Gut Immune Function: How to Balance Our Ancestral Genome

Does your gut need a reset?

Yes, I'm Ready

Do you want to start feeling better?

Yes, Where Do I Start?

Do you want to start feeling better?

Yes, Where Do I Start?

Gut Immune Function: How to Balance Our Ancestral Genome with Our Modern Day Environment for Optimum Gut and Immune Health

Disorders in immune function are a modern day epidemic which manifest as a litany of immune and autoimmune conditions like hypothyroidism, celiac disease, IBD, RA, IBS, and depression. The gut is possibly the most impactful organ influencing the immune system. By understanding how to optimize gut health and gut immune function, we can unlock a powerful method for improving this array of immune and autoimmune conditions. However, what was healthy for our ancestor’s immune systems may not be healthy for a Western immune system. This talk will outline where we should replicate the ancestral environment for optimum immune health, but also where we should make important modifications to better suit the modern-day immune system.

Subscribe for future episodes

  • Apple Podcast
  • Google Podcasts
  • Spotify

Download this Episode (right click link and ‘Save As’)


Dr. Michael Ruscio: Today we’re going to talk about gut immune function, how to balance our ancestral genome with our modern-day environment for optimum gut and immune health. And I think when you look at this issue from the perspective of the immune system, you start to see why I’ve made some recommendations that have been counter to what you may hear in other places.

And this is because I think one of the things that has been left out of the picture is looking at how our immune systems are formed, and how our immune systems are not hunter-gatherer immune systems, so therefore creating a hunter-gatherer gut may not be a great idea, because the immune system and the gut may not get along. And I’m going to expand on that posit here throughout the body of the talk today.

So, here is the outline we’ll go through.

  1. Replicating ancestral dietary and lifestyle practices can clearly be helpful. Claims suggesting otherwise are clearly not taking into account all the data.
  2. Some ancestral practices are mismatched with our immune systems and can make people ill. Creating a gut environment suitable for the immune system may involve a reduction of some seemingly healthy foods.
  3. Imbalances in the microbiota are sometimes adaptations to protect the host. Attempting to force change to these imbalances can be damaging.
  4. Overtesting is one of the most damaging practices in natural, functional, or complementary and alternative medicine. And a sound process can used to optimize one’s gut and immune system health.

So let’s jump in!

The point one, let’s expand on this slightly. All diets that reduce processed food and focus on whole fresh foods can improve health. It’s important that we’re clear on this. Any diet that’s a shift from a processed food-laden standard American-type diet shows health benefit in clinical trials. It doesn’t matter if it’s vegetarian, Mediterranean, Atkins, Paleo. They all tend to work.

Now, comparative trials have found, many of them, have found that Paleo or low-carb diets often have a slight edge, but the effect size is minimal, significant but minimal. Meaning, taking weight as one parameter, low-carb diets produce more weight loss, but oftentimes the effect size in terms of the difference between a vegetarian diet from weight loss and a low carbs diet may only be three pounds. So, they do work better, but they all work. And this is important to keep in mind so we don’t have dietary dogma. We are little bit open-minded.

And some other things that have helpful outside of an ancestral-type of diet, which would be a Paleo-type of diet: fasting, we can argue that’s something that falls in the ancestral paradigm; sleep, and I mean sleep according to circadian rhythm, and also good sleep hygiene, a dark room – I just see Harvey sitting down. He’s the godfather of that. Also, time and nature has shown to have health benefits. For example, observational trials have clearly shown that people that live in blue zones or green zones, oceanic or forest-type of environments have a lower all-cause mortality.

And walking has been shown to be, arguably, the foundation of fitness, making sure you get enough steps. And this may be because it’s more important to have a large amount of low level activity rather than a short, punctuated burst of high level activity. So this fits back to the ancestral paradigm, right? So, all this supports that many ancestral practices are health promoting.

That’s an easy point to substantiate. Let’s move on to point two, and this is where we get more controversial.

Some ancestral practices are mismatched with our immune systems and can make some people ill. The foundation that’s important to understand here is that much of the immune system is programed in early life. They’ve done studies where they’ve shown that the earlier antibiotics are administered – twelve months, nine months, six months, three months – the earlier they’re administered, the more damaging they are.

Conversely, the same thing holds true with probiotics. The earlier they’re administered, the more beneficial they tend to be. And this can even mean for when someone is a teenager or in adulthood. The effects of early life programming are somewhat locked in for the perpetuity of your life. C-section and breastfeeding has either a negative or positive impact depending on if you’re natural birth and you breastfeed, that’s protective. If you’re caesarean birth and you’re bottle fed, that’s a detriment. And also living on a farm has also been shown to be health promoting.

