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Below is a transcript of the interview with Dr. Yanuck on a phased approach to COVID-19
Dr. Hedberg: Well, welcome, everyone, to Functional Medicine Research. I’m Dr. Hedberg. And I’m really looking forward to my conversation today with Dr. Sam Yanuck. And Dr. Yanuck is the CEO and Director of Education for cogenceimmunology.com. It’s an online functional immunology course whose growing community includes nearly 5,000 clinician participants from more than 60 countries around the world. He’s an adjunct assistant professor in the program on integrative medicine in the Department of Physical Medicine and Rehabilitation at the University of North Carolina School of Medicine where he teaches topics in functional immunology. Dr. Yanuck is clinical director of the Yanuck Center for Life and Health, a functional medicine clinic in Chapel Hill, North Carolina where he sees patients with complex autoimmune disorders and other immunologically challenging cases. Dr. Yanuck has been seeing patients from everywhere since 1992. He also provides online consultations to clinicians around the world. And you can connect with the Yanuck Center at yanuckcenter.com. And today, we’re gonna be talking about Dr. Yanuck’s paper and his colleagues. They recently published a functional medicine perspective on COVID-19. And that paper is entitled “Evidence Supporting a Phased Immuno-Physiological Approach to COVID-19 From Prevention Through Recovery.” Dr. Yanuck, welcome to the show.
Dr. Yanuck: Thanks, Dr. Hedberg. It’s a pleasure to be here.
Dr. Hedberg: Great. So, this is an excellent paper outlining four phases of approach to COVID-19. Before we jump into those phases, why don’t we just talk a little bit about who is at the greatest risk of developing COVID-19? And what would make someone at a greater risk for contracting the virus and having a difficult time with this particular virus?
Dr. Yanuck: Sure. Well, this is really a moving multifactorial equation. There are ways that a person can be surprisingly predisposed to having a severe case of the illness that may not be obvious. Those are kind of wild cards that relate to things like antibodies against interferon, and so on. And so the challenge here is that we can come up with a sensible sort of view of who is and is not at higher risk, and yet, it’s important to understand that those views, those descriptions are going to be inherently imperfect because of this wildcard effect where there are cases that have been characterized where the idiosyncrasies of a person’s own diminished capacity to kill this kind of virus may only become apparent when the person is in the ICU, when the person gets the virus. And despite the fact that there are, you know, 22 or something, they may nonetheless have a terrible time of it and end up dying of COVID-19, surprisingly, despite not meeting the usual profiles. So, that’s kind of a caveat to any such attempt to describe or profile who is or is not at risk. And I can tell you just personally that I’m personally connected to someone, you know, by about a two-steps level of separation, a person who was, you know, feeling flu-like on a Friday. This is like a guy in his 40s who’s healthy and fit and so on. Feeling flu-like on a Friday and found dead on Monday.
So, that’s a kind of a cautionary tale about any attempt to say, “Here’s who is and here’s who isn’t at risk.” Now, having said that, one of the main things about risk has to do with the way that the virus drives pro-inflammatory mechanisms that drive excessive clotting. So, in the SARS-CoV-2 virus, one of the key factors is that a mechanism called the inflammasome, which is this structure inside cells that turns on and starts pouring out inflammatory cytokines. When you have inflammasome activation, one of the things that that drives is an excessive clotting effect. And that clotting effect thickens the blood and yields micro-vascular damage. And if you get micro-vascular damage in your lung parenchyma in the substance of a lung, it means that you can’t circulate blood through the lung. And if that goes…if your ability to do that goes way down, then you can’t oxygenate your blood. And that’s where a lot of the real trouble comes in. Now, there are a lot of other parts of this we can talk about, but this is a very central part. Now, the kind of inflammation, in particular, that’s involved in COVID-19 is driven by something called the NLRP3 inflammasome. And so people who have other diseases known to involve the NLRP3 inflammasome are people who are likely to already be tipped in the direction of an overexpression of NLRP3 and therefore a greater susceptibility such that when they get the SARS-CoV-2 virus that causes the COVID-19 disease, the likelihood is that those folks would have a greater expression of disease, a more severe disease expression. And the people for whom NLRP3 expression is already likely upregulated are people who have obesity, hypertension, diabetes, chronic kidney disease, chronic liver disease. All of those are diseases driven by NLRP3 inflammasome activation.
