Tag Archives: before and after

Harvard Trained Immunologist Demolishes California Legislation That Terminates Vaccine Exemptions


The following open letter by a PhD Immunologist completely demolishes the current California legislative initiative to remove all vaccine exemptions. That such a draconian and cynical state statute is under consideration in the ‘Golden State’ is as shocking as it is predictable.  After all, it was mysteriously written and submitted shortly after the manufactured-in-Disneyland measles ‘outbreak’.

The indisputable science that is employed by Tetyana Obukhanych, PhD ought to be read by every CA legislator who is entertaining an affirmative vote for SB277.  Dr. Obukhanych skillfully deconstructs the many false and fabricated arguments that are advanced by Big Pharma and the U.S Federal Government as they attempt to implement a nationwide Super-Vaccination agenda.

When the California Senate refuses to consider authoritative scientific evidence which categorically proves the dangerous vaccine side effects on the schoolchildren, something is very wrong. Such conduct by the Senate constitutes criminal action that endangers the lives and welfare of children. Their official behavior must be acknowledged for what it is — CRIMINAL — and prosecuted to the fullest extent of the law.

An Open Letter to Legislators Currently Considering Vaccine Legislation from Tetyana Obukhanych, PhD in Immunology


Dear Legislator:

My name is Tetyana Obukhanych. I hold a PhD in Immunology.  I am writing this letter in the hope that it will correct several common misperceptions about vaccines in order to help you formulate a fair and balanced understanding that is supported by accepted vaccine theory and new scientific findings.

Do unvaccinated children pose a higher threat to the public than the vaccinated?

It is often stated that those who choose not to vaccinate their children for reasons of conscience endanger the rest of the public, and this is the rationale behind most of the legislation to end vaccine exemptions currently being considered by federal and state legislators country-wide. You should be aware that the nature of protection afforded by many modern vaccines – and that includes most of the vaccines recommended by the CDC for children – is not consistent with such a statement. I have outlined below the recommended vaccines that cannot prevent transmission of disease either because they are not designed to prevent the transmission of infection (rather, they are intended to prevent disease symptoms), or because they are for non-communicable diseases. People who have not received the vaccines mentioned below pose no higher threat to the general public than those who have, implying that discrimination against non-immunized children in a public school setting may not be warranted.

  1. IPV (inactivated poliovirus vaccine) cannot prevent transmission of poliovirus (see appendix for the scientific study, Item #1). Wild poliovirus has been non-existent in the USA for at least two decades. Even if wild poliovirus were to be re-imported by travel, vaccinating for polio with IPV cannot affect the safety of public spaces.  Please note that wild poliovirus eradication is attributed to the use of a different vaccine, OPV or oral poliovirus vaccine. Despite being capable of preventing wild poliovirus transmission, use of OPV was phased out long ago in the USA and replaced with IPV due to safety concerns.
  1. Tetanus is not a contagious disease, but rather acquired from deep-puncture wounds contaminated with C. tetani spores. Vaccinating for tetanus (via the DTaP combination vaccine) cannot alter the safety of public spaces; it is intended to render personal protection only.
  1. While intended to prevent the disease-causing effects of the diphtheria toxin, the diphtheria toxoid vaccine (also contained in the DTaP vaccine) is not designed to prevent colonization and transmission of C. diphtheriae. Vaccinating for diphtheria cannot alter the safety of public spaces; it is likewise intended for personal protection only.
  1. The acellular pertussis (aP) vaccine (the final element of the DTaP combined vaccine), now in use in the USA, replaced the whole cell pertussis vaccine in the late 1990s, which was followed by an unprecedented resurgence of whooping cough. An experiment with deliberate pertussis infection in primates revealed that the aP vaccine is not capable of preventing colonization and transmission of B. pertussis (see appendix for the scientific study, Item #2). The FDA has issued a warning regarding this crucial finding.[1]
  • Furthermore, the 2013 meeting of the Board of Scientific Counselors at the CDC revealed additional alarming data that pertussis variants (PRN-negative strains) currently circulating in the USA acquired a selective advantage to infect those who are up-to-date for their DTaP boosters (see appendix for the CDC document, Item #3), meaning that people who are up-to-date are more likely to be infected, and thus contagious, than people who are not vaccinated.
  1. Among numerous types of H. influenzae, the Hib vaccine covers only type b. Despite its sole intention to reduce symptomatic and asymptomatic (disease-less) Hib carriage, the introduction of the Hib vaccine has inadvertently shifted strain dominance towards other types of H. influenzae (types a through f).These types have been causing invasive disease of high severity and increasing incidence in adults in the era of Hib vaccination of children (see appendix for the scientific study, Item #4).  The general population is more vulnerable to the invasive disease now than it was prior to the start of the Hib vaccination campaign.  Discriminating against children who are not vaccinated for Hib does not make any scientific sense in the era of non-type b H. influenzae disease.
  1. Hepatitis B is a blood-borne virus. It does not spread in a community setting, especially among children who are unlikely to engage in high-risk behaviors, such as needle sharing or sex. Vaccinating children for hepatitis B cannot significantly alter the safety of public spaces. Further, school admission is not prohibited for children who are chronic hepatitis B carriers. To prohibit school admission for those who are simply unvaccinated – and do not even carry hepatitis B – would constitute unreasonable and illogical discrimination.

In summary, a person who is not vaccinated with IPV, DTaP, HepB, and Hib vaccines due to reasons of conscience poses no extra danger to the public than a person who is.  No discrimination is warranted.

How often do serious vaccine adverse events happen?

It is often stated that vaccination rarely leads to serious adverse events. Unfortunately, this statement is not supported by science. A recent study done in Ontario, Canada, established that vaccination actually leads to an emergency room visit for 1 in 168 children following their 12-month vaccination appointment and for 1 in 730 children following their 18-month vaccination appointment (see appendix for a scientific study, Item #5).

When the risk of an adverse event requiring an ER visit after well-baby vaccinations is demonstrably so high, vaccination must remain a choice for parents, who may understandably be unwilling to assume this immediate risk in order to protect their children from diseases that are generally considered mild or that their children may never be exposed to.

Can discrimination against families who oppose vaccines for reasons of conscience prevent future disease outbreaks of communicable viral diseases, such as measles?

Measles research scientists have for a long time been aware of the “measles paradox.” I quote from the article by Poland & Jacobson (1994) “Failure to Reach the Goal of Measles Elimination: Apparent Paradox of Measles Infections in Immunized Persons.” Arch Intern Med 154:1815-1820:

“The apparent paradox is that as measles immunization rates rise to high levels in a population, measles becomes a disease of immunized persons.”[2]

Further research determined that behind the “measles paradox” is a fraction of the population called LOW VACCINE RESPONDERS. Low-responders are those who respond poorly to the first dose of the measles vaccine. These individuals then mount a weak immune response to subsequent RE-vaccination and quickly return to the pool of “susceptibles’’ within 2-5 years, despite being fully vaccinated.[3]

Re-vaccination cannot correct low-responsiveness: it appears to be an immuno-genetic trait.[4]  The proportion of low-responders among children was estimated to be 4.7% in the USA.[5]

Studies of measles outbreaks in Quebec, Canada, and China attest that outbreaks of measles still happen, even when vaccination compliance is in the highest bracket (95-97% or even 99%, see appendix for scientific studies, Items #6&7). This is because even in high vaccine responders, vaccine-induced antibodies wane over time.  Vaccine immunity does not equal life-long immunity acquired after natural exposure.

It has been documented that vaccinated persons who develop breakthrough measles are contagious. In fact, two major measles outbreaks in 2011 (in Quebec, Canada, and in New York, NY) were re-imported by previously vaccinated individuals.[6] – [7]

Taken together, these data make it apparent that elimination of vaccine exemptions, currently only utilized by a small percentage of families anyway, will neither solve the problem of disease resurgence nor prevent re-importation and outbreaks of previously eliminated diseases. 

Is discrimination against conscientious vaccine objectors the only practical solution?

The majority of measles cases in recent US outbreaks (including the recent Disneyland outbreak) are adults and very young babies, whereas in the pre-vaccination era, measles occurred mainly between the ages 1 and 15. Natural exposure to measles was followed by lifelong immunity from re-infection, whereas vaccine immunity wanes over time, leaving adults unprotected by their childhood shots. Measles is more dangerous for infants and for adults than for school-aged children.

Despite high chances of exposure in the pre-vaccination era, measles practically never happened in babies much younger than one year of age due to the robust maternal immunity transfer mechanism. The vulnerability of very young babies to measles today is the direct outcome of the prolonged mass vaccination campaign of the past, during which their mothers, themselves vaccinated in their childhood, were not able to experience measles naturally at a safe school age and establish the lifelong immunity that would also be transferred to their babies and protect them from measles for the first year of life.

Luckily, a therapeutic backup exists to mimic now-eroded maternal immunity. Infants as well as other vulnerable or immunocompromised individuals, are eligible to receive immunoglobulin, a potentially life-saving measure that supplies antibodies directed against the virus to prevent or ameliorate disease upon exposure (see appendix, Item #8).

In summary: 1) due to the properties of modern vaccines, non-vaccinated individuals pose no greater risk of transmission of polio, diphtheria, pertussis, and numerous non-type b H. influenzae strains than vaccinated individuals do, non-vaccinated individuals pose virtually no danger of transmission of hepatitis B in a school setting, and tetanus is not transmissible at all; 2) there is a significantly elevated risk of emergency room visits after childhood vaccination appointments attesting that vaccination is  not risk-free; 3) outbreaks of measles cannot be entirely prevented even if we had nearly perfect vaccination compliance; and 4) an effective method of preventing measles and other viral diseases in vaccine-ineligible infants and the immunocompromised, immunoglobulin, is available for those who may be exposed to these diseases. 

