Autoimmune Disease: The Infection Connection

In this interview I discuss the connection between infections and autoimmune disease which I call the Infection Connection.

That being said, let’s get on with it. Let me introduce our speaker for tonight. Dr. Nikolas Hedberg is a good friend of mine. I’ve known Nik for, I think somewhere around 10 years now, we both went to one of the same schools in our careers, not at the same time, but we, I guess, met at a, I think, an internal disorder conference in New Orleans, I think was the first time about 10 years ago. I’ve followed Nik’s work and his career and he’s done some outstanding work. Nik is a board certified Chiropractic Internist by the American Board of Chiropractic Internists, he received his bachelor training in Exercise Science from the University of Florida, received his Doctor of Chiropractic from the Texas Chiropractic College in Houston. He currently practices in Asheville, North Carolina and focuses on Lyme disease, thyroid disorders and autoimmune disease. He’s the author of the book “The Complete Thyroid Health and Diet Guide“, which is a comprehensive guide to diagnosing and treating thyroid disorders. He lectures at a lot of integrated medicine conferences, and he’s published in a lot of journals. He teaches Functional Medicine concepts through many forms including Functional Medicine Town, Professional Co-op, and with Hawthorn University. His particular interests lately is the role of stealth infections in chronic disease and in that effort to get this message out, he’s created a program called “The Infection Connection” and does some online training in these concepts, and he’ll tell you more about that as the night goes on. Little known to everyone in the professional world but known to me, Nik is an accomplished opera singer actually, so you’ll hear that when you hear him talk, you can hear that come through in his voice. Anyway, Nik thank you for being on. I know you’ve been on Clinical Rounds before and thanks for coming back and being a guest again.

Autoimmune Disease Infection Connection

Nikolas: Thanks for having me on David, it’s good to be here.

David: Great. I mean this is a fascinating topic and a topic that’s been really been, sort of, obsessing me for the last couple years. As you can see by the content or the topic of our Core III seminar. I’ve recently written pretty extensive articles on these concepts in Townsend Letter and Naturopathic Doctor News and Review and in other forms. I’m really interested and jazzed about tonight’s call and interviewing you because I hope to learn more about this as well because it’s literally emerging science day by day. I think it would be a full time job just to keep adequate surveillance of the literature on just what we’re going to talk about tonight and stay current with it. Anyway, I know that I kind of started having to really school myself on this stuff out of sheer necessity by virtue of my patient population and how it’s changed over the years. I guess we’ll talk about that a little bit more but I wanted to really learn a little bit more how you got started in managing patients with chronic infections or stealth infections and how you found your way into really almost sub-specializing in this area of functional and integrated medicine.

Nikolas: Right, it was actually about eight or nine years ago that I was actually listening to you, David talk about the connection between [inaudible 00:08:55] and autoimmune thyroid disease, and ever since then this has really been an interest of mine. I knew it was something that I need to learn a lot about, started seeing more and more patients with Hashimoto’s, and chronic fatigue and various autoimmune diseases. You start doing all the things you know in functional medicine, sealing the gut, vitamin D, you know etc. etc., and you can do all that but there’s that group of patients, that population that they just don’t respond to those things and I found with a lot of those patients when you dig a little bit deeper, a lot of times you’ll find an underlying infection that’s been overlooked.

You know, I saw my first Lyme patient back then and didn’t really know how to treat it. Sent the patient out for treatment, you know, heavy doses of antibiotics, to an integrated medical doctor, and the patient came back about nine months later and she was just worse off than she was going in, she couldn’t handle the treatments. Started seeing some more Lyme patients after that and realized that I had to learn to treat that as well, you know, from a functional medicine perspective, The way I think about it is a lot of times it’s not that there are more infections out there, obviously there’s more Lyme infections, but a lot of us have these infections in us and it’s the consequences of our modern day lifestyles, high stress, poor diets, environmental toxins, things like that and our immune systems just can’t keep up with it. Then the infections that we have either emerge, because they are opportunist infections, or we’re not just able to fight them off. That’s how I got started in treating these types of disorders.

David: That’s interesting because, you know, it is food for thought. I often wonder, are these infections more prevalent, are we just better at finding them, are we more aware of them since people have started talking about them and connecting the dots with the associations between certain infections and certain chronic pathologies? Is it, like you just said, you know just another straw on the camel’s back, and the back is so ladened with different stresses and pressures in modern patients that the infections that otherwise wouldn’t really cause much of a problem in a stronger individual become clinically significant? I don’t know what the right answers are but I can tell you one thing, I’ve been practicing now for 21 years and I think, personally, I think patients are getting sicker in many more complicated ways.

I’ve sat back and tried to analyze that too, it’s just because compared to 20 years ago even 10 years ago, I get probably more complicated patients because almost virtually my entire patient base is referrals from other practitioners and a lot of it is from other integrated and functional practitioners and I tend to get sent, I think, the worst of the worst or the complicated ones, the ones that just don’t respond and don’t get better. Maybe my patient cohort is skewed but overall I just think patients are more complicated in their illnesses and whole systems biology are wed, if you will, or swirling around their presentation is more complex.

