Recently I interviewed Dr. Nikolas Hedberg, as we chatted about infections in Graves’ disease and Hashimoto’s, and below is the written transcript. If you would prefer to watch the interview you can access it by Clicking Here [1]:
With me, I have Dr. Nikolas Hedberg. Dr. Hedberg, we are going to discuss infections and thyroid health. How are you doing today, Dr. Hedberg?
Dr. Nikolas Hedberg: Great. Thanks for having me on.
Dr. Eric: You are welcome. Thank you for being on. Before we start, I am going to dive into Dr. Hedberg’s bio. He is a chiropractic physician, a board-certified chiropractic internist, board certified in nutrition by the American Clinical Board of Nutrition, and an herbal medicine fellow. Dr. Hedberg is also the founder of the Immune Restoration Center in Asheville, North Carolina, where he consults with patients worldwide. He is the founder of the Hedberg Institute, an online functional medicine education platform for practitioners of all types who want to build a highly effective and successful functional medicine practice. He has also been a speaker for many years in the functional medicine arena, presenting on autoimmune disease and the connection between infections and chronic illness, which is what we’ll be discussing here. He is also the author of the book The Complete Thyroid Health and Diet Guide, a comprehensive guide to understanding thyroid disorders from a functional medicine perspective.
Doc, if you don’t mind, I’d like you to start out by discussing your background, how you started working with people who have autoimmune thyroid conditions with more of a focus- Currently, you focus a lot on infections. Of course, with Hashimoto’s or Graves’, if they have infections, that’s a potential trigger. Why don’t you tell everyone how you got started?
Dr. Nikolas: I first started practicing 18 years ago. I was building my practice and giving lectures around Asheville. I realized that the thyroid lectures always drew standing room only crowds compared to all of the other illnesses I was talking about. I knew there was something there that I really had to look into. Patients started coming in who were taking Synthroid, and it really wasn’t working, not feeling much better. The combination of those two factors drove me into the direction of focusing on thyroid.
Once you start to focus on thyroid, you realize the vast majority of people with hypothyroidism have Hashimoto’s Disease. There really is no medical treatment for Hashimoto’s. Those patients are really left without many answers from the conventional side of medicine. As you dig deeper into Hashimoto’s, you find out that a lot of practitioners are overlooking chronic stealth infections as the driver of autoimmunity. A lot of practitioners are focusing on important things like gut health and Vitamin D, but the infectious aspect, I found over the years, is usually overlooked. That has just always been a main interest of mine, the immune system, chronic infections, especially viruses. I am most interested in chronic viruses.
Dr. Eric: The same applies with Graves’. Most patients with hyperthyroidism have Graves’ Disease. People with Graves’ Disease tend to have viruses. This is not just my clinical experience, but in the literature, too, there is a correlation with both Graves’ and Hashimoto’s for different infections. Of course, we’ll talk about some of the different infections here.
Why don’t we start out by discussing how an infection can trigger an autoimmune thyroid condition such as Graves’ or Hashimoto’s?
Dr. Nikolas: The immunological description is very complex. There are six potential different mechanisms. I will break it down so that people can understand it and not go into tremendous technical detail.
Basically, your immune system recognizes viruses, bacteria, parasites, fungi, things like that. Those immune cells attack those particular microbes. In autoimmunity, the immune system is unfortunately making antibodies against your own tissue. For the thyroid, it’s thyroid tissue. There are particular types of infections that can look similar to thyroid tissue. The immune system is looking at amino acids. What those look like on the surfaces of particular infections and on the thyroid. It makes antibodies against whatever has those same amino acid sequences. That is basically how it happens.
There are other ways it can happen, such as there can be a pretty strong infection in a particular organ like the thyroid. There is a lot of debris in that area due to inflammation. In that soup, the mix of debris and infection and self tissue, the immune system gets confused, and it starts to tag the self tissue and the microbe that is in that particular organ as foreign. Both get attacked. That is called molecular mimicry. We have known about that for quite some time. Actually in about 1972, it was discovered that cytomegalovirus was connected to lupus. That was the first discovery. It’s not something new. That’s almost 50 years we have known about it. That’s basically how it works.
Dr. Eric: Besides potentially causing autoimmunity directly through that molecular mimicry mechanism, some pathogens, such as H-pylori and parasites can increase the intestinal permeability of the gut. Could that also be a mechanism, through the triad of autoimmunity? Maybe it’s not a trigger, but it’s making the person more susceptible.