Dr. Hedberg: Yeah. I mean, if you look at the landscape of the…well, you just take the U.S. population, it just seems like a recipe for some very difficult cases dealing with a virus like this if you just look at the sheer number of people who are obese, overweight, diabetic, inflamed going into this. It just seems like we’re… And I could be wrong, but we could be just one of the top, you know, populations in the world to be predisposed to having a difficult time with this virus just because of our health status. Do you have anything to add there?
Dr. Yanuck: Well, first, I think that’s exactly right. I think the way that we manage our food as a culture, as a society, and so on, has so many problems with it. One of the things that’s emerged in the past year or more, I suppose, that one of my co-authors, Dr. Joseph Pizzorno, has done a great job of bringing to our attention is that there’s a profound set of differences between organic and sort of what we would think of as regular food, but really is kind of industrial farm-style food. And he talks about the fact that if you compare organic, especially organic heirloom foods, sort of old cultivars, if you compare that with what we think of as regular food, which is more sort of industrially grown with pesticides and so on, that there’s been a decision along the way to only compare some nuts and bolts kinds of things like the vitamin and mineral content.
Well, the vitamin and mineral content is about the same. And there are, you know, fewer than 100 of those. So, that’s what gets measured and that’s the comparison that gets made and everyone says, “Well, it’s about the same, so what’s the big deal? Maybe, okay, there’s less pesticide, but whatever.” But what gets missed there is that the polyphenolic compounds and other bioactive compounds in organic and especially heirloom organic foods is enormously greater than in what we think of as regular foods. And what those substances do is that they reduce inflammation and they promote robustness of anti-pathogenic immune response. So, here you have a population of people who just, as you said, are eating crappy food, they’re eating deep-fried things, they’re eating, you know, glycemicaly dysregulated foods, they’re eating inflammatory foods. And not only are they in a nuts and bolts way eating problematic foods, but there’s this whole other layer of the process that we’re just coming to appreciate where when you eat foods that are, you know, the way food used to be, you get anti-inflammatory and anti-pathogenic chemistry built into your food in a way that’s highly protective, not just in relation to SARS-CoV-2, but across the board.
Dr. Hedberg: Why don’t we veer right into the paper now and begin with the prevention phase, talking about what we’re really looking to do as far as a foundational approach to preventing this illness. So, there’s probably some obvious things to a lot of the people out there like getting good sleep, managing stress, things like that. Can you talk about what we’re really looking to do in the prevention stage of this virus?
Dr. Yanuck: Sure. Well, the key thing is that if a person gets the SARS-CoV-2 virus and they have an expression of COVID-19 disease, and from a nomenclature point of view, this is the same as HIV is a virus and AIDS is a disease. There are people who have HIV virus who don’t express AIDS as a disease. Same thing. You can catch the virus and not have a full-on expression of the disease. The key thing is that a person who contracts the virus, if their starting point, from an inflammatory point of view, can be very, very modest, then there’s plenty of room as the immune system gets going to kill the virus, which is an inherently inflammatory thing to do. As that immune response gets going, you wanna have plenty of room to get inflamed enough to kill the virus without getting into a dangerous level of inflammation where you start getting the stuff I was talking about before with the blood getting thicker and the micro-vascular damage, and so on. So, at baseline in the prevention phase, it’s useful to think about ways to get rid of all the sources of non-purposeful inflammation. So, that would be just as you say, making sure that sleep is adequate, making sure that stress levels are low. And if the stress level can’t be modified in a fully efficient way, then you might consider giving a person adaptogens so that the person’s capacity for tolerating stress has increased and the extent of their manufacture of the chemistry of stress is diminished. So, stress is important to pay attention to. Making sure that their diet is low glycemic and doesn’t have a lot of alcohol, and so on. So, all of that is on the, you know, things to prevent…things to subtract, let’s say. Get rid of crappy stuff in the diet and so on.
