Dhru Purohit Show - Cancer Biologist Explains the Importance of Early Cancer Detection and Top Lifestyle Tips For Cancer Prevention with Joseph Zundell

Episode Date: March 25, 2024

This episode is brought to you by Cozy Earth, Lifeforce, and Lumebox. Despite significant strides in cancer research over the past two decades, there remains a vast realm of uncertainty surrounding the impact of various cancers on individuals. Amidst the proliferation of cancer discourse on social media, distinguishing evidence-based information from conjecture can prove challenging. Today’s guest is here to untangle all the complexities. Today, on The Dhru Purohit Show, Dhru sits down with Dr. Joseph Zundell to discuss the research behind cancer prevention. Dr. Zundell shares the lifestyle factors that influence the development of cancer and the cutting-edge technologies for early cancer detection. Dr. Joe Zundell received his Ph.D. in cancer biology through the University of the Sciences and The Wistar Institute in Philadelphia, PA. He has over ten years of cancer research experience as a cancer biologist. Much of his published research has focused on finding new therapies for the treatment of many different cancer types based on the epigenetic and metabolic characteristics of cancers. In this episode, Dhru and Dr. Zundell dive into (audio version / Apple Subscriber version): Technology for early detection of cancer (4:55 / 4:55) Obesity and visceral fats link to cancer (22:56 /19:30) Exercising to build muscle and for longevity (28:57 / 25:06) Protein intake and the metabolic process  (35:00 / 30:23) Fasting mimicking diet before chemotherapy (47:14 / 42:17) Otto Werberg’s research (53:17 / 49:39) Cancer as a metabolic disease (58:15 / 53:40) An overview of Dr. Thomas Seyfried’s work and Dr. Zundell’s viewpoint (1:07:07  / 1:02:08) Dr. Zundell’s views on what needs additional research (1:09:43 / 1:05:09) Dr. Zundell’s origin story (1:18:54 / 1:13:00) Socioeconomic status and its impact on disease (1:30:37/ 1:26:38) Rapid fire community questions (1:34:02 / 1:28:35) Also mentioned in this episode: Dr. Zundell’s research  Get $300 off Prenuvo at prenuvo.com/dhru (not an affiliate link) Ezra Test  Fasting and Caloric Restriction in Cancer Prevention and Treatment Professor Valter Longo's Study  Right now, get 40% off your Cozy Earth sheets. Just head over to cozyearth.com and use code DHRUP. Right now, you can save $250 on your first diagnostic and get personalized suggestions. Optimize your longevity and track your progress go to mylifeforce.com/dhru!  Lumebox is offering my community $260 off their FDA-approved portable Red Light device!  That's over 50% off! Go to thelumebox.com/dhru and get your Red Light device. Hosted on Acast. See acast.com/privacy for more information. Learn more about your ad choices. Visit megaphone.fm/adchoices

Hi everyone, Drew Prode here. Today we're talking about cancer again. Yes, again. And there's a reason why. If you look at the stats, it's actually pretty freaking mind-blowing. Cancer diagnoses are slowly increasing every year. And if you look at it, almost 50% of men in their lifetime will end up with some sort of cancer diagnosis. And for women, it's not that far behind.

It's like almost 40%. And the rates continue, especially amongst young people. This is scary. That's why cancer is on the top four list. They call it the four horsemen of chronic disease. Cancer's up there right along with heart disease, neurodegenerative diseases like Alzheimer's dementia, and things like metabolic dysfunction.

Those are the four killers and cancer is on there. That's why we're talking about it. And today we have a very special guest reminding us about the most cutting edge, but also fundamental things we all need to know when it comes to cancer. and we're talking about it in two major categories. The first one is early detection. There's been an explosion of new technologies that have launched in the last like five to 10 years,

and now all of us have access to early diagnoses and early detection tools that can help us catch cancer earlier. The earlier you catch cancer, the easier it is to address it using, hopefully a combination of traditional medicine as well as precision and functional medicine. And the second category that we're going deep in today are the tried and true, most fundamental,

most basic things that so many people ignore when it comes to helping us lower our potential risk for developing cancer. Who is this special guest? Some people call them the cancer daddy. I'm going to introduce him as Dr. Joseph Zendell. Now, a little bit more about Joe. Joe Zendell received his PhD in cancer biology,

through the University of Sciences and the Wistar Institute in Philadelphia, Pennsylvania. He's been a cancer biologist for over 10 years now and has a deep expertise in the field of cancer research and cancer research experience. Much of his published research has focused on finding new therapies for the treatment of many different types of cancers using both epigenetic and metabolic characteristics of these cancers. Currently, he's a research scientist at a biotherapeutic company near Philadelphia, where he's examining immunotherapies for treating cancers. Joe's mission in life is to develop and characterize therapies

to enhance cancer patients' outcomes. And he's incredibly committed to producing educational tools to help enable better scientific understanding with instruction. One of his big goals in life is to have his own lab with his own projects to progress cancer research. You know, lastly, before we go into the episode today, I want to say one of the reasons I'm excited to have Joe on this podcast, and that I appreciate him, is that Joe, in a very polite way,

reached out to me on social media and shared that one of the clips that I'd posted on Instagram that was starting to go very viral on cancer information, talking about one of the studies that our guest had mentioned around breast cancer and toxins, didn't give the complete and full story. Not that there wasn't validity to what our guest was saying, but that there needed to be more context added to the conversation. And that's what Joe is going to do on today's episode. when it comes to topics around cancer,

he's going to help push and help us understand that there's more nuance to the conversation of cancer, and he's going to add to hopefully the conversations we've had with past guests by bringing his deep 10 years of research expertise in this field to the audience today. Stay tuned for a fantastic conversation with Dr. Joe Zendell, aka the Cancer Daddy. Most people will get some form of cancer in their life

so that's something that we all need to pay attention to this subject. Cancer is a very scary disease. And there's, of course, prevention with cancer, which we're going to go into what is the evidence show are the top most important things. You've written about this a lot. And there's also early detection, which is really something that's been getting a lot of traction in the last, you know, especially I think like five years, you've seen an explosion of conversations around early detection.

I've heard different individuals in this space say that, you know, there's a lot of There's things that we can definitely do for prevention, but there's a lot that is out of our control with prevention. But early detection is something that we can hope that more and more people have access to. Right now, unfortunately, it typically is somebody if you have resources, right, financial resources, you're going to have access to some of the most cutting edge early detection tools that are there, diagnoses. Talk to us about a couple of those that seem most promising.

especially if people do have some resources to put into this area that most of us will end up dealing with a cancer diagnosis in our lifetime. Yeah, and it's important. I want to start this off by talking about the importance of socioeconomic status in relating to those preventative measures we can put into place. Obviously, socioeconomic status, the amount of money we have is going to play a role in terms of our access to these things. But in terms of technology that I think is at the forefront of preventative measures or reducing risks for cancer, I would put companies like Prunovo and we've we've spoken about this offline at the forefront of that in terms of changing the way that we use imagery analyses or scanning methods to detect for for cancers in

earlier stages. As far as I understand, Prunovo doesn't use contrast agents. They use a specialized image algorithm to basically generate high resolution images without having to inject contrast. which is different than most PET scans or CT scans or radio labeling imaging or radio labeling image-based methods. Yeah, it's a full-body MRI. Yeah. We had the CEO on, no affiliation to the company. Yeah.

I'm guessing you as well, no affiliation with the company. Zero affiliation, yeah. And there's many of these companies that are entering the space. So who is or who could be thinking, if they have the resources, right? And you've already given the disclaimers that not everybody does. who should be thinking about using this and when from everything that you've come across. Yeah. So I think everyone should realistically be thinking about this. Anywhere from, you know, I just turned 32, well, not just turned 32 last year. I'm almost 33.

I think anywhere from the age of 30 onward, because we are seeing a prevalence of cancer rising in younger ages, which we can talk about a little bit later. But, you know, I think it's important to think about these things early on and try and put ourselves, if we can, in a position to be able to afford these things. Now, right now, while Pernuvo isn't covered by insurance, I think eventually as it becomes more mainstream, it will eventually be covered by insurance. There's a lot of issues regarding insurance, too. But I think eventually, you know, the more we discuss these things, even on podcasts or in

mainstream media, the more of these things will be generally accepted in society and become a part of patient care because they are super helpful, companies like Prenuvo or companies like like grail, which is doing blood-based tests. There's a variety of different types of those which detect circulating tumor DNA. And again, the earlier you can detect any sort of cancer, the better your outcomes are going to be in any case. The same would be true with any disease. But, you know, since we're talking about cancer, that's my expertise.

The earlier you can detect any cancer, the better off your outcomes are going to be. So per new one of these other full-body MRI companies, are there cancers that they're better at detecting and do you know anything about like how early certain cancers can be detected? I don't know all the specifics regarding MRIs, sorry, per NUvo's technology for their MRI capabilities in detecting cancers. I imagine an MRI service would be better at detecting some of those more challenging cancers that we've had issues detecting before like pancreatic cancers, like liver cancers, ovarian cancers, you know, things that there aren't. aren't good screenings for in the oncology space.

But, you know, there's every test has its pros and cons, right? So where you wouldn't use an MRI to find one type of cancer, you could use another blood-based test to try and offset the false positive or false negative risks that come with with a test. So you could do an MRI and then you could also do something like a blood-based grail test to see you know, if you're getting the same sort of measures in terms of if a tumor is detected. Yeah. And I think multiple tests will be able to answer questions. The more evidence or more data you have to support something, obviously the stronger conclusions can be. For sure. And for those that didn't see that episode, I paid for Pernovo. I went in and did it myself. I was just curious.

I'm always curious about these things. I think the cost was like somewhere around like $2,000. Yeah. Something like that. So not cheap. And also. or two, I'm totally willing to sacrifice, you know, I'm not like a drinker or anything like that, but I'd rather sacrifice like, you know, as somebody who's paying attention to space, seeing cancer rates rise amongst young people, seeing just how it's also in the top four, right, of the top diseases that are there. I think cancer is number two. Cancer is number two.

