Welcome to this video and I'm delighted to welcome Dr. William Mackus all the way from Alberta in Canada. Dr. Mackus, 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 fact, things that often seem to be surrounded by a deafening silence. which is rather strange. Hopefully we can bring that up today.
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. Makas, if you like, just a little bit about yourself, your background. 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 Communist Party in Czechoslovakia. He had been targeted as a university professor. They wanted him, of course, to promote communism, and he did not want to. And so he felt the only option was to flee.
And 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 does have a very significant oncology component. And so my detractors will often say, well, Dr. Marcus, you're not an oncologist.
What are you talking about? 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 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 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 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 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 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 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 Prague last year and I paid homage to the Yang Palak Memorial in Wenceslas Square, who, of course, burnt himself to death after the Soviet invasion. Very moving. A very moving memorial still there and well visited by local people. It's good to see.
Prague is one of the most beautiful cities in the world and certainly it's 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 to think a bit about the work. that you were, you had a, well what's the word I'm looking for, there's a word in academia that 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 affinity molecule would then hook onto the cancer and 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 the radioactive molecule would give off beta particles. It was chelated to 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 hit the cancer cell. It would render it enabled of... 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, get their injection, and then they would go home, minimal side effects. And so I was a big fan of, of next generation cancer treatments, more targeted cancer treatments, instead of, you know, the old style chemotherapy, where you would be hitting everything, that was replicating rapidly, but you'll 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 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 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 kill a person in a matter of six months. And so the behavior was very different. I alerted the Canadian Medical Association of this in September of 2022. I had alerted them that I had seen a number of my physician's 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 it's a term that, you know, someone who's sort of not aware of this phenomenon. of these aggressive cancers may not take seriously. You know, it's a term 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 stage 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 you see... Young women in their 20s present with stage 4 breast cancer and they have no family history and they have no genetic markers that you can detect, no BRCA1 or 2 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.
I always refer to the case of cholangiocarcinomas. These are bile duct cancers where the average age was 70, the average age of presentation. This is a cancer of the elderly, and yet we have 20, 25-year-olds presenting with stage 4 cholangiocarcinoma, something that I'd never seen in my career.
And so there is something new happening. The term turbocancer... Cancer has stuck.
I believe it appropriately describes 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 re-scan 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 thing moves. And 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 very shocking resistance to chemotherapy. And so you will get either no response or partial response.
The oncologists really struggle with these cancers, these terrible cancers. They struggle with them because they throw everything at it. The oncologists are genuinely trying to get these cancers under control as they used to in the past.
And so imagine, you know, you would have A breast cancer patient who could live another five years, ten years with conventional treatment, and then that patient dies six months later, and you're left wondering what is going on. Why are these patients dying so soon after diagnosis? 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 mainstream oncology. And so Professor Deglish, for example, talks about this.
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 Dr. Ryan Cole, Dr. Professor Burkhart in Germany, 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've seen young cancers, we've seen childhood cancers, 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 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 they seem to be resistant to existing treatments, again, is indicating a new pathology, really.
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.
Just run us very briefly through, if you don't mind. What is stage one, two, three, four cancer? Well, so the stages represent the… Really the size and extent of the tumors. And so if we take breast cancer as an example, stage one would be a small tumor, one centimeter, two centimeter.
Then stage two would be a larger tumor. And then usually you often have spread to local lymph nodes. And then that'll be stage two.
Stage three, you might get 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. 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. When we talk about stage four, we're talking about metastatic disease. The cancer will be in the primary site. It will probably have grown and expanded in the primary site, but it will 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. Please. And I do believe that we are dealing with a brand new pathophysiology. 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. And I believe, you know, again, this is where the pathologists come in, you know, like Dr. Ryan Cole, Professor Burkhardt, where they're trying to look at these tumors and see what's different about these tumors, what's different about the patients who develop these cancers. 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. And so when you come in and you're a certain type of breast cancer patient, let's say stage four, we know that you are hormone positive, for example, the oncologist is very good at giving you a prognosis, saying, look, if you follow the conventional treatments, we know you're gonna live another five years or 10 years or three 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 when they offer conventional treatments to patients. Well, this is where they've been completely off, and 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 person who's been affected by a terrible cancer. And they will say, the oncologist told us we had five years and our loved one died within two, three months.
I have never seen my oncology colleagues be off by a factor of 10 in prognostication. I have never seen that. You don't get it that wrong. or colon cancer, for example, where you could live another five years, and then the person, again, dies two, three months later after diagnosis.
And it catches the oncologist off guard, and it catches the family off guard because they've told the family, you know, we can, with conventional treatments, you'll have at least another two years, three years, five years, and the person dies a few months later. That shocks everybody, and that throws everybody off. And so why are my colleagues now off?
in their prognostication by a factor of 5 to 10, there's something wrong here. I believe we are dealing with a brand new pathophysiology. I believe it's something that should be seriously looked at.
And unfortunately, we're stuck in the situation where some of my colleagues who are seeing this, like Professor Deglish, 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, you know, the manner by which they may be arising, and there are case reports and so on. And yet, on the other hand, when, you know, you'll have doctors 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 doesn't exist, right? It's not a thing, it doesn't exist.
