Ivermectin after vaccine injury, Dr. John Campbell
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Sir Jonathan Symonds CBE: Moments of Genius | Global Healthspan Summit 2023, Riyadh
Governments have to recognize the economic case for investing. And we've had some fascinating conversations in the UK and asking them, how do your economic models deal with the year on year decline in productivity that comes from an aging population with increasing chronic disease and an increasing proportion of the population that are caring for those who have got either aging or chronic disease. And until you recognize the cost, you can't put the investment case forward. And I believe that that's where we have to go in the UK. We have to build the investment case for prevention and early detection because economic growth depends on it.
Ivermectin after vaccine injury, Dr. John Campbell
.
A warm welcome back to, professor Robert Clancy in Sydney, Australia. Robert, thank you so much for coming back on. Thank you for having me, John. Robert, of course, is a is a friend and a friend of the channel. He's a doctor of medicine, a doctor of philosophy, a doctor of science, holder of the Australian medal, and, long term consultant physician and and professor.
So his insights are really quite, quite unique into this situation. And recently, Robert, you've had clinics where, I I know this because I I was at one with you, where where you were assessing and treating patients with long COVID and and long vaccine injuries? That's true. It was wonderful having you, John. I do remember that occasion.
We you you probably saw how how my practice has become dominated by, post vaccine injury. It's it's become a a real pandemic on its own. Mhmm. Now I'm a bit confused between the clinical pictures in people with ongoing long covid, which does seem to exist as a phenomena, and people with vaccine injuries. Is is there a commonality in presentation and there's a commonality is there a commonality in response to treatment?
Yes. It's it's a very good question. Traditionally, traditionally, in this business is only a couple of years, because remember, COVID is a pretty new, still very new challenge, and this conditions how we think about it, what we understand about it, and how we treat it. So, it's very much a thing in progress. I think many of us started seeing patients who had vaccine, but never had COVID, and noticed great similarity between the symptoms of people following a vaccine and symptoms of those who have traditionally called long COVID, which is a sort of catch all phrase to basically say, look, you never really got over COVID.
And this has been a real issue, and I'm glad you brought it up because, it's been a focal issue of a very big, extensive investigation by the Australian government, which was just reported a couple of months ago, where they denied that there was any, connection, and they denied there was any connection with the broader range of chronic fatigue illnesses, which was I think a great disservice to all all three of these components. And I think that what brings the 3 of them together, and now we're just talking about post COVID, infection and post COVID vaccination, not only is the clinical similarity, but secondly, the fact that we now have much evidence that the essential cause is the same, and that is that the spike protein, which viewers will remember, is that part of the virus that binds to the cell, so that it can get into the cell, and then becomes the antigen or the part of the, the various vaccines, that's used to stimulate immunity. So spike protein is really very important functionally and in terms of management, but it's not so important if you don't clear it from the body. And the real issue with, COVID as an infection is that, in about 50% of people with significant COVID remember that post COVID, or long COVID is particularly seen in people with quite severe or more severe COVID, is that they get a viremia, which means the virus spreads through the vascular system, through the body, and we call that systemic spread, and so it sits, and the messenger RNA of the vaccine, goes into all the cells potentially in the body, producing the spike protein.
So you've got a persistence of the spike protein, and in some people, it we know it it lasts well over 12 months, and possibly a lot longer. And with the vaccine, you've got the same messenger RNA, with the infection, you've got the virus going into the cell, making this white protein. With the vaccine, you've got messenger RNA, which is part of the genetic apparatus, producing spike protein in potentially all the cells. So you have this persistence of the spike protein, and that's been very amply demonstrated over and over again. And so you've got this common cause, and so with common symptoms, common cause.
But but the problem that came up in the Australian review was that people giving information, and it's a bit hard to blame the politicians here because they're trying to synthesize the information they're given. They were given, I thought, very, superficial and restricted information. It was all about, oh, these people have symptoms. How on earth can you say the symptoms of long COVID are the same as the symptoms of vaccine damage? And so they put it aside, but again, that's really because people did not quite understand what why there's, people getting different symptoms.
And the cop the important point is that the common factor to all these fatigue illnesses is fatigue that's made worse when you exercise or do something. I've always called it energy activated fatigue. That is the common feature. Many, if not most, will also get brain fog. But what happens with the long COVID is that many of these patients have structural damage.
They have cardiac damage. They have brain damage. They have, probably the commonest one I see is peripheral nerve damage. I did a clinic yesterday, and I saw 3 patients, all with what we call small fiber, neuropathy as part of their problem. These structural damages didn't seem to fit with the fatigue, and they became the major factor that individuals were looking at.
But it was simply because the mechanism of the underlying fatigue is different to the mechanism of structural damage, and we may come around to to look at that. So I think the answer to your question is that they're essentially the same condition. Therefore, one looks at similar mechanisms and looks at similar therapies. So if there's ongoing production of spike protein, let let me clarify that. Is the spike protein hanging around, or has there got to be ongoing production of spike protein?
Oh, I think that, I think you must be having ongoing production because Yeah. We know that the messenger RNA vaccines are basically designed to keep producing, antigen. I think the hope was that they wouldn't, but the reality is that they do. And, I and in fact, in in so many of these people with post vaccine, damage, you can actually find the messenger RNA still still present, months or many months, after the the the vaccination. Mhmm.
So there's on in in both conditions then, potentially, there's there there there's 2 modalities or 2 pathophysiological mechanisms. There's one which causes the small fiber neuropathy, and that kind of happens probably fairly quickly and then could take, well, we don't know, a year or several years to to to recover, if at all. And there's the other mechanism, which is the ongoing production of spike protein, and that causes the inflammation, and that's part of the the the the ongoing inflammation is perhaps what's causing the the chronic fatigue and the brain fog. Is that? Yes.
