The following transcript comes from an interview for Iconoclast: Ideas that have Shaped the Culture Wars. It was conducted by Mark Halloran with Eric Topol on October 14th, 2021. Mark Halloran is Editor of Iconoclast. He holds a PhD in biochemistry and a BA in Behavioural Science. Eric Topol is a cardiologist and Professor of Molecular Medicine. He founded the Scripps Research Translational Institute, has written three books, and has published over 1,200 peer-reviewed articles.
Mark Halloran: So I thought I’d like to pick up where the Sam Harris interview left off, and go into some of the things in more detail.
I’d like to talk about the research in relation to ivermectin, vaccines and some of the immune escape mutations like Delta. In terms of the Bryant et al. (2021) meta-analysis that was done for ivermectin, which showed that COVID-19 deaths were reduced by ivermectin; that was a moderate certainty evidence finding and there was low certainty evidence that ivermectin reduced COVID-19 infection by an average of 86 percent. I suppose I’d like to talk to you about why this isn’t compelling evidence for the use of ivermectin in the protection and treatment of COVID.
Eric Topol: That’s pretty simple. Because the two largest studies that were in the meta-analysis, were both shown to be fraudulent. That is, the data was impossible, and they had to be withdrawn. And so then, what you’re left with is a bunch of very small studies. And collectively, there’s not enough certainty to say anything. So, whether it prevents infection and prevents adverse outcomes, we're left in the lurch. It’s still possible that ivermectin does have an effect. I’m not saying it doesn’t, in fact, maybe it does? But the point is, you can’t make that judgement, based on a collection of small studies that are inconclusive. That’s very different from, for example, the drug that Merck developed recently—another Merck drug, interestingly, because ivermectin is also made by Merck. And I’m not a fan of Merck by any means, having been part of the Vioxx exposure years ago. But they had a trial of molnupiravir, a drug that had known anti-viral activity that’s potent, whereas ivermectin’s mechanisms, are still a little bit fuzzy, as far as where SARS-CoV-2 is concerned. But they did a real trial, which was intended to be quite a reasonable size, and it was judged by an independent data and safety monitoring board that it had to be stopped because it was overwhelming in its efficacy with regard to reduction of hospitalizations and deaths: 50 percent [Note: the Merck trial data for molnupiravir has been revised and it is now a 30 percent (rather than 50 percent) reduction in hospitalizations and death, and half the absolute benefit than they previously disseminated at their interim analysis]. In fact, there were eight deaths versus zero, for placebo versus the active drug. Now, you need trials like that, to be able to say something definitive. And that’s even just one trial. Usually, you like to have independent replication. And there is an ongoing trial for that drug, in relation to prevention in people with early COVID infection, confirmed.
But the problem with the story with ivermectin is that it’s a hodgepodge of studies, some of which various doses were used, there were some indications for prevention of infection, and some for prevention of outcomes. So, it’s all over the place. And it’s left in the suspension of maybe this drug could do something? But when you have fraudulent research being conducted, that is a very worrisome sign. And the fact that we haven't had reliable sources of data from the usual entities like the Recovery Trial out of Oxford, or large study groups like Solidarity or ones from the World Health Organization (WHO). A lot of the studies that have come forth had tiny numbers and are not coming from trusted sources of trialists. So, no, the way I look at it is, it’s just the zone of uncertainty is too high. And you have these zealots that are pushing this, saying it’s a panacea; it’ll end the pandemic. That makes it even worse, because you want to have definitive data, ideally; two large trials, and independent replication to say anything. And there’s not even one large trial for ivermectin, the total body of evidence was based on less than a couple of thousand people.
MH: I think that was the heart of it, aside from the fraudulent issues. I know Lawrence et al. (2021) had written a letter to Nature. And I’d like to talk to you about that. It outlines all of the issues in relation to the study: impossible numbers, mismatch of trial register, inconsistent timelines, etc. I would say outside of that, having worked in preclinical research with drugs for amyotrophic lateral sclerosis (ALS) in transgenic mice, that what people generally don’t understand is that sample size matters in relation to power and effect size. And so, I could have cited multiple drugs that looked effective in animal models that were either totally ineffective, or actually toxic in ALS patients. And that was not even fraudulent. Just bad study design, low numbers, insufficient power.
