How NOT To DIE! and How To Live!

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: http://www.drrobertyoung.com

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

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.

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

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!

David Beckham is a follower of the alkaline lifestyle and diet

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

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

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.

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

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/

 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.

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

 

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.

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.

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.

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.

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

 

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.phmiracleproducts.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

Our Next pH Miracle Event will be from November 18th to December 2nd – To learn more email us at: phmiracleliving@aol.com

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

Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

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

Jan 10, 2016

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Abstract

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

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

Introduction

Sodium and potassium bicarbonate are excellent agents for a natural alkaline approach in the treatment for all sickness and disease, including cancer. Sodium bicarbonate is the universal mainstream treatment of acidosis. It is used every day by oncologists to neutralize the heavy acidic nature of their chemical and chemotherapeutic agents which are often quite toxic. Sodium bicarbonate is also used routinely in many clinical situations as herein noted including many peer–reviewed journals: 1) Severe diabetic ketoacidosis (1) 2) Cardiopulmonary resuscitation (2) 3) Pregnancy (3) 4) Hemodialysis (4) 5) Peritoneal dialysis (5)6) Pharmacological toxicosis (6) 7) Hepatopathy (7) 8) Vascular surgery operations (8) Medics and emergency room medical doctors are accustomed to participating in a flurry of activity when trying to save a persons live after a cardiac arrest–inserting IVs and breathing tubes, performing defibrillation to restart the heart, etc. Sodium bicarbonate is a constant performer under such conditions and is more commonly used than magnesium injections, which is traditionally at the top of every doctor’s protocol for cardiac arrest. Mainstream oncologists recognize the routine involvement of late stage infections which I refer to as outfections in all cancerous conditions. Medical savants also recognize that bacteria, yeast and mold is present in over forty percent of all cancerous conditions. (9) The most recent research in this area demonstrates how even viruses, which I describe as crystallized acid, is present in fifty percent of certain types of cancerous conditions. (10) Sodium and potassium bicarbonate increases the hydroxyl ions or electron levels through increased alkalinity to the cells buffering the metabolic acids that can cause cancer.(20)  It is also one of the most basic medicines in allopathic and alternative medicine we have for the treatment of kidney disease.  Research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease.(11) We don’t need a thousand years of scientific tests to understand something as simple and essential as alkaline water and it is quite the same with sodium and potassium bicarbonate. Sodium and potassium bicarbonate are always present in the best alkaline drinking waters and organic raw green foods and is constantly being produced by the cover cells of the stomach to alkalize the acidic foods and liquids we ingest, including buffering metabolic and respiratory acids in order to maintain the alkaline design of the blood and tissues at a delicate pH of 7.365.(20) What is Latent Tissue Acidosis? Medical doctors are not taught in medical school and therefore do not understand or recognize latent tissue acidosis. They understand and recognize compensated acidosis and decompensated acidosis. In compensated acidosis, breathing increases in order to blow off more carbonic acid which decreases PCO2 because of the lowered carbonate or HCO3. When the breathing rate can no longer get any faster and when the kidneys can no longer increase its’ function to keep up with the acid load, then the blood pH starts to change from a pH of 7.365 to 7.3 then to 7.2. At a blood pH of 6.95 the heart relaxes and the client goes into a coma or dies. Latent “acidosis” is a condition that exists when there are not enough bases in the alkalophile glands because they have been used up in the process of neutralizing the acids adsorbed to the collagen fibers. This leads to compensated “acidosis.” This means the blood pH has not changed but other body systems have changed. This can then lead to decompensated “acidosis” where the alkaline reserves of the blood are used up and the pH of the blood is altered. Decompensated “acidosis” can be determined by testing the blood pH, urine pH and the saliva pH. The decrease in the alkaline reserves in the body  can occur because of hyper-proteinization, (eating meat and cheese!) or too much protein, and hyper-carbonization, or too much sugar or from excessive or over-excercise. This is why young athletes fall over dead or why 80 to 90 year old folks are all shrunk up and look like prunes. They have very little or no alkaline reserves in their alkalophile glands. When all the alkaline minerals are gone, so are you and your battery runs out of charge. The charge of your cellular battery can be measured by testing the ORP or the oxidative reduction potential of the blood, urine or saliva using an ORP meter. As you become more acidic this energy potential or ORP increases. How Is Sodium Bicarbonate Created In The Body? The parietal or cover cells of the stomach split the sodium chloride of the blood. The sodium ion is used to bind with water and carbon dioxide to form the alkaline salt, sodium bicarbonate or NaHCO3. The biochemistry is: H20 + CO2 + NaCl = NaHCO3 + HCL. This is why I call the stomach an alkalizing organ NOT an organ of digestion. The stomach DOES NOT digest the food or liquids we ingest but it alkalizes the foods and liquids we ingest.  We have one instrument in the human body to digest food and it is NOT the stomach it is your teeth.  Once we swallow our food or drink the stomach begins to prepare the food by alkalizing it in a bath of sodium bicarbonate. For each molecule of sodium bicarbonate (NaHCO3) made, a molecule of hydrochloric acid (HCL) is made and secreted into the so-called digestive system – specifically, the stomach (the gastric pits in the stomach) – to be eliminated via the blood. Therefore HCL is an acidic waste product of sodium bicarbonate created by the stomach to alkalize the food and liquids ingested. Exercise Creates Metabolic Acidic Waste Products Which Are Harmful To The Blood and Tissues When one exercises or over-exercises the body needs additional alkaline bicarbonate salts to buffer lactic acids.  The additional bicarbonate is created in the stomach lining to buffer the increased amounts of lactic acids produced as a waste product of metabolism.  