And then you wanna consider some nutritional support. And by the way, it’s useful to say everything that we’re talking about is adjunctive. Right? Let me just sort of pause and talk about this for a moment. This is very important. In a functional medicine setting, since the people who are going to be, you know, listening to this and trying to understand some things about COVID-19. If the people listening are clinicians doing functional medicine, and I’m one of those, for example, we’re accustomed to working with patients at a certain pace. And there’s an expectation about the rhythm of the work. So, a person comes in, you may talk about some things, measure some things, and so on. And then you may say, “Okay. Here are some things to deploy as a strategy, land in my office again in a month, or let’s do a Zoom again in a month and you’ll tell me how you’re doing.” But it’s very important to understand that this virus can move very quickly. So, you have to be very light on your feet. You have to be very attentive to changes. So, I have patients email me a symptom inventory literally every day so that I understand what’s going on with the crescendo and decrescendo of their disease process. This is not something where you can just, you know, give somebody some ideas and send them on their way.
So, a lot of folks may decide that they don’t wanna engage with patients who have COVID-19 because it’s such a different style of work. The other thing to say is, this should really be adjunctive with their conventional care. It shouldn’t be instead of conventional care. What you’re trying to do is create a situation where the person has every possible advantage and the majority of the heavy lifting there is gonna be on the conventional side. So, what we’re trying to do is put people in a position where they’ve got optimized biology, optimized hematological function so that their conventional care can work most effectively or so that their cases are mild enough that they’re not having to use up resources in the conventional world that other folks could use who are in a more dire position. So, now having said that, nutritionally, in the prevention phase, the first thing to do is make sure that the person has adequate installation of things like vitamin A, D, C, zinc, fish oil, things like that, that have been shown in the research to have a very useful effect in modulating inflammatory process. So, you’re trying to help the person have a very modest baseline level of inflammation so, again, that there’s room for the crescendo decrescendo of their immune response against the virus. Now, some of these things like A, D, C, zinc, they have multiple roles. So, for example, vitamin D has been shown in the research to reduce inflammation, but vitamin D is also necessary for the production of lysosomal enzymes by macrophages. So, there are important ways in which you’ve got both an anti-inflammatory role and an immune-supportive role that’s very specific being accomplished by the same substance. And there are similar effects like that that relate to things like C, A, zinc, and so on.
Dr. Hedberg: Right. One of the things that has kind of worried me recently is the current, you know, plant-based movement. And I was glad to see that you pointed this out in your paper regarding beta carotene. And some people are just going to be poor converters of beta carotene to vitamin A. And so, like I said, you wrote about this in your paper. Anything you can think of for our, you know, vegan and vegetarian listeners to ensure healthy vitamin A levels if they’re not getting enough actual A from the diet?
Dr. Yanuck: Yeah. It’s a super interesting question. I mean, that question has a bunch of vectors from it, right? So, one thing is, when you have the ability to do lab work, to identify the actual levels of various substances, it’s very, very useful to do it. So, I always wanna know about A, D, C, RBC zinc levels. I wanna know about fatty acid balance. So, LabCorp and Quest have a very, very useful test called OmegaCheck that will tell you if you’ve got appropriate fatty acid balance. It’s surprising how many people do not. And so there may be a concern, let’s say, in a vegetarian that maybe there’s not enough A because that person has a genetic, like, gene defects related to beta-carotene monooxygenase 1, BCMO1. So, if a person has single nucleotide polymorphisms, SNPs, for BCMO1, then they’ll be potentially a poor converter of beta-carotene into vitamin A. Well, a blood test will show you what’s going on there. Not everybody with BCMO1 SNPs has low A. What you will see, though, is some people when they are doing poorly, biologically, when they’re having sort of a down phase in their biology, you can retest the A level and it will be much lower, suggesting that there are differences in epigenetic expression occurring at different times in the biology of that patient, and often corresponding with when that patient is doing poorly.
