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New Cancer Therapy Protocol Shows Promise in Treatment

The Mitochondrial-Stem Cell Connection (MSCC) theory integrates the cancer stem cell theory and metabolic theory to propose that cancer arises from impaired oxidative phosphorylation (OxPhos) in stem cells. MSCC highlights the critical role of mitochondria in all stages of cancer progression.


Introduction

The Mitochondrial-Stem Cell Connection (MSCC) theory integrates the cancer stem cell theory and metabolic theory to propose that cancer arises from impaired oxidative phosphorylation (OxPhos) in stem cells. This impairment leads to the formation of cancer stem cells (CSCs), tumorigenesis, and abnormal energy metabolism. MSCC highlights the critical role of CSCs and mitochondria in all stages of cancer progression.

Unlike traditional therapies based on the somatic mutation theory (SMT), which target cancer cell DNA and fail to restore OxPhos, the MSCC approach focuses on targeting CSCs, which have the strongest tumorigenic and metastatic potential. Current therapies show limited improvement in survival rates, emphasizing the need for alternative strategies.

The MSCC theory outlines several key points:

  • OxPhos impairment in stem cells can initiate tumorigenesis.
  • Cancer cells rely on glucose and glutamine as primary fuels to survive and grow due to OxPhos insufficiency.
  • The tumor microenvironment, characterized by acidity, hypoxia, and other disruptions, stems from mitochondrial dysfunction.
  • Metastasis, the leading cause of cancer mortality, is linked to the fusion of CSCs and macrophages.

To address these challenges, the MSCC theory proposes a hybrid orthomolecular protocol combining orthomolecules, repurposed drugs, and additional therapies. This approach aims to enhance OxPhos, inhibit cancer’s primary energy sources, and target CSCs and metastasis, offering a promising therapeutic strategy for all types of cancer.


Orthomolecular Medicine for Targeting the MSCC proposes the use of vitamins C, D, and zinc as effective anti-cancer therapies due to their ability to target mitochondrial dysfunction, restore oxidative phosphorylation (OxPhos), and address cancer stem cells (CSCs) and metastases.

Vitamin C

  • Demonstrates cytotoxic effects on cancer cells, reducing tumor weight, metastases, and CSC populations in various cancers.
  • Restores mitochondrial function, enhances ATP production, and induces apoptosis, including in drug-resistant and metastatic cancer cells.
  • Competes with glucose for cellular entry, disrupting glycolysis and glutaminolysis, crucial pathways for cancer cell metabolism.
  • Converts M2 macrophages (associated with metastases) to M1 macrophages, inhibiting metastatic spread.
  • High-dose intravenous administration is essential for achieving therapeutic plasma concentrations, unlike oral supplementation.

Vitamin D

  • Exhibits anti-cancer properties by regulating mitochondrial respiration, metabolism, and inhibiting glycolysis and glutaminolysis.
  • Reduces CSCs, metastases, and overall cancer mortality, with evidence of significant benefits in patients with daily supplementation.
  • Has been effective in prolonging disease-free progression in advanced cancer cases and preventing metastases in healthy individuals with regular supplementation.
  • Cancer patients, often deficient in vitamin D, benefit from supplementation, which is low-risk and can be administered orally or intravenously.

Zinc

  • Protects mitochondria from oxidative damage, enhances OxPhos, and induces apoptosis in cancer cells.
  • Reduces CSC properties, enhances sensitivity to chemotherapy, and disrupts cancer cell energy production.
  • Zinc deficiency is strongly linked to multiple cancers, while supplementation shows selective toxicity toward cancer cells without harming normal cells.
  • Plays a role in inhibiting metastases and improving survival rates in cancer patients.

These orthomolecules address critical cancer pathways, including mitochondrial dysfunction, CSC targeting, and metabolic inhibition, offering promising adjunctive therapies to standard cancer treatments.


Repurposed (Off-Label) Drugs for Targeting the MSCC explores the potential use of non-cancer drugs with anti-cancer properties, including Ivermectin, Benzimidazoles, and DON, to target cancer metabolism, CSCs, and metastases.

IvermectinCLICK to BUY

  • A safe anti-parasitic drug with significant anti-cancer properties, including inducing autophagy, apoptosis, and mitochondrial dysfunction in cancer cells.
  • Inhibits glycolysis, targets CSCs and metastases, and demonstrates pro-oxidant effects selectively on cancer cells.
  • Effective against various cancer types, outperforming standard chemotherapy (e.g., gemcitabine) in vivo.
  • High-dose administration (up to 2 mg/kg or five times the standard dose) has shown no severe adverse effects in both healthy volunteers and cancer patients.

BenzimidazolesCLICK to BUY

  • Drugs like Mebendazole (FDA-approved) and Fenbendazole show anti-cancer activity through microtubule polymerization, apoptosis induction, cell cycle arrest, anti-angiogenesis, and inhibition of glucose and glutamine pathways.
  • Effective against CSCs, metastases, and chemoresistant cancer cells.
  • Mebendazole outperforms standard chemotherapies in several cancers, including glioblastoma and gastric cancer, significantly prolonging survival.
  • Demonstrated safety in long-term use, even at high doses (up to 4 g/day), with reports of tumor regression or stabilization in cases of advanced, refractory cancers.

DON (6-diazo-5-oxo-L-norleucine)

  • A potent glutamine-specific antagonist with anti-tumor activity, inducing apoptosis in CSCs and targeting metastases.
  • Also affects glucose uptake, disrupting cancer metabolism.
  • Low daily doses of DON are non-toxic, making it a promising candidate for cancer therapy.

