It is an open secret that conventional medical theory cannot explain cancer or offer effective treatments. Cancer is the most compelling of all medical subjects.(1) For most of medical history it has been regarded as a mysterious systemic sickness with localized manifestations that is best left untreated. Its incidence has increased with industrialization to the point that nearly everybody knows someone who has suffered and died of it. In her book “The Secret History of the War on Cancer,”(2) Devra Davis details the events that reversed the traditional view of cancer, and produced the presently prevailing presumption that cancer is a localized disease with systemic effects that can be cured using toxic chemicals, harmful radiation, and mutilating surgery — despite overwhelming evidence that these counterproductive treatments cause cancer and prevent its spontaneous remission.(3-7) Prevailing treatments only temporarily shrink or destroy visible tumors, whereupon they subsequently re-appear and are more resistant than ever to treatment, or new and seemingly unrelated tumors mysteriously emerge in distant locations. Meanwhile, cancer is inexplicably accompanied by systemic hypercoagulability of blood, so that most cancer patients die quietly and prematurely of strokes, heart attacks, and pulmonary emboli that are seldom acknowledged as cancer-related, so that cancer is far deadlier than statistics reveal. The story is depressingly familiar: cancer patients bravely “fight” their cancer by undergoing torturous treatments and mutilating surgeries, only to die before their time. As Janeen Interlandi wryly observed in Scientific American, “Today’s cancer chemotherapy consists of little more than a dismal array of toxic drugs that kill healthy cells along with cancerous ones. Physicians must often play a deadly game of trial and error, hoping to find the right dose of the right medicine before time runs out.”(8)
A Fresh Explanation
The mammalian stress mechanism provides a fresh explanation of cancer that is consistent with known science: cancer is normal tissue repair that becomes self-sustaining (i.e., “malignant”) due to unrelenting environmental stress that induces harmful stress mechanism hyperactivity. Such environment stress includes toxic chemicals, smoking, alcohol abuse, excessive radiation, sepsis, surgery, trauma, fear, and anxiety.
All tissue repair is naturally hyperactive. Nature wants to get the repair job done quickly. Repair fibroblasts are drawn to an injured area by thrombin. Fibroblasts normally proliferate just like cancer cells — including, because of the speed of proliferation, the occasional cell with broken chromosomes or increased sensitivity to toxic chemicals and radiation. Eventually, the stress resolves and repair slows to a background level maintained by the stress mechanism. That is part of the mechanism’s purpose.
But when unrelenting stress is present (environmental, nociception, psychological, emotional) fibroblasts can continue their hyperactivity past the point of healing, or even if no healing is necessary. This is a cancer condition. Repair cell fibroblasts intrude into and disrupt normal tissues, which harmfully releases tissue factor and stimulates nervous activity, causing further stress mechanism stimulation. The stress mechanism hyperactivity becomes self-sustaining — but the fibroblasts are the same cells seen in “normal” tissue repair.
There is no difference between “cancer” cells and “normal” cells. There is no evidence that “defective DNA” causes cancer, and cancer cells cannot be distinguished either microscopically or metabolically from normal tissue repair cells during the most intense phase of tissue repair and wound healing. They are the same. It is stress mechanism hyperactivity from environmental stress that causes and sustains cancer.
Interestingly, mammals appear to be more vulnerable to cancer than other vertebrates, and humans appear to be more vulnerable to cancer than other mammals. I suspect that this is partly due to the exaggerated intelligence of mammals, which harmfully exaggerates fear and anxiety. The mammalian stress mechanism is better adapted to cold environments than its reptilian antecedent, but only at the price of inferior tissue repair and exaggerated food requirements. For example, mammalian red blood cells lack a nucleus, and thus cannot participate in tissue repair — as can “lower” animals. This is discussed in detail in the chapter that describes the “unified theory of biology” in my book “50 Years Lost in Medical Advance,” now available via Amazon.
Malignancy versus Normal Tissue Repair
To understand malignancy, one must first understand how the mammalian stress mechanism regulates thrombin to energize tissue repair. Thrombin is the “universal enzyme of extracellular energy transformation.” Thrombin elevations increase the ability of cells to utilize ATP (adenosine tri-phosphate), which is the “universal medium of cellular energy storage.” The stress mechanism elevates thrombin levels in damaged tissues to energize the cellular activities that repair damaged tissues, but it simultaneously prevents excessive thrombin elevations that cause dangerous repair cell proliferation that can invade and disrupt adjacent normal tissue. Such disruption of normal tissues can cause cancer.