Now, the challenge can be if a non-hunter-gatherer immune system is presented with a hunter-gatherer type environment, that can be detrimental. A quick side point, I’m using the term hunter-gatherer diet loosely, and the context here is there has been some excitement with the research in the microbiota.

And I spoke about this at the last Ancestral Health Symposium. Much of this research is coming out of areas that eat a relatively higher carbohydrate, fiber, and prebiotic diet. And so, an erroneous assumption is being made that a Paleo diet needs to be a higher fiber, prebiotic, and carbohydrate diet. So, I’m saying I’m using this term hunter-gatherer diet a little bit loosely, because you can argue against that as I did in my presentation last year. And we’ll expand on that more in just a moment.

But I want to bring you down to where it says “examples of non-hunter-gatherer’s immune systems not doing well with a hunter-gatherer-like diet or gut.” Interestingly, if a child grows up in a farm, it’s protective against many allergic or inflammatory disorders. But if they visit a farm, that can actually cause a flaring of inflammatory conditions like allergies, atopic dermatitis. So, this was a big observation for me to open my eyes to the fact that if you have a non-hunter-gatherer immune system, and then you try to force yourself in a hunter-gatherer environment, that may not jive.

Continuing, a low FODMAP diet, which reduces foods that feed bacteria, actually shows impressive clinical benefit for many people. Also, a low histamine diet has shown some impressive clinical benefit for people of various health ailments. Now, a low FODMAP diet reduces foods that feed bacteria. A low histamine diet reduces many fermented foods that we harp on as being so health promoting. And they can be health promoting, but they may not be for all people.

So, this supports the statement I made a moment ago. Essentially this is a paper by Cordain where they surveyed hunter-gatherer diets worldwide. And to quote, most, 73% of worldwide hunter-gatherer societies, derived over 50% of their energy from animal foods, whereas only 40% of these societies derived over 50% from plant foods. High reliance on animal based foods coupled with relatively low carbohydrate content of wild plant foods.

So, this is supporting my contention, which is not everyone needs to be on a higher prebiotic, higher carbohydrate diet. It’s not saying everyone should be on a ketogenic diet. Don’t take a counterpoint meaning we have to swing all the way to the other extreme. But clearly there is evolutionary evidence showing that being on a high carb, high prebiotic diet is not going to be helpful for many people.

Now, I want to just show this study really quick, because you may hear that and think, “Oh, so does this mean everyone should be on a low carb diet?” No, this study essentially showed better weight loss when going on a high carb diet for Asian women.

So, again, we need to get away from this model of thinking about one thing being the best all the time. This is the only way to do it. Because that doesn’t really help people, it confuses people. Because then you’ll hear one camp saying to do this, another camp saying no, do that. People read all this stuff. They don’t know what to do, and they feel paralyzed.

So, let’s continue developing my main contention. Creating a gut environment suitable for the immune system may involve a reduction of seemingly healthy foods. Again, so much of creating a suitable environment for one’s health does involve recommendations that we’re all probably accustomed to: Paleo diets, sleep time, and nature walking. However, it can require also the reduction of seemingly healthy foods. I made an example of low FODMAP and low histamine, so let’s develop these.

In this study, entitled “Dietary Guidance Normalizes Large Intestine Endocrine Cell Density in Patients with Irritable Bowel Syndrome,” they took, I’ll read it for you. The study includes 13 patients with IBS and 13 controls. The patients received 3 sessions of individualized dietary guidance on the low FODMAP diet.

Both the control subjects and the participants were scheduled for colonoscopies at baseline and again at three and nine months after dietary guidance. Biopsies were taken from the colon and rectum and were immunostained for all types of large intestinal endocrine cells. The daily total consumption of fruits and vegetables rich in FODMAPs decreased significantly from 16 grams before dietary guidance to 9 grams after.

Conclusion: the density of large intestine endocrine cells tend to normalize following dietary guidance, in this case a low FODMAP diet, and may have contributed to the improvements of the patients with IBS symptoms. This is some other data here that is essentially showing the main change here was an increase in serotonin cells in the colon.

We get so obsessed with the fact that a low FODMAP diet may cause a decrease of bacteria in the gut and freak out because we’ve heard that bacteria are so important, but it may not all be about the bacteria. We may be causing an improvement in the endocrine cells in the intestines that are responsible for serotonin release. And serotonin is important for not only nociception but also for motility. And this may be why the low FODMAP diet works well.

But you get confused when you try to make the recommendations based upon mechanism. The mechanism is bacteria are good, so low FODMAP diet must be bad because the low FODMAP diet decreases bacteria. This is why I repeatedly said you should not make clinical recommendations based upon mechanism. You should look at clinical data. When you look at clinical data, the low FODMAP diet is very effective for IBS and IBD, right? So, outcome always trumps mechanism.

