transcript to 69min podcast with DR Chetty - What's Hiding In The Autopsy Data Of Covid Vaccinated Patients oct 2024

Hello. Good evening to everyone. Thank you for joining us for what is going to be another fascinating discussion and interview with doctor Rory Donelligan and doctor Shankara Shetty. And we're talking about this issue about COVID and autopsies and the vaccinated cohort. Let me make it clear.

Just in case you come across anybody from the scientific community, every family has them who knows everything and telling you to stop worrying. They think that autopsies are being done, and they perceive that there are no issues. But the reality is is that only a few have been done. And how do I know? Because every week or other week, I check.

I type in COVID plus histology on Google search, plus autopsy. I am searching for them actively. So anytime a publication about anything about autopsy comes out, I find it. Why? Because I know it is that important.

My focus has always been on autoimmunity, and I know that the only way you are going to properly diagnose that is through autopsy. And so, therefore, without autopsy, there is no science. Listen. The autopsy is the equivalent of a financial audit by an independent accountant that most big companies have to do. And it's because that's the way that they ensure they're not hiding anything in the company.

That's where you really understand the profit and the losses, the implications to the company. And so that forensic audit that is required is essential. Autopsy is the same because once you see it, you can't unsee it. It is the equivalent of having a murder case and not doing the DNA, the the stuff, the basic important critical stuff that can't easily be refuted. That's the critical part about autopsy.

And so without any further ado, I'll add to the stage with me, Rory and Shankara. Rory, do you want to do a quick introduction of yourself? Yes. I'm an anatomical pathologist, of many years now, approximately twenty 5 years. 1st qualified in South Africa, but been mainly working in Australia subsequently.

Currently in the USA and Florida. On route I was on route to Bermuda to do some work there. But, yeah, I'm, specialized in, histopathology, also cytopathology. But when I started training, I did a lot of autopsy pathology in KwaZulu Natal, and, not so much subsequently. But I'm honored honored to be back with Excellent.

Excellent. Thanks, Rory. And, Shankara, a quick intro? Hi, Philip. I'm a natural science biologist in general medical practitioner, practicing where Rory used to be in KwaZulu Natal, Port Edward.

I'm a frontline COVID doctor who treated, numerous COVID patients. And, with my biologic background, I've been trying to figure out exactly what's going on in the consequences of what's transpired over the past 4 years. Excellent. You know, I I think I have to share something with the audience here. Now, we have had this discussion about 2 years ago.

We had a similar discussion. I think it was in October of 2022, we probably had that discussion about whether or not autopsies should be mandated. It may be coincidental, but within a few weeks of that, interview, I got heavily censored. They shut me down, took me. I think that we went too close to the bone.

And it will be interesting to reflect on the fact that we are back now. 2 years later, has anything actually changed? What is the situation really on the ground with regards to autopsies? Can you at least actually for the audience just give a basic overview of the autopsy and the link to histopathology? Well, yes.

Autopsy is the most complete examination, possible. And, typically, we we start with the patient file. We review everything in the file, including any ancillary studies that have been done, Radiology, you know, all the laboratory lab work, any antemortemistology as well. And, you know, based on that on those findings, we then proceed with an examination of the deceased, usually the day after we've reviewed all the charts. Initially, it would start with maybe a review of radiology that's been done, then external examination of the body.

Then we open up the body, and we and we examine each and every organ, treating the brain. And, subsequently, what should happen, and it doesn't always happen now nowadays, unfortunately, is that multiple samples should be taken at the time of autopsy, fixed in formalin, and then subsequently processed for microscopic analysis. And then those slides would be stained, typically with an H and E stain first and then multiple other stains as necessary thereafter. And we would formulate a final report based on all of those findings, the macroscopic findings and the microscopic findings and any laboratory tests that were involved. Now there are 2 main types of autopsy.

1 would be a forensic autopsy or coroner's autopsy. That would be mandated by the coroner. And those would typically be in cases where, you know, criminal malfeasance is suspected. And the other type is a is a hospital autopsy. And this could be done, you know, in any case.

They they used to be very commonly performed, you know, as a teaching tool, and and and were actually a requirement for academic medical centers to have autopsy facilities to teach doctors and and students. But unfortunately, that practice has waned over the years. Excellent. Excellent. You know, Shankara, as we we think about where we are now, can you imagine in your training coming up that autopsy wouldn't be central to medicine at this point?

I think, I think, Philip, it's absolutely vital. Steam what's what's happened. We know that the physiologic response, has changed. Doctors seeing very strange new symptoms, unusual pathologies, all that kind of thing. So we want understanding so that we can help patients.

That understanding can only come from a thorough examination of why that patient demise. Now, yes, we do understand that, it's a difficult process to do. But when you have a very unusual death, 20 something just suddenly died. A healthy, fit twenty something, and then it happens again and again and again. There's something going on.

And all we need to do is do a thorough autopsy on 1 or 2 of them. And that would then be kind of unsee it. Now we know that there's a lot of new pathology out there. We've seen the turbocancers, the clotting issues, the strange things. As a GP, I see it all the time.

But then there's also a lot of things that are going under the radar with omicron infection. Now usually, I mean, yes, you can ask a patient's question, how many people you know in the in in your family circle that seem to have been injured by the vaccination program, and a lot of people do. But, as well, simple questions like, have you noticed recently that when you get the flu, you're taking a long time to get over it, Longer than was, normal for you before. Simple things like that are going on. So we're triggering immune responses that are long lived.

People are unaware of it. That's gonna result in different pathologies that we see. So it's almost a retraining of the entirety of medicine and how we respond. And that's gotta start with how the patient demised. You know, I think that one of the things that the medical community is probably afraid of is the fact that if we have had fundamental changes to physiology across the pandemic, and you could argue whether it's from the infection or from the vaccination or the combination of both, it undoes, it it it removes the value of all the evidence that we have used for the past 30 or 40 years.

Because, say, for instance, with the clotting issues, if suddenly your anticoagulants are not as effective, in effect, you really need to go back to study all of them. Can you imagine doing those trials over and over again? It it's scary because suddenly now you don't have evidence. But we still have to ask the question fundamentally from a pathological point of view. Rory, why is it that pathologists don't seem interested in doing this kind of work?

This is what it feels like to the public. To me, I think the main issue is fear of reprisals, to be honest. They fear reprisals. And and and and and those who have done research in this field have been subjected to, you know, censorship, you know, board reviews, just as, you know, doctor Chetty has, you know, been targeted. And, I think it's that fear that maybe limits the number of autopsies.

Yeah. It it is a real issue that, the reality for many people is that the first person who does a study that finds, say for instance, significant damage, how are they gonna publish it? Because no it's one thing to do the study, then you have to put it together in a paper, then you have to submit it to a journal who is willing to put it out there as the first, say, for instance, that causes conclusive. Imagine if it showed conclusively that there was harm. Nobody will want to be the 1st to publish that.

Yeah. What do they do? Yeah. I think what it comes down to is, would you publish something that proves your financier's culpability? Yeah.

What about I I think I I think I was well said. You know, fundamentally, you you know, I do remember when, I think it was doctor Malhotra said the date is the case where the, the researchers found pretty clearly that there was clear vascular inflammation. I don't know what investigation they were doing. And they told him privately, but they said they couldn't afford to publish it because of the conflict of funding it. You know, you they were funded, and you you can't afford to do a publication that actually targets the people who fund the research that you do.

Have you seen that meme where it says 90 97% of, scientists, agree with whoever is funding them, and the other 3% are censored? Yes. Yeah. Yeah. No.

But it it it does raise very, very serious issues because I I think that I suspect that the scientific and medical community had thought that by now, everything would have probably disappeared. So even if there were issues, you know, fine. It's kinda something you leave behind, and you can go back 20 years from now and you can say, you know, this was an issue. The problem they've got is the virus is still circulating. The pathology is still evolving.

What in the world do we do? Well well, you know, Philip, there have been a couple of small series published, But even then, they were very, you know, journals were very hesitant to publish. I think, you know, they tried to publish in the most cited journals first. And then, I mean, after preprint approval, they were suddenly rejected. So there have been a few series that have somehow got through.

I think there was one, well, earlier this year by, Nicholas Helcher. And, he teamed up with a Canadian pathologist, Roger Hodgkinson, I think William Mackas, and Peter McCulloch on that paper. That was an autopsy series. It was actually basically a review, a review of the literature on, you know, of, and they they reviewed a number of studies, and they they they whittled it down to only 28 cases. I think 14 studies and 28 cases where they could basically just about everything else.

They had very, very strict criteria. So I don't know if you've seen that study. That was fairly recent. But I still think the best series is the series by Professor Arnd Burkhart which hasn't been published yet. I suppose due to his untimely death.

But he had, he had compiled 75 cases post vaccine death. And in many of those cases, it was a second opinion that had been sought from by the family because they didn't believe the initial autopsy. I think in the majority of cases, actually. And so he was called in to give a second opinion, and often oftentimes that meant, going back to fixed organs, organs that had been fixed. No histology was available in some of them and and getting histology done.

And based on those 75 cases, he came up with, you know, in a very interesting series, which he has presented at a at a number of scientific meetings and to a number of doctors groups. I still think that's the best series. He also had 50, biopsies. Not as good as autopsies, obviously. But he had 50 biopsies as well, from from lesions post COVID vaccination.

But those were in live patients. So I still think those are the, that's the best series. But, yeah, there's, I mean, all this all the all these little reports that are coming through, they suffer from a dearth of numbers. There should be way more numbers. Pathologists should be encouraged to be performing autopsies like doctor Chetty said, especially in young people where there's, you know, no obvious concomitant pathology.

In those cases, it should be mandated, really. You know, I I I I was thinking about what you said about doctor McCullough, and, I'm glad you mentioned that paper. And for people who don't know, what he did was that they got all the published cases where someone had died and that there was some kind of report, not necessarily all with histology that had been published. He then collated them together, and they got a couple of independent people to review each case and say whether or not they thought based on each case, this was likely to be secondary directly to the vaccine. Mhmm.

I remember the big fuss about it. And so it interestingly and, if if I wish I could find it, I I hadn't thought about it. I would have pulled it up. But in the sub have you got it? Well, I just pulled out some pictures from the study.

I can, if you allow me to screen share, I could probably Yeah. You can screen share. But what I want is that supplementary report. Because what the supplementary report had in it was it had the details, the age, the comorbidities, essentially what happened and what were the organ findings. And when I went through it, I so I did myself.

I just looked at the cases. I've never presented it. I I probably should. I had to agree with them. Meaning that you you you didn't you found somebody.

They had this condition. They died, and the only abnormality you find is a myocarditis. You know? Who are you going to say that this is not the cause? You know?

It is the most obvious cause. And so when you when you go through it sequentially and you go through each case and you think objectively, if somebody put in front of me this case where this happened, this happened, here is the histology. Is there any other cause you can find? No. Why would you therefore say it wasn't potentially?

Because you can't say conclusively it was. You can say, as they say in in medicine, it's just a 51% leaning towards a diagnosis that makes it a diagnosis on a a course of death. You know? And so you don't have to be absolutely sure it's a diagnosis. It's just whether or not on balance, this is the most likely diagnosis based on the clinical presentation.

Yeah. You know, in in that study, I think, the mean age of, the deceased was 44 years. So there was predominantly younger people, and they had very strict criteria so that it had to be the death had to have occurred, you know, very approximate to actual vaccination. So I think the mean the mean time of death from the last vaccine was 3 was 3 days or the median could have the median could have been 3 days, and I think the mean 6.2 days or something like that. So it was very close to the time of last vaccination.

Otherwise, they, you know, they excluded cases where there was any concom concomitant pathology. And, yeah. So, after that, you know, a very highly selected review, yeah, I don't think anyone could, argue. I think all 28 cases had myocarditis. And in 2 cases, there was multisystem inflammatory involvement as well.

But, you know, one of the tools that we that we use is immunohistochemistry. And this was a great strength of the the series by Professor Arne Burkhardt was, we use immunohistochemistry for the Spark protein. I can, I can just show you Yeah? If you if you just click share and Okay. You should be able to share your screen.

I'll just get back to the, let me go down here. I'm sorry. I can't see kick share. But, basically, what we what we, what we do is we take an antibody to a spike protein antibody, and and attach a chromogen to that, antibody, which then reveals a brown color wherever there is spike protein deposited. So we can detect spike protein in the tissues.

Now, the spike protein that the immunohistochemical tests, highlight is not specific to the vaccine in that, you know, COVID infection itself, would produce spike proteins. Obviously, the the spike proteins are on much greater number, after vaccination because they're being produced. You know, the the cells are, forced to produce a spike protein. But what we use is other ancillary tests because, the coronavirus has 29 different, proteins. But the spike the the the spike protein is is, the vaccines only produce spike protein.

None of the other, 28 of the 29 proteins that are present in coronavirus are produced by the vaccine. And, it's it's very interesting that they would choose the most, like, toxic part of the organism to, you know, to produce vaccines. That's I think was a bad mistake. But, so we can use antibodies to other proteins that form part of coronavirus. So, if we find nucleocapsid protein or membrane protein in addition to spike protein, that would be a very strong indication that this is COVID infection.

Where we find only the spike protein and no nucleocapsid, and no membrane protein, for instance, that would be a very strong indication that this is vaccine related. And, you know, when you think about it, Shankara, from a a practical point of view, people are dying all the time. The deaths are still up. What can you say to families when they have concerns? Look, Philip.

Everyone knows someone that, has died untimely. And we, as doctors, need to try and mitigate what's going on. So with families, they have to put pressure on the coroners to get us the information we need so that we can do the right things to mitigate the deaths. Now, yeah, family should push for young young especially in young patients that die untimely for autopsies to be done. Look, it is an expensive affair.

And sometimes you have to pay yourself to have these things done. So yeah, there are the limitations that are there. But I think the state and the scientific regulatory authorities should take a more active interest in trying to understand the evolution of this new pathology and provide us the resources that we need as clinicians to make head or tail of what's going on to help people that are not in danger. So simple things for them. Like, a simple thing like making it mandatory to note the vaccination status, the thorough vaccination status of an individual on their autopsy report.

Now that would have delineated all the autopsies done so far based on vaccine status. I've been talking about phenotype, that I saw different phenotypes being affected by different variants and different organ systems. So a simple thing like a blood group and correlating blood group, we might find that certain blood groups have certain types of vaccine injuries, types of long term COVID, sequelae. And if we don't do those kind of tests, we're never gonna figure out how these the the exact correlation, who are the at risk groups in society itself. But when I speak to my patients, a lot of them on their own would say, look.

I had a flu, and I'm taking forever to get over it. They're seeing these new and unusual symptoms that are presenting. So we can't ignore the fact that it exists. There's a new whole range of pathology out there, and we need to make a real tail of it. Like, Rory said, the staining is important.

We need to find new ways of both diagnosing with, either, chemistry or histology or serology. The both the diagnosis and the extent of injury that's occurring. So we need new novel technologies. Doctor Peter McCullough used a PET scan when he found that all the other cardiac, tools that we have were not showing up myocarditis. We were having people with the normal troponins and normal markers and normal FOTCGs suddenly dropping dead on the sports field.

So the tools we have, we have to realize, are no more the sharpest tools in the shed. We've gotta find new ways of actually assessing the situation and getting the information we need. When he did the PET scan, which looks at glucose uptake, which usually occurs in tissue, he found the majority of patients with the vaccine had some uptake of glucose from their myocardial tissue. So every person that's almost every person that's taken the vaccine has some form of myocardial injury, be it minute to, life threatening. It's the adrenaline in a big match that caused them to go into cardiac arrest.

You wouldn't have figured those things out if you didn't use new and novel ways to look at the problem, and we need an interest for that to occur. Unfortunately, it is public that needs to rise when they feel the pain of the death around them and the disease around them to impress on governments and regulatory bodies to do what is necessary. You know when it moves the public. You know, I I think here, one of the interviews I did recently was with a Hetty Simoes. And what happened is that her recently was with a Hetty Simoes.

And what happened is that her young fit son, he was about 30, collapsed and died. And he had, a dissection of his thoracic aorta. And that was a cause of death. But she was saying, why did it happen? You know, he was fine.

He had been vaccinated 10 days before, but, of course, everyone says it wasn't connected. And she now this is an example of how it works. She refused to accept that. They they wouldn't do the autopsy on I mean, they did the autopsy, saw the evidence of the dissection, but they didn't want to do histology because they didn't think it was necessary. But all the information she had from her family showed that he had no risks.

He had no family history of of anything that would predispose him. He was not using any drugs or anything that would put him at risk. And the only thing that happened was the temporal association with the vaccine. Eventually, what she had to do was that she had to get his samples sent to Germany where they were then studied, and I don't know I don't think it was it was doctor Burkhard. It was someone using his techniques, looking at the spike protein, and being able to analyze if this was a a a spike protein from the vaccine as opposed to from infection.

What they found was that it was infiltrated in the vasovosorum of the large arteries. So what they what in effect had happened is that he had an, what's the word for it now? He had an aortitis, inflammation of the aorta through the vasovascorum that weakened the muscle and then caused the dissection of the aorta. Now if she had not pushed and if she did not have a doctor who was willing to help her, I think that was doctor Balbona, they would have never gotten the clear association for which they published. They managed to get it published as a case report.

You know? And this is what needs to happen, but they had to battle themselves as the family in order to get this done. Most people don't have that that capability. Is it that the pathologists are just so busy at the moment? Is it that we don't have pathologists anymore?

That's what I was told is that they are having less and less pathologists trained. The standards are changing where it's no longer as important to look at histology. Everybody is trusting everything else. Their work is now concentrated on diagnosing cancer and staging it. And so, therefore, this kind of research is no longer a priority.

Is that true? Well, it is true. The numbers have dropped. The numbers of autopsies have markedly dropped. But I think that, it's still an essential tool and, particularly in in in young people where there are no other cause.

I think in those cases, where no other cause is is apparent, in those cases, it should be mandated. And, in in hospitals, in general, it should be encouraged because it's such an important, teaching tool. So you you mentioned, dissection, aortic dissection. Interestingly, the series of professor on Burkhard, I think he had 5 or 6 cases where they found aortic dissection. And in many of those cases, the initial the initial pathology, report, you know, raised raised the possibility of maybe a genetic disorder, cystic medianecrosis, maybe, like, Marfan syndrome or one of those.

But the thing with those is that it doesn't incite an inflammatory reaction, and you don't see this vas this lymphocytic vasculitis or the, the vessel of the sorum. And then on top of that, he had, the, immunohistochemistry, which showed, spark protein deposition in all the vessels of the, you know, surrounding the aorta. And, also, within the aorta itself, within the, within the endothelium and the medial layers of the aorta. So there was extensive, spike protein deposition and an inflammatory reaction. So those pointed against, you know, some sort of genetic disorder causing these dissections.

But it was a it was it was quite a common finding in a series. Yeah. I I think that, one of the things I wanted to show you something here. This was a a study, that was was done. I think, actually, this was done, if I remember rightly, in in Trinidad, but they found that the seems to be targeted even by infection.

So this is where the spike protein comes in. And I explained to people it's not just the vaccine spike protein or there's any spike protein. And in it, they found essentially that the vasovosorum of the large pulmonary vessels seem to be targeted with thrombosis and inflammation, which can then lead either to pulmonary thrombi or if it occurs in the aorta, then aortic dissection. So there is something specific about the vasovosaurum. It's almost as if the spike protein triggers a Kawasaki type disease with with inflammation of this area of the of the body.

And, I think that this means that if we don't start figuring out how this impacts. So what you may find, and I don't know if people are looking at this, is that based on this kind of pathology, you expect to have more cases of aortic root dilatation. You know? So you should find that a lot of patients are now having on routine echocardiograms, aortic root dilatation. Now if we knew the pathology, you would then be able to say, whoops.

This suggest that they may they may have underlying inflammatory process, which needs to be addressed. But if you haven't got the histopathology in the first place to give you the guidance as to what to look for, you will never respond to it. You will just think it's coincidental that all these patients suddenly are getting aortic roots dilatation, and, you know, it it's nothing. We are flying blind without autopsy. You know, back in the day, we saw, in in in Africa, we we'd see a bit of, aortic root dilatation and proximal aortic aneurysms from from tertiary syphilis.

And it had a very similar finding of vasovosorum lymphoplasmacytic infiltration. So that was caused by Treponema pallidum, obviously, untreated. But, in in in this case, it post COVID vaccination, it seems that it's mainly, CD 4 positive t cells that accumulate around, around the small blood vessels, the vaso vosorum, but also in in vessels in the myocardium itself. And so this points to autoimmune damage. I think that's, like, one of the features of the small autopsy series that have been either presented or published at the moment is, the accumulation of CD 4 positive t cells.

You know, it makes you think, Shankara. Just imagine for a second that what we are anticipating, that means that what we're having is widespread autoimmune pathology. And the thing about autoimmunity is that it doesn't present quickly, and it tends to be very insidious. And so you have to be looking for it to find it. When you reflect on that, just imagine from a clinical point of view, drive us 5 years forward.

What would what do you think you'd be seeing? I think, Philip, we we, well, I said, what we've done is almost an extinction level event. You don't go playing around with your immune response because your immune response is how you tolerate your environment, and that will determine whether you thrive in that environment or not. So there's a learning phase in your immunity with an immune, immature immune, system to tell you about maturity. And then you don't learn anymore.

You gotta use that immunity to thrive and reproduce. So now we've influenced the immunity of the planet in a very unusual kind of way, and we need to we need to relearn how we're going to deal with this. Now understanding autoimmunity, what I see for and the way I the way I look at our immune response, there's the short and the long term. And there's those that are immune and susceptible as well, depending on how well your immunity was developed from that immature state where you're allowed to, be exposed to a lot of things and tolerate a lot of things where you shelter and have would have more immune response to new things. Now in understanding that, we see patients have COVID and have no problems, and we've seen patients take 10 doses of the vaccine and have no spike protein.

We've seen on the opposite end of the spectrum, patients that took one vaccine and are making a ton of spike protein. And we've seen patients where when they get the flu itself, it lasts a long time, and it presents in that long period with an immune response. So arthritic pain, chronic sinusitis, hay fever, chest inflammation, like like like asthma, irritable bowel syndromes, irritability in the gut through histamine release. So we see a lot of these immune mediated kinds of prolongation of the ordinary COVID infection with Omicron. And then you're getting pathology in people that are chronically exposed to spike protein through the vaccination program.

Now, clearly, when you look through that, we got autoimmunity because we're going to respond to different organ systems. But we need to be able to quantify and delineate who's gonna get what. And so, clearly, certain phenotypes might be more prone to certain types of autoimmune responses. So you might find that blood group a all have a certain kind of autoimmune response, either renal or that kind of thing. Blood group b have a different kind of autoimmune response that results in a different pathology.

So it's a reunderstanding and recalibrating of what we know so that we can find ways to find those at risk and mitigate the risk. So, yes, aortic die dissections are on the rise, But then it's impossible to screen every patient for those kind of things. But if we could find a particular phenotype, blood group, spike protein level, something something that goes up is like this. Yeah. For some reason, your mic just went dead.

Say something else? Can you hear me now first? Yes. Yes. I'm hearing you now.

I just want to you know, one of the big problems we have is that the histology that gets done and the research that gets done is commercially funded. So when you want to stage a cancer, stage a tumor, patient pays for that. And it's based in treatment, so it's a money spinner for the hospital itself. Right? So, yes, I'd understand why hospitals would do that.

But when a 20 year old drops dead, then there's no money involved in it. It's spending to try and understand the pathology as to why this person dropped dead, and there's no incentive for the hospital to spend in that direction. So, research needs to be well funded and directed. It cannot be well funded and directed if it's left to commercial interests. It's publicly taxpayers' money that's going to have to look we're gonna have to look to that to figure out why we're so sick and how we're gonna solve the problem.

I'm gonna give you an example now as to why the autopsy issue is so feared by industry. And I'd mentioned it before, so I'm just going to share it, for the audience is that in this very interesting study, which is only about a couple weeks, old, so this is they were looking at SARS COV 2 specific plasma cells not durably established in the bone marrow long lived compartment after mRNA vaccination. And this is the slide that they showed where they compared flu, tetanus, this is SARS COV 2, 2.5 months, 14 months, 23 months. Additionally, they looked at the non long lived plasma compartment, so that's the spleen lymph nodes, and they compared it to the long lived in the bone marrow. And you can see within 2.5 months, the flu vaccine had long lived plasma cells similarly with tetanus.

None for the mRNA. At 14 months, still none for the mRNA. At 20 3 months. And in some patients after 5 doses, only a slight response, but strong response in the non long lived compartment. Now this is the kind of thing that you get with regards to histology and autopsy.

Once you see this, you cannot unsee it, and you cannot ignore it. Based on these findings here with no durable long lived plasma cells, can you call this a vaccine? No. You can't. You can't.

Philip, there's there's no durable immunity. And I can almost guarantee you in the non long lived plasma cells, the reaction we're seeing is more allergenic than antigenic. Mhmm. And so we're getting us inflammation tending towards an allergenic response, which tends to propagate the IgG 4 and make you tolerate the allergen rather than an antigenic response, propagating long term memory to fight it again. And so I want Rory, what are your thoughts from a pathological point of view?

Well, I I just wondered if I could just briefly present slides that were previously presented by professor Erne Bach, Arne Burkhart. Just Yeah. Can you can you share it again? Try and click share. Okay.

Yeah. Let me try that. Try again and stay and click share. Is that, you'd sometimes have to click share again. And if you can't do it, what you can do is email it to me, and I can share it for you.

Share entire screen maybe. Yeah. Click on entire screen. Okay. And then look down and click share.

Okay. It's not allowing me to. Oh, okay. If you email it to me, I I will be able to share that. But yeah.

So it the the the the issue with regards to this pathology and the histology, this is what I'm saying is that when you see these kinds of scientific outcomes, you can't this is forensic. This is this is not something you can argue about. It's not something that you can dismiss. It is very, very clear that the long lived part of the immune system does not want to remember spike protein. The question is whether or not it's related just to spike protein or if it's related to the technology of mRNA.

And I think they have to go back to the drawing board on this one because this is what you get when you do detailed histological analysis. Yeah. Actually, there there is a technique now, to identify mRNA, and they can do vaccine specific mRNA, you know, because, I think the the vaccine has somewhat modified RNA. I think there's a methyluridine inserted. I know there's, so there is, there are immunofluorescence, methods that can be employed to detect vaccine specific mRNA, And and and shortly, there should be, methods to detect vaccine specific spike protein as well, because the spike protein produced by the vaccine is slightly different to spike protein produced by, native infection, in that there's a double proline inserted, which affects folding.

That's a genetic modification. So, yeah, those technologies are becoming available, so we should be able to learn more. But we do need the tissue. That's the main thing that I think we we should stress is that we do need the tissue. We do need, extensive sampling.

We do, well, first of all, we need, more autopsies, and then we need, more extensive sampling of tissues to be preserved for microscopy. Because, you know, even 10 or or 15 years later, we can still perform microscopic analysis and and ancillary studies on that formalin fixed paraffin embedded, tissue. Yeah. Yeah. That's a very important point, you know, Rory, is that it even even if people didn't have the time now and they weren't interested.

Yeah. You're right. 5, 10 years down the line, those pieces of tissue could be absolutely critical to being able to understand the disease and a trajectory of disease. You know? I'll I'll I'll tell you a story that, I thought early in the pandemic was one of the big gaps in terms of histology is that we didn't have we only had a few samples of patients who had COVID and were asymptomatic or subclinical.

Okay? But there was an inflammatory response in their lungs even though they had limited symptoms. And I was saying that to get the pathology of the lungs at that stage was exceptionally important because it would tell you what was the first immune response before you then went on to have severe COVID 19. And this this is the kind of thing that without that sample, that you you can't even go back in time and analyze it because it wasn't collected. Yeah.

I think, Philip as well, the nature of the problem is such that we have many tools, but nobody seems to want to accept that there is a new technology that's been used and a novel virus that's in our environment, and we need to figure a way to separate and delineate everything we have. So like Rory said, we have a vaccine specific spike protein stay. Right? They should make it mandatory that all histology that gets done gets stained with that. So even if you're dealing with the breast cancer, you stain it for virus, for for a vaccine specific spike that's done routinely in hospitals.

