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Treatment Approach

Strategic Warfare Against Cancer: Redefining Cancer Treatment by Outmaneuvering the Disease

Our innovative cancer treatment protocol represents a paradigm shift in oncology, drawing inspiration from military strategy to create a comprehensive, two-phase approach to cancer therapy. This protocol addresses a critical gap in contemporary cancer treatment, where despite significant advances since the 1971 National Cancer Act, metastatic disease continues to claim millions of lives annually.

On December 23, 1971, President Richard Nixon signed the National Cancer Act, officially declaring America’s “war on cancer.” This watershed moment marked an unprecedented national commitment to combat what had become the country’s second leading cause of death. Nixon’s declaration promised to mobilize the nation’s resources against this formidable enemy, much like the Manhattan Project had done during World War II. The Act significantly increased federal funding for cancer research and established what would become a comprehensive national cancer program.

Yet more than fifty years later, while we have won significant battles—notably against certain blood cancers, early-stage breast cancer, and some pediatric cancers—we certainly have not won the war. Cancer remains one of humanity’s most formidable adversaries, with metastatic disease in particular continuing to claim millions of lives annually. Contemporary cancer drugs, as research published in both 2004 and 2023 demonstrates (click here and here), often have a limited impact on enhancing the quality of life or prolonging survival in metastatic cases. This persistence of cancer as a leading cause of death suggests that perhaps we need to take the warfare analogy more literally.

If we genuinely wish to win this war, we must think like military strategists. Just as Sun Tzu wrote in The Art of War over two millennia ago, “Invincibility lies in the defense; the possibility of victory in the attack.” This ancient wisdom holds remarkable relevance for modern cancer treatment. Before launching major offensive operations against cancer cells, we must first secure our position and weaken the enemy’s strongholds. This requires understanding the battlefield conditions—the tumor microenvironment—and implementing a coordinated strategy that combines both defensive and offensive measures.

Our novel approach draws inspiration from military doctrine, viewing cancer treatment as a carefully orchestrated campaign rather than a series of isolated interventions. This strategy recognizes that, like any successful military operation, cancer treatment requires:

Thorough intelligence gathering about enemy territory (understanding the tumor microenvironment)
Securing defensive positions (neutralizing the acidic environment that protects cancer cells)
Disrupting enemy supply lines (targeting cancer’s metabolic dependencies)
Coordinating multiple simultaneous attacks (combining therapeutic approaches)
Protecting civilian populations (minimizing damage to healthy tissue)

In addition to important diet and lifestyle changes (click here), our approach involves a carefully sequenced deployment of two powerful therapeutic strategies: bicarbonate therapy as the defensive foundation, followed by enhanced high-ozonide oil as the offensive strike.

To learn more about the treatment protocol, please read below, and listen to this 15-minute podcast: Click here.

The Tumor Microenvironment: Understanding the Battlefield Conditions

Before engaging the enemy, we must understand the hostile territory where this battle takes place. The tumor microenvironment is characterized by two critical features that promote cancer progression: acidosis and hypoxia. These conditions create an ideal environment for tumor growth while hampering normal cellular function and immune responses, essentially creating a fortress that protects cancer cells while weakening our body’s natural defenses.

In the acidic environment of tumors, cancer cells develop remarkable metabolic flexibility through specific adaptations triggered by the acidic conditions. The acidic environment activates key regulators like SIRT1 and HIF2α, which orchestrate a shift away from glucose dependence toward the ability to use multiple fuel sources. Rather than relying solely on glucose, these acid-adapted cells enhance their capacity to take up and utilize fatty acids, storing them in specialized droplets and boosting their machinery for fatty acid breakdown through PPARα signaling. At the same time, the acidic environment promotes increased glutamine usage by upregulating specific transporters and enzymes, allowing cells to either burn glutamine for energy or use it for building cellular components. This acid-driven metabolic rewiring creates cells that can efficiently switch between different fuel sources as needed, helping them thrive in the challenging conditions of the tumor microenvironment while maintaining their growth and survival.