So, I would certainly also recommend genetic testing, and genetic testing that is, you know, thorough enough to tease out things like what we’re talking about here with A or with D or colleen or, of course, the other parts of methylation. And then also, sometimes you’ll see people, for example, who have a gain of function gene defect for interleukin 6. And interleukin 6 is a key mechanism by which that NLRP3 inflammasome is activating this clotting effect in blood. And that’s something else we can talk about in more detail if you want to. But back to the main question about, you know, vegans or vegetarians. I think lab testing is very, very important to see where people are, and especially things like B12 are very, very important in that regard as well. And you may not be able to get everything from food. I mean, patients will often say to me, and I think very appropriately, they’ll say, “Shouldn’t I just be able to get all this from my food?” And the answer ought to be yes, but the answer is no. And so if you don’t have any gene defects and if your stress level is not super high, and if you don’t live in a polluted world, and if you don’t live in a world where the food is depleted of nutrient density, and on and on, if all of those ifs were taken care of, then, yeah, you get all your nutrient density from food, you get everything from food. You don’t have to take any supplements. But that sort of idealized image may also get you a lifespan that’s more typical of the lifespans that people had back in the old days. Their food was much better, so that was good, but they had all these other disadvantages that shortened lifespan. So, it’s a very mixed… It’s a very mixed equation. Still, I think there is some intuitive appeal to the idea that we should get everything from food. It’s just not the reality now.
Dr. Hedberg: Let’s move into the infection phase. So, if we could talk a little bit of immunology. So, when this virus enters the respiratory tract and it binds to the lung epithelium, what exactly is happening immunologically at that point? What is the immune system doing? And what is it trying to do to the virus? And does the virus have any kind of evasion strategies?
Dr. Yanuck: Yeah, absolutely. So, early in the infectious phase, the main problem is that the virus will delay macrophage activation and will kill macrophages. So, you have the innate immune response and you have the adaptive immune response. And doing the heavy lifting in the innate immune response are the macrophages. Macrophage means big eater. So, these macrophages are very much front-line in the innate immune response which is the sort of right away immune response. The problem is that if the virus can delay responsiveness of macrophages and can even kill macrophages, then the first thing is that the virus will tend to get ahead of the immune response. That’s the first problem. The second problem is that if there’s a delay and if the populations of macrophages are being killed off, then what you have is the innate immune response may not be able to trigger an adequate adaptive immune response. And if you can’t trigger an adequate adaptive immune response, then the entire picture of the ability to respond becomes more muted.
So, this is crucial. There are studies that came out of China even in March, there’s a very good study in signal transduction on target therapies, March 27th of 2020, called lymphopenia, predicts disease severity of COVID-19. And what they found was that if they measured at time point number one in the patient’s lymphocytes, their TMB cells, if the patient had a differential white blood cell count greater than 20% lymphocytes, then they would do well. If they had less than 20%, then they would do a second-time point measurement. The first time point measurement was at day 10 to 12. Second-time point measurement, day 17 to 19. If at the second time point measurements they had greater than 20% lymphocytes, they would do well. And that meant that their adaptive immune response or TMB cells had come around. And so they were gonna be okay. If they had between 5% and 20% lymphocytes, they had more severe disease, but they could still be cured. If they had less than 5% lymphocytes, they were in the intensive care unit and they were in real trouble. So, the key thing then is that in the early stage, if the virus gets ahead of the immune response, ahead of the innate immune response, then you have the greater potential for trouble. Whereas if you can get the immune response going so that its crescendo is sooner and stronger than the crescendo of the viral population in the body, then you would do well. And this is largely a feature of getting the interferon response going. And the interferon response is largely a function of Th1 cells and also natural killer cells. These are the interferon gamma-producing cells that stir up the adequacy of the immune response to get that whole piece of the puzzle going.