Yeah, hard disease first. I'd rather sacrifice some, you know, bullshit luxury thing or experience. to like prioritize my health. And from what I understood about Pernuvo and other full body MRIs, we'll link to some of the other ones in the show notes below. So, you know, we're not favoring one particular company from my medical team, my medical doctors that were there is that, you know, because no cancer was detected and we went through my full sort of screening, in addition to like looking for cancer,

all the other stuff they'd look for, it's generally something that I personally probably do once every five years maybe. I think that's reasonable. And so maybe a little bit more frequency or greater frequency as you get older. Yeah. Until you're 60s or 70s when you would expect the rates of cancers to arise. Yeah. And as you said, you know, early detection with all these diseases, even a heart disease.

Any disease. Any disease? Like that's going to be our ticket for getting to the root of it. You know, there's the classic story that people hear of, especially when we're, when it comes to things like breast cancer. This was my mom's case. She's in the shower, right? She's showering and washing her body.

And, you know, one day just kind of actually feels a lump in her breast. And that was the decision to go in. It's a self-detection sort of situation. I don't know exactly the timeline of when she had had her last mammogram, you know, in context of her own sort of self-detection test. and then she went in and even though it was early, you had, you know, that tumor had been growing for a little while. Yeah. I mean, they don't just pop up.

I mean, some cancers are more aggressive than others or they don't just pop up at a thin air. Right. Yeah. So anything that we can do to get to it early. You mentioned another one that a few, some of our audience might have heard some other guests talk about, but it's worth getting into. And it's like the blood biopsy test, the grail says. Yeah. What are they good at?

Where are they maybe still limited or, or, or, or, or, or, or, you know, or, or, or, or, you know, potentially, yeah, what are they good at and what are they not good at right now? Yeah. So like we've mentioned, any test is going to have its pitfalls. Grail, the thing that I really respect about them is they're very science driven, they're very data driven. They've published all of their results in terms of the cancers that they're good at detecting and the cancers that they're not so good at detecting. Now, I did a post on this a while ago. I can't remember all the specific details because it's quite a bit of data about which cancers they were better at detecting. But I will say that from their data, what I do remember

is that they're better at detecting, again, some of the more deadly cancers in society, like pancreatic and liver cancer, that we don't have great treatments for in the clinic, typically, compared to, you know, things like breast cancer that have other, or even ovarian cancer that have other more effective treatment strategies. And again, the way that this test works is it detects circulating tumor DNA. So you give blood. You give blood. You give blood.

They take blood. They take the blood and they purify DNA from it and you can detect mutated sequences of DNA because whether Thomas Seyfried and I agree on this, I'm not or not. There are some cancers that have initial mutations that you can detect in an early stage because there's a thing called and I want to talk about the biology behind this because I think there's a lot of misunderstanding there. There's this thing called the two-hit hypothesis. You need multiple events to cause a cancer.

It could be either a DNA mutation or it can be spontaneous or it can be epigenetic driven, so your environment, things like smoking or drinking. And so if you can catch one of those early mutational events by utilizing one of these blood tests, you can reduce your risks for cancers. This episode is brought to you by Cozy Earth. I've recorded over 400 podcasts to date,

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slash d hr you to save $250 off your first diagnostic and optimize your health and longevity today. With some of these grail tests and a lot of the clinicians that are ordering them, they tend to be more in the concierge space, precision medicine space, functional medicine space, integrative space. And there are obviously a lot of practitioners that are like at hospitals or in the latest up and up. I've heard of people in like executive health programs, but generally speaking, it's not like your, you know, standard, you know, primary care physician is ordering these tests that are there, right? They're not going to be educated on it. And it's not something that's typically covered by insurance. Right. So that's why it's not going to be.

It's one of the issues of insurance. Yeah. Yeah. For the doctors that are ordering this and just to be clear, things like per Nouveau full body MRIs, they're direct to consumers. So you can order it directly, right? These grills test, from my understanding, you have to get somebody to authorize it, like write a prescription for you to be able to do that. One of the things that they'll often talk about is the importance that the results need somebody who's educated to be able to go through it with you because it's not clearly like, you have cancer, you don't have cancer.

There's a, from my understanding, and you tell me if you know anything about this, there can be sometimes what are false positives. Yeah, and that would be true with an MRI test as well. So I think even Pernuvo has a series of experts that look at their, or even your imaging data that you acquired from when you did it to be able to make the assessment that they didn't find any cancer. It's the same with the grail test. And again, that utilizes circulating tumor DNA, which once they purify that DNA from blood, they run it through a sequencer and they can detect variants of genes to see if there's mutated sequences there. And that's the basics of how it works. They can also check for, I don't know if they're, actually, I think their test checks for

DNA methylation status, which can also be indicative of which genes are turned off in certain, and relate to certain cancers. But that's just my general understanding of how their technology works. Yeah. Do you know the cost of the test? I actually haven't looked into it. I haven't looked up. I haven't looked into it.

I don't know if that's on their website. But again, I think once that test is collected, it has to go back to Grail to be analyzed by their experts. And then that information is sent off to a physician or a physician to distribute to the patient. Yeah. Nonetheless, we're highlighting these two because these two are an example of early detection that has strong evidence behind it. Not necessarily accessible to everybody yet. But if you do have some resources, you would generally say these could be things to not only think about, but potentially prioritize if you have a history of cancer or you're worried about sort of getting

cancer one. Yeah. Yeah. I think it's super important for those who have a history of cancer to try and integrate these things into their health plan or their health protocol, so to speak, in terms of trying to reduce their risks for cancers. Because some people do have heritable diseases. Like maybe they're relatively rare. So someone could have like Lynch syndrome, which is HNPCCC, another name for the disease. They have mutations in DNA repair enzymes or you could have Leframany syndrome, which is a rare disease again. Mutations in P53, the guardian of the genome as we learned it in cell biology or cancer biology. And if you know that you have these heritable mutations that, you know, they increase your risks for cancer up to 50 to 60% in your lifetime.

I think Leframani patients, they have pretty much a 90% chance. They're going to get cancer at some point in their lifetime. But if you know that you have these risks, trying to integrate some of these early detection strategies into your plan would be super helpful for those people. And also educating yourself about other behaviors and things that you can do to reduce your risks alongside something like that. So we just talked about early detection, which is a new toolbox that we all have, hopefully, increasingly more access to.

And there's also the topic of prevention. You had a fantastic post on this topic that I'd love to kind of go through a little bit. And before I share the title of this post, I want to say you're really great at making sure that while people might get distracted about one thing or another or get hyper focused on some emerging idea but has no evidence around it, they should never forget about the basics when it comes to cancer. And the post started off with saying people always ask me, what's the best? way to prevent cancer. And you had five basic concepts inside of there that you really wanted to dial home. I want to touch on these a little bit out of order, starting with the first one, which was number four on your list. Can I just stop you for a second and say that the reason that I did this post is because of YouTube commenters from my podcast episodes saying that my

advice on episodes was banal or not interesting or not novel? Got it. Got it. So it's a response to I'm a response to that because it's like the basics are really all you need to know. The basics are what you need to know. And I think what you did well in this post and what you've continued to do on podcasts and other places is that you're reminding. It's like you're getting us excited as a teacher to the public. You're getting us excited about the basics. Yeah. Right.

Your doctor could tell you, hey, exercise more. Don't eat too much. That's one way. Yeah. But then somebody can go into some aspect of that that. that fully explains the details and the how to and how to avoid the pitfalls. And now all of a sudden you're energized as a patient. Sure.

Right. So I feel like you did that a little bit with this post. Yeah. And some of your other content that's there. So going a little bit out of order, out of order, the number one item that I feel that really stood out on here is number four in your list. Excess visceral adiposity is linked to 13 cancer types. And then you went on to continue to explain with beautiful cat images inside of

there. Yeah. that obesity is linked to 13 different cancer types. Talk to us about that. Sure. Yeah. I mean, it's as it says, right, so it is linked to obesity is linked to 13 different cancer types. And that's directly related to the amount of visceral adiposity, someone who says, or someone has, because there's a lot of negative stimulation or negative associations to the BMI. So that's why I emphasize using specific words like visceral adiposity. So that way there's no preconceived notion about the limitations of BMI.

But what we do know, and I'm going to try and keep this simple, excess visceral adiposity can lead to dysregulation in pancreatic metabolism, liver metabolism, kidney metabolism. And you see a lot of those cancers arise in chronically obese people, people that don't resolve their obesity, the levels of visceral adiposity. So those chronic associations to having excess amounts of visceral adiposity can lead to those specific types of cancers by messing up the metabolic balance between those organs because they all need to work together to keep you healthy. That's the short of it. So again, visceral adiposity can screw up the metabolic rate and collaboration between organs like the liver, the pancreas, the kidney, which can lead to

cancers. And so that's why I frequently tell people exercise, one of the most important things you can do, sleep, you know, circadian biology relations to sleep and metabolism directly, because my wife, we spoke about this as a circadian biologist as well. And that's just, again, that's just trying to keep it simple. We have all the fancy mechanisms behind how these things can mess up the metabolism in various organs like the kidney, pancreas, liver, heart even, and the list goes on. So trying to reduce the amount of visceral adiposity that someone might have, you know, to a relatively natural level because you need some visceral adiposity can increase someone's or I guess increase someone's longevity. And you're talking about being chronically obese.

Does the same apply to people who are, obviously there's different levels to how much visceral fat somebody might have? Sure. And there's different ways to describe somebody's body composition, body mass, etc. Is there a healthy or an optimal level of body composition that people should be shooting for and it would be different in men and women? Of course it's different. So that's the first thing I was going to say. It's very different between men and women because typically women hold more fat than males.

It's a lot easier for males to lose weight than it is females because of our metabolic differences largely surrounding estrogen metabolism, largely not only. But I mean, I can't say specifics because that's going to vary on a person by person basis in terms of fat percentage that would be considered healthy. But I think as long as someone is integrating those behavioral traits that are associated with the basics in terms of their health outcomes and they're doing the best they can to prevent chronic obesity, then that's all you can realistically expect of somebody. And that's why I try and make my advice realistic on my mind. platform, I don't want to just tell somebody you have to get down to this level of body fat because that's going to be optimal for you. Because it's hard for me to determine that without all of their medical information as well, which is another danger of being on social media.

