Diet, immunomodulation and Coping - Understanding IBD

Welcome to The Perfect Stool: Understanding and Healing the Gut Microbiome. This is your host, Lindsey Parsons, and today I'm talking about the naturopathic treatment of inflammatory bowel disease, or IBD, with Dr. Stephen Sandberg Lewis, a practitioner of naturopathic gastroenterology in private practice at Hive Mind Medicine in Portland, Oregon. He's been in practice for 40 years, and in 1999, he 1996, he joined the full-time faculty of the National University of Natural Medicine in Portland. Now adjunct faculty, he continues teaching, seeing patients, and supervising student doctors in complex digestive disorders. His areas of special clinical and research focus include irritable bowel syndrome, SIBO, GERD, hiatal hernia, inflammatory bowel disease, biliary dyskinesia, the sterile biome, gastroparesis, and chronic nausea and vomiting. He's also the author of the textbook entitled Functional Gastroenterology: Assessing and Addressing the Causes of Functional from GI disorders. But before I get started, if you haven't yet followed or subscribed to the show, be sure to do so. And if you wanna get transcripts of the podcast, pop over to my website, HighDesertHealthCoaching.com, and sign up for my newsletter. You'll also get my free ebooklet, Finding Your Root Cause Through Stool and Organic Acids Testing, when you sign up. Now onto the show. Welcome so much to the podcast, Dr. Sandberg-Lewis.

Mm, thanks for having me.

So I know that you guys had some pretty extreme heat when I was talking to you in preparation for this up in Oregon. Has that all passed now?

It is. It's a beautiful top 81 degrees and cool at night. And we're back to Cree apocalypse. I'm worried that this will be the new occasional norm, but other than that, it's great.

Yeah, well, that's good to hear. So today we're gonna be talking about inflammatory bowel disease, and I know you've got Crohn's and colitis under that title, and that there's different types of colitis, including like ulcerative, microscopic, and collagenous, but I think collagenous is a type of microscopic colitis. And so anyway, if you could just go over the different types of IBD and how they differ in terms of what's going on and the symptoms, just to start us off.

Well, if you use the term colitis, you're focused on the colon. And of course, Crohn's disease can cause something called Crohn's colitis, which is when Crohn's disease is present in the large intestine. It can also be present anywhere else in the gut, and most commonly in the small bowel, but there is Crohn's colitis. So There's also ulcerative colitis, which by its name is always in the colon. The big difference between these two main forms of inflammatory bowel disease in terms of the actual location and nature of the disease, the biggest one is that in Crohn's disease, you typically have areas of colon that are completely normal. By biopsy, by visible exam on a colonoscopy, any other form of imaging, you have these areas that look completely normal interspersed with areas that are diseased. Whereas in ulcerative colitis, it's a continuous process. It starts in the rectum if it's the mildest form, which is called ulcerative proctitis.. And then if it's going to get more advanced, it moves gradually up into the sigmoid colon, the whole left side of the colon, or even the entire colon. And there it's called pancolitis. So they look very different in that you don't have any areas that are spared like Crohn's colitis would have. There are a lot of other differences too, like one of the most striking differences in terms of lifestyle is smoking tobacco. And tobacco, it doesn't even have to be smoked. It could be a transdermal patch or some other delivery of tobacco, but tobacco actually reduces the risk of recurrence and severity of ulcerative colitis, whereas Tobacco increases the risk for bad outcomes, the need for eventual surgery, and general aggravation of the condition in Crohn's. Even though they affect the same areas and they're both called inflammatory bowel disease, we could go on with things that make them very, very different, and I'm sure we'll talk more about that.

That's interesting that you brought up the tobacco right off the bat because I think of that as like, okay, no, we've tried absolutely everything out there. And then maybe say, hey, maybe a nicotine patch. Is that something that you use with patients?

I'm not supposed to say that we do that.

Okay. Got it.

But I certainly remember very clearly a patient who was not responding to any standard medicines. Or natural medicines. And she came in to see me, and after we talked, she started smoking 5 cigarettes a day, and it completely put her in remission, and she stayed that way for years. She could have used a patch, she could have done something else, but she thought that was cheaper and just did that. So yeah, I'm not telling people to do that. We don't tell people to do that. But an interesting finding is that the nicotine receptors, nicotinic receptors, in the gut do respond to nicotine and have opposite effects in Crohn's and ulcerative colitis.

Interesting. And so how is, like, collagenous different from ulcerative colitis or microscopic?

