Welcome to Pushing the Limits, the show that helps you reach your full potential, with your host Lisa Tamati, brought to you by lisatamati.com.

Lisa Tamati: Everyone, welcome to Pushing The Limits. This week, I have an amazing author, researcher, cancer survivor, Jane McLelland, to guest. Now, she is the author of a book called How to Starve Cancer. Many of you will know who listened to my show regularly that I am on a cancer journey with my mum who has been diagnosed with high-grade B-cell lymphoma, which is a blood-based cancer. She's had a tumour removed in the brain, and now we're fighting the lymphoma part of it. 

This lady was put onto my radar by Dr Elizabeth Yurth who I had on the show a number of times. Her work is absolutely astounding. If any of your loved ones have cancer, if it runs in your family, you need to listen to this episode. Her story is remarkable. 

She has survived three times terminal cancer herself, and she has been a relentless researcher for the past 20 years developing different protocols in different ways to starve cancer — not just with food starving it, but blocking different pathways that feed cancer, and cancer tumours and cancer cells. 

It is a well-known fact that cancer uses glucose and sugars extraordinarily highly, so you need to avoid that. But it gets a lot more complicated than that. Cancer is very clever at changing its fuel source. We go into a little bit into the details here. You really should read this book, How to Starve Cancer, if you're at all affected by cancer in your family, if you have high-risk factors. 

And one in six of us is going to get cancer at some stage in our lives, and you need to know this stuff. We discuss the problems with the current standard of care, oncology, versus the metabolic approach to cancer, and some of the limitations that we are facing, the latest in research, and her knowledge is absolutely amazing. I do hope you enjoy the show with Jane McLelland. 

Before we head over to Jane, if you're interested in DNA testing, or in epigenetics and understanding your own genes, and how they impact your health and your life, and your optimal performance, and we'd love you to check out our epigenetics program. You can head over to lisatamati.com and hit the ‘Work With Us’ button in the navigation. That will take you to our page that tells you all about our epigenetics program. 

We've taken over 1000 people through this program now, and it's been game-changing for many people. It's like getting a user manual for your body. It's all the information about your genetics and how to optimise those genetics from a food perspective, from an exercise perspective, supplements perspective, from your predispositions to different disorders — a whole raft of things, even your mood and behaviour, your personality, and so on and so forth. Make sure you do check that out — go to lisatamati.com. 

If you wouldn't mind giving us a rating and review on the show, we would love that to happen. Please do that either on iTunes, or Apple, or any other good podcast apps that you listen to. Or, you can head on over to our YouTube channel. We have a really big YouTube channel where we publish the podcasts but also lots of other stuff. I have all my documentaries from my ultramarathon days on there as well. We'd love you to subscribe on there. 

If you want to give back to the show, that's one way you can do it by subscribing on YouTube and doing ratings and reviews. Thank you very much for your attention, and now over to the show was Jane McLelland.

Hi, everyone! Welcome back to Pushing The Limits. Today, I have someone that I'm just super excited. I can’t sort of contain myself. I've even dragged my sorry ass out of bed really early in the morning to do this interview because I'm super excited. I have a lovely Jane McLelland with me. 

Now, Jane is a cancer expert. I don't know what to call you. I was going to call you ‘Cancer Queen’, but it doesn't really sound very nice. Jane, welcome to Pushing The Limits. Welcome to the show. I am super honoured to have you. I've been talking to a number of doctors, and I said, ‘I've got Jane coming on the show.’ And they're like, ‘Oh my God! Really?’ Because you're a superstar in this world. Thank you very much for taking time —

Jane McLelland: I like it. But anyway, thank you so much.

Lisa: You are. You're absolutely amazing. Now, just to put the people in the picture, I'm on a cancer journey with my mum. She has lymphoma. We've just had her brain tumour removed, and this is how I came across Jane's work because an amazing doctor in the states pointed me in the direction of How to Starve Cancer, which is Jane’s book. Jane, for people who don't know you, can you explain a little bit your backstory, and why you got into this and your amazing book?

Jane: Well, my book is kind of two halves, really. The first half is my journey of how I discovered my metabolic protocol and the approach. Then, the second half is kind of the science behind why you need to block particular pathways and starve the cancer in a particular way. I was first diagnosed with cancer back in 1994 — cervical cancer — and I was a trained physio at the time, so I had some medical background. 

But I totally relied on the medical profession to get me better, not realising that it had spread to my lymph nodes. Actually, it was quite advanced when they found it. There's a lot of areas with the screening and colposcopy clinic — the whole thing was a shambles, frankly, and I should never ever have got that far. 

My doctor was eventually removed from the NHS. There was a massive national recall of all his patients, and it was a horror show. I sort of fell between the gaps there in that process, and ended up with quite an advanced cancer. They treated me with chemoradiotherapy — normal kinds of stuff — surgery, obviously. Couldn't have children, which was kind of — I was only 30 at the time. It was hugely devastating for me. 

That actually, to me, was the big thing. I mean, I didn't really see death as a problem back then. I was engrossed with the fact that all my dreams and hopes for the future had kind of almost gone in an instant. That was my big hope. 

I was really devastated, and in a really gloomy place for a long time. To compound things, my mother then got stage four breast cancer and died in 1996. But that was kind of a wake-up call to me. Then, I investigated a whole load of stuff for cancer and realised that I really wasn't doing enough for myself. 

When I was diagnosed with stage four, which was in ‘99 because it had spread to my lungs. Normally, you're given a sort of a 12-week death sentence at that point — my type of cancer. I kind of knew that what they were giving me was not enough, and I always felt that the answers were out there somewhere buried in papers and research, and that we just weren't using a big enough cocktail to blitz the cancer. 

I'm not against traditional treatments. I'm all for chemo, radio — they do work because they reduce the tumours. But on their own, they don't get rid of the cancer stem cell. The cancer stem cell had only really been discovered back in the 90s. This was new stuff. I didn't really know much about this at that point. But my instinctive knowledge was that to starve the cancer cell was probably the way forward. I knew that glycolysis and Otto Warburg — the research behind that was already available to me. 