The production of sodium bicarbonate will always leave an acidic waste product of hydrochloric acid in the gastric pits of the stomach leading to nausea, light headedness, dizziness, muddle thingking, and poor circulation.  If the excessive exercise continues this can then lead to a dificiency of mineral and bicarbonate salts (electrolytes lost through perspiration or urination) which may lead to latent tissue acidosis, pain, edema, hyponatrenia and death. But how does something like sodium and/or potassium bicarbonate, so seemingly innocuous have such a dramatic effect? During prolonged or intense exercise muscles produce large amounts of acidic waste products, such as lactic acid, that lead to soreness, stiffness, fatigue and possible edema if these acids are not buffered and eliminated through urination or perspiration. Because sodium and potassium bicarbonate naturally reduces metabolic acids, it acts as a buffer against these performance-limiting by-products. Current research suggests that supplemental sodium bicarbonate, like the pH Miracle pHour Salts (contains sodium and potassium bicarbonate) is particularly helpful in speed-based events, including sprints, football and other fast-moving games, and middle-distance (up to 10km) running, swimming and cycling. “Essentially, sodium bicarbonate is an alkaline substance that increases the pH of the blood,” Dr Folland says. “This seems to reduce and offset the acidity produced in the muscles during intense, anaerobic exercise that produces lactic acid most quickly, such as fast running or swimming.” In Dr Folland’s study, swimmers who took the sodium bicarbonate knocked 1.5 seconds off their time for 200m, a difference that may seem insignificant to recreational swimmers but which is substantial at elite level. “At the last Olympics, the top four swimmers in the men’s 200m freestyle were separated by just 1.4 seconds,” Dr Folland says. “So, in theory, it could be the difference between winning a medal and not.” Anyone can try it, he says, but only those who are serious enough to monitor their times and progress in sports such as running, swimming or cycling may notice the few seconds advantage it might provide. “The increments of improvement are relatively small to the average person, although significant to someone who competes,” Dr Folland says. Athletes for years have sworn that taking a spoonful of bicarbonate of soda (baking soda) helps them to keep going for longer. For years, experts doubted that there was anything other than a placebo effect to these claims until they subjected the substance to rigorous examination. Most exercise scientists investigating the trend for “soda-doping” among athletes and gym-goers have shown that it offers significant benefits for endurance and speed.” At Loughborough University, for instance, physiologists reporting in the June issue of the International Journal of Sports Medicine showed that swimmers who took baking soda about one hour before a 200m event were able to shave a significant time off their usual performances. Dr Jonathan Folland, who led the study, says that it is not uncommon for top swimmers to take sodium bicarbonate (another name for the substance) before a competition to give them an edge. Indeed, he showed that of nine swimmers tested, eight recorded their fastest times after ingesting a supplement of the common baking ingredient – sodium bicarbonate. Where are Bicarbonates Created In The Human Body and Why? The chloride ion from the sodium chloride (salt) binds to an acid or proton forming HCL as a waste product of sodium bicarbonate production. HCL has a pH of 1 and is highly toxic to the blood and tissues and the cause of indigestion, acid reflux, ulcers, diabetes, cancer, hyponatremia, edema, tonsilar herniation and death.  When large amounts of acids, including HCL, enter the stomach from a rich animal protein or dairy product meal, such as meat and cheese, or from starchy foods from root vegetables like potatoes or during extreme exercise, acid is withdrawn from the acid-base household. The organism would die if the resulting alkalosis – or NaHCO3 (base flood) or base surplus – created by the stomach was not taken up by the alkalophile glands (salivary glands, pancreas, kidney, pylorus glands, Brunner’s glands, Lieberkuhn glands and liver) that need these quick bases in order to build up their strong sodium bicarbonate secretions. These alkalizing glands and organs are the stomach, pancreas, Brunner’s glands (between the pylorus and the junctions of the bile and pancreatic ducts), Lieberkuhn’s glands in the liver and its bile with its strong acid binding capabilities which it has to release on the highly acidic meat, cheese, potato, acid water or metabolic and/or respiratory acids from over-exercise to buffer its strong acids of nitric, sulphuric, phosphoric, uric and lactic acids in daily metabolism, respiration and excessive or over-exercise. Bicarbonate acts to stimulate the ATPase by acting directly on it.(12) The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating disease that it prevents patients from having to be put on kidney dialysis. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. Bicarbonates of sodium and potassium are a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash. Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa, Florida stated, upon seeing the research on sodium bicarbonate and kidney disease, “I am glad to see confirmation of what we have known for so long.  I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”. A dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.” The Stomach, Pancreas and Kidneys Naturally Produce Sodium Bicarbonate Every Day The exocrine section of sodium bicarbonate from the stomach and the pancreas have been greatly ignored in the treatment of diabetes and cancer even though its impairment is a well documented condition. The stomach and the pancreas is primarily responsible for the production of sodium bicarbonate necessary for normal alkalization of food and liquids ingested. Sodium bicarbonate is so important for protecting the kidney’s that even the kidneys get into the act of producing sodium bicarbonate.  We now know the common denominator between hyponatremia, inflammation, edema, diabetes, kidney disease, and cancer is the lack of sodium and potassium bicarbonate or the body’s inability to produce sodium and potassium bicarbonate because of a lack of mineral salts in the diet. When the body is hit with reductions in sodium bicarbonate output by these three organs,’ acid conditions build up and then the entire body physiology begins to change from a state of oxygenation to fermentation. Likewise when acid build-up outstrips these organs normal sodium bicarbonate capacity, cellular, tissue, glandular and organ deterioration begins. The stomach, pancreas and the kidneys alone produce about five hundred grams (about one pound) of sodium and/or potassium bicarbonate per day in an attempt to neutralize dietary and/or metabolic acid in the blood and interstitial fluids that surround the body cells. The stomach, pancreas and the kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood and tissues. If the blood and tissues are too acidic, the stomach and/or the kidney’s make sodium bicarbonate to restore the blood and tissue pH back to a delicate pH balance of 7.365. If the blood or tissues are too alkaline, then the kidney excretes sodium bicarbonate into the urine to restore the 7.365 alkaline balance. Acid-base balance is the net result of two processes, first, the removal of sodium bicarbonate subsequent to hydrogen ion production from the metabolism or dietary constituents; second, the synthesis of “new” sodium bicarbonate by the stomach and/or the  kidney’s.