Biofilms Can Cause Infections That Won’t Clear – What to Do About It with Dr. Paul Anderson

Biofilms are protective coatings that bacteria and fungus form to protect themselves from antibiotics and herbal treatment.  Biofilms may be at the root of infections that won’t go away like Candida, fungus, H. pylori and SIBO.  Today I speak with Dr. Paul Anderson on how to identify if biofilms are affecting you and what you can do about it.

In This Episode

Episode Intro … 00:00:39
What Are Biofilms … 00:05:13
Biofilm Phases … 00:08:00
Symptoms … 00:09:32
Infections Commonly Associated With Biofilms … 00:15:10
Methane Producers … 00:21:08
Candida … 00:22:15
Testing … 00:24:00
Treatments … 00:27:06
Dietary Treatment … 00:30:50
Natural Treatments … 00:35:05
Prescription … 00:41:00
How To Know If Treatment Is Working Or Not … 00:49:00
Die-Off vs Intolerance … 00:55:48
Other Tips and Tricks … 01:01:00
Episode Wrap-up … 01:03:00

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Episode Intro

Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. Today, I am here with Dr. Paul Anderson who is one of my cohorts with a lot of information on SIBO. And despite his great knowledge on SIBO, we’re not talking about SIBO specifically today. We’re actually talking about biofilms, another area where he’s got quite a bit of expertise.

And so, I’m excited to have this conversation and pick his brain a little bit more. So, Paul, welcome to the show.

Dr. Paul Anderson: Thank you so much for having me on.

DrMR: Absolutely. Absolute pleasure. And despite some technical difficulties that were thwarting our start, we got through them.

DrPA: Yeah, it’s always the way it is, but we’re here now. So that’s good.

DrMR: Absolutely. So, Paul, before we jump into the topic, can you give us a brief synopsis of your background and how you got into the field of biofilms, specifically.

DrPA: Ok. I’ll try and give the short version. So my entry into medicine actually goes back to 1976 when I started working in the laboratory end of medicine in both hospitals and clinics and things like that. And so, I kind of come from that research, nerdy background. And then a number of years ago, when my children were young and they’re all in their late 20s or 30s now, so they were having some trouble. And I was getting bored with the lab world, so I went into naturopathic medicine.

So I went back to medical school, finished that. For those of you listening at home, don’t do that when you have young children. It’s very, very difficult, but we made it. And I really felt like I wanted to bring forward my past experience in lab and all that business into this.

So practiced in Oregon for a number of years and Arizona and now in Washington for almost 13. So the thing with biofilms was always one of those things that—it’s kind of one of those things you hear about and you think, It sounds like I’ve got to learn something new. So you wait.

And I started getting sicker and sicker patients, more digestive tract things, SIBO, all sorts of other stuff. And it got to the point where I knew something about biofilms because I had heard what a lot of us hear, I think, in our training, if we hear about it at all, which is a piece of the story. And I realized, as I started doing more research into what was going on in what I call the big-time biofilm researchers, there was a whole other story I’d never heard.

Somewhere along the way, I ran into someone doing research in the biofilm area for treatment-resistant infections. And that got my attention because that was an area I had been kind of working in. As you and I have seen, people, whether it’s in their gut or other places, you can kill things. And if it doesn’t die, there’s some reason it’s not dying.

So I really started to look into this research that was going on and realized that it wasn’t just something that we in the integrative medicine community are interested in. The CDC and a couple of other government agencies are very keenly interested in biofilm research, because they know that this is one of the main drivers for drug resistant infections and hospital infections and stuff.

So that’s kind of what got me up to saying, “I’ve got to dive back in and see where the research has gone since the last time I looked a decade ago.” So that got me down a very interesting pathway into how complex biofilms are, how they can be either normal or pathological, and both at the same time. So it really opened my eyes up and started an odyssey that’s been, well, now about the last 10 years to getting to where we’re at.

DrMR: And you make a good comment that I want to kind of hinge on to ask my next question which is they can be, biofilms that is, normal or pathological. So I just want to reiterate that because sometimes when we learn about something it’s easy to completely vilify and lose the context that, for example, in the GI tract a lot of our healthy commensal, resident bacteria are protected by a biofilm, and that prevents us from losing all of our bacteria from a course of antibiotics.

So they can be helpful.

DrPA: Right.

DrMR: But they can also be pathological.

DrPA: Yeah.

What Are Biofilms?

DrMR: So can you define, I guess, just a simple definition of a biofilm and then we can get into more of the particulars.

DrPA: And I think that is a really good place to start because it’s human nature that we want to make something either good or bad. And in this case, it’s part of nature. And it’s part of why the planet is held together, really.

So biofilms exist anywhere really pretty much where there’s microbes and moisture. And so, you can find biofilms on the bottom of the ocean. You find them in the mucus membranes of any animal that has them in the digestive tract, even in blood vessels. You’ll find them in water treatment systems, etc., etc.

So they’re a natural outgrowth of—and here’s the thing that we’re learning more and more about. They’re kind of a natural outgrowth of certain types of bacteria in particular. And you mentioned the good guys in our digestive tract and it’s a way to protect themselves. And so, the normal biofilms are actually part of us staying healthy. So it’s not like we want to scrub away all the biofilms, just like we don’t want to take all the bacteria out of our digestive tract. And that’s where most of the biofilms in humans are is in digestive and respiratory tract.

So it’s a way for a commensal or at least a resident bacteria, usually—and then we’ll talk about other stuff later—to have a home so that it’s resistant to what would normally maybe knock it out or take it away. It starts as a good resistance strategy, a good stability strategy for mostly bacteria but some other stuff.

There’s plenty of healthy people in the world, and they have healthy biofilms and that’s part of their biome balance, let’s say, if we’re talking about the gut specifically.

What happens is—and we can get deeper into this later—but to kind of give people a big picture, I usually tell them if you think of a spectrum in front of you, going from your left to your right, on the left side are these healthy, normal biofilms. So they’re there. That’s your base. You may have nothing else, and we call you a healthy person.