The key to thrombin regulation during tissue repair is the viscoelastic blood clot.
Mammalian tissue repair occurs in a predictable sequence of events beginning with viscoelastic clot formation. Tissue damage disrupts the vascular endothelium, a delicate layer of cells that lines the inner surface of all blood vessels and isolates blood enzymes from extravascular tissues. Trauma thus exposes tissue factor in extravascular tissues to blood enzymes. This activates blood enzyme factor VII. Trauma simultaneously activates nervous tissue disruption sensors called “nociceptors” in the skin and internal organs. These generate nervous activity called “nociception.” The nociception is communicated via sensory nerves and the spinal cord to sympathetic ganglia in the chest and abdomen. This releases von Willebrand Factor hormone (VWF) into flowing blood. The nociception is also communicated to the brain, where consciousness interprets it as “pain,” which further exaggerates the release of VWF. The VWF stabilizes and activates blood enzyme factor VIII, which enables viscoelastic clot formation. The resulting enzymatic interaction of blood enzyme factors VII, VIII, IX and X is focused on the site of tissue damage because factor VII activation is the “trigger” of the enzymatic interaction. The other enzymes remain inert in the absence of factor VII activation, and factor VII is activated at the site of tissue damage. Therefore, clot formation occurs at the site of tissue damage rather than throughout the vascular system. The enzymatic interaction accelerates thrombin generation to energize the conversion of fibrinogen (a protein continuously produced by the liver) to strands of insoluble fibrin that bind blood cells into a viscoelastic clot that covers the site of tissue damage and isolates damaged tissues from blood enzymes.(9-11) The viscoelastic clot is impermeable to Factor VIII because of its gigantic molecular size. Since factor VIII is essential for generating insoluble fibrin, this limits clot formation to the site of tissue damage.
The viscoelastic clot regulates tissue repair. It allows the slow penetration of factors VII and X, which interact with exposed tissue factor in the damaged tissues beneath the clot to generate moderate amounts of thrombin which energize the cellular activities that repair tissues. The thrombin elevations also activate TAFI (Thrombin-Activated Fibrinolysis Inhibitor) that strengthens the clot and reduces its permeability. The clot thus governs thrombin generation in the damaged tissues beneath its protective surface. This prevents excessive thrombin generation that causes malignancy, and maintains optimal thrombin levels to repair tissues.
Thrombin is the “universal enzyme of extracellular energy transformation.” It governs the cellular utilization of extracellular ATP (adenosine tri-phosphate) by activating specialized thrombin receptors on the outer surface of repair cells that are called “protease activated receptors” (PAR). Thusly energized and activated, the repair cells normally proceed to repair and replace damaged tissues in a predictable sequence:
- Repair cells produce electromagnetic signals and release chemokines, cytokines, prostaglandins, bradykinins, and other cellular hormones to communicate with one another and enable their tissue repair activities.(12, 13)
- The cellular hormones dissolve the basement membrane that holds cells in tight formations and loosens cell connections to enable repair cells to move from adjacent undamaged tissues into the traumatized tissues.
- Thrombin elevations in damaged tissues attract repair cells from adjacent undamaged tissues into the area of tissue damage. They move through the tissues loosened by inflammation to begin their repair activities in the damaged tissues.
- Fibroblast repair cells proliferate and produce collagen to form “granulation tissue” that fills empty spaces and binds damaged tissues together.
- Angiogenesis produces capillaries that perfuse the repair tissues with oxygen and nutrients.
- Immune activity generates antibodies that resist infection and immune cells that engulf and remove bacteria and foreign debris.
- Elevated metabolic activity entailed by intense fibroblast mitosis and activity generates heat and elevates the temperature of the healing tissues.
- Proliferating fibroblasts differentiate and de-differentiate to repair and replace damaged tissues.
- As the repair process nears completion, the proliferating vascular endothelium restores the normal barrier between flowing blood and healing tissues, and this gradually lowers thrombin generation to normal levels.
- As thrombin generation declines toward normal, thrombin starvation triggers cellular apoptosis, which causes the granulation tissues to shrink and draw wound edges together.
- Declining thrombin levels cause the viscoelastic clot to disintegrate and disappear.
With cancer, this sequence is slightly different.
