Breaking Myths: What Really Fuels Cancer Growth, with Dr. Fung and Dr. Seyfried | TCP Ep. 71

Target Cancer Podcast
19 Sept 202480:24

Summary

TLDRThe Target Cancer podcast features Dr. Jason Fung and Dr. Thomas C. Fried discussing the metabolic theory of cancer, challenging the traditional genetic mutation theory. They argue that cancer is a mitochondrial metabolic disease fueled by glucose and glutamine, and stress the importance of diet and lifestyle interventions. The doctors also critique the focus on genetic mutations in cancer treatment, advocating for a shift towards metabolic therapy to improve patient outcomes.

Takeaways

  • 🧬 The somatic mutation theory of cancer is questioned in the podcast, with guests arguing that it's not genetics but mitochondrial metabolism that's at the core of cancer development.
  • 🍬 Insulin and sugar levels are highlighted as significant factors in cancer pathogenesis, with high levels potentially leading to faster cancer growth.
  • 🔒 The National Cancer Institute's serious consideration of the somatic mutation theory is criticized for hindering progress in cancer treatment.
  • 🌱 The role of diet, obesity, and inflammation in cancer development is emphasized, with evidence suggesting that environmental factors play a more significant role than genetic mutations.
  • 🔝 Obesity is becoming a leading risk factor for cancer, similar to how smoking was in the past, and is associated with insulin and glucose issues.
  • 🏃‍♂️ Exercise is mentioned as a way to lower blood sugar and insulin levels, which can help reduce the energy available for cancer cells to grow.
  • 🧪 The fermentation metabolism of cancer cells, which relies on glucose and glutamine, is identified as a key target for cancer therapy.
  • 💊 There is a call to re-evaluate the standard of care in cancer treatment, advocating for flexibility to adapt to new findings and a shift towards metabolic therapy.
  • 🌐 The cancer establishment and current research focus on genetic mutations are criticized for not addressing the root causes of cancer, leading to suboptimal outcomes.
  • 🔬 The importance of understanding the bioenergetics of cancer cells is stressed, as it provides a more promising pathway for treatment than the current genetic-focused approach.

Q & A

  • What is the main issue discussed in the podcast regarding cancer treatment?

    -The main issue discussed is the reliance on somatic mutation theories for cancer treatment, which the speakers argue is misguided and has led to a lack of progress in treating cancer effectively.

  • Why do the podcast guests believe that the National Cancer Institute is misguided in their approach?

    -The guests argue that the National Cancer Institute takes the somatic mutation theory too seriously, focusing on genetic mutations as the primary cause of cancer and overlooking the significant role of diet, obesity, inflammation, and metabolism.

  • What is the role of insulin and sugar levels in cancer pathogenesis as discussed in the podcast?

    -Insulin and sugar levels are discussed as significant factors in cancer pathogenesis because high levels can cause tumors to grow faster. The嘉宾主张降低血糖和限制胰岛素水平,以减缓癌症生长。

  • How does obesity relate to cancer risk according to the podcast?

    -Obesity is presented as a major risk factor for cancer, potentially replacing smoking as the leading cause. It contributes to inflammation and high insulin levels, which can stimulate cancer cell growth.

  • What is the 'trunk mutations' theory mentioned in the podcast?

    -The 'trunk mutations' theory refers to the idea that certain fundamental metabolic changes, rather than just genetic mutations, are the root causes of cancer development.

  • Why do the speakers argue against the focus on genetic mutations in cancer treatment?

    -The speakers argue that the focus on genetic mutations distracts from the more significant environmental and metabolic factors that contribute to cancer growth and progression.

  • What is the significance of the Warburg effect mentioned in the discussion?

    -The Warburg effect is significant because it highlights how cancer cells predominantly use fermentation (glycolysis) rather than respiration for energy production, even in the presence of oxygen.

  • How does the podcast discuss the role of diet in cancer?

    -The podcast emphasizes the importance of diet in cancer development, suggesting that dietary changes can either contribute to or help prevent and treat cancer by affecting insulin, glucose levels, and overall metabolism.

  • What is the proposed strategy for cancer treatment by the guests?

    -The proposed strategy is to focus on metabolic therapy that targets the root causes of cancer, such as glucose and glutamine metabolism, rather than solely relying on genetic mutation targeting.

  • Why do the speakers believe that current cancer treatments are not effective?

    -The speakers believe that current treatments are not effective because they are based on an incorrect understanding of cancer as a genetic disease rather than a metabolic disorder, leading to treatments that do not address the core issues.

  • What is the importance of mitochondrial function in cancer as discussed in the podcast?

    -Mitochondrial function is crucial in the discussion because disruptions in mitochondrial function lead to fermentation metabolism, which is a hallmark of cancer cells and a key driver of unregulated cell growth.

Outlines

00:00

🤔 Critique of Somatic Mutation Theory

The speaker expresses skepticism about the Somatic Mutation Theory, questioning its validity given the numerous issues associated with it. They are surprised that it's still taken seriously, especially by the National Cancer Institute. The podcast introduces two guests, Dr. Jason Fung and Dr. Thomas C. Frieden, to discuss the impact of diet, nutrition, and metabolism on cancer's pathogenesis and treatment. The dialogue emphasizes the importance of considering factors beyond genetics, such as insulin and sugar levels, in cancer development.

05:01

🔍 The Overlooked Role of Metabolism in Cancer

In this paragraph, the conversation delves into the role of metabolism in cancer development. The speakers discuss how obesity and inflammation are linked to cancer and how insulin acts as a growth factor, stimulating cancer cells. They criticize the focus on targeted genetic mutations in cancer treatment while neglecting the metabolic processes that fundamentally drive cancer growth. The discussion highlights the need to address the root causes of cancer, such as glucose and insulin levels, rather than just targeting symptoms.

10:01

🌿 The Environmental Factors of Cancer

The speakers emphasize the significant impact of environmental factors, particularly diet and obesity, on cancer risk. They argue that these factors outweigh genetic mutations in contributing to cancer and criticize the medical community's focus on genetics. The paragraph includes a discussion of how changes in diet and lifestyle have led to increased cancer rates, especially among younger people. The speakers also touch on the role of mitochondria in cancer cell energy production and the potential for limiting glucose and insulin to control cancer growth.

15:05

🧬 Challenging the Somatic Mutation Theory

This section critiques the Somatic Mutation Theory of cancer, suggesting that it is not the mutations themselves but the cellular environment and metabolism that drive cancer. The speakers discuss how mutations are a downstream effect of mitochondrial dysfunction and how targeting these mutations in treatment has not been as effective as hoped. They argue for a shift in focus towards the bioenergetics of cancer cells and how they obtain energy.

20:05

🔬 The Centrality of Mitochondrial Metabolism in Cancer

The discussion focuses on the importance of mitochondrial metabolism in cancer cells. The speakers explain how disruptions in mitochondrial function lead to fermentation metabolism, which is prevalent in cancer. They discuss the accumulation of lactic and succinic acid as a result of this metabolism and how it protects cancer cells. The paragraph also addresses the idea that cancer cells revert to ancient, inefficient energy production methods due to mitochondrial dysfunction.

25:05

🏥 The Failure of Current Cancer Treatment Paradigms

This section criticizes current cancer treatment approaches that focus on genetic mutations rather than the metabolic processes of cancer cells. The speakers argue that these treatments are not effective because they do not address the fundamental issue of how cancer cells obtain energy. They discuss the need for a shift in thinking towards metabolic therapies that target glucose and glutamine, which are essential for cancer cell growth.

30:07

🌟 The Promise of Bioenergetic Therapies for Cancer

The speakers discuss the potential of bioenergetic therapies that target the metabolic processes of cancer cells. They highlight the importance of understanding how cancer cells generate energy and how this knowledge can be used to develop more effective treatments. The paragraph includes a discussion of how certain metabolic interventions can make cancer cells more susceptible to radiation and chemotherapy.

35:08

🛡️ The Protective Role of Acidification in Cancer

This section discusses how the acidification of the tumor microenvironment, due to fermentation metabolism, protects cancer cells from various treatments. The speakers explain that this acidification prevents the effectiveness of radiation, chemotherapy, and immunotherapy. They argue that targeting glucose and glutamine metabolism could reduce acidification and improve treatment outcomes.

40:09

🌿 The Impact of Diet and Lifestyle on Cancer

The discussion turns to the impact of diet and lifestyle on cancer, emphasizing the need to manage cancer as a metabolic disorder. The speakers suggest that dietary changes, such as calorie restriction and ketogenic diets, can help control cancer growth by limiting the availability of glucose and glutamine. They also touch on the importance of maintaining a healthy microbiome for overall health and cancer prevention.

45:10

🔬 The Cellular Biology of Cancer Metastasis

This section delves into the cellular biology of cancer metastasis, explaining how certain cells within a tumor acquire the ability to invade and spread. The speakers discuss the role of macrophages and the fusion of different cell types in creating metastatic cells. They also address the challenges in treating cancer due to the heterogeneous nature of tumors and the presence of various cell types with different characteristics.

50:10

🌐 The Need for a Paradigm Shift in Cancer Research

The final paragraph discusses the need for a paradigm shift in cancer research, moving away from the somatic mutation theory towards a focus on mitochondrial metabolism. The speakers express frustration with the current state of cancer research and treatment, arguing that a new approach is necessary to improve patient outcomes. They emphasize the importance of understanding cancer as a metabolic disease and the potential for metabolic therapies to transform cancer treatment.

Mindmap

Keywords

💡Somatic Mutation Theory

The Somatic Mutation Theory is a concept in cancer research that suggests cancer is primarily caused by genetic mutations occurring in somatic, or non-reproductive, cells. These mutations accumulate over time and can lead to uncontrolled cell growth. In the video, there is criticism of this theory as being overly simplistic and not accounting for the complex metabolic factors that contribute to cancer development.

💡Mitochondrial Metabolism

Mitochondrial Metabolism refers to the process by which cells produce energy (ATP) through the mitochondria, typically through a process known as oxidative phosphorylation. The script suggests that disruptions in this process, such as a shift towards fermentation due to mitochondrial dysfunction, may be a root cause of cancer.

💡Fermentation Metabolism

Fermentation Metabolism is an ancient, less efficient method of energy production that occurs in the absence of sufficient oxygen, where glucose and glutamine are converted into energy through processes like glycolysis and glutaminolysis. The transcript discusses how cancer cells often rely on fermentation due to mitochondrial damage.

💡Cancer as a Bioenergetic Disorder

This concept from the video script suggests that cancer should be viewed as a disease of cellular energy production and regulation, rather than purely a genetic disease. It emphasizes the importance of understanding how cancer cells obtain and use energy as a key to treating cancer.

💡Metabolic Therapy

Metabolic Therapy is an approach to cancer treatment discussed in the script that focuses on disrupting the energy production pathways of cancer cells, particularly targeting their reliance on glucose and glutamine fermentation. It is positioned as an alternative to traditional genetic-focused cancer treatments.

💡Insulin

Insulin is a hormone that regulates blood sugar levels. In the context of the video, it is highlighted as a growth factor that can stimulate cancer cell growth by promoting glucose uptake. High insulin levels, often associated with conditions like obesity and diabetes, are suggested to potentially increase cancer risk or progression.

💡Obesity

Obesity is mentioned as a significant risk factor for cancer, potentially due to its association with chronic inflammation and high insulin levels. The video suggests that obesity may be supplanting smoking as a leading preventable cause of cancer.

💡Glucose

Glucose is a simple sugar that serves as a primary source of energy for cells, including cancer cells. The script discusses how high glucose levels can fuel the fermentation metabolism of cancer cells, contributing to their growth and making them resistant to certain treatments.

💡Ketogenic Diet

A Ketogenic Diet is a high-fat, low-carbohydrate diet that shifts the body's energy metabolism from glucose to ketone bodies. In the transcript, it is suggested that such a diet could potentially starve cancer cells of their preferred energy source, glucose, thereby inhibiting their growth.

💡Acidification

Acidification in the context of cancer refers to the lowering of pH in the tumor microenvironment due to the accumulation of acidic byproducts like lactic acid from fermentation metabolism. The script discusses how this acidification can protect cancer cells from treatments like radiation and chemotherapy.