Dr. Hedberg: I wanted to mention a paper. This was published this year out of Sweden. And they were looking at how pollen weakens the innate defense against respiratory viruses. And they found that just pollen independent of allergy puts people at a higher risk because there’s a significantly diminished interferon-gamma and pro-inflammatory chemokine response to viruses. And one of the lead authors, Dr. Dahl, out of Sweden, he made a statement that he’s found people with allergies tend to have the most difficult time with this particular virus. So, we might be looking at issues with Th2 here and its effects on Th1. Can you talk a little bit about how a Th2 dominance could potentially inhibit these mechanisms that you were just talking about in fighting a virus?
Dr. Yanuck: Yeah. Yeah. Certainly. So, a naive T cell is going to respond to the cytokines in the tissue environment. And particularly, the naive T cell is going to be instructed by dendritic cells that are handing that T cell fragments of antigen. And that T cell is going to multiply, it’s going to go back to the site of where the thing that got handed to it was harvested from. And the gist of it is that these T cells are in not a fixed and firm state forever, but they’re in a flow of oscillation. So, you have a T cell. And in the early 2000s, we used to think of this differently. We used to think that once a T cell became a Th2 cell, it was always and forever a Th2 cell as if it had been drafted by, you know, the New York Giants and so it would always wear a Giants’ jersey. But we know now that it’s more about an oscillating set of states. So, if a light blinks 100 times a second and 85 of those times it blinks blue and 15 times it blinks orange, pretty much that’s a blue light.
Now, there are reinforcing factors in the tissue chemistry for each of these T cell polarizations. So, a patient who has allergies or who has responses to environmental pathogens or even to food pathogens and so on, that’s a person who’s going to be generating chemistry that further entrenches Th2 dominance. That means there are going to be a lot of Th2 polarizing cytokines around. And all the T cells, even those that got influenced originally in a different polarization, all of the T cells will become the subject of that influence. And they may be flipped to Th2. Now, the problem is that Th2 cells make interleukin 4. And interleukin 4 inhibits the ability of Th1 cells to make interferon-gamma. And so people who are Th2 dominance have a poorer Th1 response. When you have a poor Th1 response, you can’t make interferon-gamma efficiently. But if you can’t make interferon-gamma, then you can’t spin up the antiviral immune response to the level you want it to be at, and so you’ll have a poorer outcome.
And so the question then becomes, what things make a person susceptible to being Th2 dominant? And it’s a whole range of things, right? And the simplest way to think about it is that problems involving hollow spaces tend to make people Th2 dominant. So, the sinuses, intestines, the lungs, vaginal tract, bladder. These are hollow spaces lined with epithelial cells. And in the context of chronic inflammation in those hollow spaces, the epithelial lining cells actually make Th2 cytokines that push a person further into Th2 dominance. The chemistry of stress induces apoptosis, which is programmed cell death of Th1 cells and natural killer cells. So, people who have chronic stress also end up being Th2 dominant. When a person gets a head injury, the outpouring of cortisol and norepinephrine, likewise induce programmed cell death of Th1 cells and natural killer cells. So, pesticide exposure is another one. People who live on golf courses who are essentially in a cloud of pesticide. Their glutathione levels go down. When the glutathione level goes down, you can’t have an efficient Th1 response. And there are other factors that go into it, but that’s a reasonable sort of shortlist.
Dr. Hedberg: Excellent. Right. And I’ve been reading a few papers, one just came out that I reported on. This was a gentleman in Singapore who developed the Hashimoto’s thyroiditis immediately following COVID-19. And so we’ve known since, I think, it’s about 1970 the connection between viruses and autoimmunity. And in this particular case, the authors do point out there were four other autoimmune disease connections that they’ve found thus far connected to this virus. Can you talk a little bit about how an infection like a virus can potentially trigger an autoimmune disease?
