Epstein-Barr Virus and Autoimmune Diseases

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by Dr. Nikolas Hedberg, D.C., D.A.B.C.I., D.A.C.B.N.
drhedberg.com

In this interview I discuss the connection between Epstein-Barr Virus and Autoimmune Disease

You can listen to the interview above or read the transcript below:

Dr. Brady:  Dr. Hedberg lectures all over the place, a lot of integrative medicine conferences. He’s published in many journals. He teaches advanced functional medicine courses with Functional Medicine Town, professional co-op and as adjunct faculty with Hawthorn University. Dr. Hedberg has found that many chronic diseases are a result of stealth infections and that’s what we’re going to focus on tonight. Basically, he’s also formed a website and a community known as “The Infection Connection” and I’ll have him tell you a little bit more about that later in the call. You can learn more at infectionconnection.net.

Nick’s a good friend of mine. I’ve known him for probably, I don’t know, over 10 years I would say. He has the perfect radio DJ voice, as I always say, and you’ll hear in a minute. When you hear that voice, I didn’t know this at first, I learned this only in few years ago, but it did not surprise me when I found out that he’s quite an accomplished opera singer. Nick, do you want to do a little tune for us to lead off or not?

Dr. Hedberg: No singing tonight Dave, LOL.

Dr. Brady: Okay. All right.

Dr. Hedberg: Yeah. Yeah.

Dr. Brady: All right. Well, thanks for being on, Nick, I appreciate it.

Dr. Hedberg: Yeah. It’s great to be on again.

Dr. Brady: Great. Well, let’s dive right into the topic. We’re going to talk a lot about thyroid issues and stealth infections. We’re going to look specifically tonight at the connections between Epstein-Barr virus and autoimmune diseases. I know that Epstein-Barr virus is certainly not the only virus out there implicated as an autoimmune potential trigger. Let’s explore EBV first, so just give us an idea how you first started making the connection between EBV and autoimmune diseases, and just lay the groundwork for us, if you don’t mind.

Dr. Hedberg: Right. So the first connection in the literature between EBV and autoimmune disease was actually in 1971. So a little over 40 years ago when they found that patients with Systemic lupus erythematosus had elevated antibody levels to EBV. It was actually about 10 years ago, David, you were talking about the connection between Yersinia and thyroiditis and that just kind of got me into looking at this molecular mimicry. So I just started noticing patterns on blood chemistry in patients with autoimmune diseases like low white blood cell counts, and then the class that has got elevated lymphocytes and low neutrophils which is the classic picture for a chronic viral activity. So I was seeing that a lot in the patients with autoimmune disease.

The other thing that shows up a lot in these patients were chronic low-grade fevers, getting fevers of unknown origin. A fever is basically an infection until proven otherwise. Then one of the other major red flag was, of course, cancer, but in these patients, cancer was not suspected. There was something going on there causing these chronic low-grade fevers. And then just started doing more and more Epstein-Barr virus panels on the autoimmune patients and seeing them coming back positive, reactivation of the Epstein-Barr virus. And then when I started focusing on that, the viral activity, that’s when we started seeing excellent results in a lot of these patients.

Dr. Brady: I see. Did you happen to hear my interview earlier this year, in January sometime, with Derek Enlander, by any chance, from Columbia?

Dr. Hedberg: No. I didn’t hear that.

Dr. Brady: Well, many of you on the call may have heard that. We talked about Myalgic Encephalomyelitis which is basically Fibromyalgia Chronic Fatigue Syndrome of viral origin. Of course, a lot of different viral agents are being studied and have been studied in relation to that, even though you wouldn’t consider that necessarily an autoimmune disease classically. I think it’s living in the same kind of sphere or camp and actually Enlander was first brought to the US by Stanford to study the relationship between Epstein-Barr virus and Cancer. So I thought it’s kind of interesting. These calls kind of dovetail a little bit.

If you want to know more about his work, you can just look up Derek Enlander, you can go on our library and listen, download and listen to that Clinical Rounds call and some of the research he’s doing at Columbia on Fibromyalgia Chronic Fatigue patients related to viral ideology and immune dysfunction from virus. But certainly this is in play in classic autoimmune conditions as well. So tell us just a little bit more about Epstein-Barr virus, some of the characteristics of the virus, the epidemiology of it out there, mechanisms, and can you share anything, anything meaty like that on EBV?

Dr. Hedberg: Right. So a lot of people forget that Epstein-Barr virus is a herpes virus. It’s in that family. It’s a gamma virus and it’s very different from the other herpes virus in that it’s the only one to infect B cells. It’s these naive B cells that get infected. The other thing to know about it is that unlike, for example, say the flu virus where when the flu multiples and it expands, the cell is destroyed. There’s almost instantaneous cellisis and viruses are spread into the system. The herpes viruses are very slow. What they do, it’s called budding. The budding is just basically the virus is using the DNA to replicate itself, but the cell is actually not destroyed, and that’s one of the main…

Dr. Brady: So that’s why there’s not such a virulent course or a obvious acute illness like there is with something like the flu, I would imagine.