I wonder, you know I practice in Connecticut too so it’s even more complicated because the whole Lyme and co-infection thing is so prevalent here and it’s so hard to really treat this stuff and it’s hard to test adequately for it, it’s hard to treat it adequately, it’s hard to know you have it. How much is that in play that we’re just not aware of? You mentioned fixing the gut and vitamin D and all the normal functional medicine kind of approaches that used to work almost miraculously with the majority of chronically ill patients, I find that it works with a smaller and smaller percentage of my patients, we’ve got to go digging into other very complicated stuff. Do you see that same phenomena, do you have any feelings on that?

Nikolas: Definitely see the same phenomenon. Doing all the functional medicine things that we should be doing, patients aren’t getting better, and they’re coming in with just all kinds of, they’re almost things that you can’t even label. So-called mystery illnesses, chronic fatigue, fibromyalgia, all the different autoimmune diseases, and then in some cases there’s nothing really showing up, even on a comprehensive blood chemistry. I mean there is nothing there but they’re still sick. When we scratch a little bit deeper, you know, a lot of times you do find infections and a lot of these infections will mimic those conditions that I was just talking about. Where conventional medicine says, well, you know, we don’t really know the cause of chronic fatigue syndrome or autoimmune disease, it’s just a consequence of the relationship between genetics and our environment. There’s also not a lot of profits to be made in long term antibiotic use and that could be another reason why it’s not as looked at as heavily as it should be. Speaking in regards to the connection between infections and somebody’s chronic illnesses.

David: It’s also amazing in the history when you do an intake on a patient fact, honest injun, it happened twice today. I had three new patients today in my patient load, two of them had the onset of these kind of chronic things as they tell the story. The onset was immediately after they had a significant, like, kind of viral infection that came out of nowhere like an upper respiratory type of infection that just didn’t want to go away and since then they’d never quite been right. That whole connection between a viral insult then it became a chronic smoldering thing. It’s been something that’s been known in chronic fatigue circles for a long time with CFIDS or Chronic Fatigue and Immune Deficiency Syndrome and people who looked at lymphocyte sub-sets forever, but I think maybe that phenomena is much more broad based than just in that one. How do you go about identifying infections, particularly stealth infections, clinically or in a laboratory?

Nikolas: Of course you start with a comprehensive history, like you just said, I’m finding that as well someone will have a really bad cold or flu or GI infection, tick bite you know etc., etc., and they just never were able to recover. That’s a good indicator in the patient’s history and of course where they live, history of tick bites, and some of these patients will come in and will have just a fever of unknown origin and there’s really no signs of cancer so just a basic fever that’s an infection, until proven otherwise, and a lot of them will say, “I just always run a temperature,” or they’re opposite, they’re just extremely cold all the time. Then of course if they have any of these conditions that, you know, we’ve mentioned, that is of course another major red flag.

Then under blood chemistries obviously looking at the CBC, you’re probably finding a very, very low white blood cell counts in a lot of these patients across the board and then just changes in their differentials. A lot of monocytosis, you’ll see neutrophils coming down, lymphocytes going up and it’s just kind of always there. Then a lot of markers of inflammation, sedimentation rate, highly sensitive C-reactive proteins, fibrinogen. A lot of times if there aren’t really a lot of signs of what’s causing their inflammation, if they’re eating well, low stress, because you’re probably seeing some of these patients as well who come in, and they’re doing everything right on paper, everything looks good but they just can’t break through and start feeling better.

David: I got to tell you, the majority of my patients these days come in and they’re on really good diets, they’re doing all the right things, lifestyle wise, they come in with rattling bags of supplements, they’ve been to a million providers, it’s none of the easy low hanging fruit stuff that we learn on fixing them. There’s a piece of the puzzle that a lot of people are missing, and I think the stealth infections are a big thing, but even some of them, I do some of the tests you were just talking about and even they’re clean. Even the CBC, the diff is fine, none of those things I learned on chronic infection presentation. Clearly there’s something just dragging them way, way, way down, they’re very reactive to a lot of things immunologically. Do you get into specific viral titers, do you do lymphocyte subsets, do you look at any of those things routinely?

Nikolas: I do routinely do the viral titers looking for reactivation of Epstein-Barr virus, herpes simplex virus, things like that, so I do test for those.

David: Is there a specific panel that you use in doing that with commercial lab or do you just, you do EBV, and CMV, HSV, Hep-C, is there any kind of pattern to what you do?

Nikolas: I just do a combination of PCR testing and also IGT IGM and it’s just a matter of interpreting it the right way just because it’s IGT positive, of course that doesn’t really tell you that it’s active so that’s how I interpret those.

David: And how about, let’s talk about mycoplasma, because that’s been talked about a lot in autoimmune disease and people sort of with these chronic long term issues. What’s your thought on mycoplasma playing any kind of role?

Nikolas: Mycoplasma I think is playing such a huge role especially in rheumatoid arthritis, lupus, chronic fatigue and fibromyalgia especially. Mycoplasma is interesting because when they first discovered it they actually thought it was a virus, because it was so stealth. Mycoplasma is the smallest known bacteria in the microbiology world, so it’s very, very stealth. All of these bacteria that we’re talking about are Gram-negative and just to take everyone back to micro, you know, you have a Gram-positive and Gram-negative bacteria. The Gram-positive bacteria only have one cell wall, it’s very thick and the Gram-negative bacteria, they have two cell walls and they have a peri-plasmic space in between the cell walls. Antibiotics may penetrate the first cell wall but they can actually get stuck in the peri-plasmic space while the bacteria learns how to deal with it. Then if it does break through the second cell wall, these microbes have what are called efflux pumps, they will just pump it right back out.

