The Most Important Article I Have Ever Written!

What Causes Cancer, Heart Attacks, Strokes, Diabetes, MS, Lupus, Dementia, Sepsis, Multiple Sclerosis and the list goes on and on and on?

A rise in the alkalinity of the blood plasma above pH 7.365 (alkaline phosphate)–any rise–is a result or a compensatory reaction due to over-acidity in the interstitial fluids of the Interstitium (I call this dis-ease latent tissue acidosis) as the blood attempts to maintain its delicate pH at 7.365.

There is no exception for the rule of alkalinity.

The body will ALWAYS overcompensate for the excess acidity in the Interstitium fluids (the largest organ of the human body) by over-alkalizing the blood to maintain homeostasis.

I call this the “teeter-totter” effect.

Along comes the traditional medical attendant and perceives that there is too much alkalinity, when really there is not.

This is an important concept to grasp, so let’s oversimplify a bit. The Interstitium fluids have become acidic.

The blood “knows” that!

So, it pours out extra alkalinity or alkaline phosphate into the blood and the blood pH spikes up to a higher than normal pH.

It’s like when we get the bejeebers scared out of us by something innocent, we over-react.

When suddenly alarmed, a person might scream, holler, faint, get mad, strike out, drop the vase, kick the dog, or even have a heart attack. The blood does the same thing. A knee-jerk reaction…well, actually, a blood-jerk reaction.

Alternatively, how many times have you heard of a car going off the shoulder of the road and the driver over-reacts, jerks the wheel back, and flies into the other lane of oncoming traffic. It happens all the time. Incidentally, if that does happen to you, you’re better off not to interfere. Stay on the shoulder. Let the wheel stay there for a moment. Slow the car down. But don’t overreact.

Mainstream medicine, not understanding the cause of the excessive alkalinity pouring into the blood, may try and stop the rushing over-alkalization. But that’s the wrong move.

We’re better off not to interfere.

Once more. When your little boy falls down, sees mama going out the door, or is scared of the boogey man, what happens? He not only cries, but how often do we see a child go into a big, fat over-reaction?

Sometimes, they really get worked up. It’s a natural over-reaction to a typical situation.

Now it’s Dad’s turn to over-react. Along comes Dad and says to keep quiet, don’t be such a little sissy, put a lid on it, grow up, stop that crying, OR ELSE…

Since I have digressed to make a point, I may as well digress all the way. Wrong move, Dad. If you do that often enough, the message you send to your child is don’t have feelings, don’t express your feelings, you are not acceptable, don’t act like a child even though you are a child, and don’t be who you are. So don’t over-react Dad. Better to let the child get it out, stay in the room, validate their feelings, and use a little Active Listening (www.gordontraining.com).

Strong feelings can come and go…or come and stay. If you’re really klutzy, you could be orchestrating chronic emotional issues for a lifetime.

Gee, thanks Dad.

Now, back to the blood and Interstitium fluids.

Interstitial fluids of the Interstiitum are acidic. Here comes a flood of alkalinity–even so much that the pH rises in the blood plasma and concerns the western medical establishment.

But whatever it was that caused the pH to over-react must be understood. Acidic Interstitium fluids mean problems ahead, correct? (We are the only research group in the World measuring the pH of the Interstitium)

Not only do we need alkalinity but lots of it!

The acidic Interstium fluids will soon even out the rise in

blood pH, and we will need additional alkalinity to wipe out the acidic Interstium fluid problem.

Cancer, heart disease, stroke, diabetes, MS, sepsis, etc. are not diseases of alkalinity but are diseases of acidity!

The body uses the calcium of the bones as well as other buffers (bicarbonate, hemoglobin, sodium, magnesium from the muscles, etc.) to chelate or buffer acidity! That is why there are always microcalcifications found in the liver, pancreas, breast, bowels, bladder, bones, prostate, muscles, joints, blood vessels and brain before the liver, pancreas, breast, bowels, bladder, bones, prostate, muscles, joints, blood vessels and brain cancer tumor shows up.

Why prior to the tumor?

Because the body will always try and protect and preserve the blood and Interstitium by buffering acids with the alkalinity of calcium. The bones are always affected in any cancer, heart condition, stroke, diabetes, lupus, arthritis, MS, sepsis, etc. because the bones are an excellent source of calcium for buffering dietary and

metabolic acids.

So is Cancer, Heart Attack, Stroke or Diabetes, MS, dementia, ALS, sepsis, HIV, etc., the disease?

No!

Then is the loss of bone mass the disease or the calcium deposits in the liver, pancreas, breast, brain, etc. the disease?

NO! NO!

Is the increase in the alkaline phosphates the disease?

NO! NO! NO!

These are all symptoms, not diseases!

Then the disease must be the over-acidity?

Well yes, and no.

Then what is the disease?

The “yes” part I call acidosis or hyperacidity. That is an acceptable term for the condition.

But it is really much more.

The “no” part is that it’s more than acidity. It’s a psychological disorder. It’s a sociological malaise. It’s a cultural-anthropological phenomenon. And once people understand the truth and the scientific foundation of “New Biology”TM, and once people understand the science of what I have been writing about for three, the better part of 4 decades, it may then become to be understood as a “moral disease” as well.

And why is that, you ask?

Is committing suicide a moral issue?

Well, yes.

Is drinking yourself to death a moral issue?

Well, yes.

Is allowing your children to become obese flying in the face of natural law?

Well, yes, assuming you are aware of what’s happening and have other options.

If you say “yes” to these last few questions, then we are looking at a very, complex psychological, sociological, cultural, biological and moral phenomenon.

Once you know and believe that over-acidity causes every disease and ALL dis-ease, then to ignore that fact is a form of suicide!

Just like Samson who killed a 1000 Philistines with the jawbone of an ass, every day people use same instrument with their daily lifestyle and dietary choices – the jawbone.

When you eat poorly, you pull the trigger every day of your life, and eventually, the gun fires. The bullet might hit you square in the head like a massive heart attack or stroke, or it may kill you more slowly like a cancer, or it may simply put you in a fog for the next 15 years like Alzheimer’s or dementia.

This “disease-phenomenon” is an inverted way of living, eating, drinking, breathing, thinking and believing!!!

Yes, this is the cause of ALL disease–ALL that disturbs the central balance of organized matter that leads to excess acidity in the blood and then the Interstium fluids that then leads to genetic mutations and the death of the cell, the tissues, the organs and the glands. In other words the death of the whole body, physically, emotionally and spiritually.

It is ALL that leads to increases in alkaline phosphates.

It is ALL microcalcifications in the liver, pancreas, breast, brain, prostate, and so on, and so on.

ALL liver, pancreas, breast, bladder, bowel, prostate, brain, etc., tumors. ALL liver, pancreas, breast, bladder, bowel, prostate, brain, etc. cancer and ALL potential bone cancer!!!!

First, we must understand that ALL of the above sicknesses and diseases are NOT sicknesses or diseases but a symptom of acidosis and catarrh that has built up in the blood and intestitial fluids that has significantly effected the white blood cells’ ability (the janitorial and garbage collectors for the blood and tissues) to remove metabolic, dietary acids and degenerative matter.

When we are dealing with any symptom or any biological effect, we need to look to the cause. To understand the cause is not difficult nor is the understanding of the treatment.

The “New Biology”TM explains the cause and effect of all sickness and disease in addition to explaining how to improve the quality and quantity of life.

For example, enervation (the deprivation of force or strength) and muscle weakness per se is not a disease.

Weakness, or lost power, is not a disease; but, by causing a flagging of the elimination of tissue-waste which is toxic, the blood becomes charged with acids.

I call this Acidosis–poison in the blood and then the Interstitium fluids. This is disease and when the acidic toxins accumulate beyond the toleration point, a crisis takes place. This means that the poison or acid (the so-called virus) is being eliminated–often through the skin, the third kidney.

We can call this disease, but it is not!

The only disease is systemic Acidosis which localizes in the weakest parts of our body.

And what we call disease, are symptoms produced by the forced vicarious elimination of acids from the interstitial fluids of the Interstitium through the mucous membrane.

When the elimination takes place through the mucous membrane of the nose, it is called a cold–catarrh of the nose. And where these crises are repeated for years, the mucous membrane thickens and ulcerates, and the bones enlarge, closing the passages.

At this stage, hay fever or asthma develops.

When the throat and tonsils, or any of the respiratory passages, become the seat of the crises of acidity, we have croup, tonsillitis, pharyngitis, laryngitis, bronchitis, asthma, pneumonia, etc.

When the acids locate in the cranial cavity we have dementia, Parkinson’s, Alzheimer’s, muddle thinking, forgetfulness, and even depression.