Malignancy
Excessive, unrelenting stress on account of combinations of toxic chemical exposure, excessive radiation, surgery, smoking, trauma, fear, anxiety, and sepsis can induce excessive thrombin generation that harmfully exaggerates fibroblast mitosis and proliferation, and causes proliferating fibroblasts to invade and disrupt healthy adjacent tissues. The invasion and disruption exaggerates the exposure of tissue factor to blood enzymes, stimulates nociception, and elevates thrombin generation. This sometimes causes a self-sustaining (i.e., malignant) process of tissue disruption, tissue factor release, nervous activity, and tumor formation that continuously maintains harmful thrombin elevations and prevents apoptosis and resolution of the repair process.(14, 15)
Cancer seldom kills by invading critical organs and tissues or causing catastrophic bleeding. On the contrary, once this malignant state gets underway, it continuously sheds tissue factor into systemic circulation, causing systemic thrombin generation, inflammation, and conversion of fibrinogen into soluble and insoluble fibrin that elevates blood viscosity and coagulability, undermines tissue perfusion, tissue oxygenation, and organ function, and invites sudden death due to infarction. Alternatively, cancer sometimes culminates in critical illness that manifests as ARDS (adult respiratory distress syndrome) or MOFS (multi-organ failure syndrome).(16, 17)
Tissues with high concentrations of tissue factor are targets for both primary and secondary (metastatic) malignancy as well as primary malignancy. These include lung, brain, retina, autonomic ganglia, nerves, gonads, cervix, placenta, retina, skin, mucosa, and glomeruli.(18) For example, smoking typically causes primary cancer in the lung that metastasizes to the brain. Blood and lymph circulation also influences metastasis. For example, bowel adenomas typically metastasize to the liver, which receives all venous blood drainage from the bowel, causing metastatic liver tumors even though the liver is poor in tissue factor.
Conventional cancer dogma assumes that cancer is caused by “defective DNA” and that mutilating surgery, harmful radiation, and toxic chemicals can cure cancer by eradicating the deranged cells containing the defective DNA. If this dogma were true, then one might expect that malignant tumors would consist of a single type of abnormally proliferating cells. Instead, malignant tumors invariably consist of multiple cell types, all proliferating at various rates.(19) Fibroblast repair cells are prominent, because these cells are especially sensitive to thrombin elevations. Fibroblasts and other cells are sub-specialized to optimize their function in various tissues, so that their microscopic appearance is distinctive. This gives rise to numerous cancer “diagnoses” but these are meaningless, because all cancer is caused by systemic stress mechanism hyperactivity regardless of which type of cell is affected. Eradicating the prevailing cells using surgery, chemotherapy, or radiation doesn’t cure the cancer; it only aggravates the stress mechanism hyperactivity and hastens death.(20) Conventional cancer treatments might thus be compared to pouring gasoline on a fire. If the gasoline is poured fast enough it will smother the fire, but it leaves smoldering embers that threaten to re-ignite explosively and unpredictably. Conventional treatments (surgery, radiation, and chemotherapy) are harmful and counterproductive, because they promote stress mechanism hyperactivity that promotes and sustains malignancy even as they destroy or temporarily shrink cancerous tumors. The systemic malignant state lurks and causes recurrence of the original cancer, or new forms of cancer in distant locations.
The key to curing cancer is treatments that mitigate stress mechanism hyperactivity, halt the self-sustaining malignant state, and restore normal tissue repair that culminates in apoptosis and resolution of the tissue repair process. In theory, this can be safely accomplished within 24 hours using presently available machines, monitors and medications, but before this can be tested and confirmed there must be a revolutionary reversal of the presently prevailing (and profitable) medical dogma.
Here is the cancer treatment implied by the stress mechanism:
- Patients should never be frightened by being told that they have a life-threatening diagnosis.
- Endotracheal anesthesia to enable respiratory support and control inhaled gases.
- Intensive monitoring equivalent to modern anesthesia practice.
- General anesthesia using ½ MAC isoflurane to minimize toxicity and inhibit consciousness and abolish fear and anxiety that elevates harmful sympathetic nervous activity.
- Intravenous fentanyl to maintain respiratory rate between 8-12 breaths/minute and maintain end-tidal CO2 in the range of 60-100 torr to optimize cardiorespiratory function, tissue perfusion, tissue oxygenation, and organ protection.
- Magnesium sulphate under dosage protocols used to treat eclampsia to inhibit thrombin activity.
