POST-COVID Research Drama & CV- Genetics for Bad Outcomes

This is contacttalkradio.com, consciousness in action, and you are taking action into your consciousness by tuning into Contact Talk Radio. And on tunein.com, ping.fm, and UpSnap Mobile. Contact Talk Radio. Welcome to Medicine and Health with Dr. Paul Anderson. This is a show about opening the often mysterious world of how doctors think and how science works. This program exists to educate and empower you, the listener. Now here's your host, Dr. Paul. All right, welcome. I'm Dr. Paul. Today we're going to talk about, uh, 2 COVID-related updates or summaries, etc. One is some, uh, drama in the research around post-COVID syndrome or post-acute COVID syndrome, etc. I want to kind of go through that because I had a lot of people, um, making comment on one or both of these studies, but also a bit confused. And then the other is, um, a little update through the last 3 years on the, uh, genetics and some of the associations that we see in the genetic profiles of people who do better and do maybe worse with a COVID infection. And so, uh, what I did is I chose sort of 3 generations of genetic information, and, uh, we're going to look at, uh, something published in 2020, 2021, and then just very, very recently, kind of see where they're thinking as far as that goes. But I want to get right into— let me get right into the world of post-COVID and the research around post- COVID syndrome. Some of the papers now will say post-acute COVID syndrome, which is a post-viral syndrome, as we've been talking about for 2 and a half years now on the channel. And, uh, 2 particular papers that were published— so one was published, uh, in March and one was published in May, so they're very, very, uh, recent. Of course, if you're listening live, it's June 30th, 2022. If If you're listening like on the podcast later, on YouTube, etc., it is whatever date it is for you. So keep in mind, everything that we're talking about here is up to date as of June 30th, 2022, and we'll get into it. Now, a couple of things to consider. One of them is that it's very obvious that there is a long COVID, COVID long haul, post-COVID syndrome, post-acute COVID syndrome, whatever you like to call it, uh, it's very well established that that does exist. Now, if we had other things that maybe went around the world, uh, and, uh, had as many people infected as we do with COVID We probably would have other named items where there is a post-infectious or post-viral syndrome, and we know that there are other things that have post-viral syndromes that go on with people. It's just that we've had a lot of people in the last, uh, year since 2019 infected with COVID and we have a reasonable percent of people— and the percent is not well known as far as exactly how many people have it and all that, and we've done other programs on that, you can go back and Look at those, but we know it's it's not zero; it's more than a few folks. So there were really two papers, and there's many now, but two papers that I think contrast one another. And what I wanted to do is talk about them not just from a dry point of view of well, this is sort of a research debate or how the research is done. We'll do a little bit of that, but because I talk to people and counsel other doctors and work with patients who have post-COVID. I wanted to really talk about the implications of these papers for both medical understanding, so the world of the physicians out there, and also then what does it mean to you patients if you're dealing with post-COVID syndrome? So what's the good and the bad that we can get from these papers? If we look at it, the first one I wanted to talk about is from May 2022. This is in the Annals of Internal Medicine, Drs. Sneller, Lang, et al. There's a number of people published on these papers, so we won't read all their names. I will on the YouTube channel, We move this over to YouTube, I'll put the links to all these things we're going to talk about today down in the description box. So if you're on your phone, it's usually a little down arrow or upside down, you know, V over on the right-hand side of the phone. If you're on your, you know, your computer or a larger device, it's often on the left-hand side, right down below the title, and it'll say more or show more. So if you're looking, that's where it is now. Just so that you know, you might be listening to this on the live feed on Facebook. You might be listening on our home network, which is CTR Radio Network, and you might be listening on one of the many pod burners that there are. We're on just about every podcast service. So all of those will not have show notes attached. The show notes I put onto the YouTube channel, and the YouTube channel is under DRA Online, Dr. A Online. And you can go over to YouTube and search that. And you usually will find me. You see my, my face there. Uh, if you don't find it there, you can go to my hub website, which is dranow.com, D-R-A-N-O-W dot com, and there's links to all of the media that I do, and YouTube is there. So if you're looking for these links, go to the YouTube channel and they'll be in the description. Now, why do I want to go in reverse time order? Because we have a May paper and Looks like a March paper here. Um, the reason is, is these are published contemporaneously. They're very, very close in publication time, and the work was done really at about the same time. And they have sort of 2 different, uh, points of view that they're offering. And the reason I want to go with the newer one first is it's making some waves that are making some of the post-COVID or long COVID community of patients a little worried. And I want to, I want to discuss why that is, why people would or might be worried, and also what the limitations of