These repurposed drugs demonstrate potential as adjunctive therapies by targeting critical cancer pathways, including metabolism, CSCs, and metastases, with minimal toxicity and enhanced efficacy compared to conventional treatments.


Dietary Interventions for Targeting the MSCC highlights the potential of fasting and ketogenic diets in combating cancer by altering metabolic pathways essential for cancer cell survival and growth.

Fasting

  • Enhances mitochondrial activity by increasing oxidative phosphorylation (OxPhos), autophagy, and inhibiting glycolysis and glutaminolysis.
  • Promotes the regeneration of normal stem cells while disrupting CSCs through autophagy and glucose deprivation, leading to CSC death.
  • Demonstrates anticancer effects in vivo, boosting the efficacy of combined therapies.
  • Researchers suggest fasting may eventually be prescribed as an anticancer treatment following confirmation of its safety and efficacy in clinical trials.

Ketogenic Diet and Ketone Metabolic Therapy (KMT)

  • Induces therapeutic ketosis, which inhibits CSC growth, restores apoptosis, enhances cellular respiration, and suppresses glycolysis.
  • Shows antitumor effects in vitro, in vivo, and in humans, particularly for glioblastoma multiforme.
  • Works synergistically with drugs like DON and Mebendazole, enhancing their efficacy and reducing toxicity.
  • Restricts glucose and glutamine pathways critical for cancer cell metabolism while increasing OxPhos.
  • Case studies report prolonged survival in cancer patients using a ketogenic diet, including a glioblastoma patient surviving over six years without chemoradiotherapy.
  • Ketone supplementation independently enhances mitochondrial function, suppresses tumor growth, and targets metastasis and other cancer hallmarks.
  • Lifestyle changes, including dietary modifications, have been linked to spontaneous cancer regression in some cases.

Both fasting and ketogenic interventions target cancer metabolism, particularly glycolysis and glutaminolysis, providing promising adjunctive strategies for cancer therapy with minimal toxicity


Proposed Hybrid Orthomolecular Protocol for Cancer Treatment

This protocol integrates orthomolecules, drugs, dietary interventions, and additional therapies to target the mitochondrial substrate-level phosphorylation of cancer cells (MSCC), promoting apoptosis in cancer cells while protecting healthy cells.

Key Components:

  1. Intravenous Vitamin C
  2. Oral Vitamin D
    • Dosage depends on blood levels:
      • ≤30 ng/mL: 50,000 IU/day
      • 30-60 ng/mL: 25,000 IU/day
      • 60-80 ng/mL: 5,000 IU/day (maintenance dose).
    • Blood levels should reach 80 ng/mL and be monitored regularly.
  3. Zinc
  4. Ivermectin
    • Doses vary by cancer grade:
      • Low-grade: 0.5 mg/kg, 3x per week.
      • Intermediate-grade: 1 mg/kg, 3x per week.
      • High-grade: 1-2 mg/kg/day.
  5. Benzimidazoles and DON
    • Low-grade cancers: Mebendazole 200 mg/day.
    • Intermediate-grade: Mebendazole 400 mg/day.
    • High-grade: Mebendazole up to 1,500 mg/day or Fenbendazole 1,000 mg, 3x per week.
    • Combine with DON (optional for metastatic cancers), administered orally or intravenously.
  6. Dietary Interventions
    • Ketogenic Diet:
      • Low carb, high fat (60-80% fat, 15-25% protein, 5-10% carbs).
      • Target glucose ketone index (GKI) of ≤2.0, measured postprandially.
    • Fasting:
      • Advanced cancers: 3-7 days water fast repeated every 3-4 weeks.
      • Alternative: Fasting-mimicking diet (300-1,100 kcal/day).
  7. Additional Therapies
    • Moderate physical activity: 45-75 minutes, 3x per week.
    • Hyperbaric oxygen therapy: 1.5-2.5 ATA, 45-60 minutes, 2-3x per week for advanced cancers or patients unable to exercise.

Add-on Nutrients (Optional):

  • Vitamin K2, vitamin E, coenzyme Q10, methylene blue, niacinamide, riboflavin, melatonin, NADH, magnesium, etc. (Antioxidant dosages should be avoided).

Mechanism:

The protocol targets fermentable fuels (glucose, glutamine), CSCs, and macrophages, inducing apoptosis through a pro-oxidant effect while preserving healthy cells by increasing OxPhos activity.

Duration:

12 weeks on average, with adjustments by physicians based on patient response and accessibility.

Recommendations:

Comparative studies in animals and humans are needed to validate the efficacy and safety of this hybrid approach versus standard cancer treatments.


Conclusion
The mitochondrial-stem cell connection (MSCC) is a pivotal element in cancer therapy. The proposed combination of orthomolecules, drugs, and therapies aims to restore OxPhos activity, target cancer stem cells (CSCs), and inhibit glycolysis and glutaminolysis, addressing metastases caused by CSC-macrophage hybridization. Evidence from cellular, animal, and human studies supports the effectiveness of targeting the MSCC for both cancer prevention and treatment.


Courage Against Cancer offers several of the above mentioned drugs on our Store page via our affiliate relationships with several pharmaceutical providers. Your purchase through our links helps generate operational funds to keep the CAC wheels turning. Your support is greatly appreciated and feedback welcomed.

This article is a chatGPT generated summary of the research findings from The Journal of Orthomolecular Medicine. You can link to the cited published article HERE.

Below is our revised Ivermectin and Fenbendazole dosage guidlines – CLICK specific link to download PDF file.

Ivermectin Dosage Guide for Cancer Treatment

CLICK HERE TO DOWNLOAD Guideline


Fenbendazole Dosage Guide for Cancer Treatment

CLICK HERE TO DOWNLOAD Guideline



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