Coronavirus Conversations - Day 36: Remdesivir, Ivermectin, Estrogen, and Smoking

In this live YouTube broadcast Dr. David Perlmutter provides a rapid COVID‑19 update covering a wide range of topics. He reviews the latest remdesivir trial showing a 31 % reduction in hospital stay, discusses ongoing experimental hormone therapies (estrogen and progesterone) that may modulate immune responses, and examines the controversial ivermectin data (in‑vitro viral suppression and a retrospective mortality analysis) while cautioning against self‑medication. He addresses reports of possible reinfection or PCR‑positive retests, the promise of convalescent plasma, and the misleading claim that nicotine might be protective, emphasizing that smoking markedly increases severe outcomes. Perlmutter explains leptin resistance in obesity and its impact on immune competence, outlines the global research landscape (hydroxychloroquine, lopinavir‑ritonavir, traditional Chinese medicine, ACE‑inhibitors, etc.), and reviews vitamin D and C supplementation rationales. He describes the Oxford vaccine platform and the control‑vaccine design, and compares Sweden’s “personal responsibility” approach to stricter lockdowns. Finally, he highlights COVID‑19‑associated coagulopathy, stroke risk, and the importance of blood thinners, before taking audience questions on PCOS, ivermectin availability, antibody testing, exercise, diet, and other practical concerns. The session ends with a preview of a forthcoming interview with Dr. Kellyann Petrucci.
Chapters
Well, hi everybody. Unexpectedly, here I am. I was doing another interview and I thought I would just check in with everybody and go ahead and give you an update in terms of, in terms of what's new. A lot is new. I mean, all the buzz right now seems to be talking about Remdesivir, antiviral medication that we talked about now going back at least a month. We've been talking about Remdesivir, an antiviral. And what did the results of yesterday's report tell us? It showed us that the recovery rate was about 31% quicker in individuals getting the dosages of remdesivir, an intravenous antiviral medication, obviously not anything you would take at home. Does that sound like a home run? Let me just put it into perspective. In my view, 31% less time in a hospital, for example, I think is huge. That will have a huge impact on the ability to have resources in the hospital, and it certainly means that people are far more likely to recover or survive, although that wasn't looked at. Mortality was not an endpoint of this study, but the idea is that the longer you spend in the hospital, the more likely you are not to survive. So we're going to watch this very closely. It's nice that we at least have a validated treatment of sorts. We talked a couple of days ago how it looks like in China that they're using a lot of things at one time, multiple antiviral treatments using Arbidol, the antiviral from Russia, using lopinavir as well, which is from Japan as an antiviral, and now we're seeing, we're going to see a lot of usage of remdesivir. And a powerful amplification of the production of remdesivir so it can be made available aggressively to hospitals that need it. Well, there are a few things I want to cover today, and I want to promise to all of you that I'm going to get to as many questions today as I possibly can, because I know that, you know, there's a lot of news, a lot of things we want to cover, and I don't always get to every question. Not that I will today either, but— First, I'd like to revisit a study we talked about a week ago, and that was a study published in the New England Journal of Medicine that looked at admitting 215 women to deliver their babies to various hospitals in New York, testing them for COVID-19, and they found that a small percentage were positive, but that's not the real take-home message. The take-home message was that 90%— this is really important because we're going to develop this— 90% of the women getting ready to deliver babies admitted to the hospital who tested positive for COVID-19 had no symptoms at all, didn't even have a fever. And so it's telling us that while it was a small study, it was only 215 pregnant women, But it's telling us that there may be something very, very protective in terms of what's going on during pregnancy and moving towards the time of delivery, in terms of being able to carry this virus, be infected by it, and yet not have symptoms, which is, you know, if you're going to get this infection, wouldn't it be great to not have symptoms? Though, you know, the problem with that is, of course, you're at risk for spreading it to others, but nonetheless, what is going on? What is happening with estrogen and progesterone that may be protective? Well, doctors, and as I said at the time I presented this study the other day, wouldn't it be great to start to evaluate why that might be? Well, what we learned was that a study now was brought underway in New York on Long Island where doctors are now going to treat patients with COVID-19 experimentally by giving them estrogen to hopefully enhance their immune function. And as we've just learned, study going to get underway in Los Angeles treating COVID patients in