this study are and what it does and doesn't mean. Because as you can see, you know, when we're looking in today, we have this whole stack of research papers that I'm going to go through. As you know, on this program, sometimes we do a lot of research stuff, sometimes we just talk about things in general from the clinical point of view. So whenever you have these things come out in major publications like these, they can be very helpful to your healthcare providers. They can also be confused or misconstrued, and I think that the first one we're going to talk about might have something to do with that. So this first one is called the Longitudinal Study of COVID-19 Sequelae and Immunity. in Annals of Internal Medicine, published May 24th, 2022. And the thing that we're hearing about this and the concerns that come from it are they did a lot of testing. And if you look at this paper and if you look at everything that they did, they got into looking at so many biological markers and so many other things. that you might think, well, gee, there's almost nothing they didn't look at in here. And so when they come up with their conclusions, and the conclusions essentially say, um, that there is, based on the extensive diagnostic and other workup that they did looking at people with post-COVID syndrome or long COVID and controls which didn't have it, obviously Uh, that there are no specific causes of the reported symptoms in most cases. Okay, and then they go on to say that the only difference or correlation that they found in the post-COVID patients is they were more likely to be diagnosed in the past with an anxiety disorder. So what this is concerning a lot of folks in the long COVID community is that, uh, well, now they're, you know, we're going to get gaslit even more by our doctors because they're going to read this and say, well, you see right here, here's a, uh, you know, a study with, you know, a whole bunch of people that did the study and they measured all of these different biological markers and they didn't find any biological reason for post-COVID. And so a concern that comes up there is now, you know, your healthcare provider, your doctor may look at that and say, well, there might be other things to look at, or there may be other cause areas. And that would be really great because I'm going to propose that's what we do. But other doctors are looking at this and saying, well, see, here we have proof there is nothing to post-COVID, there's nothing to long COVID, and maybe, you know, maybe it's a neuropsychiatric problem or something like that. Well, you obviously have people who are quite ill, and you have people who have quite a bit of symptomatology and problems in post-COVID or long COVID. And so there obviously seems to be something more than a, you know, than a pure psychiatric diagnosis going on there. But why did this particular paper not come up with anything of substance? Well, a couple of things. The first thing is we have to look at what are the real gems of this paper. Well, a lot of the gems of this paper are all of the things that they did look at and thought, well, Group A doesn't have long COVID, they're the controls, and Group B does have long COVID, they are the study group, and we're going to compare them. And so we did all of these tests to see, is there a difference in the biochemistry and the biology of the people between the control group and the concern or the test group. And we looked and, you know, we don't see anything there that's different between the 2 groups. Well, a silver lining there is that they did test a whole lot of analytes, a whole lot of different factors. And when you don't see a difference from the group without the disease to the group with the disease, It's, uh, some evidence that that may not be part of what creates a disease. Now, one of the limitations is this was done in a certain time frame, and it is possible sometimes that you can test people either too early or too late to find a difference if you have 2 groups, especially with something dynamic like a post-viral syndrome. So there is a possibility there's a timing error here. Okay, there's also a really good bit of data that says maybe anything that they checked in here isn't normally a place we should look. But did they check actually everything in the world that you can check with people? The answer is no. So then the next level that we can get to and look at as far as what's going to help, etc., is are there things on here on this study that says there's no difference in what we, you know, all these tests that we ran on no COVID and people with long COVID? And there's all these things that don't seem to be in association. Well, the silver lining there is that might be the place then we don't start, all of those things that don't have a lot of difference between the two of them. And then It begs the question— 2 things really. One is, is anybody looking at the areas that this paper did not look at? And then the other question it begs is, what are the areas that this paper did not look at? Okay, so before we get into that, because no one paper can look at every variable and every analyte and everything— This reminds me a lot of a paper that I did a review on probably 10 years ago, long before the days of YouTube and me and, and, uh, and most of the other audio versions of me. Uh, but it was, it was an interesting paper about, uh, multiple chemical sensitivity patients, and they did all of this really intricate assessment of the multiple chemical sensitivity patient, uh, and then matched it to people who didn't have multiple chemical sensitivity. And they came up with a, um, uh, a note that said, well, there, there's no, uh, there's no obvious reason for multiple chemical sensitivity. And I laughed because, well, you