Turbo cancers and repurposed drugs, Dr Makis

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Turbo cancers and repurposed drugs, Dr Makis
YouTube video by Dr. William Makis (https://www.youtube.com/watch?v=0gIYQCjB_NU). Transcript is the auto-caption track — verbatim ASR, not a certified transcript.

Welcome to this video and I'm delighted to welcome Dr. William Marcus all the way from Alberta in Canada. Dr. Marcus, thank you so much for coming on. Thank you very much for having me. Now, we want to talk today about well, matters of life and death basically. Things of immense importance that aren't being discussed in mainstream media, that often aren't being discussed by regulatory agencies and in in fact, things that often seem to be surrounded by a deafening silence, which is is rather strange. Hopefully, we can bring that up to date. This is of course a purely academic discussion. We won't be making any medical recommendations or giving medical advice. That's between you and your own personal health care provider. But start us off, Dr. Marcus, if you like, just a little bit about yourself, your background. What what what professionally is your background? What do you do? What's your day job? That kind of thing. Certainly. I was born in communist Czechoslovakia and my family and I fled communism in 1988 through a United Nations refugee camp in Yugoslavia. And so we were in a refugee camp for a year. This was before the Berlin Wall fell. And my father had been persecuted by the by the Communist Party in Czechoslovakia. He had been targeted as a university professor. They wanted him of course to promote communism and and and he did not want to and so he felt the only option was to to flee. And we we were fortunate enough to be accepted by Canada and so I grew up in Toronto in Canada. I went to University of Toronto. I have a four-year undergraduate degree in immunology. Then a four-year medical degree at McGill University in Montreal and then a five-year specialization in nuclear medicine, radiology and oncology. Which is a branch of radiology, but it it does have a very significant oncology component. And so my detractors will often say, well, Dr. Marcus, you're you're not an oncologist. What are you talking about? And and I have oncology training. I've run oncology clinics for many years and I have over 100 peer-reviewed publications in cutting-edge cancer diagnostics and cancer treatments. So that is my that is my educational background. I worked in Alberta in a large cancer center and then unfortunately, as soon as Justin Trudeau's government was elected, my cancer program was targeted, sabotaged and I had only learned the later that the Trudeau government actually ended up copying my cancer program and my cutting-edge cancer work in another province in British Columbia for several hundred million dollars worth of government funds and the technology that I was working with was targeted radionuclide therapy. So targeted radiation. So you know, when when cancer patients get radiation therapy, we refer to it often as external beam radiation therapy. It's external radiation. You're irradiating, you know, for example, breast breast cancer patient will have the area irradiated to make sure that they're killing any cancer cells that might have been left behind or any lymph nodes that are too small to be detected and so I was working with targeted radiation that you inject. It's radiation that's attached to molecules or proteins that would deliver the radiation directly to the cancer and not irradiate healthy tissues. And so it was a much more advanced technology than external beam radiation and unfortunately, the Trudeau government took it over and you know, what's very interesting is that the the Trudeau government in Canada was getting into pharmaceuticals. It was getting into the pharmaceutical industry, investing heavily into various cutting-edge technologies and as we found out later, you know, they would also invest into the mRNA vaccines as well. We have some mRNA vaccine factories being built in Canada. And so I've been involved in a legal battle with the provincial government here in Alberta about the sabotage of my cancer program and so I was in a I was in a semi-retirement and in a legal battle when the pandemic hit. And really that allowed me to be very objective about the nature of the pandemic and what I saw going on around me. And I think that objectivity I then brought to social media and platforms like X and like Substack. Indeed. Just before we go on, I was actually in in Prague last year and I paid homage to the Jan Palach Memorial in Wenceslas Square, who of course burnt himself to death after the the Soviet invasion. Very moving. Very moving memorial still still there and and where where well visited by local people. It was good good to see. Prague is one of the most beautiful one of the most beautiful cities in the world and and certainly uh sort of it's sort of sort of the heart of Europe in a way. Not only that, it's got fantastic beer. Yes. And it's cheap. Absolutely. So just just to just to think a bit about the work that you were you had a or what's the word I'm looking for? There's a word in academia it begins with P, doesn't it? Sounds like major plagiarism of your work. You had some sort of radioactive molecule, something that gave off radiation. And that was hooked onto some molecule presumably that had a high affinity for a cancer tissue. That that that affinity molecule would then hook onto the cancer and the the molecule emitting the radiation would only be a molecule's distance away and would directly radiate the cancer. Have I got the essence of that correct? Exactly. So so the radioactive molecule would give off beta particles. It was chelated to a a peptide that would deliver it directly to a receptor on the cancer cell. You know, the half-life was six hours so it was a short half-life. It would it would hit the cancer cell. It would render it in in enabled of replication or it would damage the DNA of the cancer cell. Meanwhile, you know, you wouldn't get any damage of the surrounding tissue. The patient would pee out the rest of the radiation and it was done as an outpatient. They would get their injection and then they would go home. Minimal side effects and so I I was a big fan of of next generation cancer treatments, more targeted cancer treatments instead of, you know, the the the old style chemotherapy where you would be hitting everything that that that was replicating rapidly, but you would also be hitting healthy tissue as well. Yeah. In recent years, have you seen an increase in aggressive cancers, higher grade cancers, cancers affecting younger people, what is sometimes called turbo cancer? And is that a term you like? I have seen this honestly and and I first saw this phenomenon in 2022. That was when I first realized that there's something else going on since the start of the pandemic that hadn't been properly characterized or looked at. I saw it among my colleagues, physician colleagues who were coming down young colleagues who were coming down with these extremely aggressive cancers and cancers that behaved unlike anything I had seen before and I have seen that since. I've seen that I've seen that in nursing. I've seen that among teachers. You know, these these various professions that faced mandates at some point and I'd seen this phenomenon, these very aggressive cancers and they would kill the person very quickly. You know, they would they would kill a person in a matter of six months. And so the behavior the behavior was very different. I alerted the Canadian Medical Association of this in September of 2022. I had alerted them that I had I had seen a number of my physicians colleagues come down with these extremely aggressive cancers and the term turbo cancer started to be used around that time as well. It's not a term I like. I don't like the term turbo cancer. It's not a medical term and and it's a it's a term that you know, someone who's sort of not may not take seriously. You know, it's a term that that doesn't sound professional. But it's a term that I think really appropriately describes what I believe is a brand new phenomenon in cancer. Which is that some people are now developing extremely aggressive cancers that present at four usually. We're not catching them early on. We're catching them quite late. Stage three, stage four presentations. Young people. These are shocking when when you see young women in their 20s present with stage four breast cancer and they have no family history and they have no genetic markers that you can detect, no BRCA1 or two mutation. That's when you realize that something is really wrong here. Colon cancers presenting in young people in their 20s and 30s. We shouldn't be seeing that. You know, I always refer to the case of cholangiocarcinomas. These are bile duct cancers that where the average age was 70. The average age of presentation. This is this is a this is a cancer of the elderly and yet we have 20, 25-year-olds presenting with stage four cholangiocarcinoma, something that I'd never seen in in my career. So there is something new happening. The term turbo cancer has stuck. I believe it appropriately describes the the very aggressive nature of these cancers. They grow very rapidly. They metastasize and spread. So even when surgeons are trying to go in and get the primary tumor out, by the time they rescan the patient after the surgery, they realize it has already spread to multiple organs and they didn't catch it in time. That's how quickly this this thing moves. And one one one particular feature of it which I think is very shocking but very characteristic is these cancers are resistant to conventional chemotherapy, conventional radiotherapy, and even conventional immunotherapy. And so you see this this very shocking resistance to chemotherapy. Um and so you will get either no response or partial response. Uh the oncologists really struggle with these cancers, these turbo cancers. They struggle with them because they throw everything at it, you know? The oncologists are genuinely trying to get these cancers under control as as they used to in the past. And so imagine you know, you would have a breast cancer patient who could live another 5 years, 10 years with conventional treatment, and then that patient dies 6 months later. And you're left wondering, what is going on? Why are these patients dying so soon after diagnosis? Why Why are they resistant to conventional treatment? And that's just not being looked at. It's not being studied. It's really being ignored by by mainstream oncology. And so Professor Daiglish, for example, talks about this. Um yes. You know, he has noticed this phenomenon in the last few years as well. And the pathologists, you know, I'm really proud of my pathology colleagues like like Dr. Ryan Cole, Mhm. uh Dr. Professor Burkhardt in in Germany, uh who who've really been, you know, raising the alarm about this, telling us there is something wrong here. These turbo cancers are real and they are claiming thousands of young lives, and no one is studying it, no one is looking into it. It almost sounds like a new pathology, doesn't it? I mean, you know, tragically in clinical practice, we we've seen young cancers. We've seen childhood cancers. But but very often young adult cancers are associated with a specific mutation or genetic disorder. You mentioned there the BRCA1 or 2 mutation which predisposes to uh tragically early life breast cancer, ovarian cancer. But now we're seeing cancers of an aggressive nature in young people without these genetic mutations. That's right. It's almost like a new pathology. And the fact that it's they seem to be resistant to existing treatments again is indicating a new pathology, really. Um I want to talk about that a bit, but just before that, you mentioned stage three and four there. We talk about this a lot. You just run us very briefly through, if you don't mind, what what is stage 1 2 3 4 cancer? Well, so the stages um represent the really the size and extent uh of of of the tumors. And so if if we take breast cancer as an example, uh stage one would be a small tumor, 1 cm, 2 cm. Then stage two would be a larger tumor. And and and then usually you often have spread to local lymph nodes. Uh and then uh that'll be stage two. Stage three, you might get uh spread to further lymph nodes. It's now you're not you're not in the