30 Years Lost in Medical Theory
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Allostasis is explained by the activity of emotional mechanisms in the brain that affect SRM and HPA axis operation by altering autonomic balance. The brain retains a complete audiovisual memory of all waking moments, but this memory is normally suppressed. During normal sleep, the dreaming process sorts through these audiovisual records and automatically identifies circumstances that are associated with danger. The emotional mechanism then automatically activates the autonomic nervous system when similar circumstances are encountered during subsequent waking moments. The autonomic nervous system activates the SRM and the HPA axis, causing the various manifestations of the "fight or flight" syndrome.
Atherosclerosis is caused by inadequate turbulence and mixing in the blood. The SRM governs blood levels of insoluble fibrin, which elevates blood viscosity and coagulability and decreases blood turbulence and mixing. Inadequate turbulence and mixing allows blood particulates to form deposits on the inner walls of arteries, and this initiates an inflammatory process that results in the formation of atherosclerotic plaque. This explains how diseases, surgery, and emotional stress can accelerate atherosclerosis.
Amyloidosis I caused by abnormal Fibrin Split Products (FSP). These are "breakdown products" of insoluble fibrin that are produced when the enzyme plasmin attacks and disintegrates the insoluble fibrin molecule. Normally FSP is benign and inert, but under certain circumstances these protein fragments can undergo conformational (shape) change that causes them to interact with Factor X. This interaction depletes Factor X and causes the generation of still more amyloid protein in the form of a "vicious cycle". Amyloid proteins cause a variety of pathologies. They collect into "rheumatoid nodules" in rheumatoid arthritis. They embed in arterial walls and damage them. By depleting Factor X they can disrupt hemostasis and tissue repair. I hypothesize that all forms of Rheumatoid Disease, including Rheumatoid Arthritis, Sjogren's Disease, and Systemic Lupus Erythematosis represent manifestations of amyloidosis. These diseases are not caused by a disorder of the immune system, as often assumed, but instead the immune system is secondarily activated by the abnormal activity of the SRM, which generates thrombin that energizes and activates immune activity as well as the various inflammatory symptoms and manifestations of the Rheumatoid Diseases.
Apoptosis is caused by declining tissue levels of thrombin. Thrombin is the "Universal Enzyme of Energy Transformation" because it converts the energy stored in ATP (Adenosine Tri-Phosphate) into cell and enzyme activities. Thrombin is necessary for the survival as well as the function of tissue repair cells such as fibroblasts, osteoblasts, and myoblasts, and declining levels of thrombin cause these cells to slow their rate of replication and other activities. When thrombin levels fall below a critical threshold, the repair cells begin to die. This is called "apoptosis", or "programmed cell death." It is often attributed to DNA or RNA signaling pathways, but no such pathways have been found. Apoptosis has been intensely studied, and the death of cells due to declining thrombin levels has been documented in numerous cell types. The apoptosis phenomenon takes place in a series of distinctive stages and is very different from cell death caused by poisoning or trauma etc. The objective of cancer chemotherapy treatment is to induce apoptosis in cancerous tissues, but most chemotherapy agents inadvertently increase thrombin generation, so that even if the chemotherapy treatments succeed in killing the "malignant" cells (see malignancy below) they simultaneously increase the risk of some other, seemingly unrelated, type of cancer that may appear at a later date.
Malignancy is an abnormal state of tissue repair cell activity that is self-sustaining and potentially lethal. It is strongly associated with environmental stress factors such as toxic chemical exposure, trauma, surgery, and radiation. Combinations of environmental stress factors can induce SRM hyperactivity that causes tissue repair cells to invade adjacent tissues, causing nociception, pain, and the release of tissue factor both locally and systemically. Under certain conditions, SRM hyperactivity becomes self-sustaining, and this explains the malignant state. Malignancy is invariably accompanied by hyperviscosity and hypercoagulability of the blood, which reflects the SRM hyperactivity that causes the malignancy. Most cancer victims die on account of stroke, infarction, and pulmonary embolus rather than the actual disruption of tissues and organs by invading cancer tissues. Because of this, many cancer deaths are blamed on causes other than cancer.
Cancer is often believed to be caused by "deranged DNA" that causes cells to behave in an abnormal "malignant" fashion and invade adjacent tissues etc. However, genetic pre-disposition has been discovered in only rare types of malignancy. The notion that cancer is caused by defective DNA does not explain metastasis, and it is not consistent with the observation that cancer treatments increase the risk of other, seemingly unrelated, forms of cancer that appear at different locations and times.