So you may be saying to yourself, “But what about the small intestine?” Maybe you’ve heard me talk about how important the small intestine is and how the small intestine is oftentimes left out of this conversation. Another study has been done, changes in duodenal, so small intestine, enteroendocrine cells in patients with Irritable Bowel Syndrome following dietary guidance. The densities of enteroendocrine cells are abnormal in patients with IBS. However, they tend to change toward normal levels in the stomach, ileum, and colon following dietary advice. The aim was to identify types of duodenal enteroendocrine cells affected after receiving dietary guidance, again low FODMAP, in this group of patients.

In conclusion, the densities of several duodenal enteroendocrine cells in IBS change toward the values measured in controlled subjects following dietary guidance. The changes in serotonin and somatostatin cell density may have contributed to the improvements in IBS, and particularly pain and diarrhea.

So now we’re showing not only in the colon but also in the small intestine you can have improvement in cells that secrete things like serotonin. So, well yes, the low FODMAP diet may decrease bacteria. That may not be a bad thing because you may see an accompanying improvement in some of the wiring, in some of the hormones, in some of the cells in the intestines in patients who go on a low FODMAP diet.

But wait! There’s more!

A low FODMAP diet has also shown the ability to decrease leaky gut as assessed by LPS (lipopolysaccharide). In another study showing—and this I think is a very key—metabolic profiling of urine showed group of patients with IBS differ significantly after the diet. And this is a low FODMAP diet again, as you see there with three metabolites, histamine, p-hydroxybenzoic acid, and azelaic acid, being primarily responsible for discrimination between the two groups.

Histamine, a measure of immune activation, was reduced 8-fold on a low FODMAP diet. Again, I don’t want to paint myself as a low FODMAP fanatic. But it’s important, I feel like I’m one of the few people saying, “Hey, maybe not everyone needs to try to feed their bacteria.” And you see this. If you work with patients and you’re objective and you’re not married to a particular philosophy, you clearly see that bacterial-reducing approaches work far superior for many patients with IBS, with IBD, and other food sensitivities, health ailments, gut involvement, what have you.

Again, it’s not to say that low FODMAP is the diet that every patient in my office gets in a dogmatic way. But it’s important that we’re familiar with some of this information, because I don’t think it’s getting the attention that it deserves. And it’s coercing us into this thinking that everyone needs to be feeding their gut bugs when I don’t think that’s really supportive.

And one more—so, in this study, “Concomitant Prevalence of Low Serum Diamine Oxidase Activity and Carbohydrate Malabsorption,” 22 percent of patients showed histamine intolerance, making it as common as lactose intolerance in this group. Abdominal pain, bloating, and diarrhea are some of the leading symptoms associated with histamine intolerance.

Histamine is a signaling molecule in the gut, not only in the gut, but it’s involved in the immune response. Now, when people have overly zealous immune systems, especially in their gut, they will have a predilection towards high levels of histamine.

A low FODMAP diet can lower histamine by 8-fold. So what does that tell you? It tells you that somehow, by decreasing bacterial load in the gut, you are calming down the immune system. Does that make sense? Low FODMAP and low histamine diets though, call on and want to restrict foods that we oftentimes associate being the beacon of healthy diets. So, it’s important that we understand this, because by understanding this, we can get people to recommendations that will be more beneficial for them.

This study essentially took patients that had been non-responsive to other IBS therapies, and they assessed them for things like fructose intolerance, lactose malabsorption, histamine intolerance. And they essentially found about just under a third of patients had histamine intolerance, making it about as common as lactose intolerance. So, it’s important that we understand this.

These are IBS-type symptoms: abdominal pain, bloating, and diarrhea, abdominal pain and altered bowel function being the two most predominant symptoms associated with IBS.

So let’s review. Normalization of intestinal enteroendocrine cells can occur in a low FODMAP diet, and these cells are responsible for the release of serotonin and sematostatin. We also see with a low FODMAP diet a normalization of immune activation via reduction of a leaky gut and reduction of histamine.

Now, I do have a clinical newsletter for anyone in the audience or listening to this who is a clinician who wants to get more into this. Because I do think it’s important that clinicians are aware of this information. We’ve done a number of case study write-ups in our clinical newsletter. And this is one of them. I’m not going to go through this case study, but if you go to that URL there, drruscio.com/review, you can access case studies where we go through “What does histamine intolerance looks like? How does it present clinically? And, how do people respond?”

I’ll tell you, one of the most common flags is when someone says, “The healthier I eat, the worse I feel.” That’s oftentimes a flag for histamine intolerance, because what are they eating? They’re having lots of soups and bone broth. Or they’re having lots of fermented foods. And these things can be very problematic for people that are histamine sensitive. So they keep trying to eat these foods because the community keeps harping on how healthy they are. And they can be healthy for many people. But for people who have this immune dysregulation in the gut, that can actually make this subset of people worse.