(13)  The stomach and kidneys pull salt, water and carbon dioxide from the blood to make sodium bicarbonate to maintain the alkaline design of the body during all functions of the body from the ingestion of food or drink to exercise.  The chemical formula is as follows:  NaCl + H2O + CO2 = NaHCO3 + HCL.  The waste product of sodium bicarbonate is hydrochloric acid which is eliminated by kidneys as an acidic excretion of the urine. It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging or rotting process. Acidosis occurs often when the body cannot produce enough sodium bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and eating and drinking highly acid foods and drinks like chicken, pork, beef, dairy products, coffee, tea, alcohol, chocolate, soft drinks, just to name a few.  We are also testing bottled mineral water and finding that these waters are acidic and may contribute to overall tissue acidosis. Acid-buffering by means of base supplementation (The pH Miracle pHour Salts) of sodium bicarbonate is one of the major roles of dialysis. Sodium bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum sodium bicarbonate concentration of 22 mmol/l.(14)  Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality.  Sodium bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.(15) One of the main reasons we become over-acid is from over-consumption of animal protein, dairy products, high sugar fruit, grains, alcohol, coffee, tea, chocolate, soft drinks and over-exercise or under-exercise. Eating meat and dairy products may increase the risk of prostate cancer, research suggests.(16) We would find the same for breast and other cancers as well metastatic cancers.(17) Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of alkaline minerals you have a dis-ease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids, such as, nitric, uric, sulphuric and phosphoric acid. Unless a treatment actually removes acidic toxins  from the body and increases oxygen, water, and nutrients most medical interventions come to naught. These metabolic and dietary acids must be excreted by the kidney’s because they contain sulfur, phosphorus, and/or nitrogen which cannot break down into water and carbon dioxide to be eliminated as weak acids. In their passage through the kidney’s these strong acids of ntric, sulphuric, phosphoric and uric acid must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn or destroy the kidney’s on their way out. This would happen if these strong acids were excreted in their free acidic form. Substituting a sodium bicarbonate solution for saline infusion prior to administration of radiocontrast material seems to reduce the incidence of nephropathy.(18) Dr. Thomas P. Kennedy American Medical Association Sodium and potassoum bicarbonate ions neutralize the acids that cause chronic inflammatory reactions. Hence, sodium and potassium bicarbonate are of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium and potassium bicarbonate are well-studied and used salts with known effects. Sodium and potassium bicarbonate are effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects.(19)  It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy. Sodium and potassium bicarbonates possess the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with healthy tissue from the same person shows that the cancer tissue has a much higher concentration of toxic chemicals, pesticides, etc. Sodium and potassium bicarbonate intravenous infusions are indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest, tonsillar herniation due to cerebral edema, severe primary lactic acidosis and hyponatremia due to excessive or over-exercise.  During heavy exercise, if the the resulting lactic acid is not adsorbed by the collagen fibers, the specific acid catchers of the body, the blood pH will drop and the body will go into a coma and the person will die. The total collection of these fibers is the largest organ of the body called SCHADE, the colloidal connective tissue organ. NO liquid exchange occurs between the blood and the parenchyma cells, or in reverse, unless it passes through this connective tissue organ. This organ connects and holds everything in our bodies in place. This organ is composed of ligaments, tendons, sinew, and the finer fibers that become the scaffolding that holds every single cell in our bodies in place. When acids are stored in this organ, which includes the muscles, inflammation or edema and pain develop. The production of lactic acid is increased with excessive exercise and the ingestion of milk, cheese, yogurt, butter, ice cream, high sugar fruit and starchy root vegetables like potatoes. That is why I have stated, “acid is pain and pain is acid or acid is edema and edema is pain”.  You cannot have one without the other. This is the beginning of latent tissue acidosis leading to irritation, inflammation, edema and degeneration of the cells, tissues and organs and eventual or sudden death.  It is why we are seeing so many amateur and professional atheletes pass out and die on the playing fields.  Metabolic, respiratory and gastrointestinal acids can and do kill and death can be overted by simply maintaining the alkaline design of the body fluids with protective hydration of alkaine sodium bicarbonate fluids. The acid/alkaline balance is one of the most overlooked aspects of diagnostic medicine. In general, the world population is heavily acidic, excepting alkalarian vegans (those who ingest raw, organic green fruit, vegetables, mineral salts, alkaline water and unsaturated seed and nut oils), and even their bodies have to face increasing levels of environmental toxic exposure, which may contribute to an acidic pH condition of the blood and then tissues. With over 30 years of research and testing over 100,000 individual samples of blood and over 100,000 samples of urine and saliva, I have come to the conclusion that the human body is an acidic producing organism by function – yet, it is an alkaline organism by design. Eating animal protein, especially meat and cheese, sugar, fermented foods, starchy foods like potatoes, acidic water, alcohol, coffee, tea, chocolate,  and excessive exercise or under-exercise, obsessive behaviors, lack of rest, lack of sunshine, and emotional stress are deadly acidic lifestyle choices. All enervation, under-performance, sensitivity, irritation, inflammation, edema, catarrh, induration, ulcerations, degeneration, aging and cancerous conditions are caused by a four letter word – ACID, which is an acronym which stands for: A = acidic food and drink, attitudes and activities, C = compromised internal acidic environment, I = illness and dis-ease, and, D = desire for more acidic foods, drinks, attitudes and activities, and the cycle repeats itself.[20] We ingest acidic medicines to lessen the symptoms of our illness. We stimulate the body with unhealthy forms of energy providing quick, often temporary relief from our symptoms which begins the cycle all over again creating a very powerful pattern of poor health and dis-ease. Conclusion The pH Alkalizing Lifestyle and Diet is a low acid producing diet and lifestyle that focuses on the foundational principal that the body is alkaline by design and yet acidic by function. This makes this program the ultimate program for preventing and reversing aging and the onset of sickness and disease. I would say that the pH Alkalizing Lifestyle and Diet is the perfect diet and lifestyle for a longer healthier life.(20)

