COVID Therapy Confusion

Dr. Paul. Or Dr. A, whatever, whatever way you like. And, uh, today, in keeping with the let's answer questions that come in, uh, way of putting together shows, uh, I wanted to answer some questions that, you know, are, I think, very common. I see them posed a lot on various social media places and just in person with people, etc. And I thought I'd put them all together here and put them under the umbrella of COVID therapeutics confusion, or COVID therapies confusion, because there seems to be a lot of kind of muddled language. And a lot of the therapies, to be fair to everybody, kind of have similar sounding names, but they do different things. A lot of stuff going on. Okay, so I took the top— I don't know what over here on the easel I've got— probably the top 7 or 10 questions and thought I would go through them. Well, as soon as I decided to do that, and I put this all on a list I got from my friendly county health department— they send you these emails if you have a license in their county. And so you get these emails like this. And that came literally, I think, right after I decided on the topic here, and it feeds into the topic. So I thought I'd start with that. And this is the monoclonal antibodies, which you hear a lot about right now, that are being used as mostly treatments, but also in high-risk contact situations. Okay, and so I got a lot of questions about these. This is before the county sent us this information about who to give them to and how much and all that stuff, and they're very much encouraging doctors to do that. But prior to that, I was getting a lot of questions because the, the type of drug which we've talked about on these podcasts before is called a biologic drug or a biological or biosimilar drug. And so their naming sounds similar to other biologic drugs, but the naming and the mechanism of what they do can be completely different, which is very important to keep in mind. And so a lot of the confusion that I was getting in questions and things, I don't know, a couple weeks ago or something, was around, well, wait a minute, how are these being used for a patient who has COVID or has a high exposure to COVID? When they're immunomodulating drugs. Well, the thing about these monoclonal antibodies is they're not really immunomodulating drugs, so they don't dampen your immune system or do other stuff. We've got other drugs to do that that we're going to talk about today. And I think because especially, you know, when, when the public health department sends doctors these things and says, hey everybody, make sure that you've got these, make sure that you're giving them to your patients or at least referring for them, make sure that you know the rules and who should get them, who shouldn't get them. And we're really, you know, the public health is really pushing the use of these, which I think is a great idea. You start to get more and more like news reports and stories, and then people start to get a little bit confused 'cause it is, you know, pharmacology, especially when you get to biologic drugs can be a little or a lot confusing. So what I wanted to do was clear up some detail around these things. Now, one of the things is when you have a biologic drug or a biosimilar drug, what it's trying to be similar to is usually something your body does. Not always, but in this case, it tries to be identically similar to what your body does. So what that means is if you or I contract COVID or any other infection, we will make a B cell response that makes antibodies and a T cell response that makes a cell-mediated immune response. And you can go back on my YouTube channel and you can look for COVID B and T cell response, or just the general B and T cell, and we get into that stuff. What this biosimilar biologic drug is trying to do is to take the antibodies a human like you or I would make to COVID and synthesize it in a lab. Now, there's a whole bunch of ways to do this, and there's a whole bunch of different types of prefixes and suffixes and names, and that, unless you're in a pharmacology course, is really nothing terribly interesting. But do know that we have all of this capacity in modern times to make synthesized antibodies and synthesized all sorts of other things too, which we'll get to some other kinds. But why would this be beneficial? Okay, well, one of the things that a monoclonal antibody— so what does that mean, monoclonal? So you've heard of like a clone, though. So you take, you know, a sheep and you clone it and then the clone is pretty much identical to the parent sheep. You can take antibodies and do the same thing. So you can take a COVID antibody from a human and clone it, and then you make a billion of them, and that becomes a monoclonal antibody. What it means is that every child antibody that has been cloned and is now in that drug is exactly the same as the parent antibody with at least a few respects. It might be cloned on a footprint that is a little different, but the binding sites— so an antibody is like a Y, so the binding sites usually are the open ends of the Y or places around there. It's a little more complex than that, but let's just go with that. So the open ends of the Y and the places for the binding are going to be identical to whatever you cloned. Now, in the case of these monoclonal antibodies, there's a few different types, but you should know that the reason that these are being, um, really promoted and pushed towards the, the medical profession and you if you're sick is that the federal government has procured from the people that make these things many, many, many, many doses and sent them all out