Phenomenal defense stealth mechanism by some of these pathogens especially mycoplasma. There’s two studies here, I just wanted to quote briefly, the first one’s called “Multiple Mycoplasmal Infections in the Blood of Patients with Chronic Fatigue and Fibromyalgia” and basically they looked at about 91 patients for four different strains of mycoplasma for maintenance, pneumonia, hominis, penetrance. They found that 54 out of 91 patients with chronic fatigue and/or fibromyalgia had mycoplasma pneumonia, 44 out of 91 have mycoplasma for maintenance, 28 out of 91 had hominis, and 18 out of 91 had penetrance. The interesting thing is that those that have multiple mycoplasma infections have a much longer history of the illness. What I found is that once mycoplasma takes hold in the system, it’s very, very hard to break through and I think some of these people with chronic fatigue and these other disorders have these underlying mycoplasma infections.

The other study is looking at the distribution of mycoplasma in patients with arthritis and basically they just aspirated the synovial fluid of patients with rheumatoid arthritis, non-rheumatoid arthritis, and osteoarthritis and 79% percent of the patients with rheumatoid arthritis had mycoplasma in the synovial fluid, 100% of the patients with non-rheumatoid arthritis had mycoplasma and 80% of patients with just your general osteoarthritis had mycoplasma in the joints. It makes sense, there’s something that’s causing the inflammation in these joints. This is an area that I think is really overlooked, not only in these arthritic patients but in chronic fatigue and fibromyalgia patients as well.

David: Yeah, well that gets into a whole other can of worms, I mean, is it really fibromyalgic patients or is it the people in the studies that were mislabeled as fibromyalgia patients? Are they really fibromyalgia patients, do they really have central [inaudible 00:24:22] and disruption and descending [inaudible 00:24:25] deception or are they just incorrectly diagnosed and labeled [inaudible 00:24:29] fibromyalgic and then they found out they have mycoplasma? It’s really dirty literature, so it’s hard to make really a strong, come up with a really strong takeaways on these different labels and how they associate to different things because the inclusion criteria for fibromyalgia is all over the map, I mean literally and the diagnostic criteria is terrible. That brings up some interesting other confounding factors but, back to mycoplasma for a minute, how are you determining if that might be in play in your patients?

Nikolas: Right, just blood testing and again doing serum PCR and IGT, IGM for the…

David: Are you doing that through a regular commercial laboratory like Quest or Labcor, or something like that or a specialty lab?

Nikolas: I’m doing that through Medical Diagnostic Laboratories. They’re a fairly large lab and they have a really excellent infectious disease arm and they’ll test for many different strains of mycoplasma.

David: And then when you find it how are you trying to treat it and eradicate it? You already said these are really resistant organisms even to prescription, pretty powerful antibiotics so what is your approach?

Nikolas: Right, so there are a few really good herbal antibiotics that work well for mycoplasma. Interestingly enough, outside of the herbal world, silver, the Silvercillin product that Designs for Health has, works very well for these inter-cellular Gram-negative bacteria. Some of the big gun herbs are cryptolopis is really good for systemic bacterial infections, sida and alchornea, also noni and neem can work very well for mycoplasma as well. Then of course doing all your other functional medicine basics supporting the immune system, but those have worked quite well for these patients.

David: What about chlamydia? I know Charles Stratton at Vanderbuilt has done a lot of work on chlamydia or chlamydophila, I guess the more proper way to say it now, and it’s role as a stealth pathogen, I guess most of his work is centered around multiple sclerosis, as an etiological agent in multiple sclerosis but also he has found it in other autoimmune type of disorders. What’s your thought on chlamydophila?

Nikolas: Yeah, there’s been many, many papers out there on chlamydia talking about it’s connection with autoimmune diseases and a lot of neurological disorders as well. Chlamydia, you know, it is also an intercellular bacteria, Gram-negative and most people are going to be more familiar with chlamydia pneumonia causing infection in the lung. There is strong connections there with cardiovascular disease, central nervous system disorders and a lot of neurological issues like Alzheimer’s disease, multiple sclerosis, and it’s interesting because what we know about chlamydia is that monocytes can actually traffic chlamydia pneumonia across the blood brain barrier. Once the monocyte carries the chlamydia across the blood brain barrier, it will shed the organism in the central nervous system and induce neural inflammation and that could end up being a chronic issue. Late onset Alzheimer’s disease, dementia, that’s also been connected with chlamydia. I guess the theory is obviously it’s active in the central nervous system but you have this chronic, low grade, persistent brain infection that’s obviously causing a lot of oxidated stress and inflammation in that area leading to various mental and even some neural behavioral disorders. That’s definitely something to look at and I think these neurological disorders and of course cardiovascular.

David: How do you broach it with patients, because the minute they hear chlamydia, they’re thinking chlamydia tracomatis and, “What do you mean, I have a sexually transmitted disease?” and yadda, yadda, yadda, even though it’s estimated that one in four men with chlamydia have no symptoms, for instance, so how would they even know right? Do you have to deal with that at all with them just not understanding that?

Nikolas: Yes, sometimes they do have a surprised look on their face. Trachomatis is the sexually transmitted chlamydia, the other two big ones that you’ll see are chlamydia pneumonia and then chlamydia saatchi and those are the ones that are non-sexually transmitted so I just explain that to them.

David: How do you test, are you testing for chlamydia?

Nikolas: Yes, yes same as mycoplasma, doing PCR and IGT IGM.

