Category Archives: Traditional Medicine

The Real Truth About How NOT to DIE and DIE-IT!

20 Ways on How to Live Longer and Healthier – Free from ALL Sickness and Disease and Old Age

Have you heard about the ravages of acid rain in Australia and the loss of the coral reef or in Alaska and the loss of millions of pine trees or maybe you have heard about the oceans and the pH dropping because of acid rain. The cause is the result of toxic acidic carbon emissions in the global environment. Acid rain damages the leaves and needles on trees, reduces a tree’s ability to withstand cold, drought, disease and pests, and even inhibits or prevents plant reproduction. The oceans of the World are dying because of acidic carbon emissions from cars and cows. In an effort for the Earth and the oceans to stay alive and combat increased acidic pollution, as tree roots pull important nutrients such as calcium and magnesium from the soil and calcium and the oceans are pulling calcium and magnesium from the coral reefs and sodium from the ocean water increasing acidity. The extraction of alkaline minerals from the soil and water is necessary for all living things on the earth and oceans to stay alive and avoid sudden death. These alkaline nutrients help to balance the increased effects of acid rain, but as they become depleted from the soil or from the ocean, the trees’ and marine life’s ability to survive is strained and placed in certain danger of extinction. Just look at the pictures below and see what is happening to the forests of Denali, Alaska and the great barrier reef in Queensland, Australia. The forests in Alaska and the great barrier reef in Queensland, Australia are both headed towards irreversible extinction because of acid rain.

We Are All Subject to Acid Rain!

What if I told you that most ALL people living today are unknowingly doing similar things to their body? A highly acidic lifestyle and diet is like acid rain in our blood, interstitial fluids and intracellular fluids that constitutes over 65% of the whole body. While the body has an alkaline buffering system (headed up by the stomach) in place to ensure that the blood and the interstitial fluids stay slightly alkaline at 7.365 pH, the depletion of alkaline minerals from the bones, muscles and other parts of your body may leave YOU vulnerable to health issues leading to ALL sickness and disease.

What is pH – The Power of Hydrogen or Perfectly Healthy or Both?

The pH (potential of hydrogen) is the measurement of acid (a measurement of hydrogen ions or protons) or alkalinity (a measurement of reduced hydrogen or electrons) on a scale from 0 to 14 with a midpoint of 7. The lower the number the higher the acidity (or the greater the concentration of hydrogen ions or protons) based upon a logarithm to the power of negative 10! For example, the pH of a healthy ocean environment free from acid rain would be 8.350. If the ocean pH drops 1 point due to acid rain to a pH of 7.350, which is a 10 times drop in pH, all life as we know it in the oceans would die. In fact, if the ocean pH drops from 8.350 to 8.100, which is a .235 drop, ALL life in the oceans would die! That is all it takes for ALL marine life to cease in our Oceans! JUST a small drop of 2/10’s of 1 point for ALL life to end! Here is another very important example that I truly want you to understand. The healthy pH of the human blood and interstitial fluids which makes up 80 percent of ALL body fluids is 7.365. This pH of the blood and interstitial fluids is a dynamic and is always changing. How do I know this? Because Dr. Galina Migalko, MD, NMD and I are the only scientist in the World measuring and comparing the pH and chemistries of the blood against the pH and chemistries of the interstitium. This is critical to truly understand when you are moving toward metabolic alkalosis or metabolic acidosis and preventing and/or reversing any sickness and disease as well as determining the efficacy of any non-invasive or invasive treatments. In other words, are the treatments for any sickness and disease making you sicker or better, whether conventional or traditional? This can now be measured and determined with certainty.

Why is YOUR Stomach So Important to the pH of the Blood and Interstitum

So why does the body, primarily the stomach work so hard to maintain the delicate pH of the blood and interstitial fluids of the interstitium? Here is the most important answer YOU will read in YOUR life! If the blood and interstitial fluids drop below 7.100 from the ideal healthy pH of 7.365 you would go into a coma. When the blood and interstitial fluid pH drops to 6.900 you are DEAD! From what? Not global warming but from body warming or in other words acidosis! The key to avoid death is to maintain the alkaline design of the blood and interstitial fluids at a precise pH of 7.365 which can be measured without drawing one drop of blood or interstitial fluid. The technology is here and the science is real!

What is the Common Denominator of pH in Relationship to the Cause of ALL Sickness and Disease

This is the common denominator for ALL sickness and disease – ALL sickness and disease are caused by acidosis or acid rain or body warming! Therefore, there are NO specific diseases, there are ONLY specific disease or sickness conditions. All sickness and disease is caused by acid rain from within and is exactly what is happening in the oceans, the soils of our planet and in all humanity. Planetary and human sickness and disease is on the rise because of personal acidic lifestyles and dietary choices and because of ignorance. Name any disease and that disease or sickness is caused by metabolic, respiratory, gastrointestinal or environmental acidosis.

Check out this YouTube video on the 7 signs YOU and TOO Acidic

I hope you can see NOW how important it is to understand and then monitor your pH daily by having your your blood and interstitial fluids tested. Unfortunately, this new science and technology for testing the pH of the blood and interstitial fluids is limited Worldwide. (For more information concerning the testing of the blood and interstitial fluids or to make an appointment email: phmiraclelife@gmail.com) In the meantime, there is a simple, inexpensive and noninvasive way for testing the fluids of the interstitium, but not of the blood, for those of you who desire to monitor your interstitial fluid pH daily. You can test the pH of the morning urine, since this urine is a product of the interstitium and NOT of the blood, by using special pHydrion strips (www.phoreveryoung.com). When you measure the pH of your urine using these special pHydrion strips it is important to achieve each morning a pH of at least 7.300 by following the suggested lifestyle and diet as described below. When you are testing your morning urine, which is the most acidic time of the day, you are testing the pH of the interstitial fluids which makes up over 60 percent of the body fluids (25 liters). You can also test your saliva using the same special pHydrion strips. When you are testing your saliva pH you are testing your body reserves available for buffering acid rain. Both the urine and saliva pH should be at least 7.300 and must be tested daily as you follow the pH Miracle alkaline lifestyle and diet in order to achieve an ideal pH for “Perfect Health!”

What Does the Stomach Have to Do With pH

An acidic pH of the blood and then interstitial fluids is what causes acid reflux—a condition in which the stomach creates when it is trying to buffer dietary acids from your toxic acidic food or drink ingested or metabolic acids from all functions of the body or respiratory acids from your respiratory system to maintain the pH of the blood and interstitial fluids at a delicate pH of 7.365. The following is the stomach chemistry as it creates sodium bicarbonate to buffer excess acid rain on your blood, interstitial fluids and intercellular fluids: H20 (water) + NaCl (salt) + C02 (carbon dioxide) = NaHC03 (sodium bicarbonate) + HCL (hydrochloric acid).

This may be the first time you have ever heard this, but I have been saying this for many years, “the stomach DOES NOT DIGEST FOOD it ALKALIZES FOOD and protects ALL of our body fluids, organs and tissues from dietary, metabolic, respiratory and environmental acidosis! In other words, the stomach is an organ of contribution and NOT an organ of digestion. Eat any food without chewing it, like a piece of corn and see what happens. The corn comes out of your anus the same way it went into your mouth. The stomach digests nothing. The hydrochloric acid in your stomach is a waste product of sodium bicarbonate production for buffering acid rain or acidic waste from what you eat, what you drink, what you breath and what you think. This is why when an athlete goes into lactic acidosis they throw-up to rid their body of all the hydrochloric acid build-up in the gastric pits of the stomach. You see the body is working hard to buffer the increased lactic acid from increased metabolism so the athlete doesn’t die from acidic rain from a declining pH in the blood and interstitium. Even when a pregnant woman throws-up (generally in her first trimester) her stomach is producing sodium bicarbonate to buffer the acidic loads in her and her unborn child’s blood and interstitium. The increased need for alkalinity during pregnancy is significant and is NOT understood or even considered by medical savants. They think, unknowingly that the body just takes care of the pH of the blood and tissues and that what you eat, what you drink, what you breath, and what you think cannot effect this delicate pH balance. You see, morning sickness is nothing more than increased acids from diet, respiration and metabolism! It requires twice the energy to make a baby and with that the pregnant Mother has increased acid rain. So I want you to understand that the stomach’s main purpose is to maintain the alkaline design of the body to keep it alive. That is IT! Get IT?

To learn more about the physiology of the stomach read the following book. You can order this book online at the following link:

How is acid/base created in the body?

a) The parietal or cover cells of the stomach split the sodium chloride of the blood. The sodium 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 you ingest it alkalizes the food and liquid you ingest.

b) 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. Therefore HCL is an acidic waste product of sodium bicarbonate production created by the stomach to alkalize the food and liquids ingested and to maintain the delicate pH of the blood and interstitial fluids at a pH of 7.365.

c) 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 body and the cause of indigestion, acid reflux, ulcers and cancer. In fact HCL is in all pharmaceuticals and most dietary nutritional supplements.

d) When large amounts of acids, including HCL, enter the stomach from a rich animal protein or dairy product meal, such as meat and cheese, 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 (pancreas, gallbladder, Lieberkuhn glands in the liver and the Brunner glands between the pylorus and the junctions of the bile and pancreatic ducts), that need these quick bases in order to build up their strong sodium bicarbonate secretions. These glands and organs, once again 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 and cheese to buffer its strong acids of nitric, sulphuric, phosphoric, uric and lactic acids.

e) When a rich animal protein and dairy product meal is ingested, the stomach begins to manufacture and secrete sodium bicarbonate (NHCO3) to alkalize the acids from the food ingested. This causes a loss in the alkaline reserves and an increase in acid and/or HCL found in the gastric pits of the stomach. These acids and/or HCL are taken up by the blood which lowers blood plasma pH. The blood eliminates this increase in gastrointestinal acid by throwing it off into the Pishinger’s spaces or what recent scientist are calling the Interstitium pictured below.