There is abundant evidence that "malignant" cells are thrombin-dependent. This suggests that the best way to treat cancer is via methods that reduce SRM activity and thereby reduce thrombin generation. If thrombin generation can be reduced below the threshold of repair cell requirements, then cancer should spontaneously resolve via apoptosis. There is considerable evidence that cancer often spontaneously disappears in exactly this manner
All forms of cancer treatment currently used, including surgery, radiation therapy and chemotherapy, have been shown to increase thrombin generation. This may explain how and why these treatments are strongly associated with the subsequent appearance of other, seemingly unrelated, forms of cancer even though they may eradicate the original cancer. This explains the notorious unreliability of cancer treatments.
Contrary to common belief, cancer cells do not usually replicate faster than other tissues. Cell division and differentiation occurs far faster during embryological development than observed in "malignant" cells. It is impossible to distinguish between malignant cells and normal wound healing cell activity at certain stages of normal wound healing.
Rheumatoid Disease can be explained by a defect in SRM function wherein "Fibrin Split Products" (FSP) undergo conformational change (a change in shape or configuration) that causes them to interact with Factor X, causing a "vicious cycle" of production of abnormal or defective forms of insoluble fibrin that disintegrates into abnormal forms of FSP. The abnormal FSP is called "amyloid" protein.
- Diabetes may be the same disease as Essential Hypertension. Both are caused by accelerated deterioration of capillary beds that simultaneously interferes with glucose uptake and tissue perfusion and blood flow resistance. This explains why diabetic patients usually suffer from hypertension, and hypertensive patients usually exhibit evidence of diabetes. There is no evidence that glucose causes tissue toxicity, as often assumed by both doctors and patients. Reducing blood glucose levels does not benefit the diabetic patient unless this is accomplished by increasing capillary flow and tissue perfusion so as to enable cells to absorb glucose from the blood. This explains why sulfonamide drugs, which reduce blood sugar via unknown mechanisms, are associated with increased morbidity and mortality in diabetic patients.
Exercise Conditioning is commonly called "cardiac conditioning" because it is assumed that it strengthens the heart muscle and thereby increases the ability of the heart to forcefully pump blood. In fact, the hearts of trained athletes differ little from the hearts of sedentary persons. Instead, athletic conditioning is explained by angiogenesis, or the proliferation of capillaries in the muscles affected by exercise. This reduces blood flow resistance, which enables the heart to expel a greater percentage of its contents with each heartbeat and function more efficiently. This explains why trained athletes have reduced blood pressure and pulse rate compared to sedentary persons. In classical stress terms, exercise induces "Eustress"; it induces the SRM to generate thrombin in affected muscle tissues that energizes angiogenesis, or capillary formation.
- Multi-Organ Failure Syndrome (MOFS) is caused by SRM positive feedback and hyperactivity that leads to the production of excessive quantities of thrombin, soluble fibrin an insoluble fibrin. Thrombin causes systemic inflammatory effects that increase tissue permeability. Soluble fibrin invades vital organs and tissues via thrombin-inflamed capillaries, causing organ failure. Insoluble fibrin increases blood viscosity and coagulability, so that there is increased risk of infarction, stroke, and pulmonary embolus.
- Adult Respiratory Distress Syndrome (ARDS) is typically the earliest manifestation of MOFS, the lung being a "target organ because it is rich in tissue factor, so that it tends to be affected sooner than other organs. ARDS often occurs as the first manifestation of eclampsia, which is a special form of MOFS.
- Eclampsia is analagous to MOFS, except that it occurs in pregnant women and the stress of pregnancy is a prominent cause of SRM hyperactivity. Typically the victim is obese, diabetic, or suffers from an occult urinary tract infection. The combined effects of these various stresses causes hyperactivity of the SRM that is the cause of the syndrome. Its "target organs" are the brain, the lungs, and the placenta, because all of these tissues contain large concentrations of tissue factor that activates Factor VII, causing the production of excessive quantities of soluble fibrin and thrombin. Thrombin causes inflammatory effects that increase the permeability of affected tissues. In the brain, soluble fibrin causes seizures or coma. In the lung soluble fibrin manifests as copius exudates that fill alveolar air spaces and disrupt gas exchange. In the placenta soluble fibrin can suffocate the fetus by coating placental villi and disrupting the exchange of gases and nutrients. Excessive soluble fibrin generation can also afflict the liver, causing it to burst. Excessive production of both soluble and insoluble fibrin are generated in the blood, which increases the risk of DIC and amniotic fluid embolus (see below). Eclampsia is essentially the same as Multi-Organ Failure Syndrome (MOFS), except that the patient is pregnant, which causes a unique form of stress.
- Surgical Stress Syndrome
- Disseminated Intravascular Coagulation (DIC)
- Amniotic Fluid Embolus
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