know, of course there's multiple chemical sensitivities, a real problem. But if you are looking at it from a narrow point of view, if you're looking for the silver bullet to as the cause of multiple chemical sensitivity, you usually aren't going to find it, number one. And the same with long COVID, it's not one cause, right? But the other thing about that paper was when we did the review on it, we looked at it, we said, well, that's great. I mean, there's, there's some things that are not a factor in most people's multiple chemical sensitivity. But what didn't the paper look at? There was a whole bunch of other things that turned out to be the area where multiple chemical sensitivity comes from biologically. in humans, and those were areas that the paper didn't look at. Okay, they looked at logical things, just like this paper, didn't look at everything. So you always have to look at these things when they come out with, well, there's no association. And the first thing that you have to be careful of is not to say, well, then it's all in your head. And that's the medical gaslighting that we see a lot. And certainly not all healthcare providers are this way, and we should, you know, all of us healthcare providers should take what our patients say very seriously. and investigate it. But a lot of people are frustrated in the medical community by post-COVID because it's multifactorial. They want one cause, and they want one reason and one thing to treat, and that will never ever happen. It's the same as we see in chronic fatigue syndrome, fibromyalgia, and a number of other poly or multifactorial things They do these studies looking for, you know, the one thing we can go after, and it doesn't work that way because these problems are polyfactual or multifactorial, and the human is a very large number of variables biologically that can go right or wrong. So I do— before we get into the other paper, I just want to go through and go through, you know, they had about 100 and close to 190 people with documented, um, COVID-19, uh, that they started out with, um, and, uh, they had post-COVID in about, uh, half of those folks. And, uh, then they were looking and they said, well, the first thing was, what about the theory of persistent COVID infection? Meaning maybe these people with post-COVID just never cleared the COVID And essentially that was the first thing they looked at, and they showed that that really was not a factor. So persistent COVID infection was not a factor in anybody's symptomatology. And the next thing that, you know, they— and they go through, and this is a very long study with lots of charts and all of that, and they did a lot A lot, a lot, a lot of testing. They looked at a lot of different things. Um, and so some of the things that they looked at, just to summarize, that were not different: physical examination findings were largely the same in the control group and the, in the study group. Routine laboratory tests were the same in the control and the study group. Levels of inflammatory markers in the plasma were basically the same. Levels of biomarkers for heart and brain inflammation were roughly the same, or injury. Um, certain autoantibodies were same in both groups. Pulmonary function and other tests were normal in both groups. And then mild to moderate abnormality in lung and heart function were seen in both the normal groups and the abnormal groups. That wasn't a real discriminator there either. The other thing that they looked at was memory and neurocognitive scoring. That, that was the same. And when I say they looked at a lot of inflammatory— they looked at a ton of inflammatory markers that went along. So they did not see a difference. Okay, now they do come out and talk about some of the immunologic things. They say, well, there's this factor of immune persistence of COVID infection. And they said, well, you know, we don't see a persistent COVID infection in blood testing, etc. maybe there could be COVID in the deep tissues and it might be persisting there. They said, we, you know, they didn't test that because that would require biopsies of the inside of you, and they didn't want to go to that point. And, you know, there were a few other things like that that they said, you know, there's not a, not a huge bunch of discriminators. Now, one of the things that they did see was there's an enzyme, uh, and a particular subset of the T cells. So remember, we go back and you can go back in the YouTube archives and look at B and T cell differences, but the T cells are part of your cell-mediated immunity. And we know that they've been part of the resistance that we developed to COVID, but also part of the pathology we developed with COVID And it turned out there was a particular type of the CD4 4 subsets that, that did show a difference between the 2 groups. Now that's going to become important for the other paper we're going to look at. Okay, but basically when they get down, you know, to the end of it, you know, they say, well, we have some limitations. The first thing is, is that the patients in the study were largely moderate to mild illness patients. They didn't have a lot of hospitalized patients. And we do know one of the statistical things that we do know is that people who've been hospitalized are, are more likely to have post-COVID syndrome. Um, the other thing was that, uh, there may have been a little bias in the enrollment because you're more likely to get people who have post-COVID syndrome to enroll, uh, than, you know, your control group. And the other was that they didn't really match the control group to age or gender with the study group, and that can make a difference. So for example, let's say if all of my— and this is not what they had, but I'm just going to give you an example— let's say all of