Some writers and researchers still don't put microscopic colitis in the same category as IBD or inflammatory bowel disease, but I do. I make a little Venn diagram with Crohn's and ulcerative colitis, and I put microscopic colitis over on the side as a separate circle. But I do call them all inflammatory bowel disease. And the difference— microscopic colitis is the general term, and by the name you can tell that it means You can only see it with a microscope. This is the kind of thing that gets biopsied for when someone, especially someone over 50, starts to have copious, many times a day, non-bloody diarrhea. It can be very serious and can be a lot of weight loss and malnutrition. So microscopic colitis is the term for It's a normal colonoscopy for this kind of condition, but when you biopsy it, either the left or the right side of the colon, you take a biopsy, you will see microscopic inflammation, and that shows up as many lymphocytic white blood cells in the lining cells. And there's two forms. As you mentioned, one is called lymphocytic because you just see those lymphocytes. And the other is called collagenous. You see the lymphocytes there too, but in addition, there's a thick layer of collagen tissue, which is the tissue that normally makes up most structural parts of the body, but a thickening of that collagen protein in the deeper layer, just underneath all those lymphocytes. And to the best of the research, it seems as if collagenous colitis is probably a later stage because it has that same inflammation that you see with the lymphocytes, but now it's starting to thicken up. Generally, what happens in the body when there's chronic inflammation is there's a thing called fibrosis, or you might call it scarring, where fibrous tissue is laid down to try to patch things when there's a long-term inflammation. And I mean, that's one of the things that destroys the liver in cirrhosis. It's actually the healing process that can affect the function of the liver because of this fibrosis. So that's what's happening in microscopic colitis, both collagenous and lymphocytic.

Got it. Okay. And then in just regular ulcerative colitis, like on a colonoscopy, you'll see visible ulcers along the colon.

Right. You see either redness, which is called erythema. You might see erosions, which are shallow denuding of the surface, or you may see actual ulcers and bleeding and other signs.

So in terms of treating these diseases functionally, which ones do you see the most success with and which the least? Or are they all potentially reversible if patients are willing to stick it out and follow your treatment plans?

Well, I used to say that I have a 3-pointed approach. My latest lecture that I did a couple months ago for our gastroenterology course, I made it into a 5-pointed star. But for most people, I like to just talk about a 3-pointed approach of treatment. So that involves number 1, diet is one of the corners of the triangle. The next one is some kind of immunomodulation, something that helps to balance the immune system in the gut, which is where most of the immune system is anyway. And then the third corner is stress and coping. I tell people that right away, that these are the things we're gonna be focused on, you know, see if they wanna buy into that kind of approach. I don't like to leave out anything that's essential if it's there. So what's the most effective? Depends on the person. You know, I've had people who really needed to go to a counselor or have some hypnosis or self-hypnosis or mindfulness and maybe put that piece off and it just had to wait until they finally did that. For things to really improve. If you're walking on eggshells every day of your life because your boss is a jerk, or your primary relationship at home makes it so you don't ever really relax, you always feel on edge and ready to jump. If you have old tapes playing in your head and colon from childhood or earlier in life that haven't been resolved, those are key things to work on. I teach a course at the naturopathic college within the university called Gastroenterology Lab. It's a lab course because we do things, physical things. I teach them how to use Emotional Freedom Technique to clear unresolved emotional states and eye movement clearing techniques for the same thing. I teach them other physical techniques like ileocecal valve and hiatal hernia syndrome techniques and things like that, visceral manipulation. I just think it's really important. I think of gastroenterology as a, a physical medicine process as well as emotional and organ-based. That's one thing. That's one corner. The other corner, like I said, would be diet. And the gold star first one you think of diet would be either the specific carbohydrate diet that was created by Sidney Haas back in the 1940s, a New York pediatrician before they knew what celiac disease was. Specific carbohydrate diet was invented by Dr. Haas as a way to treat celiac disease. Gluten had not been discovered. They didn't know what caused celiac disease. Celiac means abdominal, so it was the abdominal disease. It's not anything that they knew, and gluten wasn't really discovered as a substance until, I think, 1952. So kids were dying of malnutrition because of celiac disease, and he created this diet that had only specific kinds of carbohydrates, hence the name, ones that were not highly fermentable by intestinal bacteria. And that was extremely successful in treating celiac disease as well as IBD.

Now, why would that be for celiac?