through the U.S. In almost every instance, with the type of antibodies that they're telling us about here in the county health update, they're being provided free. And the only interaction you may have with any cost would be wherever you go to get them. Okay. Now, if you have health insurance, these are reimbursable. The injection of them is reimbursable, but the actual drug itself is not costing directly the patient anything. I said directly the patient because it's costing all of us, right? The federal government's buying it, which means we're buying it. So do know somebody's paying for it. But if you've got 1,000 people in a city that need them, there's going to be 1,000 doses available that we all bought through the federal government. And so, you know, that, that has some distribution benefits too. So the other thing, you know, I just would say about that, because it's sometimes a little easier to get confused, and early in COVID we heard a lot about this, the manufacturers of these monoclonal antibodies are not giving them away. They are being purchased by the federal government or you and I through the federal government. And so they're not losing money on this either. And that's neither really here nor there, but it's a factor because, you know, you hear a lot of, uh, interesting news stories about that sort of thing, and most of them aren't true. But, you know, these people worked hard to come up with this. They should get paid for the work that they did. So according to the latest bulletin from the health departments that tell us doctors how to use such things, it says consider using monoclonal antibodies for post-exposure prophylaxis of not fully vaccinated, uh, high-risk folks, preferably within 7 days of exposure. vaccinated with one shot out of 2, or in future days, probably 2 out of 3. Okay, and I'm not going to comment at all on vaccines here because that's prevention, so-called. That's not really treatment. We want to focus on treatment. But there's a very important thing here, and this goes to wherever the antibodies come from, whether they're human or humanized in this case, and that is preferably within 7 days of high-risk exposure. Okay, the other group that is included is anyone who's fully vaccinated but has an immunosuppression going on. Now, the last, uh, one of these I did that we put up on YouTube, it was Q&A, uh, immune Q&A, and I talk about there's different ways to have immune suppression. One of the ways you get immune suppression is you have an immunodeficiency. That's not uncommon. But the other more common way is you're on drugs that cause immunosuppression. And so I've had people say, well, why would I take these monoclonal antibodies when they're associated with immunosuppression? Well, you have to stop right there and say, no, these are not the kind of monoclonal antibodies that are associated with immune suppression. That's a different kind of biologic drug. They sound the same, but they're not. But you might have a disease like Crohn's or colitis or lupus or multiple sclerosis, and you might be on another type of biologic drug where it doesn't matter almost how many immunizations you've had, you're probably still very open to a fulminant case of COVID because your immune suppressive drugs take that barrier away. So our friends at the health department are saying, you know, also let's include people who have immunosuppression. They also give you some tips. If you don't have an infusion center, so you can't hook IVs up, you can give these subcutaneously, which is actually kind of nice because almost every health clinic can give subcutaneous type injections. And of course they say, you know, you need to be ready for reactions, but that's anything that you inject, you probably ought to be ready for reactions. So then they go into a really nice little summary that says, well, how do these things work? Well, what you want to remember is, remember I said this is a clone of the human antibodies that we make, but there's a little bit of a difference. If you have made your own antibodies, to— we'll just stick with COVID-19 because that's our topic today. If you made your own antibodies to COVID-19, those are going to have antibodies to different parts of the virus. Okay, this particular monoclonal antibody is a clone of one type of binding site on the virus, which is not bad. It's just we don't want to misappropriate and say it's an exact clone of what you make as a human because it's not. Okay, so it has a binding at the spike protein receptor domain, but there's other domains if you made the, the antibody that would happen. Now what they will say is a lot of times these are mixed, so there's 2 clones together And they do the 2 clones together so that you get less resistance developed to the drug and a better outcome from the drug. So, with the ones that the government and us all paid for, for everybody who needs them, what are the stats on how these things work? Well, if you use them early, meaning usually in the first 7 days after exposure, It reduces the risk of hospitalization by 70%. That's pretty good. Okay. Um, reducing the risk of hospitalization through any means that you do it is a wise move. So why would it do that? Well, if I get exposed today to COVID, and then I start to develop an immune response, but there's a bit of a delay, which is normal, but I am a high-risk exposure person and you give me an injection with these things, not only is my body going to make its own antibodies that have multiple binding sites, but I'm going to have one or two of these monoclonal antibodies already in my system, and it's going to go around and start to