I knew that glucose was strongly linked to the progression of cancer. If you stopped particular glucose pathways, then the cancer would be stifled in some way. But I kind of, then, got to the point where I realised that starving — if you just starve glucose, and people would be getting better. It's more than that. 

What I'd worked out was it — cancer — does rewire itself. It reroutes itself. It finds new metabolic pathways, and not just glucose. It uses glutamine, which is an amino acid — so protein. Also, it can use lipids, so fat as well. All of those can provide fuel for the cancer cell. But the trick was trying to find ways that would actually starve the cancer without having to go on starving yourself, which is why I called my book ‘How to Starve Cancer Without Starving Yourself’. 

Because yes, diet is important. But if you've got cachexia, or you’re really wasted from cancer, it can be really hard to try and do this approach without actually — particularly the dietary thing. But what I used was off label drugs, supplements, intravenous vitamin C which helps block glycolysis which is the Otto Warburg thing. 

Intravenous vitamin C on its own doesn't work. Again, it's got to be that combination of blocking different pathways at the same time, and it's important to get that in your head that it's not just one thing. It's never one thing that's going to cure cancer. 

I did this cocktail — kind of put together my own little cocktail of things that would block the glucose, the glutamine, and the fat in this little cocktail of mine — targeting multiple pathways. I've kind of since then — I’ve done endless research. But to actually understand cancer metabolism, I'm kind of self-taught. I started off from a position of no knowledge at all, and I just basically built up my knowledge. But I think because of that, I've seen it from a different perspective. 

Doctors come from this sort of a, ‘It's genetic. Blah, blah, blah.’ And they're kind of indoctrinated in that thought, and they don't see that actually, the metabolism is more important, actually, because the genetics — if you have a genetic mutation, like the p53, for example, which is commonly mutated or deleted, well, there's something wrong with it in pretty much every cancer. 

That relates to glycolysis to glutaminolysis, and in fact, to ferroptosis to this xCT and T porter, which kind of pulls in cysteine, which is another amino acid which creates an antioxidant environment for the cancer cell to withstand a lot of treatments like chemo and radiotherapy — all those things which create a lot of oxidation. 

The cysteine through making glutathione in the cell will actually protect it from those things. It's the whole protection element of the cell that we need to break down and focus on the cancer cell, and actually work on treatments that target the cancer cell, but leave your healthy cells untouched. This is where starving cancer is really so important because cancer cells are really hungry. 

Your normal cells can survive and withstand starvation for long periods of time. We're talking sometimes — but your cancer cells can't. They really don't like that at all. An extended fast has worked for some people, but it can again be a little bit tricky because you can then stimulate… 

Lisa: Autophagy? 

Jane: Autophagy. You've learned a lot? You've been studying this. Autophagy, generally, sort of is a good thing, and it's kind of in phases. You have early autophagy and late autophagy, and actually stimulating one is better than… You're trying to get an autophagy to kill the cancer cell, but you don't want salvage autophagy which kind of brings in new nutrients. It learns to scoop up the environment.

Lisa: Can I stop you there just for a second? Because, my God! We just covered the whole lots of things.

Jane: I know. I know. I’ve got verbal diarrhea. 

Lisa: Let’s unpack some of these things. Yes, because of the journey that I've been on — my listeners know — about my story with my mum. Actually, this is what the book that I've written, RELENTLESS, which was a six-year journey back from massive aneurysm. We were told that she would never do anything again, that she had massive brain damage. In that journey, I learned that the medical profession has blinkers on when it comes to anything that is outside. Like you, I went to PubMed, and I went to podcasts, and I went to scientists and doctors, and I found ways because I knew like you, that the answer was out there somewhere, and I just had to dig it up. 

I had no background in this either. I just dived straight on in. Three years later, my mum was back to full health, full power of attorney, full driver's license — like really back from the brink of nothing. Absolutely amazing. Now, we're on the second journey. I’m diving in… 

Jane: A new learning process. 

Lisa: And I'm diving into this world of cancer, which to be honest, I hadn't ever got — I'd done a little bit of research because I was always fearful that someone in my family might get it, but I hadn't… I was very much aware of the metabolic versus the genetic — the two models, if you like, or two theories. 

I just wanted to touch on Otto Warburg, for starters. Because back in 1931, he won the Nobel Prize, and basically in 1924, I think it was when he worked out the Warburg effect, which was basically showing — and this is what we use for PET scans today that sugar is sucked up, or glucose I should say, is sucked up like 20 times more or something ridiculous in cancer cells than in your normal cells. 

This was the first sign really that this is a metabolic disease, first and foremost. Then, your work looking at the genetic component, and how that's actually started. Because the argument has been weird, where is the origin? Is the origin in the mitochondria? Is the origin in the genetics?

Jane: I don't think it is. I think it's the tumour microenvironment. It's the influence on the stem cells. We have normal healthy stem cells, but if they are in an environment which is actually promoting cancer, so you have inflammation which is always implicated with every single cancer. IL-1 or IL-6 is an inflammatory what's known as cytokines. These are kinds of signals that go into the cell. 

Now, they don't arise from nowhere. These come from things like obesity, carcinogens — you can have lots of different factors that will cause interleukin-1 and interleukin-6 to be raised, and the wrong type of fat with obesity is what does it. Not everybody is fat who gets cancer. I wasn't. There were other factors. 

Many have also got things like Toll-like receptors, and these are kind of ancient pathogen receptors. These trigger as well. And these are always upregulated in cancer as well. These things actually come together alongside other factors as well. There may be too much estrogen, the hormonal influence may be completely wrong, and it may be promoting — because estrogen promotes growth. It may not be the initiator — I don't think always — but it is a promoter of cancer. 

