Dr. Ali’s Course on Healing – Part 2

Majid Ali, M.D.

Cellular Fermentation Forms the Foundation of Disease

I define disease in two ways: (1) disease is a state of separation from one’s nature; and (2) disease is evolution in reverse. These simple definitions are the culmination of my search for the boundary between a state of health and a state of absence of health during fifty-four years of my studies in the fields of surgery, surgical pathology, clinical pathology, immunology, environmental medicine, nutritional medicine, and energetic healing.

Disease Is a State of Separation from One’s Nature

Separation from one’s nature can be environmental (habitat-related elements), energetic (related to cellular energy generation and utilization), or ethical-spiritual (stress-anger-hate-related). Regardless of the initial triggering factors, every additional insult adds to the cumulative burden. Separation from one’s nature fans its own fires. This is one of the core tenets of holism in integrative medicine.

Disease Is Evolution in Reverse

I have had some eureka moments. I define a eureka moment as an experience that begins with a common (and old) observation but compels one to see things in an altogether different light. The most important of these was what I call the Oxygen Moment in which I had two insights. First, nature chose oxygen to drive all aspects of human evolution. Second, oxygen’s hand should be visible in all diseases. Then followed over thirty years of diligent searching of scientific literature to see if there was any evidence that would challenge or refute any aspect of these insights. This search did not reveal any such evidence.

Our ancestors two billion years or so ago were fermenting microbes. They lived in a toxic soup of acids. There was no free oxygen in the air at that time. Nature chose oxygen to drive all aspects of evolution and development of human cells—from fermenting primordial cells to modern cells. Cellular disease begins when cells start to ferment due to lack of oxygen. This is the core tenet of my Oxygen Model of Disease. The crucial clinical importance of this model is it requires that any and all threats to oxygen functions (homeostasis and signaling) must be detected and effectively addressed in all chronic diseases, regardless of the diagnostic label used for it. I return to this subject repeatedly in all seminars included in Dr. Ali’s Course On Healing.

List of Articles in the Series

Seminar 1: Dr. Ali’s Course on Healing Part 1 – Introduction
Seminar 2: Dr. Ali’s Course on Healing Part 2 – Cellular Fermentation Forms
the Foundation of Disease
Seminar 3: Dr. Ali’s Course on Healing Part 3 – Inflammation 101
Seminar 4: Dr. Ali’s Course on Healing Part 4 – Dr. Ali’s Breakfast
Seminar 5: Dr. Ali’s Course on Healing Part 5 – Dr. Ali’s Seven Top Priorities
Seminar 6: Dr. Ali’s Course on Healing Part 6 – Dr. Ali’s Anti-Inflammatory Remedies
Seminar 7: Dr. Ali’s Course on Healing Part 7 – Dr. Ali’s Bowel Detox
Seminar 8: Dr. Ali’s Course on Healing Part 8 – Dr. Ali’s Liver Detox

The text below is highly technical and should be skipped by individuals without a strong biology background. I include it here because it is the abstract of my original paper on the subject. Professional and advanced readers will find it valuable.

Oxidative Regression to Primordial Cellular Ecology (Evolution-in-Reverse)

In 1998, I presented a very body of morphologic observations—made with high-resolution phase-contrast microscopyg—to deal with contentious issue of whether or not the circulating blood is a sterile field. Following is an abstract of that article published in The Journal of Integrative Medicine:

In clinical states characterized by chronically accelerated oxidative stress, enzyme systems involved in oxygen transport and utilization, redox regulation, and acid-base equilibrium are severely impaired. Such oxidative states include fibromyalgia, chronic fatigue syndrome (CFS), Gulf War syndrome, severe immune disorders, and malignant neoplasms. It is proposed that normal “oxygenative” cellular ecology in such states undergoes an “oxidative regression to primordial cellular ecology” (ORPEC) in which state progressive anoxia, acidosis, excess reactive oxidative species, and accumulation of certain organic acids create cellular ecologic conditions that closely simulate the primordial state. The ORPEC state results in rapid multiplication in blood and tissues of pleomorphic anaerobic organisms with yeast-like morphologic features, which are designated “primordial life forms” (PLFs) for lack of precise nucleotide sequence and taxonomic data. PLFs are readily observed with high-resolution phase-contrast and darkfield microscopy in freshly prepared and unstained smears of peripheral blood. Strong homology among yeast and mammalian DNA sequences indicates that the genetic codes for PLF growth may already exist in human cells and that organisms observed in this study may not indicate an infection from an outside source. Rather, the clinical syndromes associated with PLF proliferation may represent a novel “microecologic-genetic” model of illness. Organic acids and other toxins produced by the growing number of PLFs further feed the oxidative flames of the ORPEC state, thus generating oxidative cycles that feed upon each other and are damaging to antioxidant and oxygenative enzyme systems of the body.

Clinical Significance of the ORPEC State (Evolution-in-Reverse)

The clinical significance of the ORPEC hypothesis is that: (1) it provides a sound scientific model for a clearer understanding of the pathogenesis of syndromes associated with accelerated oxidative molecular injury, such as fibromyalgia, CFS, Gulf War syndrome, severe autoimmune disorders and malignant tumors; and (2) it provides a framework for a rational and logical approach for repairing oxidatively damaged cellular ecologies and for restoring health. Notwithstanding the lack of nucleotide sequence and taxonomic data concerning PLFs, the ORPEC hypothesis has strong explanatory power for: (1) the morphologic patterns of growth of PLFs documented in this report; (2) the pathogenesis of clinical syndromes characterized by accelerated oxidative injury; and (3) the sound scientific basis and/or rationale for the empirical efficacy of “anti-PLF” oxygenative, antioxidant, and other therapies employed to restore cellular ecology from the ORPEC state to a physiologic, healthful condition.

To support the ORPEC hypothesis, I drew its primary support from the microscopic findings presented in this paper when these are considered in light of the following: (1) the fundamental “oxygen order” of human biology; (2) the history of oxygen during the primordial era; (3) the primordial cellular ecology as reconstructed from the origin-of-life studies; (4) morphologic evidence of accelerated oxidative injury to all components of circulating blood (oxidative coagulopathy), and to cell membranes, intracellular matrix, and cell organelles such as mitochondria (AA oxidopathy); (5) oxidative oxygenative dysfunctions (pathologic states characterized by impaired cellular oxygenation and caused by oxidative injury); (6) a high level of homology among yeast and mammalian nucleotide sequences (reflecting conserved primordial nucleotide sequences) that may lead to de novo growth of PLFs under primordial conditions; (7) phenomenon of gene swapping in nature that may enlarge the cellular genetic pool; (8) oxidative enzymatic cascades that contribute to and perpetuate primordial conditions; (9) evolving concepts of mycosis and PLFs; (10) increased urinary excretion of certain organic acids that provide biochemical evidence of overgrowth of yeast and PLFs in patients in the ORPEC state; and (11) clinical syndromes of accelerated oxidative molecular injury.

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