People are so quick to ask for advice, but realistically, there's so much personalization to a person's health care plan that we need to consider that we don't have all that access to. So that's why I can't give those specific percentages. Yeah, you may not be able to give the specifics, but you can give the themes and the theme that I took away from this, you tell me if if this is right, being significantly overweight and being obese, and you might have to look up what that is because there's so many people that are obese today that I often see that people who may fall into that category. And it's very complicated sometimes of how people end up there. It's extremely complicated, yeah. They may not recognize, just like if you go to the average person,

you say, hey, do you eat healthy? Yeah. And they'll say, yeah, yeah, I eat healthy because their friend smokes a pack of cigarettes a week and they only smoke two cigarettes a day. Yeah. Right. Or their friend drinks a liter of Coca-Cola a day and they only have two or three sodas a week, right? So everybody has a different variation that's there.

So people would have to maybe look up, but there's a lot of individuals that may fall into this space. Absolutely. And it's worthwhile to pay attention. So I will also add there are genetic predispositions to obesity too. So those people would have hypothetically a harder time losing that visceral adiposity. So that's another reason why I can't give the same advice to everybody. But in general, being overweight and chronically obese is linked to an increased incidence of cancer.

Yes, absolutely. Yeah. Okay, great. Let's go to another one of the basics that are there. Number four kind of gets into number three, which is there, is maintaining a healthy weight, right? But there's a part of that that you've been highlighting a lot. and you kind of touched on it too, is that exercise is going to be one of the most powerful tools in the toolbox.

Now, even the concept of exercise and what it can do for weight loss versus weight maintenance has been, you know, debated and talked about from what I understand, and you correct from wrong, besides exercise giving so many different benefits to the body, it may not necessarily be the best strategy of losing weight, but it's a great strategy of maintaining your weight. Is that the way that you see it? That's the way I see it, but I also align with Dr. Gabriel Lyon's message in this and that, like, it's shifting this paradigm of thinking of not being so hyper fixated on fat metabolism and trying to emphasize that exercise will also help to build muscle, muscle tissue.

And we know that up to a certain degree, the amount of muscle tissue that somebody has will also increase their longevity, their health into, you know, age, to older age. And I think a lot, we have mechanistic implications from, but from a physiological perspective, your skeletal muscle is directly tied into how your immune system works, your lymphatic system. You know, how your heart has, you know, pumps blood throughout your body. Your, your skeletal muscle or your lymphatic system doesn't have a pump like your heart to move lymphatic fluid throughout your body. So your muscle contractions actually do that. So if you go and you exercise, or even just like sitting still, like your muscles have slow and fast switch fibers,

they'll stimulate lymphatic fluid movement, but exercising can can increase the rate at which lymphatic fluid is moving throughout your body. In your lymphatic fluid, you have immune cells moving through lymph nodes. They go into lymph nodes. They interact with antigens or damaged materials to help clear it from your body, in essence, to try and keep you healthy and free of infection. So I can't emphasize this enough. Exercising is one of the most important things that you can do for your health.

I don't care if it's walking. I don't care if it's jogging in place. I don't care if it's going to the gym and lifting, you know, as much as Lane Norton or some of these other power lifters lift. If you enjoy it and it's something you can consistently do for the end of time, that's what you do. And it's going to change as you age. So your fitness plan needs to change as you age as well to meet those exercise demands

so that you can be healthy and produce risks of cancers. That's great. So just being active and looking to be a little bit, be more active than you are if you're not that active and you're living a sedentary lifestyle. And for those that are not sort of familiar, we've had multiple experts on the podcast come who are deep in the space saying, you know, people need to remember that like getting less, getting 4,000 or less steps a day is like considered sedentary. And a lot of people don't realize they're probably around like that 4 to 5,000 average,

even if they think that they're moving around a lot in a day. When you finally put on an Apple Watch or a aura ring or something. you are not getting as many steps as you think you are. Yeah. So, I mean, I have to personally admit this too because as I've ventured into my own career in the biotech space, my lab is like right next to the lab that I work in is right next to my desk. So I found that since I've started working there, I haven't walked nearly as much as I previously

did like in grad school. In grad school, I was getting like 20,000 steps a day walking around in Philadelphia between the lab and different buildings and stuff. but as I ventured and I've gotten older into, you know, the workforce outside of academia. At the ripe old age of 32? The ripe old age of 32. I already feel like a veteran. I'm not definitely.

But as I, you know, as I ventured into, you know, my own business endeavors and things like that, I found that I'm moving a lot, a lot less. My watch is, my Apple watch is an indicator of that. I'm maybe maximally getting like one day I looked at my watch. I was shocked to find. I only had 2,500 steps that day. And it was already 6 p.m. I'm like, Jesus, we need to go for a walk. So my wife and I went for a walk.

And, you know, I got up to around 4,000, 4,500 steps that day, but I was like, this ain't going to fly. And when I went to Dr. Lyons Forever Strong Summit, she was actually picking on me because my cardio respiratory capacity has taken hit because of that. I used to run like crazy. And when we were doing the training session with Don Saladino and, and that crew, it was, it was embarrassing. She's like, Joe, what hell happened to you?

But yeah, so again, important to move, increase cardiorespiratory capacity, get those steps up. This episode is brought to you by Lombox. Red Light Therapy with Lombox is a part of my daily practice. If you've tuned into my conversations with experts like Dr. Anthony Yun, you're already familiar with the incredible benefits

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Just go to the loombox.com slash Drew to get your device. That's the L-U-M-E-B-O-X.com, the loombox.com slash D-H-R-U to start stimulating your mitochondria today. One of the ones you touched on, and again, you mentioned Dr. Gabriel Lyon, also a close friend of mine just like you, love her work. She's been on this podcast and shared a lot of her great messages. When it comes to cancer in particular, you know, jumping around a little bit,

there's an area of her message outside of cancer. I loved your guys' podcast together. Thank you. Is why it's so important to maintain muscle, muscle-centric medicine and how protein is a big part of that in addition to, you know, working out. You've added in that especially for patients that are diagnosed with cancer, you know, there's a lot of questions that people have about protein, but you've mentioned why it's so important to maintain muscle mass, both, you know, hopefully to knock on wood,

avoid cancer. I'll knock. But then also, if you are diagnosed, why it's so important to maintain muscle mass through the process. Can you chat about that a little bit? Sure. Yeah, I think a lot of times in the cancer space, especially in academic works, because we need publications to be able to be considered as scientists and move through the academic track.

As part of that, we tend to hyperfixate on mechanistic implications because those mechanisms get us into the big journals. You can have the phenotype, but at the end of the day, nobody gives a shit about phenotype in the academic world. You need a mechanism to support the things that you're seeing. This specific thing does this. This specific thing does this. So I can show that X drug kills cancer cells. Small journals only care about that. But I want to show most people want me to show, you know, how that drug is killing the cancer cells. Is it affecting a specific process which is leading to cell death? Or maybe it's not cell death.

It's causing them to stop dividing and just be cytostatic versus toxic. The variables there are enormous. But we tend to hyperfixate on these mechanisms. One of those would be like mTOR metabolism, which is directly related to protein metabolism or muscle protein synthesis. Oftentimes in many diverse types of cancers, we'll find that they'll increase the metabolic rates through EMTOR to enable cancer cells to utilize amino acids to feed into metabolic processes, which enable cancer cells to continue growing.

That is an extremely oversimplified way of saying, and I'll simplify it even further, I guess, it's a more simplified in saying that amino acids have been shown to fuel cancer cell metabolism. And so a lot of people take this mindset and they say, okay, if I starve a cancer patient of amino acids or protein sources, because proteins are amino acids linked in chains, called polypeptides, if I deprive them of those amino acids, reduce cancer growth. That's not how it works. If you deprive a cancer patient of protein, you're going to reduce their chances of survival significantly because there's a lot more to physiology. regarding normal cell health and cancer cells that if you deprive someone of those nutrients

like protein, you're going to negatively affect the healthy cells more so than the cancer cells. And you also may not get the protective benefit if they are not as active, they're not having enough protein, they have a lot of muscle loss, their body's going to be more frail. Exactly. And it's not going to be as metabolically healthy because they don't have as much muscle. Yeah. And you also have to think about behaviors that come along with, you know, consuming protein. That person's more likely to exercise as well. So those compounding factors will increase their response to not only therapies, but also increase their lifespan as they

go through or survival chances through cancer. So again, we need to stop hyperfixating on these mechanisms. They're very important in terms of how we decide to treat the disease, but they're a very small fraction of the total human health picture. And I think that why that's important to talk about, and we'll kind of get into the landscape a little bit more, is that when you hear different researchers as a layperson, which I am, I have no degree in this space at all, no expertise, no nothing. Every so often I get lucky enough to have somebody like you on the podcast and I can ask these questions to.

I'm lucky to be here too. But when you have somebody on that speaks with authority, it feels like it's a settled deal, right? We're here in Los Angeles, not too far away. is the research lab and work of Dr. Walter Longo, you mentioned him. He's come on this podcast, and he was one of the first people that I had heard about talking about how mTOR specifically leads to, and I believe it was through his mice research that they were feeding mice and that because they saw this mTOR continuously being spiked, and then it's connection with the cancer cell tumor growth.