💡Macrophages

Macrophages are a type of immune cell that engulfs and消化s foreign particles. In the transcript, it is suggested that certain cancers, particularly those that are metastatic, may originate from macrophages that have fused with cancer cells, gaining the ability to invade and metastasize.

Highlights

Critique of sematic mutation theories in cancer research.

Discussion on the influence of diet, nutrition, and metabolism on cancer pathogenesis.

Insulin identified as a growth factor that can stimulate cancer cell growth.

Importance of considering environmental factors beyond genetics in cancer development.

The impact of obesity and inflammation on cancer risk, potentially surpassing that of smoking.

The role of glucose and insulin in untreated cancer growth.

The potential for metabolic activity agents to control cancer pathogenesis.

The misconception among oncologists about the role of glucose in cancer.

The need for a shift in thinking about cancer as an environmental and not just a genetic disease.

World Health Organization's stance on obesity-associated cancers.

The increase in young people getting cancer and its link to obesity and diet changes.

The role of mitochondrial function in cancer cell energy production and its implications for treatment.

The impact of diet on cancer development, supported by global population studies.

The theory that cancer is a mitochondrial metabolic disease rather than purely genetic.

The potential for metabolic therapy to improve cancer treatment outcomes.

The economic factors that may contribute to the persistence of certain cancer treatment paradigms.

The role of the microbiome in cancer development and treatment.

The potential of caloric restriction and ketogenic diets in managing cancer.

The importance of understanding cancer as a metabolic disorder for effective treatment.

Transcripts

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we spend so much time on you know

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sematic mutation theories which is such

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a bad Theory there's so much wrong with

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it that I'm I'm surprised anybody still

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takes it seriously unfortunately the

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National Cancer Institute takes it very

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very

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serious that's why we have no progress

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that's what I thought

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too welcome to Target cancer podcast

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this is Dr Sun janer I'm going to skip

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the intro because I am so excited and

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humbled

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that we have two of our guests that

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everyone's asked for uh multiple times

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because of this culture shift on

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thinking about what is causing cancer

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and can we do better and what does diet

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and nutrition and Metabolism have to do

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with its pathogenesis how we treat it

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when it

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recurs and if you're thinking that I'm

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going to say this yes it's true I have

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Dr Jason fun and Dr Thomas C freed today

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to discuss the things that we've been

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hearing in the news you know and seeing

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the data about cancer becoming uh you

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know a diagnosis younger it's it's in

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higher volume and if you have not

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listened to these podcasts before highly

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recommend doing so probably before this

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podcast because it has really opened my

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mind up as an oncologist on not only

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what is causing it but what should we be

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considering while we are treating it uh

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something called trunco mutations root

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causes so without any further Ado Jason

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Thomas thank you so much for being here

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thanks for me y yeah thank you very much

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for having me also we're in a world

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right now of this glp1 stuff and

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everyone's talking about zic and

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bringing you know body fat reduction and

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obesity down and we've talked a lot

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about how obesity and inflammation you

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know in the past shows data on causing

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cancer but also uh in Jason's podcast

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especially about how insulin is a growth

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factor and kind of stimulates these

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cells to say grow grow grow cancer is

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unregulated growth I'd love to start on

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talking about

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in an untreated cancer um how does

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insulin and sugar levels play a role in

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its you know pathogenesis quickly and

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then also do you think that the

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pathogenesis will go down when we have

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agents that are able to better control

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our metabolic activity um well no I

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think these are important issues because

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I I what we're seeing now I think um

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this obesity issue is uh now seems to be

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replacing smoking as the uh as a major

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cause of uh linkage too let's put his

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way a risk factor and uh for cancer and

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and you're right there's an insulin

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issue uh there's a glucose issue and um

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uh the the systemic

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inflammation in many people that are

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obese and let's not let's not include

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every every obese person on the planet

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in the same basket we know there are

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some obese people that are actually very

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very very healthy they have unbelievably

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healthy blood work and all this kind of

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stuff but that doesn't is that's the

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exception rather than the norm um and if

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your insulin is high and your blood

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sugar is high and you have uh a tumor uh

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it will generally cause that to grow

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faster and and I think that's uh pretty

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much obvious to those of us who

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understand this issue but apparently not

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obvious to a majority or I don't want to

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say majority but to many

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oncologists who have never heard that

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that glucose has anything to do uh with

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cancer and often encourage their

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patients to drink infel or sweet things

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to maintain weight um uh which is just

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the opposite the advice that you would

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want to give someone so why how is it

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possible uh that uh people treating uh

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cancer would not know that glucose and

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insulin levels uh elevation

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are provocative to driving the

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disregulated cell growth so Sanjay you

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are an oncologist you are the voice of

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your profession how do you explain this

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because I know Jason has spent a lot of

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time on many podcasts telling us about

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this and apparently uh they might not

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have heard him either so I'm not really

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I'm not really sure to how to explain

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this give me an ex you tell you should

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ask you that question what do you think

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I I think part of I to be honest I don't

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I don't have an explanation other than

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you do internal medicine and then you go

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on oncology so internal medicine it's

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not necessarily A pre-cancer Internal

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Medicine training we just learn about

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you know the consequence on diabetes and

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how that has to do with you know

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vascular stuff and kidney disease and

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stroke da d da endothelial stuff and

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then you just kind of jump into the

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treatment of cancer which is you know

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predominantly immune therapy

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chemotherapy replication cycle and then

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now this whole excitement about targeted

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mutations uh or targeted therapies that

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both of you have kind of taken you you

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you spoiled the the joy of for me

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because you know at first I was like

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great we have all these targets and if

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it's showing blueberries we you attack

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blueberries rather than trying to hack

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away the whole limb because that causes

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toxicity and you're like no SJ both of

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you hack away the limb or go ahead and

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go at the trunk of the tree but do so

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without necessarily poison because what

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we forget is the trunk of the tree

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actually requires things to grow right

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it has to be uh watered and it has to

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have some kind of fertilized ground

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that's why hydrangeas never do well in

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my house because I can't even keep uh

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the constituents to make that thing grow

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which further Downstream are blueberries

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strawberries and I'm saying that as if

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it's a positive thing but in these cases

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the reason that the cancer is growing

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we're chasing this all in targeted

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therapy world and and and oncologists

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have a lot of pressure to make sure

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they're up to date with the standard of

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care of assessing way down on the limb

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what different things are growing uh and

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making sure that they're adhering and

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and buying the molecular test so that we

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can make sure the therapy attacks it um

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and and that's why I think this these

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conversations are so important we are

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not it is not in our repertoire or in

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nccn to really think about are these all

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just Downstream problems because the the

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ground in which the trunk and The Roots

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exist are continuing to be watered and

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part of it is because we believe well

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all ground has to be watered so you

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can't really influence too much the

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glucose and Insulin which is obviously

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wrong yeah I mean the thing is that you

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get all these sort of exciting things

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about oh there's this mutation and this

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mutation and we're going to Target this

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and this so I think what happens is that

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you get the idea that cancer is caused

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by these genetic mutations and it's a

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genetic disease and it's just bad luck

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and and that feeds in but it's

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completely untrue because when you step

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back and you say okay well what causes

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cancer and they they've done studies on

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this what is the biggest uh attributable

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population attributable risk to cancer

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and smoking's up there around 30% but

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what everybody forgets is that way way

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up there as Tommy you're saying diet and

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obesity is also about 30% and it

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completely dwarfs everything like you

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know radon and you know chemicals and

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chemical carcinogens and stuff right

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it's it's a huge huge risk factor and

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that's all

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environmental um not genetic right so

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you have to look at the environment and

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then you look at what you talked about

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earlier which is that hey we're getting

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young people getting tons of cancer and

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if it was a genetic disease you'd say

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you know the

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genetic you know the genetic uh makeup

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of the population has not changed in the

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last 10 years um other than through

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immigration right but it that's not what

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we're talking about so what is it that

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has changed and of course diets have

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changed obesity has changed and the

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entire thing so so I think what has

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happened is because of the advances in

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the genetic you know Technologies and

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the treatment you get this idea that

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it's 90% genes and 10% but it's not it's

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like you know 80% environmental a lot

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has to do with your diet and and and

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weight and and we know this because the

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World Health Organization has 13

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different cancers that are obesity

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Associated uh one of them for example is

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coloral and now you see this shift

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younger people are getting col rectal

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cancers and bad ones too well why well

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not so hard to understand if obesity is

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a related Factor then there's more

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obesity so therefore you're getting more

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you're getting more obesity younger

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right kids are getting obese in their

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teens now so therefore you're getting

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more just like you have more type 2

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diabetes uh in young people now same

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thing right pediatric clinics used to be

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90% uh type 1 and 10% type two now it's

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like a 50/50 type one and type two right

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you get like 15 year olds with type two

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diabetes so so this whole thing is it it

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does require this whole shift in

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thinking that hey this is not just a

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genetic disease that's not to say that

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genes have nothing to do with it because

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it's not to it's not to say that these

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targeted therapies aren't good because

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they are good obviously it spend a lot

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of money on it but you have when you're

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thinking about how the these things

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develop you have to think about what is

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important so one of the things obviously

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is glucose and Insulin then and it's

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like you look at breast cancer and it's

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been known for like 50 years okay at

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least that breast tissue doesn't really

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have a lot of insulin receptors why

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would it right it doesn't need it but

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breast cancer has like piles of insulin

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receptors well why well because if it

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has lots of insulin receptors then get L

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and you have lots of insulin then you

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can open up the glute four you know

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Channel pour in the glucose into this

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into this cancerous cell and it can grow

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because we know again that it uses

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glucose to grow I mean warberg talked

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about that ages ago so it's like okay

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well if that's important then limiting

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glucose and limiting insulin is

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important in the development of colal

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and breast cancer which which which for

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some reason just gets lost in this whole

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it's all about genes it's all about

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genes it's all about genes so it gets so

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blind insided into this one sort of you

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know view that forget about everything

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else that's gone on and even when you

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look at what causes cancer like genetic

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factors um you know and they've they've

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done a big study uh on this it's still a

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relatively small factor in um in in

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causation of cancer it's it's it's like

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5 to 10% versus 30 for diet yeah and you

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both you both mentioned this in your

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podcast about how that was pretty much

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nailed on the head when we transplanted

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people from other parts of the world

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because we said wow they don't get

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cancer at all they don't get colon

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cancer they don't get this whatever the

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cancer was were like they have some

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golden you know tp53 that can't be hurt

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like or or eight of them like an

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elephant does and and then when we

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brought them here or the diets that were

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American were introduced to where they

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were all of a sudden they started having

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canc like like and I'm saying it Loosely

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but literally transplanted them to study

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they were eating American food and and

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had a much richer different nature food

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and C started to appear I mean that in

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itself was very uh memorable that both

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of you mentioned yeah remember the story

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of um Burkett right so Burkett was uh he

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did a lot of missionary work that's what

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they called him back then in the 40s and

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50s right so I think he Ireland or

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somewhere and he went to Africa and then

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he's like hey you know white people are

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getting all this color rectal cancer but

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the Africans don't they get like zero

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colon cancer but then when you take

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those African people and you westernize

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them they start getting Coline cancer

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right and that was observed like in the

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50s 40s and 50s so obviously the diet

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was a huge Factor now he thought it was

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all about fiber and maybe it wasn't all

