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Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease

Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease
Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease

Abstract

This article suggests that the use sodium and potassium bicarbonates are non-toxic primary alkalizing agents in the prevention and  treatment of all cancers, kidney disease, liver disease, Type I & Type II diabetes, Lupus, heart disease, Pharmacological toxicosis, vascular surgery operation, tonsillar herniation due to cerebral edema, lactic acid toxicosis, and hyponatremia or low salt or loss of salts due to excessive or over-exercise!

[Key words: cancer, diabetes, lupus, heart disease, vascular surgery, herniation, cerebral edema, lactic acid toxicosis, liver disease, kidney disease, hyponatremia, Pharmacological toxicosis]

Introduction

Sodium and potassium bicarbonate are excellent agents for a natural alkaline approach in the treatment for all sickness and disease, including cancer. Sodium bicarbonate is the universal mainstream treatment of acidosis. It is used every day by oncologists to neutralize the heavy acidic nature of their chemical and chemotherapeutic agents which are often quite toxic. Sodium bicarbonate is also used routinely in many clinical situations as herein noted including many peer–reviewed journals:

1) Severe diabetic ketoacidosis (1)

2) Cardiopulmonary resuscitation (2)

3) Pregnancy (3)

4) Hemodialysis (4)

5) Peritoneal dialysis (5)6) Pharmacological toxicosis (6)

7) Hepatopathy (7)

8) Vascular surgery operations (8)

Medics and emergency room medical doctors are accustomed to participating in a flurry of activity when trying to save a persons live after a cardiac arrest–inserting IVs and breathing tubes, performing defibrillation to restart the heart, etc. Sodium bicarbonate is a constant performer under such conditions and is more commonly used than magnesium injections, which is traditionally at the top of every doctor’s protocol for cardiac arrest.

Mainstream oncologists recognize the routine involvement of late stage infections which I refer to as outfections in all cancerous conditions. Medical savants also recognize that bacteria, yeast and mold is present in over forty percent of all cancerous conditions. (9) The most recent research in this area demonstrates how even viruses, which I describe as crystallized acid, is present in fifty percent of certain types of cancerous conditions. (10)

Sodium and potassium bicarbonate increases the hydroxyl ions or electron levels through increased alkalinity to the cells buffering the metabolic acids that can cause cancer.(20)  It is also one of the most basic medicines in allopathic and alternative medicine we have for the treatment of kidney disease.  Research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease.(11) We don’t need a thousand years of scientific tests to understand something as simple and essential as alkaline water and it is quite the same with sodium and potassium bicarbonate. Sodium and potassium bicarbonate are always present in the best alkaline drinking waters and organic raw green foods and is constantly being produced by the cover cells of the stomach to alkalize the acidic foods and liquids we ingest, including buffering metabolic and respiratory acids in order to maintain the alkaline design of the blood and tissues at a delicate pH of 7.365.(20)

What is Latent Tissue Acidosis?
Medical doctors are not taught in medical school and therefore do not understand or recognize latent tissue acidosis. They understand and recognize compensated acidosis and decompensated acidosis. In compensated acidosis, breathing increases in order to blow off more carbonic acid which decreases PCO2 because of the lowered carbonate or HCO3. When the breathing rate can no longer get any faster and when the kidneys can no longer increase its’ function to keep up with the acid load, then the blood pH starts to change from a pH of 7.365 to 7.3 then to 7.2. At a blood pH of 6.95 the heart relaxes and the client goes into a coma or dies.

Latent “acidosis” is a condition that exists when there are not enough bases in the alkalophile glands because they have been used up in the process of neutralizing the acids adsorbed to the collagen fibers. This leads to compensated “acidosis.” This means the blood pH has not changed but other body systems have changed. This can then lead to decompensated “acidosis” where the alkaline reserves of the blood are used up and the pH of the blood is altered. Decompensated “acidosis” can be determined by testing the blood pH, urine pH and the saliva pH. The decrease in the alkaline reserves in the body  can occur because of hyper-proteinization, (eating meat and cheese!) or too much protein, and hyper-carbonization, or too much sugar or from excessive or over-excercise. This is why young athletes fall over dead or why 80 to 90 year old folks are all shrunk up and look like prunes. They have very little or no alkaline reserves in their alkalophile glands. When all the alkaline minerals are gone, so are you and your battery runs out of charge. The charge of your cellular battery can be measured by testing the ORP or the oxidative reduction potential of the blood, urine or saliva using an ORP meter. As you become more acidic this energy potential or ORP increases.

How Is Sodium Bicarbonate Created In The Body?

The parietal or cover cells of the stomach split the sodium chloride of the blood. The sodium ion is used to bind with water and carbon dioxide to form the alkaline salt, sodium bicarbonate or NaHCO3. The biochemistry is: H20 + CO2 + NaCl = NaHCO3 + HCL. This is why I call the stomach an alkalizing organ NOT an organ of digestion. The stomach DOES NOT digest the food or liquids we ingest but it alkalizes the foods and liquids we ingest.  We have one instrument in the human body to digest food and it is NOT the stomach it is your teeth.  Once we swallow our food or drink the stomach begins to prepare the food by alkalizing it in a bath of sodium bicarbonate.

For each molecule of sodium bicarbonate (NaHCO3) made, a molecule of hydrochloric acid (HCL) is made and secreted into the so-called digestive system – specifically, the stomach (the gastric pits in the stomach) – to be eliminated via the blood. Therefore HCL is an acidic waste product of sodium bicarbonate created by the stomach to alkalize the food and liquids ingested.

Exercise Creates Metabolic Acidic Waste Products Which Are Harmful To The Blood and Tissues

When one exercises or over-exercises the body needs additional alkaline bicarbonate salts to buffer lactic acids.  The additional bicarbonate is created in the stomach lining to buffer the increased amounts of lactic acids produced as a waste product of metabolism.  The production of sodium bicarbonate will always leave an acidic waste product of hydrochloric acid in the gastric pits of the stomach leading to nausea, light headedness, dizziness, muddle thingking, and poor circulation.  If the excessive exercise continues this can then lead to a dificiency of mineral and bicarbonate salts (electrolytes lost through perspiration or urination) which may lead to latent tissue acidosis, pain, edema, hyponatrenia and death.

But how does something like sodium and/or potassium bicarbonate, so seemingly innocuous have such a dramatic effect? During prolonged or intense exercise muscles produce large amounts of acidic waste products, such as lactic acid, that lead to soreness, stiffness, fatigue and possible edema if these acids are not buffered and eliminated through urination or perspiration. Because sodium and potassium bicarbonate naturally reduces metabolic acids, it acts as a buffer against these performance-limiting by-products.

Current research suggests that supplemental sodium bicarbonate, like the pH Miracle pHour Salts (contains sodium and potassium bicarbonate) is particularly helpful in speed-based events, including sprints, football and other fast-moving games, and middle-distance (up to 10km) running, swimming and cycling. “Essentially, sodium bicarbonate is an alkaline substance that increases the pH of the blood,” Dr Folland says. “This seems to reduce and offset the acidity produced in the muscles during intense, anaerobic exercise that produces lactic acid most quickly, such as fast running or swimming.”

In Dr Folland’s study, swimmers who took the sodium bicarbonate knocked 1.5 seconds off their time for 200m, a difference that may seem insignificant to recreational swimmers but which is substantial at elite level.

“At the last Olympics, the top four swimmers in the men’s 200m freestyle were separated by just 1.4 seconds,” Dr Folland says. “So, in theory, it could be the difference between winning a medal and not.”

Anyone can try it, he says, but only those who are serious enough to monitor their times and progress in sports such as running, swimming or cycling may notice the few seconds advantage it might provide. “The increments of improvement are relatively small to the average person, although significant to someone who competes,” Dr Folland says.

Athletes for years have sworn that taking a spoonful of bicarbonate of soda (baking soda) helps them to keep going for longer. For years, experts doubted that there was anything other than a placebo effect to these claims until they subjected the substance to rigorous examination. Most exercise scientists investigating the trend for “soda-doping” among athletes and gym-goers have shown that it offers significant benefits for endurance and speed.”

At Loughborough University, for instance, physiologists reporting in the June issue of the International Journal of Sports Medicine showed that swimmers who took baking soda about one hour before a 200m event were able to shave a significant time off their usual performances. Dr Jonathan Folland, who led the study, says that it is not uncommon for top swimmers to take sodium bicarbonate (another name for the substance) before a competition to give them an edge. Indeed, he showed that of nine swimmers tested, eight recorded their fastest times after ingesting a supplement of the common baking ingredient – sodium bicarbonate.

Where are Bicarbonates Created In The Human Body and Why?

The chloride ion from the sodium chloride (salt) binds to an acid or proton forming HCL as a waste product of sodium bicarbonate production. HCL has a pH of 1 and is highly toxic to the blood and tissues and the cause of indigestion, acid reflux, ulcers, diabetes, cancer, hyponatremia, edema, tonsilar herniation and death.  When large amounts of acids, including HCL, enter the stomach from a rich animal protein or dairy product meal, such as meat and cheese, or from starchy foods from root vegetables like potatoes or during extreme exercise, acid is withdrawn from the acid-base household. The organism would die if the resulting alkalosis – or NaHCO3 (base flood) or base surplus – created by the stomach was not taken up by the alkalophile glands (salivary glands, pancreas, kidney, pylorus glands, Brunner’s glands, Lieberkuhn glands and liver) that need these quick bases in order to build up their strong sodium bicarbonate secretions. These alkalizing glands and organs are the stomach, pancreas, Brunner’s glands (between the pylorus and the junctions of the bile and pancreatic ducts), Lieberkuhn’s glands in the liver and its bile with its strong acid binding capabilities which it has to release on the highly acidic meat, cheese, potato, acid water or metabolic and/or respiratory acids from over-exercise to buffer its strong acids of nitric, sulphuric, phosphoric, uric and lactic acids in daily metabolism, respiration and excessive or over-exercise.

Bicarbonate acts to stimulate the ATPase by acting directly on it.(12)

The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating disease that it prevents patients from having to be put on kidney dialysis. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. Bicarbonates of sodium and potassium are a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash.

Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa, Florida stated, upon seeing the research on sodium bicarbonate and kidney disease, “I am glad to see confirmation of what we have known for so long.  I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”.

A dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.”

The Stomach, Pancreas and Kidneys Naturally Produce Sodium Bicarbonate Every Day

The exocrine section of sodium bicarbonate from the stomach and the pancreas have been greatly ignored in the treatment of diabetes and cancer even though its impairment is a well documented condition. The stomach and the pancreas is primarily responsible for the production of sodium bicarbonate necessary for normal alkalization of food and liquids ingested. Sodium bicarbonate is so important for protecting the kidney’s that even the kidneys get into the act of producing sodium bicarbonate.  We now know the common denominator between hyponatremia, inflammation, edema, diabetes, kidney disease, and cancer is the lack of sodium and potassium bicarbonate or the body’s inability to produce sodium and potassium bicarbonate because of a lack of mineral salts in the diet. When the body is hit with reductions in sodium bicarbonate output by these three organs,’ acid conditions build up and then the entire body physiology begins to change from a state of oxygenation to fermentation. Likewise when acid build-up outstrips these organs normal sodium bicarbonate capacity, cellular, tissue, glandular and organ deterioration begins.

The stomach, pancreas and the kidneys alone produce about five hundred
grams (about one pound) of sodium and/or potassium bicarbonate per day in an attempt to neutralize dietary and/or metabolic acid in the blood and interstitial fluids that surround the body cells.