Taken together, these four facts make it clear that discrimination in a public school setting against children who are not vaccinated for reasons of conscience is completely unwarranted as the vaccine status of conscientious objectors poses no undue public health risk. 

Sincerely Yours,

Tetyana Obukhanych, PhD

Tetyana Obukhanych, PhD, is the author of the book Vaccine Illusion.  She has studied immunology in some of the world’s most prestigious medical institutions. She earned her PhD in Immunology at the Rockefeller University in New York and did postdoctoral training at Harvard Medical School, Boston, MA and Stanford University in California.

Dr. Obukhanych offers online classes for those who want to gain deeper understanding of how the immune system works and whether the immunologic benefits of vaccines are worth the risks:  Natural Immunity Fundamentals.


Item #1. The Cuba IPV Study collaborative group. (2007) Randomized controlled trial of inactivated poliovirus vaccine in CubaN Engl J Med 356:1536-44


The table below from the Cuban IPV study documents that 91% of children receiving no IPV (control group B) were colonized with live attenuated poliovirus upon deliberate experimental inoculation.  Children who were vaccinated with IPV (groups A and C) were similarly colonized at the rate of 94-97%.  High counts of live virus were recovered from the stool of children in all groups.  These results make it clear that IPV cannot be relied upon for the control of polioviruses.

polio chart

Item #2. Warfel et al. (2014) Acellular pertussis vaccines protect against disease but fail to prevent infection and transmission in a nonhuman primate model.Proc Natl Acad Sci USA 111:787-92


“Baboons vaccinated with aP were protected from severe pertussis-associated symptoms but not from colonization, did not clear the infection faster than naïve [unvaccinated] animals, and readily transmitted B. pertussis to unvaccinated contacts. By comparison, previously infected [naturally-immune] animals were not colonized upon secondary infection.”

Item #3. Meeting of the Board of Scientific Counselors, Office of Infectious Diseases, Centers for Disease Control and Prevention, Tom Harkins Global Communication Center, Atlanta, Georgia, December 11-12, 2013


Resurgence of Pertussis (p.6)

“Findings indicated that 85% of the isolates [from six Enhanced Pertussis Surveillance Sites and from epidemics in Washington and Vermont in 2012] were PRN-deficient and vaccinated patients had significantly higher odds than unvaccinated patients of being infected with PRN-deficient strains.  Moreover, when patients with up-to-date DTaP vaccinations were compared to unvaccinated patients, the odds of being infected with PRN-deficient strains increased, suggesting that PRN-bacteria may have a selective advantage in infecting DTaP-vaccinated persons.”

Item #4. Rubach et al. (2011) Increasing incidence of invasive Haemophilus influenzaedisease in adults, Utah, USA. Emerg Infect Dis 17:1645-50


The chart below from Rubach et al. shows the number of invasive cases of H. influenzae(all types) in Utah in the decade of childhood vaccination for Hib.

Hib chart

Item #5. Wilson et al. (2011) Adverse events following 12 and 18 month vaccinations: a population-based, self-controlled case series analysis. PLoS One 6:e27897


“Four to 12 days post 12 month vaccination, children had a 1.33 (1.29-1.38) increased relative incidence of the combined endpoint compared to the control period, or at least one event during the risk interval for every 168 children vaccinated.  Ten to 12 days post 18 month vaccination, the relative incidence was 1.25 (95%, 1.17-1.33) which represented at least one excess event for every 730 children vaccinated.  The primary reason for increased events was statistically significant elevations in emergency room visits following all vaccinations.”

Item #6. De Serres et al. (2013) Largest measles epidemic in North America in a decade–Quebec, Canada, 2011: contribution of susceptibility, serendipity, and superspreading events. J Infect Dis 207:990-98


“The largest measles epidemic in North America in the last decade occurred in 2011 in Quebec, Canada.”

“A super-spreading event triggered by 1 importation resulted in sustained transmission and 678 cases.”

“The index case patient was a 30-39-year old adult, after returning to Canada from the Caribbean.  The index case patient received measles vaccine in childhood.”

“Provincial [Quebec] vaccine coverage surveys conducted in 2006, 2008, and 2010 consistently showed that by 24 months of age, approximately 96% of children had received 1 dose and approximately 85% had received 2 doses of measles vaccine, increasing to 97% and 90%, respectively, by 28 months of age.  With additional first and second doses administered between 28 and 59 months of age, population measles vaccine coverage is even higher by school entry.”

“Among adolescents, 22% [of measles cases] had received 2 vaccine doses.  Outbreak investigation showed this proportion to have been an underestimate; active case finding identified 130% more cases among 2-dose recipients.”

Item #7. Wang et al. (2014) Difficulties in eliminating measles and controlling rubella and mumps: a cross-sectional study of a first measles and rubella vaccination and a second measles, mumps, and rubella vaccination. PLoS One9:e89361


“The reported coverage of the measles-mumps-rubella (MMR) vaccine is greater than 99.0% in Zhejiang province.  However, the incidence of measles, mumps, and rubella remains high.”

Item #8. Immunoglobulin Handbook, Health Protection Agency




  1. To prevent or attenuate an attack in immuno-compromised contacts
  2. To prevent or attenuate an attack in pregnant women
  3. To prevent or attenuate an attack in infants under the age of 9 months

[1] http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm376937.htm

[2] http://archinte.jamanetwork.com/article.aspx?articleid=619215

[3] Poland (1998) Am J Hum Genet 62:215-220


“ ‘poor responders,’ who were re-immunized and developed poor or low-level antibody responses only to lose detectable antibody and develop measles on exposure 2–5 years later.”

[4] ibid

“Our ongoing studies suggest that seronegativity after vaccination [for measles] clusters among related family members, that genetic polymorphisms within the HLA [genes] significantly influence antibody levels.”

[5] LeBaron et al. (2007) Arch Pediatr Adolesc Med 161:294-301


“Titers fell significantly over time [after second MMR] for the study population overall and, by the final collection, 4.7% of children were potentially susceptible.”

[6] De Serres et al. (2013) J Infect Dis 207:990-998


“The index case patient received measles vaccine in childhood.”

[7] Rosen et al. (2014) Clin Infect Dis 58:1205-1210


“The index patient had 2 doses of measles-containing vaccine.”

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 Robert Young PhD

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


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].


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.


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 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.

BowelCancerLive Blood Dried Blood_0166









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

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

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









[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.


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.




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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

[23]  Ibid.

[24]  Ibid.

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

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

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

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

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

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

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

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

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

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

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

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

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

[43]  Rapaport, op. cit. (Ref. 4).

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

[45]  Rapaport, op. cit. (Ref. 4).

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

[47]  Ibid.

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

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

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

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

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

[53]  Ibid.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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


  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


  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


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

Table5aTable 6


  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



Table 8


Table8Table 9



Table 10



Table 11



Table 12



Table 13



Cystic Fibrosis and Pulmonary Adenocarcinoma Lung Cancer – Stage Seven Metabolic and Dietary Acidosis

Robert Young PhD

Robert Young M.Sc., D.Sc.,PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa


Cystic fibrosis (CF)[1][2] and Pulmonary Adenocarcinoma (PAC)[3] have similar symptomologies and are chronic, progressive, and frequently fatal acidic conditions of the respiratory system (lungs), lymphatic system (lymph nodes), intestines, pancreas, urinary tract system, reproductive organs and the skin as the alkaloid glands (the salivary glands, stomach, and small and large intestines) produce and secrete alkaline compounds, such as sodium bicarbonate to buffer and preserve the alkaline design of the body and the specific organs and glands affected.  These metabolic and dietary acidic conditions resulting in the buildup of mucous[3] can affect any organ or organ system but primarily affects the respiratory, lymphatic system, digestive, and reproductive tracts in children and young adults with CF and the lungs and surrounding lymph nodes in PAC.  I have suggested from own clinical research that both of these conditions are the result of latent tissue acidosis (LTA) from metabolism, diet and environmnent and may be successfully treated and reversed with an alkaline lifestyle and diet (ALD).[4]

Key Words: Cancer, Terminal Cancer, Lung Cancer, Cystic Fibrosis, Pulmonary Adneocarcinoma, Bronchitis, Asthma, Shortness of breath, Thick mucous, Wheezing, Chronic sinisitits, Nasal Polyps, Weight loss, Water retention, Abdominal pain, Excessive sweating, cirrhosis of the liver, Inflammation of the pancreas, Pancreas, Liver, Liver disease, Latent tissue acidosis, fatigue, smoking, air pollution, chemical exposure, alkaline lifestyle and diet, alkalizing, nutritional IV’s, massage, infrared sauna, colon hydrotherapy, nebulizing, alkaline nebulizing, L-arginine, glutathione, N-actyl-cysteine, detoxification, live and red blood tests, acupuncture.