local area of the tumor anymore. You start spreading to more distant lymph nodes. Um and then stage four, of course, you get spread to other organs like liver, bones, brain, and so on. And so each cancer has its own staging system, stages one to four, that describe the size of the primary tumor and the spread to the surrounding It starts, you know, usually spread to surrounding lymph nodes, and then eventually spread to other organs as well. But when we talk about stage four, we're talking about metastatic disease. They'll be the cancer will be in the primary site. It'll probably have grown and expanded in the primary site, but it'll have metastasized, spread to distant parts one or more distant parts of the body, making it much harder to treat, presumably. Exactly. And I think I want to go back to this idea, and you'd mentioned that it almost looks like a new pathology. Mhm, please. And and I do believe that we are dealing with a brand new pathophysiology. We're not We're not dealing with just cancers that are more aggressive. We're dealing with something brand new, something that has a new mechanism by which it's arising. Uh and I believe um you know, again, this is where the pathologists come in, you know, like Dr. Ryan Cole, Professor Burkhardt, uh where they're trying to look at these tumors and see what's different about these tumors, what's different about the patients uh who develop these cancers. Uh and so we are dealing with something new. And another marker or another feature of these turbo cancers that I find fascinating that has come up over and over, and really no one talks about it, is that oncologists tend to be very good at giving you a proper prognosis. Uh and so when you come in and you're a certain type of breast cancer patient, let's say stage four, you know, we know that you are you know, hormone positive, for example, the oncologist is very good at giving you a prognosis, saying, "Look, if if you follow, you know, the the the conventional treatments, we we know you're going to live another 5 years or 10 years or 3 years, whatever the case may be." And so the prognostication in oncology is quite good. My oncology colleagues are really quite good. And this is based on studies of hundreds of thousands of people. Usually these are the large trials that they look at uh when they offer conventional treatments to patients. Well, this is where they've been completely off. Uh and you will see this You will see this thousands of cases on GoFundMe where families of cancer patients are raising funds, and they will share the medical story of the persons who's been affected by by turbo cancer. And they will say, "The oncologist told us we had 5 years, and our loved one died within 2 3 months." I have never seen my oncology colleagues be off by a factor of 10 in prognostication. I have never seen that. You you you don't get it that wrong. Um you know, or colon cancer, for example, where you could live another 5 years, and then the person again dies 2 3 months later after diagnosis, and it catches the oncologist off guard. It it and it catches the family off guard uh because because they've told the family, you know, we we we can with conventional treatments, you'll have at least another 2 years, 3 years, 5 years, and the person dies a few months later. That that that shocks everybody. And and and that throws everybody off. And so why are my colleagues now off in their prognostication by a factor of 5 to 10? Uh there's something wrong here. We I believe we are dealing with a brand new pathophysiology. Uh I believe it's something that should be seriously looked at. And and and unfortunately, we're stuck in the situation where some of my colleagues who are seeing this, like Professor Daiglish, for example, we will look at the literature. We will look at the published literature and understand that there are dozens of papers that are looking at aggressive cancers and and, you know, the manner by which they may be arising. Uh and there are case reports and so on. And yet uh on the other hand, when you know, you'll have doctors in in in the mainstream and in academia saying, "Well, there's no such thing as turbo cancer." And when you put it in the search engine, no literature comes up. And you have Wikipedia, which will say turbo cancer is a conspiracy theory. It's a alternative medicine, fringe medicine. It's It doesn't exist, right? It It It's It's not a thing. It doesn't exist. And And that's not science. You know, that that's not science when when you have a phenomenon in front of you uh to say, "This doesn't exist. This is not happening, and this is not real, and cancers are not increased, and you know, cancers are unchanged." To deny a phenomenon, you know, that's right in front of your face and where you have thousands of cases with families coming to social media saying, "Yes, this happened to us." Uh that's not that that's not science. That's not how science should work. It is quite bizarre, isn't it? It It is denial of that which is patently obvious. It's a bit like saying Australia doesn't exist. I mean, it's you know, we're we're we're into the realms of of incredulity here, really. It's uh So you mentioned the these accelerated cancers, turbo cancers, for want of a better term. Um are are we seeing like a group of turbo cancers and a group of what you might call traditional cancers as well? So are we seeing a group of cancers that still carried on where the oncologists are still getting it right? Absolutely. So we kind of get two streams of cancers, really. Exactly. Exactly. And and and and so you I I see both. I I I see both. I see your your typical cancers where a patient has been struggling with with stage four breast cancer, and they've been struggling for years. They've been struggling for years, but you know, there's they go to various chemotherapies and immunotherapies, and they're effective for a while, and then at some point, you know, they're not effective anymore. They get a bit of progression of disease, but but they've had stage four for 4 5 years, and they're still they're still battling it. Uh and then you have, you know, a similar situation where a stage four breast cancer patient will come in, you know, this cancer's growing extremely rapidly. Nothing seems to work. Anything that the oncologist tried, nothing seems to be working, and then they pass away after a few months. And so both of these are going on at the same time. And it is it is it is confusing. Um I think if if if you're not open to the idea that something has changed in the last few years um where we might be seeing a brand new pathophysiology, whatever the reason behind it may be, if you're not open to the idea that something has drastically changed in the last few years where you have this subset of of cancers that are behaving completely differently, then I think you will be caught If you're If you're in medicine and you're not open to to this, um I think you'll be completely caught off guard. Which seems to be happening on a huge scale, I I think it has to be said at the moment. Uh now, what sort of If If we If we use this term reluctantly use this term, turbo cancer, what sort of primary sites are we seeing? Where are these cancers originating? And is there a typical sort of metastatic pattern? So, for example, in the colon, you would expect it to go to the liver. Um if the prostate, you might expect it to go to the bone. So, for for first of all, um what sort of primary sites are we seeing with with what we could call turbo cancers? There have been articles published. Uh I believe there was one published by Memorial Sloan Kettering uh Cancer Center in the United States that talked about a a wide variety of cancers uh that uh sort of exploded recently and are affecting young people. So, it's not one type of cancer, one or two types of cancer. I'm seeing an explosion of lymphomas, uh brain cancers that are even more aggressive than than what we were used to uh in the past. Breast cancers Uh the big ones are breast and colon. Breast and colon, and I can tell you uh in fact how the mainstream medicine and oncology are reacting to this explosion of of breast cancers and colon cancers in a much younger cohort. And so, I do believe that this new pathophysiology affects all ages, but when you see it in a younger cohort, people in their 20s and 30s, that's when you say, "Wait a minute, something's really really wrong here." This is not a cohort that should be presenting with stage four breast cancers or colon cancers. And so far, the response uh of of mainstream oncology has been to lower the screening age. So, we've seen this in the United States, and we've seen this in Canada, and I don't know about the UK, to be honest. But uh the screening age for breast cancer has already been lowered from 50 to 40. Not as far as I'm aware in the UK, but it's interesting that's happening in the in the States and Canada. That Yeah, that has already happened. Uh the screening age has been lowered for breast cancer from 50 to 40 for for mammography. And now there's there's significant debate going on about uh decreasing the screening age for colon cancer. Uh and then the the the debate is, well, what age are are we lowering it to? Are we lowering it from 50 to 40 or even to 30, you know, to to to to have the Yeah, it's still 60 still 60 in the UK for um fecal occult blood screening. And and and so And again, this doesn't get a lot of uh attention or it doesn't get a lot of a lot of, you know, media attention because I think the cancer that centers themselves can't make, you know, they don't know what to make of this situation with these turbo cancers. But And so, they talk about lowering the screening age, but we should be finding out what the pathophysiology is behind these We should be looking at these cases specifically. We should be analyzing them. I mean, pathology is the specialty, you know, that that could look at these tumors in detail, analyze them, and see what is different about these tumors um that is causing such a rapid progression and such poor prognosis. Well, that's why we have pathologists. That's why they're useful people to have to do pathology. So, it's it's fairly obvious. So, I mean, I I take your point there entirely. So, 72-year-old woman gets turbo cancer of the breast. Can breast cancer is common at that age anyway. 22-year-old woman, it kind of stands out. It's more of an obvious outlier. But it's you believe it's occurring at all ages. I do see it in all in all ages, exactly. And and you're absolutely right. When it happens in someone who's in their, you know, 60s, 70s, 80s, you don't pay as much attention to it. And you say, "Well, you know, cancer is much more common in these age groups." And it doesn't catch it doesn't catch your attention. It doesn't stand out. And yet when you see a a 20-year-old, and and I've seen I've seen women as young as 18, 19 presenting with stage four breast cancer with no family history and no genetic markers to go on. And if that isn't a red flag or an alarm bell for the medical community and for oncologists, I don't know what is. I mean, that that that that is that is unheard of unless you're in a post-to-Russia situation. Well, I mean, it's just unheard of, isn't it? It just Absolutely. just doesn't happen. Absolutely. Yeah. Now, I want to think about temporal correlations. You started noticing this early 2022. Um so, what what what possible uh changes could there have been in the environment in the years before that? And and and what do you suspect the lag period might be? So, for example, we had we had COVID in uh 2020, we had COVID vaccines in 2021. Um if we postulate that this is a post-COVID, post-vaccine event, do you think that one or two years is a significant lead time for the pathological changes induced potentially by COVID infection or by vaccination? Uh is that enough for that to transpose into the overt pathologies that you're seeing? Well, I think this is where this is where I think the the discussion gets quite heated because um you will have people saying, "Well, you know, if someone develops an extremely aggressive cancer, maybe they had a COVID infection a few months before. May maybe they had Maybe they had a vaccination." And you will have people saying, "Well, well, there's that's not enough time, you know, for for an aggressive colon cancer to arise, you know, a colon cancer takes many years to develop um or even a breast cancer." And and yet I am I am I am seeing some of these temporal correlations in some cases, but in some cases, you know, this cancer will arise years later. And and and so, there's not there's not a clear picture of of a temporal uh correlation. Uh but, you know, you bring up the point, well, what has what has changed in the last few years uh that could be contributing to this, you know, to to this dramatic rise uh and this potentially new pathophysiology. And I I and I really think, you know, you've got these two two main things that have happened in the last um four or five years is we have this COVID virus, this somewhat somewhat novel virus. Um and and we had a pandemic with with multiple waves of infections. Uh you know, this was a this is not a one-time thing where you could you could say, "Well, you know, we had we had one wave of uh COVID-19. We've had multiple waves, unfortunately. And we've had different variants, you know, we've had Delta variant, you know, the various Omicron variants. And then then also, we've had we've had the the COVID-19 vaccines and different types as well, you know, we had the DNA-based vaccines, we had the mRNA-based vaccines. And and so, these are things that that are different uh that that have affected a large segment of the population in one way or another uh in the last four years, let's say. And so, I think it's it's it's it's worth looking at looking at those things. Um but but, you know, it it seems to be somewhat of a of a taboo subject, particularly because there's this um you know, there's this overall desire of people to just move on. People want to move on from the COVID pandemic um and and and they don't want to talk about they don't want to talk about what's happened in the last few years. But I've really I really noticed this phenomenon in 2022, in the summer of 2022, but I could trace back some of these extremely aggressive cancers to 2021 um as well. And when some of some of my colleagues were being diagnosed with these extremely aggressive cancers, these turbo cancers, in 2021, and uh and really no one realized that there was anything different about these cancers, and they would die six months later, and, you know, people would say, "Well, that's unfortunate. You had bad luck." Uh it's Okay, well, you could have bad luck in a few cases, but when it's happening when it when you have thousands of cases of bad luck, that's when science has to come in. That's when you have to investigate. And you have to investigate with an open mind. You have to look at all the possibilities. You know, could could there be something from a COVID infection that might be contributing? It's very possible. Could it be something from the COVID vaccine? That's also very possible as well. We have to approach this with with an open mind. And look at all and look at those possibilities. Um and and yet those of us who are raising the concerns, raising the questions, you know, we get attacked, we get censored. I was censored for about a year off the Twitter platform. Um I only started my Substack, where I published a lot of articles uh talking about this phenomenon. Um I started my Substack in early 2023 because I wasn't being allowed back on the Twitter platform. I thought I would never get my Twitter account back. Unfortunately, Elon Musk bought the entire platform for $44 billion and brought uh a number of us, you know, physicians back, like Dr. Robert Malone, Dr. Peter McCullough, Dr. Pierre Kory, and and Dr. Ryan Cole, and so on. Donald Donald Trump. Exactly. So, I'm somebody could be mentioned. I I you know, I I feel blessed and fortunate to to to have my voice back because in 2022, when I was raising these concerns, I was writing letters to the Canadian Medical Association. I was being ignored. I didn't have a social media platform. So, I was effectively censored during a time when when I was trying to raise concerns about turbo cancer, about this new pathophysiology that was affecting people, you know, these stage four cancers that no one can quite explain why they behave the way they behave. I didn't have a platform. I was completely censored at the time. You were being censored at the time we most needed people with your expertise and your background. It really is quite paradoxical and bizarre. My my my simplified way of looking at this, if there is a new pathophysiology here, then it's not unreasonable to say that there could be an accelerated oncogenesis, you know, an accelerated development of cancer. I mean, you know, very often with cancer, we think about a long progression. There might be changes in tissue, so-called metaplasia before the malignant change. There might be multi-hit ideas. If we're dealing with a If we're dealing with what we might call a complete carcinogen, an initiator and a promoter, that can do both things really quite quickly. It's not ludicrous to me at all that someone could have no pathophysiological changes, no anatomical changes, be exposed to an initiator and promoter of cancer and develop clinical pathology within a year. I find that quite quite credible but based on my limited experience and understanding of the pathology. Absolutely. So so that that's definitely I think a component of this. Another component that I think is is relevant is the state of a person's immune system. And so you know, when we have something that impacts a person's immune system dramatically. Now we see this We see this in AIDS and HIV Patients who have HIV infections, they develop some very aggressive cancers because their immune system is compromised. And I think again we've we've we've been in a situation in the last 4 years where people's immune systems have been compromised whether they were compromised by a virus or a vaccine. I think we we see a lot of people who are struggling. People who are struggling with infections. They get repeated infections. They get repeated COVID infections or they may get repeated influenza infections. I have I have seen an explosion of of strep. I have seen an explosion of sepsis and young healthy people dying of these things. Young healthy people dying of influenza. Young healthy people dying of of strep throat and and septicemia and septic shock. And and and so I do believe that a compromised immune system you know, may may play a role in in in some of these cases. And and we don't have a good way of measuring a compromised immune system. Someone whose immune system has been damaged in some way. We don't have a great way of measuring it. You know, we measure the CD8 and CD4 cells in in AIDS patients. The white blood cell profile. Exactly. But but we don't have a good way of measuring you know, if someone's immune system has been compromised in some way. And so I think that also also plays a factor in in some of these cases. I suspect personally that that the coronavirus was not the cause of these turbo cancers because we've been exposed to different coronaviruses for a long time. Okay, this one was quite novel. It had some unusual features that are difficult to explain. There's no obvious predecessor in the natural world for this particular one. But at the end of the day, it's still a coronavirus. And the small components of that, the bits that the immune system recognizes, what we call the epitopes of that, a lot of those would already be somewhat familiar to the immune system. So I suspect we're looking at something other than the coronavirus that occurred in 2021. That that That that that seems to be the Occam's razor, if you like. I think so. And and and I think and and and the other part of it is is also looking at you know, populations that that are affected. I see you know, university students, college students who've been impacted by turbo cancers. I've seen certain professions, doctors, nurses, teachers, police officers, firefighters, military. And and so you know, you you have to ask the question, well, why? Why are we seeing the this in certain groups? You know, there there were there were man mandates in in some of these groups, especially in 2021. You know, we we had we had mandates that affected a lot of these people, a lot of young people or or some of these professions in health care for example. You We had health care workers who who who faced mandates as well. And and the entire profession faced it. So I think it it's definitely something that that we have to look at and and and really consider possibility where where there were mandates. You know, is that something that contributed to this phenomenon? And and to to understand that, we really need full data release and release of primary source data that in the UK at least, we simply don't have access to. So I'm optimistic that in the United States, this data can be made available. Now I've talked to people who know about this and they assure me categorically that this data can be completely anonymized and yet is amenable to very rigorous quantitative analysis. So and when we're dealing we're dealing with millions of people. Yes, we have that opportunity in the United States. I I And you know, and I and I don't see I don't see this opportunity in Canada for example. I I know that the government There's been no transparency from whether it is the federal governments or the provincial governments that are responsible for health care. If anything, you know, I had actually started my Substack with a series on of articles on how the government was deleting data, uh crucial data from the government websites where where people could could no longer make an informed decision in terms of their own personal health because the government was either hiding or deleting data outright. So I think you know, there's a very unique opportunity now in the United States with RFK Jr. being confirmed, which I believe he will be confirmed and I think he's expressed a strong desire to to look into this and and really a strong desire for transparency in science. And that's what we need. We need transparency in science to do proper science. Across the whole field, this is just one particular example really. But let's hope there's been no data accidentally deleted in the United States in the past in the past few weeks. Let's hope that is is the case. Dr. Marcus, that that was absolutely fascinating. I've let that run a while to to unpack that. I think that's really well worth doing. Absolutely important to to document that. But we do want to go on and talk about novel approaches to treatment, to treating cancers and particularly I want to talk about repurposed drugs. Drugs with a known safety profile. Very often very safe. Drugs that have been used for decades. Drugs that have been used on without exaggeration in the case of ivermectin, billions of people. Drugs which are very cheap. Drugs which can be manufactured literally by the ton. Relatively cheap because they're often fairly simple molecules. And drugs which may well be highly efficacious against the disease they were originally designed for or developed for or isolated for. But then out of lucky accidents really, serendipitously, amenable to treating other conditions. And we have we have a lot of precedent for this. So aspirin for example from willow bark was initially used for treating fevers. Now we realize it reduces platelet viscosity and help can prevent blood clotting and various other anti-inflammatory things. So this is not unique. This has happened quite a few times. I mean There was a drug introduced for for treating myocardial ischemia for angina and it was later used for treating impotence as a surprise as a surprise finding. So this isn't this isn't unusual. But what first arose your interest in repurposed drugs I I've started getting into repurposed drugs in when I started my Substack in early 2023 and and I I really wanted to do a a deep dive into early treatments for COVID-19. Uh treatments such as ivermectin, hydroxychloroquine. And and I wanted to know for myself, you know, you know, were these were these effective in COVID-19? Were they not? What was the science? What was What was the research telling us? And and and of course, you know, when you whenever you want to do a deep dive into a topic like that, you have to read the papers. And so I went and I read paper after paper and I and I read dozens and dozens of paper and I was particularly fascinated by ivermectin. Why? Why this antiparasitic drug was the focus of so much attention in the United States to the point where the FDA is telling people not to take it. And yet we have, you know, as you as you mentioned, we we have decades of of prescriptions given of ivermectin. I think 4 billion doses at this point. You know, excellent safety record around the world. Unquestionable safety record established around the world. And yet why was why was this a focus focus of such, you know, controversy and attention? And and as I dove into that research into ivermectin, hydroxychloroquine and so on, I discovered a large body of literature specifically with ivermectin and cancer. And ivermectin in the use of cancer. And I found that very odd and very unusual. And I and I of course, you know, I was naturally curious, well, why why would ivermectin work in cancer? How does it work in cancer? And so Um, you know, I I did a a PubMed search and and I think something like over 300 peer-reviewed papers come out. And and and you know, um, in regards to Ivermectin and cancer. Now, it's all preclinical research. And then you start looking at well, where are the human trials? You know, I want to see the human trials as well. But you see preclinical research where they, you know, where they where they're studying the the the cancer cell lines or they're studying it in in mice or rats. Um, but this preclinical body of research on Ivermectin and cancer is so impressive. It's not one or two papers, you know, some a group of researchers tinkering in the lab. You know, these are dozens and dozens of paper, you know, extensive research done uh looking at the various mechanisms of how Ivermectin might act in cancer uh and what cancers Ivermectin impact. And it really seems to be a broad anti-cancer agent uh that that can be used in in in in a variety of cancers, anything from blood cancers to to solid tumors as well. And um it's it's just uh such a fascinating uh it's just such a fascinating molecule because when you look at the mechanisms of action. Now, this is an antiparasitic a very successful antiparasitic. And yet it has different mechanisms of action in cancer. It targets cancer stem cells, for example. Something that I find really fascinating where it's it's able to uh attack these cancer stem cells that don't necessarily proliferate rapidly. But you know, these are cells that could cause problems in the future, that could cause metastases in the future, that could cause cancer recurrence in the future. And I and I believe that when you have standard chemotherapy, standard chemotherapy will kill the rapidly dividing cells. Um, just based on the nature of of of the rapid proliferation, but they will not kill slowly dividing cells often uh and they the chemotherapy may not kill cancer stem cells. And so you often hear chemo being referred to as palliative instead of curative. The intent is palliative to, you know, the the they will tell you you cannot cure stage four uh pancreatic cancer, for example. You cannot cure stage four ovarian cancer. We can buy you time with chemotherapy, which will kill most of the cancer and and shrink a lot of the tumors and so on, but it will not kill the cancer stem cells and it will not kill cancer cells that are resistant to that chemo because cancer cells can develop a resistance to certain chemotherapy. They might have, you know, these pumps that just pump the chemotherapy right out of the cell. And so in in some cases like ovarian cancer specifically, these tumors can develop a resistance to chemotherapy. That's why the oncologist has to change the chemo and go to the next agent and so on. Well, Ivermectin can kill cancer stem cells that chemo can't. Ivermectin can also reverse what's called multi-drug resistance in cancer cells. And so it can actually sensitize cancer cells to chemotherapy. It's also a radio sensitizer. It can it can sensitize cancer cells to radiation therapy, for example, as well. Now, it has other actions. It can inhibit the tumor's ability to form new blood vessels. So it can inhibit angiogenesis. Uh Ivermectin also inhibits certain enzymes called the matrix metalloproteinases, which are enzymes that detach cancer cells from the tumor and allow it to metastasize and spread to other parts of the body through the bloodstream. And so Ivermectin will actually inhibit those enzymes um so that it inhibits metastasis of the tumor, for example. So when you look at it, there's a dozen different mechanisms by which Ivermectin acts acts on the molecular level on cancers. And so then you ask the question, why where are the human trials? Because that's what it ultimately comes down to. Yes, preclinical research is nice. We have hundreds of papers on Ivermectin and cancer. Where are the human trials? And there aren't any. Uh there are case reports. There's a case series on three patients with leukemia. Uh I believe two of them were able to achieve some form of remission uh with Ivermectin. Um, and that's it. And we don't have any randomized control trials. We don't have any large studies in humans. And then you find out well, Ivermectin's been off patent since the 1990s. I believe Merck held the patent uh the patent expired in '96, I believe. And so it's a cheap drug that's off patent. And then you realize, okay, well, there's no money to be made in in studying Ivermectin in humans for cancer. And where there's no money to be made in oncology, tragically, there the research just doesn't follow. Yeah. And so and so you see this this focus and this this happens to a lot of repurposed drugs. And so for example, you look at something like another antiparasitic uh fenbendazole or mebendazole. Now, this is a different family of antiparasitics than Ivermectin. Fenbendazole was actually interestingly discovered by a terminal cancer patient uh from Oklahoma, uh Joe Tippens. And Joe Tippens had stage four small cell lung cancer, which is one of the most aggressive cancers uh known. And he had stage four small cell lung cancer diagnosis, you know, terminal diagnosis. And I I believe he was he was put on a trial of Keytruda at the time. And uh friend Is that a regular cancer drug? It is a regular cancer drug, yeah. Um, and and uh sort of what they call an immune checkpoint inhibitor. Yeah. And and um so he was put on Keytruda and and and he tells the story later on that everybody on that trial died. He was the only one who survived. Um, and he tells the story of of of how he had a friend who was a veterinarian who said, "Look, we there's this parasitic drug, this dog dewormer called fenbendazole. Uh it's been accidentally found to have anti-cancer properties in mice. It's cheap. It's it's it's safe to take. Why don't you why don't you try it?" And the story goes that, you know, he went he tried this this dog dewormer, dog medicine, I guess you could say. And he cured his stage four small cell lung cancer, which is completely unheard of. I think his his he was given a survival of less than 1%, you know, sort of a five-year survival of less than 1%. And he's still here to this day, seven years later, he's cancer-free with a stage four small cell cancer diagnosis. And so he at the time he would actually go on news news uh shows and talk about his experience of trying fenbendazole, which was not FDA approved for use in humans. Uh and how it cured his his uh or or he believed that it cured his stage four cancer. Um and and then, you know, I look into that research, that body of research. See, again, there's a ton of preclinical research on fenbendazole. And there's now been cases published by Stanford University Medical Center of three patients who cured their stage four cancer with fenbendazole. And the Stanford group looked into it, analyzed it, you know, monitored these patients. These patients had all failed three or four lines of chemotherapy. They were terminal. They took fenbendazole and they are now cancer-free. And the Stanford group published this. Now, the Stanford group itself, they were not allowed the researchers were not allowed to recommend that drug, fenbendazole, because it's not FDA approved. But they were at least I This is how This is what I love about science is that they saw something fascinating. They saw something that they thought other doctors and scientists should know about and they published it. And they published this case series. You had actually talked about this the you had you had you had talked about this paper Yeah. from 2021, this this series of of three people who'd cured their cancer with fenbendazole. And so there is an FDA approved version of fenbendazole called mebendazole. Uh there is it's structurally almost identical. There's one atom difference between fenbendazole and mebendazole. Mebendazole has been approved by the FDA as an antiparasitic drug for use in children and adults. And so it it has an an incredible safety profile, very safe to use. And mebendazole actually has a dozen uh clinical trials uh in which it's being looked at as a as a cancer agent, as a repurposed drug for cancer. And so I think because of its status as an FDA approved drug, there was much more willingness in the oncology community to do trials with it. And so there are trials in adults looking at colon cancer, various prostate cancer. And there's also trials in children looking at brain cancers with mebendazole. Um, and and and again, this is an antiparasitic drug that has a dozen mechanisms of action. One of the fascinating mechanisms of action in cancer is that it blocks glucose transporters on cancer cells. And so it it sort of starves the cancer cell from being able to use glucose as a fuel source. Specifically in cancer cells and not on normal cells. Yeah, exactly. Glucose transporting in cancer cells. That's amazing. So there must be something biochemically different about the glucose transporter in cancer cells compared to ordinary cells that it's able to specifically target. Exactly. And what's fascinating about these repurposed drugs is they are very specific to cancer cells. They are able somehow identify a cancer cell from from a normal cell. And and and this has been studied in Ivermectin as well is is Ivermectin is actually able to identify lymphoma cells and act on them. And it's able to also identify normal cells and it doesn't have that same effect on the normal cells. Um It's what we call a magic bullet. It It It is It is absolutely fascinating. I encourage anyone look you know, look into the the preclinical research. It is It is absolutely fascinating. And And the the the the the mechanisms that we're talking about here that you're talking about are based on known biochemical pathways. This is not something new. This is This is understood biochemistry. And this interfere These These drugs interfere in a particular biochemical mechanism in a in a known biochemical way. This is not speculation. I mean, biochemistry is a Biochemistry is basically a hard science. I mean, medicine is a bit soft around the edges, but but biochemistry is a hard science. It's It's bench chemistry. And you can't really argue with that. And the fact that it's got multiple mechanisms of action on multiple biochemical pathways. And that's true for Ivermectin and the mebendazole and fendbendazole group. That's right. It's just It's just absolutely incredible that these natural molecules seem to have these multiple modalities of action. And yet and yet we're staring the gift horse in the mouth. Exactly. And and the research is very very solid. The research on the mechanisms, the preclinical research is very solid. This is not one or two papers. This has been you know, replicated. This is hundreds hundreds of papers for these antiparasitic drugs. So So this is not you know, this is not a conspiracy theory. This is not This is not fringe medicine. You know, this is actually science. This is This is hard as it gets. This is hard science. Um and and I and I love you know, I I'm always fascinated by by by preclinical research because that is what we That is what we stand on. That is what the rest of medicine stands on is is the preclinical research. That's what we rely on as as physicians. And that's what gives us the plausible mechanisms of action. Because if you can't give a plausible mechanism of action, well, you're not fulfilling an essential Bradford Hill criteria apart from anything else. But you know, if you can say, "Well, this is the way it's working." then that that's what takes you into science away from mumbo jumbo. Because we've got we've got existing science and this this pharmacodynamic effect, the way this drug is working is dovetailing with what we already know with multiple points of consistency with what is already known. Exactly. And and so I found myself in a situation where I was writing articles on on on Substack and I was writing articles about turbo cancer, potential mechanisms. You know, we talked about this brand new pathophysiology of turbo cancers. And so I have I have a paper that I co-authored on the IgG4 shift that could be one of the potential causes of turbo cancer where we see someone who's had let's say multiple vaccines, they they end up with an an immune immune system shift where they start producing different types of antibodies. And instead of producing IgG1 and 3, they start producing IgG4, which is an antibody that creates tolerance to something like the spike protein, but it also starts to tolerate cancer. And and so I've I've I've been you know, I've been involved in some of this research in trying to figure out the mechanisms, but now I'm shifting towards I'm shifting towards treatment and I'm shifting towards looking at well, can we help patients with turbo cancer? How can we help them? And certainly you know, I I encourage everyone to pursue all the options in mainstream oncology. You know, pursue all the options whether it's chemotherapy, radiation therapy, immunotherapy. You know, you have to pursue all those options. You have to have those discussions with your oncologist, but what else can you do? What if you're out of options? What What other options are there? And I think this area of repurposed drugs, you know, is something that that we can try as clinicians. Something that we can look into, advise patients on. And a lot of patients themselves are you know, they look at look at some of these repurposed drugs and and they start taking them. They they start you know, they start taking them themselves. So as I was writing about as I was writing about Ivermectin and fendbendazole and mebendazole in cancer, I had patients who actually started taking them. And then they would come back to me 6 months later and say, "Dr. Makius, you know, I read your articles and I I took these on my own. Um you know, there was no patient you know, doctor relationship or anything like that. They took them on their own and they come back to me and they say, "My cancers are shrinking. My oncologist is shocked. My oncologist told me I shouldn't be alive anymore and yet I'm here. My cancer stable." And so I keep I kept getting story after story. You know, I want a two stories. You say, "That's fantastic. I'm you know, I'm I'm really happy for you. You know, that's really terrific. But when you get a dozen or two dozen stories like that and that's what happened to me as I started having so many patients coming back to me that I thought, you know, there's something here where I could actually be helping patients with. I could be helping them with Ivermectin. I could tell them about the side effects, potential side effects. I could guide them in dosing for example. How do you dose these things? Right? How do you find the appropriate dose for the appropriate condition? And so this is what I've been working on for the last 2 years. I did start a cancer clinic or or sort of a cancer coaching or health coaching program with repurposed drugs where you know, I I have clients, cancer clients that come to me. We discuss the research. We look at the research. And we talk about repurposed drugs and what repurposed drugs they might use and want to try themselves. And and so this is where I've been trying to go from just identifying the problem saying, "Look, we've got this explosion of cancers, these turbo cancers, aggressive cancers." to actually helping patients and give them some options that they can use. And I've had some fascinating results. Patients I've had you know, a number of stage four pancreatic cancer patients who've been now declared cancer-free, cholangiocarcinoma patients, ovarian cancer patients whose tumors are shrinking even though they failed multiple lines of chemotherapy. And I mean, these are cancers that were absolute death sentences. Exactly. Exactly. And and and another feature I wanted to just mention is that these repurposed drugs, when you look at the preclinical research, they have synergy with chemotherapy. They have synergy with immunotherapy and even radiation therapy in some cases. I was I was I was amazed at the radiotherapy one that you can actually sensitize a drug to sensitize a cell to radio-induced cell death is just incredible. It's just brilliant. It's It's fascinating you know, because because when you look at some of these mechanisms, some of them are known and some of them are still unknown. And you see you see all these all these all these all these biochemical pathways that Ivermectin acts on and all these pathways where you know, it it it changes the expression of certain proteins and then suddenly you you stimulate apoptosis of of the cancer cells. The cell just goes pop and dies. Exactly. The programmed cell death. And and so a lot of these pathways that Ivermectin, fendbendazole, mebendazole act on are pro-apoptotic pathways where you are you're bringing that cancer cell towards this programmed cell death. And you're also you know, this idea of of of being able to remove drug resistance. A cancer cell that has developed drug resistance to me is absolutely fascinating. Yeah, how can you possibly reverse that? That's just It's just It means wonderful, but it's uh It's biochemistry well beyond my level of understanding. That's for sure. It really is. It's pure biochemistry and it it's Sometimes even I have a hard time understanding some of these pathways, you know, but I certainly do. But it really you know, the fact that it can affect expression of certain proteins and so on. And it's just It's just It's incredible. And and so it I think repurposed drugs, I think there's there's a big future in repurposed drugs. And and I think repurposed drugs can give patients hope in situations that are very dire. And and and where in the past would be considered hopeless. I'm I'm We're dealing with drugs very safe, very limited side effect profile. Can nearly always be given with all the regular what you might call standard cancer treatments. Exactly. And and and for people who've exhausted the standard cancer treatments, stage four pancreatic cancer for example, um What What Why not Why not try something that's not going to do you any harm? You know, if you want to change the brand of whiskey that you drink in the last days of your life, then then fine. Fine. Try it. You know, but but something like this that is potentially can potentially improve the condition is is is is is just incredible. And I am optimistic again in in the states that that the right to try is going to be reintroduced. That people who are terminal can basically try whatever they want. And I agree with that. Um One of the things I always used to teach my students was in in acute care, some sometimes patients are going to die. And you you always have to be in a position where you can walk into the relatives. You can tell them about this tragic death. And you can say we tried absolutely everything at our disposal. Now, that's not always true, tragically. But we should always work to that situation. We tried absolutely everything we've got in 2025. Nothing else we could have done. And so many people are dying now, and that is not That cannot be said. You're absolutely right. I I I I I I I'm trying not to get cross now, but um it's it's not acceptable. You're absolutely right in in that the state of oncology in in let's say in North America, for example, cuz I'm very familiar with state of oncology in North America. But I do have patients in the UK, in Ireland, in Australia. I have a global I have a global clientele. And so I do get insight into how oncology is practiced elsewhere. But the state of oncology in North America is that oncologists have these rigid guidelines and protocols that they follow. And and same in the UK. Yeah. And and you have you know your first-line chemo, second-line chemo, maybe you can you can throw in some immunotherapy in there, of course radiation where appropriate and so on. But but they go step-by-step through these rigid guidelines and they come to the end and they tell the patient, "Sorry, there's nothing else we can do for you." But but that's not true. That's not true. There there is a whole body There's a whole area of of let's say repurposed drugs that you you don't even know about, that you you don't even tell your patient about. And and we run into the situation I have patients from Mayo Clinic. I have patients from Johns Hopkins, Memorial Sloan Kettering, MD Anderson, you know, Dana-Farber. These are Leading centers. leading cancer centers in the United States. And the patients come to me and they say, "You know, my doctor's saying, you know, I'm out of options or I'm running out of options or they have nothing else to offer me." And it's not true. There is something that they can offer, but I I always have this discussion with with patients that, you know, your your oncologist probably is not allowed to offer you anything else or to suggest anything else because there may be retaliation. There may you know, their their licenses may be targeted, their jobs may be targeted. And they the oncologist It's true, the oncologists don't have the freedom to go off-script, as I would say, or go outside of the guidelines. True, but there's still big ethical questions there. Oh, absolutely. If I know If I know something that might save someone's life and I don't tell them, that's got big ethical questions. But I want to I want to go into a completely academic discussion now and look at doses of these drugs. If we start off with with Let's start off with ivermectin. What what sort of doses might we be thinking about for what's Maybe just give some examples of conditions that you've where you've got personal experience. The starting dose that I look at with ivermectin is 1 mg per kilogram per day. Quite high. And it is a little bit high. I always say this is about five about five times the dose that you would use for COVID-19 or or a parasite infection, for example. Is this Is this this with What level of cancer is this with, sorry? This would be with with with most cancers, sort of intermediate to high-grade cancers. Now, for low-grade cancers, you could certainly start lower at at a half a half a milligram per kilogram per day. And so for a 60-kg person, a typical starting dose would be about 60 mg of ivermectin. But for low-grade something like CLL, chronic lymphocytic leukemia, that's been, you know, simmering for many years or maybe maybe multiple myeloma, I start lower at at half a milligram per kilogram. So that'll be something like 30 mg of ivermectin a day. And that's more in the range of a dose for a viral infection or a parasitic infection. And is that 6 days a week? That's 7 days a week. 7 days a week. For how many weeks? Well, so I suggest patients try ivermectin for cancer for 3 months. And I'll tell you the reasoning behind that. And then with a reassessment of some kind, looking at blood work, cancer markers, for example, or looking at follow-up imaging. The reason why I say 3 months is because from my experience, I have seen a response to ivermectin on cancer markers as early as 3 4 weeks. So this is markers like prostate-specific antigen, PSA. We could see a drop in the PSA. We could see a drop in CEA or CA 125 or these other more specialized markers for breast cancer, for example, like These are basically chemicals given off by the cancer cells. Exactly. And you can see And you can you can see those start to drop. Now, they are they're not perfect tests, but they are surrogates for cancer activity the level of cancer activity or the level of tumor burden. How much cancer how much active cancer is there that where these cancer cells are producing these markers. You could see those markers start to drop. And you can actually start to see the activity of the tumors start to drop on a on a PET scan, a positron emission tomography scan, in about a month. But it takes a little bit longer to start seeing tumors physically shrink, lymph nodes shrink, you know, primary tumors shrink. That takes about 2 to 3 months to see that to start seeing that on imaging like MRI, PET CT, or CT. So you want to give it a good 3 months to see if if you've got If you have a response, you could you could you could monitor it on the blood markers within a month or so you could start seeing if there is a response. And then after 2 3 months, you could actually start seeing responses on imaging. And I'll tell you the most dramatic results that I've seen. And I get attacked from both sides. I get attacked from conventional oncology on this. And I I get attacked from the sort of health freedom movement on this. But the best results I've seen in my patients are patients who are doing a combination of chemotherapy and ivermectin. And then combine it with either a fenbendazole or mebendazole as well. And when you do the combination treatment, there's a certain synergy. And and that synergy is documented in preclinical research where you get a lot more cancer cell killing with the combination than with any of those agents by themselves. Well, it's consistent with what you were saying before about the sensitization of the malignant cells. Exactly. It does It does make sense. And there's precedent for this again. Things like low-dose naltrexone can can sensitize people, too. Exactly. Conventional chemotherapeutic agents. So those sort of doses of ivermectin We're talking about ivermectin on its own or with traditional cancer treatments. That's right. Yeah. So so that's kind of almost like a monotherapy, isn't it? With ivermectin. Well, in the sense the fact that you Monotherapy in terms of of of the the repurposed therapy. You can be giving it with a range of other traditional oncologist-prescribed drugs. Yeah. And and and so, you know, when you are giving it with with chemotherapy, it's sort of an adjunct in the sense that that you're sort of adding it into you're adding it into your chemotherapy regimen. And and patients will take the ivermectin throughout their chemotherapy regimen. I'll tell you another fascinating story of a physician's assistant I have in the United States who had already done four cycles of of of chemotherapy and started taking ivermectin. And um you know, I had suggested some dosing for him and so on. And the first thing he told me was, "With my fifth cycle, I had no chemo symptoms." And he was playing golf the next day. And and he said, "Usually the chemo will knock me out for 3 days. I can't do anything for 3 days. And you know, I started taking ivermectin and then I all my chemo chemo symptoms were gone." And he was playing golf the next day. And he couldn't believe it. And the same thing happened the next cycle and then the next cycle after that. And you know, and then his markers were were dropping as well. And and he was having a fantastic response. So if if you If If you only took it to to reduce the side effects, that would have been worthwhile. Exactly. And so the ivermectin in many cases actually is able to reduce the side effects of the chemotherapy. And I think part of that may be because ivermectin does seem to have a very powerful anti-inflammatory component as well. And so I have I have other patients who don't who don't have cancer, who I've I've I've guided with ivermectin, for example, patients with rheumatoid arthritis, whose symptoms improve dramatically. Patients with fibromyalgia, patients with Lyme disease, for example. I've seen dramatic improvements in these situations where patients been suffering with with this with a chronic inflammatory condition for many many years. And they they get, you know, rapid relief with ivermectin within a few weeks of taking ivermectin. And this would be again at at a lower dose, about a half a milligram per kilogram for, you know, these inflammatory conditions. So I've seen dramatic response for inflammation. But like you said, even if it was just for, you know, improving the the patient's quality of life during chemotherapy, it would be worthwhile because the side effect profile of ivermectin is so favorable. Quite incredible. This the anti- I wasn't aware of that such a strong anti-inflammatory effect, I must say. Now the the the side effects with these sort of higher doses, um are you seeing side effects? What side effects do you see? I'm seeing some transient side effects. When If you've never taken ivermectin before and you you start at 1 mg per kilogram per day, for a 60-kg person, that's 60 mg of ivermectin, you may have some transient visual symptoms. The The visual symptoms have been described as uh uh seeing colors a little bit more vividly or seeing a little bit of stars. Uh it's almost as if when you get up too quickly and you have that that effect that you might you might faint. Uh so there's been visual symptoms described. Now these are temporary. Uh they may last anywhere from from a few minutes to a few hours and they do go away with time. You know, after 1 or 2 weeks of ivermectin use, the body seems to get used to it and they go away. E- E- even maintaining the same dose of ivermectin. Exactly. Right. A- A- A- A- And so there's there's reports I mean there's reports in the literature um of of ivermectin being used at 1 mg per kilogram for up to a year with with a no side effects and there's been no long-term effects uh reported with ivermectin use either. Now if And no no no no no no no no no no no no no no no non-reversible neurological effects that you've ever come across. None. Now you could push the dose higher to 2 mg per kilograms per day, but you have to be cautious uh when you go to those higher doses. Now I've had I've had some successes going to the higher doses especially with very aggressive cancer pancreatic cancer for example. I had a patient who who who cleared his pancreatic cancer with a few months of ivermectin 2 mg per kilogram per day. Uh but there you can start to get uh especially in in more elderly patients, you might get some confusion, you might get some instability on the feet. Uh and so you have to be more careful going into the higher doses. Uh again, ivermectin has a half-life of 18 hours. So if if you run into some side effects, you stop, it's out of your system within 2 days. Um and again, no no long-term effects. But you have to be a little bit more careful with ivermectin if you want to push the the higher doses. I did hear I think it was on Joe Rogan. Um there was a doctor on on there um I forgot his name now. Anyway, um he said that someone got benefit with just from prostate cancer with just 12 mg of ivermectin a day for uh several weeks. Is that biochemically feasible or do you think that dose is too small to No, it is. And I And I I have seen I have seen some really uh impressive responses um to a low-dose ivermectin as well. So there is a wide range of dosing and it really does seem to vary from person to person. And it it really varies from from I I I would almost say I'll say cancer cell type to cancer cell type. Cuz I could have two prostate cancer patients and one will respond to 12 mg of ivermectin and the other one may not respond to 60 mg of ivermectin. And And so there's a wide range of dosing. That That's where this becomes a little bit tricky and I think where patients need some guidance uh in terms of dosing and response because the cancer cell killing is dose dependent. It is dose we need to learn of course. This is not established pharmacology, is it? Absolu- I think this is where we need we need those human trials. We need researchers to be supported in this kind of work. Uh and and regardless of the fact that there's no money to be made at the end of this, right? That there's no money to be made for some pharmaceutical company or shareholders of a pharmaceutical company, this is for patient benefit. Absolutely. And this is where you know where where a physician or a scientist is doing something for a patient's benefit rather than for financial interests or corporate interests. And we need support of this kind of research. I think repurposed drugs there's so much research that that so much good research that needs to be done. And so with this dosing of ivermectin, you know, there is a there's there's a wide range uh of effectiveness. And I have seen effectiveness as low as 12 mg. I can tell you if you're combining it with chemotherapy, you can get away with lower doses of ivermectin. Fantastic. Uh and you will see a dramatic response. And the way most of my patients are not telling their oncologists that they're taking ivermectin. And I always you know, I'm of the opinion you want to be honest with your doctor. You should be honest with your doctors. But if your doctor doesn't have your best interests at heart, uh then you run into this complicated So a lot of patients are not telling their doctor and the situation the data's not being collected really. That's true. If this is working, you know, the oncologists are going to be thinking they're a lot cleverer than the cleverer than they actually are. Exactly. And so what happens is the oncologist then has a genuinely shocked reaction Mhm. when they see an outcome of their chemotherapy regimen that they're not used to seeing. And And And And I've seen this even with radiation oncologists where tumors are shrinking after two or three radiation treatments and the radiation oncologist is is shocked. They're like, "Wow, you had an amazing response to just a couple of radiation treatments." Because they're not used to seeing that kind of response. They have no idea that there's synergy going on with ivermectin where the ivermectin sensitized the tumor and that's why the radiation is shrinking the tumors dramatically, but the radiation oncologist doesn't know that and the and the patient is too scared to tell them because most of the time when my patients have told their oncologist that they're taking ivermectin or fenbendazole or mebendazole, the oncologist has a very bad reaction to the point and this happens in the UK, this happens in Canada, this happens in Australia, to a lesser degree in the United States. The oncologist will actually threaten the patient that if they do something like this that they'll drop them as a patient. Which to me is very unethical. But this is what patients face. That's bully boy behavior to me. Bullying. It's bullying. Exactly. Yeah. And but this is This is what patients face. And And you know, I'll have patients tell me, "I made a mistake. I shouldn't have told my oncologist. You know, I wanted to be honest. I wanted to be open. And now they threatened me. They said, 'We'll kick you out of the trial. You know, we'll we'll we'll stop treating you.'" This doesn't happen as much in the United States. I find in the United States that culture i- i- it's not as it's the bullying behavior is not there. The The oncologists are more open. I had oncologists say, "You know, that's perfectly fine. You can take ivermectin with this regimen, no problem." But once you go go outside of the United States, especially in countries like Canada, UK, Australia, there's a lot more of this bullying behavior. And the oncologist idea that a doctor should threaten their A doctor should threaten their patient is just It's unethical. unconscionable. It's unethical. It's unprofessional. It shouldn't happen. But unfortunately, it does. It does, yeah. Uh so patients have learned that it's better not to tell their oncologist and their oncologist doesn't even want to know. So when they have a good response, my patients will tell me, "My My oncologist didn't ask any questions. Didn't ask if I was eating different, if I was doing anything different, didn't want to know, didn't care." Yeah, we have a name for this in England. It actually comes from Australia, but it's called curiosity deficit disorder. And uh it's quite a debilitating condition. Absolutely. And especially in in in oncology is to not have curiosity, to not Yeah, this this is what science and medicine's all about. Ooh, why's that happen? Ooh, what's going on there? Ooh, you know, it's Cuz imagine you know, as as an oncol- I mean, you know, you you could publish it as a you could publish it as an interesting case report. You know, or maybe even a case series. Uh why why not why not ask the questions? Um you know, there there was a situation uh a couple of case reports that have been published with with CBD oil cannabidiol um where where patients There was a couple of 80-year-old patients. They had They had re- lung cancer and they refused chemotherapy. They said, "Look, I'm 80 years old. I don't want chemotherapy." And And the oncologist said, "Okay, well, we're going we're going to continue monitoring you anyways." And then suddenly the lung lung lung cancer shrinking shrinking and it's gone a few months later. And of course, now that this These oncologists actually asked the question. They're like, "Okay, what are you doing? Yeah. We're not treating you. Why is Why is your cancer gone?" And the patient tells them, "Well, I've just been taking CBD oil a few drops a day, you know, under the tongue for the last few months." And they went and they published those case reports. That is what oncologists should be doing. They should be inquisitive. They should be asking the question. They should be willing to learn. And there's this just absolute absence of willingness to learn. Obtuse. Yeah. Mhm. Yeah. So mebendazole and fenbendazole both end in azole. So they're they're in the same group. Uh do they have similar doses? They do. Uh so it's a family of antiparasitics called benzimidazoles. Mhm. Two of them are FDA approved and that's mebendazole and albendazole. And so you will you will find albendazole is also uh available um and and some doctors are willing to even prescribe mebendazole and albendazole. And then fenbendazole is is sort of the almost like the stepchild or the you know, it's it's not FDA approved and yet it's in the same family with very similar almost identical mechanisms Almost identical molecule, yeah. of action. And so uh incredible family um extensively researched. And there are a number of I would say about a dozen clinical trials ongoing right now with mebendazole in cancer looking at pediatric cancers, looking at adult cancers. Um and so it it This is again, this is not fringe medicine. This is not fringe science. This is something that's being seriously looked at. Nothing published yet that I'm aware of though. Uh in terms of mebendazole, you're right. I I think there's there's some phase two phase two trials ongoing. Mhm. Um so it's Yeah, you're you're right. But um it is being looked at seriously. At least mebendazole But that's encouraging. A- A- And so that that is, you know, that is great. Now fen- fenbendazole gets attacked because it's a medicine commonly used you know, it's a dog medicine. It's a as they call it a dog dewormer. And yet it it's got an excellent safety profile just like mebendazole. I I can tell you having advised over a thousand patients on the use of ivermectin, fenbendazole, and mebendazole. Um there's there's this myth that uh the fenbendazole mebendazole are difficult on the liver that they can damage the liver and so on. Uh they can raise the the the liver function tests, liver enzymes. Indeed. And it's it's quite rare. It's very rare. Um I just don't see it. But if it did happen and you stopped the drugs or reduced them, the liver's got remarkable powers of regeneration, hasn't it? So Well, absolutely. So if if you do get elevated liver function tests and I see it in less than maybe less than 3% of patients Right. I see elevated liver function tests. You stop it for a few weeks and those liver function tests, if it was the fenbendazole or mebendazole, they go right back down to normal. This has been published in peer-reviewed literature as well that that there's this sort of transient you could almost call it an irritation of of the liver in the sense where you get this sort of transient spike in liver enzymes. You stop it for a few weeks and it comes right back down. And then you can start again. Exactly. And so and again excellent safety profile uh established. And um really just uh I've seen some incredible incredible responses and I combine the ivermectin with either a fenbendazole or mebendazole. I do a combination. It just seemed to be a synergistic effect there, isn't it? But can we look at the doses first of all? So if you treat I've been treating worms with mebendazole for probably about 40 years. 100 mg tablets. Um So so what what sort of doses of mebendazole and fenbendazole might you be using for for uh the various types of cancers? A typical dose I suggest is a thousand milligrams a day split in two doses. And that's the same whether it's mebendazole or fenbendazole. Exactly. So either a thousand of fenbendazole and and you know the the the Stanford uh case series that you had you had talked about um on another program, uh they had done a thousand milligrams of fenbendazole. I believe it was three days on, four days off uh and achieve remarkable success achieved remission from stage four cancer. days on, four days off? Yes. So that was what what what the group of patients were doing at Stanford. I tend to use six days on, one day off. Um a little bit a little bit more aggressive dosing and same thing with mebendazole, thousand milligrams six day on, one day off. One day. Is that just to give the liver a bit of a break? Exactly. You you you give the liver a bit of a break um and again incredible results. Now you could you could you could go less, you could go either 500 of fenbendazole and 500 of mebendazole if you're dealing with a low-grade cancer. Yeah. Uh maybe a very early stage situation. I have a lot of patients coming to me with early stage prostate cancer. Maybe they don't want the surgery and radiation therapy and they're looking for a way that they can maybe shrink the tumor or get rid of it altogether um without having an intervention and the risks of of those interventions. So you could you could do lower doses like 500 mg of mebendazole. for how long? Again, I I I design my protocols for three months. And I and I always and I and I I've I've done this with ivermectin and fenbendazole mebendazole and it's roughly the same idea is is you can start to see changes in in cancer markers in about a month. Takes about two to three months to start seeing shrinkage of lesions and typically oncology patients, especially when you're dealing with active disease, chemotherapy, immunotherapy, they will have follow-up imaging every three months or so. Yeah. And so you will automatically have that imaging from your oncologist. If not, I I encourage patients to make sure that they have imaging follow-up from their oncologist. And so you can see after three months or after six months if there's been a response to the lesions. And so I had I had a situation recently with a breast cancer patient who had her surgery was delayed for whatever reason and and she had a several months of wait time to her surgery. She had a 7 cm breast tumor. By the time uh so she was taking ivermectin and mebendazole. By the time her By the time her surgery came around and there were some enlarged lymph nodes as well. By the time her surgery came around, the tumor was less than 3 cm and there were no positive lymph nodes where they were certain that they were going to be positive lymph nodes based on based on the imaging appearance. So she had shrunk her tumor by more than half and managed to eliminate some of those lymph nodes entirely by the time she had her surgery. And this was a matter of maybe three months. It's amazing. So so in things like breast cancer and prostate cancer, the the the traditional treatments will involve hormonal modification. Yes. So so for example, testosterone blocking for prostate cancer. Um what sort of interactions, if any, are possible there with with say fenbendazole and testosterone blockers? There's no documented interactions that I'm aware of. Um and you know what's interesting when you look at drug drug interactions with whether it's ivermectin, whether it's mebendazole, there's not a lot of drugs that that they interact with in in a negative way. And so for example, for ivermectin, you have to be aware that ivermectin does interact with warfarin. Um and so you have to be aware of that. Doesn't seem to interact with any of the other um anticoagulants. And then there's certain um antipsychotic medications I believe that also interact with ivermectin. So um you know, there's a few drug interactions to be aware of. Warfarin's pretty uncommon these days. We tend to use more the more modern generations of anticoagulants. Exactly. So so it it really hasn't come up as as an issue the drug interaction. So there doesn't seem to be any interaction with any of the hormone therapies uh whether it's for breast cancer, whether it's for prostate cancer. Um you know, you are you are getting that you're getting that benefit of the other mechanisms anti-cancer mechanisms from the ivermectin or the mebendazole that you're not going to get that from chemo, you're not going to get that from immunotherapy, you're not going to get that from hormone therapy. Yeah. Um is is there is mebendazole or fenbendazole preferable for treating human cancers or they're much of a muchness? They are When it comes to preclinical research, they are very very similar especially at higher doses. Yeah. Mebendazole mebendazole is preferred. Um now mebendazole has has better penetrated penetration through the blood-brain barrier than fenbendazole. So it would be the preferred agent for any kind of brain tumors. nervous system. Exactly. Or or brain metastases. And there are certain cancers in which uh there is more preclinical research for mebendazole and this would be the squamous cell carcinomas, breast cancers, sarcomas. Um I'm just trying to think of some. It's interesting that you're getting really quite specific there. Particular drug for particular pathology. So so knowledge is accumulating rapidly in this area. That's right. And I and I do I do still lean heavily on on peer-reviewed research even if it is preclinical research. You know, if there is preclinical research, I do want to lean on that. And I can tell you I can give you one example actually for ovarian cancer for example. Uh ovarian cancer, I prefer mebendazole over fenbendazole. And and why is that? Well, there's researchers in South Korea who've discovered that when they um when they researched fenbendazole for ovarian cancer, there's excellent response um in in in vitro studies, but it doesn't translate to in vivo studies when they were looking at mice. You the effect didn't didn't translate to the same degree. And so they've been experimenting combining putting fenbendazole into various kinds of nanoparticles Yes. uh as as delivery mechanisms so they could deliver the fenbendazole to the tumor in a much more efficient way. And there's been three studies that have come out looking at various delivery mechanisms, various types of sort of nanoparticle uh formulations with fenbendazole. But the solubility is fairly low, isn't it? That's probably why you need the higher doses. Exactly. And so I'm aware of that research. I'm aware that there's been struggle with fenbendazole, you know, getting that drug to the ovarian cancer cells or to ovarian tumors. And yet when you look at the mebendazole research in ovarian cancer, there is evidence that you know, it is quite effective uh in halting proliferation and so on. So I do lean on existing research uh to decide whether I'm going to use or suggest mebendazole versus fenbendazole. Interesting. How optimistic are you that as we know more, we'll be able to give for example ivermectin and fenbendazole together enjoying the synergistic effect and being able to lower the dose? You know, I I think in a way I would say the cat is out of the bag in in the sense that uh this information is getting out. Yeah. And and it's getting out on platforms like X, it's getting out on platform you know, it's getting out on subs through substacks. Uh there's other authors you know, writing about using ivermectin fenbendazole or combinations thereof. And so so once information gets out and you no longer have this um suppression because I I would say the oncologists in a way are suppressed in that oncologists who did pursue uh non-conventional treatments historically have been targeted. Their licenses have been targeted. They they've they've they've their reputations have been targeted. They often have to flee the country. You know, we have a doctor in Canada who was using repurposed drugs, Dr. Khan, who had to flee Canada after years of battling with the College of Physicians and Surgeons, and now he's in Florida and he's got a clinic in Florida. He He had to leave the country. And And other doctors look at that and say, "Well, why would I risk my career and the well-being of my family to pursue repurposed drugs? I'm just going to stick with the guidelines that I get from the American Cancer Society or Canadian Cancer Society, and I'll be fine, right?" And so So, the culture The culture has been very um uh uh unfavorable towards repurposed drugs or unconventional treatments. And But, that's changing, and I think it's just the sheer amount of information that is getting out right now. Um I think um I I think it's going to change medicine. And And And I do believe that that with the new administration in the United States, with with, you know, RFK Jr. being confirmed and and bringing in people based on again, based on merit and and and bringing freedom back to science and medicine, I think I think we have We're going to have a whole new era in medicine where you know, I I think we will have research into repurposed drugs, and I think it will become part of the mainstream. I think it will become become a part of mainstream medicine and mainstream cancer treatments. Just to picture that a lot of people are going to die in pain before we get to that point, which is a is quite tragic. How important do you think it is to be vitamin D replete when you're getting these repurposed drug treatments? Vitamin D is is is very crucial. Um and I've I have found that uh it was crucial for COVID-19. Uh I I think there was a lot of evidence that most of the patients who did very poorly uh with COVID-19 infection, who had severe infections, ended up in the ICU, or died, were vitamin D deficient. Uh and I and I think that's been borne out by many studies. And you know, it seems to be the case in cancer as well. Uh Vitamin D seems to be protective uh for cancer. So, being having high enough levels of vitamin D seems to be protective for you developing certain types of cancers. Uh but, I think also as as a cancer patient, um it's important for you to have uh high levels of of vitamin D. And And so, I always ask my patients, "Well, have you had your vitamin D levels checked?" And they always say no. And And they they always say, "My oncologist hasn't even brought it up. Uh my oncologist hasn't tested me for vitamin D." I find that bemusing. I just can't explain. Why wouldn't you test for an important immunomodulator? And it's such an easy test. It's It's not that it's a highly specialized test or an expensive test. It's a simple test. Uh and I think it it it's it's crucial. And so, I suggest, you know, high doses of vitamin D uh supplementation, at least 10,000 uh units uh a day. If someone's low, for sure, yeah. Exactly. And And And And And And to have their levels checked. And I said, "Look, if your oncologist is not willing to do it, get your family doctor uh to check your vitamin D levels." But, very very important for the immune system. Well, it would It wouldn't work in the UK because GPs have been told not to test for vitamin D unless someone's got rickets. Wow. Which again is quite inexplicable. Um But, but things like zinc, vitamin C, you know, good nutrition's clearly vital in addition to to to to these things. Uh I've just got a couple of naughty questions at the end. Feel free Feel free not to answer. But, you mentioned CBD there. Um and there's no reason why you should have looked into this, but I went to the Isle of Wight Mushroom Farm where they're growing various mushrooms, and one of them's called turkey tail. Ah, yes. And this does seem to have anti-cancer properties. So, Remer, the dog, for example, came in with a nasty malignant tumor on his lip. It was going to cost 1 and 1/2 thousand pounds to be removed. The owner couldn't afford it. So, Alex at the Isle of Wight Mushroom Farm gave him a bottle of uh tincture of turkey tail, and within a month the tumor had had gone. Uh absolutely incredible. Um And I've I've also heard it used in uh colon cancer and possibly other ones. So, one to watch. And another fascinating one I've come across, and I know nothing about it. It's called Uh please With with with uh turkey tail because turkey tail is something that I that I highly recommend in my protocols uh as well. Uh and and I'm glad you brought that up because I I've I've I've heard these uh anecdotal stories as well um in in in dogs uh responding to turkey tail. There is There's There's again, a ton of preclinical research on turkey tail. And what's fascinating about turkey tail mushroom is that it's it's it's it's an immunomodulator uh as well. And And And it And it it stimulates the My understanding is that it stimulates the immune system to produce more cytotoxic cells, immune cells, that attack and fight cancer. Uh you know, whether it's CD8 cytotoxic Exactly. Cytotoxic T cells or natural killer cells that will then help the patient fight fight cancer. And so, I do suggest that take taking that as as a supplement uh if you have cancer. I I think the whole area of of of medicinal mushrooms, I think, is fascinating as well. Whether it's reishi shrooms, lion's mane, uh chaga um I could tell you some stories It's not for this video, but I could tell you some amazing stories about lion's mane. Uh quite quite neuroregeneration stories that are really quite quite that's another incredible area of of research that that that we should be We should be looking into and researching. So, so the the guy at the Isle of Wight Mushroom Farm, Alex, he he he makes turkey tail because it's very woody. You can't chew it. You could grind it, of course, but he actually makes it into a tincture. So, he basically soaks it in vodka for 3 months. And And And And And And you know, you end up with about 30%. You don't need much. Um and he he thinks that you get more out of it in the tincture form than you do just dried. So, I think that's an area for for future research, but it makes sense that the alcohol can get more of the intracellular component of the turkey tail out. That That That's Absolutely. You You You get more of of the bioactive compounds out. Uh and I believe there's you know, in each of these, I find whether it's turkey tail mushroom or some of the other mushrooms is is there there's such a rich variety of of bioactive compounds, the polyphenols and so on, the turpentines, that that, you know, with with the alcohol, you can extract some of these really quite nicely and and get the benefit get the benefit of of of it through extraction. We really need more artisan growers. There should be like a mushroom grower at the end of in every suburb, so you can just trot along and you get some nice fresh lion's mane and slice it up and eat it for your tea. Um it's a pity that it's not more readily available. And the other one, just just to close really, um artemisia annua is another one I've started looking at. That's right, yeah. It's um It's got another more popular name. I can't remember now, but again, it does seem to have anti-cancer properties. I know nothing about it, but What's fascinating Yeah, what's that? cheap, readily available. Exactly. So, artemisia annua is is another one of these um So, that that's a plant that actually won the Nobel Prize. 2015, yeah. Exactly. And And it's been it's widely used uh as an antimalarial agent. And it's being looked at for cancer. Uh there is a lot of preclinical research now building uh on artemisia and cancer. Now, some of some of the compounds, bioactive compounds in the plant artemisia annua um have been extracted and and sold as supplements on their own. So, that's artemisinin. Artemisinin is one of them, and artesunate is another one. And so, uh you can get either the whole plant You can get supplements of the whole plant where you have the variety of of the bioactive compounds, or you can get Just just just eating the leaves, basically. Yeah, or you could make tea tea out of it. And so, it's something that I've been trying to to incorporate, uh but patients, they just, you know, they don't They don't Most patients don't know about it. Uh and they find it very confusing. And And And you know, when it's something that you've never heard of, it's always hard to to to to convince someone to try. Uh but, I think this is another one that that it's a sleeper. It's not It's not well known in North America. It's It's much more known outside of North America. That would be my experience. Uh a lot of the research I think, it's fairly well known. Italy, um yeah, in other countries around the world. And again, a big one um I'll tell you a little story a quick story about about artemisia. Um when the COVID pandemic hit, uh people in other countries started taking artemisia annua to treat COVID-19. And it does treat COVID. And so, the WHO came out and said, "Don't take it uh because you don't know what you're getting, and you you know, you you know, if you're if you're taking the plant, you don't Anyways, it So, there was an advice This is This is the This is the plant that won the Nobel Prize along with ivermectin in 2015. But, apart from that, yes. Exactly. And And And And so, we we've seen this. We've seen this before that that cheap things that people could use to treat COVID-19, whether it was vitamin D, which was very effective, whether it was artemisia annua, whether it was hydroxychloroquine, ivermectin, zinc, uh quercetin, these things that that people used successfully to treat COVID-19 were attacked, were maligned by the by the various authorities. And it's just such a shame that that that that that happened. You know, we we refer to them as early treatments for COVID-19. If you had, you know, started some of these very early on, you would not have had I've talked to doctors in Africa, Roob. There was one hospital in Zimbabwe where they didn't have any oxygen. No oxygen. So, they they they used they used Ivermectin as an early treatment and the oxygen saturations increased within about 6 to 12 hours. Just on just without any oxygen therapy. Very very hard to argue against. Yeah, exactly. So, Artemisia was one one of these uh plants that that was maligned uh you know, when when the COVID-19 pandemic hit. But but you're absolutely right. Another incredible plant to look at in in cancer. I did try to grow some last year. It got to about that high then it died. Yeah. So, but I'm I'm going to order the The seeds are absolutely tiny. Oh, wow. Smallest seeds I've ever seen. I'm going to try again as soon as soon as spring comes and see if I can uh get some nice bushy Artemisia growing. We're also going to try and grow it in Africa in in in all the back gardens in Africa because uh you know, if if if the local population in rural areas can't get to medical help sometimes and if they get malaria, then making tea out of Artemisia could give them the extra hour or two they need to get to the clinic to get to get proper treatment. So, there's no reason why it should shouldn't be everywhere. And again, Absolutely. We're just in favor of encouraging that. Dr. Marcus, I am just blown away by that information and how clearly it was expressed. Um We'll put any links, of course, to to the sites that you want below this video. If people want to contact you or and of course links to the Substack and Twitter and X and all these things, but um I I mean thank you for for what you're doing. And thank you for this information and uh I know it's come at some personal cost. Thank you very much for having me. I appreciate it. I I love I love these topics. I love talking about especially repurposed drugs because that that's something that that I think gives gives a lot of people hope. Uh and and and gives it gives people options. It gives them more tools to to help their health. And it doesn't have to be cancer. You know, it could be it could be autoimmune diseases. It could be various, you know, inflammatory conditions, chronic inflammatory conditions. But I think repurposed drugs are such a fascinating field. And thank you very much for for this conversation. No, not at all. It's the whole risk-benefit thing, isn't it? If the risk is small and the benefit is potentially there, what the heck? Absolutely. let's just do it. And I think this is this is the future. I I think this is this should be the future of medicine. You know, I I think it it we we have to move away from the sort of the the what's pharmaceutical in what pharmaceutical industry puts in front of us and what the pharmaceutical industry tells the doctors that those are the only options that they can give their patients. I think I do I do hope it's the future of medicine. I'm not 100% convinced, but it's really we are fighting for that to be the future of medicine. I hope so, too. Yeah. Wonderful. Thank you so much. Thank you very much.