Basics of Dysautonomia – Dysfunctional Autonomic Nervous System
Majid Ali, M.D.
Autonomic nervous system (ANS) is a part of the nervous system which directly or indirectly affects the structure and functions of nearly all body organs.
Dysfunctions of the autonomic nervous system (dysautonomia) is caused by toxicities of food, environment, and thought. What binds the effects of all such toxicities together in the final analysis is dysfunctional oxygen metabolism. This simply stated is my Oxygen Model of Dysautonomia.
Four Questions About Dysautonomia
I repeat the words with which I begin this first article in my Dysautomia Series to raise the following four questions about the disorder:
1. How often are autonomic symptom-complexes encountered in medical clinics?
2. How often do those complexes fit into any of the established “disease.”?
3. How often are molecular basis of autonomic symptomatology clearly recognized by the practitioners?
4. How often do the commonly prescribed symptom-suppressing drugs address the underlying energetic-molecular basis of autonomic symptoms?
The role of dysautonomia can be recognized in the production of symptom-complexes of nearly all chronic disorders. My statement is likely to be challenged only by those who take a very narrow view of the diverse functionalities of ANS. I return to the above four questions after revisiting the classical teachings of the ANS in the various articles of this series to provide a frame of reference for presenting a broader view of the autonomic dysfunctions. The components of the autonomic nervous system are exceptionally vulnerable to unrelenting and cumulative oxidative stresses of modern life. The symptom-complexes of such autonomic dysfunction—oxidative dysautonomia, in our terminology —are widely experienced by individuals who are often told there is nothing wrong with them. That is regrettable. The oxidative nature of their symptom-complexes can generally and readily be established by the examination of their peripheral blood smears with high-resolution phase-contrast microscopy and urinary excretion of organic acids. Increased excretion of acids of glycolytic, Krebs cycle, and hepatic detoxification pathways proves the existence of dysoxygenosis discussed in an earlier chapter. In recent years, there has been a disconcerting increase in debilitating autonomic symptoms in the spreading epidemics of chronic fatigue-fibromyalgia complex, chemical sensitivity syndrome, the Gulf War syndrome, and the September Eleven syndrome—the clinicopathologic entities characterized by relentless oxidative-dysoxygenative stresses.
My holistic and integrative view of oxidative-dysoxic dysautonomia is based on the fundamental molecular-energetic considerations of the functions and dysfunctions of ANS. Regardless of how the various entities characterized by autonomic dysfunction may be initiated or perpetuated, a deeper study reveals that the common denominator in all causes factors is dysfunctional oxygen homeostasis (dysox, for short).
In 1999, that was the primary reason why we introduced the term oxidative dysautonomia.1 It may be added in this context that oxidative dysautonomia affects the health/dis-ease/ disease continuum just as globally and profoundly as oxidative coagulopathy and oxidative lymphopathy presented in an earlier chapter.