But you make it sure that when you're doing staging, grading of cancers, whatever, all you gotta do is stain that tissue for vaccine specific spike. And if it's there, that becomes a likely possibility or a cause to that pathology. Now if you start looking at pathology across the board and take one simple thing, like, insisting on spike specific or vaccine specific spike staining of all histologic samples, we get a true understanding of the extent of the problem as a start. Yeah. Well, just just to clarify, the vaccine specific spike, I don't know if it's commercially available just yet.

It's under development. At the moment, what we use is we use, multiple immunohistochemical antibodies. So we use the spike protein with membrane and nucleocapsid protein to exclude, COVID or coronavirus infection. But, the vaccine specific antibody should be, you know, should be easy to develop because it there is a double proline and a different folding of the, vaccine specific spike protein. There's double proline insertion and a different folding.

But I I I have just discovered how to share this screen. So Oh, I've got it now. Yes. Yes. Yes.

So let let me let me add this to this stage. Oh, sorry. There you go. This is, this is from the talk given by Professor Arnie Burkhart where he showed, you know, the multiple, areas of endotheliitis is what he called it, and disturbance of elastic tissues aorta larger vessels. Subsequently, we've seen them even in the skin.

And, then these displaced vacuole and crystal particles and then pertinaceous deposits, basically functional amyloidosis, the clots that we've seen before that we've spoken about, and, you know, these unusual calamari type clots, and then true foreign bodies. And, so this is this this is, the spike protein. I'm not sure if you can see the arrow, but this is the spike protein. Oh, click on the I mean, you're not you're not on the just click on the next slide down. You you haven't you you're still showing the, just move the slides down 1.

Oh, the slide we're seeing now is still general lesions affecting more than one organ. Can you can you, click it and move it move it along? Can you see? Click again or, I am seeing the left hand side of your screen. So I'm seeing all the other slides on the left.

So if you just click on one of this the the other slides, the second slide down, we should be able to then see it. No? I think we're having, some some technical difficulties there, with Rory temporarily. But yeah. So I I think the point he was making, Shankar, is that the there is the capability of being able to look for these things.

There is just not the will from the scientific community. And I think part of it is fear, fear from the repercussions of actually doing something like that, and also fear from the perspective of what do we do if we then demonstrate clearly something like that is an issue. I mean, the implications are just so serious that I can I can see that they would actually be quite scared to, to do it? Sorry, Rory. You you you we lost you there in the midst of that.

Yes. But, anyway But And it it was dominated by, as I said, an autoimmune, lymphocytic population, and cardiovascular damages, particularly. This, obliterative, in endotheliitis, obliterative vasculitis, and then, you know, lymphoid tissues just about everywhere. They had cases of Hashimoto's thyroiditis in patients that had, never had, had that diagnosis before, Sjogren's syndrome. And they described this thing, what they called lymphocytamock.

That was lymphocytes everywhere where you're not not supposed to see them. And, they showed lymphocytes, basically lymph lymphocytes almost like in fading. The these were a polyclonal population of lymphocytes, not a monoclonal. So it wasn't a malignancy, but they were they looked to be like invading vessels in the spleen. In the spleen, they they, describe like a concentric onion skin type lymphocytic vasculitis, which you'd normally see in, autoimmune diseases, but specifically lupus.

So it was a very interesting constellation of findings. Even, you know, lymphocytic populations within the brain. Now we know the nano the lipid nanoparticle was actually devised to deliver chemotherapeutics beyond the blood brain barrier. And, so, yeah, so it's no surprise that you're having the spike protein detected within the brain, inciting a lymphocytic reaction. Sorry.

Sorry. I couldn't show you further images. Yeah. No. I I I wouldn't want you to share it with me afterwards.

But this is this is the problem that they would face with autopsy is that I suspect because as I said, from an autoimmune perspective, this is why I look out for histology because I know what I expect to see. I just need histology done. And if everything that you are saying there fits, you know, it it it makes sense. This is also what we saw when we did animal models, and we gave them because what happened in the animal models with SARS COV in 2012 is that they vaccinated them, then exposed them to the virus, challenged them, and every single vaccine candidate, and they tried 4 different types ended up with type 2 helper cell, immune pathology. Mhmm.

And so the obvious question is, what would be different now? And the only way you're going to diagnose that is by histology and autopsy. I I'm beginning to wonder, do you think they know this? Philip, I think they do. I think they know what the outcome's gonna be.

This was done for profiteering. There was more financial motive. And if they're not going to go down the line and figure out where we went wrong, what the issues are, then I don't think the interests that I play should be in health care in the first place, then profiteering from health care. So at the end of the day, whatever they've done, if they claim to be in the business of health care, then you should be caring for patients' health. And we're seeing some unusual things, and they need to be investigated.

So you if you're truly invested in patient health, then you stick your hand deep in your pocket to figure out the mistake you've made that's caused the injury in the first place. But if you're about profit, then you're just going to try and sweep it in the carpet and pass the buck onto someone else. So the people that made the money need to be forced to do the research. You know prove the claims. You you know what is so sad?

In the context of medicine, we have forced upon us the duty of candor. And what that means is that if we make a mistake and we have caused harm to a patient, we have to tell the patient and the family. We're not allowed to sweep it under the carpet. So how in the world is everybody else allowed to get away without the duty of Canada? They didn't take the Hippocratic Oath, William.

Well, so, I mean, so as as we as we're coming to the the end here, I'm trying to now think what is the way forward. I'm I'm gonna share with you an idea, and you can tear it apart. But I I I've come to the conclusion that this is never going to happen except if the public doesn't do it themselves. Okay? Nobody is going to do it for them.

Similar to what Hetissimo is found and did, she took the samples. She sent them off. She got them assessed. She got the diagnosis. So the public, I think they need to realize that it seems that either people are too afraid to ask questions or they are conflicted in asking questions.

So the public is going to have to insist. So here is my thought. Just as you said, Rory, that once it is fixed and put on formalin, that slide can be there for 15 to 20 years. Okay? And so here is the point to the public.

If you were to find 15 years down the line that there were huge litigation things. If you do not have a sample fixed in formalin, secured, it will mean nothing about your loved one. And so what I think needs to happen now is that the public needs to finance getting these samples themselves. Somehow, they need to ask the coroner or whoever is just say, listen. We don't want you to do anything to it with it.

Just do the biopsy, put it in the formalin, give it to us. We will then send it privately to get it fixed, looked in a slide, and assessed. And if needs be, if there are huge volumes, we will ask artificial intelligence with the international corporation of pathologists who are willing to help, but it will therefore still get done. But I am realizing more and more, if the public thinks that somebody is going to do this for them. No.

Any better ideas? No. Unfortunately, I have to agree with you. I I think, I think the recommendations you've made are very good. Interestingly, I did have a family that contacted me, who who insisted on an autopsy, and what a business it was to get it done.

They asked me to assist in the procedure. I didn't really have to assist because, I I managed to get hold of the pathologist performing the autopsy and and just instructed him very clearly just take as many tissues as you can for histology, and then I can look at the histology later. And that's exactly what he did. He he sampled extensively, and, it was very instructive to the case. But, yeah, I think that's the key.

Anyone, who's a pathologist, anyone involved with autopsies, sampling extensively, not just taking one, block for histology would be the key. But, yeah, unfortunately, like, doctor has said, I think there's issues with ethics, especially when money's involved. You know, I mentioned syphilis as a cause of proximal aortic aneurysms previously. I don't know if you remember the Tuskegee Syphilis study, you know, where they where they left all these, Tuskegee Indians and specifically didn't treat them for syphilis even though they knew they had syphilis and were spreading syphilis. You know, I mean, that was in, that was just one example.

And now we said we'd well, we'll never let that happen again. But look what's happened. You know, people are being experimented on without their knowledge, and results are being hidden from people. And I think by by not, by not requesting autopsies, results are being hidden. K.

So, Shankara, as we we close out, what what do what are your thoughts here? What do you say to the audience who at the moment because they're stuck. It's kinda like if the police are not investigating the crimes, what do you do? Do you get a private investigator? How how do they move forward?

I think it's a complex issue, Philip, because a lot of people have taken the vaccine. And so when they see loved ones and things pass away, they're too afraid to even know the truth. So they're terrified to go look for the truth because it impacts on their health as well and their decisions as well. But what we can do, I think, as a scientific and medical fraternity, is to understand that we might be dealing with a global criminal act. And as such, we might have litigation that's pending in future.

So with that understanding, we should formulate a forensic investigation collection kit like you do for a rape kit, like you do for certain other forensic, kits where you can collect evidence. And those forensic kits that we suggest should be based on the evidence that we have of pathology so far. So for loved ones in the family, you get a forensic kit that you could insist gets fulfilled when you send that patient for an autopsy. So you gotta take specific samples. It'll limit it'll limit the cost, but it'll also direct where histology samples are kept.

Whether we look at those samples 15 years down the line or not, we're just directing them where to look. So remember, we're dealing with the criminal case, and so we know where the, pathology lies. And so we can make forensic investigative kits for people to use so that they know what samples will be required in future to hold up their case. And, Rory, any any thoughts similar to that? Very practical stuff because there will be a lot of people who have had loved ones die even recently, and they have questions.

They are concerned. You know? Practically, is there anything that they can do? Well, I I agree with, doctor Chetty. I think that, you know, having a kit would be a good idea.

Obviously, the autopsy is is the is the is the gold standard and sampling extensively at at the time of autopsy, as I said. But if it cannot be done or it's prevented for some reason, we we we can obtain tissues by other means. Skin biopsies, maybe limited liver biopsy, things like that. Maybe those are other avenues that could be explored if, it becomes almost impossible to get an autopsy, which shouldn't be the case. Personally, I would like to see autopsies being encouraged, not just for medical legal reasons, but I agree this could be a medical legal situation going forward, but also just for hospital learning and teaching.

Yeah. I think that's a a very important point. I think the pathology has changed, and I think that if we don't understand the characteristics of the diseases that we are facing. So in a sense, what I usually say to people is that from this point on, you're not just dealing with heart disease. You're dealing with heart disease plus COVID heart disease.

You're not just dealing with renal disease. You're dealing with renal disease plus COVID renal disease. So for every specialty, there now requires a new learning objective to understand how their specialty has been impacted in terms of its trajectory and pathology by both factors, both the infection and the vaccination campaign. It it my view, it's a responsibility for clinicians to get this work done. I'm not sure if in 15 to 20 years time, when people look back and they ask, did the clinical staff do everything that they could to advocate for patients?

Based on what I'm seeing today, I don't think that they could say yes. That will come back to haunt us. And I think that for our own protection, we need to find a way to insist that from a clinical point of view, this kind of work is done. So many challenges ahead as usual, very interesting discussion. So thank you both very much for joining us.

Thank you audience for being with us during this time. And if you stay with me for the outro, for everyone else, have a great evening. Thanks, Gareth. Yeah.

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transcript to 2hr podcast - Long Covid & Post Vaccination - a Science-based Approach with Dr. Chetty
https://rumble.com/v5cheoj-long-covid-and-post-vaccination-a-science-based-approach.html

Joachim Gerlach and Dr. Shankara Chetty will present an in-depth discussion on the persistence of spike protein and the virus in the body following infection and vaccination, with a focus on its effects on immune cells and other targets. Dr. Chetty will share his clinical observations from the past four years, while Joachim will review the Covid-related data gathered to date, emphasizing the significance of understanding the ongoing presence of spike protein in the body and the potential future trajectory of this disease. The presenters will offer a thorough analysis of the neurological and cardiovascular consequences of SARS-CoV-2 infection, including structural brain damage, cognitive impairment, and the acceleration of neurological and cardiovascular diseases. They will also explore potential treatment avenues. Please note that this webinar is strictly for educational purposes, and no medical advice will be provided.

I will I will just start right now if that's okay. Yeah. Yeah. Okay. Then welcome, everybody.

Thank you so much for interrupting your sunny weekend and listening to what we have to say here. And I'm very happy to have with me today doctor Shankarasheti from South Africa. And, I will open up a slide so that you can or maybe, Shankar, why don't you start introducing yourself and then I show the slide of your about any kind of what has happened in 2020? Please go ahead. I'm doctor Shankar Chetty.

I'm a natural science biologist and a general practitioner. I work in a town called Podedwood, South Africa in a rural, rural community, but a very diverse population. It's a holiday destination, far away from, other medical service, 45 k's away from the nearest hospital. I'm a frontline doctor. Started seeing COVID from the start, physically examining patients.

Noticed a bi phasic nature to the illness. The second part was an immune dysregulation, which occurred very suddenly and could be timed quite precisely, but did occur with every patient. I used that information to warn patients. I treated it as a hypersensitivity trigger on that day and got great results. The second phase, showed the same.

The 3rd phase showed, again, immunity. So I knew, with my biologic science background that we're dealing with the man made virus with unusual pathology. That helped me meet people like Joaquin along the way, where of the similar mindset that we're under attack from various, pathophysiologic processes that are poorly understood by medical science. And so I think over the journey, we've developed different strategies. We found different mechanisms with which the, spike protein and the virus can injure us.

And in that understanding, we found ways to actually negate the problems, in a very scientific way. We're lucky that we were led along the way, when we encountered new problems. I think, my biologic science background, allowed us to know where to look. So I've been just part of the group helping along with biologic science and pointing direction as to where we might find solutions. I always knew that allopathy will save lives, but it won't solve the problem.

Spike protein, persistence. And that's where the nutraceuticals come in, and that's where my collaboration with walking from the start of the pandemic has occurred. We know the mechanisms. We know what we need to be doing. Joaquin has the knowledge of all the different nutraceutical compounds.

And using my, pathophysiology, biologic understanding, we've worked together now for 4 years, putting together a package of solutions to the problems we've encountered. And I don't think it's the end, but it's ongoing, but it's promising. Thank you. Thank you so much, Shankara. Let me also show you something that whoever doesn't know Shankara, people are not aware.

Shankara has treated more than 18,000 patients so far, correct me if I'm wrong, in his own practice and taught many, many doctors in the, Indo Pacific region, how his his methodology and saved a lot of life. I was present, like, a few years ago in a Thanksgiving Zoom meeting with hundreds of doctors that were in tears, thanking Shankara for preventing so many people from dying. So I would say that that thank you so much, Shankara, that you were wise enough and smart enough to understand very quickly the true nature of that disease, and millions of people would have been saved if that would have been a global initiative, and nobody would end up at the ventilators and and die horrific deaths in in the in the hospital. So that needs to be mentioned because they are attacking you enough for medical malpractice, which is the craziest thing I've ever seen. Yeah.

Because I think, I think, Joaquin, the the biggest problem was that I identified spike protein as the primary pathogen, and it's part of the vaccine. And I, inadvertently negatively affected a multi $1,000,000,000,000 global industry before they made the first vaccine. So I was, yeah, on ground 0 from day 1. Too close to the target, I'd say. Which is just fine.

Then maybe, first of all, to about today. So today, we're gonna do a dive. We will not be able to really go far beyond the surface. We would just scratch the surface of different disease expressions, some interventions that we deem important to understand. Maybe to myself very quickly, my name is Joachim Gerloff.

I'm a COVID researcher. I have published quite a lot of papers. You can find me on ResearchGate, and it's touching practically most of the biggest topics, in in long COVID, COVID condition, and postdoc conditions. I work out of Germany. My partner in the development is professor Hans Rausch with his laboratory with having 6,000 reference substances.

And so whatever you see from us has been throughout the research, and I'm gonna say only 1 minute something in in our own cause because when I speak, I see on the in the comment sections that people say, oh, then I can buy some Corsetine and I buy some and everything will be hunky dory. It won't. We have spent thousands of hours and huge amounts of money and time before we even start, and we have most of our products are in liquid form. And this is very expensive and difficult to make, so why would we go through through such lengths? And so in the beginning, in 2020, we were testing all these pairings and triple, combinations and looking at different molecular sizes, purity, plant matrix, which plant does it come from, which kind of excipients, etcetera.

And then we don't look at bioavailability in the normal sense of just measuring something in the in the in the in the bloodstream, in percentage wise. So we did directly in vivo testing, and here is just one example. We didn't stop until we reach these results. That means this was a a provoked myocardial infarction, and we had untreated animals. And we wanted to see in vivo on the tissue, on the organ, how good is the bioavailability.

And that is pretty I don't know if you know any normal medication that can achieve this, for example. So leave it at that, and let's continue. So in the course of the years, Shankara and myself, we have met many, many very capable colleagues. I wanna ex present some of them very briefly. Doctor Beatelier in Germany is far the final hope for many long haulers.

Many of her patients come in wheelchairs. He she's practicing in the with the help of a rhesus blood cleansing system and ex extracorporeal blood cleansing with the help of the heparin. Professor Malan Vegas working with her now in that clinic. Doctor Carlo Bronya, outstanding scientist and medical doctor, discovered that our own bacteria is being infected by SARS CoV 2 as a reservoir with, of course, a lot of consequences that nobody's aware of. Kevin McKern, doctor Kevin McKern is a neuroscientist.

We have set up together a laboratory in Japan right now to to look at the deeper impact of the spike protein in the brain, especially in the context of neurological disease expressions and especially to disprove, hopefully, that there are no traits for Jacob Reins being formed out of that protein. Doctor Stephanie Senef is my mentor since 10 years. She has been taking myself under her wings, so so to speak. She's an MIT research scientist, very famous because of her glyphosate research. And then maybe mention, was mentioned as Charles Riggsy, 15 years experience in biowarfare defense in the in the United States Marine Corps, and he has done more research than anybody I know, and he testified in con congress on the gain of function inserts in the spike protein of SARS COVID 2.

So the idea of this coming from a fish market is ridiculous. Wanna show shine a light to how big is the problem. Nature Magazine a few weeks ago, if we can believe these numbers, then we're looking globally at 400,000,000 long haulers. I guess that the vaccine injuries are just, like, let's say, conveniently being inserted into that number, but 409,000,000. So we can expect by the end of middle of mid of end of next year to reach half a 1000000000 people already suffering and being symptomatic.

And they are not only sick. Many of them die. So the death rate per 1,000 individuals from long haulers is 16.4. That means 6 and a half 1000 6 and a half 6,400,000 people are dying from long COVID every year. That makes it 17,000 per day.

So to think that we have all the time in the world to develop something here and and to bring that out to the patients is not correct. So if you look at the scope of the disease itself, it Shankar, correct me if I'm wrong. There's practically no body region being spared by spike protein and or SARS CoV 2. Even the hair and I I just saw another report on the on the on the jaws and even in the in the teeth. I mean, it goes everywhere, and it makes trouble everywhere.

Yep. If you look at the mechanisms by which, it influences, our physiology, Joaquin, from From the perspective of the vaccine, we know that it bio distributes everywhere. And, that's gonna make spike protein everywhere in your body. And the vaccine will have a far longer production, greater production, greater persistence, more diverse organ damage, more diverse, autoimmune responses because of it being produced in all these different areas. With the virus itself, it's dependent on where the virus actually can invade.

And, of course, that's dependent on your immunity as well. So you get some patients who have mild symptoms. You get some patients who never get COVID. And you get those patients who get, moderate disease, but becomes persistent. And those are the dangerous ones.

And then you get those with very severe disease that require urgent treatment who will demise very quickly if we don't, treat them. So we see these different acute long symptoms, persistent symptoms, recurrence with the vaccine itself. And, almost every system in the body is affected and as well has an interaction with other systems that actually present with a diversity of clinical pitches that are confusing the medical fraternity today. Yeah. Thank you, Shankara.

I think that it's correct to name these 4, 5 pillars of main pillars of disease in postvac and long COVID condition and neurodegenerative disease, cardiovascular, myocardial disease, immunosenescence. I call it that way. I'll explain later why I do that. Autoimmune disease and metabolic disorders and cancer. So we will have a brief look at all of that and see, but but first, we need to understand the true nature of this, little bugger, and, we had to change our complete flowchart after we met Shankara.

Maybe you want to explain that with me, what we're looking at here. Okay. Look. I I saw different cases, Joaquin. And, initially, everyone presented in the viral phase of the illness with typical viral symptoms.

There was a large proportion of patients who just recovered and had absolutely no further sequelae, and that's the reason the viral phase you can see stops, right, with some patients. There were others who had viral assistance in their gut wherever they, the the and then they had long term symptoms, and the severity could be different in those patients. Some severe, some mild, but persistent, but not life threatening. The life threatening part came in when after the viral phase, we triggered hypersensitivity reaction. That hypersensitivity reaction was occurred in the first three waves exactly on the 8th day, one week after the first symptom occurred.

You got better and then you got worse. So I knew there was a second part to this in a different phase. So we got hypersensitivity, and I treated it and got very good quick responses almost immediate. I had patients' actuation starting to improve on the minute they took the medication. And I had patients where they were with interleukin values of 500, where within a week they were back to normal, with everything settled.

So hypersensitivity became the trigger for whatever was gonna follow, but hypersensitivity must be treated timorously and aggressively and stopped immediately. We don't tell the patient to wait at home for 14 days before we decide to do something. Because as you can see from your chart, day 14 is the start of a whole lot of other problems. So if you don't treat the hypersensitivity, you're gonna get persistent mast cell activation. Those patients will end up with chronic long term allergy.

It can also contribute with the viral phase 2 hyper inflammation because the cytokine release. That hyperinflammation as well will trigger a whole range of issues as well, leave the hypercoagulation. And with that, sorry, the hyperinflammation, in the 3rd wave, I think we saw a lot of immune complex kind of immunity triggered by the spike protein. So there we saw coagulation come into play because I think it was free ACE in the blood that was being attacked. And so we saw all the hypercoagulation, the eating up of all your platelets with this microvascular clotting.

So you don't see the plots. You don't see the big normal plots that we see. It's all tiny. It'll block the smallest vessels in your body. So I've seen patients come with burning over their skin that seems like their skin's not getting blood supply.

But the rest of the hand is fine. The pulse is fine. Everything else is fine. There's microvascular clotting. That microvascular clotting, yes, on your hands, tip tips, or fingers, all that, I can see it.

And you present to me, and I can treat it. But that clotting is also occurring in the microvascular of your brain, and we're calling it brain fog and all these other different kinds of things. And when you look at the microvascular plots eating up all your platelets, if you do not address it quickly, early, then you got a patient that's platelet deficient. And if you got a platelet deficient patient and you give them anticoagulation, they bleed to death. So we saw a lot of that where patients were put into ICU, anticoagulated, and bled to death simply because they had no more platelet test.

It was microvascular plots we were dealing with at the start. So we saw all these different things playing out, but there's a simple central pathology. It's viral persistence, it's immune dysregulation, and it's vascular damage, or let's call it, circulatory injury that play a part in every symptom we see in COVID, and this can occur anywhere in the body. We found the virus in almost every part of the body. We found inflammatory process in almost every part the body, and we found vascular compromise in almost every part of the body.

And it tends to occur in the finest of vessels because the clots are the tiniest. The immunology affects every organ and even the tiniest. And, of course, the, microvascular, clotting influences the tiniest of vessels in the body. So sometimes I think, our eye symptoms must not be ignored. Our eyes got the smallest vessels in the body, and if you're sitting with a steadily deteriorating eyesight, don't ignore that symptom.

These are symptoms that are easy to ignore. They will have consequence very quickly. Thank you, Shankaran. One one remark. You you're talking in past sense that the virus did the virus still does.

It still does. Yes. Yeah. With the with the Omicron, we don't develop a robust immunity, some of us. I've got patients who've never picked up Omicron.

But, like with myself, I seem to be prone to picking up Omicron, and I've had it many times, I think, 8 times already. So, some of us are prone to picking it up. It is a neurotropic virus because so you gotta be very cautious with it. So I think, even those that are unvaccinated, of a particular phenotype are still at very high risk of exposure to this virus and the toxic effects of both the virus and the exposure to the spike protein. Omicron is a new platform.

It doesn't work like the others did. But in some cases, I still see the biphasic nature, the viral phase and then a follow-up. But even if the biphasic nature is a little bit less expressed in Omicron, the your core treatment was actually to address the hypersensitivity, and you were heavily criticized for that and ignored by large parts of the medical community. But, wait. Okay.

We I think, importantly, with the neuro, with the histamine. Yeah. There we there we have it. The h one receptor. Right?

And the h one receptor being that trigger, and the h one receptor is found, all over. Right? Now when you talk of the h one receptor and you're talking about how we can use that understanding of the binding to the h one receptor and this flood of histamine that starts to trigger everything else, an h one receptor blocker is an ideal medication to use in 3 different ways, which we have shown. We found that the h h one receptor blockers prevent viral binding, so it can be used in a profile active way. There's a study on azelastine and desalaractidine that showed it, it could this, prevent viral entry into the cell, and it showed very high, virucidal effect.

I managed to find an azelastine nasal spray early on in the pandemic and prescribed it regularly to my patients who were exposed. The second thing that it, that, it did evolve. The second thing is its vericidial effect. Prophylactic and vericidial effect. So when you get the symptom, you can use it, and it will help stop the virus replicating and moving on.

And then, of course, in treating patients, when they've had the h one receptor stimulated and you got the release of antihistamines, an h one blocker becomes vital in preventing that h one release of histamine triggering other cascades down the road. So antihistamines are became vitally important in that treatment of preventing that cascade. Anyway, in this cascade, you can stop it. But the longer you wait from the start, the harder it becomes to stop it. One other point with histamine, walking there, I think, h one receptors.

We know that we're sitting with neuro COVID and demyelination of the, of the, nerve fibers. And that demyelination is the root cause of a lot of the problems we see with what we see now and aging itself. But we've been trying for many generations decades to to try and find methodologies to restore the myelination of these demyelinated fibers. Because once it happens, it happens. You can't get the myelin back.

But there's recent publications that have shown that certain antihistamines used chronically have shown to demyelinate nerve fibres. Now that's that's a twofold, revelation. One is that, yeah, we can use antihistamines as prophylaxis against COVID and to heal our nerves. So a constant h one blocker in your regimen might be something vitally important in the long term, benefit. But secondly, the fact that an h one antihistamine can cause your myelin to regrow means that the biggest injury to your myelin is probably caused by histamine Yeah.

Because you're taking away the biggest trigger. That understanding that histamine triggers the demyelination of nerves takes the understanding of neurology and neuropathophysiology into a whole different realm and the treatment modalities that we could be using. Because this could be histamine release in certain areas of the brain triggering certain psychotic or psychiatric conditions. And understanding where the histamine is being released and how to address that might be the way to treat these you unusual forms of, psychosis and, of course, depression, anxiety, or the other mild forms of of mental illness. That makes a lot of sense so far, I would say.

And it's that was my little little present to you in July this year because you were attacked so heavily on the usage of and it was a a real a bombshell that this this paper here showing that you can inhibit viral replication just with an h one, blocker. And which are the 2 ones I I we wanted to mention the 2 antesamine? Azulasta. Azulasta. Azulasta and desloratidate showed vericidal effect.

Yep. Acelastine was the only one I could find in a nasal spray, because you want to address it directly on the surface itself. Desloratadine is is a tablet, and, it's it's not found in a nasal spray. And so, well, you're not gonna get that much of a prophylactic effect from it, even though because it needs to bind receptors on the mucosal surface. I have a friend of mine who's developed a nasal spray with trofiniramine, commonly known as Alergix.

That as well has shown to be very virucidal. And, of course, you're getting the antihistaminic effect from it as well. So, as prophylaxis and as treatment, it shows a great benefit, but we've got this organization called the FDA that decides what flies. Okay. But, yeah, somebody might have a COVID and hay fever at the same time.

You know? Yeah. Yeah. Yeah. And so you're using a may I are you using a drug with you, actually?

Yeah. So Yeah. Thank you for that. So I'm gonna go now into I have we have to gain some grounds. I have to go quick now with some sort of a monologue.

And after we've, go through that, then we we discuss again. So, the first, thing, we we have we don't believe anything. So we tried this ourselves. That is in India. We did, we took fluorescent.

We took fluorescent dye and combined it with a recombinant spike protein. This was injected into the tail vein of these mice, and 72 hours later, you can see the disaster for yourself. The whole organism of that poor little animal is full with spike protein. They they these mice don't have receptors as we do, so it was degraded, and ex excreted after a while, but still even after 11 days, it was still a lot there. We tried different binders already in that stage to see if we can catch the spikes and get them out, so that was going well.