Right. Again, super oversimplification. That was just the way that I was understanding it. That's correct. Yeah. Correct interpretation. And then I would see different analysis. I think I saw Lane, a buddy of yours. Yeah. And Dr. Lyons, Lane Norton, PhD researcher. We haven't had him on this podcast, but we've had his PhD advisor and Dr. Lyons program advisor, Don Lehman. Don Lehman. Yep. Dr. Donald Lehman on the podcast to talk about protein. And I saw Lane's analysis. of it that he discussed and wrote about with Peter, where he said that, you know, we have to understand that in that type of study, and I'd love to hear your thoughts on this, you know, they're, first of all, these are mice. Mice are not human beings, but they're still our contribution. And we have to, it's a stepping stone. It's a stepping stone in the right

direction. But those mice that are being fed, this higher protein diet or whatever it might be, those mice were being continuously fed throughout the day, no restriction. So if you're constantly eating, as mice would do if they have access to a lot of food, you're going to constantly be spiking mTOR in this example versus, let's say, if they were meal fed where you had a meal, you gave your body some time, and you had a meal again. Like everyone eats? Like everybody eats. It would be different or I don't know if it would be different or it has been proven to be

different. I don't know about that. It has. So those dietary and metabolic considerations have been shown across a variety of different disease contexts. And then the secondary component was that there are other things that also spike mTOR like exercise. Vigorous exercise will spike mTOR. And then naturally it'll come down after that process. But if I made you vigorously exercise for 24 hours a day, besides not getting good sleep, you would probably have. have a spiked emitor. That would also cause kakeasy at some point, though, too. So part of what you're saying, and obviously what Lane was saying there and Peter and him were reflecting on is that we have to sort of stress test some of these ideas from all angles

and see if they make sense in context. A lot of people took that. I know individuals like David Sinclair took that and would talk about on the Joe Rogan podcast, hey, this is why I'm eating a lower protein diet. I think at one point in time he even maybe went, not that plant base and low protein have to be synonymous, but I think he even went more in that direction and started reducing a lot of the protein in their diet. And so the person who's out there who's just like, well, I don't want to get cancer one day. I, what do I need to do? Okay, protein causes mTOR spike. MTOR leads to tumor cell growth. I guess I got to go on a low protein diet. Yeah. There's so many people that employ this sort of unrealistic messaging on social media. Again, the science is fun.

The mechanisms are fun. It's really cool to think about these things. But as Peter and Lane have pointed out and a few of my other colleagues, not that they're colleagues, I don't know personally. I don't personally know Peter, but Lane as an example, you know, we need to stop hyperfixating on these mechanisms and try and put it in the grander scheme of how things are going to actually translate to human health outcomes. As you point out, you know, in our research, we need to stress test certain things, which means we need to flood the system with, in this case, mouse models, with the thing that we're trying to study to see if it can cause that phenotypic change.

Because if you do those physiological considerations, if you just gave the appropriate dose of something, and you've heard this many times, the dose of something makes the poison, if you give that appropriate dose, you're going to have to be in that lab for, years, many, many, many years, like 10, 20 years. And as an academic professional, you don't want to do your postdoc for 10 to 20 years doing observational studies over 10 to 20 years just to try and dwindle down a mechanism so you can publish in nature. So oftentimes we flood the system with a substrate or a material or with trying to answer whatever question we're doing, whether it's protein, we feed them chronically with a ton of protein or a ton of fat. I studied liver cancer. You give them

ridiculously high fat diet to cause deatosis and liver damage mice mice mice mice models of course and even then they'll still develop tumors within like small tumors within 56 to 60 weeks still takes a ton of time and what if you don't get tumors because the heterogeneity of model research of mouse model research sometimes you don't get those tumors and so it's hard to get mechanistic stuff from that. So that's why we stress test these systems to be able to exacerbate a phenotype that we're trying to see. But this also takes away from the physiology of that thing because we're stressing it out so much. And so that's why it's important to corroborate those findings to human studies to see if there's been clinical trials that support the things that we're

finding from a mechanistic perspective. And the best papers do that. When I was asking Dr. Longo about this a little bit. Not as in in much detail because I didn't know about it as much of the time when he first came on the podcast. He was saying, okay, look, the mice research is one part of it, but we also have these food survey questionnaires amongst this sort of healthier populations that he studies. And then we also have the centenarian data in places like Italy, where he's doing a lot of his work and research. And so we can look at those. And so we can look at those across the board, it could say that generally these people that are living longer, there's some component to, you know, obviously making sure you have, he said, he was said adequate

protein. I think he means by like dietary guidelines. Which actually we're learning is, is relatively low. We should be increasing that. But right, right. It's another argument. So that was not in defense of him, but to sort of make sure that I sort of communicated. What do you think about some of those in sort of the hierarchy of evidence that's out there? So, and I'm fairly certain Volta or Dr. Longo would agree on this too is that's purely correlative evidence and not causative evidence. Questionnaires are a pretty poor metric of data quality because you can't control for how people answer those questions.

And a lot of times people don't know if they're answering the questions appropriately too. So while they can give you a decent metric to be able to say that there's something interesting going on, it's just that. it's just something interesting going on. Until you have multiple sets of data to corroborate those findings, you can't make conclusive statements from them. And I think that, you know, when people try and understand the complex research of people like

myself, my own metabolic works or people like Dr. Seyfried or Volta's studies, they're very mechanistically complex. When they try and understand those, it's kind of lost in translation because they are very complex. And so people tend to hyperfixate on those simplistic evidence that they gather because they can understand them. But they're not as causative as they think in terms of disease risk and outcomes. Have you seen it all when I was looking at Longo's work, not to make this about him, but just kind of continue.

I respect him very much. Yeah. One of the things that I felt asking around that people were most excited about was the fasting, mimicking diet and their papers that were published, I believe in some prominent journals of doing fasting mimicking diet right before introduction of chemotherapy if somebody was using chemotherapy to address their cancer and how there was something like, and we'll link to it in the show notes below, but if I'm remembering correctly, there was like a 25% improvement if somebody had done the fasting mimicking diet that they sort of recommend before doing chemotherapy. Had you come across

said at all? I've come across similar findings even regarding ketogenic diets and stuff too. So is there any truth to that? And is there any, you know, what's real or what's not real? I will always tell you this. The context always matter. Yeah. There is truth behind it. Currently, we have evidence to suggest that these diets in combination with, not the diets alone, diets in combination with treatment, can help shift the metabolism of tumors to be sensitive to that chemotherapy. But those have to be, be determined in very clinical settings. They can't be determined objectively outside of the clinic in like case studies. It's important to do that stuff, obviously. But right now we can't conclusively state that these things are going to be super helpful in most cancers. We need to understand the

context. I would say that these dietary interventions alongside chemotherapeutics or immunotherapies or even surgery, are there these variety of different methods to treat cancers, they're going to be more helpful in later stage disease, I think, to deal with things like metastasis, not necessarily an earlier stage. And I had sent you a paper that kind of pointed out that cancer cell metabolism is actually slow, especially as the disease progressives. Yeah, actually talk about this for a second because you did a big post on this. Yeah.

This was kind of like in the world of cancer, it was kind of a big deal the way that I understand that you're writing about it. Yeah. And the way that I would set up the conversation was that for a long time, the assumption was that cancer cells are way more active than sort of healthy cells inside the body. And there was a paper that I understand to be kind of groundbreaking in the space that showed that actually cancer cells are sort of slower or not as active as healthy cells. Is that true? And what are the implications of that? So again, there remains a lot to be determined about how true that is, but essentially they did, this is Caroline Bartman, Dr. Caroline Bartman at UPenn now. Their work established a mathematical model to determine the rate of how molecules move

from glycolysis, the breakdown of glucose through glycolysis into the citric acid cycle, which is in the mitochondria, and through the electron transport chain to produce energy called ATP. And now for a long time, we've just generally made the assumption that, you know, from Otto Warburg's findings back in the 1920s, which we've named the Warburg effect. Because of those findings, we've seen that cancer cells dramatically taking glucose, and we've always assumed that because they dramatically taking glucose, they must have increased rates of glycolysis, the citric acid cycle, and the electron transport chain to make energy so that they can grow.

But what this new study found was that the glycolysis part is very fast. So they take in glucose, they rapidly break it down. But the output for the output. from glycolysis doesn't directly go into the citric acid cycle. It goes to producing lactate, which is why the Warburg effect exists. So they kind of like proved the rate associated with glucose intake and the Warburg effect, supporting Warburg's findings, but they showed that the downstream components of glycolysis were much slower than a healthy cell because a normal cell will go at a normal rate through glycolysis, citric acid cycle, ETC to make ATP. But cancer cells, they kind of slow down very

dramatically the citric acid cycle and the electron transport chain dramatically and that was the counter evidence to what we we thought was happening it turns out that they're taking materials from glycolysis because they're getting a lot of glucose and they're putting it into other pathways like other biochemical pathways like the pentose phosphate pathway and while all these pathways don't necessarily mean anything to the layman essentially it tells us that the energetics of cancer cells aren't what we thought they were so that's why going back to the dietary components, we need to be careful about the advice that we give because it's not like cancer cells are utilizing the fuel sources the way that we thought they were. And so in late

stage disease, if they've adapted this metabolic characteristic of slowing down the citric acid cycle and we give an inhibitor against an enzyme in the citric acid cycle and they've slowed it down, the likelihood of that inhibitor doing something is going to be lower. So we want to consider the context of when those therapies will be useful. And that's why I say like those dietary interventions can change the metabolism of cancers too. So there is some evidence of these dietary interventions, but the context is we don't know when to apply them, when would be most helpful, and a lot more research is needed on that

side. Yes, but it is very promising. And there are clinical trials going on examining, you know, fasting in chemo and ketogenic diets in relation to combinations with. chemotherapeutics in pancreatic cancer, I believe, actually. So we were talking a little about Longo's work and jumping around. Sorry, I went on a tangent there. No, no, not at all. This is why we're here, you know, long format. I want to come back to

Safe Free. You know, he was on this podcast. And again, I'm just using him, but cancer as a metabolic disease, that concept, there's obviously other people that are talking about it, right? And from what I understand from Safrey, you know, he mentioned Otto as well in his research. It's hard not to. Can you just talk a little bit about that? Because I don't think our audience knows about it that much. About Otto Warburg? Otto Warburg, who he was and what he found and why it was such a game changer for the understanding of cancer.

Okay. So we'll take a trip back to the 1920s, right, where Otto Warburg was doing his research, actually between Nazi Germany at the time. And so basically, Otto's studies show. that, you know, cancer cells, they're producing lactate. And he was confused by that. And so he essentially metabolically characterized that they increase the amount of glucose they take in. And glycolysis is essentially sped up. And that fuels their metabolism. Of course, they made the assumption at the time that it... And just one question on that. So healthy cells don't produce lactate? Or they should? Okay, got it. Typically. So that's... So cancer cells were producing lactate.

Lactate is something you typically see as a process of fermentation. Okay. When there's no oxygen around. Healthy cell, if you deplete an environment of oxygen, healthy cells will even make lactate. But they saw that even when there was sufficient oxygen presence, cancer cells were still making lactate. And that's incredibly confusing because they have sufficient oxygen around. They're fermenting something. So that was essentially coined to the Warburg effect.