Acidosis, a key feature of cancer’s metabolic strategy, results primarily from increased glycolysis and lactic acid production in cancer cells. This acidic microenvironment creates a selective advantage for cancer cells, serving as both a shield and a weapon. It promotes local tissue invasion through protease activation and matrix degradation, essentially dissolving the surrounding tissue’s defensive barriers. More critically, acidosis severely compromises our immune system’s front-line defenders by inhibiting T-cell and NK cell activity, reducing cytokine production, and impairing antigen presentation. This acidic environment also stabilizes acid-base transporters and enhances glycolytic metabolism, further fortifying cancer’s defensive position.

The second battlefield condition, hypoxia, develops as tumors outgrow their blood supply, leading to areas with insufficient oxygen. This oxygen-deprived state triggers multiple adaptive responses through HIF-1α activation, essentially forcing cells to adapt to siege conditions. Cancer cells shift to glycolytic metabolism (the Warburg effect), increase angiogenesis through VEGF upregulation, and enhance their invasive potential. Hypoxia also promotes the development of cancer stem cells and epithelial-to-mesenchymal transition (EMT), creating elite forces capable of establishing new tumor colonies. Furthermore, hypoxic conditions impair immune cell function and infiltration while increasing the expression of immune checkpoint molecules, creating an immunosuppressive environment that helps tumors evade detection and elimination.

The Defensive Phase: Neutralizing Enemy Territory

Our defensive strategy begins by systematically dismantling these hostile conditions through bicarbonate therapy. This phase targets cancer’s acidic fortress, neutralizing the acidic microenvironment and forcing cancer cells to expend precious energy trying to maintain their preferred acidic state. Through this process, we achieve multiple strategic objectives:

Normalization of tumor blood vessels, improving oxygen delivery, and creating supply lines for our offensive agents
Inhibition of matrix metalloproteinases, blocking cancer’s ability to break through tissue barriers and establish new colonies
Enhancement of immune system function by creating conditions where T-cells and natural killer cells can operate effectively
Reduction of cancer stem cell populations, cutting off the enemy’s ability to regenerate and rebuild
Disruption of acid-dependent survival mechanisms, weakening cancer’s defensive capabilities

Progress in this defensive phase can be monitored through urine pH. A target of 7.5-8.0 signals successful neutralization of enemy territory and confirms our defensive preparations are complete. This measurement serves as our battlefield intelligence, indicating optimal conditions for launching the offensive phase.

The Offensive Phase: Launching a Multi-Front Attack

With our defensive preparations secured, we launch a coordinated offensive using enhanced high-ozonide oil (HOO) as our primary strike force, supported by multiple specialized agents. This phase delivers a powerful oxidative assault through several simultaneous attack vectors:

Primary Strike Force (HOO):

Direct targeting of cancer cell mitochondria through exploitation of structural vulnerabilities in cardiolipin
Release of oxygen species within cancer tissue, disrupting hypoxia-driven adaptations
Reduction of HIF-1α activation and angiogenic signaling, cutting off enemy supply lines
Triggering of apoptosis and calcium-mediated cellular destruction

Supporting Strike Teams:

Sulfasalazine: Blocks glutathione synthesis, eliminating cancer’s primary antioxidant defense
Auranofin: Disrupts the thioredoxin system, neutralizing secondary antioxidant defenses
Chrysin: Suppresses Nrf2-mediated responses, preventing adaptation to oxidative stress
Niclosamide: Creates additional mitochondrial stress and promotes cellular self-destruction

The synergistic benefits of this two-phase approach are significant and multi-faceted. The defensive preparations optimize offensive impact, with multiple simultaneous attacks overwhelming cancer cells while drug delivery and effectiveness are maximized, and immune system support is strengthened. Importantly, healthy cells maintain their natural defenses and are better equipped to handle oxidative stress, while the targeted nature of the attack spares healthy tissue, creating selective toxicity toward cancer cells.