And then there are stages of biofilm development that we now know… Here’s the other thing that kind of I think messed with a lot of the integrative practitioners learning about biofilms. We extrapolated a lot from oceanography where there’s certain types of biofilms and stuff. And they’re a little more static. But in people and most mammals, they actually can be very different across the spectrum of not helpful or pathological or bad or whatever.

Biofilm Phases

So there’s sort of an early pathological or not-so-good-for-you one that grows. And you think of it like the good one that’s the base adds on some components, and you get the wrong bacteria and they get in there with the good bacteria. And then, they start to create their own little scaffolding and hold onto stuff. And over time, you move from the left which is normal to kind of the middle which is what we call an early phase or a phase 1 type biofilm. That’s not so good but actually fairly easy to deal with.

And then, if you get sick and rundown and you lose your good bacteria or they get rundown, the bad ones create a bigger scaffolding which is harder to get through. And then, you can actually have—actually, the researchers liken it to like a hive community, where you can have viral parts in there and parasites, protozoans, regular bacteria, all kinds of stuff. And they actually can move all the way to the right-hand side of the spectrum where they are their own new pathogen. And it’s actually a family pathogen, and they all trade DNA and all this weird stuff.

So it’s actually a spectrum. And what you do to prevent or treat them has to be on a spectrum, which most of us never heard about because we heard about sort of the easier ones.

Symptoms

DrMR: Ok. So we have this spectrum. Now, as someone’s listening to this, they are likely trying to take a mental stock or assessment of, is this something that might be inflicting me?

Are there certain symptoms or any other indicators that may suggest someone should be paying more or less attention to this conversation?

DrPA: This is a question I get a lot from other healthcare practitioners, “How do I know when to worry about this in a patient?” And here’s kind of the keynotes that I see in people where it’s maybe more or less of an issue. I want to make a point that there are things built into traditional diets, and we can develop this later. But there are things built into traditional diets that tend to stop these earlier phase pathogenic ones from ever forming anyway. It’s kind of like having good bacteria stops it and all that good stuff.

But the people that I’m more concerned about are people who have had one of the following. So one would be they have a known lab-verified pathogen, such as H. pylori that’s giving them ulcers, gastritis, whatever. They’ve treated it, treated it, treated it with all the standard of care stuff and natural stuff. It’s never leaving. That’s usually a sign that there’s biofilm protecting a pathogen.

The other one though is people who have been sick for more than a year or two, your more chronically ill folks. And this is whether they have something like SIBO that’s going on, that’s definitely changing the landscape. Or whether they maybe have some chronic peripheral infections. But the bottom line is that their gut gets dysfunctional because of all the inflammation from the illness. Nothing kind of brings that back to balance.

And then, the bad actors can get in and start to build these more advanced kinds of biofilms that can become actually truly pathogenic. There’s nothing good about those guys.

So it’s kind of long-term illness we start to raise our suspicion. Infections that will just not clear. For instance, in the SIBO world, your people who you’ve done phase 1, 2, 3, and then mixed phase 2 and 3 and 4 and 5. And nothing ever comes back to normal. Those are the people where I start to have a higher suspicion that this is going on.

DrMR: There’s a few things there that you say that I think are really great. One is lab-verified, because sometimes people read about “insert pathogen or item here” and they convince themselves that they have it and it was really actually quite a simple change, like thinking about your diet less or getting a little more sleep or getting a little more exercise that was actually the issue. So I do think it’s important to just verify these things.

It’s also interesting that you say the length of time is important. And of course, that makes sense. But I guess what struck me—and I just want to make a quick recapitulation on that—is we do know that inflammation, for example, will allow unhealthier strains of commensal bacteria or just bacteria in general to thrive and that kind of dwindles the healthier populations.

And so it would make sense that with prolonged time in an inflammatory state, you’d have more of a dominance of these unfavorable bacteria. And the longer they’re in dominance, the longer they have to build this kind of protective fence, which is a biofilm, around them and protect them. So certainly, the lab verification and also the timing or length of illness make a lot of sense.

DrPA: In looking backwards at, gosh, where did I have treatment failures or this or that and when did it turn out that biofilm was really an important part of it, yes, A, finding the pathogen is the first thing. We’ve all had patients that they come in, they’ve been trying to kill something that’s actually not there for a long time, and that’s sort of a dead-end road.

But if you do indeed find them and there’s been a long term of inflammation, that’s the person who’s set up for the real bad, kind of the right-hand end of the spectrum of big biofilms. And the thing that I learned from I guess you’d call them the more traditional biofilm researchers is it sort of becomes a positive feedback loop at that point.

The bad bacteria invite more, and then you get all these other forms that just are there and they hide too. So you truly get more trouble.

DrMR: Now, do you like the kind of simple definition that I use of just calling it a protective fence? We could get more detail, but would you say that’s a decent way of describing this conceptually?

DrPA: That’s a good idea. Fence or like I use the word scaffolding because it kind of… So sort of like a hive. Yeah, protective fence I think is a good way. So the stuff on the left side that’s normal, it’s a little fence that keeps your dog in the yard. The stuff in the middle, it’s a little higher fenced and they’ve invited some bad friends in. And then, the stuff on the right, it’s sort of like a cage match where there’s fence all the way around and it’s just full of all sorts of bad actors. It’s probably the best way to think. Yeah.

Infections Commonly Associated With Biofilms

DrMR: Ok. So you alluded that in the respiratory tract and in the gut are where the biofilms are very common. So along those same lines, are there certain infections specifically that are most prone to formation of biofilm. Now, there’s been one landmark study on H. pylori. We actually have performed a retrospective chart analysis that we’re late to the party… I’m publishing, and I apologize to the audience. I know I’ve been talking about that for a while, but I’ve been very sidetracked with the book.

We’ve been able to document biofilm agents will help with SIBO clearance. I’ve heard some discussion, although I haven’t dug too deeply, regarding some of the Lyme and Lyme coinfections. I’m wondering again, to try to provide the audience, whether they’re a lay person or a clinician a little bit more clarity on when to think more or less of biofilm.

Are there certain types of infections that you find to be more prone to biofilm formation than not?