my people in my post-COVID study group were between the ages of 40 and 60 years old and were predominantly female, and then my control group was a group of people between the ages of 20 and 30 years old, and it was half males and half females, there could also be an artifact in there in saying these are not 2 equally matched groups that we can make a lot of conclusions about. And you could see that where if you have a group that is less statistically likely to develop post-COVID, and that's largely your control group, maybe the control group isn't a great control group. Okay, and there's no way to answer that question. They're just pointing out, well, you know, this might be one of the problems with the study. The other thing that they went on to say is that they, they recognize that this is very similar to things like chronic fatigue syndrome, other post-infectious disease syndromes, etc., and, and also certain mental-emotional disorders as well. So, you know, I think they did a good job of being self-critical. Uh, I think that we have to be careful of holding this study up and saying, see, there's, there's nothing wrong with you post-COVID people. That would not make any sense to me at all. Uh, what we do know is it's probably not these things that they looked at. Now, going back just a couple of months prior to that, so March 2022, uh, published in the journal Cell, That first one was in the Annals of Internal Medicine. Cell is another big-time journal. This is largely work done by people at the University of Washington, Swedish Medical Center, Fred Hutchinson, Stanford, a lot of groups that some of my old cancer research crossed over with a lot of the research groups that did this work here. These guys published, and they— the title is Multiple Early Factors Anticipate Post-Acute COVID-19 Sequelae. And so a sequelae is just anything that happens after a disease state because of the original disease. Well, that's interesting. So when they're looking here, they're saying a couple of things. One of them relates to the timing issue. So remember I said earlier that one thing that may be going on that we might want to keep an eye out on is we might be testing people too late after their illness. Okay. So one of the things that these guys did in their paper in Cell was to look for testing strategies that we might be able to test people on the front end. And people come into us and they say, uh, you know, I'm just getting over COVID, I'm concerned about long COVID, is there something we could look at? Okay. So this is more of a preventive strategy as opposed to a post hoc or an after disease strategy, which becomes very So the thing to keep in mind there is this is looking at different things, and of course it finds different conclusions. And so one of the things that you have to be thoughtful of is you, you can't really compare the outcome of 2 studies, even though they're about the same thing, if they're really looking at 2 totally different groupings of issues that go on. So again, what we can learn from this paper is, globally speaking, it would speak to the fact that there are things we probably should be thinking about. There are differences between, uh, non-post-COVID and post-COVID patients, and some of them are things that are— that were not looked at in the other paper, which would make total sense. If you got one paper that's done well and it doesn't find anything and it looked in area X, Y, and Z, but then the second paper finds things but it didn't look at X, Y, and Z, it looked at A, B, and C, you're looking at 2 totally different groupings of things to be looking for. Also, there's the timing issue where this one was really looking at what could we do early to be predictive of post-COVID so that we get the jump on the post-COVID and we don't have problems down the road. That becomes a very important thing. Now, in this group, they did find just like one of the factors was just like with other comorbidities of COVID proper, that one of the associations with people with post-COVID is more likely in somebody with type 2 diabetes. Now, type 2 diabetes is normally an acquired diabetes. It's a diabetes of insulin resistance. We used to call it adult onset diabetes. We don't anymore because children now have type 2 diabetes, sadly. It's a problem where your genetics and your dietary habits, et cetera, all collude to make you more and more insulin resistant, and it's, it's a continuum or a spectrum. The important part about that is that on that spectrum, in addition to this paper finding type 2 diabetes, which is a hard diagnosis, you could have some insulin sensitivity problems that are pre-diabetic, and you would be in the same boat. We've seen that with a lot of people. Insulin control, insulin management turns out to be— normally we're talking about dietarily here— one of the predictive factors of severity of COVID And it turns out that it's associated with people who are more likely to develop post-COVID. So that would be people who have more insulin resistance. They also had a shift in a particular type of SARS-CoV-2 um, analyte in the blood. Um, there was also a difference in Epstein-Barr virus, and that is the EBV, the Epstein-Barr virus, the virus that when you're young you get mono from it. You also can get other problems like chronic illness, etc. And, uh, that's the one where, you know, 95-plus percent of people are exposed to Epstein-Barr virus and have it at one level, but there's a fraction of people who become chronic reactivating Epstein-Barr patients. And those folks have a lot of other chronic issues if that happens. So it's not surprising to see that was more common. There were some other autoantibodies. Remember the first paper said they didn't find any autoantibodies, but they were looking at specific