ET: Absolutely, you need big numbers. Remember, you’re talking about treating millions, if not tens of millions of people. And you don't want to make the wrong call on a thousand people or a couple of thousand people, not that you have to have 10 million people in a study, but you want to be sure. And you also don’t want to be making false claims. So, the ivermectin zealots were saying this was 99 percent effective, and having an emergency podcast with Joe Rogan. That should get you scared, because there is no drug in the world that has 99 percent success. Even if ivermectin someday is proven to have some efficacy, it’s not going to be 99 percent. We know that. So, these are the things that really are disturbing, actually.
MH: Lawrence et al. called for a paradigm shift in relation to how meta-analysis is done. That, in fact, the meta-analysis should occur on individual patient data. What do you think of that?
ET: That's really important. That's been part of the meta-analysis story for years. When you pool data, it isn’t just like it’s on the back of the envelope, or you just take the total numbers from each of the publications. In this case a lot of them were preprints. You actually have to have the data from each individual participant in the trials; in the patients. So, they didn’t have the data. And had they had it, a lot of these mistakes would have been preempted. So, one of the rules of what would now be considered for a top tier meta-analysis would be that you have talked to the authors of each of the papers, you've had them submit their data; the actual raw data for each person, so that when you do your pooling, you have all that information and then you can actually look at the granular aspects of each person. But when you don’t do that, and you just have basically kind of bottom-line data from papers without you connecting with the authors, you have a weak meta-analysis that has to be automatically suspect.
MH: The point made in the Bryant et al. paper which Tess Laurie is a coauthor on, is that corticosteroids were put forward as a treatment for COVID based on one randomized controlled trial, whereas ivermectin has had dozens. How would you respond to that?
ET: I think you said it well, when you said that sample size is so important. If you have 20 studies, and there are about 20 people in each group, of the placebo and the ivermectin; adding those things up—it’s not a lot of veracity in that data set. So, the problem is you really want to bank the determination of whether a drug works on large bodies of data, rigorous studies and you can’t just lump all the different doses together too which has been a problem with these meta-analyses of ivermectin. So, no matter how you look at it, this data doesn’t cut it. Ivermectin is still a big question mark. And maybe someday we’ll get the truth about it. But it’s discouraging how it’s gotten so much mileage, and you have these people that are basically saying, if you’re not giving the drug, you’re hurting people. When in fact it could be just the opposite.
MH: I think that the people who are the advocates for it, if I’m to look at them as good actors, are simply looking at all the data and making a mistake based on the data they’re looking at. They’re looking at studies like the ones in the Peruvian states where they’ve introduced ivermectin along with multiple other safety protocols, and there’s been reduction in infection and death. How much weight would you give to those observational studies?
ET: You’re going to have a reduction just on a basis of time as we get smarter about how to treat people, just simple things—like putting people prone to avoid mechanical ventilation. And we make all these points of progress in the course of the pandemic. And if you just study a drug along the way, there’s just the time, learning, wisdom, that comes along with it. So, you can’t make judgments about that either. The only way you get the answer is randomized trials done with both the active drug, placebo, contemporaneously. Randomized, large numbers, with rigorous collection of the data, and sharing of the data. That’s important. I’ve been involved in some of the largest randomized trials in cardiovascular research—Global Use of Strategies to Open Coronary Arteries (GUSTO)—and had over 41,000 people in 18 countries looking at death as the endpoint and heart attack. We know how to do these trials, they are not hard, but they have to be large. And they have to be rigorous and subject to audit. And these are things that we haven’t had any of for ivermectin. It falls short on every box you want to check. Ivermectin data falls short on.