I I think that's, in both instances, you've got an immune response to the persistence of an antigen. This is common to all chronic fatigue illnesses, and what's happened because the immune response is not doing the job as well as we'd like it to, you get what we call inflammation, and and I think we probably can tease that out a little bit later too. Please. But, the the difference between the fatigue component and, say, heart or brain damage is it's a different type of immune response in each case. They're both immune responses.
And what's different between the post COVID infection and post COVID vaccine fatigue illnesses is they tend to have a lot more structural damage, and this is because the antigen, the spike antigen, is sitting on the cell surface, of the cells that for whatever reason, messenger RNA or the virus in the cell somehow, are producing this, antigen. Antigen means it's foreign, it's going to be attacked by the T cells of the body, And so you get this response of T cells actually against the spike protein embedded in the cells, and so you're going to get damage of the cells. This was shown very clearly by German pathologists oh, now it must be about 18 months ago where they looked at people dying from, post vaccine damage, and they found the spike protein in the heart, and they found the T cells clustered around them, causing the damage. We call it myocarditis. If it's in the lining around the heart, we call that pericarditis.
So, we we have very clear data on this, and a very clear evidence that, for the structural damage, you've got, like an autoimmune disease, exactly like an autoimmune disease, whereas the fatigue illness, you don't get that structural damage. The, we we don't really understand the the precise parameters of this inflammatory response, but it's producing various mediators of inflammation. We call them cytokines or chemokines, depending on what those particular mediators do, but they're often small proteins that float around, and they seem to have an impact on on various tissues. Mhmm. Well, we know that these inflammatory cytokines and chemokines can make you feel pretty awful, because that's a big part of why you feel sick when you've got an infection or Absolutely.
After tissue damage or, you know, you you can feel you can feel pretty rough. I mean, I was knocked off my push bike once, and I damaged a lot of tissues, and I felt terrible for days, you know, as well as the pain. Just because you're releasing what whatever it is, these inflammatory cytokines. And, of course, if you're ill, you you feel pretty awful as well. Is is is am I right there?
Is is that is that the same mechanism? I was, giving a series of lectures in, Singapore, many years ago, and, I got, the flu. Now that flu virus almost certainly never got outside of my lungs, but I was so sick, I couldn't even get out of bed. They came and found me because I didn't turn up for the lectures I was supposed to give. I I thought I was dead.
I really thought I was gonna die. Now that was this massive release of the cytokines and whatever. Now if you do it in a very small amount, you're gonna get fatigue, and, that seems to be, the the common factor Mhmm. In all these patients. That makes sense.
And because we now know that this systemic the systemic distribution of the the messenger RNA that codes for the spike protein, The mechanism of damage on the peripheral nerves and the mechanism of damage in pericarditis, myocarditis for example, It's probably the same mechanism. It's the t cells beating up on on the cells that are expressing this foreign protein. Yes. I I think you're absolutely right. And so, therefore, it's not surprising that you get a combination of two patterns of disease.
You get the classic features that you see in anyone who's got chronic fatigue illness, going back, you know, back to the flu pandemics of of 19th century. And and on top of that, you're getting structural damage. In this case, because of the persistence of expression of the spike protein on the surface of cells in nerves and heart, etcetera. So it's not a secret. It's not a mystery.
It makes enormous sense, and, I mean, every day, more and more evidence is is supporting that that paradigm, that set of sequence, that leads to disease. I think the problem is Just make one quick point, and that is that spike protein itself is not just an ordinary antigen, it's a particularly nasty one, it itself can have cause damage, and so you've got 2 components to this tissue damage aspect: the intrinsic toxicity of the spike protein, and it's present as an autoantigen, if you like, on the surface of cells. Mhmm. Indeed. And the spike protein that's embedded in tissues have been attacked by t cells.
So we we know, for example, if a myocardial cell is destroyed, there's no effective repair there. There's no effective mitosis in in myocytes, and again with peripheral nerves although they can recover, the the rate of recovery is remarkably slow. So, even though even though the spike protein's gone from those patients, the damage can persist. And I think that's been demonstrated that we know that the myocardium, the the muscle of of of the heart, doesn't have the same repair process that, say, liver cells and certain other organs have. And and this has been pointed out by, you know, some of the the the prominent cardiologists, like Peter McCullough in in the United States, that, if you get a significant damage, a young boy gets a vaccine, gets a significant damage, he then has a scar, be it microscopic, for life potentially, and, if you have excessive exercise or emotion, certain times when you're sleeping, the adrenaline level goes up, and adrenaline, plus these scars, can lead to a abnormal heart rate and sometimes even fatal tachycardias ventricular fibrillation or ventricular tachycardia.
And this has been attributed to the increase in deaths in, athletes on the field, which has been noted over the last couple of years. I mean, it it's it's a hard thing to pin down, but it's certainly been widely described. And so I'm convinced I'm convinced that's true, but I suspect that the the time that people are most vulnerable to these arrhythmias, dysrhythmias, is is in the relatively acute phases when the myocardial cells are actually in the process of dying. Because when they're actually in the process of dying, they'll have difficulty controlling the electrochemical balance across their cell membranes, and be more likely to throw out ectopic electrical activity. And I think that's why it's so important that we should advise people who who are prone to who might be a risk of this not to take vigorous exercise for a period of time.
Absolutely. After Yeah. It? I have no idea. Infection or after well they shouldn't be vaccinated of course but after infection or if you were vaccinated after after vaccine.
Yes. I I think there's good evidence, isn't there, John, that that there's a a sort of peak of of unexpected mortality, following, vaccines, what, a week or 2, after. So, you know, they've they've had the damage, they're getting an inflammatory response, they're irritable, they're they're getting up and they're moving around, increasing their adrenaline. This is a well shown mechanism in mice, I think it was, that they found that they the mice poor mice were dying if they had minor cardiac damage and they were pushed and exercised. So, you know, it's not as though this is a fanciful idea.