Because it's a gluten-free diet. Gluten is, is highly fermentable, and especially wheat because of the fructans in it. So that's the Primo diet. And then other diets have been designed off of that, versions of it. So there's the GAPS diet, the Gut and Psychology Syndrome diet, which took the Specific Carbohydrate Diet and added Price-Pottenger types of high fat to support the brain and fermented foods. And Bifidobacterium was added. Before that, only lactobacillus-containing foods were on the specific carbohydrate diet. So it just kind of advanced it to, to work more on autism and bipolar and depression and other mental conditions. Also, the brilliant Dr. Allison Siebecker, who I work with a lot and, uh, teach an advanced gastroenterology course with— she put together the Monash University FODMAP diet together with a specific carbohydrate diet, because we know based on research that both the FODMAP diet and the specific carbohydrate diet are very effective at treating both irritable bowel syndrome and inflammatory bowel disease and getting people out of flares. So she put the two of them together into one diet and one set of charts, which is really helpful. And then Dr. Nirala Jacobi took it one step further in Australia, again like the FODMAP diet, And she created what's called the biphasic diet, which is basically Dr. Sebecker's diet, but it has two phases. One that's a little stricter that you do first, and then the reintroduction phase. There's the second phase. So diet of some sort like this is extremely important and really helps in every way. Helps emotions, helps the physical structure, helps the microbiome. And it's really hard to get around not using diet. Often you can use a diet all by itself and get excellent results. And then the third piece is immunomodulation. In standard gastroenterology, this is all done by suppressing different parts of the immune system, either with prednisone, which kind of lays down a blanket over the almost entire immune system and decreases its activity. To bring down inflammation, or more specific types of immunomodulators. But they all are designed to suppress the immune system. In my approach, if I don't need to use something like that because we don't have time and there's too much tissue damage going on, I'll get them started on the diet, which can work as fast as prednisone in my experience. But I'll also, if I have time, I'll do something different. And that might be something like low-dose naltrexone. It is a prescription drug, but we use it in 1/10 to 1/15 of the normal dosage, and it works to raise endorphin levels in the body, which helps to balance the immune system's function. Uh, I like to say to people that the opiate receptors— that's what you're stimulating with your endorphins— in the digestive tract and in the nervous system. These endorphin receptors, when you block them for short periods of time with low-dose naltrexone, it actually stimulates the immune system and the pituitary gland to make more endorphins. And when you have higher levels of endorphins It helps to sort of orchestrate the whole immune system so that you don't have one part overreacting and another part underreacting. It helps balance it by stimulating certain types of cells called regulatory T cells, and the low-dose naltrexone is really good at doing that. So we'll use something like that, or we'll use herbal medicines such as turmeric or Boswellia. The common name would be— what were the 3 things that the wise men brought from the, from the East?

Frankincense, myrrh, and what was the first one?

Gold? Yeah, gold. Yeah. Well, it's frankincense. You don't have to take the gold. Yeah, frankincense is Boswellia.

So just to back up and sort of state the obvious, these are all autoimmune conditions.

Right. It's funny though, there are autoimmune conditions, especially Crohn's and ulcerative colitis. We know there are specific autoimmune markers that you can measure in the blood. The interesting thing is that a lot of textbooks of medicine still don't admit that in articles. They say, well, it's not known. We call it idiopathic inflammatory bowel disease, which means we don't know the cause. Really, I think it's almost overwhelming proof to say that these are autoimmune.

And what are the markers that you look for for the various conditions?

There's a lab called Prometheus that specializes in GI tract, and they do all kinds of advanced GI testing. They test, interestingly enough, for Crohn's disease upwards of 60 to 70% of people with Crohn's disease will have a marker in their blood, which is an antibody against Saccharomyces cerevisiae, which is baker's yeast. So they're called ASCA, anti-Saccharomyces cerevisiae antibodies.

They have that in a basic IgA panel even through like LabCorp though.

Other labs have started to do it. Prometheus was the one that initially did it. And then in ulcerative colitis, a large percentage of people will have p-ANCA antibodies, which is a substance made by neutrophilic white blood cells that you can have antibodies against, which is an autoimmune marker for ulcerative colitis. So, you know, you can do this panel where you check for these various— and there are other ones as well, but these are the main ones— where you can check the blood for these different antibodies and see if there's a pattern that looks more like Crohn's or ulcerative colitis or neither.

And in terms of your treatment, your natural treatments, does it matter whether it's one or the other?

It really matters. Now, with the diet, not so much. Although if we know someone has Crohn's, We're going to make sure they don't get gums and thickeners. I mean, that's true for probably both conditions, but carrageenan is a definite no-no for people with Crohn's.

So they want to make sure that's not in their diet, including thickeners like hydrolyzed guar gum or partially hydrolyzed guar gum. Or is that an okay one?

Well, see, that one's modified. It's like modified citrus pectin. It's different. Rather than xanthan gum or carrageenan or guar gum, which can really be problematic. The partially hydrolyzed guar gum, as far as we know, is not fermentable the way regular guar gum is.