 

f) The space enclosed by these finer and finer fibers is called the Pishinger’s space, or the spaces of the interstitium that contains the fluids that bath and feed each and every cell while carrying away the acidic waste from those same cells. There is no mention of this organ in American physiology or medical school text books. There is mention of the space but not of any organ that stores acids from metabolism, respiration, environment and diet, like the kidney. I call this organ the “pre-kidney” because it stores metabolic respiratory, environmental and gastrointestinal acids until they can be buffered and eliminated via the skin, urinary tract, or bowels.

g) After a rich animal protein or dairy product meal, the urine pH becomes alkaline.The ingestion of meat and cheese causes a reaction in acidic fashion in the organism by the production of sulfuric, phosphoric, nitric, uric, lactic, acetylaldehyde and ethanol acids, respectively, but also through the formation and excretion of base in the urine. Therefore eating meat and cheese causes a double loss of bases leading to tissue acidosis and eventual disease, especially inflammation and degenerative diseases.

h) During heavy exercise, if the the resulting lactic acid was not adsorbed by the collagen fibers, the specific acid catchers of the body, the organism would die. The total collection of these fibers is the largest organ of the body called SCHADE, the colloidal connective tissue organ or the interstitium. NO liquid exchange occurs between the blood and the parenchyma cells, or in reverse, unless it passes through this connective tissue organ or the interstitium. 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 (just discovered by American science in 2018. Dr. Robert O. Young with Dr. Galina Migalko published their pH findings of the blood, interstitial fluids of the Interstitium and the intracellular fluids in 2015. Their publication is pictured below), which includes the muscles, inflammation and pain develop. The production of lactic acid is increased with the ingestion of milk, cheese, yogurt, butter and especially ice cream.

 

That is why I have stated for years, “acid is pain and pain is acid.” You cannot have one without the other. This is the beginning of latent tissue acidosis leading to irritation, inflammation and degeneration of the cells, tissues and organs.

i) The more acidity created from eating meat, cheese, milk or ice cream the more gastrointestinal acids are adsorbed into the the collagen fibers to be neutralized and the less sodium bicarbonate or NaHCO3 that is taken up by the alkalophile glands. The larger the potential difference between the adsorbed acids and the amount of NaHCO3 generated with each meal, the more or less alkaline are the alkalophile glands like the pancreas, gallbladder, pylorus glands, blood, etc. The acid binding power of the connective tissue, the blood, and the alkalophile glands depends on its alkali reserve, which can be determined through blood, urine, and saliva pH testing, including live and dried blood analysis. (Currently we are the only two scientist in the World that are doing non-invasive testing of the stomach, blood, interstitium and intracellular fluid pH with results in less than 15 minutes) The saliva pH is an indication of alkali reserves in the alkalophile glands and the urine pH is an indication of the pH of the fluids that surround the cells or the Pishinger’s space.

 

j) The iso-structure of the blood maintains the pH of the blood by pushing off gastrointestinal or metabolic acids into the connective tissue or the Pishinger’s space or the Interstitium. The blood gives to the urine the same amount of acid that it receives from the tissues and liver so it can retain its iso-form. A base deficiency is always related to the deterioration of the deposit ability of the connective tissues or the Pishinger’s space or interstitial fluid spaces. As long as the iso-structure of the blood is maintained, the urine – which originates from the blood – remains a faithful reflected image of the acid-base regulation, not of the blood, but of the tissues. The urine therefore is an excretion product of the connective tissues or the interstitium, not the blood. So when you are testing the pH of your urine, you are testing the pH of the tissues or the interstitial fluids of the Interstitium.

k) A latent “acidosis” is the 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 occurs because of hyper-proteinization, (eating Meat and Cheese!)or too much protein, and hyper-carbonization, or too much sugar. This is 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 down. 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.

l) If there is not enough base left over after meat and cheese or surgary meal, or enough base to neutralize and clear the acids stored in the connective tissues or interstitium, a relative base deficiency develops which leads to latent tissue acidosis.When this happens the liver and pancreas are deficient of adequate alkaline juices to ensure proper alkalization of the food in your stomach and small intestine.

m) Digestion or alkalization cannot proceed without enough of these alkaline juices for the liver and pancreas, etc., and so the stomach has to produce more acid in order to make enough base, ad nauseam, and one can develop indigestion, nausea, acid reflux, GERD, ulcers, esophageal cancer and stomach cancer. All of these symptoms are not the result of too much acid or HCL in the stomach. On the contrary, it is the result of too little base in the form of sodium bicarbonate!

n) Therefore the stomach is NOT an organ of digestion as currently taught in ALL biology and medical texts, BUT an organ of contribution or deposit. It’s function is to deposit alkaline juices to the stomach to alkalize the food and to the blood to carry to the alklophile glands!!!!

o) There is a daily rhythm to this acid base ebb and flow of the fluids of the body. The stored acids are mobilized from the connective tissues and Pishinger’s spaces or the spaces of the interstitium while we sleep.

These acids reach their maximum (base tide) concentration in this fluid, and thereby the urine (around 2 a.m. is the most acidic). The acid content of the urine directly reflects the acid content of the fluid in the Pishinger’s spaces, the interstitial fluid compartments of the body. On the other hand, the Pishinger’s spaces become most alkaline around 2 p.m. (the base flood) as then the most sodium bicarbonate (NaHCO3) is being generated by the cover cells of the stomach to alkalize the food and drink we have ingested.

p) If your urine is not alkaline by 2 p.m. you are definitely in an ACIDIC condition and lacking in alkaline reserves. The pH of the urine should run between 6.8 and 8.4 but ideally 7.2 or greater.

q) After a high protein meal or meat or cheese, the free acids formed such as sulfuric, phosphoric, uric, and nitric acids stick to the collagen fibers to remove them from the blood and protect the delicate pH of the blood at 7.365. The H+ or proton ions from these acids are neutralized by the next base flood, the sodium bicarbonate produced after the meal. The H+ or proton ion combines with the carbonate or HCO3, converts to carbonic acid, H2CO3, which converts to CO2 and H2O. The sulfuric and other acids from proteins are neutralized as follows where the HR represents any acid with the R as its acid radical (SO4, PO4, or NO3) HR + NaHCO3 <=> H2O + NaR (Ca, Mg, K)+ CO2.

r) Medical doctors are not taught the above science in medical school and therefore do not understand the complex chemistry between the stomach, blood and interstitium or even recognize the effects of an acidic lifestyle and diet leading to latent tissue acidosis in the largest organ of the body called the Interstitium. They understand and recognize compensated acidosis and decompensated acidosis in the blood but do not know about or even understand a single thing about the Interstitium. 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.

s) Metabolism of a normal adult diet results in the generation of 50 to 100 meq of H+ or proton per day, which must be excreted if the urine acid-base balance is to be maintained. A meq is a milliequivalent which is an expression of concentration of substance per liter of solution, calculated by dividing the concentration in milligrams per 100 milliliters by the molecular weight. This process involves two basis steps; 1) the reabsorption of the filtered sodium bicarbonate or NaHCO3 and, 2) excretion of the 50 to 100 meq of H+ or proton produced each day by the formation of titratable acidity and NH4+ or ammonium. Both steps involve H+ or proton secretion from the cells of the kidney into the urine.

t) Sodium bicarbonate (NaHCO3) must be reabsorbed into the blood stream, since the loss of NaHCO3 will increase the net acid load and lower the plasma NaHCO3 concentration. The loss of NaHCO3 in the urine is equivalent to the addition of H+ to the body since both are derived from the dissociation of H2CO3 or carbonic acid.

u) The biochemistry is: CO2 + H2O = H2CO3 = HCO3 + H+. The normal subject must reabsorb 4300 meq of NaHCO3 each day! The secreted H+ or proton ions are generated within the kidney cells from the dissociation of H2O or water. This process also results in the equimolar production OH- or hydroxyl ions. The OH- ions bind to the active zinc-containing site of the intracellular carbonic anhydrase; they then combine with CO2 to form HCO3- ions which are released back into the kidney cells and returned to the systemic circulation. Second, the dietary acid load is excreted by the secretion of H+ or proton ions from the kidney cells into the urine. These H+ or proton ions can do one of two things: the H+ or proton ions can be combined with the urinary buffers, particularly HPO4, in a process called titratable acidity (The biochemistry is: H+ + HPO4 = H2PO4), or the phosphate buffering system or the H+ or proton ions can combine with ammonia (NH3) to form ammonium as follows: NH3 + H+ = NH4.

v) This ammonia is trapped and concentrated in the kidney as ammonium which is then excreted in the urine.

w) In response to acid load, 36% of the H+ or proton goes intracellular in exchange for the release of Na+ (sodium) into the blood stream. 15% of the acid goes intracellular in exchange for K+ (potassium) – common in diabetics. 6% of the H+ or proton or acid goes directly into the cell to be buffered by intracellular processes. 43% is buffered by the interstitium as NaHCO3- or sodium bicarbonate combining with H+ or proton to form H2CO3 or carbonic acid which breaks down to CO2 or carbon dioxide to be released by the lungs. 10% of CO2 or carbon dioxide is excreted through the lungs and 90% is used by the body to reabsorb alkaline minerals and make sodium bicarbonate for buffering gastrointestinal, respiratory, enivronmenta and metabolic acids.

