Category Archives: Science Based Medicine

Are YOU Following a LIVE-IT or a DIE-IT?

An Acidic Diet and Lifestyle Is More Deadly Than Smoking and the Cause of Heart Attacks, Diabetes and Cancer!
0-23
 
A new landmark study published in the Lancet found that, poor or acidic diet is responsible for more than 1 in 5 deaths globally, making it more deadly than tobacco.
56490433_2279593142307593_6088655710231461888_o
 
Consuming both low amounts of healthy alkaline foods and high amounts of unhealthy acidic foods are key to these findings.
 
These unhealthy highly acidic foods include, beef, chicken, pork, duck, turkey, fish, dairy, eggs, vinegar, sugar, alcohol, vinegar, carbonated drinks, energy drinks, coffee, black tea, just to name a few.
56757529_2279600538973520_7246026650633109504_n
 
The healthy alkaline foods include, low sugar fruit like tomato, avocado, grapefruit, cucumber, peppers of all colors, lemon and lime and vegetables, such as broccoli, spinach, arugula, celery, cabbage, cauliflower, brussels sprouts, just to name a few.
56664585_2279600528973521_7437041455652143104_n
 
What you put on your plate can play a serious role in how likely you are to die before your time: According, to the study, a poor or acidic diet is actually the leading cause of death worldwide, contributing to more of them than conventional risk factors like tobacco use.
Screen Shot 2019-01-22 at 1.52.33 PM
 
In the study, researchers analyzed food consumption habits of adults ages 25 and older from 1990 to 2017 in 195 countries and compared how their diet affected their chances of premature death.
Screen Shot 2019-04-07 at 7.43.21 AM
 
They found that in 2017, 11 million deaths—or 22 percent—worldwide were caused by a poor acidic diet. More specifically? Of these deaths, 9.5 million were due to cardiovascular disease, over 900,000 to diet-related cancers, over 330,000 to diabetes, and over 136,000 to kidney diseases.
 
On the other hand, more commonly known risk factors like high blood pressure and tobacco use was linked to 10.4 million and 8 million deaths, respectively. Researchers also found that a poor acidic diet is linked to more years lived with disability, too.
 
According to Dr. Robert O Young at the pH Miracle Research Center, USA, “an acidic diet is an equal opportunity killer and the number 1 cause of ALL sickness and disease!”
download-11
 
The following are the references to this very important 27 year Lancet published study validating the work of Dr. Robert O Young, who suggested in 1984 that there is only one sickness, one disease and one treatment.
 
This one sickness and one disease was described by Dr. Young as the over-acidification of the blood and interstitial fluids of the Interstitium due to an inverted way of living, eating, drinking, breathing, thinking and believing. He then suggested that there was only one treatment in order to restore the alkaline design of the body fluids by using an alkaline lifestyle and diet as described in his research, published papers and books, such as, A Nutritional Approach to the Prevention and Treatment of Any Cancerous Condition, The pH Miracle, The pH Miracle revised and update, The pH Miracle for Weight Loss, The pH Miracle For Diabetes, The pH Miracle for the Heart and The pH Miracle for Cancer.
0-73
 
You can find Dr. Young’s published research and books at: https://www.amazon.com/Robert-O.-Young/e/B001ILKCSU?ref=dbs_p_ebk_r00_abau_000000 or on his website at: drrobertyoung dotcom
0-69
 

References

 
1. Health effects of dietary risks in 195 countries, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017
GBD 2017 Diet Collaborators
Open AccessPublished:April 03, 2019DOI:https://doi.org/10.1016/S0140-6736(19)30041-8
 
2. Willett WC Stampfer MJ
Current evidence on healthy eating.
Annu Rev Public Health. 2013; 34: 77-95
 
3. Norat T Chan D Lau R Aune D Vieira R Corpet D
The associations between food, nutrition and physical activity and the risk of colorectal cancer.
Date: Oct, 2010
Date accessed: December 12, 2016
 
4. World Cancer Research Fund/American Institute for Cancer Research
Diet, nutrition, physical activity and cancer: a global perspective. Continuous Update Project Expert Report.
Date: 2018
Date accessed: February 19, 2019
 
5. Micha R Shulkin ML Peñalvo JL et al.
Etiologic effects and optimal intakes of foods and nutrients for risk of cardiovascular diseases and diabetes: systematic reviews and meta-analyses from the Nutrition and Chronic Diseases Expert Group (NutriCoDE).
PLoS One. 2017; 12: e0175149
 
6. Micha R Kalantarian S Wirojratana P et al.
Estimating the global and regional burden of suboptimal nutrition on chronic disease: methods and inputs to the analysis.
Eur J Clin Nutr. 2012; 66: 119-129
 
7. Colditz GA
Overview of the epidemiology methods and applications: strengths and limitations of observational study designs.
Crit Rev Food Sci Nutr. 2010; 50: 10-12
 
8. Nishida C Uauy R Kumanyika S Shetty P
The joint WHO/FAO expert consultation on diet, nutrition and the prevention of chronic diseases: process, product and policy implications.
Public Health Nutr. 2004; 7: 245-250
 
9. Lloyd-Jones DM Hong Y Labarthe D et al.
Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association’s strategic Impact Goal through 2020 and beyond.
Circulation. 2010; 121: 586-613
 
10. McGuire S
U.S. Department of Agriculture and U.S. Department of Health and Human Services, Dietary Guidelines for Americans, 2010.
7th Edition. U.S. Government Printing Office, Washington, DC; January 2011Adv Nutr. 2011; 2: 293-294
 
11. Lim SS Vos T Flaxman AD et al.
A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010.
Lancet. 2012; 380: 2224-2260
 
12. Forouzanfar MH Alexander L et al.GBD 2013 Risk Factors Collaborators
Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013.
Lancet. 2015; 386: 2287-2323
 
13. GBD 2015 Risk Factors Collaborators
Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015.
Lancet. 2016; 388: 1659-1724
 
14. GBD 2016 Risk Factors Collaborators
Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016.
Lancet. 2017; 390: 1345-1422
 
15. Mozaffarian D Fahimi S Singh GM et al.
Global sodium consumption and death from cardiovascular causes.
N Engl J Med. 2014; 371: 624-634
 
16. Singh GM Micha R Khatibzadeh S et al.
Estimated global, regional, and national disease burdens related to sugar-sweetened beverage consumption in 2010.
Circulation. 2015; 132: 639-666
 
17. Singh GM Micha R Khatibzadeh S et al.
Global, regional, and national consumption of sugar-sweetened beverages, fruit juices, and milk: a systematic assessment of beverage intake in 187 countries.
PLoS One. 2015; 10: e0124845
 
18. Micha R Khatibzadeh S Shi P et al.
Global, regional and national consumption of major food groups in 1990 and 2010: a systematic analysis including 266 country-specific nutrition surveys worldwide.
BMJ Open. 2015; 5: e008705
 
19. Micha R Khatibzadeh S Shi P et al.
Global, regional, and national consumption levels of dietary fats and oils in 1990 and 2010: a systematic analysis including 266 country-specific nutrition surveys.
BMJ. 2014; 348: g2272
 
20. Wang Q Afshin A Yakoob MY et al.
Impact of nonoptimal intakes of saturated, polyunsaturated, and trans fat on global burdens of coronary heart disease.
J Am Heart Assoc. 2016; (published online Jan 20.)
DOI:10.1161/JAHA.115.002891
 
21. Schmidhuber J Sur P Fay K et al.
The Global Nutrient Database: availability of macronutrients and micronutrients in 195 countries from 1980 to 2013.
Lancet Planet Health. 2018; 2: e353-e368
 
22. Gakidou E Afshin A Abajobir AA et al.
Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016.
Lancet. 2017; 390: 1345-1422
 
23. Singh GM Danaei G Farzadfar F et al.
The age-specific quantitative effects of metabolic risk factors on cardiovascular diseases and diabetes: a pooled analysis.
PLoS One. 2013; 8: e65174
 
24. Mente A O’Donnell M Rangarajan S et al.
Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies.
Lancet. 2016; 388: 465-475
 
25. Trinquart L Johns DM Galea S
Why do we think we know what we know? A metaknowledge analysis of the salt controversy.
Int J Epidemiol. 2016; 45: 251-260
 
26. GBD 2016 Causes of Death Collaborators
Global, regional, and national age-sex specific mortality for 264 causes of death, 1980–2016: a systematic analysis for the Global Burden of Disease Study 2016.
Lancet. 2017; 390: 1151-1210
 
27. Djalalinia S Saeedi Moghaddam S Moradi-Lakeh M et al.
Prevalence and years lived with disability of 310 diseases and injuries in Iran and its neighboring countries, 1990–2015: findings from Global Burden of Disease Study 2015.
Arch Iran Med. 2017; 20: 392-402
 
28. WHO
Global action plan for the prevention and control of noncommunicable diseases: 2013–2020.
Date: 2013
Date accessed: December 12, 2016
 
29. WHO
2008–2013 action plan for the global strategy for the prevention and control of noncommunicable diseases: prevent and control cardiovascular diseases, cancers, chronic respiratory diseases and diabetes.
World Health Organization, Geneva; 2009
 
30. Afshin A Penalvo J Del Gobbo L et al.
CVD prevention through policy: a review of mass media, food/menu labeling, taxation/subsidies, built environment, school procurement, worksite wellness, and marketing standards to improve diet.
Curr Cardiol Rep. 2015; 17: 98
 
31. Mozaffarian D Afshin A Benowitz NL et al.
Population approaches to improve diet, physical activity, and smoking habits: a scientific statement from the American Heart Association.
Circulation. 2012; 126: 1514-1563
 
32. WHO
Interventions on diet and physical activity: what works. Summary report.
World Health Organization, Geneva; 2009
 
33. Cobiac LJ Veerman L Vos T
The role of cost-effectiveness analysis in developing nutrition policy.
Annu Rev Nutr. 2013; 33: 373-393
 
34. Bibbins-Domingo K Chertow GM Coxson PG et al.
Projected effect of dietary salt reductions on future cardiovascular disease.
N Engl J Med. 2010; 362: 590-599
 
35. Smith-Spangler CM Juusola JL Enns EA Owens DK Garber AM
Population strategies to decrease sodium intake and the burden of cardiovascular disease: a cost-effectiveness analysis.
Ann Intern Med. 2010; 152: 481-487
 
36. Owen L Morgan A Fischer A Ellis S Hoy A Kelly MP
The cost-effectiveness of public health interventions.
J Public Health. 2012; 34: 37-45
 
37. Lachat C Otchere S Roberfroid D et al.
Diet and physical activity for the prevention of noncommunicable diseases in low- and middle-income countries: a systematic policy review.
PLoS Med. 2013; 10: e1001465
 
38. Downs SM Thow AM Leeder SR
The effectiveness of policies for reducing dietary trans fat: a systematic review of the evidence.
Bull World Health Organ. 2013; 91 (69H): 262
 
39. Anand SS Hawkes C de Souza RJ et al.
Food consumption and its impact on cardiovascular disease: importance of solutions focused on the globalized food system: a report from the workshop convened by the World Heart Federation.
J Am Coll Cardiol. 2015; 66: 1590-1614
 
40. Brown GW Yamey G Wamala S The handbook of global health policy. Wiley, Hoboken; 2014
 
41. Tilman D Clark M
Global diets link environmental sustainability and human health.
Nature. 2014; 515: 518-522
 
42. Auestad N Fulgoni VL
What current literature tells us about sustainable diets: emerging research linking dietary patterns, environmental sustainability, and economics.
Adv Nutr. 2015; 6: 19-36
 
43. Heller MC Keoleian GA Willett WC
Toward a life cycle-based, diet-level framework for food environmental impact and nutritional quality assessment: a critical review.
Environ Sci Technol. 2013; 47: 12632-12647
 
44. Sabaté J Soret S
Sustainability of plant-based diets: back to the future.
Am J Clin Nutr. 2014; 100: 476S-482S
 
45. Food and Agriculture Organization of the United Nations
Food consumption database.
Date accessed: December 12, 2016
 
46. Hill RJ Davies PS
The validity of self-reported energy intake as determined using the doubly labelled water technique.
Br J Nutr. 2001; 85: 415-430
 
47. McLean RM
Measuring population sodium intake: a review of methods.
Nutrients. 2014; 6: 4651-4662
 
48. Illner A-K Freisling H Boeing H Huybrechts I Crispim SP Slimani N
Review and evaluation of innovative technologies for measuring diet in nutritional epidemiology.
Int J Epidemiol. 2012; 41: 1187-1203

Three Ways to Reduce YOUR Chronic Pain

“Pain equals acid and acid equals pain. You cannot have one without the other. So get off your acid and go to health!”  Dr. Robert O. Young
download-30
Chronic pain is reaching epidemic levels because interstitial fluid acidity of the Interstitium is reaching chronic levels. Statistics show that either you or someone you are close to suffers from chronic acid causing pain.
​And that number dramatically increases if you are 60 years and older. Why? Because older people and their body cells are generally swimming in a pool of acid! You have probably heard me sat, “you don’t get old you mold! or When the fish is sick don’t treat the fish change the water!”
And chronic acidic pain, caused by what you eat, what you drink, what you breathe, what you think, and what you believe is not just a daily inconvenience, it makes almost every important area of your life more difficult.
 

​Chronic Acidic Pain Can:

Make it difficult to do your favorite activities, so you might feel powerless and out of control in your life;

Cause you to have a bad mood so you don’t really enjoy time with friends and family;

Make it harder to achieve your goals because you have trouble getting around and staying focused on what you are doing.

Chronic acid causing pain is so serious that some people are choosing to get surgery. For example, some people with chronic acidic pain in their rotting knees are choosing replacement surgery. The challenge with knee replacement surgery is that it can cost $50,000 per knee and require 3 months to heal – if you ever heal because you are still living an acidic lifestyle.

And, in addition recovery is impossible until you give up the acidic lifestyle and diet that is responsible for the pain.

BUT, I have some good news for you…

There are ways that you can reduce and even eliminate your chronic acidic pain without expensive or painful surgery.

3 Ways to Reduce or Eliminate Your Chronic Pain

1: Physical Therapy and Exercise

This is a great option for two reasons, first because it works, and second because it improves your overall alkaline health.

For example, did you know that exercise can open up the channels of elimination to remove the dietary and metabolic acids that are causing bone and muscle loss and ALL your pain?

And as you might know from reading The pH Miracle, removing acidic waste from the interstitial fluids of the Interstitium can help you heal throughout your body and significantly reduce and eliminate your pain.

The best way to pursue effective physical therapy and exercise for chronic acidic joint pain is to see a specialist or a pH Miracle Coach.

2: Avoid Inflammatory Acidic Foods (Check out the List Below)

A lot of chronic pain is caused by chronic inflammation. and chronic inflammation is caused by acidic lifestyles and diets. For example, many cases of arthritis are caused or triggered by chronic inflammation from eating beef, chicken, pork, duck and fish.

 
​It is important to remember that the food that you eat, drink or even think about is one of the biggest causes of inflammation.

Here are three foods that are causing massive inflammation, and therefore contributing to chronic acidic pain:

A. Eliminate Sugar in All of its Forms!

Check out the list below for all the sugary fruit you need to eliminate in order to reverse chronic acidic pain.

 

B. Eliminate Saturated Acidic Vegetable oil and Trans Acidic Fats

Vegetable oils and trans fats are high in damaging saturated acids (not to be confused with healthy unsaturated oils that can adsorb and absorb the metabolic and dietary acids that causes inflammation that leads to chronic pain.

And, generally saturated acidic oils don’t even taste that good!

There are lots of healthy and tasty alkalizing oils you can use instead:

avocado oil

extra-virgin olive oil

walnut oil

hemp oil

flax, and

borage oil,

just to name a few.

 C. Eliminate All Animal Flesh (bacon, bologna and lunch meat)

A lot of “conventional” acidic meat causes inflammation because ALL animal muscle is highly acidic and causes a double loss of alkalinity in the body fluids that leads to ALL sickness and disease.

download-29

For example, many cows today are fed genetically modified corn, but cows did not evolve eating corn, they evolved eating green alkalizing-blood building grass. Feeding a cow food that isn’t healthy undoubtedly produces negative acidic side-effects for the animal, just like you eating unhealthy food causes negative acidic side-effects in you.

Highly-processed meats like bacon, bologna, and lunch meat are some of the most inflammatory meats because of their high concentrations of acidic nitrates. Not only are the animals often raised in unhealthy ways, but the meat is often treated with acidic chemicals that cause inflammation.

So, if you want to reduce and eliminate your chronic acidic pain, any animal flesh or animal blood you eat should be completely eliminated!

3: Start Alkalizing with the pH Miracle Protocol NOW!

Perhaps the easiest and longest-lasting solution to your chronic acidic pain is get a copy of the pH Miracle revised and updated and start reversing your chronic acidic pain NOW!

To order YOUR pH Miracle revised and updated book go to: https://www.amazon.com/gp/product/0446556181/ref=dbs_a_def_rwt_bibl_vppi_i0

Tom Brady’s pH Alkaline Lifestyle and Diet

New England Patriots quarterback Tom Brady — a five-time Super Bowl Champion and three-time NFL MVP — is widely considered to be one of the greatest athletes of all time. Lately, however, Brady has been following an alkaline lifestyle and diet.

In September 2017, Brady released his book, The TB12 Method: How to Achieve a Lifetime of Sustained Peak Performance. In this book, Brady detailed exactly what he eats every day. One main feature of his diet is liberal amounts of alkaline foods and liquids.

 

In the mornings, Brady doesn’t eat a full meal. When he wakes up at 6:00 am, he drinks 20 ounces of alkaline water infused with electrolytes, including sodium, potassium, magnesium and calcium. He then drinks a smoothie and/or juices containing alkalizing grasses, vegetables, fruit, nuts and seeds. Two hours later, he has another glass of alkaline electrolyte-infused water, and a post-workout protein shake. Brady claims to drink somewhere between 12 and 25 glasses of alkaline water per day.

 

He also heavily encourages snacking. He usually snacks at around 11:00 am, just before lunch. For lunch, Brady will usually have a piece of fatty fish like salmon and a lot of green vegetables. In the afternoon, he may have another protein shake or protein bar, and around 6:00 pm, Brady eats dinner, which, again, consists of mostly green vegetables.

His book provides recipes for green juices, green soups, green salads, and a few carbohydrate recipes such as his pasta dish — which is odd, considering that he supposedly rarely eats carbs. But even Brady treats himself sometimes. He doesn’t often eat dessert, but he does give a recipe for his famous alkaline avocado ice cream.

 

His book also contains several alkalizing rules for eating. Brady won’t eat carbohydrates and protein together. He recommends eating carbs or protein with green vegetables instead, as he knows that this is better for assimilation and elimination.

Brady’s chef Allen Campbell says that 80 per cent of his diet is green vegetables and the rest of his diet is grass-fed organic steak and wild salmon.

Brady follows what he refers to as an alkaline lifestyle and diet created by Robert O. Young PhD, in order to minimize muscle inflammation caused by the buildup of lactic acid in the interstitial fluids of the Interstitium (see illustration below). This entails limiting ‘acidifying foods,’ which mostly includes starchy foods like potato, pasta, bread and ALL dairy products.