The success of this approach lies in its systematic nature and the synergy between its components. By first securing our position through defensive measures, then launching a coordinated offensive enhanced by multiple strategic strikes, we effectively corner cancer cells while protecting healthy tissue. Carefully monitoring battlefield conditions through urine pH ensures that the offensive phase begins only when optimal conditions have been created, maximizing its effectiveness. This methodical, two-phase approach represents a sophisticated strategy that leverages our understanding of cancer cell biology and vulnerability to create a comprehensive treatment protocol with the potential for improved outcomes in cancer therapy.

Note: To review the anti-cancer mechanisms of action and scientific validation for each of the components in our strategy, please scroll down to the reference list below.

Treatment Indications

Based on this comprehensive approach, our treatment may be particularly beneficial for:

Patients seeking to enhance the effectiveness and/or minimize the side effects of conventional cancer treatment, including surgery, chemotherapy, radiation, targeted therapy, hormone blockade, and immunotherapy.
Patients who have not responded to or can no longer tolerate conventional treatment.
Patients who do not qualify for a drug trial or failed to respond favorably to a trial drug.
Patients wanting to prolong their remission with health-enhancing strategies.
Patients seeking to improve their quality of life.

Patient Care and Treatment Cost

Dr. Thomas ensures exceptional personalized care by limiting his practice to no more than 50 patients, in contrast to the typical oncology practice of 250-500 patients. This focused approach allows for both individualized attention and ongoing research to optimize patient outcomes. The treatment approach described above requires close medical oversight by Dr. Thomas. Following an initial physical examination in his office, patients commence their treatment. Monthly follow-up appointments are scheduled and can be conducted through telemedicine or in-person visits. Patients enjoy unrestricted email access to Dr. Thomas throughout their treatment, ensuring they receive continuous and responsive support. Treatment progress is closely monitored by obtaining tumor markers and imaging (CT, MRI, or PET/CT) every three months.

The cost for our services is a flat rate of $2250 per month. This includes custom-synthesized oral liposomal niclosamide and ongoing medical management and continuous access to Dr. Thomas’s expertise. This is less expensive than alternative cancer treatment often sought in Mexico, Central America, the Caribbean, and Europe. In these locations, clinics typically charge $7,000 to $20,000 weekly for medical treatment or $40,000 to $120,000 for highly-experimental procedures that have limited scientific validation. Other costs are for online items (bicarbonate, high-ozonide ozonated oil, and liposomal chrysin) and retail pharmacy items (auranofin and sulfasalazine). Treatment continues until achieving remission or disease stabilization, typically within a 12-18-month timeframe. Other than covering the cost of bloodwork, health insurance and Medicare do not pay for integrative cancer treatment.

References

Auranofin:

Mechanisms of action:

Cell cycle arrest and apoptosis induction: In multiple myeloma, auranofin induces cell cycle arrest and apoptosis, reduces Mcl-1 expression, and down-regulates NF-κß activity.
Oxidative stress induction: It increases reactive oxygen species (ROS) levels, leading to DNA damage and caspase-independent apoptosis, particularly in cells dependent on the Trx1 system.
PI3K/AKT/mTOR pathway inhibition: Auranofin inhibits this pathway, essential for cell proliferation, apoptosis, and angiogenesis, affecting tumor growth and metastasis.
Protein homeostasis disruption: It inhibits proteasome and deubiquitinases (dubs), inducing apoptosis in liver hepatocellular and breast cancer cells.
FOXO3-dependent apoptosis: In ovarian cancer cells lacking p53, auranofin triggers apoptosis through FOXO3 activation, indicating a p53-independent pathway.
IKK-β inhibition and NF-κß signaling modulation: Downregulates IKK-β, reducing NF-κß signaling and promoting apoptosis via FOXO3 nuclear translocation.
Mitochondrial dysfunction: Leads to loss of mitochondrial membrane potential, resulting in cell death through apoptosis or necrosis.