the hospital with progesterone, pro for gestation. We know that progesterone levels are high during pregnancy. And for me, I want to tell you that we've seen over the years interesting research done in individuals with head trauma also being treated with progesterone. So I want to just get you all away from the notion of thinking about that progesterone is just for gestation, and estrogen is a female hormone, and testosterone is a male hormone. Au contraire, these are hormones that are found in both men and in women and have differing effects. They're not just sex hormones or related to pregnancy. As an example, we know that cells throughout the body have estrogen receptors. And guess what? The immune system has a powerful influence imparted by things like estrogen and progesterone. We know that research shows that estrogen activity has a powerful role to play in regulating both the innate immune system, which is what first comes online when we have an infection like COVID-19, and the adaptive immune system, which is the part of our immune system that kicks in later on, that starts to produce antibodies and hopefully gives us immunity. Estrogen influences those 2 systems, so it might be therefore a good idea that estrogen is being explored. We know that estrogen signaling problems or weaker estrogen signaling is related to worse outcome in men as it relates to having a pulmonary virus infection. So that speaks to this whole notion of estrogen being immunoregulatory. So who knows, you know, we may all be taking a little estrogen if we get infected with COVID-19. The point I would also make is that there may well be some synergy of an estrogen or progesterone protocol along with something like remdesivir. What we talked about a couple of days ago was the protocols being done in China where they throw a lot of things at people. A lot of different medicines are used when patients are hospitalized. Now the next update I'd like to give you has to do with this medicine called ivermectin. Now ivermectin is an anti-parasitic drug. We give ivermectin to our dogs to treat them with— dogs that have heartworm. We know that horses are treated with ivermectin. We know that humans are treated with ivermectin if they have a parasite, and it's even used as a treatment for head lice— ivermectin. And what I reported to you last week was a study coming from Melbourne, Australia, from the Monash University by a woman named Kylie Wagstaffe, showing that ivermectin, this anti-parasitic drug, caused a 5,000-fold reduction in this virus, this coronavirus, but it was done in vitro. These are cell cultures. They used ivermectin, and lo and behold, there was a 5,000-fold reduction. So it looked like, at least in the laboratory, that ivermectin was powerful in terms of getting rid of coronavirus. COVID-19. Since that time, there has not been an interventional trial yet completed, but a retrospective study, meaning a study that looked back at people who were taking ivermectin versus those who were not. And the death rate in individuals who had to go on a ventilator who were not treated with ivermectin was 21%. But those who did happen to receive ivermectin, was only 1/3 of that, 7.3%. The overall mortality risk of dying in people taking ivermectin was 1.4% versus 8.5% people who were not taking ivermectin. I want to be as clear as I can be. I'm not recommending in any way, shape, or form that people begin taking Don't take your dog's heartworm pills. Don't get a prescription for ivermectin from your doctor as yet. I don't think we have good enough data to say that it's worthwhile, but it may be in the future. But please, the take-home message from me right now is not telling you go and get ivermectin and take it. And I know that I'm going to have— you guys are going to be asking me questions. What dosage should I take? Please, not a great, great question to ask me because I'm not going to answer that question because we don't have data for it yet. The next thing that's become very interesting is this report from South Korea that in a study of 7,821 individuals, a small— who had tested negative. They had COVID-19 and then they got through it, they tested negative, then they tested positive again, and that was 2.1% of people, and that raised a lot of eyebrows, and rightfully so. I mean, if you have something like this, you hope that you become immune to it, and yet the read on that was that about 2% of people had either reinfection or reactivation of the virus. In other words, it was still in their bodies even though they had tested negative. And so new research now, or interpretation, indicates that some of the new testing that these individuals may have had saying that they are now positive again, this PCR testing, may be not accurate because apparently There's some discussion that the virus, even though there's no longer virus, it can leave a genetic fingerprint on cells of the lung that can be coughed up into the nasopharynx, and that can then cause a positive test. Well, I'm hoping, hoping that's true, because my hope is that when you get coronavirus, this coronavirus, COVID-19, that you develop immunity. Big question out there. Big question is, if you now test positive with the antibody