As I said earlier, antimicrobial therapy is oftentimes more effective than pro-microbial therapy. And this is very important for us to understand. Low FODMAP, low carb, low histamine, herbal antimicrobials, or antibiotics, if you look at all of the literature – I’m not saying that there’s one cherry-picked study. But if you look at the evidence at large and you weigh it, those therapies are generally more effective than higher FODMAP diet, higher carbs, prebiotic supplementation, and fiber. Again, for some, but not for all. So this is not an absolute.

But you do see a trend in the data. When you look at clinical trials, there are tending to be more benefit for antimicrobial strategies than pro-microbial strategies. The more symptomatic someone is, the more ill you are, the more important this is. The more likely you are, in my observation, to do better with antimicrobial approaches rather than pro-microbial approaches.

Now, what about probiotics? Probiotics are more likely to be net antimicrobial, amongst other things, than they are pro-microbial. Most probiotics do not colonize you. They’ve been trying to reduce SIBO, combat candida fungus, and assist in the clearance of H. pylori and various protozoa. We oftentimes don’t realize that by taking a probiotic, we may actually be taking a pseudo antimicrobial. It doesn’t colonize you, and kills stuff in the gut.

Elemental diets can also be very helpful. As you continue on this spectrum of people who are progressively more ill, or more challenged with their diet or with their gut health, elemental diets, which are essentially hypoallergenic liquid diets that have essentially zero fiber and prebiotics in them, can be very helpful for these highly sensitive patient subgroups.

And ironically, at least one study showed the ability of an elemental diet to somehow increase microbial diversity in the small intestine. Now, why might that be? How could something that starves bacteria increase diversity of bacteria? What’s probably happening is, by starving bacteria, you’re calming down the immune system. And it’s the immune system attacking the bacteria in the gut that’s causing the low diversity to begin with. When you calm down the immune system, you reduce the insult on the microbiota and allow the microbiota to then flourish.

Now, this is maybe suddenly off topic, but I think is worth mentioning. When all else fails and we can’t create the right environment in the gut for the microbiota, we can replace the microbiota. So if you can’t fix it you can replace it. And this is where FMT can come in. I just want to touch on this briefly.

This is a retrospective analysis of 406 patients who underwent FMT. And I’ve listed here for you from the study the cure rates and the improvement rate. So (RCDI) Recurring Clostridium Difficile Infection, 85% versus 95% cure rate and improvement rate. Now that probably doesn’t apply to many people here, but constipation may: 40% cure rate, 67% improvement rate. Ulcerative Colitis: 34%, 68%. IBS: 47%, 72%. And Crohn’s.

We see some hopeful benefit here for people that fail out of all other therapies. But I want to be clear in saying this is something that should be reserved for people who fail out of all the therapies, not, “I read two books on gut health and now I’m going to do a FMT.” You should definitely get yourself to a highly skilled gut doctor like myself or someone else who knows what they’re doing and have them help you before you think about doing a FMT. Also here, I’m cautious with this regarding IBS, because IBS is extraordinarily prone to placebo effect.

So this is a systematic review with meta-analysis showing benefit of about 45% for IBD. I think the next FDA approved condition that FMT will be sanctioned for will be for Inflammatory Bowel Disease because the data is there.

But this is why I cautioned, adverse events do occur. A systematic review of adverse events, in contrast the incidence of serious adverse events were 2% and 6% for upper and lower gastro intestinal administration routes. A total of 44 kinds of serious adverse events occurred in 9% of patients, including death in 3 ½%, infection in 2 ½%, relapse of inflammatory bowel disease in 0.6%, and Clostridium Difficile infection.

So, it’s not to say this therapy is not without its risks. And this is why I get admittedly irritated when I hear people talking about this being the next weight loss cure. “Oh, my cousin is skinny. Can I just do an FMT with her poop and lose weight?” I mean, come on!

So review. Antimicrobial therapy is often more effective than pro-microbial therapy. If no therapies work, we can replace the microbiota. Or imbalances in the microbiota are sometimes adaptations to protect the host. Attempting the force changes to these imbalances can be damaging.

So there are a few things I hope you will consider. So, treatment of diabetes improves the microbiota. They did nothing but gave type 1 diabetics insulin and the microbiota improved. Is that possible? Yes, it’s possible, because the health of the host is the environment for which the microbiota lives. And if you improve the environment, you improve what lives inside of you. Type 2 diabetics on a low-carb diet saw an improvement of their microbiota as their blood sugar became more normal. Exercise has been shown to correlate with the healthy microbiota. In fact, cardio-respiratory fitness in one study predicted microbial diversity. And another study tracked changes from sedentary to active and showed that as you exercise it improves the health of your microbiota.