MH: When I spoke to Nobel Laureate Peter Doherty, this was at the beginning of the pandemic, we spoke about a paper released by his institute which is the molecular proof of principle for ivermectin. Caly et al. (2020), did an in vitro study that found that there was something like a 5,000-fold reduction in SARS-CoV-2. Of course, they were using super physiological levels of ivermectin that are not FDA approved and cannot even be replicated in vivo. Not to say that it couldn’t have some effect. It feels like that’s where it’s kind of gone wrong.
ET: The dosing is a big deal. There's been so many drugs, one of the famous ones was resveratrol, that would make you live forever, if you drink 10 cases of wine every day, in order to get enough resveratrol. And that totally was a bust. And whenever you have supra physiologic doses that can never be achieved in human beings, as the only real biological activity marker that’s a problem. There are so many drugs—when you repurpose them in a screen, all the drugs that could have antiviral activity, again, for SARS-CoV-2, the list is very, very long. However, at doses, the potency, that you could actually give the medicine in a pill form, it starts to get narrow; very few. And one of those just recently, it appears to have clicked with the Merck drug. And there are a couple of others that are in the process, with Pfizer and Roche. So, I think we’re going to get there. But the dose support work that you’re getting at for ivermectin, was a terrible reach, we would never be able to achieve that amount of drug in vivo. And, interestingly, some of the trials that are thrown into the bouillabaisse, which is what this is, are very low doses of ivermectin, and even the highest doses are low relative to what had a putative level of antiviral activity in the Caly et al. in vitro study.
MH: It’s a tenfold increase on the FDA approved level. I do want to talk to you about Israel and about Delta. I don’t really understand this that well, but the escape mutations and the reduction in the effectiveness of the vaccines to protect against infection are down to something like 39 percent? I know you were initially against boosters to some extent, but what’s our future look like with this? With more variants coming out that are more infectious and possibly even more lethal. What are we looking at? Constant boosters?
ET: Delta is pretty bad. Delta is something that won’t make it easy for another version of this virus to compete with; it’s so hyper-transmissible, and it also has some immune evasion features. So, to be able to beat Delta, and come up with another global strain, it’s not going to be easy. There hasn’t been one yet that has mounted any competitiveness with Delta, but we may see that because we don’t have global containment of the virus. And there’s a chance for it to evolve further, but hopefully, we won't see it. Now, let’s say we just stay with Delta as our circulating virus around the world, which is pretty much the case, the only continent that was holding out till recently was South America, and that’s also being taken over by Delta. But everywhere else, it’s Delta, almost 100 percent. So back in late June in Israel, where they had previously gotten their cases down to almost zero, that is they got it down to one per million, or 10 cases in the entire country of Israel. So, it looked like they had beaten this virus, after having really had a tough road. Then Delta started and they had a huge surge. Because there was a double hit, they’ve been very aggressive in getting the vaccine to their population early. So, they were set up for waning immunity.
Now, we knew that the vaccines weren’t going to stay effective for years, we knew there would be a third shot needed, likely maybe at one year, or two years, at some point. We didn't know it’d be six months. That was the big Israeli realization, when they first came out with that and said: “Oh my gosh, protection has dropped from 95 percent to 40 percent against symptomatic infections.” At first there was denial among the medical community. Nobody wanted to see that. So, the double whammy was both that they had gotten off to a very fast start, they had a lot of people then who were at the six-month waned immunity period, and they also had Delta. If we never had Delta, if they just had Alpha, these breakthrough infections would have probably still been much lower. It’s this combination of a very contagious form of the virus with the waning of immunity that was expected. It really basically was like a perfect storm.
And you add into that, that in Israel they gave Pfizer, at three weeks spacing, which led to a not optimal response of the Beta; the B and T cell immune response. So that now has been largely squashed by the boosters. They used boosters of the Pfizer—the same dose, the same original vaccine in millions of people. And they’re well on their way to getting back to that one case per million people, which is the ultimate—we can’t do much better than that. And I think what we’ve learned already, people over 60 need to get a third shot, that probably applies to all vaccines, or with Johnson & Johnson, that would be the second dose. But an additional dose is going to be needed around six months for people over 60. If we want to suppress symptomatic infections, instead of just hospitalizations and deaths, then we have to go down to much lower ages, possibly as low as age 20 or 18. That’s the big question: how aggressive do you want to suppress symptomatic infections because they’re going to crop up with more exposure to Delta, if we don’t give a third shot.