When the acids locate in the gastrointestinal tract we have IBS, gastrointestinal dysmotility, autonomic dysfunction, carotid stenosis and ischemic colitis.

When the acids are expressed through the skin we have psoriasis.

When the acids locate in the liver, pancreas, breast, bowels, bladder, prostate, uterus or brain tissue we have microcalcifications of these acids that then leads to tumors and liver, pancreas, breast, bowels, bladder, prostate, uterus or brain cancer.

What is in the name?

All are symptoms of the expulsion of acids from the blood, to the Interstitum fluids at the different points named.

They are of the same character essentially and evolve from the one cause, namely, systemic acidosis, as a crisis of toxemia.

The description can be extended to every organ of the body, including the largest organ, the skin, causing melanoma cancer.

For any organ that is enervated below the average standard from stress of habit, from work, or worry, from injury, or any other cause, that organ may become the location of the crises of systemic acidosis.

The symptoms presented differ with each organ affected. That fact gives color to the erroneous belief that every symptom-complex is a separate and distinct disease.

But, thanks to the new light and knowledge of being shed by the “New Biology”TM upon nomenclature involved in the naming of a disease, every symptom-complex goes back to the one and only cause of all diseases, namely, systemic acidosis of the Interstitium fluids and then the blood plasma and finally the intracellular fluids causing genetic mutation to the death of the cell.

To find the cause of all symptomologies including cancer, heart attack, stroke, diabetes, sepsis, muscular dystrophy, AIDS, sepsis, etc., start with colds and catarrh, and watch the pathology as it travels through “The Seven Stages of Acidity(TM), beginning with:

1) enervation,

2) sensitivity and irritation (IBS),

3) catarrh, (the common cold)

4) inflammation, (arthritis)

5) induration (lupus, lymes, fibromyalgia),

6) ulceration and then to (colitis)

7) degeneration – cancer, heart attack, stroke, diabetes, multiple sclerosis, polio, multiple dystrophy, ALS, etc.

How well could you try to find the cause of man by ignoring his conception, embryonic life, childhood, manhood, etc.

Nature’s order is interfered with by enervation habits until systemic acidosis of the Interstitium fluids and then the blood is established.

Then a vaccination (seen in Gulf War Syndrome and Spanish Flu Epidemic) or an infection (really an outfection) from any source will act as a firebrand. Sooner or later cause the most vulnerable organ (the bowels) will undergo organic change. The organ, however, has nothing to do with cause, and directing treatment toward the organ compounds the problem and is nonsense!

Examples of this wrong thinking yield blood transfusions for pernicious anemia, gland treatment for gland impotency, the cutting out of stones, ulcers and tumors.

There is no question that one of the most pernicious practices in vogue today is treating so-called disease with disease and immunizing with the products of disease.

Current medical science calls this form of pathological thinking a “vaccination.” This my friends is the real psuedo-science!

When the cause is not known, how is prevention or cure possible except by luck?

Producing a mild form of smallpox using vaccine is the same as introducing a poison or acidity into a healthy person.

It makes no sense!

Certainly only pathological thinking can arrive at such conclusions. Vaccine or autogenous remedies (metabolic acids) are made from the products of disease.

This also includes ALL antibiotics which are products of disease!

The idea that disease can be made to cure itself is an end-product of pathological thinking!

If prevention and cure mean producing disease, surely prevention and cure are not desirable. If prevention can be accomplished, then cures will not be needed!

It is not disease, it is cause “in all its aspects” that we need to know before we can take steps to prevent or cure “disease.”

Cause is constant, ever present, and always the same. Only effects, and the object on which a cause acts, change.

And the change is most inconstant.

To illustrate: a catarrh of the stomach presents first irritation, then inflammation, then ulceration, and finally indulation and cancer.

Not all cases run true to form. Only a small percentage evolve to ulcer and fewer reach the cancer stage. More acidic toxins exit via acute food poisoning or acute indigestion then by chronic diseases.

Most Americans are challenged with the symptomology of indigestion, which can include acid reflux, diarrhea and/or constipation.

The proper way to study disease is to study health and every influence favorable or not favorable to its continuance.

Our western system of medicine has been preoccupied with the study of disease, not health.

Disease is Perverted health!

Any influence that lowers energy becomes disease producing. Disease cannot be its own cause, neither can it be its own cure and certainly not is own prevention!

My personal discovery of the truth of ALL sickness and disease – that acidosis is the cause of all so-called diseases–came about slowly, step by step, line upon line, precept upon precept, here a little and there a little.

At first, I postulated that yeast and molds must be the general cause of disease. Then I decided that it was not yeast and molds but that the body becoming enervated. But wait a minute, enervation is not a disease; disease must be due to dietary, metabolic, respiratory and/or environmental acids.

I reasoned that localized or systemic acidosis is the true general cause of all disease and must be autogenerated. And if disease is due to autogenerated acids, what is the cause of that autogeneration?

The answer is found in understanding the nature of matter and how it organizes and disorganizes. I realized that there must be a physical or emotional disturbance to organized matter before it can begin its disorganization.

And when matter begins to disorganize, it gives rise to autogenerated acids. This is true for all matter!

To illustrate, take a physical injury to a joint which is often complicated with the prior symptom of rheumatism. The rheumatism previous to the injury was potentially in the blood and/or tissues. Just what change had taken place in the matter which, under stress of injury or shock of any kind, would cause a reaction with fever?

I could not understand until the “Acidosis Theory” suggested itself to my mind. After that, the cause of disease unfolded before me in an easy and natural manner.

I called this new paradigm for ALL sickness and disease “The Cycle of Imbalance.” You can read about “The Cycle of Imbalance” in my book, “Sick and Tired, Reclaim You Inner Terrain.” You can order this book at:

http://www.phmiracleproducts.com.

In a few words, without systemic acidosis, there can be no sickness or disease and there can be NO CANCER! NO HEART ATTACK! NO STROKE! NO DIABETES! NO DEMENTIA! NO SEPSIS, NO ALS, NO ALZHEIMERS, in other words, NO DIS-EASE!

It is also true that without systemic acidosis there can be NO PAIN!

Therefore, pain equals acid and acid equals pain.

I knew that the waste products of cellular disorganization and metabolism were toxic and that the only reason why we were not poisoned by it was because it was removed from the organism as fast as it was produced.

Then I discovered that the acid was retained in the blood and then interstitial fluids of the Insterstitium when there was a checking of elimination.

Then, the cause of the checking had to be determined. In time, I thought out the cause of all sickness and disease. I knew that when we had normal energy, organic functioning was normal.

Then came the discovery that enervation caused a checking of elimination.

Eureka!

The cause of ALL sickness and disease is NOW found!

Enervation checks elimination of the dietary, metabolic, respiratory and environmental acidic waste products!

of cellular transformation or disorganization.

Retention of metabolic, respiratory, environmental and dietary ACIDS is the first and the only cause of ALL sickness and disease!

One of the first things to do to get rid of any so-called disease is to get rid of all the acid, for it is this state of the blood and then Interstitium fluid that makes disease possible.

Infection, drugs and food poisoning may kill, but if they do not, they will be short-lived in a subject that is free from enervation and acids that are being held in the compartments of the Interstitium fluids.

Conversely, the poisoning will linger in the system until the acid is overcome. Then and only then will elimination remove all traces of outfection – ACID.

Syphilitic outfection (herpes, warts, moles of any color) is pronouncedly an acidic subject thrown into great virulency by poor nutrition, lifestyle and conventional treatment.

The same is true with HIV/AIDS. The so-called infection which in reality is an outfection of acid, is the least offender of the trio. Add fear (false evidence appearing real) wrong eating, poor sanitation and wrong lifestyle choices and we have a formidable symptom complex that serves to justify all that professional syphilomaniacs HIV/AID somaniacs say and write about these dis-eases.

Remove systemic acidosis of the Interstitium fluids, drugging, FEAR, poor sanitation, wrong lifestyle choices, and vile eating, and there is little left. What is left can be easily thrown out of the body by Nature!

Scientific research is being carried on vigorously in an attempt to find the cause of disease. The conception of disease is that the cause is individual. Here is where investigators meet their Waterloo. All of the so-called diseases are increasing symptom complexes due to repeated crises of systemic acidosis of the Interstitium and then the blood plasma.

Diseases have no independent existence!

As soon as acidity is controlled, the symptoms disappear unless an organ has been forced by innumerable crises to degenerate.

Even organic change, when the organ is not destroyed, will come back by correcting the life and getting rid of the true cause–the crisis of acidosis!

All symptoms of all so-called diseases have one origin.

All diseases are ONE!

Unity in all things is Nature’s plan.

Polytheism is gone, and everything pertaining to it and coming out of it must go.

So you NOW have the truth! No more LIES!

There is only one sickness, one disease, and NOW only one treatment.

The one sickness and disease is the over-acidification of the Interstitium and then the blood and then finally the tissues, organs and glands due to an inverted way of living, eating, drinking, breathing, thinking and believing.

The one treatment is to alkalize and energize with Dr. Robert Young’s pH Miracle Lifestyle and Diet Plan.

We all need to go back to the Garden of Eden and start living and eating GREEN. (Genesis Chapter 1 verses 28 – 30)

I call this eating like “COWS” which stands for the following:

C = Chlorophyll from green plants

O = Oxygen – nascent oxygen or singlet oxygen

W = Water – alkaline water at a 9.5 pH

S = Salt – liquid mineral ionized salts

You can learn more about this program on our website or in my books, The pH Miracle, The pH Miracle for Diabetes, The pH Miracle for Weight Loss, The pH Miracle revised and updated, The pH Miracle for Cancer, Back to the House of Health I and II and Sick and Tired, which you can also purchase through Amazon.com or http://www.phmiracleproducts.com

The complete program is a 12 to 16 week program that includes the alkaline foods outlined in Chapter 11 of the pH Miracle revised and updated book.

You start off the program with a 14 to 21 day liquid feast.

You can eat as much and as often as you like as long as the food is green and pureed and/or juiced.

The soups such as the Broccoli Soup, Aspar/Zinc Soup, The Healing Soup and the Popeye Soup with lots of avocados are excellent to eat during the liquid feast.

You also need to begin taking the nutritional supplements while drinking at least 4 to 6 liters of Greens a day.

Start out gradually drinking 1 liter of Greens per day and then work up to 2, then 3, then 4, until you are drinking 6 liters a day.

When you take the nutritional supplements, take 5 drops 6 times a day of the liquid colloids under the tongue, (except the pH drops which are taken in purified water and NEVER taken under the tongue) away from meals, or taking 1 capsule 3 to 6 times a day of the encapsulated products with meals.

I would suggest taking 4 capsules every 4 waking hours of the bowel cleansing formula.

The bowel cleansing product helps to keep acids moving through normal elimination.

After you complete the 14 to 21 day liquid feast, you can then begin introducing some solid food but it still needs to be as green as possible. Remember, when you are green you are clean. I would suggest not only the vegetable soups, but steam fry vegetables and lots of salads.

Make sure you use only lemon or lime and good oils on your salads for the dressing.

NO VINEGAR, NO ENZYMES, NO FERMENTED FOODS and NO PROBIOTICS!

NO ACID FOODS or DRINKS!

Another tip is to include liberal amounts of flax, hemp, avocado and olive oil in or with your soups and salads. I suggest a minimum of 5 to 6 tablespoons of good oils every day. And you should be supplementing pomegranate seed oil everyday.

For information on pomegranate and avocado seed oil go to:

http://www.phmiracleproducts.com

In conclusion, the medical world has been looking for a remedy to cure ALL disease, notwithstanding the obvious fact that nature needs NO REMEDY and NO CURE. She needs only an opportunity to exercise her own prerogative of self-healing.

Cures! There are NO CURES! And there will be NO CURES Found!

The subconscious builds health or disease according to OUR ORDER! And we do it with our thoughts, our words and our deeds.

If we send impulses of irritation, discontent, unhappiness, complaining, hate, envy, selfishness, greed, lust, and the biggest one of all pride, the subconscious builds us in the image of OUR ORDER!

The truth is that WE NEED NO DOCTOR and WE NEED NO NATIONAL HEALTH INSURANCE PLAN!

The movie “Sicko” suggests we need a health program for every man, woman and child in the US. This health program must start with the education on how to prevent disease with what we eat, drink, breathe, think and believe.

https://youtu.be/xaB5K-PvnSY

To insure more people in the US under the current health system does not bring more health. We do not need more medicine! We need more education on how to maintain the alkaline design of our body!

We need to empower ourselves to effect a reconciliation between our subconscious creator and ourselves.

What we need is to learn self-control, respect, poise, relaxation, deep breathing, alkaline eating and drinking, and especially alkaline exercising!

And when these impulses are sent over the sympathetic nerves to our subconscious creator, we will begin to receive images of a more ideal man or woman, until an approach to “Perfection is Attained”.

Sickness and disease, including the symptoms of cancer, heart attacks, strokes, diabetes, sepsis, tumors, HIV/AIDS, MS, lupus, depression, hyperthyroidism, Wilson’s Syndrome, fibromyalgia, pain in every joint and muscle, chronic fatigue syndrome, muscle cramps, allergies (food), asthma, bronchitis, frequent colds, candida, hypoglycemia, allergic reaction to any chemical, chronic fatiguing, food cravings, indigestion, inflamed joints, insomnia, mood swings, gas, bloating, diverticulitis, irritable bowel, pneumonia, ulcers, stomach and bowel cramps and even memory loss is the culmination of years of abuse of nutrition and years of acids from faulty elimination by forcing the bowels to move.

We don’t GET sick and tired we DO sick and tired!

The most powerful way to eliminate metabolic and dietary acids in the blood, the Interstitium fluids and finally the intracellular fluids is following the pH Miracle Lifestyle and Dietary Plan.

You are the builder of tomorrow, and you need not pay a fortuneteller, doctor, lawyer, preacher, or banker to tell you what will happen to you tomorrow.

Nothing will happen.

The inevitable will come.

You will inherit the fruits of today’s sowing.

I hope you find these thoughts and suggestions helpful when dealing with ANY symptomology, whether physical, emotional or spiritual.

Your life, Your Health, Your Fitness, Your Energy is the consequence of your daily choices and you are free to choose!

I pray that you choose wisely! The quality and the quantity of your life depends upon it.

In love and Gods healing light,

Robert O. Young DSc, Phd, Naturopathic Practitioner, Preventologist

PS My hope is that you will share this articles with everyone that you know, love and care about.

In the last days Paul prophesied, “Men ever learning, and never able to come to the knowledge of the truth” 2 Timonthy 3:7

Paul’s prophesy has been fulfilled in our day!

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For other scientific articles of Dr. Robert O Young go to: http://www.drrobertyoung.com

For non-invasive blood and interstitial fluid of the Interstitium testing for the chemistry and functionality of all organs and organ systems call: 818-987-6886 or go to: http://www.universalmedicalimaging.com or email: universalmedicalimaging@yahoo.com

Lectures From Around The World

Galina MIgalko MSc, MD, NMD and Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner 

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 phmiraclelife@gmail.com 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!

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 

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

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

Abstract

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

Introduction and Historical Perspective

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

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

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

The Mechanics of Blood Coagulation

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

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

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

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

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

Key Ingredients of Pathological Blood Coagulation

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

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

Mycotoxins and Metabolism by Fermentation

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

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

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

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

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

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

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

Endotoxins

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

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

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

Exotoxins

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

Tissue Factor

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

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

Development of Disseminated
Intravascular Coagulation (DIC)

DIC Induced by MAT and Tissue Factor

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

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

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

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

DIC Induced by Electrostatic Attraction

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

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

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

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

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

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

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

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

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

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

Endothelial Cells as Antithrombotics or Procoagulants

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

 

 

 

 

 

 

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

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

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

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

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

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

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

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

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

Detection of Disseminated Intravascular Coagulation

The Sonodot Analyzer

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

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

Fibrin Degradation
Products and Fibrin Monomer

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

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

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

Other tests include:

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

The Mycotoxic Oxidative Stress Test (MOST)

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

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

 

 

 

 

 

 

 

 

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

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

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

 

 

 

 

 

 

 

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

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

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

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

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

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

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

 

 

 

 

 

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

 

 

 

 

 

 

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

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

The MOST from Solubilized Extracellular Matrix

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

Extracellular Matrix Degradation by MAT

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

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

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

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

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

Conclusion

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

­

­

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

[23]  Ibid.

[24]  Ibid.

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

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

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

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

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

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

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

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

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

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

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

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

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

[43]  Rapaport, op. cit. (Ref. 4).

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

[45]  Rapaport, op. cit. (Ref. 4).

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

[47]  Ibid.

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

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

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

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

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

[53]  Ibid.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Tables

Table 1

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

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

Table 2

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

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

Table 3

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

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

Table 4

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

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

 Table 5

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

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

Table 6

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

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

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table 9

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

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table 12

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

Table 13

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

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

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

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

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

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

• 13 percent were found to be beneficial

• 23 percent were likely to be beneficial

• Eight percent were as likely to be harmful as beneficial

• Six percent were unlikely to be beneficial

• Four percent were likely to be harmful or ineffective.

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

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

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

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

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

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

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

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

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

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

What Causes the Elevation of Cholesterol Levels In the Blood?

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

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

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

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