So this thinking that the microbiota is the cause of all disease and treating the microbiota is the next miracle is really ill-founded. You’re taking this from a gut geek. If anybody wants it to be true, it’s me, right? But it’s not. It’s not true. And certainly, improving your gut health can be a miraculously helpful intervention. But trying to custom manipulate your microbiota to do what you think it should do doesn’t really pan out.

Vacuuming, using a sponge. One study showed that children that grow up in households using a sponge have a lower incidence of allergic diseases compared to children growing up in houses that uses a dishwasher, probably because of residual bacteria in the sponge. So another thing in your environment can affect your microbiota. The frequency of vacuuming has also been shown to affect your microbiota.

We need to get away from these things thinking that if we show a change in the microbiota, we’re going to be able to do so much. It’s a little silly. And even a calorie reduction improves the microbiota in obese subjects, probably because the calorie restriction diet improved metabolism in these subjects.

Another study showed a reduction of carbohydrates improved thyroid autoimmunity. And what’s more important here is that 80% of these patients expressed signs of carbohydrate malabsorption. So again, coming back to this thinking that feeding the gut with carbs and prebiotics may not always be the best thing to do.

Anti-inflammatory drugs also increase the diversity in the gut microbiota. And I would speculate the same thing would occur with anti-inflammatory herbs. Now, why is that? It’s likely because the anti-inflammatory drugs are toning down our overzealous immune system that is attacking the microbiota. So the diversity may not be the cause of the disease. It may be a result of the disease, the disease being an imbalanced immune system.

Now, developing this further, prebiotics caused inflammation and doubling of symptoms, but a healthier microbiota. So let’s a look at this. “Effects of Varying Dietary Content on Fermentable Short-Chain Carbohydrates on Symptoms, Fecal Microenvironment, and Cytokine Profiles in Patients with IBS.” Study purpose: to evaluate the effect of a low FODMAP diet compared to a diet high in prebiotics, and IBS symptoms, and related comorbidities. They tried IBS symptoms, general health symptoms, GI microbiota, short-chain fatty acids, and cytokines. So essentially in the intervention, they took a bunch of patients and put them on a low FODMAP diet. Then, they kept them in a low FODMAP diet.

One group took up a placebo and the other group took a prebiotic, and then they switched groups.

Here’s what they’ve found. There was a significant improvement in all IBS symptoms after three weeks on a low FODMAP diet. And overall patients’ satisfaction of 85%. Those in a low FODMAP diet also expressed a significant improvement in belching, passing gas, nausea, vomiting, and fatigue. Here is the key piece. When transitioning to either placebo or FOS, fructooligosaccharides, a prebiotic, 80% of those on a placebo maintained their improvement, whereas only 30% of those who started taking a prebiotic maintained their improvement. When on a prebiotic, patients experienced a worsening of nausea, vomiting, headache, belching, and passage of gas. Additionally, cytokines, a reduction of inflammatory cytokines was noted in those on a low FODMAP diet, but not for those on the prebiotic.

Now, the microbiota paradoxically became slightly more dysbiotic, what we think is dysbiotic. I think we still don’t really know what a dysbiotic microbiota truly looks like. And the short chain fatty acids decreased. So, we see some things that may be considered bad. But my argument would be that we don’t know how to truly label a dysbiotic microbiota yet, so I totally discount that. And short chain fatty acids decreasing is not always a bad thing, because you do see elevated short chain fatty acids in some sub-groups. Patients with IBS may have elevated short chain fatty acids. Patients who are obese may have elevated short chain fatty acids. So if you go back to the erroneous thinking via mechanism, short chain fatty acids are good. Therefore, if I increase short chain fatty acids, people become healthier. Do you see how quickly that can get you into trouble? We should look to clinical data to make decisions, not speculate based upon mechanism.

There’s also the bifidobacterium paradox, another reason why we should not make decisions upon mechanism. The low FODMAP diet saw a decrease in bifidobacterium, but people felt a lot better. Ironically though, bifidobacterium is one of the most beneficial supplemental probiotics in the IBS literature. So again that’s we shouldn’t be speculating from mechanism.

So by improving the health of the host, we can improve the microbiota; treating diabetes, exercise, stress, hormone support, and reducing inflammation can all improve the microbiota.

A diet that discourages bacterial growth can benefit the host. They can reduce inflammation and reduce symptoms. This may occur while becoming “dysbiotic” and may be accompanied by less short chain fatty acids. Neither one of these may be a bad thing.

And I’ll be brief here because I’m a little over time. Overtesting is one the most damaging practices in natural functional, complementary, and alternative medicine.