Dr. Nikolas: Definitely. There are studies on intestinal permeability and leaky gut and direct connection with Hashimoto’s and other autoimmune diseases. You mentioned H-pylori. That is going to have an impact on multiple factors, not just in the gut, but in what micronutrients are being absorbed and utilized. Some of these infections can definitely affect the gut and create dysbiosis and increased permeability, and that can lead to autoimmunity.
Dr. Eric: Why don’t we talk about some of the different infections that you see more commonly in your practice with your patients? Or you could also in addition to that bring up those in the literature. I know yersinia enterocolitica is one associated with both Graves’ and Hashimoto’s. I can’t say I see a lot of patients with yersinia when I do testing. What are some of the more common infections that you see with your patients?
Dr. Nikolas: I’ll start with yersinia because unfortunately it’s missed very often in stool analysis. It hasto be tested in blood as well. IgG, IgM, and IgA antibodies. Often, you will see the stool analysis misses it, but it’s active through blood testing. That’s one connected to Graves’ and Hashimoto’s. The connection there is the surface proteins of yersinia look just like thyroid tissue.
H-pylori is another one that is very common. The connections with H-pylori and Graves’ are stronger than they are with Hashimoto’s, but there is definitely a connection with both. You can pick up H-pylori pretty accurately with a stool test, breath testing, or blood testing. A lot of the studies on H-pylori and autoimmune thyroid disease are usually in stool.
If you get deeper into the intestine, blastocystis hominis, there used to be just one case study published in the literature on this particular parasite and Hashimoto’s. A paper just came out either last year or the year before. A very good paper with direct connections showing blastocystis hominis is connected directly to Hashimoto’s. They went a little further and actually treated the blastocystis hominis, and the patient’s symptoms got much better. Their immune markers got much better. Their thyroid health got better by eradicating the parasite.
It’s one thing to identify a particular infection connection. The other is, can we actually do something about it? Will the patient get better if we get rid of it? Blastocystis hominis, in that case, it does. With H-pylori, there are some studies that show if you treat H-pylori, the patients can reduce their thyroid medication dose, and some of their thyroid markers can improve. That is another connection there as far as treating the particular microbe.
Outside of the gut, and sometimes inside, the main one is going to be Epstein-Barr virus. This is the most common virus in all types of autoimmune conditions. There is a lot of literature on Epstein-Barr virus and both Graves’ and Hashimoto’s. Those are the most common. There are a lot of other ones like HHV-6, Herpes 6. There are good studies on that with Hashimoto’s. Unfortunately, you can’t accurately test an adult for HHV-6 reactivation. It’s an ambiguous way to know if it’s reactivated or not. Viruses can transactivate each other, meaning if EBV reactivates, it can reactivate another virus like HHV-6 and vice versa. With all the herpes viruses, the functional medicine treatment for them, if you treat one, like Epstein-Barr, that will be effective for all types of herpes viruses. Even if you don’t know for certain if one of them is positive or not, if you treat one, you will be treating the other.
Dr. Eric: Do you usually treat the viruses with an antiviral herbal approach?
Dr. Nikolas: It’s a three-pronged approach. Especially the herpes viruses and Epstein-Barr, they rely on what’s called NF Kappa B, nuclear factor kappa B, which means there is inflammation. EBV relies on that to proliferate.
The first thing to do is to use some kind of anti-inflammatory that works on NF-Kappa B. The most common ones that I’ll use are curcumin, black cumin seed oil, resveratrol, quercetin. Those are all effective here.
The second prong is you want to support natural killer cells, CD8+ T cells, cytotoxic T cells that contribute things like EBV. To support those, you want to use a mushroom. I’ll usually use cordyceps and reishi. That’s the second way.
The third is with monolaurin, also known as lauric acid. This dissolves the fatty acid envelope around the virus, so it exposes it to the immune system, so it’snot as stealth without that.
Those are the three things I’ll do to approach chronic viruses like EBCV.
Dr. Eric: Regardless of whether it’s EBV or cytomegalovirus or another one like Parvo virus, that approach seems to help. With EBV on a blood test, if someone tests positive for EBV, the IgM antibodies, that’s more of an acute infection. Maybe when they first got it years ago, the IgM marker would show up. What’s your take on people who have IgG markers? Most people do have IgG. Do you pay attention to the three different IgG markers? I spoke with Dr. Kasia Kines, who wrote the book The Epstein-Barr Solution. She pays more attention to that early antigen antibody. Others are more focused on how high the antibodies are, like if they are in triple digits or undetectable. How do you interpret the EBV markers?
