#30 - Thomas Seyfried, Ph.D.: Controversial discussion—cancer as a mitochondrial metabolic disease?

Professor Tom Seifried is an expert in the field of metabolic therapies for chronic diseases such as epilepsy, neurodegenerative lipid storage diseases, and cancer. He has extensive research and publication experience in this area, including his book "Cancer as a Metabolic Disease." The discussion also touches on the Warburg effect, which is the belief that cancer is primarily a metabolic disease originating from mitochondrial or metabolic cell machinery damage. However, it's important to note that not everyone shares this view, including Peter Attia. While Attia supports the use of metabolic therapies in cancer treatment, he also recognizes the value of immunotherapy and chemotherapy. Understanding concepts such as respiration, oxidative phosphorylation, fermentation, and substrate level phosphorylation is crucial to comprehending the discussion.

Cancer is a complex disease that requires a multi-faceted approach. Peter Attia believes that targeting cancer from multiple angles is essential, rather than focusing on just one aspect. He clarifies that biopsies do not increase the risk of metastatic cancer, disputing a claim made earlier. They also discuss glioblastoma multiforme, a particularly aggressive form of brain cancer that has historically had a low survival rate. However, there is growing interest in studying metabolic therapies for this type of cancer. While these alternative approaches may not have gained mainstream acceptance yet, there are researchers, like Tom, who have been working on them for decades and are starting to see their potential applications. This conversation highlights the need to explore various perspectives and research avenues to make progress in understanding and treating cancer.

Thomas Seyfried's initial interest in ganglioside changes in tumors ultimately led him to explore comparative studies of glycolipids in human and mouse brain tumors. He then delved into researching the therapeutic potential of ketogenic diets for epilepsy. Although his grant proposal on ketogenic diets was rejected, Seyfried later discovered that there was indeed significant interest in this area of study. This realization came after one of his PhD students attended a meeting on ketogenic diets for epilepsy and shared the positive response it received. This highlights the importance of perseverance and remaining open to new opportunities, even in the face of initial rejection or skepticism.

The initial discovery of a drug's effect on brain tumors led to further investigation into the role of calorie restriction in tumor reduction. While studying gangliosides, Thomas Seyfried and his team discovered that the drug meant to reduce ganglioside synthesis also resulted in both tumor and body weight reduction in mice. This finding caught the attention of a drug company, leading to funding for further research. Through experiments comparing mice fed ad libidum and those with restricted calorie intake, it was determined that calorie restriction, rather than the drug itself, played a significant role in tumor shrinkage. This prompted Seyfried and his team to explore the potential of calorie restriction in other conditions like epilepsy. The conversation highlights the importance of understanding the mechanisms behind a drug's effects and considering the role of calorie restriction for therapeutic benefits.

Stimulating the vagus nerve can suppress appetite and promote weight loss. Thomas Seyfried mentions a vagal nerve stimulator that was implanted in epileptic patients, which effectively reduced their appetite and helped manage seizures. This device cost around $16,000 and showed promising results. Additionally, the conversation touches upon the connection between calorie restriction, ketogenic diets, and seizure control. It is revealed that both calorie restriction and a ketogenic diet can lead to the production of ketones, which have anti-seizure benefits. The level of ketosis achieved through calorie restriction can be similar to that achieved through therapeutic fasting in humans. However, it is important to practice calorie restriction in a healthy manner to avoid entering a state of starvation.

Our bodies have the ability to adapt to periods of fasting or starvation. While the duration can vary depending on factors such as body weight, age, and overall health, it is possible for individuals in good shape to go a long time without eating. This was observed in cases such as the prisoners in MACE prison who fasted as a protest. However, it is crucial to note that starvation can have devastating effects on the body, causing muscle loss and electrolyte imbalances. The diaphragm, in particular, is the last muscle to be affected, leading to the drowning of the individual in their own bodily fluids. Despite this, our species has evolved to withstand periods of food scarcity, and our ability to survive today is a testament to this adaptation.