The stomach, pancreas and the kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood and tissues. If the blood and tissues are too acidic, the stomach and/or the kidney’s make sodium bicarbonate to restore the blood and tissue pH back to a delicate pH balance of 7.365. If the blood or tissues are too alkaline, then the kidney excretes sodium bicarbonate into the urine to restore the 7.365 alkaline balance. Acid-base balance is the net result of two processes, first, the removal of sodium bicarbonate subsequent to hydrogen ion production from the metabolism or dietary constituents; second, the synthesis of “new” sodium bicarbonate by the stomach and/or the  kidney’s.(13)  The stomach and kidneys pull salt, water and carbon dioxide from the blood to make sodium bicarbonate to maintain the alkaline design of the body during all functions of the body from the ingestion of food or drink to exercise.  The chemical formula is as follows:  NaCl + H2O + CO2 = NaHCO3 + HCL.  The waste product of sodium bicarbonate is hydrochloric acid which is eliminated by kidneys as an acidic excretion of the urine.
It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging or rotting process. Acidosis occurs often when the body cannot produce enough sodium bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and eating and drinking highly acid foods and drinks like chicken, pork, beef, dairy products, coffee, tea, alcohol, chocolate, soft drinks, just to name a few.  We are also testing bottled mineral water and finding that these waters are acidic and may contribute to overall tissue acidosis.
Acid-buffering by means of base supplementation (The pH Miracle pHour Salts) of sodium bicarbonate is one of the major roles of dialysis. Sodium bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum sodium bicarbonate concentration of 22 mmol/l.(14)  Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality.  Sodium bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.(15)

One of the main reasons we become over-acid is from over-consumption of animal protein, dairy products, high sugar fruit, grains, alcohol, coffee, tea, chocolate, soft drinks and over-exercise or under-exercise. Eating meat and dairy products may increase the risk of prostate cancer, research suggests.(16) We would find the same for breast and other cancers as well metastatic cancers.(17) Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of alkaline minerals you have a dis-ease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids, such as, nitric, uric, sulphuric and phosphoric acid.

Unless a treatment actually removes acidic toxins  from the body and increases oxygen, water, and nutrients most medical interventions come to naught.

These metabolic and dietary acids must be excreted by the kidney’s because they contain sulfur, phosphorus, and/or nitrogen which cannot break down into water and carbon dioxide to be eliminated as weak acids. In their passage through the kidney’s these strong acids of ntric, sulphuric, phosphoric and uric acid must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn or destroy the kidney’s on their way out. This would happen if these strong acids were excreted in their free acidic form.

Substituting a sodium bicarbonate solution for saline
infusion prior to administration of radiocontrast
material seems to 
reduce the incidence of nephropathy.(18)
Dr. Thomas P. Kennedy
American Medical Association

Sodium and potassoum bicarbonate ions neutralize the acids that cause chronic inflammatory reactions. Hence, sodium and potassium bicarbonate are of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium and potassium bicarbonate are well-studied and used salts with known effects. Sodium and potassium bicarbonate are effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects.(19)  It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy.

Sodium and potassium bicarbonates possess the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with
healthy tissue from the same person shows that the cancer tissue
has a much higher concentration of toxic chemicals, pesticides, etc.

Sodium and potassium bicarbonate intravenous infusions are indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest, tonsillar herniation due to cerebral edema, severe primary lactic acidosis and hyponatremia due to excessive or over-exercise.  During heavy exercise, if the the resulting lactic acid is not adsorbed by the collagen fibers, the specific acid catchers of the body, the blood pH will drop and the body will go into a coma and the person will die.

The total collection of these fibers is the largest organ of the body called SCHADE, the colloidal connective tissue organ. NO liquid exchange occurs between the blood and the parenchyma cells, or in reverse, unless it passes through this connective tissue organ. This organ connects and holds everything in our bodies in place. This organ is composed of ligaments, tendons, sinew, and the finer fibers that become the scaffolding that holds every single cell in our bodies in place. When acids are stored in this organ, which includes the muscles, inflammation or edema and pain develop. The production of lactic acid is increased with excessive exercise and the ingestion of milk, cheese, yogurt, butter, ice cream, high sugar fruit and starchy root vegetables like potatoes.

That is why I have stated, “acid is pain and pain is acid or acid is edema and edema is pain”.  You cannot have one without the other. This is the beginning of latent tissue acidosis leading to irritation, inflammation, edema and degeneration of the cells, tissues and organs and eventual or sudden death.  It is why we are seeing so many amateur and professional atheletes pass out and die on the playing fields.  Metabolic, respiratory and gastrointestinal acids can and do kill and death can be overted by simply maintaining the alkaline design of the body fluids with protective hydration of alkaine sodium bicarbonate fluids.

The acid/alkaline balance is one of the most overlooked aspects of diagnostic medicine. In general, the world population is heavily acidic, excepting alkalarian vegans (those who ingest raw, organic green fruit, vegetables, mineral salts, alkaline water and unsaturated seed and nut oils), and even their bodies have to face increasing levels of environmental toxic exposure, which may contribute to an acidic pH condition of the blood and then tissues.

With over 30 years of research and testing over 100,000 individual samples of blood and over 100,000 samples of urine and saliva, I have come to the conclusion that the human body is an acidic producing organism by function – yet, it is an alkaline organism by design. Eating animal protein, especially meat and cheese, sugar, fermented foods, starchy foods like potatoes, acidic water, alcohol, coffee, tea, chocolate,  and excessive exercise or under-exercise, obsessive behaviors, lack of rest, lack of sunshine, and emotional stress are deadly acidic lifestyle choices.

All enervation, under-performance, sensitivity, irritation, inflammation, edema, catarrh, induration, ulcerations, degeneration, aging and cancerous conditions are caused by a four letter word – ACID, which is an acronym which stands for:

A = acidic food and drink, attitudes and activities,
C = compromised internal acidic environment,
I = illness and dis-ease, and,
D = desire for more acidic foods, drinks, attitudes and activities, and the cycle repeats itself.[20]

We ingest acidic medicines to lessen the symptoms of our illness. We stimulate the body with unhealthy forms of energy providing quick, often temporary relief from our symptoms which begins the cycle all over again creating a very powerful pattern of poor health and dis-ease.

Conclusion

The pH Alkalizing Lifestyle and Diet is a low acid producing diet and lifestyle that focuses on the foundational principal that the body is alkaline by design and yet acidic by function. This makes this program the ultimate program for preventing and reversing aging and the onset of sickness and disease. I would say that the pH Alkalizing Lifestyle and Diet is the perfect diet and lifestyle for a longer healthier life.(20)

References

1. Gamba, G., “Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial.” (Rev Invest Clin 1991 Jul-Sep;43(3):234-8). Miyares Gom ez A. in “Diabetic ketoacidosis in childhood: the first day of treatment.” (An Esp Pediatr 1989 Apr;30(4):279-83)

2. Levy, M.M., “An evidence-based evaluation of the use of sodium bicarbonate during cardiopulmonary resuscitation.” (Crit Care Clin 1998 Jul;14(3):457-83). Vukmir, R.B., Sodium bicarbonate in cardiac arrest: a reappraisal (Am J Emerg Med 1996 Mar;14(2):192-206). Bar-Joseph, G., “Clinical use of sodium bicarbonate during cardiopulmonary resuscitation–is it used sensibly?” (Resuscitation 2002 Jul;54(1):47-55).

3. Zhang. L., “Perhydrit and bicarbonate improve maternal gases and acid-base status during the second stage of labor.” Department of Obstetrics and Gynecology, Xiangya Hospital, Hunan Medical University, Changsha 410008. Maeda, Y., “Perioperative administration of bicarbonated solution to a patient with mitochondrial encephalomyopathy.” (Masui 2001 Mar;50(3):299-303).

4. Avdic. E., “Bicarbonate versus acetate hemodialysis: effects on the acid-base status.” (Med Arh 2001;55(4):231-3).

5. Feriani, M., “Randomized long-term evaluation of bicarbonate-buffered CAPD solution.” (Kidney Int 1998 Nov;54(5):1731-8).

6. Vrijlandt, P.J., odium bicarbonate infusion for intoxication with tricyclic antidepressives: recommended inspite of lack of scientific evidence. Ned Tijdschr Geneeskd 2001 Sep 1;145(35):1686-9). Knudsen, K., “Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning.” (Crit Car e Med 1997 Apr;25(4):669-74).

7. Silomon, M., “Effect of sodium bicarbonate infusion on hepatocyte Ca2+ overload during resuscitation from hemorrhagic shock.” (Resuscitation 1998 Apr;37(1):27-32). Mariano, F., “Insufficient correction of blood bicarbonate levels in biguanide lactic acidosis treated with CVVH and bicarbonate replacement fluids.” (Minerva Urol Nefrol 1997 Sep;49(3):133-6).

8. Dement’eva, I.I., “Calculation of the dose of sodium bicarbonate in the treatment of metabolic acidosis in surgery with and deep hypothermic circulatory arresta.” (Anesteziol Reanimatol 1997 Sep-Oct;(5):42-4).

9. “I believe that, conservatively, 15 to 20 percent of all cancer is caused by infections; however, the number could be larger — maybe double,” (Dr. Andrew Dannenberg, Director of the Cancer Center at New York-Presbyterian Hospital/Weill Cornell Medical Center.”) Dr. Dannennberg made the remarks in a speech in December 2007 at the annual international conference of the American Association for Cancer Research.

10. A sexually transmitted virus that causes cervical cancer is also to blame for half of all cases of cancer of the penis.

11.  www.nelm.nhs.uk/en/NeLM-Area/News/2009—July/20/
Bicarbonate-supplementation-may-slow-renal-decline-in-chronic-kidney-disease/

12. Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein  1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A.

13. Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986

14.  www.uptodate.com/patients/content/abstract.do?topicKey=~G/p55S8w8sQDwqG&refNum=28

15.  www.ncbi.nlm.nih.gov/pubmed/16523427

16.  news.bbc.co.uk/2/hi/health/7655405.stm

17.  Cancer Res. 2009 Mar 15;69(6):2260-8. Epub 2009 Mar 10.
Bicarbonate increases tumor pH and inhibits spontaneous metastases.
Robey IFBaggett BKKirkpatrick NDRoe DJDosescu JSloane BFHashim AIMorse DLRaghunand NGatenby RAGillies RJ. Source: Arizona Cancer Center, University of Arizona, Tucson, Arizona, USA

18.  JAMA 2004;291:2328-2334,2376-2377.www.urotoday.com/56/browse_categories/renal_transplantation_vascular_disease/
sodium_bicarbonate_may_prevent_radiocontrastinduced_renal_injury.html

19. These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin).   Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others.

20. www.phmiracle.com. Young.R.O., Young, S.R., The pH Miracle Revised and Updated, Hachett, 2010.

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa and Universal Medical Imaging Group

Abstract

Historical analysis suggests that conventional understandings of Disseminated Intravascular Coagulation (DIC) may be misguided; further examination may be necessary.  Here, a theoretical analysis provides an alternative explanation for DIC pathology; it is suggested that the cause and mechanics of DIC are largely due to the proliferation of several intravascular microforms and their associated metabolic toxic acidic waste products — Mycrozymian Acidic Toxins (MAT) and Exotoxic-Mycotoxic-Producing Microorganisms (EMPO).  The Mycotoxic Oxidative Stress Test (MOST) is presented here as an easy, inexpensive and non-invasive alternative to conventional measurements for the detection of intravascular  acidic toxins, DIC  and oxidative stress.

Introduction and Historical Perspective

More than 150 years ago, British physician T. W. Jones asked the question, “Why does the blood circulating in the vessels not coagulate?”[1]  though a general answer to this question is now obvious, the biochemical mechanisms involved in how the blood coagulates (clots) are complex and varied, and all the intricacies have not yet been explained. A. Trousseau, recognized that the blood of cancer patients is in a hyper-coagulable state in the process of coagulation, even while confined in the blood vessels.[2]  The name given to this discovery is still in use today, as “Trousseau’s Syndrome.”[2]  Early in his career, Rudolph Virchow, the Father of Pathology, was interested in thrombosis and embolism.  He speculated that intravascular blood could be altered so it would clot as a result of a stimulus too weak to clot normal blood.[3]  In 1856 Virchow delivered a lecture setting forth this concept.

Although the concept of partial clotting within vessels reaches back to the beginnings of modern medicine, much of the discovery of its biochemical mechanisms – the activation of clotting factors – has been left to chance.  The admission of a patient to the hospital with an unceplained bleeding disorder challenged researchers to discover the cause of hemorrhaging.  Analysis of blood from normal persons helped in the study of the patient with the blood disorder. A new clotting factor was hereby discovered which was missing from the  patient’s blood.  For this reason, several clotting factors have been named after the individuals in which they were missing: e.g., Christmas factor (factor IX)[4], Hageman factor (factor XII)[4].

