Cancer treatments remain notoriously dangerous and unreliable, and no theory of malignancy has been confirmed. The following passage from “The Secret History of the War on Cancer” by Devra Davis summarizes the DNA paradigm that has come to dominate cancer research, treatment and theory:

“Slivers of complex helical chains of DNA can fix or worsen damage that comes about just from being alive.  Genes tell cells when to die, when to get fixed, and how to mesh with other signals in the body.  Ordinarily, attacks on our genetic base are fixed day in and day out by a series of well-honed repair processes that occur within the blink of an eye with a constancy that approaches the amazing.  Without these ongoing repairs, none of us would long survive.

All of us contain a remarkable array of genes, proteins and enzymes that work to keep bad cells in check and tell dangerous ones to die. As we age, the vibrancy of these repair systems and the rate at which they keep springing into action declines, just like a rubber band that eventually gives out from overuse.”

Although this passage typifies prevailing beliefs about cancer, it is based on unproven assumptions. There is no proof that DNA plays any significant role after embryological development is complete. Tissue maintenance, tissue repair, cell death (apoptosis) and hemodynamic physiology all remain unexplained. To her credit, Ms. Davis, a professional epidemiologist, proceeds to note several shortcomings in the idea that defective DNA activity explains cancer:

“But an aging population does not explain why five times more men and women get brain cancer in America than in Japan. Nor do we understand why rates of testicular cancer in men under age forty have risen 50 percent in one decade in most industrial nations, why women of Generation X are getting twice as much breast cancer as their grandmothers did, or why young black women get and die from breast cancer in greater numbers than their white counterparts.”

Having noted the inability of the DNA paradigm to explain these and other cancer phenomena, Ms. Davis proceeds to describe how environmental factors such as toxic chemicals cause cancer, and how major corporations have actively suppressed this information.  She also explains how the DNA paradigm became dominant. Cancer was a mysterious, terrifying, untreatable, excruciatingly painful, and inexorably fatal condition when Goodman and Gilman of pharmacology textbook fame began experiments to treat leukemia with toxic war gases during WWII.  The federal government funded their research. Their reasoning was that these toxic agents might be useful for treating leukemia, which is characterized by elevated white cell counts. Sure enough, the toxic chemicals reduced white cell counts. The researchers then employed this treatment on a mouse with a solid tumor.  The tumor shrank dramatically, and though their experiments were far less successful on subsequent rodents, they proceeded to treat a silversmith with lymphosarcoma with the same toxic chemicals. His tumors also shrank. Even though the patient died soon thereafter, they concluded that cancer could be treated using toxic agents. Coincidentally, Watson and Crick discovered the DNA mechanism around the same time.  It seemed obvious at that point that defective DNA was the cause of cancer, and this idea quickly became entrenched.  It provides the rationale for using radiation therapy, chemotherapy and surgery to destroy the “defective” cancer cells.  As in the case of most established medical concepts, the idea has stubbornly resisted change.  One of the most obvious shortcomings of this treatment concept is that surgery, radiation therapy and chemotherapy all increase the risk of other, seemingly unrelated forms of cancer, even if they successfully eradicate the original cancer.  Also, malignant cells cannot be distinguished from normal wound healing cells. Furthermore, malignancy is invariably accompanied by increased blood viscosity and coagulability, which increases morbidity and mortality from infarction, pulmonary embolus and other forms of coagulopathy. Deaths caused by such hypercoagulability phenomena are seldom attributed to cancer, even though cancer is the underlying cause of death.  This tends to exaggerate cancer cures and obscure the true morbidity and mortality of cancer. The DNA paradigm does not explain these observations, and the theory that defective DNA is the cause of cancer has never been proven.

Stress theory provides a simple and testable alternative explanation of disease, malignancy and apoptosis that is independent of DNA activity. A wide variety of stressful stimuli and stressful forces activate the Stress Repair Mechanism (SRM). The sum total of these stressful stimuli and stressful forces determines the magnitude, location and duration of SRM activity. Prolonged and severe stress causes SRM hyperactivity that generates pathological quantities of thrombin, soluble fibrin and insoluble fibrin. This SRM hyperactivity explains disease manifestations and disease relationships. DNA does not control SRM activity, but SRM activity can increase cell proliferation, which increases DNA replication. SRM activity can also increase immune cell activity.  This explains why SRM activity is often confused with and mistakenly attributed to increased DNA and immune activity.

Stressful stimuli activate the sympathetic nervous system, which increases blood coagulability, blood viscosity, capillary hemostasis, and blood flow resistance. Stressful forces that disrupt tissues directly expose blood enzymes to tissue factor in extravascular tissues.  The resulting enzymatic interaction forms a viscoelastic blood clot that temporarily isolates flowing blood from extravascular tissues. The selectively permeable blood clot then governs contact between the blood enzymes and tissue factor in the damaged tissues beneath its surface to regulate thrombin generation in the damaged tissues. The clot maintains thrombin levels within a narrow range to energize and optimize tissue repair. The resulting moderate thrombin elevations energize chemotaxis that attracts repair cells towards the damaged tissues, inflammation that loosens cell connections to enable repair cells to enter the damaged tissues, cell proliferation and differentiation that replaces damaged tissues, immune cell activity that removes debris and fights infection, and capillary formation that supplies proliferating repair tissues with blood. As the tissue repair process proceeds to completion, it gradually restores the normal barrier between extravascular tissues and flowing blood. As this happens, thrombin levels decline within the damaged tissues, so that repair cell activity declines below a critical level, whereupon the thrombin-dependent repair cells undergo apoptosis, or programmed cell death. This enables wound closure. The thrombin-dependent clot likewise disintegrates and disappears. This concludes the normal repair process. 

Malignancy is an abnormal state of uncontrolled, self-sustaining tissue repair activity that sometimes occurs due to a combination of prolonged and excessive stressful forces and stressful stimuli.  This exaggerates SRM activity, causing excessive thrombin generation that excessively energizes tissue repair cells, so that they proliferate at excessive rates and abnormally invade and disrupt adjacent tissues. This causes additional stressful nervous stimulation and tissue factor release that sustains the malignant process.  It also explains why the risk of malignancy is increased by prolonged and excessive exposure to environmental stresses, such as toxic chemicals, surgery, uncontrolled infection, and chronic diseases. It likewise explains why the risk of cancer is increased in the aftermath of conventional cancer treatments, including surgery, radiation therapy and chemotherapy, even if these misguided treatments successfully eradicate the original cancer tissues. The SRM explains how cancer can be cured quickly, safely, reliably and comfortably for the patient using readily conventional medications and techniques that reduce thrombin generation below the threshold necessary to sustain the malignant process.

Stress theory also explains why vitamin D deficiency increases the risk of cancer and disturbs tissue repair. Actin is an intracellular protein that is released into flowing blood by cell trauma. Vitamin D plays a major role in the breakdown and elimination of fibrillar strands of actin that become entangled in the viscoelastic clot formed by insoluble fibrin. The presence of actin within the viscoelastic clot disrupts the ability of the clot to regulate contact between blood enzymes and the damaged tissue beneath its surface, causing excessive thrombin production that increases the risk of malignancy. Vitamin D supplements enhance the digestion of actin, and therefore enhance the ability of the clot to regulate the tissue repair process and prevent malignancy.