The state of functional medicine, excessive and expensive. There is a belief that more testing equals better results, this is simply not true. There is a belief the more treatment equals better results, this is simply not true. And information has become a form of marketing. You can take a mechanism and you can find a mechanism to support whatever it is you’re trying to sell: lab tests, supplements, whatever it is. But you can’t do that with clinical data, which is why I always come back to the evidence-based pyramid where we should be making our decisions based upon high quality clinical outcome data when it’s available. And in gastroenterology we have a wealth of data available.

Empiric medicine has been forgotten. We’ve been sold a bill of goods that this fancy functional medicine testing holds that key to becoming healthier. And it preys upon the desperation of sick patients and the fear of doctors not being able to help their patients. And it’s really wrong and does a lot more harm than it does good. What’s needed is a return to practical and cost-effective care, which is progressive but also conservative.

I’m growing increasingly concerned at what’s happening. At least two times a month, I have a patient come in from another clinic, where they were required to do $3000 worth of testing or more on day one. And this doesn’t even include the consultation visit or what have you. Again, more testing does not equal better results. And a few examples not needed at all in my opinion: adrenal testing, food allergy testing, microbiota mapping, many functional GI markers like certain enzymes, fecal fat, short chain fatty acids, obscure inflammatory markers, and most gene-testing. Often not needed initially: expanded thyroid panels, Lyme, metals, molds, and female hormones.

This is a big difference between, for example, $4500 worth of testing out of the gate and $800-$1200 of testing out of the gate. Now, if you have insurance these totals will all be a little bit less. But these things make a big difference. But I know someone who did a microbiota mapping assessment and felt better on fiber and prebiotics supplementation. Great! But you didn’t need the test to do that.

A flawed assumption: the gut is important, so perform microbiota mapping, then use specially tailored diets, prebiotics, fiber, and probiotics. This is simply not true. It wastes time and money and I think worsens care. If we are treating markers that are meaningless, what are we doing? We’re wasting time. We’re wasting money, and we’re potentially harming someone.

And this is a quick aside, I was lecturing at the International Symposium on Natural Medicine in Australia a few months ago. I was there with Professor Rob Knight. And we’re both on a question and answer panel. He’s sitting right next to me. And someone asked, “Dr. Ruscio, do you use microbiota mapping like American Gut and UBiome in your clinic?” Sitting next to the guy, who pretty much invented this testing.

And I said “I really don’t, because it’s just not clinically relevant.” I was so pleased to see Professor Knight, the guy when it comes to this, nodding his head in agreement as I’m saying this and essentially being completely in agreement. Don’t take it from me if you want. Take it from the guy who has pioneered this work. The microbiota mapping is not ready for clinical practice, it’s just not.

So, If you’re doing that test, I would ask you kindly to stop and just to realize that, sometimes you think something is going to help. When we learn more, we realize, “I guess that wasn’t really helpful.” So we can just change. It doesn’t mean anything bad or foul play. But if you’re trying to treat something that does not have meaning, you are making the clinical process harder because you’ve introduced a meaningless variable into an already variable-rich process. Does that make sense?

And I’ve seen patients…I’d say there is a small contingent of patients that I see who have gone to doctors, and the doctors have treated their microbiota mapping test results instead of treating the condition or treating the patient.

And what happens oftentimes, to put it simply, someone with IBS or IBD go to see a doctor. They poop in a cup. They have low diversity of bacteria, so they are given a bunch of fiber, prebiotics, and probiotics. And guess what the clinical literature shows? People who take prebiotics and fiber, the highest adverse event that’s reported is a flaring of gastrointestinal symptoms. So, what do you think happened to these patients? They get worse. And the doctor goes, “Huh? That’s weird. Your diversity was low. I’m trying to feed your diversity. You were low in this bacteria, so I gave you this bacteria.” They are not getting that there is no clinical data substantiating that that has any effect. And that’s why they’re not getting any better.

So the last couple of slides.

A sound process can be used to optimize one’s gut health and immune system. This will be outlined in my coming book, Healthy Gut, Healthy You. It will publish in February.

But here is a brief overview. Start with the ancestral, Paleo-type of diet and lifestyle. Those who are mostly improved from this are good candidates for prebiotics and fiber. They may obtain additional benefits from this. Those who do not will most likely need to visit reduction strategies: autoimmune Paleo, low carb, low FODMAP, low histamine, probiotics, herbal antimicrobials, potentially even pharmaceutical antibiotics. Then later, reintroduce and see how much they can tolerate and how much benefit they obtained from feeding strategies.

This group B may need occasional trimming of the shrubs. Guys, some conditions have a natural ebb and flow, a natural remit-relapse-remit-relapse, and it doesn’t mean that the world is ending. If you’ve had a muscular injury, like a knee injury, you may notice every once in awhile it flares up a little bit, right? You have to take it easy. Do your stretches. Do your rehab, whatever, and then it gets better. Same things happen in IBS, in IBD, and SIBO. It’s unfortunate that people read on the internet that you can never get rid of SIBO.

