Journal of Chronic Fatigue Syndrome: Volume 5, Issue 1, 1999

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Titles and abstracts for the Journal of Chronic Fatigue Syndrome, Volume 5, Issue 1, 1999.

Volume 5, Issue 1, 1999[edit | edit source]

  • Editorial, by Roberto Patarca
  • In vitro Study of Muscle Aerobic Metabolism in Chronic Fatigue Syndrome

    Abstract - "The purpose of this study was to establish if muscle aerobic metabolism is abnormal in chronic fatigue syndrome (CFS). Myoblast cultures from muscle biopsies of 16 patients with CFS and 10 healthy controls were established. Micromethods were used to determine the lactate/pyruvate (L/P) ratio, respiratory chain function and cytochrome oxidase and lactic dehydrogenase activities. Mitochondrial DNA (mtDNA) volume was measured and mtDNA rearrangements sought. The results showed that myoblasts from ten of 16 cases of CFS had defects in aerobic metabolism: two had increased L/P ratios, suggestive of a defect in oxidative phosphorylation while eight had decreased ratios, consistent with a deficiency in pyruvate dehydrogenase. There was a statistically significant broader range of L/P ratios in the patients' cultures, compared to controls (p = 0.011). No mtDNA rearrangements were present. This in vitro study confirms that there is convincing evidence of mild aerobic defects in skeletal muscle in some cases of CFS."[1]

  • Chronic Fatigue Syndrome Progression and Self-Defined Recovery: Evidence from the CDC Surveillance System

    Abstract - "Objective: To examine the presence of symptoms associated with chronic fatigue syndrome (CFS) over the course of the illness and determine the probability of self-defined recovery by duration of illness. Design: Follow-up study. Subjects: One hundred fifty-five CFS patients enrolled in the Centers for Disease Control and Prevention's (CDC) CFS surveillance system between August 1989 and July 1993 and followed to November 1997. Measurements: Presence of symptoms, a self-defined period of recovery from CFS, and demographic differences between patients reporting and not reporting recovery. Period life-table methods were used to compute the probability of recovery from CFS for specific years of illness duration. Results: At illness onset, the most commonly reported CFS symptoms (> 45%) were sore throat, fever, tender lymph nodes, general weakness, and muscle pain. As the illness progressed, the percentages of patients reporting symptoms fluctuated. At illness onset, patients with a sudden onset of CFS reported significantly higher frequencies of sore throat, fever, tender lymph nodes, chills, hypersomnia, difficulty thinking or concentrating, and depression when compared to patients with a gradual onset. As the illness progressed, these differences disappeared, but gradual onset cases reported more hypersomnia than sudden onset cases (p = 0.001). The cumulative probability of recovery from CFS was 31.4% during the first 5 years of illness and 48.1% during the first 10 years of illness. For each year of illness through year 15, both sudden and gradual onset cases had similar recovery probabilities. Thereafter, gradual onset cases had higher recovery probabilities, but these differences were not statistically significant. Patients reporting recovery and those remaining ill were similar demographically. Conclusions: A period of recovery could be reported at any time during the course of CFS, but was more likely in the early years. Additional longitudinal studies are required to adequately describe the course of CFS in the early stages of illness, determine if the illness recurs over time, and predict the occurrence of symptoms over the course of illness. We recommend that researchers develop a standard definition of recovery from CFS and that future studies take into account the variable duration of illness and follow-up."[2]

  • Chronic Fatigue Syndrome in Psychiatric Patients: Evidence of Premorbid Anomalous Patterns of Brain Organization

    Abstract - "Forty-six patients with chronic fatigue syndrome (CFS) were matched with two control groups: one chosen on the basis of relatively good physical health (N = 92) and the other without regard to physical health (N = 46). All patients were from the same psychiatric practice. The groups were compared on 20 anomalous brain conditions or phenomena (ABCP) used as markers of patterns of brain organization. The results suggest that psychiatric patients who subsequently develop CFS have a higher number of pre-CFS ABCP, of both childhood and adult onset, than psychiatric patients who have not developed this condition."[3]

  • Cytokine Expression and Morphology of in vitro Grown Monocytes from Patients with Chronic Fatigue Syndrome

    Abstract - "Although the underlying metabolic cause of chronic fatigue syndrome (CFS) is unknown, specific defects have been proposed to exist in the skeletal muscle, the immune system and the neuroendo-crine system. Peripheral blood mononuclear cells from CFS patients and healthy controls were fractionated as adherent cells (monocyte-en-riched fraction) and non-adherent cells. We have investigated some activities of the former during in vitro culture. It was observed that the morphology (shape and size) of adherent cells from CFS patients, co-cultivated with homologous non-adherent cells, differed between CFS patients and healthy controls for 21 out of 25 (84%) paired samples (i.e., CFS patient and healthy control). Cytokine expression was examined for the adherent cell population collected from 14 CFS patients and 12 healthy controls. Unstimulated and LPS stimulated tumour necrosis factor-a (TNFa) expression was higher for monocytes from 7 out of 14 CFS patients. Unstimulated interleukin-β (IL-β) expression was higher for monocytes from 10 out of 14 CFS patients, whereas LPS-stimulated IL-β expression was higher for 8 out of 14 CFS patients. The proportional increase of IL-β and TNFa following LPS stimulation was lower for the majority of the CFS patients studied, suggesting that the monocytes from CFS patients were less responsive to LPS than the respective healthy controls. The basis for the abnormal in vitro monocyte maturation, the elevated unstimulated levels of IL-β expression and the abnormal response of the monocytes to LPS is unknown. The relevance of these findings to CFS pathogenesis is discussed."[4]