Oh, and it's not new at all. I mean, when I was on coronary care in in the late eighties, late 19 eighties As as another complication. Yeah. Yeah. I I was I was a car and mechanic nurse for a period of time.
And, that was at the height of the running boom. Everyone was jogging and running around all over the place. But every year in the local run, someone would get a cardiac arrest, and and some of the time, you wouldn't get them back. That's good news. Very often when you look back were myocarditis.
Yeah. Yeah. When you look back, they they were just recovered they had a viral infection. They just recovered from a viral infection. It it's not new.
Now the other thing that convinces me about your thinking here, Robert, is the the response to Ivermectin. Can you just unpack that a little bit for us? What kind of responses are you seeing? Well, I I think one of the big breakthroughs in our understanding in COVID, has been related to Ivermectin. Now, again, I think pretty much everyone looking at this, would understand that Ivermectin has been a stalking horse for people who, basically wanted to protect a vaccine, and, it it it it's, I mean, I've used the word shameful perhaps on your programs, but certainly outside of them, that the most shameful thing that I think has occurred in the whole COVID saga is the depriving of people, from repurposed drugs, which could have saved a lot of lives.
Now, Ivermectin, I suspect, is probably the best of of these repurposed drugs, and, the the great argument around, Ivermectin, has always been that, well, you've got to have a mechanism, you've got to use it early, all that sorts of things. And, David Schaim, who is a very interesting American scientist, has put together the scenario of what's happening with Ivermectin, and and what he's shown is it actually came from 3 clinical studies. I I had my time, and I didn't didn't contribute much except write the article, I think, on one of them. The 3 studies showed, that if you treat people with moderate COVID, with Ivermectin, within 24 hours, the oxygen saturation can increase dramatically. Now no one had an explanation for this.
First of all, people couldn't understand why it was people who were didn't appear very sick, but, had COVID early on had very low oxygen saturations, well in the eighties, so it should be up you know, 94, 95, 96. And, when you treat them with Ivermectin, over 24 hours this would pop back to normal, and what David and some of his colleagues did in France was they showed that if you take the virus and mix it with red blood cells, they all clump together, and so it started making sense that if you had, moderately severe COVID, and the virus was getting out into the gas exchange part of the of the lungs, it would clump those cells so that they couldn't efficiently take up oxygen, because that's the job of the lung, to put oxygen into the body and carbon dioxide out. So, and then what they did was very clever. They put Ivermectin into the system, and suddenly, you could stop this aggregation. In other words, Ivermectin and other people had been showing that Ivermectin tightly binds to spike protein.
So here you had a situation where the spike protein on the virus was able to clump these cells, causing low oxygen in the body. Ivermectin could actually prevent that completely, and that fitted with the clinical observation that by treating people with low oxygen, it came back, to normal. And this changed the way I think people should be thinking about Ivermectin, and that is that Ivermectin works not just late in controlling the viral, replication, but also very early, by acting, if you like, like a, like a putting a clamp over the top of the spike protein, so it can't do damage. And so a number of us I'm not the only one who did this is doing this, and you put up a graph, which was the first patient that I actually treated, who had got post vaccine damage of the long Covid type. This particular young boy was immobilised.
He was found outside of a building by one of my colleagues, Tom Barodi. Tom saw this guy, but he couldn't even stand up. He was he had what's called POTS syndrome, which is a comp a type of, the, damage that you can get following vaccination, but an absolute classic case. Anyway, we treated him with Ivermectin, knowing about this new mechanism that had been described, and I make sure that all my patients do what I call visual analog scale. They take each symptom, and what you're seeing on that graph, and this is a graph that I had nothing to do this was done by this young university student, and I asked them to grade every symptom 0 to 5, twice a week before they start the ivermectin, and then and you can see that after about 2 weeks, basically all those symptoms are nearly right down the bottom, which is set close to normal.
Now the sad thing was that after a week was then he stopped the the treatment, and the symptoms started coming back. Now, the follow-up of this young fellow is he's now back at university doing extremely well. We reintroduced Ivermectin. He's titrated that against what he needs to get acceptable treatment. If he stops the treatment, the, the symptoms come back.
So, and I think you were telling me, off off camera, John, that you've had experience talking to patients with, you know, very similar, similar types of stories. Now we've obviously treated quite a few patients now, this way, and they pretty much if it's a clear cut story of either post COVID, infection or post COVID vaccination, pretty much, if not all certainly not all, there's 1 or 2 that haven't, it, but most of these people get a graph like this. Now they're they're not always quite as as good as this, but most of them have significant improvement. And and what I think is happening here is that the Ivermectin is capping the expression of the spike protein throughout the body on the various cells. Now the symptoms that improve quickly are the ones that relate to non tissue damage.
A lot of the people we see get what's called small fiber small fiber neuropathy. That is, it's not the big whole nerve that gets destroyed, but the very small fibers, and that usually they have burning feet. I had a lady yesterday had burning hands, and then she got burning feet, but they, in our experience, many of them do improve, but it takes much longer. It might be a month or 6 weeks or 8 weeks, and again, because, we can't quite get people to do large randomized controlled trials, you're not totally certain of whether some of those effects are the natural history of gradual improvement, because we know No. I'm con I'm convinced by your your cohorts of patients, Robert, and consistency with other physicians I've, had the pleasure of talking to around the world.
The the picture is consistent. Here you've got rapid reduction in chest pain, passing out this POTS syndrome, the fatigue, the the the the brain cloudiness, the the the the brain fog, all improving dramatically. How how long after starting the Ivermectin did these symptoms improve in this young man? Well well, you can see that on the graph, John. I think it's about 10 days to 2 weeks before you can see, as I'm looking at it, the the left side when when the ivermectin was about to start, and then they're treated with, the ivermectin for 10 days, 12 days, and then they plummet down to 0 or close to 0.