According to the Cystic Fibrosis Foundation, about 30,000 Americans have CF. This condition occurs mostly in whites whose ancestors came from northern Europe, although it cuts across all races and ethnic groups. About 3,500 babies are born with this acidic condition each year in the United States. Moreover, about one in every 30 Americans suffer from CF.[1][3]

Nearly 40% of lung cancers in the US are adenocarcinoma, which usually originates in peripheral lung tissue.[5] Most cases of adenocarcinoma are associated with smoking; however, among people who have smoked fewer than 100 cigarettes in their lifetimes (“never-smokers”),[6] adenocarcinoma is the most common form of lung cancer.[7] Its incidence has been increasing in many developed Western nations in the past few decades, where it has become the most common major type of lung cancer in smokers (replacing squamous cell lung carcinoma) and in lifelong nonsmokers.[3] According to the Nurses’ Health Study, the risk of adenocarcinoma of the lung increases substantially after a long duration of previous tobacco smoking, with a previous smoking duration of 30 to 40 years giving a relative risk of approximately 2.4 compared to never-smokers, and a duration of more than 40 years giving a relative risk of approximately 5.[8]

Signs and Symptoms of CF and PAC:

CF and PAC have similar symptomologies and are often accompanied by the following signs and symptoms:

  • Thick, viscous mucus in the lungs caused by the glandular secretion of sodium bicarbonate in the chelation of excess dietary and/or metabolic acids.[3][9][[10]
  • Changes in color and amount of sputum (material coughed up from the lungs) is in direct relationship to the build-up of acidic waste products that are not being properly eliminated through the four channels of elimination – the lungs, bowels, kidneys and skin.[3][9][[10]
  • Chronic cough, possibly with blood streaking is a result of increased acidic and the lung and other elimination organs ridding itself of excess dietary and/or metabolic acids.[3][9][[10]
  • Wheezing is caused by an increase in sticky acidic mucous.[3][9][[10]
  • Bronchitis is stage four acidosis.[3][9][[10]
  • Chronic sinusitis is an acidic condition or stage two acidosis which is experienced by congestion and irritation.[3][9][[10]
  • Asthma is a higher valance of congestive acidosis leading to congestive acidic mucous.[3][9][[10]
  • Nasal polyps (fleshy growths inside the nose) are groups of cells bound together with dietary and/or metabolic acids.[3][9][[10]
  • Weight loss, failure to thrive in infants, abdominal swelling all caused by the retention of acids.  Weight loss due to dietary acids destroying the delicate villi in the small intestines.[3][9][[10]
  • Excessive salt in sweat, dehydration due to the build-up of acids that are not being properly eliminated through the four channels of elimination – lungs, bowels, kidneys and/or skin.[3][9][[10]
  • Failure of newborn in CF to pass stool is the result of ingesting acidic foods and/or drinks.[9][10]
  • Abdominal pain, flatulence are both caused by trapped acids that have not been properly eliminated through the bowels or urinary tract system.[3][9][[10]
  • Fatigue is the first sign congestion of the elimination organs and dietary and/or metabolic acids are building up.[3][9][[10]
  • Other acidic conditions that are caused by an acidic lifestyle and diet such as late onset of puberty, intestinal obstruction, inflammation of the pancreas, cirrhosis (a liver condition), and infertility may also be signs of CF.[3][9][[10]

What Causes Cystic Fibrosis According to Conventional Medicine?

CF is caused by a mutation in the gene cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, is a deletion (Δ signifying deletion) of three nucleotides[11] that results in a loss of the amino acid phenylalanine (F) at the 508th position on the protein. This mutation accounts for two-thirds (66–70%[12]) of CF cases worldwide and 90% of cases in the United States; however, there are over 1500 other mutations that can produce CF.[13] Although most people have two working copies (alleles) of the CFTR gene, only one is needed to prevent cystic fibrosis. CF develops when neither allele can produce a functional CFTR protein. Thus, CF is considered an autosomal recessive disease.

What Causes Pulmonary Adenocarcinoma Lung Cancer According to Conventional Medicine?

Pulmonary Adenocarcinoma cancer is usually seen peripherally in the lungs, as opposed to small cell lung cancer and squamous cell lung cancer, which both tend to be more centrally located,[3][10] although it may also occur as a central lesions.[10] For unknown reasons according to current medical science, it often arises in relation to peripheral lung scars. The current theory is that the scar probably occurred secondary to the tumor, rather than causing the tumor.[10] The adenocarcinoma has an increased incidence in smokers, and is the most common type of lung cancer seen in non-smokers and women.[10] The peripheral location of adenocarcinoma in the lungs is due to the use of filters in cigarettes which prevent the larger particles from entering the lung.[14][15]Deeper inhalation of cigarette smoke results in peripheral lesions that are often the case in adenocarcinomas of the lung. Generally, adenocarcinomas grow more slowly and form smaller masses than the other subtypes.[12] However, they tend to form metastases widely at an early stage.[12] Adenocarcinoma is a non-small cell lung carcinoma, and as such, it is not as responsive to radiation therapy as is small cell lung carcinoma, but is rather treated surgically, for example by pneumonectomy or lobectomy.[12]

What Causes Cystic Fibrosis According to the Research of Dr. Robert O. Young?

When I talk about disease or “dis-ease”, such as CF or PAC, I am really focusing on the state of imbalance in the body, especially the lungs, that is brought on by an inverted way of living, eating and thinking.[15][16]  I have suggested that all disease or dis-ease, including CF and PAC  are caused by individual lifestyle and dietary choice, or for children, how parents are feeding and caring for their children.  I have also suggested that you do not get sick you have to do sick by making personal acidic lifestyle and dietary choices.  In other words disease is a personal choice just like health and fitness are personal choices.

When one chooses or parents choose for their children to eat acidic foods or drinks, such as animal flesh, eggs, dairy products, like cheese, yogurt and ice cream, soda pop, sport drinks, coffee or tea you set yourself up for excess latent tissue acidosis (LTA).  This is when a serious health challenge can begin to develop, such as cystic fibrosis of the lungs for a child or young adult or pulmonary adenocarcinoma lung cancer for people that smoke, breast cancer in women, prostate cancer for men.[15][16]

Over 30 years ago I postulated a theory that ALL sickness and disease is the result of an inverted way of living, eating and thinking.  And, that genetic defects were caused by acidic dietary and lifestyle choices that caused the genetics to express themselves in abnormal ways.  In the case of CF and PAC, the alkaphile glands (salivary glands, stomach, pancreas, gallbladder, Lieberkuhn glands in the intestines) are secreting sodium bicarbonate into the acidic tissues or organs, such as the lungs to maintain the alkaline design of the body fluids and protect the lung cells and tissues from breaking down.  The result is when sodium bicarbonate binds to dietary and/or metabolic acid it creates mucous.  The mucous secretion is the effect of the body protecting itself from excess dietary, environmental and/or metabolic acid. [15][16]

The intelligence of the cell or its genetics is only as healthy as its environment.  I like to compare the intelligent expression of the cellular genetics to a dangerous game called Russian Roulette.  To play the game you put one bullet in the chamber, spin the chamber and then put the gun up to your head and pull the trigger.  The object of the game is to avoid blowing your head off.  The bullet is a metaphor for the genetics and the trigger represents your daily personal lifestyle and dietary choices.  The result in cellular genetics will always be, if you continue to pull the acidic lifestyle and dietary trigger, the genetic bullet will be fired and the symptom(s) will be expressed.  The expression of cellular genetics in producing excess mucous in the condition of CF and PAW can be stopped when you stop pulling the acidic lifestyle and dietary trigger.  The human cell is only as healthy as the fluids it is bathed in just as a fish is only as healthy as the water it swims in.  Change the water and you will change the genetic expression.[15][16]

This new science is called epigenetics and it is showing that the genetic expression of a cell can be turned on or turned off depending on changes in the cellular environment affected by lifestyle and dietary choice.[17]

It is critical to understand this foundational principal in achieving and maintaining a healthy body and a healthy respiratory function.  The foundational hypothesis of my research is the understanding that the human body is alkaline by design and acidic by function.[16]  The mucous in the body is the evidence that the body is protecting itself from its acidic functions (breathing, thinking, moving, eating) when dietary and/or metabolic acids are not properly eliminated through the four channels of elimination.[16]

When you understand that the body needs to be maintained in an alkaline state in order to have sustainable energy, health, fitness and vitality, then everything you drink, everything you eat, every activity you engage in, even your thoughts, produce acidic waste products that affect the health, fitness and vitality of the blood, tissues, organs and glands.[16]

Your health, fitness, energy and vitality is an expression of what you are eating, what you are drinking and what you are thinking.  If you are ingesting an abundance of acidic foods and liquids, or smoking cigarettes or exposed to environmental pollutants, that’s creating an internal acid environment leading to a breakdown or fermentation of the lung cells, this will lead to a host of dis-ease conditions, including CF or PAC.[16]

There are seven stages of ALL sickness and dis-ease or acidity even though there is only one sickness and one disease.

The one sickness and one disease or dis-ease theory is the over-acidification of the blood and then tissues due to an inverted way of living, eating and thinking.  This one sickness and one disease or dis-ease theory has seven stages or or seven expressions, which have been categorized by medical science as separate or different types of disease without any association or connection.  But, there is NOT many diseases only one disease and one health![18]

For example, cancer is part of that one acidic disease.  Lung cancer is an acidic condition that spoils healthy cells making them cancerous.  Multiple sclerosis is part of that one disease as acid destroys the myelin sheath.  Heart disease is the result of acid damage as is diabetes.  Cystic fibrosis is also part of this one disease as healthy body cells are being protected from dietary and/or metabolic acids creating sticky mucous.  Allergies, arthritis, osteopenia, osteoarthritis, osteoporosis, bowel restrictions and constipations, from diverticulitis to diverticulosis, IBS, ulcerated colitis, Crohn’s, all of these so-called diseases are the result of a compromised alkaline environment from individual acidic lifestyle and dietary choice.[18]

The seven stages of disease or dis-ease or excess acidity begins in the bowels, then in the blood, pushed out into the tissues, organs and glands and expressed as follows:

1) The first stage of acidosis is enervation or the loss of energy.  In this stage the body does not have the sufficient energy to completely remove dietary and/or metabolic acidic waste products which build up first in the blood and then in the connective and fatty tissues.

