Dr. Ruscio was off last week teaching his London (re)Find Health Symposium. He didn’t want everyone who could not attend the seminar to miss out, so this week’s show is a recording Dr. Ruscio did with InVivo Clinical covering topics he presented on in London. Answering all your questions about the gut, thyroid and microbiota.
In This Episode
Intro … 0:42 Dr. Ruscio bio … 1:53 Connection of the gut to other systems in the body … 5:31 Gut and immune system … 8:30 Microbiota defined … 9:41 What does our microbiota do for us? … 11:23 Microbiota in obesity … 13:18 Microbiota and autoimmunity … 27:26 IBS and SIBO … 32:14 Testing dollars and sense … 35:15 GI infections and dysbiosis … 49:43 Thyroid solutions … 50:59
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The following discussion is for educational purposes only and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking with your doctor.
Now, let’s head to the show!
Susan McCauley: Hey, everyone, welcome to Dr. Ruscio Radio. No, I’m not the doc today. This is Susan McCauley, certified nutrition consultant from EvolveNutrition.com and EvolvedRecovery.com. The reason why it’s just me here today is that Dr. R couldn’t be here because he is teaching in London, the promos that you’ve heard the couple of weeks, so we wanted to share with you a webinar highlighting what he will be teaching there all on the gut, thyroid, and microbiota. Enjoy and we’ll talk to you soon.
Humphrey Bacchus of Invivo Clinical: Good afternoon, everyone, and thank you for joining us this afternoon for the last of Invivo Clinical’s free educational webinars in 2015. Today we welcome Dr. Ruscio, who is a doctor, researcher, author, and health enthusiast who practices functional medicine with an emphasis on natural and nutritional solutions in California.
Thank you for being with us today, Dr. Ruscio. We’re very pleased to be able to host you today and particularly exploring the link between the gut, the thyroid, and the microbiota. Perhaps you can start just by telling us a little bit about your training and how you became such a specialist in this area of medicine.
Dr. Michael Ruscio: Sure. Well, first of all, thank you for having me. I’m really excited to be speaking to your audience.
Dr. Ruscio Bio
DR: Regarding my background, I actually had a health challenge myself when I was way back in college, and I think, as many people who get into this field, they have some sort of personal experience that guides them there. I went from being a very healthy 23-year-old to having very bad insomnia, all the symptoms of hypothyroid, bouts of fatigue, depression, and very bad brain fog that would occur somewhat proximal to meals. That diverted me from going down a more conventional medicine path into a more integrative and functional medicine path when I realized that after seeing three of my more conventionally trained doctors, they ran tests and told me everything was normal, which, of course, was very frustrating. Then I found a functional medicine provider that determined I had an Amoeba histolytica infection in my intestines that was really driving all of my symptoms. Coming to that realization and seeing that the proper identification of an underlying cause can make a huge difference in a patient’s life—in this case, my life—was a very cathartic event for me, so I then shifted gears in going into functional medicine with a strong emphasis on gastroenterology and different digestive and microbiota conditions.
As I was in practice for years and years, I started to both love the field, but also have some major concerns about inaccuracies, unnecessary tests, unnecessary treatments, unvalidated tests, unvalidated treatments, and so I started performing my own observational research in my patient base, which has now turned into clinical trials that we’re running in the office, where we’re really trying to help improve the field, make our treatments better, make our testing better, and make our care more cost effective. Now we have one running clinical trial and another clinical trial that we’re going to be enrolling patients in very soon. Then in addition to that, I take all this information and I write about it and I speak about it in different teaching engagements and in a podcast that I host and through my website, and I’m also writing a book right now on the microbiota.
That’s a little bit about my background.
HB: Great. Perhaps we can start. I know this is really kind of what you’re writing your book around, and I know that next month you’re coming to speak in London as well, which is really focused on the links between the gut, the microbiota, and the thyroid with a specific focus on disseminating some of the information which has been, perhaps, kind of falsely portrayed out there in the conventional land and even in the integrative and functional medicine community.
DR: Absolutely. Yeah, I’m very excited about London. I think it will be a great chance to bring more of this out your way. I didn’t really realize that there’s not a ton of functional medicine training available for practitioners in the UK, so I’m happy to be coming out there and sharing some of this. With that, yeah, let’s jump in and talk about some of the… gosh, it’s so hard to try to take five or six hours of information and highlight or showcase some things in just 40 minutes or so, but I’ll do my best to give us kind of a succinct iteration of some of this stuff.
Connection of the Gut to Other Systems in the Body
DR: We went through my background already. Just briefly here, looking at the GI, just some important notes about the connection of the gut to other systems. I’m sure clinicians are aware of this to a greater or lesser extent, but I just would like to reemphasize that if you can be very proficient in identifying and eradicating gut problems and increasing someone’s gut health, you can have such a massive impact on not only their digestive symptoms, but many other systems of their body. It’s a great place to be very well versed. As we see here in the slide, there’s a thyroid connection, as we’ll talk about a little bit later. Certain gut infections have been shown to stimulate thyroid autoimmunity, and probably more importantly, we have some preliminary data showing that treatment of certain gut infections can actually quell or dampen thyroid autoimmunity.
