InnerLight SuperGreens – by Dr Robert O. Young – The Original Super Greens Powder – 49 Grasses, Leaves, Vegetables, Sprouts & Herbs – Organic & Wild Crafted Ingredients – Great Tasting – No Cameron Fillers
About the product
Come listen and learn from Key Note Speakers, Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner and Galina Migalko MSc, MD, NMD, in four different countries around the World as they lecture on non-invasive medical diagnostics, the interstitium, pH, nutrition and their break-through research on prevention and non-invasive treatments for cancer, diabetes, heart disease, arthritis, osteoporosis, lupus, multiple sclerosis, infections, and many more acidic-caused diseases.
To pre-register for one or more World Conferences please email firstname.lastname@example.org and receive an additional 10 to 20 percent discount on the listed early-bird pricing. You can also register by phone by calling 760 484 1075.
When you enroll in one of our Conferences you will receive a credit for a live and dried blood cell analysis, valued at 1200 euros.
Please check out the Countries, Cities, Dates and Pricing below!
My own young and beautiful daughter Ashley, at the age of 21 followed the pH Miracle Alkaline Lifestyle and Diet with great success. She has now been in remission from brain cancer for over 15 years. She elected not to have brain surgery, radiation or chemotherapy.
Ashley was married and pregnant with her first child and in her 3rd trimester when she had a shocking seizure while at the movie theater. She was rushed to the hospital and after brain scans was found to have a large complex mass in her brain.
She was told that she needed emergency surgery and that since she was pregnant the Doctors recommended the termination of her pregnancy by C-section so they could begin treating her cancer.
With the help of her husband Matthew and Ashley’s strong faith and courage she decided no surgery and no taking the baby prematurely. She rested at home for several weeks until it was time to give birth.
She gave birth to a healthy boy (who is now 16 pictured below loving his sisters) and was told by the Doctors that she would not be able to have any more children because of her brain condition.
Ashley did not believe what she was hearing and had faith in God and the truth she had learned from her parents. She now has 4 beautiful healthy children – 1 boy and 3 girls. The newest addition came to their family just one year ago.
Her decision to follow the pH Miracle alkaline lifestyle and diet was her own decision and was supported by her loving husband and her parents.
As her Father who loves his daughter is so happy she is alive, healthy and able to attend to all her family needs. She is a wonderful example of Motherhood, a wonderful wife and has a strong abiding faith in God. I am so proud of Ashley and her bravery, courage and especially her faith to make such a bold decision at the young age of 21.
With love I share this very personal story that has a happy ending with many tears and trails knowing Ashley is healthy and alive today because she followed her heart with the knowledge that healing comes from within and is our personal responsibility.
Each person must decide for themselves (not the government) the path they will choose to go. It is all about free-agency to choose YOUR own healing path. Ashley listened to her parents, to her husband and especially to that still-small voice that speaks to our minds and through prayer and the support of family members made a wise choice. That choice is why she is alive today!
You might remember in the story of Alice in Wonderland when Alice came to a crossroads on her path and encountered the Cheshire Cat. As the story goes Alice asked the Cheshire Cat which road she should choose to go. The Cheshire Cat answered wisely, “If you do not know where you want to go any road will do.”
May God bless all of you who are at the crossroads of life with the depth of perception and the faith to choose YOUR own road wisely. Listen to that still-small voice that will speak to your mind and tell YOU the path YOU should choose. This voice will never deceive YOU or lead you astray!
Believe in Miracle even pH Miracles!
With sincere gratitude, love and healing light,
Robert O Young (Ashley’s Father)
PS I believe that the road Ashley chose was the road that gave her a cancer cure and a healthy life, including the protection and love of her family, friends and a living and loving Father in Heaven!
PSS Ashley’s husband Mathew operates the pHmlife.com that sells the pH Miracle alkaline nutritional products.
For decades now, many scientists have been raising red flags that chemotherapy can oftentimes do more harm than good, and in a surprisingly large number of cases, it simply does not work.
Dr. Hardin B. Jones, a former Professor of Medical Physics and Physiology at Berkeley, California, studied the impact of chemotherapy, radiation, and surgery on the survival rates of cancer patients, and found that instead of prolonging lives, these treatments actually make the patients die almost four times sooner. This was found more than 40 years ago, and yet not much has changed in the way the hospitals treat cancer.
For terminal patients as well, a 2016 study in the peer-reviewed journal of the American Cancer Society CANCER found that living at home instead of being treated at the hospital prolonged their lives by about 45%.
And now, a new study was just published earlier this month that analyzed 30-day mortality rates caused by the treatment itself: chemotherapy and chemotherapy plus radiation.
The study, published in The Lancet’s Oncology, looked at 23,228 breast and 9,634 lung cancer patients in England.
The results showed high death rates linked to the treatment, increased use of SACTs (systematic anticancer therapies – cytotoxic chemotherapy). The researchers stated it was due “poor clinical decision making.”
“Patients dying within 30 days after beginning treatment with SACT are unlikely to have gained the survival or palliative benefits of the treatment, and in view of the side-effects sometimes caused by SACT, are more likely to have suffered harm,” states the study.
The researchers write that while there a few patients who may have benefited from SACTs, there were too many who were harmed by it, or even killed by the treatment.
In 2014 , the year the study was researched, almost 1,400 patients in England died within 30 days of their first chemotherapy treatment. In some hospitals, the mortality rate was significantly higher than in the others: up to 51% of breast cancer patients died in Milton Keynes (although the number of total patients was small), and up to 29% of lung cancer patients died in Lancashire Teaching Hospitals.
“Simply reducing doses of or avoiding SACT altogether would reduce or eliminate instances of treatment-related early mortality.”
The study was done after noticing a clear lack of data analyzing the risk versus gain of using chemotherapy and mortality rates caused by it in the first 30 days of treatment. As the researchers state, this is the first time this topic has been brought up and investigated at a national level.
The “million dollar questions” (or perhaps “billion dollar” since this is the cancer treatment industry we’re talking about) raised by the researchers included: is chemotherapy use still advocated based on small clinical studies — most sponsored by the pharmaceutical industry?
And it has never been fully studied how well it works in a real hospital setting?
The study points out two problems. One is that mortality rate is high due to poor clinical decisions. Perhaps because in most hospitals chemotherapy is given in a one-size-fits all manner or a fixed-dose with no consideration to a patient’s health history, and characteristics such as weight and age.
In England’s database, it was found that for many patients, the doctors did not include why the chemotherapy was given, and the overall health of the patient and the severity of their cancers was never recorded.
Both of these factors, as the study points out, could significantly change the outcome for these patients.
In America, another study found that doctors gave palliative chemotherapy to terminal cancer patients, and in at least two-third of cases, the patient did not know that the treatment could not cure them, but it only alleviated some symptoms, such as pain.
Knowing that the treatment could not help them in the end, would they have searched for alternative options that may have worked better?
The second issue the study found is that mortality rates are hard to analyze because they are not well or properly recorded.
In England’s case, many dates of deaths were simply missing from the national database. Some were documented twice, and the two dates did not match.
In America, the national statistic of cancer mortality comes from the death certificates. This is what the National Center for Health Statistics (NCHS) along with the doctors use to see how many people are die from cancer, and how many people die from the treatment. Unfortunately, the National Cancer Institute reports “cancer” as the cause of death for almost all cancer patients, regardless of what actually caused it, as pointed out in a 2002 article.
This article raised concern that “cancer death rates are systematically underestimated, in that many patients who die as a result of cancer treatment do not have cancer recorded as the underlying cause of death.”
For example, they studied patients who died within one month after a cancer-surgery between 1994 and 1998, and 41% of these deaths were not properly recorded. The authors write that cancer treatment was the likely cause of death.
“…Many deaths subsequent to 1 month after cancer-directed surgery may be similarly miscoded.”
Unfortunately, even though the study points out that many death certificates quote some condition other than cancer as the cause of death (such as liver failure), they want the cause of death to be just “cancer.” That would lead to further incorrect data as many patients do die from cancer treatments, and liver failure that would not happen from cancer, is often caused by the toxic chemo drugs. But what this study does show us, is that because of a 1999 revision in the International Statistical Classification of Diseases and Related Health Problems (ICD), instead of a cancer or cancer-related death, death certificates now have to show the “underlying” cause of each death, such as: thromboembolism (blood vessel obstruction), infections, organ failures, and hemorrhage (excessive bleeding).This leads to improper classification and underestimated cancer death rates and statistics.
That is hard to say until every doctor and hospital begins classifying the causes of deaths correctly. Until then, it is important to keep studies like this in mind when considering pros and cons of starting a chemotherapy treatment.
There are more and more alternative options out there – and for many, they do work. (Just look up testimonials from the Nutritional Oncology Research Institute, or even studies on carotenoids antioxidants derived from natural sources, and even IV curcumin and sodium bicarbonate).
“I think it’s important to make patients aware that there are potentially life threatening downsides to chemotherapy. And doctors should be more careful about who they treat with chemotherapy,” writes one of the study’s co-authors, Professor David Dodwell, Institute of Oncology, St James Hospital, Leeds, UK.
This article is for informational purposes only. Consult a doctor before beginning any treatment. See our full disclaimer here.
Want to learn more about the most effective ways to prevent and reverse cancer? Read The pH Miracle revised and updated and The pH Miracle for Cancer –
5) Alkalizing Nutritional Therapy in the Prevention and Treatment of Any Cancerous Condition – https://www.amazon.com/Alkalizing-Nutritional-Prevention-Treatment-Cancerous-ebook/dp/B01JKCXJRY/ref=la_B001ILKCSU_1_14?s=books&ie=UTF8&qid=1528429047&sr=1-14&refinements=p_82%3AB001ILKCSU
6) The pH Miracle for Cancer: Discover the Truth about the Cause, Prevention, Treatments, and Reversal of ALL Types of Cancers – https://www.amazon.com/PH-Miracle-Cancer-Prevention-Treatments-ebook/dp/B01JJX1Q8S/ref=la_B001ILKCSU_1_6?s=books&ie=UTF8&qid=1528428158&sr=1-6&refinements=p_82%3AB001ILKCSU
7) Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of All Sickness and Disease – https://www.amazon.com/Potassium-Bicarbonates-Prevention-Treatment-Sickness-ebook/dp/B01JLHJ1Y8/ref=la_B001ILKCSU_1_30?s=books&ie=UTF8&qid=1528429161&sr=1-30&refinements=p_82%3AB001ILKCSU
The pH Miracle Performance Center powered by Acquaforte is a centre of excellence for professional and amateur sports players, who want a personalized training strategy to achieve the best results in terms of muscle balance, personalized improvement in their individual sport, weight loss and general health, fitness and well-being.
Under the guidance of an extraordinary and close-knit team of athletics trainers, sports doctors, massage therapists, osteopaths, chiropractors and nutritionists, the Performance Center provides the most accurate analysis of every pathological condition and then an effective course of treatment, even when time is short, such as on holiday.
The training method of the Performance Center, aimed at improving skills, is based on the search for a new kind of balance, the result of resolving any postural issues and at the same time introducing new training methods that are personalized on the basis of the analyses provided by the Forte Lab medical team.
Each type of training is designed to the needs of the guests and takes place in the state-of-the-art Fitness Room at Acquaforte Thalasso & Spa. Depending on the different cases in question, activity in the gym is combined with the thalassotherapy course, which, in a weightless environment, allows you to effortlessly perform a series of exercises that are totally effective for getting your body back in shape.
To learn more or to register for your personalized pH Miracle Retreat email us at: email@example.com or give us at call at: 760 484 1075 or 760 751 8321.
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The interstitial fluids are the fluid areas that surround every cell of the body and hold alkalinity or electrons for cellular energy and acidic wastes that are waiting to be removed by the lymphatic system through the 4 channels of elimination (perspiration, urination, defecation and respiration).
These fluid-filled spaces or compartments are what I call the acid-catchers of the blood and body cells and are at an ideal pH of 7.2 – just slightly more acidic than the blood at a base of 7.365. This organ makes up over 50% of the entire body fluids and contains all the evidence that validates my 30 year old theory that the human body is alkaline by design when healthy although acidic by function and the key to health and vitality. The key to health, energy and vitality is achieved by maintaining the alkaline design of the body fluids, especially the interstitial fluids and eliminating metabolic, dietary, environmental and respiratory acidic waste. This is why I continue to declare the same ideology of sickness, disease and health – “There is only one sickness and one disease and the cause is the over-acidification of the blood and then the tissues (interstitial fluids) due to an inverted way of living, eating, breathing and thinking. The cure for all disease and sickness is found in its prevention NOT in its treatment. Education not medication is the answer to empower people with their personal responsibility to manage their own health and well-being.
In my published paper, “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition” you learn of the importance of testing the chemistry (pH, minerals, proteins, etc) of the interstitial or interstitium to understand the true picture of health and wellness rather than just the chemistry of the blood. WHY IS TESTING THE CHEMISTRY AND PH of the INTERSTITIAL FLUIDS SO IMPORTANT? Because everything from the blood that is toxic or in excess is pushed out into the acid catchers or interstitial fluids in order to purify the blood and to maintain its delicate pH balance and chemistry at a pH of 7.365. If it were not so you would surely die from metabolic, dietary, environmental and respiratory acidosis.
It is extremely important to understand this organ system needs to be tested regularly (At least twice a year more frequently if you are dealing with a serious health challenge) for chemistry and pH to determine true homeostasis, metabolic alkalosis, metabolic acidosis and mineral levels for accurate picture of health, fitness and vitality. This cannot be done with current blood tests (CBC’s and Chemistry’s of the blood) because deficiencies in the blood do not show up until the interstitial fluids have been seriously compromised by an acidic lifestyle and diet.
In a study published in Scientific Reports, a New York University-led team of researchers finally described my discovery of the interstitium, which is a series of connected, fluid-filled spaces found under skin as well as throughout the gut, lungs, blood vessels and muscles.
The bubble wrap-like network only became visible when the pathologists used a new laser endoscope, called a confocal laser endomicroscope, that allowed them to see microscopic tissues in living people. Most studies of tissues missed the interstitium because they rely on biopsies of tissues that are then dried and fixed onto microscope slides; the desiccated samples never showed the fluid-filled spaces.
But when the endoscopic laser was used to remove the pancreas and bile duct in a dozen patients with cancer, the odd spaces became obvious.
In the study, the authors speculate that the spaces could be important for a number of functions, including generating the collage that supports cells in certain tissues, as well as housing the stem cells that rush in to repair damaged tissues. They may also play a role in conducting electrical signals as cells move and stretch. Because the spaces form a fluid-highway linking tissues and organs, it may also explain why some cancers, if they invade the spaces, spread more quickly than others.
The bottom-line is the compartments of the interstitial fluids are where everything is taking place when determining true homeostasis and pH balance.
The idea that you cannot control the chemistry or the pH of the blood or body fluids as suggested by current medical savants is a false theory/hypothesis. The break-through research of Prof Robert O Young will continue to prove that managing and maintaining the pH or chemistry’s of the interstitial fluids is an accurate and efficient way to prevent any and ALL sickness and disease.
To learn more about the chemistry’s of blood compared to the chemistry’s of the interstitial fluids read, “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition”.
Read “The pH Miracle for Cancer”. To order go to: https://www.amazon.com/…/dp/B01JKCX…/ref=la_B001ILKCSU_1_19…
Read the “Metabolic and Dietary Acids Are the Fuel That Lights the Fuse That Ignites Inflammation That Leads to Cancer!” https://www.amazon.com/…/dp/B01JKGP…/ref=la_B001ILKCSU_1_52…
Read “The pH Miracle revised and updated” – https://store.phoreveryoung.com/…/the-ph-miracle-original-2…
Read “The pH Miracle for Cancer” https://store.phoreveryoung.com/…/the-ph-miracle-for-cancer…
For inquires for non-invasive, non-radioactive interstitial chemistry and pH email: firstname.lastname@example.org
For health and wellness coaching email: email@example.com
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]
|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?
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
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.
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
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
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,
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.
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)
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., â€œEpinephrine 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.
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
17. Cancer Res. 2009 Mar 15;69(6):2260-8. Epub 2009 Mar 10.
18. JAMA 2004;291:2328-2334,2376-2377.www.urotoday.com/56/browse_categories/renal_transplantation_vascular_disease/
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.
Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa and Universal Medical Imaging Group
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.
More than 150 years ago, British physician T. W. Jones asked the question, “Why does the blood circulating in the vessels not coagulate?” 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. The name given to this discovery is still in use today, as “Trousseau’s Syndrome.” 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. 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), Hageman factor (factor XII).
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).
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 and Gunther Enderlein’s research into the sub cellular living elements and combining this with what is known of colloidal flocculation, it is suggested that the clotting of blood begins with the end-linking (polymerizing) of the fundamental protein unit called by Bechamp the microzyma. 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. 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.
With this background, we are in a position to consider a standard medical term: disseminated intravascular coagultion (DIC). 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.
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. 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. 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)
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. 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. 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. The culminate forms produce the lions share of acids, which are mycotoxins and the primary focus of my research. 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.
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. 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. In an attempt to buffer or neutralize MAT, the body will also bind or chelate both fats and minerals to them.
Another member of the MAT family is uric acid, which is formed by the digestion of protein and the creation of EMPO. Uric acid can also break down into secondary substance, on of which is alloxan. 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. 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.  It is the positively surface-charged bacteria, yeast/fungus, mold, exotoxins, endotoxins, and mycotoxins that MOBS bind too. 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.  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. In fact, humans and animals developed in terms of microorganisms. 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..
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.
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. 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.) 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. 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. 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. 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.
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.) 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.
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. 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). 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.
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. (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.” 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. 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. (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.
It was discovered in 1964 that blood will clot simply from contacting a negatively charged surface. 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. 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.
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. 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. 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.
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. 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. (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). 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.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.)
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.
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. 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. (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.
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).
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. Research has revealed that this compound, named leukotoxin, is highly disturbing to other cells. It causes platelet lysis, thereby releasing TF and initiating DIC. (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. 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. 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. 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.
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.
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). (See Table 4.)
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.
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. 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.
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. 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.
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, 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]
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.
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. 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.
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. 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.
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.
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The science of alkalinity and the importance of an alkaline body fluid pH for health, energy and vitality.