2) The second stage of acidosis are sensitivities and irritation.  An example of stage two acidosis are sensitivities to food and/or air-born allergies.

3)  The third stage of acidosis is catarrh or mucous buildup.  An example of stage three acidosis would be the acidic condition of the lungs called cystic fibrosis.  It is important to understand that mucous is created when the glands of the body release the alkaline compound sodium bicarbonate for the purpose of binding up dietary and/or metabolic acids.  The combining of sodium bicarbonate to acid creates a sticky mucous.  Since dietary, environmental and metabolic acids can breakdown and destroy healthy tissues and organs the glands of the body, such as the salivary glands, the pylorus glands, the pancreas and even the stomach release the alkalizing compound, sodium bicarbonate to protect and preserve healthy body cells that make up our tissues and organs.

4) The fourth stage of acidosis is inflammation.  There is only one cause of inflammation and that is acid.  Acid equal pain and pain equals acid.  There is no other cause.  Any pain or inflammation in the body is the result of localized acid that has not been properly removed by the lymphatic system.  That is why exercise is so important because the lymphatic circulation is activated by the contraction of muscle and especially the calf muscles.  Therefore, inflammation is always caused by dietary, environmental and/or metabolic acid.

5) The fifth stage of acidosis is induration or fibrotic tissue or the hardening of the tissues or organs.  This is the classic symptomology of cystic fibrosis.  The tissues and organs are turning into leather.  Another classic symptomology of induration is atherosclerosis or the hardening of the vascular system.

6)  The sixth stage of acidosis is the ulceration of tissues and/or organs such as in ulcerated colitis, or cirrhosis of the liver, or any lesion where ever it may appear.

7)  And, the seventh and final stage of acidosis prior to death is the degeneration of tissues, organs and glands.  All degenerative conditions are caused by dietary, environmental and/or metabolic acids, such as in the symptomologies of osteoporosis, multiple sclerosis, ALL cancerous conditions, heart disease and all respiratory dis-eases, including cystic fibrosis.[18]

It is important to keep in mind that whatever the disease or dis-ease condition there is only one cause.  And, that one cause is the retention of excess acids first in the blood and then the tissues and organs.  This excess acid is not eliminated through the four channels of elimination they are then deposited into the connective and fatty tissues.  This is why I call the connective tissues the “acid catchers” of the blood.[16][18]

You do not need a doctor to tell you your stage of acid imbalance. You can know this based upon your the symptom(s) you are experiencing or feeling.  If you are overweight this is an acidic condition and the body protecting the organs that sustain life from excess dietary, environmental and/or metabolic acids.  In other words, obesity is NOT a fat problem any more then cystic fibrosis is a genetic problem.  They are both an acid problem.[19]

Cystic fibrosis (CF) or Pulmonary Adenocarcinoma (PAC) are both progressive latent tissue acidosis (LTA)  conditions that begin with fatigue, then congestion, then retention, irritation, mucous build up, inflammation, induration, ulceration, degeneration and finally death.[18]

The Self-Care to a Self-Cure Can Be Simple

1) Open the channels of elimination.

2)  Heal the root system or the intestinal villi of the small intestines.

3) Build healthy stem cells and red blood cells.

4) Hyper-perfuse the blood and tissues with alkalinity.[18]

Who’s Most At Risk?

CF and PAC are caused by the genetic expression of body cells to excess dietary, metabolic and environmental acidity.[18] To change the genetic expression of the body cells one must restore the alkaline design of the body fluids with an alkaline lifestyle and diet (ALD).[18]  To have CF, a child must inherit the acidic lifestyle and diet of the parents that then causes two abnormal genes — one from each parent.  The new science of epigenetics suggests that genes can change their expression as a result of diet and lifestyle changes.[17]  In other words, when a child with CF changes his/her diet from a standard acidic American diet to the AFD diet or one stops smoking the genes will change and begin slowing down and even stopping their secretion of acid-binding sodium bicarbonate.  This in turn will reduce congestion from sticky mucous that can builds up in the lungs another organs and tissues.[20]

What to Expect at Conventional Medical Doctor’s Office for Diagnostic Testing

A baby born with the CF gene usually has symptoms during its first year, although signs of the disease may not appear until adolescence or even later.

Your child’s health care provider can help make a diagnosis and guide you in determining which treatment or combination of therapies will best alleviate symptoms of the disease. Your health care provider will perform a physical exam and run laboratory tests, including a sweat test, which checks for higher than normal amounts of sodium and chloride in the sweat. Other tests include a sputum test, genetic screening, and a stool analysis. Imaging techniques may help reveal lung conditions and abdominal obstruction.[21][22]

Tests that examine the lungs are used to detect (find), diagnose, and stage CF and PAC.

Tests and procedures to detect, diagnose, and stage CF and PAC are often done at the same time. Some of the following tests and procedures may be used:

  • Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits, including smoking, and past jobs, illnesses, and treatments will also be taken.
  • Laboratory tests : Medical procedures that test samples of tissuebloodurine, or other substances in the body. These tests help to diagnose disease, plan and check treatment, or monitor the disease over time.
  • Chest x-ray: An x-ray of the organs and bones inside the chest. An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.
  • CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, such as the chest, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography.
  • Sputum cytology : A procedure in which a pathologist views a sample of sputum (mucus coughed up from the lungs) under a microscope, to check for cancer cells.
  • Fine-needle aspiration (FNA) biopsy of the lung: The removal of tissue or fluid from the lung using a thin needle. A CT scan, ultrasound, or other imaging procedure is used to locate the abnormal tissue or fluid in the lung. A small incision may be made in the skin where the biopsy needle is inserted into the abnormal tissue or fluid. A sample is removed with the needle and sent to the laboratory. A pathologist then views the sample under a microscope to look for cancer cells. A chest x-ray is done after the procedure to make sure no air is leaking from the lung into the chest.
  • Bronchoscopy : A procedure to look inside the trachea and large airways in the lung for abnormal areas. A bronchoscope is inserted through the nose or mouth into the trachea and lungs. A bronchoscope is a thin, tube-like instrument with a light and a lens for viewing. It may also have a tool to remove tissue samples, which are checked under a microscope for signs of cancer.
  • Thoracoscopy : A surgical procedure to look at the organs inside the chest to check for abnormal areas. An incision (cut) is made between two ribs, and a thoracoscope is inserted into the chest. A thoracoscope is a thin, tube-like instrument with a light and a lens for viewing. It may also have a tool to remove tissue or lymph node samples, which are checked under a microscope for signs of cancer. In some cases, this procedure is used to remove part of the esophagus or lung. If certain tissues, organs, or lymph nodes can’t be reached, a thoracotomy may be done. In this procedure, a larger incision is made between the ribs and the chest is opened.
  • Thoracentesis : The removal of fluid from the space between the lining of the chest and the lung, using a needle. A pathologist views the fluid under a microscope to look for cancer cells.
  • Light and electron microscopy : A laboratory test in which cells in a sample of tissue are viewed under regular and high-powered microscopes to look for certain changes in the cells.
  • Immunohistochemistry : A test that uses antibodies to check for certain antigens in a sample of tissue. The antibody is usually linked to a radioactive substance or a dye that causes the tissue to light up under a microscope. This type of test may be used to tell the difference between different types of cancer.[23]

Alkalizing Treatment Protocol for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)

Prevention and Alkalizing is the Self-Care to a Self-Cure for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)

The best self-care to a self-cure for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC) will be found in its prevention NOT in its treatment. Preventing CF and PAC must begin with the parents switching to an alkaline lifestyle and diet before conception.  At birth the parents can help avoid the symptoms of CF or any other dis-ease with the Alkalizing Lifestyle and Diet Protocol.

Natural Non-Invasive Treatment Plan for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC) Lung Cancer[15][16][18]

The hope for the future is that the Alkalizing Lifestyle and Diet (ALD) therapy can repair or replace the defective CF or PAC gene and cause the gene to express itself differently by changing the environment and restoring the alkaline design of the body fluids.  This will cause the gene to express itself in an alkaline way rather than in a defensive way to protect itself from an acidic lifestyle and diet.  This environmental approach for treating CV and PAC may prove to be the cure for this acidic lifestyle and dietary symptom.

CF and PAC patients suffer from frequent lung infections that may lead to obstructed breathing caused by an acidic lifestyle and diet. So, the mainstays of a treatment plan are:

1) Open up the channels of elimination of dietary and metabolic acids.

2) Hyper-perfuse the tissues with alkalinity to buffer the retained dietary and/or metabolic acids.

3) Heal the root system or bowels of the body or the intestinal villi of the small intestines to improve the quality and quantity of stem cell and red blood cell production.

4)  Alkalizing physical therapy to remove acids out of the tissues, especially the lungs.

5) Alkalizing  exercise to remove dietary and/or metabolic acids in the connective tissues out through the pores of the skin, and

6) Alkalizing natural organic and colloidal natural medications for reducing the acids that cause mucus that is congesting and blocking the lung’s airways.

Natural Alkalizing Lifestyle and Dietary (ALD) Therapies[15][16][18]

Natural organic colloidal nutrients can by pass the alimentary canal and go directly into the blood and tissues through a process of nebulization or misted alkaline nutrients that are inhaled through the mouth and nose.[16] These include the following:

  • Nebulizing 5ml of Glutathione and 5ml of N-acetyl-cysteine to reduce acidic mucous in the sinuses and lungs 2 to 3 times a day.
  • Nebulizing 10ml of a mucolytic such as colloidal silver at 5 to 10 ppm once a day
  • Nebulizing 10 ml of colloidal silica which acts as a decongestant (which reduce swelling of the membranes of the breathing tubes).
  • Antibiotics are highly acidic and should NEVER be used with CF or PAC.  To reduce infection in the blood and tissues you reduce tissue acidity which is the cause of infections.[18]

The alimentary canal problems of congestion caused by an acidic diet leading to the symptoms of CF and PAC are managed with the following natural organic remedies.