ones. These guys looked at different ones. Um, there is also, uh, what they call gastrointestinal post-acute COVID syndrome, uh, and I'm going to be doing an interview tomorrow, uh, about that and residual virus and stuff like that. Well, in those people, there was also an increase in the amount of the cousin of Epstein-Barr, cytomegalovirus, which we now know is a very common actor in systemic problems, but also in gastrointestinal problems, that was more common in the post-COVID people. The other thing though that I think is very important is that they— and I'll just read it here. We find that immunological associations between post-acute COVID factors diminish over time, leading to distinct convalescent immune states. So one of the things that they bring up in the paper is maybe if we test these things too late, you might be really sick, but your labs might go back to looking kind of normal. Whereas if we test you earlier, we might actually find some of these things going on. So I think that's an important distinction with this particular, with this particular study. Now, um, the numbers of the people in the 2 groups are similar to the first study that we talked about, but this, this paper has just a little bit more. So the numbers are, um, similar between the 2 papers. Okay, this paper by— and I'll have the link there, you can look, there's a whole lot of really nice, uh, uh, you know, numerical things that they did, a lot of good statistics. And a lot of association things that they brought up. So when they get down to the end and they're, they're talking about their, you know, discussion, they bring up a few things here. So we talked about pre-existing type 2 diabetes, Epstein-Barr, certain autoantibodies, and then the cytomegalovirus in the GI type. The other thing that they bring up is, is that there is an association with cortisol deficiency. And cortisol deficiency is something that we see that I talk about in post-COVID training that can be a acquired. So you can go into the disease with no cortisol problem, you can come out the other side with, with a low or high cortisol, which will give you symptoms. Okay, so this is one of the first papers I've seen where, where they really nail down that this is something that creates a problem. Now, we've talked about cortisol deficiency before, and one of the things that cortisol deficiency will do is it will predispose you to having unregulated or poorly regulated immune responses. And so the next thing that they bring up, although they, uh, they have them right next to each other but they're not drawing as much conclusion as I would, uh, is that, uh, people with post-COVID syndrome also have of a more uncontrolled inflammatory response to, uh, the infection. And you think, well, wouldn't it be good to have just as big of inflammatory response as you possibly could to any infection? And the answer actually is no. Uh, what you want is you want the early response to be real high and robust, then you want things like your endogenous cortisol in your body and other things to come in and level it level you out immunologically so you can fight without overdoing it. And so, uh, the combination of an acquired low cortisol and hyper-inflammatory state is, uh, the perfect storm for creating a lot of the post-COVID syndrome signs and symptoms, which I think is very important. Um, There's also things that they found about, you know, activation of essentially autoreactive T cells. So again, the first paper, there was a little bit of T cell stuff that they found. They weren't sure if it was different one side to the other. This one, there was definitely a difference that they saw. And then there were some other things that were found, but they would only be found if you tested the person early on, such as some of the inflammatory markers. This is another reason why you have 2 papers, and these 2 papers looked at a few things that were the same. They got different results, and part of it was because they looked at them at different times. And so what their, what their point here is, is that maybe what we should do is try and figure out, could preventively we look at the blood of people who have COVID and, and assess what's going on a little sooner before they've been sick for 6 months or a year or something of that nature? And let's see if there's anything else on here. So they, they go into limitations. One is that they were looking more at the short term and a shorter grouping. They had, you know, small triple-digit but small numbers like the other study, etc., etc. You know, so again, they're, they're trying to be self-critical there. Well, so what can we make of all that? Like, it's really kind of, you know, it's cool that we have these studies. It's frustrating that one is leading some doctors to say Well, then it must be all in their head, and the other one is saying, no, it's more complicated than that. And, you know, if you're already on the, on the fence and you're a clinician who's decided that post-COVID will just go away on its own and you don't want to deal with it, you're more likely to, you know, kind of hang your hat on that first paper and say, look, see, there's no, there's no biological difference between post-COVID and non-post-COVID. The second one is basically saying, yeah, there are differences the first paper didn't look at. And what the second paper is saying without really saying it is, we need a better way of assessing and treating folks who have long syndromes, whether it's Lyme complex illness, chronic fatigue syndrome, fibromyalgia. uh, long COVID, etc. We need a better way of dealing with and assessing all of these things. And so when we think about that, it makes a lot more sense. And this is something that we've talked about in other of the long COVID