What is even more interesting is the list of acidic foods that Brady doesn’t eat. For Brady, caffeine, white sugar, white flour, dairy, and some nightshade vegetables —  eggplant and mushrooms — are completely off the table. He also won’t consume olive oil if it’s used in cooking — but he’ll have it raw. And he won’t eat high sugar fruit, unless it’s in a smoothie.

Since there are profound benefits with Brady’s pH alkaline diet, and it is clearly sustaining his play on the field, there a 100’s of specific health and fitness benefits of the pH alkaline lifestyle and diet which are backed by published scientific evidence.

 

He claims that limiting acidic foods helps control the body’s pH balance. What one eats, drinks, breaths and thinks has a huge effect on the body fluids, including the blood plasma, interstitial and intracellular fluid pH which is ideal at 7.365.

Brady also knows that the alkaline lifestyle and diet can decrease the lactic acids that causes inflammation in the body, leading to ALL sickness and disease, including connective tissue disorders that can end an athlete’s career.

 

At 41 years young, which is considered ancient in football years, Brady says he wants to play at least another five years. While he is certainly capable, his pH Miracle lifestyle and diet will be a major reason he WILL achieve HIS goal.

To learn more about the pH alkaline lifestyle and diet read The pH Miracle revised and updated – http://www.phoreveryoung.com

To learn more about the lifestyle and attend a pH Miracle Retreat in Marbella, Spain or Sardenia, Italy, go to: http://www.phmiracleretreat.com

How Healthy is Your Blood?

“Scare Forms” “Yeast” & “Parasites” in Live Unstained Blood!

The live blood cell micrograph above is showing a “scare forms” with yeast (Y-form) and a Trypanosoma brucei parasite and always an indication of metabolic acidosis or decompensated acidosis of the interstitial fluids of the Interstitium and blood. (pH below 7.365) These “scare forms” with parasites and yeast are always associated with a serious health challenge and an acidic lifestyle and diet!

Read – Nutritional Cellular Microscopy: Live and Dried Blood Profiles by Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner – To order go to: https://www.amazon.com/gp/product/B01JVK48XE/ref=dbs_a_def_rwt_hsch_vapi_taft_p1_i10

The blood micrograph also shows just under the “Scare Form” a Trypanosoma brucei parasite as seen in live human blood through the eyes of pHase contrast microscopy.

If you are eating raw or uncooked meat (beef, chicken, pork) or fish (especially raw) you are at a 99 percent risk for “scare form”, “yeast” and “parasites”.

Blood parasites are at epidemic levels today in the USA and not just in 3rd World countries. To learn more read Sick and Tired, Reclaim Your Inner Terrain by Robert O Young PhD. To order go to: https://www.amazon.com/Sick-Tired-Reclaim-Inner-Terrain/dp/1580540562/ref=la_B001ILKCSU_1_5?s=books&ie=UTF8&qid=1519008562&sr=1-5&refinements=p_82%3AB001ILKCSU

SuperGreens – The World’s First Organic Vegetable, Fruit and Grass Powder!

InnerLight SuperGreens – by Dr Robert O. Young – The Original Super Greens Powder – 49 Grasses, Leaves, Vegetables, Sprouts & Herbs – Organic & Wild Crafted Ingredients – Great Tasting – No Cameron Fillers

Screen Shot 2018-07-13 at 4.40.04 AM

About the product

ORIGINALLY CREATED IN 1988 by Dr. Robert Young (author of the best-selling pH Miracle books), this product was one of the 1st greens powders on the market and has stood the test of time, helping thousands of people maintain their health.
ALL THE GREENS YOUR BODY NEEDS – InnerLight SuperGreens is a super-concentrated organic combination of 49 different grasses, leaves, vegetables, sprouts, and herbs
Screen Shot 2018-07-13 at 4.41.07 AM
DOES NOT CONTAIN any fillers, artificial sweeteners, colorings, flavorings, additives, preservatives, spirulina, algae, mushrooms or probiotics.
MICRO FINE POWDER that makes it easy to mix with water and consume.
CHILDREN LOVE THE TASTE of the InnerLight SuperGreens powder which gets them started on the road to Optimal Health.

Product description

Screen Shot 2018-07-13 at 4.40.47 AM

 InnerLight SuperGreens is a super-concentrated organic combination of 49 different grasses, leaves, vegetables, sprouts & herbs; all the “greens” your body needs. Originally created in 1988 by Dr. Robert Young (author of the best-selling pH Miracle books), this product was one of the 1st greens powders on the market and has stood the test of time, helping thousands of people maintain their health.
Tony Robbins, internationally known motivational speaker, talked about InnerLight SuperGreens in a 1 1/2 hour “Power Talk” interview he did with Dr Robert Young in the early 2000’s. This helped get the word out about our excellent product.
Tony-robbins
InnerLight SuperGreens powder is a micro fine powder which makes it easy to mix with water and digest. The greens powder smells great and has a mild taste.
InnerLight SuperGreens DOES NOT CONTAIN any fillers, artificial sweeteners, colorings, flavorings, additives, preservatives, spirulina, algae, mushrooms or probiotics. Our product is also formulated with Non GMO ingredients.
SuperGreens powder has four times the power of ordinary green powders. Drinking InnerLight SuperGreens is the quickest way to get a high concentration of chlorophyll which can assist with building healthy cells.
As Dr Young says, “When the Fish is Sick, Change the Water”. SuperGreens is an organic, colloidal, concentrated, charged high frequency food. There is nothing else like it. We invite you to commit to a 120-day program and take your health to the next level.
0-8
If you’re worried that you’re not getting enough greens in, InnerLight SuperGreens is the answer for you.
Try some InnerLight SuperGreens today!
p.s.- We have a “no-quibble guarantee” so you have nothing to lose!
Screen Shot 2018-07-13 at 4.39.47 AM

Where There Is Salt There Is Life

0-6

Harvested from the sea or wrested from the earth, salt would appear to be one of the humblest commodities. Yet the sodium it contains is a life-sustaining element.

Sodium chloride is essential in the nutrition and physiological processes of all animals including man.

From long before the first written word, there are repeated references in records and stories to the importance of salt as an essential in the daily diet.

Salt has not only ensured the survival of mankind, but colored the species food, religions, politics and superstitions. In ancient times, because of its power to preserve and purify, salt was spilled upon legal documents to symbolize enduring agreement and freedom from deceit. Mans effort to obtain salt can be traced back through history for salt has always been essential to human life.

Salt is more precious than gold

 

Ancient manuscripts tell us that more than 5000 years ago the Chinese obtained salt by boiling and evaporating the ash from seaweed. Later, people along the Mediterranean and Red Seas discovered that when seawater was evaporated by the sun, salt was left behind.

 

This was the start of salt manufacturing and the same method of solar evaporation is used today in the production of many salts around the world.

Roman legionnaires who guarded the Via Solaria, one of the most famous military roads in history, received part of their pay in salt, their ‘salarium.’ From this came the modern word ‘salary.’

 

To this day a good man is ‘worth his salt’ and we take others’ dramatic pronouncements ‘

Many of salt’s applications, including salting of fish and meat to preserve it, have remained almost unchanged down through the millennia. Its place in our superstitions and sayings remains entrenched.

Enshrined in the World’s many cultures and a vital part of global economies, salt is as essential to life as the air we breathe and the water we drink.

Surely there can be no product purer, more natural or environmentally friendly than salt – pure salt water provided and evaporated by Nature, harvested to perfection by Man.

Making salt in open pans is not new. In Mark Kurlansky’s recent book, ‘Salt A World History’, he suggests that in 450 B.C. a Chinese called Yi Duan ‘is believed to have made salt by boiling brine in iron pans, an innovation which would become one of the leading techniques for salt making for the next 2,000 years.’

Rapid boiling is still used today but the open pans have been replaced by closed vessels, outputs have increased and the salt these plants produce has a uniform cubic crystal shape.

In a move back to the open evaporating pans of the past, I developed the Great Salt Lake

North Shore salt beds. The raw material for this salt is the combination of the snow melt run off from theRocky Mountains in northern Utah and the salty North Shore waters of the Great Salt Lake at the base of the Rocky Mountains. These waters are evaporated using the natural processes of sun and wind. From this, a colloidal salt is produced to feed the open evaporating salt beds for making the worlds only 26% colloidal liquid mineral salt we call Young pHorever pH Miracle pHlavor mineral salts!

 

http://www.phmiracleliving.com/phlavor.htm

Interesting Facts About pHorever Young pH Miracle pHlavor Colloidal Mineral Salts

1) Our bodies contain almost 450 grams of salt and each day we need to replenish the salt used by our bodies to maintain our normal health, vigor and alkaline design.

2) Salt plays a big part in helping the body to digest food and turn them into living tissues, as well as helping to transmit nerve impulses that contract the muscles. In order for the cells of the body to function normally, a salt/water balance must be maintained. Salt is also necessary for making the sodium bicarbonate the body needs to alkalize the food we eat to maintaining the alkalinity of the blood and lymph fluids.

3) pHorever Young pH Miracle pHlavor colloidal mineral salt tastes great. Minerals present naturally in the salt from the Great Salt Lake North Shore as well as the crystal shape enhances its flavor therefore the salt can be used more sparingly.

4) pHorever Young pH Miracle pHlavor colloidal mineral salt contains higher levels of calcium and magnesium than normal sea or table salts, as these minerals are also naturally present in the Great Salt Lake North Shore water. Some people believe that this balance of minerals has beneficial effects on the body. Certainly we believe these minerals help enhance the taste of the pH Miracle pHlavor colloidal mineralsalt – taste it and compare to your current salt.

5) When you are tired and/or fatigued and need energy that is the need for salt. All sugar cravings are the need for salt.

6) Salt is the ion of life in which all energy is transported. Without salt there is no life.

7) Salt is what keeps the spirit body connected or joined with the physical body and mental body.

Features and Benefits of pHorever Young pH Miracle pHlavor Colloidal Liquid Salt

1) pHorever Young pH Miracle pHlavor colloidal mineral salt is an evaporated salt that produces a unique three dimensional crystal, it is produced by being very slowly evaporated naturally by the sun, allowing the formation of a 26% concentration of a heterogeneous mineral salt solution. The concentration of this salt is greater then the Dead Sea.

 

2) It is a very light textured salt with a delicate flavor. The taste is created by the unique crystal size and shape of the Young pHorever pH Miracle pHlavor colloidal liquid mineral salt.

3) Excellent for spraying on top of foods as its light texture means it ‘sticks’ better – ideal in particular for salting salads and other vegetables!

4) High surface area and low bulk density improves the product adherence. This makes it ideal for spraying on food or in your mouth directly to begin the alkalizing process.To order your bottle of the worlds first natural colloidal liquid mineral salt spray go to:

http://www.phmiracleliving.com/phlavor.htm

To learn more about the work, research and findings of Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner go to: http://www.drrobertyoung.com

safe_image-4

To register for a health and wellness Retreat go to: http://www.phmiracleretreat.com

Screen Shot 2018-05-19 at 1.55.10 AM

Second Thoughts About Viruses, Vaccines, and the HIV/AIDS Hypothesis

HIV-budding-Color

In the sciences, people quickly come to regard as their own personal property that which they have learned and had passed on to them at the universities and academies. If however, someone else now comes along with new ideas that contradict the Credo (that has been recited for years and passed on in turn to others) and in fact even threaten to overturn it, then all passions are raised against this threat and no method is left untried to suppress it. People resist it in every way possible: pretending not to have heard about it; speaking disparagingly of it, as if it were not even worth the effort of looking into the matter. And so a new truth can have a long wait before finally being accepted.

-Goethe

Viruses

Introduction

The first isolation of a virus was achieved in 1892 by Russian bacteria hunter Dimitri Iwanowski, who gathered fluid from diseased tobacco plants. He passed this liquid through a filter fine enough to retain bacteria; yet to Iwanowski’s surprise, the bacteria-free filtrate easily made healthy plants sick. In 1898 a Dutch botanist, Martinus Willem Beijerinck, repeating the experiment, also recognized that there was an invisible cause and named the infectious agent “tobacco mosaic virus.” In the same year as Beijerinck’s report, two German scientists purified a liquid containing filterable viruses that caused foot-and-mouth disease in cattle (viruses were at one time called “filterable viruses,” but eventually the term “filterable” came to apply only to viruses, and was dropped). Walter Reed followed in 1901 with a filtrate responsible for yellow fever, and soon dozens of other disease-causing viruses were found.

In 1935 another American, Wendell M. Stanley, went back to the beginning and created pure crystals of tobacco mosaic virus from a filtered liquid solution. He affirmed that these crystals could easily infect plants, and concluded that a virus was not a living organism, since it could be crystallized like salt and yet remain infectious. Subsequently, bacteriologists all over the world began filtering for viruses, and a new area of biology was born-virology.

Historically, medical science has vacillated on the question of whether a virus is alive. Originally it was described as nonliving, but is currently said to be an extremely complex molecule or an extremely simple microorganism, and is usually referred to as a parasite having a cycle of life. (The term “killed” is applied to certain viral vaccines, thus implying an official conviction that viruses live.) Commonly composed of either DNA or RNA cores with protein coverings, and having no inherent reproductive ability, viruses depend upon the host for replication. They must utilize the nucleic acids of living cells they infect to reproduce their proteins (i.e., trick the host into producing them), which are then assembled into new viruses like cars on an assembly line. Theoretically, this is their only means of surviving and infecting new cells or hosts.

{Key words: Vaccines, Vaccination, Virus, HIV, AIDS, Ebola, Hunta virus, Hepatitis C, Pleomorphism, Yeast, Candida albicans, Koch’s postulate, Farr’s law, Virology, Louis Pasteur, Antione BeChamp, Microzyma]

Birth of Virology-a Miscarriage?

Underlying the birth of virology was the doctrine of monomorphism-that all microorganisms (herein called microforms) are fixed species, unchangeable; that each pathological type produces (usually) only one specific disease; that microforms never arise endogenously, i.e., have absolute origin within the host; and that blood and tissues are sterile under healthy conditions. This last point warrants immediate comment. Theoretically, under ideal health conditions the blood might be sterile, though it has the inherent potential to develop morbid microforms, as discussed in the main text of this book. Long and repeated observation of live blood in the phase-contrast, dark-field microscope, however, shows that the blood can contain various microforms in an otherwise asymptomatic host, or in a condition defined as normal or healthy in orthodox terms. The forms are easily visible before other physical symptoms arise. (Since long and repeated observation has correlated their presence with other disease symptoms and their disappearance with the return of health, they serve as indicators of impending outward signs of disease.)

Monomorphism was the cornerstone of developments in 20th-century medical research and treatments. Refusal by the mainstream to examine fairly, much less accept, the demonstrated facts of pleomorphism-that viruses and bacteria (and also yeast and fungi) are evolutions from the microzyma (see Section 1 of this Appendix); that microforms can rapidly change their form (evolve and “devolve”) in vivo, one becoming another dependent upon conditions in the inner terrain (environment); that blood and tissues are not necessarily sterile; and that there are no specific diseases, but only specific disease conditions-was the foundation of a latter day “Galileo debate.” It is so called because those who wore the “robes” of scientific authority, reprising the religious fanatics who punished the noted astronomer for his truths, would not be swayed from folly when presented with its contrary proofs. These proofs began in earnest with Antoine Bechamp in the last century (who also endured the indignation of a fanatical clergy).

In the early third of the 20th century, the heated debate took place over filterable bacteria versus non-filterable. This was a major battle concerning micromorphology (discussed briefly below). The orthodox view prevailed: bacterial forms were not small enough to pass, or did not have a smaller, earlier stage. What passed through “bacteria-proof filters was something else, i.e., viruses. Standard medical textbooks long made this fdtering distinction between bacteria and viruses. Subsequently, however, the cellular nature of many filterable forms originally thought to be viruses, such as some mycoplasmas, rickettsias, and various other groups, has been established. In this writer’s opinion, with the victory of the monomorphic view, deeper understanding of infectious “disease” was lost, setting the stage for cancer, degenerative symptoms and AIDS.

What You See?

A typical bacterium is about 1 micron in size. Most filterable forms now called viruses range in size from .3 microns (300 millimicrons) to .01 micron (10 millimicrons)-partially in the colloidal range (.1 to .001 micron). Most of the larger viruses are a third to a quarter the size of the average bacterium. Size is critical because .3 microns is the resolution limit of modern-day light microscopes (except for the claimed resolution of Canadian microscopist Gaston Naessens’ Somatoscope, at .015 microns). Thus, as viruses were discovered (except for the very large ones, such as mumps), they required an electron microscope to be seen, especially given the fact that Royal Rife’s microscope technology and career were destroyed by vested interests (see Section 1). Unfortunately, electron microscopes and the process of chemical staining disorganize all specimens, whereas Rife’s technology allowed life to proceed and thus evolve under its lens. As viruses became visible to advancing technology, the ramification was that the technology revealed, to minds infected with monomorphism, protein structures deemed foreign to the body.

A New Theory

Formulated by Bechamp in the 19th century, microzymian principle is the basis of a new theory about “viruses.” Briefly, this principle holds that in all living organisms are biologically indestructible anatomical elements, which he called microzymas. They are independently living organized ferments, capable of producing enzymes and capable of evolution into more complex microforms, such as bacteria. Bechamp’s thesis is that disease is a condition of one’s internal environment (terrain); that disease (and its symptoms) are “born of us and in us”; and that disease is not produced by an attack of microentities but calls forth their endogenous evolution. (The common biological basis for this is discussed below.)

My studies and research suggest that the complexes science calls viruses and retroviruses originate in the cell as microzymian principle suggests. However, they are created in response to an alarming situation (condition of disease) for the purpose of genetic repair. They are repair proteins evolved from anatomical elements (microzymas), not pathogenic organisms.

It is known that normal cell activity includes genetic repair. Both enzymes and proteins must be involved. What is the mechanism? Viruses are organized around DNA or RNA, not both. Thus, they are quite probably intended to repair genetic molecules or other structures, and show up with disease symptoms because the body needs them. Since viruses require a living cell/host for reproduction, how do we know that the scenario is not set in motion for a purpose by the cell (i.e., its microzymas), rather than being the result of invasion? Because disease (disturbance of balance in the organism) is so prevalent, especially that which has not yet become indicated by common symptoms, repair proteins may be frequently or constantly present. A toxified cell may easily suffer localized damage to the genome. Since most observers are not even aware of microzymian principle, much less understand or even consider it, and since monomorphism stresses invasion, these protein complexes are regarded as foreign and disease is attributed to them.

Another note of interest is the size of viruses compared to the microzyma. Viruses are considered to be some of the smallest biological particles and are frequently of colloidal size: e.g., hepatitis A, 27 nanometers (.027 microns); hepatitis B (.042 microns); poliovirus (.03 microns); EBV (.042 microns); fflV (.080 to .12 microns), influenza (.08 to .12 microns); mumps (.15 to .30 microns); smallpox (.30 x .24 microns); and, according to Bechamp, the microzyma (.0005 microns). This coincides with what Gaston Naessens says about the size of his somatid, which ranges from “a few Angstroms to a tenth of a micron.”[1]

In his book, The Blood and Its Third Anatomical ElementBechamp states: “The microzyma is at the beginning and at the end of all organization. It is the fundamental anatomical element whereby the cellules, the tissues, the organs, the whole of an organism are constituted living. … In a state of health the microzymas act harmoniously and our life is, in every meaning of the word, a regular fermentation. In the condition of disease, the microzymas do not act harmoniously, the fermentation is disturbed, the microzymas have either changed their function or are placed in an abnormal situation by some modification of the medium.”[2]  The virus is either a self-ordered microzymian polymerization, or (less likely) a structure made by microzymas. It is enveloped in protein which is also composed of microzymas, and could well be thought of as an autonomous molecular tool box.