And about 7 to 10 days, we then stop. What I do is I give a 2 week trial, and then we stop the Ivermectin, and pretty much all of them are in exactly the same pattern. I know that, I was talking to, you know, the colleagues in the States, where they've actually seen 3,000 patients like this, and they say that they see the same the same benefits, and most of their patients are post vaccine as opposed to post viral infection. I think you And you've actually yeah. Sorry.
I was gonna say you've actually got the double confirmation there. You've got the patient improving dramatically when you start them on the Ivermectin, while they remain on the Ivermectin, they stay improved. When you take the Ivermectin away, the symptoms come back again. That's true. That's true.
It was interesting. I really followed the idea of, that David, in the States had had pushed forward, and we're being fairly closely associated with with that story, that that this is what what was happening. But in the back of your mind, you say, well, is there something nonspecific? And I I saw a very important patient, actually, also yesterday, that I I think was important, was a patient that really had had a vaccine, but the fatigue illness began about 6 or 8 months later. So the question I had is, can this person have a delayed sort of response?
Now, this patient is the single patient that has had absolutely no benefit, and it's quite interesting that although we we we felt it was, from a medical viewpoint, a a a reasonable thing to try because this person was so incapacitated, the patient didn't benefit. But, again, it was very different to all the other patients we're seeing where there's a clear cut relationship between the the insult, be it infection or or vaccine, and the generation of the their symptoms. So this this patient that didn't fit, Robert, he he had the vaccine, then there was a long period of time that he was normal. What was the kind of history? He was a person who'd had, a relapsing fatigue illness, and and came along and said, well, look, you know, I think it might be all due to the vaccine, but, you know, I had the vaccine some months ago.
I didn't actually I've had a pretty good period of time, and now that all of a sudden the the fatigue has come back. And, we said, well, look, you know, this is a bit different to what we're seeing, but let's see what happens. Nothing happened. So I think there's a There's 2 possibilities. Sorry.
I was gonna say there's 2 possibilities there, really, isn't there? What what one is that this is a delayed vaccine injury or presentation with with a different pathophysiology. And, of course, the other is it's not related to the vaccine at all. Correct. Correct.
And and we were giving this a trial on the basis of the first of the ideas that there was Yeah. A delayed effect, and the mechanism was similar to the other people, you know, that we were seeing. Mhmm. Now I think you've been thinking more about the genetics of this, these conditions as well and, again, the commonality between the chronic fatigue and the the post vaccine and long COVID. What what what sort of what's your thinking about the genetics of this?
Well, what we noticed was in a lot of the patients that we were seeing with post vaccine fatigue or post infection fatigue had a history of episodes of fatigue illness. Now, it might have gone back years before, you know, one person I had went back 20 years before when she was doing her final year exams at school, and, we call that I call it the HSC disease, because the final year exams here are called the high school certificate, and when I was in more busy practice than I am these days, I would be seeing every year half a dozen, a dozen young kids, with this, and then they'd get through that, and they'd be okay. Other people had a viral infection, and it took them a year to get over it. So there was this story I was seeing in patients, and it it suggested to me that there was a a phenotype, a particular genetically influenced phenotype, a proneness to developing a fatigue illness when they're exposed to precipitating factors, like a viral infection, a COVID vaccine, and, it it made a lot of sense. And then I started looking at at at markers that we generally used to see as being abnormal in people with chronic fatigue illness, and that is, did they have a slight defect in the antibody production by what we call a subclass deficiency?
And, I think it was a German group showed fairly recently that there's a significant, what we call, IgG 2. If if you look at antibodies in the blood, we say, oh, that's an IgG antibody. Now, if I can just go back a little bit of a step to explain this, that if you get a virus infection, you make progressively better antibody. You start off by making an IgM antibody. The names don't matter, but it's a it's not a particularly good antibody to neutralize that virus, but the body's very smart.
The t lymphocytes, remember there are b lymphocytes that make antibody, and then there are t lymphocytes that do other things. And we talked a bit about how they can damage the expression of spike protein on cells, causing structural damage. Now the B lymphocyte then makes an IgM antibody, great big awkward sort of affair, but the T cell comes along and says, hey, this is not good enough. So it switches. The IgM goes down, and an IgG antibody comes up, and that's the signature of having had a past infection.
That will stay with you, perhaps for life. But when you look at the IgG antibody, it's also made up of different components, and they're called IgG subclasses. And there are 4 main subclasses, 1, 2, 3, and 4. Immunologists have no imagination. Anyway, I can I could remember that, though, 1, 2, 3, and 4?
1 I I can too. I can too. It's about limiting my my cue these days. But, so what we found in chronic fatigue syndrome is that people are fighting the infection with one arm behind their back. They have a reduced IgG 2 or IgG 3, subclass antibody, and what they do not switch from the IGM to the IgG.
Now, I used to be so confused. I'd see people being sent to me by family doctors saying, what's going on? This person had glandular fever. You you call it infectious mononucleosis. Most people now know that's the EB virus, the Epstein Barr virus, and, you make an IgM antibody.
In fact, that's what you use to diagnose the infection. Oh, they've got an IgM antibody, and that disappears after a few weeks, and the IgG antibody comes. I'm seeing patients who have had fatigue following, glandular fever, infectious mono, infection, years before with both IgM and IgG. It was confusing, and what's happening here is that the T cells are defective, and this is allowing the persistence of this virus. In chronic fatigue syndromes, the persistent virus is the glandular fever, the Epstein Barr virus.
In post COVID infection, it's the spike protein. And so, you can start seeing that there's this common immune deficiency with genetic factors, the persistence of the antigen, be it a white protein or a part of a virus, and an ineffective immune response, which is the inflammatory component causing the symptoms. And so one of the reasons for understanding all of these three components as expressions of the same generic type of problem is that a paradigm can be built up that explains and links them together. And so, if there's a genetic factor, it may be that if you're getting a problem with glandular fever virus sorry for those who don't live in Australia, Epstein Barr virus that, you you make an incomplete immune response, and you get over it, sort of, get over it. And then come along and you get COVID.