test, is it okay to go back to work now because you're not going to get it again and you're over it? You can't communicate it or transmit it to somebody else if you have high levels of IgG. So, um, I think that's something we need to think about. We're seeing a lot more research now in looking at plasma treatment I'm very excited about plasma treatment. In other words, taking the blood of people who've recovered, harvesting their plasma. Hopefully it's rich in antibodies against COVID-19 that can then be used to treat others. So around the country, we're seeing people now being able to donate their blood with the hopes that they can treat other people. The early results of some Preliminary studies, one published in JAMA, Journal of the American Medical Association, only 5 people, but the results looked positive. Next, I want to talk about the, the, this thing that's going around that somehow it's good to smoke cigarettes. Hmm, I'm gonna have a tough time with that one as it relates to COVID-19. There is some idea that maybe nicotine is somehow protective And I will tell you that looking at epidemiological data does show, though I don't want to admit it, but it does show that risk, for example, of Parkinson's disease is lower in smokers. There's been some discussion that risk of bad outcome, if you have COVID-19, might be lower in smokers. The bulk of the data and the research that I have seen indicates quite the opposite, that the percentage of current and former smokers is higher among those with severe cases than in nonsmokers, 17% versus 5%. So if it looks as if, if you're a smoker or a former smoker, that your risk for having a bad outcome is increased. If you get this virus. So my sense is that smoking is a bad idea. Among those with the idea of being admitted to an intensive care unit and the endpoint of either into an ICU, requiring a ventilator, or dying, the proportion of people who that happens to is much higher in smokers versus nonsmokers. In other words, into the ICU, going on a ventilator, or dying. Smokers, 26%. Non-smokers, 12%. So that's convincing enough data for me to not be even thinking about the idea of smoking, vaping, anything like that to damage your lungs. You know, it's primarily a lung condition. We don't want to do anything that's going to jeopardize our lungs. And finally, I just want to bring up for discussion today the notion, and this will be a bit of a little science, but bear with me. You know, we talk about obesity and having higher levels of uncontrollable hunger. Hunger is controlled by something called leptin. The higher our leptin levels are, the more hungry we are, maybe the more food we eat. As we have higher and higher levels of leptin, we learn that we become leptin resistant. Leptin resistant means it doesn't act as effectively anymore, and that is ultimately raising our leptin levels, and we become more and more hungry. And it turns out that we need to understand what leptin is, and that is leptin is is a hormone in the body, but it has like so many other chemicals, has multiple roles. It's not just a hunger-related hormone. It's not just a hormone that has to do with hunger, though that's what gets all the attention. It has a profound effect on our immune system. Hormone basically licenses our immune cells to engage in the immune responses, the ability of our immune cells to do what we want them to do. When they become less sensitive to leptin, then they don't work as well. They become less sensitive to leptin when we have higher and higher levels of leptin, like in obesity and overweight. So we need to think about that, that might be a powerful relationship then between overweight, obesity, and risk for bad outcome. Overweight and obesity, diabetes, coronary artery disease. Those are other problems that go hand in hand with overweight, and leptin may be the link then to immune compromise and bad outcomes. So really something to think about. One last update, and then I'll jump on some questions, and that has to do with the studies that are being done. Currently, the number one studies that are being done, globally have to do with hydroxychloroquine. The lopinavir-ritonavir combination of antivirals comes in number 2 at 53. And now traditional Chinese medicine, far less studies being done looking at that approach. So, so many things are being looked at, looking at the ACE inhibitor drugs that we've talked about, looking at anti-acid pills like Pepcid, that's being studied, estrogen, progesterone being studied, And certainly a lot of attention on remdesivir being, especially in light of Dr. Fauci's comments yesterday and the positive results showing a 31% reduction in terms of how long people need to be hospitalised. And I think that's huge. Okay, ladies and gentlemen, let's Let's take some questions. Somebody said no audio. Is there audio? I need to know that. Otherwise, we've certainly wasted our time. Okay, let's take some questions. What does the estrogen impact mean for PCOS women? That's a great question. So what we typically see in PCOS, which is a kind of a misnomer, polycystic ovarian syndrome. Uh, is, uh, you know, has to do of course with estrogen. The reason I say it's a misnomer is because we can see the metabolic