Dr. Hedberg: Exactly. So it’s slow like that and the host cell is spared by the virus. The other herpes viruses are of course, the cytomegalovirus virus and then we have herpes 1, 2, 6, 7 and 8. We’re learning a lot more about herpes 6 and autoimmune disease, and then of course the varicella-zoster, chickenpox virus. About 95% of the world’s population is infected with Epstein-Barr virus and most people get it before the age of three and they are asymptomatic.

Dr. Brady: What was the percentage you gave, Nick?

Dr. Hedberg: 95% percent.

Dr. Brady: Okay.

Dr. Hedberg: Yes. Most people will get it by the age of three, but there’s no symptoms. And then, there’s about 100% infection rate of those individuals, of course, by the time they reach adolescence. It’s usually because they’re stressed. The immune system is compromised or they get a higher viral load. Because EBV is the cause of the classic kissing disease, mononucleosis, and a lot of people will get that in adolescence, in high school and into college. So it is transmitted by saliva, and the first place that it infects is the B cells in the tonsils. That’s where it germinates and that’s where it really sets up shop.

Dr. Brady: If so many people, it’s almost just universal that we’re infected, what makes one person progress on to autoimmune disease or some other type of chronic illness and the majority of people not?

Dr. Hedberg: Right. That’s what I’m talking about tonight, Dr. Pender’s hypothesis of Epstein-Barr virus and autoimmunity. He has these eight-step hypothesis. Dr. Pender is out of the University of Queensland, School of Medicine in Australia. He breaks in down into eight steps. I just want to go through these briefly. Step one is a genetic CD8 T cell deficiency. So basically, these viral infected B cells are normally metabolized and controlled by cytotoxic CD8 T cells. If there’s a genetic deficiency there, then it allows for an uncontrolled environment of the EBV infection. So you start with the genetic deficiency. The second part is of course the primary EBV infection.

Step three is a decreased cytotoxic CD8 T cells control of the infection. Step four is an increased EBV load and increased anti-EBV antibodies. Then step five is EBV infection in the target organ. So for example, these infected B cells with EBV actually would enter, for example, the thyroid gland and germinate in that area, and progress in maintaining a low-grade infection in the thyroid gland as an example. Other examples would be say the salivary glands and Sjogren’s, the gut and Crohn’s disease, examples like that. Step six is clonal expansion of the EBV-infected B cells in the target organ. Step seven, infiltration of autoreactive T cells into the target organ.

Finally, step eight, you get these ectopic lymphoid follicles in the target organ. So for example when you see a follicle on the thyroid, what they found is that that follicle was actually filled with EBV-infected B cells. So it’s a really fascinating hypothesis that when you put it all together, it makes sense and it also would explain why if everyone has it, why doesn’t everyone have autoimmune disease.

Dr. Brady: Can you pick up this genetic lack of those specific CD8 cells with lymphocyte subset testing or do you have to do genetic testing? Can you just look at the cell population in some way? Can you offer any wisdom there?

Dr. Hedberg: Yes. Let’s just talk about the testing. And just on a side note, the Epstein-Barr virus panels that are offered through the major labs like LabCorp and Quest, et cetera, they’re looking at the three main things which is the nuclear antigen, the viral capsid antigen and the early antigen. Unfortunately, in their standard panels, they leave out the IgM from the nuclear antigen and then early antigen. So when I started doing these testing, IgG and IgM for all three, and so I’m seeing a lot more activity when I do that. Yeah, you can do, basically, just a CD4/CD8 ratio and what you’ll see, and this is one of the things he talks about it in his papers, there’s one common theme among almost everyone who has autoimmune disease and that’s a low CD8 count. So their CD4/CD8 ratio is elevated. CD4 is high, CD8 is low which indicates chronic infection and the body is really not able to deal with it. The other thing I told you…

Dr. Brady: Do you know the ratio number off the top of your head that would be considered starting to get abnormal? You use some functional ranges or do you rely on the laboratory ranges?

Dr. Hedberg: There are functional ranges available but pretty much anything above 2.0. Once you start seeing it get above that, then that’s considered your starting to see some activity, but most of these people, it’s going to be very, very obvious. You’ll see it up around four, six or eight. You’ll see it very high.

Dr. Brady: I pulled an interesting paper a while back and I’ve had it in my slides, my autoimmune presentation slides for a while. It goes back to January of 2009. It was published in Virology Journal by Rachael Desailloud, I believe is how you say it, and Didier Hober. It’s entitled “Viruses and thyroiditis: an update.” They talked about the fact that viral infections are frequently cited as major environmental factors involved in Subacute thyroiditis and autoimmune thyroid diseases. Basically, there’s been a controversy on whether these viral agents are responsible for the thyroid disease and autoimmunity or whether they’re just sort of innocent bystanders or creatures of opportunity, if you will.

They really break down the classification quite a lot. They show direct evidence of the presence of viruses through their components, and in this case, in the organ, in the thyroid. For retroviruses (HFV), mumps in subacute thyroiditis and retroviruses like HTLV-1, which is the human T-lymphotropic virus 1, I believe, that’s the virus that’s implicated in causing leukemias and lymphomas. I think one in 20, to one in 25 people infected actually go on to develop cancer; also SP40. Then they break it down interestingly. They say in Graves’ disease they find evidence through this HTLV-1, enterovirus, rubella, mumps, HSV, EBV and parvovirus in Hashimoto’s thyroiditis.

