In retrospect, I saw the first patients with CFIDS in Incline Village about 1978. The epidemic officially started sometime in 1983 in Incline Village. I left Incline Village January 1, 1980 but continued to treat patients for chronic fatigue. My treatment was mainly with massive doses of vitamin C but it also included many other nutrients. The rationale has been that CFIDS is a free radical disease involving damaged mitochondria.
My suspicion that chronic fatigue was a free radical disease involving mitochondria was because of the beneficial effect of massive doses of vitamin C. I was using the massive doses of vitamin C not for the vitamin C but for the electrons carried by the vitamin C. Ordinarily, when a vitamin C molecule gives up its two extra electrons to scavenge two free radicals, the vitamin C is refueled with two more electrons from the mitochondria. When the mitochondria are damaged and cannot provide the electrons then the spent vitamin C is rapidly irreversibly lost. By giving massive doses of C, this loss is prevented, and the continuing supply of fresh vitamin C substitutes for the inability of the mitochondria to provide the electrons to refuel the spent vitamin C (dehydroascorbate.)
Not incidentally, a major function of the mitochondria is to provide electrons in the form of ATP to the muscles. Without sufficient ATP to fuel the muscles, fatigue results.
The mitochondria are damaged by either viruses, bacteria (sometimes cell wall deficient bacteria, L-forms), yeast toxins, sensitivity to chemicals (including some drugs), allergic reactions, etc. Probably, it usually involves two or more of the above. The damaged mitochondria become the major source of free radicals. A free radical cascade results. Fee radicals from a damaged mitochondria damage adjacent mitochondria and cause them to produce more free radicals. A domino effect results. Because all this up-regulates the immune system, various autoimmune phenomena frequently result which may include aching in muscles, trigger points, etc. (fibromyalgia).
The oral doses of ascorbic acid necessary to substitute for the inability of the mitochondria to supply electrons to refuel the free radical scavengers are at least bowel tolerance doses (see my other papers on this website.) Many patients have found that intravenous ascorbate is effective and necessary from time to time. The main problem has been with insurance not paying for intravenous ascorbate. While there is some expense involved with intravenous ascorbate it has been more effective than that drug costing $15,000 to $19,000 a year. $15,000 of intravenous ascorbate would probably have a chronic fatigue patient dancing a jig.
Ascorbate is not usually a cure for CFIDS but in patients who tolerate massive doses orally (almost everyone tolerates IV ascorbate), it ameliorates the disease better than other treatments. This more effective amelioration is because replacing the mitochondria function of providing the electrons for free radical scavenging gets more at the basic pathological processes in the disease and it helps protect the mitochondria so they can try to repair themselves. The disinterest in the use of ascorbate is hard to understand and it has contributed to not discovering basic causes of the disease. I doubt that short of killing a virus that may be the cause of many cases that there will be found a more effective method of ameliorating the symptoms of the disease.
See also Dr. Catchart's articles Symptoms of Wilson's Syndrome, the effects of Chronic low body temperature, and Titrating to Bowel Tolerance on determining vitamin C dosage.
Content (C) 1995 and prior years, Dr. Robert F. Cathcart.
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