issues of PCOS in women who do not necessarily have cysts on their ovaries. Insulin resistance, the weight gain, the testosterone imbalance— testosterone, I did say, and that's what I meant to say, imbalance, excessive— uh, is seen even without the necessary in terms of the name, the presence of these cysts in the ovary. And what is really quite interesting to consider is the new research coming out that relates PCOS, which is the number one cause of infertility in American women, the relationship between PCOS and changes in the gut bacteria and the role that the gut bacteria have on metabolism and insulin sensitivity. So I think that the more we recognize that this dramatic change, shift if you will, of the gut bacteria plays a role in insulin sensitivity and plays a role certainly in PCOS, I think that will certainly play out in our understanding in terms of the estrogen manifestations and the testosterone manifestations. Nicole Snyder says, I have horses and the ivermectin was being all bought up from the feed store. I know that's happening and it makes me reluctant. Please comment on this. It makes me reluctant to present this information because I know people are doing that, and I would counsel that that is not a good thing to do. May it ultimately prove to be effective? Yes, but by all means, Let a doctor, healthcare provider guide you at the time that we finally get our arms around something like ivermectin, that that turns out to be a good choice or not. We don't have a study yet, an interventional trial, meaning we give it to people and maybe in an ideal world compare that to a placebo to prove that it's helpful in humans. The study from, from Australia that was done that we talked about only demonstrated lowering the viral load in cell culture has no necessarily relationship to what might happen to people who may take this drug. So, so not a good idea in my opinion yet. I mentioned fisetin previously. Is best taken with or without food? Don't know the answer. It is a plant-based derivative. I take it with food. We take fisetin, I take fisetin, my wife too, because it is a senolytic. It is described in the literature that I've posted previously as being able to help our bodies rid themselves of aged, less functional immune cells. Okay, diamine oxidase, interesting comment, but somebody doesn't wanna take estrogen. Okay, let me go through some of these questions. Okay. Question, if you tested positive, no symptoms for COVID, and positive antibody IgG, are you still immune and not contagious? If you're testing positive on polymerase chain reaction, in other words, a throat swab, and at the same time showing antibodies, you're likely still contagious. So when you're also talking about the antibodies, if you're only showing IgM, then you may still be contagious. What you want to hope for is the IgG. Let me explain. We have 2 antibodies that are typically part of the testing. IgM shows an acute response. You get the IgM production, hopefully, if your immune system's working well, When you have the virus, IgM will be produced first. It's the first peak. The longer peak that will give you more extended immunity, we hope, is called IgG. Turns out that I think Quest Laboratory is only testing IgG, and with good reason, because it's the IgG that may well show you that you have immunity. I'm not saying that's 100%, We don't know that just yet, but when you get your results back, if you have both IgM and IgG, likely you are covered, but if you are tested with a throat swab or nasopharyngeal swab and antibodies and you're still showing positive on the throat swab, you likely still have virus, so you need to govern yourself accordingly. Okay, question about the Oxford vaccine trial, is it true that the control group is being given the meningitis vaccine? If so, how is this true science? Wouldn't this minimise any adverse reaction to COVID-19 vax group? Not sure if it would minimise— yikes, that question went away and I can't get it back— minimise the reaction, but what did we learn by the results of this study from Oxford, and what is it, which got a lot of attention past couple of days? So the researchers at Oxford— what normally happens in the development of a vaccine, let's go back to polio, for example. What was done in polio was they took the polio organism and they altered it in such a way so it wouldn't cause polio. Then they administer it to people and they develop antibodies against this. It looks a lot like polio, but it doesn't give you the disease. So that's typically what The platform has been since the original development of the polio vaccine. But what these researchers at Oxford, Dr. Hill, did, which I think is really kind of exciting, is they used a different respiratory virus that normally doesn't cause a bad respiratory illness, and they tweaked it in such a way to allow the body to create antibodies against it, but those antibodies are cross-reactive with COVID-19. which is kind of awesome. It's really great news for 2 reasons. Number one, it may be effective. They tested it in a group of macaque monkeys and then exposed these monkeys to a very high level of COVID-19, and none of them became ill. But there was only 6, I think only 6 monkeys. But