David: Now with this lab that you’re using, are you just, are these ordered a la carte or are they part of one larger panel that you use?

Nikolas: They’re just ordered a la carte. Yeah.

David: Okay, and when you interpret them you said that you’re doing IGM, IGT and PCR, did you say?

Nikolas: Right. Yeah exactly.

David: So, if you get an IGT positive but an IGM negative you consider that as being a prior exposure and an IGM being more of an active infection?

Nikolas: Yeah, you know if the IGM’s positive and then of course it’s a pretty good indicator that it’s active but the more I read about IGM, the more I find that it may only either be positive for seven weeks. It might come on two weeks after infection and then it’s only going to be positive for about seven weeks and then it’s gone. It’s just the best that we have now.

David: So basically in this chronic stealth infection, unlike in acute infection, the IGM may not be really worth that much? Nikolas: Exactly. Yeah.

David: Then if you have an IGG, how do you know it wasn’t just an old prior exposure and not something that’s really causing them an ongoing issue. It gets a little hard to tell doesn’t it?

Nikolas: It does. You just do the best you can with history and if you’ve exhausted everything else then you just have to try and treat it and quite a number of times they start to improve.

David: And have you noticed any kind of specific correlations with the PCR testing and then these antibodies, do you find the PCR popping when the antibodies don’t or vice-versa?

Nikolas: Mainly I see it’s just going to be one or the other in most cases. There are a few times where the IGG, IGM will be positive and the PCR but usually you’ll see one or the other. A lot of times you’ll see the PCR positive and the IGG positive, IGM negative.

David: And how about H. Pilori? There’s a lot of controversy over H. Pilori because when we first really became, it became the big buzz issue with gastritis, duodenitis and ulcers and then as a potential trigger of gastric cancer the whole, the reflexes, “Oh, H. Pilori is bad, you got to get rid of it.” Well then now you see all these studies showing that H. Pilori is protective in many ways against being over reactive or having autoimmune disease in some ways, because we know the people with low levels of H. Pilori or since there’s been relative H. Pilori eradication compared to in years past there’s much higher levels of atopy and we know that H. Pilori is protective against atopic disorders. Where do you, what do you think about the whole H. Pilori issue? Personally, I’m absolutely confused by the whole thing.

Nikolas: I can give you my clinical experience with it. I think this is really a valuable clinical pearl that I’m going to give and this is based on some research that I’ve, well there’s actually quite a few papers on it but there’s actually a journal called Heliobacter, that’s just the name of it and there’s been a lot of papers in there studying the connection between H. Pilori and Graves’ disease and they do find when they do stool samples of patients with Graves’, the vast majority of them come back with active H. Pilori infection. After I learned that, I started testing the Graves’ patients and the vast majority of them do have active H. Pilori infections and when I treat the H. Pilori they get better.

David: And how are you diagnosing the H. Pilori with the stool antigen, with a breath test, with serum antibodies, how?

Nikolas: Right. All the studies that I read regarding Graves’ and H. Pilori, they’re doing stool but I like to do stool and also do it in blood.

David: So stool antigens, or detecting the DNA of H. Pilori in stool?

Nikolas: I’m doing the Metametrix stool analysis of H. Pilori, so DNA. I like to do serum IGA and many times the IGA is going to come back positive. Treating it is fairly straightforward, the GastroMend-HP, that Designs for Health has actually yielded excellent results in, I don’t want to say eradicating because it is always there, but really suppressing the infection so it comes back negative. These patients do improve, I just had a Graves’ patient last week and she’s in remission and we’re basically just doing a few things and focusing on the H. Pilori. Her endocrinologist was all for it because the patient got better. That’s just something that I’ve seen and I do treat the H. Pilori when I see it and these Graves’ patients definitely respond.

David: Have you seen the work of Alan Ebringer on proteus, stealth proteus infection and rheumatoid arthritis? It is unbelievably compelling and it goes back years. His work has now been replicated by teams all over the world to show that it’s not just a UK or even a western phenomena. There’s been multiple research teams in England, Scotland, Ireland, France, Japan, and other parts of Asia, Scandinavia, US, just all over the map showing that rheumatoid arthritis. It’s almost universal that these people have stealth proteus infections in the urinary tract. Most of us were trained in urinary tract infections, you know they’re a no-brainer if people come in with pain on urination, flank pain, urgency, you do a urinalysis, urine culture, whatever, they have leukocyte esterase, white blood cells, and bacteria in the urine and all that, you treat it and everything’s good.

However, he’s really showed that that’s not the case, that organisms like proteus can exist in the urinary tract for years and years and years without overt clinical symptoms. The proteus organism mainly as proteus mirabilis produces a bacterial hemolysin and a bacterial ureaes and the hemolysin and urease basically have sequences that are very, very similar to host sequences including the HLA-DR1, HLA-DR4 and he’s really made the connection. He has the whole amino acid motif mapped between the HLA-DR molecules and the bacterial hemolysin from proteus. Basically he shows also there’s a motif molecular mimicry between, I think, the proteus hemolysins and I think it’s type 11 collagen and type 11 collagen is unique to the small joints of the hand and the small joints that RA affects.