Dr. Yanuck: Sure. Yeah. And there’s a quick good paper on this called “Broadly-Targeted Autoreactivity is Common in Severe SARS-CoV-2 Infection” by Woodruff et al. So, as you said, I think, quite appropriately, we’ve known for a long time that viruses can be triggers of new autoimmune expression. And essentially, the thought process goes something like this. And I would say it’s more than a thought process at this point. I think it’s a pretty well-understood thing. So, you have virus in tissue. Excuse me. And the virus is going to induce some damage in that tissue. Now, whenever there’s damage to tissue, it’s the job of immune cells, white blood cells to come into the area and clean up. So, most simply put, cleaning up means that white blood cells are going to be in possession of self-tissue debris. And if mistakes are made, in signaling, about how to handle that debris and specifically, if the mistake is… So, think of that debris as the debris of pathogens instead of the debris of your own tissue, then the immune system essentially has decided that the thing it’s in possession of is something you should be fighting against. And that’s autoimmunity. Now, more specifically, an antigen-presenting cell, which is the kind of white blood cell we’re talking about, an antigen-presenting cell, and that antigen-presenting cell could be a dendritic cell or a macrophage, either of them do antigen presentation, the professional antigen-presenting cell is a dendritic cell. Now, let’s say a dendritic cell takes up some debris and now it has internalized that debris in a phagosome and it’s got a couple of different kinds of debris. It’s got virus and it’s got a fragment of self-tissue. Now, it has to hand the fragment of self-tissue to a T cell whose receptor matches that fragments of self-tissue. And it has to hand the virus to a T cell whose receptor is a shape-based match for the virus.
So, it’s done antigen presentation to two different T cells, one of which recognizes the self-tissue as antigen, one of which recognizes the virus as antigen. Now, we have a problem because this antigen-presenting cell now has to release some cytokines into the tissue environment and those cytokines are going to be signaling for either a kill signal or a tolerate signal. But that antigen-presenting cell has handed fragments of two very different things. And in one case, a kill signal would be appropriate. And in the other case, a tolerate signal would be appropriate. Now you can see where the trouble is gonna start coming in. If that antigen-presenting cell releases a kill signal, it’s telling the virus to kill the… Sorry. It’s telling the T cell that’s specific to the virus to kill the virus. That’s good. But it’s also telling the T cell that has the fragment of self-tissue to kill the self-tissue and now you have autoimmunity. Excuse me. Or if the signal that gets released is a tolerate signal, the T cell that’s in possession of self-tissue tolerate the self-tissue, that’s good, but the T cell in possession of virus tolerates the virus, and that’s not good. So, this is the inherent problem of viral illness that if it goes on long enough, you’re probably going to have some instances of each of these signaling choices and you’re gonna generate some autoimmune process along the way.
Dr. Hedberg: Excellent. Great explanation. Let’s get into the third phase. And so let’s say the virus has taken hold, so to speak, because there’s an insufficient type-one interferon response or the viral titer is too much for the immune system to deal with, and now we’re looking at what you with the other authors called escalating inflammation. So, once we’ve reached that point, how does this change our strategy as far as mitigating this illness and potentially enhancing the recovery period?
Dr. Yanuck: Yeah. Well, so, the challenge there is that if the immune response has spun up so much that now you have NLRP3 inflammasome activation that’s excessive and you have neutrophils releasing excessive amounts of what are called neutrophil extracellular traps or nets. The problem is that these nets which are part of the antimicrobial immune response, they also provide a third scaffold for clotting, right? So, you’re supposed to just have fibrin and you’re supposed to have Von Willebrand factor. But if you have the formation of these neutrophil extracellular traps, then you’ve got a third scaffold for clotting, and now you’re thickening up the blood, now you’re getting micro-vascular damage, now the lungs stop working, you get damage to the heart, the kidneys, and so on. You may have effects in brain as well. Microvasculature throughout the body is affected. The risk here is death. And also the risk is sequelae that we haven’t yet come to grips with, I think, from the point of view of understanding the long-term impacts of this disease on the population. So, whereas in the second phase, the infection phase, the goal clinically is to support the adequate activation of the Th1 response and the natural killer cell response. In the third phase, the escalating inflammation phase, the concern is that pushing too hard on that in the third phase would not be suitable. You have to back that off and push much harder on downregulating the pro-inflammatory mechanisms to try to move the patient away from the excess of expression of NLRP3 and neutrophil extracellular trap biology.
Dr. Hedberg: Right. So, the supplementation strategy that was used to enhance natural killer cells and supporting Th1, we would want to just discontinue at that point, but we could continue with our foundational supplementation, antioxidants, and anti-inflammatory support. Would that be correct?
Dr. Yanuck: Yeah. That’s absolutely right. And in fact, one of the things that runs all through here is the importance of glutathione because glutathione is normal to the body. And in this escalating inflammation phase, there’s a kind of a nasty cyclical co-activation cycle between NLRP3 and transforming growth factor-beta which ramps up fibrosis and reactive oxygen species formation because TGF beta and reactive oxygen species drive each other’s activation. So, you’ve got this NLRP3 mediated inflammation, and the NLRP3 also pushes the TGF beta mediated activation of fibroblasts, so now you have more fibrosis going on. The TGF beta also pushes reactive oxygen species formation. But ROS also has a feedback activation of TGF beta. So, the whole thing starts to spin up into the patient being too inflamed, having too much fibrosis, having too much reactive oxygen species activation, and, of course, the reactive oxygen species are gonna deplete the glutathione status. And the glutathione is anti-inflammatory and the glutathione is necessary for activation of Th1 response. So, throughout this process, glutathione is of enormous importance.
Dr. Hedberg: And once the inflammation has come down and the patient is entering the recovery period, are there any changes made during that period or is everything pretty much the same?
Dr. Yanuck: I think what’s crucial about the recovery phase is as you have this crescendo decrescendo in terms of disease severity, there is a tendency, I think, to think that when the patient feels like they’re coming through it and like they’re gonna be okay, there’s this tendency to think, “Okay. Game over. You win.” But during that decrescendo phase, there’s still plenty of active process going on so that if you were to draw a crescendo decrescendo curve on a piece of paper, you can see that even during that decrescendo, there’s plenty of area under that curve. It’s not a straight line drop vertically down to nothing. And that area under the curve represents a gradually fading but nonetheless important process during which the person can get more fibrosis and more scarring of tissue and more long-term loss of function. So, because inflammation and fibrosis are still pretty crucial there, I’m always inclined to keep the process going in terms of support to try to do as much as we can to down-regulate fibrosis and down-regulate inflammation. And from the point of view of the biology of fibrosis, that TGF beta fibroblasts mutually reinforcing loop is very important and is crucially driven by the reactive oxygen species. So, again, glutathione plays an important role there.
Dr. Hedberg: We’ve done a great job covering the four phases and your paper. Did you have any final thoughts for the listeners, anything new you’ve learned recently about the virus, any parting thoughts?
Dr. Yanuck: Well, I think, inevitably, part of this conversation has to do with what we should do as a strategy going forward not only about nutrition and so on, but from the point of view of how we should conduct ourselves. And I think it’s important to notice that we’ve been in a certain kind of ongoing experiments about how we handle it and how it turns out. And other countries likewise have been in similar experiments. I think the most interesting one is Taiwan. And Taiwan, you know, they have 23 million people. So, they are about one-17th the size of the U.S. And one of the interesting things about Taiwan is that their, I believe it’s the Vice Premier with a sort of the equivalent of our Vice President, is an epidemiologist. And so they handled the situation in a very, very different way than most countries did. Now, granted, Taiwan is an island, so it makes it easier from the point of view of control of ports of entry and so on. But they’ve had a total of 533 cases. And so it’s just interesting to see that we can do things that are very practical to influence the process in terms of the spread of the disease because the most decisive way to help patients not get into trouble with this is to have them not get infected in the first place.
Dr. Hedberg: Well said. Well, this has been really excellent. If you go to drhedberg.com and search for Dr. Yanuck, I will have links to his published paper and also his functional immunology course, cogenceimmunology.com, and his website, yanuckcenter.com. So, thanks for tuning in, everyone. This is Dr. Hedberg. Take care, and I will talk to you next time.