  • Whole leaf cold pressed aloe vera juice will reduce inflammation caused by increased amounts of hydrochloric acid when the stomach is producing sodium bicarbonate to buffer the retention of tissue acids.[24]
  • Alkalizing hydrocolon therapy or colonics and enemas with mucolytic agents such as magnesium oxide, magnesium chloride, sodium bicarbonate, potassium bicarbonate, calcium glutamate and Vitamin C to treat intestinal obstructions and to infuse alkalizing compounds into the blood stream via the messenteric blood vessels.[25]

Food and Nutritional Supplements in the Prevention and Reversal of Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)[26]

Natural organic colloidal nutrients can by-pass the alimentary canal and go directly into the blood and tissues through a process of nebulization or misted alkaline nutrients that are inhaled through the mouth and nose. These include the following:

Following these dietary nutritional tips will help reduce ALL acidic symptomologies associated with CF and PAC:[15][16][18]

1)  Eliminate all inflammatory acidic liquids and foods that increase sodium bicarbonate and the formation of mucous, including dairy products (milk, cheese, sour cream, and ice cream), wheat (gluten), processed soy except for non-GMO organically sprouted soy, corn, potatoes, all high-sugar fruit including bananas, oranges, pineapple, berries, apples, all forms of sugar including honey, maple syrup, fructose, maltose, dextrose, glucose, preservatives, food additives and excessive salt and all animal meats including fish, poultry, beef and pork.[15][16][18]

2)  Eat more foods that decrease acids and the formation of mucous, including garlic, onions, watercress, horseradish, mustard, parsley, celery, cucumber, broccoli, spinach, rose hips tea, lemon, lime, tomato, avocado and anti-inflammatory/anti-acid oils from nuts and seeds.[15][16][18]

3)  Eat more foods that are high in potassium, such as avocado sprouts and kale.[15][16][18]

4)  Avoid all processed and refined foods, such as white breads, pastas, and sugar.[15][16][18]

5)  Eliminate all red meats and lean meats, pork, poultry, fish, processed soy and all legumes.  Increase plant based proteins from avocado, hemp and sprouted organic soy.[15][16][18]

6)  Use healthy oils in foods, such as cold pressed olive oil and avocado oil.[15][16][18]

7)  Eliminate trans fatty acids, found in commercially baked goods such as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.[15][16][18]

8)  Eliminate all grains from the diet.[15][16][18]

9)  Eliminate all corn products.[15][16][18]

10)  Eliminate peanuts.[15][16][18]

11)  Eliminate all forms of vinegar.[15][16][18]

12)  Eliminate all forms of mushrooms.[15][16][18]

13)  Eliminate coffee, black teas and other stimulants, alcohol, and tobacco.[15][16][18]

14)  Eliminate sport drinks, energy drinks and soft drinks.[15][16][18]

15)  Drink 4 to 6 liters of 9.5 alkaline water daily based upon 1 liter per 30 kg of weight.  Add 10 grams of pH Miracle green powder with 5 drops of pH Miracle puriphy in each liter of water.  This will help build healthy stem cells and blood in the crypts of the small intestines and reduce latent tissue acidosis which may be the cause of CF and PAC.[15][16][18]

16)  Alkalizing exercise moderately, for 60 minutes daily, 6 days a week.  Choose from walking, jogging, elliptical machines, rebounding, swimming, biking, Younga Yoga, isotonic weight lifting, just to name a few.[15][16][18]

Address nutritional deficiencies and excess latent tissue acidosis (LTA) with the following supplementation to the daily diet:[15][16][18][36]

1)  Omega-3 fatty acids, such as Hemp, Flax and Borage oils, 4 – 6 capsules or 1 tablespoonful of a 2 to 1 to 1 (Omega 3 to 6 to 9) combination of these three oils at least three to four daily, to help decrease inflammation caused by dietary and/or metabolic acids and improve the health and strength of the lipid membranes of stem, blood and body cells.[15][16][18][27][28][29][31]{34]

2)  A multivitamin daily, containing the acid chelating antioxidant vitamins A, D, E, K, the B-vitamins and trace minerals, such as sodium, magnesium, potassium, calcium, zinc, and selenium.[15][16][18][31]

3)  Digestive acid buffers of sodium bicarbonate, potassium bicarbonate, magnesium chloride and calcium chloride to reduce hydrochloric acid in the stomach, bowels, blood and tissues, 1 – 2 capsules 4 times daily with 9.5 pH alkaline water.[15][16][18][31]

4)  Magnesium oxide with Vitamin C to breakdown undigested acid foods of animal protein, dairy products and mucous in the 9 yards of the small intestines.[15][16][18][31]

5)  Coenzyme Q10, 100-200 mg at bedtime, for antioxidant and supporting the white blood cells in removing bacteria, yeast and solidified acids from the the blood and tissues.[15][16][18][31]

6)  N-acetyl-cysteine (NAC), 2000 mg daily 3 times a day, for antioxidant effects for buffering metabolic acids of acetylaldehyde and ethanol alcohol that effect the respiratory and neurological systems. NAC can also be given by IV at 5ml where each ml equals 200mgs.[15][16][18][31]

7)  Grapefruit seed extract (Citrus paradisi), 100 mg capsule or 5 – 10 drops (in alkaline water) 3 times daily, for buffering the acids of diet, metabolism, bacteria and yeast for increasing the alkaline pH of the gastrointestinal system to 8.4.[15][16][18][31][32][33][34]

8)  Methylsulfonylmethane (MSM), 3,000 mg twice a day, to help decrease the acids that cause inflammation.[15][16][18][31]

9)  Organic hemp protein, 10 – 20 grams daily mixed in fresh organic hazel or almond milk, for supporting the white blood cells and blood building.[15][16][18][31]

10)  L-Arginine, 10 grams 3 times a day to break up solidified acid crystals causing circulation problems of the vascular and lymphatic system.[15][16][18]

11)  Magnesium chloride, 2 grams 3 times a day to oxidize dietary and metabolic acids.[15][16][18]

12)  Pure organic chlorophyll from sprouted Moringa,  5 to 10 drops in 4 ounces of 9.5 pH alkaline water 3 times a day.  This mixture at 10ml can also be put into a nebulizer to reduce acid congestion in the sinuses and lungs.[15][16][18]

13)  Glutathione, 2000mg 3 to 4 times daily, neutralizes harmful acids or oxidants introduced into the lungs from the air or blood or those released by cells. Exotoxins from bacteria can overload the endobronchial terrain and feed the fires of acidic inflammation. This staggering burden increases the oxidative sensitivity of the CF lung, resulting in further injury of lung parenchyma. Data supports evidence of a decrease in the antioxidant tri-peptide glutathione. [15][16][18]

Glutathione is always in great demand and is rapidly consumed when we experience any sort of emotional or physical stress, fatigue and even moderate exercise. Some well-known causes of glutathione depletion are as follows:[15][16][18][30]

1) Acidic lifestyle and diet

2) Air and Water pollution

3) Prescription and recreational drugs

4) Ultraviolet and Radiation from cells phones, computers, electrical cars, power lines, hair dryers, etc.

5) Emotional and physical stress

6) Injury, trauma or burning

7) Heavy metals

8) Cigarette smoke

9) Household chemicals

10) Acetaminophen poisoning

11) Exhaust from motor vehicles

12) Septic shock caused by the retention of metabolic and/or dietary acid.

All of these above factors lead to a build up of acidic toxins that cause the loss of glutathione as a non-nutritive buffer leading to cellular aging, dis-ease and finally death.[30]

Alkalizing Medicinal Herbs and Organically Sprouted Grasses

1)  Medicinal herbs, grasses, fruit and vegetables is a safe way to strengthen and tone the body’s alkalizing buffering system, detox the alimentary canal and build blood in the crypts of the small intestines. You should use the whole unprocessed or non-fermented herbs, grasses, fruit and vegetables titrated to a fine powder so they that can be mixed in 9.5 pH alkaline water or put into veggie caps to be taken orally.[15][16][18][31][34]

2)  Ginkgo (Ginkgo biloba), 40 – 80 mg 3 times daily, for inflammation and as an antioxidant to buffer acids in the blood, tissues and organs.[15][16][18][31][34]

3)  Wheat, Barley and Kamut rrganically sprouted grasses, 250 – 500 mg daily, for building blood, detoxing the alimentary canal,  buffering dietary and metabolic acids and supporting the white blood cells in the removal of solidified acids. You may also prepare teas from these grasses.[15][16][18][31][34]

3)  Cat’s claw (Uncaria tomentosa) , 20 mg 3 times a day, for inflammation caused by dietary and/or metabolic acids,  supporting the white blood cells and reducing acids from bacteria, yeast and mold in the blood and tissue fluids.[15][16][18][31][34]

4)  Milk thistle (Silybum marianum), 80 – 160 mg 2 – 3 times daily, for detoxification of acids in the blood, liver and kidneys.[15][16][18][31][34]

5)  Bromelain (Ananus comosus), 40 mg 3 times daily, for pain and inflammation caused by dietary acids.[15][16][18][31][34]

6)  Ground Ivy (Hedera helix) , 50 mg 3 times daily, to decrease acids and the build-up of mucous and to loosen phlegm.[15][16][18][31][34]

Intravenous (IV) Alkalizing Therapy

The main purpose of IV therapy is to hyper-perfuse the tissues with alkaline compounds of sodium bicarbonate, magnesium chloride, potassium bicarbonate and calcium glutamate and thus buffer the retention of excess dietary and/or metabolic acids in the body tissues, especially the lungs reducing inflammation, mucous, solidfication of tissues, and cysts.