References 1. Gamba, G., “Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial.” (Rev Invest Clin 1991 Jul-Sep;43(3):234-8). Miyares Gom ez A. in “Diabetic ketoacidosis in childhood: the first day of treatment.” (An Esp Pediatr 1989 Apr;30(4):279-83) 2. Levy, M.M., “An evidence-based evaluation of the use of sodium bicarbonate during cardiopulmonary resuscitation.” (Crit Care Clin 1998 Jul;14(3):457-83). Vukmir, R.B., Sodium bicarbonate in cardiac arrest: a reappraisal (Am J Emerg Med 1996 Mar;14(2):192-206). Bar-Joseph, G., “Clinical use of sodium bicarbonate during cardiopulmonary resuscitation–is it used sensibly?” (Resuscitation 2002 Jul;54(1):47-55). 3. Zhang. L., “Perhydrit and bicarbonate improve maternal gases and acid-base status during the second stage of labor.” Department of Obstetrics and Gynecology, Xiangya Hospital, Hunan Medical University, Changsha 410008. Maeda, Y., “Perioperative administration of bicarbonated solution to a patient with mitochondrial encephalomyopathy.” (Masui 2001 Mar;50(3):299-303). 4. Avdic. E., “Bicarbonate versus acetate hemodialysis: effects on the acid-base status.” (Med Arh 2001;55(4):231-3). 5. Feriani, M., “Randomized long-term evaluation of bicarbonate-buffered CAPD solution.” (Kidney Int 1998 Nov;54(5):1731-8). 6. Vrijlandt, P.J., odium bicarbonate infusion for intoxication with tricyclic antidepressives: recommended inspite of lack of scientific evidence. Ned Tijdschr Geneeskd 2001 Sep 1;145(35):1686-9). Knudsen, K., “Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning.” (Crit Car e Med 1997 Apr;25(4):669-74). 7. Silomon, M., “Effect of sodium bicarbonate infusion on hepatocyte Ca2+ overload during resuscitation from hemorrhagic shock.” (Resuscitation 1998 Apr;37(1):27-32). Mariano, F., “Insufficient correction of blood bicarbonate levels in biguanide lactic acidosis treated with CVVH and bicarbonate replacement fluids.” (Minerva Urol Nefrol 1997 Sep;49(3):133-6). 8. Dement’eva, I.I., “Calculation of the dose of sodium bicarbonate in the treatment of metabolic acidosis in surgery with and deep hypothermic circulatory arresta.” (Anesteziol Reanimatol 1997 Sep-Oct;(5):42-4). 9. “I believe that, conservatively, 15 to 20 percent of all cancer is caused by infections; however, the number could be larger — maybe double,” (Dr. Andrew Dannenberg, Director of the Cancer Center at New York-Presbyterian Hospital/Weill Cornell Medical Center.”) Dr. Dannennberg made the remarks in a speech in December 2007 at the annual international conference of the American Association for Cancer Research. 10. A sexually transmitted virus that causes cervical cancer is also to blame for half of all cases of cancer of the penis. 11.  www.nelm.nhs.uk/en/NeLM-Area/News/2009—July/20/ Bicarbonate-supplementation-may-slow-renal-decline-in-chronic-kidney-disease/ 12. Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein  1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A. 13. Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986 14.  www.uptodate.com/patients/content/abstract.do?topicKey=~G/p55S8w8sQDwqG&refNum=28 15.  www.ncbi.nlm.nih.gov/pubmed/16523427 16.  news.bbc.co.uk/2/hi/health/7655405.stm 17.  Cancer Res. 2009 Mar 15;69(6):2260-8. Epub 2009 Mar 10. Bicarbonate increases tumor pH and inhibits spontaneous metastases. Robey IF, Baggett BK, Kirkpatrick ND, Roe DJ, Dosescu J, Sloane BF, Hashim AI, Morse DL, Raghunand N, Gatenby RA, Gillies RJ. Source: Arizona Cancer Center, University of Arizona, Tucson, Arizona, USA 18.  JAMA 2004;291:2328-2334,2376-2377.www.urotoday.com/56/browse_categories/renal_transplantation_vascular_disease/ sodium_bicarbonate_may_prevent_radiocontrastinduced_renal_injury.html 19. These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin).   Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others. 20. www.phmiracle.com. Young.R.O., Young, S.R., The pH Miracle Revised and Updated, Hachett, 2010.

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 

Robert Young M.Sc., D.Sc.. Ph.D

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.

 

 

 

 

 

 

 

[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.

 

 

 

 

 

 

 

 

[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.

 

 

 

 

 

 

 

[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.)

[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.

 

 

 

 

 

[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}

 

 

 

 

 

 

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.

[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 Medicine, Volume 28, Issue 12, 15 June 2000, Pages 1685–1696

 [12] Chang JC, van der Hoeven LH, Haddox 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 Fernandes, Carlos 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]

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.

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.

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.

 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.

Table 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.

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table 9

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

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table 12

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

Table 13

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

What Happens to ALL the Disappearing Can

What Happens to ALL the Disappearing Cancer Patients?

It’s been almost 20 years since I met my first disappearing patient — a nurse in her early 40s, let’s call her Kate. Kate was diagnosed with breast cancer. As a nurse, she had seen the results of breast cancer treatments. She was terrified, and determined. She was not heading for surgery, nor chemotherapy, nor radiation.

But Kate worked in a hospital. She worked with the doctors who diagnosed her cancer, and she worked with the surgeon, who wanted to schedule her into surgery “as soon as possible.”

The first thing Kate did was slow down. She did some research. It didn’t take her long to remind herself that in Canada, and in the USA, the treatments for cancer are akin to law. No hospital would dare deviate from the deadly three (cut, poison, burn).

Kate’s cancer was not large. She had been tested for cancer last year and no cancer was found. She knew it took many years for cancers to develop. At first, she was furious, “If it is here today, it must have been here last year. Why didn’t you find it last year?” It had not metastasized. It was not growing rapidly and was not affecting her health in any way. In theory, she had lots of time. So, she took some time.

But Kate didn’t look for magic cures. She didn’t search for the latest “cancer medicine.” She wasn’t interested in curing herself. She knew she was a nurse, not a doctor. She searched instead for the “cured” – patients who were diagnosed with cancer, and no longer had cancer. She knew from her work in the hospital, from conversations with patients, and with some staff, that these people existed — but from the perspective of the medical establishment, they seemed to disappear.

It didn’t take her long to find some patients who claimed they were cured. They hadn’t disappeared from life. They were eating, drinking, loving, and living full healthy and prosperous lives. But according to the medical records, they didn’t exist. They were “never cured.”

The medical system treated their cures as “anecdotal.” It ignored them. There was no attempt by any doctors to understand what happened to these cancer patients. They were no longer sick. The medical system looks after sick patients, treats sick patients. These patients were not sick.

Kate looked and listened. Her interest was not clinical science vs. anecdotal evidence. Her interest was personal. She talked, listened, compared stories. From several, she learned about a clinic that did not claim to cure cancer. It did not use medicines to treat cancers. But patients were cured, somehow. This clinic was not in Canada. It was not in the USA. She would have to go to Mexico to learn more.

There are lots of alternative treatment clinics in Mexico. Are some of them valid, using important techniques to cure cancers? Are some of them scams, wanting to take money from desperate clients? Do some of them have a cure that works sometimes, but might not work for her? Kate didn’t know. She did more research. She called the clinic.

The staff did not claim to cure cancer. Claiming to cure cancer is dangerous, even for a clinic outside of North America. They suggested Kate visit the clinic and see what happens there, no charge for a visit, but she would need to pay for her travel to Mexico. Kate had done her research. She had met and talked to patients whose cancers had disappeared.

Kate made her decision. She was familiar with cancer diagnosis techniques in Canada. She had undergone a physical examination, a mammogram, that detected a lump in her breast. Then she had a biopsy, where tissue was taken from the lump and was sent to a lab for analysis. The lab technician tested and examined the sample and issued a diagnosis “cancer” or “not cancer.” Once the diagnosis is issued, everybody swings into action. Kate knew that the mammogram had a high false positive rate and a false negative rate. Many people who are diagnosed with a “possible cancer” by a mammogram do not actually have cancer. She was also aware that cancer biopsies have a false positive rate and a false negative rate, as well. Her work in the hospital, with real patients, had made this very clear.

She didn’t really know for certain if she had cancer. Her surgeon, on the other hand, was still pressing her to schedule treatment.

Kate knew one thing. She had time. She cashed out some savings and booked a “holiday” in Mexico.

At the clinic, Kate was surprised that there was no “cancer diagnosis.” They did check the presence and size of the lump on her breast. But they didn’t repeat the biopsy. The clinic read her diagnostic reports, but did not investigate them further. There was instead a very thorough analysis completed by a suite of doctors. It took two full days of tests and interviews, if I remember correctly.

Kate was asked about her family’s medical histories. She gave blood samples. She was questioned extensively about her diet, about what she eats on a regular basis. What foods does she like and eat often. What foods does she not like and never eat. Doctors examined her lungs, her heart, liver, and other bodily organs with various tests. Her immune system was tested. Extensive interviews about her life, her work, her relationships, and more.

At the time I talked to Kate, I didn’t realize that she was not getting a “medical analysis,” she was actually getting a “healthicine analysis.” Her tests and questions fit perfectly to the hierarchy of healthicine: genetics, nutrition, cells, tissues, organs, bodily systems, body, mind, spirit, and community.

Kate’s genetics were analyzed through family history. There may have been further genetic analysis, I don’t remember all of the details. Her nutritional status was analyzed, not just by analyzing what she ate, and what she preferred to eat, but also by studying what she didn’t like to eat, what she deliberately never ate, what foods she believed she was allergic to. Her cells and tissues were analyzed directly, through blood samples and physical examination, and indirectly through medical history and other tests. Many of her organs were tested for healthiness. Her bodily systems, immune system, circulatory system, respiratory system, hormonal systems and more were analyzed and assessed. Her physical body was measured, weighed, and examined. Her mental health was assessed, as well as her spiritual healthiness. She was in good spirits, even in light of a potentially life threatening illness. Her community health was analyzed as well. Her family, her relationships with her children, her spouse, her parents, her work community, and more.

After a few days, Kate met with a group of doctors to discuss her health, not her illness, her healthiness. Diagnosing illness is difficult. Analyzing healthiness is more complex. It took several doctors and several hours for Kate to learn and understand what they had learned about her healthinesses and her unhealthinesses.

They then “prescribed” two weeks, if I remember correctly, of healthiness training, tailored to Kate’s specific situation. She spent the next two weeks at the clinic, learning to be healthier, not learning how to be “healthier in principle,” rather – learning what Kate needed to do to make her diet, her body, her mind, her spirits, and even her relationships with her communities healthier. She could not change her work community. But she could change how she reacted to and interacted with it – to improve her own health. After two weeks of learning at the clinic, her breast lump had started to shrink.

Kate went back to Canada, to put her learning into action. The lump disappeared. Her diagnosis was still there on paper. But her “cancer” had disappeared. She was retested at her hospital and no cancer was found.

Then Kate began to disappear.

When the surgeon asked again, she explained that she was not going to surgery. The surgeon looked away. He refused to look her in the eye after that.

But Kate didn’t disappear from her family. She went back to her family. She didn’t disappear from her job. She went back to her job. She disappeared from the cancer system. Her cancer disappeared, so, as a cancer patient, she disappeared.

Was she cured? We don’t know. There is no useful definition of a cancer cure. No medical or scientific test that can prove a patient has been cured of cancer. Our cancer treatment statistics have no count for people who are cured of cancer. Patients that are cured, whether they are cured with medicines or not, are not counted. No breast cancer patients are officially cured by medicine. If their cancer goes away without treatment, they disappear from statistics. If their cancer is killed by radiation, chemotherapy or surgery, they are not cured, they are a “survivor.” Everyone knows that cancer survivors are always waiting for the cancer to reappear. Their symptoms are in remission, but their cancer is not cured. They are not cured. With no proof of a cure, it might just be hidden.

Kate no longer has cancer. She paid, from her own pocket, for her trip to a clinic in Mexico. After the trip, her cancer disappeared. She had medical insurance. But her insurance wouldn’t pay for her trip. Insurance pays for treatments, not for cures. It pays for treatments, even if they fail. But it does not pay for success. Success disappears.

There are two ways for a cancer patient to disappear. You might be cured by health. Or you might be cured by a medicine that is not approved. In both cases, the medical system will ignore the cure, and ignore the patient.

In healthicine, there are no incurable diseases. If it is not curable – it is not a disease, it is a handicap, a disability, a deficiency, or simply an attribute of the person. All diseases can be cured by definition.

I have since met several cancer patients who have disappeared, and not just cancer patients. Maybe you have too? I’ve met more by internet, email, etc. There is no way for me to determine if a disappeared patient actually had cancer, if their treatment cured their cancer, if their body cured their cancer or if they still have cancer. We can only tell if there is another cancer diagnosis. Nothing can be told from the absence of a diagnosis.

There is no way for any doctor to tell either. There are no tests for a cancer cure. There is no way to recognize, much less document a cancer cure. There are no statistics for cancers cured.

Many cured patients don’t disappear quietly. They speak out. They write books and newspaper articles. They blog. But it doesn’t matter. They still don’t count. Once cured, they disappear. The medical system does not study their cases, does not study their diagnosis, does not study their cures. For chronic diseases, like cancer, arthritis, diabetes, heart disease, even obesity, and many more, there are no techniques to document “cured patients.” As a result, there are no statistics for “cured patients” of any chronic illness.

Once they are cured, they disappear. Health doesn’t cure illness, it disappears illness. And medicine doesn’t count people who have disappeared.

To your health

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

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

Lose Acidic Weight Eating Pink Organic Grapefruit

Women around the United States tried to burn off body fat by following some version of the Grapefruit Diet. (also known as the Hollywood Diet & the Mayo Clinic Diet)

Dismissed as a fad, the theory behind the Grapefruit Diet was that if you ate half a grapefruit or drank a glass of grapefruit juice with each meal (while reducing your caloric intake down to 800 calories/day), you would lose weight.

And while the 1970s version of the Grapefruit Diet did wonders for grapefruit farmers, it wasn’t very successful at delivering long term weight loss.

Fast forward to 2010….. and the latest scientific research which suggests that eating grapefruit contains phytonutrients that protects the body from acids that make us sick, tired and fat.

Naringenin, an antioxidant flavonoid which chelates dietary and metabolic acid, is derived from the bitter flavor of grapefruit and other citrus fruit, may cause the liver to chelate acid and release fat while increasing insulin sensitivity.

The Theory

• Normally, after a “normal” meal (consisting of carbs, fats & proteins), your blood is flooded with the metabolic and dietary acid called sugar.
• This boost in blood acid or sugar results in the activation of your Liver X Receptor Alpha – LXRα.
• Which results in the production of healthy fats by your liver to bind up the increased acidic sugar for long term storage – ie belly fat, saddle bags, love handles, etc…. The body does this to protect itself from excess dietary or metabolic acid.

The chelation of the acid sugar is good but if not eliminated through the bowels, urine or skin it ends up on you belly, thighs or buttocks.

And, up until this latest research into Naringenin, the only way to prevent this from happening was by reducing your intake of carbohydrates – via fasting or eating low carbohydrates.

But, with Naringenin, you would be able to increase your carbs while still receiving the health benefits of eating low carb:

• acids being released from your fat cells….
• resulting in the PPARα receptor being activated in your liver…
• leading to your body acid stored in the fatty tissues being broken down, while also…
• causing a reduction in over-all cholesterol production, which is created to bind up toxic acidic sugar.

And that’s not all.

Another benefit of Naringenin is that your PPARγ receptor is activated – resulting in an increase in sensitivity to insulin.

Taken together, all of this good stuff adds up to:

• No more Type 2 Diabetes
• No more high cholesterol
• No more love handles

Naringenin – remember the name and the incredible delicious organic pink grapefruit from the Rancho del Sol and the pH Miracle Living Center.

Organically Grown at the Rancho Del Sol
**Shipping included in price for orders shipped within the continental US**

100% organically grown (without synthetic pesticides, herbicides, or fertilizer), Ruby Red Grapefruits from sunny Southern California. These succulent members of the citrus family are grown in Dr. Robert and Shelley Young’s private orchard, Ranch Avorado. With its unmistakable flavor, these grapefruits offer a subtle sweetness and signature tartness that everyone can enjoy.

Nutritionally, the bitter flavor comes from limonene, a limonoid that gives grapefruit its proven anticarcinogenic properties. Naringine, a flavonoid found in grapefruit, is also effective in preventing cancer. Furthermore, narigine improves blood circulation, while pectin (a soluble vegetable fiber) unclogs arteries.

These organic grapefruits are waiting patiently – remaining on the tree until we receive your order. They are then hand-picked and packaged. Thus, the organic, natural freshness is impeccably preserved. Do your health, taste buds, and the environment a favor – Order today!

Estimated shelf life: 1 week at room temperature
1 month refrigerated
(20-25 grapefruits per box)

Nutrient Composition (100g of raw edible portion) Energy – 30 kcal
Protein – 0.55 g
Carbohydrates – 7.68 g
Vitamin A – 26 Fg RE
Vitamin B1 – 0.034 mg
Vitamin B2 – 0.02 mg
Niacin – 0.224 mg NE
Vitamin B6 – 0.042 mg
Folate – 12.2 Fg
Vitamin C – 38.1 mg
Calcium – 11 mg
Phosphorus – 9 mg
Magnesium – 8 mg
Iron – 0.12 mg
Potassium- 129 mg
Zinc – 0.07 mg
Total Fat – 0.1 g Saturated Fat – 0.014 g

To order your freshly picked grapefruit go to:

http://phmiracleliving.com/p-510-grapefruits-organic-box-of-9.aspx

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 anemia, kidney 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

Will Soy Prevent or Reverse Disease?

Will Eating and/or Drinking Soy Prevent or Reverse Dis-ease or So-called Disease?

Cancer is a group of dis-eases characterized by the uncontrolled fermentation and degeneration of body cells. Over 10 million Americans today are cancer survivors, and about 1.4 million Americans are expected to be diagnosed each year.¹

“Diet plays an important role in the prevention and treatment of ALL cancerous conditions, and soy protein is one of the leading anti-acid or alkalizing and therefore anti-carcinogenic foods being studied,” stated Dr. Robert O. Young, Director of Research at the pH Miracle Living Center.

SOY FOODS & CANCER

There has been much focus during the past 15 years on the anticancer effects of soy foods.²There are several presumed chemopreventive agents in the soy bean,⁶ but the isoflavones have received the most attention.³ A particular interest lies in the role of soy foods and isoflavones in reducing the risk of breast and prostate cancer.²

SOY & BREAST CANCER

Data modestly supports the hypothesis that soy food intake may reduce the incidence of breast cancer. A recently published analysis found the relative risk for breast cancer was 95 percent when comparing high- vs. low-soy consumers.⁵ However, many of the case-control and prospective studies included in this analysis were of poor quality.⁶

Rodent studies have generally shown that isoflavones, or soy protein, inhibit chemically induced mammary tumors when given prior to tumor initiation^7-9, although there are a number of exceptions.^10-12 Interestingly, the chemopreventive effects of isoflavones appear to be affected by the background dietary choices.

When the isoflavone genistein was added to the semi-purified diet, chemically induced rodent mammary tumors were not inhibited, but when added to the regular chow diet, tumor development was suppressed by approximately 50 percent.¹³ This suggests that animal research, which most commonly uses semi-purified diets, may actually underestimate the potential anticarcinogenic effects of soy and other foods.

Soy & Markers of Breast Cancer

In contrast to the animal and epidemiologic data, there is little clinical evidence that soy or isoflavones favorably affect markers of breast cancer risk including breast tissue density,^{14, 15}serum estrogen levels,^{16, 17} and breast cell proliferation.¹⁸ There is limited evidence that estrogen metabolism is favorably affected¹⁹ and that menstrual cycle length is increased (which decreases cancer risk).¹⁶

Nevertheless, there remains considerable enthusiasm for the possibility that soy food intake contributes to the low breast cancer rate in Japan.

Early Intake of Soy May Reduce Breast Risk

There is both epidemiologic ^20-22 and animal ^{23, 24} data in support of the hypothesis that early soy intake reduces later risk of developing breast cancer. This hypothesis is consistent with mounting evidence that early life influences — parity, lactation, age at menses, birth weight, etc. — impact risk of developing breast cancer.^25-36 Studies of migrants suggest that the first 20 years of life have an especially profound impact on risk.^36-38 The epidemiologic data suggest just one to two servings of soy foods is protective.

Breaking News – Soy Breast Cancer Study

Soy Breast Cancer Study Holds Promise, But Calls for Further Research

For more than 15 years, soy foods have been actively investigated for their possible role in reducing breast cancer risk. Initial enthusiasm about this hypothesis was based on several observations. These include the low breast cancer rates in Japan, early animal research indicating that soy beans in rodent diets reduced mammary tumor development and evidence suggesting that the isoflavones (phytoestrogens) in soy foods may exert anti-estrogenic effects.

However, establishing a relationship between cancer risk and diet – especially specific foods – is much more difficult than establishing such links in the case of other chronic diseases such as coronary heart disease. This is because there are few well-established non-invasive indicators of cancer risk, and studies are very rarely conducted for long enough to measure actual differences in tumor incidence. Consequently, it is difficult to claim with confidence whether a particular intervention increases or decreases the chances of developing cancer.

Epidemiologic research is a useful mode of investigation for exploring a relationship between diet and cancer. Epidemiology is the study of the patterns, causes, and control of disease in groups of people. There are two primary types of epidemiologic studies, case-control and prospective studies. In case-control studies, scientists compare people with cancer to those without in hopes of identifying characteristics such as lifestyle or diet that are more common to one group than the other. In prospective studies, scientists first evaluate the characteristics of a large group of healthy people, then follow those subjects for many years in hopes of identifying whether certain factors are more common to those who develop cancer than to those who don’t. Generally, prospective studies are considered more credible than case-control studies. It is important to recognize, however, that epidemiologic studies cannot establish cause and effect relationships. Only clinical trials can do that. But epidemiologic studies are often used as a basis for clinical research.

To evaluate the relationship between soy intake and breast cancer risk, Bruce Trock and colleagues from the Johns Hopkins School of Medicine and Georgetown University conducted a meta-analysis of epidemiologic studies. A meta-analysis is the statistical analysis of a large collection of results from individual studies for the purpose of integrating the findings. This particular analysis included 12 case-control studies and 6 prospective studies. The major finding of this analysis was that when all women (Asian and non-Asian, pre- and postmenopausal) were considered, soy intake was associated with a 14% reduction in breast cancer risk. That is, women consuming higher quantities of soy were 14% less likely to develop breast cancer than women who consumed relatively little soy. However, subgroup analysis revealed that soy was more protective against pre- compared to postmenopausal breast cancer, and was protective in studies involving non-Asian women but not Asian women.

The analysis by Trock and colleagues provides modest support for the notion that soy may protect against breast cancer. A 14% reduction is certainly noteworthy, but for several reasons the study results should be interpreted with caution.

First, in many studies, soy intake was not actually quantified. Rather, it was estimated based on the urinary excretion of isoflavones. Because urinary isoflavone excretion varies so much from person to person, it provides only a rough approximation of soy intake. Furthermore, although soy was found to be protective in studies involving non-Asian women, the intake of soy by the women in these studies was quite low. There is some doubt as to whether such low intakes are sufficient to exert biological effects. Since soy foods are still consumed by only a minority of people in non-Asian countries – and are often favored by especially health-conscious individuals – we must consider the possibility that the perceived cancer-protective effects of soy may result from an overall healthy lifestyle, rather than soy consumption per se. Although the researchers employed statistical techniques to try to separate the effects of soy from other factors common to people who eat soy, this is very difficult to do.

While some evidence, including the new analysis by Trock and colleagues, suggests soy foods may reduce breast cancer risk, no conclusions can be made at this time. Nevertheless, because soy foods provide excellent nutrition, they can play an important role in an overall healthy diet, regardless of their possible relationship to breast cancer protection.

SOY & PROSTATE CANCER

The soy bean isoflavone genistein inhibits the growth of both androgen-dependent^39-42 and androgen-independent^{39, 42-45} prostate cancerous cells, depending on the level of soy doses administered. In addition, genistein inhibits the invasive capacity of prostate cancerous cells ⁴²and enhances the ability of radiation to kill these cells.⁴⁶ However, the concentration of genistein required to exert these effects is higher than the serum isoflavone levels of people who eat soy foods.^47-49 Nevertheless, several observations suggest these effects are biologically relevant.^39,44-49

Regional Diets Can Impact Prostate Cancer

In Japan, although many men have prostate cancer, few die of this dis-ease. This is because the small tumors often referred to as latent prostate cancer, not uncommon to Japanese men, rarely progress to the more advanced form of this disease.^{51, 52} Isoflavones in combination with tea extracts were shown to reduce tumor growth in mice more effectively than either agent alone.⁹

In Asia, and especially in Japan, where prostate cancer mortality rates are low, both soy foods and tea are important components of their diet. There are likely several factors that contribute to this clinical situation in Japanese men and according to the International Prostate Health Council, and isoflavone intake from soy foods may be one.⁵³

There has been limited epidemiologic investigation of the relationship between soy intake and prostate cancer. These studies have produced mixed results but can be said to be consistent with the hypothesis that soy intake reduces prostate cancer risk.

A recent analysis of 10 epidemiologic studies found that soy intake was associated with a one-third reduction in prostate cancer risk.⁵ However, many of the epidemiologic studies involved a small number of cases^{54, 55} and/or did not comprehensively evaluate soy food intake. However, a recent comprehensive Japanese case-control study found that when comparing the highest with the lowest soy food intake cases, risk was reduced by nearly 50 percent.⁵⁶

Soy May Help Treat Existing Prostate Cancer

Data suggests that soy foods may be useful in the treatment of existing prostate cancer, but this remains speculative. A study of 11 trials, three involving healthy subjects^57-59 and eight involving prostate cancer patients,^60-67 examined the effects of isoflavones on PSA levels. No benefits were noted in healthy subjects, but among the cancer patients one-half noted favorable effects.⁶⁸Recent intervention data demonstrate that reducing prostate cancer risk is not dependent upon reductions in PSA levels.⁶⁹

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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).