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http://www.majidali.com/Hypothesis.htm

Majid Ali, M.D.

ABSTRACT: A hypothesis is proposed that chronic fatigue is a state of
accelerated oxidative molecular injury. Evidence supporting the hypothesis
includes the following: 1. Spontaneity of oxidation in nature is the basic
cause of the aging process for organisms capable of aerobic respiration. Redox
dysregulations represent the initial events that lead to clinical disease
processes. 2. Incidence of chronic fatigue is increasing, as is the oxidant
stress in the Earth's atmosphere. 3. Evidence for oxidative cell membrane
injury in chronic fatigue is furnished by changes in intracellular and
extracellular ions. 4. Immunologic abnormalities that occur in chronic fatigue
are consistent with initial oxidative injury. 5. Commonality of association of
antigens of HLA-DR3 region with chronic fatigue syndrome and with other immune
disorders such as rheumatoid arthritis, pemphigus vulgaris, systemic lupus
erythematosus, and IgA and gold nephropathies. 6. Direct morphologic evidence
of increased oxidative stress on the cell membrane is shown by the fact that we
have found membrane deformities in up to 80% of erythrocytes in blood from
chronic fatigue syndrome patients. These deformities are quickly reversed by
administering ascorbic acid intravenously. 7. Changes in electromyopotentials
observed in chronic fatigue patients are consistent with intracellular ionic
and membrane changes. 8. Clinical entities commonly associated with chronic
fatigue are known to increase oxidative molecular stress. 9. Clinical evidence
obtained with relief of fatigue and related muscle symptoms with the use of
oral and intravenous antioxidant nutrient therapy. From a clinical standpoint,
this model for the molecular basis of chronic fatigue is useful for making
therapeutic decisions for successful management of chronic fatigue without drug
regimens.

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