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Treatment Approach

Strategic Warfare Against Cancer: A Combined Defensive and Offensive Approach

In research published in 2004 and again in 2023, many contemporary cancer drugs were found to have a limited impact on enhancing the quality of life or prolonging the lives of those with metastatic cancer (click here and here). Such cancer is often associated with reduced survival rates because alternative approaches are limited when cancer cells evolve and acquire multi-drug resistance. New treatment approaches are needed to substantially improve outcomes. Fortunately, research scientists and forward-thinking physicians have been hard at work developing innovative approaches to fight cancer and improve the chances for long-term remission.

Our novel approach draws inspiration from an unexpected but powerful source: ancient military strategy. As Sun Tzu, the Chinese military strategist (544-496 BCE), wrote in his enduring treatise The Art of War, “Invincibility lies in the defense.” This principle, which has guided military campaigns for over two millennia, can be powerfully applied to cancer treatment through a strategic combination of defensive and offensive measures. Before launching a major offensive against cancer, we must first secure our position and weaken the enemy’s strongholds. 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.

The Defensive Phase: Creating an Inhospitable Environment for Cancer

The defensive phase employs bicarbonate therapy to systematically weaken cancer’s position through multiple mechanisms. Cancer cells create and thrive in an acidic environment, and bicarbonate therapy neutralizes this acidic fortress, disrupting cancer’s protective barrier and forcing cancer cells to expend extra energy maintaining their preferred acidic state. Through this process, abnormal blood vessels in tumors are normalized, which improves oxygen delivery to the tumor site, enables more effective drug delivery, and reduces tumor hypoxia. Additionally, matrix metalloproteinases (enzymes that enable cancer spread) are inhibited, reducing cancer cells’ ability to break away and spread, effectively blocking escape routes and preventing cancer from establishing new colonies.

The neutralization of the acidic environment profoundly affects immune function and cancer stem cells. Acidic environments typically suppress immune cell function, but by neutralizing the acidity, T-cells and natural killer cells can operate effectively, allowing the immune system to better recognize and attack cancer cells, improving overall immune surveillance. Furthermore, the alkaline environment reduces the population of cancer stem cells, which are responsible for tumor regrowth and treatment resistance, effectively cutting off cancer’s ability to regenerate and diminish treatment resistance potential. Progress in this defensive phase can be monitored through urine pH, with a target of 7.5-8.0 signaling successful alkalinization and confirming defensive preparations are complete, giving the green light for proceeding to the offensive phase.

The Offensive Phase: Launching a Precision-Guided Attack

Once the defensive groundwork is laid, the offensive phase employs enhanced high-ozonide oil to deliver a powerful oxidative assault through multiple mechanisms. The primary attack mechanisms include direct targeting of cancer cell mitochondria, cardiolipin oxidation in mitochondrial membranes, triggering of apoptosis (programmed cell death), and calcium release causing cellular destruction. This core offensive strategy is enhanced by several compounds, each targeting specific cancer defense mechanisms. Sulfasalazine blocks glutathione synthesis, removing the primary antioxidant defense and making cancer cells vulnerable to oxidative stress. Auranofin disrupts the thioredoxin system, eliminating secondary antioxidant defense and further weakening cancer’s protective mechanisms. Chrysin suppresses Nrf2-mediated responses, preventing adaptation to oxidative stress and blocking cancer’s ability to develop new defenses. Niclosamide induces additional mitochondrial stress, promotes autophagy (cellular self-destruction), and creates multiple paths to cancer cell death.

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 approach also effectively prevents resistance through multiple simultaneous mechanisms that prevent adaptation, block escape routes, and disable survival mechanisms. This comprehensive strategy creates a “perfect storm” against cancer cells while protecting normal cells, with the carefully sequenced deployment of defensive and offensive measures maximizing the therapeutic impact while minimizing the potential for resistance or escape.

The success of this approach lies in its systematic nature and the synergy between its components. By first creating an inhospitable environment for cancer cells through bicarbonate therapy, then launching a powerful oxidative assault enhanced by multiple defensive system disablers, the strategy effectively corners cancer cells while protecting healthy tissue. The careful monitoring of progress 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.

Our comprehensive monthly fee of $1850 includes custom-synthesized oral liposomal niclosamide and provides continuous access to Dr. Thomas’s expertise. This represents a significant value compared to international treatment options, which often range from $7,000 to $20,000 weekly or $40,000 to $120,000 for experimental procedures with 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). In cancer cells, cardiolipin’s altered structure 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 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 that 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:

Selective toxicity against p53-deficient cells: Niclosamide preferentially impairs the growth of p53-deficient cells and p53 mutant patient-derived ovarian xenografts, highlighting its targeted action against cancer cells with specific genetic vulnerabilities.
Mitochondrial uncoupling and energy metabolism interference: It induces mitochondrial uncoupling, affects mitochondrial function, and disrupts energy metabolism in cancer cells, leading to metabolic stress, cell death through apoptosis, and autophagy.
Induction of apoptosis and cell cycle arrest: Niclosamide triggers apoptosis in cancer cells, disrupts cell cycle progression, and enhances cleavage of caspase-9, caspase-3, and PARP1, contributing to the inhibition of tumor cell growth.
Alteration of metabolome profile and arachidonic acid accumulation: It alters the metabolic landscape, particularly leading to the accumulation of arachidonic acid in p53-deficient cells, which is implicated in apoptosis.
Perturbation of Ca²⁺ homeostasis: By triggering intracellular calcium fluxes, niclosamide affects calcium-dependent processes, leading to changes in cell signaling and metabolism.
Inhibition of various signaling pathways: Niclosamide downregulates critical cancer signaling pathways, including NF-κB, Wnt/β-catenin, Notch, ROS, mTORC1, STAT3, and HIF-1α, suppressing cancer cell energy metabolism, proliferation, growth, and survival.
Targeting cancer stem cells: Niclosamide targets cancer stem cells, addressing the challenges of tumor recurrence and metastasis.
Inhibition of tumor growth and metastasis: It exhibits anti-metastatic properties, inhibiting cancer cell migration, invasion, and overall tumor growth.
Enhancing chemo and radio sensitivity: Niclosamide improves the sensitivity of cancer cells to chemotherapy and radiotherapy, making it a valuable adjunct in cancer treatment.
Synergistic effects with cancer therapies: Demonstrating synergy with existing cancer treatments, niclosamide can potentiate the therapeutic effects against cancer.
Modulation of epigenetic regulation: It influences epigenetic mechanisms, altering gene expression related to cancer survival and resistance.
Altering tumor microenvironment: Niclosamide may improve the therapeutic response by modulating the tumor microenvironment and affecting the cancer’s immune evasion capabilities.
Induction of lipid oxygenation genes in wild-type p53 cells: In cells with functional p53, niclosamide induces genes involved in lipid metabolism, which helps in counteracting the metabolic stress imposed by the drug.
Inhibition of glutathione synthase (GS): Inhibits GS, reducing glutathione levels and increasing oxidative stress, contributing to cell stress and death.
Downregulation of nuclear factor of activated T-cells (NFAT) activity: Decreases NFAT activity, impacting cell growth and viability.
Decreased runt-related transcription factor 2 (RUNX2) expression: RUNX2’s central role in the growth and spread of various cancers makes it an attractive therapeutic target.

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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