the other thing is, it shows that this technology is quick, can work very quickly, and if this works, they can ramp up production in terms of producing hundreds of millions of dosages very quickly. Now, I know that there will be comments about people being fearful of vaccines. You know, there's always a risk-benefit discussion and consideration, and I'm open to that. I do recall that when the swine flu vaccine was created, a not insignificant number of people got Guillain-Barré syndrome, from the swine flu vaccine. So again, we've got to make sure that these immunisations are really, really safe until they are released. Now, let me digress on something, if I may, and that is this idea that Sweden, for example, is not deeply involved in keeping people at home, and doing all the things that— and shutting down businesses, shutting down schools like has happened here. Restaurants are open in Sweden. And what do we expect? What are we seeing happening in a country like that versus what happened here, although that's now being reversed? What do we learn? And we really need to keep our ears and eyes open and watch what happens in countries like Sweden because we're learning a lot of valuable information. The death rate per 100,000 in Sweden is around, I guess, 24 to 27 deaths per 100,000 members of population versus being dramatically lower in Finland and in Denmark, which are adjacent countries. It's useful not to look at the number of people who have died or even the number of people who have contracted the virus as much as it is useful to look at the number of people who have died in comparison to the total population. In a country that has a lot of people, you're going to see more death in comparison to a country that has less people. So that's why it's good to do these numbers in comparison. However, and this is really important to get your arms around, so we might say, gee whiz, they should be doing— they should be really taking this more seriously and instituting closing of schools and restaurants, et cetera. Their argument is that yes, we're seeing an explosion of this transmission and problems related to COVID-19 exposure, and they are. But they're also telling us that their rate of herd immunity, that the number of people who are now testing positive in Sweden is around one-third. Now that's the long game. What does it mean? It means that they are basically accepting the higher death rate now because it's going to lead them to get to a higher level of percentage of their population who develops immunity in a shorter timeframe than in other countries that are practising the lockdown, practising the quarantines and the restaurant closures. I don't know which is a better solution to the problem. I will say, though, that as we look at what is happening in Sweden, recognize that what is being portrayed is it's basically a free-for-all, do whatever you want, go to every store, restaurants are all open willy-nilly. It isn't like that, to my understanding, that even though the government is keeping these— allowing every place to be open, like we're now seeing happening in our country. Nonetheless, plenty of people are aware of it and practicing distancing, social distancing, many of whom are actually wearing masks, and handwashing in Sweden is strongly recommended. Handwashing is probably the biggest thing that we can do to help reduce risk of contracting this virus, one of the biggest. Certainly staying away from people who are sick and people And doing the 6 feet distancing from people is very, very appropriate. So I would say that look at Sweden, follow it closely, see how it plays out, but understand that they're accepting more infections on the front end with the idea that they're going to get to a place of herd immunity sooner, at which point the virus becomes much less able— in their population to spread. We want herd immunity here as well. And the only 2 ways to get herd immunity are getting the virus, having the virus spread, or, and/or a meaningful immunisation or vaccination programme. That's how we develop immunity that will last. Now, the idea of getting immunity from a plasma transfer or from getting plasma from someone who's had the disease is interesting, But that will not necessarily be fully protective, nor will it last. So, 2 ways: have an immunization, or at least— or get the disease. I'm not advocating that you go out and get the disease. I'm still doing my very best not to contract this virus for good reasons. Can I speak to leptin a little bit more? Can we— how can we lower leptin? You absolutely can. Various things that we do to increase our insulin sensitivity will work to increase leptin sensitivity. That's what we want. We want our cells to become leptin sensitive again. So ketogenic diet, exercise, getting a good night's sleep—all of these things can work to lowering our blood sugar and to also improve leptin sensitivity. Excellent. Question, Jessica Carter, you get points for that one. How important is daily exercise? Very important. Exercise, we'll talk about it in a moment. Actually, I have a blog that I just wrote on exercise and diabetes risk. I think that comes out on Sunday. So, Stacey, read that, but you really want to involve yourself