or post-COVID, uh, videos that I've done, has been my personal experience and actually the research that I see when I look at the big pool pool of research out there is that, number one, when we look at populations who don't have post-COVID and who do, that's an indication for us that, uh, we have areas we should or shouldn't maybe look in for the general public. So should we test everyone in the, you know, 40 different things the first paper did? when there really isn't a big difference? Probably not. But should we look to the things where there are differences, such as Epstein-Barr status, cortisol status, etc., that we find in the data, blood sugar control, etc.? Yeah, we should be looking at those things. But we need to take it a step further. And a step further is we need to also recognize that one thing that larger studies that look at big groups of people, uh, can kind of smooth over, which is good for some things, not good for other things, is that you as an individual might be what we call an outlier. And we have so many people with post-COVID, the numbers of people who are all going to be exactly the same in the middle of bell curve is going to be a certain number, but there's going to be room for more outliers out there. And what that means is that your own personal biology is going to be important in this, um, calculus of trying to figure out what's wrong with you. So the first thing that I would say is, if you are a post-COVID patient and you are being assessed by your healthcare providers, They need to take these things into consideration, but they also need to take your personal health history into account and your constitution, how your body works, into account. So when you're thinking about that, one of the things that you have to consider is the things that we do find as positive differentiators between a non- and, and a disease group. Those we should definitely be doing. Okay, so cortisol levels, uh, looking at Epstein-Barr and CMV status, other stuff like that that they found. But then there's other things such as the fact that just like with cortisol, you could go into COVID with your thyroid being totally normal, you come out the other end with something that we call thyroid resistance. And you have to do particular laboratory tests to look for thyroid resistance. Not everybody does that. There are also things such as we know, and if you go back and look at COVID and co-infections in the archives there, we know we've got papers, you know, there's well over 20 or 30 published papers now on co-infections with COVID but they're not all the same. So wherever you look for infections that happen with COVID or that COVID allows, you find them. And so there are certain viral infections, there are parasitic infections, there's bacterial infections. So one of the things that you then have to do with a patient is say, you know, where are their symptoms? Let's start out looking for the obvious things. The HHV family is well known now— the Epstein-Barr and cytomegalovirus. But if they have a lot of GI stuff beyond cytomegalovirus, maybe we need to look at some GI testing for pathogens, because pathogens that are going on a long time after you have COVID are going to cause problems. They cause a drain on your immune system, they cause their own symptoms, and they can make you have all sorts of symptomatology that if you don't look for them, you don't realize they're there. Chronic infectious things can create pain, they can create fatigue, sleep disturbances, any number of other problems that come along. Now there's other things that come up that, that were not directly looked into, which in more severe cases should be looked into. One is in the area of cellular function. It would be good then to know, you know, is there How are the mitochondria functioning? Is there damage to the cell's DNA? Those can be tested. In some cases, the status of your genomics can be important. There are certain nutrigenomic associations with fatigue and depression and other things that could be looked into. Most people by now have heard of things like the MTHFR and the methylation cycle and all of that. Well, there's things there and there's things related to that that can create problems as well. And that's something that if you already have the data is good to look at, but also if you have somebody who's not getting better, sometimes it's good to, you know, go down that road and look there. Then there are things beyond chronic infections and cell function and stuff like that. One of the things I talk about that was a little more theoretical in the early days, and now we're seeing it a little bit more, is it's possible for people during the COVID infection state, the acute COVID infection state, to uncover by becoming more sensitized to certain other stressors. One of those are environmental toxins. So in some people, they may have been more robustly strong before COVID and then they go and they get COVID, and it lowers their, their resistance to these things. So they're maybe exposed at the same level, but now they're sensitive to things. That could be things such as mycotoxins from mold, certain chemical toxins that we can get in our food and our water, and even some metal toxins, and those can be screened for as well. We talked about hormonal things like cortisol levels and thyroid resistance. Those are certainly, you know, in a long COVID patient, those are kind of non-negotiable things we should be looking at. But then other hormonal things can get thrown off as well. If you're 2, 3, 4 6, 12 months into a long COVID scenario. The longer you've been sick, the more of these things you need to look at. And that would also include broadening the hormonal look. So we now, from this and some other papers, have cortisol, something we should