So the Warburg effect is they're taking it. They upregulate receptors that take exogenous glucose from the environment, and they utilize that continuously to fuel glycolysis to keep the energetics of cancer cells so they can continue dividing. That's the Warburg effect. There's a lot of mechanistic components there that were assumed at the time, but he did some really elaborate and very, at the time, groundbreaking studies, which showed that it was present in most human tumors. such now it's become a hallmark of cancer. So this is something I've broken down on my channel as well. We've got a variety of different hallmarks of cancers, whether it's the Werberg effect to name one, angiogenesis. Angiogenesis, which is the idea that cancer, it's creating new blood vessels. Right.

And one of the things that cancer tumors are good at is basically rapidly being able to create these blood vessels, as I understand, to be able to like... They're not good at it. Okay, they're not good at that. I will say that they're good at doing it, but the efficiency of the process is extremely poor. So the angiogenesis component ties into the Warburg effect because cancer cells as they grow, they develop into tumors.

A solid tumor will have different regions like an apple. You know, you have a core of an apple. Tumors can also have a core. It's hard for oxygen to get into the core of that tumor. This is what we call hypoxia. lower oxygen tension. And so hypoxia, low oxygen, can stimulate a response to cancer cells where they'll secrete materials to recruit blood vessels to grow towards a tumor.

But because the tumor is so dense and that oxygen diffusion throughout the tissue is dysregulated and it's quite hard to diffuse oxygen through that tissue because of a variety of different physiological opponents of a tumor, the blood vessels end up being very poor integrity compared to a normal blood vessel. Like you can look at your arm and see, you know, healthy blood vessels. The ones in a tumor, if you look at the blood vessels in a tumor, they're leaky. They're not good at diffusing oxygen into the tissue. And it worsens. You'll see a lot of turnover in cancer. Like there's a lot of cancer cells in a solid tumor that are dying at the same rate that they're also growing in some cases. And it's because of,

faulty oxygen tension within a tumor. And so the blood vessel recruitment is an attempt to bring oxygen that realistically it's not getting enough of. But it's trying its best to get more because it requires oxygen to grow. Got it. So taking it back, you know, these are the hallmarks of cancer. And those are just two of them. Those are just two of them. There's a Wallberg effect. The, the angiogenesis, there's a bunch of others. We'll link to some of your content where you sort of break this down. But you were going down this idea of like these, hallmarks of cancer are now the standard sort of understanding of what is cancer and why is cancer essentially. Is that correct? Yep. And a lot of Warburg's findings stimulated a lot of our

understanding of the hallmarks. Got it. So one of the things, you know, while I have you here, there's a good opportunity to sort of clarify and put things into context. Sure. So when we have somebody like Seafreed coming on and summarizing the research of his group and other groups that are out there that are doing similar work and are saying that there is, and going to his sort of early book, which is based on some of his early studies, the individuals listening to that would walk away. And also we recently had on, you saw the Hippocrates Research Foundation, and they have somewhat a few case studies of individuals doing the Pulse Press protocol. you would walk away and you think, okay, cancer is a metabolic disease, right?

Is there truth to that or is that a limited understanding of what cancer is? So, you know, I think, so I'll start by saying this. There's 100% truth to that. I think if you asked any oncologist or any cancer biologist, they would tell you that cancer is not only a genetic disease. There are genetic components, but it is driven by a metacologist. metabolism in many, many ways. And if you look at, you know, the past, you know, 30, 40 years of therapeutic development,

a lot of the drugs that we've developed have been designed to target the metabolic components associated with the disease. So I don't think any oncologist or cancer biologists will argue that it, that it's not a metabolic disease. It is 100% a metabolic disease. But it doesn't mean that we can ignore the genetic components that are associated with, you know, things like mutational burden on metabolic processes in the cell. A good example that I like to give is K-RAS mutation.

And I point back to this. I'll talk about a paper briefly. They did a paper, I think it was back in 2016, showing that in lung cancer mouse models, You can give them a, again, stress test the system with cigarette smoke condensate, healthy mice. They gave them a bunch of cigarette smoke condensate, and eventually they developed a mutation in KRAS. KRAS is significantly mutated in many types of lung cancer.

Now, that KRAS mutation alone, despite it being present because the carcinogen induced the mutation wasn't sufficient to develop the tumor. This points back to the two-hit hypothesis. need more than one event. In this case, the spontaneous event of smoke exposure induced a mutation, which led to dysregulation in a metabolism associated with K-RAS, which then destabilized metabolism even further like a domino effect, which cause other things to happen, which can lead to cancer. So it's not just one event. It can be a genetic event. It can be a spontaneous event if it's a heritable mutation or if it's like chronic exposure to smoke or you know drinking alcohol but you need

these events to essentially enable tumor formation and so again it's it's hard to dissociate the genetic component from the metabolic component because they do both play with each other hand at hand so any again any cancer biologist any oncologist would tell you that both play together in disease formation for cancers. So hopefully that clarifies things. No, it does. I mean, the thing that I take away from it is that yes and but, right? It's like all those components together for all aspects, but especially cancer.

And I think what's important, and I haven't heard you say it exactly like this, but this is the takeaway that I got from you. Like we think of cancer as one thing. But each and every cancer is like almost like its own disease. It is. They're very different. Yeah. So things that would work, which you have said, and maybe really well for one particular type of cancer, may not work as well for another particular type of cancer.

That doesn't mean that we poo-poo the emerging stuff that's there. But where you are most, you know, sounding the alarm, sometimes you'll feel frustrated about this. And I would feel frustrated if I was in your same boat, too, is when people exaggerate claims. And that leads to a false sense of hope for people who have cancer. or a sense of blame for people who also have cancer, whose family members have passed away from cancer, like your mom, that,

oh, it's because of this exact one thing that he or she or they didn't do, and that's why they got cancer. That's what you're really trying to make sure that, you know, in addition to people not ignoring the basic advice that's there, that you call out because it's quite damaging.

Did I get that correctly? Absolutely. And so that's why it's super important for me as a communicator to communicate effectively to people and honestly with 100% transparency. I find that the controversy isn't because the scientists are conveying a specific image. Like, again, you know, safe read and they all have their own agenda in terms of, you know, what they want to do in their research. But at the end of the day, they do great work.

A lot of the controversy comes from, I don't know how polite to say this, but there are charlatans on social media that come out and they try and interpret my work. They try and interpret Safe Reads work. They try and interpret Longo's work. And they don't have the expertise to do so. And this isn't me bashing their intelligence. I wouldn't expect myself to go into whatever field that they do and expect to be an expert at it, just as I wouldn't expect them to come into my field of study and be a pro at reading, you know,

Walter Longo's cell papers. I can barely understand cell papers half the time because they're so complicated. I need weeks to digest it. The paper I sent you, I needed weeks to digest, months to digest to where I was able to effectively communicate the findings from that study. And so that's where the controversy arises when you have these charlatans that come out and they make bold claims about things they essentially don't understand. A good example of this is Benazotti tried to interpret Walter Longo's statements and Thomas

Saferied studies. And he went on and was talking about a seven-day water fast. and Saferied wrote an article later in counter, countering Benazadi's statement, was like, I never said any of that. It's because Benazati doesn't have the foundations to be able to understand Safe Ried's work, but he's making such strong and conclusive statements from something that we don't have the ability to make those statements about. And that's, honestly, that's what pisses me off about social media.

And that's why in a recent reel that I made, I was like, you know, people need to understand that as professionals in a specific field. We can't know everything there is to know about every field. That should be common knowledge to people. So why would we expect that somebody outside of my field of study is going to be able to accurately interpret my field without a proper education? I would have thought this was common sense, but it's so easy nowadays to go online and see people talking with such confidence

that we see confidence. We stop to question whether or not that what they're saying is actually accurate. because it sounds simple. It sounds logical, but at the core of it, it's not. And so that's what my content seeks to correct. I don't like calling people out. I hate it. I don't want to diminish anybody's intelligence.

I don't like talking about Benazade in this light. I respect the guy. But at the same time, it's like some repercussions need to be had because the information that they're giving is inaccurate and it can lead to a cancer patient dying. And that's what kills me. Because there's nothing that hurts me more. that when a cancer patient comes to me and says, you know, my mom or somebody took this advice

and they ended up essentially dying because they stopped responding to their treatment because they took some nutritional advice or they went on like a juicing fast and did all these crazy coffee enemas and garbage that you see online that has very little scientific foundation and it hurts their outcomes. And that's why we need to be super accurate about what we say. Well, I appreciate you coming on this podcast to be able to do that. And I want to give you the platform to be able to make it happen. Thanks, man. There's a few things that I want to get a chance to sort of address to that in a kind of

continuation. And I'm not familiar with this gentleman, Ben Azadi. I'll look him up. Don't bother. Well, I'm just curious. He means well. Yeah. I'm curious.

I like to understand the landscape. What is the history? What motivates people? You know, there's probably crazy things that I believed before. Not probably. There was crazy things. I used to believe that. Aspartame caused cancer at some point, too.

Yeah. It doesn't, just for anybody listening. So continuing on that idea, there's, I want, you know, for just because it was, we featured a recent case study, I put multiple disclaimers on there saying that it was a case study. But I also, because Thomas Saferied's work in particular has blown up on YouTube, I think our original video with him has a million views. Nice.

I want to give you an opportunity to sort of provide a disclaimer for. anybody watching, let's say, I'm going to take you through a few different sort of interview types that are there. Because again, you do a good job of saying, hey, what do we know? What do we not know but is potentially promising? What do we not know but is potentially harmful? And what do we know that is straight up harmful? Right. So for anybody that has watched Safe Reed's work, the case study that we had recently on, what is an important sort of overall message that you want to share with them that we can refer back to and link to? Sure. I think that there's a lot of promise to be had there in terms of safe reeds finding, in terms of combining nutritional strategies or

metabolic strategies, as he calls them, with standard of care treatment. Regarding how much we know about them right now, it's limited, but the studies show, like, really extensive promise. I would feel confident in saying that, you know, in certain contexts, like pancreatic cancers or maybe even liver cancers, kidney cancers, those sorts of things, that there's a lot of promise to be had there regarding dietary interventions and in combination with chemotherapeutics. And again, that's just oversimplifying things so people can understand the degree of what, and I think Thomas is in agreement with what, what, what, he's trying to show.