Dr. Nikolas: Let’s talk about what’s very clear in the literature on EBV diagnosis and interpretation. You’re right. The IgM is elevated during acute infection. On average, IgM is gone in about seven weeks. In the vast majority of people, that will not return for life.
The two IgGs that you’re talking about where people are looking for elevations, the nuclear antigen and the viral capsid antigen, those alone can’t tell you if there is reactivation. The only thing that can tell you there is a high viral load or high immune response. That doesn’t mean there is reactivation. You do have to mainly look at the IgG early antigen. Unfortunately, the major labs like Labcorp and Quest don’t have the early antigen on their standard panel. They just have the other three. You have to request to add the early antigen in. Labcorp used to include the early antigen for the last 16-17 years, and they just took it out a year or two ago. You do have to look at the early antigen.
A few caveats there: There are some individuals genetically who will just have elevated early antigen for life, IgG, even when the virus is no longer active. You do have to take that into account. Then it becomes more of a clinical diagnosis. You also have to look at the complete blood count, looking at the white blood count, neutrophils and lymphocyte ratios. If you see the lymphocyte screeping up toward neutrophils, that can be an indicator of chronic viral activity.
The early antigen, you could run it, and it could be high. But it takes about six months for the early antigen to calm down and become negative once the virus is successfully deactivated. You could also be in the middle of a successful deactivation of the virus, but it is still positive.
Those are all really important things to know, that alot of people aren’t looking at or don’t know. You don’t want to jump to conclusions if the early antigen is high.
Dr. Eric: Do you test for EBV and other viruses with pretty much all of your patients?
Dr. Nikolas: Not all of them. It depends on how ill they are. A lot of them come in and already have had EBV testing. 99.999% of the time, the early antigen is not included. A lot of times, if I am testing, I am just doing the early antigen, not looking at the other markers. I couldn’t give you an exact percentage, but the vast majority, I’m looking for viral activity in patients with autoimmunity. The vast majority come back positive.
Dr. Eric: Going back to the gut infections, you mentioned yersinia being positive more in the blood testing. When H-pylori is positive and you treat it, from what I understand, you don’t want to retest in the blood because those antibodies could take a while to get rid of. Is it the same with yersinia? If you detect that it’s positive in the blood, and you treat someone for it, do you just put them on the protocol for a specific amount of time? How does that work as far as the retesting for yersinia enterocolitica?
Dr. Nikolas: I had to call the lab. If you test yersinia through Labcorp, say, they send it out to a specialty lab called ARUP Lab. I called them and had a long conversation with a pathologist there. If you really want to know about laboratory diagnosis, you want to talk to pathologists. We talked about it for a while.
There is no real definitive way to be certain if the infection is successfully treated if any of the markers are still elevated or not. You run the IgG, the IgA, and IgM. Now you can be pretty confident with the IgM it will only be around for seven weeks. If you see that elevated, you know it’s arecent yersinia infection, so they got it from some contaminated food or water. Most of the time, you’re not going to see the IgM elevated. These people are chronic.
That leaves you with IgG or IgA. IgA can still be high if the yersinia is successfully eradicated. It can take a long time, over a year, for that to become negative.
The IgG is the last thing to look at. Once they have had it, that can actually go away completely. It’s different from a lot of IgG tests, where usually they’re elevated for life once someone has had it. Someone can have a negative IgG test in this case. The main purpose of the blood test is to identify if they have it, and if it’s relatively recent. If you see both the IgG and the IgA are both positive, that’s a really strong indicator that it is an active infection.
Dr. Eric: With H-pylori, how commonly do you see that in your patients?
Dr. Nikolas: It’s very common because of my patient population with Hashimoto’s. Probably anywhere from 60-80%, somewhere in that range, it’s positive. H-pylori is a little bit tricky with the interpretation. Especially if you are doing stool testing. I use the GI map from Diagnostic Solutions. I’ve had long conversations with the lab developers there. It becomes a clinical diagnosis if you see it. You will see a particular number. That does mean there is some H-pylori, there is some activity, which we would expect because such a large portion of the world has it.