So they’re almost breaking down different variants of thyroid autoimmunity and implicating… well, not implicating in causality, they are certainly coming up short of that. They’re showing an association between the presence of these viruses in the thyroid tissue and these sub-variants of autoimmune disease of the thyroid. Do you have any comments on that? Can you really break it down to which virus in which sub-variant? Have you seen that clinically?

Dr. Hedberg: Yeah. I actually did discuss that paper in our call in the fall, that Virology 2009 paper in… One of the things they do say in that paper is that you can have chronic viral activity in an organ with no systemic consequences. That can make it very difficult to identify if the virus is, in fact, driving the autoimmunity, because if nothing is happening systemically, if there’s no fever, if there’s nothing happening on the CDC, and if you’re not even able to pick it up on the Epstein-Barr virus panel, then yeah, that can definitely be difficult. As far as separating the viruses and identifying exactly which one is there, just in my clinical experience, it’s really the Epstein-Barr virus that tends to be the most active, especially with thyroiditis, but in the majority of the autoimmune diseases.

Dr. Brady: We see so much information flying at us now on environmental antigens and their potential to cause crossover autoimmunity to specific target host tissues. Certainly, thyroid’s very high up on that list showing multiple types of environment . You’ve talked about the Yersinia connection, Yersinia enterocolitica overgrowth in the GI microbiota and its strong association with autoimmune thyroid activity, but also food antigens. We know that celiac patients are 10 to 20 times, depending on what study you look at, more likely to have autoimmune thyroid phenomena. So it seems like there’s a lot of different potential triggers that can cause autoimmunity against one target tissue and that because it’s not a nice, tidy, neat thing for medicine to wrap their hands around. They really love the one pathogen, one disease kind of model. The minute they can’t prove that every patient with disease X has infection with organism Y, they kind of abandon that even in play. They think it breaks down.

There’s been some interesting papers that attack that whole way of thinking and one of them is a Japanese researcher, last name begins with M, I can’t remember. Basically, it was done on MS. Basically, what they showed that there were certain types of structural peptides or proteins expressed across a broad spectrum, they were looking at bacteria in the gut against a broad spectrum of bacteria, not just one organism but sort of the same type of structural patterns presented by organisms that are conserved by organisms across a whole phyla sometimes of bacteria that can cause this autoimmune phenomenon. In this case, it was against myelin basic protein in MS. So they showed that the whole concept of trying to implicate one organism, one disease with this molecular mimicry phenomena, it breaks down, because there’s more than one environmental antigen that can get the train rolling, essentially.

So I think standard orthodox medicine that’s kind of opened up the blinders a little bit to think more dynamically and less in a reductionist way about the pathogenesis of some of these autoimmune phenomena.

Dr. Hedberg: I’m glad you brought up the point about the gluten and celiac disease, because, I mean, I don’t know about you, but I’m seeing just a large number of patients with autoimmune diseases who they’ve already been on a gluten-free diet for three, four or five years. They haven’t had a single nanoparticle of gluten for five years. They’re taking vitamin D. They’ve done VG gut reparative strategies. They’ve done everything and they still have autoimmunity and they’re still sick.

Dr. Brady: Oh, yes.

Dr. Hedberg: So they’ve already done everything that’s out there. Then when you take a closer look, in a lot of these cases, we do find chronic stealth infectious activity and that’s just sort of the tipping point that gets them feeling better, based on my experience.

Dr. Brady: Let’s talk a little bit about vitamin D since you brought it up. As you know, it’s a very controversial thing in autoimmunity, all the sort of conventional vitamin D experts throw a lot of the data at you showing that vitamin D deficiency, suboptimal vitamin D is very, very common. You look at the epidemiology of latitude, if you will, with MS and all of that. It’s kind of very interesting concept to gather nicely and a lot of people with autoimmune disorders of various types certainly do have low 25-hydroxy D3 levels, and there’s even a lot of literature showing that when you put them on vitamin D replacing, get their levels up, a lot of them clinically do better.

Then you have the other camp, sort of the marshal camp, if you will. Talking about that maybe the fact that all these people have low vitamin D is simply because they have a stealth pathogen that’s infected their immune cells, particularly, their monocytes and some other specific cells that over convert 25 to 125. They basically activate vitamin D in an accelerated fashion. So if you look at the 125, you’re going to find where all those D reserves are and the 25 is, low because it’s all been converted already. If you give vitamin D, you’re actually driving the pathology harder. It’s definitely an interesting concept and it’s been somewhat rejected by the experts but so was Kilmer McCulley and so was Robin Meade, the stories go on and on about that.

Marshall had some interesting ideas about that. It seems like the data is strongest in sarcoid but not in some of the other autoimmune phenomena. He really paints the picture for potential pathological model for stealth infection causing these autoimmune disorders, but basically activating immune cells and causing over conversion of vitamin D which destabilizes the immune system in and of itself. So do you have any thoughts on that whole concept, in that controversy?

Dr. Hedberg: Yeah. There’s two sayings that I love, that I sort of live my life by and also what I kind of drive my practice under. The first is by Oscar Wilde. Oscar said, “Everything popular is wrong.” The second is Mark Twain and Mark Twain said, “Whenever you find yourself on the side of the majority, it’s time to pause and reflect.” So whenever I see something that’s very, very popular and everyone’s doing it like everyone’s doing gluten-free, everyone’s doing vitamin D, everyone’s doing these things but why aren’t they working in so many people.