Along with Drs. Glen Dettman and Archie Kalokerinos, I wonder, “whether Bechamp’s writing anticipated, in some respects, the discovery of RNA and DNA?” Could the genetic structure be the construct, thus a tool, of the microzyma? They quote a personal communication (1974) from a Professor Bayev of the USSR Academy of Sciences, who discusses his work showing that molecular self-restoration from its parts of pure transfer RNA from brewer’s yeast is possible (see Section 1 of this Appendix for full quotation).[3]

In my own research I have found molecular restorations similar to that described by Bayev. In my experiment I used five-year-old coagulated capillary blood from a woman with cancer. With one drop of 0.9% of sodium chloride, the blood was restored to an appearance and level of activity characteristic of a freshly drawn sample. In other words, the anatomical microzymas of the dried blood were restored to activity. Even the white globules became active. One might eagerly ask for an explanation of the reversal of polymers made during clotting. It is unclear at this point how this reversal takes place, except to say that what can evolve apparently has the potential to devolve. It is observable, however. For example, I have seen, and recorded on video, rod microforms retrograding without any visible decomposition from 10 microns in length to the vicinity of .1 micron.

This research supports the very important postulate that the cell is not the smallest living biological unit, as promulgated by conventional medical science. In fact, a smaller biological unit is the imperishable microzyma, which is an organized, living being “of a special category without analogue,” said Bechamp, who found them ready to become active in chalk deposits at least 11 million years old.[4]

The Pleomorphic Cycle

I suggest a developmental cycle in vivo consisting of three macrostages: (1) a primitive stage comprising the repair protein complexes; (2) an intermediate, or bacterial, stage including filterable forms such as the cell-wall deficient forms described by Lida Mattman, Ph.D. (in Cell Wall Deficient Forms, Stealth Pathogens); and (3) a culmination stage consisting of yeast and fungal phases, and then mold, the end phase. The usual course of development would be from microzyma to repair protein and then to bacterium, etc. However, under certain conditions, such as trauma for example, it is highly likely that the microzymas can skip the primitive stage and become bacteria directly. Although these transformations are as astounding as that of a larva to a butterfly, what is equally impressive under observation is the rapidity with which they can take place-in minutes, even seconds, sometimes. By the same token, when provoked by conditions and the cycle proceeds to yeast, fungus and then mold, it may occur so rapidly that the bacterial stage, if it happens, has no time to be of any significance.

Thus, symptogenic microforms can originate within higher organisms without invasion, via a permutation of the endogenous microzymas when the situation calls for such change. The situation is an imbalance referred to by Bechamp as a “modification of the medium.” Endogenous evolution is evident under the microscope when bacterial, yeast, and fungal forms are seen coming out of red blood cells which initially appear normal.

Biological Basis for the Pleomorphic Cycle

There is a common biological basis for the pleomorphic cycle and its increasing complexity of organization: More complex forms evolve inherently upon the death of an organism for the purpose of recycling its anatomical and chemical structures in the carbon cycle. The process of rapid evolution (which is reversible) is an essential life process which, beyond the repair stage, is necessary to return a dead organism to the earth. The second and third-stage microforms degenerate the body’s vital substances and tissues via putrefaction (bacteria) and fermentation (yeast and fungus). Fermentation results in acid waste products, which further break down tissue. Disease symptoms, then, especially the degenerative type, are not produced by viruses, but manifest as chemical decomposition, or attempted recycling via fermentation and acid toxins, but with “host” survival processes still operable (see Section 3 and discussion of pH in the main text). Obviously, certain other factors may play important roles in producing symptoms, such as heavy metal toxicity, or state of mind, for example. Some of the body’s survival methods also produce symptoms commonly called diseases. An example is eczema, an emergency expulsion of acid toxins via the skin.

The aforementioned causal (alarming) situation, or modification of the medium, is chronic acidification (pH imbalance) and oxygen deprivation in the blood and tissues due to acid-forming foods, adverse lifestyle, emotional stress, and environmental stress. This is not oversimplification. Acidification/hypoxia biochemically signals a dead host to the microzymas, while creating collapsed areas (dead zones) of the colloidal system in the intercellular fluid (see Section 2), and it is the primary physiological disease condition out of which the symptoms commonly called specific diseases arise.

Thus, we distinguish between this disease condition and its consequent symptoms, which include both the morbidly evolved microzymas and the physiological signs commonly thought of as specific diseases. As they develop, microforms (bacteria, yeast, fungus and mold) are actually scavenging forms of the microzyma, developed when disease in the cell life requires tissue to be broken up. These upper development forms are the ones easily visible in the blood before physical symptoms arise. They disappear (devolve) when the recycling task is complete, once again becoming microzymas of the earth and/or air.

Virus or Toxin?

Regarding the early period of virus isolation, a question is whether the unseen entities isolated in filtered fluids were accompanied by the waste products (mycotoxins) of fermentation by yeast and fungus of cellular elements, such as DNA. If virus filtrates are injected into a host to prove virulence, it is almost certain that easily filterable molecular toxins will be introduced as well. Could Dr. Stanley’s “pure crystals of tobacco mosaic virus” have been crystallized toxins? If so, they would certainly be highly symptogenic, as are exotoxins at the intermediate stage of the cycle, for example. However, it is not proof of anything that you can create illness by poison injection, except proof of that tautological fact.

In my research utilizing dark-field and phase-contrast microscopy, it is common to see crystallizations in the blood. It is normal for the body to use calcium or other mineral salts, and fats as well, to chelate the waste products from the morbid fermentation of body proteins, fats and sugars. Such crystal deposits are found in cancer tissue as well. A malignant tumor removed from the breast of one of my research clients was found to have numerous calcium deposits attached to it. It is an attempt to render inactive the substances that make our inner streams filthy, poison our cells, and coagulate colloidal systems in blood and intercellular fluid.

The term “virus” is the Latin word for poison, and gives us insight into the immediate cause of disease symptoms-poisons: mycotoxins, endotoxins, exotoxins, and toxins from environmental sources (many of which are primary or secondary mycotoxins). Orthodox medicine is well aware that it is bacterial toxins more than the bacteria themselves (they feed in us), that cause the symptoms referred to as infectious disease. Little if any emphasis is placed on this fine but important distinction. Always, the germ is emphasized. There is little to no awareness (or acknowledgment), either, of the same role played by toxins of the culminate microforms of the pleomorphic cycle. Their action and the body’s response to them are frequently ascribed to viruses, which do not produce toxins but are said to wreak havoc by a number of other means. However, if they participate in symptogenesis in a host it is because they are stimulated to evolve into more complex, toxigenic forms. Somewhat less likely is the possibility that they cause damage as a result of erroneous construction or function, for one reason or another-missing mineral nutrients leading to enzyme deficiencies, for example.

Misconception Breeds Contempt

In addition to chemical toxicity, however, what is the impact of the fear (emotional toxicity) that the word “virus” brings to mind and heart? It has been said that fear is the most deadly of disease conditions. If a “disease” kills one person, the fear of it may kill twenty. General prejudice concerning the danger of viruses is fundamental biological error based on Louis Pasteur’s germ theory, and is itself a perpetrator of auto-suggested illness. For example, in Africa doctors attribute some AIDS sickness to “voodoo death” syndrome, the term for illnesses induced psychologically. According to one nurse, “We had people who were symptomatically AIDS patients. They were dying of AIDS, but when they were tested and found out they were negative they suddenly rebounded and are now perfectly healthy.”[5]  Ironically, if the germ theory were founded on facts it would be correct to fear viruses, except there would be few, if any, humans living to discuss the issues. These socalled pathogenic entities are to researchers, medical practitioners and the press what criminals are to detectives-the focus and justification of their existence.

The Encyclopaedia Britannica has this to say about bacteria, which relates also to viruses:

The common idea of bacteria in the minds of most people is that of a hidden and sinister scourge lying in wait for mankind. This popular conception is born of the fact that attention was first focused upon bacteria through the discovery, some 70 years ago, of the relationship of bacteria to disease in man, and that in its infancy the study of bacteriology was a branch of medical science. Relatively few people assign to bacteria the important position in the world of living things that they rightly occupy, for it is only a few of the bacteria known today that have developed in such a way that they can live in the human body, and for every one of this kind, there are scores of others which are perfectly harmless and far from being regarded as the enemies of mankind, must be numbered among his best friends.

It is in fact no exaggeration to say that upon the activities of bacteria the very existence of man depends; indeed, without bacteria there could be no other living thing in the world; for every animal and plant owes its existence to the fertility of the soil, and this in turn depends upon the activity of the micro-organisms which inhabit the soil in almost inconceivable numbers. It is one of the main objects of this article to show how true is this statement; there will be found in it only passing reference to the organisms which produce disease in man and animals- for information on these see Pathology and Immunity. {Encyclopaedia Britannica, 14th ed., Vol. 2, p. 899)

The general message of the foregoing article applies even more aptly to viruses in the sense that much fear has been bred and cultivated around them, although they never produce disease symptoms, whereas some bacteria do. The writer of the above understands bacteria, with the exceptions that symptogenic bacteria found in man and animals do not produce disease (only secondary symptoms), that their precursors are endogenous to higher organisms, and they have not “developed in such a way that they can live in the human body.” If anything, the reverse is true. According to one theory of microbiology, microforms have colonized over eons to become higher organisms. In one sense, then, the human body has developed as a specialized environment for them.

An important dimension of the bacterial dependence of higher life forms is the floral population in the human digestive tract. Literally, these “foreign species” keep us alive.

Most bacteria have the same underlying function, whether found in soil, sewage, in the human digestive tract, or elsewhere in nature: they are an essential part of the life processes of higher organisms. They will not or cannot attack healthy cells or tissues, but certain ones will recycle sick or dead tissue in much the same way insect pests are drawn to weaker plants. As Bechamp said, “Nothing is the prey of death; all things are the prey of life.”

Following in the wake of misconceptions arising from the fundamental biological error known as the germ theory of disease, defining the filtrates of diseased tissue as a newly discovered infectious microform was the birth of a major corollary error in bioscience.

Viral Behavior Reconsidered

Listed below are ways viruses are said to disrupt or destroy host cells according to orthodox medical science and the germ theory. Following each in italics is a different interpretation following from microzymian principle:

1. Viral proteins insert into the host cell’s plasma membrane and directly damage its integrity to promote cell fusion (HIV, measles, and herpes viruses).

Proteins are attempting to repair membrane damage, or enter cells to make other repairs. There is the question as to whether viruses on cell walls are coming or going. In both cases it would be a matter of whether or not a cell has been disturbed by excess fermentation and acidity. But in the former case the cell would be dysfunctional before attachment occurs, thus requiring the repair complex. Another possibility, perhaps remote, is that dysfunctional receptors on cells are in need of repair, or they are covered by these complexes to inactivate malfunctioning cells. Positive electrical charges in a compromised terrain, primarily on acid molecules from fermentations, discharge cell membranes and act as mortar to stick cells together.

2. Viruses inhibit host cell DNA, RNA, or protein synthesis. For example, poliovirus inactivates cap-binding protein, which is essential for protein synthesis directed by capped host cell mRNAs, while allowing protein synthesis from uncapped poliovirus
mRNAs.

Protein inactivation is probably being done by fermentation or by acidic toxins from fermentation, while “poliovirus” is produced in the cell to reverse the damage.

3. Viruses replicate efficiently and lyse host cells, e.g., liver cells by yellow fever, and neurons by poliovirus.

Highly unlikely. The lysing is more likely caused by acid mycotoxicosis, or by free radicals (ROTS) released in response to mycotoxic stress, or from other sources (ionizing radiation, for example). Repair particles are residual after cell wall disruption.

4. Slow-virus infections (e.g., subacute sclerosing panencephalitis, caused by the measles virus) culminate in severe progressive diseases after a long latency period.

How is this demonstrated? Perhaps “latency” is a period of successful or attempted repair that eventually falters. Symptomology naturally appears in the weakest parts of the body. Excess acidity is always a systemic problem that localizes, just as cancer is a systemic condition that localizes, even though its symptogenic influence may later spread.

5. Viral antigen proteins on the surface of the host cells are recognized by the immune system, and the host lymphocytes attack the virus-infected cells (e.g., liver cells infected with hepatitis B).

Liver cells are damaged beyond repair by mycotoxicosis, and the immune system, our elaborate janitorial service, is cleaning up the garbage. Perhaps the repair protein antigen is expressed to signal immune response (because the cell is beyond repair), which is one explanation for why there are antibodies to these proteins.

6. Viruses damage cells involved in host antimicrobial defense, leading to secondary infections.

The function of immune cells is damaged by fungal infestation and/or overwork by toxic overload, preventing proper cleanup and elimination of disharmonious, symptogenic elements.

7. Viral killing of one cell type causes the death of other cells that depend on them, e.g., degeneration of muscle cells enervated by the attack of poliovirus on motor neurons.

Once again, a misinterpretation and lack of understanding that it is not viral microforms that damage neurons. Toxins from bacteria, yeast, fungus and mold-as well as the fermentation of glucose, proteins, hormones and fats-produce, or influence the body to produce, disease symptoms. Not recognizing the “virus,” for what it is, observers attribute disease to it.

8. Host cell responses to viruses include metabolic derangements and transformations resulting in neoplastic changes.

Metabolic derangement has occurred prior to the appearance of repair proteins, due to toxic overload in the cell. It is more likely that the proteins attempt to prevent cell transformation, and that cancerous development is cell conversion from primarily oxidative to wholly fermentative metabolism, mediated by fungus and mold.

Listed below are further orthodox views regarding virus replication, etc., with alternative interpretations in italics.

9. According to orthodox theory, viruses enter a host cell and replicate at the host’s expense. Replication is accomplished using enzymes which are distinct for each virus family. For example, RNA polymerase is used by negative-stranded RNA viruses to generate positive-stranded mRNA, whereas reverse transcriptase is used byretroviruses to generate DNA from their RNA template and to integrate that DNA into the host genome.

It is normal for repair proteins to generate enzymes to do their work.

10. One reason suggested for viral tropism (the tendency to infect some cells but not others) is the presence or absence of host cell receptors that allow the virus to attach. It is said, for example, that HIV binds to the protein (CD4) involved with antigen presentation on helper T-lymphocytes, that Epstein-Barr virus binds to the complement receptor (CD2) on macrophages, that rabies virus binds to the acetylcholine receptor on neurons, and that rhinoviruses bind to the adhesion protein (ICAM-1) on mucosal cells.

See number 1 above.

Theoretically, once attached, the entire virion, or a portion containing the genome and essential polymerases, penetrates into the cell cytoplasm in one of three ways: (1) Translocation of the entire virus across the plasma membrane; (2) receptor-mediated endocytosis of the virus and fusion with endosomal membranes; or( 3) fusion of the viral envelope with the cell membrane. Theory suggests that within the cell the virus uncoats, separating its genome from its structural components and losing its infectivity before replication. In either the nucleus or cytoplasm, newly synthesized viral genomes and capsid proteins are assembled into progeny virions, which may then bud through the plasma membrane. Unencapsulated viruses may be released also, directly through the membrane.

It is interesting, however, that viruses can somehow choose the “infection” to be abortive, latent or persistent, meaning respectively: (1) viral infections with incomplete replication cycles; (2) persisting in a cryptic state, like herpes zoster within a dorsal root ganglion, which suddenly becomes active to produce shingles;( 3) continuously synthesized virions, with or without altered cell function (e.g., hepatitis B). These three ideas, especially latency, have arisen as feeble excuses for the untenable virus theory.

11. In order for viruses to reproduce, they must complete the following four steps:

a). Adsorption and penetration of a cell. The viral particle binds to the host cell membrane. This is usually a specific interaction in which a viral encoded protein on the capsid or a glycoprotein embedded in the virion envelope binds to a host cell membrane receptor and is then internalized. This internalization occurs by endocytosis or by fusion of the virion envelope with the host cell membrane.

This is the mechanism whereby the viral particle enters the cell for the purposes of carrying out repairs to the damaged DNA orRNA.

b). Uncoating of the virus, so that the nucleic acid can be released from the capsid into the nucleus or cytoplasm.

Repair work may require uncoating. An uncoated “virus” in the cytoplasm may have come from the nucleus and not yet have a coat, as in the case of hepatitis B according to medscience. A coat is then created to protect the nucleic acid, to make a communicative or responsive protein complex, or to allow exiting the cell for remote function or for neutralization and recycling by the immune system.

c) Synthesis and assembly of viral products as well as inhibition of the host cell’s own DNA, RNA and protein synthesis.

Protein complexes produced in response to an alarming situation-fermentative and mycotoxic stress-are capable of self-ordered replication. As suggested by Bechamp, the microzyma is specific for each organ, therefore specific repair proteins will be needed for specific cells that make up specific organs that are being disturbed. There is the question of why the great numbers in some cases. One possibility is simply overreaction; for example, fever can be extreme.

d) And finally, release of virions from the host cell either by budding or lysis.

(1) Complexes leave the cell for remote function or to be neutralized; (2) Repairs have failed, and complexes are released prior to or during the breakdown of the cell by acid toxins or the immune system.

Further Considerations

Virologists refer to certain microforms as passenger viruses, which are present in asymptomatic situations, riding on their host’s genetic molecule like a passenger. To the conventional mind searching for new diseases or for a viral cause of unexplained ones, they are most interesting, because the status of virologists in the scientific community depends upon the pathogenic potential of the viruses they study. Due to their location, passenger viruses are thought to have much disease potential, thus their true function goes unnoticed. These colloidal passengers are the silent majority of animal and human intranuclear proteins essential for genetic repair.

Kalokerinos and Dettman quote Dr. Fred Klenner regarding the changeability of viruses: “I am of the opinion that virus units have the potential of going from one type to another by altering their protein coat. We see chicken pox at Thanksgiving, mumps at Christmas, red measles in the spring, and polio and Coxsackie in the summer.”[6]  Seasonal appearance of different forms may be mediated by variations of imbalance in the biological terrain or nutritive medium due to the fermentation of dietary excesses such as sugar and animal proteins that accompany holidays and seasons, calling for different repair proteins.

For example, outbreaks of polio have been associated with sugar consumption in summer. Various psycho-emotional stresses correspond to these seasons as well.

Supporting the general idea of dietary culpability is a statement published by the great English physician, Sir Robert McCarrison in 1936: “Obsessed with the invisible microbe, virus, protozoa as all important excitants of disease, subservient to laboratory methods of diagnosis, hidebound by our system of nomenclature, we often forget the most fundamental of all rules for the physician, that the right kind of food (nutrition) is the most important single factor in the promotion of health and the wrong kind of food the most important single factor in the promotion of disease.”7

Six years before Bechamp identified the microzyma as a ferment and, with his devoted associate, Professor Estor, began a 13-year odyssey of research into its nature, Florence Nightingale published a statement about the germ theory. In Notes on Nursing, 1st ed., 1860, she said of infection:

Diseases are not individuals arranged in classes, like cats and dogs, but conditions growing out of one another.