Now, of course, if there is a gut infection, that gut infection can cause problems with thyroid hormone conversion—the conversion of T4 to T3—usually because of the increased inflammation that is associated with that. As part of that inflammation, we see a stress response, and this stress response can cause adrenal fatigue. One of the most overlooked factors I see in my patient base that is struggling with adrenal fatigue is they have an unidentified underlying gut issue and so they’re on adrenal fatigue, they keep doing adrenal testing, they keep doing adrenal treatment, and they don’t ever really see a marked response in their adrenal symptoms because they’re treating a symptom of a deeper underlying dysfunction in the gut. That’s a key item to be able to identify.
Coming to the male hormones, inflammation can upregulate aromatization, which is where a male will turn testosterone into estrogen, and of course, that inflammation can oftentimes come from the gut. This inflammation can also increase 17,20 lyase activity, which is the enzyme that is responsible for a woman turning estrogen into testosterone and causing things like polycystic ovarian syndrome or signs of high androgens like scalp hair thinning, facial hair growth, acne, and the like. Of course, if we can’t detoxify hormones through the gut effectively, then that can cause problems with estrogen dominance and similar types of problems.
There are also neurological connections, mainly between the gut-brain barrier and the blood-brain barrier. They tend to function together. This is why many patients will see brain fog get better once their gut heals and they have less food reactivity, and I learned that personally.
Then also blood sugar. The impact of what you eat, which is, of course, absorbed through your gut, has an impact on blood sugar, and blood sugar can drive many things, including inflammation and adrenal stress.
Gut and Immune System
DR: Then looking at a slide that kind of helps symbolize the connection between the gut and the immune system, I should mention—and I’m sure many practitioners listening are already aware of this—that the largest density of immune cells in the entire body is housed in the small intestines as the gut-associated lymphoid tissue, or GALT, and other cells known as Peyer’s patches.
This is a slide that was stained to show immune cells that was published in The American Journal of Pathology in 2008, where we can see that, yes, we have epithelial cells, which are lining cells essentially, which are non-immune, in red, but then are our dendritic cells in green, our B cells in blue, and our T cells in white are all immune cells. (1) Trusted SourcePubMedGo to source You can easily see from this slide here that there’s quite a large density of immune cells in the lining of the intestines. This is why there is such an important tie-in between autoimmune conditions and autoimmunity and the health of the gut.
DR: Now, talking briefly on some aspects of the microbiota—and just to clarify, sometimes the term “microbiota” is used very broadly. The way I define the microbiota, just to help us with kind of clinical clarity, is when I refer to the microbiota, I typically refer to the thousand-some-odd species that inhabit the gut, the world of bacteria that inhabit the gut. Sometimes it is used to also canvas and encompass things like SIBO, which, yes, are part of the microbiota, but typically microbiota research, microbiota testing, and proposed microbiota treatments are more so concerned with kind of modulating and assessing all of your commensals, and so I just want to draw that distinction if it maybe helps people stay connected with me here. I’ll outline some of these clarifications as we move through here.
Here’s just a quote and anytime you see one of these links, the NCBI, these are just links to PubMed, so if you just were to enter this link into your web browser, it would take you to the abstract that I’m citing. Even more simply, you could just take this number here at the end, the 22861802, and enter that into the PubMed search box, and it would produce the abstract that I’m referencing. This makes it pretty easy for people to grab references. But a quote: “The gut microbiota has coevolved with humans and can be considered an organ of similar size as the liver.” (2) Trusted SourcePubMedGo to source
What Does Our Microbiota Do For Us?
DR: What does our microbiota do for us? Well, digestion—roughly 10 percent of our calories are from bacterial fermentation, and the production of B and K vitamins, and it enables us to survive and adapt faster using bacterial genes. This is actually a very interesting evolutionary perspective. It seems that the changing food supply was shifting faster than our digestive tracts could evolve, but we could borrow from the rapidly adaptable genome of bacteria and allow the bacteria that digest this new food supply to colonize our gut to allow us to digest a broader array of foods. We couldn’t adapt our gut quickly enough through some points of evolution to digest the changing food supply, but if we paired up with bacteria that can evolve much more quickly, then we could capitalize on their fast evolution to allow us to survive and thrive. This is, I think, one of the most deepest lines of symbiosis that we see regarding our gut and gut bacteria. There’s also production of short-chain fatty acids, which are reparative to intestinal cells.
There’s also immune system tone, and also having a healthy microbiota helps to crowd out pathogens. There’s also detoxification of certain chemicals and regulation of metabolism, as we’ll talk about later. Interestingly, there’s some preliminary data being published showing that the treatment of, say, small intestinal bacterial overgrowth can help with decreasing cholesterol levels, increasing insulin sensitivity, and with weight loss. There are also some very interesting clinical observations that support that as well.
Microbiota in Obesity
DR: With the topic of metabolism and weight in mind, let’s briefly talk about the microbiota in obesity. During the weekend, I will go through a very detailed narrative about the microbiota in obesity because unfortunately this is an area where I think a lot of false promises are being made. Outlining the inaccuracies and what the factual information is in this presentation would be a bit too lengthy, but I did want to present people with a couple of important thoughts.
This comes from journal Nutrition Reviews, and this is actually a histological sampling of intestinal tissue. As you can see at the top in green, germ free compared to germy, or just a mouse raised in normal conditions. What we see is the mice that are raised in germ-free conditions actually have different intestinal architecture than the mice raised in a more germ or bacteria or normal type of environment. What may be happening here—again, this is an area we still have much to learn and don’t understand everything, but what appears to happen is when you have a mouse raised in germ-free conditions, the villi of the intestines—that’s what we’re seeing here; we’re seeing two of the villi—the villi can become thinner and longer, and this gives the villi a greater absorptive surface so they can absorb more calories but also makes them more prone to infection, whereas in a germ-rich environment, we see the villi are shorter, which gives them less surface area and less of an ability to absorb calories but also makes them less prone to infection.
