The Biophysics of Cancer

Cancer is often misunderstood as a genetic disease, but at its core, it is a disorder of cellular energy and signaling. Despite the $7.3 billion spent annually on cancer research in the United States, the prevailing medical model remains locked in outdated paradigms, emphasizing genetic mutations while overlooking the fundamental biophysical processes that drive oncogenesis. This reductionist approach has led to standardized treatments that yield limited success, while alternative models exploring the metabolic and biophysical roots of cancer have gained traction.

Cancer is not a singular disease but a complex, adaptive biological state driven by fundamental disruptions in energy metabolism, cellular signalling, and environmental interactions. At its core, cancer emerges from mitochondrial dysfunction and metabolic inflexibility, forcing cells into a survival-based fermentative metabolism (Warburg effect) rather than efficient oxidative phosphorylation. This metabolic shift fuels uncontrolled proliferation, immune evasion, and genomic instability, hallmarks that allow cancer cells to thrive despite hostile conditions. Cancer cells bypass apoptosis, induce angiogenesis for sustained nutrient flow, and hijack inflammatory and immune pathways to create a microenvironment conducive to their survival. Additionally, cancer exhibits epigenetic plasticity, allowing it to adapt rapidly to therapy by silencing tumor suppressors and activating oncogenes. Beyond genetic mutations, cancer must be understood as a dysregulated energy state, where biophysical and biochemical alterations in water structure, circadian rhythm, and electromagnetic signaling create the conditions for malignant transformation. Without addressing these foundational disruptions in cellular energy and environmental coherence, conventional treatments will continue to target symptoms rather than the true origins of cancer

The Biophysical and Biochemical Path to Cancer

A healthy cell maintains strict control over its volume, redox state, and metabolic pathways through mitochondrial function and structured water. Mitochondria, often called the powerhouse of the cell, are far more than energy producers they regulate apoptosis, redox balance, and energy transduction turning on or off genes in the nucleus, forming the backbone of cellular integrity. When mitochondrial function declines, the cell experiences an energy deficit and compensates by enlarging and oncogenes can turn on. If this deficit persists, the cell shifts from oxidative phosphorylation to predominantly glycolysis (Warburg metabolism), regardless of oxygen availability, as a last-ditch survival mechanism and if this goes on for long enough hypoxia occurs, apoptosis is inhibited opening up proliferative and uncontrolled cell growth as a survival strategy.

At the molecular level, cancerous transformation is deeply tied to deuterium fractionation. Inside a healthy cell, water exists in two primary forms: light water (low-to-no-deuterium H₂O) and heavy water (D₂O-enriched H₂O). Light water is the preferred biological medium, making up 99 out of every 100 molecules. It facilitates intracellular and extracellular communication, oxygen transport, nutrient delivery, waste removal, and energy generation, forming the structural and functional foundation of the human body. Crucially, this structured water is primarily produced within mitochondria and continuously recycled to sustain life.

In a healthy cell, mitochondria establish a highly structured exclusion zone (EZ) water network, optimizing proton transfer, ATP synthesis, and charge separation. However, when deuterium levels rise above 120 ppm, this structured network begins to collapse, setting off a cascade of metabolic dysfunction. Excess deuterium slows proton transfer, impairs enzymatic function, and disrupts molecular kinetics, initiating membrane permeability changes, oxidative stress, hypoxia, and mitochondrial inefficiency. This deuterium burden collapses energy production kinetics, disturbing the urea cycle, TCA cycle, and ATP synthesis and pushing the cell into a cancerous state characterized by inhibited apoptosis, metabolic dysregulation, unstructured water, glucose dependence, and cellular swelling, the hallmarks of malignancy.

The loss of structured water means the very medium that sustains coherent biological function is compromised, leaving the cell trapped in a self-perpetuating disease state where survival overrides regulation the final step into cancer pathology.

Cellular Volume, Ion Transport, and Energy Decline

Cancer cells exhibit unique biophysical properties compared to normal cells. They universally upregulate the sodium/hydrogen exchanger (NHE1), disrupting intracellular pH, ion balance, and hydration states. This shift leads to increased sodium influx, intracellular swelling, and a loss of net-negative charge. In a healthy cell, structured EZ light water and functional mitochondria maintain a robust redox potential across the mitochondrial inner membrane (between -400 and -200mV), but cancerous mitochondria and water now containing more deuterium (heavy water) exhibit a reduced electrical charge (below -200mV), reflecting metabolic inefficiency and excessive ROS (reactive oxygen species) production. This altered environment promotes uncontrolled cell division and prevents normal apoptotic mechanisms from engaging, meaning they become zombie-like cells that don’t die.

Cancer cells exhibit high mitotic indices, meaning they divide rapidly and uncontrollably, a direct consequence of cell swelling and metabolic rigidity. The Warburg effect, which shifts cells toward dominant glucose metabolism, is an extremely inefficient energy production method, requiring up to 60 times more glucose to produce the same ATP as a healthy cell. This excessive glucose demand places extreme stress on surrounding tissues, creating a hypoxic, acidic, low voltage microenvironment that further fuels cancer progression.

Cancer’s Relationship with Water and Light

Water plays a crucial role in cancer development. Blood, which is 93% water, serves as the primary medium for nutrient transport, waste removal, and bioelectrical signaling. Albumin, the main carrier protein in blood, is produced in the liver and contributes to oncotic pressure, which maintains fluid balance between blood vessels and tissues. Chronic hypoalbuminemia leads to a progressive loss of structured water, reducing the EZ and compromising redox signaling, ultimately paving the way for oncogenesis.