Is it not living in a continual mistake to look upon diseases, as we do now, as separate entities, which must exist, like cats and dogs, instead of looking upon them as conditions, like a dirty and a clean condition, and just as much under our own control; or rather, as the reactions of kindly Nature against the conditions in which we have placed ourselves?

I was brought up … distinctly to believe that smallpox, for instance, was a thing of which there was once a first specimen in the world, which went on propagating itself in a perpetual chain of descent, just as much as that there was a first dog, (or a first pair of dogs), and that smallpox would not begin itself any more than a new dog would begin without there having been a parent dog.

Since then I have seen with my eyes and smelt with my nose smallpox growing up in first specimens, either in close rooms or in overcrowded wards, where it could not by any possibility have been “caught,” but must have begun. Nay, more, I have seen diseases begin, grow up, and pass into one another. … I have seen, for instance, with a little overcrowding, continued fever grow up; and with a little more, typhoid fever; and with a little more, typhus, and all in the same ward or hut.

Would it not be far better, truer, and more practical, if we looked upon disease in this light? For diseases, as all experience shows, are adjectives, not noun-substantives.

That is, symptoms (called diseases) are describers of a situation.

I find legitimate Bechamp’s conclusion that what are called germs of the air are fundamentally microzymas of beings which are being consumed by the recycling process, i.e., some kind of vegetative digestion-putrefaction or fermentation. In short, there are no pre-existing disease-germ species. The principles of microbian medicine constitute a fundamental biological error. As Bechamp said, “The microbian doctrine is the greatest scientific silliness of this age.” This is not to say that there is no transmission, only that invasion is not necessary for symptogenesis, nor is it the primary mechanism for illness. It is to say that for transmission to take place, susceptibility in the form of a compromised terrain must pre-exist in the receiver, who is then likely to be ill anyway. With the exception of the immune component in the mucosal barrier, primary host “resistance” is a function of terrain condition rather than immunity per se.

Phantom Viruses Hepatitis

Hepatitis can be a painful symptom that has yielded profitable virus-hunting opportunities in recent years. Although there are several categories of this disorder, three main varieties of what is called “acute viral hepatitis” exist: Type A (formerly “infectious hepatitis”), Type B (formerly “serum hepatitis”), and hepatitis C (formerly “non-A, non-B”). The corresponding viruses are HAV, HBV, and the non-A, non-B “group,” now called C. Type A is said to be caused by an RNA virus, spread primarily by fecal contamination of water and food, with blood and secretions also possibly being infectious (but it is due to the toxins associated with unsanitary conditions). Hepatitis B, discovered in the ’60s, is said to be caused by a DNA virus which replicates in the hepatocyte nucleus and receives its surface coat in the cytoplasm. It is said to be transmitted by transfused blood or blood products, or via common use of needles by intravenous drug users (but it is due primarily to over-acidification from the drugs, especially heroin. The exchange of body fluids into the blood, whether by unsterilized needles, abusive sexual activity, etc., can also play a role over time because of repeated immune stress caused by foreign proteins. See Section 1 for Bechamp’s view of the invasion of blood by injection of proteins). Third World babies with poor nutrition and unsanitary conditions around the time of birth are also susceptible.

The third type of hepatitis, discovered in the ’70s, is found among drug users and alcoholics, and accounts for 80 to 90% of hepatitis caused by blood transfusion. It is thus akin to B type and was at first thought by scientists to be hepatitis B until thorough testing of subjects revealed no virus B-nor A, for that matter. It was thus called “non-A, non-B” hepatitis and thought to be at least two viruses and perhaps more.

In 1987 scientists believed they found a single virus causing the third type, what is known today as the hepatitis C virus. However, what they identified was an antibody they associated with a virus. Now, just as with HIV, they could test patients for antibodies against an elusive or invisible virus. With this new observation, however, new paradoxes confronted the viral hypothesis. Huge numbers of people testing positive for the phantom C virus never developed any symptoms. Hepatitis is truly the result of over-acidification or toxification of the largest filter in the human body by such substances as lactic acid, acetic aldehyde and ethanol-not the disease of a pathological virus. It is interesting to note also that all these hepatitis viruses have incubation periods of 2 to 25 weeks, violating Farr’s Law (see below), yet are not classified as slow viruses. Also, the point at which a “natural invasion” takes place, as opposed to a highly artificial injective one, and thus, how true incubation periods are determined, is another interesting question.

Hantavirus

A recent example of unwarranted panic in American biomedicine was the eminent hantavirus of 1994. Presumably it had jumped species, from mouse to man (the American Navaho Indians). However, after supposedly killing a number of people, this phantom virus apparently made peace with the Indians and retired to its mouse reservoir. The virus failed to materialize.[8] A front-page article in the San Francisco Chronicle reported that CDC “epidemiologists across the nation are carefully monitoring the deer mouse population and the level of virus within it.” But all that was left to discover of the former “Navaho flu” by the CDC epidemiologists (shown in their space suits) were healthy mice in the mountains.[9]  The Navaho flu is nothing new to the native Americans and is most likely tied to sanitation, nutrition and lifestyle.

Ebola

In May 1995 the CDC announced the new, threatening Ebola virus. The deadly killer virus was expected to leave its hidden reservoir in the rain forests of Africa to claim Europe and the United States. An article in Time magazine was peppered with men in space suits and colored electron micrographs of the virus (even though electron microscopes cannot take color pictures). A CDC virologist suggested the virus could leave the rain forest if “we get a virus that is both deadly to man and transmitted in the air.” We are thus asked to fear the image of viruses somehow being launched into the air, perhaps by ejection from a host, and then floating on killer breezes to other lands. A more imaginable scenario was suggested by a European epidemiologist who heads the United Nations AIDS program. Echoing the CDC’s alarm, he stated, “It’s theoretically feasible that an infected person from Kuwait could go to Kinshasa, get on a plane to New York, fall ill, and present transmission risk there.” But within a month the virus had disappeared in Africa, and not a single Ebola case was reported in the United States or Europe. [10]

The World Health Organization announced on December 19, 1995 that the Ebola virus epidemic that killed 245 people in West Africa was over. All tests on any remaining suspected cases were negative. A somewhat unsettling revelation was that every Ebola outbreak in Africa “is associated to have spread through public hospitals.”[11]  As it turned out, it was associated with re-used hypodermic needles in these hospitals. Just like hantavirus, Ebola vanished, never to be heard from again. Most interesting is that this epidemic, as epidemics will, stopped without vaccines or other drugs. But consider the impact such stories have made upon our minds and on the way we view and understand germs. What’s next in virodrama, the Andromeda Strain?

There is one insidious possibility that must be mentioned in passing. Some mysterious outbreaks of the past have been shown years later to have been man-made. In some cases, government agency has used the public to test releases of organisms and weak biochemical toxins in order to verify, through medical reports, expectations of biowarfare activity. These incidents and the whole story of such behavior is well documented in the book, A Higher Form ofKillingby Robert Harris and Jeremy Paxman (Hill & Wang, 1982). In this scenario, the cause of such an incident would be constructed officially, or left as a mystery, in order to draw attention away from the truth.

Vaccines

Haphazard Beginnings

The greatest danger of the germ theory half-truth is its promulgation and acceptance as the whole truth, thus diverting attention from endogenous factors, primarily host ecology-resistance and susceptibility. Such factors are highly significant if Bechamp and his many followers, including me, are correct. Distraction from host factors has been quite thorough, with the exception of the false notion that the immune system is the “first line of defense” against infectious symptoms.

Louis Pasteur is credited with improving and successfully using the technique of vaccination, a practice blindly begun in 1796 by British physician Edward Jenner. Jenner happened to notice that dairy maids who had contracted the relatively mild disease cowpox did not later contract smallpox. On a hunch, he took pus from the running sores of sick cows and injected it into the blood of an eight-year-old boy. As the story goes, the boy developed cowpox. Several weeks later Jenner inoculated the boy with smallpox, but the disease failed to develop. Upon this single anecdotal event was based the supposition that this practice was safe and effective. The process has changed little to this day except perhaps to have been worsened with additives. Its understanding is still clouded by Pasteur’s theory, and it is as recklessly pursued as it was begun.

Theoretically, vaccination works by introducing a diluted and weakened (attenuated) or “killed” version of the pathogen into the body, causing the immune system’s memory function to prepare for any subsequent contact, which is met with much greater response. It is commonly thought that infectiosity, or germ-virulence, tests are performed on laboratory animals and then vaccines are made which boost the immune system against germs. However, like Jenner’s, the tests are primarily toxicity tests, and vaccines, especially viral ones, activate the immune system primarily in response to injected toxins. Whether the response is to toxins, microforms, or both, it is a misguided approach at best. Bypassing the mucosal barrier and thus the segment of the immune system which is the organism’s interface with the environment, makes such experimentation, and vaccination itself, flawed, unscientific practice ipso facto.

A Toxin Pathway

Bacteria secrete a variety of enzymes (leukocidins, hemolysins, coagulases, hyaluronidases, fibrinolysins), any of which are disruptive in the body. For example, diphtheria toxin is composed of the enzymatic fragment A, which is at the amino end of the molecule, and fragment B at the carboxyl end, which allows entry into host cells. The two fragments are linked by a disulfide bond. Once bound diphtheria accesses the cell cytoplasm, the disulfide bond is broken, releasing fragment A. This enzyme catalyzes the covalent transfer of adenosine diphosphate ribose (ADPR) from nicotinamide adenine dinucleotide (NAD) to EF-2. The latter, a ribosomal elongation factor involved in protein synthesis, is thus inactivated. One molecule of diphtheria toxin can kill a cell by ADP-ribosylating more than a million EF-2 molecules. In diluted form this toxin, along with other toxic chemicals and fragments of bacteria, is what is introduced directly into the blood of infants under the guise of a health measure.

Diphtheria toxin creates a layer of dead cells in the throat, on which Corynebacterium diphtheriae outgrows competing bacteria (the diphtheria microform is an intermediate stage of a morbidly evolved microzyma, and competing bacteria also evolve out of sick cells). Subsequent wide dissemination of diphtheria toxin causes the characteristic neural and myocardial dysfunctions. Diphtheria toxin also causes disseminated intravascular coagulation, which activates the various alarm responses of the body. Thus, we know that toxins produce symptoms, but what is it that produces the condition which creates or supports the toxin producer?

Bordetella pertussis is a fascinating organism to study. A certain amount of empiricism, as opposed to logic, is required for success with pertussis. Diagnostic cultures are difficult and sometimes unreliable. Different lots of vaccine, made in the same way from the same strains, sometimes show different properties. Experimental work is not always reproducible from one laboratory to another, but this is common in biological research. The diagnostic culture problems and the unexpected variability in vaccines and in pertussis strains themselves are not easy to explain.

-Charlotte Parker Department of Microbiology, U. of Texas at Austin

Vaccine Recipes

To make a vaccine you need to acquire the disease germ-a toxic bacterium or a live virus. The mumps virus is a sterile, lyophilized preparation of the Jeryl Lynn (B level) strain of mumps virus. It is adapted to, and propagated in, cell cultures of chick embryo, free and stabilized with sorbitol and hydrolyzed gelatin. The rubella virus (Wistar RA 27/3 strain) is grown in human diploid cell cultures. Measles (from Eners’ attenuated Edmonston strain) is grown in cell cultures of chick embryo.[12]  The various so-called virus strains are stored by pharmaceutical companies for later culture. Where these stockpiles come from and the specific methods used seem to be guarded secrets, but as Bechamp emphasized, they must originally be obtained from diseased higher organisms, for they are found nowhere else in nature. If protein complexes exist in the viral stores, their replication in culture is simply the behavior pattern of the repair proteins they are. It is highly likely that toxins accompany these strains as a means of stressing the culture cells.

To make a live vaccine, the microform must be attenuated, or weakened. This is accomplished by serial passage-passing the microform/toxin many times through animal tissues, e.g., monkey kidneys, human diploid cells (the dissected organs of an aborted fetus), chick embryos and calfs.[13]  Killed vaccines are prepared with heat or radiation, or else chemically, usually by using the mycotoxin formaldehyde.[14]

The weakened microform must be mixed with antibody-boosting and immune-activating adjuncts such as the antibiotics neomycin and streptomycin, as well as stabilizers such as sodium chloride, sodium hydroxide, aluminum hydroxide, aluminum hydrochloride, sorbitol, hydrolyzed gelatin, formaldehyde, and thimerosal (a mercury-based antiseptic).

For example, diphtheria, pertussis and tetanus (DPT) vaccine consists of a combination of tetanus and diphtheria exotoxins with pertussis microforms. Diphtheria toxin is produced by growing Corynebacterium diphtheriae in a medium composed of pig pancreatic hydrolysate of casein. Tetanus toxin is produced by growing Clostridium tetani in a medium composed of pig tryptic digest of casein. Both toxins are combined with formaldehyde, ammonium sulfate (a mycotoxin), and diluted with saline containing thimerosal. They are then adsorbed on aluminum phosphate and combined with a suspension of Bordetella pertussis organisms.[15]

The first pertussis (whooping cough) vaccine was created in 1912 by two French bacteriologists, Jules Bordet and Octave Gengou, who wanted to use it on the children of Tunisia. After growing the pertussis bacteria in large pots, they killed them with heat, preserved the mixture with formaldehyde, and injected it into the children.

One change made in the original Bordet/Gengou recipe was to add an “adjuvant.” This material, usually a metal salt, somehow heightens the capacity of the pertussis vaccine to produce antibodies in the host. In 1943 a pioneer American pertussis vaccine researcher, Pearl Kendrick, reported that alum had this adjuvant effect. The vaccine was said to be more protective, and fewer pertussis bacteria had to be included. After her report, alum or alum-based substances were added to the vaccine. Kendrick was also instrumental in having pertussis combined with diphtheria and tetanus vaccines already in use in the 1940s.

The vaccine is made in essentially the same way today as in the time of Bordet and Gengou, although each manufacturer prepares it differently, and the exact processes and formulas are considered trade secrets. Pertussis bacteria are usually grown on a casein hydrolysate medium with yeast dialysate, supplemented with agar and charcoal. The mixture is prepared in vats, then washed, and the bacteria killed with heat and formaldehyde The resulting toxoid is preserved with thimerosal. Other possible ingredients are hydrochloric acid, the adjuvant (usually an aluminum compound), sodium hydroxide, and salt.

In the past, human blood was often added. This is now prohibited by federal law, but manufacturers are still permitted to add blood from “lower animals other than the horse.” The microzymas of horse blood destroy human blood.

The vaccine is stored for a while at near-freezing temperatures, then combined with the diphtheria and tetanus exotoxins and poured into vials for distribution. Ultimately it is shipped to pharmacies, private physicians, and public health clinics, whence it is injected into the blood of infants.

Calf Serum

The precedent of cruelty to animals, promoted, if not set, by Louis Pasteur, is apparently a hallmark of germ theory. It is not better demonstrated than by the following description of the preparation of so-called calf serum dreamt up in the early days of vaccine manufacture, and continuing, as far as I can tell, into the late 1980s, if not to this day:

A calf is strapped down to an operating table. A space on the abdomen of about 12-15 inches is shaved with a razor, then about 100 slashes are cut into the flesh. The seed virus, consisting of a culture of smallpox passed through a solution of glycerine, is rubbed into the wounds.

Made to stand in a headstock so it cannot lick its belly, the calf grows very sick and the wounds become swollen and inflamed. In a few days, as the body reacts to the poison, small blisters appear, scabs form over the wounds and fill with pus. In five to seven days, the wounds are ulcerated, issuing pus and morbid cells. The calf is again strapped to the operating table, and the infested area is washed with warm water. Each scab is scraped off and its contents are pressed out of the sores into a container. An equal amount of glycerine is added to the pus, and the whole is stirred. Once thoroughly mixed, the concoction is passed through a sieve to remove solids such as pieces of flesh, scabs and hair. After being stirred once again, the mixture is put into vials, sealed, and distributed as “pure calf lymph,” commonly known as smallpox vaccine.[16]

These aforementioned concoctions are obviously poisonous products of disease. By injecting these products into the blood of school children, physicians, via legal manipulation of health boards and school boards, potentiate illness and ensure that medical products and services will continue to be in high demand.

It is interesting to note that the vaccine given to those considered to be at high risk for hepatitis A (such as highly overactive homosexual males, users of illicit injectable drugs, residents of a community experiencing hepatitis A, hemophiliacs and other recipients of therapeutic blood products), or those testing positive for hepatitis A, is made of immune serum globulin obtained by ethanol fractionation of plasma pooled from hundreds of donors. Considering that microzymas and morbidly evolved microzymas are being transferred from one individual to another, one might conclude that this could have disastrous consequences. (The fact that animal blood and fluids are transferred to humans by vaccination bears no further comment, except to say that Frankenstein would be proud.)

It is also very interesting that the vaccine given to those testing positive for hepatitis B is created by cloning the antigen HBsAg in a bed of yeast {Saccharomyces cerevi’s Jae, the culminate stage of the morbidly evolved microzyma) and formulated as a suspension of the antigen adsorbed on aluminum hydroxide. [17] Such morbid, poisonous vaccines are given to infants at 2, 4, and 15 months of age. The vaccine is enough to disturb the central balance of the biological terrain and cause an array of symptomologies in anyone, especially an infant. That more people are not quickly poisoned to death by this practice is testimony to the astounding resilience of human physiology.

Vaccination Results

Does the vaccinal approach produce wellness or any health benefit? Kalokerinos and Dettman point out that statistics in England and Wales, presented at the Presidential Address of the British Association for the Advancement of Sciences (Porter, 1971), show that deaths of children under 15 years of age attributed to scarlet fever, diphtheria, whooping cough and measles saw a 90% decline from 1850 to 1940. Yet, antibiotics and compulsory (i.e., widespread) vaccination against diphtheria were not introduced until 1940. The death rate due to these illnesses dropped from over 6,000 per million children in 1850 to under 1,000 per million children in 1940, a period marked by vastly improved public health, sanitation and nutrition.[18]

Along the same lines, an English doctor, D. Powles, observed: “The major contributing factor toward improved health over the past 200 years has been improved nutrition. Nearly 90% of the total decline in the death rate in children between 1860 and 1965 due to whooping cough, scarlet fever, diphtheria and measles occurred before the introduction of antibiotics and widespread immunization against diphtheria.”[19]  Also, it has not been well publicized by authorities that infectious epidemics are naturally cyclic in populations. The procedure has generally been to introduce vaccines as the downcurve begins, giving the impression of effectiveness. In addition, there are numerous instances in history of violent outbreaks of illness following near-total immunizations of population groups.

Once I looked into this subject and its history, microzymian principle brought it into focus for me. Since germs evolve out of, or take advantage of, the susceptible state, and are symptoms themselves, drugging or vaccinating susceptible individuals cannot render them immune, and may have the reverse effect. When and if a vaccine works as intended, the result is only to suppress the appearance of a specific set of symptoms, not to prevent disease. Therefore, it is not conferring wellness, nor reducing susceptibility, but simply creating an effect in a highly artificial and dangerous manner, while allowing the disease condition to worsen. Is there a price to pay for this invasive and unscientific approach? In this writer’s view, it is what we’ve got-pandemic degenerative disease, cancer and AIDS, because we are not dealing with the foundational disease, which may then get worse and re-expresses itself in more intense ways.