DrPA: The first one you mentioned, H. pylori, it may be one of the best known. I would put the kind of footnote to what I’m about to say to say this is an area where there’s a lot of unknowns because nobody thought to look there, not because maybe they don’t exist. And as people are more interested in super infections and stuff, you’re going to see more data come out about it. But a real, very well-researched and potentially very pathogenic bacterium, the Pseudomonas family, which can cause persistent lung infections and death from pneumonia, all kinds of bad things there. Also, Pseudomonas can get in other places.

Pseudomonas is a huge biofilm producer. And it turns out that’s one of the reasons it’s so pathogenic or likely to cause treatment-resistant problems. So Pseudomonas is in that family. Some of the common gram-negative type bugs that you see a lot in the gut, as you’ve probably talked a ton about. Like the E. coli is a huge family, and there’s different genetics across the E. coli spectrum. Some of them make biofilms better than other ones do, for example, the latent pathogen ones.

And then, to the degree we understand it right now, although I will say people studying biofilms are starting to see, well, there’s stuff we thought that didn’t make biofilms that now maybe does, and they need to look into it. But it becomes an opportunistic advantage. So let’s say H. pylori or let’s say a Pseudomonas relative sets up the initial deeper fence with little higher walls. Other bugs can get in there of different types. They start to share genetic information, and they make the fence taller to protect themselves.

And then that’s when you tend to wind up with, I would say probably certain of the Lyme and coinfections we’re probably going to find. They like those. There are certain parasitic infections that like those. Like Blastocystis hominis and some of the other ones, they’re on the fence of are they bad or are they not bad? Well, it’s situational. If they get into a biofilm, they become persistent and then they bring other guys with them.

And this may be jumping ahead a little bit, but I just want to point this out because of the research I’ve done with my patients over time. There’s a lot of press that was given to, well, these are in the blood vessels, and the real bad biofilms are disseminated through the body. And we thought that for a long time too. Certainly, there’s actual studies of biopsies of blood vessels with biofilms. So we know they’re there.

But what I’ve noticed using biofilm agents is I’ve used them intravenously on the same people and gotten very little response. And then I’ve used them as, say, an oral agent to hit digestive biofilms and gotten a completely different, much more aggressive response that would indicate to me that I think the gut is ground zero for biofilms. Respiratory system is number two, and then everybody else follows after.

So the gut bacteria… And then it becomes this piling-on effect of one or two of the biofilm—the ones that have the DNA to produce the biofilm, produce a biofilm and then some bad guys get there, chronic inflammation like you mentioned, and then it’s off to the races. And then, they’ve got the big cage built.

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Methane Producers

I would be curious to hear your thoughts on this because I don’t think this is an area we know much about. In the research that I’ve done, although there’s not a lot of data here, it does seem that we have documentation that methane-producing archaea can produce biofilm. Any thoughts on that in particular?

DrPA: I know that there’s not a ton of—and really, we’d have to say with very few exceptions like Pseudomonas or H. pylori, there’s not a ton of research on a lot of things in humans and biofilms. But it makes complete chemical sense, and I believe from what I’ve seen clinically that the methane producers would be really high on the list of things that’s easy for them to do. Yeah.

DrMR: Sure. And a follow-up to that, Allison Siebecker, one of our mutual friends, she’s made the remark…And I tend to agree with this, at least from what I’ve been able to parse together from some clinical observations, which clinical observations are not always perfect. They’re definitely amenable to bias, even if you’re very objective, as I like to think I am. Even if you think you’re being objective, sometimes there’s that hidden bias that you can’t get out of your head.

DrPA: Sure.

Candida

DrMR: But her remarks were that she feels Candida tends to be one type of infection or dysbiosis, however you want to term it, that is more prone or tends to more aggressively form biofilms. What are your thoughts on that?

DrPA: Maybe it’s a chicken and egg kind of thing. I have seen that I believe clinically. And one of the times that I’ve seen that, or maybe fold this into something we already talked about, is the people who have had lab-verified intestinal Candida that’s been treated very appropriately, very broadly, first, second, third line. It just never goes away. There’s reasons that that seems to be happening.

Now, there’s a couple of biochemical ideas about that. One is they’re hijacking and getting into other people’s biofilms, and so that gives them some resistance. The other is maybe they can do it on their own. And then the third thing is that they’re either trading some DNA with biofilm producers which allows them to do it and/or they’re using other fuel sources from maybe other things that you’re killing off.

So I think that’s a deep well. I think that there’s a biofilm piece. But Candida and other fungal forms that are pathogenic or at least problematic, I think they have multiple resistance strategies once you get a sick person.

DrMR: Now, I know again that H. pylori study, I believe it was an electron microscope or micrography that they were essentially able to scan the stomach mucosa and show biofilm pre and post eradication or show it and then show a great diminishment of it after the treatments with n-acetyl cysteine. So that may be one way of “testing.”

Testing

But I’m assuming when we get into other areas of the body, the testing gets much hairier. But are there any practical tests for this other than just using a treatment as a test?

DrPA: I think right now our state-of-the-art is pretty low as far as testing goes. Now, on the research end, I’ve seen some really cool, like intravascular biopsies that show biofilms, scaffolding all this stuff. You’re not going to do that on your patient. I’ve seen GI scope biopsies that really showed and they do microscopy and it’s plain as day. None of those are practical really for my purposes.

There’s a lab that we use sometimes that is very good. The pathologists there are very into the biofilm world, and they know what to look for and all this business. It’s called Fry Labs in Arizona, and they can do certain assays. But they’re still not perfect.

So essentially and even in the case of—so kind of behind the scenes, biofilms are such a problem with hospital iatrogenic, doctor-induced infections. You go to the hospital for surgery. You didn’t have biofilms when you went in. You do now. And for drug-resistant infections. The way that the science and pharmacology is going is we know it happens. We have proof it happens in certain instances such as surgery, etc., where there’s trauma. Where they’re evolving the pharmacology is if you have a procedure done, if you’ve had a dirty wound, if you’ve had an untreatable chronic, recurrent infection, we’re just going to treat you for it because it’s probably the biofilm behind it.