In this article, the causes of pathological (intravascular) clotting will be described, as will various methods of detecting this condition, especially a blood test I call the Mycotoxin Oxidative Stress Test (MOST).

The Mechanics of Blood Coagulation

Blood clotting is a highly detailed chemical-mechanism involving many distinct components.  The problem for the hematologist hs been to understand it at the biochemical level.  Undoubtedly, efforts to fully understand blood clotting will continue for many more years.

Recalling Antione Bechamp’s[8] and Gunther Enderlein’s[9] research into the sub cellular living elements and combining this with what is known of colloidal flocculation[6], it is suggested that the clotting of blood begins with the end-linking (polymerizing) of the fundamental protein unit called by Bechamp the microzyma[8].  A chain of these living units constitutes fibrinogen, which is still dispersed 9micro-hetergenous0 in the blood, and it may or may not be further processed.  If processing continues, it will be either by continued end-linking or by cross-linking.  End-linked fibrinogen is referred to here as fibrin monomer, which I have suggested is a repair protein also dispersed in the blood. Due to a number of blood clotting factors, the process may continue until the excess fibrin monomer and/or until fibrin becomes excessively end-linked.

Cross-linking the polymerized strands to form a three-dimensional network results in what is called the hard clot (fibrin – the major protein of clotting blood).  Factor XIII, which instigates the forming of these blood networks. is always present but latent in the blood, and must be activated before the formation can occur.  Persons who are producing fibrin monomer or excessively linked fibrinogen are said to be in a hyper-coagulable state, while those having diminished  ability to form clots are in a hypo-coagulated state.  It is the activation of the colloidal clotting factors which is so complex.  Blood clotting may occur through many pathways and be initiated by many different stimuli.  Regardless of initiation factors, the process is a sequence of events in which the activation of one factor triggers another, until, after a series of discrete steps, fibrin is formed.

When blood is clotted prematurely, and the factors involved are consumed (incorporated into) the body recognizes a deficiency of clotting agents and generates more.  Thus, people with a tendency to clot excessively will alternate between a hyper coagulable state and a hypo-coagulatable state.  When in the hypo coagulated state, such people hemorrhage until the deficient clotting factors are replaced.[4]  When only fibrin monomer or excessively linked fibrinogen is formed (no cross-linking), it is quite subtle and may go undetected.  It may be detected by a change in blood viscosity (sedimentation rate), by the Mycotoxic Oxidative Stress Test (described later), or by other more subtle means.  If strands of fibrinogen are cross-linked, however, a suggicient amount of insoluble precipitate of fires may result, and these can be detected microscopically using a phase contrast and dark-field microscopy in prepared slides of fresh tissue or blood.  An excessive formation of fibrin leads to  an impairment in circulation, and eventual organ failure usually results.[5]

With this background, we are in a position to consider a standard medical term: disseminated intravascular coagultion (DIC).[6]  This term encompasses the hyper coagulable state, i refer to as pathological blood coagulation which consists of both insoluble and excess dispersed polymers of colloidal proteins.

Key Ingredients of Pathological Blood Coagulation

Before discussing DIC in more detail, it si necessary to introduce its fur important ingredients according to this view – mycotoxins, endotoxins, exotoxins, and tissue factor.  Any of these elements, or any combination of them, can play a major role in initiating unwanted DIC.[6]  However, mycotoxins or the acids from yeast have been found to be the underlying element which instigates and intensifies the participation of the other three.[6]  Each will now be described in turn and brought into the clotting picture.

(Micrograph 1: left, shows normal hyper-coagulated blood in a healthy blood clot sample and right, hypo coagulated blood in an unhealthy blood clot sample)

Mycotoxins and Metabolism by Fermentation

As discussed in the main text of my published book, Sick and Tired book[7 ]. acidification of blood and body tissues and organs and the accompanying lack of oxygen lead to pathological metabolic fermentation, which is carried out primarily by yeast and mold.  Such pathological microorganisms, or their precursors, ar inherent to the human body and to all higher organisms.  Their precursors according to Bechamp, the microzymas, carry on a nominal and homeostatic fermentation themselves. under healthy conditions.[8]  The primary function of yeast and mold is to decompose the body upon the death of the animal or human organism.  Their premature overgrowth indicates a biochemical environment akin to death.  During pathological metabolic fermentation, high concentrations of several acidic substances called mycotoxins are created.  They are highly damaging, always acidic, metabolic products.  If not immediately buffered by specific antioxidants, such as hydrogen peroxide and the hydroxyl free-radical, mycotoxins can seriously disrupt the physiology by disrupting normal metabolism and by penetrating blood and body cells and poisoning them.  As will be seen, they interact with many of the mechanisms for DIC in various pathological symptomologies.

In my published article called The Finger on the Magic of Life: Antoine Bechamp, 19th Century Genius (1816-1908),  I discuss pleomorphism in some detail.[7] Understanding this phenomenon – the rapid evolution of microorganisms across traditional taxonomic  lines is helpful in getting a complete picture of DIC.  Briefly stated, collodial living microzymas evolve intracellularly into more complex forms (microorganisms), beginning with a healthy primitive stage comprising of repair proteins.  As the disease condition worsens, morbid intermediate forms (filterable bacteria or viruses, cell-wall deficient forms and full bacteria) develop from repair proteins, or directly from microzymas.  A third macrostage comprises the commonly recognized culminate microorganisms which are yeast, fungus to mold.  In terms of pleomorphism, all of these microorganisms represent a single family of variously functioning forms.[8]  The culminate forms produce the lions share of acids, which are mycotoxins and the primary focus of my research.[7][8][9]  For convenience, bacteria, yeast, fungus and mold that produce acidic metabolic wastes and protein cellular fragments called exotoins, endotoxins and mycotoxins will here be referred to collectively ash EMPO, or exotoxic, mycotoxic-producing microorganisms.

What follows is a shortened description or the description and origin of several exotoxins and mycotoxins, referred to collectively microzymian acidic toxins of MAT, which are involved in the processes leading to DIC.  The bio-effects, or the pathology of cellular fermentation, of these toxic metabolites are know as mycotic illness, mycotoxicosis, or mycotoxic stress as seen in the MOST and described and published by Dr. Bolin in the 1940’s.[10]

One such metabolic product is acetyl aldehyde, which is formed by  cellular breakdown of food, especially carbohydrate and the birth of  EMPO.  Acetyl aldehyde can also break down into a secondary substance know as ethyl alcohol.  Although acetyl aldehyde presents an immediate hazard to health and well-being, nature has provided a means of buffering of neutralizing this acidic by-product of cellular digestion and fermentation almost as soon as it is created.[11] The controls of acetyl aldehyde (and ethyl alcohol) are the sulfur amino acids, cysteine, taurine, methionine and the peptide glutathione which is found in red blood cells and almost all cells utilizing oxygen.[12]  In an attempt to buffer or neutralize MAT, the body will also bind or chelate both fats and minerals to them.[12]

Another member of the MAT family is uric acid, which is formed by the digestion of protein and the creation of EMPO.[13]  Uric acid can also break down into secondary substance, on of which is alloxan.[14] This has been shown to damage the insulin-producing pancreatic beta cells leading to diabetes [Refer to Tables 1 and 2]

A shortage of alkalizing nutrients or an excess of MAT initi­ates an immune response in which a special class of free radicals which I call microzymian oxidative buffering species (MOBS) are released.[15] These oxygen metabolites carry unpaired electrons and are intended to disrupt bacteria, yeast, fungus and mold, and buffer exotoxins, endotoxins, and mycotoxins. Current medical savants believe that they can disrupt just about any­thing they contact, including healthy cells and tissue: this is not accurate. The fact is that MOBS carriers a nega­tive surface-charge and repel healthy cells, which also have a negative surface-charge. [16] It is the positively surface-charged bacteria, yeast/fungus, mold, exotoxins, endotoxins, and myco­toxins that MOBS bind too.[17]  This aspect gives some insight into autoimmune phenomena, which are not, as is often maintained, the result of an overburdened immune system. They result either as a side-effect of the immune system’s attempt to remove foreign or toxic ele­ments, or as a direct attempt by the immune system to remove cells or tissue rendered useless or disturb­ing to the body by MAT.

In every degenerative symptomatology I have studied, I have found excessive MAT and MOBS (see Tables 1-3). Some of these degenerative symptoms and their underlying disease conditions, including cancer are described in my recently published paper on a deficiency on alkaline nutrition and cancer. [15] But the fact that myco­toxins cause harm to humans and other animals is purely a secondary effect, since, as noted, the prima­ry function of the microorganism is not to cause illness. We know from the fossil record that pleomorphic microforms existed long before animals.[19] In fact, humans and animals developed in terms of micro­organisms.[20] The reverse, however, is not true. Since micro­organisms appeared first in the developmental sequence, they are not physiologically aware of humans and animals. There is much evidence that human and animal physiologies are highly aware of, and respond to MAT – these acidic compounds signaling the presence of bacteria, yeast, fungi and/or mold or  EMPO.[21].

Endotoxins

Also involved in the process leading to DIC are endotoxins, substances endogenous to symptogenic (i.e., “pathogenic” in orthodox terms) bacteria. Endotoxins are a family of related substances having certain common characteristics, but differing from one bacterial form (or strain) to another. Endotoxins are lipopolysaccharides (LPS). LPS form a widely diversified group because of (1) the number of long- chain fatty acids composing lipids; (2) the number of individual sugars as well as their modes of linkage to one another; (3) the branching of sugar chains; and (4) the number of possible arrangements of these units. Endotoxins also contain proteins, further com­pounding the structural diversity.[22]

One theory on endotoxin states that its purpose is to act as a semi-permeable membrane for the bac­terium, limiting and regulating substances entering the organism.[22] Endotoxin resides solely on or near the interior surface of the cell membrane and is shed into the surrounding medium only upon the death of the bacterium. Thus, as these microforms die off, or are lysed by bodily activity, endotoxin is released. (This fact may well be an explanation for the Herxheimer reaction, in which a patient becomes worse following the administration of toxic drugs or other forms of treatment that drastically alter the associated organ­ism.[23]) Another endotoxin theory states that LPS are a constituent of the membrane, and as the organism grows, endotoxin fragments are repeatedly sloughed off into the medium. This phenomenon has been observed in the digestive tract.[24] Since bacterial translocation into the blood is not only possible but common where epithelial hyperpermeability exists, one can assume that the process will continue there. Both theories may be correct if we think of the first one as true of “adult” forms, and the second as true of newly developed and expanding ones.

Basic to the structure of an endotoxin is the lipid common to all forms, designated lipid A, to which is attached a “core” polysaccharide, identical for large groups of bacteria. To the core polysaccharide is attached the O-antigen, consisting of various lengths of polysaccharide chains which are chemically unique for each type of organism and LPS. These chains pro­vide endotoxin specificity.[25] Experiments conducted over many years indicate that most, if not all, of the toxic effects of an endotoxin may be attributed to the lipid portion, and it is sometimes used per se in experiments rather than the entire molecule.[26] An important additional feature of lipid A is its phos­phate content. Each phosphate group carries a nega­tive charge, and since lipid A is a rather large mole­cule, it provides, essentially, a negatively charged sur­face. The importance of this will be seen shortly.

Exotoxins

These are the metabolic excretions of bacteria. While endotoxin’s ongoing effect is, in a manner of speaking, in the background, exotoxins, like myco­toxins, present a double-edged sword. Not only do they initiate DIC, but they produce, or influence the body to produce, the various and numerous infec­tious symptomatologies, such as typhoid fever, diph­theria, etc. (See “Vaccination Reconsidered” in Section 4 of the Appendix of Sick and Tired for details on the action of diphtheria toxin.)[7] By comparison, mycotoxins not only initiate DIC, but there is much evidence to sug­gest that they produce, or influence the body to pro­duce, degenerative symptomatologies, such as arthri­tis, diabetes, etc., and cancer and AIDS as well.

Tissue Factor

Crucial to the understanding of DIC is recogni­tion of the role of tissue factor (TF), formerly known as thromboplastin. This transmembrane lipoprotein exists on the surface of platelets, vas­cular endothelial cells, leukocytes, monocytes, and most cells producing EMPO.[27] It plays a major role in several biochemical mechanisms leading to DIC.