Citations:

Bicarbonate:

Mechanisms of action:

Neutralization of tumor acidity: Bicarbonate buffers the acidic tumor microenvironment, increasing extracellular pH. This disrupts the acidosis that supports cancer progression, metastasis, and therapy resistance.
Inhibition of cancer cell invasion and metastasis: Acidic conditions facilitate extracellular matrix degradation, aiding cancer cell migration. Bicarbonate reduces extracellular acidity, impairing the invasiveness and metastatic potential of cancer cells.
Enhancement of immune response and reduction of tumor microenvironment immunosuppression: Acidosis suppresses immune cell functions, including T-cell activation and cytokine production, while lactate accumulation directly inhibits cytotoxic T lymphocytes. Bicarbonate neutralizes acidity and reduces lactate levels, restoring immune activity and enhancing responses to immunotherapies such as anti-CTLA-4 and anti-PD1.
Improvement of chemotherapy efficacy: Acidic environments reduce the effectiveness of weak-base chemotherapeutic drugs. Bicarbonate neutralizes tumor acidity, improving drug delivery and efficacy.
Reversal of metabolic advantages of cancer cells: Cancer cells rely on the Warburg effect (aerobic glycolysis), producing lactic acid and creating an acidic microenvironment. Bicarbonate disrupts this metabolic adaptation, limiting cancer cell survival and proliferation.
Reduction of hypoxia-driven tumor adaptations: Hypoxic and acidic conditions drive tumor metabolic reprogramming and aggressive behavior. By increasing pH, bicarbonate disrupts these adaptive mechanisms.
Suppression of acid-sensitive pathways: Bicarbonate interferes with the function of acid-regulating proteins such as carbonic anhydrase IX, monocarboxylate transporters, and proton pumps, which are critical for cancer cell survival.
Restoration of cellular processes: Acidosis disrupts key cellular processes like adhesion, proliferation, apoptosis, and histone acetylation. Bicarbonate restores these processes by maintaining a more alkaline intracellular and extracellular pH.

Citations:

Chrysin:

Mechanisms of action:

Suppressing Nrf2-mediated defenses: Chrysin enhances the effectiveness of ROS-mediated cancer treatments by suppressing the Nrf2-mediated antioxidant response in cancer cells, preventing them from upregulating defenses against oxidative stress, thereby increasing their vulnerability to ROS-induced damage and improving sensitivity to pro-oxidative therapies.
Induction of apoptosis: Chrysin activates apoptotic pathways, often involving caspase activation and the inhibition of anti-apoptotic proteins such as Bcl-2. It induces apoptosis through both intrinsic and extrinsic pathways, enhancing cancer cell susceptibility to programmed cell death.
Cell cycle arrest: It disrupts the cell cycle by regulating cyclins and cyclin-dependent kinases (CDKs), effectively halting cancer cell proliferation.
Inhibition of angiogenesis: Chrysin downregulates hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF), which are critical for tumor angiogenesis.
Anti-inflammatory effects: By suppressing NF-κB activity and reducing levels of pro-inflammatory cytokines such as TNF-α and IL-1β, chrysin creates an unfavorable environment for cancer progression.
Anti-metastatic properties: Chrysin inhibits epithelial-to-mesenchymal transition (EMT), reducing cancer cell migration and invasion. It also downregulates metalloproteinases (MMPs) involved in metastasis.
Regulation of autophagy: Chrysin affects autophagy through pathways such as CDK1/ULK1, modulating the tumor microenvironment and cancer cell survival mechanisms.
Sensitization to chemotherapy: Chrysin sensitizes cancer cells to chemotherapeutic agents by overcoming drug resistance mechanisms, enhancing the efficacy of combination therapies.
Inhibition of pro-survival signaling pathways: It targets critical signaling pathways like PI3K/Akt, STAT3, and MAPK, which are involved in cancer cell survival and proliferation.
Suppression of tumor-associated macrophages (TAMs): By inhibiting TAM-mediated autophagy and their pro-tumor effects, chrysin reduces the supportive role of the tumor microenvironment.
Epigenetic modulation: Chrysin exhibits inhibitory effects on histone deacetylases (HDACs) and influences the expression of microRNAs involved in cancer progression.