Contaminants

The November/December 1995 issue of The Vaccine Reaction, Volume 1, No. 5, issued by the National Vaccine Information Center, reveals that Swiss scientists have reported finding the enzyme reverse transcriptase (RT) in the live measles/mumps/rubella (MMR) vaccine. This has been traced to the chicken embryos whose cells are used to create the vaccines. It has reportedly been detected in yellow fever and some influenza vaccines, also prepared in chicken embryo cells. No disease has been attributed to RT in the MMR vaccine, but it is a factor in retroviral disease theory and its presence in this case is a mystery. RT, which is officially said to be produced by many “tumor-producing” viruses, supposedly the retroviruses, catalyzes the transformation of RNA into DNA. However, there is no proof of viral production of tumors-only theory.

I suggest the following process to explain how it gets into the vaccine, based on microzymian principle: Disruption of the embryo cells, by toxins or other means, probably damages their DNA. The response is endogenous microzymian production of repair protein complexes (“retroviruses”), which in turn produce RT in order to effect repairs. As the toxification process continues, central balance in the embryo cells is disturbed sufficiently and the ensuing endogenous pleomorphic development of upper development forms results in excess fermentations, with corresponding increase in the level of toxins. In order not to “spoil the broth,” however, preservatives are added at a certain point to arrest development.

Experiments with fertile eggs, which I later discovered were described by Bechamp, provide evidence of endogenous microzymian development. I have observed that the hypodermically extracted serum of a fresh egg looks normal under a high powered light microscope. However, when the central balance is disturbed by shaking the egg, which is then allowed to sit for a period of time, extracted serum shows the presence of bacteria, yeasts, and their associated toxins, i.e., acetic, sulfuric and butyric acids. An equally elegant, but even simpler, demonstration is bruising an apple without breaking the skin. Soon the area begins to turn brown and rot from the inside. This is a life process mediated by endogenously developed microforms.

The enzyme that orthodox researchers associate with retroviruses is being found in live vaccines such as MMR and polio. But RT does not cause disease. It is toxins which taint the vaccine, whether produced in culture or introduced as ingredients, that have the potential to interact with each individual’s immune system and DNA and disrupt the body such that various symptoms are produced. This practice of introducing foreign (genetic/viral) proteins directly into the blood may result in morbid pleomorphosis with further potential for toxification. Of course, that is precisely what has been occurring for many years, with the blessing of the allopathic medical system, whose financial health depends on disease.

Another example of unwanted or unpredictable vaccine contaminants: polio vaccines grown on monkey kidney have been identified as a source of simian viral (SV40) and spherical retroviral structures.[20]  Such stray protein structures and fragments in vaccines can be regarded as a large, uncontrolled, cross-species genetic experiment in which a gene from one species might be spliced as a repair protein into another.

Reactions

Though secondary to the failure to address disease, vaccine reaction has become the more common issue because of its immediacy. It results from the aggressive willingness of medical authorities to play Russian roulette with people’s lives. When asked about potential, dangerous reactions, officials reply, “The benefits outweigh the risks.” The simple fact is, there are no benefits, even before we get to the fact that this assertion is based upon statistical information that seems far from complete. According to the U.S. National Vaccine Information Center, more than 54,000 adverse events following vaccination, including convulsions, encephalitis and deaths, were reported to the FDA during a three-year period ending October 1993. However, since the FDA estimates that only 10 percent of doctors report adverse events, the real number could have been extremely high, more than half a million, including 50 or 60,000 serious injuries and 10-11,000 deaths. Connaught Laboratories, a vaccine manufacturer, estimates a 50-fold under-reporting of adverse events.

I can find no accurate statistical estimate for how many deaths and serious injuries are caused by vaccinations each year in the United States. It appears as though the government would rather not release such information, although a federal fund has been set up to cover the millions of dollars in lawsuits that are always pending. Thus, the law has been constructed so that perpetrators of this damaging practice cannot be sued, but continue to profit, while the government shields them with the people’s money.

Perhaps the government feels that with no way to enforce accurate reporting from doctors, it is futile to indulge in a guessing game. From the doctors’ perspective, there is little to gain from reporting, except an inexorable and embarrassing statistical slide toward collision with the truth. Consider these words from Kalokerinos and Dettman 20 years ago: “Moreover, it is disappointing to observe the futility and ineffectiveness of many ‘flu’ vaccines that have been accepted by an unwary public.”[21] In this writer’s opinion, the statement applies to all vaccines.

Taken in the Rear

Montague R. Leverson, M.D., Ph.D., M.A., an American physician, happening to come across some of Professor Bechamp’s writings in New York, became fascinated with his views. Realizing that the dated works anticipated Pasteurian “revelations” in certain important points, he decided to go to France to meet Professor Bechamp, where he heard the story of Pasteur’s plagiarism of the professor’s work directly. In a lecture entitled “Pasteur, the Plagiarist,” delivered at Claridge’s Hotel, London, on May 25, 1911, he outlined briefly Bechamp’s claim to be the first to produce a ferment in a medium containing no albuminoid matter, something thought impossible up to that time. (Ethel Douglas Hume’s book about Bechamp was based on work begun by Leverson, who is also the translator of Bechamp’s masterwork, The Blood.)

Understanding microzymian principle, he had this to say about inoculation:

When a drug is administered by the mouth, as was beautifully pointed out by Dr. J. Garth Wilkinson, in proceeding along the alimentary canal it encounters along its whole line a series of chemical laboratories, wherein it is analyzed, synthesized, and deleterious matter is prepared for excretion, and finally excreted, or it may be ejected from the stomach, or overcome by an antidote.

But when nature’s coat of mail, the skin, is violated, and the drug inserted beneath the skin, nature’s line of defense is taken in the rear, and rarely can anything be done to hinder or prevent the action of the drug, no matter how injurious, even fatal it may be. All the physicians of the world are incompetent either to foresee its action or to hinder it. Even pure water has been known to act as a violent. . . poison when injected into the bloodstream. How much more dangerous is it, then, to inject poisons known to be such, whether modified in the fanciful manner at present fashionable among vivisectionists or in any other manner. . . . Inoculation should be regarded as malpractice to be tolerated only in case of extreme danger where the educated physician sees no other chance of saving life.

Now the forcing of these inoculations upon individuals by law is one of the worst of tyrannies imaginable, and should be resisted, even to the death of the official who is enforcing it….

. . . The entire fabric of the germ theory of disease rests upon assumptions which not only have not been proved, but which are incapable of proof, and many of them can be proved to be the reverse of truth. The basic one of these unproven assumptions, the credit for which in its present form is wholly due to Pasteur, is the hypothesis that all the so-called infectious and contagious disorders are caused by germs, each disease having its own specific germ, which germs have existed in the air from the beginning of things, and that though the body is closed to these pathogenic germs when in good health, when the vitality is lowered the body becomes susceptible to their inroads.

Dr. Leverson goes on to describe disease as nature’s attempt to eliminate waste, and diseased tissues as being due to improper living. He suggests plenty of fresh air, the best sanitation, scanty clothes, and a scientific study of diet. He saw overeating as the precursor to “an enormous number of diseased conditions.”[22]

Vaccine Causes Polio Symptoms

Although Leverson is correct in his criticism of inoculation, even the body’s amazing “coat of mail” sometimes fails to be enough, as oral vaccine also poses danger. In a report on the Internet by Nando.net/Associated Press, we have a statement by Dr. Rebecca Prevots of the Center for Disease Control in Atlanta (Jan. 30, 1977) that almost every case of polio in the United States between 1980 and 1994 was caused by, or related to, the oral vaccine itself, “which consists of a live but weakened virus,” the CDC said. But, they hasten to add, there is a new, safer plan. “This emphasizes the timeliness of the change in policy,” said Prevots. Time is said to pass in a different manner for different personalities, but it still seems a bit of a stretch to apply “timeliness” to a period of 14 years with 133 impacted lives involved.

The new policy is “expected” not to eliminate risk but to cut it in half. In the official oddsmanship game of risk versus benefit, this is tendered as comfort to those yet to be afflicted. It consists of two preliminary killed-virus injections given to infants in the first four months “… to build up their immunity to polio. Then they are given two oral doses of ‘weakened-virus’ vaccine between ages 1 and 6.” One can only hope that these microbists desist from this folly because, in addition to their misplaced belief in germ theory, they do not yet understand that the extent of vaccine risk goes beyond reaction.

Compulsory Vaccination

As Leverson emphasized, people are forced to this abomination by law in many cases, especially schoolchildren. Overcoming this assault on human rights usually requires extreme persistence, courage and a knowledgeable approach. (I don’t recommend his approach, but it is self-defense!) The argument is literally that those at risk for damage must be sacrificed to save millions of others (i.e., “the benefits outweigh the risks”). But there is no science or even logic to this. If one is vaccinated, theoretically one is safe. If one chooses not to be vaccinated, then s/he does not threaten vaccinated people, but only those who have chosen that risk. Yet, the responsibility for the decision has been stolen from families under the guise of government responsibility to protect children from parents.

The unvaccinated, threatened by medical authority with the risk of developing a serious “disease,” are not told that said risk is greatly increased by germ theory mentality itself. It’s the medical equivalent of a mob protection racket, and the law has been manipulated to maintain the profitability of ill health produced by this practice. Holistic means of preventing or dealing with these symptoms are not even in the equation.

To summarize, if we consider Bechamp’s thesis that bacteria are evolved forms of anatomical elements called microzymas, that there are specific disease conditions rather than specific diseases, and that the microform is not the antecedent of disease, but arises in it; and if we add to this my thesis that the primitive stage of evolution, viruses, are apathological and created as response to structural breakdown, and that yeast, fungus, mold and their symptogenic poisons produce the symptoms attributed to viruses, is it possible that medical science is misdirected, if not malfeasant, in its intense pursuit of vaccinal answers? Was Bechamp on the right track? Are his many followers, including myself, correct as well? Is this why we cannot make a successful vaccine, and have, in fact, made dangerous and deadly ones?

On a final note of sanity, Edgar Cayce, the renowned psychic who could diagnose illnesses and treatments while in trance, was asked and answered the following question during a diagnostic session:

Q. Can immunization against contagious diseases be set up in any other manner than by inoculations?

A. If an alkalinity is maintained in the system-especially with lettuce, carrots and celery, these in the blood supply will maintain such a condition as to immunize a person. In an alkaline system there is less effect of cold and congestion.[23]

HIV/AIDS and the Monomorphic Disease Model

In 1960 a veteran retrovirologist urged his peers to “raise questions whether the known facts about viruses suffice to account for it.” The subject was cancer, the veteran was Peyton Rous, and the quote is from a paper in Cancer Research. Mindful of that example, in 1987 I asked a similar question in a paper likewise published in Cancer Research: whether the known facts about two human retroviruses suffice to account for leukemia and AIDS.

Clearly, following Rous’s example did not make me very popular with the multinational club of retrovirologists. My article was officially ignored and not “dignified” with a response because the AIDS virus establishment was “too busy . . . saving lives” and testing for antibodies to HIV. I was often shunned like an AIDS patient by my former fellow retrovirologists. My views were unwelcome for several reasons: after a frustrating, twenty-year-long search for a human cancer virus, the retrovirologists were craving for clinical relevance and hence happily adopted HIV-“the AIDS virus”-as the cause of AIDS. The discovery of HIV was announced in the U.S. at a press conference and the virus-AIDS hypothesis became instant national dogma. On this basis, the retrovirologists convinced their governments to spend billions of dollars to stop the predicted viral epidemic, already being labelled “the epidemic of the 20th century.” The virus was also the immediate darling of the biotechnology companies. Due to its very low complexity, it can be readily cloned for diagnostic test kits and vaccines. In turn, the virus was a hit with the press because it mobilized in readers the instinctive fears of a contagious disease, and appealed to the public prejudice that all evil comes from without.

-Peter H. Duesberg, Ph.D.

What Proof?

Perhaps the foremost thing that should be said about HIV is that it has never been proven to be the cause of AIDS, or any human illness for that matter. Not one scientific paper exists that demonstrates it. Based on activity in contrived situations in test tubes, among other illogical things, its culpability was a pronouncement handed down by an authority figure at the National Institute of Health. It is the same authority (Dr. Robert Gallo, head of NTH cancer labs) behind the expenditure of around a trillion dollars in cancer research which has produced nothing but an epidemic that is virtually out of control. (One wonders what it will take before people finally get the idea and stop creating walks, rides, telethons and cake sales to contribute money to the bottomless pit of biased, misdirected, wasteful and cruel orthodox medical research in cancer and degenerative disease.) And it is the same authority who has taken out two patents whose value depends upon HIV being accepted as the cause or a co-factor. One patent is for the technique of testing for HIV, and the other for a method of laboratory cultivation. No one in a position to do anything about it questions this obvious conflict of interest.

Kary Mullis, microbiologist inventor of the Polymerase Chain Reaction, says, “I can’t find a single virologist who will give me references which show that HIV is the probable cause of AIDS …. If you ask a virologist for that information, you don’t get an answer, you get fury.”[24]  Mullis has continued his outspoken criticisms of the AIDS establishment: “Where is the research that says HIV is the cause of AIDS? We know everything in the world about HIV now. There are 10,000 people in the world now who specialize in HIV.

None have any interest in the possibility HIV doesn’t cause AIDS, because if it doesn’t, their expertise is useless.”[25] Their embarrassment would also be considerable.

AIDS exists on paper. It is just a new label applied to a defined combination of immune-deficiency symptoms, which are not new, and a group of existing “diseases.” Intense public attention has been focused on the combination using statistical manipulation and fear that is bred in a general lack of understanding about health and disease. The question is whether all the destruction of AIDS can be laid at the feet of a nearly undetectable virus that defies every rule of medical microbiology. For example, HIV is said to cause AIDS after the appearance of antiviral immunity. Furthermore, the establishment has shown irresponsibility in referring to this syndrome as a disease. And the fact that it has been given the handy four-letter word encourages others to do likewise. This reinforces programmed notions, especially the idea of a single evil entity causing the whole thing. To emphasize these important points, AIDS will be here designated as “AIDSyndrome” in many instances.

A Medical Establishment on the Elastic Band Wagon

The HIV/AIDS theory is so elastic it stretches to embrace all reasonable criticism. Typical of this elasticity is the so-called latent period of the virus, which has gone from about one year to twelve, and shows potential of going to twenty. The elasticity is equaled only by the degree of credulousness required to accept HIV dogma. For example, it is said that in spite of the extremely low incidence of HIV in the body, it (mysteriously) tricks the immune system into attacking itself! I use the term HIV/Elastic Theory, or HIV/ET.

Another major factor is oppressive socio-economic and political conditions. Such conditions exist in the Third World particularly, but in their own way in sections of the United States. This aspect will not be detailed here, but includes such phenomena as corporate dumping of banned drugs on unregulated Third World markets, pesticide manufacture and use with frightening disregard for safety, squalid living conditions, and rainforest destruction. These, not HIV, are among the primary causes of what is labeled AIDSyndrome in the Third World. Pharmaceutical companies are heavily involved in the pesticide market. The corporate-interest connection with these abominations goes: pharmaceuticals, pesticides, agriculture, petroleum, international banking. Therefore, since the HIV/ET hoax has to cover a lot of financial territory, it must have considerable stretchability.

AIDSyndrome Scenarios

1. The first recorded AIDSyndrome case in history, one of five reported by the CDC in June 1981, was a 33-year-old Los Angeles male. He was engaged in a lifestyle which we now consider high risk; but there are reasons for risk other than those defined by AIDSyndrome “viromania” (a word coined by microbiologist Peter Duesberg). For one thing, he admitted using “poppers,” the aphrodisiac amyl nitrite (a poisonous secondary mycotoxin), then popular in homosexual bathhouses and discos. We are familiar with nitrites, used in tiny amounts as a preservative in meat. Sodium nitrite, a relatively weak member of the family, has been regulated for years as a potential carcinogen. It is well known that once in the body it is converted into carcinogenic nitrosamines (via its reaction with mycotoxins-not so well known).

Few mycotoxins, however, are more toxic than the organic nitrites (poppers), which react violently with almost anything. In water, they form the unstable nitrous acid, which destroys any biological molecule within reach. Nitrites and their breakdown products have long been known to scientists for their ability to mutate DNA, a point recently verified by direct experiment.[26]

During the 1960s and ’70s, poppers and other drugs were heavily abused, especially by sections of the male gay community. As a result, in 1969 prescription laws were tightened, and as usual, contaminated illegal products appeared on the streets adding insult to injury. In addition, impure products were marketed as “room odorizers.” According to a former nitrite researcher with the CDC, doses from inhalation are likely to exceed those from eating preserved meats by a million times.[27]  Yet this massive insult to the body, and the drug abuse factor in general, including filthy street injectables, OTC drugs, and especially prescription drugs such as antibiotics, antifungals and other immunosuppressive chemicals, are not considered causative, in favor of a scarce, barely detectable, inactive, difficult-to-transmit retrovirus. However, HIV/ET would respond by saying that, if anything, the drug factor increased susceptibility to a virus that invaded him and destroyed his immune system.

Popper use has been associated with one “AIDS indicator”- Pneumocystis carinii pneumonia (PCP)[28] – officially said to be caused by a protozoa. But the corresponding organism is not a protozoa; studies show the DNA sequencing of PCP to be identical to that of the Saccharomyces cerevisiae yeast.[29]  PCP is responsible for 62% of all AIDSyndrome mortality in America and Europe, candidiasis is responsible for 23%, and Cryptococcus neoformans is responsible for 12%. This means that yeast and fungus-the culminate microform symptoms of disease-contribute 97% of all AIDS-related mortality in those continents.

Thus, in the first recorded AIDSyndrome patient, a yeast infestation of the lung instigated pneumonia (symptom of over-acidification from fermentation processes), and oral thrush, a thick overgrowth of Candida albicans, choked him to death. He died, not from the ravages of a scapegoat retrovirus, but from an overdose of mycotoxins-nitrites-and the mycotoxins of yeast and fungal infestation-acetyl aldehyde, alcohol, and uric acid.

In Kenya, Africa, a 39-year-old woman from Zaire entered the hospital for treatment of her lung condition, which had begun with a relatively innocent cough and an unexpected drop in weight. Soon her coughs began to bring up blood, and tuberculosis was the diagnosis. But the patient had a strong allergic reaction to prescribed drugs, and her condition progressed from bad to worse, producing diarrhea, uncontrollable fever, swollen lymph nodes, and anemic blood disorders (all symptoms of a compromised biological terrain, as described in the main text). The woman was then diagnosed with AIDSyndrome (but not I-AIDS-Iatrogenic-AIDS).