We have we have the whole documentation if somebody's interested. But let me explain one thing that is a big misconception in all these approaches to get rid of spike, spike detox, etcetera. The the idea of having a virus and or a spike protein floating around freely in the blood is a misconception. It is designed to stick to our cell membranes and to our receptors. So it's like a super magnet, and it will not circulate long.

So whatever you find in the blood means that you have an ongoing production by default. You cannot have a spike protein floating around for 3 months and detect it in the blood. Also, because it's like a burdock. It'll it'll stick to anything. So that that is as a starter because now we got getting to the nitty gritty details here.

So Carlo Bronner, the nice colleague and capable colleague from us and from Italy US discovered these bacteria being infected by SARS CoV 2 has done also another groundbreaking work. He was the first one to prove beyond any doubt with a double proline insert spike that he could detect after 187 days in the blood of patients that were vaccinated. So if we remember now that spike cannot circulate longer than maximum 72 hours, if you wanna have an educated guess, then how can you find 187 days later, you can find spike? That means there must be an ongoing production of spike protein in these transfected cells. So that's one problem, plus the spike, of course, that has been produced during the first phase of real proliferation, is has settled somewhere in the organism.

That's one thing. But not to underestimate the virus is that you can see also in COVID 19 patients after recovery, 654 days later, you can still see strong viral presence in the organism persistent nesting and especially in the olfactory system and the brain periphery, which is very worrisome that's we're gonna get to that in a second. Then you see that there is another phenomena. When SARS CoV 2 touches a cell, it turns the cell into a kind of to wanna say phrase it simply into a zombie cell. That means that cell turns into a senescence state and into an inflammatory senescence.

That means the cell cannot go into apoptosis, the cell cannot do autophagy, and the cell cannot replicate anymore. It's not dead, not alive, but it will not be cleared. It's gonna sit there and harbor the spike protein and the virus for a long time. And, unfortunately, it's not like only one cell. Some many most of the cells start to fuse together into so called sensation, into cell conglomerates, which is being more and more measured.

In this case, 67% of the patients were having that in their in their lung pathology to be found since they're in conglomerate like a porridge of cells, and that is the, let's say, harboring spike and and, and, and persistent virus. And you can see that also in more and more papers and more and more examinations. And so that can be one of the root causes for this, impaired oxygen exchange in the in the lungs of many patients. You you had that patient last week, Shankara Jazz from from Britain. She was the worst in that study.

Now from all the patients that were tested, she had the poorest gas exchange in her lungs. So that needs to be addressed, and that is where that is what we wanna talk about today. And so we have to enable the organism to clear this all out. So let's at first, a quick look what we what we find here and go through the different body regions and see how it plays out. So this and I really like, postmortem histopathology because that doesn't die.

And 60% of all SARS CoV 2 infected patients had persistent spike in the bone marrow of the skull and the meninges. So that is a clear finding here, and that is because it's owed to the olfactory system and the influx of of viruses directly to the brain or shedding of spike proteins. And they speak and this is a very German a very conservative German institute, the Helmholtz Institute. When they start to speak about enormous amounts of spike, then this should raise our eyebrows. And because this is a place where you don't a location where you don't wanna have, enormous amounts of spike, in my opinion, especially on the bone bone marrow of the skull.

So we are at the at this moment, we just built up this laboratory together with Kevin, and we are going now in a hamster model because the hamsters have a very similar receptor landscape as we humans have because we have to simulate a lot of receptors. You know? We we are not only having ACE 2. We have more than 20 reported receptors for SARS CoV 2, and the hamsters are necrosis from the rodents. Plus, they are excellent animals to try, and investigate all the neurodegenerative disease.

For example, prion diseases are preferably being studied on hamsters, okay, especially in the US. And so that's what we wanna hopefully disprove that we don't look at, like development here. But what I wanna do here is a very quick case. So this will be the only error area that we will dive in a little bit deeper today is the neurological sequelae after exposure to spike protein, and I'm daring to, yeah, challenge the medical community to to phrase neuro COVID in its first phase classified as a vascular dementia. Yeah.

In order to clear out this narrative that it's only some brain fog, there are we we we have we talk to patients that we sent home, because the the the the neurological clinics said this is a, psychological problem, and this is ridiculous. They should do something else with their lives and not run clinics like that anymore. Now because if you see so let's do the test here. What is vascular dementia? How is it being defined?

Impaired blood flow to the brain, microplots, coordination issues, and you'll see the dysfunction, disruption of the blood brain barrier, lymphatic system impairment, electronic inflammation are hallmarks to be so that this can be classified as a vascular dementia. And if you look at the pressure cooker hypothesis that we have developed over the last years, it shows you that the brain periphery, especially the neurovascular system, is completely full out, filled with spike proteins in the endothelium, that you have endothelium inflammation, a disrupted blood brain barrier, a transmigration of immune cells into the brain, lot of toxic peptides being able to get into the brain, the astrocytes being directly infected, and the end feed of the astrocytes that hold the valves for the lymphatic system also are clearly impaired. And if you look then at MRI scans of the blood flow to the brain of patients recovered from mild mild COVID 19, everything you see here, yellow, orange, and red, shows you an impaired blood supply to the brain, which will result in hypoxia and a diminished supply with nutrients and, of course, anything else that the brain needs to start with. So how can this happen? So to give the okay.

The the spike protein can't do anything to the endothelium if you have an intact glycogenics, the inner layer of the artery. And that is probably what is distinguishing the patients that develop symptoms and don't develop symptoms because a damaged glycocalyx is a hallmark of diabetes, chronic inflammation, intestinal bowel disease, etcetera, etcetera. So all the chronic diseases you see, especially in the US with 50 more than 50% of the population being already chronically ill, have a degree of glycogenics degradation. But to make things worse, Omicron actually directly and strongly interacts with the heparan sulfate of the glycocalyx and slowly starts to punch holes into the glycocalyx. So it's not waiting for your chronic disease to degrade your glycocalyx.

The little bugger is doing that himself actively, and he does it well, twice as good as delta. No? So let's look at that first because that's the precondition for everything else. So what what else can degrade the glycogenics? And it's a bombshell that I just was revealed when I was listening to Charles and Kevin speaking about gain of function.

And and I was wondering for 2 years, what is what about this super antigen, motive in the spike protein? And it's actually that's why you have some conflict conflicting studies. It's embedded inside the spike. It's not on the outside. And only the cleavage with furin will then separate the s one part of the 2 s two part of the of the spike protein and expose the receptor binding domain with the super antigenic motive in there.

So it's a, again, a biphasic weapon. Now you need furin to leave the spike, and furin is elevated in all chronic disease, highly elevated. You can even measure certain disease just by looking at the furin level in the blood of these chronically ill people. So there will be plenty of urine. And if you have plenty of spike protein, then it will be cleaved.

And then you have these superantigens out there, and they will trigger a super response from the t cells, and that is what you were mentioning before, a hyperstimulated immune system attacking especially the glycocalyx. So how can you mitigate that? You need strong furosem inhibitors, and that's what we're doing. So with some of these compounds we're using, you can practically I don't know exact percentage here, but it looks really good. How you can prevent the cleavage of of the spike protein into 2 parts.

So keep it closed. You know? That don't let it open. That's number 1. Number 2 is, okay, that's really funny.

Okay. So they they studied the countermeasures against because, super antigen SEB, stethoscope corpus SEB is considered a bioweapon. It was stockpiled in huge amounts in the sixties seventies, probably still is today. So they did a lot of research in Fort Detrick. Fort Detrick is the biggest bioweapon laboratory in the world.

And what did they come up with? Epigallocatechin, green key extract, and resveratrol as the 2 most potent inhibitors of of supranidine. So thank you guys. You were doing our job by the it saved me a lot of time. Very nice.

And then another thing that nobody's aware of, you have an enzyme called heparinase, and that is degrading heparin and heparin sulfate. And that is highly elevated in COVID 19. Never saw that before. I just found this morning that. And so heparinase is being used for studies on how to you know, anything that has to do with glycogenics degradation.

If they artificially want to degrade, the glycogenics, they use that enzyme. And it's very high, look at this here, compared to healthy. And so we're looking I was looking today again, can some of our compounds be coming handy here, and they can. And here you see that. They take heparinase, and then they they they the glycocalyx couldn't take on, the sorry.

The endothelium couldn't be infected with SARS COVID 2 as long the glycocalyx was intact. Then they used the heparinase to degrade the glycocalyx, and then it worked. And so that's what's happening. And if you if you wanna prevent this shit storm, you you have to protect that. And so another factor degrading the glycocalyx and also the blood brain barrier is an MMP 9 metalloproteinase.

And we did lot of research on that, and you can see here how the natural compounds here that we use are strongly inhibiting MMP 9. So that will also help, you know, here was, healthy glycolytics, diabetes glycolytic glycolytics, and then they use here an MMP 9 inhibitor similar to what we do. And you can see it restored the glycolytics. And then, of course, the heparan sulfate mimicking, we are using we are using those not to rebuild per se the glycocalyx. We use those as a decoy and as a chelator for spike protein that we come to that later.

But at the same time, it is also rebuilding the glycogenics. Look at that here. And that is the thickness of the glycogenics if you consume these fucoidans or or these algae products. And that all can prevent or is you you need to degrade the glycocalyx in order to cause this. And the findings from doctor Burkhard were mind blowing.

That is after vaccination. People that died after vaccination. Look at the vasculitis and the damage, this incredible damage done to the vascular system with a lymph lymph cell infiltration and a complete degradation of the elastic fibers. We come to that later. And so if you lose your your, if if you start to get into an arterial stiffness, now that's another point that will lead to this vascular dementia.

But first, let's look at this now. Now after the glycogenes has been freed or in a patient that it was weak already, then you see the intrusion of spike protein. This is a cut through an arterio arteriole, and you see with the spike staining, every spot here is an endothelial cell full of spike protein without any doubt. And that, of course, will then turn these cells into senescence cells, which are of a secretory phenotype. That means they are highly inflamed, and they attract also immune cells.

So it's gonna be a battle right in your endothelium, and that will, of course, through various factors, strongly feed into the microplotting that we're observing. And the microplots are somewhere between 5 oh, no. Yeah. I think, yeah, 5 micron to a 100 micron. So if you look at our at our neurovascular system, you have, like, 300 plus miles of vascular system in 1 and a half gallon volume.

You can imagine how how fine they have to be and so that anything between 5 a 100 micron will will con will, as a consequence, close-up depending on the size. Size will close-up these these vessels. And so that that is one of the problems. Then another one that is adding into that is the spike protein itself. When it meets fibrinogen, it's already starting.

You see this here. Even if you just add spike protein into blood of healthy donors, look at this. This will develop. So it's, again, a a multisystemic attack on our health happening here, all leading to coagulation. And let me shine light on this one here that most people are not aware of.

The arterial stiffness is a huge problem. I'll explain in the next slide why. But it's clearly documented that the arterial stiffness, even after mild inflection, is happening. And our colleague, Martin Krita, from German Max Planck Institute has was the first one to show that we don't only have arterial stiffness, we also have stiff red blood cells. So they turn stiff and they use their deformability.

And you in the very small vessels, a a blood cell can only pass through if it is flexible. But if you combine both, you have the arterial stiffness and you lose your elasticity in your red blood cells, then disaster is 100% sure, like in this study. They could only cause thrombosis when it was combined with the loss of the elastin layer with arterial stiffness. That is one of the preconditions. So So we see all that in COVID.

Then we see another problem where the neuro invasion directly into the brain, especially with Omicron, is mind boggling. You see here, these are different areas in the brain, 18 hours post infection, and it's not yet in the blood at all after 18 hours, but it's already in your brain stem for Christ's sake. After 42 hours, you have some in the blood. The brain stem is going through the roof, and, actually, your lacrimal gland, you mentioned the eye before, you you your lacrimal gland has holds the highest virus data from all. Interesting.

Yeah. So we see that all happening in parallel during neuro COVID. We are very lucky that we have chosen these phenolic compounds because I was not aware of that in the time when we developed all this. But you see here, phenolic, these phenolic compounds like quercetin and, what it says here, Resveratrol and and so on would would restore the glycocalyx and at the same time, restore the atrial stiffness. And so this is really good news.

Plus, we see here even with the MMP 9 inhibition would do a lot of more other really good, blockages on the inflammation and everything that's happening in the endoshelium, including the degradation of the elastic lamina and the, the blood brain barrier. Again, this MMP 9 inhibition is here is imperative. And then we look very quickly now at the glymphatic system. Been now multiple studies out there clearly showing that the the, let's say, the drainage system of our brain is blocked. Now so if you look at the at the brain, you have an artery.

Here's the sub subarachnoid space. This is the bone marrow of the skull, and here we have a vein. And all the toxins that have come in here cannot get out because the astrocyte NFE that drain everything into the lymph system are directly hit by spike and SARS CoV 2. And so these aquaPeal 4 channels are responsible as valves to open up the drainage for toxins, and that's what I meant with the pressure cooker in the beginning. You were having an influx of toxins.

You have an a buildup of toxic peptides in the brain, in the brain, where you have inflammation, and it cannot get out. So you are breathing neuro neurological disease much faster than usual. That's why we see so many young people now suffering from end of life diseases like Alzheimer's or Parkinson's. And it can be seen even in the early phase of neuro COVID in brain scans, and this one is really that knocked me off my socks. Even without subjective or objective neurological symptoms at the time of the MR scan, the COVID subjects had changes in cortical thickness and subcortical brain matter volume in mild COVID 19 in healthy young people.

My god. Yeah. So how can we classify this as a as a psychological problem? And we can now say, after we looked at these very quickly, just at these surrounding circumstances, we are looking at some sort of vascular dementia here. And then in the phase 2, I think we won't even go much further into that.

That's the inside of the pressure cooker. That is being accelerated. Microgliosis, astrogliosis, senescence, demyelination, the, ferroptosis, the calcium influx. So all that and I'm not even talking about any biochemical disturbances like, you know, renin, tryptophan pathways, and all the neurotransmitter glutamate overshot, and all these things. But the then in this phase 3, you will see amyloid beta tau proteins, alpha synuclein, and other aggregates that will lead to severe neurodegenerative damages.

Yeah? And one study here I will highlight very quickly now is, again, postmortem control brain, light microglia in activation, Alzheimer brain, SARS COVID 2 disease. Looks very similar, doesn't it? And if you look at the Alzheimer patient that has this was that is that died of SARS COVID 2, it looks almost like you take this slide and this slide and you put it on top of each other. Yeah?

So clearly indicating that we have a huge problem here. I will skip some no. I'm not gonna make a break. Shankara, what is your your take on on this hypothesis that we are dealing with a vascular dementia in the in the first phase of neurocognitive disease. Could you agree with that?

Yeah. I would, I would agree with that, Wavin. I think, it all comes down to the, affectation of the glycocalyx itself, which is all the membranes in the body, all the cells in the body, and how they actually function. Your glycocalyx is a lipopolysaccharide chain. And, if you look at the integrity of that glycocalyx, it's been challenged for many generations with the types of sugars that we've been exposed to or the lack of certain kind of sugars with the polysaccharide chain.

And the polysaccharide chain not only identifies the kind of cell, but also is involved in cell to cell communication in a microenvironment. And so it tell it it directs homeostasis. It directs healing. So it's all little communities of cells talking to each other through this glycocalyx, and we're disrupting that glycocalyx. So it impacts on the body's ability to do everything.

Now with the blood pressure control that we see, we see stiffness of our arterials. Look. A lot of this can be, if, diagnosed early, reversed. So I see a lot of patients coming to me post vaccination with fluctuant blood pressure where doctors are struggling to control it. It drops too low and then suddenly is too high.

Now I don't I think what's being misunderstood is that we've got this kind of microvascular coagulopathy occurring in peripheral circulation, and that's causing a feedback mechanism to the heart to increase pressure to keep circulation going. And when there's good enough circulation, then the the pressure comes down. But you're trying to control the pressure. You're not trying to control the problem, which is the blockage, the terminal vessel blockage. So a lot of these patients when they come to see me, when I put them on medication to thin down those microvascular clots and address that kind of issue, I find that their blood pressure stabilizes back to pre vaccination levels.

So there's a lot of different, kinds of symptoms we're going to see. And when you look at, the pressure cooker that you speak of for walking, the effect again is glycocalyx, but we're affecting the entrance of nutrients, toxins, fluid, all that into the blood brain back into the blood brain by disrupting the blood brain barrier. And we're also disrupting the drainage out of the brain by, again, affecting the glycocalyx of cells of the of the lymphatic system. And so you're developing a as as as a problem where there's an increased diffusion of whatever it is, nutrient or toxin, into the brain and a decrease in the ability of the brain to clear it because of the affectation to the lymphatics. That's where the pressure cooker, system comes in.

And to to understand that, it it's to it's to understand that you are treating a kind of vascular dementia. Yeah. Thank you. I'm gonna skip now the rest of the, neurological slides and go directly to the next topic. Otherwise, we will never finish today.

And so is everybody knows now, myocarditis and myocardial necrosis. We sometimes are discussing. Everybody says, okay. Myocardial necrosis comes exclusively from the vaccines. And I I argue that my my cardonecrosis can also happen from infection.

And so if you can't really separate the 2 topics, you have to find a way to deal with anything that comes your way. And, again, like I've mentioned before, we have done through our testing on that. You can look it up as it's it's a peer reviews paper. And, again, there is this idea of what can we do to protect the heart. And here on this one, every cardiologist will understand that if you can bring down troponin levels in infarction animals by orders of magnitude, that is not a bad sign.

I would say that that is something you should keep an eye on and maybe use it. And then, also, these kind of damages you see in the in the in the heart apart from inflammatory damage, which is, is the spike itself. So and you don't wanna have a cardiomyocyte fusion like sensation formation in your cardiomyocytes for Christ's sake. Now because one spike protein can now use several cells, it is leveraging the damage. Now it's like a bomb.

You know? It's like not killing 1 is killing now a whole group. So that is dangerous. So whenever you see syncytial, all alarm bells should go off. Yeah.

But because in the the only cell there there are few certain cells that we will have problems even if we can clear them out. You can't replace so easily cardiomyocytes or as many many of the tissues in the in the in the heart cannot be restored. So you have to protect them from being damaged in the first place if you can. Yeah. K.

Then let us go jump to the next problem here. That is the coagulation cascade. And, I think Philip is here today as well as a as a member. Maybe we can talk later. The the project is called calamari project.

It's a it's a project where we try to figure out how these clots come about, and it's starting actually at the microscopic level. This is an electron microscopic picture of a spike protein that has been degraded with an enzyme called neutrophil allersteins. And I met these scientists here. Hammersdrom said he has never seen so scary fibroes in his whole life. So that means when spike protein is degraded by these enzymes, it turns into something much more toxic, not only neurotoxic, but also thrombogenic.

Now this can be the at the at the initial point of why the spike protein is doing is causing so many clots and and microclotting. And then, of course, what we talked about before, the endoscereal inflammation and platelet activation and many, many other factors play into these microclots. And it could be that, eventually, these microclots will slowly assemble into these rubber like clots. Maybe later when we have gone through the presentation, Philip wants to say something from his side because he has been investigating that with, Richard Hirschman, to a to a quite large degree. What we did so far is with our protocols, we could show that we could bring down this microtrotting without using any blood thinners because the normal therapy, in South Africa developed by Pretorius, Laufer, and Kel would be to to use anticoagulants on this.

Yeah. It works, but it it doesn't address the root cause. The root cause is actually persistent spike and especially persistent spike in the endothelial cells. So by removing the spike, we could bring down the measurable micro plotting. And that I find very interesting because we we we it is kind of already proving that we're on the right track here.

And so because if you you you can't use anticoagulants forever, and you were rightfully mentioning that we have a mixed bag here, you can have microbleeds in your brain and vascular leakage with occlusions in the same artery system or vessel system at the same time, and then it becomes really tricky. So you wanna go other another route. Yeah. So what is your experience with the you you also when you when you were sick yourself last time from from the virus, you had some coagulation issues, and you addressed that in the correct manner. Maybe you wanna speak a little bit about that, Shankar?

In the first episode that I had, Omicron, I got over the viral phase of the illness very easily. But I noticed, on the exact 8th day, I lost my smell. And, I thought it's strange, but I felt well enough. And, of course, ignored it, Joaquin. Doctors are not the greatest of patients.

I advise all my patients never to ignore those symptoms on the 8th day. I didn't bother to check. It triggered a reaction. The following day, I lost consciousness. I was rushed to hospital.

I'm the only patient I've ever hospitalized, twice so far. But, what they found was that my d dimer had gone up not too significantly from 500 to about 900. I spent the night in hospital on heparin, checked my platelets, and the next day was discharged. But it somehow made me realize that, coagulation is gonna be an issue going forward whenever I get an infection. My, coagulation system seemed to have been primed.

And I had in the 3rd wave of, COVID, a lot of my first, close, paternal cousins get COVID and have coagulation issues. So there seems to be a phenotype there. In the second time, I had the same kind of infection. Ignored it, got better, thought I was fine. But this time, just to be sure, on the 6th day, I did my d dimer interleukins.

It all looked fine. But I do know on 8th day is when it starts to suddenly rise. On 8th day, I was walking back to my car and I started to get double visioned. And, of course, eye symptoms are very worrisome with microvascular coagulation. They tend to be the first symptom.

But, of course, I came home. I thought it may be my sinus. I ignored it. The following day, I had 3 episodes where I had severe spinal seizures, that caused my spinal muscles to contract and caused me to lose consciousness. The first one lasted for a few, few, about a minute.

The second, a little longer. Took me longer to regain consciousness. The third occurred in, ICU in the emergency unit. I didn't recover consciousness from that. I did, however, in the lucid interval, explain to the doctors that it's my 9th day.

I'm probably developing microvascular clots. They need to do my d dimer. I had taken 10 prednisone that morning realizing that it's my 9th day. So my interleukins and my, CRP should be normal, but please check my d dimer. And they're not gonna find a clot because these are microvascular clot cell exam.

You're not gonna see them on an angiogram. When I lost consciousness, they ran all my bloods again. My d dam over 2 days had gone up from 421 to 6,000. But every single other blood test that they did, and they did everyone that they could think of came back normal. Absolutely normal.

Only my. They were then concerned as, mainstream medicine would be that I might be bleeding. So they still refused to anticoagulate me and decided that they want to do angiograms. So they did an angiogram CT on my brain, MRI angiogram on my heart. They checked, and they couldn't find a single clot anyway.

They did ultrasounds on my entire body and couldn't find a single problem besides my d dimer being high. So by Tuesday, this started on a Monday morning. By Tuesday, they decided to give me heparin after checking my platelets. And by Tuesday, I had to anticoagulate me. And by Tuesday afternoon, I had started regaining consciousness again.

By Wednesday, I was lucid, back to my old self, had no neurologic deficit. I seemed to be perfectly fine except for a pain in my spine, which upon MRI on that day showed that the, spinal muscular paraspinal muscular chest seizure was so severe that it caused a fracture of the, vertebral body of my t 8 vertebra. So I recovered from COVID after the anticoagulation relatively quickly, but, it's taken a little while to recover from the spinal fracture. So I think as an unvaccinated person who's worked to through COVID, never got any infection in the 1st, 2nd, and 3rd wave, understood clearly that Omicron was a completely different platform, and now see that I'm prone to being infected by it, puts me and my phenotype at high risk. Mhmm.

So I think people need to be careful. But, nonetheless, we should all take Omicron serious, and it it's not it's not a mild flu like. It's it's it's it has some anger. We get to that. Then let let us get in thank you, Shankar.

Let's get into the next chapter. We won't be able to e go deep, but immunodeficiency, widespread opportunistic infections, and reactivation of retroviruses, bacteria and fungal infections, and widespread damages to the biome by SARS CoV-two bacteriophage behavior. So these are points that need to be looked at and need to be addressed somehow. We won't have time to really go into details today. Just one example here is some, opportunistic infections in Australia from 2022 on skyrocketing, for example, and it can be due to immunodeficiency and intestinal dysbiosis in large parts of the population.

Yeah. So it's not that we see now a a new waves of monkeypox and whatever they wanna sell us. It is just the overall immune defense of the population, very similar to AIDS, has been lowered for many different reasons, which I cannot explain today. But one of the reasons, of course, is this. If you see that the biome, this is a bacteria full with SARS CoV 2 Virons.

When they are finished replicating, they burst the bacteria and come out. And so how can you ignore this? Now it will there are several severe implications. One is, of course, is an additional reservoir. We have 35,000,000,000,000 own cells and around 35,000,000,000,000 bacteria in our body.

So it's as big as a reservoir as our own body cells. The virus, unfortunately, does not infect the bad boys like the staphylococcus and other E. Coli bacteria. No. And it it infects very targeted probiotic, bifido, lactobacillus, and butyrate producing for us beneficial bacteria.

And I don't know any other virus doing that. So how does that happen? Now what it leaves you with an impaired biome with an imbalance biome, which by itself makes you prone to opportunistic infections. So it's part of the immune deficiency is the is the, the dysbiosis. And this one here just Charles yesterday brought it to my attention.

I need to open up the authors here. So here you see a direct infection of t lymphocytes by SARS CoV 2, ACE 2 independent. That means they use other receptors. And you see this lymphocyte is full of coronaviruses. Yeah.

And the funny thing is that this paper was published by the bat lady that is under suspicion of having developed this weapon in the first place in the Warhorn Institute of Technology a biology. Yeah. How bad can it be? And here, we published on that that got a lot of attention in the German press, even the health minister, and and it was fought to the nail. They don't want this to be known.

Now that our immune system is directly infected, we described all many of them, not all, but many of the mechanisms, the receptors involved, and why this is the case. And you can tell that these PBMCs and all these immune cells are loaded with spike protein for a very long time, and they don't die. Yeah. This is Bruce Patterson here, 245 days post vaccination in monocytes. You see a strong elevation of these, viral proteins in the monocytes.

We are discussing with him since long time. I told him, Bruce, it's not only a phagocytosis process. It's not that the spike is being chewed up. Only it can be, but these these cells all are displaying all the receptors needed for SARS to enter and for the spike to enter. So what we're doing at the moment, ongoing project here in Germany, thanks god she has done that.

She she has now a laboratory that for patients and doctors, you can send blood samples and have a quantification of spike protein in the free blood, in exosomes, in PBMCs, in the stool, and in the urine. So that is the first time now that we are working on proving how a spike detox can work and does it work. So apart and that that's leave the Trevor, you wanna mention you wanna explain something on the immunodeficience? I've I've forgotten one thing. So it's not an immunodeficiency in the classic sense because all these cells are full of viral fragments or virus themselves.

They will turn by default into senescent zombie cells that are becoming dysfunctional. So the organism, it's not the lack of cells. It's these cells are not functioning anymore, and they even are more inflammatory from the phenotype than they normally would be. And so it's like you have to clear them out. So that's what we're trying here and trying to prove with brigantine in UrLab.

Yeah. But we we we will selectively try to kill these cells now, and it looks like it's working. And by doing that, the spike will be liberating. We get to that later what why we do that and how we do how we then take care of that process. Yeah.

So but this is to be understood that we are dealing with a immunosenescence that is normally only happening in people that are very old when the immune cells reach their biological age and telomere attrition is is preventing them from from producing new immune cells. You know? Yeah. I think the the the issue of senescence is vitally important. Just just just for people to understand, Joaquin, the immunological implications we're dealing with, because spike protein has such a high ability to trigger, an immune disruption tending towards allergy.

All different forms as far as it being a super antigen. So when we're talking allergy, we're talking a wide diversity of things. All the way from hypersensitivity, which can be quick and aggressive and life threatening, to, immune complex disease, where it will cause coagulopathies and things like that, to autoimmunity, where you start to self attack. So you got this entire range of your immune system all shifted refocus towards allergy, and not fighting anything else but allergy. So whether we shouldn't talk of a strong or a weak immune system.

Yes. A strong or a weak immune system just means you got more soldiers. What we have here is an immune immune refocusing. So you took all your soldiers, and they perceive we're operating in a a a solving allergy. And none of them are left to suppress cancer, to suppress infection, to do all those other things your immunity should be doing.