Well, the same sort of genetic immune defect is there, and so you get the problem. Now that's been I've been finding in a number of the patients with, post COVID, fatigue illnesses that they've got an IgG subclass deficiency, many of them do, and many of them still have the signature of a defective response to the F star bar virus by still having an IgM, IgG, combination of antibodies saying, hey, I've got a phenotype. I'm around to get problems if I run into COVID. Now, to me this is incredibly important because should we be vaccinating those patients, should we be doing these simple screening tests? I don't know the answer.
These are issues that the people who, have, access to large, funding thing, they should be looking at this. And when we started talking, I was talking about the the the great disappointment of the outcome of our review, government initiated review of long COVID, where none of this sort of aspect was looked at. It was all very superficial stuff. You know, we need rehab, more rehab, so they put a $100,000,000 in into that sort of research, not a statement about, let's looking at what's going on and how we can understand and maximize the the benefits by looking broadly at this issue of phenotypic, fatigue illness syndromes, if you like. So quite a few of the patients that you're seeing with with post vaccine long COVID, whatever we want to call that, these these two things, Quite a few of them still have IgM, immunoglobulin type n to m to Epstein Barr virus.
Not a few not quite a few, but some. Some. Some. Yeah. And are you are you seeing IGM few do have IgG subclass deficiencies.
Yes. Right. And are are you seeing ongoing IgM 2 spike protein as well? Do we know that? Alright.
Look. I that it's the absolute obvious question, and, unfortunately, the routine pathology labs, don't do that as a routine. I wish they did. My problem, of course, is that, in the past, I had a laboratory with something like up to 60 sinus, and, I could simply say, look, guys. Just go and do an IgM antibody, but, I'm seriously old these days, John, and, I don't have that laboratory access anymore because I've retired from the university, but, that's desperately needed desperately needed and so easy to do.
Yeah. It's just so so obvious. I mean, well, if I can think of it, it's got to be totally obvious. It's a Yeah. Well, I think it's a probably probably answer to the question you asked, which was the genetic aspect, right, we have to look at what I think is very exciting, and that is the current what's called computational genetics.
Now, if we look at genetics, we understand there's DNA, there's messenger RNA, there's expression on proteins, and if we go back to Mendelian genetics, people were looking at big chunks of genetic change so that you didn't get that gene, you got a rare disease, it could be phenylketonuria, all these things little kids can get, and, Single gene conditions very often. A single gene causing a disease. But, of course, things changed when in the early 2000, we brought in, the piece using PCR technologies, you could start analysing genetics, and this, of course, led to the Human Genome Project, and we started looking at what's called SNP's. SNP's were identifying a single genetic defect that may not lead to albinism or or some major disease, but could influence the outcome of a disease. And these were called, single base replacements.
So you you know you've got these 4, base components in DNA or RNA, and if one of them was just missing, it could not necessarily lead by itself to a major disease, but could influence. And when they started using SNP analysis in, post COVID, there there were rare findings, so but not not a lot, and it was a bit disappointing. And so we've moved from the Mendalian to the SMPs, using, genome what's called genome wide analysis, using PCR technology. And then more recently people said, Wait a second, maybe we should be using analytic methods that look at the interaction of genes. And this is called computational genetics, where you actually look to see how this gene, is there a minor defect here that works with another gene to actually have an expression?
And when they did that, they started finding in chronic fatigue illness, post COVID vaccine fatigue, and post infection fatigue, very similar genetic abnormalities. And this, to me, was a huge breakthrough. And there were clusters of these, and the clusters tended to relate to 2 different biological, aspects. The first was the development of an immune response, and that made a lot of sense. We've got a cluster of these interactive gene abnormalities related to not making a great immune response to get rid of that spike protein or the Fstarbar virus or the Ross River virus or, CMV, any of these other viruses that can cause a fatigue illness.
But they also found a second cluster, which related to defects in mitochondria. Now, mitochondria are little tiny organelles in the cell, which are like the batteries of the cell. This is where you generate the energy. You make the, it's like a bouncing electron chain, and these electrons, bring together phosphate bonds that are high energy, and they can be used by the metabolic processes of the cell. And so this was really, really exciting because for the very first time, there's a potential mechanism of the major symptoms that characterize every person with pretty much every person with chronic fatigue illness, no matter what the cause, and that is energy activated fatigue.
So if you've got a lousy battery, then the energy, particularly when you're stressing it by wanting to use it in muscles and whatever, makes a lot of sense. I'm not saying this is the course, but to me, I found that extremely exciting, and the other really important thing is the same clusters of genetic abnormalities were present in those who got post COVID infection, long COVID, following post COVID vaccination, and in people with chronic fatigue illness. Not identical, but very similar. So all of a sudden now, the story is starting to evolve that, as a result of clinical, metabolic, and genetic studies, we've got this FINNA. People are born with, a proneness, if you like, in certain circumstances to get a fatigue illness, and so it's not surprising that when you've got something, like, messenger RNA vaccines, which cause up a cystine antigen, and you've got a nasty virus that's likely to, get expressed, on a longer term basis, that, you're going to get up to 5 to 10% of people getting chronic fatigue illnesses, plus of course the structural problems due to a second type of immune response to these persistent antigens.
Does that make sense? It does. So we we have these one or several of these single nucleotide polymorphisms, these the the a t c t a c g t letter could be switched. So the a c g several a, t, c, and g. Yeah.
Yeah. Glamydia had the same guamette. Yeah. Yeah. Exactly.
Yeah. I always remember it's a to t and c to g. That's how I remember it. I won't tell you how I remember it, John. I I took a I took a year off in doing medicine.
