Oxygen, Oxygen, Oxygen

Majid Ali, M.D.

My Oxygen Model of Diseases are extensions of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of chronic diseases—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of Diseases provide a simple model that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of xxxxxxxx.

The crucial importance of the Unifying Oxygen Model of Diseases are that they:

* Explain the scientific basis of physiology and pathology of various chronic diseases;

* Shed light on various contributory causative factors fan each other’s fires;

* Elucidate how toxicities of foods, environments, and thoughts set the stage for various chronic diseases;

* Reveal the mechanisms by which various detox therapies restore functions of injured body organs;

* Allow the formulation of rational and effective designs for reversing chronic diseases; and

* Provide explanations of mechanisms by which time-honored natural remedies work.


For more info, please consider:

*  “Darwin, Dysox, and Disease” (the 10th volume of my textbook entitled “The Principles and Practice of Integrative Medicine” available at www.aliacademy.org.

* Ali, M. my Aging and Oxygen (2000)

* Oxygen Model of Diabetes  at http://www.alidiabetes.org

* Oxygen Model of Insulin Toxicity at http://www.alidiabetes.org

Linking Diseases

Is there a connection between xxxx and xxxx? If so, what is that connection? These are the two questions I received from a reader. I thank that reader. Such letters allow me to enhance he value of video and textual parts of my Science, Health, and Healing Encyclopedia.

My Oxygen Models of XXXX and XXXX

The Oxygen Models of Preeclampsia and Autism

The Oxygen Model of Autism and The Oxygen Model of Preeclampsia are both extensions of my Oxygen Model of Health and Disease. They are unifying models that explain all aspects of the two disorders—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of Autism and The Oxygen Model of Preeclampsia provide simple models that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

These models predict that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of preeclamsia and autism. .

The crucial importance of the Unifying Oxygen Model of Preeclampsia and Autism are that they:

* Explain the scientific basis of primary mechanism of cellular energetic dysfunction in the two disorders;

* Shed light how health can be restored by addressing all relevant oxygen-related issues;

* Elucidate how toxicities of foods, environments, and thoughts cause tissue injury and disease;

* Reveal the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

* Allow the formulation of rational and effective designs for preventing, arresting, and reversing these disorder; and

* Provide explanations of mechanisms by which time-honored natural remedies work.

The Oxygen Model of XXX and The Oxygen Model of YYYYare both extensions of my Oxygen Model of Health and Disease. They are unifying model that explains all aspects of the two diseases—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Models of XXX and The Oxygen Model of XXX provide simple models that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of xxxxxxxx.

The crucial importance of the Unifying Oxygen Model of XXXXX and XXXXare that they:

Explain the scientific basis of primary aging processes in the body;

Shed light how health can be preserved by addressing all oxygen-related issues;

Elucidate how toxicities of foods, environments, and thoughts cause tissue injury and disease;

Reveal the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

Allow the formulation of rational and effective designs for reversing chronic diseases; and

Provide explanations of mechanisms by which time-honored natural remedies work.

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The crucial importance of the Unifying Oxygen Model of Nuropathy is that it:

* Explains the scientific basis of physiology and pathology of peripheral nerves;

* Sheds light on various contributory causative factors fan each other’s fires;

* Elucidates how toxicities of foods, environments, and thoughts set the stage for neuropathy;

* Reveals the mechanisms by which various detox therapies restore functions of nerves;

* Allows the formulation of rational and effective designs for reversing neuropathy; and

* Provides explanations of mechanisms by which time-honored natural remedies work.

My Oxygen Model of XXXXXX is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of XXXXXX—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of XXX provides a simple model that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of xxxxxxxx.

The crucial importance of the Unifying Oxygen Model of Disease is that it:

* Explains the scientific basis of physiology of sleep;

* Sheds light how healthful sleep preserves health and prevents disease;

* Elucidates how toxicities of foods, environments, and thoughts disturbs sleep;

* Reveals the mechanisms by which various detox therapies restore healing effects of optimal sleep;

* Allows the formulation of rational and effective designs for reversing sleep sleep disorders; and

* Provides explanations of mechanisms by which time-honored natural remedies work.

Explains the scientific basis of primary aging processes in the body;

Sheds light how health can be preserved by addressing all oxygen-related issues;

Elucidates how toxicities of foods, environments, and thoughts cause tissue injury and disease;

Reveals the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

Allows the formulation of rational and effective designs for reversing chronic diseases; and

Provides explanations of mechanisms by which time-honored natural remedies work.

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Oxygen is the organizing principle of human biology and governs the aging process. I began my book Aging and Oxygen (2000) with these words. I followed that volume with a series of articles in which I marshaled evidence for the Unifying Oxygen Model of Disease.

Oxygen is the organizing principle of human biology and governs the aging process. I began my book Aging and Oxygen (2000) with these words. I followed that volume with my twelve volume textbook entitled “The Principles and Practice of Integrative Medicine” devoted to looking at the subjects in the fields of molecular biology, pathology, immunology, and dclinical medicine through the prism of “Oxygen Thinking.” Specifically I presented oxygen models of inflammation, pain, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and other disorders. The crucial importance of the Unifying Oxygen Model of Disease is that it:

Explains the scientific basis of primary aging processes in the body;

Sheds light how health can be preserved by addressing all oxygen-related issues;

Elucidates how toxicities of foods, environments, and thoughts cause tissue injury and disease;

Reveals the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

Allows the formulation of rational and effective designs for reversing chronic diseases; and

Provides explanations of mechanisms by which time-honored natural remedies work.

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ECOLOGY

I first recognized the need for cellular ecologic thinking in the science and philosophy of healing in the late 1970s and taught the subject as a part of the curriculum of the American Academy of Environmental Medicine. In 1980, I published a monograph entitled “Altered States of Bowel Ecology. (monograph.”

I proposed Oxygen Model of Cancer in 1990s as integration of my perspectives on evolutionary design of cellular energetics, micro-ecologic relationships among cellular population, and tumor biology. Our primordial cellular ancestors were fermenting cells. This is the scientific basis of my view that cancer is evolution in reverse. The core clinical application of this view of cancer that every effort must be made to alter the micro-ecologic conditions of malignant cells and healthy cells that surround them

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Dr. Ali’s Start-Low-Build-Slow Principle

I offer all my guidelines for healing therapies for chronic illness after extensive clinical evaluation. If understood and properly put into use, these therapies are simple, safe, and effective. It is, of course, crucially important to rule out the presence of a tumor or serious acute underlying disease. Still, I ask readers to follow the golden “Dr. Ali’s Start-Low- Build-Slow Principle.” Specifically, I recommend that readers beginning natural remedies starting with 1/4 of the amounts of ingredients used and time allocated. After the first use, the amounts and times can be doubled if there are no questions about the safety and tolerance. Only then should readers consider the full protocol.

The Cellular Grease and Detergent Model of Disease

I proposed my Cellular Grease and Detergent Model of Disease as a unifying model to explain the basic mechanism of diseases and their signs and symptoms. This model is based on my evolutionary view of structural and functional integrity of cells and matrix. I illustrated it with the example of insulin resistance and diabetes. The insulin receptor is a large protein embedded in normally fluid cell membranes. It becomes resistant to the action of insulin when it becomes immobilized in chemicalized and hardened cell membranes—plasticized, so to speak—by toxicities of foods, environment, and thoughts. The cell membrane hardens as a result of deposition in it of cellular grease, which is made up of cellular waste, molecular waste, toxic fats, tangled proteins, and sticky sugars. The process of cellular grease buildup begins with mitochondrial dysfunction caused by dysfunctional oxygen dysfunction (dysoxygenosis or dysox for short. This model predicts that oxygen mal-signaling will be found to cause grease buildup on cell membranes, cell innards, and matrix in all chronic diseases. It will involve excess acidity (acidosis), increased oxidative stress (oxidosis, and clotting-unclotting dysequilibrium (CUD) as the primary mechanisms of diseases, which play central roles in the pathology and clinical features of all chronic diseases.