MH: It seems that that’s a balance then because even though there’s a decrease in approximately 39 percent for the ability to stop infection, there’s still an 89 to 93 percent protection against hospitalization and death.
ET: It’s really a little lower than that. But if you zoom in on the people over age 65, then it drops down, and for the people in their 70s it dropped from 95 to 85, which is substantial. So, the point I am getting at is that most of the hospitalizations and deaths occur in people over age 60. So that's where you see the big bang of the booster.
MH: Because the immune response is just not going to be as good with older people, even with a good vaccine, they’re just not going to be able to produce antibodies the same way.
ET: Exactly. So then with the younger age group it’s two things going on. One, they make better antibody and cellular responses; B and T cells, and they don’t have as much of a risk to wind up in hospital or die. So, for those people as you get younger and younger, the benefit of an additional shot is lower. But it is consistent about the symptomatic infections. We just learned that data this week from Israel. There’s one other point—if we get containment of the virus, where it’s at very low levels, then the need for these additional shots is much lower, especially in younger healthy people. So, a lot of this story about the additional shots is dependent on us getting our global vaccination rates way up, achieving containment, and the unknown as to whether neutralizing antibodies at high levels is going to be required to prevent infections and transmission. That is still out there, dangling, because we finally have spacing between vaccinations; now that we’ve given a six month third dose, and we have this really good cellular immune response generated—that might be enough to carry us years. We’ll have to see.
MH: If you’ve got something as infectious as Delta doesn’t it become sort of a pandemic of the unvaccinated? But then the unvaccinated can also affect the vaccinated if you’ve got a significant proportion of them. If we thought 70:30 percent—if we had 30 percent unvaccinated, we would get away with it at Alpha or Beta, we’re not going to get away with it at Delta. I'm wondering whether if we vaccinate everyone, say, down to 16 years old, then doesn’t it becomes a pandemic of children? The virus then starts to circulate in really young children and become more infectious and deadly in children? That’s the concern.
ET: I haven’t been a fan of the pandemic of the unvaccinated just because we’re all in this together. And as you said, aptly, people who are vaccinated are not necessarily durably protected. So, they’re involved. And they can transmit, maybe not as frequently, but if you’re vaccinated, and you get a breakthrough infection, you may transmit before you have any symptoms, or you may never get symptoms, and you may be capable of transmitting particularly with Delta, because it’s such high copies of the virus that you harbor in your nose and upper airway. And then you get to the children. Now, even if we were to get 80 percent of the total population, and there’s some more people that have prior COVID who have immunity—it still may not be as ideal as if those people got one dose of a vaccine—but then you start getting up to the 90 percent ballpark. And with the children basically then they get the drag effect of having most of the population build up this great Delta immunity wall. We don’t have that yet. We’re seeing it maybe in places like Spain and Portugal and the UAE, where they are at 80 percent and prior COVID, unlike Singapore, which had almost no prior COVID. So that may be the ticket to getting containment, Israel may get that now because they've gone through so much to get through this recent Delta wave.
The Delta problem changed the dynamics. We need 90–95 percent of a Delta wall of immunity; a combination of some type of vaccination, plus prior COVID in people who didn't get vaccinated, and particularly if it’s within the last six months or a year of that prior COVID. And then the kids will basically benefit even without having to necessarily get vaccinated. But in the US, we’re so short; we’re at 56 percent of the total population. We need those kids vaccinated to be part of the 90 percent because they are a vector of transmission. Places that have done really well, like Spain or the UAE, it’s not as vital for them to get young children vaccinated as it is in the US.
MH: I think because the safety profile hasn’t been established for certain subgroups. So, children are one, pregnant women are another, and then there are the immunocompromised. Are we going to be able to get vaccination in those subgroups without an appropriate safety profile?
