The True Science of Cancer

Describe metabolism: glucose becomes ATP in mitochondria to fuel activities, while lactate, a waste product, enables cancer cells, influenced by bowel movements, overeating, enzymes, and fruit and vegetables.

Discover how cancer cells derive energy mainly from mitochondrial oxidative phosphorylation, with a smaller share from substrate-level phosphorylation, enabling growth under hypoxia and lactate fermentation.

Learn how glucose fermentation forms lactate in low oxygen, contrasting with oxidation via the TCA cycle. Discover how glycolysis and NADH drive lactic fermentation and its effect on cell function.

Explore glutamine fermentation under hypoxia, where mitochondria convert glutamine to glutamate and alpha-ketoglutarate via glutaminase, with NH3 detoxified to succinate through succinyl-CoA.

Explore whether glucose or glutamine drives cancer progression under hypoxia, and show that glucose primarily fuels progression through fermentation and glycolysis.

Explore whether cholesterol affects cancer progression alongside glucose and glutamine as fuels. Under normal oxygen, tumor cells can grow without cholesterol, but under hypoxia they require cholesterol to survive.

Explore the normal mitochondrial structure and function, detailing the outer and inner membranes, crests, and electron transport chain that drive oxidative phosphorylation to produce ATP, contrasting with dysmorphic cancer cells.

Explore how cancer cell mitochondria differ in number, size, and shape, with lower counts and smaller, abnormally shaped organelles, and reduced respiratory capacity linked to higher malignancy.

Explore how protein defects and lipid abnormalities in tumor mitochondria impair mitochondrial function, focusing on the inner membrane lipids cholesterol and cardiolipin, electron transport chain, and their impact on oxphos.

Identify cancer causes by linking factors like fermentation from excess sugar, chronic inflammation, carcinogens, pathogens, and radiation to mitochondrial damage that drives cancer through respiratory insufficiency and compensatory fermentation.

Demonstrates that mitochondria in the cytoplasm suppress tumor growth, not the nucleus, via sufficient respiration. Supports Warburg's view through cybrid studies showing that normal cytoplasmic mitochondria curb malignant progression.

Explore how Warburg's view of respiratory insufficiency as the origin of cancer shows mitochondrial disruption triggering RTG retrograde signaling to the nucleus, altering nuclear genes and promoting oncogene-driven growth.

Show how cancer arises as a metabolic disease, linking mitochondrial function to calcium homeostasis and mitosis, and explaining that chromosomal missegregation reflects mitochondrial health and respiration.

Examine the first hypothesis that chromosomal imbalance and disrupted mitosis may cause cancer, framing cancer as a genetic disease, while recognizing abnormalities as effects rather than causes.

Compare how normal cells undergo apoptosis after cellular insults and how cancer cells evade apoptosis, continuing fermentation and substrate-level phosphorylation to fuel growth and metastasis.

Define metastasis as the spread of cancer cells from the tumor to distant organs, via detachment, invasion of circulatory and lymphatic systems, immune evasion, exit at capillary beds, and proliferation.

Explore the origin of metastasis, comparing tissue stem cells and myeloid cells as sources, with evidence from stem cell similarities and hematopoietic lineages, and whether macrophages drive metastasis.

Macrophages from myeloid cell family can fuse with epithelial cells in the inflamed environment to drive metastasis; hematopoietic stem cells may metastasize through fusion with neoplastic tumor cells or transformation.

Explore how macrophages activated by inflammation acquire properties that drive metastasis, including secreting growth factors and cytokines, with M1 promoting inflammatory damage and M2 fusing with tumor cells.

Examine how macrophages may drive metastasis by exhibiting cancer hallmarks and phagocytosis in mouse brain tumors, melanoma, and other cancers, while crown gall plants lack metastasis due to absent macrophages.

Explore whether cancer is many diseases or an energy-driven disease, via Warburg's sugar and glutamine fermentation in cancer cells. Learn why metastasis targets lung, liver, and bone with macrophage involvement.