Guys, that’s not really how this works. The analogy I like to use is, think about the shrubs, the bushes, outside of your house. They grow, and then sometimes you have to trim them. And then they grow, and you trim them again. It doesn’t mean that you need to rip out your shrubs, right? There are some people that I think don’t have a good ability to keep the shrubs trimmed, because their immune system may not be highly attuned at doing that. Or they may have certain genetic polymorphisms.

And so they need you to occasionally visit something like a couple of days on an exclusive elemental diet or a short low-dose gentle course of antimicrobials. Or a low FODMAP or low histamine diet, right? They kind of keep that proper environment in the gut. And there’s nothing wrong with that. And we should stop painting that as SIBO is this chronic condition that you can never clear because of autoimmunity in the gut. And it’s just way too much.

So getting off my soapbox, improving gut health is not a cure-all, but it’s a great place to start. Why? GI problems can manifest solely as non-GI symptoms: fatigue, pain, depression, skin lesions. And so, you may be chasing down what you think is hypothyroid, and it’s actually not. It’s actually a problem in the gut. More in-depth testing and treatment has a time and a place, but we’ve become way too exotic with our approach. More does not equal better.

Resources for you: the link for my book, which will publish in February, the link for the training newsletter, which is active, and the website there with podcasts, articles, videos. And I’ll open it up now for questions. And thank you guys for your time and your attention.