  • Treatment of Chronic Fatigue Syndrome with Chinese Medicine

    Abstract - "Chronic fatigue syndrome (CFS) is a severe, debilitating disorder, which prominently features self-reported impairments in concentration and short-term memory, and disturbances in sleep and emotions, all of which can affect any one and seriously affect quality of life. In 1987, the Centers for Disease Control and Prevention (CDC) defined CFS as persistent or relapsing fatigue, with at least 50% reduction of baseline activity level lasting for at least 6 months, as one of the main symptoms. Since its cause is still unknown, treatment of CFS has been palliative and has included usually orally administered products, such as vitamin B12, vitamin C, folic acid, iron, magnesium, essential fatty acids, coenzyme Cho and nicotinamide adenine dinucleotide (NADH), among others. The latter therapeutic modalities can only relieve some symptoms to some extent, but cannot fundamentally eliminate fatigue. It is, therefore, urgent to seek safe and effective drugs for the treatment of fatigue. We propose here that regulating homeostasis and enhancing immunity are important for the treatment of fatigue. In China, many Chinese herbs with such functions have been proven effective, an observation which opens the possibility of a new therapeutic method of eliminating fatigue with traditional Chinese medicine (TCM)."[5]

  • A Nutrient/Toxin Interaction Theory of the Etiology and Pathogenesis of Chronic Pain-Fatigue Syndromes: Part I

    Abstract - "Recent research suggests that Chronic Fatigue Syndrome (CFS), Fibromyalgia Syndrome (FMS), and Persian Gulf Syndrome (PGS) may represent the effects of dysfunctions involving the central and/or peripheral nervous system, neuroendocrine system, neuromuscu-lar system, immune system, metabolism, or sleep patterns. Each systemic dysfunction is accepted here as being central to these syndromes but not causal. This two-part review introduces the theory that the syndromes listed above represent finitely variable combinations of multiple systemic dysfunctions which all share a common underlying etiology at the subcellular level: magnesium deficiency plus concomitant fluoride excess (MDFE). The theory is introduced in Part I; detailed evidence which supports the theory is presented in Part II. Treatment suggestions are listed at the end of Part II through a call for clinical trials to test this theory."[6]

  • A Nutrient/Toxin Interaction Theory of the Etiology and Pathogenesis of Chronic Pain-Fatigue Syndromes: Part II

    Abstract - "This second part of the review paper covers the evidence in favor of the theory which proposes that Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Persian Gulf Syndrome represent finitely variable combinations of multiple systemic dysfunctions which share a common underlying etiology at the subcellular level: magnesium deficiency plus concomitant fluoride excess (MDFE). Treatment suggestions are listed at the end of the manuscript through a call for clinical trials to test the theory presented."[7]

  • Letter to the Editor by Leslie J. Findley & Diane L. Cox[8]
  • Patient Column about Young Action Online.

See also[edit | edit source]

References[edit | edit source]

  1. Behan, Wilhelmina M.H.; Holt, Ian J.; Kay, David H.; Moonie, Pamela (1999). "In vitro Study of Muscle Aerobic Metabolism in Chronic Fatigue Syndrome". Journal of Chronic Fatigue Syndrome. 5 (1): 3–16. doi:10.1300/J092v05n01_02.
  2. Reyes, Michele; Dobbins, James G.; Nisenbaum, Rosane; Subedar, Nazerah S.; Randall, Bonnie; Reeves, William C. (1999), "Chronic Fatigue Syndrome Progression and Self-Defined Recovery: Evidence from the CDC Surveillance System", Journal of Chronic Fatigue Syndrome, 5 (1): 17-27, doi:10.1300/J092v05n01_03
  3. Noble A. Endicott. (1999). Chronic Fatigue Syndrome in Psychiatric Patients: Evidence of Premorbid Anomalous Patterns of Brain Organization. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 29-45. http://dx.doi.org/10.1300/J092v05n01_04
  4. H. B. Gimenez, P. Cash, R. B. S. Laing & J. G. Douglas. (1999). Cytokine Expression and Morphology of in vitro Grown Monocytes from Patients with Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 47-60. http://dx.doi.org/10.1300/J092v05n01_05
  5. Chen Jiaxu & Yang Weiyi. (1999). Treatment of Chronic Fatigue Syndrome with Chinese Medicine. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 61-65. http://dx.doi.org/10.1300/J092v05n01_06
  6. Julia A. Laylander. (1999). A Nutrient/Toxin Interaction Theory of the Etiology and Pathogenesis of Chronic Pain-Fatigue Syndromes: Part I. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 67-91. http://dx.doi.org/10.1300/J092v05n01_07
  7. Julia A. Laylander. (1999). A Nutrient/Toxin Interaction Theory of the Etiology and Pathogenesis of Chronic Pain-Fatigue Syndromes: Part II. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 93-126. http://dx.doi.org/10.1300/J092v05n01_08
  8. Leslie J. Findley & Diane L. Cox. (1999). Letter to the Editor. Journal of Chronic Fatigue Syndrome, Vol. 5, Iss. 1, pp. 127-128. http://dx.doi.org/10.1300/J092v05n01_09