ET: I think the pregnancy thing has played out. Pregnancy is an immunocompromised state. And right now, in the UK, one in five of the intensive care unit patients with COVID are unvaccinated pregnant women. So, it’s a very serious matter. And we know that the safety has been assured and efficacy is short. And so pregnant women do benefit from getting vaccinated. The real immunocompromised patients are the ones that have an autoimmune disease or are taking drugs that are basically interfering with their immune system. That’s tricky, because they’re variable, and we need to probably do lab tests to see that they are really getting protection. So that one’s a bit of a wildcard because it’s quite heterogeneous. I think the benefits of vaccination, though, are much bigger than the average person is appreciating. Because it’s not just the individual, of course, it's the ability to break the chain.
And then there’s the children, you’re right, we don’t have the safety data we would like. Let’s say we saw in the teenagers that the myocarditis cropped up. And that wasn’t expected. We didn’t know that was going to happen, we still don’t know the mechanism of it. And most of those are boys, most of them do really well. It’s mild, it’s self-limiting. The number of cases is, let’s say, one in 50,000. But if you get down to teenage boys, it gets higher, but almost always, they recover well. And it’s usually the second dose. Now, what if that was even more common in children? We don’t know. And the only study we have is with Pfizer with five to 11-year-olds. And it’s only 1,500 people who got the vaccine. Now we’re back to like ivermectin numbers. But now we’re talking about safety issues. And if it’s one in 50,000, or one in 10,000, and you only have 1,500 people studied, well you can get a misread. So, there wasn’t any myocarditis in the 1,500 children in that study. But we need more data to be certain about that.
MH: In relation to the instances of myocarditis from the mRNA vaccines, it has been suggested that there may be some degree of molecular mimicry between the spike protein and self-antigens.
ET: Everything under the sun has been touted as a putative mechanism, and we have nothing yet to rule in or out. It’s very elusive. I think that there was the idea that somehow the mRNA was getting into a vein during the injection, but that doesn’t explain why it’s just boys. And then why the second shot, and the age thing? There are so many unknowns here, whether it’s an actual autoimmune, proinflammatory. This mimicry. I've heard testosterone being put forward as a factor. Well, there’s young women getting myocarditis, so testosterone doesn’t do this. Why is there an imbalance of the genders? It’s puzzling. The good thing about it is if you get COVID, the chance of you getting the real deal myocarditis is relatively high, much higher than if you get it from the vaccine, which is very mild if it occurs, and self-limiting.
So COVID of the heart is not a good thing; from the infection. COVID caused myocarditis of the vaccine, even though we don’t know why it occurs, I think we can at least say it’s not likely to be of a durable, adverse impact. The rarity of myocarditis from the mRNA vaccines being a problem is notable.
MH: What are the comparable rates between myocarditis from COVID versus myocarditis from the vaccine?
ET: If you just looked at all people, without segmenting teenagers or older people, it’s more than a 10-fold difference, much more than 10-fold of myocarditis from COVID than you would ever get from a vaccine. And it was a New England Journal of Medicine paper from Israel that found this and others have confirmed it. It’s orders of magnitude difference. And it’s also a different type with COVID. The heart problem you get through a COVID infection is much more worrisome than the one you get through the vaccine.
MH: People talk about getting natural immunity through catching COVID versus some type of artificial immunity from vaccines. The issue is that people don’t take into account that after previous pandemics the increase in neurological illness, things like Parkinson’s disease, have skyrocketed. So COVID is not something that you want to go out and catch to get natural immunity because you don’t really know what’s down the track for you.
ET: So, I think this is a really important topic, the so-called prior COVID immunity, or natural immunity...
MH: The problem we’ve got is none of it is long term.
ET: The immunity that you get from a COVID infection, in some people, can be quite durable. You just don’t know that until it's too late—when you actually wind up getting a reinfection. Over time, even prior COVID—what some people like to call natural immunity—I don’t think it’s natural to get COVID. I don’t think anybody wants to get COVID. And just like I don’t want to have a chicken pox party to get chicken pox, you don't want to have a COVID party. The issue here is the immunity you get is very different. With COVID infection you’re getting exposed to the entire virus, you’re getting different antigens that you’re making antibodies to, and different cellular immunity. It’s very different from you just getting the spike protein to fight against. So, it does have, in some people, more durability and more breadth. The best of all, you can’t beat this, is you get COVID, you have a good immune response, and then you get one dose of vaccine. That’s unbeatable. That’s better than two doses of any vaccine known to mankind. That’s hybrid immunity. But again, you don’t want to get COVID. It’s only if you had missed an opportunity of getting the vaccine, because when you get COVID, there’s a wildcard. The wildcard is what you’re getting at which is long COVID.
Long COVID is a mosaic of many things. Some of the constituent symptoms are brain fog, and cognitive impact. Obviously, fatigue is a central part of this, but also breathing difficulty, and many other things. Now, recent studies have shown that this is not uncommon at all, more than 10 percent of people who get COVID, even young, healthy people are getting long COVID symptoms. Diverse, debilitating symptoms, and they often can’t return to work, or if they do go back to work, they’re troubled. They really have limitations. So, this is the legacy of the COVID pandemic; there is going to be millions of people around the world who have long COVID. And who knows how long it will last for?
MH: Well even beyond long COVID. What we’ve seen from previous pandemics is that there’s a correlation after the pandemics with people developing severe neurological illnesses.
ET: To pinpoint that further, there’s one really important study that came out of the UK. So, in the UK they have the Biobank. And they have taken hundreds of thousands of UK citizens who volunteer to participate and a large number had a brain scan. And by happenstance, they had it before the pandemic. Then they repeated their brain scans, if they had COVID, or they didn’t have COVID, and they saw marked grey matter loss in the COVID group. And it gets to your point, which is that it takes a long time after losing brain cells to see the impact. And the fact that it’s already been documented from that UK study, that’s one of the most worrisome studies we’ve seen about COVID. Beyond the deaths, and the sickness that induces, is the implications of what it could do to some people’s brains. Young, healthy people who happen to have brain hits or involvement. So, this is yet another reason why we don’t want people to get COVID. Many will wind up unscathed, of course. But what about the people who unknowingly have this hit to their brain, which we still need to learn a lot more about?
MH: I wanted to address some of the claims that were made in Bret Weinstein’s DarkHorse podcast with Dr. Robert Malone and Steve Kirsch. So, the first one is that the spike protein that’s produced by the mRNA vaccine is cytotoxic. And then, the claim is that the transmembrane domain that is supposed to anchor the spike protein to a localized spot fails, or can fail to some extent, and that the spike protein then cleaves, and then Steve Kirsch talks about a Japanese study that shows the distribution of the spike protein throughout the body, bloodstream, the ovaries and in bone marrow. Tell me what do we make of this? What evidence is there for this?
ET: It’s all false. It’s all unacceptable lying; making things up. For example, Bret Weinstein on one of his podcasts said that the reason people get headaches post vaccination is because the mRNA from the vaccine crosses the blood brain barrier, and that’s what’s causing it. That’s ridiculous. This is what, in many ways, has ruined the American vaccination campaign, why we’re sitting at 56 percent fully vaccinated instead of 80 or 90 percent. Is this kind of fabrication. Now, I want to make sure that your listeners know that Dr. Malone, who claims he’s the inventor of mRNA vaccines, is a charlatan; he’s not the inventor of mRNA vaccines. He’s already admitted to that. So, anything he says is suspect. And for whatever reason, he’s on a campaign to take down the mRNA vaccines that he says he was the inventor of—when he wasn't the inventor. He had some involvement with the delivery of nanoparticles with mRNA. But he was not the inventor of the vaccines. And he continues to make false assertions, and team up with people like Bret Weinstein and others, to make stuff up. And all this stuff is made up. It’s unacceptable, and it’s scaring people from getting the vaccines.