The available evidence indicates that this treatment should be maintained for a minimum of 24 hours to reduce stress mechanism hyperactivity and induce apoptosis.(21)
Ideally, the magnesium sulphate could be replaced by an intravenous antidote to tissue factor. Research evidence indicates that such a treatment is theoretically possible, and would be extremely useful for treatment of all types of critical illness, but despite this evidence pharmaceutical companies have inexplicably failed to develop such a product.(22, 23)
Notes
1. S. Mukherjee, The Emperor of All Maladies. (Scribner, New York, NY, 2010), pp. 573.
2. D. Davis, The Secret History of the War on Cancer. (Perseus Books Group, New York, N.Y., 2007).
3. T. Jessy, Immunity over inability: The spontaneous regression of cancer. J Nat Sci Biol Med 2, 43-49 (2011).
4. A. D. Janiszewska, S. Poletajew, A. Wasiutynski, Spontaneous regression of renal cell carcinoma. Contemporary oncology 17, 123-127 (2013).
5. P. H. Zahl, P. C. Gotzsche, J. Maehlen, Natural history of breast cancers detected in the Swedish mammography screening programme: a cohort study. Lancet Oncol 12, 1118-1124 (2011).
6. P. H. Zahl, J. Maehlen, H. G. Welch, The natural history of invasive breast cancers detected by screening mammography. Arch Intern Med 168, 2311-2316 (2008).
7. C. Maltoni, M. A. Mehlman, Carcinogenesis bioassays and protecting public health : commemorating the lifework of Cesare Maltoni and colleagues. Annals of the New York Academy of Sciences, (New York Academy of Sciences, New York, 2002), pp. xii, 231 p.
8. J. Interlandi, in Scientific American. (New York, NY, 2007), chap. 24, pp. 1.
9. L. S. Coleman, Insoluble fibrin may reduce turbulence and bind blood components into clots. Med Hypotheses 65, 820-821 (2005).
10. L. S. Coleman, A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand’s factor may function as a “capillary gate” and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance. Med Hypotheses, (2005).
11. L. S. Coleman, A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand’s factor may function as a “capillary gate” and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance. Med Hypotheses 66, 773-775 (2006).
12. R. O. Becker, G. Selden, The body electric : electromagnetism and the foundation of life. (Quill, New York, ed. 1st Quill, 1985), pp. 364 p.
13. P. J. Rosch, Bioelectromagnetic and subtle energy medicine: the interface between mind and matter. Annals of the New York Academy of Sciences 1172, 297-311 (2009).
14. H. Schiller et al., Thrombin as a survival factor for cancer cells: thrombin activation in malignant effusions in vivo and inhibition of idarubicin-induced cell death in vitro. Int J Clin Pharmacol Ther 40, 329-335 (2002).
15. J. Wang, I. Weiss, K. Svoboda, H. C. Kwaan, Thrombogenic role of cells undergoing apoptosis. British journal of haematology 115, 382-391 (2001).
16. A. A. Khorana, Cancer and coagulation. Am J Hematol 87 Suppl 1, S82-87 (2012).
17. M. E. McFadden, S. E. Sartorius, Multiple systems organ failure in the patient with cancer. Part I: pathophysiologic perspectives. Oncol Nurs Forum 19, 719-724 (1992).
18. R. A. Fleck, L. V. Rao, S. I. Rapaport, N. Varki, Localization of human tissue factor antigen by immunostaining with monospecific, polyclonal anti-human tissue factor antibody. Thromb Res 59, 421-437 (1990).
19. J. F. a. M. P. O. H. Leon Bradlow, Cancer: Genetics and the Environment. J. F. a. M. P. O. H. Leon Bradlow, Ed., Annals of the New York Academy of Sciences (New York Academy of Sciences, 1997), vol. 833, pp. 209.
20. C. N. Pagel et al., Inhibition of osteoblast apoptosis by thrombin. Bone 33, 733-743 (2003).
21. J. F. Kerr, C. M. Winterford, B. V. Harmon, Apoptosis. Its significance in cancer and cancer therapy. Cancer 73, 2013-2026 (1994).
22. K. E. Welty-Wolf et al., Coagulation blockade prevents sepsis-induced respiratory and renal failure in baboons. American journal of respiratory and critical care medicine 164, 1988-1996 (2001).
23. R. S. Kasthuri, M. B. Taubman, N. Mackman, Role of tissue factor in cancer. J Clin Oncol 27, 4834-4838 (2009).