This hints at potentially a mechanism of why Western societies are seeing an increase in weight gain and obesity. Now, there are certainly several factors that would potentially be reasons why a Western type of lifestyle would cause or be correlated to obesity. I’m not trying to say this is the only one, but from a gut and from a microbiota standpoint, there may be some unintended consequences of our increasingly hygienic Western environments that may come all the way down to the architecture of our intestinal villi.
Now coming to more clinical information and in supporting this point, when antibiotics are used in early life, it’s a risk factor for obesity (3) Trusted SourcePubMedGo to source. Clearly antibiotics used early in life—the earlier in life, the more harmful. Six months compared to a year compared to two years, the earlier you go with looking at infant administration of antibiotics, the more deleterious the effects seem to be. Part of this is likely because the microbiota is forming in a child and usually somewhat fully forms by around age three. Once the microbiota is formed, it tends to be somewhat resistant to perturbations. When adults take antibiotics, they seem to have the ability of their microbiota to bounce back, but in children, especially in infants, since the microbiota is still forming, then an antibiotic administration can really disrupt the formation of the microbiota, and this may cause the architectural changes we saw in the last slide and certainly has been correlated to cause many different types of immune and microbiotal problems later in life.
Also reinforcing what we saw in the previous slide, if one has diverse early exposure, that may be protective (4) Trusted SourcePubMedGo to source(5) Trusted SourcePubMedGo to source. Antibiotics would reinforce kind of a germ-free environment, and diverse exposure to dirt, germs, bacteria, what have you, would reinforce more of a germ-rich environment.
Looking at some treatments or interventions that may modulate the microbiota, low-carb diets show promising results. I’d like to be clear in saying that I am not someone that has a position in terms of dietary macronutrients one way or the other. I’m not vested in the low-carb camp. I’m not vested in the high-carb camp. I think that we clinicians need to guide our patients through the process of determining what their ideal carbohydrate consumption should be and not be vested in one camp of thought. But I like to pose the low-carbohydrate diet as a healthy starting point because it does tend to be a good starting point for many gastrointestinal conditions, and it also tends to work very well for weight loss.
Not in these notes, but recently there was published a systemic review—and systemic reviews are studies that examine many other studies, oftentimes clinical trials, and systemic reviews attempt to summarize what the majority of the available studies on a topic show. Looking at the results of a systemic review is akin to maybe reading 30 studies and averaging out what those 30 studies found, so a systemic review is very high-level scientific information.
A recent systemic review concluded that low-carbohydrate diets tend to have a better effect on weight loss than higher-carbohydrate diets (6) Trusted SourcePubMedGo to source. Both can work for certain patients, but again, we see a trend where low-carb diets tend to be a bit more effective. How this ties in with the microbiota is that a very-low-carbohydrate diet may actually prune some of the microbiota or may cause a decrease in bacteria in the intestines (7) Trusted SourcePubMedGo to source(8) Trusted SourcePubMedGo to source. This is oftentimes vilified as a bad thing, especially when we look at the microbiotas that we see in African cultures that have very rich and diverse microbiotas; however, a Western population has a completely different gut, probably different gut architecture as we showed a moment ago, and completely different metabolisms, so to try to take a diet of another culture and force that into a Western population, like Americans or Europeans, can likely cause deleterious effects.
The big message I’m trying to articulate here is that with the bolus of microbiota literature that we’re seeing right now, there’s almost an obsession to increasing bacteria in the gut; however, we have to be a little bit practical in our analysis and look at what the interventional data shows. When we look at the interventional data, it seems that approaches that actually prune back bacteria, like a low-carbohydrate diet or even administration of antibiotics or antimicrobial herbs, in Western populations can have a very powerful effect on weight loss.
With that as a transition point, let’s look at interventions that feed the microbiota, feed bacteria, and what kind of weight loss results they produce (9) Trusted SourcePubMedGo to source. The hypothesis that is circulating is that if we had more diverse gut bacteria, we’d be more like some of these non-Westernized societies, like hunter-gatherer bands in Africa, and that would cause us to lose weight and be at a healthy weight like they are. To either reaffirm or disprove that hypothesis, if we look at what happens in a Western population when we put them on treatments that increase microbiota diversity, we should see weight loss.
Let’s have a look now at fiber. The best results using fiber for weight loss were using a compound known as glucomannan, and 8.3 pounds were lost more than the control group, so that’s actually fairly impressive (10) Trusted SourcePubMedGo to source. One review—and again, a review paper is a paper that will look at many studies—one review showed the average weight loss effect from fiber is about 4.2 pounds (11) Trusted SourcePubMedGo to source, and viscous fiber may be better (12) Trusted SourcePubMedGo to source. Not bad, but not what I would call anything alarming or anything super substantial.
Now looking at prebiotics, which would be maybe even a more powerful method of feeding the microbiota, feeding of bacteria, the best results show 2.5 pounds of weight loss (13) Trusted SourcePubMedGo to source. This is very important for clinicians to be aware of because it will help us have a more intelligent dialogue with our patients who may be reading media stuff talking about how the microbiota may be the next cure to weight loss. Not to say that the microbiota or modulating the microbiota can’t help with that, but we as clinicians should know what a reasonable expectation could be. From prebiotics, it’s about 2-1/2 pounds.