Oh, okay. So that's the issue is that they're fermentable. So Crohn's patients are more susceptible to having problems with those gums and thickeners. This is like polysorbate 80 and— other things too, right?

Well, there's even some very fascinating research articles that look at the kinds of substances that help water and soap kind of sheet out in layers, like you use in your dishwasher. Detergents. Detergents, yeah. And that's a good word for it. I was thinking of some fancier word. Oh, surfactant. Detergents definitely often have surfactants in them. And there is some very interesting evidence from research that that may be a factor in either type of IBD. You know, again, when we talk about the differences between the diseases, ulcerative colitis really appears to be a mucus problem. In Germany, they've done a series of studies to look at phosphatidylcholine, common name lecithin, normally produced in the last portion of the small intestine, the terminal ileum. It's secreted there and it becomes part of the mucus that then flows in through the ileocecal valve through into the large intestine. You know, the large intestine has a special kind of mucus. It has two layers of mucus. The stomach and the large intestine have these two layers of mucus because the stomach has to protect itself from acid so it doesn't get digested, because it produces acid. And the large intestine— you really don't want the billions of bacteria per gram of material in the large intestine to touch the mucous membrane to actually touch the cells that line the colon, because that could stimulate an immune reaction which looks a lot like ulcerative colitis. So the large intestine has a very dense, deeper layer right up against the cells that line the intestine that's very dense and hard for bacteria to move through. And then it has a less dense more superficial layer that some bacteria can live in it, especially things like Akkermansia, a type of bacteria that really likes mucus. Then others live out in the opening, in the air, so to speak, even though there's no air there. It's an anaerobic environment, but in the space. We think that, at least according to these series of German studies, that if you're not having phosphatidylcholine, which is the stickiest, gooeyest substance in the world, mixed in with your mucus and then have that flow through your large intestine, you're not going to have normal mucus in there. You're not going to have these very important layers. And then bacteria are more likely— normal flora, of which, like I said, there are billions per gram in the large bowel, normal to have that much— they can actually end up touching some of the cells, and that's a no-no. That's going to stimulate a big reaction by the immune system.

So is that something that you tell people to supplement with?

Well, we're not doing that, mostly because I think we would pull that out if nothing else was working. But we have to have it specially formulated and triple encapsulated to get to the large intestine. Yeah, to make sure it isn't absorbed too soon.

So in other words, if you're, if you're eating processed food with soy lecithin, that's not gonna be helping you.

That's right. That's good for your gallbladder. It'll go to your liver and get used and put into your gallbladder to help prevent gallstones. But no, not otherwise. It's also a good source of choline, which your body can turn into acetylcholine, which is a very important neurotransmitter for the gut. So it's, it's really helpful thing, but not for the colon directly.

Forgive this brief interruption, but I just wanted to let you know that if you're struggling with a gut health issue like IBD, IBS, SIBO, Candida, gastritis, or GERD, or you don't have an official diagnosis but are dealing with chronic diarrhea, constipation, acid reflux, nausea, bloating, gas, or other GI symptoms, my specialty is helping clients with those issues. Together we discuss different testing options and the information that you'd get from them. Then I show you how to order tests yourself and educate you on what the results mean and the protocols that practitioners use to resolve those issues. If you want to share what you've been going through and see if a 5-appointment gut health coaching program is for you, you can set up a free 30-minute breakthrough session by going to the link in the show notes. Or if you can just afford one appointment at a time, or you think your issue may be resolved with one appointment, you can set up a 1-hour consultation, and that's also linked in the show notes. Let me just back up and ask about the antibodies to S. cerviciae. Because, you know, I think about Saccharomyces boulardii, which is Saccharomyces cervisiae subspecies boulardii, as a, a very common probiotic. Is that a problematic one then for people with Crohn's?

I'm not aware that it is, but certainly yeast overgrowth in general and Candida and Rhodotorula, some of these other forms of yeast that can overgrow in the gut. Can definitely be a big problem. Bacterial overgrowth, normal flora, especially in the small bowel, as well as yeast overgrowth in the small or large bowel, can be a big issue in Crohn's, even more so than ulcerative colitis, right? I don't tell people never take Saccharomyces cerevisiae or boulardii because it'll make your Crohn's worse. I'm not aware of that.

Okay, but you do tell them presumably to avoid gluten as part of the SCD diet, or which one do you use? You, you sort of gave me a series of them, but do you use the biphasic diet then?

Depends on the patient. One thing I want to mention too is I highly, highly, highly suggest that if they're eating gluten on a regular basis, before they discontinue it, get a blood test, a thorough blood test for celiac, non-celiac, and wheat allergy, because you'll never be able to get an accurate test again if you quit eating it.