Now, vitamin D, one of the things we know is that CD8 T cells, of all the immune system cells in the body, they have the highest number of vitamin D receptors. We know that if we expose someone to natural sunlight or we put them in a solarium, that increases their CD8 T cells, so that brings the CD4/CD8 ratio back into balance. Dr. Pender talks about how it’s inversely proportional. When vitamin D goes down, then you see changes in the cytotoxic CD8 T cells and vice versa. So low vitamin D is, as he says, is just more of an aggravating factor for autoimmune disease, because you start to see that shift. When you see the shift, then you lose the ability to control the chronic infection if it’s there.

I just want to make that very clear that I’m not saying that everyone with autoimmune disease has it because of Epstein-Barr virus. I don’t want to come across like that. What I’m saying is that you really need to be aware of it and you really need to look for it very, very closely, because it’s going to be there and it’s going to be active in many of these patients. So you talked about the high latitudes. You know you see more autoimmune disease with no map, like about MS and rheumatoid arthritis, for example. So there’s definitely something there. I found, clinically, that vitamin D supplementation, it does really help, but it’s, obviously, not the whole picture.

Dr. Brady: Do you have any specific thoughts about Marshall’s ideas that you might actually be doing them harm by reinforcing the pathology, if you will. Yours is the ACE inhibitors and all these different things that manipulate the vitamin D receptor in pulsed antibiotic to deal with the stealth infection, and claims a lot of success. I’ve played around with Marshall Protocol. I have some colleagues that have but really don’t have enough clinical experience directly using it to make any firm conclusions, partially because I’m still up in the air on whether I buy the whole thing or not, because you have equally compelling, if not more, data suggesting the opposite. So it really is confusing for the practitioner.

Dr. Hedberg: Yeah. Back when I was really getting into Lyme disease, I read all of Marshall’s material and studied it. I’m just very open-minded about it for a couple of reasons. Number one, I’ve seen patients with Lyme who have really tried the antibiotic routes for years. They tried the natural route. They tried both. Then they went to a practitioner who’d use the Marshall Protocol and they got well. Then there’s also just as many people who have tried the Marshall protocol and it didn’t work for them, and antibiotics or herbs and things like that worked. So I mean I can’t say definitively if either side is right or wrong. I don’t think we really know enough at this point to make a really strong conclusion there.

Dr. Brady: We talked about vitamin D, but how about the role of estrogen? I always found that really interesting, because there are some exceptions, but usually you look down the list of autoimmune diseases and the epidemiology is clearly apparent that the female predominance is striking. No one’s really wholly or adequately explained it. I’ve heard various theories. Certainly heard some of the theories on estrogen’s role, but do you have anything to add on that?

Dr. Hedberg: Yeah. There’s some brief information on that. Basically, what we know is that the connection between estrogen and the cytotoxic CD8 T cells, they are inversely proportional. So as estrogen levels rise, CD8 T cell levels drop; and then when estrogen levels drop, obviously the CD8 count rises and the CD4/CD8 ratio comes back into balance. So just part of the theory is that, of course, one of the reasons why women are more prone to autoimmune disease is because of the estrogen which suppresses cytotoxic T cells.

The other thing we sometimes see is that when women go into menopause and their estrogen levels are dropping, you’ll see a lot of changes in their autoimmunity and their autoimmune disease. There’s a lot going on there hormonally, but you will see shifts in the CD4/CD8 ratio as the estrogen levels shift as well.

Dr. Brady: Well, we talked about different autoimmune diseases and different predilections and different potential triggers and the like. Epstein-Barr virus is what we are concentrating on tonight and we did mention thyroid quite a bit, but how about the other autoimmune conditions? What does the literature say tying EBV specifically to various autoimmune diseases? Are there somewhat stronger associations or connections than others?

Dr. Hedberg: Right. So the strongest connections in the literature, and this can be difficult to do when everyone has the virus. so they look at age-matched controls and B studies and so they’re looking at people who are of similar age who have it and don’t have it. So what they call the big five autoimmune diseases connected with EBV are Hashimoto’s thyroiditis, Graves’ disease, multiple sclerosis, systemic lupus erythematosus, and this may surprise people, but actually, celiac disease is number five. There’s just some really interesting research on the connection between Epstein-Barr virus and celiac disease.

The other aspects that they look at are how well is the immune system controlling Epstein-Barr virus infections. What they found is there are six main autoimmune diseases where they found, specifically, that the immune system control of the EBV infection was significantly compromised. Those six were lupus, rheumatoid arthritis, Sjogren’s, multiple sclerosis, primary biliary cirrhosis and suspended sclerosis . So those are some of the most common autoimmune diseases that we see, and there are some pretty strong connections there.

The third aspect that I wanted to talk about was when they go in and they want to look specifically at EBV infected T cells and target organs, they are able to do that with various methods like PCR and things like that. So when they go in and they extract B cells from the thyroid glands of Graves’ disease patients, salivary glands of Sjogren’s patients, the colons of patients with Crohn’s, the myelin and the brain of MS and the finest, in my opinion, graph is they found very, very high levels of Epstein-Barr virus DNA in those tissues. So those are some pretty strong connections there as well. Compared to controls, they don’t find that at all in those tissues in patients who don’t have the autoimmune diseases. So that’s pretty compelling evidence.