Oxygen is the organizing principle of human biology and governs the aging process. I began my book Aging and Oxygen (2000) with these words. I followed that volume with a series of articles in which I marshaled evidence for the Unifying Oxygen Model of Disease. Specifically I presented oxygen models of inflammation, pain, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and other disorders. The crucial importance of the Unifying Oxygen Model of Disease is:

It explains the scientific basis of primary aging processes in the body;

It sheds light how health can be preserved by addressing all oxygen-related issues;

It elucidates how toxicities of foods, environments, and thoughts cause tissue injury and disease;

It reveals the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

It allows the formulation of rational and effective designs for reversing chronic diseases; and

It provides explanations of mechanisms by which time-honored natural remedies work.

V

My Oxygen Model of XXXXXX is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of XXXXXX—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of XXX provides a simple model that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of xxxxxxxx.

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The Oxygen Protocol for Cancer

My Oxygen Model of Cancer an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of cancer—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of Cancer provides a simple model that allows one to reduce complexities of diverse clinical manifestation of cancer into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of cancer.

In controlling and eradicating XXXXX, the Oxygen Model requires that all relevant “oxygen issues” in a case—whether or not related to the recognizable aspects of XXXXXX—must be effectively addressed. In my experience, the clinical results for individuals with cancer are far superior when all relevant nutritional, environmental, and stress-related threats to oxygen signaling are effectively addressed. Specifically, these issues include fermentation, increased gut permeability (leaky gut state), and glucose-insulin-roller coasters.

13. Ali M. The Crab, Oxygen and Cancer. Volume I: The Dysox Model of Cancer. 2007. New York, Canary 21 Press.

14. Ali M. The Crab, Oxygen and Cancer. Volume II: The Oxygen Protocol for Cancer. 2007. New York, Canary 21 Press.

The Oxygen Protocol for Reversing Chronic Disease

In clinical medicine the Oxygen Model requires that all relevant “oxygen issues” in a case—whether or not related to what appears to be the target organ of the disease process under consideration—must be effectively addressed. To cite one example, in my experience clinical results with individuals with mental issues are far superior when all relevant nutritional and environmental issues are effectively addressed. Specifically, these issues include fermentation, increased gut permeability (leaky gut state), and glucose-insulin-roller coasters.

The Oxygen Model of Diseases

My Oxygen Model of Diseases are unifying models that explain all aspects of specific diseases—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of Diseases provide a simple model that allows one to reduce complexities of diverse clinical manifestation of cancer into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of specific diseases.

In controlling and eradicating specific diseases, the Oxygen Model requires that all relevant “oxygen issues” in a case—whether or not related to the recognizable aspects of specific diaseses—must be effectively addressed. In my experience, the clinical results for individuals with cancer are far superior when all relevant nutritional, environmental, and stress-related threats to oxygen signaling are effectively addressed. Specifically, these issues include fermentation, increased gut permeability (leaky gut state), and glucose-insulin-roller coasters.

T.Pain.TOP7

Pain Control and Cure – Dr. Ali’s Top Seven Natural Remedies

Majid Ali, M.D.

The Grease-and-Detergent Model of Cell Membrane Dysfunction

I proposed my Grease-and-Detergent Model of Cell Membrane Dysfunction to explain the basic mechanism of diseases – the clinical features of which begin with injury to cell membranes. I illustrate this model with the example of insulin resistance and diabetes. The insulin receptor is a large protein embedded in normally fluid cell membranes. It becomes resistant to the action of insulin when it becomes immobilized in chemicalized and hardened cell membranes—plasticized, so to speak—by toxicities of foods, environment, and thoughts. The cell membrane hardens as a result of deposition in it of cellular grease, which is made up of cellular waste, molecular waste, toxic fats, tangled proteins, and sticky sugars. The process of cellular grease buildup begins with mitochondrial dysfunction caused by dysoxygenosis (dysox, dysfunctional oxygen dysfunction). This model predicts that ongoing research will reveal that contributors to the dysox state (acidosis [excess acidity], oxidosis [increased oxidative stress], and CUD [clotting-unclotting dysequilibrium]) will be found to play central roles in the pathology and clinical features of all chronic diseases.

These subjects regrettably are not parts of the prevailing vocabulary of drugs. Nor are they brought up in deliberations of drugs that block various cell membrane receptors.

My Oxygen Model of Polycystic Ovarian Disease (PCOS) is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of PCOS—causes, clinical course, consequences, and reversal—on the basis of disturbed oxygen functions. The most important among there are: (1) impaired or blocked oxygen signaling; (2) interrupted oxygen’s ATP energy generation; (3) diminished oxygen’s detergent functions; (4) interrupted oxygen’s cellular detox functions; (5) impeded oxygen-governed cellular repair mechanisms; and (5) oxygen-regulated cell membrane and matrix functions. These abnormalities usually begin in early life but may develop at any time during life
Is there a Link Between XXX and YYY?

Majid Ali, M.D.

I answer this question with a question you are not likely to anticipate: Is this a good question? My answer: No, it is not a good question. Now I anticipate your question: Why not? Here is my answer:

* Obesity is a state of excess of acids , free radicals, and thickened bodily fluids. All of that is caused by perverted oxygen signaling.

* Multiple sclerosis is a state of excess of acids , free radicals, and thickened bodily fluids. All of that is caused by perverted oxygen signaling

* Perverted oxygen signaling is caused by toxicities of foods, environments, and thoughts.

If you accept the above facts, then the question in the title of this article becomes “not good.” I expect some readers are likely to be disappointed, even annoyed, by the above.

My Oxygen Model of AXXXXXX is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of XXXXX—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among there are: (1) impaired or blocked oxygen signaling; (2) interrupted oxygen’s ATP energy generation; (3) diminished oxygen’s detergent functions; (4) interrupted oxygen’s cellular detox functions; (5) impeded oxygen-governed cellular repair mechanisms; and (5) oxygen-regulated cell membrane and matrix functions. These abnormalities usually begin in early life but may develop at any time during life.

Updated Sept. 1, 2012

The Oxygen Model of Mental Health and Disorders

I proposed my Oxygen Model of Mental Health and Disorder as an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of mental health and mental disorders—causes, clinical course, consequences, and control—on the basis of impaired oxygen signaling, diminished oxygen’s detergent functions, and interrupted oxygen’s cellular detox and repair functions. altered oxygen signaling. These abnormalities essentially begin during fetal life and continue through infancy, and childhood. This model is based on a biologist view of the brain development and neurotransmission. Autism is not a psychological or psychiatric disorder.

My Oxygen Model of Mental Health and Disorders Autism is a unifying model that explains all aspects of autism—causes, clinical course, consequences, and control—by disruptions of oxygen homeostasis occurring during fetal life, infancy, and childhood. This model is based on a biologist view of the brain development and neurotransmission. Autism is not a psychological or psychiatric disorder.

Models in science are proposed to: (1) explain such natural phenomena; (2) offer workable simplicity to reduce complexities of such phenomena; (3) predict natural phenomena hitherto unrecognized. These models are tested, validated, or refuted with ongoing scientific observation. In clinical medicine, I add a fourth criterion for a model’s validity: it must facilitate health and healing.