I did a bachelor of medical science research, and we were doing the the really the first, messenger RNA, analysis in metasoan multi cell systems, and I had to work with chickens, chicken egg, embryonic, 12 day old embryonic chicken eggs, and I never ever, ever can eat an uncooked egg anymore, but one thing I did learn was, the base, the base ratios of nucleic acids, and that was in just 1963, a long time ago. Wow. Some some of the pioneering work into into RNA. That's that's amazing. But so but but what what is is now becoming obvious, really, is this computational genetics where it's not a single gene or even 2 genes or 3 genes or 4 genes.
It's a whole interaction, genes, some genes switching on, some genes regulating, some genes down regulating. Yeah. And it's almost like a complex emergent biochemistry that emerges from this from this whole thing giving varying degrees of of of predisposition. It makes it makes perfect sense. Yep.
What what what I would like though is some way to upregulate the immune system so that the the body itself can down regulate the spike protein production. Any way we could possibly do that? Well, I as you you possibly know, I I have certain views on on all of this, and and that is that the, I think we're taking some concerning roots in how we manage conditions like COVID. I think what probably the biggest mistake we made, was to, I'm an immunologist, so I'm all for vaccination, but I think what we did hereand I'm not buying into messenger RNA, I've obviously got views on that too, but I think that what the biology, the history of biology shows, from 80 years of flu vaccination is that a vaccine will never be a central the central the central component for managing a pandemic to an inhaled virus, because you're straightaway looking at trying to overcome the biology of 2 separate systems. You're injecting 1, and you're getting infected in the other, and they don't talk to each other very much.
And when they do, you get incredible suppression coming from the, mucosal root. Now that that was all known right at the beginning. Now the, and so, the vaccine was never going to be the the central component, and so The vaccine's only working systemically. Yeah. It's not working it's not working where the virus gets in in the mucosal.
Impact is is important because they will help when that virus gets into the gas exchange part of the body, in the lungs. That that is handled by the systemic IgG circulating T cell response. And so there is no argument from me that you do get benefit against serious disease, but, it's it's transient. It's in the early stages at least, and I'm not sure it would work. Yeah, the vaccine producers have never ever kept up, and in any case, vaccine's got other issues.
So, what I'm really saying is that I don't think that is going to be any more productive than we have had over 80 years of flu vaccine, and the Chinese vaccines are just as good. The Australian vaccine produced, at Flinders University is just as good, at preventing without without the dangers, but they're not going to change the course of the disease. They won't affect getting infected or giving the infection to someone else because you're vaccinating inside the body, not the mucosal surface, which is talking about getting infected and getting other people infected. So you have to think of something different. Now, the way we've thought about this is that, trying to answer the question, why is it that if you get a 100 people getting a virus, flu or COVID, 90 5% really do very well.
You know, I've had COVID twice and, or have treated myself, but but even so, in my health anyway, none of us have got particularly sick, but I've got friends who have got very sick, and, I know obviously of people who who have died from this. It's only a small percentage, but when you start off, we're all sitting there in a room. We all look the same. We think we're we've got the same immune system, but we don't. So what is the difference?
So my group, over many years, we've we've been looking at where there's a difference, and what we showed was that the way the the body protects itself against these and how virus is by swallowing the virus, and there are little organelles in the lining of the the gut called Peyer's patches. They're little limp like little lymph nodes, And that's yeah. They're they're little organs. Organelles or what, you know, organs. And and they make t cells and b cells, antibody producing cells, the b cells and the t cells, and they then go through the bloodstream to the lung.
The lung is a very clever organ. It doesn't want to be bothered with having to learn how to protect itself. All it wants to do is put oxygen into the body and take the carbon dioxide out. That's what the lungs are there for. They do a few other things, but that's really what they're there for.
And so they, if you like, have this off-site system where you you make all the immune cells, and you tell them what to do by swallowing what you've got. Sitting here, John, for if we sit here for 24 hours, and I won't do that to you, we'd swallow at least a cup full of secretions without knowing it. And, of course, all the bugs that we have are in that cup full of secretions. Now, what we found is that 1 in 4 people do this process very inefficiently, and we can make that far more efficient, by actually feeding the the one of the bugs that, make this system work well. It's so simple.
It's so ridiculously simple, and yet what it does, it dramatically changes the way in which the airways control an infected virus or a cell, so that you actually look at the idea of immune resilience. And while immune resilience is not something that's easy to measure, it can be done. Some people are over here, and what if you can push their resilience over to, the other side, you're actually preventing them getting serious disease. So my view is that that what we have to start doing a lot more is looking at making people more able to resist getting serious disease, using what we do know about the the biology. And this is something, obviously, my group and others I hope there's others, seriously looking at, so that we we when a pandemic comes, no matter what that pandemic is, you've helped that person respond to the pandemic in a mile away than they would have if they were sitting there without by making their processes, physiological process, far more, efficient.
And this will boost their mucosal immunity whether it was a bacterium, whether it was a virus, whether it was something cooked up in a lab in Russia or wherever, it it would it would just increase our ability to resist inhaled mucosal surface exposure to antigens. Exactly. Exactly. We've been developing this for 40 years, really, and, you know, we've shown that in people with chronic damage to the lung, people with COPD, M5, Zima, we actually reduce admission to hospital by 50 up to 50% in people who have got chronic, cough and sputum, with they're called exacerbations there. When they get a virus infection, they get an exacerbation, and that's the thing that puts these individuals into hospital.
We can halve that by making their process work more efficiently. We've now started thinking much more about, as a result of COVID, the normal healthy, so called healthy individuals, particularly people with risk factors like smoking, older age, who could do with, improving their delivery systems. And we are not short of people with acute exacerbations of chronic bronchitis in hospitals. We have. Oh, yeah.
Well, we've got plenty of those. I mean, with the surgical wards fill up with them every winter, and I know. Surgical patients don't have space to fit in. So 75% of us aren't really very good at this. 75% of us are sitting there swallowing these bugs.