The woman’s husband, whom doctors assumed must have transmitted AIDSyndrome to his wife, was suffering entirely different symptoms. He had pneumonia, a Candida infestation in his mouth, and lesions of Kaposi’s sarcoma on his now irregularly pigmented skin. He lost weight to a relentless diarrhea and was constantly fighting off episodes of gonorrhea. Their children had no symptoms.[30]

We are asked by national public health officials to believe that the Los Angeles case and the two Zaireans all suffered the same affliction from the same cause. The irony is that in terms of germ theory this is highly questionable, but when considered in the light of microzymian principle, it is highly plausible. With one instance of overlap, each person was affected with radically different symptoms-a Pneumocystis pneumonia (as noted, yeast in the lungs); a tuberculosis (symptom of exotoxin from an intermediate pleomorphic stage); and a Kaposi’s sarcoma, or papular tumors of the skin and mucous membranes (caused by mycotoxins). Before AIDSyndrome, these conditions never would have been connected by clinical doctors. Now they are struggling to believe that the common factor is the presence of nearly undetectable antibodies against HIV, and they could not be at a much worse disadvantage.

African AIDS

The World Health Organization’s definition for African AIDSyndrome includes some opportunistic infections, like tuberculosis; also, the African version of wasting called “slim disease,” a composite of weight loss, diarrhea, and fever; plus such conditions as persistent cough, skin problems and swollen lymph nodes. These signs comprise old, indigenous African health problems. But here is another example of HIV/ET. Compromised immunity makes “diseases” worse, so whatever “diseases” are already common become the indicators. All we have to do is plug HIV into the equation and we have AIDS. This makes sense to most people.

On the other side of the coin, malaria, for example, the leading killer in the Third World, produces fever and other symptoms frequently misdiagnosed as AIDS.[31]  Tuberculosis, also a common killer and part of the defined African syndrome, presents a challenging situation there, as described by a Nigerian medical professor: “The serologic demonstration of HIV infection in patients with tuberculosis in Africa is very important because it aids the separation of seropositive from the seronegative patients, since such a separation may be impossible in all cases on clinical grounds.”[32]

According to a Ugandan doctor treating AIDS cases, “A patient who has TB and is HIV-positive would appear exactly the same as a patient who has TB and is HIV-negative. Clinically, both patients would present with prolonged fever; both patients would present with loss of weight-massive loss of weight, actually; both patients would present with prolonged cough, and in both cases the cough would equally be productive. Now, therefore, clinically I cannot differentiate the two.”[33]  What can be the difference? Of course, a major one is that the AIDS case may be given expensive poison drugs which are nearly certain to end the patient rather than the illness, while filling pharmaceutical coffers.

Doctor Konotey-Ahulu has illustrated the confusion created by the HIV/ET: “Immunosuppressive diseases, of course, there always have been in Africa and elsewhere before antiquity was born. … I have clinical photographs from 1965 of a Ghanaian man who looked like some of the AIDS patients I saw in Africa recently. The man, who was like a skeleton, had severe nonbloody diarrhea (more than twenty bowel actions a day); he had what looked like fungus in the mouth [candidiasis], skin changes, periodic fever and cough-all the classical features of African AIDS. . . . The patient (according to relatives) had literally consumed on average one and a half bottles of whisky [a mycotoxin] every single day for the previous eighteen months before admission. We found it difficult to believe the story, but there are photographs today showing a complete reversal in 1966 of physical signs and symptoms, including the diabetes, when hospitalization cut short his alcohol supply and active treatment was administered, with gradual protein calorie buildup and pancreatin supplements.”[34]

Ongoing HIV testing since 1985 has revealed that eight times more Africans than Americans are infected (6 to 8 million)[35], yet the continent has produced fewer AIDS cases: 129,000 by 1992 and 345,639 as of December 1994.[36]  By contrast, several large studies recently published findings that among thousands of randomly selected Africans with standard AIDS diseases, fewer than half were HIV-positive.[37]  What does this say about a supposedly raging epidemic?

A completely separate epidemic seems to affect rural Africans, this one having no identified risk group. Some reports suggest a correlation between AIDS there and the symptoms of malnutrition. Doctors observe that AIDS patients who eat least often, or whose diets are skewed by food availability, suffer the most rapid decline in health. This should surprise no one. In rural Africa, the most important aspects to be considered, as in the entire history of epidemics, are: sanitation, which rarely exists; clean water supplies, also rare or nonexistent; and decent nutrition. It would seem that HIV/AIDS has created no new epidemic in Africa. But since HIV/ET is such a well-received hoax, it jumps in and “takes credit,” while obfuscating relevant issues.[38]

In 1985, 250 patients from a local hospital in a remote area of Zaire, none of whom had clinical AIDS, were tested for HIV. Twelve percent clearly showed positive, while another 12 percent were borderline; but there was no correlation with any health complaints. The researcher concluded, “Thus, if antibodies indicate prior exposure to [the AIDS virus], this population must have had and survived [AIDS-virus] infection without lasting health problems.”[39] In a similar situation in Venezuela, Indians who live cut off from the rest of the country’s people were found with from 3.3 to 13.3 percent infection, with no symptoms.40 Being so isolated, they are highly unlikely to have been infected within the latent period. In both these cases, investigators concluded that people could have been living with the virus for a generation or more.

One might be challenged, as the Ugandan doctor was, to distinguish between an AIDS/tubercuIosis and a traditional one. Since the clinical symptoms are identical, the CDC has stipulated in its current definition that tuberculosis must be renamed AIDS if HIV antibodies are also found. In the absence of HIV antibodies, the disease is classified under its old name, tuberculosis, and treated accordingly. Therefore, simply by definition/elasticity, HIV antibodies can never be found apart from AIDS, and vice versa; and any symptomology has the potential to become an AIDS indicator with HIV around. In general, if doctors can tell the difference between AIDS on the one hand, and non-AIDS presence of its indicator diseases on the other, only by testing for antibodies to HIV, which sometimes don’t even have to be present (discussed below), it would seem we have a syndrome of contrived or arbitrary origin, circularly defined.

HIV/AIDS and Koch’s Postulates

Koch’s postulates is a set of conditions long accepted as the requirements for establishing a fixed microorganism as the cause of a specific disease. The case for HIV as the AIDS virus, as with the identification of any causative infectious agent, should depend upon meeting these parameters, of which there are four. (Keep in mind that researchers disagree about what constitutes proof that any germ causes a disease.)

1.  The germ must be found in all cases of the disease. Tissues said to be affected by HIV include primarily the white blood cells of the immune system, particularly the T-cells, the brain neurons in dementia, skin cells in lesions of Kaposi’s sarcoma, as well as, theoretically, any cell in the body expressing the CD4 surface receptor said to be the key to HIV cell entry. But no trace of the virus can be found in either the Kaposi’s sarcoma or the neurons of the central nervous system. HIV/ET has now moved from involving only immune cells to other types of cells in order to explain certain AIDS-defining symptoms which are not immune deficiencies anyway, including the cancers, dementia and wasting diseases, and which have not been, or cannot be, explained in terms of a germ-theory virus model that involves destruction of the immune system.

And if HIV were actively infecting T-cells or other members of the body’s immune system, extracellular virions should easily be found circulating in the blood. But in most individuals suffering from AIDSyndrome, no particles can be found anywhere in the body.

Another aspect of HIV/ET is that now several HIV “reservoirs” have been suggested. One encyclopedia, which will go unnamed, says: “Researchers have also been able to show direct infection of bone-marrow cells-the precursors of circulating blood cells-and the proliferation of the virus within these cells. Thus bone marrow may represent an important reservoir of HIV in an infected person and provide a potential mechanism for dissemination of the virus through the body.” This is misinformation, pure speculation, a conclusion based on laboratory pyrotechnics, or scientific fraud. It is also said that macrophages can support HIV replication while harboring the virus from immune surveillance. Circulating macrophages are said to play an important role in the distribution of HIV throughout the body, including the brain. The question is, wouldn’t there be significant amounts of virus in a reservoir? The fact remains: it is nearly impossible to recover HIV from its “victims.” (See below under “Autoimmune Theory.”) One paper published in March 1993 reported two individuals with about 100,000 particles per milliliter of blood, among dozens of patients with little or no detectable extracellular particles.[41]

The abundance of uninfected T-cells (about one in 500) in all AIDSyndrome patients is the definitive argument against the false claims for high cell-wall particle “loads,” or “burdens,” in AIDS patients. The absence of active, infectious virus automatically disqualifies HIV as a player in the AIDSyndrome.

2.  The germ must be isolated from the host and grown in pure culture. Even for the most experienced virus hunters, a virus that is so extremely scarce is difficult to find. Only with rare luck and extreme persistence has HIV been extracted from an antibody-positive person. This amounts to finding the proverbial needle of HIV in a haystack of human DNA. This difficulty speaks to HIV’s lack of potential in disease.

3.  The purified germ must cause the disease again in another host. There is no animal or human model for HIV and AIDS, and where there is no animal or human model, you cannot establish Koch’s postulates. (It is more than disconcerting to think of the number of primates that have been injected to this day in an attempt to produce AIDS.) HIV/ET jumps in and says that HIV should receive special dispensation from Koch’s postulates. A major stumbling block is the latency which is claimed, but whose modus is not explained by authorities. In 1989 the official latent period between HIV infection and the onset of AIDS was one year. This period of “incubation” has since been stretched to 1012 years. For each year that passes without the predicted explosion in AIDS cases, approximately one year is added to this period. Even this is insufficient; with only 5 percent of infected Americans developing AIDS each year, the average latent period would have to be revised to more than 20 years for 100 percent to become sick.

HIV should cause AIDS within two weeks of infection at most, but it does not, and with the complete lack of a demonstrated process by which HIV diminishes immune function, belief in a decade or more of unexplained latency requires a level of “faith” beyond this writer’s capacity. Another major stumbling block is that even once the latent period is apparently over, there is still precious little development of the virus.

4. The germ must then be isolable from the newly infected host. We are now back to the problem of meeting requirement number 2.

The Antibody That Isn’t

According to germ theory, an antibody is a certain antidote to a pathogen. According to HIV/ET, however, the more antibodies you have to HIV, the sicker you are said to be. AIDSyndrome is the only “disease” in the allopathic file cabinet in which antibodies to the causative agent mean you’re in trouble; and it defies just about every known law, rule, guideline, fact, and behavior in the germ theory book. This includes, as we have seen, Koch’s postulates, and, as we will see below, Farr’s Law. Furthermore, vaccine research proceeds on the basis of producing antibodies to HIV in the patient. Apparently, these “synthetic” antibodies will signal recovery, while one’s own signal death.

The Autoimmune Theory

One explanation put forth for the deadliness of such a scarce pathogen is that it somehow induces a self-destructive immune response (the system attacks itself). Evidence for this is said to be low white cell counts in people with AIDSyndrome; however, there is nothing to support the hypothesis, i.e., no plausible process by which this occurs has been suggested (see “What’s Overlooked” below).

For the sake of discussion, let us allow germ-theory interpretation of immune function and autoimmunity. With only one in 500 immune cells said to be infected in HIV positives, it would seem to require a virus of extraordinary cunning to get uninfected cells to attack each other and not infected ones, which would be self-defeating for the virus. Or in the latter event, such cunning could be matched only by the adroitness required to move quickly from one host cell to another just before destruction. Or, if macrophages are involved, the process should lead either to increasing titers of virions in the blood, lymph, etc., as infected cells are lysed, or to increasing concentrations in macrophages if they are ingesting T-cells. This supports the reservoir notion (if there were any viruses to be found in them). It is thus easy to expand HIV/ET.

HIV/AIDS and Farr’s Law

Established in the early 1900s, Farr’s Law, which is fundamental to virology, states that viral disease develops exponentially, and dictates that illness will strike soon after infection. The rate-determining factor of the exponential growth of viruses is viral generation time, which is between 8 and 48 hours. Since laws are made to be broken or excepted, viruses with incubation periods longer than allowed by Farr’s Law are called “slow viruses.” And since HIV joins an exonerated class of viruses by not multiplying according to this law of virology, virologists stretch HIV/ET to accommodate it. The question arises, though, of how anyone can determine or demonstrate when a “natural” HIV infection takes place, and thus determine latency, since no one is being tested daily or weekly, etc., and there is no animal model. Within the slow-virus concept, adopted as an exception to Farr’s Law, retrovirologists can find refuge, hold on to their theory, hibernate in their labs, and hope the long winter of HIV latency is over before they expire.

According to expert retrovirologist Dr. Peter Duesberg, “The slow virus concept has never been reconciled with the short generation time of viruses and the immune system. Once the virus lies totally dormant, an intact immune system will never allow any virus to be reactivated to multiply into numbers that would threaten the host. For a virus to be reactivated, the immune system first must be destroyed by something else-the real cause of a disease. A reactivated virus would just contribute an opportunistic infection. Thus, there are no slow viruses, only slow virologists.”42 Also, says Duesberg, “Retroviruses are all very similar. I mean, there are differences, but as far as pathology is concerned, you don’t see a marker in one which is going to explain why it supposedly wakes up from sleep and becomes active.”[43]

The Chemotherapy Drug Azidothymidine (AZT)

HIV-antibody-positive individuals suffer major health risks from AIDS medications routinely administered by physicians uncritical of drug-company propaganda. AZT, an isolate from herring sperm, was first synthesized in 1964 by Jerome Horwitz, heading a lab at Detroit Cancer Foundation and financed by an NIH grant. Designed to kill cancer cells, Horwitz’s creation is a chemically modified form of a DNA building block. When a cell divides, it must copy its complete genetic code, which is stored in long chromosome chains. The DNA components (nucleotides) are linked to one another in a sequence. But Horwitz’s altered DNA building block enters the growing DNA chain while a cell is preparing to divide and acts as a premature terminator, blocking addition of DNA components. Being unable to copy its DNA sequence, the cell dies.

AZT was the perfect killer of dividing cancer cells. When the compound was tested on cancer-ridden mice, however, it failed to perform as expected and instead revealed its extraordinarily deadly nature. The experimental drug was withdrawn from testing and never approved for human use-until AIDSyndrome. Side effects of AZT include ulcerations and hemorrhaging; damage to hair follicles and skin; destruction of mitochondria, the energy dynamos of cells; wasting of muscles; and the destruction of the immune system and other blood cells. Children are affected more severely, because many more of their cells are dividing than in adults.

Amid scandal-(l) the single, human trial that was ruined, yet was claimed to have proven effectiveness; (2) free corporate (Burroughs Wellcome) acquisition of large amounts of National Cancer Institute (taxpayer) raw material and technology; and (3) government stonewalling of other, potentially less expensive antivirals-AZT was first approved for treatment of AIDS in 1987.44 The cost was $250 a shot, or about $18,000 per year, per case. In 1990 it was approved for AIDS prevention, and has currently reached an average cost of $6,000 per year.

I have worked with many HIV-antibody-positive individuals who have for years remained completely free of any AIDS-indicator symptoms or any other significant ones. When treated with medications like AZT, however, people are observed to sicken and die from “wasting disease” in a short period of time. I, as well as other molecular cell biologists, know of no one who has been treated with AZT and lived for more than around one year. Fortunately, it has begun to fall out of favor as the drug of choice.

Use of AZT is a good example of two other medical phenomena: (1) the odds game called the therapeutic index, or the relationship between a drug’s effectiveness and its toxicity; and (2) the dependence upon destruction that informs “scientific medicine.” The acceptable toxicity of a drug is directly proportional to, and established by, the deemed deadliness of the disease. However, to this date the Physicians’ Desk Reference quotes the low toxicity of AZT reported by Broder, Barry, Bolognesi, and colleagues in 1986. According to at least four independent studies published since, however, the toxicity of the drug is a thousand times higher.[45]

Broder, Barry, Bolognesi, and colleagues overlooked or disregarded two basic factors in their lab experiments: (1) In the test tube in which they tested AZT, there was a high concentration of “infected” cells. But, as noted earlier, in a person with HIV, titers are very low, and the ratio of infected to healthy cells is very low (only 1 in about 500 T-cells in HIV antibody-positive persons is ever “infected”); (2) Like all other chemotherapy drugs, AZT is unable to distinguish between target cells and healthy cells. The disastrous consequence is that AZT must poison 499 good T-cells in order to poison one inhabited by the AIDS “virus.”

Real Fallout

Various individuals diagnosed with AIDS who were paraded in the media, trapped into following the AIDS “company line,” later died of AIDS-related symptoms. Many were treated with AZT from the very beginning, even though they showed no signs, or few signs, of ill-health at the start of the program. Two examples are Kimberly Bergalis (featured in the October 22, 1990 issue of People magazine) who supposedly “caught” HIV from her Florida dentist, and Arthur Ashe, the heterosexual tennis professional. (Kimberly had only a minor yeast infection at the start of her AZT program.) In typical fashion, the news media focused upon, and widely broadcast, the details of their gradual degeneration and painful deaths, which exhibited all the classic symptoms of AZT poisoning. “AIDS” death and AZT death are outwardly indistinguishable. Here is a perfect combination: an illness incorrectly billed as universally fatal, treated by a useless, frequently fatal drug.

What’s Overlooked

Shades of doubt concerning HIV/ET validity in terms of germ theory have arisen since three-quarters of the 20,000 hemophiliacs in the United States were infected by HIV through the blood supply a little more than a decade ago. During that period, clotting factor VIII doubled life expectancies, while relatively few developed AIDSyndrome. HIV has made no measurable impact on the well-being of hemophiliacs, except for devastation of those who are treated with AZT.[46] No evidence has shown that death rates from blood transfusions ever increased from HIV transmission, nor has anyone demonstrated that death rates declined once the virus was screened out of the blood supply.

Even if AIDSyndrome does exist as a new phenomenon, perhaps insufficient scrutiny has been paid to the idea that it is not virus-based, but related to an inverted way of living and eating. For these reasons, and the sociopolitical ones mentioned earlier, illness is simply on the rise in general, and individual cases are often more intense and intractable. Cancer is now epidemic, for example. “Flesh-eating” bacteria have made an appearance. Disease intensity and statistics must also be considered in terms of the ineffectiveness and iatrogenic influence of the orthodox approach to illness-the equivalent of trying to remove a screw with a hammer. HIV/ET attempts to divert responsibility for health disaster from an inept, sometimes malfeasant, pharmaceutically controlled medical tradition. A century of medical practice and health concepts based on the scientifically erroneous germ theory is as much the cause of AIDS as any single factor-probably more. AIDS could easily have been predicted epidemiologically as an aspect of the burgeoning crisis in health. It had to be blamed on a virus on order to distract attention from the real problems.

Speaking of prediction: Several doctors and writers have made a strong connection between AIDSyndrome and syphilis. The consequences of misdiagnosed or improperly treated (including penicillin) syphilis may be misinterpreted as AIDS indicators. According to one researcher, almost every AIDSyndrome indicator has been seen in syphilis.[47]  An interesting corollary here is the Tuskegee Alabama Syphilis Study, in which 400 Alabama sharecroppers were allowed to suffer and die with untreated syphilis (which they were not told they had) for 40 years until the study was exposed in 1972. Did a medical establishment (CDC, Public Health Service, NIH) capable of such behavior learn anything about syphilis which might have helped predict, and formulate a description of, the “new” AIDSyndrome epidemic?