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about fiber it may have been all these

play12:17

other things you know the refined foods

play12:19

and all that stuff they didn't have the

play12:21

same chemicals and stuff but probably

play12:23

the stimulating the hyperinsulinemia the

play12:26

glucose um at least played a role it but

play12:29

same thing right you take and and same

play12:31

thing in um in the north and in in the

play12:35

Arctic you had all these in the 40s you

play12:38

had people going up into the Arctic

play12:40

researchers going up there why don't

play12:42

these native uh peoples get cancer

play12:45

there's zero cancer then of course you

play12:48

yes they start to westernize them and

play12:50

give them sugar and refined flour and

play12:52

stuff and they start getting weight gain

play12:54

and all this type two diabetes hey their

play12:57

rates of cancer are actually worse than

play12:58

ours now right so it's like well

play13:00

obviously it had to do with diet right

play13:02

that's that's the key factor and when

play13:05

what you all one that's the cause and

play13:07

two which y both mention in the podcast

play13:09

Jason you talked about and I've never

play13:10

been the same since then about dcis and

play13:13

are we overtreating because we know to

play13:15

your point cancer you know needs fuel

play13:18

and oncologists still Community

play13:20

oncologist roll their eyes when they

play13:21

hear well doesn't it fuel cancer but you

play13:23

need fuel to grow cancer is unregular

play13:26

cell growth and you're like are we

play13:27

overtreating dcis when we could have

play13:30

modifications to

play13:32

possibly temperate or not give it the

play13:34

the gas that needs to go uphill and then

play13:36

let our immune system you know do what

play13:38

it does and then Dr cpri you took that a

play13:41

step further and said okay even if it's

play13:44

invasive can we limit the fuel or or

play13:49

nutritional sources to hard types that

play13:53

need something else electric cars need

play13:55

the charge station that's why I don't

play13:56

have one I probably need one and do a

play13:57

lot of driving I have to use gas and you

play14:00

were like okay we know that one of those

play14:02

if we the Tes can't be charged it can

play14:04

take away electricity but that half and

play14:06

half you're like I want to be able to

play14:08

take on something additional and and

play14:10

went into these kind of uh amino acids

play14:13

or other kind of Escape uh means to be

play14:16

able to process quote unquote Fuel and

play14:19

energy uh due to their mitochondrial

play14:22

changes so if we could talk about that

play14:24

for a second mitochondria how that gets

play14:26

changed and influenced uh with diet uh

play14:30

sugar insulin and then and that strategy

play14:32

Dr CP that you were talking about yeah

play14:34

well I I think to follow up on this uh

play14:37

with respect to the genes and also to

play14:40

segue into what you what you just said

play14:43

um we have to look at the theory that's

play14:46

driving the the approach which is the

play14:49

somatic mutation theory of cancer now

play14:52

for those who would think cancer is a

play14:54

genetic disease they would say and argue

play14:57

that that that smoking and obesity and

play15:00

inflammation induce somatic mutations in

play15:04

the DNA so it's the abnormal yeah you're

play15:08

you're you're you have an abnormal diet

play15:10

you have obesity is infl

play15:13

inflammatory uh and inflammation uh can

play15:17

lead to uh DNA repair problems and and

play15:21

these kinds of things and therefore even

play15:24

though we're seeing a linkage with diet

play15:26

earlier onset it's still considered a

play15:29

genetic disease because if we look at

play15:32

the tissue itself we see uh all kinds of

play15:36

different

play15:37

mutations in in the tissue uh even even

play15:41

the young people when you when you look

play15:42

at the the tissue from the young people

play15:44

or the Africans going from one or the

play15:48

anuit going from one diet to another

play15:50

when you look at their cancer it's

play15:52

loaded with all different kinds of

play15:54

mutations so they say well that see it's

play15:56

a somatic mutation as opposed to

play15:59

germline mutations which uh like Jason

play16:03

said you know it's it's it's the

play16:06

germline so what we have done is we have

play16:08

explained uh where all those mutations

play16:11

and how they link to disregulated cell

play16:13

growth um the somatic mutations are

play16:16

coming from this from the mitochondria

play16:18

itself when the this

play16:20

inflammation uh coming from obesity and

play16:23

all these other things or from smoking

play16:25

or from virus infections or whatever uh

play16:28

they lead to reactive oxygen species in

play16:31

the cells

play16:32

r r are carcinogenic and mutagenic so

play16:37

they lead to the mutations that you see

play16:39

in the DNA they break proteins they am

play16:42

dist disrupt lipids um all of these

play16:44

things uh lead to uh problems in the

play16:48

energy utilization and homeostatic state

play16:51

within within within the cell but every

play16:54

every cell in someone's tumor has a

play16:57

different constellation of mutations

play16:59

from any other cell there's no uh all my

play17:02

tumor cells have can be identified by

play17:04

having a singular kind of mutation

play17:07

that's not true and we've seen that over

play17:08

and over again but what every cell in

play17:11

that tumor does share is a dependency on

play17:14

a fermentation

play17:15

metabolism um which is in one part the

play17:18

glucose is fermented to lactic acid and

play17:22

this is what we see in all major cancers

play17:25

uh uh an accumulation of lactic acid and

play17:28

the second thing we is accumulation of

play17:29

suic acid which is coming from amino

play17:32

acid fermentation uh when the

play17:34

mitochondria become defective the cell

play17:36

has to fall back and getting energy from

play17:38

some someplace else uh and that energy

play17:41

has to come from fermentation it's

play17:42

called substrate level phosphorilation

play17:45

and in the cytoplasm it's through the

play17:47

glycolysis pathway and in the

play17:49

mitochondria it's through the

play17:50

glutaminolysis pathway D and glutamine

play17:53

is the most abundant Amino so we have

play17:54

shown that glutamine is actually

play17:56

fermented it's a fermented it's a

play17:58

ferment mented amino acid um now the

play18:01

mutations are accumulating in the cancer

play18:04

uh different from every other cell in

play18:05

the tumor so but but according to the

play18:07

sematic mutation Theory we'll try to

play18:10

Target some of those mutations in the

play18:13

tumor cell with the hope of of reducing

play18:17

uh and and you often don't find complete

play18:19

cures from targeting mutations mainly

play18:23

because you have other cells in there

play18:24

that may not have those mutations and

play18:26

therefore they bypass the targeting and

play18:28

the same time now we're realizing that

play18:31

many of these driver mutations which are

play18:34

different P passenger mutations were the

play18:37

mutations that were thought to be the

play18:39

ones responsible for triggering the

play18:41

disregulated cell growth now when you

play18:43

try to Target driver mutations new

play18:46

information says and shows clearly from

play18:49

numerous studies that normal cells in

play18:51

our body and our tissues have these same

play18:54

driver mutations that do not lead that

play18:56

are not associated with disregulated

play18:58

cell

play18:59

so when you use an immunotherapy a

play19:01

targeted approach to managing cancer yes

play19:04

you may slaughter a large number of the

play19:06

tumor cells but but then you have

play19:09

promiscuity and you start destroying

play19:11

your liver and kidneys and some other

play19:13

organs that also may have that same M uh

play19:16

epitope from the mutation and therefore

play19:18

it's no longer what we consider a precis

play19:20

a t a precise targeting it's a imprecise

play19:23

targeting and what we do know is that in

play19:27

every single cell cancer cell and and

play19:30

tissue that we have found they are all

play19:32

have abnormalities number structure and

play19:35

function of mitochondria and I our most

play19:37

recent paper shows that all major

play19:40

cancers accumulate cytoplasmic lipid

play19:43

drops in the cytoplasm and those

play19:46

cytoplasmic lipid drops triglyceride

play19:48

accumulation is there to protect the

play19:51

cell from Death because they can't use

play19:53

the fatty acids so they store them in

play19:55

these vacul in the in this in the

play19:58

cytoplasm and that's all due to

play20:00

disregulated mitochondrial function so

play20:02

if the mitochondria can't respire they

play20:04

ferment but fatty acids if their fatty

play20:07

acids or go into the mitochondria

play20:09

they'll create tremendous oxygen

play20:12

radicals and kill the cell so to protect

play20:14

the cell they store the fatty acids as

play20:16

lipid drops and what we did is we went

play20:18

through all major human Cancers and we

play20:21

compared mitochondria structure and

play20:23

function with cytoplasmic lipid drops

play20:25

every major cancer has those two

play20:28

characteristics and they're all

play20:30

fermenting and they're all dependent on

play20:32

glucose and glutamine regardless of what

play20:34

the mutations happen to be all germ line

play20:37

mutations p53 Leaf manyi braco one all

play20:41

of these every one of those genes

play20:43

damages number instruction function of

play20:45

mitochondria leading to a fermentation

play20:47

metabolism so whether it's in the germal

play20:49

line and the mutations the cyto the

play20:52

somatic mutations are secondary

play20:53

Downstream effects and germline

play20:55

mutations cause disruption of

play20:58

mitochondria function uh leading to

play21:00

disregulated cell growth as the result

play21:02

of the product of the inherited Gene

play21:04

none of them are 100% penetrant meaning

play21:06

they can only be secondary risk factors

play21:09

we have never found an inherited

play21:11

mutation in the genome that is

play21:13

associated with 100% the highest is Lea

play21:16

manyi which is about 80% but 20% of the

play21:18

people that have never developed the

play21:20

cancer so they're all considered

play21:21

secondary risk factors just would be a

play21:23

viral infection smoking obesity any of

play21:26

these they're all secondary risk factors

play21:28

the primary risk factor for the origin

play21:30

of cancer is a chronic disruption of

play21:32

oxidative phosphorilation coupled with a

play21:34

trans compensatory fermentation driven

play21:37

by amino acid and glucose fermentation

play21:41

processes exactly and I appreciate you

play21:43

explaining that so granularly uh Tom

play21:46

Jason when we talk about insulin and

play21:49

obviously it being a growth factor is

play21:51

there a relationship on

play21:53

hyperinsulinemia I'm asking this you

play21:55

know for for a non-medical person and

play21:58

mitochondrial health and what are some

play22:01

strategies to either do or avoid when it

play22:04

comes to thinking about and should we be

play22:07

thinking about preservation of

play22:08

mitochondrial Health when it comes to

play22:11

metabolic disregulation and

play22:13

hyperinsulinemia and then even now I'm

play22:16

thinking you know increase acidity with

play22:18

dialysis patients and and and their

play22:20

impaired ability to be able to uh you

play22:23

know take care of that regulation that

play22:25

could potentially cause a metabolic

play22:27

injury to uh to the

play22:29

mitochondria should we be seeing

play22:31

increased cancer levels in people that

play22:33

have impaired renal function um it's not

play22:35

the acidity so much but I mean for sure

play22:38

I mean to get back to the in I I think

play22:40

they work at slightly different levels

play22:42

because insulin is a sort of a hormonal

play22:44

level whereas Myra is a cellular level

play22:46

so they're not they're not directly

play22:47

interactive but I always think it's

play22:49

funny because it points to the

play22:52

importance of looking at the sort of

play22:56

bioenergetics of cancer which is very

play22:59

striking because we spend so much time

play23:01

on youo sematic mutation theories which

play23:04

is such a bad Theory like honestly it's

play23:07

it's you know there's so much wrong with

play23:10

it that I'm I'm surprised anybody still

play23:13

takes it seriously Jason unfortunately

play23:17

the National Cancer Institute takes it

play23:19

very very

play23:20

seriously that's why we have no progress

play23:23

that's what I thought too it's

play23:25

unbelievable I agree with you 100%

play23:28

understand how Ral Minds can believe

play23:32

that and and yet uh when you go to the

play23:35

National Cancer is to

play23:37

website 100 different genetic

play23:40

unbelievable don't those guys ever read

play23:42

the literature this what I learn what I

play23:44

learned in the 90s in medical school was

play23:46

this two hit hypothesis that's what

play23:48

they're talking about back then right so

play23:50

you have it's not a genetic disease like

play23:52

polycystic kidney disease or CLE cell

play23:54

you don't have one hit you have can get

play23:56

one hit then a second hit and that's

play23:57

fine that was the theory that I was

play23:59

taught and probably a lot of people grew

play24:01

up on but it's go so completely wrong

play24:03

because there are you know you look at

play24:05

the average you know cancer uh and he

play24:09

did this I think Bert vogelstein did a

play24:12

study and he looked at took cancers and

play24:14

said how many mutations are there right

play24:16

and it wasn't one it wasn't two it

play24:18

wasn't three it wasn't four the average

play24:20

breast cancer I think had like 50 and

play24:23

you know the some of the the brain

play24:24

cancers that you see in young people

play24:26

there are like 200 mutations right so

play24:28

it's like okay that's ridiculous right

play24:30

50 50 different genetic changes and you

play24:34

still think this is a viable Theory like

play24:36

how are you going to do that give them

play24:38

50 different agents to attack all these

play24:40

these different mutations can't do it on

play24:42

the other hand you look at bioenergetics

play24:44

and every single cancer cell I mean not

play24:47

every but almost all share the same

play24:51

difficulty described ages ago by warberg

play24:54

right that hey there's a real difference

play24:57

here in the way they generate energy

play24:59

fermentation versus respiration and why

play25:02

is that and everybody says well you know

play25:04

with the sematic mutation Theory it's

play25:07

just a quirky problem that happens it's

play25:11

just a mistake it's like what so every

play25:13

single cancer in history makes the same

play25:16

mistake and you think it's just a coinky

play25:19

dink right like what are you talking

play25:21

about clearly this is at the heart of

play25:25

the the cancer is the bio energy etics

play25:29

whether you're talking about

play25:30

mitochondrial Health which is important

play25:32

and it does influence it so things like

play25:34

autophagy and mitophagy and stuff

play25:36

influence it uh you know uh so when you

play25:39

do talk about intermittent fasting and

play25:41

stuff it does influence it but insulin

play25:43

and glucose you're still talking about

play25:45

the same thing bioenergetics right how

play25:48

do cells get energy and I I also think

play25:51

that it's always funny to me that they

play25:53

say okay so these these cells produce

play25:55

lactic acid these cancer cells produce

play25:57

lactic acid and it's like okay and if

play26:00

that's just another big coinky Dink and

play26:03

it has no relevance it's like I don't

play26:05

think so if every single cancer cell is

play26:08

producing lactic acid it must be because

play26:10

lactic acid is good for the cancer cell

play26:13

right so basically I think the cancer

play26:15

cell produces it I think there's you

play26:18

know they they say okay it's not

play26:21

generating as much energy because

play26:23

oxidative phosphorilation generates way

play26:25

more ATP per glucose right than than

play26:29

than fermentation then than um but

play26:31

that's only a problem if you don't have

play26:34

enough glucose if you have a lot of

play26:36

glucose it doesn't matter how many ATP

play26:39

you're generating per glucose because

play26:41

you have a ton of glucose sitting out

play26:44

there so again thinking about it that

play26:46

way you say well okay then why doesn't

play26:48

the cancer if if the cancer can choose

play26:50

either one then it must be producing

play26:53

lactic acid for a reason and I think

play26:55

it's a very good reason the lactic acid

play26:57

protects the cancer cell cells it breaks

play26:59

down you know the cell membrane so it

play27:01

allows it to expand it protects it

play27:04

against attack from other you know

play27:06

immune cells and other cells that want

play27:08

to destroy it right because you know

play27:10

your own body has a natural immunity

play27:13

natural killer cells and stuff that try

play27:15

to attack it so the lactic acid must be

play27:17

beneficial and we need to look at why

play27:19

it's beneficial so you can attack it but

play27:21

nobody looks at this nobody looks at

play27:23

this these sort of really logical sort

play27:26

to me logical sort of questions and

play27:29

answers about how we can do this they're

play27:32

all stuck in this it's all about the

play27:35

genes it's like so you so you basically

play27:38

you can't explain any of what's happened

play27:40

to these different populations right

play27:42

when when you move a Japanese person

play27:44

from Japan to America right their risk

play27:48

of certain cancers goes up tenfold and

play27:50

you know other cancers gastric cancer

play27:52

went down tfold well you can explain the

play27:55

gastric cancer right that was H pylori

play27:57

probably right so it's like okay well

play27:59

you're talking about environmental

play28:01

factors what's the increase in risk of

play28:03

say breast cancer right and and so the

play28:06

whole idea of of genetics and sematic

play28:09

mutation Theory it's it's just like the

play28:11

sematic mutation like there's so much

play28:13

wrong with it even in the New York Times

play28:15

there was an article a few years ago

play28:17

talking about how they took

play28:19

esophageal uh cells from sort of uh they

play28:24

they took normal people non-cancerous

play28:25

people took these cells and and just

play28:27

looked at them and compared it to cancer

play28:30

patients like Cancers and they had all

play28:32

the same genetic mutation this is the

play28:35

same it wasn't it wasn't any different

play28:37

so if normal people are getting

play28:39

mutations but not getting cancer then

play28:41

what's the difference right and that's

play28:43

where I think I think um you know

play28:45

mitochondrial health is probably the

play28:48

underlying cellular sort of mechanism

play28:51

and then on a hormonal level which is a

play28:53

little bit higher because you're talking

play28:54

about hormones not individual self then

play28:57

I think you're talking about hey what's

play28:59

what's what's the energetics what's the

play29:00

glucose what's the insulin what's and

play29:02

also things like glutamine can uh can be

play29:05

important and and and triglycerides as

play29:08

well so I mean I'm sitting here thinking

play29:10

like should I yeah I'm like I'm like

play29:13

there' be a study on you know a high

play29:15

volume presentation like just springly a

play29:17

little sodium bicar po Wes day P I'm

play29:20

sure you're thinking like North kidney

play29:22

are going to fix that that's not going

play29:23

to do anything but the point is these

play29:24

are things that you want to think about

play29:25

and consider and I think one good

play29:28

example that I believe Utah had

play29:30

mentioned I you Jason uh forgive me for

play29:33

not remembering but there just so much

play29:35

wealth of information about cardiac

play29:37

tissue like that is a nice way that I've

play29:39

been explaining since talking to you

play29:40

about about how it's like oh this is a

play29:42

prim primary heart tumor right that in

play29:46

itself Clues you in that the heart is

play29:48

the one tissue in your body that cannot

play29:52

have fatigue so you could lift all day

play29:54

in the gym you could do a 10 pound a 50

play29:55

lb you could do more with the 10

play29:57

eventually

play29:58

lactic acid builds up and you're just

play30:00

not able to Contin however the heart is

play30:02

the only thing and we don't talk about

play30:04

that enough that doesn't you know have

play30:06

that same phenomenon and is able to

play30:08

sustain for the entirety of your Decades

play30:10

of life God willing and also ironically

play30:15

just doesn't have seem to be that common

play30:16

of an organ to have a primary you know

play30:18

cancer type in those on those myocytes

play30:21

yeah that's true and and that and

play30:22

neurons in the brain e you in order in

play30:25

order in order to have cancer as warber

play30:27

said you have to have cell that can

play30:29

compensate oxos inefficiency with

play30:32

fermentation and uh cardiac meiocytes

play30:35

and neurons uh can't do that for very

play30:38

long um they can do it over a short

play30:41

period of time if you were to have a

play30:42

heart attack or or one of these kinds of

play30:44

things uh but when you have a heart

play30:46

attack you generally die from massive

play30:48

brain Dam failure um even if you can get

play30:51

the person's heart back because the

play30:53

neurons are dead uh they can sustain a

play30:56

massive upregulation of fer ation a jolt

play30:59

for a short period of time and you see

play31:01

massive amounts of lactic acid uh being

play31:03

produced um but it can't sustain it

play31:06

can't sustain that one one thing that's

play31:08

very interesting is when people do have

play31:11

heart attacks uh the two things that you

play31:13

see massively accumulate in the blood uh

play31:16

are lactic acid and succinic acid this

play31:19

is well known and the succinic acid

play31:21

accumulates from glutamine fermentation

play31:23

in the mitochondria it's called

play31:25

mitochondrial substrate level

play31:27

phosphorilation

play31:28

the cancer cells are locked into this

play31:30

fermentation they they can't get out of

play31:32

it because their mitochondria are

play31:35

inefficient when you accumulate the

play31:37

lactic acid in the mic you call the

play31:40

acidification that's that's the that's

play31:42

the result of mitochondrial inefficiency

play31:45

so lactic acid lactic acid soyic acid

play31:48

accumulation in the micro environment is

play31:51

the direct result of mitochondrial

play31:54

chronic mitochondrial

play31:56

insufficiency that

play31:58

acidification is due to the fermentation

play32:01

of glucose and glutamine together it

play32:03

also makes your immunotherapy's

play32:05

radiation therapy and a lot of other

play32:07

therapies ineffective they can't break

play32:09

through this

play32:10

acidification so question is how do you

play32:13

reduce the acidification you have to

play32:15

take away the glucose and the glutamine

play32:18

um we have not yet been able to find any

play32:22

canc cell that can survive in the

play32:24

absence of glucose and glutamine they

play32:26

can't grow on fatty acids they can't

play32:28

grow on Ketone bodies we can't find

play32:30

anything uh that will in in other words

play32:33

if you take glucose and glutamine and

play32:34

grow them on fatty acids Ketone bodies

play32:37

anything you want they die um and how do

play32:40

we know that you know what we did we

play32:42

took cancer cells from a range of human

play32:45

and mouse

play32:46

cancers and we grew them in Saline just

play32:49

salt water just salt solution no nothing

play32:52

and we timed them with a how long did it

play32:54

take for them to die Mouse cells die

play32:56

quick because they have a high basil

play32:57

metabolic rate human cells took actually

play33:00

few days for them to completely die just

play33:02

in Saline Solution can you believe it

play33:04

then we add stuff back one after another

play33:07

what perks them up uh what allows them

play33:10

to grow and survive again and we did all

play33:12

20 amino acids we looked at a bunch of

play33:15

carbohydrates and stuff and we found

play33:17

that it was glucose and glutamine were

play33:19

the only two major fuels that allowed

play33:22

those tumor cells to perk back up if you

play33:24

throw a little glutamine they get a

play33:25

little bit of burst you put glucose and

play33:27

glut to me together and it's it's

play33:29

unbelievable um and you have a few

play33:31

vitamins in there and a few other things

play33:33

so clearly we have interrogated the

play33:36

cancer cells to know precisely what they

play33:39

need to grow in a disregulated way and

play33:41

it's the two products uh uh driving the

play33:44

fermentation metabolism in these cells

play33:47

making this not a complicated disease at

play33:50

all and as Jason said the all the major

play33:53

cancers have the same problem it's not

play33:55

like brain is different from bladder

play33:57

different from they they all can't live

play33:59

without glucose and gluty so why are we

play34:02

focusing on thousands of different gene

play34:04

mutations when we're Downstream effects

play34:07

and they have almost nothing to do with

play34:09

the disregulated Cil

play34:11

growth now why doesn't somebody tell the

play34:13

NCI this how is it possible that those

play34:16

guys sitting at the National Cancer

play34:17

Institute have no clue they sit there

play34:21

doing out hundreds of millions of

play34:23

dollars in Grant support for things that

play34:25

and we got 1,700 people people a day

play34:28

dying from cancer in the United States

play34:30

that's 70 an hour about 70 an hour and

play34:34

everybody's chasing gene mutations that

play34:36

have almost nothing irrelevant to the

play34:38

nature of problem I think tell me what

play34:42

is wrong what is wrong like telling on

play34:44

growing I'm just kidding I'm not gonna

play34:46

put that original original Gene

play34:48

treatments were so good you know the um

play34:52

you know the GAC and the uh you know the

play34:57

herself in and stuff they were really

play34:59

good right so then everybody thought

play35:02

this is the answer I remember this

play35:04

because I I was doing going through

play35:06

medical school at the time it was like

play35:08

oh this is great we're just going to

play35:10

find okay this Gene and treat it with

play35:13

this drug which was like okay you have

play35:15

CML we get dreu with GC because that's

play35:18

the G mutation was so logical right and

play35:22

I think everybody got seduced by that

play35:24

that they forget that after those couple

play35:26

of drugs the first couple drugs there's

play35:28

been like zero drugs in the last you

play35:30

know what 20 years now that have made

play35:33

that kind of a difference right

play35:35

everything else these all targeted gene

play35:38

mutation they're not transformative

play35:40

right if you think about the way LC

play35:43

transformed uh the treatment of cmml it

play35:46

was like night and day the thing turned

play35:49

on a dime right from a bad disease to

play35:52

like nothing at all practically right it

play35:54

was a pill you just took it and that you

play35:57

know so that's why it was so seductive

play35:59

that the story was so seductive the

play36:02

treatment was so seductive that

play36:03

everybody keeps looking but if you

play36:05

haven't found it in 20 years and you

play36:06

know how much money has gone into cancer

play36:08

research well it probably ain't there

play36:11

those were like the way outliers of the

play36:14

genetic Paradigm and they're just not

play36:17

true for most cancers but the initial

play36:21

promise was so alluring that people are

play36:24

still going down this pathway despite

play36:26

the fact that there's just way better

play36:29

you know this whole evolutionary uh

play36:32

thought that it's an evolutionary

play36:34

disease I mean changes everything right

play36:36

it it it changes how you think about the

play36:38

disease it changes how you should

play36:40

approach the disease bioenergetics like

play36:42

thinking about bioenergetics because

play36:44

it's so core to all cancers it just

play36:47

changes then like then you can start

play36:49

asking the questions how can you affect

play36:51

it right because we don't have great

play36:52

treatments right people say can you

play36:54

starve cancers by just changing your

play36:56

diet that's pretty it's pretty broad

play37:00

right because if you think about cancer

play37:02

CIA the cancer really takes what it

play37:05

wants from your body right because when

play37:08

you lose weight what you see in the

play37:10

normal non-cancerous is that you see

play37:12

that the uh as you lose weight your

play37:14

metabolic rate goes down because you

play37:16

have less and less energy stored right

play37:19

you don't see that in canceri it's a

play37:21

totally different disease the cancer

play37:22

just takes whatever it wants it will

play37:24

completely catabolize your your muscles

play37:27

it'll burn out everything you have

play37:29

that's why these people get so skinny

play37:30

it's a different disease it's not just

play37:32

weight loss that's why people who say

play37:33

well you should eat sugar and stuff so

play37:35

you gain weight it's like okay this

play37:37

cancer is taking all your amino acids

play37:39

breaking down your muscles and you're

play37:41

gaining fat cells does not a good

play37:43

strategy and you're actually not even

play37:45

getting that much of it so that whole

play37:47

idea of oh you should eat more have some

play37:49

candy because you're losing weight

play37:51

that's not it doesn't actually pass any

play37:54

kind of logical thing like that's third

play37:57

GR thinking right like we're supposed to

play37:59

be doctors right it's like you're

play38:02

operating at a level that's way too low

play38:05

right because cancer CIA is not just

play38:07

weight loss it has nothing to do with

play38:10

normal weight loss it's these cancers

play38:12

that are sucking all your energy out no

play38:15

matter what you do so when you see um

play38:18

you know people losing weight and

play38:20

they're 80 pounds they're metabolic rate

play38:22

has not gone down at all their metabolic

play38:24

rate should have gone from 2,000

play38:26

calories a day to like 12 100 a day

play38:28

because that's what happens in every

play38:29

other person who tries to lose weight

play38:31

that's the whole problem with losing

play38:33

weight right is that when you reduce

play38:35

your calor intake your metabolic rate

play38:37

goes down because the body is trying to

play38:39

match it that doesn't happen in cancer

play38:41

totally different disease so again

play38:43

pointing to the fact that bioenergetics

play38:45

like how this cancer generates energy

play38:47

which is you know gets back to the power

play38:49

you know the the energy Supply which is

play38:51

mitochondria and stuff is sort of core

play38:54

to the entire problem right and

play38:57

obviously we don't have all the answers

play38:58

but at least it's a much more promising

play39:01

pathway than going on and on about

play39:04

genetics and same as Tom I'm like I'm

play39:06

always stunned when I go to any of these

play39:09

websites and it's a genetic disease it's

play39:11

like the first sentence they say it's

play39:13

like goodness I know it's bad and and I

play39:17

know hard stops Tom I'm let you finish

play39:19

that out I'm sorry I want to ask on that

play39:21

point from both of you and your thought

play39:24

P please sorry um speaking on that

play39:28

if somebody had a malignancy stage two

play39:30

stage three or it's just like a strong

play39:33

family history and really worried what

play39:35

are some more granular things to

play39:37

optimize obviously like the insulin

play39:39

levels mitochondrial injury Downstream

play39:43

in the way of antioxidants and berries

play39:45

like even conceptually what are the

play39:48

things why does working out help what

play39:50

are the things we can do to protect the

play39:52

much more rooted cause of what seems to

play39:55

be the you know elicitor of all these

play39:57

mutations in the plasms um well let me

play40:00

just follow up on Jason's CIA issue

play40:03

which is really a core issue in cancer

play40:06

um and he's right the the the cancer uh

play40:09

will take your muscles the muscles begin

play40:11

to lose their uh composition and what

play40:14

happens the amino acids uh will go back

play40:17

into the bloodstream and go to the liver

play40:20

and the liver will use it to make uh

play40:22

through gluconeogenesis you can actually

play40:24

make sugar from the dissolved amino

play40:26

acids from the from the muscles and the

play40:28

glutamine itself is just a a pure gold

play40:30

fuel uh for the tumor and our work has

play40:33

shown that all metastatic cancers are uh

play40:37

of maccrage origin a maccrage is part of

play40:39

our immune our immune cell um they are

play40:42

the only cells that can actually move in

play40:44

in and that one of the few they're part

play40:46

of the immune cells move in and out of

play40:48

tissues um so you have two different

play40:50

kinds of cancer cells you have the stem

play40:52

cells that grow like crazy uh and then

play40:55

you have the metastatic cells and they

play40:57

all of macro every every major human

play40:59

cancer that we have studied has maccrage

play41:02

characteristics and they are the cells

play41:04

that are already programmed to enter and

play41:06

ex exit the bloodstream this

play41:07

intravasation extravasation their

play41:10

immunosuppression um and they they they

play41:12

they'll lead to the cic phenotype and

play41:15

getting their energy from dissolving

play41:16

muscles and and Jason it's very

play41:18

interesting when when you're in CIA your

play41:21

insulin is high when you go under

play41:23

calorie restriction therapeutic fasting

play41:25

your insulin and glucose go down and

play41:27

it's like just it's just a blown out

play41:29

opposite thing you're you're you're

play41:30

right so we have to look at this as a

play41:32

bioenergetic problem uh linked

play41:35

intrinsically to to the mitochondria and

play41:38

and when you say well how do we manage

play41:41

well if we know that the cells can't

play41:43

grow without fermentation fuels that are

play41:45

driving the disregulated growth then the

play41:48

strategy to manage cancer would be to

play41:50

simultanously Target the two fuels that

play41:54

are leading to this disregulated growth

play41:56

and they can't use fatty acids and

play41:58

ketones as I've said they store them

play42:00

they don't use them so uh when we look

play42:03

at calorie restricted ketogenic diets or

play42:05

ketogenic metabolic therapy we lower the

play42:08

blood sugar and this's another very

play42:09

important thing people always say oh we

play42:11

can never lower sugar enough to starve

play42:14

the tumor that's not true because when

play42:16

you lower the blood sugar what are the

play42:18

organs that take in the available sugar

play42:20

it's the muscle and there you go back to

play42:22

your exercise again muscle does not

play42:24

share sugar muscle builds glycogen

play42:27

because if the Beast is evolutionarily

play42:29

if the if the bear is chasing you you

play42:31

must run away that comes from the energy

play42:34

if your muscle shares glucose with other

play42:36

organs and the Bears you have no energy

play42:38

to run so the muscle takes glucose out

play42:40

of the blood stores it as glycogen for

play42:43

the muscle use the brain is the biggest

play42:45

consumer of glucose in our body so what

play42:48

little glucose is left when you lower

play42:50

blood sugar the brain's going to get it

play42:51

who's going to get it last the tumor

play42:53

cell gets the last so you have to

play42:55

realize you're marginalizing their

play42:57

ability to survive and then when you hit

play42:59

them with the GL the glutamine targeting

play43:01

on the other end which has to be done

play43:03

very strategically and carefully you Mar

play43:05

you completely destroy the capability of

play43:08

this tumor to grow you reduce the

play43:10

angiogenesis you reduce the inflammation

play43:12

and gradually your body power to heal

play43:15

will eventually go after and dissolve

play43:17

those tumor cells themselves and use

play43:20

that fuel for the energy for the rest of

play43:21

the body it's unbelievable it's called

play43:23

un autolytic cannibalism where the body

play43:26

will actually turn on the tumor and use

play43:28

the fuels for itself everything is

play43:30

related to bioenergetics if you know why

play43:33

and we and then we take poor patients

play43:35

and we treat them with all these

play43:36

terrible toxic poisons reducing the our

play43:39

own ability of the body to do what I

play43:42

just said you compromise the body's

play43:44

ability to heal itself by the very

play43:47

treatment she using to manage the

play43:48

disease makes absolutely no sense now

play43:51

I'm not throwing out immunotherapies

play43:54

because they're based on the sematic

play43:55

mutation Theory they're based on the so

play43:57

based on an incorrect Theory but they

play43:59

could be a powerful tool if used

play44:01

correctly if you can use a metabolic

play44:04

approach to shrink the tumor down to a

play44:05

few cells that are still alive they must

play44:08

share something in common because

play44:10

they've survived together as a group

play44:12

they may now be appropriately destroyed

play44:15

by a targeted immunotherapy but not at

play44:18

the beginning because at the beginning

play44:20

you have all this hodge podge like Jay

play44:22

said there just a total hodge podge of

play44:23

stuff you may get some people to respond

play44:26

well but you also create

play44:27

hyperprogressive disease not knowing the

play44:29

tool that you're use making the situa a

play44:32

bad situation much worse so I I think we

play44:34

just have to know how to use all the

play44:36

tools that we have in the appropriate

play44:38

way with our understanding that this is

play44:40

fundamentally a metabolic disorder a

play44:43

bioenergetic disorder that we have to

play44:45

use the entire body's resources together

play44:47

with our understanding with the

play44:49

foundational principle of what's going

play44:51

on inside the neoplastic cell itself

play44:53

once we understand this the solution to

play44:56

the cancer problem problem will be

play44:57

obvious to everybody and you're going to

play44:59

see drops in death rates like you can't

play45:01

imagine but as long as the National

play45:03

Cancer Institute thinks it's a genetic

play45:05

disease yeah ain't G to get any progress

play45:08

It's just that simple and the other

play45:09

thing that was if you go back and look

play45:11

at the NCI history you find in

play45:15

1984 they invited the pharmaceutical

play45:17

industry to help the scientists of the

play45:20

national cancerous who find cures to

play45:22

cancer that was putting the fox in the

play45:24

an house how's that working out for us

play45:26

so far

play45:27

right we have more cancer today let me

play45:30

tell you something else that smoking

play45:31

thing in in the early days of the smoke

play45:34

anti-smoking campaign get alone they

play45:36

they in 1991 they had this no more smoke

play45:39

because you second sand smoke was

play45:41

bothering people so we stopped smoking

play45:43

now what they say is all the advances

play45:45

we've made since 1991 this giant 33%

play45:49

drop was because we stopped smoking the

play45:51

the the issue is is that had we not

play45:53

smoked we would have 33% more cancer

play45:56

deaths today than we that we actually

play45:58

have so it's all smoking mirrors if you

play46:00

want if you want to know what's going

play46:02

on it's unbelievable prevention was the

play46:05

only thing that really gave us some grip

play46:07

on the whole thing it wasn't targeting

play46:09

gene mutations or any of that crazy

play46:11

stuff that that seems to be uh the

play46:13

subject of millions of dollars uh thrown

play46:16

at these insane grants that are having

play46:19

no significant impact on survivability

play46:22

for cancer with a majority of people

play46:24

it's as I said it's the greatest tragedy

play46:25

in the history of Medicine what we've

play46:27

had happen with this cancer fias yeah I

play46:30

I mean I agree I have to leave in a

play46:31

minute but I I I completely agree with

play46:33

you I think that you know using you know

play46:36

understanding about glucose and amino

play46:38

acids and then trying to do sort of more

play46:41

fat-based therapies I to me it's it's

play46:43

the only way but but to me it's a very

play46:45

sort

play46:46

of you know ham-handed sort of way to

play46:49

approach things and I think that if we

play46:52

had more research then we could develop

play46:54

much more sort of targeted ways like I

play46:56

know Tomia talked about hyperbaric

play46:58

oxygen and stuff and I think there's

play47:00

still something in there uh but it just

play47:02

hasn't been fleshed out and nobody's

play47:04

thinking about these things that such a

play47:06

promising

play47:07

pathway you know that that that needs

play47:10

the research because we're we're dealing

play47:11

with very primitive tools when we're

play47:13

just trying to sort of do this diet

play47:15

thing compared to you know oh we're

play47:17

targeting this Gene you get we have so

play47:19

much money poured into the genes that we

play47:21

are so specific treatments of genes and

play47:24

yet we can't we know nothing and can't

play47:27

do anything about the bioenergetics

play47:28

which sort of um does it so yeah I mean

play47:32

such a lost opportunity so well that's

play47:35

that's predominantly because of the

play47:37

theory that's driving the industry the

play47:39

sematic mutation theory is the is the

play47:42

theory driving research and development

play47:45

in the academic and pharmaceutical

play47:47

Industries and therefore if cancer is

play47:50

not a genetic disease it's a

play47:51

mitochondrial metabolic disorder you're

play47:54

never going to achieve Optimum outcome

play47:56

for the majority of patients the theory

play47:58

is wrong just as the geocentric theory

play48:02

of the solar system was not correct

play48:04

until you put the sun in the center of

play48:05

the solar system all the planet

play48:07

movements made sense when as soon as you

play48:09

put the mitochondria in the center of

play48:11

the cancer problem you're going to see

play48:12

major drip

play48:14

drops sorry about that it's great

play48:16

talking to you I appreciate it when you

play48:18

mentioned the point about the acidity

play48:21

around the tumor or the lactic acid and

play48:24

how radiation isn't as effective I'm

play48:27

really almost frustrated because I've

play48:29

never heard the next step we've hear

play48:31

about radio resistant or radio

play48:34

refractory tumors and they become very

play48:36

challenging especially when they're in a

play48:37

bad stubborn place can we talk about

play48:40

that a little bit more on how is there a

play48:43

way that we could potentially make a

play48:45

radio classically or traditionally radio

play48:48

refractory uh tumor more susceptible to

play48:52

radiation delivery number one and number

play48:55

two um what like how do we how do we do

play48:58

that well I mean it's very clear what's

play49:01

responsible for the um acidification of

play49:04

the micro environment in impeding uh

play49:07

radiation therapy and immunotherapy for

play49:10

that matter and chemotherapy for that

play49:11

matter it's this

play49:13

acidification um what what what happens

play49:16

when you're fermenting uh there's a

play49:18

pglycoprotein on the surface of of

play49:21

cancer cells that as soon as the drugs

play49:23

come in they pump them right out so and

play49:25

that's driven by a fermentation

play49:26

metabolism and the and causing the

play49:28

acidification so what is that as I said

play49:31

we have interrogated these cancer cells

play49:33

and it's the availability to convert

play49:35

glucose into lactic acid through the

play49:38

glycolysis

play49:39

cytoplasmic gly in the in the cytopl in

play49:42

the in the cytoplasma glycolysis pathway

play49:44

dumping out lactic acid and also

play49:47

glutamine uh dumping out succinic acid

play49:50

so those are acids where the protons

play49:51

come out along with the with the lactate

play49:53

the succinate and you have acidified the

play49:56

micro environment thereby serving it's

play49:58

it's not purposeful in the sense the

play50:00

cancer cells don't do this as a designed

play50:03

mechanism to provide they're doing it as

play50:06

as a as a response to a failure in

play50:07

oxidative energy metabolism but it also

play50:10

prevents other therapies from working so

play50:13

if you were able to significantly reduce

play50:16

glucose and Elevate Ketone bodies um you

play50:19

then make these tumors extremely

play50:21

vulnerable to radiation uh therapy you

play50:24

make them far more vulnerable to

play50:26

immunotherapies and some and you can use

play50:29

half the dosage of chemotherapies and

play50:31

still have them have tremendous

play50:32

therapeutic benefit so again you have to

play50:36

to remove that protection that Shield of

play50:38

acidification where is it coming from

play50:41

it's coming from the fermentation of two

play50:43

fuels glucose and glutamine simultaneous

play50:45

targeting of glucose and glutamine while

play50:48

under nutritional ketosis will allow

play50:50

radiation and all these other therapies

play50:52

to work infinitely

play50:54

better case period it's no question

play50:58

about that because everybody knows the

play51:00

acidification is blocking how do you get

play51:01

rid of the acidification where is it

play51:03

coming from it's coming from the

play51:04

fermentation of two fuels only now

play51:06

Sanjay listen to this no one anywhere is

play51:09

doing what I just said they want to test

play51:12

drugs in clinical trials double blind

play51:14

crossover One Drug this guy gets it then

play51:16

we're going to that cannot be done that

play51:19

kind of a a trial must be booted out

play51:22

those trials have been Monumental

play51:24

failures uh for a long period of time

play51:26

obviously we had 1,700 people a day

play51:28

dying from cancer in the country I mean

play51:30

this is a tragedy why because we're

play51:32

testing drugs in the wrong way it's a

play51:34

diet drug combination that you're

play51:36

looking for to make the tumors

play51:38

vulnerable the ultimate goal ultimate

play51:40

goal in all this is how do we keep

play51:42

cancer patients alive longer with a

play51:45

higher quality of life and it's

play51:47

metabolic therapy man that's what's

play51:49

going to do it and you got to Target

play51:51

these fuels and then you're going to

play51:52

find all these things that didn't work

play51:54

all of a sudden are going to work

play51:55

dramatically well

play51:57

under a different kind of it so we're

play51:58

not throwing anybody out of the boat

play52:00

we're just telling them to reposition

play52:02

where you're sitting you're you might

play52:04

not have been as important as you

play52:05

thought but we still need what you're

play52:06

going to do so uh um so this is the

play52:09

thing you're going to find dramatic I

play52:11

have no doubt about it but what I'm

play52:13

talking seems to be uh too many there

play52:16

too many issues to stand in the way

play52:17

especially the theory when the theory is

play52:19

incorrect the outome will never be

play52:21

optimal and that's seems like this

play52:23

podcast and what I hope to achieve even

play52:25

in the next six months for myself but

play52:27

meaning like on transition of where I

play52:29

can put my manand withd that that will

play52:31

hopefully really catalyze this because I

play52:32

know you have made it your mission the

play52:36

man that is Thomas C freed has you have

play52:38

you have spent now decades on trying to

play52:42

debunk this thing and I I cannot express

play52:45

my deep admiration for you for that well

play52:47

we we we need guys like you you you're

play52:51

going to be the guy you're the guy in

play52:53

the in the trenches that's actually

play52:54

going to implement the the Paradigm

play52:57

change because we we have when we go to

play53:00

oncologists and they never heard that

play53:02

glucose has any role in cancer and diet

play53:04

has no relevant and that we're going to

play53:06

use all these expensive drugs we have to

play53:08

re-educate the oncology Community to

play53:11

know that the disorder that they thought

play53:13

was a genetic disease is actually a

play53:15

mitochondrial metabolic disease well Tom

play53:17

Tom I worry I worry it's deeper than

play53:19

that I worry that

play53:20

it's ultimately economic and

play53:23

capitalistic issue which I know you said

play53:25

but I really deeply think well then then

play53:28

then then we have to give every cancer

play53:30

patient that comes into the clinic has

play53:32

to be given a little brochure to say we

play53:35

thank them for their disease because

play53:36

it's a very powerful uh driver of the of

play53:39

the medic I know nobody's gonna say that

play53:42

nobody's going to tell cancer patients

play53:44

we're going to thank them because their

play53:45

disease is supporting a massively

play53:47

profitable industry um I think it should

play53:50

be patient outcome first and

play53:52

profitability second not not the reverse

play53:55

but how do we do that we have to have

play53:58

entrepreneurs who come into the picture

play54:00

and figure out how we can uh generate uh

play54:04

a comparable profits from something that

play54:06

actually works and helps the patient I

play54:08

don't think people are opposed to paying

play54:10

a large amount of money for something

play54:12

that actually works uh but it's paying a

play54:14

lot of money that causes Financial

play54:16

toxicity and death th this is this is

play54:19

this is an a program that's not going to

play54:22

work uh eventually people are going to

play54:23

wise up and say we can't we can't do

play54:25

this anymore it's actually threat threat

play54:28

to National Security for crying out loud

play54:30

I honestly think and I've never said

play54:33

this in my life before I honestly think

play54:35

in a weird way if you have this

play54:37

beautiful big torch of passion and and

play54:40

and Science and and understanding you

play54:43

have lit one for me that I now feel as

play54:47

like my primary Mission I've never felt

play54:48

in my core like what is the primary

play54:50

Mission I just like do what the univers

play54:52

tells me I feel like I want to I want to

play54:54

help uh everything that You' done to

play54:57

really go full force on this very

play55:00

important issue um I really I'm going

play55:03

say that in a second I'm going to ask

play55:05

one thing real quick to put back right

play55:07

when you went on that about the aid V

play55:10

and I'm afraid to ask this question but

play55:13

I'm really afraid to ask this question

play55:15

but is that why and I could be wrong

play55:18

liposarcomas are generally very chemor

play55:20

refractory and even like radiation's not

play55:23

great uh and is pancreatic cancer which

play55:25

we know is called classically a stubborn

play55:27

tumor is that also an uh uh

play55:30

environmental we know they hijack the

play55:32

immune system and hijack you know

play55:34

extracellular Matrix stuff but do you

play55:36

think there's a role on the a acidity of

play55:38

the micro environment for these way more

play55:40

stubborn tumors that's reducing our our

play55:43

whole yeah well certainly for pancreatic

play55:45

cancer and and gasto and some of the

play55:47

lung C well they're all like you know

play55:49

driven um with with a a macras component

play55:53

fuse hybridization and these kinds of

play55:55

things um making them making them

play55:58

exceptionally uh dependent on both

play56:00

glucose and glutamine the

play56:02

liposarcomas uh on the other hand

play56:04

they're not nearly as aggressive uh as

play56:06

some of these other more um uh what we

play56:09

call malignant kinds of things and I've

play56:11

always been interested in liposarcomas

play56:13

they they kind of they can come from

play56:15

certain kinds of mitochondrial

play56:16

abnormalities I have I I put that

play56:19

section in my book where you have

play56:21

certain kinds of impacts on

play56:23

mitochondrial F you get some some kinds

play56:25

of these postar and they can be a

play56:28

to to manage they just hang

play56:31

on just just hack them away maybe

play56:34

surgery might be the only but but it's

play56:37

like the Cockroach

play56:38

ofy uh they have an interesting slightly

play56:41

different kind of metabolism from some

play56:43

of the more invasive malignant kinds um

play56:46

but that's kind of the interest of of

play56:48

Cell Biology and uh you know I become

play56:51

less less concerned about a liposarcoma

play56:55

than I become concerned by a pancreatic

play56:57

or a glol blastoma these kinds of tumors

play57:00

you know these are the ones that and the

play57:01

ones that are lung cancer and breast

play57:03

cancer the ones that are killing most of

play57:04

us is cholon cancers and bladder and

play57:06

this kind of thing um but uh uh yeah but

play57:09

I mean I I did dress the liposarcoma a

play57:12

little bit in my in my canceris a

play57:14

mitochondrial metabolic disease paper

play57:16

but I I didn't do a deep dive on it and

play57:20

yeah it's just unique because things

play57:21

don't work on it and that usually

play57:23

happens when things are slow because

play57:25

tools we use on rep the funny thing when

play57:27

you talk about liposarcoma is my my

play57:29

sister many years ago had a had a dog

play57:31

with a liposarcoma and we try to use our

play57:34

metabolic therapy on it uh you know what

play57:36

was U it was you know the the dog was

play57:40

given calorie restricted food usually it

play57:42

works on on a lot of different kinds of

play57:43

malignant cancer and and what happened

play57:46

was that you had a liposarcoma on this

play57:48

on this dog it was attached and we put

play57:49

him on metabolic therapy then we found

play57:51

out it was a dog attached to a lightos

play57:53

saroma

play57:56

oh my gosh you know it worked on the dog

play57:59

but it didn't work on the lifeo sarom

play58:01

but but uh that was an interesting uh n

play58:04

of one uh but but you're right I I think

play58:08

we we we need to figure that out a

play58:09

little bit more I'm not I'm not claiming

play58:11

that we have a solution it's just so

play58:13

unque yeah compared to other we study a

play58:16

little bit more we'll figure it out real

play58:18

quick it's funny you said that about

play58:20

dogs I had uh a gentleman from uh

play58:22

Harvard yesterday uh Dr San Lim and they

play58:27

found a workaround around their AI

play58:29

enabled you know uh tumor sensitivity

play58:32

workup stuff they do on live cells and

play58:34

they started with dogs one because you

play58:35

it kind of bypassed all of this uh you

play58:38

know difficulty on that's another whole

play58:40

another podcast on on even proving

play58:43

something its utility because of of all

play58:45

the red tape but at least to blood

play58:48

cancers dogs apparently have a much

play58:52

faster um response to treatments like

play58:55

the chemotherapy anyway I didn't know if

play58:56

there was a metabolic reason for that or

play58:58

if they just proliferate more or what

play59:00

but apparently it's it's it's far more

play59:02

prompt and brisk uh than what we have to

play59:04

wait for with a couple of Cycles in

play59:06

humans for things like Hotchkins and

play59:07

other things yeah well dogs you know I

play59:09

published that paper on the mass cell

play59:10

tumor on the dog's face published in in

play59:13

I think it was frontiers of nutrition or

play59:15

something and uh that was the only thing

play59:17

we actually cured um I mean we keep

play59:20

people alive very long but who knows if

play59:22

they're cured or not uh but but the dog

play59:25

had complete resolution of the mass cell

play59:28

tumor using a metabolic therapy um and I

play59:31

have all the details in the paper itself

play59:33

it's unbelievable the dog died from old

play59:35

age from heart disease so the cancer

play59:37

never can't that's the only way you know

play59:38

you're cured if you live really old and

play59:40

you die from something other than the

play59:42

cancer then you can say oh I was Cur

play59:44

somebody say I cured my cancer when I

play59:46

died from but that's okay if you're 98

play59:48

years old Dro dead of a heart attack

play59:49

when you had bladder cancer when you're

play59:51

40 you know obviously metabolic therapy

play59:55

tour kept you alive for that long to die

play59:57

from something else I mean we're all

play59:59

we're all terminal in one way or another

play60:01

that we just want to we just don't want

play60:03

to make it too premat we don't want it

play60:05

to be premature um but but like and I

play60:08

like I like I like that that's what you

play60:10

say you're like look I'm not claiming to

play60:12

cure cancers but what I can tell you is

play60:14

we can have them in a deep durable

play60:17

control just keep them quote unquote in

play60:19

check for a long time like that's what

play60:21

that's our guy from England Pablo Kelly

play60:23

he's had three three uh debulking for

play60:25

his

play60:26

Blasta I idh1 and and and he's he's just

play60:30

celebrating 10 years of survival now

play60:32

he's married two kids he never had that

play60:34

uh but his cancer is there he's not Ted

play60:37

he's just has it and it grows slow and

play60:40

he gets into de bulk periodic uh what do

play60:43

you have to have a cure do you want to

play60:44

just live longer and have a somewhat of

play60:46

a normal life I mean be thankful man if

play60:48

you did standard of care you would have

play60:50

been dead nine years

play60:52

ago right right and I mean it's I'm

play60:56

laughing and I'm I know that person I'm

play60:58

the person that's doing this you know

play60:59

like I'm the one it's like Gallow humor

play61:02

for Christ's sake you know

play61:04

it's yes nail it um gosh I I I really if

play61:09

I can say I have a bromance love for

play61:11

someone it is 100% you lastly if if you

play61:14

have the time so sparing what I believe

play61:17

is is also understated got microbiome

play61:19

health and its intimate relationship

play61:21

with the dexterity of the immune system

play61:23

because I do believe having these narrow

play61:25

diet of just mac and cheese and chicken

play61:27

nuggets without the kind of

play61:29

heterogeneous stuff when it comes to

play61:31

different fruits and fibers not the

play61:33

fiber itself but but fiber RIS things

play61:36

that have uh introduce kind of a

play61:37

dexterity to your immune system short of

play61:39

that on a cellular metabolic level when

play61:42

it comes to optimizing the health of our

play61:44

you know mitochondria and and cellular

play61:47

injury I hope anyone can appreciate one

play61:51

in your discussions the role and why

play61:53

we've been saying antioxidants for a

play61:55

long time

play61:56

right you do support like that supports

play61:59

what you're saying oh we you know we you

play62:01

know it helps radical uh Ros injury Etc

play62:05

T like working out what is that it helps

play62:10

cardiovascular you know

play62:13

processes what are the things that make

play62:16

theoretical Sense on someone that is

play62:19

trying to avoid a recurrence or prevent

play62:21

cancer to optimize this mitochondrial

play62:25

metabolic health that you were talking

play62:26

about well that's you know the late uh

play62:29

Richard V from NIH I had many

play62:30

discussions with him and and George

play62:32

kahill from the diabet josin diabetes

play62:35

center and when we look at what what

play62:37

prevents reactive ox or oxidative stress

play62:41

uh when you say antioxidant uh

play62:43

capabilities while water only fasting uh

play62:46

uh and and these kinds of things when

play62:49

the body switches from glucose to Ketone

play62:51

bodies they're powerfully antioxidant um

play62:54

they actually improve the Delta G Prime

play62:56

of ATP hydrolysis within the

play62:58

mitochondria itself which means you're

play63:00

for every for every breath of oxygen for

play63:03

every mole of oxygen you take in you

play63:05

actually get more efficient energy uh

play63:08

with minimal reactive Ox species so this

play63:11

is don't forget we as a species evolved

play63:14

to always been in a sem a semi-state of

play63:16

nutritional ketosis where cancer was

play63:18

unheard of uh well I not going to say we

play63:21

knew what was going on in the

play63:22

Paleolithic period but we certainly know

play63:24

from modern modern humans live according

play63:26

to traditional ways they're generally in

play63:28

in in semi ketosis that's powerfully

play63:31

antioxidant so um and you can supplement

play63:35

that with your berries and things like

play63:37

this and certain things like that so

play63:39

again it's never one thing it's a

play63:41

cocktail of things all go together to

play63:43

give you Ma maximum metabolic efficiency

play63:46

maximum homeostatic efficiency it's like

play63:49

a it's like a hypo oxidant State almost

play63:51

that's a word it's it's not yeah you can

play63:53

kind of touch it every now and then like

play63:55

pull out weed here and there in your in

play63:57

your in your house with antioxidants

play63:59

that's a Bist that you're talking about

play64:00

just like ketotic State a ktic state can

play64:03

double over as a homonym to a hypo

play64:06

oxidant State yes yes and you know the

play64:08

other thing people are always talking

play64:09

about is their microbiome they love this

play64:11

to soon as just mentioned microbioma you

play64:14

know has keep our microbiome healthy and

play64:16

then when you get cancer you Jim know

play64:18

you know what chemo does to your

play64:19

microbiome God Almighty what are you

play64:22

talking about your microbiome and then

play64:23

you take some toxic chemical and you

play64:25

can't get off the pot and kill it when

play64:27

are your microbiome is screaming out

play64:29

please no more no

play64:31

boss right no it's true I think that's

play64:34

the factor it makes no damn sense you're

play64:36

always talking about then you give

play64:37

somebody this radiation and chemo and

play64:40

and it knocks the crap out literally

play64:42

next to your

play64:44

microb I mean when you think of the

play64:46

absurdity of stuff that we do to human

play64:48

beings in the name of trying to help

play64:50

them it just makes no sense at all but

play64:53

um yeah there's so many different uh

play64:55

ways you can you can look at this and

play64:57

our our goal has always been how do we

play64:59

manage a chronic CA disease like cancer

play65:02

in a logical way based upon the hard

play65:04

science that we know is there and and

play65:07

and all I have done is looked at the

play65:10

science I'm trained biochemist and

play65:13

geneticist we go back and you look and

play65:15

and all of a sudden you can see all this

play65:16

thing and how wonderful it works and

play65:18

doesn't hurt people and then you go out

play65:19

you're looking say everybody what are

play65:21

they doing out in the real world what

play65:23

are you guys doing to these poor cancer

play65:25

patients it's like they exist in two

play65:27

different worlds it's like the

play65:28

biochemists and the phds do something in

play65:31

some other country with a different

play65:33

passport and somehow it's like get that

play65:35

and you get you trickle into another

play65:37

country and they see it off and then

play65:38

they take what was done in this country

play65:40

when it's the clinical stuff now and

play65:42

that's the problem is there is just not

play65:44

a nice uh you know inner stitching of

play65:47

that world it's more of a handoff and I

play65:49

think that's where things are lost

play65:50

there's nobody in the middle that's

play65:53

actually kind of putting these things

play65:54

together like you are yeah well that's

play65:56

the whole thing our work is directly

play65:58

translational better better than any

play66:00

anyone else's that we can find uh and

play66:02

the NIH oh you got to do translational

play66:04

work and then they build all these crazy

play66:06

models genetically engineered cells and

play66:08

genetically engineered hosts and you get

play66:10

all these things and it makes it it's

play66:12

just doesn't make a lot of sense

play66:14

everything has to be done with natural

play66:15

natural natural natural as close to the

play66:17

real world as possible will give you the

play66:19

better the better uh uh outcomes uh and

play66:23

you know translational and and and

play66:25

almost none of this stuff is

play66:27

translational uh when you look at it um

play66:30

and they say oh you know you cure these

play66:31

mice all the time and you go to the

play66:33

clinic and you never get the well

play66:35

they're not using the right the right uh

play66:38

tools they're not using the right models

play66:40

they're getting it like like like I said

play66:42

in my in my in my in my book uh the uh

play66:46

when you when you bait when you bait the

play66:48

um the mouse trap with a picture of a

play66:50

piece of cheese what you catch is a

play66:52

picture of a mouse you don't really get

play66:55

the you don't really see the real what's

play66:57

really happening yeah and what we're

play66:59

doing is we've just got you know

play67:01

pictures of cheese everywhere in our in

play67:03

our uh in our preclinical model systems

play67:06

I mean the cheese is like the tumor

play67:08

micro environment we know that's

play67:09

important it seems to be a problem and

play67:10

you're like yes and this is this is the

play67:12

cellular level and the kind of

play67:14

communication we know why the micro

play67:16

environment is screwed up we just don't

play67:18

do anything about it and and we're

play67:19

making it worse in most of the case in

play67:21

most cases so again you have to have a

play67:23

re-evaluation of what's going on you you

play67:25

really need to I don't know what the

play67:27

hell they're doing down at the National

play67:28

Cancer Institute they they keep backs

play67:31

slapping and coming up with all this

play67:32

kind of crazy stuff and and and people

play67:34

are dying out there um uh they're

play67:37

miserable uh suffering that I can't even

play67:40

I get all these emails dozens of dozens

play67:42

I sometimes I have to walk away I say

play67:44

what are we doing to these poor people

play67:46

um we're not treating them the way we

play67:48

should be treating them when you say are

play67:49

and we can you just tell us anyone

play67:51

that's listening that that that is

play67:53

driving and can't like ghoul you

play67:56

what do you mean by us and we and our

play67:58

well I would say it's the it's the

play68:00

establishment what is the cancer

play68:03

establishment doing no I mean for you

play68:05

when you say what we're doing and what

play68:06

our focus is what what our our focus is

play68:08

to manage are uh what well the people

play68:11

that understand maybe maybe one of you

play68:14

maybe you'll become one of these guys in

play68:15

the I'm I I think this podcast did it

play68:17

for me actually understand what cancer

play68:20

is and how it should be treated yeah uh

play68:22

and then and then not being allowed to

play68:24

do that because of a of a a standard of

play68:26

care written in Granite and standards of

play68:28

care should have never been written in

play68:30

Granite uh they have to be flexible as

play68:32

new information comes along we should be

play68:34

able to modify the standard of care you

play68:37

know when we do clinical trials you you

play68:39

have the standard of Care standard care

play68:42

with metabolic therapy and metabolic

play68:44

therapy by itself why is the missing

play68:46

control group never allowed to be done

play68:49

this is this is the the the crazy stuff

play68:51

so anyway I I have no long I don't know

play68:53

how long it's going to take to break

play68:55

down the walls uh but I'll tell you one

play68:57

thing people want to live and their

play68:59

their motivation to want to live and

play69:01

know that there's an alternative to what

play69:02

we're doing uh may may help change the

play69:05

system and I and I'm hoping for that

play69:07

Dred I just I really hope I would love

play69:09

to shake your hand one day I hope like

play69:11

that's something you find were you live

play69:12

in Foxboro uh yeah I live in Foxboro I'm

play69:16

right now right now I'm at the

play69:17

University at Boston College gotcha I

play69:20

just I really respect so much what

play69:21

you're doing have you met GRE Greg Simon

play69:24

uh no I haven't I I don't think the

play69:26

first cancer moonshot director yeah if

play69:28

you time one day I would love to

play69:30

introduce yall too I honestly think

play69:32

y'all would be best friends like it's

play69:34

like it's unbelievable how much I like

play69:35

he was the first cancer moonshot uh

play69:37

director under Obama and um and uh Gore

play69:41

and y'all are just so unbelievably

play69:44

similar you appreciate the NCI shadiness

play69:47

and and y'all are just very you know

play69:50

globally just kind of mission driven

play69:51

he's a cancer patient he's actually not

play69:53

a scientist he used to get like a rock

play69:55

star I believe it or not but he's he's

play69:56

deeply respect I think once the once the

play69:58

theory changes and you realize that it's

play70:01

a mitochondrial metabolic disease then

play70:02

everything will begin to change until

play70:04

that theory is and and and all the

play70:06

textbooks say it's a genetic disease so

play70:08

you're you're just perpetuating the the

play70:10

the lack of knowledge on the part of the

play70:12

industry uh all the as you said when you

play70:14

went to medical school you never heard

play70:16

that cancer was a was anything other

play70:18

than a genetic disease so clearly the

play70:20

education in the medical schools have to

play70:22

change as well it's a big mission but

play70:25

anyway I'm I'm here I'm not going

play70:26

anywhere um we have a lot of stuff going

play70:29

and all of our work is supported by

play70:31

philanthropy and private foundations so

play70:34

uh not the nation they they did it when

play70:36

you do certain things they're very very

play70:38

valuable to support research there's no

play70:40

question about it you know National

play70:42

Institutes of Health has been a great

play70:44

resource for the nation um but right now

play70:48

in the cancer field and the cancer thing

play70:49

it's it's just not working and and and I

play70:52

think it can work once they realize the

play70:54

theory the theory that they're working

play70:55

under uh is incorrect and they once they

play70:57

switch the theories then you're going to

play70:59

see massive changes in the outcome and

play71:01

Improvement for patient uh survival when

play71:04

we talk about like contiguous or cancers

play71:07

that like in lung on smoker or in

play71:10

Colon to Jason's point about the double

play71:13

hit to me there it kind of makes sense

play71:17

because it's like if you have a tubo

play71:18

villis adoma or an environment where

play71:21

there was one portion that's invasive

play71:23

and the other is not that's the one

play71:26

challenge I can think about what it

play71:28

relates to the switch or a mutation

play71:31

because what is it that Mak something

play71:34

that's screwed up actually become

play71:36

invasive cancer versus pre yeah that's

play71:39

what we we in my book on the origin of

play71:41

metastatic in my paper this is another

play71:44

thing that's very I published the paper

play71:47

uh in 2013 I believe u on the origin of

play71:50

metastatic cancer which talks about

play71:53

exactly what you just mentioned why some

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cells are not invasive where other cells

play71:57

are invasive and that comes from the

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fusion hybridization of of our immune

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cells coming in cancer is viewed as by

play72:03

the body as an unhealed wound and and it

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it sends out singings cyto and factors

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that cause the immune system to come in

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and facilitate wound healing and those

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cells are largely macras and they throw

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out growth factors in cyto but it

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stimulates the the stem cells to grow

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stem cells are not in invasive they grow

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like crazy but don't have the

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capabilities of metastasizing

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intravasation extravasation this kind of

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thing but when the macras is fused

play72:32

together with themselves and with one of

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these stem cells you now have a cell

play72:37

that's not only disregulated in in cell

play72:39

growth but also has the genetic

play72:41

apparatus to spread around and invade in

play72:43

in a different way because when when

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macrofagos come out of your bloodstream

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as monocytes they come right through the

play72:49

tissue to heal the wound right they're

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in they're uh uh intravis intravasation

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extravasation all this is macras

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behavior this exactly what metastatic

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cancer cells but stems and one sub part

play73:01

of the tumor can't do that because

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there's mostly stem cells so you can

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have very this is why when you're

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looking at a cancer you have a hodg

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podge of different kinds of cells in

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that you have normal Max you have Fus

play73:13

Max you have stem cells you have a whole

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big what they call Cellular heterogen Hy

play73:17

blasts yeah they're all in there and and

play73:20

and the ones that blast out and become

play73:22

metastatic every one of them has has

play73:24

macro characteristics I published all

play73:27

this I I showed everything and that

play73:29

paper has been cited over 1,300 times

play73:33

now listen to this they never read the

play73:35

paper I put I only said in there

play73:37

metastasis is responsible for most

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cancer deaths and that's the only reason

play73:41

they site the paper without without ever

play73:43

reading what I actually said this is

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amazing so the the folks in the field

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aren't reading the literat are just

play73:50

they're just taking little chunks of

play73:51

what this so I call it broken science

play73:54

it's a problem where we have everything

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there to explain it but people either

play73:59

are not reading it or don't understand

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it so it's really yeah metastasis why

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you have certain parts of the tumor uh

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they grow fast but they don't spread the

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other part little thing spreads all over

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the place this is all due to the cell

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biology that exists inside that um uh

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organ a tumor is kind of an organ it's

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own blood system Ed yeah yeah yeah yeah

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so that cell that cell is the cancer

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cell or the even pre cancer cell is a

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thing that eventually actually puts out

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the signaling to make that stem cell

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around it differentiate yeah it's not

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differenti EnV yeah they well and don't

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forget when you interrogate the

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metabolism of the of the stem cell and

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the metastatic cell they're they're both

play74:41

fermenting the the problem is the stem

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cell does not have the genetic apparatus

play74:46

to allow it to pen local Invasion

play74:48

intravasation extra these are all very

play74:50

sophisticated biological processes this

play74:53

just doesn't happen by chance and the

play74:55

thing the the field calls it the E

play74:57

epithelial meenal trans transition which

play75:00

is complete nonsense but yet that's

play75:02

based on the sematic mut mutation theory

play75:04

if you ever sit down and look at what

play75:06

the EMT me is have in that paper it's

play75:09

complete nonsense and yet everybody is

play75:11

brainwashed into thinking about this um

play75:14

so yeah it's a metastatic cancer is a m

play75:17

is a maccrage disorder with with macr

play75:20

fases fermenting with that and their

play75:22

fused hybrid hybrids has been shown many

play75:25

many times so you know what the

play75:27

metastatic cell is driven heavily by

play75:29

glucose and glutamine you know how to

play75:31

kill metastatic cells just because you

play75:33

understand their biology yeah stem cells

play75:35

grow like crazy too they'll kill you

play75:37

from Mass Effect by by just being a big

play75:39

a big bringing in more immune cells it's

play75:42

a as I wrote it's a it's a it's a

play75:45

situation of of escalating biological

play75:48

chaos all these different cells are

play75:50

doing what they're doing in the wrong

play75:52

context so biology is now they're all

play75:55

cells are screaming at each other in

play75:56

different ways trying to figure out

play75:57

what's going on and it's all uh things

play76:00

that were programmed into cells but done

play76:02

in a completely wrong context yeah this

play76:04

is the first time ever of two years

play76:07

doing this podcast every two weeks that

play76:09

I finally made a connection to what

play76:12

Michael Levan Dr Michael L I know if you

play76:14

know him yes I know him well yeah he's

play76:16

doing what you're doing basically but

play76:18

not metabolic but the on the electric

play76:20

bioelectric kind of you know concept

play76:22

this is the first time I've finally been

play76:24

able to make a connction ction because

play76:25

when you said the tomare you know I

play76:29

guess I knew but I didn't know until you

play76:30

said it like this is basically like a

play76:32

wound and it's trying to heal the wound

play76:34

and and and that entire process one can

play76:37

now conceive Michael 11's podcast on

play76:39

saying all that's happening is the

play76:41

cancer cell is actually just a regular

play76:43

cell that's doing what it supposed to do

play76:46

which all the cells have been doing

play76:47

since we were like

play76:48

protozoans uh which is once it believes

play76:52

it's autonomous it will do anything to

play76:54

survive that's what evolution has done

play76:55

inside of our bodies so if you have this

play76:58

basically Detachment from the electric

play77:01

or bioelectric Harmony that in itself

play77:04

has its own communication outside of

play77:07

exosomes and and signaling uh you know

play77:10

with cells around the environment then

play77:12

it's almost like can you blame it for

play77:14

doing exactly what we're programmed to

play77:16

do when it now feels you know foreign or

play77:19

or autonomous I I don't like to give the

play77:21

cancer uh uh a brain a brain

play77:25

that's more theological which doesn't

play77:28

doesn't fit with our understanding

play77:30

evolutionary biology but when you say

play77:32

it's if falling back all the all the

play77:34

cells that existed on the planet before

play77:36

oxygen came into the atmosphere were

play77:37

fermenters uh so the fermentation

play77:40

pathways are the most ancient Pathways

play77:42

for energy there was no oxygen so when

play77:44

you have no oxygen how do you get energy

play77:46

and it's through substrate level

play77:48

phosphor relations which are ancient

play77:50

Pathways and as I said when you are

play77:52

fermenting glucose and glutamine you're

play77:54

using substrate level phosphor relations

play77:56

these are ancient Pathways um uh and the

play77:59

cancer cells are simply falling back on

play78:02

on these and they exist in all of our

play78:04

cells in tiny little they don't play a

play78:06

major role but they're there but in the

play78:08

cancer they become dominant because the

play78:10

organel that was controlling the

play78:12

differentiated state has lost control

play78:14

cells fall back on their default state

play78:16

which is proliferation driven by

play78:18

fermentation energy through substrate

play78:20

level phosphorilation this is ancient

play78:23

Pathways of energy met metabolism that

play78:25

the that the cell and they cify the

play78:28

micro environment creating a world of

play78:30

difficulty for those trying to manage

play78:32

the disorder but once you understand

play78:33

biological evolution and biochemistry

play78:35

all the stuff to to manage cancer makes

play78:38

should be done and can make a lot of

play78:39

sense and be very very effective problem

play78:42

is most people don't know that or can't

play78:44

I don't know it's just I know it I

play78:46

understand it and uh uh uh I'm trying to

play78:49

tell the world that this is not an

play78:51

insurmountable problem this is a very

play78:53

logical way to manage this dis disase

play78:55

based on your understanding of

play78:56

evolutionary biology and biochemistry

play78:58

and and warberg had it right mostly and

play79:00

we're correcting where he made his

play79:01

mistakes oh he C made a couple of

play79:03

mistakes but we're fixing those mistakes

play79:06

and we're going to come out with a new

play79:07

uh uh showing how warberg hypothesis

play79:10

merge now into the mitochondrial

play79:12

metabolic theory of cancer and it will

play79:14

replace the somatic mutation theory of

play79:16

cancer and then you're going to see

play79:17

death rates drop and people living

play79:19

longer and being healthier and and this

play79:23

is just the future and you you will be

play79:25

part of this future once you once you

play79:27

get to know this your patients are going

play79:29

to love what you're doing to them and

play79:30

helping them out but if if the system

play79:33

allows you to do that if the system

play79:34

doesn't allow you to do that then you're

play79:36

going to be a very frustrated person

play79:39

yeah Tom I appreciate it so much I'm

play79:41

just always humbled mind blown M mind

play79:45

rattling after speaking of you this is

play79:48

it's exhausting in the sense in all the

play79:50

good reasons but it's almost like an

play79:52

existential it's a professional

play79:53

existential crisis that's the way I

play79:55

would Define it well I wish other

play79:57

members of your profession would have

play79:58

the same feeling we'll get there we'll

play80:00

make it out hope so

play80:05

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Cancer MetabolismDiet ImpactOncologyInsulin LevelsSugar LevelsMitochondrial HealthFermentation MetabolismGenetic MutationsCancer TreatmentMetabolic Therapy
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