Clinical Significance of the Oxygen Model

In clinical medicine the Oxygen Model requires that all relevant “oxygen issues” in a case—whether or not related to what appears to be the target organ of the disease process under consideration—must be effectively addressed. To cite one example, in my experience clinical results with individuals with mental issues are far superior when all relevant nutritional and environmental issues are effectively addressed. Specifically, these issues include fermentation, increased gut permeability (leaky gut state), and glucose-insulin-roller coasters.

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The Oxygen Model of Health

The Oxygen Model of Disease

Models in science are proposed to: (1) offer workable simplicity to reduce complexities of natural phenomena; (2) to explain such phenomena; (3) to predict natural phenomena hitherto unrecognized. These models are tested, validated, or refuted with ongoing scientific observation. In clinical medicine, I add a fourth criterion for a model’s validity: it must facilitate health and healing.

My Oxygen Models of Health and Healing, as well as my Oxygen Models of various diseases are based on my “Oxygen Eureka Moment” described briefly on my YouTube video encyclopedia. I discuss these subjects at length in Darwin, Dysox, and Disease Triology (2008), the 10th, 11th, and 12th volumes of my text book entitled The principles and Practice of Integrative Medicine.

How does my Oxygen Model of xxxxxxxx Disease stand up to these criteria? I leave that to your imagination. After you take a stab at it, below is a list of my articles on the web and video articles on my YouTube Science, Health, and Healing Encyclopedia:

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I propose The Oxygen Model of XXXXX as a unifying model that recognizes disturbances of oxygen functions as the fundamental commonality of all elements that cause T4-to-T3 conversion abnormalities seen in the syndrome. For treating the syndrome, this models offers a workable simplicity to cope with the complexities of the reverse T3 thyroid syndrome. It requires that all threats to oxygen homeostasis (inflammation, infections, chemical toxicity, stress) be recognized.

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In the Oxygen Model of Diabetes, insulin can be visualized as a crank—a device that transmits rotary motion—and the insulin receptor protein as a crank-shaft embedded in the cell membrane. In the Dysox Model of diabetes, insulin resistance can then be seen as a “rusted”crank-shaft of insulin receptor which is “impacted” in a “hardened” cell membrane, and so cannot be turned by the insulin crank

Is diabetes mellitus a sugar problem? No. The abnormalities of blood sugar seen in diabetes are the consequences of the derangements of cellular energetics and toxicity which collectively create what is commonly called diabetes. Is diabetes an insulin problem? No. The abnormalities of insulin functions are the consequences of plasticized (chemicalized) and hardened cell membranes which immobilize the insulin receptors embedded in them. Is diabetes a problem of blood vessels which cause blindness, kidney failure, stroke, heart attacks, and neuropathy? No. The abnormalities of blood vessels are the consequences of oxidizing and deoxygenizing

influences in diabetes.

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OLD Models in science are proposed to: (1) offer workable simplicity to reduce complexities of natural phenomena; (2) to explain such phenomena; (3) to predict natural phenomena hitherto unrecognized; and (4) to improve the human condition. These models are tested, validated, or refuted with ongoing scientific observation.

Below, I explain how the Oxygen Model of XXXXXXXXXX meets are all four criteria.

Diseases are states of energy imbalance. Energy in the human body is produced by oxygen. From these simple facts of science, I establish that health is a state of “energy-oxygen balance.” Diseases are states of “energy-oxygen imbalance.” This, simply stated, is the core of the Unifying Oxygen Model of Health and the Unifying Oxygen Model of Disease

In 1996, in a series of three large article I published by Oxygen Model of Diabetes. Fourteen years later, Dr. Keertik Fulzele and colleagues of Johns Hopkins University School of Medicine, Baltimore, provided incontrovertible experimental evidence to fully validate the core tenet of my oxygen model of diabetes: the insulin receptor dysfunction caused by toxicities of food, environment, and thoughts.

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Holism in Healing Arts

The core tenet of my notion of holism in medicine is: No part can be understood without understanding its relationships with the whole. In 1987, I wrote my monograph “The Altered States of Bowel Ecology” to underscore the need for ecologic thinking among physicians. I asserted that all rational measures for the prevention and treatment of chronic disease, first and foremost, require a clear understanding of all relevant “oxygen issues” in the context of healthful aging and reversal of chronic disease.

My describe the evolution of my ecologic thinking in my various books over the years.

tail rcologic thinking understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.

Will my prediction be proven wrong? Oh, how I wish it might be so. Might Darwin surprise us again? Might Nature yet have another card up its sleeve? Might evolution yet unfold a new order of life—of ethics, learning, knowing, and compassion for all planetary life

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Dysox Is Energy and Detox Failure in Cells

Majid Ali, M.D.

In 1998, I introduced the term dysox—short for dysoxygenosis—for a state of fundamental failure of energy generation and detox in the cells. I showed that dysox is caused by impaired function of enzymes involved in oxygen-driven chemistry (“oxyenzymes”) and leads to buildup of acids and toxins in the body. My original data published in Townsend Letter was entitled “Respitarory-to-fermentative shift in ATP Production” and that paper is included at this site. With passing time, the enzyme defects altered expressions of genes involved with oxygen functions—”oxygenes” was the term I chose to refer to them.

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The Origin of Life Explains the Origin of Disease

A diseases is a state of regression—evolution in reverse, so to speak. In 1998, I conceived this simple idea and the possibility that the origin of diseases, at its core, could be understood through an understanding of the origin of life on the planet Earth. I recognized that the origins of both life on the planet and disease share one fundamental commonality: fermentative metabolism. That was a eureka moment for me. In that year, I published a long article in The Journal of Integrative Medicine entitled “Oxidative Regression to Primordial Cellular Ecology (ORPEC)” to link the fermentative mode of primordial life to the degradative metabolic shift in cellular energetics. Simply stated, in a a disease state the high-efficeincy respiratory-ATP generation is degraded to a low-efficiency fermentative ATP production. I introduced the term dysoxygenosis—dysox for short—to refer to this degrative metabolic shift. To explain the basic idea to my patient, I also introduced the term dysfunctional oxygen metabolism for dysoxygenosis.

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OXYGEN SIGNALING

In 1998, I introduced the term dysox—short for dysoxygenosis—for a state of fundamental failure of energy generation and detox in the cells. I showed that dysox is caused by impaired function of enzymes involved in oxygen-driven chemistry (“oxyenzymes”) and leads to buildup of acids and toxins in the body. Soon after I defined dysox as energy and detox failure, I recognized other biochemical defects (and their clinical consequences) caused by blocked oxygen functions in the body, including:

Oxygen-driven cellular energetics,

Oxygen-driven cellular development and multiplication,

Oxygen-driven removal of cellular grease (oxygen’s detergent functions),

Oxygen-activation of the enzyme systems of the body,

Oxygen-driven cellular detox mechanisms.

In 1998, my primary purpose in introducing the term dysox was to compel the readers to reach beyond the then-prevailing practice of naming diseases—choosing a diagnostic labels that reveal nothing about the real underlying causes—to justify the use of the so-called “drugs of choice.”