block the viral activity in the body. So it gives my body an immune head start. Okay, so that's very, very important. So reducing the risk of hospitalization by 70%, and in, um, so that's in high-risk patients. And then in contact, so non-high-risk but high-contact people, Let's say you found out, oh no, you know, I went to a birthday party or whatever and everyone there had COVID. They didn't know it. And then the next day they found out they had COVID. I've actually been to events like that since COVID And it's a little disquieting to, you know, you get back home and the next day you get these phone calls and it says, oh, you know, really sorry, but we need to notify you that, you know, 5 of the people there have developed COVID. So that's a lot of good news. So that would be an eligible contact. These monoclonal antibodies reduce symptomatic infection in those people by 80%. There's not much else that does that. So these things— and I'm certainly not in the business of selling them, I don't make any money off of monoclonal antibodies— I'm just trying to explain some confusion I heard from people. Because some of the confusion I heard was, you know, and people are getting a little cantankerous or a lot cantankerous at this point. in COVID, but it was like, well, you know, why don't we just rely on our human antibodies? Or why don't we use convalescent plasma, which was our next topic? And that's all true. We should use whatever's available to us. But these things, even though they're more limited than a human antibody, they are clones of part of the human antibody, and they work really well. Okay. They also— every injectable drug that you ever take, it doesn't matter what it is, has a chance for allergy and anaphylaxis, bad outcomes. So everybody is, of course, reminded, if you're going to inject these things, don't, you know, do it at a place where you can medically treat an allergic reaction or anaphylaxis. That should be anything you're injecting, okay? That should be just universal. So that's not really a big difference there. 85 pounds or, or higher, symptom duration under 10 days, high risk with illness, not hospitalized, and you don't need supplemental oxygen. Now, why would we say, you know, don't go 15 days, don't go out too, too many days into the disease, don't need supplemental oxygen, all this stuff? It's because Think about it. When your body makes these things naturally, which is what your body ought to be doing when you're exposed to something that makes you sick, these things are going to be in the early response phase. So the immunoglobulins are going to be dumped out into your body along with the cytotoxic T cells, so the T and the B cell activity early on. If you have a viremia that has lasted 7, 10, 15, 20 days, the longer you go in your viremia, the less effect that the binding antibodies have on it. So we really want this in there early and, and kind of early and hard, which is why, you know, a known exposure is a great time, or early in, you know, you get a fever, cough, etc., whatever your symptoms are, get a positive test, that's the perfect time for someone to give you these things. Okay, so people who are in the hospital already, people on oxygen and steroids and everything else, these things don't work as well, and that's why they're often not given. Now, I mentioned that the, the one, the Regen-Cov branded one that we're all paying for, so it's free to everybody except that we're all paying for it, that's 2 non-competing IgG antibodies. So Ig is immunoglobulin G is the subclass, and that's the type that they are. And as I said, 70 to 80% effective as they go along. Now, the, the nice folks at the Department of Health do tell us about some other things that are available, and, um, but they go on to say, well, you might read about these, but the government hasn't bought any, so your likelihood of finding these is Very, very low. So, so there's that. So then comes the next group of things which the people questioning me a few days ago were asking about, which is what about convalescent plasma? Early on in COVID, we were hearing about, well, you know, the government said if you've had COVID and you're still alive, let us take some blood out of you, we'll filter the plasma out. We'll put your blood cells back in your body, but we'll keep some of the COVID antibodies. And so they call it convalescent plasma, meaning you've been ill, we're going to suck the blood out of you, filter out the antibodies, and put the blood back into you. Makes a ton of sense. We do this with other things in infectious disease. Used to be more common. Now with us having, you know, lab-made antibodies, we do it a little bit less. But convalescent plasma, there were no monoclonal antibodies for, you know, spike protein or anything else early on. So convalescent plasma became the thing that we all were using. Now, why would that be better or worse? Well, here's the thing. If you have convalescent plasma, you've got a couple of criteria that you have to think of. On the plus side, you have a human-made set of antibodies, meaning your body's B cells did it. And so that means if they were exposed to COVID, they're going to have the full complement of human binding site moieties, the binding site, you know, kind of sticky places on the antibody, and it's going to be more binding sites than on a lab-made one. So that's the upside. The downside is, and what we saw early on, 2 things. One is, how concentrated can we get these? So can we get the same delivery of the same number of billions of antibodies into your body as we do with the monoclonal lab-made ones? And then the other one, which