Dr. Brady: We have a lot of association data and they are starting to connect the dots on what’s associated to what statistically. But what is lacking, there are a lot of great hypothesis on mechanisms of actual causality or ideology of these organisms, but have you seen a lot of really good, hard data? For instance, what’s the connection with EBV and celiac? We’re always told, well, it’s the gluten/gliadin antibodies and this is how the destruction occurs in the GI tissue and yada yada. What’s EBV doing? Do we know? Or does it just happen to be along for the ride?

Dr. Hedberg: Yeah. As far as the studies with celiac disease and EBV, there may be a connection there between when the patient was infected, if there’s actual reactivation of the Epstein-Barr virus and then the onset of celiac disease. Then of course, if you we’re taking direct tissue samples from the gut tissue in celiacs, they’ll find extremely high levels of Epstein-Barr virus in the follicles, in the guts, the patients with Celiac disease so…

Dr. Brady: You can argue, listen, this is a compromised patient with a dysfunctional immune system with a lot of inflammation there. This is an opportunistic passage and that’s ubiquitous, pretty much. Boom! It’s just flaring up because this person is compromised and it seizes opportunity. It’s not causing the problem. It’s just feasting on it, if you will. That’s…

Dr. Hedberg: Right. Right.

Dr. Brady: It’s going to be interesting when we know a little bit more how to answer those questions. Well, let’s say EBV is in play. Interesting, obviously, in integrative medicine, nutritional medicine, there are a lot of different ways we attack viral issues, acute and chronic, depending on the type of virus. With encapsulated viruses, you can use things that try to dissolve the encapsulation on the virus. You can use things that up-regulates natural killer cell function, direct immunity enhancers, direct antiseptic steps, there’s a lot of different things you can do. What do you do and what do you have success with?

Dr. Hedberg: Right. So everything else aside, everything else that we do on functional medicine, once we’ve done all that or we are doing it, then we want to go and directly target the Epstein-Barr virus. So the first is we’d like to use monolaurin which is a fatty ester. It dissolves the fatty acid envelope around the virus and that basically exposes it to the immune system. It takes away its stealth abilities. Now, we do that in a pyramid-style. Start out very slowly with the monolauric acid and then you build up to extremely high levels and then taper back down.

Dr. Brady: What kind of dosing are you talking about where you start the high level and then… you know.

Dr. Hedberg: Yeah. So we’ll just start at 600mg three times a day. Each capsule, 600mg and you’ll slowly work up to three capsules, three times a day. So you are up to nine capsules a day at the top of the pyramid, so to speak, and then working your way back down to two or three as far as maintenance goes. That’s done over about a four to six week period.

Herbally, there’s tremendous amount of things that you can use. The first one, one of my favorites is Larrea tridentata also known as chaparral. That was used a lot by the Native Americans for infections, but there’s been some really good research on Larrea and it’s deactivation of the herpes virus. The second one is olive leaf extract, just a classic anti-viral, also a good anti-bacterial. And then one of my favorites is reishi mushroom. The thing about reishi is that it does stimulate the immune system, but it also contains what are called triterpenes. The triterpenes have been shown to directly deactivate the Epstein-Barr virus. So you get kind of a nice stand on there. You get support of the immune system and you get direct action on the Epstein-Barr virus. Schisandra berry’s good and moranga, also known as milkweed is another great herb.

Then just some other great antivirals are, of course, lysine, the amino acids, zinc, vitamin C, quercetin, and actually, silver, silvercillin, colloidal silver, the silver products are excellent in some cases for these viruses as well.

Dr. Brady: What about the other mushroom fractions that are in NK cell pushers, you said ray-shaped, but what about maitake, take, all of those kinds of things?

Dr. Hedberg: I’ve never used any of those, but I’m sure they are very effective. It would be interesting to see if they have like the triterpenes or any other compounds that directly affect the virus as well.

Dr. Brady: What about Larch?

Dr. Hedberg: Yeah. That’s a great compound for the immune system. I haven’t’ used it really in practice, but I’m sure that could work well, too.

Dr. Brady: Then how about beta-1, 3-glucan, have you used that at all?

Dr. Hedberg: I haven’t just used it by itself. I know that the mushrooms contain glucans, and so they’re just kind of being used there indirectly. That brings up another point. I think a lot of practitioners might be scared to use immune stimulants in autoimmune disease, but…

Dr. Brady: That was the next question.

Dr. Hedberg: I just really haven’t seen that clinically. They get concerned about the whole TH1/TH2 balance, stimulating one side or the other. But I haven’t really seen it exacerbate people especially with the reishi mushroom which is a pretty strong TH1 stimulant. In some cases, they’d say, “Well, if the autoimmunity is TH1-driven, then you shouldn’t drive further,” but… There are some really good papers out there.

Dr. Brady: that are really complex substances tend to have a balancing effect, not heavy-handed one side or the other. Even that whole classification system of TH1-dominant, TH2-dominant autoimmunity, if you really look at the research, a lot of that is kind of falling by the wayside a little bit as we learn more about the complexity of the immune bonds. Not totally, but it is being chipped away to a large degree.