Then from probiotics—I should mention that what I’m showing you is after an exhaustive review of the literature. Probiotics, the best weight loss results we see are with Lactobacillus gasseri at 2.2 pounds (14) Trusted SourcePubMedGo to source or with Lactobacillus rhamnosus at 3.7 pounds (15) Trusted SourcePubMedGo to source.
Collectively, when we look at some of the available microbiota treatment options, we see that we can produce weight loss, but the amount of weight loss is fairly marginal.
Now, I should also mention that recently a study was done using fecal microbiota transplant therapy, and this study was in a group of overweight and diabetic subjects. The authors concluded that fecal microbiota transplant therapy may be a viable method for lowering blood sugar, but when you actually read their paper, you see that fasting blood glucose, which is, as clinicians, probably the most important marker for us to track, and hemoglobin A1c, neither one of those changed over the course of over a month, nor did weight loss. The only metric that changed was what I consider a somewhat obscure glucose absorption kinetic marker, and so, again, we have to be careful even with the conclusions we draw, unfortunately, from reading an abstract because sometimes an abstract will make what seems like a promising conclusion, again, using FMT for weight loss or for diabetes, but really if we go through the laborious process of a patient going through FMT and they see no weight loss and no change in their fasting blood glucose, that’s not a very good recommendation for us to be making as clinicians, whereas something like berberine, an herb, has been shown to be as effective for lowering blood sugar as metformin.
I should also mention that, in terms of microbiota manipulations, some of the studies using prebiotics for lowering blood sugar have been quite impressive. We’re talking 20 to 40-point reductions in fasting blood glucose using prebiotics. I hope I’m not rambling here, but one of the things that I’m trying to bring to clinicians is a very precise understanding of what the available treatments for the microbiota are, what conditions certain interventions work well for, and what conditions certain interventions don’t work well for.
Humphrey, with that, are there any questions that you’d like to ask?
HB: No. You’re covering a lot of ground. I think one of the things that we see routinely, unless people read into the specifics of the research or the literature, is just more kind of broad swaths of research around probiotics, but not necessarily looking at particular species or looking at the microbiome as a whole and looking at different patient groups or different groups in different parts of the world and quite rightly, as you say, directly trying to link them and say that if you just translate their diet to kind of where we are now then eventually you’re going to see improvements, but as we know, there are all sorts of bacteria which are specific to different parts of the world as well, different strains, so it’s very difficult to directly translate what you see in one patient population in one part of the world directly into what we’re doing in the West.
DR: Absolutely, and you make a great point that reminds me of something else I should mention here without, hopefully, getting too tangential. When we look at the gut microbiotas of some of the African populations, we see a very high density of Methanobrevibacter smithii colonization, which tends to help the Africans survive in their environment. However, in Westerners, high levels of this Methanobrevibacter smithii cause methane-positive SIBO, which can cause fairly remarkable constipation and abdominal pain and may also cause weight gain and high blood sugar levels. Again, to your point, another important point for us to be aware of as clinicians is that we have to understand that we can’t take observations from another culture and try to replicate those in a different culture because, with this African example as an example, if we try to do that, we actually may make Westernizers constipated and overweight by doing that. It’s definitely an important point and an important thing for us to be aware of.
OK, I’m going to skip forward to the next slide here.
Microbiota and Autoimmunity
DR: The microbiota and autoimmunity—and this begs a question I’m sure many people have heard of or thought about, which is, parasites—friend or foe? People may have heard conflicting things about what may be a parasite and it being detrimental or it being beneficial.
An example of that is H. pylori. From the journal Inflammatory Bowel Diseases, essentially we see a narrative being published showing that increased incidence of H. pylori infections seem to correlate with a decreased incidence of inflammatory bowel disease (16) Trusted SourcePubMedGo to source. H. pylori here seems to be protective. Now, this may be because H. pylori may be a proxy of a dirtier environment, which can be healthy for the immune system, but we see some evidence showing H. pylori is protective.
HB: Yeah, that’s one of the things that we ceased to report H. pylori as a strict pathogen and offer numbers and the associated virulence factors rather than just a positive or a negative simply based on that because of the potential protective benefits that it has, and specifically look at the strains or the cytotoxins associated with individual strains rather than looking at it just as a group of, like, “Oh, H. pylori, it’s bad.”
DR: Right. There are definitely many nuances to H. pylori, and another thing that makes it even more complicated is there’s some discussion in the literature right now that a major factor may be the compatibility of the genes of the H. pylori and of the host, if they’re compatible. Essentially this means that if you have, like, an African strain of H. pylori that is residing in a European host, that may be deleterious; however, if you have an African strain of H. pylori that’s residing in an African host, that may confer protection. But there are other concepts in there, too, that can help us clinically determine what to do, and I’ll come to one of these in just a moment.
However, here’s a really interesting study (17) Trusted SourcePubMedGo to source. They looked at 10 patients with Hashimoto’s that also had H. pylori infections. Half of these patients were treated for the H. pylori infection, and the other half weren’t. Those that were treated for H. pylori saw a decrease in thyroid autoimmunity. This kind of contradicts the earlier point.
Here’s what this looked like. This slide is a little bit involved, but if you look on the right side here, you can just see the net change in the treatment group’s antibodies compared to the non-treatment group’s antibodies. You see that there was over a 2000-point reduction in the treatment group compared to only a 500-point reduction in the non-treatment group. What we see is—in this study, anyway, of 10 patients—we see quite a marked ability of treating H. pylori to dampen thyroid autoimmunity.