Review current cancer treatments—surgery, chemotherapy, and radiation—and their limits for malignant and metastatic cancer, and introduce immunotherapy as a promising newer option.

Explore FDA-approved immunotherapy drugs for cancer, focusing on ipilimumab for malignant melanoma, its side effects and dexamethasone management, cost, and survival outcomes.

Explore targeted cancer therapies like Vemurafenib for BRAF V600E melanoma (50% response, 12-month survival) and Gefitinib targeting EGFR, plus biomarker-integrated approaches in lung cancer.

Explain the standard of care for glioblastoma multiforme, including surgery, radiation, and chemotherapy, and describe how glucose and glutamine fuel tumor growth and the glutamine glutamate cycle.

Investigate how radiation contributes to cancer progression by damaging tumor mitochondria, upregulating the p13 K Akt pathway, and promoting glycolysis, vascularization, invasion, and risk of recurrence.

Explore gamma therapy and its side effects, review chemotherapy drug classes—alkylating agents, antineoplastics, antimetabolites, hormonal agents, mitotic inhibitors, immunomodulators, misc. agents—and bevacizumab as an anti-angiogenic.

Explore how chemotherapy causes oxidative damage and side effects like mouth sores, magnesium loss, and taste changes from radiation, and learn antioxidants, glutamine, zinc, and ginger strategies.

Explore how cancer is a metabolic disease and how dietary energy reduction, via fasting, calorie restriction, and ketogenic diets, targets tumor cell energy metabolism by reducing glucose and glutamine availability.

Discover how lowering glucose and raising beta hydroxybutyrate through fasting, low calorie, and ketogenic diets can inhibit cancer progression; ketone bodies fuel metabolism and can be toxic to tumor cells.

Explore how a restricted ketogenic diet, with a 4:1 fat-to-carbohydrate-protein ratio, may modulate brain cancer by altering energy metabolism, mitochondrial function, and glutathione redox balance.

Calorie restriction exerts anti-angiogenic effects, delays tumor growth, and targets abnormal tumor vessels marked by alpha smooth muscle actin, with brain tumor studies showing up to 80% growth reduction.

Explore how calorie restriction triggers proapoptotic pathways via Bad/BCL2, promotes apoptosis over necrosis, and reduces nfkb-driven inflammation to slow cancer progression.

Calorie restriction targets advanced cancer and exerts anti-invasive effects by downregulating the IGF-1 Akt HIF-1α signaling pathway, reducing tumor growth, invasion, and Ki-67 positive cells.

Restrict glucose and glutamine through a calorie-restricted ketogenic diet in phase 1 to shrink tumors while sparing normal cells, with blood glucose and ketone monitoring and defined target ranges.

Phase two presents optional surgical resection after shrinking the tumour with fasting and kdr therapy. Opt for watchful waiting before surgery to reduce inflammation and microenvironment changes promoting cancer progression.

Control surviving tumor cells in phase three maintenance with a low calorie diet, monitor glucose and ketone levels, and use mr imaging with spectroscopy to extend survival to 36 months.

Explore how corticosteroids, fasting, and Cd-R therapy affect cancer progression, glucose control, inflammation, and cachexia via interleukin-6 and hepcidin pathways.

Identify factors that provoke cancer and protect mitochondria as the primary way to prevent cancer. Limit sugar to prevent fermentation and inflammation from smoking, alcohol, obesity, radiation, and carcinogen exposure.

List and discuss anti-cancer plants, herbs, and vitamins that may complement a ketogenic diet, including cannabis leaves, curcumin, turmeric, vitamins C and D, selenium, quercetin, and moringa leaves.

Show how damaged mitochondria drive cancer by respiratory failure and fermentation, with sugar as cause; manage through calorie restriction, fasting, a ketogenic diet, plus sunlight, fresh air, water, and sleep.