Dr. Hedberg: I agree.

Dr. Brady: Just before we go into questions, because we’re getting late, any kind of interesting cases where you’ve had success with this approach or anything there?

Dr. Hedberg: Yeah. This was a woman in her early 30s who developed Hashimoto’s thyroiditis and alopecia areata, and for those of you who don’t know, the alopecia, people start losing these big patches of hair. This woman came in and she just had these just large bald parts on her head from the hair loss, because it is an autoimmune condition. She had been gluten-free for about two and a half years, with doing vitamin D, had gone through some protocols, tried a lot of things, a lot of things that are done in functional medicine. We just looked a little bit deeper and the EBV was in fact active in her and we didn’t really do a lot. She had already tried so much so when patients come in like that, we don’t want to redo things that they’d done before.

So really, we just focused on the Epstein-Barr virus. And within about six weeks, the hair started growing back. She had started feeling much, much, much better. I’m actually going to write this up with some photographs, before and after of the hair, the bald parts and then it all filling in. She’s feeling great now. The hair is back. Like I said, we didn’t really do a whole lot. We just worked on the Epstein-Barr virus and we just used the monolaurin and the reishi and really, that was it. It’s really fascinating where you can go in and you can just use two products, two supplements, nothing else and really turn someone around. They’re obviously not all like that, and they’re not all that easy, but that was just a really, really interesting case and a direct connection there with the EBV.

Dr. Brady: Now, you mentioned some of the standard testing that Quest, LabCorp or whatever, the EBV titer test that you can get through the commercial labs, are they of value, are they usually high when there’s a significant problem or in your…?

Dr. Hedberg: Yeah. LabCorp & Quest and labs like that, they have an EBV profile and they have a little chart with positives and minuses and it says it’s active or it’s a past infection or it’s reactivated. But I have a paper that was published, I believe it was last year, I can send this to you, it’s a complete review of how to interpret an Epstein-Barr virus profile. So you look at the paper and you look at what the labs are offering and they just don’t click, because they leave out the IgMs of the nuclear antigen and the early antigen. So you’re not really getting the whole picture with their standard profile, so you have to add the IgMs in. When you see the IgM, that’s an excellent indication that there’s reactivation. You’re going to see high IgGs in everyone, because everybody has it. So you are looking for the IgM for a reactivation.

Dr. Brady: Yes. If you can send me that paper, Nick and send it to our people to post to the calls, so the download for the call, you’ll be able to find the supporting documents, of course, and we’ll put that one up there as well. Well, before we go to questions, tell us a little bit more about, I know you’ve been running some postgraduate kind of education courses through your infectionconnection.net for people who want to dive a little deeper into some of these specific concepts. You want to just tell everyone about that.

Dr. Hedberg: Yeah. So this just basically stemmed out of just a lack of really good educational material out there on this topic, studying functional medicine, going to seminars, things like that. A lot of the training just sort of kind of glanced over it, mentioned it, not a lot of details. So I just put together this course online and we just get heavily into Lyme disease and co-infections, viruses, parasites, just all the infections that are out there and their connection with autoimmune diseases and chronic illness and then we get into how to manage these patients and how to identify if an infection is truly there and we have a forum. And I’m going to be updating this on a regular basis as we learn more. It’s at infectionconnection.net. People who have signed up so far, they are really enjoying it at this point.

Dr. Brady: Can they find your thyroid book there as well or is that a different place?

Dr. Hedberg: Yeah. The thyroid book is on amazon.com. Then anyone who has signed up for the course, I just send them a copy, complimentary.

Dr. Brady: Good. Okay. It’s “The Thyroid Alternative,” right? That’s what they would search.

Dr. Hedberg: Yeah. Yeah. “The Thyroid Alternative,” it’s on kindle now, too.

Dr. Brady: Let’s go to questions if you have some time. Is that okay?

Dr. Hedberg: Great. Yeah. Plenty of time.

Female: I was just wondering if when you go through the whole procedure of reducing this Epstein-Barr, do you have to stay on a maintenance for the rest of their life or…?

Dr. Hedberg: That’s a really good question. Like I mentioned earlier, we talked about the antivirals that we use and things like that, and if I just preface that by saying that we’re already doing everything else, because a healthy, robust immune system should be able to maintain the infection. So after you’ve done everything else, optimized gut function, amino acids, vitamin D, all those things that we do on functional medicine, as long as they can maintain health and keep their stress levels very low, no, they don’t have to stay on something forever. There are some cases though where people just feel better taking something to suppress the infection and keep it at bay. The answer to the question, that’s just really going to be based on the individual, sometimes yes, sometimes no.

Female: Thank you.

Male: I have CIDP, chronic inflammatory demyelinating polyneuropathy, have you seen any patients with this disease with the Epstein-Barr and I’m just wondering what the results were with your treatments in these cases. Thank you.

Dr. Hedberg: I’ve never seen a patient with that condition. I know that there is research out there on H. pylori and that particular condition and I also believe herpes 6 and possibly some other viruses, but I can’t remember directly off the top of my head. So yeah, there is research out there on some connections there, but I don’t have any personal experience with that condition.

Male: Thank you.

Female: I was wondering if you have been using any of these genetic panels now available to look at people’s predispositions to being more susceptible to these reactivations of viral infections or being unable to feel the infections.