I think a lot of people stop the estrogen, and I think it's a good idea, in many cases, to reduce or your estrogen exposure. That can be plastics, it can be cooking in the microwave, just all sorts of, you know. Now, it's just about everywhere. We've got tiny bits of microplastic in the air as well now. It's just pervasive.

Lisa: Xenoestrogens everywhere. This also goes to — because I studied genetics and epigenetics, and understanding your estrogen pathways or your hormonal pathways generally because that plays into it whether you've got the inflammatory type of estrogens predominantly, or the normal type of estrogens. This is especially for cervical cancer, which you had, and breast cancers, and those types of things that are hormonally driven.

Do you not think that it starts in the actual mitochondria because there is a big argument, I know that—

Jane: I don't. I don't believe it does. I think the mitochondria is affected by the signals that come in from the outside. There may be bacteria, things like that, that we haven't actually detected, and viruses. Viruses convert your cells into — and I think the viral component is pretty much in every cancer as well. 

Again, we haven't detected what all of them are. you know, Epstein-Bar.

Lisa: That’s what mum’s got.

Jane: Exactly. It’s going to make the virus — the HPV. But I think these things actually affect other cancers as well. We just haven't detected all of them. I think it's a sort of this grand concoction of many things. Liver cancer — classic one, hepatitis, and things like that. 

There are these viruses that can cause cancer, and I think it's a combination of the influence of kind of like these things acting a bit like a parasite. They change, they affect the mitochondrial DNA because you have the circle of DNA in the mitochondria, as well as DNA in the nucleus of the cell. 

These things talk to each other. The mitochondria talks to the nucleus, and nucleus talks to the mitochondria. But you get things called microRNA which are triggered by epigenetics. Changes in the surface and the environment around the cell triggers this microRNA, to then go in and trigger certain changes within the DNA of the mitochondria and also of the nucleus as well.

Lisa: It’s actually what's going on in the COVID vaccine, isn’t it?

Jane: It's kind of a cross-talk between one part of the cell and another. They're all linked together. I don't think — people who always say, ‘It’s dysfunctional mitochondria.’ Yes, you get dysfunctional mitochondria, but that's the downstream effect. As far as I'm concerned, that's the way I see it. 

How I work it out in my head and how I can see, I know about the microRNA. They don't arise from nowhere. They are triggered, and now they're now looking at RNA and microRNA as ways of detecting early cancer. 

Before it turns into a proper full-blown cancer, this is a new detection route that we are going to see come through in the next five to ten years. It'll start becoming accessible for people to actually find out if in five years or ten years, you're going to actually have lung cancer or colorectal cancer. A bit scary, but actually, you can prevent it. People are saying, ‘Oh, you can't prevent cancer.’ Of course, you can prevent cancer. You just have to understand — 

Lisa: Don’t tell Jane she can't do something. She'll find a way around it. 

Jane: Absolutely.

Lisa: The mRNA — this is outside of your warehouse probably. The mRNA that's in the COVID vaccines. That is actually telling the instructions of the nucleus what to do to produce certain proteins. Isn't that frightening because —? The connection between that and possible cancers? That has been our thought.

Jane: Actually binding, it helps them with their cancer. It's interesting to see what will happen there. I know a lot of people are scared of it. I'm not particularly keen on the — and I've had to have the Pfizer one because I've just had my booster, and I wasn't given an option on it. I had AstraZeneca, actually, to start with because I didn't want the mRNA particularly because we don't know the long-term effects. 

Lisa: This is my concern because just connecting the dots in my own head with my own research. Is it the toll-like receptors that you mentioned earlier? The innate immune system can be hurt by this. There are some preliminary studies coming out now that the innate immune system has been hurt in this way, and that we are changing. We don't want to go into that bloody deep — but

Jane: I know. That’s another rabbit hole to go down.

Lisa: It is cause for concern, though. I’d say that we haven't got — 

Jane: I just think we don’t know enough about it yet, and just the long-term effects of how it affects our immune system with dealing with other infections, and how — we don't know yet and…

Lisa: So you would have prepared your body having to have it? I mean, we're in the position to, now, where we're being mandated left, right and centre. I've lost my ability to work a lot about sort of holding out at the moment. I'm doing my research. I'm just doing more studies. I'm just open to both sides of the argument, but I want more data. I'm seeing is concerning me, and I think we needed more longitudinal studies on this. Probably, we should —

Jane: We shouldn't dash into it. I'm not an anti-vaxxer. I think most of us do need to have a vaccine. We just don't know. 

Lisa: It is an experiment at the moment. 

Jane: It is. It is an experiment. We definitely need some herd immunity. We need something. I think it does. It's helping protect a lot of people. If you're prepared to go ahead and get the natural infection and whatever — a lot of people are. People should have the choice of doing that if they want to run that risk. But the problem is it's putting other people at risk, and you get slated. 

Lisa: That’s a big argument. It's a big ugly hole at the moment.

Jane: It is. It really is because it seems like you don't really have a choice at the moment.

Lisa: But it's just interesting to see somewhat when you start to study something like cancer and understand the implications of things that you're putting into your body a bit more on a deeper level. When I was reading your work, I was like, ‘Oh my God! I've been giving things like vitamin E and NAC — N-acetyl cysteine — which is perfectly fine for a person who hasn't got cancer. But in the state that ‘I didn't know that she had cancer’, I'd been doing the wrong thing.

Jane: Well, there are arguments for having small doses of NAC just to sort of boot your immune system at times and to actually detox, and things like that. It's not all bad. But if you're trying to go for a ‘kill phase’ and kill the cancer, yeah. Also, after chemo, it can be very useful just as a short hit just to try and boot the immune system up. The same with glutamine, people get very scared about glutamine. But actually, that’s taken up by the gut. 

Actually, what you're trying to stop is the glutamine getting from the blood circulation into the cancer cell. You can't stop glutamine. In the system, you've got glutamine everywhere. But it's actually the transport into the cancer cell, and the use of the glutamine, and the breakdown of the glutamine in the cancer cell. 