And a thorough test would go beyond just tissue transglutaminase, or what, what all would you test to get a thorough test?

So a basic test that would test everything that would make it thorough I mean, there's some really thorough tests by Cyrex Labs and the Wheat Zoomer that's done by Vibrant America that are incredibly detailed and check for every possible kind of reaction you could have to gluten. But the basics would be tissue transglutaminase, both IgA and IgG, deamidated gliadin peptide, IgA and IgG, total secretory IgA.

And that's to check if the immune system's working in the first place?

That's just to make sure they don't have an IgA deficiency, which is quite common in celiac.

Right.

And also, so you'll know to forget— you'll know to ignore the TTG IgA and the deamidated gliadin IgA because they're not accurate if Total IgA is low.

And they would then be low as well.

Most likely. I mean, if they're still high, then they're high, but if they're normal, it doesn't mean anything. And that's why you have the IgG to back it up. Also, if you wanted to check for non-celiac gluten intolerance, which I think is a great idea, you would do anti-gliadin antibody IgA and IgG.

And that's blood. Right.

These are all blood.

Just cuz I know there's in the GI-MAP, there's an anti-gliadin from the stool. Is that worth anything?

Yeah, there are two labs that I know of that do that. The GI-MAP and then also the original lab that does all the testing from stool.

Genova?

No, not Genova. It's been so long since I saw one of those that I can't even remember the name of it. It's like EnteroLab, I think it is. And they do the TTG in the stool as well, as well as anti-gliadin antibody. So the last one, if you want to check for wheat allergy, is wheat IgE. That's the only one that's IgE because it's an allergy.

But do you think the stool ones are, are useful markers?

I don't know, they're not standard. I certainly take them to heart, but they're not standard ways of diagnosing celiac.

Right, right.

If it's anti-gliadin antibody that's elevated in the stool, that's pretty indicative of non-celiac gluten intolerance. And I think it makes sense to use saliva or stool rather than blood to do these tests because you're in the right compartment, you know, you're in the gut., but the standard tests are the ones to also do, and those are blood.

So do you, as a naturopath, do you do endoscopies and colonoscopies and that type of thing, or do patients come to you having already typically seen an allopathic doctor and gotten a diagnosis?

Do you mean do I order the tests or do I do them?

Do you perform them?

So I don't. Our license allows us to do that, but most gastroenterologists, they spend several days a week doing these procedures and I just don't think that's the highest calling for a naturopathic doctor when we have so many tools for actually, once we have the diagnosis, to treat it. But yeah, we could if we wanted to. In fact, Mark Davis, a former student of mine, who specializes in IBD in Bethesda, Maryland. He took the training, the 80-hour training to do it. He just decided after that that probably had other things that he should do. But yeah, we can do it, but we don't.

What is a typical functional testing regime for someone with IBD?

The first thing I do if I'm thinking, hmm, does this person have IBD. Let's say they have Crohn's, or they have the rare kind of ulcerative colitis where there's no blood in stool. Crohn's can have blood or not. Ulcerative colitis almost always does, sometimes doesn't. And you're not sure, but based on their other symptoms, you're really thinking about it. The first thing I do is a stool calprotectin. I think of the calprotectin as a really good way to decide if somebody needs a colonoscopy and biopsy or not. And if the levels are under 50, then we're thinking about other things besides IBD. Definitely, I think all labs at this point, for some reason, use the number 165 and above. Seems to be a really accurate number for indicating someone's in a flare, definitely when calprotectin's over 250, that's definitely an active flare of Crohn's or ulcerative colitis. Anyway, levels between 50 and 100, usually repeat it again in 3 or 4 weeks and see if it's going down or up because it's kind of in the equivocal maybe range. I do that, and again, if it comes back high And if there's not time because someone's really acute, you're going to just start treating them as if, right? But you can also get a stool sample and send it off as you're starting to treat them and see what the calprotectin is. I've had patients with calprotectins to over 2,000. That's almost typically, you know, someone who has a really severe flare. And so it's a great marker, non-invasive., and I like to use the calprotectin once I start treating someone. I like to do it every 6 to 8 weeks to see if the treatment's working. You know, someone's symptoms could be better, but they could still have pretty severe inflammation if you're kind of controlling it with the treatment. So I like to see if the marker's actually coming down. Calprotectin is another immune substance produced by neutrophilic white blood cells., and it's a really accurate marker for that. So how else do we diagnose? We send for colonoscopy if we think that's what's going on.