And that's not science. You know, that's not science. When you have a phenomenon in front of you 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, that's not science. That's not how science should work.
It is quite bizarre, isn't it? It is denial of that which is patently obvious. It's a bit like saying Australia doesn't exist.
I mean, we're into the realms of incredulity here, really. So you mentioned these accelerated cancers, turbo cancers for want of a better term. 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're going to get two streams of cancers really? Exactly, exactly and so I see both.
I see both. I see your typical cancers where a patient has been struggling with stage four breast cancer and they've been struggling for years. They've been struggling for years but you know 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 they've had stage four for four or five years, and they're still battling it.
And then you have, you know, a similar situation where a stage four breast cancer patient will come in, you know, this cancer is 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. I think if, if, if you're not open to the idea that something has changed in the last few years, 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 think it has to be said at the moment. Now, if we 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.
If the prostate, you might expect it to go to the bone. So first of all, what sort of primary sites are we seeing with what we could call turbo cancers? There have been articles published.
I believe there was one published by Memorial Sloan Kettering Cancer Center in the United States that talked about a wide variety of cancers that have exploded recently. 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, brain cancers that are even more aggressive than what we were used to in the past, breast cancers. The big ones are breast and colon, breast and colon. And I can tell you, in fact, how the mainstream medicine and oncology are reacting to this explosion 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 of mainstream oncology has been to lower the screening age.
And 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 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 States and Canada.
That, yeah, that has already happened. The screening age has been lowered for breast cancer from 50 to 40 for mammography. And now there's significant debate going on about decreasing the screening age for colon cancer.
And then the debate is, well, what age are we lowering it to? Are we lowering it from 50 to 40 or even to 30? to have that.
Yeah, it's still 60 in the UK for fecal or cold blood screening. And so, and again, this doesn't get a lot of attention or it doesn't get a lot of, you know, media attention because I think the cancer centers themselves can't make, you know, they don't know what to make of this situation with these turbo cancers. And so they talk about lowering the screening age, but we should be finding out what the pathophysiology is behind these cases. We should be looking at these cases. Specifically, we should be analyzing them.
I mean, pathology is the specialty that could look at these tumors in detail, analyze them, and see what is different about these tumors 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.
It's fairly obvious. So, I mean, I take your point there entirely. So, 72-year-old woman gets... Turbo cancer for the breast. 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 you believe it's occurring at all ages. I do see it in all ages, exactly.
And you're absolutely right. When it happens in someone who's in their 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 your attention.
It doesn't stand out. And yet when you see a 20-year-old, and I've seen women as young as 18, 19, presenting with stage 4 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 is unheard of unless you're in a post-Hiroshima situation. I mean, it's just unheard of, isn't it? Absolutely.
It just doesn't happen. Absolutely. Yeah. Now, I want to think about temporal correlations.
You started noticing this early 2022. So what possible changes could there have been in the environment in the years before that? And what do you suspect the lag period might be? So, for example, we had we had COVID in 2020. We had COVID vaccines in 2021. 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?
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 discussion gets quite heated, because 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, maybe they had a vaccination, and you will have people saying, well, that's not enough time, you know, for an aggressive colon cancer to arise. You know, a colon cancer takes many years to develop, or even a breast cancer, and yet I am seeing some of these temporal correlations in some cases. But in some cases, You know, this cancer will arise years later.
And so there's not a clear picture of a temporal correlation. But, you know, you bring up the point of what has changed in the last few years that could be contributing to this, you know, to this dramatic rise and this potentially new pathophysiology. And I really think, you know, you've got these two.
Two main things that have happened in the last four or five years is we have this COVID virus, this somewhat novel virus, and we had a pandemic with multiple waves of infections. You know, this was not a one. Time thing where you could you could say, well, you know, we had we had one wave of COVID-19.
We've had multiple waves, unfortunately. 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 COVID-19 vaccines and different types as well. You know, we have the DNA based vaccines. We have the mRNA based vaccines. And so these are things that that are different, that that have affected. a large segment of the population in one way or another in the last four years, let's say.
And so I think it's worth looking at those things. But, you know, it seems to be somewhat of a taboo subject, particularly because there's this, you know, there's this overall desire of people to just move on. People want to move on from the COVID pandemic. And they don't want to talk about they don't want to talk about 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 as well. And when some of some of my colleagues were being diagnosed with these extremely aggressive cancers, these turbo cancers in 2021, and, 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. It's okay, well, you could have bad luck in a few cases.
But when it's happening, 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 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 an open mind and look at those possibilities.
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. I only started my sub stack where I... published a lot of articles talking about this phenomenon.
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. And fortunately, Elon Musk bought the entire platform for $44 billion and brought a number of us, you know, physicians back like Dr. Robert Malone, Dr. Peter McCullough, Dr. Pierre Corey, and Dr. Ryan Cole, and so on.
Donald Trump. Exactly. So it could be mentioned.
I feel blessed and fortunate 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 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 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 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 credible, based on my limited experience and understanding of the pathology.
Absolutely. So that's definitely, I think, a component of this. Another component that I think 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 because their immune system is compromised. And I think, again, we've been in a situation in the last four years where people's immune systems have been compromised, whether they were compromised by a virus or a vaccine.