Dr. Hedberg: No. I haven’t done any of that testing. I don’t have any experience with it.

Dr. Brady: Are you talking about genetic SNPs of some kind or are you talking about predictive autoantibody?

Female 2: More the genetic SNPs. There seems to be some that deal with people not being able to — like zinc wasters, people that just can’t handle, that need a lot more zinc than typical or there seems to be… as I’m learning there’s these generic SNPs that seem to make people more course of detoxification, but also in terms of susceptibility to immunity issues.

Dr. Hedberg: Does the genetic testing change how you would treat the patient? If they have a generic predisposition, is there anything that you can do about it?

Female: Yeah. I think so. I think the whole area is still very new, but it looks like if people have certain, either heterozygotes or homozygotes issues because of these particular SNPs that, for instance, if they have this problem of the zinc that they’re going to need a lot more zinc than a typical patient to keep their immune system in a better place. I’m still learning, but I was just curios if that was something that you looked at all.

Dr. Hedberg: Yeah. It sounds very interesting.

Female: Yeah. There’s this one test out now called 23andMe which will look at basically all your raw data, but then knowing what’s what is still hard to figure out unless you have somebody that’s a little more knowledgeable and so I’m still learning, but I was just curious if you have looked at that as well yet.

Dr. Hedberg: Yeah. I’d like to learn more about it.

Female: Yeah. Okay. All right. I have more questions, I’ll come back around.

Dr. Brady: Thanks.

Female: Thanks.

Female: Hi. I would like for you to hit that estrogen component again. I was wondering also about the estrogen, the EBV and possibly herpes 2, if there’s a connection between all of that.

Dr. Hedberg: Yeah. Basically, the connection with the estrogen is inversely proportional to the cytotoxic CD8 T cell levels, so the higher the estrogen levels in a woman or even a man for that matter, the lower the cytotoxic CD8 T cell levels. Then when estrogen levels drop, the CD8 levels rise, so that’s the connection there. I haven’t read anything on estrogen and herpes 2.

Female: Okay. Thank you.

Dr. Brady: Thanks.

Dr. Hedberg: Thanks.

Male: Hi. When we are targeting the EBV with the monolaurin and the antivirals, do we have to worry about die-off reactions, and if so, what would you use for that?

Dr. Hedberg: Right. That’s one of the reasons why you do the pyramid scheme with the monolaurin. That’s why we just start out, two or three capsules a day and then you slowly build up and that eliminates any kind of die-off reaction. Then with any of the other herbs that we talked about, kind of the same thing, you can just start out slowly and work your way up.

Male: Okay. Great. Thank you.

Dr. Brady: If refer to it as the pyramid scheme with the patient, they might get

Dr. Hedberg: Yeah. Yeah.

Todd: Hi Nikolas, this is Todd LePine calling. Have you had any experience in reading a literature clinically with Epstein-Barr virus and DNA methylation, because apparently, in my reading of literature, the Epstein-Barr virus uses methylation of DNA to sort of hide itself from the immune system and a lot of us are using folic acid, activated folate supplement? Do you know of anything on a literature or clinically related to possibly looking at taking script, Epstein-Barr virus versus maybe MTHFR? Is there any connection there? And then, one other side question is have you found the monolaurin as effective for some patients using antiviral Valtrex?

Dr. Hedberg: We do run the MTHFR blood test for the folate metabolism polymorphism. Doing that sometimes, usually 5000 to 10,000 micrograms a day, and then also looking at the mean corpuscular volume and the methylmalonic acid, forming glutamates, seeing if there’re any issues there. I’m just trying to think off the top of my head if I’ve seen any correlations there. Obviously, not in every one, but it is there sometimes. Now, my understanding of Valtrex, I’m a non-prescribing physician, so I’ve never used it, but my understanding is that it also destroys the host cell which may or may not be a bad thing. I know that it works. I know that it’s highly effective for herpes viruses, so it may be effective for EBV as well.

Todd: Great. Thank you.

Dr. Brady: Hey, Todd, are you still there?

Todd: Yes.

Dr. Brady: With the stuff relating to methylation, they are saying that methylation is used by EBV to sort of stay still. Does that mean that the more the better or the more efficient you are as a methylator, the more the EBV has a way to survive? Would polymorphism be a good thing or a bad thing? I’m kind of confused by that.

Todd: Yeah. I’m not exactly sure either, but apparently my reading, and I can actually send this to you, Dave, you can actually put it on the web after the conference call, is that when DNA is methylated, it sort of goes silent. Apparently, the Epstein-Barr virus can actually utilize methylation pathways such that it silences the body’s own immune system so it can state more stealth. That’s my understanding.

Dr. Brady: Beside Todd, you know how I love to find issues like with polymorphisms or pathologies where they actually serve a purpose. I love that whole concept, survival of the sickest. Why we need all these stuff we think of as being really bad and none of us should have it. A lot of the times, there’s a method to the madness.

Todd: Exactly. Exactly. Yeah. I’ll forward to both of you.

Dr. Hedberg: Yeah. That’s fascinating. I’d like to read about that.

Female: Hi. Thanks so much for the great talk. I just had a question about… to kind of clarify you’re your testing. Do you even bother with the EBV titer profiles that just leaves out the IgM or do you still do that and then do just the CD4/CD8 ratio or are there other things you do to kind of confirm the EBV?