Furthermore, mitochondrial function including the electron transport chain (ETC) is deeply responsive to light absorption from our biological surfaces (eyes, skin gut and lungs). Light frequencies in the infrared (IR-A, 780nm to 1,300 nm) and ultraviolet (UV-A, 320-390 nm) wavelengths regulate mitochondrial size and energy output. We know this from Roeland van Wijk, Dr. Alexander Wunsch’s and Dr. Fritz Albert Popp’s research. Cancer cells lack proper light absorption dynamics, leading to mitochondrial swelling and disorganized respiratory proteins. The absence of coordinated Biophotonic signaling within cancer cells means they emit excessive Ultraweak UV Biophotons, the key biophysics indicator of disease progression.

The Role of Calcium and Mitochondrial Dysfunction in Cancer

Mitochondria have an insatiable appetite for calcium (Ca²⁺), which regulates apoptosis, bioenergetics, and metabolic signaling. However, excessive calcium influx leads to mitochondrial depolarization and structural expansion, triggering stress responses and altering ATP synthesis. Blue light (400-480 nm) and nnEMFs exacerbate calcium efflux, further damaging mitochondrial integrity. The MICU1 and MCU (mitochondrial calcium uniporter) proteins tightly regulate calcium homeostasis, but in cancerous states, this balance is lost, leading to further metabolic dysregulation.

Interestingly, the relationship between calcium, amino acid codons, and seasonal light exposure is well-documented. Aromatic amino acids (tryptophan, tyrosine, and phenylalanine) absorb UV light and regulate dopamine synthesis, which is why a Warburg metabolism is inherently a light-based disorder. In cancerous conditions, the codons responsible for biogenic amine synthesis become dysregulated, altering hormone panels and neurotransmitter production.

Cancer as an Evolutionary Regression

Cancerous tissues exhibit traits reminiscent of embryonic placental cells, which aggressively divide, form new blood vessels (angiogenesis), and evade immune detection. This phenomenon suggests that cancer is a form of evolutionary regression—cells reverting to primitive survival strategies when faced with chronic environmental stressors. The placenta, which grows unchecked until fetal pancreatic enzymes signal it to stop, shares striking similarities with malignant tumors. Both exploit metabolic reprogramming, immune suppression, and hypoxic adaptation to sustain unchecked growth.

This perspective raises critical questions about the evolutionary role of cancer and why standard treatments fail. If cancer represents a deeply ingrained survival mechanism, then conventional cytotoxic treatments which indiscriminately target rapidly dividing cells fail to address the root cause of mitochondrial dysfunction. This gap in understanding has led to the rise of alternative therapies, some with varying success, as patients seek solutions outside the mainstream oncology framework.

While xenoestrogens from plastics and other endocrine disruptors synthetically mimic natural hormones, and factors like heavy metal toxicity, glyphosate and pesticide exposure, persistent viral, fungal, or bacterial infections, and disruptions in DNA methylation or histone modifications (epigenetically turning genes on or off) contribute to cancer, the biophysics and biochemistry of mitochondria and water must be addressed first, as they form the foundation for true cancer reversal and long-term survival.

Spontaneous Remission, Screening, and the Unanswered Questions

One of the most perplexing aspects of cancer is spontaneous remission—cases where advanced tumors regress without medical intervention. These occurrences are actually quite common and usually go unreported. This is evidence that the body can heal even from the most toxic states if given the opportunity to do so. These occurrences deeply challenge, and I would say prove wrong the centralized medicine deterministic view of cancer as an irreversible genetic condition. The biophysical understanding of cancer suggests that restoring coherent energy flow, cellular hydration, and mitochondrial efficiency play the key role in these remissions for which centralized medicine has no explanation.

Every single human on earth has cancer cells within them, when we sleep and undergo apoptosis (programmed cell death) and autophagy (cellular renewal) these cancer cells or cells about to turn cancerous are cleared out and replaced with better functioning cells. If sleep has gone awry in your life leaving you unable to sleep through the night without waking or getting up to go to the bathroom, low amounts of deep and REM sleep, low Heart Rate Variability (HRV) or less than 6h sleep duration consistently, then your well on your way to turning on your oncogenes and allowing cancer cells to continue being created in numbers the body will struggle to control. However, if you begin reversing this process, the body can get on top of this cancer cell creation and begin to heal once again. The body thrives when the number of cancer cells remains low but can be significantly affected if just a few too many accumulate or grow. However, out of 100 trillion cells in the body, if 500 billion (0.05%) are cancerous, you still have far more well-functioning cells to overcome the dysfunctional ones. The choice is yours if you want to heal or not.

Cancer screening, while valuable for early detection, is a double-edged sword. Overdiagnosis often leads to unnecessary interventions, reinforcing a fear-based medical model that prioritizes treatment over understanding. The widespread reliance on genetic screening and tumor markers fails to account for the dynamic nature of mitochondrial function, epigenetic signaling, and environmental interactions, the real reason cancer grows and metastasizes.

Conclusion

Cancer is not a random event but a predictable consequence of biological energy collapse, mitochondrial dysfunction, and disrupted biophysics. The centralized traditional oncological framework, despite its vast funding, has yet to integrate biophysics, circadian medicine, and water science (aquaphotomics) into its models where the mitochondrial genome is under the microscope rather than the nuclear genome. Until these paradigms shift, mainstream treatments will remain ineffective at addressing cancer’s true origins.

Understanding cancer requires a fundamental reexamination of life at the molecular and atomic levels, integrating biophysics, metabolism, and environmental influences. Only then can we begin to grasp why cancer emerges, how it varies across tissues, and why conventional treatments continue to fall short despite decades of research and hundreds of billions of dollars. 

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