No. 75% of us are very good. It's a 25%. Percent are very good. Yep.
25% aren't very good. Yeah. But we all get a boost if you increase the number of bugs that we're swallowing by giving these attenuated bacteria to swallow, that's going to give everyone a boost to some extent. That's right. Exactly.
Exactly. What we're doing is shifting the resilience, so we're making them more able to control the response to a in hard virus, be it a Mhmm. Flu, coronavirus, or whatever. So interesting questions there. Very obvious questions because I I I can think of some of them, and and, obviously, you've thought about these in more detail.
Things that could easily be tested with basic laboratory testing, with with, I think, pretty basic research techniques. We're talking about pretty basic prospective research methodologies here, and these things could be completely answered if if if there was the will to do so. Yeah. It's it's interesting. I think about this a lot.
What I've noticed, is that science has been dominated increasingly by people doing PhDs in maybe a single cytokine, a single chemokine, and the literature is peppered with fascinating observations in the lung. You know, why have they got these funny cells? What, is not happening is that young scientists, and unfortunately some of the people who are responsible for the training, don't seem to understand that you need to understand the big picture. You need to understand the broad physiological framework, so that you can interpret and understand the, the specific specifically identified abnormalities, like a particular chemo kind, and what is a TH17 cell suddenly found in a lung? What does that mean?
Well, if you don't understand that that's the cell that's been delivered from the payers' patches, I mean, it sounds so basic and simple, but but it happens all the time. Yeah. Well, that, and and in combination that that and and in combination with the fact that a lot of research is done for commercial ends. A lot of research is is done by people that can afford to pay for it or companies that can afford to pay for it. That kind of epistemological problem that you've identified and this sort of, I don't know what what you would describe it as, an unfortunate financial situation.
There's there's a a deficit between the, the money to sense ratio, in in a lot of in a lot of these, situations. And, and Yeah. It's hard. It's the way in which people allow Short short short term commercial interest. Yeah.
I mean, we're responsible for allowing this to happen. We've, you know, a a company, they see their responsibility is they're focused on rewarding shareholders, and they're gonna reward shareholders by having a patented product. It doesn't really matter in a sense from the shareholders' viewpoint whether it's very effective or not effective or causes more damage. It's gonna be sold at great rate. I mean, let me let me give you an example.
I'm just writing a thing at the moment on on different ways of really repurposed drugs, and this is data that's in the literature, that the cost of saving a life with Ivermectin in COVID is 25 US dollars a life. Now, I mean, this is a terrible way to look at medicine, but but just to give you an idea, the cost of saving a life with Paxlovid or Molyupiroviv, not that there's too many lives saved with them, but is $1,500. $1,500. No. Actually, no.
It's more than that. It was more than that. It was much more than that. I I can't. But we're talking It's it's probably it's it's that without for for a course, a short course, I would think.
Oh, $25,000. No. That's That sounds more like it. Well, no. No.
A 150,000. I mean, it was massive amounts of money. Massive. Massive amounts of money. Now this is all based on, relatively objective analysis.
Not And even if these drugs are absolutely brilliant, which, of course, they're not, but even if they were brilliant drugs, the the the cost precludes whole swathes of the world's population. Well, that's right. Absolutely. I mean, we we look look, it's interesting. Looking at the big studies that are coming out with these specific antivirals, you know, with their patents, they're all repurposed drugs, by the way.
They're they're not brand new, wonderfully, identified drugs because of COVID. You know, they've been tried out in flu. They've been tried out in HIV, found to be pretty ineffective, so they recycle them, but they've still got their pattern. Now, there's a big study, showing that pexlobbered, which was probably the better of the 2, has zero impact, 0 impact in resolution of symptoms or prevention of going to hospital. Now that's with the current isolates.
So in other words, the earlier studies which showed some benefit, even that was argued by many with the Paxlovid, But the early studies in your country, John, with Molnupiravir looking at 25,000 patients, I think it was the Oxford group that did this, 0, 0, effect, and yet every family practitioner in Australia is writing scripts for these every day at $1,200 a a time. I mean, it it's just and it's worse than that because of the problems that that are being seen with some of these people with the antivirals. And and no one seems to want to talk about it or or or do anything about it. It shows you what pain live. Ivermectin, we've got this obvious example and, in acute and chronic.
And, I mean, nothing's Again, in treating treating your patient, you you I think you got down to 12 milligrams twice a week, you know, really, really Well, so some of the people, when they stabilize, these are the post COVID, damaged patients. What we do is we we titrate to see how little you need, because remember, you know, this is all new. We we haven't this is a new problem. We we, you know, no one wants to be on a drug for a long period of time, but I think what it's showing is that if Ivermectin is acting the way that people like David Schein, are showing, then that as long as you need it, all it's doing is is preventing the immune response getting to the spike protein. That's how long the spike protein is sitting here.
It's an indirect index of how long the spike protein is persisting. Yep. And you you mentioned there, Robert, that a lot of this is new, but people like yourself who've got a lifetime's experience in research and treating patients, who are a lifelong physician and consultant physician, researcher, you're in the ideal position to transpose your existing medical knowledge onto this new condition, and as a result of that it really disappoints me that more people aren't listening to, people that are able to synergize the old and the new together, like yourself. And it just seems the height of arrogance not to listen, to to people to people with with high levels of medical, practical, and and theoretical experience. It's just we just seem to be in a bizarre situation.
Why do we bother having professors if we're not going to listen to them? It really is. Well, you know, this one's a a bit of an ex professor these days. But, look, I I I don't know. I can't talk about myself, of course, but what what I can say is that it's fascinating to look at the decision tree, the individuals involved in making decisions as you go down through all aspects of of any medicine, but particularly now it's COVID, where you've got this incredible, over overpinning, financial and political components.