Dr. Hedberg: Just I run the all the IgG and IGMs that are available. The CD4/CD8 ratio, I don’t run those anymore. Just because, when you kind of know what it’s going to look like, there’s no real reason to run it. The other one I forgot to mention is the CD57 which I’ve always for Lyme disease, but I just started using it for just any kind of chronic infection. If there’s almost no chance that the patient has Lyme, I am seeing very low CD57 counts in a lot of these reactivated Epstein-Barr virus patients. So that’s another thing that I’m looking at.

Female: Okay. Thank you.

Dr. Hedberg: Thanks.

Male: Yeah. I have two quick questions. One, if one has a positive EBV antibodies and is symptomatic, are you assuming there’s an autoimmune condition present? Number two, is there any known relationship between diabetes type 1 and stealth infections?

Dr. Hedberg: Right. So if someone has an activated EBV infection, then that does not necessarily mean they have an autoimmune disease. So that it could be active and there’s no autoimmunity. I’m sorry, what was the second part of that?

Male 6: Is there any known relationship between Diabetes Type 1 and Stealth Infections?

Dr. Hedberg: Yeah. I have quite a few papers on that, Type 1 diabetes, various viruses especially through sensitivities, of course, mercury…

Dr. Brady: Or vinoburic peptides, very strong in genetic or individuals. There’s a lot of stuff on viruses, too.

Dr. Hedberg: Yeah. Lots of , cow’s milk.

Male: Right. Okay. Very good. Thank you.

Dr. Hedberg: Thanks.

Female: Hi. My question is about thyroid receptor and sensitivity. I’m an acupuncturist and I see a lot of patients whose thyroid treatment just isn’t working. They still have full blown hypothyroid symptoms. Some of those are on standard thyroid replacement and I try to direct them to better care, but some of them are on updated and a prescription, custom compounded prescription and still they’ve got the hypothyroid symptoms. Do these people have poor receptor sensitivity and if so, what’s it do to, is it the toxic, allergic, infectious causes and what can be done about it?

Dr. Hedberg: Thyroid disrupting chemicals, kind of affect the thyroid receptor, it’s really difficult to pinpoint. There’s chemical toxic to thyroid receptor. But the other thing that I’ve been looking at a lot is the total T3 to the reverse T3 ratio and I’m seeing a lot of these where, obviously, the reverse T3 is high. And that can make the numbers look fine, but the patient still has severe signs of hypothyroidism. So we divide the total T3 divided by the reverse T3 and looking for a number between 10 to 14, and a lot of times, it’s going to come in lower than that. So that can be an indicator that they just need more T3, and by pushing the T3, you are obviously making more available to the thyroid receptors, and then you will also push down the reverse T3 by doing that. So that’s just the kind of approached that I’ve been using that’s been working pretty well.

Female: To paraphrase, you said total T3 to reverse T3 ratio, not 3T3 to reverse 3T3 ratio.

Dr. Hedberg: Right. Yeah. Not, the total T3 and dividing that by the reverse T3.

Female: Very interesting.

Dr. Brady: Thank you.

Female: Thank you.

Dr. Hedberg: Thanks.

Female: I wanted to ask what lab you use for all the IgMs and IgG testing board that you do get.

Dr. Hedberg: I use medical diagnostic laboratories. They’ll do the IgG and IgMs for the nuclear antigen and viral capsid antigen and the early antigen.

Female: Okay. All right. Can you just review this, total T3 to reverse T3 ratio? You said you want it to be about 10 to 14?

Dr. Hedberg: Exactly. Yeah.

Female: In another word, if it’s more than that, it’s a problem or if it’s less than that? Explain that a little.

Dr. Hedberg: If it’s less than that. So what you’re going to see is a lot of them are going to come in between four and eight. So we’ll consider that low and it’s just going to function much, much better if it’s between 10 and 14.

Female: Okay. Okay, I got it. Okay. All right very good. Thank you.

Dr. Brady: Great. Thank you.

Dr. Hedberg: Thanks.

Dr. Hedberg: Okay. Well, great. Thank you, Nick. Wonderful Clinical Rounds call again. We really appreciate you taking your time this evening to be with us and I’m sure you’ll be with us again soon. Wanted to remind everybody, if you’re at HIS, in New York, coming up here during the first weekend in March, come say hi. I’ll be speaking on Saturday the 2nd, in the morning, on this very topic on autoimmunity. We have Core III on Autoimmune Conditions and Stealth Infections in South Florida in the Fort Lauderdale-Hollywood area on March 23rd and then in Philadelphia in June. Andy, do you have that date? I don’t remember off the top of my head.

Andy: Yeah. It’s actually June 15th.

Dr. Brady: June 15th. Then we have our Thyroid, Adrenal Thyroid, Diobesity Core II seminar with Dr. Alan Weiss and Becky Murray. And what was the date of that Andy?

Andy: That is going to be April 6th in Nashville.

Dr. Brady: April 6th in Nashville. Great and then, Glacier Fest, of course, come join us at Glacier Fest and first weekend in August and we really appreciate everyone being on Clinical Rounds and we’ll have another great call for you next Wednesday night. So thank you, everybody, and goodnight.

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