Citations:

High-ozonide oil (HOO):

Mechanisms of action:

Re-activation of intrinsic apoptosis: HOO oxidizes mitochondrial membranes in cancer cells by exploiting structural differences in cardiolipin (a key phospholipid in mitochondrial membranes). Cardiolipin’s altered structure in cancer cells due to lack of cytochrome c binding creates gaps that allow HOO access, while normal cells’ intact cardiolipin structure blocks HOO. This selective targeting triggers the release of cytochrome c and calcium, leading to apoptosis, specifically in cancer cells.
Inhibition of tumor-associated macrophage activation: HOO inhibits the oxidative burst and inflammatory cytokine release from macrophages, which typically support tumor growth.
Increase of oxygen availability in tumor tissue: HOO releases oxygen species inside cancer tissue, counteracting the hypoxic environment that triggers angiogenesis and metastasis.
Competition with mitochondrial fat oxidation pathway: HOO may compete with fatty acid oxidation, which provides energy to cancer cells. Its catabolism leads to oxidative stress, mitochondrial damage, and apoptosis.
Targeting cancer stem cells: HOO depletes the high antioxidant levels in cancer stem cells, reversing their chemo/radioresistance.
Anti-inflammatory effects at the systemic level: HOO induces anti-inflammatory effects without immunosuppression by inhibiting macrophage oxidative burst.

Citations:

Niclosamide:

Mechanisms of action:

STAT3 pathway inhibition: Blocks STAT3 phosphorylation at Tyr705, reducing transcription of survival proteins like Bcl-2, Mcl-1, and Survivin).
Wnt/β-catenin pathway suppression: Degrades β-catenin, inhibits Dishevelled expression, downregulates LRP6, and reduces transcriptional activation of Wnt target genes.
NF-κB Pathway inhibition: Blocks IκB phosphorylation and nuclear translocation of NF-κB, reducing inflammatory and pro-survival signaling.
PD-L1 modulation and immune checkpoint inhibition: Inhibits HuR-mediated stabilization of PD-L1 mRNA, reduces PD-L1 levels, and promotes T-cell activation, enhancing the efficacy of immune checkpoint blockade.
Mitochondrial dysfunction and metabolic disruption: Uncouples oxidative phosphorylation, decreases mitochondrial respiration, and disrupts ATP production, inducing apoptosis.
Hypoxia-Inducible Factor-1α (HIF-1α) and VEGF suppression: Reduces HIF-1α levels and VEGF signaling, impairing angiogenesis and enhancing radiosensitivity.
TGFBI expression inhibition: Suppresses TGFBI via ERK signaling pathway, reducing migration and invasion in osteosarcoma.
Cancer stem cell targeting: Reduces stem cell markers like CD44 and CD24, inhibits tumorsphere formation, and disrupts cancer stem cell-associated signaling pathways.
Autophagy activation: Promotes autophagic cell death via ER stress and disruption of cellular homeostasis.
Induction of apoptosis: Activates cleaved caspase-3 and downregulates anti-apoptotic proteins, leading to apoptosis in multiple cancer types.
Epithelial-to-mesenchymal transition (EMT) inhibition: Upregulates E-cadherin while downregulating vimentin and MMPs, reducing invasion and metastasis.
Immune evasion reduction: Decreases immunosuppressive cells, such as myeloid-derived suppressor cells (MDSCs), in tumor microenvironments, enhancing immune responses.
Combination therapy potential: Enhances sensitivity to chemotherapeutic agents like cisplatin and erlotinib, and synergizes with radiation to improve efficacy.
Reactive oxygen species (ROS) generation: Elevates ROS levels, causing oxidative stress and apoptosis in cancer cells.
Radiosensitization: Enhances the effects of radiation therapy by sensitizing cancer cells to radiation-induced damage.
Notch signaling suppression: Reduces Notch receptor expression and downstream effectors, contributing to decreased tumor growth and stemness.
Cell cycle arrest: Induces G1 or G2 phase arrest by modulating cyclin-dependent kinases and their inhibitors.
Protein ubiquitination and degradation: Facilitates proteasomal degradation of key oncogenic proteins, including androgen receptor variants.
Selective toxicity against p53-deficient cells: Niclosamide preferentially impairs the growth of p53-deficient cells and induces metabolic alterations like arachidonic acid accumulation in such cells, leading to apoptosis.
Energy metabolism interference: Disrupts macropinocytosis, SLC38A5-mediated amino acid entry, and H⁺-coupled nutrient transport pathways, leading to nutrient starvation and metabolic disruption in glucose, glutamine, and fatty acid utilization.
Perturbation of Ca²⁺ homeostasis: Triggers intracellular calcium fluxes, affecting calcium-dependent signaling and metabolic processes.
Modulation of epigenetic regulation: Influences epigenetic mechanisms, altering gene expression linked to cancer survival and resistance.
Induction of lipid oxygenation genes in wild-type p53 cells: In cells with functional p53, induces genes involved in lipid metabolism, which counteract metabolic stress imposed by niclosamide.
Inhibition of glutathione synthase (GS): Reduces glutathione levels, increasing oxidative stress and contributing to metabolic and cell death.
Downregulation of nuclear factor of activated T-cells (NFAT) activity: Reduces NFAT activity, impacting cell proliferation and survival.
Decreased RUNX2 expression: Downregulates RUNX2, which is crucial for cancer growth and metastasis.