TF is the primary cell-bound initiator of the blood coagulation cascade. Its gene is activated in wound healing and other conditions. By itself it is capable of initiating clotting, but also becomes active when complexed with factor VII or activated factor VII (Vila).[28] TF has been described as the receptor for factor VII because of the close association between the two proteins and because it causes a shape change (conformational) in factor VII, allowing it to attain activity. Both factor Vila and the TF/VII com­plex activate factors IX and X, which initiate the clotting cascade and the formation of thrombin.[29]

Development of Disseminated
Intravascular Coagulation
(DIC)

DIC Induced by MAT and Tissue Factor

An infusion of toxins into the blood has a direct effect on TF gene expression in leukocytes. Contact of MAT, endotoxins (lipid A), or exotoxins with leukocytes, activates proteins that bind to DNA nucleotide sequences, thereby activating the TF gene.[30] (See Tables 4-6.)

Endothelial cells damaged in culture by exotoxins, endotoxins, or mycotoxins attract polymorphonuclear leukocytes (PMNs), which adhere to the damaged cells. Once the leukocytes are bound, they can still have their TF gene activated if it hasn’t yet occurred, and they may release MOBS in response to toxins and to organisms of disease, possibly creating further dis­turbances. (Cellular disorganization then releases acti­vating proteins into the blood, which is discussed in more detail later.) Research shows that exotoxic and mycotoxic stress resulting in bound PMNs can be blocked by “antioxidants.”[31] These might better be called anti-exotoxins or antimycotoxins. Both observa­tion and study have led the author to conclude that cellular disorganization is initiated and primarily caused by fermentation pathology, not, as is the cur­rent belief, by the MOBS, or free radicals, generated to destroy toxins and microorganisms. MOBS or free radicals, because of their negative charge, are released to chelate or bind EMPO and MAT. It is suggested by current savants that free radical tissue damage is the secondary, “shotgun” effect of intense immune response to EMPO toxification and MAT-damaged cells. This could not be the case since healthy cells or their membranes carry a negative charge and would resist any electromagnetic attraction because of simi­lar charge. The concentration and instability of MAT generated in a compromised terrain, as opposed to the fleeting existence of free radicals, especially exoge­nous ones, also lead to this conclusion.

Endothelial cells grown in culture can be induced to express tissue factor. In one experiment, no procoagulant activity could be detected in the absence of toxins. However, the addition of mycotoxins from Aspergillus niger or Micrococcus neoformas (Mucor racemosus Fresen) resulted in procoagulant activity which reached a maximum in four to six hours and was dose-dependent. The same experiment was applied using E. coli and Salmonella enteritidis endo­toxin with a similar result.[32] A single intravenous injection of a mycotoxin from Aspergillus niger into experimental animals resulted in circulating endothelial cells within five minutes. In other exper­iments with the mycotoxin, detachment of endothe­lial cells from the basement membrane was noted.[33] (See Table 8.)

Removal of endothelial cells has dire conse­quences from two standpoints: First, the surface of these cells is covered with a specific prostaglandin (PGI2) known as prostacyclin. If blood contacts a surface not covered with PGI2, it will clot. For example, surfaces devoid of this prostaglandin are formed whenever a vessel is cut or punctured. An abrasion or other injury may also expose a surface on which PGI2 is lacking. The removal of endothelial cells by exotoxins or mycotoxins creates a surface devoid of PGI2, leading to blood clotting (see Table 7). Secondly, disorganization of endothelial cells cre­ates increased levels of EMPO and MAT which are attracted to an exposed surface (basement mem­brane) which expresses a negative charge. This also leads to clotting.

DIC Induced by Electrostatic Attraction

It was discovered in 1964 that blood will clot sim­ply from contacting a negatively charged surface.[34] Previously it was believed that the clotting process comprised a cascade of enzyme activity in which one activated the next, etc. The discovery that blood could be clotted simply by contacting a negatively charged surface ruled out the purely enzyme hypoth­esis. Only some of the known clotting factors have been shown to be enzymes.[35] As a result of this sur­prising discovery, detailed research was conducted in an attempt to describe the process. In some experi­ments, the negatively charged surfaces of selected, finely divided, inorganic crystals, including alu­minum oxide, barium sulfate, jeweler’s rouge, quartz, and titanium oxide, were considered.[36]

The clotting factor eventually shown to be activat­ed when whole blood contacted negatively charged surfaces was factor XII, also known as the Hageman factor. This is a positively charged protein migrating in an electric field (electrophoresis) toward the anode.[37] It is believed that factor XII is normally in the shape of a hairpin which binds to the negatively charged sur­face at the bend. Electrostatic attraction forces the two arms to lie flat on the surface, thereby exposing the inner faces and activating the molecule.

It was discovered that if the negatively charged particles were smaller than the clotting factor itself, activation was minimal. Or, if the concentration of clotting factor was too great, there was little or no activation.[38] Both of these observations indicated that the process was one of electrostatic attraction between the negatively charged surface and the clot­ting factor, which is a “basic” protein, that is, posi­tively charged.[39]

Activation of factor XII allows the activation of factor XI, which then activates factor IX. Thus, the blood clotting cascade continues to the formation of fibrin in the normal manner.[40] However, due to a series of activations begun by contact of factor XII with a negatively charged surface, trace amounts of factor Xa also show up in the blood. Factor VII is activated to Vila by factor Xa. Factor Vila then acti­vates factors IX and X, leading to the formation of thrombin. Factor Xa, with co-factor Va, continues the clotting cascade until fibrinogen is activated, leading to fibrin formation.[41] (See Table 5.)

As discussed earlier in terms of prostacyclin, beneath endothelial cells is another surface—the basement membrane. Called the extracellular matrix, it is a thin, continuous net of specialized tis­sue between endothelial cells and the underlying connective tissue. It has four or more main con­stituents, including proteoglycans (protein/polysac- charide).[42] The removal of endothelial cells by’MAT exposes this membrane, which is negatively charged by virtue of its sulfonated polysaccharides in the pro­teoglycans. This brings a reduced negatively charged surface into direct contact with the blood, which activates factor XII and the clotting cascade.[43]The positively charged toxic components of MAT also activate factor XII, as do disturbed disorganized cells, yeast/fungus cells, moldy cells, and the phos­phate groups in the lipid A component of endotoxin. (See Tables 2-5.)

To summarize this section, exotoxic, mycotoxic, and oxidative stress resulting from the overgrowth of bacteria, yeast/fungus, and then mold, has multiple actions, all leading to disseminated intravascular coagulation:

MAT activation of tissue factor gene in leukocytes; subsequent activation of factors VII, IX, and X, resulting in the blood clotting cascade.

MAT activation of tissue factor gene in endothelial cells, again leading to the clotting cascade.

MAT damage to endothelial cells, resulting in neu­trophil attraction, with TF gene activation and generation of MOBS, which, in turn, neutralize MAT, protecting healthy endothelial cells or the basement membrane and supporting the janitorial services of the leukocytes.

Removal of negatively charged endothelial cells by positively charged exotoxins, endotoxins, and mycotoxins, creating a surface devoid of PGI2, also exposes the negatively charged basement membrane, leading to the activation of factor XII and initiation of the clotting cascade. Positively charged components of EMPO, exotoxins and mycotoxins, and several other elements, including the lipid A component of bacterial endotoxin, also activate factor XII and the clotting cascade.

Endothelial Cells as Antithrombotics or Procoagulants

Normal, resting (unstimulated) endothelial cells show antithrombotic activity in several ways: (1) by the inhibition of prostacyclin (platelet adhesion and aggregation); (2) the inhibition of thrombin genera­tion; and (3) the activation of the fibrinolytic system, leading to clot lysis.[45] We will take a brief look at the thrombin aspect.

On the surface of endothelial cells is a protein called thrombomodulin, which acts as a receptor for thrombin. When bound to thrombomodulin, throm­bin can activate protein C. Activated protein C then catalyzes the proteolytic cleavage of factors Va and Vila, thereby destroying their participation in blood clotting. Thus thrombin, which normally activates fib­rinogen, plays an opposite role in this case and inhibits the clotting process.[46,47] (See Table 7.)

On the other side of the coin, the endothelial cell becomes a procoagulant agent when acted on by cer­tain lymphokines, such as interleukin-1. Not only can interleukin-1 induce TF gene expression, but it also suppresses transcription of the thrombomodulin gene in endothelial cells. As in other situations, the lymphokine-activated endothelial cell expresses TF on its surface as a result of TF gene activation. This leads to the production of thrombin and the trigger­ing of the blood clotting cascade.[48] (See Table 5.) Many lymphokines also stimulate adhesion of leuko­cytes to endothelial cells damaged by MAT, resulting in recycling of the cells by MOBS, as described later.

DIC Induced by Intracellular Exotoxic, Mycotoxic, Oxidative Stress by Bacteria, Yeast/Fungus and/or Mold

Any cell which has gone from an oxidative to a fer­mentative state can biochemically cause macrophage production of the lymphokine tumor necrosis factor (TNF). This protein has been shown to activate the gene for TF in fermenting cells, which are so behaved due to morbid evolution of bacteria, yeast/fungus, and then mold.[49,50] In the author’s view, a cell having been switched entirely to fermentation metabolism as a result of a physical or emotional disturbance of that cell, is what constitutes cancer (see Tables 5 and 13). (One might argue that this definition does not fit all “forms” of cancer, such as leukemia, for example. This is because leukemia is not cancer, but an immune response to the rise in EMPO and MAT in the body, and a relatively easy compensation to correct.)

The surface of many disorganizing or fermented cells (cancer cells) is characterized by small projec­tions in the plasma membrane which pinch off, becoming free vesicles containing toxins as well as TF complexed with factor VII. These vesicles can aggre­gate and/or lodge anywhere, ultimately releasing their contents. Also, the presence of excessive amounts of TF/factor VII complexes on the surface of fermented cells allows the formation of a fibrin net around the cell and around the entire mass of cells (tumor). This seems to be an attempt by the body to encapsulate and contain the mass. However, fermented cells do escape from the primary fibrin net, perhaps due to some electromagnetic effect, and become free-float­ing in the circulation. They may thus lodge elsewhere and instigate the fermentation of other cells by fungal penetration or by poisoning them and provoking a morbid evolution of their inherent microzymas.

Because of the surrounding fibrin net, these mobi­lized fermenting cells are protected from collection by the immune system while in transit.[51,52] (See Table 4.) The blockage or dissolution of fibrin net forma­tion by an anticoagulant such as heparin allows freed, fermenting (metastasizing) cells to be dismantled by natural killer cells and other immune cells (see Tables 5, 12 and 13).

DIC Induced by MAT/EMPO and Immune System Response (Release of MOBS)

Unsaturated fatty acids are highly susceptible to EMPO as well as MAT. Linoleic acid, a long-chain fatty acid present in white cells, has 18 carbons and 2 unsaturations. Subjected to MAT, linoleic acid binds the exotoxin, endotoxin, or mycotoxin, there­by forming an epoxide at the first unsaturation.[53] Research has revealed that this compound, named leukotoxin, is highly disturbing to other cells. It caus­es platelet lysis, thereby releasing TF and initiating DIC.[54] (See Table 10.) The fact that MAT result in fermented fats lends further credence to the sugges­tion that the initial and primary degenerative damage to structures and substances in the body is caused by exotoxins and/or mycotoxins, and that damage by MOBS, or by other free radicals, is not possible.

Another mechanism leading to DIC is the release of a special glycoprotein, sialic acid, from the terminal ends of cell-membrane polysaccharides, where it is always found. Polysaccharides play a highly significant role in biochemical processes, with both enzymes and membrane receptors recognizing various groupings of specific sugars linked in highly specific ways.

Immediately preceding the release of sialic acid in the polysaccharide chain is the sugar galactose. The sialic acid/galactose arrangement is utilized as a biolog­ical indicator of cellular and molecular aging. As cells age, sialic acid is naturally expressed from the terminal ends of polysaccharides, thereby exposing galactose. A membrane-bound enzyme from the liver, galactose oxi­dase, recognizes galactose and eventually disorganizes it, disrupting cell function integrity and hastening demise. Aged red blood cells, which have expressed a significant amount of sialic acid, are removed from the blood by this process. (I theorize that the biological ter­rain may be at work in normal cell aging. That is, the rate at which sialic acid is expressed is determined by the levels of corrosive acids in the system and the body’s ability to remove them, although there are no doubt intracellular factors at work as well.)

