Testing: Liquid Biopsy TruCheck

Circulating tumor cell isolation for cancer diagnosis and prognosis

‘According to the Warburg effect, cancer cells do not produce energy via oxidative phosphorylation in the mitochondria, but through the process of aerobic glycolysis characterized by high level of glucose uptake and secretion of lactic acid. The cross-membrane movement of lactate results in removal of the labile inorganic cations, leaving a net of negative charges on cancer cell surfaces which distinguishes them from the normal blood cells except for red blood cells. The level of the negative change is dynamically regulated by glycolytic capacity.‘







Tryptophan, Cysteine

What is Cancer Metabolism?

Cancer metabolism refers to the alterations in cellular metabolism that occur in cancer cells compared to normal cells. These changes enable cancer cells to sustain higher rates of proliferation and survive in the often harsh microenvironment of a tumour. The metabolic reprogramming of cancer cells is not just a consequence of cancer but also a driving force in its progression.

One of the most well-known aspects of cancer metabolism is the Warburg effect, named after Otto Warburg, who observed that cancer cells tend to ferment glucose into lactate even in the presence of oxygen, which is a less efficient way to produce energy compared to the normal process of oxidative phosphorylation used by most healthy cells. This phenomenon is also referred to as aerobic glycolysis.

Cancer cells have a high demand for nutrients to support their rapid growth and division. They primarily use glucose and the amino acid glutamine for synthetic purposes, such as building the macromolecules they need to proliferate. While normal cells primarily use glucose for energy, cancer cells are more reliant on fats as their energy source. This is partly due to the metabolic inefficiency of cancer cells, which synthesize fat from glucose and amino acids and then oxidize the fat, a process that is energetically costly and can lead to systemic stress, immune failure, and weight loss.

Estrogen plays a significant role in this metabolic inefficiency. It promotes the uptake of water by tissues, stimulates fat synthesis, and tends to produce lactic acid. The activation of transhydrogenases by estrogen shifts metabolic energy between glycolytic and oxidative systems, allowing cells to continue growth and repair processes even in a hypoxic (low oxygen) environment.

The metabolism of cancer cells is also characterized by an increased uptake of fatty acids from their environment. The extracellular acidity created by cancer cells’ emission of acid increases the ability of fatty acids to enter the cell. While cancer cells synthesize fat, they also consume it avidly, particularly polyunsaturated fats, to the point that they can induce their own death in vitro. This has led to the misconception that fish oil, which is rich in polyunsaturated fats, can kill cancer cells. However, saturated fats have been shown to have a calming effect on cancer cells, inhibiting their aerobic glycolysis and allowing them to resume more normal energy production.

The dietary implications of cancer metabolism suggest that foods that nourish the patient without interfering with hormones or causing excitation of tissues are beneficial. Saturated fats are anti-inflammatory and do not interfere with mitochondrial function, while polyunsaturated fats can suppress the immune system. Carbohydrates, particularly sugars, may be more favorable for the immune system than starches, and a sugar-free diet is not necessarily beneficial for cancer patients since the tumor can increase the rate at which it consumes the host’s proteins in the absence of sugar.

In summary, cancer metabolism is characterized by a shift towards less efficient energy production, a reliance on fats for energy, and an increased uptake of fatty acids. These metabolic changes are influenced by hormones like estrogen and can be targeted through dietary interventions that support the patient’s overall health and immune function.


Cancer metabolism refers to the alterations in cellular metabolic pathways that are observed in cancer cells as compared to normal cells. These changes enable cancer cells to sustain higher rates of proliferation and survive in the often harsh microenvironment of a tumor. The metabolic reprogramming in cancer cells is complex and involves several key characteristics:


1. **Aerobic Glycolysis (Warburg Effect):** Cancer cells preferentially use glycolysis for energy production even in the presence of oxygen, which is less efficient than oxidative phosphorylation used by most normal cells. This phenomenon is known as the Warburg effect. The lactic acid produced from this process can lead to an acidic microenvironment around the tumor.


2. **Glucose and Glutamine Addiction:** Cancer cells have a high demand for glucose and the amino acid glutamine. Glucose is primarily used for biosynthetic processes to build the macromolecules needed for new cells, while glutamine is a key nitrogen source for nucleotide and amino acid synthesis.


3. **Fatty Acid Metabolism:** Cancer cells also reprogram their lipid metabolism. They can synthesize fatty acids from glucose and amino acids, and then use these fats as an energy source. The uptake of fatty acids from the environment is also increased in cancer cells.


4. **Mitochondrial Dysfunction:** Many cancer cells exhibit mitochondrial defects that affect normal oxidative phosphorylation. This can lead to an increased production of reactive oxygen species (ROS) and further genetic mutations.


5. **Altered Energy Production:** Due to the inefficient metabolism, cancer cells produce a large amount of heat and can cause systemic stress, immune failure, and weight loss (cachexia).


6. **Estrogen’s Role:** Estrogen can influence metabolic processes, leading to increased fat synthesis and water uptake in tissues. This can contribute to the metabolic inefficiency seen in cancer cells.


7. **Hypoxia and Metabolic Flexibility:** Under low oxygen conditions (hypoxia), cancer cells can adapt their metabolism to continue growing. For example, they can use glutamine to fuel parts of the tricarboxylic acid (TCA) cycle even when glucose is scarce.


8. **Acidic Microenvironment:** The production of lactic acid by cancer cells leads to an acidic extracellular environment, which can promote the invasion of fatty acids into the cells and further support cancer metabolism.


9. **Immune System Interaction:** The altered metabolism of cancer cells can affect the immune system. For instance, polyunsaturated fats are known to suppress the immune system, while sugars might be more favorable for immune function.


10. **Therapeutic Implications:** Understanding cancer metabolism has led to the exploration of new therapeutic strategies, such as targeting the metabolic pathways that cancer cells rely on, using drugs that affect glucose and glutamine metabolism, or manipulating hormone levels to influence metabolic pathways.


The context provided emphasizes that while some dietary recommendations like fish oil or sugar-free diets are popular, they may not be based on a complete understanding of cancer metabolism. For example, depriving tumors of essential fatty acids can retard their growth, and saturated fats can have a calming effect on cancer cells, contrary to the effects of polyunsaturated fats. Additionally, the context suggests that a well-nourished state, supported by the right balance of nutrients and hormones, may help in managing cancer by not exacerbating the metabolic inefficiencies that cancer cells exploit.

Why lipolysis is undesirable for mitochondrial health and cancer

Lipolysis, the process of breaking down lipids or fats into fatty acids and glycerol, plays a complex role in metabolism and has been studied for its effects on health, including mitochondrial function and cancer. The relationship between lipolysis, mitochondrial health, and cancer is intricate, with both beneficial and detrimental aspects depending on the context. However, I’ll focus on the concerns you’ve mentioned regarding why lipolysis can be considered undesirable in some contexts for mitochondrial health and cancer.

Mitochondrial Health

Mitochondria are known as the powerhouses of the cell, generating most of the cell’s supply of adenosine triphosphate (ATP), used as a source of chemical energy. Healthy mitochondrial function is crucial for energy metabolism, cellular signaling, and the regulation of apoptosis (programmed cell death).

  1. Increased Reactive Oxygen Species (ROS) Production: Excessive lipolysis can lead to an increase in fatty acid oxidation in mitochondria. This process can elevate the production of reactive oxygen species (ROS), which are harmful byproducts that can damage cellular structures, including mitochondrial DNA, proteins, and lipids. Over time, this oxidative stress can impair mitochondrial function and lead to mitochondrial dysfunction.

  2. Mitochondrial Overload: Mitochondria have a limited capacity to process fatty acids. High levels of fatty acids resulting from excessive lipolysis can overwhelm the mitochondrial processing capacity, leading to incomplete oxidation of fatty acids and the accumulation of toxic intermediates. This situation can further exacerbate mitochondrial dysfunction and contribute to cellular stress and damage.


The relationship between lipolysis, mitochondrial function, and cancer is multifaceted. Cancer cells often exhibit altered metabolism, including changes in lipid metabolism and mitochondrial function, known as the Warburg effect, where cancer cells preferentially rely on glycolysis for energy production even in the presence of oxygen, a less efficient way to produce energy.

  1. Fatty Acid Availability for Cancer Cells: Excessive lipolysis can provide an abundance of fatty acids, which can be utilized by cancer cells to support their rapid growth and proliferation. Fatty acids serve as building blocks for the synthesis of new membranes and signaling molecules, facilitating cancer progression.

  2. Altered Metabolic Signaling: Lipolysis and the release of fatty acids can also alter metabolic signaling pathways within the tumor microenvironment, promoting tumor growth and survival. For instance, fatty acids can activate peroxisome proliferator-activated receptors (PPARs) and other signaling pathways that support tumor growth and metastasis.

  3. Immune Suppression: Fatty acids released during lipolysis can have immunosuppressive effects, impairing the body’s ability to mount an effective immune response against cancer cells. This can facilitate the evasion of cancer cells from immune surveillance and contribute to tumor progression.

It’s important to note that the context and balance of lipid metabolism, including lipolysis, are crucial. While under certain conditions, excessive lipolysis and its consequences can be undesirable for mitochondrial health and may promote cancer, lipolysis is also a normal and essential process in energy homeostasis. The impact of lipolysis on health depends on a range of factors, including the metabolic state of the organism, the presence of disease, and lifestyle factors.

Research in this area is ongoing, and a nuanced understanding of lipid metabolism’s role in mitochondrial function and cancer is essential for developing targeted therapies and interventions.


Is there any link between cancer cachexia and lipolysis

Yes, there is a significant link between cancer cachexia and lipolysis. Cancer cachexia is a complex metabolic syndrome associated with underlying illness and is characterized by loss of muscle with or without loss of fat mass. It is a serious condition that affects many patients with advanced cancer, leading to significant weight loss, muscle atrophy, fatigue, weakness, and a decrease in quality of life. The pathophysiology of cancer cachexia involves a multifactorial process with alterations in energy and protein metabolism.

Link between Cancer Cachexia and Lipolysis

  1. Increased Lipolysis: One of the hallmarks of cancer cachexia is an increase in the breakdown of fat stores through lipolysis. Cytokines and factors released by tumors or as a response to tumors can stimulate the lipolytic pathway, leading to an elevated release of free fatty acids into the bloodstream. These substances include tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and other inflammatory mediators that can increase lipolysis and contribute to the cachectic state.

  2. Energy Imbalance: The increased lipolysis seen in cancer cachexia is part of a broader metabolic dysregulation, where the energy balance is disrupted. Despite the mobilization of fatty acids from adipose tissue, patients often experience a decrease in overall energy availability due to reduced food intake and altered metabolism. The body’s attempt to provide energy by breaking down fat stores through lipolysis is insufficient to counteract the weight loss and muscle wasting.

  3. Fatty Acid Utilization: In cancer cachexia, despite the increased availability of fatty acids from lipolysis, there is often an inefficiency in utilizing these fatty acids for energy production by the mitochondria. This inefficiency contributes to the energy deficit and promotes further muscle wasting, as the body may start to consume lean body mass in an attempt to meet its energy needs.

  4. Insulin Resistance: Cancer cachexia is also associated with insulin resistance, which can exacerbate the condition by impairing the uptake of glucose by cells, further increasing the reliance on lipolysis and fat oxidation for energy. This insulin resistance complicates the metabolic situation, making it harder for the body to maintain weight and muscle mass.

  5. Effect on Mitochondrial Function: The increase in lipolysis and the associated rise in circulating fatty acids can also impact mitochondrial function, as discussed previously. The overload of fatty acids can lead to mitochondrial dysfunction, contributing to the muscle wasting seen in cachexia through mechanisms such as increased oxidative stress and impaired ATP production.

In summary, the link between cancer cachexia and lipolysis involves a complex interplay of factors that lead to increased fat breakdown, altered energy metabolism, and muscle wasting. Understanding this link is crucial for developing targeted treatments to manage or mitigate the effects of cachexia in cancer patients, focusing on nutritional support, metabolic modulation, and potentially targeting specific pathways involved in lipolysis and energy balance.

Can limiting lipolysis be treatment for cancer?

Limiting lipolysis as a therapeutic strategy for cancer treatment is an area of interest but requires careful consideration due to the complex role of lipid metabolism in cancer progression. The rationale behind targeting lipolysis in cancer therapy lies in several key aspects of cancer metabolism and the tumor microenvironment:

  1. Energy Supply to Cancer Cells: Cancer cells have high energy demands to sustain rapid growth and proliferation. Limiting lipolysis could potentially restrict the availability of fatty acids, which are important energy sources for cancer cells, especially under conditions of hypoxia or altered metabolism such as the Warburg effect.

  2. Lipid Signaling in Cancer: Lipids are not only energy sources but also play critical roles in signaling pathways that promote cell survival, proliferation, and metastasis. By reducing lipolysis, it may be possible to influence these signaling pathways and inhibit tumor growth.

  3. Modification of the Tumor Microenvironment: The tumor microenvironment, which includes cancer cells, stromal cells, and immune cells, is influenced by the availability of nutrients, including lipids. Limiting lipolysis could alter the lipid content of the tumor microenvironment, potentially affecting tumor growth and the immune response to cancer.

  4. Cancer Cachexia Management: Since cancer cachexia is associated with increased lipolysis and fat mass loss, targeting lipolysis could help manage this condition, improving the quality of life and possibly the survival of cancer patients.

Challenges and Considerations

  • Selective Targeting: One challenge is selectively targeting lipolysis in cancer cells without adversely affecting normal cells. Many tissues rely on fatty acid oxidation for energy, particularly during periods of fasting or stress. Therefore, therapies designed to limit lipolysis must be carefully developed to minimize harm to normal metabolic processes.

  • Cancer Heterogeneity: Different types of cancer may have varying dependencies on lipid metabolism, making it difficult to develop a one-size-fits-all approach. Personalized medicine, where treatments are tailored based on the metabolic profile of the tumor, may be necessary.

  • Potential Resistance: As with many cancer therapies, there is the potential for tumors to develop resistance. Cancer cells may adapt to treatments limiting lipolysis by altering their metabolism to rely more on other nutrients, such as glucose or amino acids.

  • Clinical Evidence: The concept of targeting lipolysis is still under investigation, with most evidence coming from preclinical studies. More research, including clinical trials, is needed to fully understand the potential benefits, risks, and mechanisms of such a treatment strategy.

In conclusion, while limiting lipolysis presents an intriguing potential therapeutic avenue for cancer treatment, it is not without its challenges. It underscores the need for ongoing research to better understand the role of lipid metabolism in cancer and to develop targeted therapies that can safely and effectively exploit these pathways for cancer treatment.

Can you look up Pyrucet from idealabs DC and if this is relevant for cancer treatment

Pyrucet, offered by Idealabs DC, is a mixture of the ethyl esters of pyruvate and acetoacetate. These compounds have been shown in numerous studies to have beneficial effects on glucose metabolism, fatty acid oxidation, ATP synthesis, and redox status, among other health-related areas. Ethyl pyruvate (EP), a component of Pyrucet, has been identified for its potential anti-inflammatory, anti-coagulant, and antioxidant effects, which could have implications for cancer treatment. Specifically, EP has been highlighted for its ability to ameliorate systemic inflammation and multiple organ dysfunctions in various animal models, and its anti-tumor activity is thought to be associated with its anti-inflammatory effects. Prolonged treatment with EP has been shown to ameliorate experimental ulcerative colitis and slow multiple tumor growth in studies.

However, discussions on forums such as the Ray Peat Forum indicate that while there is interest in the potential of Pyrucet for cancer treatment, concrete evidence or widely accepted protocols specifically for cancer treatment with Pyrucet appear to be limited or anecdotal. One thread mentions an interview that discussed Pyrucet as a treatment for cancer, but the video was removed, indicating that while there is some discussion and interest, robust clinical evidence or mainstream acceptance may still be lacking.

Given this context, it’s important for individuals considering Pyrucet for cancer treatment to consult with healthcare professionals to understand its potential benefits and risks fully. While the components of Pyrucet have shown promise in various health-related areas, cancer treatment decisions should be based on comprehensive medical advice, considering all available evidence and treatment options.

What is redox and how do we achieve redox balance for health?

Redox, short for reduction-oxidation, refers to a type of chemical reaction in which the oxidation states of atoms are changed. These reactions are fundamental to numerous processes in biology, especially those involved in energy conversion and utilization within cells. Oxidation involves the loss of electrons or an increase in oxidation state by a molecule, atom, or ion, whereas reduction involves the gain of electrons or a decrease in oxidation state.

Redox balance in the body is crucial for maintaining health as it is central to the metabolic processes that provide energy to cells, the detoxification processes, and the immune response. An imbalance, particularly oxidative stress (where there’s an excess of reactive oxygen species or ROS and insufficient antioxidants to neutralize them), can contribute to the development of various diseases, including cardiovascular diseases, neurodegenerative diseases, cancer, and the process of aging.

Achieving redox balance involves:

  1. Antioxidant Intake: Consuming a diet rich in antioxidants helps maintain redox balance. Antioxidants can neutralize excess ROS, preventing cellular damage. Foods high in vitamins C and E, selenium, and phytochemicals (found in fruits, vegetables, nuts, and seeds) are excellent sources.

  2. Physical Activity: Regular exercise can enhance the body’s natural antioxidant defenses and improve overall metabolic health, helping to maintain redox balance. However, it’s important to balance exercise intensity and recovery, as excessive physical stress can increase oxidative stress.