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Derangements of those primary oxystatic and energetic mechanisms set the stage for all subsequent autonomic, endothelial, inflammatory and atherogenic responses encountered in patients with chronic insidious as well as acute ischemic coronary artery syndromes.2-4 Of crucial significance to the dysox model of CHD are: (1) morphologic changes of oxidative coagulopathy5; (2) oxidative dysautonomia 6; (3) patterns of oxidative regression to primordial cellular ecology7; and (4) biochemical profiles of increased urinary excretion of metabolites of the Krebs cycle and glycolytic pathways indicating the presence of the dysox state.8,9 In 1998, those observations led to the hypotheses of the oxidative-dysoxygenative model of coronary artery disease (ODCAD)10 and subsequently to the dysox model of atherosclerosis,1 which has the following two core tenets:

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  1. ALI’S FIVESOME

FOR OXYGEN HEALTH

  1. Dr. Ali’s Breakfast to prevent sugar-insulin-adrenaline roller coasters
  2. Dr. Ali’s Insulin meal plan to prevent and reverse insulin toxicity
  3. Dr. Ali’s Feather Breathing for more oxygen
  4. Dr. Ali’s Peroxide Oxygen Therapy with foot soaks or baths
  5. Dr. Ali’s Anti-inflammatory topical oils rubs and Anti-inflammatory spices
  6. ALI’S LIST OF FIVE MOST CRITICAL HEALTH HAZARDS
  7. Chronic disappointment with life conditions
  8. Sugar-insulin-adrenaline roller coasters
  9. Insulin toxicity
  10. Chronic low-grade overbreathing (hyperventilation)
  11. Impaired oxygen homeostasis (chronic oxygen deficiency)
  12. Chronic inflammation

ICastor / sesame oil rubs

(3 days castor, one day sesame rotation)

Dr. Ali’s Breakfast

Dr. Ali’s Insulin Reduction Recipies

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For a full discussion of the Oxygen Model of Disease and the scientific basis of my xxxxxx protocol, I refer professional readers to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine for a detailed discussion of the above subjects, as well as for extended citations.

I refer professional readers to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine for a detailed discussion of the above subjects, as well as for extended citations.

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OXYGEN SIGNALING

Oxygen-driven cellular energetics,

Oxygen-driven cellular development and multiplication,

Oxygen-driven removal of cellular grease (oxygen’s detergent functions),

Oxygen-activation of the enzyme systems of the body,

Oxygen-driven cellular detox mechanisms.

In 1998, my primary purpose in introducing the term dysox was to compel the readers to reach beyond the then-prevailing practice of naming diseases—choosing a diagnostic labels that reveal nothing about the real underlying causes—to justify the use of the so-called “drugs of choice.”

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Three Unifying Principles

I devote all twelve volumes of my textbook entitled The Principles and Practice of Integrative Medicine to two unifying principles:

First, no part can be understood without understanding its relationships with the whole—the Darwin Principle is my designation for this principle—and so relatedness of natural phenomena must be the basis of all efforts to understand and treat all diseases;

Second, oxygen is the organizing principle of human biology and governs all healing in the body—hence all relevant oxygen issues must be addressed in all diseases for best long-term results;

Third, each individual is a unique person and requires an individualized application of the principles of relatedness and The Oxygen Model of Disease.

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The Oxygen Model of Polycystic Ovary Syndrome

Deranged oxygen functions increase insulin production,. Excess insulin causes premature aging. That includes early slowing of ovaries and shrivelling of eggs in them. That, simply stated, is one of the important ways in which polycystic ovary syndrome (PCOS) begins and young women lose their fertility.

The Oxygen Model of Polycystic Ovary Syndrome

Derangements of oxygen’s energetic, detergent, and development functions are caused by the cumulative consequences of toxic foods, toxic environment, and toxic thoughts. This is the scientific basis of my Oxygen Model of Polycystic Ovary Syndrome. The crucial importance of the oxygen-PCOS link is:

It explains the scientific basis of how ovaries and eggs age prematurely;

It explains how toxicities of foods, environments, and thoughts cause cellular injury and clinical features of PCOS—men-like features (acne, facial hair, excess testosterone), high insulin, loss of ovulation, and infertility;

It reveals the mechanisms by which various direct and indirect oxygen therapies (including bowel and liver detox) work. (Oxygen is the primal

It compels us to focus on all threats to oxygen homeostasis (balance) to restore ovarian health and the health of eggs;

It explains how all bodily functions improve when oxygen therapies reverse PCOS; and

It provides explanations of mechanisms by which time-honored natural remedies work.

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So for understanding molecular biology of all diseases and for rational measures for the prevention and treatment, first and foremost, we must understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.

what re devoted twelve volumes of my textbook entitled The Principles and Practice of Integrative Medicine.

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In began my book Oxygen and Aging (2000) with the following words: oxygen is the organizing principle of human biology and governs the aging process.

See P-Physician files (Oxygen’s Three-Legged Throne” and The Origin of Diseases” for finalized versions.

Recommended Readers for Professional Readers

I refer physicians and other readers with special interest in deeper understanding of diverse issues in the treatment of Crohn’s colitis, as well as the pertinet citations to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine.

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Darwin’s Message

Darwin’s message for us is: No part can be understood without understanding its relationships with the whole. So for understanding uric acid biology and for rational measures for the prevention and treatment of gout, first and foremost, we must understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.

Will my prediction be proven wrong? Oh, how I wish it might be so. Might Darwin surprise us again? Might Nature yet have another card up its sleeve? Might evolution yet unfold a new order of life—of ethics, learning, knowing, and compassion for all planetary life?

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For citations and detailed information on the biology of oxygen, I refer professional readers to Darwin, Oxygen Homeostasis, and Oxystatic Therapies (2009), the tenth, volume of my textbook entitled The Principles and Practice of Integrative Medicine.

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Contains basic definitions and concepts

Oxygen is the organizing principle of human biology and governs the aging process. I began m book Aging and Oxygen (2000) with these words. I followed that volume with a series of articles in which I marshaled evidence for the Unifying Oxygen Model of Disease. Specifically I presented oxygen models of inflammation, pain, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and other disorders. The crucial importance of the Unifying Oxygen Model of Disease is:

It explains the primary aging processes in the body;

It sheds light how health can be preserved by addressing all oxygen-related issues;

It elucidates how toxicities of foods, environments, and thoughts cause disease;

It allows the formulation of rational and effective designs for reversing chronic disease can be developed; and

It provides mechanisms by which time-honored natural remedies work.

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A prism splits white light into a luminous rainbow—then emboldens the colors. For me, the “oxygen prism” splits the energetic domains of the body—then sparkles them. This is the core of oxygen thinking. It de-fogs issues

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The Grease-Detergent Model of Disease Part – I

Majid Ali, M.D.

http://www.ethicsinmedicine.us/the_grease-detergent_model_of_disease.htm

The spectrum of diseases in medical textbooks is vast. Is there any common underlying energetic or metabolic derangement that applies to most, if not all, acquired diseases? Is there a workable simplicity that can help us cope with the seemingly mad complexity of diseases? Is there a unifying model of disease with an explanatory power for all acquired diseases? Can such a model be supported by sound scientific evidence? My answer to these questions is an unequivocal yes. Simply stated, it is The Grease-Detergent Model of Disease.

Every living cell breathes oxygen and produces waste and cellular debris. In this process, fats turn rancid, sugars become sticky, and proteina are pulped (chains of amino acidsmaking forming proteins are cut, turned, and twisted). In health, these substances are rapidly cleared so that cells can breathe oxygen, expel waste and toxins, and stay healthy and happy. In disease states, rancid fats, sticky sugars, and pulped proteins accumulate on cell membranes. Sometime ago, I introduced the term cellular grease for the layer of such materials that builds on cell membranes in all diseases.