And so, it seems that the “standard medical community” is moving in the direction of just empiric work, because I don’t think we have really great things beyond very invasive stuff to test.

DrMR: And as you make those remarks, there’s a couple things maybe just as some background. And again, please correct me if I’m off on any of this. But as I understand it, our initial understanding or our predominant initial understanding of biofilms came from both oral plaque biofilms and also for prosthetic devices that would form biofilms. Is that correct?

DrPA: Yeah. So kind of the evolution was oceanography where we first noticed them and then those two things. Really, the dental plaque was the first one because that’s easy and then devices like in-dwelling IV catheters and implanted devices, etc. So stuff that shouldn’t be there, but it is. So that’s true.

DrMR: And also, in a lot of cases, easy to see and easy to access but not, again, super relevant for the purposes of our conversation today.

DrPA: Right.

Treatments

DrMR: Now, as we kind of segue into treating, there’s one question I’d be curious to kind of get your take on. What I see sometimes and I’m sure many clinicians out there see this is sometimes you simply have to treat an infection a few times to clear it. You have SIBO; you may have to treat it two or three times and then you clear it. You have Candida; you may need to treat it a few times to clear it.

And I know that many natural agents and some pharmaceutical agents have inherent anti-biofilm properties. So I’m assuming that with a light case you may be able to treat again and not need to add the co-administration of anti-biofilm agents and potentially, as you go more down the spectrum of severity of illness and length of illness, the co-administration of an anti-biofilm agent makes more sense.

That’s kind of how I look at it, but I guess, and pardon my long lead-in to this question, what are your thoughts versus treating again versus re-treatment plus anti-biofilm agents? How do people kind of distinguish between when to do either one?

DrPA: I guess in a sense I kind of proceed clinically like what you just described. And that’s because it’s very rational to me that if we exclude the sickest of the sick people and take the normal bell curve of people who we know they have infection X, Y, Z. The middle of that bell curve is going to clear with whatever your standard go-to treatments are. And as you mentioned, many of them, probably part of the reason they work is they weaken biofilms.

So one of the ways that I kind of get to an empiric or sort of a trial-and-error, if you will—we’re beyond the normal pathogenic biofilm level here—is you treat it, not quite done. You back up. You treat from a different direction. Still there. You’re having more trouble or they’ve just been sick a long time. That’s when I start thinking, Look, there’s probably more biofilm acting here than not.

So I don’t tend—unless a person like we talked about has been sick for a long time, I tend to just treat with regular, standard things that work for most of the people and let their body prove to me that that didn’t work. And then I try the clean-up or the phase 2 sort of therapy. And if that doesn’t work, then I think, It’s probably time to bring in a bigger gun as far as the biofilm goes.

DrMR: Good. I’m glad you said that. And one of the reasons I wanted to ask, I was thinking we’d probably be on the same page there. But after I presented on biofilms for the first time, I think, two years ago, all my patients were asking on day one, “Are we going to use anti-biofilm agents?” And so, I said, “I appreciate the enthusiasm and I appreciate your level of education on this. But we don’t have to go right to the most severe, most robust treatment right out of the gate.”

DrPA: I am totally like—yeah, because that’s just what you find clinically is for most people you don’t need it because it’s going to clear. And like you said, and I want to point this out and it sort of segues back to, ok, so why is this not a problem for a lot of people, at least traditionally, because humans and biofilms have been around a long time.

Dietary Treatment

Most traditional diets—and it doesn’t matter whether it’s northern or southern hemisphere or east or west or whatever. In most traditional diets, there are anti-biofilm things that are either part of the food or part of the additives to the food that are just part of what people eat, such as aromatic compounds that we use as spices or herbs or something or curcumin or oregano.

You think about almost every kind of native diet to a particular area, whether it’s certain parts of certain peppers that people eat in certain areas or it’s oregano or it’s rosemary or it’s curcumin or whatever, they are all actually are anti-biofilm to the degree they don’t wipe out your base ones, the good ones we talked about. But they don’t allow new ones to form on top.

And the same goes for a lot of natural anti-infectives. We use a lot of aromatics. We use oregano and all these other things that are aromatic type herbs. Well, those naturally have what I term like a phase 1 or early pathogenic anti-biofilm built in. So I always tell the patient, “Look, we are doing biofilm stuff. It’s just mixed in with your therapy here. It’s a bonus part of what’s killing it.”

It’s when those don’t work that I feel we need to take it up a step, and that’s actually what I had to learn as a next step in my evolution of trying to figure out what’s protecting these real bad bugs.

DrMR: I’m glad you made that note about diet because it is important to mention the foundation, not just again jump right to the most aggressive treatments, which I actually do want to get to in just a second. But just a couple other things just from a big-picture perspective to help orient the listener or the reader, you mentioned earlier starting with the gut. And so, that would be predominantly oral anti-biofilm agents to address that endpoint, correct?

DrPA: Certainly, yes.

DrMR: Ok. And then, after that, you might consider using IV dosing, and I know there’s also some nasal sprays that can be used. So would you say that’s kind of your second consideration is IV and/or spray dosing?

DrPA: So the nasal sprays make a lot of sense because, of course, if I take an oral agent, whether it’s an aromatic or whatever it is, I’m not really going to get into my upper respiratory system. So the sprays and that sort of stuff, that makes a lot of sense because we build lots of biofilms in the sinuses and the paranasal areas.

And actually, something that will tip me off is—I don’t know how it is in your area, but in our area, for some reason a lot of the more traditional ENT docs and other people have gotten into the idea of, oh, maybe there’s something to these nasal biofilm things. So they’ll use like BEG Spray or something that’s got a little biofilm action in it. And the patient will just flare up like crazy. They’ll have a great day, and then they’ll crash. And the ENT doesn’t know what to do about it.

That’s a sign to me that they have a lot of biofilms going on. So I will sometimes use the use of a nasal biofilm agent as kind of a canary in the coal mine. And a lot of times that’s when they come to see me. I will usually do gut first and then work my way up to respiratory. And honestly, with very few exceptions, I used to think that in the beginning of doing the actual human research with people, I used to think I would get the best and most amazing immune responses using IV biofilm agents. I actually don’t.

It’s the oral ones that make the biggest immune response. And I really think they start in the gut. Yes, if you have a lot of respiratory issues, they’re probably there too. But I think the gut is ground zero. And, yeah, as you mentioned, you also have to dig down and get real with the person about if they’re eating inflammatory foods and a lot of sugar and a lot of other stuff, you can’t out-treat that. They’re feeding the problem. So that’s really got to be a base.

Natural Treatments

DrMR: So regarding natural…And what I’d like to do is try to partition the treatment options for biofilms in natural and then prescription. What do you feel to be some of the more effective natural treatment options?

DrPA: Kind of working with our left-to-right spectrum. The herbs that we find in a lot of cooking instances, actually the aromatic ones, seem to be very good anti-biofilm agents. Like my top ones I tend to use are oregano and then thyme, rosemary, all those ones that have a lot of kind of the volatile, smelly good oils that come out.

There’s some information about the turmeric family, curcumin. There’s some information about the deeper red peppers like capsaicin-containing peppers, etc. Also, sometimes olive leaf. Olive leaf, if you get the right extract, actually has some effect.

And then there’s sort of this middle-of-the-road one that appears—there’s actually been some decent research on it. And it’s less likely found in a diet. And that would be black cumin. I keep telling people black cumin is going to be the new curcumin. Everyone’s going to be taking it for everything pretty soon because they keep researching black cumin, and it’s like, “Oh, it’s anti-autoimmune and, oh, it’s anti-biofilm, and all this.”

But black cumin’s actually pretty useful as a supplement. And in my mind, it bridges the gap between the weaker biofilms and the stronger biofilms. So that’s one. Now, you also mentioned thiols like n-acetyl cysteine, alpha-lipoic acid is also a thiol which can have that effect.

And just because probably you have so many listeners, and I’m sure this has happened to some of them. If anyone has ever gone and gotten treated for “heavy metals” and used something like DMSA or DMPS orally and they had a very aggressive either immune or digestive reaction to that, that’s probably because those are actually quite strong biofilm disruptors themselves.

And so, like NAC is a simple thiol, and it’s one we use a lot. I use NAC a lot to prep people for stool tests and things just to kind of rough up the biofilms before we do test their stool. So thiols become important. And then, kind of circling back to I think maybe the bug with the most or some of the neatest data, H. pylori, bismuth has always been a part of the triple and quad therapies. And one of the reasons is bismuth itself, although it can be toxic if used wrong, bismuth is a biofilm disruptor as well which is why they put it in with H. pylori therapy.

So there’s lots of those at that end of the spectrum that are quite useful, most of them pretty safe really.

DrMR: Gotcha. And so, for the NAC, alpha-lipoic acid, and the bismuth, would you classify those medium-to-heavy or would you consider those lighter? I’m assuming medium or heavy at least but just to try to help organize this for the listener.

DrPA: I think all of those—so the thiols, like alpha-lipoic acid, NAC, bismuth and some people now even use like EDTA and other things. They’re in the middle to the stronger end of the spectrum. And actually, to my reading, but also just to using it with people once I figured out there was research out there on it, I think black cumin kind of is in that middle to stronger end of the spectrum as well.

DrMR: So are there any, what you would consider, highly strong natural agents before we leave the natural spectrum?

DrPA: Anything stronger than what we just talked about becomes actually new molecules that are developed from individual natural things that become something not found in nature.

DrMR: Gotcha.

DrPA: At the point where we stop getting responses, say, to NAC and bismuth or cumin or whatever, now you’re having to look at things that are actually two natural things put together with the design of actually breaking into the deeper, the thicker fences, if you will.

DrMR: Gotcha.

DrPA: So they’re natural, but nowhere in nature do they come together naturally.

DrMR: Gotcha.

DrPA: So they’re made somewhere. Yeah.

Dr. Ruscio Resources

DrMR: Hey, everyone. This is Dr. Ruscio. I quickly wanted to fill you in on the three main resources that are available to you in case you need help or would like to learn more. Of course, I see patients both via telemedicine, via Skype, and also at my physical practice in Walnut Creek, CA.

There is, of course, my book Healthy Gut, Healthy You, which gives you what I think is one of the best self-help protocols for optimizing your gut health and, of course, understanding why your gut is so important and so massively impactful on your overall health.

And then, finally, if you’re a clinician trying to learn more about my functional medicine approach, there is the Future of Functional Medicine Review which is a monthly newsletter which is a training tool to help sharpen clinical skills.

All of the information for all three of these is available at the url, DrRuscio.com/resources. And in case you’re on the go, that link is available in the description on all of your podcast players. Ok. Back to the show.

Prescription

Ok. So good transition, I guess, then to the prescription versions or the isolate versions. So what do you think are some of the options there for people to consider?

DrPA: One of the ones that been probably available the longest, even in an over-the-counter/professional supplement-y kind of way… There’s a couple. There’s things like Biocidin and that whole family of things that are combinations of… They’re all natural things, but they’re combined in a way that are probably in the middle to strong end. So that’s one.

The other is there’s a couple of combos that are used with enzymes. And we didn’t mention enzymes. But enzymes are another natural way to keep biofilms at bay. So they mix enzymes and actually EDTA together which is a chelator. And it turns out EDTA—now, if you go in the blood stream, EDTA is one of the best chelators there actually is. And it’s also one of the best biofilm breakers. But in the gut, it always needs a helper. So EDTA, your people have probably seen the supplement called InterFase. One of them’s got EDTA in it. That’s why they put EDTA in that one.

Now that one is I consider kind of still in the middle, but it’s a mixture. Biocidin and some of those other guys, kind of mixture like that. What the drug development world has actually known for well over a decade—and I was surprised when I found out that this was even widely publicized but nobody cared about it in like 2000… I don’t know. This was like 10-12 years ago—is that when you get to treatment-resistant ones where, say, bismuth on its own or cysteine on its own or whatever isn’t working, you have to come up with a stronger molecule that’s like a wedge.

So what they started to do is just experiment with, well, we know all these things individually work. Chemically, can we put them together and make a new molecule that will be a better biofilm breaker? And the one that won out really was a combination of bismuth and a sulfur molecule, thiols, an example being n-acetyl cysteine or alpha-lipoic acid, then some of the complex ones like DMSA or DMPS. And what they were writing about 10+ years ago was, well, we finally found this combo.

And here’s what people kind of get confused about. It’s no longer really just bismuth and it’s no longer really just, say, DMPS. It’s actually bismuth and DMPS bind together and form a new molecule. And that actually sits and, for chemical reasons, it likes the outer edges of the biofilm fence, and it just drives a wedge in it. So the purpose of it is not really to kill anything; it’s actually to open the fence up so the immune system or the drug or whatever can get in there.

So they call them bisthiols just for short. The drug that they are develop—so there’s actually a drug in the pipeline right now that’s in final human trials that will come out. And it’s going to be the kind of thing that you’ll be given after surgery and no one’s even going to tell you about it because they know they’re sending you home with biofilms already.

So it’s just going to be part of all surgical procedures. It’s going to be part of a whole bunch of stuff. And it is two super-strong versions of a bismuth molecule and a thiol molecule that binds so tightly together they’re literally like little wedges. That particular molecule has a patent on it, and it can’t be replicated anywhere for many reasons, partly because the government wants it for itself.

But, right below that, there are some both prescription and then there’s actually an OTC version of those that a friend of mine in research put me onto a number of papers by the people who developed the drug. And the papers are hard to find because the government doesn’t really want us to find them. But we found them.

And they give the chemistry of how to combine these things. So what we found were things that are still available to either a compounding pharmacy or an over-the-counter place and made a prescription version and we made an OTC version of a bismuth-thiol complex and tried to make it as tight and strong as possible.

And so, we’ve been using that for, oh, gosh, probably three, three-and-a-half, four years now. And here’s, I think, the punchline. I did it because it looked good on paper, but I had people with the most treatment-resistant things, kids with PANS/PANDAS syndrome, people with treatment-resistant whatever. Tried everything. Got to be something wrong. Used these types of molecules on them.

And somewhere within a week to sometimes four or five weeks, they start to have massive immune responses. And the reason is, is the biofilm opens up. The immune system, especially in the gut, suddenly says, “Wow, there’s a lot of pathogens here we never knew about.”

And it’s an amazing response. It’s a little uncomfortable, but it’s an amazing response. We didn’t change anything else. We didn’t give any anti-infectives. Your immune system’s actually starting to fight something.

So in those cases, these bisthiol complexes are what we use. Think of them as a first strike to break down those real bad ones. And they’re not supposed to be used for super long term. They’re kind of early phase use. And unless a person’s been sick for 10 years or something, weeks to months of use. And then you work your way back to the aromatic herbs or Biocidin or whatever. And then you work your way back to not needing any of these other than prevention.

So the prescription or the quasi-prescription ones really are these bisthiol molecules where you take a bismuth and you stick it about 90% irreversibly to a sulfur molecule, a thiol, and they become a wedge.

DrMR: And what are the names of the OTC version and the Rx version if you can provide those?

DrPA: The OTC comes from Priority One who’s a supplement maker. And I gave them a formula for it, and it’s called the Biofilm Phase 2 Advanced. So the idea of phase 1 and phase 2 biofilms is left-hand spectrum, right-hand spectrum we’ve been talking about.

So because it’s OTC, it can’t have a super-strong thiol. So we used an ALA combo with a bismuth nitrite which is a good binder. And then we put black cumin in it. We get pretty good traction with that.

The prescription one is—it’s compounded, so any compounding pharmacy can make it. The first pharmacy that decided to buy all the products just on faith that I knew what I was doing and put it together called it Biosolve. And actually, that formula I gave away, so any pharmacy can have it for free.

But Biosolve, it’s become a real common thing with infectious disease people because the trade drug that’s going to be similar, only stronger, is not through testing yet. So doing it through a compounding pharmacy is the way to kind of get ahead of the curve on that. And the Biosolve is actually a combination of DMPS and bismuth sub-nitrite and then there’s lipoic acid in it as a synergist.

So when you combine DMPS which is a super-strong chelator and bismuth, they don’t fall apart. They don’t become their individual components in about 95% of the molecules. So you don’t get the effects of either one. You get the stronger effect. Yeah.

How To Know If Treatment Is Working Or Not

DrMR: So zooming this way out, because it’s tempting to get into all these details which I think are fantastic. But how can people—if they’re starting to go down this road, maybe they’re a clinician overseeing a patient, maybe they’re someone just trying to do it themselves, are there some key indicators that someone knows that it’s working compared to maybe that it’s not working?

DrPA: I think the first thing is let’s exclude people who have been sick for five or more years where there’s been inflammation on inflammation. But let’s take the person where we’ve done what normally works in phase 1 and phase 2 of our treatment of the problem, whether it’s SIBO or Lyme or whatever, and nothing’s happening. We’re just not getting anywhere. That’s the first sign to me that we know there’s biofilms but maybe they’re a little more advanced, a little trickier than we thought they were.

The other is this phenomenon of we’ve tested, we know there’s a bug there, we’ve appropriately treated it, we retest, and it’s just as bad when we started. That’s another kicker. Anybody who’s been sick with, say, “chronic Lyme,” or whatever you want to call that, where they’re just sick for five or more years, that’s another group that I’ve found just empirically there’s biofilm because they’re doing something.

And I think the other one would be is people who have a lot of digestive symptoms that ought to come out, say, on a stool test or something like that and they’re not getting—like the stool test looks so clean, but their symptoms are not clean. Those people, we go back, we give them one of these more advanced kind of biofilm treatments for, say, a week or two, redo their stool and all kinds of stuff is coming out. So that’s one of the actual linear sort of testing things you can do, sort of like a challenge test in a sense.

But those are the groups of people that I look at. And then, I assume anybody who’s been chronically ill for more than five years probably has built them up.

DrMR: That’s a very interesting one to hear the note about—and it makes sense. Someone that’s got a clean bill of health from a gut testing perspective, SIBO normal. Your other breath testing might be normal. Blood testing might be normal. Stool testing might be normal, yet they’re still symptomatic. Yeah, it makes a lot of sense to try a short course of anti-biofilm agents empirically to see if they respond. I like that.

But when they do start treating themselves, let’s say someone has—because I’m sure there’s people who fit this proximate bill listening or reading this—they’ve treated Candida or H. pylori or SIBO a few times and now what they’re going to do is they’re going to go on some herbal medicines like, let’s say, oregano and berberine. And they’re going to add in along with that something like n-acetyl cysteine and maybe something like InterFase.

Have you found that when this is the right treatment approach for someone that they noticeably feel improvements within days to weeks? Is it maybe more common for people to have a little bit of a die-off reaction and is that kind of an indicator that it’s working? Can you drop some pearls that may help people know “I’m on the right track or I’m not on the right track”?

DrPA: Right. And this is a conversation that we have really very carefully with our patients when we’re guiding them through this because if it’s one of the cases where it’s a little more advanced than it looks like from the outside, you don’t know what all is hiding inside of a biofilm.

And if your immune system is at all working, as soon as the biofilm starts to open up, you can get a very aggressive immune response which can be not only uncomfortable but scary. And so, A, yes, that’s a good sign. It means you’re on the right track. But, B, what it normally means is that you need to then support the immune response that’s going on.

You have now opened the biofilm up and you may need to back off a little on whatever you’re doing there. But now you need to… And normally, natural, especially herbal agents you mentioned, etc., are broad-spectrum enough they can take care of helping to kill the stuff. But I do tell people, especially if you have someone who’s very sensitive.

And for instance, we’ve had an older child with a long, undiagnosed PANS syndrome where they have infections that create neurological inflammation and stuff. And in cases like that, you have to watch out because you open up the GI tract kind of Pandora’s box of bugs that you’re going to now go after and kill. And the inflammation that goes systemic hits them wherever they’re weakest. And so, in PANS it’s neurological. In people with other stuff, it might be their joints hurt or whatever.

Yeah, those are all great signs, but that means you’ve got to then go in and say, “We need more things to help the immune system, to support it. We might need more things to kill stuff because now we have the availability to kill it.” And the other thing I would say is if people who are doing this who’ve been sick for more than, say, a year, a lot of times they’ll need a lot of adrenal support during this time because the adrenals then have to start to respond to immune activity that they haven’t been seeing. It’s so suppressed. So adrenal support is another kind of important thing.

But, yes, I always tell people if we haven’t—like, let’s say it’s more on the “you’ve been sick a long time” end of the spectrum, 5+ years. If we get to eight to 12 weeks doing some biofilm stuff, especially the heavier duty stuff and we see no change, no immune response, no nothing, I just quit that stuff because we’re barking up the wrong tree there.

In every case where it empirically worked, it’s been somewhere between one and six weeks usually before we see that. And usually, it’s one or two weeks. But there is that die-off thing. And that can be scary and uncomfortable. So people need to know that it’s not always just all getting better. Your immune system, when it reacts, can give you a lot of unpleasant symptoms.

Die-off Vs Intolerance

DrMR: So a follow up question for you then. Is there a certain way that you distinguish between on the one hand this is a die-off and on the other hand this reaction that I’m seeing is actually an intolerance to something that they’re taking?

DrPA: Yeah. Now, one of the things is the chemistry that creates the reactions for an intolerance and/or die-off can sometimes be exactly the same. So in those cases, sometimes it’s very difficult to tell. But normally, and this is just what we’ve seen kind of from watching people with—most of the time, it’s die-off, etc., or whatever you want to call that. Sometimes it’s actually just a reaction.

So the minority of the times it’s a reaction to what you’re taking. In those cases, you tend to get sensitivity-type reactions which are more… In the case of NAC or ALA or maybe DMPS or one of the other sulfur molecules, the person may get flushing of the skin, itchy rashes, maybe headaches, stuff like that. That’s usually not die-off. That’s usually actual reaction to the sulfur-y molecules or that sort of thing.

Normally, if I’m going to be combining things and adding oregano or one of the stronger aromatics, before we do any biofilm stuff, I just have them try it and make sure they don’t have some bizarre reaction to that stuff. But when we—and if your listeners are into irony, I am the only person who’s actually had an actual allergic reaction to the drug I developed. I’m the only person ever. It’s me. And it makes total sense, I’m sure, in some weird calculus in the world.

We don’t see a lot of true allergy outside of in myself, but when people react in that way, they get allergic-like. So itchiness, maybe a little respiratory agitation, that sort of stuff. The die-off tends to be very kind of core immune stuff. And it’s like achy joints, almost like the things you see with Herxheimer-type reaction where they have flu-like symptoms, etc. That’s more you’re getting at things. Your immune system is active.

The sensitivity stuff tends to be more sulfur-y things, sulfur-y rashes or headaches or other peripheral kind of things. I can tell you from just watching lots of people go through it, the intensity of the reaction if they’re sensitive or allergic to it, except in my case, is very low really. It’s irritating, but not bad.

If you open up biofilms in the gut and there’s a lot of bugs in there, your immune system gets super active. And it’s almost like you’re getting the flu or something like that.

DrMR: Ok. So Herxheimer or a die-off reaction tends to be stronger than an intolerance-type reaction?

DrPA: Yes. And less organ systems involved. It tends to kind of be focal as opposed to—your sensitivity or allergy-type reaction tends to be focal. Whereas, Herx-ing or die-off tends to be like lots of parts of you. Joints light up that were very painful that weren’t before or whatever.

DrMR: And are you ever recommending someone use something like an antihistamine or an over-the-counter antihistamine to help get through the die-off reaction phase?

DrPA: Especially if we’re pretty sure that’s what’s going on. And this is I would say about 20% of the people that we’ve worked through this with with bad infections that were indeed biofilm protected. In that first week, you kind of do whatever it takes to get them through and kind of calm their system down, because it’s literally like someone just ripped the biofilms open and the immune system is going from zero to 100 miles an hour.

So what I always tell people is let’s say they’re already on an adrenal support. This is common with people. They’re taking some kind of adrenal support. If they start getting a reaction, I’ve had them quadruple their adrenal support for the first two weeks. And that actually helps. That takes it down. Antihistamines acutely, like the first couple of days, can kind of be very, very helpful. Sauna can be very helpful. Hydrating. All those normal things.

But, yeah, in the first week, you do what you’ve got to do. And the one caveat I would say is, because I’ve seen this in people with kind of your deeper, more pervasive infections that have a lot of other problems, if you have a doctor who has you on, say, something like a low dose of prednisone or hydrocortisone or whatever because they’re not quite sure what’s going on and your adrenals aren’t working so well, that might need to be adjusted if you start having die-off. If you’re not on a steroid, you don’t need a steroid. But if you are on one, it might need to be adjusted.

Other Tips And Tricks

DrMR: Gotcha. Ok. Are there any other tips or tricks that you’ve found to be helpful that people might want to keep in mind?

DrPA: I think, honestly, the biggest thing has been trying to avoid human nature, which is, gosh, I finally found something that moved the needle here and knowing that this is a moderately short-term treatment. So when you do finally get biofilms open and you finally kind of wear down the bad guys, get the good guys built up, you’re theoretically, from everything we know about what goes on at least in the gut and the respiratory system, you’re moving back towards the weaker forms of biofilms, the lower fences.

And so, what we do there is we do withdrawal trials of the heavier stuff. So let’s say whether it was a la carte, some bismuth and NAC together that worked for you or some berberine and bismuth or whatever or you did one of the supplement kind of things that’s got EDTA or bismuth thiol in it or whatever or prescription. Once you get past that phase, so there’s no more die-off. The killing is going on, etc. We don’t want people on those heavier things long term because they don’t need them.

They need to keep the pressure on and keep killing stuff off and getting the good guys established. But it’s literally an early first strike. In your average person who’s been sick less than five years, that means a couple to three months at the most. In your super sick people who’ve been sick for 10-20 years, I’ve seen a year.

But I think that the best tip is this is not like a forever. You don’t have to do this forever. You think of it as you open them up. The immune system and whatever you’re taking clears the stuff up, and now the guys who built the big high fences are gone. So now, we can go back to aromatics and some of the kind of easier-on-the-body players. And then, eventually, it goes back to diet and the other preventive things. So you literally think of working towards the left, towards the weaker stuff.

Episode Wrap-up

DrMR: Yeah. I think that’s very sage advice. As we draw to a close here, are there any thoughts that you want to leave people with? Any big-picture, closing thoughts that you want to leave them with?

DrPA: One would be that if this is something—from my experience taken these last 10 years, this is something that I think one should investigate if they’re in that situation like you and I talked about where they’ve had appropriate testing and treatment and it’s not going anywhere. They’re with a good practitioner or whatever they’re doing. I think this is something to keep on the list of possibles. I think that’s number one.

Number two is, because I’ve gotten so many questions about this over time, next month there’s an online periodical for doctors but anyone can get it. So literally NDNR, so N like Nathan, D like dog, N like Nathan, R like your last name. NDNR. If you just go to NDNR.com, a paper I wrote in there is pretty well-referenced about biofilms. And it goes through all of this. So if you had to go to a practitioner, you can take it and it’s got references. It explains the spectrum thing and low versus high-level things.

Normally, they publish all that. It’s free online. It comes out later in January of 2018. And it’s just called “Biofilms: What Have We Learned from the Research?” And it’s my name, Paul Anderson. So you can get that at NDNR.com. And actually, that’s probably the best—any patient will be able to read it, understand it. And if they have to interact with a doctor, they’ll be able to have something that has references that they can share with them.

So I think that’s probably—it’s the kind of thing that I’m sure what you and I learned about biofilms and what reality is, is very different. And it’s the same with all things in health. So you go to your doctor and unless they happen to have kept up on this, they’ll either not know what a biofilm is or say that doesn’t happen in people. Or maybe say, “Well, oregano should take care of it.” So it’s a little bit deeper well than that.

DrMR: Awesome. Thank you for referencing that paper. Would you do me a favor? When that becomes available, if you have a moment, would you send that over to us? And we’ll make sure to include that in the links, because I think this will publish probably shortly after your paper publishes. So I think the listener or reader would love to have that link to click through to.

DrPA: Yeah, I will definitely. I’ve already kind of let the people at the publication know, and they’re all about it. So I’ll put that on the to-do list.

DrMR: Awesome. And then, I know you have a website. I know you have some clinical training materials. So tell people more about where they can learn more from you.

DrPA: Yeah, the website, which it has portals to all the other stuff that I do, is ConsultDrA.com. And that has links to a whole bunch of free things I’ve written and podcasts and other things of that nature that they can find. There’s also—a coauthor and I have written a book about integrative cancer care coming out in early 2018, I think the end of March. And it’s called Outside the Box Cancer Therapies and it’s through Hay House publishing. And it’s written for patients, but it’s very well referenced.

So if they take it to their doctor, it’s not just opinions. There’s lots of references for doctors to check into. It’s just called Outside the Box Cancer Therapies. You can preorder it from Hay House or at Amazon. There’s not really any other book that’s quite like this one, as far as integrative cancer therapies, coming out. So we’re pretty excited about that.

DrMR: Awesome. I didn’t know that you were involved in integrative cancer therapy. That’s terrific. I might have to have you back on to talk about that because I have been looking for someone to have that discussion and have not been very impressed with some of the names I’ve come across in my initial search.

DrPA: Yeah. So I was the kind of child that got in trouble because I was always doing things I shouldn’t. And so, in addition to this infectious disease bent that I have, I actually did NIH-funded research in integrative cancer medicine. So that’s what led to writing this book and took up a lot of my time for 10 years. Yeah, we should probably talk about it sometime.

DrMR: Awesome. That would be absolutely fantastic. I’ll put that on my list to reach back out and get you locked in here.

DrPA: All right.

DrMR: Well, Paul, thank you so much for taking the time. This has been a great conversation. And until I see you at the next SIBO symposium or wherever, keep up the great work that you’re doing.

DrPA: All right. Hey, thanks a lot.

DrMR: You got it. Take care.