in daily exercise, improve your insulin sensitivity. improve your immune regulation, decrease your production of cortisol, and that has a role to play in immune regulation. Although we call it a stress hormone, it actually has an important role in immune regulation as well. I'm a smoker that have a serious problem in getting this virus. I've been doing a lot of steaming because this virus definitely attacks the lungs. Okay, and I'm not gonna say your name, probably you don't want me to. So I would say that as a smoker, I believe you're at increased risk, and therefore the message then is to do everything you can to reduce your risk of contracting the virus right now. Don't be hoping that these new treatments that we are learning about, or proposed ideas, will necessarily ultimately be available to you, much less prove effective. And, you know, I'm not easing up on the restrictions. Nobody's coming into the house. We're meeting with our neighbors and friends in the front driveway. They bring their own chair. They sit across the driveway. They bring their own appetizers. And it's a different way of socializing with people, but that is what is called for. We call that the new normal. Will it get back to how it was? I don't know, but for now, this is a serious virus. I think the death rate is lower than we had thought it was, but still, when you get it, you know, you're at risk for significant complications, especially if you are older like me, or if you have underlying conditions like overweight, diabetes, other chronic conditions. Okay, let's go through. What do I eat on a normal day? Okay. Well, a lot of times I don't really eat a whole heck of a lot, but lately I've been having. I've been eating a little earlier earlier in the day after I exercise. So typically around noon or one o'clock, I've been eating, and several times a week I've been having as my breakfast. I've been having eggs that are cooked in a frying pan. I also go out and harvest a little bit of kale. I take the kale leaves and put them in the frying pan with a lid so that they are steamed and lots and lots of olive oil. My wife often makes me a green drink that has added collagen and prebiotic fiber. And I really appreciate that. I do have coffee during the day, But breakfast is, is for me, that's the meal that I then have nothing else until suppertime. And then we have a protein of some sort. It could be lentils or mung dal and as much fresh vegetables as we can get. Our garden is becoming more and more productive, but here in Florida, I don't know how long it's going to last because it gets really hot and growing food Growing a vegetable garden is very challenging. I'm having a lot of problems with our tomato plants. They look great, but they're not bearing fruit. Our string beans are not bearing fruit either. So anybody has any brilliant ideas? I don't know what to do. Maybe it's more fertilizer. Maybe I'm watering too much, maybe watering too less. But we're getting wonderful eggplants, that's for sure. And the lettuce that we're growing upstairs on the balcony seems to be growing. Really well. Okay. All right. Let's a couple more questions, and we'll take it from there. All right. And what is your take on the vitamin D study that shows that the correlation between vitamin D levels and the severity reaction to COVID-19, and this is a question that we've been asked actually quite a bit, and the real question is what does vitamin D, what is the role that it has in immune function, and there are many. We know that the activity of our immune cells is highly influenced by the binding of vitamin D to what are called vitamin D receptors. We also know that vitamin D is important in the creation of what are called antimicrobial peptides. Well, what are those? Those are the body's short protein-like molecules that tend to isolate and help us get rid of bacteria and viruses. So one of them that is getting a lot of attention is something called cathelicidin. But anyhow, I am in favor of vitamin D. I think it would be good, Michelle, to know how you might be genetically, because we know that some people have changes in their vitamin D receptors that might cause them to need more or less vitamin D in terms of how much they are producing and/or supplementing in their bodies. I'm currently taking around 5,000 IU of D3 each day. And there you go. Anyway, let me look a little bit more and then we're probably gonna call it a day. Why not promote vitamin C to prevent getting the virus? I have seen 3 people turn around 180 in hours with 3,000 to 5,000 milligrams a day of vitamin C. There are actually several studies going on right now looking at vitamin C as an intervention. Giving it intravenously. And I think there are a couple of studies actually looking at vitamin C levels in terms of outcome. So I don't have any problem with that whatsoever. I'm taking at least 2,000 milligrams of vitamin C each day. I don't have good data on it. I think overall it makes sense. That's why I'm doing it, knowing what I know about vitamin C and basically for immunity. So there you go. I would love to be able to— I'd love to be able to quote a study on vitamin C. I can't, but I'm gonna tell you that I am taking vitamin C. Well, let