➕ References
  1. Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000 Mar;71(3):682-92. doi: 10.1093/ajcn/71.3.682. PMID: 10702160.
  2. Wan Y, Wang F, Yuan J, Li J, Jiang D, Zhang J, Huang T, Zheng J, Mann J, Li D. Effects of Macronutrient Distribution on Weight and Related Cardiometabolic Profile in Healthy Non-Obese Chinese: A 6-month, Randomized Controlled-Feeding Trial. EBioMedicine. 2017 Aug;22:200-207. doi: 10.1016/j.ebiom.2017.06.017. Epub 2017 Jun 20. PMID: 28655596; PMCID: PMC5672080.
  3. Mazzawi T, Hausken T, Gundersen D, El-Salhy M. Dietary guidance normalizes large intestinal endocrine cell densities in patients with irritable bowel syndrome. Eur J Clin Nutr. 2016 Feb;70(2):175-81. doi: 10.1038/ejcn.2015.191. Epub 2015 Nov 25. PMID: 26603880; PMCID: PMC4744244.
  4. Weber B, Bachmann CC, Braun R, Abraham AG, Serra AL, Hofbauer GFL. 25-Hydroxyvitamin-D3 serum modulation after use of sunbeds compliant with European Union standards: A randomized open observational controlled trial. J Am Acad Dermatol. 2017 Jul;77(1):48-54. doi: 10.1016/j.jaad.2017.02.029. Epub 2017 Apr 14. PMID: 28416344.
  5. Enko D, Meinitzer A, Mangge H, Kriegshäuser G, Halwachs-Baumann G, Reininghaus EZ, Bengesser SA, Schnedl WJ. Concomitant Prevalence of Low Serum Diamine Oxidase Activity and Carbohydrate Malabsorption. Can J Gastroenterol Hepatol. 2016;2016:4893501. doi: 10.1155/2016/4893501. Epub 2016 Nov 30. PMID: 28042564; PMCID: PMC5155086.
  6. Li N, Tian H, Ma C, Ding C, Ge X, Gu L, Zhang X, Yang B, Hua Y, Zhu Y, Zhou Y. [Efficacy analysis of fecal microbiota transplantation in the treatment of 406 cases with gastrointestinal disorders]. Zhonghua Wei Chang Wai Ke Za Zhi. 2017 Jan 25;20(1):40-46. Chinese. PMID: 28105618.
  7. Colman RJ, Rubin DT. Fecal microbiota transplantation as therapy for inflammatory bowel disease: a systematic review and meta-analysis. J Crohns Colitis. 2014 Dec;8(12):1569-81. doi: 10.1016/j.crohns.2014.08.006. Epub 2014 Sep 13. PMID: 25223604; PMCID: PMC4296742.
  8. Wang S, Xu M, Wang W, Cao X, Piao M, Khan S, Yan F, Cao H, Wang B. Systematic Review: Adverse Events of Fecal Microbiota Transplantation. PLoS One. 2016 Aug 16;11(8):e0161174. doi: 10.1371/journal.pone.0161174. PMID: 27529553; PMCID: PMC4986962.
  9. Mejía-León ME, Petrosino JF, Ajami NJ, Domínguez-Bello MG, de la Barca AM. Fecal microbiota imbalance in Mexican children with type 1 diabetes. Sci Rep. 2014 Jan 22;4:3814. doi: 10.1038/srep03814. PMID: 24448554; PMCID: PMC3898044.
  10. Yamaguchi Y, Adachi K, Sugiyama T, Shimozato A, Ebi M, Ogasawara N, Funaki Y, Goto C, Sasaki M, Kasugai K. Association of Intestinal Microbiota with Metabolic Markers and Dietary Habits in Patients with Type 2 Diabetes. Digestion. 2016;94(2):66-72. doi: 10.1159/000447690. Epub 2016 Aug 10. PMID: 27504897.
  11. Bressa C, Bailén-Andrino M, Pérez-Santiago J, González-Soltero R, Pérez M, Montalvo-Lominchar MG, Maté-Muñoz JL, Domínguez R, Moreno D, Larrosa M. Differences in gut microbiota profile between women with active lifestyle and sedentary women. PLoS One. 2017 Feb 10;12(2):e0171352. doi: 10.1371/journal.pone.0171352. PMID: 28187199; PMCID: PMC5302835.
  12. Estaki M, Pither J, Baumeister P, Little JP, Gill SK, Ghosh S, Ahmadi-Vand Z, Marsden KR, Gibson DL. Cardiorespiratory fitness as a predictor of intestinal microbial diversity and distinct metagenomic functions. Microbiome. 2016 Aug 8;4(1):42. doi: 10.1186/s40168-016-0189-7. PMID: 27502158; PMCID: PMC4976518.
  13. Hesselmar B, Hicke-Roberts A, Wennergren G. Allergy in children in hand versus machine dishwashing. Pediatrics. 2015 Mar;135(3):e590-7. doi: 10.1542/peds.2014-2968. PMID: 25713281.
  14. Avershina E, Ravi A, Storrø O, Øien T, Johnsen R, Rudi K. Potential association of vacuum cleaning frequency with an altered gut microbiota in pregnant women and their 2-year-old children. Microbiome. 2015 Dec 21;3:65. doi: 10.1186/s40168-015-0125-2. PMID: 26687338; PMCID: PMC4685603.
  15. Ruiz A, Cerdó T, Jáuregui R, Pieper DH, Marcos A, Clemente A, García F, Margolles A, Ferrer M, Campoy C, Suárez A. One-year calorie restriction impacts gut microbial composition but not its metabolic performance in obese adolescents. Environ Microbiol. 2017 Apr;19(4):1536-1551. doi: 10.1111/1462-2920.13713. PMID: 28251782.
  16. Zhang X, Zhang D, Jia H, Feng Q, Wang D, Liang D, Wu X, Li J, Tang L, Li Y, Lan Z, Chen B, Li Y, Zhong H, Xie H, Jie Z, Chen W, Tang S, Xu X, Wang X, Cai X, Liu S, Xia Y, Li J, Qiao X, Al-Aama JY, Chen H, Wang L, Wu QJ, Zhang F, Zheng W, Li Y, Zhang M, Luo G, Xue W, Xiao L, Li J, Chen W, Xu X, Yin Y, Yang H, Wang J, Kristiansen K, Liu L, Li T, Huang Q, Li Y, Wang J. The oral and gut microbiomes are perturbed in rheumatoid arthritis and partly normalized after treatment. Nat Med. 2015 Aug;21(8):895-905. doi: 10.1038/nm.3914. Epub 2015 Jul 27. PMID: 26214836.
  17. Busquets D, Mas-de-Xaxars T, López-Siles M, Martínez-Medina M, Bahí A, Sàbat M, Louvriex R, Miquel-Cusachs JO, Garcia-Gil JL, Aldeguer X. Anti-tumour Necrosis Factor Treatment with Adalimumab Induces Changes in the Microbiota of Crohn’s Disease. J Crohns Colitis. 2015 Oct;9(10):899-906. doi: 10.1093/ecco-jcc/jjv119. Epub 2015 Jul 4. PMID: 26142465.
  18. Hustoft TN, Hausken T, Ystad SO, Valeur J, Brokstad K, Hatlebakk JG, Lied GA. Effects of varying dietary content of fermentable short-chain carbohydrates on symptoms, fecal microenvironment, and cytokine profiles in patients with irritable bowel syndrome. Neurogastroenterol Motil. 2017 Apr;29(4). doi: 10.1111/nmo.12969. Epub 2016 Oct 16. PMID: 27747984.

Need help or would like to learn more?
View Dr. Ruscio’s, DC additional resources

Get Help

Discussion

I care about answering your questions and sharing my knowledge with you. Leave a comment or connect with me on social media asking any health question you may have and I just might incorporate it into our next listener questions podcast episode just for you!