Note: Standard niclosamide should not be used due to its poor bioavailability, which limits its absorption from the gastrointestinal tract into the bloodstream. While this characteristic is advantageous for treating intestinal parasites, it is unsuitable for cancer treatment. Liposomal niclosamide, on the other hand, significantly enhances the drug’s absorption and extends its duration of action. This version offers superior therapeutic efficacy for cancer treatment (click here).

Citations:

Sulfasalazine:

Mechanisms of action:

Targeting xCT antiporter and redox homeostasis to induce oxidative stress: Sulfasalazine inhibits the xCT cystine/glutamate antiporter, reducing cystine uptake essential for intracellular glutathione (GSH) synthesis. This disruption of cystine availability depletes GSH, leading to oxidative stress through increased reactive oxygen species (ROS). The imbalance in redox homeostasis undermines cancer cells’ antioxidant defenses, triggering nutrient starvation, autophagic processes, apoptotic cell death, and heightened susceptibility to oxidative damage.
Reduction of tumor growth across multiple cancers: Sulfasalazine suppresses growth in various cancers, including prostate cancer, hepatocellular carcinoma (HCC), lymphoma, and breast cancer, both in vitro and in vivo.
Selective cytotoxicity: Sulfasalazine preferentially affects cancer cells due to their higher dependency on extracellular cystine, sparing normal cells and minimizing toxicity.
Targeting cancer stem cells: Sulfasalazine effectively eliminates cancer stem-like cells by disrupting redox balance, reducing tumor recurrence and aggressiveness.
Suppression of chemotherapy resistance: By depleting GSH, sulfasalazine enhances the efficacy of chemotherapeutic agents, overcoming glutathione-mediated drug resistance.
Synergistic effects with other treatments: Sulfasalazine enhances the efficacy of ROS-inducing therapies, such as vitamin C and chemotherapeutic drugs, by complementing their mechanisms of action.
Inhibition of tumor microenvironment support: Sulfasalazine disrupts the tumor microenvironment by reducing macrophage-mediated cysteine supply and impairing stromal cell support, starving cancer cells of critical nutrients.
Induction of autophagy and apoptosis: Sulfasalazine-mediated ROS accumulation activates autophagic pathways and apoptotic signaling, contributing to cancer cell death.
Reduction of metastasis and invasiveness: By inhibiting xCT-related signaling, sulfasalazine reduces cancer cell invasiveness and metastatic potential, particularly in aggressive cancers.

Citations:

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