Chronic Fatigue is a disorder of unknown cause that lasts for prolonged periods and causes extreme and debilitating exhaustion as well as a wide range of other symptoms such as fever, headache, muscle ache and joint pain, often resembling flu and other viral infections. Also known as Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS), Chronic Epstein-Barr Virus (CEBV), Myalgic Encephalomyelitis (ME), “Yuppy Flu” and other names, it is frequently misdiagnosed as hypochondria, psychosomatic illness, or depression, because routine medical tests do not detect any problems. Chronic fatigue syndrome is exactly what its name implies, namely an overwhelming sense of fatigue. Symptoms may represent several ongoing disorders which begin abruptly, tend to come and go, and may last for 6 months. Because there are no specific laboratory tests, diagnosis is made by the presence of chronic fatigue that does not resolve. The clinical disorder is defined by fatigue severe enough to decrease daily activity by at least 50% for at least 6 months. In order to have this condition, it is necessary to eliminate all other clinical conditions, including possible psychiatric problems.
Oxidative Stress and Chronic Fatigue Syndrome
Studies have shown that oxidative stress plays a role in the development of Chronic Fatigue Syndrome (Fulle et al. 2000; Richards et al. 2000; Logan et al. 2001). Oxidative stress is a term used to describe the body’s prolonged exposure to oxidative factors that cause more free radicals than the body can neutralize. Free radicals are produced as a byproduct of normal metabolic functions. When there are enough free radical scavengers present, such as glutathione and vitamins C, E, and A, along with zinc and other nutrients, through normal metabolic functioning, the body will “mop up” or neutralize the free radicals. When free radicals are not neutralized, the body can become vulnerable to cellular destruction. A relationship between abnormal oxidative stress and Chronic Fatigue Syndrome can be found in the literature. An article in the journal Life Science described a study that showed that patients with Chronic Fatigue Syndrome had lower serum transferrin levels and higher lipoprotein peroxidation. These results indicate that patients with Chronic Fatigue Syndrome have increased susceptibility of LDL and VLDL to copper- induced peroxidation and that this is related both to their lower levels of serum transferrin and to other unidentified pro-oxidizing effects of Chronic Fatigue Syndrome (Manuel y Keenoy et al. 2001). Exercise has been shown to increase the production of oxidants. Fortunately, regular endurance exercise results in adaptations in the skeletal muscle antioxidant capacity, which protects myocytes (muscle cells) against the deleterious effects of oxidants and prevents extensive cellular damage (McCully et al. 1996; Powers et al. 1999). A study of the oxygen delivery to muscles in patients with Chronic Fatigue Syndrome found that oxygen delivery and oxidative metabolism was significantly reduced in Chronic Fatigue Syndrome patients after exercise (compared with sedentary controls) (McCully et al. 1999).
Metal Sensitivity and Chronic Fatigue Syndrome
The effect of dental metal (amalgam) removal was studied in 111 patients with metal hypersensitivity and symptoms resembling Chronic Fatigue Syndrome. After consultation with a dentist, the patients decided to replace their metal restorations with nonmetallic materials. A significant number of patients had metal-specific lymphocytes in the blood. Nickel was the most common, followed by inorganic mercury, gold, phenyl- mercury, cadmium, and palladium. As compared to lymphocyte responses in healthy subjects, the Chronic Fatigue Syndrome group had significantly increased responses to several metals, especially to inorganic mercury, phenyl-mercury, and gold. Following dental metal removal, 83 patients (76%) reported long-term health improvement; 24 patients (22%) reported unchanged health; and two patients (2%) reported worsening of symptoms. Following dental metal replacement, the lymphocyte reactivity to metals decreased as well (Stejskal et al. 1999) (see “Mercury Amalgam Toxicity” in the May 2001 issue of Life Extension Magazine).