I think 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 seen an explosion 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 strep throat and septic shock. And so I do believe that a compromised immune system may play a role in some of these cases. 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.
And, you know, we measure the CD8 and CD4 cells in AIDS patients. The white blood cell profile. Exactly.
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 plays a factor in some of these cases. I suspect personally 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 seems to be the Occam's razor, if you like. I think so. And the other part of it is...
Also looking at populations that are affected, I see university students, college students who've been impacted by turbo cancers. I've seen certain professions, doctors, nurses, teachers, police officers, firefighters, military. And so you have to ask the question, well, why?
Why are we seeing this in certain groups? There were mandates in some of these groups, especially in 2021. We had mandates that affected a lot of these people, a lot of young people, or some of these professions in healthcare, for example. We had healthcare workers who faced mandates as well. And the entire profession faced it. So I think it's definitely something that we have to look at and really consider a possibility.
Where there were mandates, you know, is that something that contributed to this phenomenon? 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. 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 with millions of people. Yes, we have that opportunity in the United States.
And I don't see this opportunity in Canada, for example. Nor in the UK. There's been no transparency from whether it's the federal government or the provincial governments that are responsible for health care. If anything, I had actually started my Substack with a series of articles on how the government was deleting data, crucial data from the government websites where people 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 look into this 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. Makkas that's absolutely fascinating I've let that run a while to unpack that I think that's really well worth doing absolutely important 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 cheaply 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, are amenable to treating other conditions. And we have a lot of precedent for this.
So aspirin, for example, from willow bark was initially used for treating fevers. Now we realise it reduces platelet viscosity and can help prevent blood clotting. 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 treating myocardial ischemia, for angina, and it was later used for treating impotence.
So there's a surprise finding. So this isn't unusual. But what first arose your interest in repurposed drugs in the field of oncology?
I've started getting into repurposed drugs when I started my Substack in early 2023. And I really wanted to do a deep dive into early treatments for COVID-19. Treatments such as ivermectin, hydroxychloroquine. And I wanted to know for myself, were these effective in COVID-19?
What was the science? What was the research telling us? And... And of course, you know, 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 read dozens and dozens of paper. And I was particularly fascinated by ivermectin, why this anti-parasitic 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 mentioned, we have decades of...
Prescriptions given of ivermectin, I think 4 billion doses at this point, excellent safety record around the world, unquestionable safety record established around the world. And yet, why was this a focus of such controversy and attention? 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, of course, you know, I was naturally curious, well, why would ivermectin work in cancer? How does it work in cancer? And so, you know, I did a PubMed search and I think something like over 300 peer-reviewed papers come out and, you know, in regards to ivermectin and cancer.
Now, it's all preclinical research. and then you start looking at, well, where are the human trials? I want to see the human trials as well. But you see preclinical research where they're studying the cancer cell lines or they're studying it in mice or rats.
But this preclinical body of research on ivermectin and cancer is so impressive. It's not one or two papers, a group of researchers tinkering in the lab. You know, these are dozens and dozens of paper, you know, extensive research done looking at the various mechanisms of how ivermectin might act in cancer and what cancers ivermectin impacts.
And it really seems to be a broad anti-cancer agent that that can be used in a variety of cancers, anything from blood cancers to solid tumors as well. And 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 able to 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 believe that when you have standard chemotherapy, standard chemotherapy will kill the rapidly dividing cells just based on the nature of the rapid proliferation. But They will not kill slowly dividing cells often, and 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, they will tell you, you cannot cure stage four 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 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 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 multidrug resistance in cancer cells. And so it can actually sensitize cancer cells to chemotherapy. It's also a radiosensitizer.
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. Ivermectin also inhibits certain enzymes called 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 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 on the molecular level on cancers. And so then you ask the question, 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. There are case reports. There's a case series on three patients with leukemia. I believe two of them were able to achieve some form of remission with ivermectin.
And that's it. We don't have any randomized control trials. We don't have any large studies in humans.
And then you find out, well, ivermectin has been off patent since the 1990s. I believe Merck held the patent. 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 studying ivermectin in humans for cancer.
And where there's no money to be made in oncology, tragically, the research just doesn't follow. And so you see this focus. And this happens to a lot of repurposed drugs.
And so, for example, you look at something like another antiparasitic, fenbendazole or mebendazole. Now, this is a different family of antiparasitics than ivermectin. Fenbendazole was actually interestingly discovered by a terminal cancer patient from Oklahoma, Joe Tippins.
And Joe Tippins had stage four small cell lung cancer. which is one of the most aggressive cancers known. And he had stage four small cell lung cancer diagnosis, terminal diagnosis. And I believe he was put on a trial of Keytruda at the time. Is that a regular cancer drug?
It is a regular cancer drug, yeah. And sort of what they call an immune checkpoint inhibitor. Yeah.
And so he was put on Keytruda 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 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 shows and talk about his experience of trying fenbendazole, which was not FDA approved for use in humans, and how it cured his, or he believed that it cured his stage four cancer. 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 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 here.
You had actually talked about this. You had talked about this paper from 2021, this series of three people who had cured their cancer with fenbendazole. And so there is an FDA approved version of fenbendazole called mebendazole.