Yeah, no, I'm saying assuming they have the diagnosis, right? Like, so they've seen someone, they, you know, they have some form of IBD. I'm talking about what kind of testing you might do to look for other things going on.

Oh, yes. And that's where stool testing can be really helpful. Like I said, I will use the calprotectin as a a marker of inflammation. But then I'm also going to culture for yeast. I'm going to look under the microscope for yeast because it doesn't always culture. If it cultures, the labs will give us culture and sensitivity. The sensitivity testing will check for natural substances that would kill that particular yeast, as well as prescription. We'll also check for certain kinds of viruses such as cytomegalovirus, which can really kick up inflammatory bowel disease in ulcerative colitis patients. If diarrhea is a strong component, we'll do a Clostridium difficile toxin test because you gotta really treat that specifically if they have that and they won't get better. Until you do. And we'll check for small intestine bacterial overgrowth, especially if they have significant bloating and abdominal pain, which in Crohn's disease is sometimes all you have is sort of a tendency toward constipation, bloating, and abdominal pain. And abdominal pain can be the main symptom.

And will you check for SIBO with like a breath test or a Triosmart?

So the breath test of course measures for hydrogen and methane, and the Triosmart adds the third gas, which we had a lot of trouble getting a test for. They worked on that for over 15 years, and that's hydrogen sulfide. And I'm actually— I meet with physicians and researchers around the country every third Wednesday of the month for an hour, and we talk about the TrioSmart tests that we've done in this previous month, and we're trying to really understand how to use this. And how to treat it, because it's treated a little differently than other kinds of bacterial overgrowth.

So when you were talking about the stool testing, whose stool test do you use typically?

Well, if I order it for a patient, meaning someone who lives in Oregon or who has come to see me in Oregon physically, then they can actually be a patient. I can order lab work and prescribe medicines. I'm going to use— usually going to use Dr. Z's data. I like culture-based testing, first of all, because like I said, you can get a sensitivity. If you can culture the organism, you can get a sensitivity for a stool test and see what would be most specific for treating that bug to bring the numbers down. You can't do that if you just check PCR, the gene testing, the DNA testing, which many of the other labs have dropped the culture altogether and just do the, the genetic testing. Genova is probably the oldest lab. I've been using them since the 1980s. I think it was started by naturopathic doctors, which is kind of cool, but they still have options for doing culture as well as testing for genes.

So just to make sure people understand what sensitivity means, that is where it tells you which natural substances and antibiotics and such would kill the thing that you're testing.

I really need to ask how they do it. When I was being trained back in the 1970s, they would take the stool and spread some on a petri dish, and they would grow the bacteria or the fungus. And then once they grew it, they would put little paper circles that were impregnated with the different natural treatments or drug treatments. They lay those on top and they'd see how big an area of clearing occurred around those treatment discs. And that's how you knew if it— the bug was sensitive to it and it would be killed by it or not.

When it comes to culture, I've heard it argued that it's not as valid as PCR because it tends to just culture those bacteria that are aerobic and those will grow and proliferate, whereas the anaerobic ones won't.

Yeah, it also grows the facultative anaerobes, the ones that can, like Lactobacillus, that can live in some oxygen. But you're right, if you want to check all the anaerobes, you really have to do both kinds of testing. That's what I would suggest until we know more about what to do with some of these dozens and dozens of fully anaerobic organism markers. I think at this point, you know, we have the microbiomes kind of mapped out for both the colon and now for the small intestine. We know how to test for all kinds of bacteria using their DNA. But the thing to know about the colon, when you're looking at stool, you're looking at colon. Doesn't tell you about the small bowel. And according to researchers and all the textbooks, about half the bacteria in the colon are dead. So it's like 50/50 living and dead. So when you're looking at DNA, you're looking at dead and live bacteria. That's what you're looking at. When you do a culture, it won't culture if it's dead. You know, it's only living that will grow. So I still like that idea that I'm looking at what's alive and what's able to grow, as opposed to everything dead and alive. Because I think it's a real shame when doctors do PCR, you know, this DNA testing on stool, they find something that's high and then they treat it with strong drugs to try to kill it, or even strong herbs to try to kill it. I think they may be doing nothing except maybe some damage. You know, they're going after something that's already dead, at least half of it's dead.. So I just think that we have a lot of information about the microbiome, but we're like little infants, you know, squashing bugs that they see on the floor. And it, we're not really doing anything very intelligent. Not that infants aren't intelligent, but we're not doing anything that's maybe that meaningful or intelligent at this point by strictly using PCR. Until we have about 20 years experience with this, I think we're probably going to be making a lot of mistakes. So I like to go with what I know is alive. That's just my prejudice.