Nature also created a system of grease-cutters—detergents, in common language—that remove cellular grease and allow cells to breathe again. The primary detergent in the human body is oxygen. Secondary detergents are hydrogen peroxide, superoxide, singlet oxygen, nitric oxide, and others. The third layer of detergent is provided by enzymes. The Grease-Detergent Model of Disease explains the beginning of all acquired disease with either excess of grease or deficit of detergents

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Darwin’s message for us is: no part can be understood without understanding its relationships with the whole. His message to physicians today would have been simple: no disease of any organ can be understood or prevented without understanding the structural and functional relationships of the organ with all other organs of the body. relationaor treat any disease heart diseasHe teaches So,

for understanding uric acid biology and for rational measures for the prevention and treatment of gout, first and foremost, we must understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.

******

This article presenting outlining the Oxygen Model of xxxxxxxxxxxxxxxxxx is an extension of that work.

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OXYGEN ORDER OF HUMAN BIOLOGY

An oxygen order governs human biology. In this order, oxygen provides the primary oxidative drive for human redox equilibrium. Oxygen is the currency of molecular communications, of energy dynamics, and of anabolism (tissue buildup) and catabolism (tissue breakdown). The basis of life is energy, and the basis of energy in humans is oxygen. (Other forms of energy undoubtedly influence human health, but technology for measuring such energy dynamics is not yet available.) Oxygen initiates and regulates all digestive-absorptive, energy, and detoxification enzyme pathways. Accelerated oxidative molecular injury is the core mechanism of molecular and cellular injury in all disease processes. Nascent oxygen is the primary defense of human tissues in countering both xenobiotic load and microbial threats. In the context of the ORPEC hypothesis, the author considers oxygen to be the primary antiPLF agent of the human defense system. Oxidation is a spontaneous process in nature—it requires neither expenditure of energy nor any outside stimulus. Reduction, by contrast, requires an expenditure of energy.

The major components of the oxygen order of human biology included in this article have been discussed previously.1-19 To provide a framework of reference for presenting the ORPEC hypothesis, some essential aspects of that order are presented below under the following headings: (1) spontaneity of oxidation in nature; (2) molecular duality of oxygen;; (3) anoxic air, anoxic water; and (4) clotting-unclotting equilibrium (CUE) and clotting-unclotting dysequilibrium (CUD) of the health-disease continuum.

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THE OXYGEN THRONE

Oxygen is the king of human biology. It maintains law and order in the body by organizing and coordinating its three “executive branches: acid-alkali balance, oxidant and antioxidant regulation, and clotting-unclotting equilibrium (CUE). The law and order in oxygen’s kingdom is threatened by the trio of toxicities of environment, foods, and thoughts. The failure of its executive branches lead to acidosis, oxidosis, and clotting-unclotting dysequilibrium (CUD) respectively.

” for maintaining law and order in the body. This analogy has four trios:

To explain the two core tenets of the Oxygen Model of Diabetes—oxygen removes grease and restores functions of cell membranes, matrix, and mitochondria—I offer an analogy of the “oxygen king” and its three “executive branches” for maintaining law and order in the body. This analogy has four trios:

The trio of balancing acts in the body for keeping diabetes in the normal range;

The trio of toxicities that cause diabetes (environment, foods, and thoughts);

The trio of functional derangements; and

The trio of structural abnormalities (membranes, matrix, and mitochondria).

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The Oxygen Model of Disease

The Oxygen Model of Disease is a unifying model of enormous explanatory power—for understanding the basic nature of the disease processes, as well as for designing testable, rational, and scientifically sound integrative plans for restoring health. The primary strength of this model is that so little explains so much.

Specifically, I point here that the common denominator in the cause of all non-developmental disorders is cellular dysox (dysfunctional oxygen homeostasis). Every pain is some cells’ cries for oxygen. Cellular dysox is the primary cause of all disease-causing inflammation, which sets the stage for the beginnings of all forms of bowel disorders, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and degenerative disorders.

The primary strength of this model is that so little explains so much. On close scrutiny, the common elements in all mechanisms of injury by noxious agents—metabolic waste toxins, environmental toxins, microbial species, anger neurotranmitters, and others—are oxygen-driven host defenses.

This article presenting outlining the Oxygen Model of xxxxxxxxxxxxxxxxxx is an extension of that work.

I urge readers to consult an experienced integrative physician to guide them in the clinical applications of the the Oxygen Model of Disease for tissue regeneration and healing.

I point here that the common denominator in the cause of all symptom-complexes of Crohn’s colitis iis cellular dysox (dysfunctional oxygen homeostasis) in the various cell populations of the body. I urge readers to consult an experienced integrative physician to guide them in the clinical applications of the the Oxygen Model of Disease for tissue regeneration and healing.

I refer physicians and other readers with special interest in deeper understanding of diverse issues in the treatment of Crohn’s colitis, as well as the pertinet citations to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine.

Trilogy

I refer physicians and other readers with special interest in deeper understanding os the issues presented in this column to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine.

X Ali M. The Principles and Practice of Integrative Medicine Volume III: Darwin, Oxygen Homeostasis, and Oxystatic Therapies. 3 rd. Edi. (2009) New York. Insitute of Integrative Medicine Press.

x Ali M. The Principles and Practice of Integrative Medicine Volume XI: Darwin, Dysox, and Disease. 2000. 3rd. Edi. 2008. New York. (2009) Insitute of Integrative Medicine Press.

x Ali M. The Principles and Practice of Integrative Medicine Volume XI: Darwin, Dysox, and Integrative Protocols. New York (2009). Insitute of Integrative Medicine Press.

Ali M. The Principles and Practice of Integrative Medicine Volume XI: Darwin, Dysox, and

I point here that the common denominator in the cause of all of the above symptom-complexes is cellular dysox (dysfunctional oxygen homeostasis) in the various cell populations of the body. Hence the enormous explanatory power of the Dysox Model of Hashimoto’s Disease (see dysox models of other disorders on this site for a comparative study of the cause of various diseases and a broader context).

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OXYGEN, CHEMICALIZED UNBORNS,

AND PROSTATE CANCER

Majid Ali, M.D.

March1, 2010

I look at the problems of unborn babies and children through the prism of oxygen homeostasis. This “oxygen view” of the problems of infants and children—adults in later years —has a strong explanatory power for diverse health issues that otherwise remain unexplained. I began my book Oxygen and Aging (2000) with the following words: Oxygen is the organizing principle of human biology and governs the aging process. I incorporate this central message in all articles in this series. At times I make strong claims that require strong evidence. I refer physicians and readers interested in pertinnet bibliography to my Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine.

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atSome of my statements discussions of the heart rending problems of unborns, newborns, infants, and children—who grow up to become uwell and sick adults. Specifically, I point here that the common denominator in the cause of all non-developmental disorders is cellular dysox (dysfunctional oxygen homeostasis). Every pain is some cells’ cry for oxygen. Cellular dysox is the primary cause of disease-causing inflammation, which sets the stage for the beginning of all forms of bowel disorders, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and degenerative disorders.

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Dumbing Down Science

The inclusion of oxygen in the title of this article on Crohn’s disease may seem odd to some readers. Doctors do not look at this disease—nor at any other disease, for that matter—through the prism of oxygen homeostasis. So, it is not surprising that people in general do not think of oxygen when they think of Crohn’s disease. Doctors can disregard oxygen only at the cost of dumbing down science of their profession. I assert that the last thing we can afford to dumb down in healing arts is the science of medicine.

Below is text from my forthcoming book entitled Darwin’s Drones, Oxygen, and Diabetes: to make my larger point:

In our toxic preoccupation with daily intramural murders, we are missing the central story of our time: an epic planetary struggle between the oxygen-loving (“oxyphils”) and oxygen-shunning species (“oxyphobes”) and the incremental victories of the latter. A monumental tragedy of mass extinction of species is playing out on the global stage. Oxygen-loving frogs and related amphibian species are being decimated by oxygen-shunning fungi. The oxygen-shunners are also responsible for the plight of butterflies, bees, and bats—for disappearing butterflies, collapsing bee colonies, and bat that fly out of their caves in daylight and drop dead. Their fungus-ridden noses foretell things about the shape of the future.

For hundreds of thousands of years, the planet Earth was in equilibrium in terms of its acid-alkali balance, oxidant-antioxidant regulation, and atmospheric gas homeostasis. Now it is fermenting because it is:

Chemicalizing;

Acidifying;

Oxidizing;

Carbonizing; and

Deforesting (“De-lunging)”

Humans are also fully engaged in this struggle, and losing with spreading epidemics of mystery maladies—chronic fatigue, brain fog, fibromyalgia, polycystic ovary syndrome, gender devolution, memory deficits, and rising incidences of cancer. Regrettably, the main body of physicians, under the influence of The New England Journal of Medicine, is totally oblivious to the man-microbe conflicts that are at the root of these disorders.

The observable elements of climatic chaos—as well as those that will almost certainly occur—are further shifting the equilibrium in the favor of oxyphobes and against oxyphils. Among the most vulnerable on the planet are its children.

In 1994, 94 pounds of synthetic chemical were produced for every child, man, and woman worldwide in the United States. The planetary acidification and oxidation is being caused by incremental chemicalization and carbon dioxide accumulation. Forests, shrubs, and gases are the Earth’s lungs—exchanging carbon dioxide for oxygen—and spreading deforestation is literally planetary de-lunging.

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Diabetes Is An Oxygen Problem

Below is a brief explanation of the above statement:

Diabetes is an insulin toxicity problem before it becomes a sugar problem.

The insulin toxicity is an insulin excess problem before it becomes a toxicity problem.

Insulin excess is a blocked-insulin-receptor problem before it is an insulin excess problem

The insulin receptor problem is a cellular grease problem before it becomes an insulin receptor problem.

The cellular grease problem—buildup of rancid lipids, sticky sugars, and pulped proteins—is a “cellular-detergent-deficiency problem” before it becomes a cellular grease problem.

The cellular detergent deficiency problem is the trio of toxicities—toxic foods, toxic environments, and toxic thoughts—problem before it becomes detergent deficiency problem.

The trio of toxicities problem is caused when the toxicities disrupt oxygen homeostasis.

The above, succinctly stated, is the Oxygen Model of diabetes. I present The Grease-Detergent Model of Disease in a companion article on this site.

Disease is separation from one’s nature. I close this essay by repeating my earlier words. Disowning disease is a part of this larger vision. It is not an easy road. Earlier in my work in integrative medicine, I recognized that we have choice: We can spend little time to heal, or we can waste much time in being sick.

I refer physicians and other readers with special interest in deeper understanding of diverse issues in the reversal of chronic kidney failure and diabetes to Darwin and Dysox Trilogy (2009), the tenth, eleventh, and twelfth volumes of my textbook entitled The Principles and Practice of Integrative Medicine. 4-6

The Dysox Model of Insulin Toxicity

The Dysox Model of Insulin Toxicity is an extension of the Dysox Model of Disease. In 1998, I introduced the term dysoxygenosis for the state of dysfunctional oxygen metabolism (dysox) characterized by disrupted oxygen signaling. Specifically, it includes: (1) oxygen-driven cellular energetics; (2) oxygen-driven detox pathways; (3) oxygen signaling for cellular development, differentiation, and demise; and (4) oxygen detergent functions. I began my book Oxygen and Aging (2000) with the following words: oxygen is the organizing principle of human biology and governs the aging process. Within that broader context, below is the core of the Dysox (Oxygen) Model of Insulin Toxicity in simple words.

Insulin toxicity is an insulin excess problem before it becomes a tissue injury problem.

It is an insulin receptor problem before it becomes a tissue injury problem.

It is a cellular grease—rancid lipids, sticky sugars, and pulped proteins—problem before it becomes an insulin receptor problem.

It is a cellular detergent—oxygen, oxyradicals, and oxyenzymes—problem before it becomes a grease problem.

Since evolution chose oxygen to drive all its detergent functions, insulin toxicity, at its core, is an oxygen problem.

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OXYGEN IS THE ORGANIZING PRINCIPLE OF HUMAN BIOLOGYAND GOVERNS THE AGING PROCESS

Dysox (dysoxygenosis) is a state of disrupted oxygen signaling. Specifically, it includes: (1) oxygen-driven cellular energetics; (2) oxygen-driven detox pathways; (3) oxygen signaling for cellular development, differentiatiomn, and demise; and (4) oxygen detergent functions.

x Oxygen-driven cellular energetics

x Oxygen-driven detox pathways

x Oxygen signaling for cellular development, differentiatiomn, and demise

x Oxygen detergent functions

V

A 4

DYSOX

DYSOX IS BLOCKED OXYGEN-DRIVEN ENERGETICS.

DYSOX IS DERANGED OXYGEN SIGNALS.

DYSOX IS LOSS OF OXYGEN’S DETERGENT FUNCTIONS

DYSOX IS IMPAIRED OXYGEN-DRIVEN DETOX

PATHWAYS.

v

V

A 4

DYSOX

DYSOX IS BLOCKED OXYGEN-DRIVEN ENERGETICS.

DYSOX IS DERANGED OXYGEN SIGNALS.

DYSOX IS LOSS OF OXYGEN’S DETERGENT FUNCTIONS

DYSOX IS IMPAIRED OXYGEN-DRIVEN DETOX

PATHWAYS.

v

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OXYGEN HOMEOSTASIS, DYSOXYGENOSIS,

AND THE SCIENTIFIC BASIS OF OXYSTATIC THERAPIES

Majid Ali, M.D.

Author,

The Principles and Practice of Integrative Medicine (12 volumes)

This presentation will present and discuss at length seven aspects of human biology.

x First, oxygen is the organizing influence of human biology and governs the aging process. It is also a molecular Dr. Jekyll/Mr. Hyde par excellence—ushering life with one sleight of hand and terminating it with another.

x Second, human biology is an enormous web of webs—a vast and intricate network of energetic-molecular pathways. Everything in that web is connected to everything else.

x Third, the webs of human biology form a panoramic kaleidoscope. A singular change within that kaleidoscope causes everything to change.

x Fourth, spontaneity of oxidation in nature—sustained by oxygen above all else—provides the primary metabolic drive for all human life processes. It also assures that no oxygen-utilizing life form lives forever.

x Fifth, persistent and progressive oxidosis sets the stage for dysoxygenosis—a state of dysfunctional cellular oxygen metabolism resulting from an impaired function of enzymatic pathways involved with oxygen utilization.

x Sixth, the spiritual serenity that is essential for long-term good health; and

x Seventh, chronic anger and sadness that fan the fires of oxidosis and dysoxygenosis. The so-called mind-body-spirit trio is an artifact of thinking. I have never seen anyone dissect a human and delineate where the body ends and the mind begins , nor where the mind ends and the spiritual begins.  The mind cannot ordain healing on injured tissues. Preoccupation with clever thinking, in reality, is an expression of our inability to sense, feel, and know the wholeness of the human condition. This presentation will address some aspects of spiritual serenity and chronic anger.

All clinical work of a practitioner of integrative medicine—in my view—should be based on a clear understanding of the above seven energetic-molecular aspects of human biology. To illustrate the core clinical points, I will present the following three models:

  1. The Three-Legged Throne of Oxygen Model
  2. The Grease and Detergent Model of Disease
  3. The Sun-Soil Model of health/dis-ease/disease continuum.

The Three-Legged Throne of Oxygen Model will elaborate the following:

  1. Oxygen-driven cellular energetics
  2. Oxygen-driven detox pathways

C Oxygen signaling for cellular development, differentiatiomn, and demise

  1. Oxygen detergent functions

The presentation will include discussions of oral biofilm formation, systemic effects of oral pathology, and offer clinically-validated oral hygiene protocols.

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Redox homeostasis, redox stress, and oxidative stress

Cellular respiration (the transference of electrons between oxygen species) allows each of us to survive on this planet not only at the cellular level but also as an organism. Homeostasis is a key element to all healthy physiologic functions throughout the body and when there is loss of homeostasis, there is usually disease.

Redox homeostasis describes the normal physiologic process of reduction and oxidation in order to re-pair unstable, damaging, reduced, reactive oxygen species (ROS) which will include the following oxygen free radicals (O2′ – superoxide, H2O2 – hydrogen peroxide, -OH’ hydroxyl radical, and singlet oxygen) and organic analogues which include reactive nitrogen species (RNS) primarily peroxynitrite ONOO’.

This homeostatic balance between ROS and antioxidant capacity is in contrast to redox stress (redox imbalance) which implies a loss of this unique homeostasis resulting in an excess production of ROS (tables 1 and 2) either through the process of reduction or oxidation.

Table 1. Courtesy [9] origins of reactive oxygen species (ROS) which produce redox stress

Table 2. Courtesy [9] Origins of reactive oxygen species (ROS) and cellular location

Oxidative Stress implies a loss of redox homeostasis (imbalance) with an excess of ROS by the singular process of oxidation. Both redox and oxidative stress may be associated with an impairment of antioxidant defensive capacity as well as an overproduction of ROS.

It has been known for some time that ROS are detrimental and toxic to cells and tissues as a result of injury to lipids, nucleic acids, and proteins: (A). Lipid peroxidation of membranes (loss of membrane function and increased permeability) and generation of lipid autoperoxidation reactions. (B). DNA damage leading to mutation and death. (C). Cross linking or vulcanization of sulfhydryl rich proteins (leading to stiff aged proteins specifically collagen of the extracellular matrix). [7]

The evolutionary process of redox homeostasis allows humans to survive in an atmosphere of high oxygen content. In addition our bodies have become “hard wired” to utilize the mechanism of redox stress injury to fend off invading infectious organisms and survive our environment.

Paradoxically, (when there is loss of homeostasis resulting in redox or oxidative stress) this protective mechanism turns on our own cells; tissues and causes damage, especially the intima in the atheroscleropathy associated with MS, IR, PD, and overt T2DM. This constellation of MS, IR, PD, and T2DM is associated with an elevated tension of redox stress within the intima (also the islet in MS, IR, PD, and T2DM) due to multiple toxicities. (table 3) Each of these A-FLIGHT toxicities result in the formation of damaging ROS. [8,9]

Table 3. Courtesy [8,9] The manifold toxicities of insulin resistance, metabolic syndrome and T2DM

Not only are ROS involved in the development of type 1 diabetes mellitus (T1DM) and T2DM but also play an important role in the long-term development of the associated complications: The multiple diabetic-opathies (A – DINNER: atheroscleropathy, angiogenesis (accelerated) and arteriogenesis (impaired), diabetic cardiomyopathy and dermopathy, intimopathy, nephropathy, neuropathy, enteropathy, retinopathy (table 4). This review will focus primarily on the association of redox stress in the intima and how it interacts with MS, IR, PD, and T2DM.

Table 4. Multiple diabetic-OPATHIES.

Metabolic syndrome and insulin resistance

IR describes the condition whereby there is a resistance to insulin mediated glucose uptake by cells and is central to the clustering of multiple metabolic abnormalities and clinical syndromes (figure 3). The clustering phenomenon was first described by Kylin in 1923 when he described the clustering of three clinical syndromes: hypertension, hyperglycemia, and hyperuricemia. [10]

Figure 3. The cluster of multiple abnormalities are associated with the metabolic syndrome and insulin resistance is central to the development of ATHEROSCLEROPATHY, cardiovascular disease, and events in the patient with MS, IR, PD, and overt T2DM.

In 1936 Himsworth [11] noted that a large number of diabetic patients were insulin insensitive and suggested that diabetics be divided into groups that were insulin sensitive and insulin insensitive.

Yalow and colleagues in 1965 [12] were first to discover an insulin assay and reported that IR was a condition in which insulin does not produce the same glucose lowering effects seen in insulin-sensitive individuals.

These concepts were rejuvenated and immortalized by Reaven in 1988 given as the Banting lecture.[13] The clustering phenomenon has gone by many names since Dr. Reaven first described the metabolic and clinical associations of the many names of Syndrome X. (table 5)

Table 5. Courtesy [8,9] The myriad names of the metabolic syndrome

By 1999, the World Health Organization had chosen a unifying definition for this syndrome of many names and elected to use the term metabolic syndrome rather than the insulin resistance syndrome because they felt it was not well established that insulin resistance was the cause of all components of the syndrome.[14]

Additionally, there are at least a dozen factors that link clinical suspicions to the metabolic syndrome. (table 6) Factors and findings in this syndrome occur together all to frequently to be considered a coincidence and there are common underlying factors that may explain this coexistence. Namely, the well documented hyperinsulinemia story and the more recent hyperamylinemia and amylin derived islet amyloid story. [8,9]

Table 6. Courtesy [53] Factors that link clinical suspicions to insulin resistance, metabolic syndrome, and a proclivity to develop T2DM.

MS affects approximately 47 million or greater Americans. [15] Of these 47 million, only 20% will develop T2DM and the remaining 80% will be able to compensate (at least for a period of time) through the process of beta cell expansion, hypertrophy, and hyperplasia (utilizing the replicative pool of periductal cells). [16,17]

The resulting hyperinsulinemia, hyperamylinemia (37.6 million = 80% of 47 million) does not come without a price to pay as this compensatory mechanism places these patients at risk for hypertension, atheroscleropathy, and subsequent coronary artery disease. [18,19] (figure 3) See section (A). Ang II, (A). Amylin toxicity, and (I). Insulin toxicity.

The manifold – A-FLIGHT toxicities

(A). Angiotensin II toxicity

Angiotensin II (Ang II) is associated with hypertension, MS, IR, PD, and T2DM both systemically and at the local tissue level. Currently, there is evidence that a local tissue renin angiotensin aldosterone system (RAAS) is operative within the intima and islet as angiotensin type one (AT-1) receptors have been identified as being present on smooth muscle cells, endothelial cells, and the beta cells within the intima and islet [20,21] Insulin is known to upregulate the AT-1 receptor [22] and there exists cross talk between the insulin and the Ang II signaling systems [23] In 1995, Copper et al. were able to demonstrate that amylin activates the RAAS with elevations in renin and aldosterone in humans [24] and, in 2001, Ikeda et al. were able to demonstrate that insulin, proinsulin and amylin infusions resulted in significant increases in renin release and that proinsulin and amylin enhanced this insulin-stimulated renin release in the perfused rat kidney [25].

Taken together, these data support the strong influence of a local RAAS mechanism operating within the intima and islet for the local production of excess Ang II. The islet is quite vascular with an abundant supply of intra islet capillaries and endothelial cells and the intima is lined by a continuous monocellular layer of endothelial cells (additionally, the arterial vessel wall becomes highly vascular through the process of plaque angiogenesis as the vulnerable plaque evolves during the process of atheroscleropathy).