Full disclaimer, as Thomas has said as well, he doesn't expect all of these people to, you know, get off their standard of care and try these nutritional strategies. I think it's important for people to do that. But the overall premise behind what we're learning how this works is that cancer cell metabolism is very different than healthy cell metabolism. We can exploit those metabolic things. by using diets to change their metabolism from kind of like an epigenetic perspective.

So they after before a diet and after a diet, they'll have very different metabolisms. Blanket statement. One metabolism to the next after that diet, we can then give them a chemotherapeutic that would make them sensitive. But if we didn't apply that diet, they wouldn't have responded to that chemotherapeutic. That's where the importance of these dietary interventions appears to be coming out. in combination with chemotherapy because the diet sensitizes the cancer to the drug. Got it.

That's the pulse press thing that he's going with. Yeah. If you wouldn't mind, I'd love to just go through maybe a couple more of these. Sure. You know, and it's not to, as you mentioned, you know, this is not to call anybody out, but it's to sort of add to the conversation that's there. Maybe in some cases it is to call some individuals out. But another person that's been on this podcast and actually wrote a book about cancer is Jason

and Fung. And what do you want individuals to know about some of the core concepts that you've heard from him? In particular, obviously, he's written about diabetes, and he's written about blood sugar, diabetes code, cancer code. And the cancer code is primarily about like the seed and soil theory of cancer. Let's start off with that and then you can continue on with anything you might want to add. Sure. The seed and soil hypothesis is mostly about metastasis. But regarding, Jason Fung, I will say that in general, he branches out of his area of expertise. There's a lot that he understands about cancer, but he, you know, a lot of people rely on his expertise because he sounds confident that what he says is accurate. And so when he talks about

the seed and soil hypothesis, these things sound intelligent, but he doesn't always convey them in an accurate sense. And this isn't, again, this isn't an attack on him or his character. He means, well I'm sure of that but we need to understand that he's going to have limitations in his background he wasn't trained as a cancer biologist you know so I wouldn't expect again that I would have the same level of understanding in his field of study I think it was diabetes is his his realm of research where he was trained so his diabetes code book is probably going to be better than his cancer code book the level of understanding there is going to be different

But regarding the seed and soil hypothesis, that's largely related to metastasis. So the origin of a tumor as it grows, the characteristics from where it originates is going to be very different than where it metastasizes too, because it's going to have to change characteristics to be able to get into a different organ. And this sounds super basic, but can you explain the difference between origin and metastasies? is like metacetaceous is like the full encapsulation of the tumor? Or can you explain the difference between those? Basically a tumor where it originates is the organ that it starts growing in,

the solid primary tumor, or if it's a blood-based tumor. It's kind of different because it's obviously it's in the blood. But the point of origin of a tumor is where it starts growing. Metastasis is when that tumor basically packs its bags and moves to different organs. Got it. It spreads. It spreads. Yeah.

And so in order to metastasize, again, this is also a hallmark of cancer. It's basically called epithelial to mesenchymal transition is a long way of saying that cancer cells change their cell surface to be able to detach from a solid tumor and reattach to another type of tissue. And that's essentially metastasis in a long, in a short, component. So in order to do that, it needs to, the cells themselves, they degrade the membrane below it so it can detach on a solid tumor from its primary origin site. So it decades the membrane below it to detach. And then it also needs to change characteristics to move through holes in cell

walls to be able to get into the bloodstream through blood vessels. So it kind of has to squeeze through. And so all of these things need to happen for a cancer cell to metastasize. Once it gets into the bloodstream and it gets to a different tissue of origin, it then needs to go through another change to be able to live in an organ. Certain cancers, they metastasize to specific areas because they can't survive in other organs. So, you know, lung cancers often go to the brain because they can live in the brain. They can't live in other tissues. So they often go to the brain. They form, you know, brain cancers or brain tumors. And that's only because they develop abilities where they can survive there.

So basically take up a new seed and replant its soil, so to speak. Does that make sense? I think it makes sense. The sort of the conclusion of that that you want our audience to understand about the seed and soil hypothesis is that there may be some truth to it, but it's not universally applicable in every single case of cancer? Is that kind of... No, I would say that there's a strong degree of truth

to the seed and soil hypothesis regarding metacetasis. It's just the mechanistic components vary between tumors. They don't all utilize the same means of packing up their bags and going to different tissues. They might have the same sort of methodology, but the mechanistic components about how they degrade the basement membrane, the enzymes associated with that, the characteristics at which they extrovisate or move through blood vessels into the blood and travel are going to be different between cancers,

but the overall premise is the same regarding metastasis as a whole. So all cancers in late stage try to metastasize, and they utilize similar characteristics. Metastasus is a fact. Got a seed and soil hypothesis. Despite being called a hypothesis, because it's complicated, there's a variety of different mechanisms, it is very well supported. So then when somebody like Dr. Jason Fong says, largely when I look at a lot of his advice, he's not out there advocating for people to go on water fast. He's not doing some of these extreme things from having him on,

kind of going through the book, the cancer code, when he makes recommendations of reducing visceral fat, which is something that you're on board with in general, right? Sure. We are in agreement. And typically, Dr. Jason Fung,

with his background and probably his also, his healthy bias of working in diabetes, He sways more low carb. So he generally recommends people obviously staying off of ultra-processed foods, moving towards a more lower-carb diet and reducing their visceral fat. And in some instances, obviously reducing toxin exposure. You generally would be on board with that. But the challenge is when people speak with confidence that, well, actually, let me ask you, you know, are there any recommendations that you have seen? not that you know every single recommendation he's made,

that in that particular instance, you would feel, hey, I'm not on board with that? Or is it primarily somebody stepping out of their lane and describing something in detail that maybe they don't have the fullest understanding of it? It's mostly that. So I've heard him describe things outside of his lane in detail where he doesn't have the expertise to do so.

And if he mentioned that thing about toxins, I would say that that's one of those cases. it's hard to educate people about, you know, what is and isn't a toxin. Because from my understanding, when I've studied microbiology, there's a very big difference between what a toxin is from microbial-produced species like bacteria or fungi. Things like botulinum. Botulinum is a toxin. People get Botaninjections as fillers.

But there's a very difference between getting like a filler and being infected by Botox to where it's making a toxin that's going to be essentially a paralytic. So that's why I try and not use those words without providing sufficient context. And I think when some people hear somebody like Jason Fung use specific jargon without identifying what that means and how that applies to reducing toxin exposure or maybe why somebody might go low carb, then it's easy to make blanket assumptions about it. that's where the confusion and the um that's just where the confusion comes from yeah got it makes perfect sense you know i want to talk a little bit while we have still some time here i want to talk a

little about origin story uh you know you've shared before on multiple podcasts that a big part of your why and what drove you to be in this position where you're not only highlighting and showcasing the research that we know of, right? We never finished the list before, but it was minimizing quits, minimize slash quit smoking, minimize alcohol, maintain a healthy weight, you know, sleep, sleep, increased fiber intake. Yeah, it's a big one. Get your visceral fat, you know, down, don't be obese, get into a healthy body composition, and obviously practice sun safety. That was another one that was out there with skin cancers being on the rise. There's a few others that are in there that maybe I didn't acknowledge.

Those are it. But a big part of your recommendations of doubling down on the basics, people being on guard about sensational claims, and then being optimistic about categories that might have some promise, but to understand where they have promise and where they may not have promise, a lot of what's inspired that is your own personal experience with cancer with your mom. Can you just chat about that for a minute? Sure. So when I was

Excuse me When I was 15 I was in high school obviously It was 15 Ripe old age of 15 My mom got diagnosed with esophageal cancer It was actually a misdiagnosis She her doctor who had his medical license

Stripped later Misdiagnosed her for acid reflux Which does run in the family But it was He was being very adamant not to check her esophagus or do an endosopy. And when they found the esophageal tumor, it was pretty late in terms of its development. And so, of course, with that comes very few treatment options.

All this is to say that my mom eventually went about a year and a half to where, you know, she had chemotherapy. She went into remission. But as with a lot of cancer. cancer patients, the cancer comes back with their vengeance. Remission means that there's no detectable cancer. So cancer went away and then it came back with a vengeance. And whatever tumor cells were left over that couldn't be detected, didn't respond

to the initial therapy, chemore resistance is another term for that. And they just outgrew and her body was so frail at the time that she passed away after two years of battling with cancer. So, you know, when you're young, she passed when I was 17, December 18th, 2008, 1030 a.m. Excuse me. It's hard to talk about. When you're young, it's hard to cope with that. So when she passed away, I didn't know what to do. I was on track to, man, I've always been fascinated with marine biology. And so I was on track to go to marine biology in school. At that time, I had also done ROTC. I got, I was commanding officer in my unit in high school, went, signed the paperwork to become,

you know, an army officer through ROTC in college, got a full ride scholarship that was revoked that year. They gave it to somebody else, basically. At that time, I didn't know what to do. My mom just died, went to school. My world was just ripped apart. My stepdad abandoned us, basically. My sisters and I, I had nobody.

And so when I went to school, I was alone. I had nobody. And the Army revoked my scholarship, so I had no money. I had to transfer schools to go somewhere else. Marine biology thing just wasn't working out anymore. And I was just pissed off, man. You know, cancer took my hero. And so when I started taking my biology courses,

because they didn't have a marine biology course at the school that I transferred to called St. Leo in Florida, St. Leo University. just outside of Tampa. I was just addicted to biochemistry. And a great model to study biochemistry is cancer because things are kind of f***ed up in cancer. Excuse my language. They're messed up in cancer regarding metabolic perspectives.

And so I became addicted to studying biochemistry from a cancer perspective. And so for me, it was a coping strategy. And I would just stay up until like, 2 a.m., 3 a.m. Not sleeping as I probably should have, which has probably taken some years off in my life. But I couldn't sleep until I had answers because it just was a way that put into perspective what my mom was going through, the level of hopelessness. I felt as a 17-year-old kid, I couldn't do anything. I didn't know anything about the disease. So researching it gave

me solace, peace. So that's why I do what I do. And so then I tried getting into the Moffat cancer research center after I graduated undergrad I did a spark internship there and just kept going down that path of you know getting rejected from that got a technician position was the hardest working experience of my life the guy worked for at the time was a slave driver i'm already a hard worker i'll work all ends uh all hours of the night if i need to this guy required minimum 12-hour work days nights and weekends. I did that for two years and three months of hell until I finally got into graduate school when he moved us to the Wistar Institute, Philadelphia.

And I learned of a grad school program there at the University of the Sciences. And that's when I applied to the cancer bioprogram there. And so, again, a lot of my mission about why I got into cancer biology stems from my experiences with my mom and the level of hopelessness that I felt. So now, like, the reason I do what I do is I don't want to make money off this. No offense to you. I don't care to be a public figure. I don't want to be on podcast.

I just want people to better understand this disease so they can make better choices about how they reduce disease risks, whether that's cancer, heart disease. I don't care. If there's any way I can help with that, that's why I do what I do. If you don't remember my name at the end of day, I don't care. Just do what I say and know that the level of ethical and moral responsibility behind that is of the utmost importance to me. I want people to feel less hopeless and just take their life into control. So that's why I do what I do.

And it all stems from my personal experiences with my mom. And actually the first time in my life, and I'm sorry to get emotional on this, but it is an emotional topic. Of course. So you know what? I'm going to stop apologizing. No need to apologize. The first time I felt relief from the amount of grief that I've had since I was 17 was when I defended my thesis. You know, I don't think I've told anybody this, which is kind of surprising.

you know, I walked out of the room after I defended my thesis and I just thought to myself, what do I do now? I achieved the highest degree that there is in cancer biology. What do I do with this? This is what I do. This. Yeah. So fuck all the noise.

This is how to see through that bull. Your mom sounds amazing, first and foremost. She was a character. My heart goes out to not just you now, but also 17-year-old you. And on the drive over here, we were chitch chatting a little bit about life growing up, the socioeconomic status. You know, you've kind of found yourself in limited resources. And I can even imagine losing a parent. and needing to navigate life

and all the questions that have brought up in addition to the loss. Yeah. My heart goes out to you, but also the 17-year-old you, you have a sibling. I have four sisters. You have four sisters.

All of them crazy. Crazy, amazing, I'm sure. Yeah. I love them to pieces. But yeah, brother, my heart goes out to you. And I appreciate you opening up. because, you know.

It's a two-way street. You experienced this as well. So no matter what age you're at, a cancer diagnosis, as you pointed out, early in this podcast episode, it's terrifying. It's terrifying. It's scary. It brings up so many questions. And I'm just so happy that you are doing the work that you're doing to highlight because

it is probably the most scariest disease that people can imagine. Probably that Alzheimer's, right? I'm biased in the argument. Yeah, yeah. But both those up there, I know when my mom first called me and privately told me, she didn't want to tell my sisters at the time because she was worried about how to share with them and she didn't know what to do. And I was living here in California and she was visiting in town. She had just received a diagnosis about four weeks earlier. Yeah. She said, I want to tell you this. And my mom is like such a strong individual. And I genuinely in her eyes, I saw that she was both trying to be strong because she wanted to be strong for me. She's your mom. And she was completely unsure of where to go from there. And that feeling that you see anybody going through, let alone your mom, it's so terrifying. Yeah. So I just want to acknowledge you.

And I want to give props to you keeping your mom's legacy alive through the work that you do. And being able to share the message on such an important topic that people, so many people are being touched by. and if we can create a little bit of unneeded suffering by people having access to more information, especially on the topics of prevention, which really never got that much attention minus the kind of smoking side of it.

I mean, our healthcare system isn't exactly designed in a great way that would emphasize prevention that well. It isn't. And, you know, things are changing. Yeah, it's getting better. It's getting better. There's a lot of options. I'm not the type of person that feels that I believe that technology, when we look at the history

of technology and humanity, which has led to so many advancements for our species, the solutions come from a lot of different places, right? Like, it's not just that I'm waiting for the government to figure it out, right? I'm not just waiting for insurance to figure it out. I'm not waiting for nonprofits to figure it out. I'm not waiting for just the private sector. we need everybody working on all aspects of health. It's that important of an issue.

And we're truly in America, especially, but increasing around the world, we're at a crisis moment. Yeah. Where the quality of life is going down. Life expectancy is going down. Obviously, cancer rates are going down. We spoke about that. Yeah.

Going up or going down. Going down. Well, going down with age. Yeah, going down with age. Yep. They're increasing for people who are younger. Yeah, increasing in prevalence. So we need to do something about this and we need people to first and foremost talk about

it. The other thing that I want to acknowledge. is that because of your background that you kind of hinted towards a little bit, your stepfather abandoning you, your mother, you know, passing away early, you being 17, not growing up in a household that had financial stability, I also just super appreciate how often into your writing about things, especially things like the start of this conversation where we were talking about preventative measures, things that are often out of pocket right now.

now, which by the way, for everybody who's also listening, typically technology throughout humanity has been that way. It always starts with people who have the resources, even indoor plumbing, even antibiotics, even antibiotics, even electricity. It always starts off with the people that have the resources. That's how you establish a market. But we can't let it end there. It has to be able to come. So I feel like as I have had all these DMs back and forth with you and I've been binging your content over the last couple months of us getting to know each other. I want to acknowledge you for how often you and your writing hint to the fact that we have to understand the socioeconomic component of why people don't have access to the same potential for a healthy

life. And so you talk about that a lot. And I just want to acknowledge you for that because it's true. I mean, if you don't have money to spend on healthy foods, you're not going to be as healthy. You're going to buy cheap food that's there because that's what you have access to and you're just trying to survive. Yeah. I mean, it's obviously no surprise you see increased risks for most diseases in places where there's low income. Right. So that's, again, there's not as much access to health care. Right. You don't have insurance. Lower education. Lower education. Higher amount of ultra-processed foods in the diet. Higher amount of sugar, sweetened beverages, right, in some of these communities, depending on which, you know, group you're

looking at. I think that's why you wrote one of your posts that I came across was why there are such much, there's such higher rates, especially in like the Native American populations here in America. Yeah. In addition to obviously different pockets of the black community and Latin community as well. Yeah. Right. And then in some cases also cultural differences too. Like cultural differences. Yeah. Yeah. So I just, I just want to acknowledge you for being able to, you know, work that into your writing and recommendations. I appreciate that. I think it's an important part of the conversation.

We don't talk about enough. Yeah. But again, you know, I also want to point out that that none of this is about me. So I appreciate the acknowledgement. But, you know, again, I can't realistically expect that everyone's going to have access to this information. So if I can share that in any way and talk about, you know, how these very diverse aspects of our health are going to play a role in our ability to receive.

receive good health care, I mean, I have to talk about those things because it's a more full picture. I can't just hyper fixate on the cancer component without considering the psychological component, the socioeconomic component, you know, those sorts of things. Would you be up for it while we have a little bit of time left here for our interview for me to go through a rapid fire round of a few topics that my community has shared with me that they'd love to have you chime on? Sure. So actually, a really important. thing for me that I've tried to strive for on my platform is consistent communication with my followers. You see a lot of people as they get big pages. They don't interact with their followers at some point.

So I've tried to maintain that to the best of my ability. And I very strongly moderate discussion. So it's important for me to address people's questions because this is how I stay connected with the people that I'm trying to help. It's fantastic. I really appreciate that. I love these kinds of questions. Red meat and cancer. Can you chime in on that? I love red meat. I had a steak last night actually at the hotel restaurant. Red meat doesn't intrinsically cause cancer. I don't know how many more times I need to say that.

Any meat, no matter if it's fish, chicken, red meat, pork, doesn't matter. The heat at which you cook it will generate carcinogens. So if you're cooking it under an open flame, high heat all the time, and you consume it primarily in relation to, you know, your total diet, let's say you're a carnivore diet. and pretty much all you eat is meat-based products. And you cook those under an open flame, like our ancestors, like they claim. The dose makes the poison. If you're chronically cooking like that, you're going to generate carcinogens, which you're consuming, polyeromatic hydrocarbons to name, you know,

some jargon associated with this that people like to think about. Consuming more and more of those will generate specific types of cancers. And does that mean that the meat has to be charred? Like you're looking for charing. So you're looking for blackening. Yes. The more black. It's delicious.

Nobody denies that. Like I love a good grilled steak with the blackened sears across it at a steakhouse. Phenomenal. Taste amazing. Medium rare. That's it. But that charing is associated with producing carcinogens and meats. The same chicken.

But isn't that also true for vegetables as well? Exactly. Chared vegetables. Yes. Heavily char them. Yeah. That is the same instant. too. We just want to avoid heavy charing. Yes. Yeah. Whether meat or weather vegetables. Yes. And consuming

one more than the other in our diets. Can you can you explain that again? So like balancing, like having a nutrient diverse and rich diet. So having you can you can have those meats. If you if you prefer to cook your steak that way, you can you can eat it that way every day. But there's going to be other nutritional considerations that you should take into account like consuming lots of veggies for not only the other micronutriates and veggies, vitamins and things, but also for things like fiber. Those can help to offset some of the effects that you would get from exposure to carcinogens. What about some of the conversation around how applying a healthy level of spices to your meat may offer some sort of protective benefit with the charing? Have you heard

that at all? What do you mean by that? That spices offer, like if you like. Nutrition, nutritional recommendations? Not nutritional recommendations, but that spices actually have a protective kind of coding that can help out a little bit. I'll find, like, I'm not just pulling this off like some real on Instagram. Logically, I've heard of some people mention that, that, besides a shield. There's a little bit of a shield component that could come from making sure your food is appropriately spiced. Not that that's going to get rid of the complete blackening of any product that's there. But that there may be. Okay, maybe. You'd hear that you maybe haven't heard about that.

Yeah, but there might be a protective effect associated with adding spices to to meats and grilling them. So that way the flame maybe isn't coming into direct contact. It's reducing the heat generation through the meat and the production of those carcinogens. Maybe. Yeah. I haven't seen any research. I'll see if I can find some papers.

I'll send it your way. I'd be surprised if there were. Okay. Fun to think about, though. Yeah. Cool. Well, that's why we have you here. All right.

You made a video about this one, coffee and cancer. Yeah, that was interesting. So there's a correlation, not a causative correlation, just a correlation between those who drink coffee and reduced risks for cancers. And as I like to point out, there's a variety of ways to think about this, though, too, is from like a psychological perspective. You know, oftentimes, like, I love drinking coffee every morning when I wake up and it helps to relieve stress. So that could be one way that it can reduce risks if people associate coffee drinking with stress relief. but also just drinking it alone coffee has some really interesting nutrients in it that have been associated with decreased risks things like little polyphenols

those sorts of things but you can get those in a variety of different food sources it just so happens we see a trend that you know the the more coffee someone drinks the the reduced risks of specific cancers it was just an interesting trend that I thought you know could be beneficial for people a little bit biased though too because I again I love coffee I think a lot of people do as well So just a fun little fact to share that's supported by evidence. How much alcohol is too much when it comes to cancer? I'm not going to act like I don't drink.

I like alcohol. I have the occasional drink. What's your drink of choice? I like whiskey sours. I love tequila. Margaritas are my thing. Actually, I have a nickname that I gained. It's called I'm called Tequila Joe in some space.

because I love tequila that much, especially during grad school. Ticilla Joe is crazy. But alcohol is a carcinogen. There's no way around that. When it's brought into your body, it's metabolized to produce the carcinogen from aldehyde in the liver, just naturally from metabolic purposes. It's a two-step enzymatic reaction. Aldehyde dehydrogenase is the first step.

Alcohol dehydrogenase is the second step. I might have reversed those biochemists out there will correct me if I'm wrong. Other way, it's a two-step enzymatic reaction that essentially produces formaldehyde. If you drink excess amounts of alcohol, of course the dose makes the poison, the more formaldehyde in your system that requires clearance and further metabolization and break down to be excreted by the body. This is why people who chronically consume alcohol have increased risks for liver cancer because those enzymes are within the liver.

They break down alcohol. So any amount of alcohol is strongly associated. with cancer. But it doesn't mean that we can't deal with it. You can metabolically handle a certain load. Like if I have a drink, two drinks a week, I would say that's two drinks being like a whiskey sour. Two drinks a week would be okay. Try and minimize it to one if you can. You can deal with that. But I think the current recommendations are still too high. I think it's like a drink a day is considered light drinking. And when you say a drink, you're really talking about a serving. Yeah. Yeah. So a serving of either liquor, beer, wine. The volumes are going to vary depending on

alcohol content. Got it. And a lot, I bring that up because a lot of people, there's some different charts. Maybe we can pull one up and show it on on YouTube here. But a lot of people think that they're having one serving, but they're having like two. Yeah. Yeah. I mean, it's easy to get a double shot of whiskey too. It sounds so smooth, you know. But also there's cultural role considering here too because there's certain races that have genetic polymorphisms or genetic changes in the things that make the enzymes that break down alcohol. So the Chinese culture, they have polymorphisms in the alcohol, sorry, aldehyde dehydrogenase gene that slows the rate of breakdown of alcohol. So they will build up. Have you ever seen when someone of Asian descent gets the flushing?

Yeah. they likely possess that polymorphism. They don't digest alcohol or metabolize alcohol as efficiently as somebody has both of those enzymes working efficiently. So those people would probably not want to drink really a lot. They'd want to drink a lot less alcohol than the standard recommendation in general because they can't metabolize it as efficiently. Got it.

All right. Last one or two that we have here. getting extra antioxidants into your diet through supplemental form, like outside of like food and appropriate dietary and sort of polyphenol exposure from having good fruits and vegetables. Sure. Thoughts on that. I think it can be helpful. I think people should generally try not to rely on supplementation, but they're just that.

They're supplements. So if you know that you're not eating a lot of foods that have high amounts of antioxidants and you have supplements and they're maybe more easy to acquire for you, depending on your society, then yes, I think antioxidant supplements can be helpful. There's a variety of different types. Some are going to have different abilities than others. I will say that antioxidant supplements like glutathione are generally useless in both IV and pill form because your body makes so much of that in general. Glutathione is probably the most abundant antioxidant in your body in millimolar concentrations at a cellular level that is ridiculous amount in order to reach millimolar concentrations

in the blood is high. But there's a reason for that physiologically. So realistically, unless you have some rare disorder where you don't make enough glutathione, hypothetically wouldn't need supplementation with it. But in general, they can be helpful if you know that you're not consuming enough foods high in those antioxidants. All right. last one here, before we conclude, you mentioned something that might be a little shocking to

people that are listening to this podcast, which is about aspartame. And you said it is not linked to cancer. Can you just expand on that? No, no, no. It is linked to cancer. It is considered, if you go to the International Association for a probable carcinogen. It's a probable carcinogen, which means we've stressed test Aspartame in mouse models and in some case correlative models to humans. And we found that there's an association to aspartame consumption at extremely high doses. Again, extremely high doses in association to cancers. But most people don't consume that much aspartame, unless you're drinking like, I don't

know, like, it's Coke zero even have aspartame in it. Let's say you drink an aspartame related drink. You'd have to drink hundreds of cans of calories. a day, I think. And I don't know anybody that can physiologically handle that. You'd have other issues if you drank that much coke outside of the aspartame or out of the, yeah, no, aspirame realistically won't cause anyone cancer. Got it. This has been great, brother. Yeah. Thank you so much for going down the whole rabbit hole of all things cancer. We talked about preventative strategies. We talked about early detection, which I'd love to have you back on in the future as you come across

additional things and you start to go down that rabbit hole. I think a lot of people who listen to this podcast typically are people that have some time and maybe other financial resources. And so they want to spend their money on things that matter. They'd rather instead of getting, not that my audience is getting bottle service out there, but they'd rather, you know, avoid some sort of luxury experience and instead invest in their temple, their own body. So they're very interested in topics like that. We talked about your opinion on some of the viral videos that are out there on YouTube, whether they've been on my channel or other people's channel, including some of the main

sort of people that might be in the sort of what I would call integrative, alternative cancer sort of space. What truth is there, what's unknown, and what may be potentially bogus or harmful. And you also super kindly took us through your origin story. Yeah. And shared about your incredible mom and also your crazy sisters. Yeah. We can talk more about that.

Yeah. Shout out to your sisters. Shout out to my sisters. But really what was important through that is you showed the humanity behind what you do and why you do it, which is so important. Because I think that when we understand why people will do what they do, do and the mission that's behind it, there's a sacredness that's there for their work. Even if we might have difference of opinions that people have, there's an honoring and there's

an understanding of like, wow, I get why this person cares that much. Yeah. So I want to appreciate you. And you also answered our rapid fire questions. Thanks, man. Which is super helpful. Yeah. Final question, which I actually never really understood.

I know you have a cat. I have two cats. You have two cats. Yeah. And cats are all over your social media. Yeah. Is there more to the story? besides the fact that you have two cats?

You know, when I started creating my page, I was trying to get people interested in cancer biology, and it's hard to do just because it's cancer. You know, like you said, it's scary. It's kind of crazy to talk about. It can be very complicated at times. And I was like, you know, one day I was sitting down and talking to some friends,

and, you know, I was trying to find ways to establish myself in the space because there, you know, there really aren't, many pages, not to like pat myself on the back, but there aren't many pages that are doing what I'm doing. Right. Just devoted to cancer, going deep into it. Yeah, but like, you know, the way that I choose to do things too, I think is a little bit unique in terms of what it brings to the space of health. But I ultimately just started using cat pictures because it helped in the creation process because I love cats. Like, there's no denying that given my content. But it made the creation process more enjoyable for me. And then I started finding that people liked those pictures that I was just

throwing in there. And they were like, oh, I'm here for the cats. Or at some point, it was like, come for the science, stay for the cats. Yeah, yeah, yeah. It was a slogan there. I had it in my bio for a little bit. I might even put it back. But, you know, ultimately it's just like a creative outlet. You know, like I've told you, everything I do on my social media is free. I don't have, I'm starting to acquire sponsorship. So it's something I'm looking into to help kind of offset the cost that I put into you know, the image production software that I use and organizational stuff that I pay for. But ultimately, the cat thing is just, you know, fun trying to keep people engaged so they can swipe to the next slide and see like another cute cat picture and learn something new about cancer

they didn't see before. I love it. Well, it's working. Congratulations to you. Joe, where can our audience follow you and continue to stay in touch with your work? So I'm mostly on Instagram because it already takes me a stupid amount of time to make a post. So mostly on Instagram, I have a Patreon. I can send you those links for the show notes later. I have an X or Twitter account that I don't really use. I was booted off a Twitter a long time ago for sharing PubMed articles. I don't know what Twitter's algorithm was like, but I was recently regained Twitter X access or whatever.

But again, primarily on Instagram. So this is where people can find me and communicate with me. Awesome. Well, we'll have the links to all those that you mentioned. Sure. So that people can stay on the journey and can continue to get their catfix. Yeah. As well, too.

Brother, thank you so much for coming to town, being on the podcast. I'm a huge fan of your work. And we're going to continue to be in touch. Yeah. Thank you again so much for this opportunity. It's been incredible. Everyone should also follow Drew if you aren't. My audience included.

Thank you so much. I really, really, really appreciate it. Thank you. Hi everyone, Drew here. Two quick things. Number one, thank you so much for listening to this podcast. If you haven't already, subscribe, just hit the subscribe button on your favorite podcast app. And by the way, if you love this episode, it would mean the world to me.

And it's the number one thing that you can do to support this podcast is share it with a friend. Share with a friend who would benefit from listening. Number two, before I go, I just had to tell you about something that I've been working on that I'm super excited about. It's my weekly newsletter. And it's called Try This. every Friday, yes, every Friday, 52 weeks a year, I send out an easy-to-digest protocol of simple steps that you or anyone you love can follow to optimize your own health. We cover everything from nutrition to mindset to metabolic health, sleep, community, longevity,

and so much more. If you want to get on this email list, which is, by the way, free and get my weekly step-by-step protocols for whole-body health and optimization, click the link in the show notes that's called Try This or just go to drew perot.com. That's D-H-R-U-P-U-R-O-H-I-T dot com and click on the tab that says, try this.