me take one more, and that is a report from George Ann Nugent, Mount Sinai report, and several other institutions, I might add, stroke in young people with COVID Yeah, it is worrisome. We're seeing stroke not only in young people, but in many people across the age spectrum being admitted to hospitals with COVID-19 symptomatically. In other words, in terms of what they're presenting with. But also, interestingly, one study showed a high prevalence of individuals showing strokes on their MRI scans of their brains Who are admitted just because of this infection. So why might that be? A couple of reasons. Inflammation in the body is irritating to the blood vessels. As an example, coronary artery disease is an inflammatory disorder, and it's the response to inflammation of the lining of the arteries that narrows the the arteries in the heart causing a heart attack or angina, and in the brain causing a stroke. Strokes are inflammatory, but not all are inflammatory. Some strokes are what we call embolic, meaning they represent the blockage of an artery caused by a fragment of something breaking off from lower down, traveling all the way up into a part of the brain and occluding a small artery. That's called an embolic stroke. That's the type of stroke that we see, for example, in people who have atrial fibrillation. We see other types of stroke, thrombotic or closing off of artery strokes as another type of stroke, and also a type of stroke called hemorrhagic stroke where there's actually the breakdown or falling apart of an artery and then there's a hemorrhage into the brain. That's called a hemorrhagic stroke. Well, we're seeing a lot of blockage strokes in COVID-19 more than expected. And understand, this is a little technical, but we had a discussion several weeks ago as to why was the heart so involved in this infection. And it turns out that the research that I quoted back then looked at the binding sites for COVID for this virus on cells, and it binds to a receptor called the ACE2 receptor. And what the study demonstrated was that the ACE2 receptor, where the virus binds on the cell, is found in some of the lining cells of the heart arteries. I'm not going to be surprised once the work is done that it's in the arteries going to the brain as well. But in addition, understand that this is a profound inflammatory event going on head to toe throughout the body. So the idea that stroke can be inflammatory and that, you know, this is inflammatory event is therefore not surprising. Let me tell you one last bit of information that's relevant to that comment. Georgiann, and that is that COVID induces coagulation changes in the bloodstream, and that's very worrisome. It makes the blood in many cases hypercoagulable or increases coagulation, hypercoagulable, and this can really become accentuated to the extent that the blood will actually coagulate throughout the body, and therefore we can't— it'll the body can't receive oxygen. We call this DIC, or disseminated intravascular coagulation, or coagulopathy. And that is, you know, a very, very life-threatening event. So just by nature of the ability of this virus to increase the, I hate to say thickness of the blood, but the coagulation aspects of the blood that can be increased by this virus is very worrisome. It's why many protocols now have people being treated as they go into the hospital, and especially those going into the intensive care units, with blood thinners like heparin, because of the fear that these individuals may develop this coagulation issue, which can be lethal. So that is the answer to that. And I guess let me take one last comment because I think it's a very good point. It's from Kathy Allen Hendricks, and she says Sweden is practicing personal responsibility. That's actually a very good point. They're calling upon their population to do the right thing as opposed to saying the government says you're going to stay indoors, we're going to shut your business, and etc. So that's the tact that they took. And it looks like a lot of people are practicing this social responsibility. And, you know, here things were shut down. I don't know which is best. I think we're going to learn which is best. I'm not coming down on either side of this. I'm not by any means ever going to make a political statement as to what we're doing. We'll see how it all plays out. Again, They may get to herd mentality or herd immunity rather via their herd mentality sooner than we do. And therefore, in the long run, it's the right thing to do or not. We'll follow it closely. And I promise to report back in terms of that very interesting observation. Well, everyone, thank you for watching today. I know this was unannounced, but I was doing a podcast for somebody else and I got dressed. I put on the shirt, so I figured I'd connect with everybody. And, uh, oh, here's the thing. On Facebook, on my site here, I'm doing a live broadcast with Dr. Kellyann Petrucci tonight at 7. We'll be taking questions. She's got a lot of questions to ask me as well. So, uh, join us then. And, uh, for now, that's all I've got. Love you all. Thanks for paying attention, and we'll talk soon. Bye-bye. Bye.
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