The biochemistry is: CO2 + H2O = H2CO3 = HCO3 + H+.

You can order the following book on sodium and potassium bicarbonate at: http://www.phoreveryoung.com or https://www.amazon.com/gp/product/B01JLHJ1Y8/ref=dbs_a_def_rwt_hsch_vapi_taft_p3_i9

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x) Of all the ways the body can buffer metabolic and dietary acids, the excretion of protein (the eating of meat and cheese) generated acid residues is the only process that does not add sodium bicarbonate back into blood circulation. This creates a loss of bases which is the forerunner of all sickness and disease. In the long run, the only way to replace these lost bases is by eating more alkaline electron-rich green foods and long-chain polyunsaturated fats. Eating meat and cheese is definitely hazardous to your health. That is why I say, “a cucumber a day keeps the doctor away while eating meat, cheese and even an apple creates more excess acid in the colloidal connective tissues of the Schade or the Interstitium, leading to latent tissue acidosis and then sickness, disease and finally death.

y) With over 30 years of research and testing over 500,000 samples of blood and over 1,000,000 samples of urine and saliva I have come to the conclusion that the Human Body is an acid producing organism by function – yet, it is an alkaline organism by design. Eating animal protein, especially meat and cheese and sugar from any source are deadly acidic choices – unless you interested in becoming sick, tired and fat over time.

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z) Bottom line – the pH Miracle Lifestyle and Diet is a program that focuses on the foundational principal that the body is alkaline by design and yet acidic by function. These are my two greatest discoveries. This make this program the ultimate program for preventing and reversing aging and the onset of sickness and dis-ease. I would say that the pH Miracle Lifestyle and Diet is the diet for a longer healthier life free from all sickness and disease. That is why you are seeing a slew of celebrities (Harry and Meghan, Tom Brady, Rhianna, Elle Macpherson, Gwyneth Paltrow, David Beckham, NeNe, Tony Robbins, just to name a few) can attest to the benefits of a pH Miracle alkaline lifestyle and diet and the drinking of alkaline water for improving the quality of their skin, hair and body and to avert over-acidity which often leads to breakouts of the skin and many other health challenges.

Harry and Meghan live an alkaline lifestyle and diet

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Tom Brady is an avid supporter of the alkaline lifestyle and diet and states it is keeping in the game playing the best football of his life!

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David Beckham is a follower of the alkaline lifestyle and diet

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Ellie Macpherson drinks her green drink and tests her pH daily at the age of 54 enjoying extraordinary health and fitness

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Tony Robbins has been teaching Dr. Young’s pH Miracle Lifestyle and Diet to Millions Around the World for Over 20 Years!

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Gwyneth Paltrow has been following the pH Miracle Lifestyle and Diet for over 10 years and attributes her health, energy, vitality, fitness, and anti-aging benefits to this lifestyle and diet.

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Rhianna attributes her glowing skin to the alkaline lifestyle and diet.

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Please remember this very important truth, hydrochloric acid in the stomach is not the cause of digestion but the result of alkalization. Start alkalizing today and begin improving the quality and quantity of your life today.

The Break-Through Research of Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner

My research has linked acidity to every sickness and disease, including enervation, irritation, catarrh, inflammation, induration, ulceration and degeneration. People do not die from disease they die from the inability to maintain the alkaline design of their body. The key to living a long and healthy life is managing the alkaline design of the body. For example pain equals acid and acid equals pain. You cannot have pain with acid. It is that simple! Remove the acid and you remove the pain.

 

The following are 20 suggestions on how to manage the alkaline design of your body and to increase your energy, vitality and quantity and quantity of life which is in your complete control! YOU determine YOUR Destiny!

20 Suggestions for Maintaining the Alkaline Design of YOUR Body for a Longer and Healthier Life

1. Start your day with a large glass of 9.5 alkaline water with the juice of a whole, freshly-squeezed lemon. While lemons are wrongly considered acidic, they are NOT! They are loaded with sodium bicarbonate which means they contribute to your alkaline reserves and protect the blood and interstitium from acid rain.

Be Alkaline and be healthy and loving

Get weekly alkaline tips of the day for leading a long and healthy and compassionate alkaline life when you sign-up as a member of our pH Miracle Fan Club on our facebook page at: https://www.facebook.com/groups/50864627953/

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 2. Better yet, invest in a water filtration system that alkalinizes the water and increases the pH of the water to a 9.5 or greater. Pure water found in nature, which is hard to come by now thanks to acid rain, is quite alkaline. If you’re already drinking purified water, you can also purchase water alkalinizing drops to add to your water bottle and to raise the pH of your water to pH or 9.5 or greater. Here is the link to purchase alkaline pH drops for you water: https://store.phoreveryoung.com/collections/supplements/products/activator-by-ph-miracle-2-fl-oz-59-14ml

3. Eat a large green vegetable salad tossed in alkalizing lemon juice and olive oil. Greens are among the best sources of alkaline minerals like calcium and are high in chlorophyll for building hemoglobin and red blood cell counts.

4. Drink raw organic almond milk. Almonds are packed with natural alkaline minerals like calcium, magnesium and potassium which can help to balance out acidity while buffering another acid called glucose or blood sugar.

5. Drink an Avocado smoothie daily. Using a Vita-mix blender you can blend an avocado with spinach greens, cucumber, celery, ginger and almond milk for an incredible alkalizing and energizing green shake.

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6. Add green powder like wheat grass, barley grass, moringa grass or other greens to your daily diet since these foods that are highly alkalizing and energizing. It’s easy to throw a tablespoon of these greens into your Avocado based almond milk smoothie. To order the best green powder in the World go to: https://store.phoreveryoung.com/collections/supplements/products/innerlight-supergreens

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7. Take a brisk walk, bicycle ride, swim, rebound or some other exercise for at least 30 minutes everyday. Exercise helps move acidic waste products out of the interstitium and through the pores of the skin via perspiration.

8. Breathe deeply. Ideally, choose a spot that has fresh, oxygen-rich air. And, sorry, air filled with Febreze, Glade and all the other so-called “air fresheners,” is not what I’m talking about here. Take a deep breath in through your nose and then switch to breathing through your mouth without letting go of your first inhalation through your nose.

 

9. Go for Meatless and Eggless Mondays. Better yet, opt for meat-free Tuesdays, Wednesdays and other days throughout the week. During the chewing of meat, acid residues like uric acid, nitric acid, sulphuric acid and phosphoric acid residues are left behind for the stomach to address. There is zero health benefits from eating the flesh of another living being. All flesh is acidic and causes a double-loss of alkalinity in the blood and interstitium.

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10. Skip the sugar-laden soda and drink some iJuice Wheat Grass Juice.(www.ijuicenow.com) Sugar is one of the most acidic foods we consume. Sugar is a waste product of metabolism and fermentation. You need over 30 glasses of alkaline water at a pH of 8.4 just to neutralize the acidity (sugar and carbonic acid) of ONE can or bottle of soda.

 

11. Skip the artificially-sweetened diet beverages and other diet products. They contain artificial sweeteners like aspartame (now known as NeoTame), sucralose (also known as Splenda) or saccharin (also known as SugarTwin) and they all cause body warming and acid rain inside your body.

12. Add more green fruit and vegetables to your diet. No, fried potatoes don’t count, including sweet potatoes. Asparagus, green peppers, green string beans, kale, spinach, beet tops, carrot tops, wheat grass, barley grass, broccoli, cucumber, avocado, and lime and other green fruit and vegetables are also excellent choices for supporting the alkaline design of the body.

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13. Instead of slathering your vegetables in acid-forming butter, drizzle alkaline flaxseed oil, hemp seed oil, and/or green olive oil over them.

14. Sprout it out. Add more sprouts to your daily diet like bean sprouts, sunflower seed sprouts and broccoli sprouts. They are extremely alkalizing and supercharged with nutrients and energy-boosting electrons.

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15. Skip ALL desserts or reserve them as occasional treats instead of daily habits. Sugar consumption has been linked to a whole host of health problems and is best minimized or eliminated. If you are in body warming then removing all acidic foods and drinks are a must.

16. Avoid all alcoholic beverages or so-called nutritional supplements that contain alcohol. Alcohol is a devastating acid that causes pancreatic and liver cancer.

17, Avoid corn and peanuts because they are loaded with bacteria, yeast and mold and the cancer causing acid lactic acid.

18. No acidic beverages like coffee, black or green tea or chocolate. They all contain food acids that robs your body of its alkaline reserves causing many diseases, including cancer.

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19. Stay far away from vinegar. Vinegar is pure acid and steals years off your life! Do not believe the so-called health experts to state the vinegar is good for digestion. Remember this very important point. There is only one instrument in the human body that can digest or breakdown food and the is your teeth. When you pour vinegar into your body all you have done is poison yourself. The stomach has to rob alkalinity from the blood, interstitium, organs and glands to buffer this highly toxic chemical setting the stage for enervation, inflammation, induration, ulceration , degeneration and finally death. Vinegar is death in a bottle.

20. Test your urine and saliva and drink pHour Salts every morning. Your ideal pH of your urine and saliva should be at least 7.300. If your pH is lower than 7.300 take a scoop of pHour salts in a small glass of alkaline water. Ideally, you should drink a glass of phour salts which contains sodium bicarbonate, potassium bicarbonate, magnesium chloride and calcium at least 3 times daily. To order pHour salts go to: https://store.phoreveryoung.com/collections/supplements/products/phour-salts-per-case

 

You can also order saliva and urine testing strips at the following link: https://store.phoreveryoung.com/products/phydrion-strips-5-5-8-0?variant=2085775876

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To learn more about the work, research and discoveries of Robert O Young go to the following websites: http://www.drrobertyoung.com, http://www.phmiracleretreat.com, http://www.ijuicenow.com, http://www.innerlightblue.com and http://www.phoreveryoung.com

To learn more read The pH Miracle, The pH Miracle revised and updated, The pH Miracle for Diabetes, The pH Miracle for Weight Loss, The pH Miracle for Cancer and Sick and Tired, just to name a few of Robert O Young’s published books. To order any of these books go to: http://www.phoreveryoung.com

Dr Galina Migalko and I will be key note speakers sharing our research and findings at the 3rd World Congress on Advanced Cancer Science and Therapy on October 15th and 16th in Osaka, Japan.  If you would like to attend our lecture on our break-through science you can email: phmiraclelife@gmail.com
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Our Next pH Miracle Event will be from November 18th to December 2nd – To learn more email us at: phmiracleliving@aol.com
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Could Sodium or Potassium Bicarbonate save your life? Low levels of bicarbonate ‘are linked to a 24 % higher risk of early death!

Could Sodium or Potassium Bicarbonate save your life? Low levels of bicarbonate 'are linked to a 24 % higher risk of early death!

Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

Could Sodium or Potassium Bicarbonate save your life? Low levels of bicarbonate ‘are linked to a 24 % higher risk of early death!

  • Compound in baking soda – bicarbonate – reduces early death, study found
  • Baking soda – or sodium bicarbonate – helps regulate pH levels  
  • People with low bicarbonate levels have 24% higher risk of early death
  • People should ingest fruit and green vegetables to get more bicarbonate!

Many of us think of baking soda as little more than a vital part of the recipe to making a cake or baking cookies.

But two new studies have found that the ingredients of sodium and/or potassium bicarbonate plays a far more important role in human health: It can help save lives.

Older people with low levels of sodium and/or potassiumbicarbonate – which is found in baking soda – have a 24 per cent higher risk of dying an early death!

The findings suggest increasing bicarbonate levels can prolong a person’s life.

Study author Dr Kalani Raphael, of the University of Utah, said: ‘What we found was that generally healthy older people with low levels of bicarbonate had a higher risk of death.’

Sodium bicarbonate, a main component of baking powder, reduces the risk of premature death, scientists revealed. Older people with low bicarbonate levels are 24 per cent more likely to die young, a study found

The kidneys and lungs work together by varying the levels of sodium and/or potassium bicarbonate – a base or alkaline compound – and carbon dioxide – an acid – in the blood, interstitial fluids and intracellular fluids.

Sodium and potassium bicarbonate helps keep the body’s pH in a healthy range (7.365), which allows the body cells that make up our organs to work properly.

Critically ill patients with severe acid-base abnormalities have very low levels of sodium and/or potassium bicarbonate and are very unlikely of surviving their illness, according to the study.

RELATED ARTICLES

  • Using Sodium and Potassium Bicarbonate in the Prevention and Treatment of ALL Sickness and Disease – Dr. Robert O. Young – www.phoreveryoung.com 

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Yet, it has been unclear whether more subtle changes to the body’s acid-base status affect the longevity of relatively healthy older people.

A team of scientists investigated how measurements of pH, carbon dioxide and bicarbonate are associated with long-term survival in healthy older people.

They analyzed data from 2,287 participants in the health, aging and body composition study.

That data focused on well-functioning black and white adults between the ages of 70 and 79.

Data started being collected in 1997 – with collection efforts extending through February 2014.

Each of the participants were followed for an average of 10.3 years.

Scientists recommend people with low levels of sodium and/or potassium bicarbonate should increase their intake of foods that produce it in the body, including fruit and green vegetables.

Because of the study’s results, blood bicarbonate concentrations – which are already commonly measured – may allow clinicians to better identify people with a higher risk of premature death.

Those with low sodium and potassium bicarbonate levels may benefit from increasing their intake of foods that produce bicarbonate in the body – including fruit and vegetables, according to the scientists.

The study was published in the Clinical Journal of American Nephrology.  The study by Dr. Robert O. Young has been approved for publication in The International Journal of Complementary and Alternative Medicine.

Read more: http://www.phoreveryoung.wordpress.com

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

The Truth About Science-Based Medicine! Fact or Fiction?

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The current healthcare debate has brought up basic questions about how medicine should work. On one hand we have the medical establishment with its enormous cadre of M.D.s, medical schools, big pharma, and incredibly expensive hospital care. On the other we have the semi-condoned field of alternative medicine that attracts millions of patients a year and embraces literally thousands of treatment modalities not taught in medical school.

One side, mainstream medicine, promotes the notion that it alone should be considered “real” medicine, but more and more this claim is being exposed as an officially sanctioned myth. When scientific minds turn to tackling the complex business of healing the sick, they simultaneously warn us that it’s dangerous and foolish to look at integrative medicine, complementary and alternative medicine, or God forbid, indigenous medicine for answers. Because these other modalities are enormously popular, mainstream medicine has made a few grudging concessions to the placebo effect, natural herbal remedies, and acupuncture over the years. But M.D.s are still taught that other approaches are risky and inferior to their own training; they insist, year after year, that all we need are science-based procedures and the huge spectrum of drugs upon which modern medicine depends.

If a pill or surgery won’t do the trick, most patients are sent home to await their fate. There is an implied faith here that if a new drug manufacturer has paid for the research for FDA approval, then it is scientifically proven to be effective. As it turns out, this belief is by no means fully justified.

The British Medical Journal recently undertook an general analysis of common medical treatments to determine which are supported by sufficient reliable evidence. They evaluated around 2,500 treatments, and the results were as follows:

  • 13 percent were found to be beneficial
  • 23 percent were likely to be beneficial
  • Eight percent were as likely to be harmful as beneficial
  • Six percent were unlikely to be beneficial
  • Four percent were likely to be harmful or ineffective.

This left the largest category, 46 percent, as unknown in their effectiveness. In other words, when you take your sick child to the hospital or clinic, there is only a 36 percent chance that he will receive a treatment that has been scientifically demonstrated to be either beneficial or likely to be beneficial. This is remarkably similar to the results Dr. Brian Berman found in his analysis of completed Cochrane reviews of conventional medical practices. There, 38 percent of treatments were positive and 62 percent were negative or showed “no evidence of effect.”

For those who have been paying attention, this is not news. Back in the late 70’s the Congressional Office of Technology Assessment determined that a mere 10 to 20 percent of the practices and treatment used by physicians are scientifically validated. It’s sobering to compare this number to the chances that a patient will receive benefit due to the placebo effect, which is between 30 percent and 50 percent, according to various studies.

We all marvel at the technological advances in materials and techniques that allow doctors to perform quadruple bypass surgeries and angioplasties without marveling that recent studies indicate that coronary bypass surgery will extend life expectancy in only about three percent of cases. For angioplasty that figure sinks to zero percent. Those numbers might be close to what you could expect from a witch doctor, one difference being that witch doctors don’t submit bills in the tens of thousands of dollars.

It would be one thing if any of these unproven conventional medical treatments were cheap , but they are not. Angioplasty and coronary artery bypass grafting (CABG) alone cost $100 billion annually. As quoted by President Obama in his drive to bring down medical costs, $700 billion is spent annually on unnecessary tests and procedures in America. As part of this excess, it is estimated that 2.5 millionunnecessary surgeries are performed each year.

Then there is the myth that this vast expenditure results in excellent health care, usually touted as the best in the world (most recently by Rush Limbaugh as he emerged from a hospital in Hawaii after suffering chest pain). But this myth has been completely undermined. In 2000 Dr. Barbara Starfield, writing in the Journal of the American Medical Association, estimated that between 230,000 and 284,000 deaths occur each year in the US due to iatrogenic causes, or physician error, making this number three in the leading causes of death for all Americans.

In 2005 the Centers for Disease Control and Prevention reported that out of the 2.4 billion prescriptions written by doctors annually, 118 million were for antidepressants. It is the number one prescribed medication, whose use has doubled in the last ten years. You would think, therefore, that a remarkable endorsement is being offered for the efficacy of antidepressants. The theory behind standard antidepression medication is that the disease is caused by low levels of key brain chemicals like serotonin, dopamine, and norepinephrine, and thus by manipulating those imbalanced neurotransmitters, a patient’s depression will be reversed or at least alleviated.

This turns out to be another myth. Prof. Eva Redei of Northwestern University, a leading depression researcher, has discovered that depressed individuals have no depletion of the genes that produce these key neurotransmitters compared to people who are not depressed. This would help explain why an estimated 50 percent of patients don’t respond to antidepressants, and why Dr. Irving Kirsch’s meta-analysis of antidepressants in England showed no significant difference in effectiveness between them and placebos.

You have a right to be shocked by these findings and by the overall picture of a system that benefits far fewer patients than it claims. The sad fact is that a disturbing percentage of the medicine we subject ourselves to isn’t based on hard science, and another percentage is risky or outright harmful. Obviously, every patient deserves medical care that is evidence-based, not just based on an illusory reputation that is promoted in contrast to alternative medicine.

We are not suggesting that Americans adopt any and all alternative practices simply because they are alternative. These, too, must demonstrate their effectiveness through objective testing. But alternative modalities should not be dismissed out of hand in favor of expensive and unnecessary procedures that have been shown to benefit no one absolutely except corporate stockholders.

Source: The HuffPost Healthy Living, November 18th, 2014, http://www.huffingtonpost.com/dr-larry-dossey/the-mythology-of-science_b_412475.html

Political Science! – The Politics of Medical Science and Research

The Politics of Science (Part 1)

The following last chapter in Robert O. Becker’s book, The Body Electric” should give some insight into the politics of science. How and why some researchers and their research gets funded while others don’t. Maybe, it will explain why many researchers in CFS continue to bark up the wrong tree and will not dare delve into truth of the matter – into the Big Lie – since this might very well cut their funding, ruin their reputations, and even end their careers. This has happened to many honorable and brilliant scientists such as Dr. Antione BeChamp, Dr. Livingston Wheller, Dr. Royal Rife, Dr. Gunther Enderlien, Dr. Duesburg, Dr. Robert Becker, Dr Nassens and finally Dr. Robert O. Young.

Postscript: Political Science

An important scientific innovation rarely makes its way by gradually winning over and converting its opponents: it rarely happens that Saul becomes Paul. What does happen is that its opponents gradually die out and that the growing generation is familiarized with the idea from the beginning.-Max PlanckDispassionate philosopher inquiring into nature from the sheer love of knowledge, single-minded alchemist puttering about a secluded basement in search of elixers to benefit all humanity – these ideals no longer fit for most scientists. Even the stereotype of Faust dreaming of demonic power is outdated, for most scientists today are overspecialized and anonymous – although science as a whole is somewhat Mephistophelian in its disregard or the effects of its knowledge. It’s a ponderous beast, making enormous changes in the way we live but agonizingly slow to change its own habits and viewpoints when they become outmoded.

The public’s conception of the scientist remains closest to its image of the philosopher – cold and logical, making decisions solely on the basis of facts, unswayed by emotion. The lay person’s most common fear about scientists is that they lack human feelings. During my twenty-five years of research I’ve found this to be untrue yet no cause for confort. I’ve occasionally seen our species’ nobler impulses among them, but I’ve also found that scientists as a group are at least as subject to human failings as people in other walks of life.It has been like this throughout the history of science. Many, perhaps even most, of its practitioners have been greedy, power-hungry, prestige-seeking, dogmatic, pompous asses, not above political chicanery and outright lying, cheating, and stealing. Examples abound right from the start. Sir Francis Bacon, who in 1620 formulated the experimental method on which all technical progress since then has been founded, not only forgot to mention his considerable debt to William Gilbert but apparently plagiarized some of his predecessor’s work while publicly belittling it. In a similar way Emil Du Bois-Reymond based his own electrical theory of nerve impulse on Carlo Matteucci’s work, then tried to ridicule his mentor and take full credit.

Many a genius has been destroyed by people of lesser talent defending the status quo. Ignaz Semmelweis, a Hungarian physician who practiced in Vienna during the mid-nineteenth century, demanded that his hospital colleagues and subordinates wash their hands, especially when moving from autopsies and sick wards to the charity childbirth ward he directed. When the incidence of puerperal fever and resultant death declined dramatically to well below that of the rich women’s childbirth ward, proving the importance of cleanliness even before Pasteur, Semmelweis was fired and vilified. His livelihood gone, he committed suicide soon afterward.

The principle figure who for decades upheld the creed that dedifferentiation was impossible was Paul Weiss, who dominated biology saying the things his peers wanted to hear. Weiss was wrong, but along the way he managed to cut short a number of careers.

For many years the American Medical Association scorned the idea of vitamin-deficiency diseases and called teh EEG electronic quackery. Even today that august body contends that nutrition is basically irrelevant to health. As the late-eighteenth-century Italian experimenter Abbe Alberto Fortis observed in a letter chiding Spallanzani for his closed-minded stance on dowsing, “… derision will never help in the development of true knowledge.”In the past, these character flaws couldn’t wholly prevent the recognition of scientific truths. Both sides of a controversy would fight with equal vehemence, and the one with better evidence would usually win sooner or later. In the last four decades, however, changes in the structure of scientific institutions have produced a situation so heavily weighted in favor of the establishment that it impedes progress in healthcare and prevents truly new ideas from getting a fair hearing in almost all circumstances. The present system is in effect a dogmatic religion with a self-perpetuating priesthood dedicated only to preserving the current orthodoxies. The system awards the sycophant and punishes the visionary to a degree unparalleled in the four-hundred-year history of modern science.

This situation has come about because research is now so expensive that only governments and multinational corporations can pay for it. The funds are dispensed by agencies staffed and run by bureaucrats who aren’t scientists themselves. As the system developed after World War 2, the question naturally arose as to how these scientifically ignorant officials were to choose among competing grant applications. The logical solution was to set up panels of scientists to evaluate requests in their fields and then advise the bureaucrats.

This method is based on the naive assumption that scientists really are more impartial than other people, so the result could have been predicted decades ago. In general, projects that propose a search for evidence in support of new ideas aren’t funded. Most review committees approve nothing that would challenge the findings their members made when they were struggling young researchers who created the current theories, whereas projects which ponder to these elder egos receive lavish support. Eventually, those who play the game beome the new members of the peer group, and thus the system perpetuates itself. As Erwin Chargaff has remarked, “This continual turning off and on of the financial faucets produces Pavlovian effects,” and most research becomes mere water treading aimed at getting paid rather than finding anything new. The intuitive “lunatic twinge,” the urge to test a hunch, which is the source of all scientific breakthroughs, is systematically excluded.

There has even been a scientific study documenting how choices made by the peer review system depend almost entirely on whether the experts are sympathetic or hostile to the hypothesis being suggested. True to form, the National Academy of Sciences, which sponsored the investigation, suppressed its results for two years.

Membership on even a few review boards soon establishes one’s status in the “old boys’ club” and leads to other benefits. Manuscripts submitted to scientific journals are reviewed for validity in the same way as grant requests. And who is better qualified to judge an article than those same eminant experts with their laurels to guard? Publication is accepted as evidence that an experiment has some basic value, and without it the work sinks without a ripple. The circle is thus closed, and the revolutionary, from whose ideas all new scientific concepts come, is on the outside. Donald Goodwin, chairman of psychiatry at the University of kansas and an innovative researcher on alcoholism, has even put it in the form of exasperation: “If it’s trivial, you can probably study it. If it’s important, you probably can’t.”Another unforeseen abuse has arisen, which has lowered the quality of training in medical schools. As the peer review system developed, academic institutions saw a golden opportunity. If the government wanted all this research done, why shouldn’t it help the schools with their overhead, such as housing, utilities, bookeeping and ultimately the salaries of the researchers, who were part of the faculty? The influx of money corroded academic values. The idea arose that the best teacher was the best researcher, and the best researcher was the one who pulled down the biggest grants. A medical school became primarily a kennel of researchers and only secondary a place to teach future physicians. To survive in academia, you have to get funded and then get published. The epidemic of fraudalent reports – and I believe only a small percentage of the actual fakery has been discovered – is eloquent testimony of the pressure to make a name in the lab.There remain today few places for those whose talents lie in teaching and clinical work. Many people who don’t care about research are forced to do it anyway. As a result, medical journals and teaching staffs are both drowning in mediocrity.

Finally, we must add to these factors the buying of science by the military. To call it a form of prostitution is an insult to the oldest profession. Nearly two-thirds fo the 47-billion 1984 research budget was for military work, and in the field of bioelectricity the proportion was even higher. While military sponsors often allow more technical innovation than others, their employees must keep their mouths shut about environmental hazards and other moral issues that link science to the broader concerns of civilization. In the long run, even the growth of pure knowledge (if there is such a thing) can’t flourish behind this chain link fence.

If someone does start a heretical project, there are several ways to limit this threat. Grants are limited, usually for a period of one or two years. Then the experimenter must reapply. Every application is a volumous document filled with fine-print forms and meaningless bureaucratic jargon, requiring many days of data compilation and “creative wriiting.” Some researchers may simply get tired of them and quit. In any case, they must run the same gauntlet of peers each time. The simplest way to nip a challenge in the bud is to turn off the money or keep the reports out of major journals by means of anonymous value judgements from review committees. You can always find something wrong with a proposal or manuscript, no matter how well written or scientifically impeccable it may be.

Determined rebels use guerrilla tactics. There are so many funding agencies that the left hand often knoweth not what the right hand doeth. A proposal may get by an obscure panel whose members aren’t yet aware of the danger. The snowstorms of paper churned out by the research establishment have required the founding of many new journals in each subspecialty. Some of these will accept papers that would automatically be rejected by the big ones. In addition, there’s an art to writing a grant proposal that falls within accepted guidelines without specifying exactly what the researchers intend to do.

If these methods succeed in prolonging the apostasy, the establishment generally exerts pressure through the schools. Successful academics are almost always true believers who are happy to curry favor by helping to deny tenure to “questionable” investigators or by harassing them in a number of ways. For example, in 1950 Gordon A. Atwater was fired as chairman of the American Museum of Natural History astronomy department and curator of the Hayden Planetarium for publicly suggesting that Immanuel Velikovsky’s ideas should receive a fair hearing. That same year Velikovsky’s first book, Worlds in Collision, was renounced by his publisher (MacMillan) even though it was a best seller, because a group of influential astronomers led by Harvard’s Harlow Shapley threatened to boycott the textbook department that accounted for two thirds of the company’s sales. No matter what one may think of Velikovsky’s conclusions, that kind of backstairs persuasion is not science.As the conflict escalates, the muzzled freethinker often goes directly to the public to spread the pernicious doctrines. At this point, the gloves come off. Already a lightning rod for the wrath of the Olympian peers, the would-be Prometheus writhes under attacks on his or her honesty, scientific competence, and personal habits. The pigeons of Zeus cover the new ideas with their droppings and conduct rigged experiments to disprove them. In extreme cases, government agencies staffed and advised by the establishment begin legal harrassment, such as the trial and imprisonment that ended the career and life of Wilhelm Reich.

Sometime during or after the battle, it generally becomes obvious that the iconoclast was right. The counterattack then shifts toward historical revision. Establishment members publish papers claiming the new ideas for themselves and omitting all references to the true originator. The heretic’s name is remembered only in connection with a condescending catchphrase, while his or her own research programs, if any remain, are defunded and the staff dispersed. The facts of the case eventually emerge, but only at an immense toll on the innovator’s time and energy. To those who haven’t tried to run a lab, these may seem like harsh words, unbelievable, even paranoid. Nevertheless, these tactics are commonplace, and I’ve had personal experience with each and every one of them.

I got a taste of the real world in my very first foray into research. After World War 2, I continued my education on the GI Bill, but those benefits expired in 1947. I’d just married a fellow student named Lilian, who had caught my eye during our first orientation lecture, and I needed a summer job to help pay expenses and set up housekeeping. I was lucky enough to get work as a lab assistant in the NYU School of Medicine’s surgical research department.I worked with Co Tui, who was evaluating a recently published method for separating individual amino acids from proteins as a step toward concentrating foods for shipment to the starving. Dr. Cok, a tiny man whose black, spiky hair seemed to broadcast enthusiasm, inspired me enormously. He was a brilliant researcher and a good friend. With him I helped develop the assay technique and began to use it to study changes in body proteins after surgery.

I was writing my first scientific paper when I walked to work one morning and found our laboratory on the sidewalk – all our equipment, notes, and materials in a junk pile. I was told neither of us worked there anymore; we were welcome to salvage anything we wanted from the heap.

The head secretary told me what happened. This was during a big fund drive to build the present NYU Medical Center. One of the society surgeons had lined up a million-dollar donation from one of his patients and would see that it got into the fund, if he could choose a new professor of experimental surgery – now. As fast as that, Co Tui and his people were out. I vowed to Lilian: “Whatever i do in medicine, I’m going to stay out of research.”I’m happy that I wasn’t able to keep my promise. The research itself was worth it all. Moreover, I don’t want to give the impression that I and my associates were alone against the world. Just when hope seemed lost, there was always a crucial person, like Carlyle Jacobson or the research director’s secretary to help us out. However, right from my first proposal to measure the current of injury in salamanders, I found that research would mean a constant battle, and not only with administrators.Before I began, I had to solve a technical problems with the electrodes. Even two wires of the same metal had little chemical differences, which gave rise to small electrical currents that could be misinterpreted as coming from the animal.

Also, the slightest pressure on the animal’s skin produced currents. No one understood why, but there they were. I found descriptions in the older literature of silver electrodes with a layer of silver chloride applied to them, which were reported to obviate the false interelectrode currents. I made some, tested them, and then fitted them with a short length of soft cotton wick, which got rid of the pressure artifact. When I wrote up my results, I briefly described the electrodes. Afterward I received a call from a prominent neurophysiologist who wanted to visit the lab. “Very nice,” I thought. “Here’s some recognition already.” He was particularly interested in how the electrodes were made and used. Some months later, dammed if I didn’t find a paper by my visitor in one of the high-class journals, describing this new and excellent electrode he’d devised for measuring direct-current potentials.

A couple of years later, while Charlie Bachman and I were looking for the PN junction diode in bone, I was asked to give a talk on bone electronics at a meeting in New York City. The audience included engineers, physicists, physicians, and biologists. It was hard to talk to such a diverse group. The engineers and physicists knew all about the electronics but nothing about bone, the biologists knew all about the bone but nothing about electronics, and the physicians were only interested in therapeutic applications. At any rate, I reviewed some bone structure for the physicists and some electronics for the biologists, and then went on to describe my experiments with Andy Bassett on bone piezoelectricity.

I probably should have sat down at that point, but I thought it would be nice to talk about our present work. The rectifier concept was tremendously exciting to me, and I thought wwe might get some useful suggestions from the audience, so I described the experiments showing that collagen and apatite were semiconductors, and discussed the implications. After each talk, a short time was set aside for questions and comments, generally polite and dignified. However, as soon as I finished, a well-known orthopedic researcher literally ran up to the audience microphone and blurted out, “I have never heard such a collection of inadequate data and misconceptions. It is an insult to this audience. Dr. Becker has not presented satisfactory evidence for any semiconducting property in bone. The best that can be said is that this material may be a semi-insulator.”

Semiconductors are so named because their properties place them between conductors and insulators, so you could very well call them semi-insulators; the meaning would be the same. My opponent was playing a crude game. Where saying these derogatory things about me, he was actually agreeing with my conclusion, merely using a different term.This man’s antagonism had begun a couple of years before. When Andy Bassett and I had finished our work on the piezoelectric effect in bone, we wrote it up, submitted it to a scientific journal, and got it accepted. Unbeknownst to us, this fellow had been working on the same thing, but hadn’t gotten as far in his experiments as we. Somehow he learned of our work and its impending publication. He called Andy, asking us to delay our report until he was ready to publish his own data. Andy called me to talk it over. What counts in the scientific literature is priority; he was asking us to surrender it. There was no ethical basis for his request, and I would never have thought of asking him to delay had the situation been reversed. I said, “Not on your life.” Our paper was published, and we’d acquired a “friend” for life.

Now there he was at the microphone trying to scuttle my presentation with a little ambiguous double-talk. I thought, “He must be doing the same work as we are again. If he wins this encounter, I’ll have trouble getting my data published, and he’ll have a clear field for his.” Instead of defending the data, I explained that semi-insulator and semiconductor were one and the same. I said I was surprised he didn’t know that, but appreciated his approval of my data! Someone else in the audience stood up in support of my position, and the crisis was past. The lab isn’t the only place a scientist has to stay alert.In 1964, soon after the National Institutes of Health approved the grant for our continuing work on bone, I received the VA’s William S. Middleton Award for outstanding research. That’s a funny story in itself. The award is given by the VA’s Central Office (VACO), whose members had already decided on me, but candidates must be nominated by regional officers, and the local powers were determined I shouldn’t get it. Eventually, VACO had to order them to nominate me.

The award put me on a salary from Washington instead of Syracuse, and due to the pressure from VACO I was soon designated the local chief of research, replacing the man who signed all the papers at once. I was determined to put the reseach house in order, and I instituted a number of reforms, such as public disclosure of the funding allocations, and productivity requirements, no matter how prominent an investigator might be. Many of the reforms have been adopted throughout the VA system. They didn’t make me popular, however. Over the next several years there was continuous pressure from the medical school to allocate VA research funds for people I felt were of little value to the VA program itself; thus the money would have constituted a grant to the school. I knew that if I didn’t deliver I would eventually be removed from my position as chief of research. In that case, I would go back on a local clinical salary and my research program would again be in jeopardy. Therefore, at the beginning of 1972 I applied for the position of medical investigator in the VA research system, a post in which I would be able to devote up to three fourths of my time to research. I was accepted. The job was to begin a few months later; in the meantime I continued as chief of research.

Apparently, my new appointment escaped the notice of my local opponents. I’d accepted several invitations to speak at universities in the South and combined them all into a week’s trip. I left the office a day early to prepare my materials and pack. While I was still home, my secretary called. She was crying, and said she’d just gotten a memo firing me as chief or research and putting me to work as a general-duty medical officer in the admitting office. This not only would have closed our lab, but also would have kept me from practicing orthopedic surgery.

It was a nice maneuver but, fortunately for me, it wasn’t legal. As medical investigator, I could be fired only by Washington, and the local chief of staff soon got a letter from VACO ordering him to reinstate me. Soon I began to get on some “enemies lists” at the natinal level too. In December 1974 I got word that our basic NIH grant (the one on bone) hadn’t been renewed. No reasons were given. This was highly irregular, since applicants normally got the “pink sheets” with at least the primary reviewer’s comments, so they could find out what they’d done wrong. Instead I was told I could write to the executive secretary for a “summary” of the deliberations.

The summary was half a page of double-spaced typing. It said my proposal had been lacking in clarity and direction, and that the experimental procedures hadn’t been spelled out in enough detail. The main problem seemed to be that I was planning to do more than the reviewer thought I could do with the money I was requesting. In addition, my report on the perineural cell research with Bruce Baker was criticized as “data poor.” The statement concluded: “On the other hand, there are some areas which appear to be worthy of support and are reasonably well described, e.g., bone growth studies, regenerative growth, and electrical field effects.”

I was, to say the least, puzzled. The subjects “worthy of support” were precisely the main ones we were working on. It didn’t make any sense until I reflected that this was just after I’d helped write the first Sanguine report and had begun to testify about power line dangers before the New York Public Service Commission. Perhaps the Navy was pressuring the NIH to shut me up.If someone at the federal level was trying to lock me out as early as 1974, he forgot to watch all the entrances, for my proposal of that year on acupuncture was approved. I’d originally tacked this on to the main NIH application, where is was criticized as inappropriate. I merely sent it off to a different study section, which funded it. After a year we had the positive results described in Chapter 13, and I presented them at an NIH acupuncture conference in Bethesda, Maryland. Ours was the only study going at the problem from a strictly scientific point of view, that is, proceeding from a testible hypothesis, as opposed to the empirical approach of actually putting the needles in and trying to decide if they worked. To the NIH’s basic question – is the system of points and lines real? – our program was the only one giving an unequivocal answer: yes.

Nevertheless, when the grant came up for approval in 1976, it, too, was cut off. The stated reasons were that we hadn’t published enough and that the electrical system that we found didn’t have any relation to acupuncture. The first was obviously untrue – we’d published three papers, had two more in press, and had submitted six others – and the second was obvious pettifogging. How could anyone know what was related to acupuncture before the research had been done? I happened to know the chairman of the NIH acupuncture study section, so I wrote him a letter. He said he was surprised, because the group itself had been pleased with our report. By then it was obvious that something was up.As of October 1976 we would have no more NIH support. As the money dwindled, we juggled budgets and shaved expensese to cover out costs, and with the help of Dave Murray, who was now chairman of the orthopedic surgery department at the medical school, we kept the laboratory intact and enormously productive. We actually published more research than when we hadn’t been under fire.Early in that same year, however, my appointment as medical investigator had expired, and I had to reapply. Word came back that my application had been “deferred,” that is, it had been rejected, but I had the option of reapplying immediately. In her accompanying letter, the director of the VA’s Medical Research Service wrote, “While your past record and strong letters of support [the peer reveiws of my application] were considered favorable, the broad research proposal with sketchy detail of technique and methodology was not considered approvable.” Now, the instructions for medical investigator applications clearly stated that I was to spell out past accomplishments and indicate future directions only in broad outline. Instead, the director was applying the criteria for first-time grant applications just entering research. She invited me to resubmit the proposal in the other format. But that would not have helped. Even if the second application was approved, the money would arrive six months after the lab had been closed and we had gone our separate ways.

There was another strange thing about the rejection. By that time all federal granting agencies had to provide the actual reports (with names deleted) of the peers who had done the reviewing. Three out of the four were long, detailed, well-thought-out documents in the standard critique format; they’d been neatly retyped, single spaced, on “reviewers’s report” forms with an elite typewriter. One was absolutely lavish in its praise, saying that the VA was fortunate to have me and that the proposed work would undoubtedly make great contributions to medicine. Another was almost as laudatory.One name had inadvertently been left on one page of the third review. It was the name of a prominent orthopedic researcher with whom I had disagreed for years about commercialization of bone-healing devices. Since our mutual disregard was well known in the orthopedic service, I feel it was indefensible for the director to ask him to review my application in the first place. Perhaps she expected a more damaging critique from him. He did complain that the proposal was insufficiently detailed. However, his appraisal was quite fair and even said my proposed work was of “fundamental importance to the field of growth and healing.” It obviously led up to a recommendation for approval, but the last sentence of that paragraph had been deleted.The last review was half a page of vague objections, typed double-spaced on a pica machine with no semblance of the standard format. There was a revealing mistake (“corrective” tissue instead of connective tissue) that showed the writer had glanced at my proposal for cues but really didn’t know what it was about. Strangest of all was the phrasing of this pseudoreview: “[Becker’s proposal] is broad and sweeping in scope and contains little documentation for technique and methodology. However, in view of his past record and strong letters of support, a decision should be deferred…” The director had used it almost word for word in her letter.

She certainly had no motive for such conduct herself. I’d met her briefly a few years before. In 1966 she’d been appointed chief of research at the Buffalo VA Medical Center and had visited Syracuse to see how I’d organized the program there. Our conversation was pleasant but quite innocuous….

A Natural Healthy and Legal Way To Increase Blood Volume – Pass It Along To Lance

There were several questions that came to mind after watching the Oprah Winfrey and Lance Armstrong interview where Lance finally admitted to using EPO, human-growth hormone, testosterone and blood doping.

So What is Blood Doping?

Blood doping is an illicit method of improving athletic performance by artificially boosting the blood’s ability to carry and deliver more oxygen to the connective tissues, including the muscules.

In many cases, blood doping increases the red blood count and its main oxygen carrying molecule, hemoglobin.  So, increasing hemoglobin allows higher amounts of oxygen to reach and alkalize an athlete’s muscles.  This can improve stamina and performance, particularly in long-distance events, such as long-distance running and cycling.

Blood doping is banned by the International Olympic Committe and other sports organizations.

What Are Types of Blood Doping?

The three widely used types of blood doping are:

1) Blood transfusions
2) Injections of erythropoetin (EPO), and 
3) Injections of synthetic oxygen oxygen carriers.

Here are some more details about each of these types of blood doping:
Blood transfusions.  In normal medical practice, patients may undergo blood transfusions to replace blood lost due to injury, surgery or chemotherapy. Transfusions also are given to patients who suffer from low red blood cell counts caused by anemiakidney failure, cancer and chemotherapy treatments.
Illicit blood transfusions are used by athletes to boost athletic performance. There are two types.
Autologous transfusion. This involves a transfusion of the athlete’s own blood, which is drawn and then stored for future use.  Most commonly this involves the removal of two units (approximately 2 pints!) of the athletes blood several weeks prior to competition. The blood is then frozen until 1-2 days before the competition, when it is thawed and injected back into the athlete. This is known as autologous blood doping.
Homologous transfusion. In this type of transfusion, athletes use the blood of someone else with the same blood type and then injected straight into the athlete.
EPO Injections

EPO is a hormone produced by the kidney. It regulates the body’s production of red blood cells.  In medical practice, EPO injections are given to stimulate the production of red blood cells. For example, a synthetic EPO can be used to treat patients with anemia related to chronic or end-stage kidney disease or cancer and its treatment with chemotherapy.
Athletes using EPO do so to encourage their bodies to produce higher than normal amounts of red blood cells, hemoglobin and blood volume called hematocrit to enhance athletic performance.
Synthetic Oxygen Carriers 

These are chemicals that have the ability to carry oxygen. Two examples are:
  • HBOCs (hemoglobin-based oxygen carriers)
  • PFCs (perfluorocarbons)
Synthetic oxygen carriers have a legitimate medical use as emergency therapy. It is used when a patient needs a blood transfusion but:
  • human blood is not available
  • there is a high risk of blood out-fection (A blood outfection is when the blood is breaking down due to metabolic and/or dietary acids or from acidic drug use.)
  • there isn’t enough time to find the proper match of blood type
Athletes use synthetic oxygen carriers to achieve the same performance-enhancing effects of other types of blood doping: increased oxygen in the blood carried by the hemoglobin in red blood cells that helps reduce tissue acidosis in the connective tissues and muscles.  This results in reduced tissue or muscle breakdown and tissue acidosis that causes inflammation and pain.

So what could have Lance Armstrong done differently to achieve athletic superiority in his sport without drugs and blood fransfusions? And, how could have Lance Armstrong naturally increased his red blood cell count, hemaglobin and hematocrit and in turn increased his VO2 or oxygen volume to his connective tissues and muscles thus minimizing acid build-up and cellular breakdown, without taking hormones, steroids, EPO and blood transfusions known as blood doping?

Having been a professional athlete myself I have been doing natural blood doping successfully for myself (My blood counts run consistently – RBC count 5.2 million/mcL, Hemoglobin 17.2 g/dl, Hematocrit 53%, White Blood Count 3.8 thousands/mcL, Platelet Count 156 thousands/mcL, Glucose 80 mg/dl, Sodium 146 mEq/L, Chloride 106 mEq/L, Potassium 5 mEq/L, and Calcium 9.8 mg/dl, just to name a few of the most important markers in the blood), other athletes (including Professional and Olympic athletes) and cancer patients around the World for years with NO negative side-effects.

IT IS SIMPLE – IT IS SAFE – IT IS NATURAL – IT IS SMART and IT IS LEGAL!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! No side-effects except for increased health, energy and vitality.

Pass this on to Lance Armstrong?

Here is the formula for natural blood building without medical drugs, hormones, steroids, or blood transfusions (based upon 70kg body):

1)  Drink 250ml of pH Miracle liquid Chlorophyll.  Chlorophyll is the concentrated blood of green plants and is identical to human hemoglobin except for the center atom of magnesium in chlorophyll.  Drinking the blood of green plants will increase hemoglobin in less than two weeks.

2)  Drink 6 liters of pH Miracle Greens with 5 drops of the puripHy per liter.  The pH Miracle greens contains concentrated (28 to 1 concentration) grasses, fruit and vegetables that will increase red blood cell count and blood volume as indicated on a Comprehensive Blood Count Test.  The pH Miracle puripHy drops will increase the pH of the green drink and help to buffer metabolic and dietary acids that break down connective tissue and weaken muscles.

3)  Ingest 16 portions of alkalizing green fruit and vegetables.  Ingesting liberal amounts of green fruit and vegetables daily will help to maintain the high levels of red blood cells, hemoglobin and hematocrit.

4)  Drink 100ml of the pH Miracle Omega 3, 6 and 9 oil.  The ingestin of polyunsaturated oils from hemp, borage and flax will provide the necessary lipids for building the membranes of stem cells and blood cells and keeping them strong.

5)  Ingest 1 scoop of pHour salts in the morning, 1 sccop at night and 1 scoop any time the pH of the urine drops below 7.2.  The pHour salts contain four foundational mineral salts for the purpose of maintaining the alkaline design of the body fluids and reduce and/or eliminate the metabolic and respiratory acids that build-up during strenuous exercise such as carbonic acid and lactic acid.

6)  Spray the pHlavor salts orally to replace electrolytes and reduce the acids that create lightheadedness, dizziness, cold hands, cold feet, poor circulation, low energy, just to name a few symptoms of low mineral salts.

7) And, finally take 2 scoops twice a day of the pH Miracle L-Arginine Max to improve blood and lymph circulation by breaking up acidic mucous, plaque, calcifications, and cysts in the blood, lymph and connective tissue.

When an athlete follows the above recommendations based upon my clinical research for over twenty years he or she will consistantly show increases in their red blood cell count approaching or exceeding 5 million/mcL, hemoglobin increases approaching or exceeding 15 g/dl, and hematocrit increases approaching or exceeding a volume of  50 percent or higher.

The following article suggests other incredible benefits for eating and drinking daily green fruit and vegetables:

http://articlesofhealth.blogspot.com/2013/01/another-reason-to-eat-and-drink-your.html

Cholesterol Lowering Drugs Cause Heart Attacks, Strokes and Diabetes!

The higher your cholesterol the lower your risk for heart attack or stroke when you are living and eating the standard acid lifestyle and diet (SAD). And, the lower your cholesterol the higher your risk for a heart attack or stroke. (1)

The first graph shows the world famous Lancet published Framingham Study after ten years and the effects of high cholesterol. The second graph shows the study after twenty years. The interesting thing is everyone knows about the first ten years but few people, including doctors have been informed about the Framingham study after twenty years. The Framingham study is the largest and longest reliable study on the effects of chloesterol on the heart and vascular system.(1)
 
Ten years later the study NOW indicates that high cholesterol is NOT a risk for heart attack or stroke. When cholesterol exceeded 300 mg/dl the risk of heart disease was significantly reduced. Eighty percent of people who developed heart disease had cholesterol less than 200 mg/dl.(1)
 
Dr Robert O. Young’s has stated in his research that all heart attacks and strokes are caused by acids from an acidic diet and metabolic acids and NOT high cholesterol. He has suggested that cholesterol, especially low density lipoproteins are created by the body to buffer and protect the blood, organs and tissues from dietary and metaobolic acids. He states the best way to protect the heart and the vascular system is to maintain the alkaline design of the body with an alkaline lifestyle and diet as outline in his book, The pH Miracle Revised and Updated.(2)
 
Just recently the Food and Drug Administration issued new safety warnings about a popular class of drugs used to control and lower cholesterol levels. The FDA says the drugs, known as statins, can cause several side effects, including cognitive problems such as memory lapses and confusion. But the agency is stressing that the side effects appear to be rare and not serious. It is Dr Robert O Young’s research that suggests taking any drug, like statin drugs that lowers LDL cholesterol without removing acidic lifestyle and dietary choices is a risk for heart attack, stroke and other dis-eases like diabetes. Dr Young has lowered cholesterol sucessfully in all cases of hyperchlolesterolemia without drugs by just changing the diet and lifestyle to an alkaline pH Miracle lifestyle and diet that restores the alkaline design of the body.(2)
 
One of Dr. Young’s research clients Maren Hale was diagnosed with familial hypercholesterolemia and hypertriglycerides with LDL’s over 400 mg/dl and triglycerides over 200 mg/dl. She was also overweight. Over a period of four years Maren lost over 70 pounds and lowered her cholesterol and triglycerides to healthy normal ranges on the pH Miracle Lifesyle and Diet. Maren and her family and extended family have been a research study of the University of Utah for familial hypercholesterolemia for over 40 years. Maren was the first of all family members to lower her cholesterol and triglycerides to normal ranges due to her commitment to living a pH Miracle Lifesyle and Diet.(2)
 

 
 
The following is an article that appeared in the Wall Street Journal:
 

The FDA raised safety concerns about the popular class of cholesterol-fighting drugs. The drugs have been taken for years by tens of millions of people and include brand names such as Lipitor and Crestor. Ron Winslow reports on the News Hub. Photo: Getty Images.

The Food and Drug Administration warned that patients taking cholesterol-fighting statins face a small increase in the risk of higher blood-sugar levels and of being diagnosed with diabetes, raising concerns about one of the country’s most widely prescribed groups of drugs.

The federal safety agency said Tuesday it plans to require drug makers to add the diabetes-risk language to the “warnings and precautions” section of the labels on statin drugs.

Statins include top-selling brand names such as Lipitor, Crestor, Zocor and a dozen or so other branded and generic versions under various names. The drugs are prescribed to more than 20 million Americans a year, at a cost of more than $14 billion in 2011, according to the research firm IMS Health.

The warning isn’t expected to prompt doctors to stop prescribing statins for patients with multiple risk factors for heart attack. Cardiologists said for many patients, the benefits of statins still outweigh these risks.

The diabetes issue is “real” but “not a huge effect,” said Robert Califf, vice chancellor for clinical research and a cardiologist at Duke University Medical Center. “Informing people is a good thing, but for the vast majority of people who really need to be on a statin, this shouldn’t change what they do.”

But some physicians cautioned that the risk wasn’t insignificant and that patients at lower risk for heart problems might want to reassess whether they should remain on statins.

“The diabetes issue is a really big deal. We’re overcooking the statin use,” said Eric J. Topol, a prominent cardiologist and chief academic officer of Scripps Health in LaJolla, Calif.

In addition, the FDA said labels for statin drugs now will contain information about patients experiencing memory loss and confusion, though this side effect was classified as an “adverse reaction” rather than one of the warnings and precautions, a more serious category.

Amy Egan, the FDA’s deputy director for safety of metabolic and endocrinological products, said “these cognitive changes can be quite dramatic” and “sustained” but that they disappear when statin therapy is stopped. Dr. Egan said the agency cannot identify a specific drug or age group of people who might be prone to such cases. She said patients should notify their doctors if these symptoms occur.

Bloomberg News

Cholesterol drugs Lipitor and Zocor are arranged on a counter of a Cambridge, Massachusetts pharmacy in 2006.

The FDA made new labeling recommendations for one specific statin, Mevacor, generically called lovastatin. It said that some medicines like protease drugs used to treat AIDS and drugs for bacterial and fungal infections shouldn’t be taken with Mevacor because of interactions that may lead to muscle injury.

At the same time, the FDA announced that drug makers could remove a label warning that liver enzymes need to be monitored during statin therapy. It cited the fact that “serious liver injury with statins is rare and unpredictable” and that periodic monitoring “does not appear to be effective in detecting or preventing this rare side effect.”

AstraZeneca PLC, which makes Crestor, the only major statin still sold exclusively as a brand-name drug, said in a statement that “the cognitive issues are generally nonserious and reversible upon discontinuation” of a statin. It said reports about increased blood sugar were already included on Crestor labels.

In addition to the pure statins, products that contain statins include Advicor, Simcor and Vytorin. Merck & Co., which makes Zocor and Vytorin, said information for those drugs was “updated” in October in a way that reflects the contents of the FDA’s Tuesday safety advisory. It revised labeling for Mevacor more recently.

The FDA’s action follows analyses of large numbers of statin studies in recent years. In one, published in the Lancet in 2010, researchers looked at 13 studies including 91,140 patients. The researchers concluded that statin therapy “is associated with a slightly increased risk of development of [Type 2] diabetes, but the risk is low both in absolute terms and when compared to the reduction in coronary events.”

Cardiologists differed on how to weigh the findings, especially for the millions of people given the drugs for the prevention of a first heart attack or stroke.

Steven E. Nissen, chairman of cardiovascular medicine at the Cleveland Clinic, said, “There is no question that statins slightly increase the risk of a diabetes diagnosis and of slightly higher blood sugar, but I think this has no impact on the risk-benefit assessment. I know I can lower the [relative] risk of death, stroke and heart attack by about 30%” in patients at high risk of such cardiovascular events.

Dr. Topol said research suggests that for every 200 people who take a statin, 1 will develop diabetes. By comparison, 1 to 2 out of 100 patients at risk for a heart attack will avoid one, he said, adding, “That’s a very narrow margin of benefit,” he said.

Rita Redberg, a cardiologist at the University of California, San Francisco Medical Center, stressed the long-term concerns about diabetes. “We know that diabetes is a significant risk factor for heart disease,” Dr. Redberg said. She said the statin-diabetes link “raises the concern that over time the diabetes risk will outweigh the cholesterol-lowering benefit on overall risk of cardiovascular disease.”

Reference:
(1) Martin MJ et al, Lancet 1986; H-933-936
(2) The pH Miracle Revised and Update, Pub. July 2010, Hachett Publishing

What Causes the Elevation of Cholesterol Levels In the Blood?

After all, what causes the elevation of cholesterol levels in blood?

The following are some suggestions from the medical literature about factors, beyond the famous but wronged and simplistic idea that foods based on saturated fats cause the development of atherosclerosis (1, 22), suggesting that stress, high carbohydrate diets (sugar acid) and smoke may raise total cholesterol and low density lipoproteins levels:

1. Stress increases metabolic acids
a) Anxiety and cholesterol elevation (2, 3, 4, 5, 6, 7, 8, 9, 10, 11)
b) Hostility and cholesterol elevation (12, 13, 14)
c) Extreme physical exertion and cholesterol elevation (15)

2) High carbohydrate diets or the acid sugar and cholesterol elevation (16, 17, 18).

Continue reading What Causes the Elevation of Cholesterol Levels In the Blood?

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