Our nutritional state plays a crucial role in our ability to access minerals and vitamins. Research indicates that our need for these nutrients tends to increase when our bodies are in a fed state. However, in today's society, many foods are depleted of these essential nutrients, leading some people to be in a state similar to starvation despite consuming food with little nutritional value. As a result, the body stores excess fat instead of efficiently using sugar for energy. Furthermore, calorie restriction has been found to be a key mechanism in the effectiveness of the ketogenic diet in managing epilepsy. While the effects may not be immediately visible, maintaining stable glucose levels is crucial in preventing breakthrough seizures. Additionally, some individuals who undergo prolonged fasting experience a lasting change in their eating habits and weight, suggesting a potential physiological shift rather than a behavioral one.

The key to managing epilepsy and cancer lies in lowering blood sugar and elevating ketones, which can be achieved through ketogenic diets. While the exact mechanism behind this is still under investigation, it is clear that calorie restriction and the Warburg effect play significant roles. Calorie restriction shrinks tumors by lowering blood sugar, and the Warburg effect refers to cancer cells continuing to produce lactic acid even in the presence of oxygen. By understanding these processes, we can potentially develop more effective treatments for cancer and epilepsy. It is fascinating to think that if Otto Warburg had known about ketogenic diets, he may have made groundbreaking discoveries in cancer research much earlier.

There is a significant difference in energy production between normal cells and cancer cells. Normal cells, when supplied with oxygen and not in excessive demand for ATP, can efficiently produce energy through cellular respiration in the mitochondria, generating over 30 units of ATP. However, cancer cells, even in the presence of abundant oxygen, continue to produce large amounts of lactic acid, indicating a defective respiratory system. This observation, made by Otto Warburg in the 20th century, led to further research and the formulation of the theory that the organelle responsible for energy production in cancer cells is faulty. Despite some controversy, Warburg's work had a profound impact on the field of biochemistry and his findings were widely reproduced by other scientists.

All cancer cells have some form of defect in the number, structure, or function of their mitochondria, which affects their ability to generate energy through normal respiration. This defect leads to the Warburg effect, where cancer cells rely on fermentation for energy production. The focus on aerobic glycolysis in cancer research is a secondary problem, as the real issue lies in the impairment of respiration. It is important to note that studying cancer cells in culture can lead to misleading assumptions and artificial results, as they are no longer connected to the tissues and are growing in an unnatural environment. Quantifying aerobic respiration can be done by measuring the amount of oxygen consumed and lactic acid produced. Overall, understanding the diverse defects in mitochondrial respiration is crucial in comprehending the complexity of different types of cancer cells.

The structure of organelles in biological cells determines their function. Abnormal structure leads to abnormal function. While some may refer to these abnormalities as mutations, Thomas Seyfried prefers to call them defects. Surprisingly, when studying cancers in mice, Seyfried's team found that the entire genome of the tumors had no genetic abnormalities or mutations that would impact function. This challenges the common understanding that cancers are caused by mutations that disrupt normal cell signaling. Instead, Seyfried argues that the primary cause of cancer is damage to the respiratory system of cells. Maintaining healthy mitochondria, which are responsible for respiration, is crucial in preventing cancer. This emphasizes the importance of avoiding risk factors like viral infections, radiation exposure, and carcinogenic exposure to protect mitochondrial health. Despite the Warburg effect, which was initially dismissed in the field, damage to respiration and mitochondria is consistently evident in cancer cells under microscopic examination.

Mitochondrial dysfunction plays a significant role in the development of cancer. Traditional biochemical analysis has shifted towards molecular biology analysis, leading to the belief that genetic defects and mutations cause cancer. However, it was not considered that viruses could also affect the mitochondria and disrupt respiration. Research shows that both direct viral infection and the integration of viruses into the nuclear genome can disrupt mitochondrial function. All cancers studied so far have shown to ferment, indicating abnormal mitochondrial function. Additionally, plants also exhibit dysmorphic cell growth following Warburg's metabolic profile, but they do not metastasize due to the absence of an immune system. This conversation emphasizes the importance of understanding and targeting mitochondrial dysfunction in cancer treatment.