is what we learned early, which is why convalescent plasma kind of got a bad name, but it's really sort of a dumb reason for it. It's a misnomer. was they didn't know really any better, and we were using convalescent plasma early, middle, and late disease. Well, obviously, if you go and you look at the data, and we already know now— remember, a couple years in— that if we give people antibody therapies, we want to do it early as possible. Well, that rule didn't change, but then we're judging convalescent plasma whether we gave it at day 3 or day 30. Obviously, day 10, 20, 30, not going to work as well. Might do something, not going to work as well. Day 1, 2, 3, 4 through 7 to 10, probably going to work really well. So there's absolutely nothing wrong with convalescent plasma. You're going to get a broader type of antibody to respond to. But the biggest thing now would be, what's our availability of convalescent plasma? Who's making it? How available is it? Is it in the distribution pipeline like My health department just told me the monoclonal antibodies are, or is it going to be hard to find? This is something that, you know, like the old commercial, only your hairdresser knows. This is something only your doctor and your hospital really are going to know, because the distribution of these drugs, although the new federally purchased monoclonal lab antibodies is going anywhere you want. Convalescent plasma depends a lot on your center, your usually hospital, and were they harvesting convalescent plasma. So again, earlier is better, going to be the same administration profile, it's all that. So then, and let's see, I'm just I'm referring to my, my notes from all over the world, including my local health department here, just to make sure. Um, so I think we kind of covered the monoclonal antibodies, whether a lab made them or whether, you know, you made them and loaned them to somebody else. And we went through the criteria for who gets them. So before I move on, Other things about high risk: 65 or older. 65 or older is pretty much high risk for everything, though. Overweight, a BMI of over 25, so heavy body habitus, overweight. Pregnancy. Chronic kidney disease. Diabetes of type 1 or type 2, so any diabetic. And if you take Diabetic and overweight. Um, you literally have about 45% of the U.S. population, and that's not a judgment, that's a statistic. So this is not a small group of people that's being targeted here. Weakened immune system— remember from our previous discussions, that could be due to medications you're on, due to previous diseases you've had or immune deficiencies. Currently receiving immunosuppressive treatment, like I said. High blood pressure and other cardiovascular disease. Now if we take all types of diabetes, being overweight, and then all cardiovascular disease, that's the majority of the United States population. Chronic lung disease, sickle cell disease, neurodevelopmental disorders, And then medical technological dependence, which could be in anything that, that is required to keep you going that is a medical technology. You can kind of fill in the blank there. And one of the experts was asked, so, you know, so let's say I'm exposed or I test positive but I don't feel sick, do I need it? Yes, get it as early as you can. So that it works as well as it can. Also, you want to know that these are not— nothing we talked about anyway— they're not FDA approved. These are all under emergency use authorization, but there's nothing wrong with that. You just need to know that it's sort of a fast-track thing. So far, as far as, you know, and again, I'm not— this is not an editorial comment about anything. I'm just saying, uh, statistically, so far, statistically, the monoclonal antibodies or the convalescent plasma, as far as adverse events, uh, side effects and things, probably lower than, you know, than other treatments going on or other, other preventive things, you know, like vaccines, etc. So Good, you know, good stuff for those where they are appropriate. Now, the next thing is, what about not monoclonal antibodies or convalescent plasma, but what about other treatments? So I go in the hospital and, you know, as we saw early on, you know, you might be given steroids, you might be put on a ventilator, You may get off the ventilator, you may not, you might die. You know, there's a lot of we're not sure what to do. So one of the things that I really wanted to drive home about the antibody treatments, whether it's convalescent plasma or monoclonal antibodies, is there is great benefit in getting diagnosed and getting these things in your body as early as possible. Because they work faster and better the earlier you use them, and 70 to 80% reduction in serious outcome, etc. This is a no-brainer medically and statistically speaking. So because of 2 things, in the past we had people going in and they wouldn't really be hospitalized till they're in respiratory distress. And then now we know that we put a lot of people on ventilators that probably shouldn't have been on ventilators, and then they would die. You know, it's a pretty fast track. Well, what muddled a lot of this around the antibodies that for treatment was they would wait to give the antibodies till the person was hospitalized, and that's too late. Okay. This is why they're saying we don't prefer to give these to hospitalized people. Let's give them to people outpatient and keep them outpatient. So you really need to keep in mind that earlier is better with these sort of things. But what about other treatments that may be used either in or out of the hospital? Well, I'm looking at a— and I'm in the— when we put this up on YouTube, I'll put links down in the description box below. Usually there's a little chevron or a down arrow and you click on that and it goes down. Just be careful, there's an ad below this, which I get nothing from the ads, but there's an ad below. and you click on the ad, you may go to, you know, whoever the ad is for and not see any of the show notes. But for example, there's a, there's a National Institute of Health panel recommendation here. It's got all these pretty colors and it's going through, okay, they're hospitalized but they don't need oxygen, we can do these things. Hospital but need some oxygen. Hospital but need You know, a BiPAP or, you know, any other sort of assist device, and then hospital but needs like ECMO or something really high level. They have different recommendations from the NIH as far as what should we give people in these cases. So like everything, you're the best off if you have to be hospitalized, if you don't need supplemental oxygen. What they will often do there is to start steroids and then depending on your level, maybe some antiviral drugs. I want to talk about— sorry, just shuffling the papers. I want to talk about steroids and antiviral drugs for a little bit. Now, a catch-22 that we have is we had all this rules and regulations I just read about convalescent plasma or monoclonal antibodies. And one of the things was, you know, you're, you're going to increase your need for these things if you're on an immunosuppressive drug. Well, one of the most commonly given immunosuppressive drugs is a steroid. So whenever you're using steroids, you always have this, uh, conundrum that you have to monitor Which is you might need to save someone's life by giving them steroids, but on the other hand, if they have an infection brewing, the infection may kind of go crazy. And I've seen this happen, you know, sometimes in emergency medicine or other situations where you can't avoid giving steroids to somebody, but then their infection starts to get very aggressive. So you'll be monitored heavily, etc., if you're on those. Also, because of co-infections, you might be, uh, being treated for other infections that aren't COVID if you're put on steroids. So there's 2 steroids I wanted to talk about. One, because it's the most likely steroid you'll be given outpatient or inpatient. called dexamethasone, also known sometimes as Decadron, but dexamethasone's its generic name. Dexamethasone is extremely commonly used in emergency medicine because you can inject it intramuscularly and it gives the person a steroid benefit for a while. And you say, well, why do I need a steroid benefit? That sounds like an odd benefit to me. Well, it is a bit of an odd benefit, but the idea behind this is That— let's say you've had an allergic inflammatory reaction and they gave you Benadryl. It's calming that down, but you're still likely to go into a rebound allergy anaphylaxis. They give you dexamethasone, uh, you're going to be able to leave the ER and they're going to have a level of comfort. You're not going to go back into another allergic reaction. Why are they giving dexamethasone to people who have COVID with respiratory symptoms? It's because it, in a nonspecific way, shuts down inflammatory processes. And that is a two-edged sword, as I said. You need inflammatory processes for your body to respond to an infection. So shutting them all down is not always a great idea. But on the other hand, one of the things that will kill you rather quickly with COVID is inflammation in places you don't need inflammation. That's everywhere, but especially your heart, your lungs, your brain, and your kidneys. Inflammation in those areas will kill you. So dexamethasone is one of these recommendations that you see almost throughout treatment. Now, there's a separate, uh, drug steroid that is normally given by a respiratory inhalation, usually an inhaler or maybe, uh, a respiratory device like a nebulizer or something like that. And that is, uh, budesonide. It's a trade name, sometimes Pulmencort. There's other ones, but budesonide is an inhaled steroid. So then you say, well, does that have the same problems that giving me systemic whole-body dexamethasone does? Kind of, you know, inhaled steroids eventually have a systemic effect. But why are we inhaling it? It's because the first place we usually get in trouble with COVID inflammation is in our lungs. There are a lot of clinical guidelines coming out now that say if you have a respiratory-centered case and they're not hospitalized especially, it might be worth looking at inhaled budesonide to help with the lung inflammation. Now, why all this business with steroids when we know that this also has an immunosuppressive effect. It's because you can do things often about the immunosuppression, but if the patient dies from lung inflammation or some other inflammation, there's nothing to treat. A dead person cannot be treated for anything. Okay, so in medicine you always have to make choices like this, and you just have to make wise choices. So if For example, I decide to give someone dexamethasone or budesonide or any other steroid, the bigger thoughts I'm going to have are going to be, uh, what am I doing to monitor for other infectious processes? What am I doing to monitor for the suppression of normal immune response? Am I covering them for other infectious things that may be going on, etc.? So steroids are you know, shouldn't really be used alone. They're generally not, but they're in some of the first-tier type of treatment recommendations that we see with COVID But then we get to other antiviral drugs and immune-manipulating drugs. So some of these are biologic or biosimilars, like those monoclonal antibodies we talked about, but they're different, and then some are engineered antiviral drugs particularly. Okay, so when we look at these drugs and we look at like the one you see the most, remdesivir— remdesivir is a drug that's been around for a while, but what they found about it as an antiviral drug. And then when they looked at it with respect to COVID, remdesivir blocks viral replication. Now here's something that you can miss. It's a subtlety about antiviral versus antibacterial drugs. Antibacterial drug, like most antibiotics, will kill the bacteria through one or another means. So they may directly kill the bacteria like penicillin does, or they may inhibit its operation so it dies off with your immune system like other antibiotics do. When it comes to viral drugs, antiviral drugs mostly work not by— now, a virus is really active or inactive. It's not really alive. It's in your cells. it uses your cells. But antiviral drugs don't kill the virus normally. What they do normally is stop it from replicating. So I used to tell patients it's like viral birth control, literally. That is the important thing to keep in mind with an antiviral drug. It is an anti-replicating drug in many cases. So you hear of drugs not used as much for things like coronavirus, but like acyclovir or Valtrex, valacyclovir, those are viral replicator inhibitors. Well, remdesivir, which is the one that we've used almost the longest, was, was developed for other things and was used for the purpose of COVID because it appears to slow down the viral replication through a mechanism that's not really that important to talk about. Now there's some Other designer drugs. Let's say remdesivir isn't cutting it. They might try some of these other ones, such as baricitinib and tocilizumab and sarlumab. These are drugs that work either to block the entry of the virus through a different pathway than remdesivir. And/or they might block the viral entry and block an inflammatory cascade. So these drugs might be given to you and they might be chosen. So let's say your front end is what? Best thing, avoid getting COVID. But let's say that didn't happen, high exposure or your early diagnosis of COVID The next wave is going to be to give you convalescent plasma or monoclonal antibodies, so antibody therapy. Then if you need to— and you want to do that in the first week to 10 days— then if you need to and you get hospitalized, you might be given steroids and other supportive treatment and remdesivir. And if it's— if you've gotten more severely ill, they may move on to the, uh, the BAR-1, the TO-1, and the SAR-1. So we'll just leave the long names out of it. Um, why might they do that? Because here you have different mechanisms of action of the drug than remdesivir or the antibodies, and you have a bigger, uh, entree into treating the more severe disease. So remember I said it could help to block, uh, the replication or uptake of a virus, but it might also do something like block interleukin-6. Now All along the way through COVID, when we first heard about COVID and the infamous cytokine storm or cytokine release syndrome, everyone said, well, that's what kills you, which is true. Well, interleukin-6 is part of what kicks off the cytokine release syndrome. Here's a problem with blocking interleukin-6 universally: it's also part of your immune response. So just like if I give you too many steroids and your immune system shuts down and you die, that's not a great thing. If I block too much interleukin-6, you might die as well. So these are very carefully balanced normally. And so interleukin-6 inhibitors are trying to do what the steroids are doing without using a steroid to slow down the inflammatory response in your lungs and elsewhere. So, uh, Things like talizumab and sarlumiab, those drugs, baricitinib, they're working through these other mechanisms, and you might be given those if you are sicker or in more peril. Okay, so you need to start to think about— we've got tiers of treatment. So you might have a family member, as I have, go into the hospital with COVID. And someone may say, well, why aren't they giving the monoclonal antibodies? Might be because it's too late. Or why did they stop the remdesivir? Well, there's a couple reasons for that. One is it may not be doing anything. The other is remdesivir can raise your liver enzymes, and sometimes that's not desirable, so they'll move to other, other drug therapies. But the important part about this is there are things that can be done And I think that one of the sort of things that made people hopeless, especially the first year, was, well, geez, if I go to the hospital, everyone I hear who goes to the hospital is on a ventilator and then they're dead. Uh, you know, I don't want to do that. Well, nobody wants— you shouldn't do that. No one wants to. Now there are more levels and layers of therapies that can be used, but the goal of any good interventional therapy is to use it when it's appropriate. If you're, you know, unless you have no other options and you're just trying sort of a Hail Mary pass, you generally are not encouraged to try and give a therapy that would've worked a month ago. You try and do things in an appropriate time, in an appropriate format and all of that. So, these other drugs that are biologics, biosimilars that mimic things in the human body or block them through biologic means, They're good drugs, they work well, but they only do what they do. Now, what does it mean when we get to antiviral drugs, the fact that they're a viral replication inhibitor versus a viral killing drug? Okay, well, if you go to the bacterial model and you have, uh, a, you know, bacteria that penicillin will kill, and that bacteria is going to kill you You give you a lot of penicillin, that bacteria all dies, or most of it will die, and your immune system clean it up. If we go to the viral model and we use most antiviral drugs and they're just replication inhibitors, then what happens is that the viral load that's already in your body is still a major player. That means your immune system has to do a lot To keep up with the viral load that's in there. Yes, the new drug is stopping— put a cap on viral replication, but if you already have billions and billions of viruses in there, they're still very active. So this is where the combination of a viral replication inhibitor and some other things that we'll talk about, especially in the world of supporting the immune system, become very important. Okay, viral replication inhibitors are wonderful, but they only do what they do. They can't get rid of the viral load that's already in you. Whose job is that? Turns out that's your immune system's job. Now, could that be helped by convalescent plasma or monoclonal antibodies? 100%, especially if it's early on. So sometimes the people on that front-end curve where they do get to the hospital They might still get monoclonal antibodies or convalescent plasma and remdesivir. Great combo there. What are other things that help your immune system? Being generally healthy, you know, not being on one of these lists that I read to you. Okay, there's not a whole lot you can do about your age. So if you're over 65, you're over 65. There you go. That one none of us can really do much about. Uh, if you have type 1 diabetes, pretty much that's not going to go away. Not much you can do about that. If you have, you know, if you're overweight, you have the ability to work on your, your weight and type 2 diabetes and stuff, great. You know, those are helpful things. But there's a lot of shades of gray in the world of things that make our immune system work better and worse. Remember, we've talked about things like not sleeping enough. Not sleeping enough is the best way to run your immune system down and get you very sick. Not eating the right things, all that stuff. Yeah. Well, let's talk, uh, for a moment now about the atypical drugs that are being used or being recommended. Well, atypical drugs include a whole bunch of different things, and some of these would be like the budesonide. The inhaled steroid is still considered a little atypical, although we use steroids all the time for people with COVID But then there's other things we've talked about that make more or less sense. So early on, you heard people using an antibiotic called azithromycin with other treatments. It's like, well, that's an antibacterial drug, how does that work? Or then you see this research, and we've talked about it, come out about doxycycline, again an antibiotic. Yeah. Uh, how does that work? Well, it turns out doxycycline has 2 big benefits. One is it actually appears to be an antiviral drug as well. We kind of knew that before, but now it's a little more popular. But 2, maybe the most important, is things like azithromycin and doxycycline kill what we call atypical bacterial infections in the lung. Why is that important? Because many people with no symptoms at all carry chronic atypical bacteria in their lungs, and those atypical bacteria give you no symptoms because you're not sick. But as soon as you get the flu, a bad cold, COVID, whatever, inflame your lungs, guess who comes out to play? The atypical bacteria that live in your your lungs. These tend to end in the word pneumoniae because they cause atypical pneumonia. Doxycycline, azithromycin, both are used as primary treatment to kill atypical bacteria in the lungs. And what I've seen with people is as soon as they light up a viral infection, whether it's COVID or any other bad viral infection, if they have these atypical bacteria in the lungs and you don't treat them The person will be 2 or 3 or 4 times as sick. So doxycycline and maybe azithromycin have some antiviral effect, but they also kill the hang-on or the superimposed infectious agents that actually can kill you if you have COVID. So whenever we're thinking about COVID we always have to think about immune suppression, all this other stuff, but also co-infections. And I've said this before, and it's not the point of this particular talk, but just so you know, you know, one of the things that we saw the earliest from all the research was the sicker you are with COVID the more likely you are to have multiple other infections going on. If your doctors are not treating those, they will be a giant hole in the immune bucket. Now, most hospitals now are very on to this because it's been so much in the research. And they will check for certain types of, you know, fungus and bacteria and stuff. And sometimes they'll just empirically treat you, meaning just treat you because you already have COVID and you probably need to kill these guys. But that's a very important thing to think about as well, is these co-infections and how these other things work, like doxycycline, azithromycin, and there's other things too. Now there's 2 other drugs, and if I say them, what I have found is there's, uh, you know, bots that read every word or hear it or whatever it is the bots do, and I'll either get this video taken down off of YouTube or it'll— some other bad thing will happen. So I'm gonna maybe give some initials and I'll let you use your imagination. One that was talked a lot about earlier starts with the same letter that horse starts with. Okay, horse, horse starts with H. That one actually is still in some treatment guidelines and not others. And what it does is a number of things. One is it kills other bugs like doxycycline does. It also is a zinc ionophore like Quercetin and EGCG. Well, this one's a strong zinc ionophore, puts the zinc in the cell. Why do we care? More zinc I put into the cell, the better my natural antiviral mechanisms go. So the H1, you know, H is for horse, that one is still going on and off different treatment recommendations around the world. It's used in some places, not used in others, but if, you know, we speak about it, stuff happens. The other starts with the same letter as ice. So I is for ice, right? This one has been in the news a lot. It's very controversial. And what I will tell you is that that particular— all of these drugs, actually, these atypical drugs we've talked about, but especially the H and the I one, I've used those in chronically ill people and people with cancer for going on 20 years now as repurposed drugs. Repurposed drugs mean it originally went for one reason and we use it for another reason. Very useful in some cancer situations, very useful in some chronic illness. They have their side effects and all that. The problem is that they've gotten a lot of kind of smear campaigns going from people who didn't ask any of us who've been using them a long time in humans. And so the data and the information goes a different direction. What I can tell you is they're not magic. They don't, you know, cure everything. They don't do all that. But they are used in many, many countries around the world, again, to augment the antiviral and the anti-comorbid or co-infectious infection issues around their COVID patient. The other thing, uh, was there have been these— there's something called a meta-analysis where they look at like all the research around one thing. And some meta-analyses that have been recently redone with their, um, statistics looked at show that in, in largely with a drug, when you have meta-analysis, it's sort of a spread from the left to the right. It's like a graph, and they look at all the different studies. And in the case of these drugs, especially the second one I mentioned that we're not using the name of, the meta-analysis shows in favor of using the drug, meaning that the research bore that out. Now, that's not what's reported in the news. I don't know why. I don't— I'm not part of the news. And Frankly, I don't care. Uh, I would like real information to be given out in the news. That's great. Or we can give it out here and just not talk about what we're talking about. Um, so that's another thing. Now I'll put the references for this stuff, uh, down in the, in the description. Again, a little chevron or down arrow when, when we put this up on, uh, YouTube. I'll, I'll only do it on YouTube. We, we live stream it elsewhere. I don't put up references in those places because it's— there's other things things that happen to those of us that mention things about COVID Anyway, there's all sorts of other stuff we could talk about. Intravenous vitamin C, remember all those new designer drugs that lower IL-6? Remember that one of the most effective lowering of IL-6 is intravenous vitamin C, which is why we try to get that used in the hospital when we can. It's hard to do, but we try to get it used when we can. And I've seen people come off ventilators using intravenous vitamin C in the hospital. Nutrients, of course, nutrients are always important. If you start taking all the good nutrients, are you sure not to get COVID? No, it doesn't work that way. But why not be as healthy as you can? And I've got YouTube, I've got tons of stuff on my channel around that. So we will put up all of the references that I was looking at, talking about here today. Or at least those that are germane to what we were talking about. So we're running down to the last couple of minutes. And I just wanna remind you that when you hear about a designer drug, a biological drug, a biosimilar drug, just because it's that doesn't mean it works the same as all the other 100 biologic drugs you might hear about. So the monoclonal antibodies are just mimicking your antibodies. Are they as good as your antibodies? No, but we can put more of them into you. And so you have a better head start. Nothing wrong with that. That might save your life. 70 to 80% reduction in disease state, etc. You can't beat those odds. Convalescent plasma, do it early, just like the monoclonal antibodies, works pretty good. You're probably more likely nowadays to find the monoclonal antibodies because you and I are paying for them through the U.S. government, so they're going to be around. They're being shipped out en masse. And like I say, whenever doctors get these flash updates about, hey, you know, the drug is here, here, use it, there's something going on behind that with, with the government. But remember, we're paying for it. I don't mind because I know that that intervention at least saves a lot of lives. So let's do it. All right, I'm Dr. Paul Anderson. This is Dr. A answering questions. Which I do on this channel. Today we were talking about, uh, COVID therapeutic confusion. Uh, for those who've joined us on YouTube, uh, you just go over there to YouTube, you can find me. There's lots and lots of videos up. Uh, like, share, subscribe, all of those things very, very important for the channel. And I want to thank you, uh, coming to you live here on Contact Talk Radio Network. But I will see you all Next week on the radio, you've been listening to Medicine and Health with your host, Dr. Paul Anderson.