So it is an immune refocusing that's triggering all these other issues that are there, and it's to the persistence of spike is keeping that going. So we got a twofold problem. We can solve it by refocusing the immunity, by stopping the release of all these chemicals and things and calming the immunity down and giving it a chance to refocus. But the minute you take away the allopathic medication, because you haven't cleaned out the spike, you'll return back to that issue of an immune response. So it's like someone with the peanut allergy refusing to spit out the peanut.

Our job is to get out that peanut. And so I think the removal of spike protein from the body is key to having long term benefit from treatment. Thank you. I will skip some slides now otherwise because we are now really running short on time. But what's worth mentioning is the cancer causing potential of SARS CoV 2.

You just mentioned that because it's not only the lack of control over cancer through the immune system. You also have a direct carcinogenic percent potential of the spike protein in the virus itself. And I wanna mention something else here. This has been reported. That was actually a vaccine promoter, Serge Goldman, the author of this.

And he had cancer in remission, and on September 8, they did this scan. He took a vaccine booster on September 22nd, and 8 days later, the scan looked like that. How is that possible? How can you develop so many tests in such a short time? That is highly unusual.

And so few months ago, finally, a paper came out that could give us a hint why this is the case. And you see here, these animals were transfected with a mRNA vaccine that contained pseudo urethane, and these ones were injected with a vaccine that was not was also mRNA, but didn't contain the pseuduridine. So pseuduridine is only in the Moderna and Pfizer. And so these were animals that had, like this person, year cancer in remission. And within days, they did develop this.

And the ones that didn't receive the pseudouridine containing vaccine didn't show this development. So that could be a clear hint that we are dealing with the pseudo pseudouridine induced, turbocancer development. So we have been Yeah. Joakim, I just wanted to quickly add to that, to explain to to explain to patients that, see, looking at sero urodine, sero urodine is a component that is used in the manufacture of messenger RNA vaccines. It has nothing to do with spike protein, the protein coded for.

So any new messenger RNA vaccine that is made using the same technology, and we can see plants being developed around the world. It's going into veterinary practice. It's just being fast tracked. But here, right in front of us, is the potential toxicity or the toxicity that we see from the technology, not necessarily the spike protein. So people around us as well need to be aware that messenger RNA technology is not fit for human purpose just yet.

It it's still a long way from being safe and but k. Just so what can we do? So we we you don't wanna cure cancer to be forced to cure cancer at all times. So a preventive approach, again, would be smart. So our, colleague here in in in the University of Sydney, professor Kamal Dua, has been conducting tests with our polyherbal formulation, but this was on noncancer cells.

And the outcome was quite astonishing because it was not very cytotoxic to the rest of the organism, but would be extremely effective in keeping the cancer cell proliferation, at bay conditions. Because the suppression of the p 53 tumor suppressor gene, the methylation of that gene, is one of the key points why you see so much cancer in post COVID and long, and and postvac conditions. So he could clearly show, at least in the cell culture, that the these phenolic compounds would bring back p 53 expression, but, I mean, significantly. And that's what you want. You wanna strengthen the organism.

You have to clear out the senescent immune cells. You have to rebuild this the the immune system. You have to take out the spike and the virus because while they're present, they're suppressing type 1 interferon, which is also controlling cancer, and they are methylating tumor suppressor genes like p 53. So all these factors, you have to address at the same time in order if you want to prevent cancer development and cancer proliferation. Once a read that, it's peer reviewed, published, and available in the in the public domain.

Let me just give you very quickly some results here before we get into the detox part. These are the the products we we have developed and we are using. The main product has been has been gone through phase 2 clinical trials in the in by the end of 2020, early 21. We were having really good outcomes in setting with a 120 patient 124 patients. It was done in India because we couldn't find another country where we would be able to work unmolested.

And in India, everybody was welcoming our work, so that's why we went there. And it showed very good baseline effects on the on the patients. We did a lot of blood markers. We took, like, 4 times around 50 biomarkers for each patient. It was very expensive and very big effort to do all that.

And, in the first thing, we could we could notice a very strong viral cycle effect. You see all these papers now. They're talking about how many patients were were turning negative after how many days. This is not you can't do that. You can't compare apples with bananas.

You have to measure the particular viral load and the diminishing of that with your virus cycle intervention per day on average. That's the only reliable marker you can take. So we were doing outstanding on on that respect. And that's also important for spike detox because you mentioned we would we will liberate viruses out of these pockets, and we have to prevent them from reentering back into healthy cells. So if you wanna do a spike detox, you'll need a very strong virus cycle.

That's imperative. And then, of course, also other, things you mentioned, d dimer. You see, this is the the yellow one is the standard treatment, and the blue one is the recidivism group. You can see that here the d dimers went shot up on day up until day 12, and here it was immediately controlled. Interleukin 6, same lung function, incredible improvements within 12 days, 75% improvement in abnormal lung X-ray findings.

And this is here from the US from our clinic in Connecticut from doctor Robin Rose. Some patient data, we're getting more. Just to give you an idea maybe for the therapist here present today, it's interesting to see which markers we are using or she is using, but most of our practitioners do that. And what as as a panel, you can see that TGF beta is highly elevated in practically all long haulers. Also, d dimers to a degree, and that it's imperative to bring down TGF beta.

It's not easy to say where does it come from. It can come from different many, many different sources, the elevation of TGF beta. But here in these patients, you see it's this one was 9,520, pretty high because the normal range of, TGF beta would be around give me a sec. I don't find it here. It should be higher here.

It should be way below that. I think it's this is the correct level here around 1500. Yeah. And interesting is the amyloid beta 4042 ratio in these patients. If it's very low, it's bad.

That means you wanna have that high that ratio. And this is an indication of ongoing dementia, Alzheimer processes. You can measure it in the blood. And all these things we see now in the patients after treatment and going through the protocol are improving. We can make it a separate webinar just together with the practitioners and with the doctors and looking at the results.

I I don't wanna do that today. It will take too much. So let's get into the part of navigating the mind field of removing Skype for Teams from the body, which in itself is a tricky business. So many people, let let let us first understand a bit about about what the nature of this. This is a SARS CoV 2 virus.

These are the spike proteins, and the spike protein is kind of the key, and the receptors are the locks on the cell membrane. And then you have also to penetrate the cell membrane, you need also some fusion enzymes. And then once the virus gets into the cell, you have more possibilities to interrupt the replication by many, many different pathways, which will be too much today to mention. But the entry mechanism is a little bit different than what we see in the vaccine. In the vaccine, you have a lipid nanoparticle carrying the instruction to build spike proteins like the manufacturing instruction RNA, and this goes fuses with any cell.

This lipid nanoparticle doesn't need any receptors. It's a forceful entry and transfecting the cell and we're converting it into a spike factory. And then these cells will excrete spike proteins either as a whole, maybe even already cleaved in s one and s two subunit, and many times in so called extracellular vesicles or exosomes. So, again, the exosome shedding of spike protein is pretty, concerning because the exosomes are like lipid nanoparticles. They can go to any cell.

Yeah. Exosomes are our own lipid nanoparticles. As you see that here, and then the retards at BioNTech, they are even proud of them. And as I said, they they they they prove them how they they their spike protein is being shipped around in highly fusogenic exosomes, and that is what we are measuring now at the laboratory of of a Saconic because this will be happening on a continuous basis if the cell is still producing spike protein because the cell is using exosomes as garbage cans to throw out things that it doesn't that's too much in the cell. And so that is important to understand.

So in principle, we are not looking at free spike. You can't just take some enzyme, throw it on the patient, and hope that it will meet enough spike protein to to resolve the problem. You have to take the terrorists out of there. So we're distinguishing between productive cells and deposit cells. A productive cell is a cell that was transfected by the vaccine and still produces spike protein or is a nesting reproducing virus, also shedding virus and spike.

Once a spike protein hits a cell, it will stay there. It will, again, like I mentioned, will switch off all the cell signaling that can become a problem for its demise. So it protects itself. It wants to stay there. It's a self preserving mechanism, and that happens with the spike from the vaccine as well as the wild type spike from the virus itself.

A few words, we we had nattokinase in the program in the US. I don't wanna say anything about any other treatment, what other people are doing. We are testing now nattokinase in Japan for its ability if it really can degrade spike protein as a whole and not lead to these fibers. So I went to the expense and bought an a real time quaking machine that we are now using to add spike and neutrophil allostase, spike and different enzymes, including nattokinase and other enzymes just to be sure that they are completely degrading the spike and not leaving these little presence here. Now and if that's the case, then I'll be the first one to fully endorse and keep promoting.

So what what are phase 1, autophagy induces? So we've seen SARS CoV 2 spike protein wants to stay with us. It doesn't want to be degraded. It doesn't wanna be kicked out. So what does it do?

It takes all the efforts possible to block any autophagy initiation and mechanism it can. Yeah. So it's an autophagy inhibitor. So, also, the idea promoted at the moment with intermittent fasting that you can get rid of spike protein, Maybe, maybe not because it is very successful in doing that as we see. So, thankfully, it wasn't me.

This time, it was another group that came up with tests and and studies on phenolic compounds that can override the blocked autophagy mechanisms that were blocked by SARS CoV 2. So maybe that's a chance. Yeah? So we should we can go this route, but we have no data, we have no experience, and we are not sure if this is happening or not. But it counter to mention it and look at it.

What we do know is that we can break up the cells and kill the cells selectively that contain spike and viruses, this we know by now. So we have to understand the the nature of this. So the spike protein when it hits the receptor or the membrane, at that moment, it switches the complete cell signaling to senescence, as we mentioned before. So this cell is now a senescent sasp phenotype inflammatory cell. It's like a bad apple in the shelf.

It will also destroy and infect and and and affect cells around it. But this cell, you can't save anymore. When the spike is in there on the membrane, the cell is, you you can call it. Yeah. So it's far beyond of being possible to be repaired.

So we have to selectively take out these cells, plus we have to do something about the, main so the main cytokines that are coming out of this thing is very famous in long COVID and COVID, is tNF alpha and interleukin 6. And so what we have been doing from beginning of the pandemic was to emphasize that we have to bring down these 2. Now look at this as significant. This is like half, almost, now that we could bring it down in the preclinical trials in the animals. And then, of course, you can start now to look at the at the, at the at the and and the, the, sorry, the the the resistance to apoptosis.

Yeah. So what we are now using is these kind of senolytics. Yeah. And the senolytics have been proven to really do a good job on this. For you, you have cell cultures.

These are mock cells that don't contain SARS CoV 2. These were the same cells containing SARS CoV 2. And when when you start treating them with senolytics, you are strongly diminishing and selectively killing, these cells. We did tests with, Barthejager doctor Barthejager and, professor Konig, and we could see a strong elevation within 2 hours in the blood. So we took blood before and after the xenonalytics.

And in in the before samples, you you didn't find any spike in the serum and blood. And after 2 hours, it will go through the through the stratosphere. I'm still waiting on the on the report on that, but it was causing a lot of confusion at the laboratory that from the same patient, all of a sudden you had it from both from the same day, you had one blood sample without spike and then one with a lot of spike. So it shows that within 2 hours, you're you're mobilizing that, and there's many other studies that confirm this. Doesn't really matter which kind of viral debris you're looking at.

It can be spike envelope, nucleocapsid, RDP, RP, protein in the cell, and it all turns out the same as senescent. So it's one of the biggest problems we have. It's the biggest problem, but it's also the Achilles heel of COVID and of this weapon. Yeah. Because now you can selectively take out these cells, but you have to do it very carefully, very slowly, not too fast, not too often because the body needs to regenerate these cells, and you need to catch, of course, all the debris that is coming out, especially from the sensation.

Yeah. The sensation are bigger cell conglomerates, and you will have also, like, different other cell debris coming out. And your monocytes and macrophages are anyhow impaired because they are full of spike at the moment. Yeah? So you have to go slowly, give the organism time, but we see the results.

It works, and the syncytia are also being cleared. Yeah. I I took out the molecules because of patent reasons. Yeah. So the last step, of course, is then to chelate the liberated virus and and spike, and you have to do you have to make damn sure that you have enough binders and chelators at the right place in the organism where you are mobilizing these viral debris or the virus itself.

We've been doing that for a long, long time, and you see all these different molecules here, and most of them are in the binders that we are using or in the products we're using. And then there are some champions here also, ciflabin, digilate, curcumin, that are very strong binders to the spike protein, but also some of them are strong senolytics. So I won't give away every molecule and what we're doing, how we do it, and it it should be, not attempted. Don't do this at home, but without without proper guidance. Yeah?

Because it is a tricky process, and there are also some regions in the organism where it's more complicated. If you look at this battlefield here, this is the epithelium of the gut and there's the intestines. Bacteria containing spike proteins and viruses, and the viruses reproduce in the bacteria and in the epithelium of the gut lining. You can see that here, a persistent spike in the epithelium of the gut lining. And so you can have a ping pong cross infection between epithelium and bacteria.

So you wanna have a strong binder in this area here to prevent the virus from jumping from epithelium to the bacteria. And there we are using several other binders that are not only ophthalmic compounds in the medicinals, it's also sulfated polysaccharides. Remember, we were talking about the glycocalyps. Yeah. So you were using heparin when you were in the hospital.

It's actually one of the best binders to spike protein known, but these polysaccharides are even 4 times better at binding to the whole spike. I found that very interesting. So these are excellent binders, and we have we use we use other ones. We also like this, zeolite kind of products that are mixed together with the algae. And look at it.

How how at how little dosage they can also completely absorb the virus. Yeah. So you wanna have that present at all times, but you wanna be sure that you also have not only in the gut, the right binders and in the normal blood flow in the organs, you also need in your brain. And melatonin have the highest binding interaction with the SARS are redo from all the tested compounds. That's wonderful because melatonin does another well, does a lot of other good things, and that's why we are using that in the detox in in larger amounts, and we are working also on the nasal spray that will come out in the course of this year.

Then we need to block the host cell receptors, not only bind the spike in the virus. We have learned that there is a multitude of receptors, and so you want to have something like this here. This is, again, a test with our product here with this line. For example, one receptor is the AXL receptor, and it's reported to be as receptive for SARS CoV 2 spike as is ACE 2, almost a little bit less. So you wanna inhibit that.

Yeah. So there's data on many, many of these receptors that we have already accumulated, and you want to interfere also with the furin inhibition. We talked about that before, the cleavage enzyme that the spike needs for cleavage. Yeah. So without a furin cleavage site, there would be no pandemic.

So why not inhibit furin? Yeah. Highest priority for me. Yeah. Catch this thing where it's weak.

And then, of course, you wanna protect your kidney while you're detoxing. So we see here that quercetin, pure quercetin would have a great effect of protecting kidney cells from being damaged by the spike protein itself. All this is documented if anybody needs or wants to have any reference papers or whatever. We are sitting on around 10,000 reference papers just for these product bundle and for the according mechanisms while we do what either describing the scientific rationale and or showing already preclinical in vitro in silico or other results on the whole composition that we were using. All this is available as a as a bundle, spike buster bundle that you can purchase at special prices, of course, for therapists and doctors, and that is a turnkey bundle.

So you can right away start treating patients with it. And, I mean, there there will be a certain triage. Maybe, Shankar, you wanna say more to that because we can't you can't just now take your worst patients that are already severely injured and in very critical condition and give them a bundle like that. But the majority of the patient is somewhere between mild to moderate, and they can they can take a a product like that without big problems. So I think I think, individual basis working.

Patients that are acute, high risk of death. We need allopathic medication to suppress the reactions that are causing the problem very quickly. But once we have them stable, we need to understand why they have what they have. Is it an infection that created a little bit of spike protein that can be dealt with relatively quickly, or is it a vaccine, you know, with long term spike production? And then, of course, we want to, besides stopping the process, we want to remove the spike.

That's where the nutraceuticals come in. Remove the spike, bind it, excrete it from the human body. That's the second part of what, vitally needs to get done. And with the nutraceuticals, restoring the balance again, the integrity of your linings, all that kind of thing. And then I think the third part that we must, constantly look at is the ongoing attack on us and how we're going to protect ourselves.

And I think that comes from, diet, going back to nature, our microbiome, and how we protect the integrity of what it actually means to be human. Yeah. Thank you so much. So if there is any questions on this, please contact, Carl will, in by the end of this. When we finish, we will give you all the contact data.

And you if you need any more information on that and guidance and intake plans and so on, Shanti and Carl will will be able to help you there. Shankar, you also wanted to explain something about your courses in South Africa for medical doctors that would like to come and learn from you more on how to treat patients. Do you do you have any contact information and some information on how people can touch with you? Joaquin, we're busy trying to, set up. There are 2 2 major issues that I face, is to treat patients around the world with, our modalities that we've developed, and I've had great success here in South Africa, but to share that knowledge with everyone around the world.

So I'm setting up a consultation platform, where I can then take bookings and start to treat patients itself. Then for doctors that want to have mentorship, I've been approached by many doctors that want to have mentorship training. So we want to set up a 2 week program where we provide them accommodation here in Port Edward, and they can come and work with me for 2 weeks, half the time, with me physically seeing patients, and the other half about the academics. I think, for us to move forward, we need to bring the understanding of biologic science back to the way we actually treat and heal patients. And I think that's where doctors are lacking in understanding the holistic, entire approach.

So Port Edwards is a very quaint, destination, a little bit of paradise where nature flourishes all the time. And so I think it's a nice, environment to realign the medical profession for those who want that realignment. So, yeah, we're trying to make it a very individual service where someone can come spend 2 weeks at a time learning about, the differences the way in the way I see medicine and the way we should be treated. Thank you, Shankara. We will try to repeat this on a biweekly basis, and Shankara and myself.

So maybe we we now you can also, write us what you wanna have in-depth so then we can go and specialize on one of these webinars onto one topic via my cardio, cardiovascular, neuro neurological symptoms, etcetera, and then elaborate deeper and explain better. And, Carl, can you please be so kind and read me some of these? Are there questions in the chat? I couldn't read that while I was speaking. Absolutely.

So one of the questions is for doctor, and it says, did your research include details on the endocrine system, specifically aspects like cortisol, ACTH, Aldosterone, renin, and thyroid functions. Okay. Sorry. I'm just putting in my there we go. I have it all.

I think, look. With my research itself, I understood that we're dealing with the hypersensitivity reaction, and that's gonna affect everything. All it's all all all it takes is time for it to cascade out of out of control. So a lot of the research that I've done focused on the interleukin 6 as a biomarker for immune dysregulation. CRP as a biomarker for generalized inflammation.

Right? Sorry. The the interleukin 6 has an immune reaction. The CRP as an, as a indicator for hyper inflammation, and the d dimer as a marker for, for the clotting. And clearly in the 1st wave and the 2nd wave, we could see a trend.

The, interleukin went up, immune start. Then the CRP started to climb, inflammatory response, and then the coagulation in D dimer went up. So my work was to look at those three markers and to figure out the most effective treatments because I felt that was the core of the trigger. So a lot of the work went into looking at different types of antihistamines, montelukast, different kinds of ways to negate the process, high dose steroids. And, of course, with Carlo Brougner's work coming into it, we realized the persistence in the microbiome.

So we had to have a add a second modality to where we treat that intensely in those patients with persistence to clear the virus out the gut and to try and restore the integrity of the gut both with the tight junctions and the appropriate microbiome. So, yeah, my work's covered to that that those those basic areas. But I think the understanding of, hypersensitivity, the immune, dysregulation that occurs with the virus, and how that cascades down the road with viral persistence, I think, is the essence of treating both acute COVID, long COVID, and viral injury. The underlying pathology is the same, but the, speed and persistence of the toxin there is dependent on the individual itself. And Okay.

We have another question from Greg Miller. What has your research shown as the optimal number of months patients need to take the program to get the results you have shown here? Yeah. So we are we are still in the middle of all that. Give me a second.

My dogs are barking. Sorry. So we're still in the middle of all that. It's, of course, depending a little bit on the, on the patient itself. It can be the preconditions.

Shankar, are you gonna say something about that? I'll I'll mute while my dogs are barking. Maybe it it it Yeah. No. I think, yeah, I think it is I think it is very patient specific.

Where the nutraceuticals are vitally important in is in both, the removal of spike protein, and in the restoration of balance. Allopathic medication is far too targeted. It might be good enough to address symptoms and to stem ongoing pathology, but it's not good enough to address the entirety and to aid in restoration of, balance itself. So I always felt that nutraceuticals were, God's way of giving us everything we need in the right concentrations rather than extracting a single chemical to have a single effect, which will, inevitably have knock on effects. Now what we found in some patients is that when we use allopathic treatment, we get very good benefit in a very short space of time.

Usually within a week, the patient notices a significant improvement. The problem is you've got a patient with a significant improvement, but stop the medication. The patient will go back. So that is where the nutraceutical comes in and the nutraceuticals in restoring good health and removing the spike protein, which is the offensive agent. That length of time, I think, to recovery and full recovery, depends on how quickly you sought, acute treatment to, limit the injury itself.

The second thing it will depend on is whether you are a phenotype that's constantly exposed to, new variants and get sick from it even though you may not be vaccinated. And I think the 3rd variable are those that are vaccinated but have an ongoing, though highly variable, production of spike. So those are the 3 kinds of, patients that you're actually dealing with. Yeah. Yes.

Thank you. Okay. Okay. The let let me okay. Let me first get to the first one, the last, point you mentioned, the ongoing production of spike protein by transfected cells from the vaccine.

So that is a hypothesis. I couldn't prove it yet. But if you look at the mechanism of action, this cell that has the mRNA, injected into it and is producing our spike proteins, that spike protein will be in the cytoplasm for a while, and it will automatically, because of its composition, change the signaling of that cell into a senescent cell. Most likely, isn't it? And so it the cells containing spike, production, lipid nanoparticle injected mRNA will be targeted as well, hopefully.

So that means we probably also kill the cells that are still producing spike. I forgot to mention that. Yeah. That's the hypothesis. Yeah?

So that's We kill the cells producing the spike, and we bind the spike so that it can go kill other cells. Yeah. But to to the question of, doctor Crick Miller, yes. So so experience has shown that the the mild patients that show light symptoms that maybe are not in such a bad condition, which is are the patients that respond quickest to this protocol within a month or 2 of of showing much better results clinically, symptomatic, and also from the blood markers. And then there are patients that take longer.

We were surprised last winter. We had some patients that took until they showed, for example, good results on the microplotting took 6 months, 5 months. And then we found out that they were infected, like was mentioned, they were exposed to the virus in between. And then you go back to square 1. When you are in the middle of the detox and you don't you don't really do something about the acute infection, then you go back to square 1.

Your your microblotting are back and your your blood markers are are off again. Yeah. So preventing reinfection of lung volus is really very important. Yeah. Even even everybody underestimates this omicron as as mild.

So it is not easy to give a conclusive answer, doctor Greg. It can be anything from 4 to 6 weeks to 6 months depending on the And I think, Joaquin, identifying the, the kind of patient as well is vitally important in, in the Absolutely. Regulatory. Yeah. Carl, are there any more questions at the moment?

I do not see any questions in the chat. If anybody would like to unmute themselves or ask a question in person, by all means, or you can place them in the chat. Is Philip there? I wanted to have he maybe he wanted to say something about the rubber like clots and where we are at the moment in the calamari project. Are you there, Philip?

Can you hear him? I just asked to unmute himself. So he is there. Let's see if he can unmute, Philip? Hop in.

Maybe he's not getting us well. No problem. So then, look, for for today, if there are no more questions, then I would like to tell you that we will be back here in 2 weeks, same time, by noon on Saturday, and, me and Shankara, and we will prepare, another presentation that goes into, let's say, into any of these 5 big fields more deeply and also from the strategies. And I I don't wanna just talk about our products. I wanna talk about what is working.

I have no problem with other things coming in. And maybe, Shankara, it's good to also show both. Many many medical doctors are listening today, so I don't say we all have to use just now dietary supplements for Christ's sake. We we can combine anything that works. We have to think in the patient interest.

Now this is such a catastrophe. So, like like I mentioned, and, Shankar, I mentioned the histamine blockers, for example, when my wife turned had COVID just the last time, I I I put her on the, on the antibiotics. That's another good information for all of you. So the, I forgot to put the publication in. The use of amoxicillin and rifaximin in acute COVID, is very useful, and we have papers now with 220 patient, retrospective report, from Italy with Carlo that it would would help, especially at early onset, at the in the first three days, it would drastically reduce viral load in the organism, in the stool samples, and in the, overall organism of the lung and in of the COVID patients.

So you you if you are allopathic doctors and you'd also wanna use some pharmaceuticals, yes, of course. That makes a lot of sense. Yeah. I'm not against that at all. I just what I don't like is so many now very famous allopathic doctors talking about natural molecules have as if they have done that all their life, and they don't understand much about natural molecules with all due respect.

That is a whole different animal. So I would say everybody should use that what he knows. And if you know pharmaceutical drugs and we find we find a gap, they are very narrow. So they're not as broadband as what we are doing, but sometimes you need also a narrow sharp knife, yeah, to push something quick and effective in a in a in a setting of, of a acute patient. Yeah.

I think, I think that the the allopathic doctors on the, on the group, need to understand that, we have to have a collaborative effect. This is not only a medical attack. Yeah. If we look broadly, it's economic, it's educational, it's spiritual. There's a whole lot of things that are going on.

And the collaboration of experts in the different fields will actually bring us together like our work did working, where I'm more of a biologist and understand mechanisms. You're more of an engineer and understand where to look for process. And, yeah, the collaboration yielded a lot of benefit and a lot of fruit. So I think, people around us just need to understand that that we we are under attack, and, it is a broad based attack more than allopathy could ever, hope to to to to to to solve. But I can use my allopathic understanding of pathophysiology to help those in naturopathy look for the solutions and where to look for the solutions.

So each one of us has a role to play. And I think, the collaboration going forward with like minded people that resonate with a common purpose would be vitally important in winning the war. Thank you, Shankara. Doctor. Greg, do you have, something to ask?

Go ahead. Greg, do do you Doctor Greg, please. Go ahead. Alright. So, Monthly, what I've been doing is I've been doing testing of d dimer, IL 6, TNFA, histamines.

What other broad test? And I do a a CBC with diff, obviously. What other testing would you recommend on a monthly basis where I have patients on the program? Did you have beta 1? Yeah.

And ferritin, if I do. You know, I obviously, we we pull up ferritin because of that. Of course, the levels of ferritin are so elevated. You know? It becomes an inflammation marker.

Doctor Biller, I think as well, we've we see some very drastic fluctuations in these levels, and it's those fluctuations that we need to, address. So you might find when when I look at those three levels, when I I usually do CRP interleukins and d dimers, and, depending on the, patient population and the affordability of those tests. But what I noticed through COVID was that the interleukins, d dimers, and CRPs in the first phase, the viral phase phase where the patient initially presents, tend to not really go up at all. The CRP goes up, and we expect that because there's a in inflammation because of the virus itself. But there's a specific point in a specific phenotype of patients where you can look back at their history and see if they've had a flu and it took 2 months to get over it.

That would give you an indication that, look, I'm dealing with a particular phenotype here. And it's those kind of patients where suddenly in the illness, after a period where they thought they're recovering in that 1st week, suddenly stopped recovering and started to worsen. And in those patients with a far more severe worsening, you you see a rise in those values. So it's a sudden uptick in those values. So besides regular testing, it's also to advise patients that a week after getting the flu, if you are still not better, do the tests and check.

Just a simple example, doctor Mala. I, on the Sunday, was perfectly fine being my 8th day. I had double vision, which should have, as a doctor, drawn my attention to microvascular clots, which I am prone to. And I should have went straight to the lab and did my d dimer and started my anticoagulation, but they left it just for one day. And the following day, I was admitted to ICU 4 days, unconscious with a great consequence.

So I think the education of patients that this is the type of pattern we are seeing and not to take new symptoms lightly, on the side of caution. In the 1st, 2nd, and 3rd wave, it was easy. On 8th day, people started to die. So everyone started talking about the 8th day, and, you know, we need to go do this. For some reason, God stuck me back in hospital on the 9th day, I think, just to remind me.

Stop forgetting about the second phase. And I think the second phase with Omicron might be so mild that we'll ignore it and call it brain fog and fatigue and just not yourself. But you got an ongoing process that in the long term and when I talk long term, I'm talking 2 years. You're gonna see consequence. And so that's, I think, as as doctors, we need to be aware of that.

To to patients, you know, it's only 15% of patients with a medical condition that actually come to the doctor. The other 85% ask their neighbor, ask the pharmacist, treat themselves, find their ways to get better. But now we're sitting with the population that's been vaccinated, and those minor symptoms that they spoke to all these other untrained medic medical professionals about and thought they will get benefit from it are now critical actually, critical symptoms that are lead gonna lead to drastic consequences if not addressed properly. Thank you, gentlemen. Great presentation today.

Thank you. Thank you. Then I thank everybody As we have one more question we have one more question here, Joaquin. Are there key things to focus on with respect to our microbiome? Sorry.

I didn't get the question. One moment. I it was acoustically wait. Let me go into the chat as well. Yeah.

Alright. The key things to focus on with respect to our Yeah. Okay. That is a tricky question. Look.

If you looked at the, again, we're talking about fubar. Yeah. That means you have the bifido lacto and other beneficial butyric bacteria, bacteria and butyric producing bacteria being infected actively by the SARS COVID 2 virus. And probably, I I'm not at liberty to speak, but it's an ongoing project is to find out if the lipid nanoparticles and the spike proteins can do something similar. And the data suggesting, for example, that pregnant mothers that were vaccinated give birth to children that have practically no bifida bacteria.

Have you ever heard that that in a little baby, which is normally full of bifido, there's no bifido. So all these things are very spooky. But so I'm reluctant to follow with all patients now the advice from doctor Carlo Bruni. I really respect him, but, you know, some experts are sometimes having the syndrome of having a big hammer and everything looks like a nail. And so we have to hold them back.

They are right with what they say, but not it's not only that one problem. There's many things to blink again. So, I think that the bacteria might exhaust itself by producing these back these virgins. It's not like a the bacteria doesn't go into a senescent cell state state. The bacteria will produce these viral and die.

And when it runs out of reservoir or if we bind these virals that are produced, then the the infection in the bacteria hopefully will seed. But as long as you have in the neighborhood, in the epithelial gut lining, you have persistent reproducing viruses, it can always start to reinfect the any bacteria that comes close. So during the spike detox, it's imperative to hit the epithelium first, but that is happening anyhow. Because if you take this analytic mix and this fine tuned product, then it will hit the epithelium first. That will first hit the epithelium and mobilize all virus and spike that's in there.

So you have to have a lot of binders in the in the in the, in the intestines, which we have. Yeah. So binders, you should not, be looking at quantity. Just take them. They they are all uncritical substances you can take.

So that is the essential. So when we when we do the detox and we get the spike in the virus out of the epithelium and we keep up the binders long enough, my hope, and we will have to see again with professor Bridget and with Carlo, is that we don't need anti antibiotics to kill half of the biome to get rid of that virus. It will kind of outbreed itself, and we will bind everything that comes out and get it out with the faecus. And then, of course, you have to follow you then then who am I to tell anybody in the field of integrative medics and the natural therapist how to restore a biome, that is being massacred? I mean, it's pretty clear you can use whatever prebiotics, probiotic mixes, etcetera, etcetera.

We will probably develop something that is more specifically targeted. But to be honest, we don't have time at the moment. We have so many urgent, really pressing things to be developed first before we get to that point that we have the luxury to to develop a symbiotic or pre and probiotic mix, will take a few more months for us to to get there. But yes. I think I think, Joaquin, just to add to what you're saying, nature has a way of balancing itself, for for for where we are at the moment.

The best we had, 3 years ago was, I think, a probiotic with about 9 or 10 strains of different bacteria in it. And these were highly marketed, put out there. But, are those the bacteria that are now the ducks? So was it, filling us up with bacteria provide host for bacteriophage activity and to cause viral replication and actually set us up for the fall itself? So I think the field of, probiotics and prebiotics has changed a little bit.

We've got to put in bacteria that are resistant to getting infected with the virus itself and are beneficial as well. And, of course, the diversity to allow nature to restore itself. So when it comes to probiotics, I think, yes, the bacteria and the active bacterial species must be there. But the best probiotics is to get out into nature and to roll around in the mud a little bit because your microbiome is from your chest into your nose, in your eyes, down your spine. It's over your entire body through your intestines.

And I think nature has a way of balancing itself. So I think that's that's, is to go back to the basics. Groundy. You know, enough sunlight at midday. Those kind of little things that will restore us.

Eat clean foods. Stay away from glyphosate. Any any lifestyle? Processed foods. Yeah.

Okay. Cool. Just just go back to anything anything in a in a supermarket or a big store that's wrapped in plastic is not food. You need to get that into your head. That's not food.

I've never seen a cake that I've baked stay on the shelf for 6 months. That can't be right. Okay. Then gentlemen, one more quest one more question here, guys. How to treat antiphospholipid syndrome, if you can see that working?

Yeah. That is, of course, a an an autoimmune disease. So we can't just not very quickly do that in a nutshell. So maybe we can pick this suggestion up for the next webinar and go there more into autoimmune disease expression. We didn't talk today much about IGG 4 and other things, and maybe, Shankar and me myself, we can invite somebody that is very knowledgeable on on this topic to come in as an expert also for certain autoimmune diseases.

And so let us prepare a nice webinar. That's a good good suggestion, sir Glenda. And, actually, I have to admit for myself, I'm that autoimmunity in all long COVID and post vax condition is a little bit not my strong side. It's so complicated, and we really don't understand it yet. And the and the molecular mimicry and the, let's say, the the b cell activation and whatever's placed into that is very complicated.

And I hope that by taking out viral debris and fragments from the cells and removing them from the membranes, because they're triggering all the time some immune response, of course. But by clearing the body from all viral debris and viruses, we will maybe help already the the basic constellation to bring down autoimmune reactions. But how to specifically treat that? I I wouldn't know yet. I'm not sure.

I mean, there's evidence that many of the compounds will be helpful in autoimmune diseases, but that is still a field. Yeah. I think, I think, to to to put more context, Joaquin, the autoimmune issues that we deal with are many fold. First of all, you've got your cells making spike protein, which is a membrane bay bound bound protein. And so dependent on the bio distribution of the vaccine, certain cells in your body will express spike protein on their membrane cell membranes.

Yeah. And those will be prone to attack. And I think the cells that express the spike protein on the membrane, whichever system it might be, might be dependent on phenotype again. So certain families will have a lot of kidney disease. Certain families will have a lot of lung pathology.

Certain families, you know, different kinds of things depending on where that spike protein is being, expressed and, of course, having triggering an autoimmune reaction to spike protein and then progresses to the cell itself. And so now it starts to destroy even cells without the spike protein in it. But as well, we also got the immune system responding to a wide diversity of spike, spike based proteins, a whole lot of other chemicals, and it's constantly learning. And because of this rush of learning to try and maintain survival, there is that risk of cross reaction again and triggering autoimmunity with antibodies that were formed to, proper antigens that needed to be addressed, but those antibodies now became cross reactive to the self. And this overproduction of antibodies will lead to an increase in autoimmunity.

But I think, I wrote about this in 2020, Joaquin, that once your immunity learns, you're sitting with the problem. You're sitting with a naughty child who's been out of jail too many times and knows how to do the crime. And that's what that's what the world is sitting with. The only way to actually solve that problem would be to reboot your immunity. That means to unlearn all the bad things it learned and start from scratch again.

And one of the ways of doing that is, if you had an outbreak of measles, it measles is one of the viruses that tend to reboot your immunity and wipe out a lot of the memory that's there, which is what we want. Some of the a lot of this memory is bad. But the other thing that can actually do that is the BCG vaccination. The live attenuated BCG vaccination that we all took as children. Please not the mRNA technology.

I'm not suggesting anything in that direction. The BCG vaccination tends to reboot your immunity and stimulate t cell response again. So, as a prophylactic, I would actually advise all older patients that are over, let's say, the age of 16 to go and get the old style BCG vaccination. It will reboot your immunity and probably give you a lot of benefit from an immune perspective in refocusing that immunity. But when it comes to autoimmunity and the treatment of autoimmunity and the modalities for the control of that autoimmunity, I think we need the experts involved that have been in that field.

Let us see. We will prepare something, get some get some homework so we will have one chapter of next week's webinar, excuse me, being focusing on our community. And I thank you everybody for your attention, for staying so long with us. It was only planned to be for an hour. We have reached 2 hours.

So thank you so much, Shankara, and everybody else. Nice. See you again in 2 weeks. Sorry. Thank you, everyone.

Thanks thanks for allowing us the opportunity to share or not. Yeah. Bye.

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transcript  to 36min podcast How do Doctors Diagnose Severe COVID-19 in 2024? dr chetty Vejon health

https://www.youtube.com/live/glBs9fd5dwQ 

Hi. Good evening. This is one of our midweek discussions with doctor Shetty. Looking at diagnosis of COVID, and you have to understand this is gonna be a clinical discussion because we are trying to understand what happens with regards to severe disease. So I'm not talking about somebody just having minor symptoms and so on.

I'm talking about patients who get really sick, end up in hospital. How do we diagnose them? That's really the question that I think is very important at this point. So, before, I start, I just wanted to mention that in the links usually below is the ability to join our newsletter. As well, coming up next week is going to be on Thursday of next week is going to be presenting storm.

This is the spike triggered autoimmune response. This is a a specific area that I think is very important as to how the disease is going to present in the near future. That's a separate clinical discussion. But for the time being, without, any further ado, let's just make sure that we have got doctor Shetty with us. Shankara, how are you?

Hi, Ty. Hi, Philip. I'm fine. I'm fine. Excellent.

Excellent. Of all our views to it. Yes. Yes. Yes.

So let's let's get into it, and let me explain what I'm trying to see if I can get my head around. At the moment or let let me put it to you, the question that I often ask people. Is the diagnosis of COVID, and I'm thinking of more severe disease, is the diagnosis of COVID a clinical diagnosis, or is it a lab diagnosis? I think at the moment, Philip, with the unreliable PCR test, it is more clinical diagnosis. Until we find better methodologies for testing and more efficient testing and, testing that's simpler, you don't have to go to a lab, I think at the at this point in time, it is a clinical diagnosis.

No. That that's a problem because at the moment, certainly, when we look at, first world countries, the PCR test, they will consider it still to be 90% effective, you know, as opposed to, say, a lateral flow test. Now I can't imagine that the same tests that we have been using over the pandemic as more and more variants come out is still gonna be as efficient. It may still pick up some cases, but based on my observation, it tends to be quite hit and miss. And so, therefore, how, from a clinical perspective, do we diagnose COVID?

So based on just your experience, Shankara, imagine you didn't have a PCR test. What would make you think that this patient has COVID? Philip, there's many little nuances that I think, clinicians need to pick up on. If you look at the first initial viral phase of the illness, there's very little that's different from all the other respiratory viral illnesses that we usually present with. Right?

You get the generalized malaise, body aches and pains, the fever. A lot of it is very simple. The one thing I noticed different with all patients who develop COVID is that the start of the infection is usually unusual. It didn't start with the sore throat or it didn't start the usual way an infection starts. It usually starts patients report they had a headache for a day, which was unusual.

You know? Or they felt very tired for a day, which was unusual. And then the other infective symptoms started. So I tend to question patients as to when and how the illness started to see whether it's the usual flu, whether there was something a little unusual about this. That draws my attention to it being COVID.

The second thing is I've mentioned from the start, Philip, the 8th day and the changes that occur on that day. And I've seen those changes occur critically even in the mildest of cases. It happened to me twice, Philip. I had very mild inflammation. I thought I was getting better.

Exactly on 8th day, almost to the hour, I had new symptoms emerge. Those new symptoms, I I I as a doctor ignored them. The first time, the only thing that happened was I lost my smell and taste. I was improving, but I lost my smell and taste. I ignored it, and the following day, it had triggered microvascular clotting that had me in ICU.

Luckily, just for a day. The second time around, exactly on 8th day, I was feeling reasonably fine. I had a trip down to the local mall, and the only symptom I had was for a few seconds intermittently, I kept getting cross eyed. And I got home that evening. That was my 8th day.

I again ignored it. And the following day, I was in ICU. So and that that took me 4 days to get out of that. And both occasions, it was microvascular coagulopathy. And on both occasions, the only test that that showed an increase was my d dimer.

Now in this last episode, they ran every test in the book, and everything came out clear. It was only my d dimer went up. It went up from 490 odd to 6000, and I can guarantee you that rise started on that Sunday when I became cross eyed. Saturday morning, always fine. I'm thinking to myself now because, as I said, I've always said that that microvascular clotting, the microclots that we said, is more like a vasculitis.

It's an inflammation in the blood vessel, which then leads to the clotting. And, generally, when we think of severe COVID, and that's what you use, you you would bring in steroids, and you have the extra thing of antihistamine because you need to shut down the immune system. That's the beginning of the cytokine storm. Yep. Now that the world has been either infected or vaccinated, I think that the presentation is different.

It's not quite the same. And I think that makes it very complicated because I've been I've been listening to patients for a while, and what I have found clinically is that especially when their presentation doesn't add up, I start looking for a prodrome where they were unwell. You know? Just like you said, they're a bit fatigued, weren't quite right. And I look for that, and it oftentimes is a range of about 4 weeks, 2 to 4 weeks before their presentation that you tend to have that.

Your presentation with the 8th day, I think that was more unusual. Yes. But I think When you have a patient who suddenly deteriorates like I did, right, a healthy patient who's had no comorbidities, had no history of illness, and you suddenly have a patient where that happens, your first consideration should be is and and if there's a history of a previous or a recent respiratory infection or some some kind of infection, your your immediate look should be towards this being COVID. Is it a reaction that this patient is having? Remember, if it is anything else, you have time.

You have time. But time isn't on your side if this is an acute presentation like it did with me. If I got if on that day that I started to notice I was cross eyed, if I drove straight to the lab and did my because it happened the first time that it was a coagulopathy problem, I would have noticed an increase and taken immediate steps to negate it. So when you talk about the vaccine, COVID infections and autoimmunity, What I think is happening is that either COVID infection or the vaccine primes certain tissue in the body because we're not sure exactly in which tissue. We know that spike proteins made throughout the body, but we're not sure in which tissue it's being expressed as a receptor.

So dependent on genetics, you might have different populations express it as a receptor in different tissues. And when exposed to the infection, present with an autoimmune response directed at specific targeted systems. Now I know mine is my blood. It's my red blood cells. So on the 8th day, it triggers an immune response that causes the clotting.

And remember, at this point in time, Philip, why I say that when this happened, I was on hydroxychloroquine and zinc through that 1st week. I was on antihistamines. I was on ecotrananacolchicine. I took the necessary precautions. Right.

On that 8th day, the symptoms started anyway. I could not prevent it. And the only thing that saved my life was heparin. Now when I look at it, it was it was gonna be heparin if we caught it immediately If the microvascular clotting proceeded to a point where it depleted my platelets, then heparin would have caused hemorrhaging, and we would have had to move to drugs like rivaroxaban that don't have the side effect of causing that kind of clotting. So there's a methodology to look at it, and I think we're gonna have to find ways of classifying patients because some present with respiratory symptoms, some present with gastrointestinal symptoms.

But I think there's a target because these patients, even when I get them well, when they have another episode, maybe 6 months down the line, they go down that same road with the same symptoms. Like, I, on 2 occasions, had blood issues. Patients tend to some have respiratory issues, some have cut issues, some have neuropathy. But I think it's to have a healthy suspicion and an understanding of the uniqueness of each patient and how they're going to present. And a lot of the time, I I look laterally.

I mean, I I I have a patient. I've had a locum working, who's been treated in the past week and a half to 2, twice for respiratory infections. He's had a chronic cough now for about 3 months. The respiratory infection was there. You could clearly see that in the first course of antibiotics.

When he returned a week later, feeling better, but still with the cough, he was given a second course of antibiotics. He came and saw me yesterday. He's not wheezing, yet he's being treated as an asthmatic. He has no sign of infection, but he has this chronic cough. Now when I look at those kind of patients, the two things that seem to persist with COVID is either a chronic allergic process or however triggered by autoimmunity, by hypersensitivity, by whatever triggered it, there's an inappropriate immune response.

And the second thing is microvascular coagulopathy. And both can present in very much the same way with respiratory symptoms, with cut issues, and that kind of thing. So when he came to see me today, his x-ray showed really nothing remarkable, which I'd sent him for yesterday. A very mild, consider bronchitis, which can be inflammatory. And so I did these d diamine to look in 6 today.

If I find either of those high, I think I know where to treat you. Either as an allergic patient or a patient who's sitting with microvasculocoaagulopathy. A very mild microvasculocoa coagulopathy, that's not enough to give him severe acute symptoms, but to cause persistent problems and probably in the long run, may lead to lung fibrosis that nobody seems to understand why it happened. So I think it's, you know, the individual you know? It's one of the things that I think I'm concerned about is the fact that this is I think that people are scared when it's acute.

Okay? So meaning that when things happen and somebody just suddenly gets on well, and in a few days, they're on intensive care, that sounds scary. But if that person is unwell for 4 weeks, and then they gradually get more unwell and then they die. People don't seem that concerned. They're okay with that.

Yeah. That's the same numbers. It's just the time frame is different. I think, you're you're absolutely right there, Philip, and I think we we need to humble ourselves as doctors, because of COVID. Right?

And because of understanding the importance of time frame and solving the problem, The patient knows what he felt like before he got sick. My aim is to get him back to that state of health. Right. So whenever I treat a patient, I give them a clear picture of my expectation to their recovery, And I make it very clear that I am not afraid to fail, and I'd like to know if I do. So when I have a patient who I'm suspicious of clotting, and I know it'll take 2 or 3 days to see some good clinical benefit, I tell the patient that.

And in the next 2 or 3 days, I expect you to see a good clinical improvement. And if we give it to 2 or 3 days more and you're still not improving, come back. Come back. I need to look elsewhere. You understand what I mean?

So I I don't mind giving the patient a clear understanding that if we're on the right journey, we'll see improvement. If we're not, don't leave it for another 3 months before you decide to address it. We need to get you good health quickly now. So I'm gonna take you outside of that environment now, Shankar, and I'm gonna imagine that I plunk you in a different environment. I'm dropping you now, not in South Africa.

I'll drop you in the US, for example. Mhmm. Okay? The most of the western world operates by protocols. So they have these protocols that you have to follow in order to treat a patient.

And usually every hospital and the system will come up with a protocol. One of the problems here is that I think it's it's an issue. I think that not just the general public, but I think clinicians are thinking that COVID is over. This is, you know, we're having a few remnant issues. They are not anticipating another wave.

Okay? Let's just suppose as Gert had been talking about, a variant comes along. The variant is not as sensitive to the PCR, so people are not testing positive, but they are presenting with lung disease. Therefore, the standard approach is maybe it's heart failure, Maybe it's just a chest infection. You're using antibiotics and you're using diuretics.

But critically, you're not using steroids. So the clinical part, the the management part is very different. So it is very important to know the difference. Yep. What happens in that situation?

What could you do in that situation? Well, I guess it's what could you do and what would you do. What I what I could do and what I would do is different things, Philip. What I would do is consider COVID, do the necessary testing, and treat that patient the way I see appropriately. The high dose steroids, if I require The, you know, there's a study that came out in Japan recently, Philip, that showed that the h one receptor is a very, strong receptor for COA for SARS COVID, virus, COVID 2 virus.

So, yeah, from the start, I've been talking about this, antihistamines, the the h one, h two receptors. They all have been proven to be true. So, yeah, if if if I had Latitude, then I would look to all those different things, and I would treat the patient accordingly. But, of course, with being protocol driven, that puts me at risk of being litigated against for doing something outside that box. And I think that's what ties western doctors' hands behind their back that they're protocol driven.

So you'd rather have a patient demise even though you follow protocol. So you have to This is this is a very this is an important point, and nobody talks about it. So I'm apologize to clinicians for, talking about the dirty laundry. But here is the reality. Patients don't know this.

But in the context of protocol driven medicine, which is there for safety of patients. That's the truth. That's why it's there to standardize therapy. It's not designed for a pandemic situation where you have strange thing happening. But the reality is that as a clinician in that environment, you are better off, you are safer to let the patient die than to try outside the box to treat them.

What is your thought on that? I think I think, Philip, it shouldn't be called a protocol. It should be called a framework. So every patient is unique in the symptoms that they present with. Even a patient that presents with a simple thing like a urinary tract infection.

Some have burning, some don't. Some have severe, smell to their urine and cloudiness, some don't. So when I put the medication together, I know what is needed to treat a UTI, but I know what is unnecessary also. I don't need to give them the whole box of medication. So I think that you need that individualization of treatment with that patient.

The problem is is that when you do that, then you open yourself up to a whole lot of litigation. And I don't think that people understand the impact of such litigation and how it ties clinicians' hands. Remember, I have a lot of patients who sign living wills with me. I have a lot of patients who, are organ donors. But the first thing I do when we go down that road with the living will and the organ donor is to explain to the patient that this is something that needs to urgently be discussed with the extended family so that when that time comes, we don't have a problem.

Because it's only after the patient demises that the family wants to sue you because they feel you didn't do what's right. But the patient was there saying do whatever you want. I wanna survive. But the family weren't there when he said that. So I got it.

I think patients need to take far more responsibility for the choices they make and for whose hands they choose to put their lives, into. And, of course, they need to understand that, yes, we might be doctors. All of us treat patients differently. I can almost guarantee you, Philip, that the same patient won't get treated the same way by 2 different doctors. We cooks.

Now we don't we don't do it the same way. So protocols go against that. And that's why I say a protocol should be a general framework for a doctor to use. It shouldn't be something to litigate against. If Yeah.

So it bring it brings the issue, though, is that within the protocols and this is a question, so I don't know if any clinicians are listening, but it is it is a really important question. If we have a situation where there is a variant that is not as easily detected or let's say it's it's 80% effective, the PCR test. 20% of people are gonna have COVID and not have a positive test. Okay? So that 20% of people who present with respiratory compromise, who are unwell, who are not responding to antibiotics.

How do we diagnose if it's COVID and they need immune suppression? That's the question. Yeah. And that's that's that's something I've been pushing from day 1. I did speak about a, a spike specific IgE test to look for titers, which might show up on the 8th day.

We might look for certain types of antibody immunoglobulin responses that we can look for that would because remember, Philip, when you're treating a patient 3 weeks down the line, the virus has long left. So looking for COVID is of no no no consequence. We need to know what's going on with the patient to treat it. We know what COVID leaves behind. It leaves behind an inappropriate immune response.

It leaves behind microvascular coagulopathy. We know what it leaves behind. So we gotta go looking for those kind of things to try and fix that kind of problem. Now when you talk about 80%, yes, I was always taught that you never use a test to come to a diagnosis. You always use a test to confirm your diagnosis.

So in those 20%, the test being negative doesn't tell you they don't have COVID. It just tells you the test was negative. I would say a positive test, I would believe. A negative test, I treat with suspicion. I'd prefer to trust my clinical judgment over the fallibility of a test.

So it it raises a question now, and I'm I'm I'm talking about, I guess, some clinical observations. My rule of thumb is that the it needs to look like a duck and quack like a duck. So if I see a patient with chest symptoms, that should be a chest infection, but their say their CRP, the inflammatory marker, instead of it being 200 is 400. That's a red flag for me. Yeah.

If I don't see if the CRP is very elevated and I don't see typical patterns of picture. Yeah. The unit, then I'm worried. The other thing that I am thinking about is that I believe that when you don't know, you investigate more. And one of the tests that I think needs to be done, therefore, very early is a scan of the chest, a CT scan, looking for ground glass changes because that kind of inflammatory change doesn't suggest a typical infection.

And so if you are I think it will for them, for clinicians to realize the ground glass appearance does not diagnose pneumonia. Yes. You know what I mean? I I if if I give you a scenario, I kept at the beginning of the pandemic sending patients for X rays, and it came back saying ground glass appearance, COVID pneumonia. Right?

And it irritated me because they kept using the word pneumonia, and this was not an infection. So when I started sending patients for X rays, I put I wrote on the request form, query hypersensitivity pneumonitis. Then I started getting x rays coming back to me from the local radiologist to say ground glass appearance confirmed clinically between pneumonia or pneumonitis. He then, when he saw my work, went ahead and started giving lectures to other pathologists in the area and radiologists in the area that ground loss appearance is not a diagnosis of a pneumonia. It is a differential diagnosis, and they should consider hypersensitivity pneumonitis.

Then I started getting x rays back saying hypersensitivity and humanitis. But it it raised it raised responses. We need to be, you know, aware. Absolutely. But this is this is why I'm I'm asking a genuine clinical question here because because the system is so weighted towards the PCR test Yeah.

For which I am worried either is not as effective as it should be or could become even less effective with new variants because you can't guarantee that the l b one is going to respond in the same way as the as the previous variant. So Yes. Yes. In that circumstance, what we need for clinicians is a framework where they can say, okay. If you find that there is nothing obvious on the chest degree or even just diffuse bilateral nonspecific changes with an exceptionally high CRP and maybe very high oxygen requirements combined with an elevated d dimer over Yeah.

Yeah. Yeah. This is what I mean is that Yeah. Yeah. I do you're right.

You're absolutely right there, Philip. I've had patients, who have suffered with either, long vaccine symptoms or long COVID symptoms for periods of, 2 years where they've had every test in the book, seen a cardiologist, seen a neurologist, everything. They come to me 2 years later with all these results, but not a single one of those doctors has done a CRP, interleukin, or a d dimer. And when they see me, those are the 3 tests I do, and invariably, one of them is high. Now how come you've run same with myself.

How come you've run all these tests and they're negative, but just 1 or 2 are high? So how hard it is how hard is it to harbor a healthy suspicion in a patient who's been unwell for more than 10 days and you are failing to or a patient, more importantly, that seemed to be improving and suddenly started to worsen and then refuses to improve, We're dependent on whether that worsening was acute and needed critical care, or it was just a slight worsening that refuses to improve. Harbor a a healthy suspicion that this might be a COVID reaction, and do those 3 tests. And sometimes when I am, in two minds, I'll do those 3 tests with the full blood count to rule out infection. Because if I'm gonna put a patient on a steroid, if there's any infection, I'd like an antibiotic coverage.

So sometimes if the patient might have had a fever, I'm suspicious there might be an infection, I do a full blood count with those 3 tests just to look at do they have elevated leukocytes, you know, those kind of things. So why are we running all angiograms and CT scans and the rest when we got 3 tests, CRP, interleukin, and d dimers? And with a full blood count will give us a good understanding of what we're dealing with and at least advise us on where to start. It's it's it's difficult times ahead because as I said, I don't think the medical fraternity is prepared enough for the complexities of the questions that are coming. And as I said that when you add on top of it, that there is a delayed response for many patients, And the patients don't even remember that they had this flu like illness for which they never tested for 4 weeks ago, but they're coming with just strange, oftentimes these days, neurological symptoms.

It just doesn't add up. And if we don't have the ability to know how to identify who will benefit from immune suppression, the outcomes are Yeah. Is the hue it's a nightmare. Yeah. But, Philip, if I had to consider my treatment for the microvascular clotting and my treatment for the inappropriate immune response, right, Prednisone, fair enough.

You gotta have a clinician to rule out, infection and use it in the right situation. So fair enough. You gotta look at the patient and make sure you're not gonna that's the one medication that can cause problems if you got a patient with an infection and you didn't cover them with an antibody. But the rest of it, antihistamines, h one blockers, h two blockers, your somatadine, ranitidine, fomartadine. Right?

Your ecotrin, your aspirin, your colchicine to cover it, because we found the combination of aspirin and colchicine tend to work with the microvascular plots. Now all those medications are generally over the counter, tend to have very few side effects, if any. And if any side effects can be withdrawn immediately and those side effects are reversible, but will show very quick clinical benefit if you're on the right track. Why aren't we trying it? You've got a patient sitting for 1 year with symptoms.

You can give them medication that's over the counter, and within 2 days notice of benefit. I'm not asking you to treat them for 6 months. All I'm asking you to do is give them a week of treatment and see if it has any improvement. And I tell this to patients. I say, look.

I'm putting you on this. It's my standard of care when it comes to treating this. After a week, you might find 10 of your 12 symptoms have subsided. The other 2 come back. Let's have a look.

There might be long term injury. There might be preexisting conditions that we undiagnosed, all that kind of thing. So I think it's to be open with the patient. But remember the treatment poses no harm to the patient. So why not try it?

My only question to the patient is, are you allergic? The next question is, do you have sedation with antihistamines? Then I know my latitudes in how I can treat you. Do you know that Phenergan, promethazine, an h one, a specific h one blocker, is one of the most effective medications I've ever used in COVID. And I mentioned this to you many times for the for the last 2 months, I can't find stock of it.

Do you know that when I mentioned Fennegan in the first wave, the World Health Organization put a red red box warning on it? There was never a red box warning, and Fennegan has always been an essential medication, a lifesaving medication that every doctor should have in his toolbox. Then I went on to mention montelukast. And for about 2 weeks, there was a red box warning on the World Health Organization site about montelukast. So now I'll, keep thinking to myself every time I find a solution, pharmaceutical industry seems to have a hand in making it unavailable.

So, there's a lot going on more than meets the eye, you know, that's going on in the background. So I think, yeah, clinicians need to understand that. You know, I've always been called a doctor Philip that uses medications from Noah's Ark. But let me tell you, I trusted the ethics of the pharmaceutical fraternity, I'd say, around the eighties and the nineties. But I thought clearly around the mid eighties to early nineties, the problems that crept in, the commercial interests, the the the lack of scientific rigor in the way they tested medication.

And so any medication that's come out, say, after 1990, I'm very cautious about ever using it. I'll use it as a last resort when everything else failed. So I get classified as this doctor who uses medications from Noah's Ark when there's supposedly better stuff out there. But, hey, it's Noah's Ark that got me here. So, hey, call me what you wish.

I prefer to use something I know was ethically made. You know? And I know the tools I have. Brilliant. Brilliant.

Yeah. Sankar. So yeah. So this, I think, is going to be an ongoing discussion. Just in case our audience, is listening.

We're only keeping it for short periods of time. But I think that as we continue to see an evolution of disease, and this is what I think is going to be happening, is that, you know, it would be great if, we could find that everything disappears, and life gets back to normal. That's not my expectation, but I don't mind. You know? It would be great.

Amen. And so we represent here the questioning minds who are looking at symptoms, analyzing it, trying to find solutions, and critically, especially for clinicians who are in 1st world countries tied by protocols that are not necessarily as effective. The hope is that just by thinking, we can find solutions that are available to patients, help patients to make their own choices. You know, if you can't prescribe it, you say use this or use that, and give them the leeway to try and make a difference for their health because the system, I think, is now like the Titanic. An iceberg is in front of us.

No matter how hard it tries to turn, it is too big, it is too slow, it's going to hit. You need the lifeboats, and that's what the thinking can I think as well I think as well, Philip, if you look at the timeline, the the, from the nineties when the scientific rigor, the commercial interest became part of the pharmaceutical industry, all those kind of things happened? It was at that point in time that the litigation against doctors increased. And now we're sitting with that problem. So we got to find some balance between the 2.

The litigation ties my hands, and the pharmaceutical industry dictates what I can and can't give you. So, there's the circle. There there there's a ring of fire there that needs to be broken. Yeah. Absolutely.

Absolutely. So yes. Wonderful. Thank you again, Shankara, and we'll have another conversation, I'm sure, again soon. And, audience, look out for these.

These are clinical, insights into analyzing, understanding COVID with one of the best in the world, doctor Shankara Shetty. So thanks, Shankara. Just hang with me. And for the audience, have a great evening.

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transcript to 1h pdf Shankara Chetty interview on PELLE-NEROTH-TAYLOR podcast-HR1_08052024

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https://ia600204.us.archive.org/33/items/read-print-13pg-pdf-of-transcript-of-40min-mp-3-dr-chetty-interview-clinical-imp/read-print%2013pg%20pdf%20of%20transcript%20of%2040min%20mp3%20Dr%20Chetty%20interview%20Clinical%20Implications%20of%20Weaponised%20Bacteria%20Against%20the%20Host.pdf 

https://ia600304.us.archive.org/31/items/read-print-5-pg-pdf-transcript-of-14min-mp-3-dr-chetty-clinical-implications-of-/READ%20PRINT%205PG%20PDF%20TRANSCRIPT%20OF14min%20mp3%20dr%20Chetty%20Clinical%20Implications%20of%20Weaponised%20Bacteria%20Against%20the%20Host.pdf 

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transcript to 67min podcast The Day Dr. Chetty Almost Died interview by Vejon Health july2024

https://www.youtube.com/live/wJTl_kbIto8 

Hi. Good evening to everyone. Thank you for joining me for this spontaneous discussion with doctor Shankar Shetty. I'm just waiting for him to join. And so in the interim, I thought I'd just share a few updates as to what's coming up, what I'm trying to see if we can get doing what I want you to join.

But as I was saying, this is an important discussion. Doctor Shetty has always been at the forefront of what's happening with regards to COVID 19. So in early 2020, he faced the pandemic full on. He took the risk himself personally and he dealt with it, understood the principle about the 8th day, and was able to help thousands of people in South Africa and across the world. This time, it's a little bit different because he got home well, and that's what we're talking about.

So for 1, it's unusual for somebody to come and share their their experience like that, but it's important. And what we'll be doing today is a a clinical dissection of what happened, trying to make sense of it, and trying to see if we can find a way to explain it. Before I bring doctor Shetty in, just to mention that, in the description below is our newsletter. Click on it. There are lots of topics that you can look at.

We've done a number of them now. Beautiful imagery from Lumenca. And so please click on the link to join our newsletter. Additionally, coming up in another few days next week, Tuesday, I'm tackling this 1 here for Celine Dion. She has just recently done her documentary.

So I'm gonna analyze it, look at it, and try and determine the question about spike autoimmunity. This is really what I've been looking at from a research point of view. So please, if you're interested, again, look in the link below, register. And this should be of value to anyone who potentially has had any kind of issue like that in the past. So let's see if we can get a doctor Shetty in straight away.

Hi, Shankara. Glad to have you here. Hi, Philip. Hi, Philip. Nice to see you.

Nice to see you. Excellent. You look exactly the same. No. Nothing has changed.

Nothing has changed. Sure. I was up. Right? Yes.

Yes. Yes, sir. I was I was explaining to the audience that this is an impromptu discussion. We were talking yesterday about what happened. And I said, you know, Shankara, this is valuable to share.

And Shankara being Shankara, he's quite willing to discuss anything in relation to health and so on. And so we're gonna try and just look at it clinically, try and analyze what we think was happening, and see if this could be relevant to anyone else. So, Shankara, just so people understand, share a little bit about yourself and what was happening in the run up with regards to this specific period of time where you were unwell, ended up in intensive care. This is what? Just a few weeks ago, isn't it?

Yeah. 2, 3 weeks ago. 3 weeks ago. 3 3 weeks ago, Philip. Look, I think, I think the audience, already, Philip, is well aware of my, if you can still call it a theory behind what happened to you during the pandemic.

I was always of the opinion that it wasn't the virus that was causing the problem, but more a pathogenic protein. And in that first wave, the very sudden trigger of such a severe decompensation by a human being led me to formulate a theory on the possibilities, 1 of them being hypersensitivity and that kind of sudden sudden response to things. But I think, hypersensitivity was a diagnosis meant to inform treatment options, treatment plans. Where do we go? How do we negate?

What happened? But from the start, my look was always in an immune direction. And why I thought that, Philip, very, vitally important, I think it's an area lacking in medical science. But, from my perspective of being a natural science biologist and understanding more the interactions between the microbiology, the biochemistry, the genetics, and all the other nuances of the entirety of life. I realized that our immunology is the most important thing in anything.

Now if you look at everything around us and how it survives, you got groups of cells exposed to their local environment. They are only contacted by those cells. They communicate in specific ways. They serve particular functions. You get those cells exposed to the outside that have to be able to replace themselves, exposed to different elements on the outside, so constantly changing environment.

Their immunologic response will be different and governed by many different things. We do understand that cells have a surface, a glycocalyx. The glycocalyx used to always be thought of in identifying different cells. The glycocalyx of a muscle cell is different from the glycocalyx of a heart muscle cell. Is different from the glycocalyx.

So we use it as identification, but I think we must also remember that the glycocalyx of a cell is involved in cell to cell communication. And so these bodies or tissues talk to each other's individual cells through these glycocalyx. Just the reason I bring in that context, Philip, the spike protein from the beginning is what I figured as the pathogenic protein of this illness. And, yes, in the first wave, I saw that it managed to trigger what typically looked like a type 1 hypersensitivity reaction. And the typical treatment of that type 1 hypersensitivity reaction negated the problem very timelessly, almost miraculously.

And there were no sequelae. There were no long term COVID symptoms. So it seemed like in that first wave, I had addressed the completeness of the underlying pathology. But then we got into the second wave of the illness, and in that second wave of the illness, I saw the clinical presentation change. I saw that it took longer to get these patients to recover.

I realized that day day seemed to remain the same, so the sudden event on a particular day never changed. It was never a build up to the 8th day. It was the sudden onset on the 8th day, And that that seemed not to change. Yeah. Can I come in here, Shankara?

Because I think it's it's probably important to highlight to people that this this sudden change, as you as you said, is very characteristic. There are only a few things that do it, especially in terms of the lungs. 1 of them is acute left ventricular failure, where the lung gets full of fluid quite quickly. And the other 1 is mast cell degranulation, like an alert And and 1 other 1 other, Philip, which involves mast cell degranulation as well, is the sudden inappropriate immune response to a toxin. Yes.

Yes. Which is the same kind of muscle degeneration. When I look at at cardiac failure, cardiac failure creates a very particular kind of crepitus, in the lung. And when you listen to a patient in cardiac failure, you hear those crepitations. It's a bubbly, crackling sound in the lung.

And what, removed that as a differential diagnosis was the lack of sounds in the lung. And, of course, no pedal edema, none of those, no 3rd heart sound, none of the things you would expect to see with a heart failure. So I'd say in those first and second waves, Philip, my view was quite cemented that I'm dealing with an immune immune response. And, of course, at that point, when we got to the 3rd wave and we started to see the clotting issues again, the standard intervention for a, type 1 type of immune response negated the problem. No 1 died in my hands, but I noticed that I needed higher steroids.

I need a longer duration to treat these patients. These patients, unlike in the first phase, in the first variant, where the illness was restricted in its initial presentation on the 8th day to the lung itself. Mhmm. There's no kidney issues. There's no other issues.

When we got to the 3rd phase, it presented with gastrointestinal symptoms with would, if not treated, became coagulation problems. It persisted even though you got to the patient on the 8th day. You had this slightly increase in length of illness and the diversity of illness, and I was of the opinion that something had changed. I knew that, yes, the variant had changed, but I was of the opinion that maybe the immune response had changed from something as straightforward as a type 1 response to something more complex like a type 3 response, where you're dealing with immune complex mediated responses. So you might have immune complex forming that can form in a far far that that distributes through your body fill up, so it will circulate with your circulation.

If that is what is the target, then when eventually the trigger happens, it'll happen in a diversity of areas. You might be able to stem the mediators that these degranulations might present with, but it'll take you a little longer to overcome the the general generalization of the injury it caused. It was not to a specific organ or a specific system. And I saw this progress through that area of the pandemic early on. As well, my concerns were around the spike protein being used in the vaccine.

Kurt, you and I have discussed that at great length as to what that might do. I think just to understand, we wanted to find the best way to negate all the mortality and morbidity in this pandemic at that point. And I had found some inroads into understanding the pathophysiology, but we all know about the censorship and the rest that transpired. But, in trying to in trying to negate the pandemic, of course, we we missed very many options in not considering prophylaxis, not considering early treatment, and not considering how that would bring us understanding of the pathophysiology, as well as in our population based measures with lockdowns and masking and the rest. In all my experience, Philip, I have not yet seen an airborne pathogen whose primary primary means of transmission is not fomites.

It is not through the air. Oxygen in the air, the ventilation in the air and sunlight do not allow viruses or even bacteria to live for any length of time. Even with TB, for you to pick up TB from someone that's infected with TB, they need to cough directly in your face while you're breathing in. Yes. You can extend the length of, survival of that virus outside the human body by keeping a room where that's poorly ventilated, maybe more humid so that it can survive a a length of time.

But the majority of patients infected by airborne respiratory pathogens happen through fomites. You shake someone's hand, it lives for longer because you have moisture on your skin, and you touch your nose and you pick it up. Now looking at the vaccine, they used the wrong thing. Why would you use spike protein? You are using a very highly mutagenic part of the virus that has the propensity to stimulate quite a great immune response to that person, and that is the most toxic part of the virus.

Yes. I did understand that there was a genetic propensity in who was being affected. That tied in with my understanding of an immunologic response because immunologic responses are tied into your genetics. Fathers and sons seem to be allergic to the same kind of things, that kind of thing. But also that immunologic response, besides being a genetic response, is also dependent on your exposures through your life and how you depend how you develop tolerance to your environment and how you develop resistance to infection, And those 2 vitally important responses of your immunity will determine your viability to survive and your ability to thrive in your environment and are the 2 most important factors in life.

And so I was under the impression that this was triggering some kind of immune response, and there's a broad diversity of different kinds of immune response. And it was triggering some kind of immune response that was causing all the mortality and morbidity. I understood through the censorship and my trying to influence what happened with COVID. I understood clearly that there's a nefarious agenda. Philip, I'm in genetics from the eighties.

I understand what biowulfy means. I understand exactly the latitudes and possibilities that exist with such platforms and what those possibilities actually are. I understand how we can use immunology and, our responses to things because, remember, in the design of weaponry, you want it to be discreet and discriminate. Otherwise, it's of no use to anyone. Now when I look at what's transpired, these are the things that have sat at the back of my head from the start of the pandemic.

It has led us into understanding a lot of the pathophysiology around the pandemic. We've also gone into understanding the, the way this virus exhibits bacteriophage activity with our looking at stool samples. It's taken us to the point where we understand the toxin production by these bacteria and how our microbiome is being targeted. And that is another means of causing mortality and morbidity. We've had many, many discussions out there about, graphene oxide and all these other things that are cons considered conspiracy theories that I would not just pass by, get ethical people to investigate.

We've had many discussions about the unusual, postmortem clots that embalmers were finding, and we now find that these are happening antimonthymly. But, luckily, confined to those who took the vaccine, so likely to be related to 1 of the constituents of the vaccine. That gives us at least a direction to look at to figure out where the problems lie. But, in totality, from my experience over these 4 years of COVID, this is what I've seen. And, to end it all, I've seen the new variants.

They are not that virulent, but they are far more contagious, and I'm seeing my patients getting them. I'm seeing some of my vaccinated patients trigger storms with either an exposure to a cold or a flu, or taking the flu vaccine. Those kind of triggering events seem to be very unpredictable. But, understanding that they are inappropriate cytokine responses, I think I have a fair handle on how to negate them for now and and how to treat them. And that extends to treating long COVID patients and vaccine injured patients as the understanding of the the the underlying mechanism that's causing these problems with these patients.

And so that's where I am I I want to pause it here a minute, Shankara, because I'm just listening to you. And I want to make the audience aware of something. People change after a near death experience. And listening to how frank and to the point you are now, you are a man on a mission with saying that, listen. I have something to say.

I have something important to give, and nobody's going to stop me. I can just I can just feel it coming through, that very clear focus that you're not afraid to speak because you already came that close. Is that about right? I'd say, Philip, what I'm saying, I've been saying from the start of the pandemic. I've been ignored.

I've been censored. I've been banned. I've been ridiculed. I understand this is new science. I understand that it's a new perspective to science, but I place my faith and my conviction in the patterns I've studied all my life in nature around me, and that is my grounding.

That I see these patterns, and I cannot take them for granted, and I understand the processes. We've come out with this vaccine, just to put some context there. I'm I'm of the opinion that while we're dealing with an inappropriate immune response to a pathogenic protein, there are many ways to attack that protein. We've made, we we've addressed many toxins in our lives in the way we treat tetanus, in the way we treat rabies, with anti rabies, toxoids. We've known how to address these things when they occur.

I'm not talking prophylactic measures, Philip. I'm talking if we realize an inappropriate trigger that's gonna cause the production of antibodies that will have implication in the future, then we know how to negate that when the event happens. That's how we negate the erythroblastosis for fat fatales by checking the blood groups of patients before they deliver and understanding that that mixing of blood, that little mixing of blood during delivery might impact on the next pregnancy. And so we make sure that patient gets an antibody injection so that if any are found, we negate it. Now that's an intervention that can only occur if you can predict a point in time where that's gonna happen.

This is cannot be done prophylactically, and it cannot be done therapeutically once the event has been triggered. Then once the event has triggered itself being an inappropriate immune response, there's nothing hard about shutting down that response and cons being considerate of the type of mediators and clearing those mediators as we're looking at the different systems that we put into place. Now what what where my gravest concern lies is that my understanding of nature and the balances that nature bring to us is something that should never be touched. And, I'm really, really not considerate of things like climate change and the rest. I don't think we are that important to this planet because I've seen the power of nature and its ability to cause balance and rectify that balance that's supposed to be there.

So I know that nature will bring back this balance. But in saying that, Philip, a lot of my study has taken me to understand and where we are thinking is a paucity of information is to understand the interaction between all these players and the equilibrium at play. A randomized clinical trial just tells you about what medication. We need to know how things interact with each other, how they enhance each other, how they suppress each other. All these minute interactions are vital importance.

1 of the subjects that I've studied quite intensively is called population genetics, and that looks at the interaction of different species and how nature grows or suppresses different species dependent on the resources that are prevalent at that time and maintains a balance. Now we have a lot of game reserves in South Africa with a large diversity of species, and we have people that settled around these game reserves that are dependent on hunting these endangered species for their livelihoods. And we went through intensive look at how to balance this, And what we did was we created a game reserve where, it was fenced. There were deliberate gaps in the fence, and these gaps were spaced exactly where the settlements were, close to where people had inhabited the place. And we made a deal with all the people around to say, we expect nature to balance whatever's in this game reserve.

If there are too many herbivores, then there will be flourishing of carnivores, and each thing will balance itself out. But the 1 thing that is limiting is the availability of resource. And as soon as resource becomes unavailable, you will get the population that's starved of that particular resource migrate out of those gaps in the fence looking for more resource, and you are allowed to kill any animal that walks out the gap in that fence and use it for your economic gain. And we found a great balance between that. We we did look at species diversity and how to maintain species diversity.

But what that taught me, Philip, was that even the slightest influence on the genetic species diversity of a population is an extinction wide event. Yeah. And what happened to people around us, I don't think humanity understands the gravity of what stands before us when we talk of biotechnical research no matter what it is. Absolutely. So now let's let's go to the meat of the matter.

Okay? Now I want to just analyze what happened with you, and let's see if we can make some clinical sense of it. Taking it back, this is how I usually start. When did you first start feeling unwell? About how long ago was that?

Oh, that was, let's say, about 4 weeks ago, Philip. I'll take you through the, look. I I was I was coping with the the first symptoms. Yeah. Yeah.

Go ahead. What what happened? It was I'll I'll tell you very clearly. It was a Sunday. I was doing some work in my practice.

And, by that evening, I developed some nasal congestion. Of course, I thought it might be exposure to the dust and the rest. I was doing some cleaning and you know? And by Monday morning, I had developed, body aches and pains and a low grade fever. So immediately, I knew it was an infection.

Right. But the sinusitis that I had developed was completely dry, unusual, completely dry. I could feel the congestion, but there was absolutely no production to it. I had this low strange, low grade headache that seemed very unusual. And besides the, generalized body aches and pains and fever, there was nothing else wrong.

I'm just just checking. What what about smell and taste? I did, on on the second day, Philip. That was the Sunday. I noticed Monday, I knew I had an infection.

Sunday being my 1st day. By Tuesday, I had noticed that my my taste had been altered a little. I could smell things, but, food didn't just taste the way it did, especially as, again, a slight bitterness to things. You know? Anything that had a bit of spice, had a bitter aftertaste, that kind of thing.

That was by the Tuesday itself. By Wednesday, the fever had broke. The body aches and pains had started to subside. I remember through this period, Philip, for the Monday, Tuesday, and Wednesday, I wasn't at work. I had a locum working for me, trying to just diversify my practice a bit.

So at least I had someone to take over those 3 days. By Wednesday, the fever had broke. The body aches and pains had subsided. I felt a world better. But the nasal congestion and the dull headache remained.

Right? They remained, but I had no other symptoms. And I kept thinking to myself, this is a very unusual, you know, feels very unusual. On the Thursday, Friday Saturday, I was actually back at work. I had no fever.

I had no constitutional symptoms. I just had the slight burning in my nose and the slight dull headache, and I kept hydrating, thinking, you know, it'll pass. That was the Thursday, Friday, and the Saturday. Uneventful, really. On the Sunday, I had some work to do, 40 days away.

So I I had to I had to go do some shopping, household chores. And on the way back walking from the store to my car, I this headache gave me a slight muzziness, I'd say. You know, they talk about brain fog. I couldn't call it brain fog, but I had this slight feeling. And as I started walking towards my car, Philip, I started to notice I'm getting double visioned.

Okay. So he double So when you say double vision, so you mean that vertical, horizontal, was it any any difference? Just It was it was it was horizontal double vision. Yeah. But it could be negated with, concentration and focus.

And what about and I guess if you covered any of the eyes, it disappeared. You were seeing normally out of the both eyes. Yeah. It did it did. When when when I covered my eye, it disappeared, but there was still, not normal, slight blurriness.

Right? Slight blurriness of vision, and it wasn't constant. It occurred, and when I blinked and it went away. Right? It happened, I'd say, 3 times, but for a period of a few seconds.

So it happened and then just disappeared. So it wasn't there was a concern, but not a grave concern. I was I'm just curious. Any change with the headache at that time, or was it the same? You know, it just remained the same.

It just remained the same, let me see. And then I I drove back home, Philip. I got home. I, at that time, remember during this week, Philip, I was on, hydroxychloroquine and zinc. I was taking, antihistamines just to III didn't see the need.

My nose was dry, but I thought, hey. God put this in front of you. Don't don't question it. And so I took it. You know?

And then on that Thursday, before this happened on Sunday, that Thursday during the week, I stopped by the lab. I did my CRPs into Lucas, d dimers just to see, everything's in order. Everything seemed absolutely normal. My d dimer at the time was 421. Below 500 is considered normal.

So so I was happy with that. And on the Sunday when this happened and I came back home and it was strange, it it dawned on me, but, I I don't think, with the appropriate gravity, Philip, for someone that's, at the front, I think doctors are the worst patients. But, yeah, it dawned on me that it was my 8th day. Mhmm. And I was getting double vision.

And in the, Omicron wave where I had a reaction, on the 8th day, I started feeling strange. And on 9th day, it triggered a widespread disseminated intravascular microcoagulopathy. Wait. Wait. Hold on.

You you're giving us a diagnosis. Give us the symptoms first. Well, at that point, Philip, I collapsed. Alright. Suddenly.

I don't know what's This is on the Monday. This is not this time. This is not this time. This was the first time this happened 2 years ago. Oh, okay.

Omicron. Right? We had So so take me through this. I did I didn't realize that. So when you had Omicron, if they That's when I let my guard down and stopped sterilizing my hand after every damn patient.

I let my guard down and I picked up Omicron. That's 1 of the worst so so just take me through that. That's important. So 2 years Omicron? Yeah.

Omicron, exactly the same kind of symptoms. The sinus inflammation was far worse, still dry, but far more burning, discomforting, all that kind of thing during that week. Again, exactly on the 8th day. On at that time, exactly on 8th day, I was improving. Exactly on the 8th day, suddenly, I lost my smile and taste.

Just suddenly. And I wondered how come I lost how come did I lose my suddenly lose my smile and taste? And then it dawned on me, hey. It's your 8th day. But I disregarded it, Philip.

I said, ah, it's your 8th day. It's not that bad. You know? The next day and I started prednisone thinking, well, you caught the tap before anything happened, and you'll treat it accordingly because I knew how to, you know, manage it along the way. And, I took some prednisone.

I had that on that day. The following day felt fine. Didn't do any bloods. Decided, well, I need to be back at work on Monday. So I took a brisk walk, which is the worst thing to do if you're suspicious of microvascular coagulopathy.

I came back, sat at my desk, and, my son was with me. I lost consciousness. He said it looks like I went into complete spasm. It took a few minutes for me to start breathing again. He said they kept checking, and I had a pulse.

But I I was completely unconscious, and I had stopped breathing. When I got my breathing back, I regained my consciousness, and it was like absolutely nothing had happened. I was completely lucid. I kept saying, no. You're lying.

When they were telling me what happened, I said, no. You're lying. No. No. No.

I'm not lying. So let me let me get this right. This was 2 years ago. This was 2 years ago. My family I didn't have any further events after that.

Nothing. I was I my my family insisted I go to hospital, and I have my bloods rechecked. Everything came out normal besides my d dimer, which was normal before, and it went up from 400 and something to about 900 and something. So I was given, epiren. I made sure I asked them to check my platelets so that I don't end end up with you know, we talk about disseminated, intravascular coagulopathy causing thrombocytopenia.

And when you anticoagulate that patient, they're gonna have a bleed, and they'll they'll probably die of a hemorrhagic stroke. And we saw a lot of that during COVID. We're trying to anticoagulate patients with heparin. So I had my concerns. Within that very day, they gave me heparin.

The very next day, my DDAM, restored back to normal. I was corpus mantis. And, of course, I was being terrified of injected or probed or swabbed while I'm asleep. So I said, look. I'm feeling fine.

I'm going home. So at that at that event, Philip, I had spent 1 night in hospital. But I I was out of the woods, and I recovered completely, and I was back to work in no time. And I understood clearly what it meant. But what that cemented for me Yes.

Go ahead. What that cemented in my mind was the importance of that 8 day. I Yep. I distinctly saw the change. I suddenly lost my small increase, and it had consequence that me as a doctor, understanding my state of health, didn't even notice it or predict it.

Okay. So let's pull it back now. For the silent issue. You know? So let's pull it back now.

So we have that background 2 years ago. We come around to this time. So this is now still about 4 or 3 weeks ago. Yeah. You have the episode of double vision on the Sunday.

You were then fine for the rest of the Sunday. Yeah. I came home. I was fine. I had dinner.

I just had the slides, slight thing going on, and I thought maybe it's my sinus to so, you know Yeah. Headiness, maybe the sedation of the medication I'm taking, you know, that kind of thing. But, the things that I was aware of, Philip, was that in that first episode, it targeted coagulopathy. I was seeing this with patients, Philip, where when a patient had COVID and it, it attacked their lungs. Now when we're getting the new variants, if they have a cytokine response, be it to a COVID variant, an influenza variant, a vaccine, vaccine, whatever the cytokine response might be, it seems to be the same as it was with the initial cytokine response.

So there's a system propensity. You know? And that seems to be different with different people. That's the reason I was speaking about, blood groups, major yeast or compatibility complexes. How do we form antibodies?

You know, those kind of things. Now, yeah. So I got home that, that evening, and I went to bed that night. And a lot of it is a is a blur. A lot of it very lucid in between.

So I had periods where I was completely unconscious, and I had periods in between where I was perfectly lucid. Knew exactly where I was, what day it was, where I was. I just missed that period that happened. And what transpired made a seizure then? Because there were many people who make sure it was conscious.

Yeah. It happened it happened, 3 times in a period of about, 20 hours. The first 1 occurred that Sunday night in the middle of the night. According, well, according to my wife, she heard me scream. She thought it was a nightmare or something like that, and she just shook me awake.

When she shook me, I was quiet. She thought, well, I woke up and you know? And then she turned to look at me, and I had my hands across my chest. I was unconscious, and I wasn't breathing. And she checked my pulse, and my son came in, and they started doing pulmonary.

I think after about a minute, I regained consciousness. But in that consciousness, I was lucid but confused. I was saying I was talking logic. Everything was logic, but I was in the wrong place. My wife said I wanted to examine her and in that few minutes.

And then suddenly, after a minute or 2 of being in that state, I regained complete consciousness, and I refuse to believe what happened. I said, no. I'm fine. What are you guys talking about? You know?

And they watched So that that does sound could be 1 of those postictal period. Thing again. Yeah. Yeah. So I probably I checked my blood pressure, and I was looking for a postictal period.

I had no lack of memory, any, focal neurologic deficit, anything. And when I questioned my son at that time, he said that it looked like your spine went into a complete spasm. The spasm was so great that you couldn't take a breath, and you lost consciousness. Right? The minute the spasm stopped admitted to the hospital?

Yeah. The minute the spasm stopped, Philip, I managed to start breathing again, and then I regained my consciousness and lucidity. My family look. I'm I'm I'm a I can be a stubborn stubborn person. And, yeah, my son and wife sat there, and I said, look.

It's it's it's a transient thing. This happened before. I know it targets my red blood cells. So right there when this happened, I took 50 milligrams of prednisone, and I took an aspirin and a colchicine. I said, look.

I know how to treat this. Let's just be, on the side of caution. Tomorrow morning, first thing Monday morning, I'll go back to the lab. I'll repeat my bloods, and I'll know where I need to act on this. Right?

But with the understanding, Philip, that in the first wave, he targeted my red blood cells, right, and triggered the coagulant. Right? At that point, I they watched me through the night. I was fine. I got up that morning, had a cup of coffee.

I was getting ready to get started with, I had a meeting with some of the doctors working for me. And I went upstairs, and my son said he was standing next to me. He saw me turn. He could see that I wasn't there. I turned.

Again, I went into that tonic spinal spasm. In that state of spasm, Philip, I'd stopped breathing. I was not conscious at that time, but I was lying there in a absolute tonic spasm, which he's he looked at as a seizure. He said that that was a seizure. You know?

That second episode, Philip, they couldn't get me out of. They called the paramedics in. The paramedics eventually managed to resize me, and they rushed me to ICU. When we got to emergency, I had fully regained consciousness by then. And I knew exactly where I was back then.

Again, denying everything that happened to me and saying, no. No. You're talking nonsense. It was a small thing. You know?

But, luckily, during that period of lucidity, well, you can imagine everyone running around me, Philip. But I had the, doctor Vishal Mirage, the physician specialist physician there. And he asked me what what I think, and I gave him a run up like I did you as to where this happened. I said, look. I think it's my, intravascular coagulopathy.

Please do my d dimer. I think that this has suddenly triggered a broad diverse intravascular coagulation, And it happened very suddenly, and I think that's where the rub is. And then I explained my work to him and why I you know, I heard you know the controversy, Philip. But at least they they respect the work that I'm doing and understand it. So I explained to him, this is what I suspect it is.

And, it seems to be central affecting the area of my brain stem because it seemed to have caused my entire core to go into spasm. There wasn't so much of peripheral spasm. There was no focal deficit. There was absolutely nothing to show a typical seizure activity or a typical focal lesion that could trigger the seizure. So III put all this on on the table with them and said, look.

This is what I think is happening to me. You know? Triggered a microvascular coagulate coagulopathy. It showed up in the smallest vessels in my body, in my eyes, in my retina, and started showing up with this crossing of my vision and my eyes trying to accommodate something. And there suddenly, I lose consciousness.

And in the strangest of way, with the spasm, in the strangest of way, They sat there scratching their heads, Philip. They at that point where we discussed everything, Philip, at that point, I had the 3rd episode. In that 3rd episode, they witnessed it. They were at that point wanting to transfer me to a high k cardiac facility because they thought it might be a cardiac issue they're dealing with. But, I discussed it to them, and I said, look.

This is neurology. Please listen to what I'm saying. This is disseminated into vascular coagulopathy. We are seeing microvascular clots with COVID, and it can be a very simple target. Right?

So they kept me there. We, when I had that second, the 3rd episode, they they witnessed it. That was a very bad episode that needed, I I called it. It needed recess. So, that Monday, I was, admitted unconscious into ICU.

I spent the entirety of Monday Tuesday unconscious in ICU. In that period, Philip, they did every possible test. I'm thankful that they listened to me, followed my instructions. I said the first thing you do is an angiogram. Yes.

You don't want to put me on anticoagulation. I understand your reservations, but I'm telling this to you telling you this is a coagulation event. So the first thing you need to do is rule out a bleed and put me on it onto anticoagulation. Okay. The only thing.

Yeah. Just just just to fill in there just to fill in there, Philip. When I went in conscious, they ran every blood test in the book. Right? My kidney function, my liver function, the whole truth.

I said, but you make sure you run the IL6, the d diamond, and the CRP. And I'm telling you that's gonna give out another diagnosis. Every single test that they ran, Philip, came out normal. Absolutely normal. Right?

My d dimer had gone from 421 to 6, 000 overnight. Mhmm. And that's the reason, and I said enalapril. Besides enalapril being an appropriate anticoagulant, it is also an antibody almost to spike protein. It has And now, you said or heparin?

Yeah. Heparin. Heparin. Heparin. Heparin.

Heparin. Heparin. Yeah. So you want to know so let me just clarify something. Yeah.

So let me clarify something here. I told them. I said, look. Injective to heparin for now. If not, you're worried about my platelets?

Xarelto, rivaroxaban. It works. Okay. Pause pause here a second. Was this intravenous heparin or low molecular weight heparin?

Any difference? No. It was subcutaneous heparin. Subcutaneous. So low molecular heparin.

Okay. But I explained to them that I've taken a vulture scene. I've taken an aspirin. I understand it's a clotting event. I do understand the risk I took by taking that, but I do understand the history I go through and the experience I've had.

So I put that on the table. I said, you do my FPC and check my platelets. You do an angiogram of my brain. If there is absolutely no bleeding event, you actively anticoagulate me to get my back to normal. Then I had that other seizure.

They resized me. They did exactly what I'd asked for. They stuck me into ICU. They started the anticoagulation. I spent the entire Monday unconscious in ICU.

I was hooked up to a 24 hour hotel. They had done an echo on my heart. They sent me for a coronary angiogram to make sure there's nothing wrong there. They hooked me up to, EEG, to a constant EEG. They did everything they they needed to fill up.

In every single thing, Philip, through that entire investigation. They were looking for a cause. By the Thurs by the Tuesday, I had started having lucid intervals. I could remember by friends or family coming in to try and feed me. By the Wednesday, I had regained complete consciousness.

I'd spoken to the doctor. I'd started to really review my blood test and what happened. By Thursday, I had insisted I want to be discharged. But what transpired as well, Philip, in that, in that time that I think was important, besides me directing them into, you know, what needed to get done, the Tuesday, I started to regain consciousness. And in that regaining of my consciousness, I was completely lucid.

I knew exactly what had happened to me. I could, you know, understand the completeness of what was there. All of them were scratching their heads simply because they had done every single test in the book from a cerebral to a coronary, MRI angiogram, an ultrasound of everything, all the relevant blood tests, everything they could think of, besides the gastro or a colonoscope. If they tried a colonoscope, I guess I would regain consciousness a lot quicker. Thank god for that.

But, you know that, Philip. In all that, they did a drugs of abuse screen. They did toxicology. They found absolutely nothing besides a raised d dimer. So quick question.

What happened to the IL 6? Was the IL 6 normal and the CR IL 6 was normal. CRP was normal. Now if I say IL6 and CRP being normal, let's put that into context. When I had that first episode at home, I took a Fennegan, I took 10 prednisone, and I took an ecotrienolacolgiase.

So that must remember, that reflects the effect of those medications. That might have been sufficient to suppress my CRP and ILCs because I've seen those kind of big recoveries, but not good enough for the, for the response I had with the, with the clotting issues. You know? So yeah. I'll be Thursday.

Just 1 other thing for the on the Thursday, I insisted to be discharged from hospital. The only thing that had happened while this this occurred, in the in the, during the seizure activity, the intensity of the muscular spasm down my central spine had caused a fracture of the vertebral body of my t 8 vertebra. And so I fractured my t 8 vertebra somewhere along this episode. Luckily, with the fracture, it was a compression fracture of the body, and there was no impaction into the spinal canal or any, affectation to the nerve, you know, impingement of nerves that surround the area. So I'm I would call it completely recovered, but for a for AT8 spinal fracture that needs to be nursed back into health.

So, yeah, I deal with I deal with the Indian pain, but, I think I can handle that. Sometimes important information. Teaching. Yeah. So so let's just just dissect something here because this is where it becomes very relevant to just in case there are clinicians who are listening.

The first thing that you seem to have identified is that this is brain stem. And I can say clinically as well that I have noticed that that when some patients deteriorate, it's it appears to be brain stem involvement that they may get this, uncoordinated. They can become semi comatose, and that has puzzled me. But you what you're saying here is seeming to to align with what I think could be happening. Now the bit that I'm trying to understand is what is driving it.

So I was doing some research before trying to piece it together, and I realized that mast cell activity certainly can occur. The mast cells are not really in the brain, but they're in the meninges. They're in the choroid plexus, and they can release histamine, which can then cause these kinds of strange responses in the brain. But what what has stood out to me here is the fact that the only therapy that reversed this was low molecular weight heparin. Yep.

Now that Looks a little, The way I look at that, Philip, yes, sir. I gotta try and make understanding of what's happened. When we got to Omicron, and, I was seeing the patterns of the different variants in the systems that they influenced, I predicted that omicron is gonna affect our nervous system. And, of course, we saw that. And we saw the way it affected it.

It could affect your nervous system from a broad diverse peripheral neuropathy to a very focused neuropathy, tinnitus, numbness in 1 arm, a very focal kind of neuropathies, to a very central kind of neuropathies that mimic diseases like Alzheimer's and dementia and acute psychosis and those kind of things. Now I've been, unfortunate enough to treat such patients. And, in in doing so, Philip, some of them very close to me, family members. And, yeah, it it it it brought a few things into stock perspective. Just to put 2 just 2 simple cases, I had a family member on the 8th day start to become aggressive.

By about 14th day, he had now been hospitalized, with acute psychosis. And by the 14th day, they were going to discharge him into a psychiatric facility. I asked his wife to bring him home. I said, look. That's a muscle deactivation in his brain, and it's caused the histamine release, and it presents as acute psychosis.

So I stopped all his medication on the Thursday. By the Saturday, I thought it's safe enough to institute my modality of treatment, which is about stabilizing muscles and mopping up histamine and the chemical mediators. And by the following Tuesday, I had a 2 o'clock 2 hour conversation with him. He had returned to absolutely normal. This has been 2 years ago.

That was a misdiagnosis that could have cost him his life. My dad got out of hospital, had a knee injury. He was, recuperating with the cousin. I got a call this Sunday morning to say for the last 4 days, he doesn't know where he is. He's, wetting himself, trying to jump out the window.

So I rushed off to Peter Maritzburg. On examining him as well, Philip, No focal neural deficits. No typical pictures that you'd see with Alzheimer's or dementia. Yes. It looked like senility, but senility to creep in over 4 days is highly unusual.

These are not the way neurologic conditions present. There's gotta be some initiating event. And so I looked at him, and I thought, did this man have COVID, and now is he having a reaction that's triggering this? So I drew his interleukin sixties d dimers and his CRPs. And on the way home, I dropped it off at the lab.

By the next morning, I got the results, and all of them were sky high. He was having a cytokine reaction to something. I immediately started him on the medication that I thought necessary to calm it down. That was on the Monday. By the Thursday, he was completely back to his old, so I knew where he was and could sit and discuss the politics of the country.

He would have been put away as a patient that had developed senility and left as a lost cause. Now these are the things we're seeing going on around us, and so I understand the diversity of, what we face. And from me going to hospital, Philip, from me, finding a way through this, from me understanding how quickly it took me, from me understanding that profile access really didn't save my life. I understand, and this is where I feel, the virus and the vaccine in the way they were designed, Every exposure to the virus in an unvaccinated patient leaves you at risk of being sensitized by the spike protein, and that sensitization can occur in any tissue in your body. And I think that that tissue is determined by some genetic predisposition, blood groups, histocompatibility complexes, exposures through your life, your tolerance to the environment, those kind of things.

That kind of, exposure is with the virus, hopefully transit. But with the vaccine, it is an exposure that, again, is targeted and will be dependent on your genetic constitution as to which organs organs actually get targeted. Remember, Philip, we know the biodistributions throughout the body, but biodistribution is 1 thing. Incorporation into a cell membrane is something else. Let's not even get into the contaminants that we saw in the vaccine and poor marketing of it and the way it was not transported accordingly and what comes with that.

But if you just look at the RNA and what it was meant to do in creating spike protein and us understanding its biodistribution, Philip, you and I from the start been talking about, spike protein being a membrane protein. And if the body makes this protein, it will then get incorporated into the cell membranes of the of the cells that make this. Now, of course, I think that there's a genetic predisposition into its cells manufacture spike. Because in some people, it's, renal tissue and in some people, it's cardiac tissue. And so so we're finding spike in a lot of different tissues, but not necessarily everywhere.

So I think the ability to incorporate spike into your tissue has a genetic predisposition. But what that actually does is it primes different people in different ways. So we're sitting with the population where some are pried, some have their livers primed, and some have their kidneys primed, and some have their hearts primed, and some have their neurology primed by their exposure to this single toxin, spike protein. Now if you have a population like that that's primed, then a virus with a very specific spike protein can act as a very effective, discreet, and discriminate trigger for the population you wish to target in the next You know, I want you to think about something here, you know, Shankar. This is very important, and a lot of people don't get it.

And it's because I look for it, why I see it. A lot of people don't even know when they were infected. Because sometimes symptoms are so mild that they just ignore them. And then 3, 4 weeks later, they have significant pathology. As you say, it could be kidney, it could be heart, it could be brain, or whatever.

And I have noticed from a clinical point of view that if you go back carefully and you look for that prodrome, you usually find it. And so Yeah. You you're right in the sense that there there is a time delay be between the exposure to the spike and the manifestations of disease. And very easily, people will not connect the 2. Unlike They won't connect the group of lip.

They will be discreet. They will be discriminate. And so so you you you even if you have a pathogen that spreads, if we have a pathogen that, liberates a certain variant of spike protein, and that variant of spike protein triggers an autoimmune response to people who have developed receptors on a particular organ system, so let's say your blood or your bath your vessels, then that particular variant will trigger all the people that we're primed in that way. And so we'll have a similar disease with a group of people presenting with hemorrhagic coagulopathy kind of illnesses, and that would tie in with what we would be sold as as a new variant causing hemorrhagic problems. So, yeah, it's it's not indiscriminate.

They can group it together, but I think it's time we realize we've been primed. In 1 of the interviews we spoke about, Philip, I mentioned that I'm of the opinion that they've changed the physiology of the entire planet. And what I mean by that is how we respond to the things around us. And what allows us to survive and thrive is our ability to tolerate our unique environments and our ability to resist the pathogens that might influence us in that environment. And it's a balancing act our immunity is more than adapted to to take care of.

It's the reason we thrive. It's the reason for our existence. Now the fact that this has happened and the fact that I am of the opinion that the root of the problem lies in the understanding of immunity or our lack of understanding of how the different immune mechanisms interplay with each other. And this is occurring throughout nature, Philip. It's balancing everything around me and our lack of understanding, and more importantly, the understanding of certain people with nefarious agendas of how this works and using it to suppress certain information and use certain knowledge for the wrong means.

We are at a place in humanity where we face an existential threat that is absolutely invisible, but it's an existential threat. And we have to figure ways to identify how people have been put at risk. Because, let me tell you, if I did not mention to the doctors disseminated intravascular coagulopathy, my d dimers, my concern about microvascular clotting, this being my 8th day, understanding how it triggers it, how this will spiral out of control before they actually understand the pathology, that there are certain things they can do without having to think about it. Rule out hemorrhage, anticoagulate me, deal with the rest as you see fit. You know?

And I think it was that little bit of advice that saved my life. It saved my life. And I think it made me stop and redirect, re understand. So now with my understanding, Philip, you must remember when it comes to immunity, we can talk about immune priming. We can talk about immune suppression.

But 1 thing we must never forget, we should also talk about immune labeling. They can use viruses and vaccines to label us accordingly. Label the target before you release the weapon, and use the genetics of the individual to specifically label the targets you wish. You're using our genetic predispositions against us. So the variance, the vaccine, all these kind of things, can act as priming and for them to release the appropriate trigger whenever they feel it absolutely necessary.

But I think I think, Philip, I understand it's a spiritual war. I've mentioned to you this to you many times. Everything that's happened to me along the journey, I think, was meant to happen, Meant for me to understand, use the knowledge I'm blessed with to gain, understanding for us to use it to save lives. I do understand, what humanity faces. I mean, last year, I did a pilgrimage to Mount Kailash to sit in front of God and figure out where are we going.

It's something I think is vitally important. I know we'll not solve this problem on our own. We might be given insights into what's happening around us. I think for the moment, humanity hasn't yet come to grasp with the gravity of what faces us. We are at the brink of extinction, and we're still far from understanding how that's gonna happen.

But a simple understanding of the nefarious agenda, how immunology works, how the how we can be targeted, how they've actually targeted us will bring us solutions. And I'm sure if we can cure things like, erythroblastosis, fetalis, snake venom, poisonings, things like, tetanus toxoids, and how to negate that. I think humanity has great potential, and I'm sure we'll solve the problem if you understand the problem and ex and and simply simply accept the extent of it. Underestimate it at your own peril. And so I prefer overestimating it and being prepared.

And so this has been a teaching experience for me. You know, just in case people listening don't understand this, I know listening to Shankara that this is somebody who is now thinking and looking at a different level. And so what he says, even though it may be controversial and, I may have to clip out bits on certain channels because they won't like it, But what he is saying is coming from somebody who has just been right to the edge and has come back with a message. And it gives us hope, you know, Shankar, because I think that that 1 thing, just in case there are any clinicians floating around, that 1 thing about heparin, I didn't realize until I started to research it a bit that heparin also stabilizes mast cells. It's anti inflammatory, as well as it is, it's anticoagulant.

And, and it was used certainly in the cytokine stone, but if they used it too late, you know, you you you can't negate it with the trigger bleeding. On its own. If you allow the coagulation to take place, the platelets get mopped up. And eventually, when you decide to use a heparin, you trigger bleeding. And so once platelets, count goes down, you've got to go to mechanisms or modalities that don't have that as a risk factor, like your rivoriboxaban, you know, that kind of thing.

Yeah, Philip. It's been a it's been a crazy journey. Yeah. I I do know the I came to the edge of my life. But it's mind you.

I think you know me. It's not the first time. I I challenge the boundaries. It is in my job to keep me alive. Strangely, Philip, my mom, and 1 of my dad's uncles, both of them came to me at the end of their lives to help me see them to their demise, and, I helped them through that.

It caused a lot of controversy in my family. But somewhere in that period, I saw my mom and, my uncle. They were in good health. They didn't speak to me, but they acknowledged my presence. And, be me being the naughty kid, I was I was under the impression I did something wrong, and they were there to admonish me.

But, yeah, I'm still here. And so, yeah, I think it, reestablished and, reinvigorated my understanding that, we're not alone. We are all joined together by a common thread, and I think that common thread is love and compassion. And yeah. So it's not a war that's argonable.

Excellent. Excellent. Like, I can't ask for a better ending. Thank you very much, Shankara, and thank you everyone who has been with us and the same wonderful words about him. I think that this is an important record.

That's 1 of the important things I thought just for people to reflect on, especially people in the clinical world. There are going to be answers that we can use. We just need to be creative, find ways, make sure we can protect as many as we can. But I think that there is something you have said. This is an existential crisis.

And the implications Mhmm. Just as Garrett had also predicted, I don't think this next year is going to be easy. It's going to be challenging, and we can only do the best we can. Yep. And, with what I've been through, I think we're a little bit prepared.

Wonderful. Great. Thank you, Shankara. Just stay with me. Let me just play a quick outro.

Thank you everyone for joining us, and look out for our next interview hopefully coming up shortly. Thanks,

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https://www.extremelyamerican.com/post/dr-chetty-covid-vaccine-intended-to-reduce-the-world-s-population-without-anyone-suspecting-it 

Dr. Chetty: "COVID Vaccine intended to reduce the World’s Population without anyone suspecting it"

Nov. 27th, 2021

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Source: Great Game India - Journal on Geopolitics & International Relations

“The deaths that are meant to follow the vaccinations will never be able to be pinned on the poison. They will be too diverse, there will be too many, and they will be in too broad a timeframe for us to understand that we have been poisoned,” claims Dr. Shankara Chetty.

According to his website, South African family doctor Dr Shankara Chetty, “has treated 7,000 Covid-19 patients without a single hospitalization or death,” combining his insights with his medical background along with his observations of government censorship orders and censorship of medias to support its conclusions.

Joining the Zoom conference (watch below) as a Doctor, Chetty began by asking the following questions:

“I think the perspective around what is happening is vitally important. We need to understand what the aim is. Everyone knows that there’s inconsistencies, that there’s coercion, but we need to understand why. Why is it there?”

He then identified the “most important” answer to these questions, “pathogen that was causing all the death in COVID illness,” the spike proteins common in both the vaccine and virus designed to be produced in a revivers body.

In my opinion of what’s going on in the world, spike protein is one of the most man-made toxins. And the purpose of this toxin is to kill billions of people without anyone noticing, he went on to add.

“What looks like transpired here, [is] they’ve engineered a virus and put this weapons-grade package onto it called ‘spike protein.’”

The allergic reaction with the initial release of the “most elaborately engineered toxin,” occurs in a small number of people, resulting in more severe cases and death when the vaccine is administered. According to Chetty, this usually happens eight days after the onset of symptoms.

Doctors say that due to the first 14-day international shutdown, people with the COVID-19 virus that caused it are arriving late to the hospital, and these facilities “to engineer death and damage in order to stir all the fear.”

“But the game that they played with this engineered virus was to justify the vaccination of the planet,” he continued.

Chetty added that these injections “expose us to the spike protein for a longer period.”

I often interview doctors online, and Dr. Pierre Kory, Ryan Cole, and Richard Urso have described how long a health risk begins to occur after death from an allergy in the first two.

“We begin to see the endothelial [blood vessel lining] injuries that this vaccine causes with its spike protein, with its influence on its ACE2 receptors. Those are the deaths that are meant to follow. And they will never be pinned onto the spike protein, a very well-engineered toxin,” he said.

“Now spike protein is also a membrane protein. So, the mRNA will distribute this throughout our body. It will be made in various tissues around our body. It will be incorporated into those membranes around our body, and those specific tissues.”

“Those tissues will be recognized as foreign and will trigger a host of autoimmune responses. So, the deaths that are meant to follow the vaccinations will never be able to be pinned on the poison! They will be too diverse, there will be too many, and they will be in too broad a timeframe for us to understand that we have been poisoned,” he went on”

“Now this toxin in the long term is going to get people with pre-existing illness to have those illnesses exasperated,” the doctor explained.

With some toxins, including “bits of HIV protein” within this “definitely engineered” spike protein, Chetty states “people with cancers are going to have their cancers flareup, and they will say they died of the cancer.”

“People with vessel injuries or predisposition like our diabetics and [those with] hypertension are going to have strokes and heart attacks and the rest at varying times, and we’ll attribute those to their preexisting conditions,” he said.

“People are going to develop, over time, autoimmune conditions, the diversity of which will never be addressed by any pharmaceutical intervention because they’re far too targeted.”

“But I think if people understand what the intention is, then they’ll understand why what’s happened has happened. The ill logic, the coercion, the suppression, is all warranted if you understand that there is a bigger plan.

"This plan is to make sure that we can control and kill off a large proportion of our population without anyone suspecting that we were poisoned,” the COVID specialist said.

“And so, I think the justification for everything we see is warranted in understanding the endgame,” he concluded.

“I think there’s a huge picture at play; otherwise, the vaccines make absolutely no sense. We were sold the vaccine as our savior from the start, and if we look at the science, the science does not play out.”

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TRANSCRIPT OF14min mp3 dr Chetty Clinical Implications of Weaponised Bacteria Against the Host

Hi. Good evening to everyone. This is a presentation that I wanted to do yesterday, but we had some technical difficulties with doctor Shetty. And, for those who don't know me, I'm doctor Philip McMillan. Based in the UK.

I've been focused on COVID 19 from an autoimmune perspective. And one of the tremendous pleasures I've had over the many years is talking with doctor Shankara Shetty about his research and critically his interventions, from a South African perspective to save the lives of all his patients. Now I think it's very important to listen to what he has to say. And today, we're gonna be focused on the potential impact of weaponization of bacteria. So we're just usually just going to chat about what some of the thoughts that we have.

And so without any further ado, with a little bit of flash, let's bring in doctor Shetty. Great. Shankara, how are you? I think Hi, Philip. Nice to be well.

And, welcome to all the people watching us tonight. Excellent. So listen, Shankara. As I said, yesterday, we were planning to have this discussion, and then we we had some technical difficulties. I started to speak about, this this recent Carla Brockner paper, which we will go into in a little bit.

But before we go into that, Shankara, I just want you to remind the people again. Part of the reason why we're speaking, regularly with Shankara is that his license to practice medicine is on the threat for saving the lives of his patients as remarkable as it may seem. I want you, Shankara, to tell us a little bit about this paper that you had done in 2020. What was this about? Philip, I knew when the pandemic arrived, transitioned from UHAN to to Italy, that there was a nefarious agenda at play.

I had seen the insert in the genome of the virus and knew that it was likely lab made, and so I had to see patients. I had to understand the clinical presentation of how patients progressed into severe illness for me to try and negate that with the treatment strategy. So I looked at basically all the information that was available around the world, how people were dying, the clinical observations that were being made, the understanding of the virus being a miss an RNA virus, how that usually, did did I I looked into the knowledge that we had already and looked at what was on the table and tried to figure out what we were dealing with. It was the reason I decided to see patients to understand clinical presentation and from that, understand why people did the pathophysiology around the illness itself. And very early on in the pandemic, when I started seeing patients, I understood the biphasic nature.

I understood that there was an immune dysregulation occurring at a point in time, and that was the critical point to address this. I also understood that that immune dysregulation might be tied into the insert into this virus. In that, it was something new. And, of course, we've been exposed to coronaviruses before, and we never have this kind of reaction. So I just looked at all the information around what was known, what was unknown, and tried to formulate a reasonable hypothesis of how to treat this.

When I got the treatment successes, my staff came to me and said, look. You gotta share this with the world. You're getting amazing results. Patients were recovering within a day overnight. And so I had decided I need to publish an academic paper, more an observational and clinical academic tour of COVID, the illness, the pathophysiology, the treatment strategies that should be employed and of course at that time I had seen about 200 patients.

This article was written in, May June 2020 and got published in September 2020 in an academic journal here in South Africa. So basically, I just wanted to direct, early treatment and understanding of what we were dealing with and of course to direct research from a pathophysiological perspective so that we could understand what we need to research in future to get a better understanding of how to more effectively treat this. I didn't expect that to morph into a commentary about pending medical interventions that might be compromised by my work. Yeah. This this is it's fascinating.

Interestingly, I put the the link to it. It's a citation, from the paper. But there you can't you'd have to probably go to the publication to read it unless you have the PDF. I didn't have a link for the PDF on it. But in it, you know, Shankara, it it's quite clear.

And strangely, as hard as it is for the academic community to to acknowledge, you are spot on because you had observed the patients at that time. You were seeing as as I'm just gonna show it here again. You were seeing because this was, as you said, by May, you had identified the unusual symptoms with the hypoxemia, the sudden onset, sudden rapidly progressive, breathing difficulties, you know, they drop in the saturations. You are looking at the autopsy findings with heavy edematous lungs and the microclots. Critically, these microclots, the multiple organ involvement, disseminated intra intravascular, complications.

You're looking at some of the chronic manifestations that could occur because of it on unusual outcomes. This this was quite profound at the time. I'm I'm I'm telling you, you know, is that it's fascinating to think that the clinical and the scientific community would find criticism of this really forward thinking document in 2020, May 2020. Just get for people to remember this was in May 2020. This was even before Oxford had realized about dexamethasone.

This is quite fascinating. You were using steroids before Oxford did the recovery trial on steroids, and people would want to punish you for that. This is this is just unbelievable. I think, Philip, that that informed my opinion of the narrative around the pandemic. That exact lack of acknowledgment, lack of accreditation, informed my decisions.

I understood that I found something remarkable, and why wouldn't the world want to listen to it? So the lack of acknowledgment was more telling than any acknowledgment I got. And so I started to look at things in a different light from that point on. I I had the knowledge that we're dealing with a the probability of a lab made, pathogen at that point. And when I noticed the, illogic of the agenda, the lack of acknowledgment for the discoveries I've made, I understood that I was dealing with a far bigger picture.

And I think the last few lines of that article are what made it controversial because I mentioned in that that, if early treatment could negate a lot of the mortality and morbidity in the pandemic, it would make an mRNA based intervention rush to market wholly unnecessary. And, of course, I did say that the messenger that the mRNA was wholly unnecessary. Even the rushing to market would have been unnecessary because we've found a way to negate the mortality and morbidity and could take our time to develop an appropriate strategy with all the safety and efficacy built into it and confirmed from it. You know, it's interesting because I did find that right at the end of your paper in mid 2020. You made the point that if you if there is a solution like this, you know, we can treat patients, and we don't need to do any other kind of intervention.

This is probably what got you into hot water with this, and this is probably why this information anyway, let let look at this. I just wanted to add. When I wrote the article, I knew that it was going to be controversial. I had seen the paper that had come out about hydroxychloroquine and, you know, there was all this false reporting by profound journals that should have been, the mainstream. And so I thought, which peers should I approach?

And I approached 2 friends of mine, 1 a senior gynecologist and 1 a a cardiothoracic surgeon. He was, the cardiothoracic was actually in Italy at the time looking at COVID, and I sent them both this article and asked their opinion. I got a response within an hour to say it's the most immaculate piece of science they've seen, but both advised me to remove that last sentence about the vaccine. And I said, no, it needs to be put there. It needs to be understood in the context of what we're dealing with.

And little did I realize that, yeah, it would be the most controversial statement in that paper. Wow. So listen, just so, people understand because we're gonna wrap up now, Shankara, as we continue to explore these thoughts, I I think that some of what we said there was so almost, what's the word? So serious. I have a feeling that those words may not necessarily want to be seen.

So if you want to see the full discussion, you must follow the link that will be put below, on the sub stack because I think I'll leave there's some parts of this that are almost too serious that, I suspect those who do not wish this kind of conversation to occur would therefore want it to be taken away. So, yes, folks who are with us, thank you. This is a Thursday evening, and so we appreciate the people who are here with us. But this is some pretty significant clinical stuff, and I still maintain that doctor Shetty has been there from the start observing the clinical patterns. I can't think of anybody better to try and work out the directions that things could go.

So, Shankara, any final words before we leave? I think, a little bit of hope for people, to understand how bacteria and viruses actually cause more morbidity and mortality in their hosts. Our immunity is a pretty remarkable thing, and it can take care of almost any virus or bacteria on the planet. We developed that immunity through exposure in childhood and build up this library of things we can ignore. So I don't think immunity is a problem.

We'll we'll be able to tackle any virus or any bacteria thrown at us. However, the mortality and morbidity from these infections is caused by a host response, not by but but not by the virulence of the pathogen itself. So the virulence of a pathogen is its ability to trigger a serious host response that eventually kills the host. So if we gain a decent understanding of how to curb these unusual host responses, then we can deal with any pathogen that's thrown at us. If you look at Ebola, you got the western variant and you got the wild type.

The western variant does not kill. The wild type does. And its its lethality rests in its ability to trigger a cytokine storm. So if we can gain an understanding of how cytokine storms are triggered by different pathogens and the treatment necessary to negate those, then we can deal with any pathogen thrown at us. So there is hope for the future.

Absolutely agreed. So listen, guys. Remember to stay with us. We are right at the front of this trying to figure it out. So if you want to join in the research journey, please continue to stay and listen with this kind of work.

Have a great evening, everybody. Shankar, if you could just hang fire with me. Thanks, Eric.

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read transcript of 40min mp3 Dr Chetty interview Clinical Implications of Weaponised Bacteria Against the Host

Hi. Good evening to everyone. This is a presentation that I wanted to do yesterday, but we had some technical difficulties with doctor Shetty. And, for those who don't know me, I'm doctor Philip McMillan, based in the UK. I've been focused on COVID nineteen from an autoimmune perspective.

And one of the tremendous pleasures I've had over the many years is talking with doctor Shankara Shetty about his research and critically his interventions, from a South African perspective to save the lives of all his patients. Now I think it's very important to listen to what he has to say. And today, we're gonna be focused on the potential impact of weaponization of bacteria. So we're just usually just going to chat about what some of the thoughts that we have. And so without any further ado, with a little bit of flash, let's bring in doctor Shetty.

Great. Shankara, how are you? I think Hi, Philip. Nice to have you. And, welcome to all the people watching us tonight.

Excellent. So, listen, Shankara. As I said, yesterday, we were planning to have this discussion, and then we we had some technical difficulties. I started to speak about, this this recent Carla Brockner paper, which we will go into in a little bit. But before we go into that, Shankara, I just want you to remind the people again, part of the reason why we're speaking, regularly with Shakara is that his license to practice medicine is under threat for saving the lives of his patients as remarkable as it may seem.

I want you, Shankara, to tell us a little bit about this paper that you had done in twenty twenty. What was this about? Philip, I knew when the pandemic arrived, transition from one to, to Italy, that there was a nefarious agenda at play. I had seen the insert in the genome of the virus and knew that it was likely lab made, and so I had to see patients. I had to understand the clinical presentation of how patients progressed into severe illness for me to try and negate that with the treatment strategy.

So I looked at basically all the information that was available around the world, how people were dying, the clinical observations that were being made, the understanding of the virus being a miss an RNA virus, how that usually did did I I looked into the knowledge that we had already and looked at what was on the table and tried to figure out what we were dealing with. It was the reason I decided to see patients to understand clinical presentation and from that understand why people did the pathophysiology around the illness itself. And very early on in the pandemic, when I started seeing patients, I understood the biphasic nature. I understood that there was an immune dysregulation occurring at a point in time, and that was the critical point to address this. I also understood that that that immune dysregulation might be tied in to the insert into this virus.

In that, it was something new. And, of course, we've been exposed to coronaviruses before, and we never have this kind of reaction. So I just looked at all the information around what was known, what was unknown, and tried to formulate a reasonable hypothesis of how to treat this. When I got the treatment successes, my staff came to me and said, look. You gotta share this with the world.

You're getting amazing results. Patients were recovering within a day overnight. And so I had decided I need to publish an academic paper, more an observational and clinical academic tour of COVID, the illness, the pathophysiology, the treatment strategies that should be employed. And of course at that time I had seen about two hundred patients. This article was written in, May, June twenty twenty and got published in September twenty twenty in an academic journal here in South Africa.

So basically, I just wanted to direct early treatment and understanding of what we were dealing with and, of course, to direct research from a pathophysiological perspective so that we could understand, what we need to research in future to get a better understanding of how to more effectively treat this. I didn't expect that to morph into a commentary about pending, medical interventions that might be compromised by my work. Yeah. This this is, it's fascinating. Interestingly, I put the the link to it.

It's a citation, from the people. But there you can't you'd have to probably go to the publication to read it unless you have the PDF. I didn't have a link for the PDF on it. But in it, you know, Shankara, it it's quite clear. And strangely, as hard as it is for the academic community to to acknowledge, you are spot on because you had observed the patients at that time.

You were seeing as as I'm just gonna show it here again. You were seeing because this was, as you said, by May, you had identified the unusual symptoms with the hypoxemia, the sudden onset, sudden rapidly progressive, breathing difficulties. You know, they drop in the saturations. You're looking at the autopsy findings with heavy edematous lungs and the microclots. Critically, these microclots, the multiple organ involvement, disseminated intra intravascular, complications.

You're looking at some of the chronic manifestations that could occur because of it and unusual outcomes. This this was quite profound at the time. I'm I'm I'm telling you, you know, is that it's fascinating to think that the clinical and the scientific community would find criticism of this really forward thinking document in twenty twenty, May twenty twenty. Just for people to remember, this was in May twenty twenty. This was even before Oxford had realized about dexamethasone.

This is quite fascinating. You were using steroids before Oxford did the recovery trial on steroids, And people would want to punish you for that? This is this is just unbelievable. I think, Philip, that that informed my opinion of the narrative around the pandemic. That exact lack of acknowledgment, lack of accreditation, informed my decisions.

I understood that I found something remarkable, and why wouldn't the world want to listen to it? So the lack of acknowledgment was more telling than any acknowledgment I got. And so I started to look at things in a different light from that point on. I I had the knowledge that we're dealing with a the probability of a lab made pathogen at that point. And when I noticed the, illogic of the agenda, the lack of acknowledgment for the discoveries I'd made, I understood that I was dealing with a far bigger picture.

And I think the last few lines of that article are what made it controversial because I mentioned in that that, if early treatment could negate a lot of the mortality and morbidity in the pandemic, it would make an mRNA based, intervention rush to market wholly unnecessary. And, of course, I did say that the messenger that the mRNA was wholly unnecessary. Even the rushing to market would have been unnecessary because we've found a way to negate the mortality and morbidity and could take our time to develop an appropriate strategy with all the safety and efficacy built into it and confirmed from it. You know, it's interesting because I did find that right at the end of your paper in mid twenty twenty, you made the point that if you if there is a solution like this, you know, we can treat patients, and we don't need to do any other kind of intervention. This is probably what got you into hot water with this, and this is probably why this information anyway, let let to you, Philip, I just wanted to add.

When I wrote that article, I knew that it was going to be controversial. I had seen the paper that had come out about hydroxychloroquine and, you know, there was all this, false reporting by profound journals that should have been, the mainstream. And so I thought, which peers should I approach? And I approached two friends of mine, one a senior gynecologist and one a a cardiothoracic surgeon. He was, the cardiothoracic, was actually in Italy at the time looking at COVID, and I sent them both this article and asked their opinion.

I got a response within an hour to say it's the most immaculate piece of science they've seen, but both advised me to remove that last sentence about the vaccine. And I said, no. It needs to be put there. It needs to be understood in the context of what we're dealing with. And little did I realize that, yeah, it would be the most controversial statement in that paper.

And just so, people can can see it, I'm trying to oops. I'm trying to see if I can I can get it here if I can, so that, people understand why this would have been a problem? So here, I have it in the conclusion here. And so you went and said with the high mortality and morbidity from COVID nineteen, A little above that, Philip. Just above.

Oh, it's here. It is oh, yes. Here we go. Oh, boy. I'm not even sure if I can read this, Shankara.

For those people who can read, you can read what he is saying. Effectively, he picked up the point that I think would have hit the industry, and it would have been unnecessary and unsafe in view of the rush to bring it to market without long term evaluation. Goodness, Shankara. No wonder you're you're getting into trouble. You you're you're too you're too close to the target.

What's the truth, Philip? Oh, boy. So, you know, so I it it's important for people to understand because, recently, we highlighted about, doctor Kuderoff losing his job, talking about lockdowns at Harvard. Doctor Carr, I don't know if you know about her from Canada, a pediatrician who, was criticizing the government with regards to some of the actions. They have pulled back from their, their targeting of her, but she's still left with a huge legal bill, which is which is very sad, and she's trying to fight to to get through that.

But it it's just showing you that, sadly, this is pretty, pretty serious. And so this is why I think I'm highlighting now, and we're gonna transition into the bit that I wanted us to talk about. You had pointed out something then, and let me see if I can get it here. Yeah. I've got it here.

So look at this here. In that same paper, you highlighted that gastrointestinal infection is common, usually preceded by a sore throat, then spontaneously results in a day or two. Heartburn, nausea, short, severe intermittent abdominal cranks with severe diarrhea. That's it slows to a poorly formed, sometimes slightly stool in four to five days. So you were noticing this gastrointestinal pattern, and it had made you think about the interaction with the microbiome at that time, didn't it?

Yes. Yes, Philip. It did. As well, I did mention in the articles that the, the Chinese at the time of early investigation had found a positive PCR rectal swab, and I had, asked for consideration of a fecal oral route of transmission. We were only talking about airborne spread.

And if we had a positive PCR rectal swab, then there is viral genome in the stool itself. And if that viral genome is there, is there a possibility of a fecal oral route of spread? And if there was, then you could pick this up from a public toilet without anyone else being in there, and the masking couldn't solve that problem. So it put the public health measures into a little bit of a different light. Subsequently, we it I think a year later, they identified it in sewage, And I still couldn't understand why we weren't looking upstream to, stool samples and trying to understand how this virus was interacting with the cuts and, of course, the microbiome.

Yeah. And so it it leads me into, important point, and I I've I've got this this paper that I'm gonna show you here. This is central to a publication we're working on about, long COVID type patterns. And it's because it's one of the at the time, it was one of the few papers that was looking at biopsies in the gut, and they were looking at viral persist antigen persistence in the intestine. And they took a number of patients with inflammatory bowel disease.

And, effectively, what they were doing so they were doing an endoscopy, forty six patients with inflammatory bowel disease. Two hundred and nineteen days after, a range of up to two hundred and fifty seven days after confirmed infection. And what they were finding is that they were having antigen persistence of many of the critical proteins, nuclear capsid, you know, spike protein, with associated symptoms from the, long COVID type picture. So what it's clearly demonstrating, and this is what we had thought before, is that there is an element of viral long term persistence that was driving symptoms. But it's not until Carla Brockner's work came out that we started to think really properly about that this may be bacterial.

By the way, let let me let the audience know something. What we're talking about here is so important and so significant that I wouldn't be surprised that you will struggle to see this discussion. It is it is such a significant discussion. This is what we're looking at now. If and let's just let's just give the presumption that Carlo maybe wasn't right.

Let's just say if if we have virus being able to replicate or even the proteins, the different, proteins being made by bacteria. Because we're talking about two hundred and fifty seven days after infection. It's almost a year. They are still finding the pieces of the virus in the intestine. Yep.

I think it's, Philip. I think there's more to this than meets the eye. Ever since biotechnology advances started occurring in the late nineteen seventies, early eighties, we should have had the regulations in place to make sure they were done for good intentions. That never happened. I don't think people realize that, biotechnology has advanced to the point where it can challenge conventional, weapons in global warfare.

Yeah. And when you look at what they found, they were breaking it down here into the different categories here. So they were able to identify so they could find the RDRP proteins. I'm not even sure what that one is. Certainly spike, nuclear capsid, and envelope proteins were all present, and this is the percentage of patients who had the so it's not just the spike.

It's a whole viral protein. And so the spike certainly is part of it. And this is one of the other things that was being found is that, you're having viral persistence that can be affected even just from the spike, but certainly from the virus. And so when we have and this is now moving into the clinical bit now. One of the problems we've got is that because the disease is mild at the moment so people either have natural immunity or they have hybrid immunity.

Okay? Now my the the research seems to suggest natural mucosal immunity blocks the virus from getting through the mucosal barrier. But we don't get the same protection with hybrid immunity because it can still penetrate the mucosal barrier, but it doesn't necessarily cause severe disease. In the context of bacteria, if you have virus being able to penetrate and get because it doesn't seem as though it can pass the stomach. So it must be getting to the gut from the bloodstream.

That's my thought. And any any thoughts on that? Do you think it can get through the stomach acid? Philip, we have many enteroviruses that actually are able to do that, that can directly get into your gut and withstand the acidity in the stomach itself. And then, of course, you have people that are on proton pump inhibitors in the rest that change the environment in the in the stomach itself that allows viruses to get through.

I think as well, immunity is half the picture when we look at what's transpiring in the gut and Carlo's work. Carlo showed that when he took the supernatant and inoculated it onto fresh healthy stool and incubated it, he got a exponential increase in both viral titer, and he got an exponential increase in toxicity in that in that sample. So it showed bacteriophage activity and the virus able to replicate in the gut using bacteria as their host. But, also, he it cuts the bacteria in the gut to produce toxins, and immunity doesn't play a part in toxicity. Now the the issue is that, toxins, peptides or toxin like peptides will be degraded by stomach acid.

But But if you could find a way to have them made directly in your colon, then you'll absorb them unchanged. And so the ideal place to implant toxin would be directly into the colon. And if you could recruit the gut microbiome to make that toxin for you, it would be the ideal environment to create toxicity without the interaction of stomach acids and the rest. And I think that is where when you look at what's transpired, it it it creates more, creates more not confusion, but more skepticism about this being for the good with good intention. Yeah.

It it it really and this is why I was saying yesterday, you know, the the building is on fire. And how do you warn people? I need you to leave the building quickly, but don't panic. You know? Yeah.

But whatever you do, don't ignore it. And so I I did an example yesterday, and I don't know if it made any sense. I said, it it's kind of like, for whatever reason, cyanide was found in your tea. You don't know how it got there. It could have fallen from the ceiling.

Somebody could have tripped and it fell in or something. But if you do not consider the possibility that someone deliberately put it in your tea, there's a pretty good chance you're in trouble. And this is where most of the world and this is what I'm trying to say to people. Listen. Whatever your opinion if if your opinion is that this could never happen, you would make a terrible detective.

Yes. I think as well, Philip, we got to look at synchronicities that we see around what's happening. When you look at toxic peptides, in general, toxic peptides influence physiology in a particular way. Toxic peptides either are cytotoxic, They damage tissue directly, on contact with them. And, of course, we know about the endothelial injuries and that kind of thing that's by protein has is caused.

Toxic peptides also cause damage through hematologic ways. So they are hematoxic, which will either cause coagulopathies or bleeding disorders, and we've seen that as well with, COVID illness. And, of course, the third mechanism by which toxins work is to cause nerve problems, paralyze their prey, and cause nerve damage, and we've seen that with COVID. So when you look at the broad diverse spectrum of clinical presentation and then understand the toxicology around gut microbiome, there seems to be too much of correlation there for it to be discounted. You know, here's an interesting thought that I I had today when I was discussing.

We're seeing a sharp rise in liver disease. And, I recently did a a a presentation about this. But as I was reflecting today, I had a number of different things, the fatty liver. Had spoken about the, the autoimmune hepatitis subclinical either from virus or any other spike routine. And I spoke about alcohol as being a toxin to damage the liver.

And I then suddenly remembered there is one other point because when bacteria in the intestine produce toxins, if they penetrate that gastrointestinal barrier, the first place they are going to hit and need detoxification is the liver. Yep. What would happen if we then had chronic low level toxin production from the intestine hitting the liver. It should be like a continuous blow to the liver, which could then accelerate underlying liver disease. I I really should put that in as part of the presentation.

Any thoughts on that? Yeah. You're absolutely right, Philip. Everything absorbed in your gut goes through the liver first to detoxify before distributing whatever it is that you've absorbed through the body itself. It's a protective mechanism.

We found ways past that through sublingual and, cutaneous routes of administration of certain drugs, patches, hormone patches, things like that. By putting it onto your skin or absorbing it through the mucosa in your mouth, you bypass the liver. That's known as first pass metabolism, a common thing in medicine. All drugs go through that. When you take a drug, we gotta know its first pass metabolism because that will tell us how much is actually getting into the bloodstream for biodistribution.

So the liver is vital in detoxing anything that's absorbed from the gut. And so the liver would be the first point of injury with any, toxic peptide being absorbed in the gut. And, you know, another area as we think about the clinical implications, one of the other things that I've been hearing about, and, initially, I couldn't make sense of it until recently, is that the issue with teeth because, again, much of the mouth is full of lots of bacteria, especially anaerobic bacteria. And they are usually below the gum line, and so they, they don't need oxygen to replicate. If this cohort of bacteria are also weaponized in the sense that they're producing more toxins, they're damaging their, the counters, bacteria because, important thing for people to understand is that bacteria keep control of themselves because there is limited amount of new of nutrients.

And so they battle for the nutrients, so no one group can outgrow the other. However, if you have a situation where one group or two groups of bacteria are able to produce toxins that destroy the other bacteria, suddenly, they are the king of the hill. And so you end up with overgrowth of bacteria, which could then potentially lead to lead to gingival disease, teeth problems, chronic gingivitis. And then what would happen from that is from for people who are susceptible, infective endocarditis. And that's another thing where the bacteria get into the bloodstream and then infect the valves of the heart.

I mean, the the the implications are, like, endless. I think, I think Philippus has been known for a long time. It's just that it's been kept from general mainstream, science and public interest. I've been talking out against the use of wheat as a source of carbohydrate. We weren't meant to eat that as a source of carbohydrates.

I haven't seen a primate eat grass. Neither have I seen a primate milk a cow. So the two commonest foods that we're allergic to are wheat and gluten gluten and milk. And when you look at gluten, wheat products, we can't we don't have the bacteria in our mouth to degrade it. But every morning, we stick some in our mouth, it gets in our teeth.

And what I found was that wheat is the commonest cause of tooth decay. We, wrongfully ascribe it to the eating of refined sugars. But we have the right bacteria and amount to degrade sugar, and sugar does not persist in your mouth. But we don't have the bacteria for wheat. And so the bacteria and the ASC food in our mouth and start to settle there.

And then, like, we say toxins, they make some of the strong strongest acids and enzymes to degrade those cell walls of this dense wheat. And those strong enzymes degrade your teeth as well and damage your enamel. So I've seen kids that don't eat sweets that have very bad teeth. It's the morning breakfast that's causing the problem. I've encouraged my son to brush his teeth after breakfast, and he's never added a a rotten tooth.

So, yeah, I think there's a lot of the microbiome or the microbiology on the planet that we don't understand, and I think it's vitally important for our survival. Sixty percent of the cells that make up you are not you. They are microbiome. So as general practitioners, we've limited ourselves to treating forty percent of the patient by not understanding the sixty percent that's so vital to our survival. We are an an ecosystem, and it's a very balanced ecosystem.

You know, as and and some people reading or listening to us would think, well, you know, the solution is just, you know, just use antibiotics. But it's not so simple because your antibiotics, whilst they do do some targeting, can quite easily wipe out even more of your good bacteria. And so you may easily go from a bad situation to a worse situation where there's also resistance. There are all kinds of problems that that occur with this. This is not necessarily easy to fix.

No. Not not not at all for them. If you look at the role of the bacteria in let's take your gut. They digest your food. So your gut is like a septic tank.

And when you put in food there, it gets digested enzymatically digested, by these bacteria. So it releases nutrients from your food that you wouldn't, normally be able to digest and absorb. The gut bacteria also process pathogens that get into your gut, and in that way, stimulate immune response to things throughout the body. And as well, they make certain chemicals that we can't make, which we readily absorb and convert into other other chemicals. So serotonin and things like that are all the starting, compounds are made by the bacteria in your gut.

So someone depressed might have a gut microbiome upset that doesn't give them the chemicals they need to make the feel good factors that cause the depression. So I think the the microbiome has been understudied, but it is is I think the the bottom line in what we're dealing with will provide us the solutions if we look at it very closely. I think that's where the solution actually dies. Yeah. It's very, very worrying, even for us from a clinical point of view because we know the complexities of this.

This is not straightforward. And if the scientific community is not even considering it, then there is absolutely no chance. Just to give some more context, I've got here, this is an image of from the paper. So this is easily over two hundred proteins scattered around inside the, the intestine. And some of it, this is just zoomed in.

You can see all of these scattered within. So some is in the lumen. Some is in the submucosal region. Similar picture here. This here is in a cell in the, in the lumen, and then you see scatterings in the sub submucosa here.

This is some pretty serious stuff to have this kind of remnant of the virus existing. And as I said, what happens is once it penetrates the mucosal barrier, it can then diffuse. So it's not even just the gut. It will be, any area that could become infected. Prostate could end up with prostatitis with this kind of, inflammation.

It it could literally be anywhere that you have the microbiome existing. And so this is what makes it so very, very complex. And and I can't see it here. Yeah. Part part of my consideration early on in the pandemic, we had a very distinct start to the second phase of the illness itself.

Like I've mentioned on numerous times, patients on the eighth day suddenly took a turn for the worse, where on the seventh day, they thought they were completely recovered. And, of course, when we have the development of, antibodies, immunoglobulins, it is a it is a process that's progressive. It's not a sudden onset of something. So I looked at that, and I kept considering, is is there something more that we're actually dealing with? And then I spoke to.

He's with, a training for the special operatives in the US Department of Defense. And, of course, there are two things. Only two, physiologic or pathophysiologic processes that are that aggressive and that, lead to such rapid decompensation in a patient. And that is an exposure to an allergen that you are highly allergic to or an exposure to a toxin. And those two things were on my mind from the start.

Now when you look at an exposure to a toxin, that is a sudden event. So I kept considering, is this an infection of the microbiome that doesn't really cause any problems due to the infection? But once the microbiome start to produce toxin, then we respond to that. Either way, the treatment is about the same. You're trying to stop the body's response to something, and it's the response to either a toxin or an allergen that kill the host.

And so the treatment intervention's pretty much similar. It's the reason TAO got in touch with me to plant that seed in my head that we might be dealing with the toxicity rather than an allergen. And, of course, I think there's an interplay. Yep. And, you know, one of the things that I remember when I was looking at some of the long COVID research around the microclotting and so on, and there was very specific abnormalities with the interaction of von Willebrand factor and from and so on.

And I then because of Carla's work, I then did a backward step and said, okay. Is there any toxin that can replicate this kind of picture? And you know what it was? Shigella. Shigella toxin definitely is associated with clotting and increased clotting.

And and suddenly you realize that suppose this kind of bacteria is then producing higher levels. And it it it's small amounts over a long period of time that will overwhelm, eventually, almost wear down the system until it causes disease. And so it's a it's like a, oh, you know what it's like in in the second World War? This is a historical reference. In the second World War.

The Germans came up with the butterfly bomb. Okay. What they did is that they dropped them. And in some parts of the UK, the planes would fly over and then they would drop these bombs that were like butterflies. So the children would then later on go out and see them and play with them and bring them home.

But these bombs had a delayed explosion on it, so within twenty four or forty eight hours, they would just explode. They were absolutely frightening. This is almost potentially that kind of really frightening picture, which you'd if you really have to be suspicious even to think about it, much less to be able to try and anticipate it. Yeah. It's like recruiting the gut microbiome to be that butterfly, that would cause secondary problems, and you'd never understand why it's why it was there.

You know, Philip, the the the clinical observation and understanding of symptomatology is vitally important, and that's the reason I did what I did. In the paper that I've that we've just went through, I mentioned a mucoid diarrhea, and that is dysentery. And, generally, infections of the gut present with a very watery diarrhea. But if you have toxicity and colonic inflammation, then you get mucus production. And now it makes sense that we're dealing with toxicity that creates the mucoid diarrhea.

And like you say, she get a, yeah, dysentery. Toxic. Wow. So listen. Just so, people understand because we're gonna wrap up now, Shankara, as we continue to explore these thoughts, I I think that some of what we said there was so almost, what's the word?

So serious. I have a feeling that those words may not necessarily want to be seen. So if you want to see the full discussion, you must follow the link that will be put below, on the Substack because I think I'll leave there's some parts of this that are almost too serious that, I suspect those who do not wish this kind of conversation to occur would therefore want it to be taken away. So, yes, folks who are with us, thank you. This is a Thursday evening, and so we appreciate the people who are here with us.

But this is some pretty significant clinical stuff. And I still maintain that doctor Shetty has been there from the start observing the clinical patterns. I can't think of anybody better to try and work out the directions that things could go. So, Shankaran, any final words before we leave? I think, a little bit of hope for people, to understand how bacteria and viruses actually cause, morbidity and mortality in their hosts, our immunity is a pretty remarkable thing, and it can take care of almost any virus or bacteria on the planet.

We developed that immunity through exposure in childhood and build up this library of things we can ignore. So I don't think immunity is a problem. We'll we'll be able to tackle any virus or any bacteria thrown at us. However, the mortality and morbidity from these infections is caused by a host response, not by a but but not by the virulence of the pathogen itself. So the virulence of a pathogen is its ability to trigger a serious host response that eventually kills the host.

So if we gain a decent understanding of how to curb these unusual host responses, then we can deal with any pathogen that's thrown at us. If you look at Ebola, you got the western variant and you got the wild type. The western variant does not kill. The wild type does. And its its lethality rests in its ability to trigger a cytokine storm.

So if we can gain an understanding of how cytokine storms are triggered by different pathogens and the treatment necessary to negate those, then we can deal with any pathogen thrown at us. So there is hope for the future. Absolutely agreed. So listen, guys. Remember to stay with us.

We are right at the front of this trying to figure it out. So if you want to join in the research journey, please continue to stay and listen with this kind of work. Have a great evening, everybody. Shankara, if you could just hang fire with me. Thanks, Philip.

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