Okay. Do you find that there are certain root causes that you find commonly with Crohn's and colitis when you do these types of tests?

I mean, there's one piece, and that is almost all these stool labs will check the short-chain fatty acid levels in the stool. And we know that short-chain fatty acids are produced by friendly bacteria, the microbiome, when they metabolize fiber or mucus. Now they'll make short-chain fatty acids. We know that butyric acid is the best understood and probably at this point the most important of the beneficial short-chain fatty acids produced in the large intestine. It's a food source. You can actually get— I think it's like 20% of your calories from your own bacterial production of short-chain fatty acids. And it does many things. We, we know that in research it really seems to help reduce the risk of inflammatory bowel disease. So certainly when you see someone who has very low butyric acid levels, that in itself isn't the cause. It's the— whatever's not producing the short-chain fatty acids, which might mean they've got a really low diversity or low number of bacteria in the large intestine, so they don't have enough bacteria to produce it. Or maybe they don't take in the right kind of fiber or enough fiber to give the bugs what they need. Or maybe they don't produce enough mucus because they have some issue with that.

That always strikes me as ironic that a lack of short-chain fatty acids that are produced from eating fiber can be a problem, and yet the solution is eat less fiber and go on these, you know, diets like SCD that has virtually no fiber, right?

Well, I wouldn't say it has virtually no fiber, and it depends how you do it. And I, I certainly recommend working with a knowledgeable nutritionist that can help you individualize the diet. But there can be plenty of fiber on these diets. It's just specific carbohydrates. So it's not all fiber, and it's certainly not insoluble fiber like bran, because that's quite irritating. You know, soluble fibers, some are less fermentable than others. And certainly vegetable fiber, if someone is lucky enough to have the ability to process vegetable and fruit fiber in a healthy way when they have IBD, These kinds of diets can have plenty of fiber from fruits and vegetables and nuts and seeds. You're just choosing the lower FODMAP versions of those things.

Which sort of points to the fact that an overgrowth of bacteria in the small intestine is likely at the top of the train, or the, you know, that that's stopping that fermentation in the small intestine is the beginning of trying to solve the problem in the large intestine.

Right. The small intestine and the large intestine are whole different worlds. Like I say, they have different microbiomes when you study them. Also, the small intestine isn't small. It's the largest part of the, of the digestive tract, right? By about a factor of 4 or 5. It's 18 to 20 feet long. Some say 22 feet long. And the large intestine's only about 3.5 feet long. So it's all about the diameter of the opening, right? That's why they call it small as opposed to large intestine. And the small intestine is designed to have very low numbers of bacteria in it because it's got stomach acid, bile, and pancreatic enzymes all dumping into the top of it and really creating an adverse environment for the bacteria. So it really keeps their numbers down. And then the migrating motor complex that moves things through the small bowel also helps kind of flush out the bacteria so they don't just sit there and multiply. So the numbers in the small intestine shouldn't be more than 1,000 to 10,000 per gram of material, whereas in large intestine you have millions or billions per gram, and that's normal. Just depends whether you're on the upside or the downside of the ileocecal valve, whether that's going to be normal.

So are you seeing then that the majority of people with IBD have either SIBO or SIFO?

I think that those conditions are extremely common, especially in Crohn's disease, but they can also be a aggravating factor in ulcerative colitis and microscopic colitis. I've seen really good results by treating adrenal problems, which we haven't talked about yet, as well as bacterial overgrowth in the small bowel in, in people with microscopic colitis as well.

And so I imagine some of your patients come to you already taking pharmaceutical immunomodulatory drugs and steroids and such. If that is the case, and, you know, you work with them and they seem to be doing better, how do you know when it's the right time to try and get off of those?

In large part, that depends on the patient. Not all patients come to me saying, my goal is to get off this drug.

Right, assuming they have that goal.

Yeah, if they come and they say, yeah, I want to get off my biologic, I want to get off my Pentasa or whatever. First of all, I look at the fact, is the drug working? Does it do what it's supposed to do? And sometimes it's really not. So I have patients who are on biologics, which are injectable drugs at this point, either as infusions at an infusion center or self-administered every couple of weeks at home. What I'll ask them, say they're on a biologic drug that has an 8-week cycle. They have an infusion every 8 weeks. I'll say, so how are you immediately, you know, the first week after you have the infusion? And how are you the last week or two when you're needing the next infusion? And if they say, no real difference, doesn't get better after the infusion and it doesn't get worse. As it's wearing off, then I'm, I'm gonna figure, you know, this drug really isn't working. That's very different than someone who comes to me and says, oh, I just feel like I got my life back the first 2 weeks after I have my infusion. And the last 2 weeks while I'm waiting for my next one, I'm kind of wondering if I should go in early because I'm getting so bad. Then that's a drug that's doing something. So it really makes a difference. If the drug's not doing anything, there's less need to worry about starting to withdraw it as long as we have something else in place. So I always, if I can, I like to get the diet in place, the emotional state starting to move in the right direction if it needs to, or coping with stress, as well as some kind of immunomodulator. And usually the first one is low-dose naltrexone that we try because it's often so effective. So I'll get that started and then we'll work with the doctor who prescribed the biologic to wean it.