With the primary U.S. AIDS groups, or with any group for that matter, if you understand microzymian principle and consider the blood as a flowing tissue, it will be seen in general that body fluids which find their way from one individual directly into the blood of another are a stress factor on the body. This is by virtue of the introduction of foreign tissue and possibly morbidly evolved microzymas. Total impact depends on the degree to which the terrain is already compromised. In fact, a major danger is blood transfusion itself, essentially a “tissue transplant,” which is a threat or irritant to immune function. There is no reason to believe that such repeated stress will not, by itself, overwork and weaken immune function and drain overall energy reserves.

Current medical science gives credence to the so-called autoimmune response, where white cells said to be deranged indiscriminately destroy and/or clear out healthy and unhealthy cells. This misconception arises as a consequence of germ theory mentality, which misunderstands the central function of the immune system. It is essentially a sophisticated janitorial service. It operates to keep the place clean and to recycle usable material. Should “self cells or tissue become useless or even dangerous to the body, the immune system will clean them out. Thus, it is not deranged, but is doing its job correctly. The host is somehow not doing its job, however, to maintain a balanced internal environment, which is the first line of defense, not immunity, against tissue destruction and infection. This is because infection can come from within. And it bears repeating that the fundamental misconception of the germ theory is that infection must be invasion, rather than an endogenous morbid change in chemistry or micromorphology.

Compromised or weakened by fungal infestation (evidence for which is obvious and strong) or by drugs and chemicals such as mycotoxins, the immune system may weaken and fail to be efficient, but it will not attack healthy cells. There is a situation where this may appear to be so-when free radicals produced by the immune system in response to mycotoxins and morbidly evolved microforms damage local cells and tissue by the “shotgun” effect – but it is not a direct attack on “self,” and is frequently an overreaction to the alarming situation.

What Constitutes AIDS in 1998?

HIV/ET responds to the question of why the syndrome hasn’t spread into the general population with the reply that it just needs a little more time. To accomplish this, however, the situation requires a little massage as well. On occasion, the definition of AIDS has been expanded (along with the latency period), with more indicator diseases being added to the list. In 1987, purportedly for surveillance purposes, a major change was made to the definition, which not only added diseases to the list, but removed, in the presence of a positive HIV test, exclusions for other known causes of immune suppression. The rationale was to provide consistent statistical data for public health purposes. Thus, a person could now be diagnosed with a surveillance case of AIDS.

In the CDC guideline, the caveat was given that clinicians would not rely on this definition alone to diagnose serious disease caused by HIV. Good medical practice, which was apparently expected to be employed later, could be expected to catch cases that somehow slip through the vast surveillance net because they have either a negative H1V-antibody test or, in the presence of HIV antibody, an opportunistic disease not listed in the definition. With the new rules, in the case of diagnosis of any one of several indicator diseases by a “definitive method,” AIDS had to be diagnosed even if the patient were HIV negative.

One question would seem to be: Why not employ good medical practice at the outset? Also, with the vast range of conditions listed, one is hard pressed to imagine what might not be included, except perhaps the common cold. But the overall effect of this change was to boost statistics and bring more people into the web of fear surrounding the syndrome. In 1992 another statistic-bumping revision was handed down.

Today the AIDS-indicator list includes, but is not limited to, Pneumocystis pneumonia, Kaposi’s sarcoma, non-Hodgkin’s lymphoma, candidiasis, cryptococcosis, tuberculosis, herpes simplex, cryptosporidiosis, coccidioidomycosis, toxoplasmosis, wasting disease and dementia. And symptomologies such as syphilis, chronic fatigue, anemia, arthritis, nephritis, pneumonitis, diarrhea, cervical cancer, and a T-cell count of less than 200 cells per microliter, or less than 14% of the expected level, have been added to the diagnostic list. It appears that when a higher rate of new AIDS cases is needed “for public health data,” the CDC expands the definition. With the stroke of a pen an illusion of the spread of AIDS is created. To include the major symptoms of malnutrition (wasting) as an AIDSyndrome indicator, especially in Africa and the Third World, is to ensure a burgeoning statistical picture.

Nor is this the first time such statistical manipulation has occurred in medical history, polio being an excellent example. According to Dr. Herbert Ratner, former public health officer for Oak Park, Illinois, prior to vaccine introduction, doctors were being paid $25 apiece by the National Foundation for Infantile Paralysis for polio case reports. Also, Ratner indicated, it was known that paralytic polio went away in 50 percent of cases within 60 days. After the arrival of the Salk vaccine, the case definition for polio was changed to require symptoms for 60 days before a diagnosis could be reported. Thus, if someone had it and it went away within that time, it was never counted, making the vaccine look better.48 After vaccine introduction, cases previously reported as poliomyelitis were differentiated as aseptic meningitis. Despite this subterfuge, case incidence increased dramatically after vaccine introduction (80 percent from 1958 to 1959) but the Public Health Service manipulated statistics and made statements to give the opposite impression.[49]

Should anyone question the idea that the CDC at any time “needed” a higher case rate, consider the following: In the early years of AIDSyndrome, while this supposed epidemic was developing, the CDC stood back and did nothing to identify and help the sexual contacts of AIDSyndrome patients. It was a departmental “do-nothing” policy. This has been documented and published by a former Public Health Adviser and AIDS researcher who worked at the CDC at the time.[50]

A Final Thought

To prove that HIV is the cause of AIDS and make HIV/ET more than a speculative hypothesis, it would be necessary to show the presence of HIV among patients with AIDS diseases whose personal history did not include: (1) chronic, abusive, male homosexual activity with associated chronic drug abuse and antibiotic dependency; (2) massive ingestion or injections of recreational drugs; and (3) use of toxic prescription medications, including AZT and antifungals. Likewise, one would have to show HIV absent among groups of healthy, asymptomatic individuals. In spite of the millions which have been spent on AIDS research, such a study has never been undertaken, although we have seen instances of long-term HIV presence with no correlated illness.

In my research, I can see only minor differences among dried blood samples of people with cancer, dementia, MS, and diabetes on the one hand, and the person with AIDS on the other. They all show excess fermentation processes and disseminated intravascular coagulation. They are all rotting from the inside out. There seems to be one model that makes sense and consistently validates clinical observation and research: There is only one physiological disease-terrain imbalance seen as acidification, due primarily to an inverted way of eating and living. Acidification leads to the one sickness, or primary symptom of disease-morbid microzymian response, or the overgrowth of microforms whose poisons result in secondary symptoms (commonly called “diseases”), these being produced in or by the body in keeping with the uniqueness of each individual. Forms of toxicity such as environmental chemicals and heavy metals also play a role, but in most cases will also disturb the central balance of the microzymas, thus complicating the situation with morbid microzymian evolution.

There are no “diseases” created by “microbes” invading from without. Viruses are not even symptogens. HIV has no causative connection with disease, and no new epidemic exists.

References 

[1]  L’Orthobiologie Somatidienne. Video by Gaston Naessens, 1991.

[2]  Bechamp, Pierre Jacques Antoine. The Blood and Its Third Anatomical Element, (Montague R. Leverson, translator). London: John Ouseley Ltd., 1912, pp. 205 and 229.

[3]  Kalokerinos, A. and Dettman, G. Second Thoughts About Disease: A Controversy and Bechamp Revisited. Warburton, Victoria, Australia: Biological Research Institute, p. 9 [booklet published from an article in Journal of the International Academy olPreventive Medicine, July 1977; 4(1)].

[4]  Hume, E. Douglas. Bechamp or Pasteur? Ashingdon, Rochford, Essex, England: The C.W. Daniel Co. Ltd., 1923, p. 109.

[5]  Farber, C. Out of Africa, Part I. Spin Magazine, March 1993: 61-63, 86-87.

[6]  Kalokerinos and Dettman, op. cit., p. 12.

[7]  Ibid.

[8]  Denetclaw, T.H. and Denetclaw, W.F.J. Is “Southwest U.S. mystery disease” caused by hantavirus? Lancet, 1994; 343: 53-54.

[9]  Russel, S. On the Trail of Hantavirus. San Francisco Chronicle, July 4,1995: AI, AI2.

[10]  Russel, S. Signs that Ebola Virus Is Fading Away. San Francisco Chronicle, May 24,1995: A6.

[11]  Kaiser, R. Africa State Hospitals Make Viruses, Not Patients, Feel at Home. Washington Post, June 4,1995: A6.

[12]  Physicians’ Desk Reference (PDR), 1997, p. 1730.

[13]  Beale, A.J. Vaccines and Antiviral Drugs. In: Topley and Wilson, Principles of Bacteriology, Virology and Immunity, (Publisher, Year?), p. 149.

[14]  Jegede, V.A. et al. Vaccine Technology. In: Encyclopedia of Chemical Technology, (Publisher, Year?), p. 629.

[15]  PDR, op. cit., p. 2650.

[16]  Rappaport, John. Touching All Bases-Exploring Alternative Theories of AIDS. The Reader (Los Angeles Free Weekly), August 7, 1987; Vol. 9, No. 42: 10. [Note: Reference pertains to evidence that calves were recently, or are still, cruelly used for this purpose. Minor details of the process differ from those described in the article.]

[17]  PDR, op. cit., p. 2656.

[18]  Kalokerinos and Dettman, op. cit. (Ref. 3), p. 13.

[19]  Ibid., p. 12.

[20]  Goldberg, B. Origin of AIDS. Lancet, 1992; 339: 1548.

[21]  Kalokerinos and Dettman, op. cit.

[22]  Pearson, R.B. The Dream and Lie of Louis Pasteur. Collingwood, Australia: Sumeria Press, 1994, pp. 32-35.

[23]  Cayce Reading #480-19. The Cayce readings are on fde at the Association for Research and Enlightenment, Virginia Beach, VA.

[24]  Hodgkinson, N. Experts Mount Startling Challenge to AIDS Orthodoxy. Sunday Times (London), April 26,1992; I: 12-13.

[25]  Carroll, John. The Weird Way to Win a Nobel Prize. San Francisco Chronicle, October 21,1993: E9.

[26]  Mirvish, S.S., Williamson, J., Badcook, D., Sheng-Chong, C. Mutagenicity of Iso-butyl nitrite vapor in the Ames test and some relevant chemical properties, including the reaction of iso-butyl nitrite with phosphate. Environmental. Molecular Mutagen, 1993; 21: 247-252.

[27]  Rappaport, John. AIDS Inc. Scandal of the Century., San Mateo, Cal.: Human Energy Press, 1988, p. 38.

[28]  Ibid., p. 40.

[28]  Fungalbionics Convention: The Fungal/Mycotoxin Etiology of Chronic and Degenerative Disease. Metro Toronto Convention Centre, September 30,1994.

[29]  Konotey-Ahulu, F.I.D. What is AIDS? Watford England: Tetteh-A’Domeno Co., 1989, p. 109.

[30]  Rappaport, op. cit. (Ref. 27), p. 73.

[31]  Williams, A.O. AIDS: An African Perspective. Boca Raton, Fla.: CRC Press, 1992, p. 238.

[32]  Duesberg, Peter H. Inventing the AIDS t7ras,(**Publisher, YEAR?), p. 293.

[33]  Konotey-Ahulu, op. cit., pp. 56-57.

[34]  World Health Organization, The Current Global Situation of the HIV/AIDS Pandemic, 1995.

[35]  Duesberg, Peter H. AIDS acquired by drug consumption and other noncontagious risk factors. Pharmacology and Therapeutics, 1992; 55: 258.

[36]  Ibid., p. 240.

[37]  Rappaport, op. cit. (Ref. 27), pp. 71-82.

[38]  Biggar, R.J. et al. Seroepidemiology of HTLV-III antibodies in a remote population of Eastern Zaire. British Medical Journal, 1985; 290: 808-10 (cited in Coulter, Harris L. AIDS and Syphilis, The Hidden Link. Berkeley, Cal.: North Atlantic Books; and Washington: Wehawken Books, 1987; p. 61).

[39]  Duesberg, Peter H. Retroviruses as carcinogens and pathogens: Expectations and reality. Cancer Research, 1987; 47: 1199-1220 (cited in Coulter, Harris L., op. cit. [Ref. 38], p. 61).

[40]  Lemonick, M.D. Return to the Hot Zone. Time International, May 22,1995; 145: 56-57.

[41]  Duesberg, Peter H. AIDS acquired by drug consumption . . . (Ref. 36), pp. 237-38, 241, 247.

[42]  Rappaport, op. cit., p. 130.

[43]  Committee on Government Operations. AIDS Drugs: Where Are They? 73rd Report. U.S. Government Printing Office; October 3, 1988. (Cited in Culbert, Michael L., D.Sc. AIDS: Hope Hoax and Hoopla. Chula Vista, Cal.: The Bradford Foundation, 1898, pp. 10-11).

[44]  Chiu, D. and Duesberg, P.H. The toxicity of Azidothymidine (AZT) on human and animal cells in culture at concentrations used for antiviral therapy. Genetica 95, 1995: 103-109. Duesberg, Peter H. AIDS acquired by drug consumption . . . (Ref. 36), pp. 201-77.

[45]  Yarchoan, R, Pluda, J.M., Perno, C.-F., Mitsuya, H., Broder, S. Anti-retroviral therapy of human immunodeficiency virus infection: Current strategies and challenges for the future. Blood, 1991; 78: 859-84. McLeod, G.X., Hammer, S.M. Zidovudine: Five years later. Annals of Internal Medicine, 1992; 117: 487-501.

[46]  Duesberg, Peter H. Is HIV the cause of AIDS? Lancet, 1995; 346: 1371-72.

[47]  Coulter, Harris L. AIDS and Syphilis, The Hidden Link. Berkeley, Cal.: North Atlantic Books; and Washington: Wehawken Books, 1987, p. 37.

[48]  Rappaport, op. cit. (Ref. 27), pp. 152-53.

[49]  Hearings before the House Committee on Interstate and Foreign Commerce. House of Representatives, 87th Congress, 2nd Session, H.R. 10541, May 1962, pp. 94, 96, 112 (cited in: James, Walene. Immunization: The Reality Behind the Myth, 2nd edition. Westport, CT: Bergin & Garvey (Greenwood Publishing Group, Inc.), 1995, pp. 35-36).

[50]  Sermos, Gus G. Doctors of Deceit and the AIDS Epidemic-A View From the Inside. McComb, Miss.: GGS Publishing, 1988, p. 3.

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 Robert Young PhD

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

Abstract

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

Introduction and Historical Perspective

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

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

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

The Mechanics of Blood Coagulation

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

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

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

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

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

Key Ingredients of Pathological Blood Coagulation

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

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

Mycotoxins and Metabolism by Fermentation

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

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

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

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

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

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

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

Endotoxins

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

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

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

Exotoxins

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

Tissue Factor

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

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

Development of Disseminated
Intravascular Coagulation
(DIC)

DIC Induced by MAT and Tissue Factor

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

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

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

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

DIC Induced by Electrostatic Attraction

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

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

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

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

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

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

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

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

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

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

Endothelial Cells as Antithrombotics or Procoagulants

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

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

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

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

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

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

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

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

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

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

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

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

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

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

allergiesbefore

 

 

 

 

 

 

 

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

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

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

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

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

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

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

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

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

Detection of Disseminated Intravascular Coagulation

The Sonodot Analyzer

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

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

Fibrin Degradation
Products and Fibrin Monomer

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

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

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

Other tests include:

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

The Mycotoxic Oxidative Stress Test (MOST)

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

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

BowelCancerLive Blood Dried Blood_0166

 

 

 

 

 

 

 

 

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

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

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

calciumpattern

 

 

 

 

 

 

 

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

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

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

sialicacid

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

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

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

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

Aspergillusnigercrystal

 

 

 

 

 

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

HIV

 

 

 

 

 

 

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

poorfibrin

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

The MOST from Solubilized Extracellular Matrix

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

Extracellular Matrix Degradation by MAT

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

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

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

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

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

Conclusion

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

­

­

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

[23]  Ibid.

[24]  Ibid.

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

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

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

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

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

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

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

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

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

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

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

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

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

[43]  Rapaport, op. cit. (Ref. 4).

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

[45]  Rapaport, op. cit. (Ref. 4).

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

[47]  Ibid.

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

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

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

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

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

[53]  Ibid.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Tables

Table 1

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

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

Table1a

Table 2

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

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

Table2a

Table 3

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

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

Table3a

Table 4

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

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

Table4a

 Table 5

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

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

Table5aTable 6

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

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

Talble6

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table7

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table8Table 9

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

Table9

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table10

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table11

Table 12

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

Table12

Table 13

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

Table13

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

10665731_1492605317673050_5545234100728925724_n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The Truth About Alkalizing Your Blood, Interstitial and Intracellular Fluids!

The following article is Dr. Robert O. Young’s rebuttal to Dr. Ben Kim’s felacous statements concerning the bio-electro/chemistry of the blood and tissues.
 

April 12, 2012

The Truth About Alkalizing Your Blood

Dr. Ben Kim states: Is it true that the foods and beverages you consume cause your blood to become more alkaline or acidic? Contrary to popular hype, the answer is: not to any significant degree.

Dr. Robert O. Young states: The pH of blood and interstitial fluids are constantly being challenged with environmental, dietary, respiratory, and metabolic acids. The body deals with blood acids by eliminating these acids through the four channels of elimination (urination, perspiration, defecation and respiration) and the buffering of acids through the alkaline buffering system in order to maintain the delicate pH balance of the blood plasma and interstitial fluids at 7.365.

Dr. Kim Ben states: The pH of your blood is tightly regulated by a complex system of buffers that are continuously at work to maintain a range of 7.35 to 7.45, which is slightly more alkaline than pure water.

Dr. Robert O. Young states: The pH of your extracellular fluids, which includes the blood plasma and the interstitial fluids are kept at a very narrow range at 7.365 to 7.385. Any pH measurement of blood plasma in excess of 7.385 indicates a condition of compensated acidosis and any pH measurement of blood plasma or interstitial fluids below 7.365 indicates a condition of decompensated acidosis.

Screen Shot 2018-11-25 at 10.08.28 AM

When the pH of the blood plasma increases above the 7.385 this is the result of the blood pushing environmental, dietary, respiratory and metabolic acids out into the interstitial fluids of the colloidal connective tissues of the schade as the blood is pulling alkaline mineral salts such as calcium ions from the bones or magnesium ions from the muscles to offset the increase of acids in the blood. It is always a sure sign that as the blood plasma is becoming more alkaline the interstitial fluids of  the colloidal connective tissues of the schade are becoming more acidic and this is the cause of ALL inflammatory and degenerative diseases.

When the body tissues, organs, cells, or the alkaline reserves (sodium, calcium, magnesium and potassium) become deficient in alkaline minerals the blood plasma pH will drop below the ideal 7.365 causing decompensated acidosis leading to hemolysis at a pH below 7.365 or a coma and/or death at a pH below 7.2.

Dr. Kim Ben states: If the pH of your blood falls below 7.35, the result is a condition called acidosis, a state that leads to central nervous system depression. Severe acidosis – where blood pH falls below 7.00 – can lead to a coma and even death.

Dr. Robert O. Young states: If pH of the blood plasma drops below 7.365 the result is called decompenated acidosis.  If the pH of the blood plasma stays at the ideal 7.365 this is called compensated acidosis. And if the pH of the blood plasma increases above the 7.365 this is called “latent tissue acidosis” in the interstitial fluids of the colloidal connective tissues of the schade.