What I mean, I was looking at the reports that were contributing to this, outcome of the government, investigation of post COVID, syndromes, and the individuals giving it were well meaning physicians, but I don't think there was one immunologist, I didn't see anyone I recognized as having an understanding of the process of the disease. And so you're you're seeing if you look at the long COVID clinics in in our hospitals, they're being run by rehabilitation doctors or respiratory physicians, all of whom are important, and I would never underpin the, the not the importance of rehabilitation, in managing many of these patients with chronic severe illnesses, at all. But what I'm saying is that that these were the individuals who seemed to be giving the information, and it's it's not surprising that, a very competent person, politician who happened to be a very experienced pediatrician, who was chairing the committee. I mean, you can't expect him to have, an intricate knowledge of the immunology of COVID, but he's getting the input from my colleagues, some of my and and that input's important, but there was no input from people who I thought understood the the disease. And this is the same with all the decision making, components of the decision making tree, that, you've got public health, physicians who, are very good at aspects of public health.
But quite frankly, I've I've yet to meet one that really understands, the immunology of of a mucosal infection, and yet they're the people we see on TV. Many of them haven't even got medical degrees, so they can't be expected to to really understand these processes. And we're having a we're having a a review at the moment of of COVID, and and an old friend of mine happens to be chairing that, who is fantastic, but, you know, she's, not a physician, not a scientist, and the 2 people are assisting individuals who are a long way from understanding the biology of of the disease. So, you know, what can I say? Yeah.
Well, we are biological entities. When the physiology goes wrong, that becomes pathophysiology, and there's no substitute for understanding those mechanisms. And then applying those to the clinical pictures that we see is, it's not something that can be dispensed. It's it's a resistance. We have a, a thing called APRA, which is, it's a commercially run, organisation for supervising, the registration of health professionals.
Now, I looked at APRA, and they were making some pretty silly decisions, and, I thought, well, I'm one person in this country who who has a background of understanding this type of problem. So on two occasions, I contacted them and said, look, I'd be very happy to help you. I mean, I'm not trying to be arrogant at all because there are other things I can't help with, but this was some area I could. I didn't even I didn't even get a reply, not even the courtesy of a reply, and that was with 2. And that is a repeating pattern.
I I tried with several other organizations, and, you know, that's just the reality. It's kind of an obtuse obtuse component to it, isn't it? Just a refusal to to learn lack of humility, arrogance, I suppose. It's, it's it's a very strange find. I think what what I've described as arrogant is having a bureaucrat telling me how to treat a patient, and, you know, this is this is getting a little bit away from what we've been talking about, but for for I got myself in hot water about 3 years ago when I wrote an article, for a very interesting, good journal called Quadrant.
And I said, look. This is I wrote it at the end of 2020, and it was published in January of 21. And I said, look. This is what I think is gonna happen as a person involved in the biology, all of which has basically happened. But, I pointed to the the value of repurposed drugs in a circumstance where people were dying and and, they were being told to go to hospital if they couldn't breathe and get oxygen.
That was the, you know, the the way they were being managed. Now I got into terrible strife over that, and we were having bureaucrats making decisions, people who wouldn't know a sick person from a non sick person, or or doctors who'd never seen a patient for a long long period of time, making decisions to basically support a vaccine, as an experimental, registration. And people died as a result of that. Now, to me, the greatest, arrogance and and shameful activities was to interfere with the relationship between a doctor and a patient, in making a decision with an accepted, safe drug that had some common sense, value of of trying because, you know, you what harm are you going to do? And all of us, use off label drugs, all the time, to to handle, patients who don't fit into textbook.
People don't fit into textbook descriptions. Textbook descriptions are you and me writing a book about a disease, which seems to put together most of the problems, but every patient's different and needs to be treated differently. Absolutely. Professor, as always, thank you so much. And next week, we are hoping to have a guest on the channel.
We won't say who it is at the moment because we're not quite sure whether we're going to get him, but it's gonna be very interesting if we can get, the 3 of us together. Do tune in next week. You won't be disappointed, and, we'll have lots more interesting things to talk about. But but for now, I'd like to say, Robert, I really appreciate the fact that this is this is pioneering material that you've chose to release through this through this medium, which is absolutely brilliant. It's going from, your experience to people around the world to consider, without having to go through the cumbersome process of writing papers.
I mean I know you are writing papers as well, but that does take much longer. So we really appreciate this sort of breaking medical news really, a bit of being released in this format. Thank you very much for that. And Well, John, I look, I'll just I know you want to finish but let me just say Let me just say one thing that the, part of the, confused process that surrounded COVID has been, the written information, at one level with the legacy press and at another level with the, the once trusted medical journals. Now a lot of what we've talked about would not be accepted by, journals that I've grown up with, that I've lived by, that I've paid for out of my own money that I because I I value valued those journals.
The level of corruption, I think, that has, seeped into, communication through the printed word, through the Trusted News initiative, with Legacy Press, with journals now that are charging 1,000 of dollars if you want to put an article in because it's only the big pharma companies that can afford that that type of money, it's it's a disgrace. And so, John, I think what you've done is you provided a third arm of evidence based medicine, and, this is respected across the world, as you hopefully know. And, people like myself really appreciate the opportunity of saying things that that we believe are are really important, and, so we're grateful for for this opportunity. Thank you. And, of course, the irony there is that that you can now not get published in journals that you've been published in all your life.
I could have a 3 hundred publications on a whole lot of this. But Yeah. Yeah. But, I know that, they wouldn't wanna publish, a lot of the stuff we're talking about. It's it's not to do with the data.
It's It's to do with, a narrative that's been so oppressively, overwhelmingly, influential. And I think people in the public around, they understand this better than, than one might expect. And increasingly so. Yeah. Increasingly so.
Yeah. Well, I'm gonna go to bed, and you're gonna start your day. So I don't have another cup of tea. Yeah. Good idea.
So so for now, professor, thank you very much as always. Great pleasure, John.