You use a various number of things and supplements as well. Green tea is particularly good for stopping glutamine transport. That's a top. It’s something I recommend that pretty much everybody has.

Lisa: It is atomic. With mum, the day that we went into hospital initially, we thought it was a stroke because the right side of your face was dropping, and she was slurring her speech, etc. We got sent home. They couldn't find anything and the CT scan. Went back and three days later, they sent me home again. I've pushed, and pushed, and pushed until I managed to get an MRI. 

Got the MRI, and there was this big tumour on the left side. We had an amazing neurosurgeon team. They took the tumour out. From the day that I knew that it was a tumour was the day that I stopped because I didn't know enough at that point. I went, ‘No, nothing but vegetables is going in your mouth while I work this out ma.’

Jane: Good. Cool. Because it is. It's like ‘Alright, okay. Start from scratch, and yeah, you do.’ It's not something that — you can't just do this overnight. Unfortunately, understanding the metabolism and understanding how particular cancers work because I'm not as sort of a one approach fits all at all. I know that different cancers feed in different ways. 

You have to tailor your approach a little bit to — is it feeding more on glutamine? Is it feeding more —? What are the mutations? How do they affect the cancer as well because these affect the metabolism? Like the p53, like we said or the MEK, the MRC will affect glutamine predominantly, but it also affects glycolysis. There are different — you have to look at the whole picture. 

Lisa: I'm still working it out. 

Jane: I know. I will be doing… Eventually, with my online course, I will be doing more little things about specific cancers. I think I’ll actually do it. 

Lisa: I think three-quarters of the way through your course at the moment, we're actually off to the oncologist after this or haematologist says we've got lymphoma — B-cell lymphoma, high-grade B-cell lymphoma. I'm still working out which mutations there are. I know there's ones like CD20 and CD45, but I don't know some of the others. I'm still working out which pathway.

Jane: I can tell you B-cell lymphoma is very responsive to ferroptosis.

Lisa: Oh, okay. Because I've been studying ferroptosis, but I haven't quite a good grip on it.

Jane: The GPX4 actually needs to be looked at in-depth with that, but we can have a little chat afterwards.

Lisa: Okay. That would be appreciated.

Jane: That's the enzyme that breaks down.

Lisa: Superoxide dismutase, isn’t it?

Jane: No. Glutathione peroxidase. You can help it with things like ashwagandha, danshen, things like that.

Lisa: Okay, we might have a quick chat afterwards. 

Jane: It’s in the book.

Lisa: It’s in the book?

Jane: I’ve got a video. They sent me at the end of my online course. I realise that — like you discussed it at the end. In fact, you have to be a little bit — there are certain things you need to do to protect the brain from ferroptosis as well. So you want to kill the cancer cells, but yet you want to protect the brain as well.

Lisa: Yes, which in her case is — 

Jane: Yes, exactly. It's important to take what's known as HDAC — histone…

Lisa: Deacetylase.

Jane: Inhibitors.

Lisa: The HDAC inhibitors. This is like the marks on your DNA — the acetylation mark. Does it have to do with like aging as well? I'm just connecting dots here.

Jane: Aging is more with the telomeres, which are at the end.

Lisa: Those too — but then there's the acetylation or methylation marks that are used are biological —

Jane: Well, you're ahead of me on that one. But yes. I'm sure they are totally related to aging. Yeah. Even methylate, probably, you are definitely not getting the best effects from your treatments. It's worth checking her homocysteine levels as well.

Lisa: That's been a question that's running around in my head about the methylation, and is it safe then to — I know her methylation genes are very, very poor, and this becoming a consult about my mum, but I can pay you for that afterwards. When the methylation is poor, do you want to be supporting it? Because I'm scared of supporting that if that's going to upregulate your cysteine and —

Jane: You need fairly normal or low homocysteine levels. In order to do that, you need to actually sort of sometimes take enough B vitamins to lower your homocysteine because the cysteine part of homocysteine can provide a backup replenishment of cysteine for the cell. If you're trying to do ferroptosis, and you have high homocysteine, the cell will just use homocysteine to replenish it instead of… 

It's important to look at making sure homocysteine levels are below before you actually start the ferroptosis. That's important. You don't want to overdo the B vitamins because, again, you can go the wrong way.

Lisa: Exactly.

Jane: They need to monitor the levels, and you also need to monitor homocysteine as well. It's important to look at that, and CRP as well. Check inflammatory, level. That’s routine.

Lisa: Those have been on my radar for a long time because I teach epigenetics, methylation in helping people understand that for a healthy person. In this case, I was just like, ‘Woah!’ Because it could be upregulating the wrong things if I — Like her, her homocysteine and CRP are actually really low. That's really good. 

Jane: That's good. 

Lisa: But they need to keep an eye that if she's got enough B12, especially with the stuff that she's on. and that we keep that in balance. Thanks for sort of clarifying that a little bit for me. I'll do a bit of a deeper thing into that whole area. Just to go back to the whole — your story, when I read your story, I bawled my eyes out through your book because I have been there with my mom and myself, actually, with my own health journeys, and with my father, who I lost last year. 

With a system that's not listening and treating you like you're an idiot half of the time, and got the blinkers on — oncology. I'm about to start on the oncology journey because we're going for our first haematology today. But this will lead to oncology. 

I'm actually really scared of this because I know that they're probably going to take all this research that I want to bring to them and shut me down. I've seen this happen before. Last year, I had my father in hospital who had a massive aortic aneurysm and survived the operation but unfortunately, developed sepsis. 

I vary upon the research around intravenous vitamin C, and I fought like a crazy woman to try to get him intravenous vitamin C in the ICU. I fought for 15 days against the ethics committees, and the hospital boards, and the whole Intensive Care Unit team to keep them on life support while I fought this legal battle. 

I won the battle, but it took me 15 days. There was a nondisclosure agreement which I've since ignored because I believe that that was coercion. I won the battle but it was 15 days into his battle. By the end, he had multiple organ failure. Despite that, the very first intravenous vitamin C that we got, he was at death's doorstep — like he could die at any moment. It turned around. 

They got him off noradrenaline. His c-reactive protein dropped massively. His white blood cell improved his kidney function went up. That was from one small dose of 15 grams of vitamin C, and you’re meant to have that every six hours in the case of sepsis, that’s the protocol — six hours and ideally much bigger dosages. 

They stopped me doing the second one. They stopped me doing the third one. I had to fight 18 hours every time to get it through. Two days later, of course, by this time, my GP, who was actually administering it because that was the only loophole that we could find in the system that she could actually come up to the hospital and do this for me. 

She then told me, ‘Look, we are now beyond what anything can help.’ And I lost my dad. This has made me very much — I never wanted to be an activist in this space, but it's made me…

Jane: Me neither.

Lisa: You don't want to say that.

Jane: No! I’m not the person that stands up makes adverse. I’m the last person to do that, but you have to fight for your rights. You really do. When it comes to this, they don't have the answer for cancer. 

They don't have the answer for sepsis. B vitamin, high B12 can actually help with sepsis, but they're just not looking at it in a natural — they're not looking at the cheap options because of course Big Pharma is pushing them into these really toxic, ‘Let's do lots of antibiotic cocktails and things.’ 

Lisa: Meager amounts of money. After my dad died, I went and got five of the world's top scientists and doctors in vitamin C and research, and actually had them on the show to share their insights to activate this information. I heard the other day that somebody used our case, and has now survived sepsis. That's my point because I want this to help — just like you with your book that's helping hundreds of thousands of people around the planet. 

Yesterday, I was on a call with a doctor in Thailand. As soon as I mentioned your name, he was like, ‘Oh, awesome! What are you on? Give me all the dosages of the things you're doing.’ They were all over it. These are integrated oncologists. these are people that have actually opened their eyes and gone, ‘Hang on a minute. Maybe, they are right.’ It's the same with vitamin C. 

When I went to the ICU to talk to them about intravenous vitamin C, they thought it was like having an orange. They didn't understand that it becomes a pro-oxidant. In these high dosages, when it's intravenous, it's no longer an antioxidant, and it acts like a pharmaceutical when it's done in those high doses. 

I came with the clinical studies in my hand to say, ‘Hey, these are the clinical studies. Read them.’ They were like, ‘We don't care about the clinical studies. It's whether this is legal for us to do this or not.’ In my opinion, my dad died because of a legal battle, and not because of the sepsis. 

Now, we had a wonderful surgeon. They did a wonderful job on all of that. I'm super grateful for all of those people that do their amazing jobs. But we have got big problems in the system. This is why you and I are both in the space now — me in a different, smaller capacity than you. But it's very, very important work. 

When I understood all these metabolic pathways that you're talking about, and there's — I don't know how many is in your Metro Map — we'll put links to all this in the show notes, by the way. Then, you can start to shut down because so many people are just told, ‘Okay, you've got a terminal illness. Go home and pack your bags. There's nothing we can do.’ That couldn't be further from the truth.

Jane: Exactly. It's not an honest answer. If they really did their research, they would know that. I just feel so sad for so many patients that are told the wrong thing by their oncologist. Immediately, they go into that negative thought process. Then, they can't be bothered to try. They're not bothered to look. They lose all will because it's been stripped — has been stripped of them. 

Unfortunately, the white coat is very powerful. As soon as something comes out of the doctor's mouth, we're indoctrinated and ingrained to think that, even though we know that what they're saying can't be right, it somehow sits in there, and puts the element of doubt in you — whatever. It really does. 

I think that they really need to — I really want, kind of like medical school, just purely on cancer metabolism for people to come and learn. Maybe my online course is going to do that — I don't know. I've got a lot of doctors who sign up for that now. I'm really pleased, and it seems to be sort of word of mouth going around the oncology. Well, certainly the integrative circles for doctors to sort of listen and —

Lisa: I have about eight doctors working on mom’s case because I want lots of different — I'm relentless. Four of those doctors were all over your work. They knew everything about it. 

Jane: In Australia? 

Lisa: In New Zealand and in America. Sorry. One of the doctors in America, she's actually who pursued me, Dr Elizabeth Yurth from the Boulder Longevity Institute. Shout out to her. She's amazing. 

Jane: She should be on my list. 

Lisa: She should be.

Jane: I should have these people on my website because — just send me all the details after this.

Lisa: Definitely. I shall connect you two ladies because you will love each other. My local GP — she had your book on her shelf. She’s done all the studies. Dr Tim Ewer down in the South Island, President of the Australasian Integrative Medical Association. 

Jane: Reeder? You got?

Lisa: I’m sorry? 

Jane: Bill Reeder? Dr Bill Reeder.

Lisa: No, I haven't got him on, but I do know who he is.

Jane: And Katie Boyd, who's brilliant. She's more sort of nutritional help, I think. But she's brilliant.

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All of these people are very much aware of your work. Sometimes, as an author, I know that my book is out there doing its job without news — sometimes you don't get that feedback. Now, you don't get any feedback.

Jane: I'm totally unaware of the impacts, really, until somebody comes back and says, ‘Oh, you do know everybody's talking about you when in the oncology clinics.’ I don’t think about that, really. The other thing is that it's all very personal because my story is very personal. You think, ‘My goodness, all these people who've read my story, and they feel like they know me.’

Lisa: And they do, and they know a piece of you. I've had that journey, too. I've written three books — I shall send you my books. You are putting it out there, but you particularly know you're walking along the street, and someone will just come up and hug you and go, ‘Oh my God, there's just so —’ And you realise —

Jane: Haven’t had that yet. 

Lisa: Maybe that I'd hug you over.

Jane: Then, there’s COVID.

Lisa: Maybe, COVID. But I get cold —

Jane: No, unless I’m at a conference.

Lisa: It's gold because then you know, ‘Maybe I am making a tiny little bit of a difference.’ The difference between my work and your work, though, is that in my book, I didn't have a full plan of attack like you have. You've developed this incredible roadmap for me to follow. Whereas my book is a story, and I have some of the things like hyperbaric and the epigenetics, and stuff in there, but it's not a roadmap per se to come back from brain injury. 

I haven't put the 20 years of work into development of that. What astounds me with your brain, you've basically taken all the knowledge from thousands and thousands of scientists who are working on the cancer problem for decades. You've come along and revolutionised the whole model, and you haven't even been to medical school.

Jane: I've simplified it and said, ‘Right, let's break it down into —’ It is the tumour microenvironment, I believe, to the cell signalling to the cancer metabolism, to how it produces growth factors that then kind of switch off the immune system, and then you get this runaway fast dividing cell. But there's a whole load of stuff which gets ignored with current treatments that is not treating those earlier phases which happens in every — to produce new cancer. 

Once you've got this ongoing, fast, rapidly dividing cell, you need to be attacking every single stage of that, really. Actually, the more the tumour environment kind of comes top, almost because that's kind of creating an environment for cancer to just continue to grow. If you can work on that, and epigenetics is the big thing there, and then you work on the pathways as well, you're making a massive difference. 

The diet side of things — it just amazes me that we haven't accepted that in mainstream oncology yet, and it's still — doctors look down their nose at you if you say, you're going to change your diet. They just laugh at you.

Lisa: They know from PET scans that they use glucose. 

Jane: But then, they say, ‘Oh, well. We cut out sugar, we will just use something else.’ Yes, it does, but you need to know how to look over things. 

Lisa: At the start, I didn't know how to block any of those, so I just sit down eat. I pretty much just have veggies. A full fast — I would have done a full fast, but she wouldn't do it. I do have a question for you. Do you know Dr Dom D’Agostino? His work?

Jane: I've met him a couple of times, but not really spoken to him much.

Lisa: He is pretty fascinating too, and he has a very clever brain that's putting different aspects. I think I should introduce you to him again to try to connect and find a little bit more. Very interesting guy. He's looking at things like hyperbaric oxygen therapy, and he stumbled into the cancer research — exogenous ketones. 

What is your take on exogenous ketones? I think melanoma and prostate cancer are a couple of exceptions. But do you think exogenous ketones have a place in this —? 

Jane: What you don't want to be having — acetate. But what you do want to have are the —

Lisa: BHB? Beta-hydroxybutyrate.

Jane: Because that is an HDAC inhibitor. That actually will help with ferroptosis. It comes part of my ferroptosis — and it will help protect the brain. Yes, I think actually, they are really useful.

Lisa: I've been diving into his work as well just in the last week, really, and I've now got mom’s —

Jane: Again, it's a kind of a ‘kill phase’ with the HBOT. You're oxygenating. But you can make it far more effective if you add the ferroptosis protocol alongside what he's doing. When he was saying that, ‘Actually, HBOT doesn't work particularly effectively unless you have it within about 15 minutes of intravenous vitamin C.’ 

I don't think you necessarily need to do that. I think you can — if you create the right environment of a sort of oxygenating environment with lots of other things, and I think the HBOT probably does help. I think he's a bit dogmatic about that. 

Lisa: I've had my mom exogenous ketones just for the last four days, and I was concerned because of the whole glutamine thing. But then — 

Jane: No, don't worry about that. I think that’s actually — start looking at… It’s a whole total new list of things to take for ferroptosis. It's working particularly on things that will create these, what's known as reactive oxygen species — free radicals. Oxygen-free radicals in the cancer because cancer really doesn't like oxygen. It creates the environment.

Lisa: This was the intravenous vitamin C. Today, we’re heading over to do a — we're following The Riordan Protocol. As far as the intravenous vitamin Cs, we're going high dose. Again, 30 grams yesterday, we're doing 60 grams today. I hope we're getting 60, and then 90 on Friday in combination with the hyperbaric oxygen therapy, and she's on the ketones, and —

Jane: Artemisinin, and there's a whole load of stuff like —

Lisa: I haven't got that yet.

Jane: Fenugreek — there's a whole load of stuff that will actually stimulate the production of free radicals, and you can really boost the effects of that massively by taking the right cocktail. But you need to avoid certain antioxidants like luteolin and genistein.

Lisa: And what else?

Jane: Green tea, actually. The EGCG is okay. But the tannins in green tea you want to avoid because it prevents ferroptosis from happening.

Lisa: I only take the actual tablets? This is very tricky. The artemisinin, I only found out about that one yesterday, again, from a doctor in Thailand who —

Jane: That all really helped the intravenous vitamin C work much better — don't panic! You can do it next time. But it's all about getting the correct effect. This is where there's a slight — you've got to be a little bit careful that what you're doing with one thing doesn't counteract something else. 

The ‘kill phase’ is a little bit more specific which is why some people manage the ‘starve phase’, and that's enough to gradually get the cancer to disappear. If you've got a much more aggressive cancer that's kind of got its own — if the materialism is that high that it actually needs a ‘kill phase’ to knock it off, then you need that ‘kill phase’ to be much more specific. 

Just doing chemo can — it can be helpful because cisplatin actually works synergistically with ferroptosis. That's actually quite a useful chemo to take.

Lisa: What about temozolomide?

Jane: Identical. It's a chemo — we all produce free radicals. You can do all these things alongside but actually, cisplatin particularly helps block something called the xCT and T Porter which is the thing that brings the cysteine in. It’s a better — in terms of chemotherapy, it can actually help a lot better. Cyclophosphamide, also I think is quite synergistic with it as well — a low dose of cyclophosphamide.

Lisa: Because with an 80-year old mummy — very fragile. The whole chemo thing scares the crap out of me, and I know that TMZ is a little bit less toxic.

Jane: It works. But it works synergistically with berberine in the brain. Brilliant. You've probably seen the graphs in my book where you've got just temozolomide on its own, and then you've got metformin on its own. Then, you get the combination of the two. Berberine is similar in that. It works actually very much like metformin, but it's actually working on more fat pathways as well, which is important because fat your brain is a really — fatty area and actually uses some of the fat to feed itself, which is a bad thing. Yeah. It's about getting the correct combo, which is really critical.

Lisa: Your particular cancer, and your particular — this is where you have to start doing some other specific work.

Jane: My brain is kind of full of stuff. Anyway —

Lisa: Tell me about it. Because I'm doing that the hyperbaric — the high dose vitamin C, hopefully going to get some chemotherapy in the mix. Not that I want to but — we're already on things like berberine and metformin.

Jane: Berberine will actually help the uptake of vitamin C as well. It helps — it upregulates those glute receptors which is where the intravenous vitamin C enters. It sort of allows the vitamin C to work better.

Lisa: Right, I'm taking berberine into the office today. 

Jane: My own personal cancer markers went down to the lowest ever when I was having intravenous vitamin C, berberine — I'm sure it's having a load of other things as well. Aspirin as well — that can really help ferroptosis.
 
Lisa: It stops the platelets. I've just got to the platelets part on your course where the platelets — that would help too, wouldn’t it? The aspirin? These are also off label drugs. People, when we're saying off label drugs, these are simple, readily available drugs that are off-patent. 

It’s usually the things like aspirin, or things like atorvastatin, or things like metformin that have a huge safety profile or have been used for years, and they block certain pathways that feed the cancer. This is what we're doing — taking a combination of these things in order to try and block all of these pathways as best we can to kill the cancer stem cell as well as the actual daughter cells. 

This is what we've been talking about, and I hope we haven't lost people in the process. There is a couple of there that — do you know, dichloroacetate (DCA) and 2-deoxyglucose? Nobody seems to know about those ones. We can get them. That's 3-bromopyruvate.

Jane: 3-BP has got I think too many side effects really, and it’s not one I would readily recommend people to take. DCA have to be a little bit careful sometimes with the brand because it can cause a little bit of inflammation which if you got a tumour pressing on in an enclosed space in the brain, that's a potential disaster. Although, I know people who have used it to good effect with the brain. 

But I just put that out there as a warning that you need to be a little bit careful with that. 2-DG  — that's kind of like an alternative. It's a fake glucose — if you know what I mean. The body recognises it as glucose, but the cancer cell can't use it. It's a bit like putting the wrong fuel in your tank in your car, and it doesn't run. It's the same principle, but it's blocking those glycolysis, in particular. 

But melatonin will help with that as well. There are lots that you — probably, you need to redo glycolysis and the glucose module in my course. I go through a lot of stuff in there. And melatonin, it's a bit — I just had this debate on Facebook this morning, actually, because I think melatonin is one of those things that may be a bit like vitamin C in low dose — it acts as an antioxidant. But at high dose, it might actually act as a pro-oxidant.

Lisa: I've done quite a lot of research on melatonin prior to this. It has some really good sides, some really bad sides. I think Dr Yurth actually has been a good person to talk to — the Boulder Longevity Institute. I personally have got my mom 20 milligrams of melatonin. Being an older adult, she's not producing your own melatonin probably. It's something to do with the mitochondrial transport pause without losing people too much. It has some really good effects in that regard as well.

Jane: It blocks some of those glycolysis pathways like lactate dehydrogenase, and things like that. It’s really good for helping to block particular parts of the breakdown of glucose. It's actually preventing the cancer cell from being able to use it. 

Lisa: Do you know, where to get 2-deoxyglucose? Is that available anywhere? Like it's not a domestic use. 

Jane: Somebody in Australia.

Lisa: Okay, thank you. Sorry. Where do you think like — from here on in… You're going to develop more resources for particular cancers because as someone going through the course, going through the book, who's loving this roadmap, but are slightly confused now — because I've been like pressure-cooking my brain trying to get all this stuff. I'm throwing the bus at it, so pretty much everything that's on your list, I'm trying to get.

Jane: We don’t need to take everything. In my course, I go through different pathways and different — so you don't need to take everything that I talked about for every pathway. What you have to do is to be a little bit more selective. In fact, if you look at the way that the cancer works, it'll — 

Say, if you block OXPHOS, it will upregulate the glycolysis and vice versa. If you block glycolysis, it will use more OXPHOS. If you block those two really effectively, you pretty much snuff the thing out if you do really well. Unfortunately, most people don’t. Then, it will start to use a bit of the glutamine more. Again, you have to look at that. 

The other things that you need to look at are things like the fat. New research comes out with pancreatic cancer that are actually — it's lipids you really need to be blocking alongside other stuff. But lipids are very powerful. That's actually how I managed to stuff my cancer out. 

One of the main two pathways that I worked on was the cholesterol pathways. We’re looking out the mevalonate pathway with statins — lovastatin. Then, I knocked out the SARPi2,which is an alternative cholesterol pathway that the cancer cell will use. They can't use the mevalonate pathway. It uses this other one called SARPi2. 

I blocked that with another drug called dipyridamole, which is this old antiplatelet drug but luteolin, there are delta-tocotrienols, which is a vitamin E, which I think is fine, but you need to stop possibly for ferroptosis. I'm not entirely convinced. Alpha-tocopherol, which is the really powerful antioxidant you need to avoid. But delta-tocotrienols, which is a different type of vitamin E. I suggest people take that to block the SARPi pathways and natural alternatives. 

But you probably do have to stop it for ferroptosis — I don't know. There a whole load at the moment. This is new stuff. It’s new stuff. I can't say I know absolutely everything about ferroptosis. But my God, I've done a lot of delving. Then, I won't stop. I keep finding out new stuff. 

Lisa: And it's evolving.

Jane: I’d like to leave cancer behind me. Here’s the book, get on with it. 

Lisa: See you later. I’m going to go sailing or something. 

Jane: Yes, exactly. I’ve got a boat and I want to go sailing around the world.

Lisa: You can’t Jane, I'm sorry. You put her on the suits to help so many people. I get that you’re like, ‘Alright, I'm done with it. It’s up to you guys now!’

Jane: Leave me alone now!

Lisa: And you see it. I mean, even if you did, honestly, the work that you've already done, have massive impact and massive effect. This is why these little podcasts, and things around the world getting this sort of messaging out is just so, so important because it might save more lives just from this one hour that we’re spending. Therefore, it's really hard to know when to stop, isn't it? 

It is still evolving. Science is always going to be evolving. In two years time, I'm sure you'll tell me more nuances about whatever to take. But this is at least a pathway for people who have been told, ‘There is no way forward. You are dying.’ Jane's been there. You were told 12 weeks to live roughly when the lung cancer hurt her. That was how many — 30 years ago?

Jane: No, that was ‘99. Then, it ended up causing myelodysplasia in my bone marrow which was really the kind of another experience.

Lisa: You should have been dead three times.

Jane: That's when I started taking the cocktail because I realised that whatever I was doing was not enough, and I had to take it up a notch. Just doing intravenous vitamin C, the supplements and everything else that I'd been doing. 

Strict diet just wasn't enough, and that the cancer had got the upper-hand again. I needed to just bring in some more big guns — as I call them in order to sort of knock it on the head, but I never thought I would survive. I just assumed that I might be buying a little bit more time.

But it was always a big leap of faith, and I had no idea whether it was going to work or not. Then, I've since worked out exactly what pathways because this is all — back when I was doing it, nobody really understood how statins worked on cancer. The whole starving cancer was just something that has emerged more and more, and people gone, ‘Oh! Yes, it does starve cancer.’ 

Then, it’s sort of working out all the different pathways and it's become more and more obvious that actually starving cancer really is the key. It’s the critical key that we're not using and conventional treatments in order to unlock that cure. You look at childhood leukemias, and they use something called asparaginase which blocks the glutamine because these cancers are very glutamine-driven. 

Once they started bringing that in, it's a metabolic drug — blocks it, starves it, boom… They went from about 20% survival to 90%. It was just like an overnight sensation. They've improved the formulation of it a little bit because it was a bit toxic to start with. They've made it less toxic now, but we should be using that with some of the other cancers that are very glutamine-driven as well. 

Lymphoma — these things are really quite… I just wish that the oncology profession would just wake up and realise we have a lot of the tools that we could use for other cancers if we just looked at it as a metabolic —

Lisa: Doesn’t make anybody rich Jane. That's the problem. With hyperbaric — I mean I’ve got a hyperbaric over in the corner there. It doesn't make you rich, and this is the problem. They want… Then, when they've spent 40, 50 years in the genetic — we started off really well with what Otto Warburg thing in the 1920s — in the right direction. Then, we took this left turn, and we've gone genetics for the next 50 years, and the whole genome project which sucked billions and bought — absolutely bugger-all a little bit.
 
Jane: They have discovered that there are some key metabolic pathways that have come out of that because we know that the p53 does this, and it does that, and the KRAS does this — has this metabolic effect, and people just get, ‘Let's target the gene.’ Well, the gene has an effect on the protein. 

The protein creates enzymes. It has things that have an effect on the cancer cell itself. The way that it expresses itself, the way it feeds, the way it metabolises — this is what we need to be targeting, and it's the epigenetics Once we stop that, and we work on those epigenetic pathways, and we can shut down the cell. The cancer cell will stop behaving like a cancer cell and revert back to behaving more normally.

Lisa: Dr Yurth said to me last week on a podcast, ‘If you take the mitochondria of a cancer cell —’ Let me get the right way around, ‘If you took the nucleus of the cell and put a cancerous nucleus of a cell into a normal cell, it will just — it's got normal mitochondria to be normal. If you go the other way, and you took faulty mitochondria —’

Jane: Mitochondria in? Then, you get an answer. It's all to do with the metabolism, and all to do with the effect of the mitochondria on the cell. If we can change dysfunctional mitochondria — and you get this… You get overabundance of mitochondria as well which are working abnormally to produce OXPHOS as well, it's not just glycolysis. 

You get too much OXPHOS, particularly in some types of breast cancer. They use much more OXPHOS than they do glycolysis sometimes. you know. You've actually got to be wary of the fact that if you're blocking the glycolysis, you also need to block the OXPHOS because it's a compensatory pathway.

Lisa: Those are real killer?

Jane: But you could use the two cholesterol pathways as a key, or you could use nucleoside salvage, and the pentose phosphate pathway. Those two are synergistic as well. Or mTOR and autophagy. Those two are synergistic. There are a lot of pairings that go on on my Metro Map. Those are all on my Metro Map. They work together — you've got one, you've got the other one as well.
 
Lisa: Have you actually developed a course for teaching practitioner? Like people coaching?
 
Jane: Haven’t got that far yet. People want trained coach, certified. It will be in the pipeline at some point.

Lisa: You need a bigger team.

Jane: I know, I do. It's just me effectively. I really do. I need to bring on board doctors to help me do this. I have got some who are willing — I had one who's unfortunately just headed off to do another project of his own invention of looking at killing off cancer stem cells in the circulation which looks terrific. But he's now totally encompassed with that. I've kind of lost him but he was going to help me, but I've got other doctors who I may team up with to do this.

Lisa: Any doctors listening to this, there's a few — if you want…

Jane: I’ve got cocktails for say, pancreatic cancer, for example. This is crying out for a really good cocktail of label drugs and supplements to actually knock it on the head. I've been — there’s something I've been working on for…I'm trying to look more specifically at different types of cancer now and just try and work out really good cocktails for each one. I haven't done the online course, updated the book. Now, I've got grand hopes to do this app