Acupuncture may alleviate symptoms of cystic fibrosis. Acupuncture may help enhance blood and lymph circulation to the lungs which in turn will help the immune function to remove cellular debris and acid crystals.  Because acupuncture improves circulation it also helps remove acids throughout the alimentary canal, and strengthen.


Therapeutic lymphatic massage can help drain acidic mucus from the lungs and remove latent tissue acidosis.

Infrared Sauna

Therapeutic infared sauna can help increase blood and lymphatic circulation and open up the pores of the skin to eliminate excess dietary, environmental and metabolic acids from the tissues.  This passive form of exercise will cause you to sweat at every pore removing latent tissue acids.  I recommend at least 30 minutes a day or until you start sweating.  Once you start sweating remain in the sauna for at least 15 minutes.  Make sure you are adequately hydrated with alkaline mineral rich water at a pH of 9.5.  To adequately hydrate drink at least 1 liter of akaline fluids for every 30 kg of weight.  You can also drink before, during and after your infared sauna. Prognosis/Possible Complications Respiratory problems due to acid build-up and the solidification of dietary, environmental and/or metabolic acids forming acid crystals and cysts in the lungs are the most common complication from CF and PAC.

Following Up

CF and PAC patients receive pulmonary function tests every 3 – 6 months. They also receive chest x-rays every 2 – 4 years, or more often if needed.

Case Study of the Alkalizing Lifestyle and Diet (ALD) for Terminal Metastatic Pulmonary Adenocarcinoma Lung Cancer

A 58 year old Danish woman was diagnosed by X-ray, Cat Scan and biopsy of the lung with Pulmonary Adenocarcinoma Lung Cancer with metastasis to the axillary lymph nodes at the Roskilde Hospital on June, 2011.  She was not offered conventional invasive surgery because the cancer had spread throughout her left lung to the lymphatic system and the axillary lump nodes.  Chemotherapy and radiation were suggested but would only extend life for a few weeks beyond her 6 month life expectancy.  She started the ALD protocol a week after diagnosis.  She was retested in October, 2015 with Ultrasound and Bronchoscopy  and found to have no pulmonary adenocarcinoma cancer in the lungs or in the axillary lymph nodes.  The medical doctors found her to be in good health and attribute her cancer remission to the Alkalizing Lifestyle and Diet (ALD) that she followed and is still following as of to date.


Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC) of the lungs are terminal chronic acidic conditions, theoretically caused by LTA with no current conventional treatments to slow-down the aggressive nature of these conditions.  The Alkalizing Lifestyle and Diet (ALD) have shown great promise in improving symptoms of both CF and PAC and in one case reversing PAC, a terminal cancer condition with a 5 year life expectancy of 1 percent.[37]

Further Research

Further research needs to be done with larger groups with CF or PAC to show that the ALD cancer treatment protocol is a viable therapy for the prevention and/or reversal of Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC).  The author of this article is hopeful that more research scientist will be open to investigating the efficacy of the ALD protocol as a potential non-invasive treatment for the cure of CF and PAC.


  1.  O’Sullivan, BP; Freedman, SD (30 May 2009). “Cystic fibrosis.”. Lancet 373 (9678): 1891–904. doi:10.1016/s0140-6736(09)60327-5PMID 19403164.
  2. Hodson, Margaret; Geddes, Duncan; Bush, Andrew, eds. (2012). Cystic fibrosis (3rd ed.). London: Hodder Arnold. p. 3. ISBN 978-1-4441-1369-3.
  3. Travis, William D; Brambilla, Elisabeth; Müller-Hermelink, H Konrad; Harris, Curtis C, eds. (2004). Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart (PDF). World Health Organization Classification of Tumours. Lyon: IARC Press. ISBN 92-832-2418-3. Retrieved 27 March 2010.
  4. Young, R.O. (25 February 2015). “The Blood Jerk Reaction – A Rise In The Alkaline pH of the Blood! What Does It Really Mean?” http://blog.phoreveryoung.com/tag/latent-tissue-acidosis/
  5. Smokers defined as current or former smoker of more than 1 year of duration. See image page in Commons for percentages in numbers. Reference:
    1.  Horn, L; Pao W; Johnson DH (2012). “Chapter 89”. In Longo, DL; Kasper, DL; Jameson, JL; Fauci, AS; Hauser, SL; Loscalzo, J. Harrison’s Principles of Internal Medicine(18th ed.). McGraw-Hill. ISBN 0-07-174889-X.
  6. Subramanian, J; Govindan R (February 2007). “Lung cancer in never smokers: a review”. Journal of Clinical Oncology (American Society of Clinical Oncology) 25 (5): 561–570. doi:10.1200/JCO.2006.06.8015PMID 17290066.
  7. Kenfield, S. A.; Wei, E. K.; Stampfer, M. J.; Rosner, B. A.; Colditz, G. A. (2008). “Comparison of aspects of smoking among the four histological types of lung cancer”Tobacco Control 17 (3): 198–204. doi:10.1136/tc.2007.022582PMC 3044470PMID 18390646.
  8. Flume PA, Mogayzel Jr PJ, Robinson KA, et al. (March 2010). “Cystic Fibrosis Pulmonary Guidelines: Pulmonary Complications: Hemoptysis and Pneumothorax”. Am J Respir Crit Care Med 182 (3): 298–306. doi:10.1164/rccm.201002-0157OCPMID 20299528.
  9. Mitchell, Richard Sheppard; Kumar, Vinay; Robbins, Stanley L.; Abbas, Abul K.; Fausto, Nelson (2007). Robbins basic pathology. Saunders/Elsevier. ISBN 1-4160-2973-7.
  10. “Profile : Lap-Chee Tsui”. Science.ca. 1989-05-09. Retrieved 2013-01-23.
  11. Mitchell, Richard Sheppard; Kumar, Vinay; Robbins, Stanley L.; Abbas, Abul K.; Fausto, Nelson (2007). Robbins basic pathology. Saunders/Elsevier. ISBN 1-4160-2973-7.
  12. Bobadilla JL, Macek M, Fine JP, Farrell PM (June 2002). “Cystic fibrosis: a worldwide analysis of CFTR mutations—correlation with incidence data and application to screening”. Hum. Mutat. 19 (6): 575–606. doi:10.1002/humu.10041PMID 12007216.
  13. Goljan USMLE Audio Tapes, 2001
  14. Young, RO, “Sick and Tired”, Woodland Publishing, Orem, Utah, 2001.
  15. Young, RO, Young, SR, “The pH Miracle Revised and Updated”, Grand Central Publishing, New York, NY, 2010.
  16. McGowan P.O., Meaney M.J., Szyf M. (2008).  Diet and the epigenetic (re)programming of phenotypic differences in behavior. Brain Research, 1237: 12-24 (subscription required).
  17. Young,R.O., Young, SR, “The pH Miracle for Cancer”, Hikari Omni Media Publishing, Alpine, Utah, 2015.
  18. Young,R.O., Young, S.R., “The pH Miracle for Weight Loss”, Grand Central Publishing, New York, NY, 2005.
  19. Rubin BK. The pharmacologic approach to airway clearance: Mucoactive agents. Paediatr Respir Rev. 2006;7 Suppl 1:S215-9.
  20. The Cystic Fibrosis Foundation, “Testing for CF”, https://www.cff.org/What-is-CF/Testing/
  21. Farrell P, Rosenstein B, White T, et al. Guidelines for Diagnosis of Cystic Fibrosis in Newborns through Older Adults: Cystic Fibrosis Foundation Consensus Report. Journal of Pediatrics. 2008;153(2).
  22. The National Cancer Institute, “Testing for Non-Small Cell Lung Cancer”‘ http://www.cancer.gov/types/lung/patient/non-small-cell-lung-treatment-pdq
  23. Young, R.O., “The Real Scientific Truth Concerning The pHysiology of the Stomach”,  http://blog.phoreveryoung.com/2015/02/02/the-real-scien…of-the-stomach/
  24. Young, R.O., “Alkalizing Colon Hydrotherapy – The Secret of the Ancient Healers”,  http://blog.phoreveryoung.com/2015/08/01/the-secret-of-…ient-healers-
  25. Adde FV, Rodrizues JC, Cardoso AL. Nutritional follow-up of cystic fibrosis patients: the role of nutrition education. J Pediatr (Rio J). 2004;80(6):475-82.
  26. Mizejewski GJ, Pass KA. Fatty acids, alpha-fetoprotein, and cystic fibrosis. Pediatrics. 2001;108(6):1370-3.
  27. Caramia G, Cocchi M, Garliardini R, et al. Fatty acids composition of plasma phospholipids and triglycerides in children with cystic fibrosis. The effect of dietary supplementation with an olive and soybean oils mixture. Pediatr Med Chir. 2003;25(1):42-9.
  28. Beckles Willson N, Elliot TM, Everard ML. Omega-3 fatty acids (from fish oils) for cystic fibrosis. Cochrane Database Syst Rev. 2002;(3):CD002201.
  29. Roum JH, Buhl R, McElvaney NG, et al. Systemic Deficiency of Glutathione in Systic Fibrosis. J Appl Physiol 1993; 75:19-24
  30. Young, R.O. “Herbal Nutritional Medications”, Hikari Omni Publishing, Alpine, Utah, 1992.
  31. Cvetnic Z, Vladimir-Knezevic S. Antimicrobial activity of grapefruit seed and pulp ethanolic extract. Acta Pharm. 2004;54(3):243-50.
  32. Heggers JP, Cottingham J, Gussman J, et al. The effectiveness of processed grapefruit-seed extract as an antibacterial agent: II.
    Mechanism of action and in vitro toxicity. J Altern Complement Med. 2002;8(3):333-40.
  33. Guo R, Pittler MH, Ernst E. Herbal medicines for the treatment of COPD: a systematic review. Eur Respir J. 2006;28(2):330-8.
  34. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002;21(6):495-505.
  35. Murray KL, Lee CK, Mogayzel PJ Jr, Zeitlin PL, Rosenstein BJ. Dietary supplement use in pediatric patients with cystic fibrosis. Am J Health Syst Pharm. 2008;65(6):562-5.
  36. The American Cancer Society, “Non-Small Cell Lung Cancer Survival Rates by Stage”, http://www.cancer.org/cancer/lungcancer-non-smallcell/detailedguide/non-small-cell-lung-cancer-survival-rates

Summary of Double Blind Research Study on the Negative Effects of Everyday Lifestyle Stressors on the Human Cell and the QLink Device to Buffer Stress1

Live and Dried Blod Analysis - Copyright ROY


A double blind study was conducted by Robert Young2, PhD, DSc, microbiologist, to investigate and validate the potential of the Clarus QLink Pendant as a device for buffering everyday stress and maintaining the integrity of the human cell.


Materials and Methods

Human blood cells are examined for cellular organization and disorganization in which live and dried blood samples are tested before and after wearing QLink pendants.

In this study, two blood microscopy tests are used to examine the organization of matter in the human blood. These tests are the “Unchanged Blood Test” , also referred to as the live blood test and the “Mycotoxic Oxidative Stress Test” 3, also referred to as the dried blood test. (See page 2, Figures 1 & 2)

The Live Blood Test examines the unstained blood. Blood is drawn from the test subject and placed on a microscope slide for examination. From the live blood micrographs, the organization and disorganization of matter present in the blood plasma such as red blood cells, white blood cells, bacteria, yeast, mold and acid crystals can be seen and characterized.

Live Blod Analysis - Crystals .Copyright ROY

The Dried Blood Test examines the coagulation of blood. Blood is drawn from the fingertip and allowed to dry and clot in a normal manner. Dr Young states that the states of imbalance are reflected by changes in blood composition and clotting ability4. When blood is allowed to clot, the pattern seen in normal healthy subjects is essentially the same. This pattern is characterized by a dense mass of red areas interconnected by dark, irregular lines, completely filling the area of the drop. (figure 2) However, blood containing abnormal artifacts will distort the normal pattern. The blood of a subject under mycotoxic oxidative stress will exhibit a variety of characteristic patterns that deviate from the normal pattern. One common characteristic observed in these abnormal patterns is the presence of “clear” or white areas seen in the dried blood. These clear areas indicate the absence of the fibrin net or red blood cell conglomerate typically found in the normal healthy blood.5 These areas are the result of cellular disorganization from factors such as EMF exposure, poor diet, etc.

Live and Dried Blod Analysis - Copyright - ROY


1 Young, Robert, Ph.D., D.Sc., Research Study for Everyday Lifestyle Stressors and the QLink Pendant, January 2001.

2 Founder of Robert O. Young Research Center, Salt Lake City, Utah

3 Young, Robert, Ph.D., D. Sc., Sick and Tired, Pathological Blood Coagulation, Woodland Publishing, January 2000.

4 The medical term disseminated intravascular coagulation is characterized by the abnormal presence of fibrin monomer in the blood.

5 These white areas are referred to as polymerized protein puddles and are the result of cellular disorganization from disturbing factors like low EMF. These polymerized protein puddles will appear in various areas of the red blood cell conglomerate based upon their molecular weight, indicating cellular disorganization in specific areas of the body.

Figure 1. Live Blood Test Micrograph Figure 2. Dried Blood Test Micrograph

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

A total of 16 adult volunteer subjects were tested. Personal history interviews were conducted for each individual case study prior to testing. The 16 subjects were divided into two groups, A & B. Subjects were given an inactive QLink (Group A) or real QLink (Group B) to wear continuously for 72 hours. Neither the test subjects nor the microbiologists conducting the blood tests knew which were wearing the dummy or the real QLink pendants.

Results and Conclusions

Live and dried blood samples are examined for cellular integrity and organization. Baseline micrographs were taken for each subject prior to wearing the real QLink or the dummy. After approximately 72 hours of wearing the QLink or dummy, each test subject was retested. The Baseline micrographs were compared against the micrographs taken 72 hours later. Significant differences or changes seen between the two conditions are highlighted in the micrographs taken. (Typical micrographs are shown in Appendix A).

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf


Based upon microscopic examination of the blood, the blood micrographs (see Example Micrographs in Appendix A) taken and comments from each individual test subject, Dr Young6 made the following conclusions.

Group A (Dummy QLink):

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

“In all 8 subjects, there was little or no impact on the morphology of the red and white blood cells and the red blood cell conglomerate while wearing QLink A. In addition, all 8 reported little or no notable improvement in increased energy and/or health experiences. No perceived beneficial effects were reported while wearing QLink A.”

6 Individual case study comments and conclusions are detailed in the original report by Robert Young, Research Study for Everyday Lifestyle Stressors and the QLink Pendant, January 2001.

2  Group B (Real QLink):

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

“In all 8 subjects, there was a significant impact on the morphology of the red and white blood cells and the red blood cell conglomerate while wearing QLink B. After 72 hours the red blood cells appeared to be more round and symmetrical which is the normal healthy profile. The major white blood cells (neutrophils) were healthy, active and streaming, collecting and removing morbid matter. There appears to be a reduction in the presence of bacteria, yeast, acid crystals and colloid symplasts in the blood plasma. The red blood cell conglomerate appeared hyper-coagulated which represents the health normal profile rather than hypo-coagulated, an abnormal profile in which clear or white areas of protein mass are present in the conglomerate.”

A notable improvement in the morphology of the live and dried blood was seen in all 8 subjects in Group B as viewed in the micrographs. This improvement is hypothesized to be a direct result of the QLink pendant mediating disturbing lifestyle stressors. The QLink achieves this by maintaining the integrity of the energy fields that surround each individual blood cell. In addition, all 8 test subjects reported experiences of increased energy and/or health.

3  Appendix A

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

Example Blood Micrographs from Test Subject in Group A – Dummy QLink

Without QLink A – Baseline Live Blood Test

Without QLink A – Baseline Live Blood Test

With QLink A ~72 Hours Later Live Blood Test

With QLink A – ~72 Hours Later Live Blood Test

Dr Young reports little or no visible changes in the live or dried blood tests between the baseline micrographs and the micrographs taken after wearing QLink A.

4  Appendix A

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

Example Blood Micrographs from Test Subject in Group B – Real QLink

Without QLink B – Baseline With QLink B ~72 Hours Later Live Blood Test Live Blood Test

In the examples above, Dr Young reports significant visible changes between the Baseline and With QLink micrographs. The baseline micrographs show irregular shaped red blood cell organization with a “stacking” condition while the With QLink micrograph indicates more symmetrical, round shaped red blood cells. The cells also appear separate and free flowing, which is necessary in delivering oxygen and the removal of cellular waste.

Without QLink B – Baseline With QLink B ~ 72 Hours Later Dried Blood Test Dried Blood Test

To micrographs go to: http://www.qlinkproducts.com/pdf/young.pdf

In the above micrographs, Dr Young reports significant changes between the Baseline and With QLink Dried Blood Test. Evidence of several “clear” or white areas through the center of the red blood cell conglomerate is seen in the Baseline micrograph. Dr Young suggests that this indicates an abnormal blood clot or hypo-coagulation condition associated with lack of exercise, diet, adrenal and psychological stress. The With QLink micrograph indicates hyper-coagulation of the dried blood, which is a normal profile. Note that the large white protein mass in the center has filled in.

Does The Radiation From A Cell-Phone or a Cel-Phone Router Destroy Life?

After this you will think twice before putting your cell phone near your head!

cell phone

Five girls in the 9th grade in a school in Denmark have performed a very interesting experiment, which drew huge attention of people worldwide. The images that are placed on the Internet caused a stormy reaction of many researchers, biologists and experts on radiation from England, the Netherlands and Sweden.

The experiment consisted in the fact that they watched the development of seed of identical plants in two rooms with identical position to the sun, an equal amount of water when they were watered and the same temperature. In one room was placed router for wireless internet that emits the same type of radiation as an ordinary mobile phone, and in another room there was none.

After 12 days, the germinated seeds next to the router, hadn’t grown, and some of them were mutated or completely dead. The plants resulting from the seeds that were in a room without radiation progressed normally and were completely healthy. The young researcher actually wanted to draw attention to how mobile phones, which most of us at keep beside the bed close to the head at night, help with sleep and concentration, but such a thing was impossible to measure in school, so they opted to show on the plants.

Ever since they saw the result of the experiment, they no longer sleep with their phone next to the bed. “It’s scary that radiation has such a negative impact on living creatures, and everyone must pay attention to this. During the night, turn your phone off or put it in another room also, turn your computer off before going to sleep, “– says Leah Nielsen, one of the young scientists.


What to say after all of this? The experiment proved how much radiation is harmful, and you may want to consider carefully whether or not you’ll continue to keep your phone close to you during the night (or day).

source: worldtruth.tv

– See more at: www.phoreveryoung.com

The Cure for Cancer? That’s an easy question to answer! The Cure for Cancer is Found in its Prevention NOT in its Treatment! – Dr. Robert O. Young

Do you know what rotten apples, grapefruit or bananas look like? If you do then you know what cancer cells look like. Cancer cells are nothing more that healthy cells that are spoiling because of a compromised environment! Look at the picture below and you will see colorized cancerous body cells rotting in their toxic acidic environment.

What compromises the internal environment of a human body that causes body cells to begin spoiling and rotting? The answer is simple! The body’s build-up of acidic metabolic and dietary waste that has not been properly eliminated through the four channels of elimination – urination, defecation, respiration and perspiration!

Cancer is not a noun but an adjective that describes what is happening to body cells in an acidic environment due to an acidic lifestyle and diet. www.phoreveryoung.com
To learn more about Dr. Robert O. Young go to: https://www.linkedin.com/in/drrobertoyoung
To read more of Dr. Young’s articles go to: www.phoreveryoung.wordpress.com
To join Dr. Young on Twitter go to: @drrobertyoung
To watch more videos on YouTube go to: https://www.youtube.com/user/pHMiracleCenter
Join Dr. Young on Facebook at: The PH Miracle Medical Association or The pH Miracle
To purchase Dr. Young’s books or nutritional productts go to: www.phoreveryoung.com or www.phmiracle.com

Research Reveals That Coconut Oil Is Great For Cleaning and Whitening Teeth!

Virgin Coconut Oil has been lauded as the miracle oil – a super food good for everything from salad dressings to morning smoothies. It’s been shown to soothe improve digestion and metabolism as well as reducing acids that cause the increase of acid-binding cholesterol and increasing energy.


Coconut oil needs a prominent place in your bathroom as well as your kitchen. Many people are discovering the benefits of virgin coconut oil for hair, cosmetic health such as soothing rashes as well as conditioning hair and skin. Now, toothpaste gets a big overhaul with nature’s pH miracle oil, too.
Coconut oil has been known to support the immune system, buffer metabolic and dietary acids, support organ health – all benefits that also translate to oral health.
Swishing coconut oil around in your mouth daily, a technique called oil pulling, also helps to remove acids from the mouth and body. Incorporating these health benefits to your daily routine will lead to healthier teeth and gums, fresher breath, and will decrease toxic acidic side-effects of commercial toothpastes.
Coconut oil toothpaste is easy and inexpensive to make. It only requires a few ingredients to make enough for several uses.
Step-by-Step guide to making your own Coconut Oil Toothpaste
-Prepare and clean a small jar with a tight lid. A baby food jar or small Mason jar will do.
-Mix 1 part Coconut Oil with 1 part pH Miracle pHour Salts of sodium and potassium bicarbonate.
-Add 3-5 drops of Sweet Orange, Peppermint, or other food-grade essential oils to flavor.
-Allow your paste to cool and set.
Then simply apply this paste to your toothbrush and brush your teeth as you normally would. Coconut oil on its own can also double as a refreshing mouth wash in between brushing.
This homemade coconut oil toothpaste will clean and whiten your teeth, with the baking soda adding a gentle abrasive agent. It will help fight gum disease and tooth decay. The health quality of this pH miracle oil means your teeth get powerful detoxifying paste without the harmful chemicals found in regular toothpaste.
To order pH Miracle pHour salts go to: http://www.phoreveryoung.com or http://www.phmiracle.com

Diagnostic Medical Thermography


Carolyn Dean MD ND

I remember speaking at the American Medical Women’s Association and getting into an argument with a woman radiologist. I was asking, and quite politely I thought, why she didn’t consider Thermography a safer tool to screen for breast cancer than radiating the body with mammogram X-rays. You would have thought I killed her first-born…and maybe that was her fear. Taking away her livelihood and her favorite tool. We have known for over a decade that Mammograms do NOT save lives. Now in the past couple of years researchers have finally come to recognize that mammograms can cause cancer with their cumulative ionizing radiation.

So, what’s a girl to do? Why are we still getting our breasts smashed and irradiated with cancer causing X-rays? Good question. My advice? Find a good Thermography practitioner and get periodic testing. Even if you have to fly to LA to do it! I’m serious.

While in LA last month I visited with my friend, Dr. Galina Migalko, a medical doctor who is skilled in Medical Thermography and Diagnostic Ultrasonography. Dr. Galina operates from her center Universal Medical Imaging Group in Los Angeles, CA and the pH Miracle Living Center in Valley Center, California.

Thermography is a painless, non invasive, adjunctive state of the art clinical test without any exposure to radiation and is used as part of an early detection program which gives women of all ages the opportunity to increase their chances of detecting breast disease at an early stage. One of the reasons Mammography doesn’t save lives is that it is too late when it detects tumors. But Thermography may detect breast cancer years earlier than Mammography. Dr. Galina does much more than breast Thermography. Looking through her computerized full body Thermography scans I was amazed at what could be discerned about a patient’s health.

Instead of chopping up the body into individual parts and doing testing, Dr.Galina prefers to get a full picture of the body and put all the pieces together to create an overall diagnosis. If she finds something on Thermography, she can immediately use Ultrasound to learn more if needed. This is far superior to having to wait and worry for weeks to do follow up testing on something that may have shifted in the meantime. Diagnostic Medical Thermography and Ultrasound are complimentary tests. When using these two diagnostic tests together the diagnostic sensitivity goes up to over 95%. And how much more sane than the latest “fad” of doing full body CT Scans with radiation doses equivalent to hundreds of chest X-rays.

Thermography is unique in that it shows physiology or “what’s happening” in the tissues as opposed to CT’s, MRI’s and other static pictures of simple anatomy. It is the only imaging test that can show pain, inflammation, lymphatic congestion, and more. This testing is not just for women! Thermography can detect early signs of arthritis, neck and back pain, dental infections, headaches and sinus infections, immune dysfunction, fibromyalgia, carpal tunnel syndrome (CTS), digestive disorders, bursitis, ligament or muscle tears, nerve problems, as well as screen for strokes and detect cancer in the very early stages.

Dr. Galina Migalko is also a trained and experienced Naturopath who can offer a treatment program based on your results so that preclinical conditions detected long before they become pathologic can be eliminated. So, I suggest that when you bring your kids to Disneyland, stop by and consult with Dr. Galina and stay “the picture of health.” For more information please go to the Universal Medical Imaging Group website: www.universalmedicalimaging.com or www.phoreveryoung.com or http://www.phmiracle.com
(818)508-8895 – 760-484-1075




If you are looking to learn more about alkalinity and would like to see the same results in your own weight loss then read The pH Miracle for Weight Loss by Dr. Robert O. Young – http://www.phoreveryoung.com. Whether you need to lose 10 pounds or 200 pounds the pH Miracle is a lifestyle NOT a die-it and you can sustain your weight loss. There are four great books to read to help you along the way The PH Miracle  and The pH Miracle for Weight Loss by Dr . Robert O Young, The Whole Heart Solution by Dr Joel Kahn and Fats that Heal and Fats that Kill by Udo Erasmus

Healthy Alkaline Eating Reduces Cognitive Decline


A healthy diet may reduce your risk for cognitive decline, according to a study published in Neurology. Researchers analyzed diet records and cognitive health tests from 27,860 men and women as part of the ONTARGET (Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial) and TRANSCEND (Telmisartan Randomised Assessment Study in ACE Intolerant Subjects with Cardiovascular Disease) studies. Those who consumed the most fruits, vegetables, and whole grains had the lowest risk for cognitive decline after a 56-month observation period. This study hopes to shed more light on diet’s potential to curb cognitive decline.
Smyth A, Dehghan M, O’Donnell M, et al. Healthy eating and reduced risk of cognitive decline: a cohort from 40 countries. Neurology. 2015;84:1-8.

A Self-Care to a Self-Cure for Oxidative Stress, Aging, and Diabetes!

The testimony and before and after pictures of Laurence Yap‎ who has been following The pH Miracle Protocol for over one year!
My 2nd round of pH Miracle intensive cleansing took place this April-May of 2015. The 1st time following the pH Miracle Whole Body Cleanse was carried out in January of 2014. Following the pH Miracle Protocol I was successful in reducing my blood sugar levels from 13 mmol (abnormal or diabetic) to 5 mmol (normal or non-diabetic). There were two pictures taken before the pH Miracle diet in 2013.
Many people asked me why am I looking younger and glowing. My ex-colleagues have told me that I looked younger than I was nine years ago.I told them I am following the pH Miracle alkaline lifestyle and  diet.
I still experience a healing crisis periodically as I continue to live the pH Miracle alkaline diet to rejuvenate and reverse the aging of my body.
If you study the research of Dr Daug Kauffman (Fungus), Dr John Bergmen (Chiropractic) and Dr. Barbara O Neil, they are all fall back to the framework advocated by Dr. Robert O. Young and  pH Miracle  Protocol for human biological Health – alkalinity, pleomorphism and thinking.
Dr Robert Young’s pH Miracle science is indeed a NEW BIOLOGY.  It has proven to be the solution for my health recovery. I have tried many methods before and the pH Miracle Lifestyle and Diet is the ONLY method that has had lasting impact on my physical and emotional health!
Bottom-line the pH Miracle Protocol works! I hope by experience will encourage others who are following or who want to follow to continue or to start pH Miracle Lifestyle and Diet.
All I can say is endure the pains for the healing will come.  It did for me!
%d bloggers like this: