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Cancer as a metabolic disease - implications for novel therapeutics

Ever wondered if cancer might be a metabolic disease? Explore a groundbreaking perspective on cancer as a metabolic disease rooted in mitochondrial dysfunction and energy mismanagement. Discover how therapies like ketogenic diets, hyperbaric oxygen, and metabolic drugs can target cancer’s weaknesses while preserving healthy cells. Join us in rethinking cancer treatment with science that challenges traditional genetic theories!

Frequently Asked Questions (FAQ)

  1. What is the main argument of this review? This review challenges the prevailing view of cancer as primarily a genetic disease, arguing instead that it is fundamentally a metabolic disease. The authors propose that disturbances in cellular energy metabolism, particularly in the mitochondria, are the root cause of cancer. They suggest that the genomic instability and other hallmarks of cancer are downstream consequences of this metabolic dysfunction.

  2. If cancer is not primarily caused by genetic mutations, then what initiates the disease? According to this review, any condition that impairs cellular respiration, specifically oxidative phosphorylation (OxPhos) in the mitochondria, without causing immediate cell death can potentially initiate the path to cancer. This includes factors such as inflammation, carcinogens, radiation, hypoxia, certain viral infections, and aging. These factors can damage mitochondrial structure and function, leading to a reliance on less efficient energy production through fermentation (glycolysis).

  3. What is the Warburg effect and how does it relate to cancer? The Warburg effect, named after Otto Warburg, describes the observation that cancer cells preferentially utilize fermentation (glycolysis followed by lactate production) to produce energy even in the presence of oxygen. This is less efficient in terms of ATP yield per glucose molecule compared to OxPhos used by most normal cells under aerobic conditions. This review supports Warburg’s theory, arguing that this metabolic shift arises from insufficient respiration due to mitochondrial dysfunction.

  4. But don’t many studies show high oxygen consumption rates in cancer cells, suggesting normal respiration? While it’s true that high oxygen consumption (OCR) is sometimes observed in cancer cells, the review emphasizes that OCR doesn’t always equate to efficient ATP production via OxPhos. Oxygen consumption might be uncoupled from ATP synthesis, or used for processes other than energy generation. Additionally, the review highlights the “Crabtree effect,” where high glucose levels (common in cell culture) can suppress respiration and promote fermentation even in non-cancerous cells, making in vitro metabolic data interpretation complex. The core argument remains that respiration is insufficient to meet the cell’s energy demands, leading to compensatory fermentation.

  5. Does the review completely dismiss the role of genetic mutations in cancer? No, the review acknowledges the presence of widespread genomic instability and numerous mutations in cancer cells. However, it posits that these mutations are largely secondary effects, or epiphenomena, arising from the chronic metabolic stress induced by impaired respiration and a reliance on fermentation. The authors propose that the initial metabolic shift triggers downstream events, including mitochondrial stress responses, reactive oxygen species (ROS) production, and oncogene activation, which contribute to genomic instability.

  6. How does this metabolic theory of cancer explain metastasis? The review references the idea that metastasis, the spread of cancer cells, could be linked to mitochondrial dysfunction in specific cell types, potentially those of myeloid/macrophage origin or through fusion events. These cells, naturally capable of migration, might adopt a more aggressive, invasive phenotype due to respiratory damage and reliance on fermentation. This metabolic reprogramming could enhance their migratory and invasive capabilities, facilitating metastasis.

  7. What are the therapeutic implications of considering cancer as a metabolic disease? If cancer is driven by metabolic abnormalities, particularly reliance on fermentation (glucose and glutamine), then therapies targeting these metabolic pathways hold significant promise. The review strongly highlights the potential of calorie-restricted ketogenic diets (KD-R). KD-R reduces glucose availability and elevates ketone bodies. Normal cells can typically adapt metabolically, using ketones efficiently for energy. However, many cancer cells, due to mitochondrial defects and dependence on fermentation pathways, struggle to utilize ketones effectively and are stressed by glucose restriction, making them more vulnerable to cell death or other treatments. Other metabolic therapies mentioned include hyperbaric oxygen and drugs targeting specific metabolic enzymes.

Resources & Further Watching

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Youtube Hashtags

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Youtube Keywords

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