It’s always been a mystery why rheumatoid arthritis only affects certain joints of the body and spares others, and Ebringer’s work explains why that happens in his proteus stealth infection model. That there’s specific antibodies made to combat the proteus infection that cross react only to type 11 collagen, which is only in these specific joint structures. He goes on to explain all the other mysteries of RA through this model too. The female predominance in RA is about three to one. Well in UTI there’s a strong female predominance because of anatomical differences, disease onset between 30 and 50 well UTIs become much more prevalent in middle and older age women. Exacerbation after pregnancy which is common, to have UTIs exacerbated after pregnancy. Low concordance rates in identical twins and fluctuating course of the disease tends to suggest not a strong genetic but a strong environmental factor and the high proportion of RA patients having positive rheumatoid factors can be attributed to a secondary phenomenon due to B-cell stimulation and the presence of antigen antibody complexes to proteus.

I mean it’s elegant work, it’s unbelievable and this guy is a major, I think he’s Sir Alan Ebringer. He’s NV Phd, major researcher, he’s a consultant to CDC, and NIH on infectious disease and yet there’s no appreciation in standard medicine and the practice of rheumatology for molecular mimicry very much at all but they are certainly not looking for stealth proteus infection and Ebringer couldn’t even find commercial lab tests that were good enough to reliably detect it so he had to basically come up with a laboratory methodology in his own labs which he then shared with these other research groups. If you read his papers, his treatment modalities are not just NSAIDS and biologicals and things, he uses those when necessary, but he’s kind of using an almost naturopathic therapies. He’s using alkolysing therapies like vitamin C, he’s using high fluid intake, he’s using diets that are high in certain herbals, like cranberry juice and others that have high blocking capability of these organisms to the mucusal linings because of the D’mannose and other kinds of sugar that are in them and he uses antibiotics. He uses Cipro to knock the heck out of the proteus infection and he’s gotten really good clinical outcomes and yet there’s nothing done like this in conventional medicine, at least I haven’t seen it. They’re just put on NSAIDS and DMARDs and biologicals and Methyltrexate and those drugs have really nasty, serious complications. Are you aware of that research? Have you seen any of it, do you have any thoughts?

Nikolas: Yes. It’s fascinating that you’ve just brought that up because I’m sitting here staring at Ebringer and Rasheed’s paper in Clinical and Developmental Immunology, March 2006. Entitled “Rheumatoid Arthritis is an Autoimmune Disease Triggered by Proteus Urinary Tract Infection.” That’s exactly what you just said. He says right here, “Patients will benefit by involved using vegetarian diets, high intact of water, cranberry juice as treatment.” Yeah, I’ve read this paper and a few other ones and it’s really fascinating.

David: How about viruses, what’s good viruses, I want to talk about Lyme a little bit and have time for enough questions but we’ve been talking a lot about bad bacterial organisms but what about chronic viruses a little bit more. Do you have anything more to say about those connections to autoimmune disease because most of the connections that you see out there in the molecular mimicry type of thing are mostly due to bacterial pathogens?

Nikolas: Right, yes the whole study of viruses and autoimmune disease is fascinating. Almost pretty much any autoimmune disease you can find research with some kind of connection with one virus or another. There’s a really good paper published in the journal Virology in 2009 and basically it’s a review of all the research out there on the connection between viruses and autoimmune thyroid disease and particularly with Hashimoto’s they did find direct evidence of Epstein-Barr virus, herpes simplex virus and parvovirus B19. I mean, the most interesting part of the paper is that the authors say that the virus can be inside the thyroid gland but there can be no systemic consequences. They’re saying that nothing may show up on the CBC, the patient might not have any symptoms at all but the virus can still be active in the glands causing an inflammation and thyroiditis. This is just a fascinating paper that blew me away and they talk about Graves’ disease and acute thyroiditis like you mentioned earlier, some people will develop thyroiditis just after they have a really bad flu virus so again pretty much any of the autoimmune diseases.

Then another fascinating area is adenoviruses and celiac disease. I’ve been reading that it’s possible that celiac disease can be triggered or significantly exacerbated by adenovirus activity, just so that whole area is really, really fascinating.

David: What was that paper you mentioned in Virology?

Nikolas: I have a copy of it, I can send it to you.

David: What was the year or anything, is it recent?

Nikolas: Virology, 2009. Virology Journal, 2009.

David: Right, send it over to me and we’ll post it on the resources for tonight’s call.

Nikolas: Yeah, yeah, it’s great.

David: Yeah I know and there’s been a lot of work with viral triggers for type 1 diabetes for instance. Everyone’s familiar with the bovine beta lactalbumin protein crossovers and all of that, but there’s a lot of stuff on viruses as well. Of course, we know there’s a lot of, you know, there’s a lot of work on viral triggers for cancers. Well beyond just cervical cancer and others, I mean there’s a tremendous amount of literature on viral triggers for a lot of the most common cancers. Cancer really, in many circles is starting to be looked at as an infectious disease and ISM did a great conference a couple of years ago on cell infections and particularly the infections aspect of cancer, which I found fascinating. Of course they did tackle Lyme, they had Burrascano and they had a couple of other people talking about Lyme. Talk to us a little bit about your experience with Lyme and some of the other co-infections and what can you share with us about those?

Nikolas: So, Lyme, the first connection that you see with Lyme is in the Hashimoto’s thyroiditis. There’s been a couple of good papers published in the journal Thyroid where they talk about homologies between Borrelia burgdorferi, surface antigens and thyroiditis. Basically those are people who are going to have genetic suspectibility to thyroiditis and you know, like you’ve talked a lot about before with usenia as well. Lyme is obviously the fastest growing infectious disease within the US. It’s grossly underreported to the CDC so the numbers are not what they really are per year.