We've hit an hour and I just wanna see if you have time to answer one more question and then our special musical finale.

Okay. Okay.

So one thing that I've found challenging with clients with IBD is that some of them just don't believe that healing is possible because they come from that allopathic background in terms of who they've seen, that they don't want to stick it out. Like, they're not willing to stick out diet for an extended period of time that's difficult, or, you know, try different things.

Diet is for life. Yeah, that's a, that's a long time to stick it out.

Yeah. So I'm just wondering if you have any tips for patient adherence.

You know, I have gotten less and less skilled at that, I think, because I don't have to. By the time people see me, I have this one guy, he keeps telling me he's seen 50 gastroenterologists before he saw me. I'm not primary, I'm not secondary, I'm not tertiary. I'm probably quaternary care.

Right. So you're getting the people who really want to get better and will do anything.

Yes. So I'm probably not as good as a primary care doctor at, at getting people motivated.

Fair enough. So we talked beforehand that you have a song about the Bristol stool chart. So I, I—

Oh, doesn't everybody?

Well, yeah, but you know, I, I'm wondering what your version is like. So I'm really looking forward to hearing the Bristol stool chart song. And just in case anybody doesn't know what the Bristol stool chart is, it's, it's the chart of, you know, how your stool looks on a scale of 1 to 7 that can help you. Determine what's going on, whether you're constipated or have diarrhea or whatever.

We use it to just get a good quick way to write it in the chart so we know what the form of their stool is. Because one thing I could say about constipation and diarrhea, people will start talking about their condition. They'll say, yeah, I got constipation. So I say, so what, what's the Bristol stool type? And, you know, 7 is liquid and 1 is a little hard ball. And they'll say, let's see. So they look at the pictures and they say, that's a 6 or a 7.

I've had the same thing.

Yeah, yeah. And you think, well, wait a minute.

So what aspect of that is constipated?

1 and 2 are constipated. So the thing is the definition of constipation according to the Rome criteria. Is it's a number of things. It can be frequency of less than 2 to 3 stools per week. So it doesn't matter what the form is at that point. And often people who have constipation take a lot of vitamin C or a lot of magnesium or Miralax or something else, and they end up overdoing it and go from having a Bristol 1 hard ground ball stool to having sometimes explosive diarrhea. So if you were to just take their history and not know that they were constipated to begin with and start taking all these laxatives, you'd think they have diarrhea. There is also, by the way, have you ever talked about overflow diarrhea on your podcast?

No, but I mean, I know about it. Yeah.

So, yeah. So For those who don't know about it, quickly, it's when people have diarrhea— often children have diarrhea, but they're really constipated. You have to treat them as if they're constipated because they have built-up stool that can show up on a CT or x-ray of the abdomen in the colon. And all that can get through that narrowed space because of all that hard stool in there is liquid. And so that's the only thing they have is liquid stool. That's called overflow diarrhea. So It's not exactly straightforward all the time, but the Bristol chart does help us at least get a sense of what the form of the stool is. It doesn't necessarily tell us whether it's truly constipation or diarrhea. I'll see if I can remember the chords. This is to the tune of Do a Deer because there are 8 notes in an octave and it seemed to work.

Okay.

It's got some interesting chords that I might— I may make a mistake. One, a ball, a hard round ball. Two, a clumping form of one. Three, a log with wrinkled lines. Four, a snake that's smooth and done. Five, An unformed bunch of flecks. 6. A pile of soft-serve mess. 7. A fully liquid stool. That will bring us back to 1.

Wonderful! Now everybody will know how to sing to their stool. Yes. Well, thank you so much for sharing all your knowledge with us today. I appreciate you coming on the podcast.

All right, it was fun.

If you'd like to connect with Dr. Sandberg-Lewis, I'll link to his practice, Hive Mind Medicine, in the show notes. And if you'd like to connect with me online, you can follow my High Desert Health Facebook page or join my gut healing Facebook group or join my newsletter list at highdeserthealthcoaching.com. Links for all those are in the show notes. Thanks for joining me today, and here's wishing you all the perfect stool.