The question is if it’s causing a problem. If it’s elevated, in the red, and the clinical picture fits with if they are having symptoms of H-pylori, then that’s the case where you would most likely want to treat it. But if they don’t have any gut symptoms at all and it’s high, I won’t do an extensive treatment for H-pylori just because of the lab tests if it doesn’t fit clinically. That’s how I approach those H-pylori markers.
Dr. Eric: When you do treat it, do you take more of a natural approach, or do you typically recommend the triple therapy consisting of antibiotics and the PPI?
Dr. Nikolas: I do a triple therapy approach with triple probiotics. I use a LactoBif blend, a saccharomyces boulardii, and a spore-based probiotic. I will use all three types. Strengthening stomach acid production, strengthening digestion, along with the probiotics is very effective for most people. If it isn’t, I would go in with a few herbal antibiotics for three or four weeks. That clears it out quite nicely.
Dr. Eric: Talking about symptoms, you mentioned that with H-pylori, you rely on the symptoms. Are there cases, when it comes to infections, where you don’t rely on symptoms, where it could potentially be a trigger, even if the person isn’t experiencing specific symptoms associated with that infection?
Dr. Nikolas: Yeah. Almost all of them, there could not be any symptoms. So HHV-6 and EBV, they might not really have any strong symptoms related to those viruses, but they are active. Yersinia, you can have yersinia in the gut, and it’s not causing any major symptoms. Again, H-pylori, if they don’t have the symptoms of it, but they have a very strong autoimmune response, and we are doing a lot of the things we would normally do, and they are not moving along the way we would like them to, I might go in there and do a trial and knock it out in three or four weeks. See if there is some improvement. You’re not really going to do any harm treating H-pylori alternatively because we’re not using antibiotics to damage the gut micro flora.
Thinking of other infections that are connected there, like Hepatitis C, there is a really strong connection between Hepatitis C and Hashimoto’s. Hepatitis C actually has a stronger connection with Hashimoto’s than any other infection that we know of. In fact, Hepatitis C can leave the liver and set up in the thyroid. It’s called an extra hepatic reservoir. It can drive autoimmunity there. Some people with Hep C, especially early on, don’t have any symptoms. It’s always a matter of doing some extensive investigation.
Dr. Eric: As far as the research, I don’t think there are any other parasites in the literature associated with either Graves’ or Hashimoto’s, but have you seen from a clinical perspective where, maybe not blastocystis hominis, but maybe another parasite is present, the person’s symptomatic, and that seems like it might be a trigger? You treat the parasite, and there is a positive correlation with their immune markers going down.
Dr. Nikolas: Yeah. Blastocystis hominis really is the only one that I have ever been able to find in the literature connected to thyroiditis of any kind. But hypothetically there would be some similarities with other types of parasites if you look at the blasto mechanism. Blastocystis hominis is going to drive TH17, which drives autoimmunity. People with parasites, not always, but a lot of them tend to have a TH2 polarization. When you successfully eliminate any kind of infection that is driving TH17 or a TH2 polarization, then theoretically, you would help the immune system and help autoimmunity. Again, no strong evidence to support that other than blastocystis hominis. I’m sure you’ve seen it, and I’ve seen it, and other practitioners have seen it, where you treat the parasite, and they do get much better.
Dr. Eric: Definitely. Of course, to be fair, many times, we’re working on other things, too. It’s not just the parasite. Sometimes it’s then difficult to make the connection, but there have been cases where I’m pretty sure it was due to a parasite that is not in the literature. That greatly helped. Thanks for sharing that.
Speaking of parasites, you said you do the GI Map, which I do as well. Would you agree that stool testing, it can be helpful, but also with parasites, it’s not perfect? Even though the GI map again is DNA-based. Arguably, it might be more accurate than other testing. Still, there is always a chance for a false negative, correct?
Dr. Nikolas: Yeah. I mean the way I explain it to patients is you have the villi in the intestine. The stool analysis, it’s mainly going to pick up the stool that is passing over the brush border of the intestine. You can have deeper infections deep in between the villi. You can have parasites in there, all kinds of things. There is no way to pick up everything that is in someone’s gut ona stool analysis. It’s just impossible. We can’t go by that exclusively just because of the depth of the spaces in between the villi.
Dr. Eric: After you treat someone for H-pylori or a parasite, it’s a little bit different with viruses, but specifically with the gut infections, do you usually retest after treatment, or do you rely mostly on the presentation of the person and some other markers like blood markers?