I suggest from my years of  clinical research  that cellular breakdown is compounded by the fermentation of the galactose by the microzyma. This is a process that begins from within and not necessarily from without. Not only does this action create more sialic acid, it creates other toxic waste products such as acetic aldehyde, alcohol, uric acid, oxalic acid, etc. The increase in cellular disturbances and fermenta­tion of the galactose creates biochemical signals for more galactose oxidase. This leads to greater cellular disorganization and developmental morbidity, espe­cially in the red blood cells, and a rise in the level of detrital serum proteins, which encourages clotting. From this perspective, diabetes, arthritis, atheroscle­rosis and other symptomatologies become more clearly “degenerative” (see Tables 2-5, 12 and 13).

Fibrinogen is a rather elaborate protein having the structure of three beads on a string. Expressed on the end beads is sialic acid, which indicates the beginning of disorganization of the fibrinogen and a declining negative charge to the positive. Prior to the declining charge and the expression of sialic acid on the end beads, fibrinogen, which is negatively charged, will not polymerize the healthy blood due to mutual repulsion. However, fibrinogen will poly­merize to damaged cells, EMPO, MAT and other positively charged areas of the body for repair pur­poses. Thus, as more and more sialic acid is expressed, there will be a significant reduction in the charge of the fibrinogen, acting as the primary requirement for the polymerization of fibrinogen (hypercoagulable state). The resulting polymer, fib­rin monomer, is the protein chain used in the repair of cells and clotting of blood.[55] End-linking will take place after the release of sialic acid (positive charge) by whatever means.

With this background, it is interesting to note that blood taken from persons suffering from anxiety is expressing sialic acid from fibrinogen, and is halfway toward clotting. Hormones released during anxiety states are easily fermented, giving more momentum to MAT and thereby resulting in this important change in fibrinogen. It leads to a clotting pattern characteristic of anxiety stress, and is readily identi­fied in the MOST. As can be seen in this picture, the pattern is a “snowstorm” of protein polymeriza­tions measuring from 2 to 10 microns.

allergiesbefore

 

 

 

 

 

 

 

[Micrograph 2: An Anxiety Profile showing a ‘snowstorm’ of 2 to 10 micron protein polymerizations starting from the center of the clot and moving out towards the edge]

As mentioned earlier, despite the attempt by the body to neutralize EMPO and MAT, an excess will initiate the release of MOBS by immune cells. A major MOBS is superoxide, designated chemically as O 2. It may exist alone or be attached to another ele­ment, such as potassium (KO’2) or sulfur (SO). Again, however, nature has provided a means of pro­tecting healthy cells—their negative charge[1]. Another protection against superoxide is the enzyme superox­ide dismutase (SOD), also found in all healthy cells.

A second member of the MOBS family is hydro­gen peroxide (H202). This molecule is very unstable and tends to react rapidly with other biological mol­ecules, damaging them. The release of hydrogen per­oxide in the body is a response to the overgrowth of decompositional organisms in a declining pH (com­promised biological terrain). The control for healthy cells against hydrogen peroxide is their negative charge and the protective enzyme catalase, one of the most efficient enzymes known.

When leukocytes and other white blood cells are stimulated by the presence of bacteria, yeast/fungus and mold, they treat these organisms as foreign par­ticles to be eliminated. During and prior to phagocy­tosis, the foregoing oxidative cytotoxins, along with the hydroxyl radical (OH’), are generated and released specifically for neutralizing microforms or harmful substances. This release is referred to as an “oxidative burst.” As a result of fermentation and the production of exotoxins and mycotoxins that fer­ment galactose from cells, the immune system is activated. An oxidative burst is released to neutralize the morbid microforms and mycotoxicity.[56] Like other biological processes faced with constantly alarming situations, the continued release of MOBS can get out of control. This may damage endothelial cells, the basement membrane, or other body ele­ments, and this activates fibrinogen to fibrin monomer (repair protein), leading to DIC [see Table 9]. Interestingly, the white blood cells capable of neutralizing MAT through MOBS production are the same ones capable of phagocytosis, the process by which foreign matter, waste products and microor­ganisms are collected and dumped in the liver.[57]

To summarize this section, pathological microforms and their acids create DIC by a number of pathways:

Leukotoxin (linoleic acid bound to mycotoxin) is highly toxic to cells. It causes platelet lysis, there­by releasing TF and initiating DIC.

The expression or release of sialic acid residues from healthy cells that have been disturbed allows for the fermentation of galactose, creating exotox­ins and mycotoxins, biochemically activating galactose oxidase, which further disturbs and dis­organizes healthy cells. This cycle loads the blood with debris.

EMPO and MAT disturb fibrinogen, which releas­es sialic acid and reduces the charge, allowing it to polymerize into fibrin monomer and fibrin nets.

The presence of exotoxins, endotoxins, and myco­toxins and their poisoning of cells activates the immune system. White blood cells generate MOBS (e.g., superoxide [0′2] or hydrogen perox­ide [H202]). These substances bind to and neu­tralize EMPO and MAT. MOBS are repelled by healthy endothelial cells and the basement mem­brane because of their negative charge. Cellular disturbances and disorganization stimulate the generation of fibrin monomer for repair purposes, leading to DIC.

Detection of Disseminated Intravascular Coagulation

The Sonodot Analyzer

The Sonoclot Coagulation Analyzer provides a reaction-rate record of fibrin and clot formation with platelet interaction. An axially vibrating probe is immersed to a controlled depth in a 0.4 ml sample of blood. The viscous drag imposed upon the probe by the fluid is sensed by the transducer. The electronic circuitry quantifies the drag as a change in electrical output. The signal is transmitted to a chart recorder which provides a representation of the entire clot for­mation, clot contraction and clot lysis processes. The analyzer is extremely sensitive to minute changes in visco-elasticity and records fibrin formation at a very early stage. The Sonoclot has been evaluated scientif­ically and shown to provide an accurate measurement of the clotting process.[58,59]

One application of the Analyzer has been the development of a test to distinguish non-advanced breast cancer from tumors that are benign. The ratio­nale for the test is the hypercoagulable state seen in cancer patients (Trousseau’s Syndrome), resulting from the generation of TF by leukocytes (mono­cytes).[60] (See Table 4.)

Fibrin Degradation
Products and Fibrin Monomer

DIC can be seen as a two-step process. First, fib­rinogen, which is always present in the blood, is acti­vated by any of several mechanisms. This activation leads to an automatic polymerization (chain forma­tion) resulting in fibrin monomer. This is not apparent in a microscope unless the blood is allowed to clot, as in the MOST.[61,62] The second step is the precipitation or deposition of fibrin (hard clot) by several other mechanisms. One of these is the formation of cross­links through the action of factor XIII. Another such mechanism may be poor circulation in an organ already blocked by deposited fibrin. The deposition of precipitated fibrin may be detected microscopically in tissue sections and diagnosed as DIC.[62]

Because fibrin monomer is not readily detected, a chemical test for it is of immense value in diagnosing DIC. Research has indicated that its detection may be very useful in the early diagnosis of DIC and MAT.[63] There are three fundamental physiologic areas related to blood clotting: (1) the prevention of blood clotting, (2) the clotting of blood, and (3) the removal of clotted blood once it has formed.

Enzymes are present that are capable of removing (lysing) clotted blood, one of which is plasmin. Another enzyme, plasminogen, is always present in the blood, but is inactive as a proteolytic agent. Plasminogen acti­vator converts plasminogen to plasmin, which can degrade deposited fibrin. This process is not specific for fibrin, however, and other proteins may be affected. When fibrin is degraded (fibrinolysis), fibrin monomer, as well as several other products, are formed. Commercial kits are available for the analysis of fibrin degradation. This test is an indirect measure of the pres­ence of DIC and MAT.[64]

Other tests include:

Protamine Sulfate: Protamine sulfate is a heparin binder sometimes used in surgery for excessive bleed­ing. The test, which indicates fibrin strands and fibrin degradation products, is conducted in a test tube, with fibrin monomer and fibrin forming early and polymer­ization of fibrin degradation products occurring later.[65] Ethanol Gelation: A white precipitate is formed by the addition of ethanol to a solution in a test tube containing fibrin monomer as a degradation product of fibrin, indicating DIC and MAT.[66]

The Mycotoxic Oxidative Stress Test (MOST)

Up to now, blood chemistries have been the prima­ry mode of diagnosis or analysis for the presence of pathology. In the view presented here, the bright-field microscope, is used to easily and inexpensively reveal a disease state as reflected by changes in certain aspects of blood composition and clotting ability. DIC is char­acterized by the abnormal presence in the blood of fib­rin monomer. When allowed to clot, blood containing such an abnormal artifact will exhibit distortions of normal patterns. The presence in the blood of soluble fragments of the extracellular matrix and soluble fibronectin, as well as other factors, will also create abnormal blood clotting patterns as described below.

A small amount of blood from a fingertip is con­tacted with a microscope slide. A series of drops is allowed to dry and clot in a normal manner. Under the compound microscope, the pattern seen in healthy subjects is essentially the same—a dense mat of red areas interconnected by dark, irregular lines, completely filling the area of the drop. The blood of people under mycotoxic/oxidative stress exhibits a variety of characteristic patterns which deviate from nor­mal, but with one striking, common abnormality: “clear” or white areas, in which the fibrin net/red blood cell conglomerate is missing.

BowelCancerLive Blood Dried Blood_0166

 

 

 

 

 

 

 

 

[Micrograph 3; An abnormal clot with striking ‘clear’ or white areas or protein polymerization as seen in the hyper coagulated blood of a patient with lower bowel imbalances]

Why the fibrin net is missing may be understood from the following: Two peptides—A and B—in the central protein bead of the fibrinogen structure become bound in the cross-linking process. There are two ways this can be configured: (1) Thrombin is capable of activating peptides A and B, resulting in the formation of a polymer loosely held together only by hydrogen bonds; (2) With peptides A and B acti­vated normally, the resulting hard clot is insoluble, indicating that the peptides are linked by covalent bonds. The difference in bonds results from factor XIII, an enzyme which links the two fibrin strands with a glutamine-lysine peptide bond.

Additional research has shown that the release of sialic acid from fibrinogen inhibits the action of factor XIII, resulting in a soft, white clot. In addition, acetic aldehyde has been shown to inactivate factor XIII directly. The soft clotting, compounded by other polymeric aggregations (described below), results in clear areas in the dry specimens. In the opposite extreme, high serum levels of calcium, for the pur­pose of neutralizing MAT, activates factor XIII, lead­ing to excessive cross-linking of fibrin to form a clot harder than normal. This is reflected in the MOST pattern characteristic of definite hypercalcemia— that of a series of cracks in the clot radiating outward from the center, resembling the spokes of a wheel. High serum calcium is the body’s attempt to com­pensate for the acidity of mycotoxic stress by pulling this alkalizing mineral from bone into the blood. This demand creates endocrine stress in turn, because reabsorption of bone is mediated by parathormone (PTH). Therefore, this clotting pattern indicates cal­cium deficiency and thyroid/parathyroid imbalance.

calciumpattern

 

 

 

 

 

 

 

[Micrograph 4: A mineral deficiency or more specifically a calcium deficiency pattern associated with an imbalance of they thyroid and/or parathyroid}

Advanced research has shown that there are seven carbohydrate chains in fibrinogen (each terminated by sialic acid). A second action of factor XIII is to ferment a large amount of carbohydrate during clot­ting. Because carbohydrate is most often water solu­ble, the loss of this material undoubtedly adds to the insolubility of a clot, while pathological retention contributes to the softness of the abnormal clot.