ET: There is no evidence that the mRNA vaccines, Pfizer and Moderna specifically, are cytotoxic. No evidence. To say this sort of thing is just outrageous. There’s never the comparison with COVID itself, which, as we’ve already discussed—what it can do to the brain, what it does do to cells, how it hijacks the cells. So, these things have scared the public, and their listeners and their followers from getting vaccinated. And this complete sham of inventing the vaccines so that that supposedly commands respect when it’s an absolute lie. It’s unimaginable that this has been happening. This is what has been happening here in the vaccine world. Yes, people are making false assertions. And you can never keep up with it. Because if it isn’t that, then it’s that it causes infertility or it causes cancer. It’s a gene therapy, it’s experimental, the list goes on, it’s infinite attempts to take down vaccines, and there’s no basis for it. These vaccines, the mRNA in particular, have been given now to hundreds of millions of people, and the number of people who’ve had any very serious untoward events, adverse outcomes, is miniscule; it’s almost nil.
MH: The thing that may have contributed to the vaccine hesitancy may have been the short development period of less than one year. The shortest period for vaccine development prior to this was the Ebola vaccine, which took five years. Do you think that this and then the emergency authorization by the FDA led to more hesitancy?
ET: It took 30 years to have the mRNA platform, and that’s with mRNA delivered by nanoparticles to get into muscle cells to then start the factory of the immune response. It took 30 years—not one year. The point being that it took a long time. The animal studies were done in non-human primates; macaques. And it was done in the largest clinical trials in the history of vaccines, 40,000 participants in one trial, 35,000 in another trial, these were conducted in a compressed way. I’ve already alluded to the fact that one thing that was done to move things fast was to do the three week dosing of Pfizer and the four week dosing of Moderna. I would have loved to see that done eight or 12 weeks, because it would have had an even better immune response. But remember, we were going into a crisis of existential threat to a large proportion of people. They needed to go fast. And they didn’t want to wait eight to 12 weeks and thought the three or four weeks was going to be enough. That was the only thing rushed.
When it came down to the FDA to adjudicate whether these vaccines are safe and effective, they actually took great pains to delay the Pfizer to make sure the trial was complete. Because at one point, under the pressure of the Trump administration, they were trying to get vaccine emergency approval, on the basis of the first interim analysis of 32 events. Thirty-two events! They wanted the administration of Trump and Pfizer to get approval. Well, the first thing the FDA said was, “No, you have to finish that darn trial, then we'll look at the data, and then maybe we’ll give you an emergency approval.” That's what happened. So, this was not rushed. This was done in a rigorous way, thank goodness, because if it had been rushed, and if Trump had gotten his way to have the October surprise, and atPfizer the CEO Albert Bourla, kept talking about getting the results out in October, if they had gotten it on the first interim analysis of 32 events, that would have been a nightmare. But since it was done right, this accusation that the trial was done too fast—it’s complete balderdash. It’s malarkey. It’s upsetting because it was actually done in a very rigorous way.
MH: I know that at the beginning of the rollout of the vaccines that they were monitoring for things like antibody-dependent enhancement (ADE). But that turned out to not be an issue. But they are the sorts of things that you look at with vaccines. Your claim is that if you’re going to see something, it’s within two months of a vaccine administration.
ET: We’ve seen everything we’re going to see with these vaccines—we saw it in the first two months. And that even includes the myocarditis that we discussed. It was seen in the first couple of months, when it’s introduced to the population at large. So, there’s not going to be any surprises. We talked about some of the pluses of a natural infection during our conversation. Let’s just be truthful about all this. And unfortunately, a lot of the damage has been done. Too many innocent minds have been inculcated with the fabrications, and disinformation. And I say dis not misinformation, because some of the perpetrators of this lack of evidence and fabricated stuff, did it purposely—to advance their own agendas. And we’re suffering because we can’t fix it now. It’s embedded. They’re programmed now to have a total aversion to getting vaccinated in the United States, and we suffer the most of any country because of that.