Dr. Nikolas: Early in my career, I would retest. As the years went on, I tested less and less. If the patient is feeling good and their symptoms are gone, I leave it up to the patient if they want to retest or not. I have some patients who really want to see on paper that everything is cleared out and they are going to be okay going forward. Other patients are feeling great. There aren’t any indications that they have any ongoing infections. I say, “You’re fine. You’re good to go. We don’t have to spend the money and retest.”
Dr. Eric: Do you use any biofilm disrupting agents, like N- acetylcysteine (NAC), or proteolytic enzymes when treating infections?
Dr. Nikolas: N-acetylcysteine the main one that I use for biofilms. The herbal medicines that I use pretty much all disrupt biofilms, if I am using something for an intestinal parasite or H-pylori or fungi. The triple probiotic approach plus the herbs, if it seems like a difficult case, then we use NAC, is all more than enough. There are products out there designed for biofilms. I’ve used those in the past. I didn’t really find an amplified successful outcome using those. The fewer the supplements, the better, is how I approach things. The things I do usually work well without using those extra products. They can definitely work, but the question for me is always, do I really need them in this particular patient?
Dr. Eric: Makes sense. Thanks for sharing that. How about stealth infections such as Lyme disease? Viruses could be considered those, too. Or co-infections such as Bartonella, babesia. Can those be potential triggers of autoimmune conditions?
Dr. Nikolas: The literature is weak on all the tick-borne infections. But there are a couple papers on Borrelia, the bacteria that causes Lyme disease and thyroiditis. Those are ambiguous. Any kind of strong infection that drives an immune response can potentially trigger autoimmunity. There are a lot of anecdotal reports of rickettsia, which is also transmitted through ticks, and other biting vectors as being connected to Hashimoto’s.
You do find in the Lyme community a fair number of them have autoimmune thyroid disease. Whether those are particular microbes from the tick, or is it just because their gut is so messed up from all the inflammation? Is it because they have been on so many antibiotics, which has caused dysbiosis and gut problems? Whether it’s all the inflammation, the stress of having Lyme disease. It could be any of those things. I can just say that the literature is pretty weak on the connections there, but you do see it a lot.
Dr. Eric: That is true. I was diagnosed with chronic Lyme three years ago. I have a history of Graves’. I was concerned it might retrigger it. Fortunately, it didn’t. I tested all the thyroid antibodies, not just the thyroid stimulating immunoglobulins.
You mentioned stress. One question is the impact of stress on infections, especially viruses. Do you agree that to some extent they are more opportunistic, if you could talk about the importance of optimizing one’s immune system health, such as improving adrenals and stress handling, how much overall does that help in preventing certain infections? Maybe not the gut infections, or maybe them as well. Especially viruses, stealth infections, Lyme disease.
Dr. Nikolas: Huge factor, not just because of what it does to the gut and the immune system, but lymphocytes have cortisol receptors on them. Chronic stress drives cortisol elevations. That causes down regulation of cortisol receptors on lymphocytes. The immune response becomes weak over time, the longer someone is under stress. That allows these opportunistic infections to grow. Stress is #1 in my practice, figuring out every potential possible stress input to the system and figuring out how to mitigate that. You won’t really get great results unless you’re addressing all those factors.
Also, adrenaline drives histamine. Histamine drives chronic viral activity. Adrenaline and cortisol both drive TH2 polarization, which drives TH17. Unfortunately, TH17 cells are the major drivers of autoimmunity. Whenever it comes to the immune system, there are always multiple factors there. You can draw out all the connections, and it looks like a big web. Stress is one of the most important fundamental aspects of chronic infections and autoimmunity.
Dr. Eric: I definitely agree with that. I had a case of shingles a few years ago, too. I’m pretty sure that was just due to a ton of stress that summer. I agree. Stress management, getting proper sleep, extremely important. Diet, lifestyle factors, very important.
All right, thanks, Dr. Hedberg. I appreciate you sharing all this information. It was great chatting with you about infections. Could you share with the audience where they could find out more about you?
Dr. Nikolas:My website is DrHedberg.com. That is where I have my articles and my podcast. That’s for potential patients. The Hedberg Institute at HedbergInstitute.com is for functional medicine practitioners. I have functional medicine courses there that they can sign up for and learn how toeffectively treat all these conditions that we’ve talked about.
Dr. Eric: Again, thanks, doc. Appreciate you taking the time to talk about infections. Hope everyone learned a lot.
Dr. Nikolas: Great, thanks for having me. Enjoyed it.