Clinical experience demonstrates that the MOST is a reliable indicator of exotoxic and mycotoxic stress and, concurrently, of various disorganizing symptoma­tologies associated with fermentative and oxidative processes. As various cellular degradation occurs, the blood-borne phenomena which accompany such symptoms as diabetes, arthritis, heart attack, stroke, atherosclerosis and cancer show up in the MOST, often with sialic acid beads in the clear areas of poly­merized proteins. (Determination of the liberation of sialic acid from carbohydrate has been approved by the U.S. Food and Drug Administration as an accept­ed indicator for cancer, and is clinically available.)

sialicacid

[Micrograph 5: Sialic acid beads are seen inside the protein
polymerization of the hypocoagulated blood as black dots]

The extent and shape of the clear areas are reflec­tive of particular symptomatologies which have arisen from the way in which the disease condition manifests in a given individual. This observation is borne out by having the patient undergo appropriate alkalizing therapy. With success of treatment based on the patient’s freedom from symptoms, sense of well-being, and live blood exams discussed in the main text of Sick and Tired, Reclaim Your Inner Terrain, Appendix C,[7] repeated analysis with the MOST reveals a progressively improving clotting pattern.

[Micrographs 6 and 7: Medically diagnosed cancer patient with large polymerized protein pools (PPP) in the hypo-coagulated blood above. In the picture below PPP’s have significantly reduced in size and the blood is moving to a more hyper-coagulated state as a result of reducing acid loads with an alkaline lifestyle and diet (7, 70)]

Because of its very nature, the MOST is emi­nently suited to reveal and measure the presence in the blood of abnormal substances, clotting factors, and disorganization of cells due to an inverted way of living, eating, and thinking, which gives rise to MAT. The MOST indicates both the direct and indirect activity of MAT on blood clotting, endothelium, and the extracellular matrix (described next), as well as on biochemical pathways, including hormonal ones. The generation of excessive MOBS in response to EMPO and MAT, the inability that accompanies all degenerative symptoms to neutralize or eradicate EMPO and MAT, and the recognized hyper- and hypocoagulable states seen in various symptomatolo­gies, will beyond doubt be revealed in the MOST.

Aspergillusnigercrystal

 

 

 

 

 

[Micrograph 8 and 9: Medically Diagnosed HIV/AIDS micrograph showing above an Aspergullus niger mold crystal using dark field microscopy and below a hypocoagulated blood clot with systemic protein polymerizations measuring in excess of 40 microns using bright field microscopy}

HIV

 

 

 

 

 

 

As mentioned, hormones are easily fermented, and this will show up as a hypocoagulated blood pattern in the MOST. It is my opinion, this hypocoagulated blood appears in the MOST as misty clouds of protein polymerizations throughout the clot, as seen in the accompanying picture.

poorfibrin

[Micrograph 10: Poor fibrin interconnection in the clot associated with endocrine or hormonal imbalance]

The MOST from Solubilized Extracellular Matrix

There is now a clearer picture of the biochemical rationale for correlating abnormal blood clotting patterns with the presence of degenerative symptoms.  A link between symptoms and the distorted clotted blood patterns has been delineated in the MOST.
Another reason for the abnormal clotting patterns accompanying pathological states, in addition to insufficient bonding of fibrinogen peptides as seen in the MOST, is presence in the blood of water-soluble fragments of the extracellular matrix.

Extracellular Matrix Degradation by MAT

The extracellular matrix (EM) is a three-dimen­sional gel, binding cells together and composed of five or more major constituents: collagen (protein), hyaluronic acid (polysaccharide), proteoglycans (pro- tein/polysaccharide), fibronectin and laminin. Also included are glycosaminoglycans and elastin.[67] In every degenerative disease studied by this author, evidence has been found for MAT activity destruc­tive of EM.

One of the proteolytic enzymes activated in response to EMPO and MAT is alpha-1 antitrypsin (capable of neutralizing MAT), normally not active in the presence of the enzyme trypsin. The active por­tion of this anti-exotoxin and antimycotoxin contains the amino acid methionine, which includes a C-S-C linkage. When chelated by the hydroxyl radical (one of the MOBS oxidants), methionine’s central sulfur atom acquires one or two oxygen atoms (forming the sulfone or sulfoxide respectively). The fermentation of methionine is a secondary effect of immune response to an alarming situation, intended to neutral­ize MAT and prevent degradation of the EM. Once alpha-1 antitrypsin is exhausted, MAT will have more access to the EM. If the EM is damaged beyond repair, then the enzyme trypsin is released to disorganize and recycle the cells involved.[68]

A similar scenario holds for the enzymes collage- nase and elastase. Thus, the absence of alpha-1 antitrypsin in the presence of EMPO and MAT activates three enzymes which degrade the extracellular matrix. Degradation of the EM by enzymes and MAT puts into the blood the water-soluble fragments (proteins and glycoproteins) of normally insoluble EM components (see Table 11). The presence of these fragments modifies the normal clotting pattern (described below), as seen in the M/OST, and is therefore an indication of EM degradation, which is always found with degenerative symptoms. (Also present is fibrin monomer, which has been found in the blood of patients suffering from collagen dis­ease.[69] See Table 11.)

Fibronectin is a molecule in EM having several binding sites for various long-chain molecules— heparin (a sulfonated polysaccharide) and collagen, for example. As such, it functions as a cellular glue, bind­ing cells together as well as various components of the EM. A soluble form of fibronectin is normally found free in the blood, and enters into the formation of a blood clot through the action of factor XIII. This form of fibronectin binds to fibrin. Elevated, bound-serum fibronectin results from EM fragmentation by MAT, and accompanies degenerative symptoms such as arthritis and emphysema (collagen diseases).

Water-soluble fragments of the EM bound by fibronectin form a three-dimensional network or gel in the pathologically clotted blood (fibrin and com­ponents of the blood clotting cascade). Since fibronectin binds to both fibrin and collagen, the two polymeric networks are superimposed and intermin­gled, resulting in a modification of the normal clot­ting pattern. Exactly how the pattern is modified depends upon the nature of the collagen abnormally present, the nature and extent of hyaluronate pre­sent, and the degree to which EM fibronectin has been released by MAT.

Conclusion

Thus, it is easily seen that there are many forms which the pattern of clotted blood may take, depending on the individual and the internal terrain that produced the modifying substances. The MOST reveals not only the presence of exotoxic and mycotoxic stress, but indicates as well the nature of the symptom(s) resulting from the stress (see Table 12). Since MAT underlie the entire complex of events which degrade the extracellular matrix, I must conclude that the absence of these exotoxins, endotoxins and mycotoxins would provide substantial improvements in tissue integrity and the overall physiology and functionality of the organism or animal and human.

­

­

References

[1]  Jones, T.W., “Observations on some points in the anatomy, physiology and pathology of the blood.”  British Foreign Medical Review, 1842. 14 : 585.

[2] Trousseau, A., Phlegmasis alba delens. “Clinque Medicale de L’Hotel Dieu de Paris.”, 1865, 3:94

[3]  Virchow, R., “Hypercoagulability: A review of its development, clinical application, and recent progress.”  Gesammelte Abhandlungen our Wussenschaftlichen Medizin, 1856, 26:477.

[4]  Rapaport, S.I., “Blood Coagulation and its Alterations in Hemorrhagic, and Thrombotic Disorders.”  The Western Journal of Medicine, 1993; 158: 153.

[5]  Hamilton, P.J. et al., “Disseminatied Intravascular Coagulation: A Review.”  Journal of Clinical Pathology, 1978, 31: 609

[6] The Harper Collins Illustrated Medical Dictionary, 1994, p.13.

[7] Young, RO, “Sick and Tired, Reclaim Your Inner Terraine,” Woodland Publishing, 1999.

[8] BeChamp, A., “The Blood and Its Third Anatomical Element,”  Hikari Omni Publishing, 1999.

[9]  Schwerdtle, C, Arnoul, F, Enerlein, G, “Introduction to Darkfield Diagnostics”, Semmelweis-Verlag (2006).

[10]  Hawk, BO, Thoma, GE, Inkley, JJ, The Evaluation of the Bolen Test as a Screening Test for Malignancy*, cancerres.aacrjournals.org on December 5, 2015. © 1951 American Association for Cancer Research.

[11]  Uchida, K., “Role of Reactive Aldehyde in Cardiovascular Diseases”,  Labortory of Food and Biodynamics, Nagoya University Graduate School of Bioagricultural Sciences, Nagoya, Japan , Free Radical Biology and MedicineVolume 28, Issue 12, 15 June 2000, Pages 1685–1696

 [12] Chang JCvan der Hoeven LHHaddox CH, “Glutathione reductase in the red blood cells”,  Ann Clin Lab Sci. 1978 Jan-Feb;8(1):23-9.

[13] Kutzing, MK, Firestein, BL, “Altered Uric Acid Levels and Disease States”, Department of Cell Biology and Neuroscience (M.K.K., B.L.F.), Graduate Program in Biomedical Engineering (M.K.K.), Rutgers University, Piscataway, New Jersey. Address correspondence to: Dr. Bonnie L. Firestein, Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854-8082. E-mail: firestein@biology.rutgers.edu

[14] Claudino, M,. Ceolin,,DS, Alberti, S.,  Cestari, TM,  Spadella, CT, Fischer Rubira-Bullen, IR, Gustavo Pompermaier Garlet, Gerson Francisco de Assis, ” Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats”,  Published: December 19, 2007. DOI: 10.1371/journal.pone.0001320

[15] Young RO (2015), “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition. Int J Complement Alt Med 2(1): 00046. DOI: 10.15406/ijcam.2015.02.00046

[16] Heloise Pöckel FernandesCarlos Lenz Cesar, and  Maria de Lourdes Barjas-Castro, “Electrical properties of the red blood cell membrane and immunohematological investigation”, Rev Bras Hematol Hemoter. 2011; 33(4): 297–301. doi:  10.5581/1516-8484.20110080 PMCID: PMC3415751

[17] Harris, JO, “The Relationship Between the Surface Charge and the Absorption of Acid Dyes by Bacterial Cells”, Department of Bacteriology, Kansas Agricultural Experiment Station, Manhattan,Kansas, Received for publication March 3, 195.

[18] Young, RO, “Metabolic and Dietary Acids are the Fuel That Lights the Fuse that Ignites Inflammation that Leads to Cancer”. https://www.linkedin.com/pulse/metabolic-dietary-acids-fuse-ignites-inflammation-causes-young. 2015.

[19] Snaders, R, “Did Bacteria Spark Evolution of Multicellular Life?” Berkeley News, Research, Science and Environment,  October 24, 2012.

[20] Wenner, M, “Humans Carry More Bacterial Cells than Human Ones”. Scientific American, November 30th, 2007.

[21} Animals and humans respond to MAT as a poison.

[22]  Morrison, D.C. et al. The effects of bacterial endotox­ins on host mediation systems. American Journal of Pathology, 1978; 93: 526.

[23]  Ibid.

[24]  Ibid.

[25]  Van Deventer, S.J.H. et al. Intestinal Endotoxemia. Gastroenterology, 1988; 94(3): 825-831.

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

[28]  Hu, T. et al. Synthesis of tissue factor messenger RNA and procoagulant activity in breast cancer cells in response to serum stimulation. Thrombosis Research, 1993; 72: 155.

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

[31]  Mackman et al. Lipopolysaccharides—mediated tran­scriptional activation of the human tissue factor gene in THP-1 monocytic cells requires both activator protein 1 and nuclear factor kappa B binding sites. Journal of Experimental Medicine, 1991; 174: 1517.

[32]  Yamada, O. et al. Deleterious effects of endotoxins on cultured endothelial cells: An in vitro model of vascular injury. Inflammation, 1981; 5: 115.

[33]  Colucci, M. et al. Cultured human endothelial cells: An in vitro model of vascular injury. Journal of Clinical Investigation, 1983; 71: 1893.

[34]  Cho, T.H. et al. Effects of Escherichia coli toxin on structure and permeability of myocardial capillaries.

[35]  Acta Pathologica Japonica, 1991; 41: 12.

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

[38]  Margolis, J. The interrelationship of coagulation of plasma and release of peptides. Annals of the New York Academy of Sciences, 1963; 104: 133.

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

[42]  Alberts, B. et al, eds. Molecular Biology of the Cell. New York: Garland Publishing, Inc., 1989 (2nd ed.), p. 818.

[43]  Rapaport, op. cit. (Ref. 4).

