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Dysox:

Energy and Detox Failure in Cells

Majid Ali, M.D.

In 1998, I introduced the term dysox—short for dysoxygenosis—for the 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 the 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.

Oxygen Signaling

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 diagnostic labels that reveal nothing about the real underlying causes—to justify the use of the so-called "drugs of choice."

The webs of oxyenzymes are vast and the webs of oxygenes are far more complex (see the series of articles listed under "Molecular Biology of Oxygen, Advanced" at this site).All such webs are exquisitely 'aware' of changes in oxygen availability in their microenvironment and vigorously respond to them. When one thing changes in those webs in one way, everything changes in some way. Dysoxygenosis, then, is discerned as a state caused by a rich diversity of elements but one that creates the same cellular oxygen dysfunction. In 1998, I also introduced the terms dysfunctional oxygen metabolism and oxygen disorder for readers without medical or biochemical background.

The webs of oxygenes actively respond to their changing microenvironment. All such webs are exquisitely 'aware' of changes in oxygen availability in their microenvironment and vigorously respond to them. When one thing changes in those webs in one way, everything changes in some way. Dysoxygenosis, then, is discerned as a state caused by a rich diversity of elements but one that creates the same cellular oxygen dysfunction. In 1998, I also introduced the terms dysfunctional oxygen metabolism and oxygen disorder for readers without medical or biochemical background.

The Webs of Oxyenzymes and Oxygenes

The webs of oxyenzymes are vast, with each entity linked to every other through multiple pathways. The webs of oxygenes are seemingly far more complex. All such webs are exquisitely 'aware' of changes in oxygen availability in their microenvironment and vigorously respond to them. When one thing changes in those webs in one way, everything changes in some way. Dysoxygenosis, then, is discerned as a state caused by a rich diversity of elements but one that creates the same cellular oxygen dysfunction. In 1998, I also introduced the terms dysfunctional oxygen metabolism and oxygen disorder for readers without medical or biochemical background.

Clinical Significance of Dysoxygenosis

A clear understanding of metabolic trade-off between the high-efficiency respiratory and low-efficiency fermentative ATP-production is crucial for a clear understanding of the clinical significance of dysoxygenosis. Simply stated, the cells in the dysox state lose about 93% energy and rapidly bloat up with acids and alcohols. Unless cellular dysox is quickly reversed, all cellular functions suffer.

The primary biochemical evidence for dysoxygenosis presented here concerns increased urinary excretion of metabolites of the Krebs cycle and glycolytic pathways for generation of ATP. In essence, such organic acid excretion represents a costly metabolic error. The acids were 'packages' of energy that were not processed in the ATP-producing pathways and were 'returned unopened.' Put in other words, urinary waste is"' respiratory ATP-producing pathway to an 'energy-inefficient' partially fermentative ATP-producing pathway. That core issue is explained at length in later tutorials of this course.

Of central importance in such analysis are the intermediates of the citric acid (tricarboxylic or Krebs) cycle. In health, this cycle is the true crossroad of both the anabolic and catabolic energetics. It is the final common pathway for oxygen-driven breakdown of sugars, fats, and proteins for serving the energy needs of the body. It also provides for the oxygen-driven synthesis of the basic building blocks for structural and functional molecules of the body. All steps in this cycle of energetics are catalyzed by a variety of enzymes and their cofactors. Metabolic pathways of carbohydrates, lipids, and proteins enter the cycle via acetyl CoA derived from pyruvic acid, fatty acids, and amino acids respectively.Theoretically, blockages at various levels in the Krebs cycle can be produced when: (1) The cycle enzymes are inactivated by endogenous and exogenous noxious substances; (2) The functions of enzymes are hampered by factors such as pH, temperature, or changes in the quality and quantity of substrates; (3) The cycle enzymes are in short supply or imperfectly produced—enzymes are proteins produced by expression of genes that encode them; (4) The enzyme cofactors are in short supply due to nutritional factors; and (5) There are mitochondrial inefficiencies that interfere with optimal enzyme functions. It may be added here that Krebs cycle metabolites succinic acid, ketoglutaric acid, and others—regarded as mere waste products in the past—are now known to serve crutially important signaling functions.

Related Learning Materials

* The Oxygen Model of Disease

* Dysox: Energy and Detox Failure in Cells

* Coronary Heart Disease - Simplified

* Being One’s Own Cardiologist

* Seeing the Heart

 

Tutorial GG.1 Ali M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit States. Townsend Letter for Doctors and Patients. 2004. August/Sept. issue. 64-65.

Tutorial GG.2 Ali M. Hydrogen peroxide therapies: Recent Insights into oxystatic and antimicrobial actions. Townsend Letter for Doctors and Patients. 2004, 255;140-143.

Tutorial GG.3. Ali M. Cancer, Oxygen, and pantotropha — Part I. Townsend Letter for Doctors and Patients. 2004;256:98-102.

Tutorial GG.4 Ali M The Oxygen View of Pain: Every chronic pain represents cells' cries for oxygen. Townsend Letter for Doctors and Patients. 2005;258:46-48-102.

Tutorial GG.5 Ali M. Prevention of the Iraq War-associated sickness (I-WAS): A prediction and a challenge to the Department of Defense- Townsend Letter for Doctors and Patients. 2005;259/260:134-138.

Tutorial GG.6 Ali M. Bone homeostasis is but one face of oxygen homeostasis. Townsend Letter for Doctors and Patients. 2005;261:86-93.

Tutorial GG.7 Ali M. Oxygen governs the inflammatory response and adjudicates the man-microbe conflicts. Townsend Letter for Doctors and Patients. 2005;262:98-103.

 

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