be checking. It's an easy blood test. I talked about thyroid resistance. Again, blood testing, fairly simple. to do that. But then if you've been sick a long time, you should probably have the reproductive hormones looked at because the balance between testosterone, estrogen, and progesterone can create a hyper-inflammatory state in the body. And none of them have really looked at that. But I found in some of the long COVID patients that those become very, very important long term. And then as you're going along, we, you know, we talked about digestive things. So there is a subset of post-COVID syndrome that is digestive, but sometimes you can have— because the digestive system has its own immune system and it absorbs your nutrients and everything, it can be messed up and it can make you kind of feel messed up in other parts of your, your biology as well. So the digestive system needs to be looked at. And then there are other things that can be contributory. So one contributory area is your physical function, right? So physical function being, you know, maybe this is not a cause of all of your problems, but because of being inflamed, because of being fatigued, because of not being well, your structural body may not be working like it used to. So working with somebody who does physical medicine to be assessed and see, you know, are you just all now tense and tight and that's where your headaches are coming from, or you're, you know, structurally not, you know, kind of moving the way that you used to, etc. Maybe, you know, those are things that ought to be looked into as well. And I would submit that they really should be. The other area, which is always you know, sort of touchy with some folks is the psychosocial or psychoemotional, neuroemotional area. Because as soon as you start talking about that, you know, someone will say, well, you're just saying this is all in my head. And no, that's not the case. Okay. If you come out the other side of an illness and you're still sick 3 months, 6 months, 12 months, 24 months later, You're going to develop— if you didn't have it before, you're going to develop a psycho-emotional, neuro-emotional issue or two. That could be a sleep disturbance, it could be anxiety, it could be depression, it could be all manner of things. So it's not to say that that is the ultimate cause, but if that is an effect of your illness, it needs to be dealt with. Because people who have developed anxiety disorder or depression or sleep disorder or any other thing, they are not going to heal and perceive their healing the same way that other people do. So it becomes very, very important to look holistically at the whole person, which is what holism means. So I think those are important parts to think about with those 2 papers. So just remember, and I'll put the links to these in if you want to read them, and they're very interesting. Uh, there is the one in, um, the, uh, Annals of Internal Medicine, and there's one in Cell, and they're sort of point-counterpoint, although they look at quite different things. One says, gee, there's no biological reason that we can find for post-COVID syndrome. The other says, well, we do see these things go on, but they You know, they change over time. And so my best advice would be— and, you know, I'm not giving medical advice here, I'm just saying what we see, and this is educational, this is not medical information. Remember, it's, it's dumb to get medical advice from people on TV or the radio. You should get that from your healthcare providers. But what I see and what I advise other doctors is Number one, earlier treatment is better. You have less post-COVID if you treat the COVID earlier. So that's not really a topic today, but just to say that again, if you're after the COVID and now you have a post-COVID situation going on, the earlier you encounter the patient and treat them, the less stuff you usually have to treat. But you should be looking in these areas of nutrient and sulfur function, digestive function, uh, collaborative or co-infections, hormonal things, and all the stuff that we talked about. But certainly the longer you've had post-COVID syndrome, the more that you need to think about, well, maybe I need to look into more of these things. So if I am consulting a doctor and they have a patient who's just been sick for 6 to 12 weeks, We're going to start simple and work our way out. If I'm consulting with a doctor or a clinic and they got a patient who's been sick for 6, 9, 12 months, 2 years, 3 years, we're going to be looking at all of those things that we talked about, including, you know, screening for toxins and all of this other stuff. And is that, you know, something you do to everybody? No, you base it clinically on how bad is the person and how are things going. We have just enough time now to bring up the second topic I said, which is the genetic, and I'll put the links to these in. But I, I have one from each of the last 3 years. So the first one is very interesting. This is in Nature, and it's the major genetic risk factor for severe COVID is inherited from Neanderthals. And it's a very interesting paper. It's not a joke paper. It's a real paper, and it goes through and it talks about, you know, Neanderthal heritage and how there's certain parts of the world where there's a lot more Neanderthal, you know, genetics still in the genome. There's other places where it's less, and that kind of matches up. And there's a particular gene that is specifically one we carry from the Neanderthal interbreeding that went on long, long time ago. And so if you have a lot of Neanderthal in your background, that is a possibility if you inherited that gene. Now, most people only have a fraction to a few percent Neanderthal, if they have any, but it's in the part that we apparently inherited. So that's, that's one if you're into that, or if you're into your Neanderthal heritage, you can go look at that one. The next one is from 2021. in the European Journal of Medical Research. And genetic susceptibility— this one is a little bit more along the lines of things that we've been seeing in the literature going on, you know, all along, at least theorized. And that is that if we have genetic polymorphisms in the ACE2, so the angiotensin-converting enzyme 2. There's a, there's a pre-ACE, and then there's ACE1, and there's ACE2. So ACE2, it's a higher risk for COVID infection. The first one was really for severe COVID. This is for infection. And this has a lot to do with the fact that at least up to this point in 2021, the main way in was through the ACE receptor complex and the preparation that that complex did for us. So as you go through that, that one kind of makes plenty of sense. And then the one that was just published fairly recently in Cell Systems, this is another big Uh, you know, one of those real, uh, brainiac kind of papers that looks at a lot of heavy-duty stuff. This one, uh, gets into looking at something that kind of ties us back to the post-COVID discussion, and that is looking at the genetic risk of COVID severity. So, so again, the first paper with severity, we the Neanderthals. Second paper with the ACE was just likelihood of getting COVID, and now we're back to severity. Well, it turns out that certain subsets of your immune system, uh, and the cells that operate that part of your immune system can have genetic changes that might make you more sensitive to a worst case of COVID So one of them is the natural killer cell, and the other is our old friend from before, the T cell. So remember, the T cells make the cell-mediated immunity. Now, natural killer cells we used to discreetly categorize as nonspecific. So a B cell for antibodies or a T cell for cell-mediated immunity or specific immunity. Natural killer cells, as their name would imply, are either in your tissues or maybe in your blood. And if they bump into a cell that doesn't look like you or that's virally infected, they will kill it. Okay? Hence the name. Well, now what we know is that natural killer cells do take some marching orders from other parts of your immune system. So the natural killer cells appear to be both nonspecific and specific. So as we go along, in this particular paper, if you're really into natural killer cells, it goes into a lot of detail here. And so they make a couple of things. We're running low on time, but one of the things that in their discussion, they— in particular, we highlight the failure of cytokine production by a particular type of natural killer cells. Well, that's— remember, too much cytokine gives you cytokine storm, but not enough cytokine does— gives you not enough immune activity. So there's a genetic predisposition for natural killer cells to not be able to trigger enough cytokine production, which becomes a problem. Um, the other is a predisposition to just lower amounts of natural killer cells. And, you know, normally when, when I'm teaching about natural killer cells to physicians, we usually talk about, well, look at natural killer cell function. Are they working like they're supposed to? Uh, which is true for the most part, but if you just don't have enough of them, they're not— they're not only not going to work, they're not going to be enough to do anything. Um, so impaired natural killer cell function, a scarcity of the capacity of natural killer cells to do their job in the early infection, and a change in your viral load. And so here we highlight the importance of T cells and natural killer cells in particular. Other immune types carried less genetic risk. So if you have B cell abnormality, it was less of a risk than T and natural killer cell. Well, that kind of came up in some of those other papers that we looked at as well earlier on. So we're just down to the last minute or so here. Just want to kind of summarize. So I'll put down in on the YouTube, uh, when we move this over to YouTube, in the description box. If you're on your phone, it's on the right side, a little down arrow, a little down V. Click on that, go in. If you go to an ad when you click on that, you click the wrong V. It's probably the one above that. On your computer, it's usually on the lower left side, and it'll say more or show more. Click on that, it'll go down and show you more, and there'll be links to all this stuff. So we've got 2 papers about long COVID. They appear to be disagreeing, but they're really not disagreeing. They're just talking about 2 different sets of data. And what we learned is the first paper showed us a lot of things that probably aren't a problem, or they're not a problem at the time they tested them. Second paper showed us there are things that are a problem in post-COVID, and we need to be looking in those areas first and then broaden our, our looking for a cause or a place to treat, uh, based on your particular, uh, medical situation, your own constitutional medical situation, which in any chronic illness is always how we should be approaching it anyway. All right, well, I'm Dr. Paul Anderson. This is Medicine Health with Dr. Paul Anderson. We do this every week here, and as I said, we put them all over onto the pod burners. Whatever favorite pod burner you have, look for Medicine Health with Dr. Paul Anderson. You look for that, you'll find me, uh, you know, whether it's Apple Play or Google or whoever. YouTube, just DRA Online, Dr. A Online. And if you can't find any of them, go to my hub website, dranow.com, and you'll find links to everything there. As always, it's wonderful speaking to you, and I will see you all on the radio or YouTube next week. Thank you.