This allows the vascular NAD(P)H oxidase enzyme to come into play. Ang II is one of the most potent endogenous stimuli for the generation of superoxide O2- via the activation of vascular NAD(P)H oxidase. [26,27]

The interruption of this mechanism by the angiotensin converting enzyme inhibitor (ACEi) ramipril in the Heart Outcomes Prevention Evaluation (HOPE) study may help to explain the 32% risk reduction for developing T2DM as well as the dramatic reduction in cardiovascular events. [28]

A special reference to Griendling and Harrison seems appropriate: “Out, damned DOT! Out I say” (where the damned DOT represents the unpaired dots on Lewis diagrams). [29] One of the best ways to prevent these dots from forming is to prevent excess substrates (table 3) which cause the multiple toxicities and the multiplicative effect of the A-FLIGHT toxicities associated with MS, IR, PD, and T2DM.

In MS, IR, PD, and T2DM the intima and islet milieu will be laden with the necessary substrates (hyperinsulinemia, hyperproinsulinemia and hyperamylinemia) to activate the damaging cascading mechanism of Ang II, NAD(P)H oxidase, superoxide (O2-) and peroxynitrite (ONOO-) production while consuming the natural endogenously produced antioxidant nitric oxide (NO) within the vulnerable intima and islet.

Advanced glycosylation endproducts: AGE

Advanced glycosylation endproducts (AGEs) are formed as a result of the non-enzymatic damaging protein glycation due to an excess of glucose (hyperglycemia) present in both T1DM, PD, and T2DM. AGEs are initially formed through the process of a glucose nucleophilic addition reaction with proteins forming a Schiff base followed by the formation of an Amadori compound which undergoes further reactions, rearrangements, dehydrations and cleavage resulting in brown insoluble, cross linked complexes called AGEs. This process is thought to liberate H2O2 through two pathways: the first is the 1,2-enolization pathway which leads to 3-deoxyglucosone forming H2O2 and glucosone; the second pathway is the 2,3-enolization pathway leading to 1-deoxyglucosone and putative 1,4-deoxyglucosone. Under oxidative conditions, the 2,3-enediol is thought to generate H2O2 and carboxymethyllysine. 3-deoxyglucosones are known to be both highly reactive intermediates in non-enzymatic glycosylation and also potent cross-linkers which are responsible for the polymerization of proteins to AGEs. These highly cross-linked proteins, especially collagen, cause a stiffening within the vessel which results in decreased compliance of the arterial vessel wall and may well play an important role in the development of diabetic diastolic dysfunction, diabetic cardiomyopathy, and the diastolic dysfunction of the arterial vessel wall. Furthermore, there are advanced fructosylation endproducts (AFEs), which actually have a greater affinity binding to proteins than glucose and follow a similar pattern in the production of the ROS. [30-33] An excellent in depth review of AGE can be found in an article by Aronson and Rayfield where they discuss how hyperglycemia promotes atherosclerosis [34].

The multiligand immunoglobulin superfamily cell surface receptor: the receptor for advanced glycation endproducts (RAGE) is up-regulated by the presence of AGE and results in the signal transduction of nuclear factor kappa B (NFkappa B) which then results in a chronically active inflammatory state and links this section to section (I). Inflammation Toxicity and atheroscleropathy. [35,36]

(A). Antioxidant enzymes

Antioxidant reserve compromised

In addition to the excess generation of the ROS seen in diabetes, there exists an impaired generation of endogenous antioxidants. Superoxide dismutase (SOD), [37] glutathione reduced (GSH), [38] and ascorbic acid (Vitamin C) [39] are all decreased and associated with atheroscleropathy in diabetes. Moreover, there is evidence of the diminished capacity of other antioxidants such as uric acid and vitamin E with a reduced activity of catalase and glutathione peroxidase (GPx). (Table 6) [40] The exact mechanisms of impairment are still not completely understood but two explanations exist. Protein glycation may be a mechanism that damages the protein within the primary antioxidant enzymes, and the antioxidant enzymes which are co-dependent on one another, may be dysfunctional if one or the other is being consumed by an overactive demand such as compromised GSH function due to the depletion of NADH in the polyol pathway.

It seems quite logical that both mechanisms may be in play at one time or another in the diminished antioxidant defense mechanisms. Another example is glutathione disulfide (GSSG) which is reduced to GSH at the expense of NAD(P)H. [41]

Absence of network antioxidant enzymes

eNOS

The absence of network antioxidant enzymes could play an additional role. A good example of this condition would be the endothelial nitric oxide synthase (eNOS) -/- knockout mouse model by Duplain and Scherrer.

They were able to demonstrate that insulin resistance, hyperlipidemia, and hypertension were present in mice lacking the specific isoform eNOS. This implicates eNOS not only in the endothelial cell (important in the regulation of arterial pressure) but also in the loss of its expression in skeletal muscle which impairs insulin stimulated glucose uptake, and that its loss (both at the endothelial and skeletal muscle sites) impairs lipid homeostasis and creates insulin resistance. [42] This represents the loss of the naturally occurring free oxygen radical scavenging antioxidant effect of endothelial nitric oxide (eNO) (Table 7). Does this apply to humans?

There is evidence of a gene polymorphism in humans and recently Miyamoto et al.[43] were able to demonstrate that a gene polymorphism, Glu298Asp in exon 7 of the eNOS gene, was associated with coronary spastic angina and myocardial infarction and found further evidence for this gene polymorphism in the statically significant association with the development of essential hypertension in two separate Japanese populations. There could be other gene polymorphisms in other populations as well as in other antioxidant genes that relate to insulin resistance, metabolic syndrome, and hypertension. As the human genome evolves, we are certain to find other alterations in various populations throughout the world.

Asymmetrical dimethylarginine (ADMA) has recently been shown to be associated with endothelial dysfunction and increased risk of cardiovascular disease. Stuhlinger, Reaven, Tsao, and colleagues were able to demonstrate a positive correlation with impaired insulin-mediated glucose disposal and elevated levels of ADMA. Plasma ADMA concentrations increased in insulin-resistant subjects independent of hypertension. Increases in plasma ADMA concentrations may contribute to the endothelial dysfunction observed in insulin-resistant patients.

Elevated levels of ADMA have been observed in IR, hypertension, hyperlipidemia, hyperglycemia, hyperhomocysteinemia, and renal failure. ADMA is formed by protein arginine N-methyltransferases and LDL-C both native and oxidized up regulates PRMT’s increasing ADMA. [44,45]

Under physiologic homeostatic conditions, eNOS is the endothelial constitutive (rate limiting) enzyme responsible for the conversion of L-arginine to NO and L-citrulline. It requires a cofactor tetrahydrobiopterin (BH4). There is a paradoxical uncoupling of the eNOS enzyme that allows this above reaction to be capable of producing superoxide (O2′) if there is insufficient BH4, L-arginine, or if there is direct interference with and/or defect in the eNOS enzyme. Uncoupling of eNOS enzyme results in the production of damaging O2′ adding to the oxidative stress within the arterial vessel wall.

Causative factors for eNOS uncoupling are as follows: Increased O2′ and ONOO’, elevations in glucose and both native LDL-C and oxidatively modified, mmLDL-C, hyperhomocysteinemia see section (H), decreased or impaired Cofactor BH4, decreased L-arginine, increased ADMA, and C reactive protein. In time there will in all probability be other causative factors that disable the eNOS enzyme resulting in increased oxidative stress. Additionally, diabetic endothelium has been shown to be a net producer of superoxide O2′ instead of nitric oxide NO resulting in a decreased ratio of NO / ROS [46-51] (figure 4)

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