Cancer cells have a unique way of obtaining both energy and building blocks for growth. While regular cells primarily rely on oxidative phosphorylation for energy production, cancer cells utilize substrate level phosphorylation (SLP) in the mitochondria to generate ATP. SLP involves the transfer of phosphate groups from organic substrates to ADP, resulting in the restoration of ATP levels. This process allows cancer cells to compensate for the damaged respiration observed in Warburg's theory. Additionally, cancer cells obtain the necessary building blocks through glucose, glutamine, and the pentose pathway. Understanding the mechanisms of energy production and building block acquisition in cancer cells is crucial for developing effective therapeutic strategies.

There is a shift in energy production from oxidative phosphorylation (oxfoss) to substrate level phosphorylation (SLP) in cancer cells. Unlike normal cells, cancer cells lack oxfoss and rely heavily on SLP for energy generation. This shift is supported by the findings of Katska's experiments on aquatic animals, where lactic acid and succinic acid (a stimulant for oxfoss) were found to be dumped into the bloodstream during periods of oxygen deprivation. The conversation also highlights the limited understanding of this phenomenon within the majority view of cancer research, which focuses more on gene expression rather than direct measurement of oxygen consumption and gas production. Thomas Seyfried believes that it is only a matter of time before this minority view gains wider recognition.

ATP production and oxygen consumption in cancer cells can be a complex and nuanced process. While measuring ATP levels can indicate whether a cell is alive or dead, it is challenging to determine the exact origin of ATP production within the mitochondria. The production of lactate and the presence of certain enzymes, such as pyruvate kinase, can provide clues about ATP generation. Additionally, structural defects in the mitochondria can impact ATP production, even in cells with normal mitochondrial genomes. Understanding these complexities is crucial in studying cancer cells and developing effective treatments. Further research is needed to unravel the mechanisms of ATP production in cancer cells and explore potential therapeutic avenues.

Glucose and glutamine are the primary fuels that drive cancer growth. While it is not possible to completely eliminate glucose from the body, therapeutic fasting and restricted ketogenic diets can significantly lower blood sugar levels. These dietary interventions make normal cells glucose hungry, forcing them to transition to ketones for energy. In contrast, tumor cells that are mitochondrial defective cannot utilize ketones and depend on glucose for survival. This creates a direct competition between normal and tumor cells for glucose. Clinically, a ketogenic or calorie-restricted diet may initially cause physiological insulin resistance, but in the long run, calorie restriction increases insulin sensitivity in the body.

Insulin resistance can be measured by the steady state plasma glucose (SSPG) level, with higher levels indicating higher insulin resistance. This test is typically performed on individuals following a standard diet, and not on those who follow a ketogenic diet. However, injecting glucose and insulin into someone on a ketogenic diet can lead to excessive insulin production. Additionally, the test results showed that even individuals with normal fasting blood glucose levels can exhibit high SSPG levels, indicating potential prediabetic conditions. It is important for individuals to be aware of their glucose and ketone levels during such tests, as administering too much insulin can lead to dangerously low blood glucose levels. Communication and transparency with loved ones is also essential in case of emergencies.

The goal of cancer treatment is to starve the tumor cells without harming the rest of the body. While some individuals may experience insulin sensitivity and glucose disposal on a ketogenic diet, this may not be the case for everyone. Many patients on a ketogenic diet fail glucose tolerance tests and appear to have diabetes-like symptoms. However, if these patients are primed with a few days of consuming carbohydrates prior to the test, their insulin sensitivity improves. The challenge lies in finding the balance between lowering blood sugar levels to starve tumor cells and avoiding harm to the individual's overall health. Insulin can be protumorgenic, but with low glucose levels and careful management, it can be used effectively without stimulating tumor growth.

Strategically targeting glutamine is crucial in cancer treatment. Glutamine, although a nonessential amino acid, plays a massive role in various physiological systems such as the gut, immune system, and urea cycle. While there is no dietary strategy to effectively reduce glutamine, drugs like Don 6 can be used to block glutamine and selectively kill tumor cells. However, it is essential to have knowledgeable experts administering these drugs, as the immune system may be compromised if not done correctly. The press-pulse concept is developed to maximize the effectiveness of treatment, where glucose is pressed hard with diets and drugs, and then glutamine is pulsed. By restoring the immune system and gut function, the normal physiological systems can be maintained while targeting cancer cells.

The energy source of cancer cells is a crucial aspect to consider in managing the disease. Thomas Seyfried emphasizes the compromised structure and function of mitochondria in tumor cells, which is supported by extensive literature. He points out that without energy, nothing grows, and the evidence strongly indicates that the mitochondria in cancer cells are defective. Peter Attia raises the question of the functional flexibility of mitochondria, suggesting that even with structural changes, there may still be optimal function. However, Seyfried argues that mitochondria are highly adaptable but have certain critical genes that control cell survival. The malfunction of these genes prevents cancer cells from undergoing normal apoptosis. Overall, understanding the energy source and structural changes in cancer cells is crucial in developing strategies to manage the disease.

Cancer cells have a unique ability to upregulate fermentation pathways, allowing them to survive and multiply under low-oxygen conditions. Before oxygen existed on Earth, all cells operated through fermentation, but with the introduction of oxygen, most cells switched to oxidative phosphorylation as their primary energy source. However, cancer cells can revert back to fermentation, which normal cells cannot do for long periods. This adaptation is what allows cancer cells to thrive and form tumors. Skeletal muscle cells, although capable of temporary fermentation, cannot sustain it permanently without dying. This is why tumors rarely form in muscle cells. The difference in adaptability to fermentation between different cell types plays a crucial role in cancer development and the probability of tumor formation in various tissues.

Brain neurons rarely become tumor cells because they are not capable of doing so. Instead, brain cells die, leading to neurodegeneration. Tumors in the brain are usually found in glial cells and microglia. It is important to distinguish between these cell types and neurons when discussing brain cancer. Additionally, it is counterintuitive that cardiac myocytes, the cells in the heart, also do not form cancer despite their ability to buffer lactate. This is because disruptions in oxidative phosphorylation, which occur in cancer cells, are catastrophic for brain and heart cells. The hypothesis suggests that the lack of metabolic flexibility in other cells, such as those found in the colon or breast, contributes to their susceptibility to cancer.

Oncogenes play a crucial role in the metabolic changes observed in cancer cells. When the respiratory system of a cell is damaged, oncogenes upregulate fermentation pathways, leading to a shift towards a fermentation metabolism. This change requires additional fermentable fuels such as glucose and glutamine to compensate for the loss of energy from oxidative phosphorylation. Consequently, the genetic behavior of the cell begins to change, and mutations and defects accumulate in the nuclear genome. The damaged respiratory system also generates reactive oxygen species, which are mutagenic and carcinogenic. Additionally, high levels of lactic acid can be seen in patients with a high tumor burden, often stemming from the tumor cells themselves or due to multiple end organ ischemia caused by defective white blood cells.

The microenvironment of tumors is complex and contributes to the fermentation behavior of cancer cells. Lactic acid and hydrogen ions accumulate, creating an acidic mess. Monocarboxillic acid transporters (MCTs) play a role in both bringing in ketones and removing lactate, protecting the cell from harm. Ketogenic diets upregulate MCTs, increasing the intake of ketone bodies. Targeting blood vessels, as in anti-angiogenic therapies, has proven ineffective because cancer cells can ferment without them. Drugs like Avastin, which target blood vessels, may actually promote invasive behavior in brain cancer. Understanding the biology of cancer is crucial for effective treatment strategies and avoiding harmful interventions.

Tumor cells, when treated with Avastin, spread throughout the brain instead of being clustered in one area. This phenomenon is not visible in radiographic images, making it seem like the treatment is effective. However, the overall survival rate remains unchanged or even lower. This false sense of improvement is due to the behavior of macrophage cells, which can fuse with neoplastic cells and make them more aggressive and invasive. Fusion involves the fusion of genetic and cytoplasmic material, and is prompted by the immune system's response to persistent wounds. The immune cells release growth factors and cytokines to facilitate wound healing, but inadvertently promote the growth of neoplastic cells. This fusion behavior and the resulting invasive nature of cancer cells are characteristics of macrophages. Ultimately, understanding this process is important in developing effective treatments for metastatic cancers.

Macrophages, which are responsible for wound healing and clearing cellular debris, do not effectively kill cancer cells because they do not recognize them as foreign invaders. Cancer cells can mimic the appearance of normal epithelial cells, making it difficult for macrophages to identify and eliminate them. Additionally, the molecules produced by cancer cells to put out the "fire" of inflammation actually stimulate the growth of the abnormal cells. This can lead to the formation of metastatic lesions, where cancer cells spread from the original site to other parts of the body. The process of metastasis varies from person to person, and it is not solely dependent on the number of mutations present in the cancer cells.

Cancer cells can exhibit highly invasive and metastatic behavior without showing the expected mutations or abnormalities. This challenges the traditional understanding of how cancer spreads. In the case of two women with similar breast cancers, one may experience metastasis while the other remains disease-free, even though their primary tumors appear similar. Needle biopsies, commonly used for diagnosing tumors, can potentially create a more aggressive environment in the tumor's surroundings, increasing the risk of further spread. This phenomenon, known as inflammatory onco-taxis, has been observed in breast, colon, liver, and brain cancers. It is essential to understand that while needle biopsies can increase the risk of metastasis in some cases, the evidence is not universal.

There is a potential risk of metastatic cancer when performing a needle biopsy following a resection. While this experiment has not been conducted, there is existing knowledge about needle biopsies facilitating tumor spread. However, it is important to distinguish this phenomenon from needle track seeding, as tract-related cancer cells can be dealt with separately. The risk of developing secondary glioblastoma after removing a low grade tumor is comparable to the risk associated with needle biopsies. To determine the control for this observation, a group of patients who do not undergo surgery would need to be included, but such experiments are not currently conducted. The philosophy mentioned is to shrink the tumor before debulking it, ultimately improving the probability of a successful cure. Thus, the question arises as to why anyone would want to put a patient at risk unless the information gained from the needle biopsy leads to a curative procedure.

There are significant flaws in the current approach to diagnosing and treating cancer. Despite advancements in gene screening and biopsy procedures, there is a lack of understanding around the biological processes at play in different types of cancers. This has led to overlooked aspects of cancer, such as extracranial metastasis in glioblastoma cases, which research has shown to be more common than initially recognized. Furthermore, there is a concerning number of daily cancer-related deaths, indicating that current treatments may not effectively address the true nature of the disease. To make substantial progress in combating cancer, it is crucial to acknowledge the limitations of existing methods and explore alternative approaches that address the complex nature of cancer at its core.

There is a fundamental misunderstanding of the biology of cancer, leading to ineffective treatments and a high death rate. Thomas Seyfried argues that by understanding the true nature of the disease and strategically approaching it, we have the potential to reduce the death rate by more than 50% within 10 years. Currently, unnecessary procedures and tests are being conducted, such as needle biopsy tumor cells for genetic profiling, which do not contribute to understanding the disease. While there may be debates on the statistics and population demographics, the fact remains that more people are dying from cancer each year. To address this, it is crucial to focus on managing the disease based on its biology rather than outdated approaches. A bold reduction in mortality is possible if we embrace the necessary changes.

Conducting an experiment to integrate metabolic therapy with standard of care for breast cancer patients may yield promising results. The goal is to combine metabolic therapy, which involves reducing blood sugar, elevating ketones, and targeting energy metabolism, with the standard treatments like chemotherapy. This approach is being done in Turkey, where the lowest dose of chemotherapy that complies with the law is employed. The metabolic therapy alone group would follow the press pulse concept, which begins with lowering blood sugar and achieving therapeutic ketosis through a ketogenic diet. Additionally, stress management techniques, such as music therapy and yoga therapy, are incorporated to address emotional stress. Further research and individualized approaches are necessary since response to therapy can vary among patients.

Metabolic ketosis, combined with strategic management techniques, can have a significant impact on cancer treatment. Thomas Seyfried emphasizes the importance of informing patients that their disease is not terminal and that reducing stress can enhance the effectiveness of medicine. By achieving metabolic ketosis, various options become available, such as insulin therapy and hyperbaric oxygen, which primarily affects tumor cells without harming normal cells. Targeting glutamine with pulse drug treatments further weakens the tumor cells' antioxidant capacity, making them more susceptible to hypobaric therapy. It is crucial to reach a significant reduction in glucose levels and lower glutamine availability. Cancer cells, which are dependent on glucose, cannot utilize ketones efficiently due to defective mitochondria. Providing normal cells with an alternative fuel source marginalizes tumor cells over time. Hyperbaric oxygen therapy, administered at approximately 2.5 atmospheres for 90 minutes daily, aims to replace radiation therapy by inducing oxidative stress and cell death in the tumor cells. Therapeutic ketosis also proves to be a potent anti-inflammatory therapy. Overall, this conversation highlights the potential of metabolic ketosis and targeted treatments in cancer management.

A metabolic approach to cancer treatment shows promise in reducing the death rate and potentially curing certain types of cancer. By targeting the tumor's microenvironment and reconfiguring it to make it less inflamed, proapoptotic, and anti-angiogenic, the tumor becomes more vulnerable and damaged. Surgery would take place at a midpoint where the tumor is visibly shriveled and less inflamed, making it easier for the surgeon to remove without extensive collateral damage. This metabolic approach focuses on the tumor's dependence on specific fuels and aims to disrupt those fuels without harming the rest of the body. One potential drug, Don, which targets glutamine metabolism, has shown promise in clinical trials. By shifting the focus from genetic mutations to metabolic therapy, the potential for treating and eliminating cancer is increased.

Current cancer therapies are not effectively targeting the metabolic nature of cancer. Traditional treatments like radiation and chemotherapy may actually worsen the condition and decrease overall survival. Metabolic therapy, specifically through the use of a ketogenic diet, has shown promising results in terms of extending lifespan and improving quality of life for cancer patients. By targeting the two prime fuels for cancer cells, glucose and glutamine, metabolic therapy offers the potential for a cure rather than just another treatment option. Implementing metabolic therapies as a standard of care could significantly reduce death rates and dramatically improve overall survival for cancer patients.

Implementing a metabolic therapy program for managing cancer could potentially extend overall survival and improve quality of life. While it may be challenging to determine if a person is truly cured, being disease-free for 10 years can serve as a good indication. Standard cancer treatments may not only have negative effects on long-term survival but also lead to other diseases. Therefore, adopting a therapeutic ketogenic diet could eliminate the toxic effects of conventional treatments and potentially offer better outcomes. In the case of aggressive brain tumors like GBM, a combination of debulking surgery and metabolic therapy could be a viable strategy to consider, even though complete disease eradication may not be achieved. It is important to weigh the metabolic risks of radiation, corticosteroids, and surgery and prioritize the least metabolically harmful options.

Eliminating radiation from the treatment plan may significantly increase survival rates for patients with glioblastoma (GBM). Thomas Seyfried suggests that metabolic therapy combined with surgery and delayed radiation can lead to better outcomes. He highlights the case of a young patient who rejected radiation and chemotherapy, opting for metabolic therapy instead. Contrary to medical predictions, the patient not only survived but also experienced tumor regression and eventually had no tumor left. Seyfried emphasizes the importance of publishing these findings and generating interest for clinical trials. By reevaluating the role of radiation in GBM treatment, there is a potential to double or triple the amount of survival for patients.

There is a need for unbiased experimentation to test hypotheses in the field of cancer research. The discussion highlights the importance of conducting dream experiments under ideal conditions with no resource constraints to examine the role of structural deficits in mitochondria and the production of lactate and fermentation in tumor cells. By depriving tumor cells of fermentable fuels, such as glucose and glutamine, and implementing metabolic therapy, it is possible to eliminate cancer cells. However, there is disagreement among researchers, demonstrating the necessity for convincing data and open-mindedness. This conversation emphasizes the significance of considering all available evidence and avoiding the dismissal of alternative facts when exploring complex scientific topics.

There is a worrying trend in the scientific community of ignoring evidence that doesn't align with preconceived notions or mainstream beliefs. Just like the Catholic Church refused to accept that the Earth was not the center of the solar system, researchers in the cancer field are disregarding massive evidence that shows structural and functional issues with mitochondria. This crisis of ignoring conflicting evidence hinders progress and stalls the development of effective treatments. To overcome this, collaboration and the generation of new experiments are necessary. By understanding the biology of diseases and basing strategies on that understanding, we can improve overall survival rates and quality of life for patients.

There is a significant roadblock preventing the advancement of alternative cancer therapies. Thomas Seyfried's proposal of metabolic therapy as an alternative to the standard of care is met with resistance and inflexibility from the medical community. Despite having data and case studies that show promise, there is a reluctance to deviate from the established treatment protocols. This is hindering progress and potentially preventing better outcomes for cancer patients. There is a need to challenge the notion that the standard of care should always be followed without question, as it may impede the exploration of potentially more effective therapies. To make a real difference, there is a call for a change in mindset and the willingness to try new approaches, even if they go against convention.

There is a potential alternative approach to cancer treatment that combines immediate surgery with metabolic therapy. Peter Attia suggests that delaying radiation and corticosteroid therapy until necessary may increase the chances of success. However, finding advocates who support this thinking is crucial. Thomas Seyfried acknowledges the need for bold individuals to set up specialized treatment clinics where patients can receive comprehensive care in one place. Peter Attia emphasizes the importance of promoting this approach from a position of pull, rather than push, by showcasing the positive results and testimonies of those who have benefited from it. Despite differing opinions on whether cancer is primarily a genetic or metabolic disease, both agree that cancer is a complex condition that requires a multifaceted strategy.

There is potential value in using metabolic therapies for cancer treatment regardless of whether cancer is primarily caused by genetics or metabolic dysfunction. Rather than engaging in unnecessary debates about the exact nature of cancer, the focus should be on incorporating various oncology specialties, including medical oncology, radiation oncology, surgical oncology, immuno-oncology, and metabolic oncology. By embracing a multidisciplinary approach, we can explore every possible therapy for cancer, including novel and innovative treatments. It is important for patients and their loved ones to support research efforts and promote funding for metabolic therapy programs, either through foundations or universities. This support can contribute to the development of effective therapies and improve the chances of accessing these treatments through clinical trials. Furthermore, creating public awareness and advocating for increased risk tolerance in clinical trials for high-stakes cancers like glioblastoma can lead to advancements in cancer treatment.

There is a difference in opinion regarding the risks involved in trying new treatments for a disease. Thomas Seyfried believes that taking risks to find potential solutions is worth it because it cannot harm anyone and could potentially have positive outcomes. However, Peter Attia disagrees, stating that the outcome of the disease is uniformly bad and there is a risk of potentially doing worse. He believes that acknowledging the risks involved when discussing treatment options is crucial for maintaining credibility. Both agree that there will always be risks involved in medical procedures, but they differ in their perspectives on the level of risk that should be accepted. Ultimately, the conversation highlights the importance of carefully weighing risks and benefits in medical decision-making.