It's structurally almost identical. There's one atom difference between fenbendazole and mebendazole. Mebendazole has been approved by the FDA.
as an anti-parasitic drug for use in children and adults. And so it has an incredible safety profile, very safe to use. And Mabendazole actually has a dozen clinical trials in which it's being looked at 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. And so there are trials in adults looking at colon cancer, prostate cancer, and there's also trials in children looking at brain cancers with Mabendazole. 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 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 to somehow identify a cancer cell from a normal cell. And this has been studied in ivermectin as well. As 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 is it is absolutely fascinating i encourage anyone look you know look into the the preclinical research it is it is absolutely fascinating and 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 understood biochemistry. And these drugs interfere in a particular biochemical mechanism in a known biochemical way. This is not speculation.
I mean, biochemistry is basically a hard science. I mean, medicine's a bit soft around the edges, but biochemistry is a hard science. 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 Mabendazole-Fenbendazole group. It's just absolutely incredible that these natural molecules seem to have these multiple modalities of action, and yet we're staring the gift horse in the mouth. Exactly.
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 replicated.
This is hundreds of papers for these anti-parasitic drugs. So this is not a conspiracy theory. This is not fringe medicine. Hard science, as hard as it gets. This is hard science.
And I love, I'm always fascinated by preclinical research. Because that is what we stand on. That is what the rest of medicine stands on, is the preclinical research. That's what we rely on 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 if you can say, well, this is the way it's working, then that's what takes you into science away from mumbo jumbo. Because we've got we've got. Existing science and 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 so I found myself in a situation where I was writing articles on Substack. 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 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 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 so 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 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 other options are there? And I think this area of repurposed drugs, you know, is something 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 some of these repurposed drugs and they start taking them. They start, you know, they start taking them themselves.
So as I was writing about As I was writing about ivermectin and fenbendazole and mebendazole in cancer, I had patients who actually started taking them, and then they would come back to me six months later and say, Dr. Maccas, I read your articles, and I took these on my own. There was no patient-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, and one or two stories, you say, that's fantastic. I'm, you know, I'm really happy for you that, 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 is 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 two years. I did start a cancer clinic or sort of a cancer coaching or health coaching program with repurposed drugs where, you know, 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 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 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. These are cancers that were absolute death sentences. Exactly, exactly.
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 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 fascinating, you know, because when you look at some of these mechanisms, some of them are known and some of them are still unknown. And you see all these biochemical pathways that ivermectin acts on and all these pathways where, you know, it changes the expression of certain proteins and then suddenly you stimulate apoptosis of the cancer cell. The cell just goes pop and dies.
Exactly. the programmed cell death. And so a lot of these pathways that ivermectin, fembendazole, and abendazole act on are pro-apoptotic pathways, where you're bringing that cancer cell towards this programmed cell death.
And you're also, you know, this idea 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, I mean, it's wonderful, but it's, it's, uh... It's biochemistry well beyond my level of understanding, that's for sure.
It really is. It's pure biochemistry. And sometimes even I have a hard time understanding some of these pathways, you know, but really, you know, the fact that it can affect expression of certain proteins and so on.
It's just it just it's incredible. And so it I think repurposed drugs, I think there's there's a big future in repurposed drugs. And I think repurposed drugs can give patients.
hope in situations that are very dire and and and in the past would be considered hopeless um 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 for people who've exhausted the standard cancer treatments stage four pancreatic cancer for example 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 fine, fine, try it. You know, but something like this that is potentially, can potentially improve the condition is just... Incredible.
And I am optimistic, again, in the States 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. One of the things I always used to teach my students was in acute care, sometimes patients are going to die.
And 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'm trying not to get cross now, but it's just not acceptable.
You're absolutely right in that the state of oncology in, let's say, North America, for example, because I'm very familiar with the state of oncology in North America, but I do have patients in the UK, in Ireland, in Australia. 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. It's the same in the UK. Yeah, and you have, you know, your first-line chemo, second-line chemo, maybe you can throw in some immunotherapy in there, of course, radiation where appropriate and so on, 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 that's not true. That's not true. There's a whole body, there's a whole area of, let's say, repurposed drugs that you don't even know about, that you don't even tell your patient about. And we run into the situation, I have patients from Mayo Clinic, I have patients from Johns Hopkins, Memorial Sloan Kettering, MD Anderson, Dana-Farber, these leading cancer centers in the United States, and the patients come to me and they say, you know, my doctor is 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 always have this discussion with patients that, you know, your oncologist probably is not allowed. To offer you anything else or to suggest anything else because there may be retaliation. Their licenses may be targeted.
Their jobs may be targeted. And the oncologists, 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 something that might save someone's life and I don't tell them. That's got big ethical questions. But I want to enter a completely academic discussion now and look at doses of these drugs.
If we start off with, let's start off with ivermectin. 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 one milligram per kilogram.
per day. Quite high. And it is a little bit high.
I always say this is about five times those that you would use for COVID-19 or a parasite infection, for example. Is this with, what level of cancer is this with? Sorry. This would be with most cancers, sort of intermediate to high-grade cancers. Now, for low-grade cancers, you could certainly start lower at half a milligram per kilogram per day.
And so for a 60-kilogram person... Typical starting dose would be about 60 milligrams of ivermectin. But for low-grade, something like CLL, chronic lymphocytic leukemia, that's been simmering for many years, or maybe multiple myeloma, I start lower at half a milligram per kilogram. So that would be something like 30 milligrams 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 six days a week? That's seven days a week. Seven days a week. For how many weeks?
Well, so I suggest patients try ivermectin for cancer for three 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 three months is because, from my experience, I have seen a response to ivermectin on cancer markers as early as three, four 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 CA125 or these other more specialized markers for breast cancer, for example. These are basically chemicals given off by the cancer cells. Exactly.
And 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 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 two to three months. to start seeing that on imaging like MRI, PET-CT, or CT.
So you want to give it a good three months to see if you have a response. 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 two, three 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 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 FN-bendazole or Mabendazole as well. But when you do the combination treatment, there's a certain synergy, 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 make sense, and there's precedent for this again.
Things like low-dose naltrexone can sensitize people too. Exactly. Conventional chemotherapeutic agents.
So those sorts of doses of ivermectin, we're talking about ivermectin on its own or with traditional cancer treatments. That's right. Yeah.
So that's kind of almost like a monotherapy, isn't it, with ivermectin? Well, in the sense... The fact that you can't... Monotherapy in terms of the pre-purpose therapy, you can't be giving it with a range of other traditional oncologist-prescribed drugs. Yeah.
And so, you know, when you are giving it with chemotherapy, it's sort of an adjunct in the sense that you're sort of adding it into your chemotherapy regimen. And patients will take the ivermectin throughout their chemotherapy regimen. I will tell you another fascinating story of a physician assistant I have in the United States who had already done four cycles of chemotherapy and started taking ivermectin.
And, 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 he said, usually the chemo will knock me out for three days. I can't do anything for three days.
And, you know, I started taking ivermectin. And then all my 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. You know, and then his markers were dropping as well. and he was having a fantastic response. So if you only took it 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 other patients who don't have cancer. who I've guided with ivermectin, for example, patients with rheumatoid arthritis, whose symptoms improved dramatically, patients with fibromyalgia, patients with Lyme disease, for example. I've seen dramatic improvements in these situations where patients been suffering with a chronic inflammatory condition for many, many years, and they get, you know, rapid relief with ivermectin within a few weeks.
of taking ivermectin. And this would be, again, a lower dose, about a half a milligram per kilogram for, you know, these inflammatory conditions. So I've seen traumatic response for inflammation. But like you said, even if it was just for, you know, improving the patient's quality of life during chemotherapy, it would be worthwhile because the side effect profile of ivermectin is so favorable.
Quite incredible. I wasn't aware of that such a strong anti-inflammatory effect, I must say. Now, the side effects with these sort of higher doses, are you seeing side effects?
What side effects do you see? I'm seeing some transient side effects. If you've never taken ivermectin before and you start at 1 mg per kg per day for a 60 kg person, that's 60 mg of ivermectin, you may have some transient visual symptoms. The visual symptoms have been described as seeing colors a little bit more vividly or seeing a little bit of stars.
It's almost as if when you get up too quickly and you have that effect that you might faint. So there's been visual symptoms described. Now, these are temporary. They may last anywhere from a few minutes to a few hours, and they do go away with time. You know, after one or two weeks of ivermectin use, the body seems to get used to it.
and they go away. Even maintaining the same dose of ivermectin. Exactly. And so there's reports, I mean, there's reports in the literature of ivermectin being used at one milligram per kilogram for up to a year with no side effects.
And there's been no long-term effects reported with ivermectin use either. Now, if there are no non-reversible neurological effects that you've ever come across, none. Now, you could push the dose higher to two milligrams per kilograms per day, but you have to be cautious 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 cleared his pancreatic cancer with a few months of ivermectin, two milligrams per kilogram per day.
Uh. But there you can start to get, especially in more elderly patients, you might get some confusion, you might get some instability on the feet. And so you have to be more careful going into the higher doses.
Again, ivermectin has a half-life of 18 hours. So if you run into some side effects, you stop, it's out of your system within two days, no long-term effects. But you have to be a little bit more careful with ivermectin if you want to push the higher doses. I did hear, I think it was on Joe Rogan, there was a doctor on there, I forgot his name now. Anyway, he said that someone got benefit from prostate cancer with just 12 milligrams of ivermectin a day for several weeks.
Is that biochemically feasible or do you think that dose is too small? No, it is. And I have seen some really impressive responses. 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 really varies from, I would almost say, cancer cell type to cancer cell type, because I could have two prostate cancer patients, and one will respond to 12 milligrams of ivermectin, and the other one may not respond to 60 milligrams of ivermectin, and so there's a wide range of dosing.
That's where this becomes a little bit tricky, and I think where patients need some guidance. in terms of dosing and response, because the cancer cell killing is dose dependent. These are things we need to learn, of course.
This is not established pharmacology, is it? Absolutely. I think this is where we need those human trials. We need researchers to be supported in this kind of work. And regardless of the fact that there's no money to be made at the end of this, that there's no money to be made for some pharmaceutical company or shareholders of a pharmaceutical company, this is for patient benefit.
And this is where you know 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, so much good research that needs to be done.
And so with this dosing of ivermectin, you know, there's a wide range. uh, of effectiveness. And I have seen effectiveness as low as 12 milligrams.
I can tell you, if you're combining it with chemotherapy, you can get away with lower doses of ivermectin 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 situation. So a lot of patients are not telling their doctor and the situation... Which means the data is 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 they actually are. Exactly. And so what happens is the oncologist then has a genuinely shocked reaction when they see an outcome of their chemotherapy regimen that they're not used to seeing. And I've seen this even with radiation oncologists where tumors are shrinking after two or three radiation treatments, and the radiation oncologist 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 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 mabendazole, 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. That's bully boy behavior to me. Bullying. It's bullying.
Exactly. And this is what patients face. 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've threatened me.
They said, we'll kick you out of the trial. You know, we'll stop treating you. This doesn't happen as much in the United States.
I find in the United States, that culture, it's not as, it's the bullying behavior is not there. The oncologists are more open. I've had oncologists say, you know, That's perfectly fine.
You can take ivermectin with this regimen, no problem. But once you go outside of the United States, especially in countries like Canada, UK, Australia, there's a lot more of this bullying behavior. The idea that a doctor should threaten their patient is just unconscionable. It's unethical.
It's unprofessional. It shouldn't happen. But unfortunately, it does. And 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 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.
We have a name for this in England. It actually comes from Australia, but it's called curiosity deficit disorder, and it's quite a debilitating condition. Absolutely. And especially in oncology is to not have curiosity, to not... Yeah, this is what science and medicine is all about.
Oh, why does that happen? What's going on there? Because imagine, you know, as an oncologist, I mean, you know, you could publish it as an interesting case report, you know, or maybe even a case series.
Why not ask the questions? You know, there was a situation, a couple of case reports that have been published with CBD oil, cannabidiol, where patients, there was a couple of 80-year-old patients, they had lung cancer and they refused chemotherapy. They said, look, I'm 80 years old.
I don't want chemotherapy. And the oncologist said, okay, well, we're going to continue monitoring you anyways. And then suddenly the lung cancer is shrinking, shrinking, and it's gone a few months later.
And of course, now, these oncologists actually ask the question, they're like, okay, what are you doing? We're not treating you. 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. Yeah.
So Mbendazole and Fenbendazole both end in azole. So they're in the same group. Do they have similar doses?
They do. So it's a family of antiparasitics called benzimidazoles. Two of them are FDA approved, and that's mebendazole and albendazole. And so you will find albendazole is also available, and some doctors are willing to even prescribe mebendazole and albendazole. And then fenbendazole is sort of the almost like the stepchild or the, you know, it's not FDA approved, and yet it's in the same family with very similar.
almost identical mechanisms, almost identical molecule of action. And so incredible family, extensively researched. And there are a number of, I would say about a dozen clinical trials ongoing right now with Mabendazole in cancer, looking at pediatric cancers, looking at adult cancers. And so 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 um so it's yeah you're right but um it is being looked at seriously at least mebendazole that's encouraging and and so that that is you know that is great now 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's got an excellent safety profile, just like Mabendazole.
I can tell you, having advised over a thousand patients on the use of ivermectin, Fembendazole and Mabendazole, there's this myth that the Fembendazole and Mabendazole are difficult on the liver, that they can damage the liver and so on. They can raise the... the liver function tests liver enzymes 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 reduce 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 three percent of patients i see elevated liver function tests you stop it for a few weeks and those liver function tests if it was the fenbendazole or benzozol they go right back down to normal.
This has been published in peer-reviewed literature as well, that there's this sort of transient, you could almost call it an irritation of the liver, in a 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, again, excellent safety profile established, and really just I've seen some incredible responses. And I combine...
the ivermectin with either a fenbendazole or mabendazole. I do a combination. There does seem to be a synergistic effect there, doesn't there? But can we look at the doses first of all? So I've been treating worms with mabendazole for probably about 40 years, 100 milligram tablets.
So what sort of doses of mabendazole and fenbendazole might you be using for 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 Mabendazole or Fenbendazole? Exactly.
So either 1,000 or Fenbendazole. And the Stanford case series that you had talked about on another program, they had done 1,000 milligrams of Fenbendazole. I believe it was three days on, four days off, and achieved remarkable success, achieved remission from stage four cancer. Three days on, four days off?
Yes. So that was what... what the group of patients were doing at Stanford. I tend to use six days on, one day off, a little bit more aggressive dosing. And same thing with mebendazole, 1,000 milligrams, six day on, one day off.
One day off. Is that just to give the liver a bit of a break? Exactly. You give the liver a bit of a break. And again, incredible results.
Now, you could go less. You could go either 500 of fenbendazole and 500 of mebendazole if you're dealing with a low-grade cancer. It may be 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 are looking for a way that they can maybe shrink the tumor or get rid of it altogether without having an intervention and the risks. of those interventions. So you could do lower doses like 500 milligrams of Mabendazole. For how long?
Again, I design my protocols for three months. And I've done this with ivermectin and Femmedazole and Mabendazole. And it's roughly the same idea is you can start to see changes in cancer markers in about a month.
It 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. And so you will automatically have that imaging from your oncologist. If not, 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 a situation recently with a breast cancer patient who had, her surgery was delayed for whatever reason. And she had several months of wait time to her surgery.
She had a seven centimeter breast tumor. By the time, so she was taking ivermectin and mabendazole. 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 three centimeters and there were no positive lymph nodes. where they were certain that there were going to be positive lymph nodes 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. That's amazing. So in things like breast cancer and prostate cancer, the traditional treatments will involve hormonal modification. Yes. So, for example, testosterone blocking for prostate cancer.
What sort of interactions... if any, are possible there with, say, fembendazole and testosterone blockers? There's no documented interactions that I'm aware of. And, you know, it's interesting when you look at drug-drug interactions with whether it's ivermectin, whether it's fembendazole, there's not a lot of drugs that they interact with in a negative way.
And so, for example, for ivermectin, you have to be aware that ivermectin does interact with warfarin. And so you have to be aware of that. It doesn't seem to interact with any of the other anticoagulants.
And then there are certain antipsychotic medications, I believe, that also interact with ivermectin. So, you know, there's a few drug interactions to be aware of. Warfarin is pretty uncommon these days.
We tend to use the more modern generations of anticoagulants. Exactly. So it really hasn't come up as an issue.
the drug interaction. So there doesn't seem to be any interaction with any of the hormone therapies, whether it's for breast cancer, whether it's for prostate cancer. You know, you are 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. Is there a... Is mebendazole or fembendazole preferable for treating human cancers or are they much of a muchness?
When it comes to preclinical research, they are very, very similar, especially at higher doses. Mebendazole is preferred. Now, mebendazole has better penetration through the blood-brain barrier than fembendazole, so it would be the preferred agent for any kind of brain tumors.
Central nervous system. Exactly, or brain metastases. And there are certain cancers in which there is more preclinical research for Mabendazole. And this would be the squamous cell carcinomas, breast cancers, sarcomas. I'm just trying to think.
It's interesting that you're getting really quite specific there, particular drug for a particular pathology. So knowledge is accumulating rapidly in this area. That's right. And I do still lean heavily on peer-reviewed. research, even if it is preclinical research.
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. Ovarian cancer, I prefer mebendazole over fenbendazole. And why is that? Well, There's researchers in South Korea who've discovered that when they researched fenbendazole for ovarian cancer, there's excellent response in in vitro studies, but it doesn't translate to in vivo studies when they were looking at mice.
The effect didn't translate to the same degree. And so they've been experimenting, combining, putting fenbendazole into various kinds of nanoparticles. 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 nanoparticles formulations with fenbendazole. Because 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 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 in halting proliferation and so on.
So I do lean on existing research 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 think in a way I would say the cat is out of the bag in the sense that this information is getting out.
Yeah. And it's getting out on platforms like X. It's getting out on platforms, you know, it's getting out through sub stacks.
There's other authors, you know, writing about using ivermectin, fembendazole or combinations. And so once information gets out and you no longer have this suppression, because I would say the oncologists in a way are suppressed in that oncologists who did pursue non-conventional treatments historically have been targeted. Their licenses have been targeted.
Their reputations have been targeted. They often had 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 had to leave the country. 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 the culture The culture has been very unfavorable towards repurposed drugs or unconventional treatments, but that's changing. And I think it's just the sheer amount of information that is getting out right now.
I think... I think it's going to change medicine. And I do believe that with the new administration in the United States, with RFK Jr. being confirmed and bringing in people, again, based on merit and bringing freedom back to science and medicine, I think we're going to have a whole new era in medicine where I think we will have research into repurposed drugs, and I think it will become part of the mainstream.
I think it will become a part of mainstream medicine and mainstream cancer treatments. Just a pity that a lot of people are going to die in pain before we get to that point, which 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 very crucial. And I have found that it was crucial for COVID-19. I think there was a lot of evidence that most of the patients who did very poorly with COVID-19 infection, who had severe infections, ended up in the ICU or died, were vitamin D deficient. And I think that's been borne out by many studies. And, you know, it seems to be the case in cancer as well.
Vitamin D seems to be protective for cancer. So being... Having high enough levels of vitamin D seems to be protective for you developing certain types of cancers.
But I think also as a cancer patient, it's important for you to have high levels of vitamin D. And so I always ask my patients, well, have you had your vitamin D levels checked? And they always say no. And they always say, my oncologist hasn't even brought it up.
My oncologist hasn't tested me for vitamin D. I find that bemusing. I just can't explain why would...
You test for an important immunomodulator. And it's such an easy test. It's not that it's a highly specialized test or an expensive test. It's a simple test, and I think it's crucial.
And so I suggest high doses of vitamin D supplementation, at least 10,000 units a day. If someone's low, for sure, yeah. Exactly. And to have their levels checked. And I said, look.
If your oncologist is not willing to do it, get your family doctor to check your vitamin D levels. But very, very important for the immune system. Well, 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.
But things like zinc, vitamin C, good nutrition is clearly vital in addition to. To these things. I've just got a couple of naughty questions at the end. Feel free not to answer.
But you mentioned CBD there. 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 is called Turkey Tail.
Ah, yes. And this does seem to have anti-cancer properties. So remember the dog, for example, came in with a nasty malignant tumor on his lip.
It was going to cost one and a half 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 tincture of turkey tail. And within a month, the tumor had gone. Absolutely incredible.
And I've also heard it used in 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 great. With turkey tail, because turkey tail is something that I highly recommend in my protocols as well.
And I'm glad you brought that up because I've heard these anecdotal stories as well in dogs responding to turkey tail. There is, again, a ton of preclinical research on turkey tail. And what's fascinating about turkey tail mushroom is that it's an immunomodulator as well. And it's... It stimulates, my understanding is that it stimulates the immune system to produce more cytotoxic cells, immune cells, that attack and fight cancer.
CD8 cytotoxic. Exactly, cytotoxic C cells or natural killer cells that will then help the patient fight cancer. And so I do suggest taking that 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 so rich yeah 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 yeah quite neuro regeneration stories that are really quite quite i think that's another incredible area of yeah of research that that that we should be we should be looking at and research So the guy at the Isle of Wight mushroom farm, Alex, 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 three months. And, you know, you end up with about 30 percent.
You don't need much. And 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 future research, but it makes sense that the alcohol can get more of the intracellular component of the turkey tail out. Absolutely. You get more of the bioactive compounds out.
And I believe that, you know, in each of these, I find, whether it's turkey tail mushroom or some of the other mushrooms, there's such a rich variety 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 it through extraction we really need more artisan growers they should be like a mushroom grower at the end of in every suburb so you can just trot along and get some nice fresh lion's mane and slice it up and eat it for your tea it's a picture that is not more readily available And the other one, just to close really, Artemisia annua is another one I've started looking at. That's right. 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 cheap, readily available. Exactly. So Artemisia annua is another one of these. So that's a plant.
That actually won the Nobel Prize. It did, 2015, yeah. Exactly.
And it's widely used as an anti-malarial agent. And it's being looked at for cancer. There is a lot of preclinical research now building on Artemisia and cancer.
Now, some of the compounds, bioactive compounds in the plant Artemisia annua, have been extracted and sold as supplements on their own. So that's Artemisinin. Interesting.
Artemisinin is one of them. And artesunate is another one. And so you can get either the whole plant, you can get supplements of the whole plant where you have the variety of the bioactive compounds, or you can get... Just eating the leaves, basically. Yeah, or you could make tea out of it.
And so it's something that I've been trying to incorporate, but patients, they just, you know, most patients don't know about it and they find it very confusing. And, you know, when it's something that you've never heard of. It's always hard to convince someone to try. But I think this is another one that it's a sleeper.
It's not well known in North America. It's much more known outside of North America. That would be my experience.
Italy, I think, is fairly well known. Italy, yeah, in other countries around the world. And again, a big one.
I'll tell you a little story, a quick story about Artemisia. When the COVID pandemic hit, 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 because you don't know what you're getting. And, you know, if you're taking the plant, you don't. Anyways, it's.
This is the plant that won the Nobel Prize along with ivermectin in 2015. But apart from that, yes. Exactly. And so we've seen this.
We've seen this before, 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, quercetin, these things that... that people used successfully to treat COVID-19 were attacked, were maligned by the various authorities. And it's just such a shame that that happened.
You know, 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... Oh, yeah. I've talked to doctors in Africa, Ruv.
There was one hospital in Zimbabwe where they didn't have any oxygen. No oxygen. So they used ivermectin as an early treatment and the oxygen saturations increased within about 6 to 12 hours, just without any oxygen therapy.
Very, very hard to argue against. Yeah, exactly. So Artemisia was one of these plants that was maligned when the COVID-19 pandemic hit. But you're absolutely right, another incredible plant to look at in cancer.
I did try to grow some last year. It got to about that high, then it died. But I'm going to order.
The seeds are absolutely tiny. The smallest seeds you've ever seen. I'm going to try again as soon as spring comes and see if I can get some nice bushy Artemisia growing.
We're also going to try and grow in Africa, in all the back gardens in Africa, because... You know, 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 proper treatment. So there's no reason why it just shouldn't be everywhere. And again, it's just a matter of encouraging that.
Dr. Mackes, I am just blown away by that information and how clearly it was expressed. We'll put any links, of course, to the sites that you want below this video if people want to contact you. And, of course, links to the Substack and Twitter and X and all these things.
But, I mean, thank you for what you're doing. Thank you for this information. And I know it's come at some personal cost.
Thank you very much for having me. I appreciate it. I love these topics.
I love talking about, especially repurposed drugs, because that's something that I think gives a lot of people hope and it gives people options. It gives them more tools to help their health. And it doesn't have to be cancer. It could be autoimmune diseases. It could be various inflammatory conditions, chronic inflammatory conditions.
But I think repurposed drugs are such a fascinating field. And thank you very much 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 the future. I think this should be the future of medicine. I think we have to move away from what the pharmaceutical industry puts in front of. and what the pharmaceutical industry tells the doctors that those are the only options that they can give their patients. I do hope it's the future of medicine.
I'm not 100% convinced, but we are fighting for that to be the future of medicine. I hope so too. Wonderful. Thank you so much. Thank you very much.
Fascinating. Thank you.