David: I had a doctor tell a patient the other day that Lyme doesn’t exist in New Jersey.

Nikolas: Really? I thought that was only in North Carolina.

David: I mean, it’s just in Connecticut and New York and it’s not in New Jersey. The deers ticks in New Jersey don’t carry it. I went, “Wow, that’s interesting.”

Nikolas: Yeah, the infectious disease doctors here in Ashville don’t believe that Lyme exists in North Carolina so these people walking around with tick bites and erythema migrans, bullseye rashes and all the Lyme’s symptoms, you know you get a positive Western blot and they just say, “Oh, that’s a false positive.” People are not getting diagnosed properly. Treatment in the acute stages is of course Oxycycline and other antibiotics which should definiately be implemented. Then in some cases and I see a tremendous amount of these when Lyme is very, very chronic I see a lot of people who they’ve tried the antibiotic route and it just hasn’t really worked for them in chronic Lyme or they’ve just not been able to tolerate them and so I have some really good herbal approaches to chronic Lyme.

David: Are these the same for the BCO Bartonella, arricular, hepsea all that stuff?

Nikolas: Yes.

David: Do they work for all of them? Well, I’m really interesting in this, talk to us about that herbal approach. What are some of the botanicals you use, how do you apply them, how aggressive are you with them, do you get die-off reactions? How long do you have to use them. I’m sure everyone is wanting to know that.

Nikolas: Let’s start with borrelia burgdorferi the bug guns for that, so to speak, herbally are sarsaparilla, also known as Smilax, stephania root, Japanese Knot Weed, noni, neem, teasle, cat’s claw, and womwood all work very, very well for borrelia. They way that I look at it, you want to figure out which infection is the most active. Sometimes the co-infections are the most active so sometimes it’s works better just going after one of the co-infections. Right, yeah, you go after the co-infections first in some of the cases and babesia, you know, it’s just like malaria so wormwood, also known as artemesia works very, very well for babesia. Red root is going to be important because that really supports the lymphatic system so it helps the body clear these infections. People with babesia they might have a lot of fever and chills so boneset works very, very well for helping people deal with those fever and chills. Some of the other big herbs for babesia are cryptolepis, sida, alchornea.

David: Can you spell that herb?

Nikolas: Cryptolepis C-R-Y-P-T-O-L-E-P-I-S It mainly comes from Africa, it works very, very well for systemic infections like babesia. Bartinella is going to be the second most common co-infection and bartinella a lot of the symptoms are going to be mainly pain based so a lot of sharp, shooting pain, pains on the bottom of the feet, things like that. Bartinella, some of the herbs that are good for that, the red root and the boneset again, you want to use those to support the lymphatic system and to deal with some of the symptoms and I like using noni, neem, usnea lichen and silver can work well for bartinella as well and then Japanese knotweed, those can all work well for bartinella.

Those are going to be the two main co-infections, the other ones like ehrlichia and rickettsia I do see a lot of rickettsia here in North Carolina but ehrlichia and rickettsia those herbs that I mentioned for borellia and the other co-infections will work well for those as well.

David: What’s your experience with the silver for borellia?

Nikolas: Right. In order for it to really work, they have to do two teaspoons three times a day, for two to three months. They really need a lot of it.

David: And what about these other herbs, are you using combinations of these herbs in tincture form? Are you using individual herbs and then how are you dosing them? Can you give us a feel for that?

Nikolas: Yes, so most of them are tinctures, some of them are capsules starting out slowly and building their way up and that’s just based on body weight, how much they take. If I’m going after one co-infection, I’ll go after it for four to eight weeks and then shift into another infection after that.

David: Are you using drop dosages? A certain amount of ounces, what’s typical? I know some of these really highly concentrated extracts out there, the Byron White formulas and things people are using, sometimes using five or six drops and people are [inaudible 00:54:09] they claim. What’s your experience with that?

Nikolas: Right, with those formulas you just start out at one or two drops a day and then you want to max at 20 drops twice a day but for all the other . . .

David: That small amount of drops of a botanical can have profound effects like that on one of these self pathogens?

Nikolas: Oh, yeah, definitely.

David: It’s hard to believe that that little of the substance would have a biochemical like conventional mechanism to be able to disrupt those pathogens systemically. Do you think it’s that or do you think it’s more like the German biological biophysics kind of medicine, think that it’s, I don’t want to say it’s like homeopathy but it’s almost just like getting the substance in the body that has the right frequency or resonance or vibrance or whatever you want to call it. Do you have any feeling on that?

Nikolas: I just think that with herbal medicine, as you know, it’s the taste, it’s the smell, it’s the formulation that’s really important. How herbs work together, I think, if they’re well formulated then you don’t need as much but for just your general tinctures, you know, where you’re at a 5 to 1 ratio will do 30, 60 or 90 drops and load every couple of hours for a few days and then drop back to five times a day and then . . .

David: Some of these Lyme ones are 1 to 1s, they’re like really, really strong tinctures.

Nikolas: Exactly. Maintenance, while you’re cruising, so to speak, is taking them three times a day. For your general tinctures but in addition to just going after the microbe, if you look back at some of the herbal literature out there when they were treating syphilis they didn’t exactly focus so much on the Treponema pallidum spirochete, they actually focused on lymphatic system and blood cleansers and diaphoretics and just really supporting the body to clear these things. That’s the question that you had earlier, why do some people get these infections, why do they take hold whereas other people can get the infections and they just fight them off?

David: Once again I practice with some really skilled people who do more the German Biological approach and they are using F:scans and they’re using coils and rice machines and their using the AV and they’re using all of these different energetic things. I see with these stealth chronic infections that they get significant results when you don’t get it with the sort of western, biochemical model and they’re even isolating the frequencies of these pathogens and then introducing neutralizing frequencies and really going at it on an entirely different kind of level, which I find really interesting but the reason I just brought that up is a lot of what they center their therapy on first is even not going after the pathogen but really going after those, using those lymphatic drainage type of remedies. I think that kind of goes back to what you were saying about that approach. Even if it’s been used, historically at least, in some conventional circles also. What about Herxheimer reactions and die-off? It’s so common when you start trying to treat these stealth infections, particularly Lyme, how do you manage that? Just slow it up?

Nikolas: The Herxheimer is the biotoxins, the biotoxins are released from the outer cell wall of the Gram-negative bacteria as they die-off and you want to use herbs that have saponins because saponins absorb those things and sarsparilla also known as Smilax is excellent for absorbing those toxins and reducing Herxheimer. Japanese knotweed works as well. For all those listeners out there Japanese knotweed has a massive amount of resveratrol in it so it does have a strong anti-oxidant effect and also a way of absorbing and reducing these toxins. Then ginger, just taking ginger as a powdered capsule really isn’t going to do much, you have to make them into a ginger juice or a really strong tea. Those three right there can significantly reduce the Herxheimer reaction.

David: How about biofilms, I mean, because this is a real controversial thing. Everybody talks about eradicating biofilms and there’s all these products to eradicate biofilms with chelating agents and all these different things. I’ve had a hard time honestly wrapping my mind around it because everyone pretends that only bad organisms live in biofilms, right. Only the things we don’t want, pathogens and opportunistic organisms. Well the reality is that good organisms live in the biofilm too including in the gut, the gut biofilm. If you came up with an agent that knocked out the biofilm, how are you just knocking out the biofilm that houses the bad things and not knocking out the biofilm that houses the good things? I’ve yet to see any literature on knocking out only biofilms of bad organisms, so that’s where I struggle with the whole biofilm therapy stuff. Do you have any…?

Nikolas: I hear you. Early on I did try and address that but I found that if I didn’t really focus on that I was still getting good results. Using EBTA and then various enzymes like lumbrokinase, serrapeptase, nattokinase, bromaline, you know all these things to dissolve the biofilms, but these enzymes that I mentioned I’m really using those anyway for coagulation because especially in Lyme, as a stealth mechanism the microbes upregulate the coagulation in the blood so it’s just harder for you to get to them. I hear you, it’s not something that I directly focus on. I think that the herbs that I’m using I know that those have an effects on biofilm and the enzymes that support coagulation are going to have an effect but again, it’s not a major focus for me, at least.

Woman: Thanks, excellent call. I had a question regarding flu vaccine, how this is affecting the whole thing in general and it’s also in the case of a patient who had a flu vaccine and it then started the herpes virus, just going crazy for him where he had problems with that. I just wanted to see if any of these herbs that you deal with for the herpes as well.

Nikolas: I’m not knowledgeable about vaccinations or what they do in this particular topic, it’s not something that I’ve studied or I don’t really have a great interest either in vaccinations but I think that there’s a lot of practitioners out there who talk about vaccines but they don’t really, they haven’t really done an exhaustive review of the literature to really talk about it and I’m definitely one of those people who doesn’t know enough to confidently talk about it.

David: I think conceptually though, an immune insult from vaccinations could be somewhat like having an infection, right? That’s what it’s meant to do so a lot of these disorders seem to come up after a viral infection or after some kind of infectious event. It seems logical that people may have problems and an immunological imbalance after they’ve been administered various vaccines which are designed to modulate the immune system. How exactly that works and how to connect those dots I’m not sure anyone knows, now.

Nikolas: And what can you do about it, if it does?

Woman: Right, okay. Then regarding the herpes, how do you treat that in terms of a virus?

Nikolas: Right. Herpes the two things that I use, that have worked really well. The first is monolaurin works very well for herpes and then a combination of olive leaf extract and larrea tridentata, also known as chaparral. That combination of those three rarely fails me with herpes.

Woman 2: Okay.

David: You said monolaurin, chapparal and then what was the other one you just mentioned, Nik?

Nikolas: Olive leaf extract.

David: Olive leaf. Okay, great.

Woman: Thank you.

Nikolas: Thanks.

Woman 2: Hi, Dr Hedberg. I think that the answer to this question may be the same as the previous question and that is what have you found to be effective for treating Epstein-Barr virus and how soon have you seen it be effective?

Nikolas: Okay. Epstein-Barr virus, what’s worked well for me again is the monolaurin and then schisandra berry works very, very well for Epstein-Barr and reichi extract.

Woman 2: Okay, and how soon have you seen this be effective in the treatment process?

Nikolas: It’s usually pretty rapid, especially if you add reichi to the mix but the monolaurin you build them up over a week, over a couple of weeks until they’re at a very high level for a few weeks and then drop back down and then the schisandra and the reichi they can just go full bore with it and those work quite well.

David: The monolaurin is for encapsulated viruses, right, because it kind of dissolves the outer lipid layer that they’re sealing themselves with?

Nikolas: Right.

David: The monolaurin you’re saying you’re giving that at high doses to kind of expose them and then these botanicals can do what they need to do once it’s exposed, in my understanding?

Nikolas: Yeah, they do their anti-viral thing and then something like reichi is really going to really . . .

David: [inaudible 01:05:56]

Woman 2: And what would be a high dose of the monolaurin?

Nikolas: Right, 600 mg capsules, three of those three times a day is really the maximum.

Man 1: Fascinating conversation gentlemen. Could you repeat what you just said about the monolaurin, was it 600 mg three times a day was the maximum dose?

Nikolas: It’s three 600 mg capsules three times a day.

James: Oh, okay, got it I wasn’t. . .

Nikolas: It’s going to be nine capsules.

James: I wasn’t quite sure. Earlier in the conversation you talked about the herbs you use for mycoplasma.

Nikolas: Right, well the first two are noni and neem, N-E-E-M and then the systemic herbal antibiotics that work well are the cryptopis, C-R-Y-P, it’s a herbal tincture. Sida S-I-D-A and alchornea , those are the systemics.

James: Okay, and you mentioned Silvercillin, was that a similar dose?

Nikolas: Silvercillin yes.

James: Was it a similar doses that you mentioned elsewhere, two teaspoons three times a day?

Nikolas: Right, two teaspoons three times a day.

James: Great. Thank you very much.

David: Thank you, James.

Man 1: Yes I have a particular rheumatoid arthritis patient with the elevated estrogen dominance and the IGG sensitivities and the H. Pilori I was able to maintain or put the person back into a normal hormonal balance lowering the estrogens and so forth and eliminating the IGG food sensitivities and also eradicated the H. Pilori. Would you at this point suggest that we go after mycoplasma? What is that connection between the elevated estrogens and these RA people?

Nikolas: I mean, it’s difficult to say with each case. At first you would obviously want to identify if there is active mycoplasma infection. Say they have rheumatoid arthritis they might not have mycoplasma, it could be the proteus we were talking about earlier or other infections but if you are able to identify an infection then I would definitely address that.

Man 2: Dr Hedberg do you still use the CD57 as a screen tool for Lyme? Do you find it effective because I’ve read where some doctors are saying that they find it totally useless in their practice and others saying it’s a really great tool. What’s your opinion on the CD57?

Nikolas: Yeah, I run the CD57 on everyone that I expect or if I suspect Lyme disease or one of the co-infections. I think it’s a very, very valuable tool. If you do find the CD57 low, let me tell you what will boost that. Catsclaw, also known as samento will raise the CD57 count and reichi will also raise the CD57 count. For those of you who don’t know it is theorized that borellia burgdorferi specifically represses the CD57 count and therefore it’s a good indicator of how much the borelia has hold in the system and how much it’s suppressing the immune system so I think it’s a good test. I’ve used it for years but, as with any test, it’s not going to definitely tell you if they have Lyme or not.

Man 2: Sure. At what low range would you start to suspect the possibility of Lyme? What are your ranges for CD57?

Nikolas: The cut off on the lab is 60 but I like it to be above 100. Some say it should be above 150 but that’s all anecdotal observation.

Man 2: All right, thank you very much. By the way, I just wanted to tell you I’ve got Japanese research showing that vaccinations can trigger autoimmunity in mice and the article is Self Organized Criticality Theory of Autoimmunity. Just to show the effect of repeated vaccinations triggering autoimmune reactions in this case a lupus type reaction in mice, so there could be your connection with vaccinations.

David: And that was in what journal?

Man 2: You know, I don’t have the name of the journal, the article is called Self Organized Criticality Theory of Autoimmunity.

David: Okay, I’ll search that and I just got a, pertaining to your question, I just got an instant message from Todd LePine saying that if you do a CD57, try to do it with Labcor because they do the most accurate count, they actually give an absolute CD57.

Man 2: Thank you very much.

Nikolas: No problem.

Andy: For some reason when I hit the tape next question it’s not working right.

David: Yes, actually all the ones still hanging are people who have already asked a question. I started doing it when you hung up so I think we may have jumbled it. Anyway I wanted to thank Nik for being on. I wanted to thank everyone else for taking time out of your precious evening to be with us and we’re honored that you were here and next week on Clinical Rounds we will have Mark Mendlecino [SP] who’s been on Clinical Rounds before he’s been a Glacia Fest [SP] speaker and he’s been a webinar guest for Designs for Health. He always has great things to say and he’s talking about natural supplements and interventions for diabetes and diabetes reversible protocols. Join us with Mark Mendlecino next week and hopefully we’ll see you at one of our upcoming seminars including Core III in San Francisco in a couple of weeks in September 29, Houston on October 27 and Andy just one more time do you have those Core II dates? I don’t have them with me.

Andy: Yup, Core II dates are September 22 in Traverse City, Michigan and also Chicago, Illinois on November 3.

David: Thank you everybody for being on and we look forward to having you on on another Clinical Rounds call and thanks for sharing everything, Nik. Nik, did you want to mention your website for some of your continuing ed stuff?

Nikolas: Yes it’s so it’s all one word, and there’s some good information on there about this topic.

David: Dot net, not dot com, right?

Nikolas: Yes, dot net.

David: Excellent. Okay, thanks everybody and have a wonderful evening.

Andy: Good night Nik, good night David.

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