Then it begs the question of, what do we do? And what does this all mean? Well, we’re still figuring out a lot of this out, but here’s what I think.
Timing seems to be a very important factor here. Exposure seems to be protective if the exposure or the colonization is before three years of age, before the gut stabilizes. If you were colonized by H. pylori before the age of three, it may be protective in you, whereas if you were colonized for the first time at 23, it may be detrimental to you.
Context is also important. Like we discussed a moment ago, the immunogenetics, if you will, has an effect, the immunogenetics of the H. pylori and of the host, the interplay between the two, and also the diversity of someone’s colonization.
With H. pylori, we see a lot of this being published in the literature that managing H. pylori may not be solely an issue of just pure eradication, but rather making sure that H. pylori is at the appropriate level and that there are other healthy commensals to keep H. pylori in check and prevent it from overgrowing. I think that’s the type of strategy that works the best. This is probably why we see very high-level science like systemic reviews with meta-analyses being published, showing that if we give a probiotic along with antibiotics, it greatly enhances the treatment results for H. pylori and the clinical outcomes because it’s more than just eradicating, but it’s also supporting the healthy ecosystem to prevent H. pylori from overgrowing, so to speak.
IBS and SIBO
SIBO—this is an area that I’m very involved in both clinically and in clinical research. Here are a couple of studies. Essentially what this first study is showing is that about 50 percent of patients with IBS may have SIBO as the underlying cause and that rifaximin, a nonabsorbable antibiotic, seems to be a safe and effective treatment for SIBO (18) Trusted SourcePubMedGo to source. Fortunately, we also have herbal medicines that work very well in this application.
Then the second study here, some studies have found that even higher levels of SIBO may be present in IBS (19) Trusted SourcePubMedGo to source. Maybe as much as 84 percent of IBS may be caused by SIBO. Clinically a simple way that we can determine this or separate this out is have someone start with a healthy diet and some simple gut interventions, like a healthy diet and a probiotic, and that may clear many cases of IBS. The ones that don’t respond fully, SIBO is much more likely.
There are some modifiable factors for SIBO, like gastroparesis, which is essentially paralysis of gastric motility, small intestinal dysmotility or just impaired motility, celiac, diabetes, stomach acid, and organ dysfunction. These are important things for people to be aware of.
This is a very interesting study (20) Trusted SourcePubMedGo to source and a study that we’re trying to replicate, not with the same treatment, with a different treatment, but we’re looking at a similar study set-up right now, looking at when a patient has cleared their IBS symptoms and cleared SIBO, can a prokinetic drug or a prokinetic intervention, something that helps stimulate and make sure that one has healthy small intestinal motility, can that prevent the SIBO and/or the IBS symptoms from coming back? This study shows that erythromycin, which is, when used in low dose, a prokinetic, or tegaserod, these medications greatly enhance the time in which patients were relapse free or extended or increased their time in remission. The mechanism here is that inhibited or impaired small intestinal motility, or the ability of your intestines to move food through at the appropriate pace down to the colon, if that’s inhibited, things slow down and it’s kind of like when water is stagnant and fosters bacteria growth. When food is stagnant, it also fosters bacteria growth, or SIBO in this case. So by giving an agent that fosters or promotes motility or movement, you prevent this bacterial overgrowth from occurring, and that’s what we’re seeing with these two medications. There are also natural agents available that can be used in this application.
Testing Dollars and Sense
I want to take a moment to just talk about something that I’m very passionate about, which is making functional medicine cost effective. I love functional medicine; however, I do have some fairly lofty concerns that it is becoming increasingly expensive because of overtesting and overtreatment.
A few things that are worth mentioning: I’ve saved my patients a lot of money by using insurance when and where possible. This is underappreciated; however, as I’ve been using some of the more conventional insurance labs, I’ve found that they do a very good job, and we don’t always need to have a patient go to a specialty lab. Definitely sometimes there are certainly a time and a place for a specialty lab, but if we can incorporate or use a hybrid of specialty labs that are cash pay and insurance labs, then we can really do a lot to drive down the bill for a patient.
HB: The only thing here, Dr. Ruscio, is here we basically have the NHS, which will just deal with acute medicine. If they think you have a thyroid problem, they’ll literally just test TSH, and you will be pulling teeth trying to get them to measure… a GP won’t even want to measure T3, free T3, TPO antibodies, thyroglobulin. They won’t even touch it, so that basically you can pretty much guarantee even insurance won’t really do that sort of thing. Here pretty much everyone that you’re speaking to will certainly be seeing from the same [inaudible] as far as making sure that they focus on things that are cost effective, but pretty much all of the patients will be paying cash out of pocket.
DR: Gotcha. Well, that makes this second bullet, then, even more important, which is focusing on the vital few tests rather than the trivial many. There are several tests that I, to be frank, just stopped doing because I was wondering if there was really any true clinical utility to these tests. Food allergy tests and adrenal tests are two of those. I haven’t done those in over a year and a half in my practice, and I’m probably getting better results with food allergies and with adrenal function or symptoms of adrenal function than I was about two years ago. Not to say that these are tests that should never be done; however, one of the things that we’ll talk about in the seminar is having a model that focuses on the cause of the problem first and the deepest cause.
If someone presents with IBS and adrenal fatigue, taking care of their IBS, testing what’s causing the IBS and treating that, is more important than testing the adrenals. We can definitely support the adrenals, but I don’t see a huge need for very elaborate adrenal treatment that’s based upon lab testing because to tell you the truth, if you do a good job pegging the cause of the adrenal dysfunction, in three months the adrenals are going to be somewhat irrelevant because they’re going to be healed. I see that all the time in my practice, where we fix a gut issue and a patient’s adrenals come right back online.
Now, I realize for some people listening that may seem like a very hard concept to accept, and it’s something that we’ll expand upon more in the weekend seminar, but it pulls at a very important concept, which is, are you focusing on treating the most root cause, or are you focusing on treating factors that are just associated with the root cause? This can be a very, very powerful clinical tool because it will enable you to get the same or better results with less time and less money. Sorry not to be able to go a lot deeper into that, but there are a few other notes that I want to just highlight.
Having a sort of linear progress that you work through, meaning, “OK, we may have SIBO, we may have heavy metal toxicity, and we may have Lyme. Do we need to test for all these things at once, or might we want to start with one factor that seems the most supported—let’s say SIBO—treat SIBO, and at the end of SIBO treatment, reevaluate? If the patient’s symptoms are nearly all gone, then we don’t need to move further toward the heavy metal testing or the Lyme testing. If they’ve not fully responded, then we would move on to other testing.
Looking at this in terms of not trying to diagnose every problem right out of the gate, but organizing or codifying these things into a hierarchy, where you focus on what you think is the most supported or the most likely first. At the end of that, reevaluate, and then only proceed if you need to to get further improvement. That model of thinking, that hierarchical model, has really done volumes to decrease my overtesting and my overtreatment.
A couple of other notes here: Personally I feel the most successful as a clinician when I can take someone off adrenal support, for example, and that patient maintains their improvement. That’s something I think we sometimes lose sight of, where we maybe get too fixated on treating a lab or treating a pathway, and we get too focused on the treatment. For me, my ultimate goal is to get a patient to a point where they need no treatment and they maintain the benefits that they were previously getting from the treatment.
Patients really do appreciate this. Many patients come to me because they’ve heard about my approach in being a bit more cost effective, and lots of patients have actually sought me out with that objective in and of itself. I think patients really appreciate if you’re going to be sensitive to cost and conservative in action because that’s really how I would want to be treated. If I came in and someone told me it was going to cost $3000 to diagnose my problem, I would be a little bit wary about that, but if someone said, “We’ll take this one step at a time, and we’ll start with testing what seems to be the most relevant and then reevaluate, and it’ll cost $600 to get started,” I’d feel much better about that approach. I’d feel much more like this was a team endeavor and me and my doctor were working together. There’s a quote that I think encapsulates this nicely, which is, “He who is the best can do the most with the least.” I think with testing and treatment, that’s an important moniker to kind of keep in mind.
HB: Can I just interject there for a second, Michael?
HB: A couple of questions have come up. One is, you talked about the timing of exposure and the timeline particularly around H. pylori. Are you currently aware of any research around exposure to any specific yeast, fungi, molds as kind of being beneficial, again in that zero to three years? Are you talking about total exposure in those first three years to all commensal bacteria and infections as being beneficial, or are you talking about just specific bacteria?
DR: That’s a great question, and it’s a very hard question to answer because there are many factors that, of course, are going to be at play in a certain individual. Here’s an example. Let’s say we have two children. One child lives in Europe. One child lives in Africa. The person living in Africa in a more hunter-gatherer-type society is likely going to have exposure to different dirt that someone who lives in a slum in Bangladesh or who lives in the States and their total environmental exposure to bacteria is low, but they have periodic punctuated exposures.
Why this is confusing is because we see a high level of observational data showing that children that grow up in less hygienic environments seem to be protected from autoimmunity. We also see that there’s some literature that shows that exposure to even infectious agents like cryptosporidium or flu or other pathogenic or potentially pathogenic bacteria in youngsters is protective against autoimmunity. However, there are also studies showing that those exposures may stimulate autoimmunity later in life.
It’s very challenging to have a specific answer to that question, and some of this may have to do, I think, with the context that someone is growing up in. Here’s an example to maybe further outline that. It’s been shown that mothers that live on farms have children with a lower incidence of autoimmune conditions and also that children growing up on farms have a lower incidence of autoimmune conditions. That would then suggest that being exposed to farms and especially farm animals, because other studies have shown that the more animals one is exposed to, the more farm animals, with every increased animal is an increased protection against autoimmunity. All this would suggest that going to a farm and being exposed to different bacteria and what have you would be protective for the immune system. However, if you live in a city but only periodically visit a farm, that may actually make autoimmunity and asthma and allergies worse. How this may unravel is that if you have continuous background exposure, it may tone your immune system, but if you have periodic episodic exposure, that may be perceived by your immune system as an attack.
There’s a lot of nuance and a lot of context here with unraveling this. Fortunately the clinical applications of this, I think, are a bit more simple, but does that kind of answer the question?
HB: Yeah, I think it does, and I think it leads in a different way to another question, which is just that one of the clinicians has just been asking, and I think this is very common. I read a lot specifically about some of what I would consider nonpathogenic parasites, particularly lots of stuff around the subtypes of Blastocystis and Dientamoeba fragilis, and one of the clinicians is asking whether seeing those positive with somebody who is presenting with chronic bowel symptoms that haven’t been favorably changed or helped with herbals, is it appropriate, in your perspective, to then start looking at antibiotics for treating those?
DR: Well, I have not had a case of Blasto that I have not been able to clear using herbs. Every case of Blasto that’s walked in my clinic I’ve been able to eradicate in one round of treatment by using the herbal protocols that I use. If someone is not able to clear Blasto and/or they’re not able to ameliorate their symptoms, they’re probably missing something. I am very open to antibiotics, and one of the things I’m hoping to do with the next wave of studies that we’ll produce through my clinic is to start doing some herb-drug comparison studies. For example, there has been one done looking at herbs and drugs in the treatment of small intestinal bacterial overgrowth. While this study may not have been perfect, the gastroenterologist that published this study, he did find about an equivalent eradication and success rate using herbs and using the antibiotics. So I am definitely open to the antibiotics; however, I think we may be missing something in these conditions that are unable to respond to herbal medicines.
HB: So you’re saying that potentially they could still be there and actually for that particular patient they might not be considered parasitic or pathogenic for them but there’s just something else going on that they’re just not able to see because there’s this kind of light going on which is saying Blastocystis when actually it’s kind of taking that focus away from actually looking at other things?
DR: Well, I think both. The Blasto may be pathogenic, and I think it’s more supported that the Blasto could be acting in a pathogenic way if someone has a healthy diet and lifestyle and still has symptoms. However, if they’re not clearing the Blasto, it may be something that they’re missing in their Blasto treatment, or it may be some other factor in tandem with the Blasto that they’re missing. That’s what I’ve found clinically, anyway.
The other thing is, from a patient management perspective, when patients feel very strongly that an antibiotic is going to be what they need to get over their health challenge, we will often have them use an antibiotic, and many times what patients will find is the antibiotic isn’t as great as they thought it was going to be. It’s not a grass-is-always-greener-on-the-other-side sort of phenomenon. Sometimes it is. I mean, we have to be open to using the different available treatments in helping personalize treatments for the patient, but I’ve found it a very freeing experience when a patient felt that inclination, to have the dialogue with them, and if they felt strongly about it, to humor them and let them use the antibiotic therapy or the hormone therapy. In many cases, we don’t see huge results from that, and we come back to, “OK, I was excited about this idea, and now I understand that it’s not necessarily a magic protocol.” It’s coming back to these clinical basics of trying to work through the problem—identify what the problem is and treat that problem. Hopefully that helps.
HB: That’s good. I know you want to get on with some of the other slides as well. You were very kind to show me the slides that you’re presenting in London.
GI Infections and Dysbiosis
HB: I know you go into a lot more depth in terms of very specific treatment protocols that you engage in with your patients, which you’re not going to have time to go into today, but you go into very, very dose-specific protocols that you engage in with your patients in the longer talk you’re going to be doing in London in January.
DR: Right, absolutely. There’s never enough time here, and I think… what do we have, maybe five minutes left?
Quickly here, this is the H. pylori biofilm. This is an interesting concept that comes back to a question from a moment ago, Humphrey, which is resistance to treatment.
This study treated two groups of patients, one with just antibiotics for H. pylori, the other with antibiotics and n-acetylcysteine, which is a biofilm degrader for H. pylori (27) Trusted SourcePubMedGo to source. As you see, with the antibiotic plus n-acetylcysteine, the clearance rate was 65 percent compared to only 20 percent without n-acetylcysteine.
DR: Natural medicines can be powerful, n-acetylcysteine being natural. It’s just knowing how to use these things.
HB: What doses were they using of the n-acetylcysteine?
DR: Oh, gosh… I don’t remember off the top of my head.
HB: Was it quite moderate, like 500 mg, something like that?
DR: Yeah, nothing unusual. Yeah, maybe 500 mg. When I checked it, it was nothing out of the ordinary. The natural medicines can be very powerful.
Coming back to Blasto, another example, there are certain antiprotozoal herbs that are very powerful for things like Blastocystis hominis and Amoeba histolytica, but it’s knowing what herbs have that effect. Also there are certain probiotics that have very strong antiprotozoal activity. It’s knowing how to pair the right antibiotic with the right herb in the treatment of Blasto to enhance treatment effect, or in this case, if it’s a resistant case of H. pylori, how to use an antibiofilm agent to assist with that treatment success.
DR: The thyroid is the other piece we’ll be talking about, and we’ve already talked about quite a bit of the gut, which has a huge effect on thyroid. I want to skip forward here to… I’m sure people know this, but Hashimoto’s is the most common cause of hypothyroidism in the United States and in many Westernized countries. Hashimoto’s is essentially a process in which your immune system attacks the thyroid gland, so these immune system cells come in and they attack the thyroid gland. What this will manifest as is a decreased amount of thyroid hormone secreted over time as you have a loss of healthy thyroid tissue. Ways to assess this are fairly straightforward with laboratory markers, which would be TPO, thyroid peroxidase, and thyroglobulin for Hashimoto’s.
There are many factors that can lead to autoimmunity. This list may look a bit daunting, but when we kind of codify things into a clinical approach like we talked about a little while ago, where we start with one intervention and then work our way to the next if we need further improvement and then work our way to the third if we need more improvement, when we codify these things into that sort of approach, it makes it much easier to take on all the potential causes and treatments of autoimmunity. Here are some supporting references for that slide.
Here is a slide maybe I can [use to] kind of bring us to a close with, which is the clinical, “What do you do with some of this thyroid stuff?” We have two patients that both present with symptoms of hypothyroid: Sarah and April.
Sarah started having thyroid problems after her second pregnancy. When we work her up, we find elevated TPO antibodies, which would diagnose Hashimoto’s, and this would diagnose her as postpartum autoimmune hypothyroid. The treatment looks like balancing of the immune system to stop the autoimmune attack, which consists of dietary changes, antioxidant therapy, and vitamin therapy.
In April, her digestion is not as good as it used to be. She has gas, bloating, and stomach burning on occasion, which started five years ago. This accompanies her hypothyroidism, her hypothyroid symptoms. In her workup, we find an H. pylori infection, and we find high reverse T3. This is infection-induced high inflammation resulting in decreased thyroid hormone activation or conversion. Her treatment looks like removal of the gut infection and repair of the gut using antimicrobial herbs, vitamin therapy, and probiotics.
What I’m trying to illustrate with this slide is if we take a moment to perform a good history and some targeted lab testing, we can get to the cause of the hypothyroid symptoms or the hypothyroidism itself and then formulate a treatment program that is specific to that.
This is just one of our patient’s labs, their TPO labs, that went from a low-level positive, 172, to negative over the course of about a year.
HB: I was going to say, Dr. Ruscio, the slide before that one, which was one of the questions that just popped up. I know we have so many questions from people, but I know we’re not going to be able to cover them. Hopefully you will cover an awful lot more in your seminar in January, but it was about the particular infections that can affect the thyroid autoimmune status, and I think this was a slide that I think would address that.
DR: Great question. There’s an important distinction I should make, which is we have a wealth of data showing association between certain infections and thyroid autoimmunity, but association does not mean cause, and it doesn’t mean that treatment will yield improvement. We have, to my knowledge, only one study of its kind, and that’s the H. pylori study that we covered a moment ago. H. pylori treatment has been documented in the peer-reviewed medical literature to help with thyroid autoimmunity, according to one study. These other infections, like Yersinia enterocolitis, which is actually more common than you might think, Epstein-Barr, cytomegalovirus, and the herpes simplex virus family, have all been associated. I certainly think it’s worth treating these infections if they’re present because we know that treating these infections will yield other benefits. Whether or not we’ll have a strong impact on thyroid autoimmunity is something that hasn’t been very well documented in the scientific literature; however, I think this is where the clinical science is ahead of the published science, and so anytime I find one of these infections in a patient with autoimmunity that does not respond to initial diet and lifestyle therapy, then they would definitely be a treatment consideration.
Then the last point here, I guess, to be very brief in this, would be regarding iodine. We’ll go into more detail about this in the seminar, but it is not a good idea to use iodine in anyone that has any kind of active inflammation because it may throw off what’s known as their sodium/iodide symporter, which helps the body regulate iodine. The reason why regulating iodine is so important is because it has been consistently shown in population studies that iodine and increased iodine intake is correlated with hypothyroidism and thyroid autoimmunity. It’s really incontrovertible. There’s so much science showing that increased iodine intake, especially when iodine intake becomes high, increases the chance of thyroid autoimmunity and hypothyroid. One of the reasons why that may be is when people are inflamed and taking iodine, the inflammation damages the sodium/iodide symporter, which is your body’s regulatory mechanism for getting rid of excess iodine if you’re intaking more than your body needs. So if that regulation system is broken, you can’t get rid of the excess iodine, and that has been very well correlated with autoimmunity.
There are two podcasts I’d like to refer people to, podcasts with full transcripts, because I had a feeling I wouldn’t be able to get into this deeply during the call here today, but if you go to my website, which is DrRuscio.com—I’ll put the link up in a second—there’s a two-part podcast on thyroid and iodine (28)(29), and it’s very meticulously referenced and, if I may say, I think it’s very well done. There’s also an episode on thyroid nodules, goiter, and iodine (30). Those might be interesting to people.
The website here isDrRuscio.com. At my website, there are a lot of resources. There are weekly updates, podcast, interviews, research updates, and articles that can all be accessed via the newsletter.
Then the event in London, which I’m very excited about, is January 16 and 17.
Just to come back to a closing quote for a moment, this is a very important, I think, philosophical concept, and it’s a quote by Harrington Emerson. “As to the methods there may be a million and then some, but principles are few. The man who grasps principles can successfully select his own methods. The man who tries methods, ignoring principles, is sure to have trouble.” I think this applies in clinical practice, that we have to understand principles of good clinical medicine, and then we can select our own methods. If we bounce from method to method to method or from protocol to protocol to protocol, not understanding the deeper principle behind it, I think we’re sure to flounder. Hopefully some of that has come through throughout this presentation.
HB: That’s great. Thank you so much. As we often find, we feel like we could have gone on for hours! There’s so much material to cover. I’m excited to hear you speak on the 17th of January in London, and I will certainly send out an invite to all the clinicians that registered with us for this webinar this evening just so if they feel like they want to come and delve a lot deeper into the material over a whole day that you just managed to touch on in fragments, then certainly I’m sure lots of them will be really keen to come and engage with you for that event.
DR: I hope so. I think it will be a good event, and I hope to see many of the people listening there.
HB: Great. Thank you so much, Dr. Ruscio, for being with us today, and I hope you have a really good break. I know you’re away from practice next week, and we look forward to seeing you in the new year.
DR: Absolutely. Thank you, and thank you, everyone, for listening. I really appreciate it.
HB: That’s great. OK, thanks very much. Thank you. Good night… or good morning!
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