SCDlifestyle.com. This episode of the RHR Show is brought to you by 14Four.me. This website and this program is a 14-day healthy lifestyle reset program that Chris Kresser has put together to help you if you're still struggling with, for instance, weight loss, maybe even weight gain, sleep issues, autoimmune conditions, digestive health. Basically if you're having any health-related conditions and you're still not where you want to be, optimizing your diet, your sleep, your movement, and your stress are really the foundational principles to getting these problems resolved, and what has Chris has done is put together a 14-day step-by-step program that's going to walk you through fitting all these new changes into your life. As we all know, implementing healthy habits can be a real struggle, so it's really good and really wise to work with somebody who has done this with hundreds and thousands of other people and using science-based principles and habit-based principles that can really make it easy for you to implement these things into your life and take your health up to the next level, so check out 14Four.me. Now, with me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, how are you? Chris Kresser: I'm great. How are you doing, Steve? Steve Wright: I'm very wonderful. It's a great day. Chris Kresser: Fantastic. So, we have a great question today. It — guess what? — revolves around the gut, one of our favorite topics, and in particular the connection between the gut and the heart, which is something we haven't talked about a lot. I mean, we know there are connections between the gut and just about everything, but this is one area we haven't explored in a lot of detail, so I'm looking forward to it.

What Chris ate today

Steve Wright: Yeah. Now, before we get to the question, Chris, people would love to know, what have you been eating all day? Chris Kresser: Yeah, I thought you might ask that. This morning I skipped breakfast and just had coffee and cream. There was a lot going on, and I had a few things I needed to get done, and so, yeah, that's what I did, as you know I'm prone to do sometimes, and then I worked out, did some exercise around 10, and then at 11 I had kind of a brunch, I guess you'd call it. I had some plantains, a raw spinach salad with carrots and beets and a balsamic vinaigrette dressing, and then I had some lamb merguez sausage from my favorite local charcuterie, The Fifth Quarter. Steve Wright: Nice. And no bottomless mimosas at brunch today? Chris Kresser: Not today. I did have a glass of kefir afterwards, but that's not quite the same. Steve Wright: Perfect. Sounds delicious, man. Chris Kresser: All right, so let's give this question a listen. It's from Simas. I hope I'm pronouncing that right. Simas: Hi, Chris. You have briefly mentioned about the gut-heart connection in one of your podcasts, and I find it really, really interesting because I've had all kinds of heart problems through the years, which include high blood pressure and heart rhythm problems like various kinds of extrasystoles and just a general feeling that something's not really right in that area, and so I wanted to hear how gut health can affect that. I mean things like H. pylori, SIBO, lipopolysaccharides, and nutrient deficiencies, do they play a role in heart rhythm problems and how it all works? I would love to hear about that. Thank you. Chris Kresser: OK, yeah, so as I said, we've talked about the gut-brain connection, we've talked about the gut-skin connection, the gut-immune connection, so of course, why not the gut-heart connection? It shouldn't surprise us that there is a strong connection between gut health and heart health. There are, in fact, a wide range of connections, and in this podcast I'm going to talk about the ones that I think are significant. I'm also going to spend a little time talking about one that I don't think is significant that's gotten a lot of attention in the media, so maybe we should probably start there.

TMAO and heart disease

All right, so I'm not sure if those of you who are listening to this know, but a year or maybe it was two years ago now — it's all a blur! — there was a lot of discussion about TMAO and heart disease. I wrote a couple articles about it at the time, but it was really kind of the latest attempt to blame red meat and foods like eggs for heart disease. It's pretty complex. As I said, I wrote two articles about it. They have a lot of detail. We'll put those links in the show notes so you can do a deep dive if you want. I'm just going to cover the basics here, and that's that there's a chemical called trimethylamine N-oxide, which is TMAO for short, and the theory is it increases the risk of heart disease, and eating red meat and choline-rich foods like eggs supposedly increase TMAO. Therefore, red meat and egg increase heart disease. That was the argument that was being made, and there were articles published in The New York Times, and there was this whole big brouhaha about it. But there were a lot of problems with that research, and, again, you can check the articles for details, but I'm going to just highlight the biggest ones here. First, most previous studies have shown that the only food that significantly increases TMAO reliably is seafood and fish, but of course, seafood and fish are inversely associated with heart disease in just about every study you can look at, and you don't hear these researchers going out and telling people not to eat fish because of TMAO. And shockingly, the researchers that were really kind of advocating this TMAO-red meat connection just entirely ignored that in their papers. This was Stanley Hazen's group out of the Cleveland Clinic, a group that's kind of notoriously anti animal product and pro-vegetarian, kind of vegan agenda. So nobody's explained that. If TMAO is increased by eating seafood and fish by orders of magnitude more than by eating red meat, than how is it that eating fish isn't killing people? Number two, even if there is an association between TMAO and red meat consumption, there's no evidence that meat consumption is actually what's causing the higher levels of TMAO. If you've been listening to the show, the most recent episode on how to do proper scientific research, you know that correlation is not causation. So if you see high levels of TMAO in people who eat more red meat, it doesn't necessarily mean that the red meat is what's causing the high levels of TMAO. We've talked before about the healthy user bias, which means that people who engage in one unhealthy behavior or healthy behavior are more likely to engage in other similar behaviors, and since red meat has been demonized for so long, typically people who eat more red meat in studies do things like smoke more cigarettes, they exercise less, they don't eat as many fruits and vegetables, they engage in all kinds of behaviors that are less healthy, so how do we know that it's not these other things that are leading to the higher TMAO levels? How do we know that people who tend to eat more red meat have a messed-up gut microbiome because of all these other behaviors that I mentioned and that's what's causing the higher TMAO levels, which is certainly possible? And third, if eggs do increase TMAO, and TMAO causes heart disease, we should see a clear association between people who eat more eggs and heart disease, and in fact, we don't. I'm sure many of you heard that for the first time ever the US Dietary Guidelines have removed dietary cholesterol from the list of foods that need to be avoided because there's just no evidence to support that link between dietary cholesterol and heart disease. Other industrialized countries removed that a long time ago. The US finally joined the club and did it this year. Along those same lines, in some of the more recent larger studies, we don't see even any association between fresh red meat consumption and heart disease, and that's in spite of all these confounding factors that I just mentioned related to the healthy user bias. If you go into PubMed and you look at studies on the connection between the gut microbiome and heart disease, a lot of the papers you'll find initially will be related to this idea that TMAO causes heart disease and meat and animal products increase TMAO, but this is not, in my opinion, something that's really significant and that we should be paying attention to, so I just wanted to start by kind of getting that out of the way. Steve Wright: Yeah, you've done a lot of research on that, and I think there have been a lot of write-ups in this community about the lack of scientific evidence there. Chris Kresser: Yeah. So now let's talk about what I think is worth paying attention to, and there's some really interesting stuff. I'm sure we're going to be seeing a lot more of it in the months and years to come.

Four gut-heart connections

There are four lines of evidence that I looked at in terms of connections between the gut and the heart. The first one is our old friend, SIBO, small intestine bacterial overgrowth. There aren't a lot of studies on the connection between SIBO and heart health, but I did see one study showing that SIBO is associated with cardiovascular autonomic neuropathy. We also know that SIBO is linked very convincingly with nutrient deficiencies, and of course, there's tons of research showing various nutrient deficiencies connected to heart disease. And then SIBO has been shown to cause both inflammation in the gut and then, by extension, systemic inflammation, which, of course, conceivably could contribute to heart disease because we know it's an inflammatory condition, and anything that causes continual low-grade inflammation is definitely going to contribute to inflammatory diseases like heart disease. The second connection is with H. pylori. This is the bacterium that's associated with ulcers, as many know, and there are a few different lines of evidence connecting H. pylori infection with higher rates of heart disease. There's observational or epidemiological evidence showing higher rates of heart disease and heart attack in people who have H. pylori, but then there are studies that have found a significant relationship between H. pylori and endothelial dysfunction, although it's worth pointing out that some other studies didn't find a relationship, so there's a little bit of uncertainty there. But most interestingly, because we can't rely on observational or epidemiological data, as we've been talking about kind of ad nauseam at this point, to establish causality, there are some studies that have found that eradication of H. pylori decreases risk factors associated with atherosclerosis; such as oxidative stress; myeloperoxidase activity; C-reactive protein, which is a marker of systemic inflammation; fat mass; and blood pressure, which is actually the single greatest risk factor for heart disease. So that's convincing evidence that there may be a causal relationship because if you observe that people with H. pylori are more likely to have heart disease, that's just an association, but then if you find that eradicating H. pylori decreases all these risk factors that are associated with heart disease, that's one factor that makes it more likely there's a causal relationship. And finally — this is another factor leaning towards showing causality — is H. pylori has been detected within the plaque in coronary and carotid artery walls using DNA-PCR analysis, so they're actually finding this bacteria in plaque. Again, that could be more a consequence of another problem and not the causal event, but it's interesting, nonetheless. OK, so we've covered SIBO and H. pylori. I'm sure many of you are wondering if there's any connection between leaky gut or intestinal permeability and heart health, and there definitely is. There was a study published in The American Journal of Cardiology that found that intestinal permeability may contribute to heart disease by increasing the production of inflammatory cytokines and weakening the stability of plaque. And as I think we've talked about before, the stability — or lack thereof — of plaque is a major factor in terms of heart disease because the initiating event of a heart attack is the rupture of plaque, which then occludes the artery and prevents blood from getting to the heart, and that causes the cells of the heart to die, and that's what a heart attack is. Instability of plaque can be the main precipitating event of a heart attack, so that connection between intestinal permeability and plaque instability is, I think, particularly significant. Then there were a couple studies showing that leaky gut is associated with an increase in visceral fat or abdominal fat. This is fat that accumulates around the viscera or the abdominal organs, and we know from numerous studies at this point that that type of fat is a strong risk factor for heart disease. And then we can kind of extend our search and look at patients with celiac disease. Even if there aren't a lot of studies directly looking at intestinal permeability and heart disease, we know that patients with celiac, especially untreated celiac, suffer from intestinal permeability. So we can look at the connection between patients with celiac disease and heart disease, and sure enough, there are studies showing that patients with celiac disease tend to have an increased intima-media thickness of their carotid artery, and that is, again, a well-known marker of endothelial dysfunction and vascular disease and a risk factor for heart disease and for stroke. So several different lines of evidence suggesting a connection between intestinal permeability, AKA leaky gut, and heart health. And then last, but not least, of course, we have to talk about the gut microbiome and not TMAO, just because there's not necessarily a strong connection between red meat and TMAO — and even TMAO and heart disease, although I'm not ruling that out, per se — I'm just criticizing the idea that our diet is the major contributor to TMAO production. But there are lots of studies linking changes in the gut microbiome with things like intestinal permeability, which we just established is related to heart disease; inflammation, which is extremely well established in terms of its connection to heart disease; insulin and leptin resistance and all kinds of different metabolic problems. I'm sure a lot of listeners have heard now, over the last few years, a lot about the connection between the gut microbiome and diabetes and metabolic syndrome and metabolic health, and of course, diabetes and metabolic syndrome are very strong risk factors for heart disease. We can link changes in the gut microbiome to heart disease pretty directly via those mechanisms. The research here is still kind of young in terms of just directly looking at changes in the gut and cardiovascular disease, but there's enough already, both direct and indirect, to convince me that there is a strong connection, and given what we know about the gut, that's not at all surprising. Steve Wright: Yeah. Not to mention, Chris — I'm guessing you have this point of view, but you'll obviously clarify — the gut sort of feeds the rest of the body. So if we want a healthy heart or a healthy brain or any healthy organ, being able to assimilate nutrients out of our food and keeping our inflammation as low as possible, the gut seems like the central player just at a high level sort of as a feeder to the rest of the organs that will never be able to be quantified, I don't think, in research. Chris Kresser: Yeah, absolutely. I mean, it probably could be quantified to some extent in the sense of just measuring nutrient absorption and things like that, but when I was talking about SIBO, I mentioned that SIBO is linked with nutrient deficiencies, and then nutrient deficiencies are strongly linked with heart disease, so, yeah, I completely agree. I think that at the most simple level if we're not absorbing nutrition from food, then our whole body isn't going to function right, including our heart! And heart disease is the number-one killer in the modern world still. And that may change. Cancer is catching up, but still right now in the industrialized world heart attack is the leading cause of death. So we want to do everything we can to protect our heart health, and a lot of people don't necessarily think about the gut when it comes to living a heart-healthy lifestyle. This is a little anecdote from my clinic and work with patients. I have quite a large number of people that come to me who have started a paleo diet and their cholesterol has gone through the roof, and in some cases I have patients — usually men, but sometimes women — who their only complaint is very high cholesterol. These are, maybe, competitive athletes, people who are at the top of their game. They don't have any other symptoms that bother them. They're just concerned about their really high cholesterol. And when they come to see me, one of the first things I do is I run a full suite of gut tests, and fortunately my patients are often up for this because they're people who have listened to my podcast or read my book and they're kind of expecting that. I think a lot of patients, if they were to go to see a health practitioner about high cholesterol, might be surprised and reluctant to go pay hundreds of dollars for gut testing when their only complaint is high cholesterol, but so far I haven't had anyone resist. But they have often been surprised to find out that they have SIBO or fungal overgrowth or something like that. For whatever reason, it's not causing a lot of symptoms for them in the gut, which is something we've talked about before. And let's say they have an LDL particle number of, like, 2400 or 2500, which is quite high. Then we treat their SIBO or fungal overgrowth, confirm eradication by follow-up testing, and then we retest their LDL particle number and it drops down to 1300, which is a huge, huge drop. It's gone from the extremely high category to the borderline high category and to a level that probably doesn't even require treatment for most people if they don't have any other significant risk factors. We've seen this a lot in our practice, and it's direct evidence between the gut and gut health and major risk factors that at least conventionally have been strongly associated with heart disease. Steve Wright: Well, it seems like for anybody who's concerned about long-term heart disease issues investigating gut health would be a top priority. What about any sort of short-term heart arrhythmia-style stuff that was mentioned in the question? Chris Kresser: Yeah, I didn't find anything direct on that, but something that can cause cardiac neuropathy, I assume, could certainly affect the rhythm of the heart. I would assume that anything that we talked about that could cause heart disease could also affect the rhythm of the heart and how the heart pumps blood. I mean, those, to me, seem pretty closely connected. Steve Wright: OK. Chris Kresser: Although I didn't find any specific studies linking SIBO and arrhythmia, for example. That's what I meant by saying I think the research is still kind of in the early phase. We're not seeing that level of specificity yet, but I imagine we will at some point in the not-too-distant future. Steve Wright: Yeah, I would think so. I mean, the amount of money that's pouring into gut health research right now is pretty staggering. Chris Kresser: Mm-hmm. Steve Wright: So I think there are going to be a lot of things that we might be chatting about in two years that are finally proven. Chris Kresser: Yeah. I agree. So that's it, the gut-heart connection. I imagine eventually we'll get through every organ or organ system in the body and its relationship with the gut. Steve Wright: I can't wait for you to do the gut-calf connection. Chris Kresser: The gut-calf connection. Well, we could do sort of, like, the gut-muscle-joint connection. I mean, there's certainly a strong connection between the gut and things like rheumatoid arthritis and muscle fatigue and exercise intolerance and things like that, so maybe you can call in and record a question, Steve. Steve Wright: All right, I might just go over to ChrisKresser.com/PodcastQuestion and give you a ring! Chris Kresser: Use a fake name, disguise your voice, you know? Steve Wright: I will use my sexy voice. All right. Well, if you'd like your question, please, as I just mentioned, go to ChrisKresser.com/PodcastQuestion and submit it there. And in between shows, make sure you're following Chris on social media, Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser. On social media is where you're going to get his latest updates on new posts, but also he's sharing things like the scientific research that he's looking at for the shows and things that don't necessarily make the blog for many months, so it's a great place to keep up with what Chris is looking at on a daily basis. Chris Kresser: All right, everybody, thanks again for listening. Talk to you next time. Steve Wright: Yeah. Thanks, everyone.

Over the last three or four weeks in my practice I’ve seen four or five kids of varying ages from about 2 years old to 10 years old, with digestive and other issues, so this has been on my mind recently. As a father myself, I know it’s just so difficult to be in a situation if your child is sick and wanting to help and not being able to help as much as you’d like to be able to.

In this episode, we cover:

2:00  Goodbye and thank you to Steve 4:22  Pre-enrollment for clinician training program 10:42  Which tests to use for diagnosing children 22:03  Rebuilding the gut [powerpress] Steve Wright: Good morning, good afternoon, or good evening. You are listening to the Revolution Health Radio Show. I'm your host, Steve Wright, co-author at SCDlifestyle.com. This episode of RHR is brought to you by 14Four.me. This is a 14-day healthy lifestyle reset program. This is for you if you’re someone who is trying to put together all the pieces of great health that Chris talks about, things like diet, sleep, movement, and stress. It can be hard to incorporate all these things into the modern lifestyle, and what Chris has done is created a step-by-step, hand-holding program, where in 14 days he’s going to walk you through how to fit them all into your life so that you can continue to make progress on your health issues, whether that’s weight gain, whether that’s fatigue or any autoimmunity, things like that. If you’re struggling with any of those areas, I’d encourage you to check out 14Four.me. All right, on with the show. With me today is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, how are you doing? Chris Kresser: Pretty well. How are you, Steve? Steve Wright: I’m excited. Chris Kresser: Yeah? What are you excited about? Steve Wright: My shoulders have been really messed up pretty much this entire year, and I’ve finally gotten to the place where I can work out on a regular basis, so it’s just great to be able to be exercising on a daily basis again.

Goodbye and thank you to Steve

Chris Kresser: I bet. I bet. Well, we have a couple of big announcements to make before we go forward with the question for this episode, and the first is that after several years of being a fantastic host on this show, Steve is going to be moving on. This will be our final episode together, and then there’s going to be a short break for the show and we’ll come back in a new format. I’ll be hosting myself, but I’ll also be having more frequent guest hosts, like Dr. Amy Nett from CCFM and others, and then more interviews with experts, researchers, people that I’m interested in talking to that are exploring various things that I’m looking into or passionate about or want to learn more about. Yet another new chapter in the evolution of Revolution Health Radio, and I just feel a lot of gratitude and appreciation for Steve and everything he’s brought to the show over the years. We’re definitely going to miss you, Steve. Steve Wright: Yeah, thanks, man. I’m going to miss doing the show, too. This is, I think, going on our fourth year of doing this together. Believe it or not, when we started, I was still an engineer back in Michigan, doing the SCD Lifestyle thing on the side, trying to make that work, and you don’t know this yet, but I used to take all of my vacation time, every time you wanted to record I’d take a half day of vacation to go home and record because I had to work those two jobs. Chris Kresser: Wow. I didn’t know that. Well, that just makes your commitment even more impressive. You’ve certainly come a long way since then, and we’re sad to lose you, but I know you have lots of really interesting things going on, and of course, we’ll stay in touch. Steve Wright: Yeah, definitely. This has been a labor of love, and it’s been amazing to just get to work with you on a regular basis. I tell this to people who ask me about it. I say basically I get to go to school for an hour every week with Chris Kresser and pick his brain, so it’s been an honor to do the show and to be able to be the guy that gets to ask all my questions.

Pre-enrollment for clinician training program

Chris Kresser: All right. So that’s number one, a pretty big announcement, and number two is another pretty big announcement, which is that after really kind of several years of development, I’m finally excited to be getting very close to opening pre-enrollment for the clinician training program that I’ve talked to you about several times now. I’m creating a new training body organization called the Kresser Institute for Functional and Evolutionary Medicine. The next announcement, we’re sending an email, if you’re subscribed to my email list, on Tuesday, July 21. I think this podcast is going to come out on the 23rd or something like that. But if you’re not on the email list, you can head over to KresserInstitute.com and watch a short video of me explaining what’s happening and what to expect in the next month or six weeks, and there’s also a little sneak peek there of what the training will entail, how enrollment will work, and a few other things that you should be aware of if you’re interested in taking part in this training. It’s going to start in January of next year, and it’ll go for one year with four breaks during the year, kind of almost like a trimester system, and I just can’t tell you how excited I am to finally be bringing this to fruition. It feels like probably one of the most important things I’m going to do in my life professionally. There’s just such a growing and unmet demand for functional medicine practitioners with an ancestral perspective, and there really isn’t a training that offers that, at least until now, so I can’t wait to share more with you. For now, just head over to KresserInstitute.com, watch the video. And if you are interested, make sure to sign up for the early notification list. The number of people we can accept in the first course is limited to about 125, I think, possibly 150, and the last time I checked there were over 2200 people on the early interest list. Unfortunately, we’re probably going to sell out, and there may not be space for everybody, so if you want to be among the first to be notified, after you watch the video and check out the page, if it looks like something you might be interested in, make sure to put your email address in the box so that we can contact you when enrollment opens up. Steve Wright: Well, congratulations, Chris. I know this has been something that you’ve been thinking about for three or four years and working really hard on in the past year, and it’s something that’s going to plug a big hole in the market, so I appreciate you doing all that hard work. Chris Kresser: Yeah, thanks, Steve. And we’ll be back in August when pre-enrollment opens. I’ll spend an episode talking a lot more about it, what the training is going to entail, giving you much more detail about it, and answering some questions that we’ve received a lot of and just try to paint a more clear picture so you can make an informed decision. But for now, we’re going to go forward with a question from Brooke, so let’s take a listen. Question from Brooke: Hi, Chris. I have a question regarding testing and treating digestive issues in small children. My son who is almost 3 years old has had loose stool and pretty significant bloating basically all of his life. We didn't realize there was an issue until a while after he was really eating a lot of solid food, and his stool was still very mushy and soft. We've been working with a naturopath since he was 18 months old, and initially the stool tests she did confirmed that he had dysbiosis and overgrowth of E. cloacae and very low good bacteria. We've done a lot of different antimicrobial herbs and Chinese herbs, enzymes for biofilms, along with a low-FODMAP diet and probiotics. These approaches greatly reduce his bloating, but as soon as we veer from the diet whatsoever, the poor guy gets so bloated he looks like he’s pregnant, in his third trimester. His symptoms also seem very similar to SIBO-type symptoms. My question with all of this is what sort of testing you suggest for digestive issues in small children — he's just learning to blow, so breath tests probably aren’t really possible yet — and specifically for bacterial overgrowths, what sort of treatment you might suggest for SIBO or bacterial overgrowths when confirmed on testing. Is there a point at which one would need to consider a medication? Thank you very much for your insight on all of this. Chris Kresser: OK. This is a good timing on this question. For whatever reason, the last three or four weeks in my practice I’ve seen four or five kids, actually, of varying ages from about 2 years old to 10 years old in my practice with digestive and other issues, so this has been on my mind recently and something I’m paying attention to. I have been, of course, for a long time, but these particular issues are front and center for me over the past couple of weeks. Steve Wright: Before you get into the answer here, Chris, I just want to let all the listeners know that RHR is predominantly built for you and by you, so go to ChrisKresser.com/PodcastQuestion to get your question on the show. Chris Kresser: Great. All right, so first of all, Brooke, I’m sorry to hear that you’re having problems. As a father myself, — Sylvie’s actually turning 4, believe it or not, in a week; it’s hard to believe — but I know it’s just so difficult to be in a situation if your child is sick and wanting to help and not being able to help as much as you’d like to be able to help, so I’m sorry that this is happening.

Which tests to use for diagnosing children

I think there are a few things that I would say here. Number one is a breath test for SIBO would be excellent. I understand that at 3 years old he may not be able to blow on demand yet, but in my experience, most kids acquire that ability right around this age, so keep practicing. Maybe turn it into a game. Do some demonstrations yourself. Maybe get a straw connected to a balloon and see if he can inflate that or even just a balloon. There are ways that you can kind of prep for doing the breath test and helping him to develop that capability because it really is the best way to screen for SIBO, and as you mentioned, his symptoms certainly are consistent with that. His symptoms could be related to simply dysbiosis, as you mentioned, or other gut pathogens that haven’t yet been detected, but certainly SIBO would be something that you’d want to rule out. You didn’t mention any risk factors, whether he was born vaginally or via C-section or if he was breastfed or formula fed or if he had to take antibiotics when he was a baby or if you took antibiotics during your pregnancy or what your gut flora was like when you were pregnant and when you gave birth. Those will all, of course, influence the risk of him developing SIBO early on, and it sounds like it did start basically from the beginning from your description in the question. The testing that we would do would be breath test as soon as he’s able to do that. We would do two stool tests. We would use Doctor’s Data Comprehensive Stool Analysis, which is a great combination of proteomic analysis and stool culture and has some other very useful markers like inflammatory markers, like lysozyme or lactoferrin or calprotectin, which are good markers for inflammatory bowel disease, some markers for absorption, short-chain fatty acid production, markers for fungal overgrowth, etc., so that’s a really good test. But then we also tend to run BioHealth 401H side by side, and that’s a stool culture, but a very good stool culture. We’ve found that that test will often pick up things that the Doctor’s Data test misses and vice versa, which is why we still run them side by side. It’s a pain and it’s certainly more expensive, but we’ve found it to be necessary. I would also consider doing urine organic acids testing. I think this is the least reliable or consistent in terms of detecting dysbiosis and bacterial overgrowth of the three methods, and the evidence supporting it for that purpose is thinner than it is with breath testing and stool testing, but I do think it can be useful when it’s combined with the breath and stool testing. I also would say that there are other markers for cellular energy production and mitochondrial function that can be really useful, and in some cases in kids with digestive issues like this, those things can be playing a significant role and actually preventing progress, and if you focus exclusively on the gut and don’t test for these other things that could be contributing, in some cases it can be one reason that progress is not happening to the degree that you would expect. Steve Wright: Chris, I’m wondering — and I’m betting that other people like Brooke or listeners might be wondering — why is it that we need to do these tests? All the antimicrobial herbs, the Chinese herbs, the enzymes for the biofilms, diet changes, probiotics — this is an approach that a lot of people take rather than spending whatever amount of money, $500 to $1000 or more on those tests. People try this approach, and then they end up in this situation. What is happening here where whatever infections, if they are there, are not going away? Chris Kresser: Well, it’s hard to say. I mean, there are several possibilities. One is that there is no infection and it’s a question of dysbiosis. I mean, dysbiosis alone can cause all of these symptoms, and really the biggest problem could be a lack of beneficial bacteria, not too much harmful bacteria or bacteria overgrown in the small intestine or fungal overgrowth or a parasite or something like that. That’s one possibility, especially if he had some of the risk factors that I mentioned earlier. And in that case, actually, a low-FODMAP diet, while it might help relieve the symptoms initially, over the long term would not necessarily be desirable because you’re then starving the beneficial bacteria in the colon of what they need to grow. I think the studies are pretty clear now — and this is consistent with my experience in the clinic — that probiotics, in most cases, don’t have a quantitative impact on the levels of beneficial gut bacteria. In other words, taking probiotics doesn’t, over the longer term, increase the levels of beneficial bacteria in the gut. They play more of an immunomodulatory role, which is very important, and they can have a really significant impact that way, and as long as you’re taking them, of course, you’ll have more bacteria there, but when you consider that we have a hundred trillion microorganisms in the gut and even the strongest probiotics are billions or hundreds of billions, it’s a drop in the bucket. So the best way to actually increase beneficial bacteria in the gut over the longer term is to eat fermentable fibers or types of carbohydrates that the bacteria can ferment. We’ve talked about this on the show before. Microbiota-accessible carbohydrates was one of the terms that’s been used in the scientific literature. But these, of course, would be FODMAPs but also other kinds of starches that have a low glycemic index and would survive the upper part of the small intestine intact and then maybe make it to the colon, where they can be fermented by gut bacteria. So that’s one possibility. Another possibility is that there is an infection present but the treatment so far hasn’t been strong enough or effective enough to get rid of it. Without knowing what of the herbs and other stuff that have been used and what dosages have been used, I can’t really comment on that, but I can say that treating these conditions both in kids and adults, they can be very recalcitrant and difficult to get rid of and can sometimes require pretty aggressive approaches, so that’s another possibility. A third possibility, as I alluded to earlier in the show, is that even though bloating is the main symptom and gut issues are the main symptom, in some cases there are other problems or conditions that can contribute to these symptoms that aren’t the expected culprit. For example, if he has a thyroid problem and low thyroid function, T3 is required to produce stomach acid, activate intestinal motility and peristalsis, and has a number of other important functions in the gut, so if T3 is low, that can cause bloating and a number of other issues. Hypothyroidism in kids isn’t super common, but it’s not rare either, so it’s something that should definitely be checked out. Mitochondrial function I mentioned. Mitochondrial disorders in kids are really on the rise, and there are a number of reasons for that. It’s another disease of civilization, and I’m going to have someone on the show in the near future to discuss this. It’s fascinating and also a little bit disturbing, but environmental toxins, in particular, and poor diet and a range of other influences that are just part and parcel of the modern world that we live in can adversely affect mitochondrial function. And then when the mitochondrial function is reduced in the gut, then that can actually produce a lot of symptoms like bloating or gas or changes in stool frequency and consistency and things like that. In some kids, if that’s present, focusing on that will be helpful and necessary in terms of moving forward. Steve Wright: And the organic acids test will let someone know about that? Chris Kresser: It certainly provides some important clues. There are organic acids that give you some hints into the Krebs cycle, the citric acid cycle, which is what happens inside the mitochondria to start producing energy, ATP, and whether there’s a defect in the processing of glucose to pyruvate. There’s maybe a problem with aerobic respiration and a consequent buildup of lactic acid because anaerobic respiration is being favored, or if pyruvate is not being shuttled into the mitochondria and oxidative phosphorylation where ATP is produced is impaired, if there’s a problem with the electron transport chain. There are a lot of genetic mutations that can affect all different stages of this process, and then there are environmental factors which can affect all different phases of these processes. All of these conversions that happen in the citric acid cycle, or the TCA cycle, and through the whole transport chain require nutrients. They’re enzymes and they require nutrients to function properly, so if the nutrients are low for whatever reason, then that whole system can get broken, essentially. Another possibility is inflammatory bowel disease. Especially if he’s had loose stools and it just continues despite all of these different interventions, I would want to screen him for inflammatory bowel disease, like Crohn’s or ulcerative colitis. Those are autoimmune conditions, and certainly they can co-present with SIBO and other gut infections, but if IBD is present, that will probably have to be addressed with additional steps above and beyond just treating SIBO or dysbiosis. Short of a colonoscopy, which is a very invasive procedure, those markers that I mentioned from the Doctor’s Data Comprehensive Stool Analysis — calprotectin and lactoferrin and lysozyme — can be helpful initial markers for determining whether active IBD is present.

Rebuilding the gut

So that’s a good place to start, looking into all of those things, getting some additional testing done, and then if you do the breath test and that’s negative and there are no parasites, no fungal overgrowth, no other pathogens, this really could come down to just a lack of beneficial bacteria, and it may be that the approach to getting well is much less about killing and much more about rebuilding. The tricky thing about this is that if he improved with a low-FODMAP diet, that does suggest that at one point there may have been microbial overgrowth, but it’s also possible that the microbial overgrowth or pathogens have been dealt with now but he still has really low levels of beneficial bacteria, and what you need to do at some point is start adding the FODMAPs back in and then start adding other types of fermentable fibers back in. Soluble fibers like glucomannan or psyllium husk or acacia tend to be pretty well tolerated. Then you have the resistant starches, which are potato starch or green banana flour or green plantain flour. And then you have the non-starch polysaccharides, which are the FODMAPs, but can be supplemented with, like inulin or FOS or larch, and you have to be extremely methodical and careful about how you add those in initially because they can cause gas and bloating if you go too quickly. And of course, you’d want to make sure that there aren’t pathogens or SIBO present before you try to do this because if they are still present, then it could get worse. I’m not sure what probiotics you’ve been taking, but if you’ve only been taking acidophilus and bifidus and those kinds of probiotics, I would definitely recommend some soil-based organisms like Prescript-Assist, some spores. MegaSporeBiotic is a product I really like, and AOR 3 is another good product. You can just rotate these in sequence so that he’s getting a lot of different types of probiotic bacteria. And then fermented foods can be, in my experience, even more potent in terms of rebuilding the gut and modulating the gut immune system. If he tolerates dairy, homemade kefir — so that there’s no lactose in it — can be really, really therapeutic and healing. You can start with as little as, like, a half of a teaspoon a day and then just gradually increase. If he can’t tolerate dairy, you could do water kefir. You can order the kefir cultures from CulturesForHealth.com. A 24-hour homemade yogurt so that the lactose is gone can be helpful, too, although I’ve found kefir to be more therapeutic than yogurt in most cases. Beet kvass can be very therapeutic if he can tolerate that. Raw sauerkraut can be therapeutic, and adding these things back in in conjunction with the fermentable fibers either in foods and/or the supplemental fibers, in some cases that kind of really focused approach is what’s necessary to rebuild the beneficial gut bacteria and heal the gut. Steve Wright: Got it. So in general, would it also be safe to say that if he’s more on the constipated side than the diarrhea side that the prebiotics might be another plus-one for potentially doing the prebiotics in the short term. Chris Kresser: Yeah, exactly. They can work for both, but certainly resistant starch can be really helpful with loose stool. One thing, too, Saccharomyces boulardii can be really helpful for loose stool presentations like this. Again, I’m not sure what probiotics you are doing, but that’s something else to consider. In sum, I think expanding the diagnostic approach to include other tests that you may not have gotten yet, like breath and the urine organic acids, looking at things like thyroid function and mitochondrial function, basic blood markers to rule out any other issues — blood sugar issues, liver function, nutrient status, etc., all of which can, of course, affect gut function — and then if there really aren’t any pathogens or gut issues present, then considering switching more toward the rebuilding-your-gut kind of approach that I described instead of the antimicrobials. Now, if SIBO is present, then the way that I approach it is with a kind of microbial reset diet, which is a combination of low-FODMAP plus reducing intake of certain starches that are likely to be fermented by the gut bacteria, the ones with the most fiber and the lowest glycemic index. And then we start with antimicrobial herbs and nutrients. We use kind of different tinctures for kids because 3-year-olds can’t typical swallow pills or capsules. As for the question of whether I would consider medication at some point, it’s tricky. I think it really depends. Rifaximin is the medication that is typically prescribed for SIBO if there’s hydrogen overgrowth without methane. If there’s methane, it’s more effective to use rifaximin plus neomycin. Rifaximin is not systemically absorbed, so it has that going for it, and it’s not a hugely broad-spectrum antibiotic that would be expected to totally wipe out the beneficial gut flora, and it is generally well tolerated and pretty safe, so I might consider that, but I would probably do a lot of other things first, all of the stuff that we’ve talked about, of course, including the reset diet plus all of the natural antimicrobials, before I moved on to that. If you did have to give rifaximin a try, again, it’s better than a lot of other antibiotics, and if you do that, I would just follow up with all of the approached that I mentioned in terms of fermentable fibers and fermented foods and probiotic rotation to help rebuild the gut. Steve Wright: Awesome, Chris. Thank you for sharing all that. I think the one question that I’m left with for all the parents out there is, “Awesome, Chris. My doctor might be able to get me a breath test and knows nothing about everything else that was said today,” so is there ability for more people to get in to see you or Amy? Are there other kid functional medicine specialists that you could point these people to that would understand? Chris Kresser: Good question. I reopened my practice a couple of months ago, and I still am accepting new patients, although I may have to close again shortly because I think I’m scheduling out into November now. Amy is still accepting new patients, and so we would definitely welcome anyone who can come see us in the Bay Area. If you live outside of the Bay Area, you just have to come in for the first appointment in person, a case review appointment, and then we can work via video conference or phone long distance after that. I’m only currently accepting patients who live in California, while Amy is accepting patients that live all over the US. As far as pediatric functional medicine specialists elsewhere, nobody comes to mind, and this, of course, Steve, is the big problem, right? I get requests for referrals pretty much every day either via email or people calling the office, social media, etc., and there’s nothing I would love more than to be able to have a long list of folks all over the country — or even the world — that my staff or I could just easily refer people to. Nothing would make me happier, and this experience that I’ve had, getting these requests for so long now, is, of course, what pushed me in the direction of creating this clinician training program, and I really don’t think there’s anything else that I could do right now that’s more important because we desperately need more clinicians that understand these things. Steve Wright: Got it. Yeah, it’s a big problem right now, and I would say that if there are some functional medicine practitioners out there who actually have experience with kids — not that you’re just a functional medicine practitioner — please leave a comment on this podcast. Try to get your name out there, and don’t think that someone commenting is an endorsement from me or Chris for anyone leaving a comment, but at least we can maybe help facilitate trying to get the word out about some people who might specialize in this area. Chris Kresser: Thanks, everyone, for listening. And, Steve, a very heartfelt thank-you and appreciation again for everything you’ve done for the show over the years. We’re going to miss you, and you’ll have to come back for a visit to say hello sometime in the future. Steve Wright: All right. Thanks, Chris. And thank you to all the listeners, everyone who has ever said hello to me at a conference or in Whole Foods and thanked me for the work here. I really appreciate you as listeners and making this possible. And, Chris, as always, man, thank you so much for this opportunity. It’s been just amazing, both from learning about health, but also growth and getting to know you, so I really appreciate the opportunity and I’d love to come back every once in a while and do a little guest episode. Chris Kresser: A little guest hosting. All right. Well, thanks again, everyone, for listening. Make sure to check out KresserInstitute.com if you’re interested in joining us in this functional medicine, ancestral nutrition revolution and radically transforming people’s health and radically transforming the way that we approach healthcare in this country and the world. I think it’s one of the most important things we can do and devote our lives to, so if you’re ready to take up the charge with me, I would love to have you in the training. Steve Wright: All right. Thanks, everyone, for listening. Make sure you’re following Chris on social media, Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser. And also remember that you could have your question live on this podcast. Just go to ChrisKresser.com/PodcastQuestion. Once again, thank you all for listening. It’s been a wonderful, wonderful couple of years. Have a great day.

Few things are more frustrating than lying in bed at night exhausted, but not being able to fall asleep because of an uncontrollable urge to move your legs. This phenomenon, known as restless legs syndrome (RLS), affects between 4% and 29% of adults in Western populations, and is a major contributor to sleep loss. (1, 2)

Pinpointing the cause of RLS has been an active research topic for years, but the condition is still not fully understood. The symptoms have been convincingly linked to impaired dopamine function in the brain, but the cause of this dysfunction is still being explored.

In this article, I’ll review four factors that could contribute to RLS, as well as steps you can take for improving your symptoms.

1. Systemic Inflammation and Immune Dysregulation

Restless legs syndrome has been associated with numerous conditions involving systemic inflammation and immune dysregulation. (3) One review paper published in 2012 investigated health conditions that were reported to cause or exacerbate RLS symptoms, and found that 95% of the 38 different health conditions that were strongly associated with RLS have an inflammation or immune component. (4) These conditions include Parkinson’s disease, multiple sclerosis, ADHD, Alzheimer’s disease, Celiac disease, Crohn’s disease, rheumatoid arthritis, sleep apnea, diabetes, and depression.

As further evidence, an elevated blood level of C-reactive protein (a marker of systemic inflammation) has been associated with increased RLS severity. (5) A small crossover trial found that a hydrocortisone infusion, which reduces systemic inflammation, reduced RLS symptoms. (6)

Researchers have proposed three potential mechanisms to explain the association between RLS and inflammatory or autoimmune states: direct autoimmune attack on the nervous system; genetic factors that could predispose an individual to RLS and be triggered by inflammation or autoimmunity; and iron deficiency caused by inflammation, which I’ll talk more about below.

What to do: If your RLS is a symptom of underlying systemic inflammation or immune dysregulation, the goal should be to find and treat the root cause. As I’ve mentioned many times in the past, gut infections are often the culprit—even if you don’t have noticeable digestive symptoms—so get your gut tested.

If you already have a diagnosed inflammatory or immune condition such as those I mentioned above, the best first step you can take is to adopt a “low-inflammatory” diet and lifestyle. This means eating a nutrient-rich, low-toxin diet based on whole foods; getting enough sleep every night; prioritizing stress management; and incorporating regular movement into your day.

You can also check out the bonus chapter about autoimmune disease from my book, as well as explore other information on my site about reversing autoimmune disease, the autoimmune protocol, the role of the microbiome, and alternative therapies such as LDN.

Do you have restless legs syndrome? Find out what might be causing it, and what to do.

2. Small Intestinal Bacterial Overgrowth (SIBO) and IBS

Some of the more recent research on restless legs syndrome has focused on a connection with small intestinal bacterial overgrowth (SIBO) and IBS, which is often caused by SIBO. One study found that 69% of RLS patients also had SIBO, compared with only 28% of controls. (7) They also found that 28% of RLS patients had IBS, compared to only 4% of controls. And according to the 2012 review I mentioned in the previous section, 32% of the 38 conditions associated with RLS are also associated with SIBO. (8)

A strong association between SIBO and RLS doesn’t mean that SIBO is causing RLS in these patients. But a few trials have found that in patients with both SIBO and RLS, their RLS symptoms improve after being treated for SIBO. (9) For example, one double-blind, placebo-controlled study reported that treatment with the antibiotic rifaximin—the standard treatment for SIBO—significantly improved RLS symptoms in patients with both conditions. (10) This, of course, does suggest a causal link between SIBO and RLS.

What to do: If you have both RLS and SIBO, the best option would be to find a functional medicine practitioner who has experience dealing with SIBO and get treated. That said, two steps you can try on your own are a low-FODMAP diet and probiotics. Low-FODMAP diets reduce the amount of fermentable carbohydrates that “feed” bacteria in the small intestine, and a couple studies have shown that probiotics can be as effective as antibiotics for treating SIBO. (11, 12) I’ve found the probiotics Prescript Assist, S. boulardii (a beneficial yeast), and MegaSporeBiotic to be helpful.

One important note about low-FODMAP diets, however, is that it’s generally not a good idea to stay on one indefinitely. Low-FODMAP diets eliminate sources of prebiotics, which can improve symptoms by starving pathogenic bacteria, but can also starve your beneficial bacteria. The best approach is to follow a low-FODMAP diet until symptoms subside (and your SIBO breath test is normal), and then gradually re-introduce prebiotic foods (or supplements) to support your gut microbiome.

3. Vitamin D Deficiency

As I mentioned in the introduction, one of the most-researched theories about the cause of restless legs syndrome is impaired dopamine signaling, which has led to the conventional treatment of RLS by dopamine agonists (i.e. chemicals that can bind to and activate dopamine receptors). Unfortunately, these treatments can become less effective over time, and can even result in a worsening of symptoms.

And while replacing neurotransmitters might be an effective way to manage symptoms in the short term, the goal should be to figure out why dopamine signaling is impaired in the first place.

This is where vitamin D comes into play. The role of vitamin D in dopamine signaling is only beginning to be investigated, but some evidence indicates that vitamin D could play an important role by increasing levels of dopamine and its metabolites in the brain, as well as protecting dopamine-associated neurons from toxins. (13)

RLS has been associated with vitamin D deficiency in several studies, and disease severity has been inversely correlated with vitamin D levels. (14, 15, 16) One study has also found that vitamin D supplementation improved the severity of RLS symptoms. (17)

What to do: If you have RLS, one of the easiest first steps you can take is to get your vitamin D levels tested. A good range to shoot for is typically between 25-50 ng/mL, but if you have an autoimmune disease or another chronic health condition, I prefer to bring vitamin D levels up to 35-60 ng/mL. One way to supplement vitamin D is cod liver oil; I recommend extra-virgin cod liver oil. You can also take a D3 supplement, such as this one that contains both vitamin D and vitamin K2. And of course, you should get regular sun exposure to bring your vitamin D levels up naturally.

4. Iron Deficiency

Iron deficiency isn’t exactly a “little-known” cause of restless legs syndrome; in fact, it’s probably one of the most well-researched areas relating to RLS. Iron is required for proper dopamine signaling, but its role is much better established than that of vitamin D, and it’s pretty clear that iron deficiency in the CNS can cause RLS symptoms by impairing dopamine function. (18)

Several studies have found that low iron levels in the cerebrospinal fluid and in the brain occur more frequently in patients with RLS compared with matched controls. (19, 20) And this difference isn’t always reflected in serum ferritin levels.

Other abnormalities in iron metabolism have also been observed in RLS patients, and many conditions that increase the risk of RLS (including pregnancy and end-stage kidney disease) are known to cause iron insufficiency. (21, 22)

Further, iron supplementation significantly improves or even eliminates the symptoms of RLS in many patients. For example, RLS patients with low-normal serum ferritin experienced significant improvements in their RLS symptoms after 12 weeks of iron supplementation. (23) And oral iron was as effective for treating RLS as pramiprexole, a dopamine agonist, although the response rate for both treatments was relatively low (46.7%). (24)

The tricky thing about iron deficiency is that the solution is often not as simple as taking an iron supplement. Iron deficiency is frequently secondary to SIBO, gut infections, or other inflammatory states, which explains at least in part the association between RLS and these conditions. Iron deficiency caused by infection or inflammation is mediated primarily by the hormone hepcidin, which at high levels can decrease serum iron and reduce iron absorption from the GI tract. (25)

One cause of increased hepcidin levels is the production of IL-6, an inflammatory cytokine present in most inflammatory diseases. Another cause of increased hepcidin levels is the presence of lipopolysaccharides (LPS), which are components of gram-negative bacteria that can enter circulation as a result of SIBO or other gut infections. Thus, increased levels of circulating IL-6 or LPS can result in iron deficiency, and subsequently, RLS.

What to do: If you have RLS and iron deficiency, the first step is to identify why you’re iron deficient. If the cause is blood loss (such as from heavy menstruation in women) or dietary insufficiency (such as in vegetarian or vegan diets), increase your consumption of iron-rich foods such as liver and red meat. You can also consider an iron supplement; I recommend Proferrin ES and bovine ferritin, because they are better absorbed and better tolerated than plant-based iron supplements. 

However, if the cause is SIBO or a gut infection, increasing iron intake can often make matters worse by creating an environment that promotes pathogen growth and inflammation. (26, 27, 28) For this reason, it’s best to address the gut before (or at least concurrently with) adding iron supplements.

As you can see, restless legs syndrome is complex, and several factors could come into play when trying to figure out the cause. As with many other health conditions, RLS is best seen as a symptom which signals that something else is amiss, and it’s necessary to dig deeper to find out the root cause, and how to treat it.

Do you suffer from restless legs syndrome? If so, has this article helped clarify what might be causing it? Share your experience in the comments.

Dr. Pimentel has been very active in research and served as a principal investigator or co-investigator for numerous basic sciences, translational and clinical studies in areas like IBS and the relationship between gut flora composition and human disease.  He is widely known and sought out for major scientific developments that he’s pioneered, including the discovery that IBS is a condition of altered intestinal microbial balance.

In this episode, we cover:

7:36  What is small intestinal bacterial overgrowth? 11:20  Testing for SIBO 18:42  The future of SIBO treatment

[powerpress] Chris Kresser:  I’m Chris Kresser and this is Revolution Health Radio. Hey, everyone.  Chris Kresser here.  Welcome to another episode of Revolution Health Radio.  I’m really excited about our guest today.  We have Dr. Mark Pimentel, a global expert on small intestine bacterial overgrowth, and I’m going to talk to him all about some unresolved questions and problems or issues with SIBO, the SIBO hypothesis, diagnosis and treatment of SIBO, and I’m really looking forward to this, and I hope it’s going to be useful for you as well. Mark Pimentel is an associate professor of medicine at Cedars-Sinai Medical Center in Los Angeles, California.  His medical training includes a fellowship in gastroenterology at the UCLA Affiliated Training Program.  He’s been very active in research and has served as a principal investigator or co-investigator for numerous basic sciences, translational and clinical studies in areas like IBS and the relationship between gut flora composition and human disease.  Dr. Pimentel is widely known and sought out for major scientific developments that he’s pioneered, including the discovery that IBS is a condition of altered intestinal microbial balance, which we’ve talked about before; the recognition that antibiotics improve IBS, irritable bowel syndrome, and this officially legitimized IBS because before these discoveries, IBS was often considered to be a psychosomatic condition; the discovery that methane produced in the gut by specific microbes produces constipation, which we might talk about today; and then his work linking SIBO to IBS and other conditions. So again, I’m really, really excited about this episode, and without further ado, let’s get to it. This episode of Revolution Health Radio is brought to you by 14Four.me.  14Four is a diet and lifestyle reset program I created to help you dial in the four pillars of health — nutrition, physical activity, sleep, and stress management.  Whether you want to lose weight, boost your energy, treat a chronic health problem, or just maintain your current good health and extend your lifespan, these are the four areas you need to focus on before anything else.  In the 14Four program, I walk you through every step of the process, from cleaning out your pantry and shopping for the right foods to recipe and meal plans to video demos of workouts that you can do at home without any special equipment to guided meditation and stress management programs to daily sleep tips to personalized recommendations for what to do after you finish the reset.  14Four is a great option whether you’re just getting started with this stuff or you’ve been on the path for a while.  In fact, I do a 14Four myself three or four times a year to hit the reset button and give myself a boost.  To learn more about how 14Four can help you achieve your health goals, head over to 14Four.me. OK, now back to the show. Chris Kresser:  Dr. Pimentel, thanks so much for being here.  I really appreciate it. Mark Pimentel, MD:  It’s my pleasure.  Thanks for inviting me. Chris Kresser:  Maybe you could start by telling us a little bit about how you got interested in SIBO in the first place.  I’m always curious to hear how people get involved in their field. Mark Pimentel, MD:  Well, it’s interesting.  I mean, when I was in residency and planning my fellowship and my career, obviously IBS was not on my radar.  I think what I learned very quickly when I started to learn gastroenterology is that IBS was an area not too many people were interested in, and as I started to see these patients, I was fascinated by the fact that they all had distention and bloating, and it seemed to me that bacteria and fermentation in the gut could be an important aspect of that.  I also began to notice under the tutelage of my mentor that these patients often had positive breath tests, and we began treating them with antibiotics, and we got some remarkable results, and so this really was the beginning of a long journey into trying to help a group of patients that really were outcasts in medicine.  Doctors just didn’t want to see them, didn’t know what to do with them. Chris Kresser:  Right.  For all the listeners, at that time, IBS was largely considered to be a psychosomatic condition, right?  Antidepressants — or maybe no treatment at all — was what was offered at that point. Mark Pimentel, MD:  Yeah, I mean, in some of the early days and some of the early patients that I saw, I remember distinctly this one retired lady who had IBS.  She brought out a paper bag full of six different psychotropic medications, and she said, “I no longer need these medications,” but that was the therapy she was given, to no avail, and it didn’t help her. Chris Kresser:  Yeah.  You were definitely ahead of your time now because I would say it’s pretty universally recognized — well, maybe I’m getting ahead of myself! — but at least within the scientific community, that altered intestinal microbiota is a major player in not only IBS, but a whole range of other diseases, both gastrointestinally and even extra-intestinally.  Things like fibromyalgia and even depression now are being linked to altered intestinal microbiota, so you were a real pioneer there, and I just want to thank you for your contribution to that. Mark Pimentel, MD:  Well, it’s humbling to actually see this evolution because even before the term ‘microbiome,’ we were kind of yelling in the wilderness and saying, “You know, microbes may be important in some of these functional disorders.”  It wasn’t very well accepted, obviously, in the beginning, but it’s really nice to see the evolution of the science, and really it’s come such a long way.  Very exciting. Chris Kresser:  It has, yeah.  We were chatting before.  Most of my listeners know that I struggled with a long chronic illness that started with an infection in Indonesia, and I saw you at some point early on in that journey, and that was enough to convince me that some alteration of the gut by a viral infection or a parasitic infection or antibiotic use — all of which were actually historically present for me — was something that could create so-called IBS or potentially even IBD.  There wasn’t much research on that at that time, but my own personal experience of it was enough to convince me! Mark Pimentel, MD:  Yeah, it’s very interesting how a lot of these patients are describing exactly the scenario you had, and we’re learning a lot from that, actually.  I have to say just briefly, my largest group of researchers are my own patients because they teach me the answers.  You have to listen to your patients because they’re telling you what they’re feeling and their experiences. Chris Kresser:  Yeah, I feel the same way.  I’m so glad to hear you say that. So let’s move on to SIBO.  This episode, since we have Dr. Pimentel here, I really want to focus on, not some of the basics of SIBO, which we’ve already covered at some length, but I want to talk to Dr. Pimentel about some of the unanswered questions, at least in my own mind, and get his take and opinion on those.  But before we dive in, maybe we can just start with what should be or would seemingly be a straightforward question but maybe is not, which is, what is SIBO?  How are you defining it now?

What is small intestinal bacterial overgrowth?

Mark Pimentel, MD:  I think the term SIBO is evolving in a sense because initially we used the term small intestinal bacterial overgrowth based on breath testing, and I think breath testing has a lot of merit, but SIBO does not equal SIBO does not equal SIBO, and I think both from a breath testing standpoint and even a microbiology standpoint we know there are different forms.  But essentially the bottom line is that it’s an overcolonization of specific bacteria, usually the colon bacteria, into the small intestine, where they don’t belong.  Ruminating animals, for example, like cows and sheep and horses, they have a lot of bacteria through their small bowel in order to help them absorb and digest grass, which they don’t have enzymes for.  Humans don’t need that.  Our small bowel is almost sterile — on purpose — because we’re sophisticated, we can digest many different things, and we have all the enzymes for that.  And when all this bacteria builds up in the small bowel, then you get this bloating, gas and distention, and a lot of changes in bowel function. But the reason I started by saying, “SIBO is not SIBO,” is because as we move forward, we’re seeing that if you have methane type of organisms in the small bowel, you’re getting constipated, and if you have hydrogen type, you get more of the loose bowel movements or mixed IBS.  And it’s going to get even more complicated because we think that the type of bugs may be associated with different diseases.  Maybe fibromyalgia has a different type of overgrowth than, say, just simple IBS.  So those complexities are emerging. Chris Kresser:  Right.  And I’ve seen some studies that show that apparently healthy controls — and of course, I always wonder about that because the definition of a healthy control has certain assumptions that I’m not sure are correct, but let’s just assume that they are healthy — up to 20% can have SIBO, at least according to breath tests or other testing methods, so what do we make of that?  Is it possible to have SIBO and be completely asymptomatic, in your opinion? Mark Pimentel, MD:  That’s a great question.  The breath test, of course, has its limitations, and that may be part of the reason why some of the healthies are positive, but I like where you’re going, and you’ve obviously put a lot of thought into this, because healthy is not healthy.  Even the definitions of what is a normal bowel habit in textbooks were based on studies that didn’t exclude IBS patients. Chris Kresser:  Right. Mark Pimentel, MD:  The range is three times a day to three times a week as a normal bowel function, but after treating overgrowth in thousands of IBS patients and all of a sudden they’re having a perfect bowel movement every day, some of the IBS patients are better than healthy people that I’ve seen. Chris Kresser:  Right! Mark Pimentel, MD:  So it really speaks to the question, OK, so what is true normal?  And if we don’t know what true normal is, then it’s really hard to define healthy and then to compare breath tests between healthy and unhealthy.  So it’s complicated, and the answer to your question is, if we take super-healthy people who are spot-on perfect, the chances of having an abnormal breath test are very low, less than 5%.  But people might critique that and say, “Well, super-healthy is not normal either.” Chris Kresser:  Well, yeah. Mark Pimentel, MD:  It’s splitting hairs. Chris Kresser:  Yeah.  It may not be common, but I would like to think it’s normal for humans.  It’s, perhaps, our default state if we don’t get in the way of that. Mark Pimentel, MD:  Right. Chris Kresser:  And certainly everyone listening to this show is looking for that super-healthy state, so I appreciate that distinction.

Testing for SIBO

Let’s talk about breath testing next because that’s something I really wanted to go into some detail on.  As some listeners will know, there are different kinds of breath tests.  There’s a lactulose breath test and a glucose breath test, and I want to talk to you about some of those distinctions.  At this point, do you look at breath testing as being kind of the best compromise available, in the sense that other test methods are invasive and if you’re sampling a part of the small intestine, if SIBO is patchy, you may miss it because you’re getting a portion of the intestine that doesn’t have the overgrowth?  Tell us just kind of in a general sense where you’re at in terms of looking at breath testing as a whole category. Mark Pimentel, MD:  Well, I think this is where is gets confusing for patients because, for example, Mayo Clinic doesn’t like breath testing, so they do a lot of aspirates.  They tend to want to take the sample.  Taking a sample is very expensive.  The validity of that is questionable, too.  I mean, we don’t really know what part of the bowel to culture for your best result. Chris Kresser:  Right. Mark Pimentel, MD:  You hit the nail on the head.  It could be patchy.  We don’t culture everything, so maybe we should be doing PCR or sophisticated genetic techniques to look at the bacteria.  Mayo Clinic doesn’t do that for their aspirates.  All they do is culture, so they’re missing stuff.  So there’s no perfect technique, but I have to say that what we’ve seen in the papers and in our own experience is that breath testing is kind of a compromise.  It’s extremely easy to do.  Patients can do it even at home, in some circumstances, with some of the kits that are available, and it’s convenient. But what I will say is that when the breath test has methane in it — and I suspect we’ll be talking about that a little bit later — that’s super accurate. Chris Kresser:  Yeah. Mark Pimentel, MD:  So in that context, when you have methane on the breath test, that’s extremely predictive.  Hydrogen is a little bit more challenging. Chris Kresser:  OK.  Let’s talk a little bit about methane detection now.  I know this is an area where you’ve made big contributions, and up until fairly recently, a lot of commercial labs weren’t even offering methane as an option.  Methane has some specific effects and characteristics compared to hydrogen, so maybe you could tell us a little bit about why it’s important to test for methane overgrowth and if you’re still using 3 parts per million at baseline as the cutoff there. Mark Pimentel, MD:  Yeah, so methane is intimately related to constipation.  In fact, there’s now a large series of studies, various investigators around the world proclaiming the same results, and a meta-analysis.  But essentially, if the methane is present on the breath test at greater than 3 parts per million at any part during the test, the association to constipation is over 90%.  The other very interesting aspect of methane is that methane is proportional.  So the higher the area under the curve on the breath test for methane, the greater the patient’s constipation severity is.  And we know from animal studies that giving methane, just the gas itself, constipation or slows transit remarkably by about 60%, so getting rid of the methane is key.  The breath test is very accurate at picking up methane, and I think, to be honest with you, there’s almost no argument about methane and breath tests in terms of the utility of breath tests in that particular circumstance. Chris Kresser:  And is it the same difference there between lactulose and glucose in terms of detecting methane?  Is lactulose more likely to detect it for the same reasons? Mark Pimentel, MD:  The interesting thing about methane is that methane is not driven by the lactulose or the glucose; it’s driven by the presence of hydrogen, because hydrogen gas from fermentation of other bacteria fuels — Chris Kresser:  It’s the food for the methanogens, right? Mark Pimentel, MD:  Right, exactly.  I would say more than 90% of the time, just at baseline, the methane is already elevated, whether you’ve given the glucose or the lactulose or not.  So it really doesn’t matter which breath test you use because the methane will be there, and you don’t see, necessarily, a rise in methane all the time. Chris Kresser:  OK, I have a bonus question for you, and this is just selfish clinician-to-clinician from a test result that I saw the other day.  It might be a little over everyone’s head, but we have a patient, and we treated them for SIBO.  They had high hydrogen levels and methane levels.  Then on the retest, their hydrogen was actually zero at nearly every time interval, but their methane was still a little bit elevated.  How is that possible since the methanogens require hydrogen to produce the methane? Mark Pimentel, MD:  There are different methane profiles, and this gets a little complicated.  There are methane profiles where methane is elevated throughout the test and hydrogen is zero all the way across the board.  The only way that can happen is if the methanogen organisms are colocalized precisely where all the hydrogen organisms are.  In other words, the methanogens are eating up every bit of hydrogen that you find on a breath test because they’re sitting beside each other throughout the gut. Chris Kresser:  Interesting. Mark Pimentel, MD:  When you see hydrogen on the breath test, it means that the methanogens are not all localized to where the hydrogen producers are, and we call that ‘hydrogen escape.’  It’s kind of a term we made up.  Let’s say there’s 3 or 4 feet of bowel where there are hydrogen producers, but there are no methane producers in the area, so you’re getting this hydrogen release and you’re picking it up on the breath test.  So maybe you’ve gotten rid of the hydrogen in that area and therefore you’re only left with areas with some methanogens colocalized with hydrogen. Chris Kresser:  Yeah, that makes sense. Mark Pimentel, MD:  That’s kind of hypothetical.  It makes sense, but of course, you can’t dissect humans to prove that.  You can only kind of theorize how it works, but that’s how we think it works. Chris Kresser:  It’s a reasonable theory, yeah. OK, great.  Before we move on to treatment,  let’s talk a little bit about what’s on the horizon in terms of testing.  I’ve read a few papers that talk about electronic nose or metabolomics.  Is there any methodology that you’re aware of or excited about that might help us to have more accurate testing without being invasive or costing too much money? Mark Pimentel, MD:  Well, I think that there are a number of people looking at volatiles in the breath for detection of cancer, for detection of getting bacterial signatures.  There’s a lot of excitement around that.  The problem is I haven’t seen anything that is kind of an aha moment yet. Chris Kresser:  Right. Mark Pimentel, MD:  I think it’s a matter of time because so many people are working on this, so I’m very excited, but I’m waiting for the aha moment that somebody says, “OK, this is very predictive of X, Y, and Z, and this is how you treat it.”  And I think those are the connections that will be made in the next few years. Chris Kresser:  Maybe we’ll have SIBO-sniffing dogs. Mark Pimentel, MD:  No doubt! Chris Kresser:  We have cancer-sniffing dogs, mold-sniffing dogs now.  I wouldn’t be surprised! Mark Pimentel, MD:  With YouTube, it’s only a matter of weeks. Chris Kresser:  Right!

The future of SIBO treatment

All right, so let’s talk a little bit about treatment now, and specifically, along the same theme here, not the treatment that goes well and works perfectly as advertised, but some of the issues that we see with treatment.  The first thing I want to talk about is some of the studies that have shown recurrent rates of up to 45% in people that have been successfully treated.  They go breath test negative, and then almost half of those people are getting SIBO again.  Do you accept that number, is that your experience, and what do you think is happening there? Mark Pimentel, MD:  The TARGET 3 Study, which is the latest rifaximin study, is the only study, really, that’s blinded and controlled for treatment and retreatment.  And what I was shocked at when I saw the results of the trial is it almost mirrors what happened in my clinic back when I started using rifaximin.  You can’t say that in my clinic now because I basically see the patients that fail, because everybody in the community is using it this way, and so I’m seeing the tougher cases.  But back when I started using rifaximin, this was exactly the rate. We see about 72% of people have some response to rifaximin, for example.  Using the FDA endpoint, the patients who responded by FDA criteria, over 18 weeks 36% of them never relapsed, and they just dropped out of the study because they were done.  They didn’t relapse.  And then the 64% who did relapse then were randomized into the double-blind phase of the trial and responded again and again versus placebo, which was good. But the point is that pretty much mirrors what I see.  I see about 70% of patients with IBS or SIBO — however you want to frame it — but definitely with the breath test, more than 70% respond to rifaximin.  What we then are looking at is relapses, and I think for sure I’m seeing about a third of patients that I don’t see them for months and months and months, and they never have a relapse, maybe more than a third.  But then the rest of them, they will have relapses.  And it depends.  Some of them relapse in six months, some of them relapse in three months, and some of them relapse in a week, and those are the tougher cases. Chris Kresser:  So what do you think is driving the relapse?  I know you’ve done a lot of work on intestinal motility and impaired motility and its contribution to SIBO and relapsing SIBO, so maybe you could talk a little bit about that and if there are any other factors that you are investigating right now in terms of the propensity for relapse. Mark Pimentel, MD:  Well, this speaks to kind of food poisoning triggering everything because this starts to get into that area, but we think food poisoning causes some kind of neuropathy or motility disturbance of the intestinal tract, and then you get stasis or slowing, and then the bacteria start to accumulate.  I would say that probably 70% or 80% of patients who come to me with overgrowth, that’s the mechanism of action, or at least that’s what we feel is the mechanism, and that it’s a reduction in the migrating motor complexes as a result of some insult in the past. Where it gets tricky is that depending upon how bad that is or how bad the motility is will probably predict how quickly the bacteria will return.  The problem is we don’t have a good grading system for how bad the motility is, so I can’t tell a patient, “Look, you have this test; you’re going to relapse in two months.”  We don’t have that kind of sophistication yet.  I’d love to see that come. When the patients relapse in one week or two weeks, then we start to be concerned that it isn’t just a motility disorder, that maybe it’s an adhesion or some other mechanical cause for the overgrowth to begin with and not just the motility disorder. Chris Kresser:  When you say ‘impaired motility,’ is that always clinically evident, like delayed transit time, or is it possible to have a defect in the migrating motor complex, but still have regular bowel movements? Mark Pimentel, MD:  The migrating motor complex is responsible for cleaning the gut — or the small intestine, specifically — when you’re not eating.  The intestines have kind of like two computer programs.  One is eating mode, one is cleaning mode, and usually it’s the cleaning mode that goes bad in terms of the bacterial overgrowth.  If you were to ingest a meal, for example, and you measured stomach emptying, stomach emptying is perfect.  But that’s not telling the whole story, so if we really want to know what the patient has, we do a manometry of the upper gut.  We put a tube in that detects motor function, and we’re able to see how many migrating motor complexes, what happens when they eat, how are the mechanics of the gut working, and we can diagnose these things.  But if you have no migrating motor complex in 6 hours, is that severe, or do I have to do it for 24 hours to know how severe it is?  The patients don’t want to have a tube in their nose for 24 hours, so it’s really hard to grade these things. Chris Kresser:  Mm-hmm.  What do you think of the idea that dysbiosis or changes in the microbiota in the colon could be a predisposing factor to SIBO and SIBO recurrence? Mark Pimentel, MD:  I can’t discount changes in colon in terms of a response to antibiotics, although I will say with rifaximin, specifically, I think this has probably convinced some of late critics who were saying, “Well, maybe it’s the colon, maybe it’s the colon,” the stool study that we did and microbiome work that has been described at meetings but will be fully presented at the ACG meeting in Hawaii, there really is no change in the flora of the colon in these patients with overgrowth or IBS after rifaximin.  So rifaximin is not doing anything to colon bacteria, at least in stool.  I can’t tell you the cecum or the higher parts of the colon.  And no increases in yeast and other things in the case of rifaximin — in the stool, again, specifically looking at that area. Chris Kresser:  Right. Mark Pimentel, MD:  We think that all along, as we’ve been saying rifaximin dissolves in bile, will work mostly in the small bowel, not in the colon when the bile is gone, rifaximin crystallizes — I think we’re all on the same page with that now.  But I can’t totally dismiss the possibility that it is a dysbiosis in the colon.  We’re going to require more work there. Chris Kresser:  Right.  OK. Mark Pimentel, MD:  One more point on that, though. Chris Kresser:  Sure. Mark Pimentel, MD:  I will say in our animal models where we give food poisoning, Campylobacter, to the rats and then we follow them over time, they develop overgrowth.  But when we do PCR of the colon, we see absolutely no differences between the colon, the cecum, or any part of the colon in the rats who got Campy and the rats who never got anything and are normal.  It’s all in the small bowel, the detrimental events. Chris Kresser:  Yeah, that’s really interesting and would definitely seem to support your argument there. Mark Pimentel, MD:  Yes. Chris Kresser:  Let’s talk a little bit about diet.  Within the, let’s call it, allied health professional world, functional medicine, alternative medicine community, it’s common to prescribe a low-FODMAP and even low-starch or no-starch diet during treatment for SIBO, and the thinking there is that these are carbohydrates that are poorly absorbed and can become food for the bacteria that are overgrown in the small intestine.  We ourselves at our clinic have been doing that for some time, but I have a couple of questions about that in my own mind, and I’m curious to get your take on it. Number one is I saw a study recently — I’m sure you saw it — that showed that rifaximin plus partially hydrolyzed guar gum was more effective than rifaximin alone, and that’s essentially a prebiotic that would seemingly be expected to feed the bacteria in the small intestine, but yet this study showed that it significantly improved the treatment. And then the second thing is that, as far as I know, there’s been no study yet that has examined the efficacy of a low-FODMAP or low-residue diet during treatment other than an abstract that was presented at Digestive Disease Week a couple of months ago, and I haven’t been able to track down the full paper, so I’m curious to hear your thoughts on that. Mark Pimentel, MD:  Well, I can say you’re extremely well read because, yes, these are issues, and these papers are very, very interesting and hard to put into the context of this.  You’ve opened up a lot of things to talk about, and I’m just trying to figure out where to start, but let me start with the guar gum aspect.  I have told my patients from day one of rifaximin or treating with antibiotics — and this goes back to the 1980s; this is an old microbiological concept — happy bacteria, happy and well-fed bacteria, are more sensitive to antibiotics and are easier to kill.  What that means is that most antibiotics work on the replicating cell wall of bacteria.  When bacteria are in hibernation, starving, distressed, they wall off, don’t replicate, and they just sit there, waiting for conditions to improve.  That’s a survival mode.  So when the bacteria are in survival mode, antibiotics won’t penetrate and won’t work as well. Chris Kresser:  Mm-hmm.  I have heard you say that. Mark Pimentel, MD:  If you give guar gum or you augment their eating — so now you’re feeding them, they’re thrilled, they’re enjoying all that food — they’ll be more sensitive to rifaximin.  So when I treat with rifaximin, or antibiotics, in general, for these IBS patients, I don’t want them to be on a low-FODMAP diet simultaneously or any kind of carbohydrate restrictions.  I want those bacteria happy and fed because they’ll respond better, in my experience, and the guar gum study kind of supports that notion. Now, speaking to low-FODMAP diets, for example, it’s kind of a joke I tell patients, and I don’t mean to be flippant, but it you don’t eat any food at all, the bacterial overgrowth will be better. Chris Kresser:  Right! Mark Pimentel, MD:  Looking at the entire spectrum of people publishing papers and/or books about diets for SIBO or for digestive health, the more restrictive you make the diet, the less the bacteria is going to be happy, or you’ll starve the bacteria out, but you want to do it within a rational and a reasonableness for the patient because we all want a relatively normal life, we all want to walk with our friends into a restaurant and at least be able to get something and not be so difficult, so that’s kind of how I start my conversation in the clinic.  The low-FODMAP diet works.  I mean, there’s no question.  Studies show it works.  I’ve experienced its benefit.  It’s just difficult for patients to maintain in the long term. Chris Kresser:  Mm-hmm.  I’ve also seen some studies — I’m curious to get your take on these — that the low-FODMAP diet over the long term may actually decrease bifidobacteria production in the colon, which would make sense, given that that’s the substrate that those bacteria use, and therefore, there may be some disadvantage to doing a really strict low-FODMAP diet.  Maybe it’s helpful for SIBO or IBS recurrence, but maybe it’s not great for the colon.  What do you think about that? Mark Pimentel, MD:  I agree.  Sometimes I think the paleo folks have it right because when we think about how we evolved, we didn’t have potato chips and various refined carbohydrates back then that we have now.  And eating whale blubber and seal meat and so forth, those were the staples, and a few berries off of the plains or whatever.  It was a very different time, and the question is, is our digestive tract honed into that type of diet more than it is to what we’re currently doing?  It’s so hard to know, but what I tell my patients is carbohydrates feed bacteria.  You can leave the bottle of oil on the counter for cooking, and it will never become contaminated because bacteria cannot live on oil alone.  You can leave your protein powder in the cupboard, and for the most part, it’s going to be fine.  As soon as you put carbs in something, if you take a teaspoon of sugar and put it in that olive oil, that olive oil’s done in 24 to 48 hours. Chris Kresser:  Right. Mark Pimentel, MD:  It’s carbohydrate related.  Now, I don’t tell my patients zero carbs.  I tell them try to eat the carbs that humans easily absorb and digest, so white bread, of all things.  It sounds like I’m telling them to eat Wonder Bread, but French, sourdough, and Italian bread are white breads, and they’re a little bit better than just Wonder Bread or the off-the-shelf, in-the-bag bread. Chris Kresser:  So you’re talking about higher glycemic carbs that would be absorbed further up in the digestive tract and less likely to feed bacteria. Mark Pimentel, MD:  Kind of like a glucose breath test versus a lactulose breath test.  You want to feed them less, as less as you can, and patients tolerate that well.  I call it kind of our low-fermentation diet as opposed to low-FODMAP. Chris Kresser:  Yeah. Mark Pimentel, MD:  But everything becomes individualized over time.  Patients will come in and say, “Well, yeah, that diet works great except for onions,” and they’ll tell me, but at least they can go to any restaurant in the country and get a meal and not feel so socially isolated. Chris Kresser:  Right.  It seems so tricky because I totally get how that diet is better for SIBO recurrence possibly and even symptomatically.  I’ve seen that in our patient population.  But I do get concerned about the longer term.  You mentioned paleo, and it’s definitely true that our ancestors ate a lot of fermentable carbohydrate, like starchy plants and non-starchy vegetables and all kinds of stuff that would provide food for that beneficial bacteria in the colon, so my dilemma is, in fixing one problem, are we causing another one?  That’s what I’m always worried about.  It would be helpful if we had any studies at all to guide us in this area, but as far as I know — and correct me if I’m wrong — there haven’t been any studies specifically about a low-FODMAP or low-fermentation diet related to SIBO.  I know there have been a ton with IBS, but nothing that actually characterizes, does a low-FODMAP diet reduce the recurrence of SIBO after it’s been successfully treated? for example.  I’d love to see that question answered. Mark Pimentel, MD:  Yeah.  It’s not been answered, but if you want to add another layer of complexity to this whole thing, just to touch on methane briefly for a second, the highest population of methane colonization in the world is Sub-Saharan Africa.  And methanogens, it turns out, based on the microbiome work that’s being done on that particular organism, are super important to help liberate calories from nondigestibles.  So let’s say you have a high-fiber diet.  Humans generally can’t eat fiber.  Cows and ruminating animals have a lot of methanogens because the methanogens help facilitate digestion of fiber.  So what does that mean?  That means that you can get more calories from a meal if you’re a methane producer because you’re liberating calories from things that people who don’t have methane can’t get. So where am I going with this?  What I’m saying is if you take a population from Africa and immigrate them into the United States, and those folks, for genetic reasons or environmental reasons, have methanogens flourishing in their gut, which is an evolutionary advantage for getting and harvesting nutrients, it’s not an advantage when food is abundant and food is so processed and easily digested that you get more calories, and we’ve seen signals between methane and obesity.  The question then becomes, does one diet fit all?  And the answer is, no, it’s not going to be that way, and maybe it does have to do with your microbial profile benefits from this diet, and your microbial profile benefits from that diet, and it’s not as simple as one suit fitting all. Chris Kresser:  Yeah, I completely agree with that.  I’ve often said there’s no one-size-fits-all approach, and it’s really interesting to hear you say that about Sub-Saharan Africa because I know Jeff Leach and some other people who are down there studying the Hadza hunter-gatherers and looking at their gut microbiome because they’re one of the last cultures on Earth that is really still living a paleolithic lifestyle.  They’re down there trying to sequence the microbiome.  It’s the last kind of intact, normal human microbiome. Mark Pimentel, MD:  Right.  At least for that area. Chris Kresser:  Right, and what they’ve found are some really interesting things, which is that some of the bacterial species that we associate with ill health in the West are actually quite prevalent there in healthy populations, and vice versa.  Bifidobacteria, which is kind of universally considered to be a beneficial species in Western people, is virtually absent in those people.  So I think that really just supports what you were saying, that a great microbiome imprint for someone living in Sub-Saharan Africa could be a total disaster for someone living in the industrialized world. Mark Pimentel, MD:  Which is probably why probiotics have been challenging to prove effectiveness in certain diseases, is because it isn’t all that simple. Chris Kresser:  Right. Mark Pimentel, MD:  I think probiotics are the way of the future, but it’s just trying to find the right key for the right lock.  Science is on to this.  This is a very exciting time in terms of the microbiome, and I have a great deal of optimism for the future in terms of characterizing it and then finding the key and locks for populations. Chris Kresser:  Yeah, exactly. I want to step back to something you mentioned when we were talking about eating prebiotic fibers during rifaximin treatment to kind of make the bugs come out to play so that they will be killed.  Different antimicrobials work in different ways, for the listeners’ benefit, and rifaximin appears to work when the antibiotics are multiplying or splitting.  Is that correct? Mark Pimentel, MD:  That’s always the way antibiotics are best effective, is when the bacteria are happy.  For example, some bacteria form cysts or they sporulate, and once they’re sporulated, it’s done.  You can’t get an antibiotic to go into the cell or do anything.  Those are the kinds of concepts I’m talking about, is that stress or starvation will force those events in bacteria. Chris Kresser:  Spore forming.  Right. Mark Pimentel, MD:  Yeah. Chris Kresser:  Given that, I suppose the same would be true for some of the botanical antimicrobial protocols.  I know there’s been at least one study, which you may have seen, that compared the efficacy of rifaximin with a botanical protocol and found that they were roughly equivalent.  We use both in our clinic.  We will tend to start with a botanical protocol, and if that’s not effective, we’ll go on to rifaximin, or rifaximin plus neomycin if it’s methane.  But would you guess the same thing is true for the botanicals? Mark Pimentel, MD:  You’re referring to the study from Johns Hopkins? Chris Kresser:  Yeah, they had the four different botanical supplements. Mark Pimentel, MD:  Yeah, that’s the one.  I think botanical supplements have some benefit, and I’ve seen some of the studies like that one which show some interesting results.  I’ve done a couple of programs for the naturopathic college, and what I’ve learned from them is incredible because — you know, the funny thing is the naturopathic physicians are giving rifaximin, and when I first met them, it kind of befuddled me.  It would seem counterintuitive, but the scientists in their group — because they have a scientific core — they say, “Well, natural antibiotics are still antibiotics.  Bacteria still get resistant.  That’s where we get our penicillins:  from the plants.”  So the plant effects and side effects are identical to the pharmaceutical effects and side effects, and that really spoke to me in a way. So I think, yes, there are botanicals — garlic, for example — that can have effects or anti-methanogen effects, and they’ve been studied.  I think the big challenge with the botanicals is not their lack of efficacy; it’s a lack of funding and ability to get good studies out in the public domain and prove their efficacy.  I think the Johns Hopkins study is a great study, it helps to demonstrate that these things are possible, but we need more like that. Chris Kresser:  Yeah, I would agree. Let’s talk a little bit about methane treatment.  I believe it was one of your papers that showed rifaximin alone is only effective about 45% of the time — I could be getting numbers wrong — but when you add neomycin, it goes up to 80-something percent.  Is that your current treatment of choice for methane, still the rifaximin-plus-neomycin combo? Mark Pimentel, MD:  Right.  With methane, rifaximin alone or neomycin alone are relatively ineffective or modestly effective, and with then the combination of the two both in vitro, meaning in the lab, and in humans, we see a dramatic effect.  That is the cocktail we’re using now.  We sometimes substitute the neomycin for metronidazole, although that’s not published, so that’s mostly anecdote.  The neomycin-rifaximin combination was a small double-blind study we published about a year and a bit ago. The new kid on the block, although it’s not available yet, is we’re in phase II trials of a product that just inhibits methane production.  It doesn’t kill the bacteria — or I should say ‘archaea’ in the case of methane.  It doesn’t kill them.  It gets in and shuts down the machinery that makes methane, because we think the methane it what’s causing the constipation.  You don’t need to get rid of the bugs.  Just stop them from producing methane. Chris Kresser:  Right. Mark Pimentel, MD:  In preliminary work, that’s highly effective.  We should have some top-line results in the late fall, so you can look forward to hearing that.  I don’t have results yet.  The study is halfway through. Chris Kresser:  Right.  Yeah, I definitely will. Since you mentioned that, any other future avenues that you’re looking into or excited about?  Prokinetics, we haven’t really touched on that yet, but what have you been looking at doing lately in terms of prokinetics for people with the impaired MMC, migrating motor complex, and who are highly likely to relapse? Mark Pimentel, MD:  There’s a variety of prokinetics on the market.  I don’t like to use domperidone because of the side effects with the heart.  Generally we resort to two potential prokinetics.  One is erythromycin at a very low dose.  It has prokinetic properties at a very low dose and no antibiotic properties at that does, so that’s what we use.  Sometimes we get Resolor, which is prucalopride from Canada, a very potent prokinetic based on serotonin.  It doesn’t have any real side effects except for headache in some patients.  Those are the two. The problem with prokinetics is we’re kind of hitting a wall.  The circuitry of the gut is not connected well, and you’re kind of forcing it to do something that — and again, it depends on how severe that is in a patient, as to whether the prokinetic will work well enough, so we’re shifting gears almost entirely.  We’ve spent the last six years kind of trying to figure out, well, why is this happening from food poisoning?  And that led to the next blood test for IBS that was just launched about eight or nine weeks ago.  Are you familiar with that? Chris Kresser:  Yes. Mark Pimentel, MD:  There are two antibodies that get created after an infection like you described in Indonesia, and these antibodies, when they go up, they’re the ones that are causing the damage of the nerves.  We, in fact, did a study in animals where we just gave the CdtB toxin from food poisoning, not the food poisoning, and the rats get bacterial overgrowth, so we know the toxin that causes bacterial overgrowth and IBS, and we can measure the antibodies in the humans now to that toxin. So what does that mean?  First of all, it will tell us why you have the overgrowth, what the mechanisms are, and that it is likely this neuropathy.  Two, the antibodies, the higher they are, the worse the patient is.  Three, our entire focus now for the next two years is trying to get that out of the bloodstream and make the nerves come back to life, so really kind of essentially curing the disease.  Will it mean a drug in two years?  Drug development takes time.  But can we prove that that will reverse the disease?  I think in two years we’ll prove that that will reverse the disease, which means drugs will be developed around that concept.  That’s the exciting part, and then you don’t have to worry about whether you’re disturbing the microflora.  We’re basically treating it at the root. Chris Kresser:  Right. I’m kind of skipping back here.  There’s a question I wanted to ask you before we finish up.  I saw a study recently that suggested that the length of treatment with rifaximin should be correlated with the severity of the breath test results.  I believe in that study, they used a course of treatment as long as 12 weeks with no adverse effects.  What do you think of that notion, and are you using longer courses of rifaximin in people who have very severely elevated breath test results? Mark Pimentel, MD:  I’ve seen various groups or research groups around the world trying different cocktails for their patients with overgrowth.  I think that in my experience, and again, I haven’t studied longer-duration therapies, except I will say just in the phase II studies of rifaximin, there was a longer arm, and the longer arm did not work well.  It was really short-term therapy. I don’t have a problem with longer therapies.  Again, this will be described at the ACG and was briefly described at DDW.  Rifaximin does not cause microbial resistance of any magnitude.  In fact, if there’s any resistance whatsoever, it disappears within a week or 10 days after stopping the rifaximin, and so rifaximin really doesn’t create any kind of superbugs or any kind of resistance, and this was epic amounts of culture, stuff that even Cipro and other antibiotics that are true antibiotics didn’t have to go through.  Rifaximin did.  And it’s not apocalyptic on the microbiome, rifaximin, compared to, like, Cipro. Chris Kresser:  Yeah. Mark Pimentel, MD:  But what I was saying is that I think using these longer therapies is fine, very experimental.  I haven’t seen the need for it in my practice so far. Chris Kresser:  Right.  I’m mostly a natural medicine guy myself, but I’ve always felt like my standard is whatever works and causes the least harm, and if that happens to be a drug, then I’m all for it, and rifaximin certainly does seem to fall into that category. Mark Pimentel, MD:  Yeah. Chris Kresser:  Well, is there anything else, before we finish up, that if you could tell folks — let’s say we have folks out there listening to this who have SIBO and it’s recurrent, any words of wisdom or advice or even just a way for them to frame it in their mind that is helpful for them to think about? Mark Pimentel, MD:  Anything specific you want me to? Chris Kresser:  Well, part of it for me is just educating patients about the things that we’ve already talked about, so I think that this will help a lot, that SIBO is not necessarily a one-time thing.  I think it helps patients.  It’s not easy to hear that, right?  Most of us would like to be able to just treat it and move on.  But once they do hear that and they accept that, I think it helps with the outcome because then they know that they have to stay a little more vigilant and it’s something that they may have to treat repeatedly, and if they understand the safety profile of rifaximin, that’s a little bit easier to accept as well. Mark Pimentel, MD:  Right. Chris Kresser:  So nothing in particular.  I guess the question was more like, is there anything else you want to say?  We’ll put it that way. Mark Pimentel, MD:  Well, I think I know exactly what you’re getting at.  Let me give you an example of something that happened in one of the clinical trials which kind of speaks exactly to your point. As a patient in phase II studies of rifaximin, you take rifaximin, if you got better, you move on and get followed through the whole trial.  If you didn’t get better, you’re out.  One of my patients went into phase II.  She got rifaximin, it turns out, after the unblinding, and she came to my clinic, and I said, “Well, it looks like you didn’t do well in the trial.”  At the time, we thought she got placebo.  It turns out she got rifaximin.  She says, “No, no, I’m doing great!”  I said, “Well, what do you mean?  If you did great, you’re supposed to stay in the trial.  How much percent improved are you?”  She says, “Well, I’m 80% better.”  I said, “Well, that’s terrific,” and I said, “Why aren’t you in the trial?”  She said, “Well, they asked me if I’m all better,” and she interpreted it as, “If it’s an antibiotic, I should be cured.  I should be 100%.” Chris Kresser:  Right. Mark Pimentel, MD:  And 80% wasn’t like her urine infection in the past.  That’s a point for your listeners to kind of appreciate, that rifaximin is going to make you better when it works, it’s going to make you a lot better than anything we’ve had before, but it’s not like a urine infection where you’re cured, because the motility disorder underlying this is still there and you’re still going to have a little bit of gas and you’re still going to have poor clearance of the bowel, and it’s a bit of a lifestyle change until we have something that gets at the root. Chris Kresser:  Yeah, that’s really helpful. Well, Dr. Pimentel, this was certainly educational for me, and I think my audience is really going to appreciate it as well, so thanks so much for joining me. Mark Pimentel, MD:  Thank you for your time.  This was a lot of fun for me as well. Chris Kresser:  That’s the end of this episode of Revolution Health Radio.  If you appreciate the show and want to help me create a healthier and happier world, please head over to iTunes and leave us a review.  They really do make a difference. If you’d like to ask a question for me to answer on a future episode, you can do that at ChrisKresser.com/PodcastQuestion.  You can also leave a suggestion for someone you’d like me to interview there. If you’re on social media, you can follow me at Twitter.com/ChrisKresser or Facebook.com/ChrisKresserLAc.  I post a lot of articles and research that I do throughout the week there that never makes it to the blog or podcast, so it’s a great way to stay abreast of the latest developments. Thanks so much for listening.  Talk to you next time.