[44] Bertz, A., et al. Modulation by cytokines of leukocyte endothelial cell interactions. Implications for thrombo­sis. Biorheology, 1990; 27: 455.

[45]  Rapaport, op. cit. (Ref. 4).

[46]  Nachman, R.L. et al. Hypercoagulable states. Annab of Internal Medicine, 1993; 119: 819.

[47]  Ibid.

[48]  Tallman, M.S., et al. New insights into the pathogene­sis of coagulation dysfunction in acute promyelocytic leukemia. Leukemia and Lymphoma, 1993; IT. 27.

[49]  Silberberg, J.M., et al. Identification of tissue factor in two human pancreatic cancer cell lines. Cancer Research, 1989; 49: 5443.

[50]  Grimstad, I.A. et al. Thromboplastin release, but not content, correlates with spontaneous metastasis of can­cer cells. International Journal of Cancer, 1988; 41: 427.

[51]  Gunji, Y. et al. Role of fibrin coagulation in protection of murine tumor cells from destruction by cytotoxic cells. Cancer Research, 1988; 48: 5216.

[52]  Sugiyama, S. et al. The role of leukotoxin (9, 10- epoxy-12-octadecenoate) in the genesis of coagulation abnormalities. Life Sciences, 1988; 43: 221.

[53]  Ibid.

[54]  White, A. et al, eds. Principles of Biochemistry. McGraw-Hill Book Co., New York, 1964, p. 648.

[55]  Mueller, H.E. et al. Increase of microbial neu­raminidase activity by the hydrogen peroxide concen­tration. Experientia, 1972; 23: 397.

[56]  Young, Robert O. Fermentology and oxidology. The study of fungus-produced mycotoxic species and the activation of the immune system and release of microzymian oxidative buffering species (MOBS). Self- published: InnerLight Biological Research Foundation, Alpine, Utah, 1994.

[57]Chandler, WL. et al. Evaluation of a new dynamic vis­cometer for measuring the viscosity of whole blood and plasma. Clinical Chemistry, 1986; 32: 505.

[58]  Saleem, A. et al. Viscoelastic measurement of clot for­mation: A new test of platelet function. Annals of Clinical and Laboratory Science, 1983; 13: 115.

[59]  Spillert, C.R. et al. Altered coagulability: An aid toselective breast biopsy. Journal of the National Medical Association, 1993; 85: 273.

[60]  Bowie, E.J. et al. The clinical pathology of intravascular coagulation. Bibliotheca Haematologica, 1983; 49: 217.

[61]  Muller-Berghaus, G. et al. The role of granulocytes in the activation of intravascular coagulation and the pre­cipitation of soluble fibrin by endotoxin. Blood, 1975; 45: 631.

[62]  Bick, R.L. Disseminated intravascular coagulation. Hematology/Oncology Clinics of North America, 1993; 6: 1259.

[63]  Bredbacka, S. et al. Laboratory methods for detecting disseminated intravascular coagulation (DIC): New aspects. Acta Anaesthesiologica Scandinavica, 1993; 37: 125.

[64]  Sigma Diagnostics, St. Louis, MO 63178; tel: 314- 771-5765.

[65]  Nachman, R.L. et al. Detection of intravascular coag­ulation by a serial-dilution protamine sulfate test. Annals of Internal Medicine, 1971; 75: 895.

[66]  Breen, F.A. et al. Ethanol gelation: A rapid screening test for intravascular coagulation. Annals of Internal Medicine, 1970; 69: 1197.

[67] Hay, E.D., ed. Cell Biology of Extracellular Matrix. New York: Plenum Press, 1981, p. 653.

[68]  Carp, H. et al. In vitro suppression of serum elastase- inhibitory capacity by ROTS generated by phagocytos- ing polymorphonuclear leukocytes. Journal of Clinical Investigation, 1979; 63: 793.

[69]  Wilson, C.L. The alternatively spliced V region con­tributes to the differential incorporation of plasma and cellular fibronectins into fibrin clots. Journal of Cell Biology, 1992; 119: 923.

[70] Young, RO, Young, SR, “The pH Miracle Revised and Updated”, Hachette Publishing, 2010.

Tables

Table 1

Expression of Sialic Acid/Galactose [MAT] from Cell and Protein Degeneration (From All Serum Proteins, RBC/WBC and Other Cell Surfaces)

  1.  Carbohydrate, Proteins, and Fats From Diet, Body Cells or Reserves
  2. As cells breakdown or ferment they give birth to bacteria, yeast, fungus and mold [EMPO] and their associated metabolic acidic waste [MAT]
  3. Exotoxins, Endotoxins, and Mycotoxins [MAT]
  4. Acetyl Aldehyde, Ethyl Alcohol, Uric Acid, Alloxan, Lactic Acid are examples of MAT
  5. MAT  Ferments Other Body Cells and their Extracellular Membranes and Proteins
  6. MAT Modifies Glycoprotein
  7. Binds to liver Galactosidase
  8. Creating an Increase in Cell and Protein Fermentation and Degeneration and Increased Amounts of Exotoxins, Endotoxins and Mycotoxins [MAT]

Table1a

Table 2

Expression of Sialic Acid [MAT] From the Fermentation of Degeneration of Insulin Producing Pancreatic Beta-Cells in Type I, Type II and Type III Diabetes

  1. Pancreatic Insulin producing Beta-Cells with no or minimal Surface Sialic Acid [MAT]A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Diet
  2. Normal regulation of Insulin Production
  3. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choicesdd
  4. Leads to cellular fermentation and degeneration and the birth of EMPO
  5. This lead to increased abnormal amounts of MAT that the immune system, the alkaline buffering system and the elimination organs has to deal with
  6. Fermenting and degenerating Insulin Producing Beta Cells
  7. Giving Rise to Surface Cell Sialic Acid [MAT}
  8. Increased Amounts of Sialic Acid Activates the Immune Response [MOBS] and Sialidase [AB]
  9. Leads to Lowered or No Insulin Production
  10. Symptoms of Type I, Type II or Type III Expressed
  11. The insulin producing beta cells of the Islets of Langerhans express silica acid on their surface as a break down metabolite.  I have suggested that when insulin producing beta cells are physically disturbed by MAT they begin to disorganize and express sialic acid on the surface of the cell.  This indicates the death of the cell and insulin production will stop.

Table2a

Table 3

HIGH BLOOD PRESSURE, ATHEROSCLEROSIS, HEART ATTACKS, STROKES, and CONGESTIVE HEART FAILURE

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the immune system to chelate the MAT.
  4. Increased amounts of MAT will cause endothelial breakdown and the expression of Sialic acid.
  5. Increased Amounts of Sialic Acid and damage to the endothelial will cause a reduction in the negative surface-charge leading to the release of Glycoproteins.
  6. The release of Glycoproteins will cause the activation of Factor XII and the blood clotting cascade.
  7. This cause the creation and formation of fibrin monomers and the increase of Platelet Deposition out of the red blood cells for clotting purposes
  8. The immune system will activate and MOBS will be released as well as sodium bicarbonate, calcium, lipids and other alkaline buffers to reduce metabolic acidity.
  9. The build-up of fibrin monomers in the clotting cascade will lead to fibrin nets and clots causing an increase in blood pressure and the risk of blockages potentially causing a Stroke or Heart Attack.

Table3a

Table 4

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
FROM INTRACELLULAR DISORGANIZATION OR FERMENTATION WHICH GIVES RISE TO MAT
 AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII (VIIa) and trace amounts of Factor Xa into the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activation of the blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated these unhealthy cells to protect healthy body cells.
  11. As body and blood cells breakdown from MAT this causes an increase of MAT and EMPO leading to systemic latent tissue acidosis and a potential metastatic cancerous condition.

Table4a

 Table 5

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
IN CELLULAR DISORGANIZATION OR FERMENTATION/OXIDATON AND THE INCREASE OF MAT AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices.
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII and Factor Xa in the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activated blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated the unhealthy cells.
  11. This leads to tumor formation of the unhealthy or cancerous cells.
  12. As the body and blood cells breakdown this causes an increase of MAT and EMPO leading to an increased risk of  systemic metastatic cancer.

Table5aTable 6

ENDOTHEIAl CELL CONVERSION FROM AN
ANTITHROMBOTIC STATE TO A PROCOAGULANT STATE
CELLULAR DISORGANIZING PATHWAY

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This leads to increased abnormal amounts of MAT that damages the protective endothelial cover cells leading to a reduction of PGI2
  4. The absence of PGI2 causes the release of Interleukin-1 and/or Tumor Necrosis Factor (TNF).
  5. In addition the loss of protective endothelial cover cells leads to Tissue Factor Gene Activation and the release of Thrombin causing a pro-coagulate state leading to DIC
  6. Another pathway to DIC would be the loss of protective endothelial cover cells and the absence of PGI2 causes the suppression of Thromomodulin, Protein C leading to procogradulation and DIC.

Talble6

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table7

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table8Table 9

ACTIVATION OF SIALIDASE AND MICROZYMIAN OXIDATIVE BUFFERING SPECIES (MOBS) BY EMPO AND MAT

Table9

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table10

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table11

Table 12

TYPICAL SOURCES OF FERMENTATION INSULT (MAT) IN BIOLOGICAL SYSTEMS INITIATING DIC

Table12

Table 13

POSITIVE CHARGE OF CANCEROUS CELLS AND TUMORS AND THE FORMATION OF FIBRIN NETS AND TREES IN RESPONSE TO MAT

Table13

A Self-Care to a Self-Cure for Type I Diabetes!

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Today is Jakob’s 8th birthday. Jakob was diagnosed with Type I diabetes and was taking daily insulin shots to regulate his blood sugar levels. Now he is following Dr. Robert O. Young’s pH Miracle for Diabetes Protocol as outlined in The pH Miracle for Diabetes. It has NOW been 241 days since Jakob needed a single daily insulin shot. His blood sugar levels have been normal for over 8 months. He is a very happy and healthy boy now. And his parents are even more happy that they have a happy and healthy boy free from high blood sugars and the daily insulin shots! I am also happy for Jakob and his family. You know who is not happy about Jakob’s self-cure from Type I Diabetes and wants Dr Young’s protocol suppressed?

In the words of Martin Luther King, Jr., “Our lives begin to end the day we become silent about things that matter.” The Self-Care to a Self-Cure for diabetes matters.

As long as I am alive i will continue to proclaim to all the World to all who will listen to the truth that there is a natural non-invasive, drug-free, self-cure for Type I, Type II and Type III diabetes, for heart disease and for cancer.

There is a natural non-invasive, drug-free, self-care to a self-cure for ALL sickness and disease. No child needs to be diabetic if the child and his or her parents are willing to follow The pH Miracle for Diabetes Protocol. UNDERSTAND?

If you have Type I, II or III diabetes or know someone who has diabetes and is insulin dependent, the pH Miracle for Diabetes Protocol will begin the process of your/their Self-Care to a Self-Cure regardless of how long you’ve/they’ve been doing diabetes! Understand?

Stand-up for health freedom! Education NOT Medication! Health Care NOT Sick Care! Read and share the truth with your family and friends. Juvenile diabetes is a world-wide epidemic and we NOW know the cause and we have the self-cure. Every child with diabetes can be healed.

Remember it is YOUR Body, YOUR LIFE and YOUR CHOICE. YOU MUST BE THE CHANGE AND THE CURE YOU WANT TO SEE!

For more information of reversing Type I, II and III diabetes go to: http://www.phoreveryoung.wordpress.com, http://www.phmiracle.com

The Sugar Fructose from Fruit Causes Diabetes!

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Credit: © flaviuz / Fotolia

Recent studies have shown that added sugars, particularly those containing fructose, are a principal driver of diabetes and pre-diabetes, even more so than other carbohydrates. Clinical experts writing in Mayo Clinic Proceedings challenge current dietary guidelines that allow up to 25% of total daily calories as added sugars, and propose drastic reductions in the amount of added sugar, and especially added fructose, people consume.

Worldwide, approximately one in ten adults has type 2 diabetes, with the number of individuals afflicted by the disease across the globe more than doubling from 153 million in 1980 to 347 million in 2008. In the United States, 29 million adults (one in eleven) have type 2 diabetes and another 86 million (more than one in three) have pre-diabetes.

“At current levels, added-sugar consumption, and added-fructose consumption in particular, are fueling a worsening epidemic of type 2 diabetes,” said lead author James J. DiNicolantonio, PharmD, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute, Kansas City, MO. “Approximately 40% of U.S. adults already have some degree of insulin resistance with projections that nearly the same percentage will eventually develop frank diabetes.”

The net result of excess consumption of added fructose is derangement of both overall metabolism and global insulin resistance say the authors. Other dietary sugars not containing fructose seem to be less detrimental in these respects. Indeed, several clinical trials have shown that compared to glucose or starch, isocaloric exchange with fructose or sucrose leads to increases in fasting insulin, fasting glucose, and the insulin/glucose responses to a sucrose load. “This suggests that sucrose (in particular the fructose component) is more harmful compared to other carbohydrates,” added Dr. DiNicolantonio. Dr. DiNicolantonio and his co-authors, James H O’Keefe, MD, Saint Luke’s Mid America Heart Institute, Kansas City, MO, and Sean C. Lucan, MD, MPH, MS, a family physician at Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, examined animal experiments and human studies to come to their conclusions.

Data from recent trials suggest that replacing glucose-only starch with fructose-containing table sugar (sucrose) results in significant adverse metabolic effects. Adverse effects are broader with increasing baseline insulin resistance and more profound with greater proportions of added fructose in the diet.

The totality of the evidence is compelling to suggest that added sugar, and especially added fructose (usually in the form of high-fructose corn syrup and table sugar), are a serious and growing public health problem, according to the authors.

The 2010 Dietary Guidelines for Americans say it is acceptable for some people to consume up to 19% of calories from added sugars, and the Institute of Medicine permits up to 25% of total calories from added sugars. In contrast, the World Health Organization recommends that added sugars should make up no more than 10% of an entire day’s caloric intake, with a proposal to lower this level to 5% or less for optimal health. Such levels would be more in line with what the authors would recommend and similarly restrictive to existing American Heart Association (AHA) recommendations–to consume no more than six teaspoons (24 grams) of sugar per day for women and no more than nine teaspoons (36 grams) of sugar per day for men.

While fructose is found naturally in some whole foods like fruits and vegetables, consuming these foods poses no problem for human health. Indeed, consuming fruits and vegetables is likely protective against diabetes and broader cardiometabolic dysfunction, explained DiNicolantonio and colleagues. The authors propose that dietary guidelines should be modified to encourage individuals to replace processed foods, laden with added sugars and fructose, with whole foods like fruits and vegetables. “Most existing guidelines fall short of this mark at the potential cost of worsening rates of diabetes and related cardiovascular and other consequences,” they wrote.

The authors also think there should be incentives for industry to add less sugars, especially fructose-containing varieties, to food-and-beverage products. And they conclude that at “an individual level, limiting consumption of foods and beverages that contain added sugars, particularly added fructose, may be one of the single most effective strategies for ensuring one’s robust future health.”


Story Source:

The above story is based on materials provided by Elsevier Health SciencesNote: Materials may be edited for content and length.


Journal Reference:

  1. James J. DiNicolantonio, James H. O’Keefe, Sean C. Lucan. Added Fructose: A Principal Driver of Type 2 Diabetes Mellitus and Its ConsequencesMayo Clinic Proceedings, 2015; DOI: 10.1016/j.mayocp.2014.12.019

The pH Miracle Self-Care to a Self-Cure for ALL TYPES of DIABETES!

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My resolution for 2015 is to share the pH Miracle for reversing ALL types of diabetes with every parent with a child, every young adult and every adult with the diagnosis of insulin dependent diabetes that there is A Self-Care to a Self-Cure for Type I Diabetes – What is the cause and how to reverse an acidic condition of the gut. When the gut is healthy NO MORE diabetes! Please watch, listen, share and like the pH Miracle self-care to a self-cure for ALL TYPES of diabetes.

Part 3 – The Key to Prevention for a Self-Care to a Self-Cure for ALL Sickness and Disease!

Health and Healing Crusade welcomed Robert O. Young M.Sc., D.Sc., Ph.D. ND who gave three incredible talks on promoting an alkaline Lifestyle and diet. He claims that health depends primarily on proper balance between an alkaline and acid environment in the human body, and that an acid environment causes cancer, obesity, osteoporosis, yeast overgrowth, flu, skin disorders, and other diseases.

Please listen carefully as he teaches some important truths about our wonderful universe, our bodies, and the importance of having an alkaline environment to keep us free from ALL sickness and disease caused by and acidic diet and our neglect to care for our body!

Part 2 – The Prevention and Self- Care to a Self-Cure for ALL Sickness and Disease!

Health and Healing Crusade welcomed Robert O. Young M.Sc., D.Sc., Ph.D. ND who gave three incredible talks on promoting an alkaline Lifestyle and diet. He claims that health depends primarily on proper balance between an alkaline and acid environment in the human body, and that an acid environment causes cancer, obesity, osteoporosis, yeast overgrowth, flu, skin disorders, and other diseases.

Please listen carefully as he teaches some important truths about our wonderful universe, our bodies, and the importance of having an alkaline environment to keep us free from ALL sickness and disease caused by and acidic diet and our neglect to care for our body!

The Prevention and Self-Care to a Self-Cure for ALL Sickness and Disease

Health and Healing Crusade welcomed Robert O. Young M.Sc., D.Sc., Ph.D. ND who gave three incredible talks on promoting an alkaline Lifestyle and diet. He claims that health depends primarily on proper balance between an alkaline and acid environment in the human body, and that an acid environment causes cancer, obesity, osteoporosis, yeast overgrowth, flu, skin disorders, and other diseases.

Please listen carefully as he teaches some important truths about our wonderful universe, our bodies, and the importance of having an alkaline environment to keep us free from ALL sickness and disease caused by and acidic diet and our neglect to care for our body!

The Game of Life and How it Ends!

The Game of Life and Death!

Odds-of-Dying

Let’s see if the odds are in your favor.

Lifetime odds of death by cause:

Most Americans won’t die of any of the below causes.

But about 56 million will die of…
Heart disease and cancer: 1 in 7
Chronic lower respiratory: 1 in 29

And motor vehicle incidents (1 in 112) will claim about as many as intentional self harm (1 in 103)

While around 4.7 million present day Americans will due of Unintentional poisoning by and exposure to noxious substances (1 in 119)
And falls (1 in 152)

Assault by firearm will claim about a 890,000 (1 in 356).
Much more than accidental firearm discharges, which clocks in at 48,000 (1 in 6,509).

There’s a chance you’ll be on the street.
Motor vehicle incidents: 1 in 112
Car occupant: 1 in 492
Pedestrian: 1 in 723
Motorcycle rider: 1 in 922

Though your safest bets are bikes, planes and spacecraft:
Pedalcyclist: 1 in 4,974
Air and space travel incidents: 1 in 8,321

Around 609,000 people can expect to die in one of these unsavory ways:
Unintentional drowning and submersion: 1 in 1,043
Exposure to fire, flames, or smoke: 1 in 1,418
Choking from inhalation and ingestion of food: 1 in 3,649

At least mother nature won’t kill many:
Exposure to excessive natural heat: 1 in 8,321
Exposure to electric current, radiation, temperature and pressure: 1 in 12,174
Contact with sharp objects: 1 in 37,566
Contact with heat and hot substances: 1 in 62,608
Contact with hornets, wasps and bees: 1 in 75,852
Cataclysmic storm: 1 in 83,922

And your much likelier to be killed by a dog than a venomous snake:
Bitten or struck by dog: 1 in 103,798
Venomous snake: 1 in 1,224,099[4]

Similar numbers of people will be legally executed as well be killed by lightning:
Legal execution: 1 in 96,203
Lightning: 1 in 136,011

Or you could die in a terrorist attack (1 in 256,410)[3]
A number comparable to your chances of being crushed to death by your own television(1 in 253,205)

Though the chances of just furniture (1 in 1,346,153) or appliances crushing you (1 in 2,025,641) are much more slim.

But it really all depends on your age

Top ten causes of death by age:

<1: Congenital anomalies, short gestation, SIDS, Maternal pregnancy complication, placenta cord membrane, unintentional injury, respiratory distress, bacterial sepsis, neonatal hemorrhage, circulatory system disease
1-4: Unintentional injury, congenital anomalies, malignant noplasms, homicide, heart disease, influenza/pneumonia, septicema, perinatal period, chronic low respiratory disease, benign neoplasms
5-9: Unintentional injury, malignant neoplasms, congenital anomalies, homicide, heart disease, influenza/pneumonia, septicemia, benign neoplasms, chronic low respiratory disease, cerebro-vascular
10-14: Unintentional injury, malignant neoplasms, suicide, congenital anomalies, homicide, heart disease, chronic low respiratory disease, influenza/pneumonia, benign neoplasms, cerebro-vascular
15-24: Unintentional injury, homicide, suicide, malignant neoplasms, heart disease, congenital anomalies, influenza/pneumonia, cerebro-vascular, chronic low respiratory disease, HIV
25-34: Unintentional injury, suicide, homicide, malignant neoplasms, heart disease, HIV, diabetes melitus, cerebro-vascular, congenital anomalies, influenza/pneumonia
35-44: Unintentional injury, malignant neoplasms, heart disease, suicide, HIV, Homicide, liver disease, cerebro-vascular, diabetes melitits, influenza/pneumonia
45-54: Malignant neoplasms, heart disease, unintentional injury, liver disease, suicide, cerebro-vasclar, diabetes melititus, HIV, chronic low respiratory, viral hepatitis
55-64: Malignant neoplasms, heart disease, chronic low respiratory disease, diabetes melititus, cerebro-vascular, unintentional injury, liver disease, suicide, nephritis, septicemia
65+: Heart disease, malignant neoplasms, cerebro-vascular, chronic low respiratory disease, alzheimer’s disease, influenza/pneumonia, diabetes melititus, nephritis, unintentional injury, septicemia.

Total deaths by age bracket:

<1: 19,229
1-4: 3,645
5-9: 2,358
10-14: 3,128
15-24: 28,677
25-34: 32,740
35-44: 69,448
45-54: 139,380
55-64: 220,404
65+: 1,471,011

Total: 1,990,020 per year
(From 2003)
That’s 1 in 145 whose time is up, every year.

Such is the game of life!

Odds-of-Dying

Citations:

Eating Eggs Will Increase Your Risk For Cancer, Heart Disease and Diabetes!

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A recent question in The New York Times Well blog created some confusion by asking how many eggs you can (or should) eat. The answer was not eggs-actly correct.

Since one egg has the same amount of cholesterol as a Big Mac, it is unnecessary—even detrimental to your health—to consume eggs or egg products. One egg has more cholesterol than your body needs. In fact, any added dietary cholesterol is unnecessary because our bodies already produce more than the amount we require. An excess of cholesterol leads to heart disease, so it’s no surprise that a 2010 study in theCanadian Journal of Cardiology found that those who consume the most eggs have a 19 percent increased risk for cardiovascular problems.

What The New York Times blog fails to explain is that eating an occasional egg might not increase health risks for people already eating a high-fat, high-cholesterol diet—just as smoking an occasional cigar might not increase health risks for people already smoking cigarettes. But if people are already eating a healthful diet without any added dietary cholesterol, eggs can contribute to many problems in addition to heart disease. Recent studies in Atherosclerosis and the International Journal of Cancershow that egg consumption can also cause diabetes and even cancer.

The misperception surrounding the necessity of eggs has even spread to the courtroom. Unilever is suing Hampton Creek Foods for using the term “mayo” in relation to its egg-free Just Mayo condiment. The argument is that “mayonnaise” is defined as an egg-based product. However, removing the egg from mayonnaise also removes the cholesterol, a win-win. The lawsuit seems to be backfiring for Unilever by helping people realize that there are more healthful alternatives to Hellmann’s mayonnaise.

No matter what you call it, egg-free is the better option.

For more information about egg consumption and health, read and share our fact sheet:http://www.pcrm.org/pdfs/health/Nutrition-Fact-Sheets/Eggs-fact-sheet.pdf

Last updated by  at November 24, 2014.

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