  3. Reducing Exposure to Environmental Toxins: Minimizing exposure to sources of oxidative stress, such as pollution, cigarette smoke, and excessive sunlight, can help maintain redox balance.

  4. Managing Stress: Psychological stress can increase oxidative stress. Practices that reduce stress, such as meditation, deep breathing exercises, and yoga, can help maintain redox balance.

  5. Adequate Sleep: Quality sleep is crucial for the body’s repair processes, including the maintenance of redox balance. Ensuring sufficient and restful sleep supports antioxidant defenses.

  6. Moderation in Alcohol and Processed Foods: Limiting the intake of alcohol and foods high in sugars, refined carbohydrates, and unhealthy fats can reduce oxidative stress levels.

Maintaining a healthy lifestyle that incorporates these elements can help achieve and maintain redox balance, contributing to overall health and well-being. However, it’s also important to note that the balance between oxidative stress and antioxidants is complex and can be influenced by various factors including genetics, age, and lifestyle.

If cancer is a chronic reductive state, what does that mean in terms of treatment?

If cancer is described as a chronic reductive state, this refers to the idea that cancer cells often exhibit altered redox homeostasis compared to normal cells. They tend to maintain a more reduced environment, which is one aspect of their metabolic reprogramming that supports their rapid growth and survival. This altered redox state in cancer cells is characterized by changes in the balance of oxidants and antioxidants, making them more resistant to oxidative stress than normal cells. This can affect how they respond to certain therapies.

In terms of treatment, understanding cancer as a chronic reductive state has several implications:

  1. Targeting Redox Homeostasis: Therapies could be designed to specifically disrupt the redox balance within cancer cells, making them more susceptible to oxidative stress and less able to proliferate or survive. This approach might involve the use of pro-oxidant drugs or treatments that further increase oxidative stress beyond the cancer cell’s threshold for survival.

  2. Antioxidant Use: There’s ongoing debate about the role of antioxidants in cancer treatment. While antioxidants are generally seen as beneficial for health, in the context of cancer, there is concern that they might protect cancer cells from the oxidative damage induced by treatments like chemotherapy and radiation. Therefore, the use of antioxidants during cancer treatment needs careful consideration and more research.

  3. Combination Therapies: Exploiting the altered redox state of cancer cells can lead to the development of combination therapies that include agents targeting the redox balance. These therapies can be designed to weaken cancer cells’ defenses against oxidative stress in combination with conventional treatments that induce oxidative stress, potentially improving treatment efficacy.

  4. Selective Targeting: Identifying drugs or treatments that can selectively target the reductive environment of cancer cells without harming normal cells is a key area of research. This selectivity is crucial for minimizing side effects and improving patient outcomes.

  5. Biomarker Development: Understanding the specific alterations in redox homeostasis in different types of cancer can help in the development of biomarkers for early detection, treatment monitoring, and the prediction of treatment response.

The concept of cancer as a chronic reductive state emphasizes the complexity of cancer metabolism and the potential for targeting metabolic vulnerabilities in treatment strategies. However, the effectiveness and safety of targeting redox homeostasis in cancer treatment require thorough investigation and clinical validation.

Hello, can you write down this?

Of course! What would you like me to write down for you?

you were just talking about the cancer as a reductive state and its implication about in

Certainly! When we describe cancer as being in a chronic reductive state, it points to how cancer cells adapt their redox balance differently from normal cells. They create an environment that’s more resistant to damage from oxidative stress, supporting their growth and survival. This unique characteristic of cancer cells has several implications for treatment:

  1. Targeting Redox Homeostasis: By disrupting the redox balance within cancer cells, treatments could make them more vulnerable to oxidative damage. This might involve using drugs that increase oxidative stress to levels cancer cells can’t manage.

  2. Rethinking Antioxidants: The role of antioxidants in cancer treatment is complex. While they’re beneficial for general health, they might protect cancer cells during treatments like chemotherapy by reducing oxidative stress. This suggests a need for caution and further research into antioxidant use during cancer treatment.

  3. Developing Combination Therapies: There’s potential in combining treatments that target the redox state of cancer cells with traditional treatments. This approach aims to weaken cancer cells’ defenses and enhance the effectiveness of existing therapies.

  4. Selective Targeting: Finding treatments that specifically target the unique reductive environment of cancer cells, while sparing normal cells, is a crucial research area. This could help reduce side effects and improve outcomes

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