The blood plasma pH always goes alkaline when the blood pushes out environmental, dietary, respiratory or metabolic acids out into the interstitial fluids of the colloidal connective tissues of the schade. These acids are always deposited into what I call the ‘acid catchers’ which are the connective tissues of the schade. This leads to what I call ‘latent tissue acidosis’.

As acids build-up in the colloidal connective tissues of the schade and if NOT eliminated by the lymphatic system and the out through the channels of elimination, including the skin, lungs, bowels or urine this will result in ALL the connective tissue diseases and degenerative diseases, including ALL cancerous conditions.

Dr. Kim Ben states: If the pH of your blood rises above 7.45, the result is alkalosis. Severe alkalosis can also lead to death, but through a different mechanism; alkalosis causes all of the nerves in your body to become hypersensitive and over-excitable, often resulting in muscle spasms, nervousness, and convulsions; it’s usually the convulsions that cause death in severe cases.

Dr. Robert O. Young states: If the blood plasma pH increases over 7.385 you are in a state of ‘latent tissue acidosis’ of the interstitial fluids on the colloidal connective tissue of the shade and a high risk for cancer. This is what I call the “tee-ter-totter effect”. The body is pulling alkaline minerals into the blood to compensate for an equal amount of acids being pushed out into the interstitial fluids of the connective tissues of the schade to keep the blood plasma in an alkaline state. The result is tissue acidosis which then leads to hypersensitivity and over-excitable nerves, muscle spasms, nervousness and convulsions that can lead to coma or even death.  All of these symptoms are NOT a result of too much base or alkalinity but the result of too much acid from the blood being deposited into the interstitial fluids of the colloidal connective tissues of the schade. The cause of ‘latent tissue acidosis’ is caused by an acidic lifestyle and dietary choices.

Dr. Kim Ben states: The bottom line is that if you’re breathing and going about your daily activities, your body is doing an adequate job of keeping your blood pH somewhere between 7.35 to 7.45, and the foods that you are eating are not causing any wild deviations of your blood pH.

Dr. Robert O. Young: The bottom line is when you understand that having an acidic lifestyle and diet does affect the blood plasma and interstitial fluid pH in a negative way.

The blood responds to increased acids from lifestyle and diet by pushing them out into the interstitial fluids of the connective tissues or the colloidal connective tissues of the schade. The foods you eat, the liquids you drink, the air you breath, even your thoughts will effect the pH of blood and then the interstitial fluids of the colloidal connective tissues. The blood is constantly responding to the acidic wastes of lifestyle and diet choices!!!!!!!!!!!

Dr. Kim Ben stated: So what’s up with all the hype about the need to alkalize your body? And what’s to be made of the claim that being too acidic can cause osteoporosis, kidney stones, and a number of other undesirable health challenges?

Dr. Robert O. Young states: The hype about alkalizing your blood and then interstitial fluids of the connective tissues is important because the human body is alkaline by design and acidic by function. This is the foundation for understanding the true cause of ALL sickness and disease.

Dr. Kim Ben states: As usual, the answers to such questions about human health can be found in understanding basic principles of human physiology. So let’s take a look at the fundamentals of pH and how your body regulates the acid-alkaline balance of its fluids on a moment-to-moment basis.

Dr. Robert O. Young states: The problems with current understanding of the basic principals of human physiology is the basic principals do NOT understand that the human body is alkaline by design and acidic by function. Current medical savants DO NOT understand that there is only one health, one sickness, one disease and one treatment. The one health is to maintain the alkaline design of the blood and interstitial fluids of the connective tissues with an alkaline lifestyle and diet. The one sickness and one disease is the over-acidification of the blood and then tissues due to an inverted way of living, eating and thinking. The one treatment is to restore the alkaline design of the body fluids with an alkaline lifestyle and diet. Remember the fish bowl metaphor? It goes like this – When the fish is sick what would you do? Treat the fish or change the water? Remember the fish is only as healthy as the water it swims in.

Dr. Kim Ben states: pH is a measure of how acidic or alkaline a liquid is. With respect to your health, the liquids involved are your body fluids, which can be categorized into two main groups:

  1. Intracellular fluid, is the fluid found in all of your cells. Intracellular fluid is often called cytosol, and makes up about two-thirds of the total amount of fluid in your body.

  2. Extracellular fluid, is the fluid found outside of your cells. Extracellular fluids are further classified as one of two types:

    • Plasma, which is fluid that makes up your blood.
    • Interstitial fluid, which occupies all of the spaces that surround your tissues. Interstitial fluid includes the fluids found in your eyes, lymphatic system, joints, nervous system, and between the protective membranes that surround your cardiovascular, respiratory, and abdominal cavities.

      Your blood (plasma) needs to maintain a pH of 7.35 to 7.45 for your cells to function properly. Why your cells require your blood to maintain a pH in this range to stay healthy is beyond the scope of this article, but the most important reason is that all of the proteins that work in your body have to maintain a specific geometric shape to function, and the three-dimensional shapes of the proteins in your body are affected by the tiniest changes in the pH of your body fluids.

Dr. Robert O. Young states: pH is a measurement of the concentrations of hydrogen and hydroxyl ions in a aqueous solution. Any aqueous solutions, including your blood plasma interstitial fluids of the colloidal connective tissues of the schade (the largest organ of the human body) and the intracellular fluids that are saturated in hydrogen ions is less or more acidic and any aqueous solution that is saturated in hydroxyl ions is less or more base or alkaline.

Once again, the human body is alkaline in its design and acidic in its function. Your blood plasma and interstitial fluids of the colloidal connective tissue of the schade needs to be maintained at a delicate pH of 7.365 for your cells to function properly.

I have found in my own blood research that when your pH is stable at 7.365 you find healthy blood which is even in color, even in size and even in shape. The red blood cell is the primary stem cell which becomes all other body cells. And the health of the blood and the interstitial fluid of the colloidal connective tissues of the shcade is directly connected to the health of all body cells. It is blood that becomes, liver, heart, brain and skin cells. All red blood cells and then body cells are made up of microzymas.

Microzymas are the foundational, indestructable matter and intelligent matter that makes up all living cells, including the DNA. The tiniest changes in the pH of the body fluids can cause the microzymas in the red blood cells or body cells to change into bacteria, yeast and/or mold. This is how germs are created – from within NOT from without.

Dr. Kim Ben states: The pH scale ranges from 0 to 14. A liquid that has a pH of 7 is considered to be neutral (pure water is generally considered to have a neutral pH). Fluids that have a pH below 7 – like lemon juice and coffee – are considered to be acidic. And fluids that have a pH above 7 – like human blood and milk of magnesia – are considered to be alkaline.

Dr. Robert O. Young states: The pH scale ranges from 0 to 14 with the pH of 7 being the midpoint (pure water may have a pH of 7 but I have found that the pH of pure water has a range of 6.2 to 7.2 – a 10 times exponential swing. I have also found that pure water has an oxidative reduction potential in a range of +50mV to +150mV) which will drain energy from the body. Lemon is an alkaline fruit not an acidic fruit. This is because of its low sugar and high alkaline mineral content of potassium bicarbonate. Lemons do not draw down on the alkaline buffering system and contributes in excess of 10 times in hydroxyl ions (OH-) in relationship to its hydrogen ion content.

Dr. Kim Ben states: It’s important to note that on the pH scale, each number represents a tenfold difference from adjacent numbers; in other words, a liquid that has a pH of 6 is ten times more acidic than a liquid that has a pH of 7, and a liquid with a pH of 5 is one hundred times more acidic than pure water.  Most carbonated soft drinks (pop) have a pH of about 3, making them about ten thousand times more acidic than pure water. Please remember this the next time you think about drinking a can of pop.

When you ingest foods and liquids, the end products of digestion and assimilation of nutrients often results in an acid or alkaline-forming effect – the end products are sometimes called acid ash or alkaline ash.

Dr. Robert O. Young states – All food and drink which has a pH of less than 8.4 will cause the production of sodium bicarbonate by the stomach and the release of this sodium bicarbonate via the salivary glands, the pylorus glands, the pancreas, gall bladder and intestinal glands to alkalize whatever ingested. The main purpose of stomach is to prepare the food in a liquid state at a pH of 8.4 for biological transformation into stem cells which takes place in the crypts of the small intestines.

Dr. Kim Ben states: Also, as your cells produce energy on a continual basis, a number of different acids are formed and released into your body fluids. These acids – generated by your everyday metabolic activities – are unavoidable; as long as your body has to generate energy to survive, it will produce a continuous supply of acids.

Dr. Robert O. Young states: Metabolism produces acidic waste products of lactic, uric, citric and glucose if not eliminated will cause dis-ease and then disease. You are only as healthy as the alkaline fluids of the body which includes the extracellular and intracellular fluids.

Dr. Kim Ben states: So there are two main forces at work on a daily basis that can disrupt the pH of your body fluids – these forces are the acid or alkaline-forming effects of foods and liquids that you ingest, and the acids that you generate through regular metabolic activities. Fortunately, your body has three major mechanisms at work at all times to prevent these forces from shifting the pH of your blood outside of the 7.35 to 7.45 range.

Dr. Robert O. Young states: There are seven main sources at work on a daily basis that can disrupt the pH of your body fluids – these forces include acids from the external environment, acids from the foods and liquids ingested, acids from the air you breath, acids from metabolism, acids from cells breaking down or catobolic acitivity, acids from endogenous bacteria, yeast and mold, and acids from respiration. Your body has an elaborate alkalizing buffering system at work at all times to help prevent through chelaton these forces from shifting the pH of the blood plasma pH as well as the interstitial fluid pH at a delicate pH of 7.365. It is important to note that when the alkaline buffering system (a new organ discovered by Dr. Robert O. Young) becomes depleted and acids are being deposited into the interstitial fluids of the colloidal connective tissues and the fatty tissues this is when dis-ease and eventual disease manifests.

Dr. Kim Ben states:

These mechanisms are:

  1. Buffer Systems

    • Carbonic Acid-Bicarbonate Buffer System
    • Protein Buffer System
    • Phosphate Buffer System
  2. Exhalation of Carbon Dioxide
  3. Elimination of Hydrogen Ions via Kidneys
 
Dr. Robert O. Young states: There are ten (10) mechanisms that the body engages to buffer excess acids from lifestyle and dietary choices that are NOT properly eliminated through the four channels of elimination (bowels, kidney, skin and lungs):
1) The sodium bicarbonate system – the main organ of production is the stomach. The stomach is the major organ for sodium bicarbonate production for alkalizing food and maintaining the alkaline pH of the blood, tissues and organs.
2) The hemoglobin buffering system – the hemoglobin is a secondary alkalizing buffer for the blood when there is insufficient elements for the production of the primary buffer, sodium bicarbonate. This is the main cause of ALL blood diseases and why most all the client/patients I see have to a lesser or greater degree anemic and unhealthy blood.
3) The pHosphate buffering system which buffers acids creating phosphoric acid which is then excreted via the urine.
4) The ammonia buffering system reacts with hydrogen ions or acids to form ammonium ions which are excreted into the urine.
5) The plasma protein buffering system helps to chelate acids. The most plentiful type of buffer in the body including glutathione, methionine, cysteine and taurine which are found in the cells, lymph fluid and plasma.  Most plasma protein activity occurs intracellularly to bind or neutralize acids during cellular metabolism and/or disorganization or transformation of the human cell.
6) The electrolyte buffering system which includes the alkalizing mineral salts of sodium, magnesium, potassium and calcium. The chelation of any acid will form a less toxic solid or a stone in the body. All stones and cysts and tumors are the result of excess acids in the extra and intracellular fluids. The electrolyte or mineral buffers work in the blood, lymph, extracellular (blood plasma and interstitial fluids) and intracellular fluids to bind acids which are then removed via the urine. These four elements are recycled by the kidneys into the blood and lymph by binding them to CO2. Over 90 percent of the CO2 produced in the body through cellular fermentation in the production of energy is used to carry out this recycling process.
7) The low density lipo-protein buffering system also referred to as cholesterol works primarily as a binder of acids in the blood, lymph, and extracellular fluids which are then excreted via the urine. If elimination is compromised the fat bound acids are removed away from the organs that sustain life into the body cavities, hips, thighs, buttocks and abdominal area. This is the cause of over-weight and obesity.
8) The endocrine buffering system releases hormones to buffer acids. These hormones include the antidiuretic hormone which regulates the rate at which water is lost or retained by the body and aldosterone which regulates the level of sodium ions and potassium ions in the blood. These two alkaline secretions help the kidneys maintain the alkaline design of the body and reduce excess acidity thus creating pH balance in the body.
9) The release of free radicals or reduced hydrogen (OH- and SO-) by the lymphocytes to buffer excess acids in the blood, interstitial and intracellular fluids.
10) The retention of alkaline water to buffer excess acids in the colloidal connective tissues of the schade. This is the cause of edema or water retention.
Dr. Kim Ben states: It’s not in the scope of this post to discuss the mechanisms listed above in detail. For this article, I only want to point out that these systems are in place to prevent dietary, metabolic, and other factors from pushing the pH of your blood outside of the 7.35 to 7.45 range.
Dr. Robert O. Young states: The blood can be stressed from dietary and metabolic acids which are eliminated through the four channels of elimination or buffered by the ten alkalizing buffering mechanisms to maintain the delicate blood plasma, interstitial and intracellular pH at a healthy 7.365.

Dr. Kim Ben states: When people encourage you to “alkalize your blood,” most of them mean that you should eat plenty of foods that have an alkaline-forming effect on your system. The reason for making this suggestion is that the vast majority of highly processed foods – like white flour products and white sugar – have an acid-forming effect on your system, and if you spend years eating a poor diet that is mainly acid-forming, you will overwork some of the buffering systems mentioned above to a point where you could create undesirable changes in your health.

Dr. Robert O. Young states; Everything you eat, everything you drink, everything you breath, everything you think and everything you do affects the blood and interstitial fluids in an acidic way to a lesser or greater degree. That is why we age. We do not get old we mold from years of acidic lifestyle and dietary choices. The key to a healthy life or a life of sickness and disease and then eventual death is in the blood! Especially the blood plasma.

Dr. Kim Ben states: For example, your phosphate buffer system uses different phosphate ions in your body to neutralize strong acids and bases. About 85% of the phosphate ions that are used in your phosphate buffer system comes from calcium phosphate salts, which are structural components of your bones and teeth. If your body fluids are regularly exposed to large quantities of acid-forming foods and liquids, your body will draw upon its calcium phosphate reserves to supply your phosphate buffer system to neutralize the acid-forming effects of your diet. Over time, this may lead to structural weakness in your bones and teeth.

Dr. Robert O. Young states: Dr Kim Ben has described the cause of bone loss correctly. It is important to remember that the activation of the pHosphate buffering system does not happen when you are on an alkalizing lifestyle and diet and hyper-perfusing the blood and interstitial fluids of the colloidal connective tissues with alkalinity.  The alkaline lifestyle and diet is outlined in my book, The pH Miracle Revised and Updated.

Drawing on your calcium phosphate reserves at a high rate can also increase the amount of calcium that is eliminated via your genito-urinary system, which is why a predominantly acid-forming diet can increase your risk of developing calcium-rich kidney stones.

Dr. Ken Ben states: This is just one example of how your buffering systems can be overtaxed to a point where you experience negative health consequences. Since your buffering systems have to work all the time anyway to neutralize the acids that are formed from everyday metabolic activities, it’s in your best interest to follow a diet that doesn’t create unnecessary work for your buffering systems.

Dr. Robert O. Young states: The protocol that will NOT unnecessarily activate the alkaline buffering systems of the body is outlined in the pH Miracle Revised and Updated by Dr. Robert O. Young.

Dr. Kim Ben states: Generally speaking, most vegetables and fruit have an alkaline-forming effect on your body fluids.

Dr. Robert O. Young states: Generally, all green fruit and vegetables are the ONLY alkalizing foods for the blood and interstitial fluids of the colloidal connective tissues and are critical in building healthy blood and then healthy body cells.

Dr. Kim Ben states: Most grains, animal foods, and highly processed foods have an acid-forming effect on your body fluids.

Dr. Robert O. Young states; All grains, animal foods, dairy products, fermented foods, algae, probiotics, enzymes, high sugar fruit, high sugar vegetables, vinegar, corn, nuts, mushrooms, alcohol, carbonate drinks, sport drinks and tobacco products are acidic to the blood and interstitial fluids of the colloidal connective tissues of the schade (the largest organ of the body) and will activate the alkaline buffering systems.

Dr. Kim Ben states: Your health is best served by a good mix of nutrient-dense, alkaline andacid-forming foods; ideally, you want to eat more alkaline-forming foods than acid-forming foods to have the net acid and alkaline-forming effects of your diet match the slightly alkaline pH of your blood.

Dr. Robert O. Young states: The only way to achieve extraordinary health and fitness is with the pH Miracle Lifestyle and Diet as outlined in The pH Miracle Revised and Updated book.

Dr. Kim Ben states: The following lists indicate which common foods have an alkaline-forming effect on your body fluids, and which ones result in acid ash formation when they are digested and assimilated into your system.

Please note that these lists of acid and alkaline-forming foods are not comprehensive, nor are they meant to be.

If you’re eating mainly grains, flour products, animal foods, and washing these foods down with coffee, soda, and milk, you will almost certainly improve your health by replacing some of your food and beverage choices with fresh vegetables and fruits.

Dr. Robert O. Young states: The four alkalizing food groups are chlorophyll from green fruit and green vegetables, mono and polyunsaturated oils, alkalizing water and finally alkalizing mineral salts. I call this the COWS Plan as outlined in The pH Miracle Revised and Updated book.

Dr. Kim Ben states: The primary purpose of this article is to offer information that explains why I believe that you don’t need to take one or more nutritional supplements or “alkalized water” for the sole purpose of alkalizing your body. Your body is already designed to keep the pH of your body fluids in a tight, slightly alkaline range.

Dr. Robert O. Young states: Your body is alkaline by design but acidic by function and that is why you would be wise to follow an alkaline lifestyle and diet to prevent ALL sickness and disease and remain strong, healthy and fit. Drinking alkaline water is essential to maintaining the healthy alkaline state of ALL your body fluids!!!!!!

Dr. Kim Ben states: The ideal scenario is to make fresh vegetables and fruits the centerpieces of your diet, and to eat small amounts of any other nutrient-dense foods that your appetite calls for and that experience shows your body can tolerate.

Dr. Robert O. Young states: The ideal scenario is to make fresh organic electron-rich green alkalizing fruit and vegetables the centerpiece of your diet with liberal amounts of alkalizing polyunsaturated oils, alkalizing water at a pH of 9.5 and finally alkalizing mineral salts of sodium, potassium, magnesium and calcium.

Dr. Kim Ben states: I hope these thoughts bring some clarity to this often misunderstood health topic.

Dr. Robert O. Young states: I hope these scientific truths brings some clarity to Dr. Kim Ben and others that are confused about the biochemistry, bioenergetics and the importance of alkalizing the blood and interstitial fluids of the colloidal connective  tissues of the schade (the largest organ of the human body) with an alkaline lifestyle and diet as outlined in my book, The pH Miracle, revised and updated.

For additional information read The pH Miracle Revised and Updated by Dr. Robert O. Young .

 

%d bloggers like this: