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Chronic Fatigue Syndrome Research Studies

Chronic Fatigue Syndrome Research Studies

The following is a list of Chronic Fatigue Syndrome (CFS) research studies:

1.  Clayton, EW. Beyond myalgic encephalomyelitis/chronic fatigue syndrome: an IOM report on redefining an illness. JAMA 2015; 313(11): 1101-1102. Abstract conclusion: This Viewpoint describes an Institute of Medicine report on chronic fatigue syndrome, the result of efforts to develop diagnostic criteria for clinical use and recommend new terminology for the disorder.

2.  Reeves WC, Jones JF, Maloney E, Heim C, Hoaglin DC, Boneva RS, Morrissey M and Devlin R. Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural Georgia. Popul Health Metr 2007; 5:5. Abstract conclusion: We estimated that 2.54% of persons 18 to 59 years of age suffered from CFS. There were no significant differences in prevalence of CFS between metropolitan, urban or rural populations or between white and black residents of the three regions. However, there were significant differences in female-to-male ratios of prevalence across the strata (metropolitan female: male 11.2 : 1, urban 1.7 : 1, rural 0.8 : 1).

3.  Filler K, Lyon D, Bennett, J, McCain N, Elswick R, Lukkahatai N, and Saligan LN. Association of mitochondrial dysfunction and fatigue: A review of the literature. BBA clinical 2014; 1: 12-23. Abstract conclusion: This review examined studies that investigated the association of markers of mitochondrial dysfunction with fatigue and proposes possible research directions to enhance understanding of the role of mitochondrial dysfunction in fatigue. A thorough search using PubMed, Scopus, Web of Science, and Embase databases returned 1220 articles. After the application of inclusion and exclusion criteria, a total of 25 articles meeting eligibility criteria were selected for full review. Dysfunctions in the mitochondrial structure, mitochondrial function (mitochondrial enzymes and oxidative/nitrosative stress), mitochondrial energy metabolism (ATP production and fatty acid metabolism), immune response, and genetics were investigated as potential contributors to fatigue. Carnitine was the most investigated mitochondrial function marker. Dysfunctional levels were reported in all the studies investigating carnitine; however, the specific type of carnitine that was dysfunctional varied. Genetic profiles were the second most studied mitochondrial parameter. Six common pathways were proposed: metabolism, energy production, protein transport, mitochondrial morphology, central nervous system dysfunction and post-viral infection. Coenzyme Q10 was the most commonly investigated mitochondrial enzyme. Low levels of Coenzyme Q10 were consistently associated with fatigue. Potential targets for further investigation were identified as well as gaps in the current literature.

4.  Behan, WMH, More, IAR and Behan PO. Mitochondrial abnormalities in the postviral fatigue syndrome. Acta neuropathologica 1991; 83(1): 61-65. Abstract conclusion: The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.

5.  Fulle, S., Mecocci, P., Fanó, G., Vecchiet, I., Vecchini, A., Racciotti, D., ... & Beal, M. F. (2000). Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome. Free Radical Biology and Medicine, 29(12), 1252-1259. Abstract conclusion: In this study, we detected oxidative damage to DNA and lipids in muscle specimens of CFS patients as compared to age-matched controls, as well as increased activity of the antioxidant enzymes catalase, glutathione peroxidase, and transferase, and increases in total glutathione plasma levels. From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia. These data support an organic origin of CFS, in which muscle suffers oxidative damage.

6.  Myhill S, Booth N and McLaren-Howard J. Chronic fatigue and mitochondrial dysfunction. Int J Clin Exp Med 2009; 2; 1–16. Abstract conclusion: Our observations strongly implicate mitochondrial dysfunction as the immediate cause of CFS symptoms. However, we cannot tell whether the damage to mitochondrial function is a primary effect, or a secondary effect to one or more of a number of primary conditions, for example cellular hypoxia, or oxidative stress including excessive peroxynitrite. Mitochondrial dysfunction is also associated with several other diseases and this is not surprising in view of the important role of mitochondria in almost every cell of the body, but this fact appears to have been recognised only in recent years.

7.  Myhill S, Booth, N and McLaren-Howard J. Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)-a clinical audit. International journal of clinical and experimental medicine 2013; 6(1): 1. Abstract conclusion: We report on an audit of 138 ME/CFS patients who at tended a private practice and took the ATP Profile biomedical test. The results revealed that all of these patients had measureable mitochondrial dysfunction. A basic treatment regime, based on 1) eating the evolutionary correct stone-age diet, 2) ensuring optimum hours of good quality sleep, 3) taking a standard package of nutritional supplements, and 4) getting the right balance between work and rest, was recommended for all patients. Additions to the basic regime were tailored for each patient according to the results of the ATP Profile and additional nutritional tests and clues from the clinical history. Mitochondrial function is typically impaired in two ways: substrate or co-factor deficiency, and inhibition by chemicals, exogenous or endogenous. For the former, additional nutrients are recommended where there is a deficiency, and for the latter, improvement of anti-oxidant status and selective chelation therapy or far-infrared saunas are appropriate. We show case histories of nine patients who have taken the ATP Profile on three or four occasions, and a before-and-after treatment summary of the 34 patients who have had at least two ATP Profile tests separated by some months. Finally, we summarize the results for the 30 patients who followed all aspects of the treatment regime and compare them with the 4 patients who were lax on two or more aspects of the treatment regime. All patients who followed the treatment regime improved in mitochondrial function by on average a factor of 4.

8.  Kaiser, JD. A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. Int J Clin Exp Med 2015;8(7):11064-11074. Abstract conclusion: Stimulant drugs and various micronutrient interventions have previously been studied in chronic fatigue syndrome (CFS) but they have never been studied in combination. This proof of concept investigation seeks to examine the clinical effects and safety profile of KPAX002 (a combination of methylphenidate hydrochloride and mitochondrial support nutrients) in patients with CFS. Fifteen patients diagnosed with CFS by 1994 Fukuda criteria were recruited and treated with KPAX002 to explore a potential synergistic effect of this combination. Fatigue and concentration disturbance symptoms were measured at baseline, 4 weeks, and 12 weeks using two clinically validated tools: Checklist Individual Strength (CIS) and Visual Analog Scale (VAS). The primary outcome objective was a decrease in the total CIS score of ≥25% in at least 50% of the subjects. The mean total CIS score decreased by 36.4 points (34%) at 12 weeks (P<0.0001), corresponding to a ≥25% decrease in 87% of the participants. Treatment with KPAX002 was well tolerated and significantly improved fatigue and concentration disturbance symptoms in greater than 50% of patients with CFS. These results were statistically significant. This combination treatment is worthy of additional investigation.

9.  Billing-Ross, P., Germain, A., Ye, K., Keinan, A., Gu, Z., & Hanson, M. R. (2016). Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome. Journal of Translational Medicine, 14(1), 19. Abstract conclusion: Analysis of mitochondrial genomes in ME/CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to ME/CFS of individuals carrying particular mitochondrial genomes or SNPs was observed.

10.  Myhill, S., Booth, N. E., & McLaren-Howard, J. (2009). Chronic fatigue syndrome and mitochondrial dysfunction. International journal of clinical and experimental medicine, 2(1), 1. Abstract conclusion: The “ATP profile” test is a powerful diagnostic tool and can differentiate patients who have fatigue and other symptoms as a result of energy wastage by stress and psychological factors from those who have insufficient energy due to cellular respiration dysfunction. The individual factors indicate which remedial actions, in the form of dietary supplements, drugs and detoxification, are most likely to be of benefit, and what further tests should be carried out.

11.  Kaiser, J. D. (2015). A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. International journal of clinical and experimental medicine, 8(7), 11064. Abstract conclusion: The primary outcome objective was a decrease in the total CIS score of ≥25% in at least 50% of the subjects. The mean total CIS score decreased by 36.4 points (34%) at 12 weeks (P<0.0001), corresponding to a ≥25% decrease in 87% of the participants. Treatment with KPAX002 was well tolerated and significantly improved fatigue and concentration disturbance symptoms in greater than 50% of patients with CFS. These results were statistically significant. This combination treatment is worthy of additional investigation.

12.  Maes, M., Mihaylova, I., Kubera, M., Uytterhoeven, M., Vrydags, N., & Bosmans, E. (2008). Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder. Neuro endocrinology letters, 30(4), 470-476. Abstract conclusion: The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population. Since statins significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation.

13.  Maes, M., Mihaylova, I., Kubera, M., Uytterhoeven, M., Vrydags, N., & Bosmans, E. (2008). Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder. Neuro endocrinology letters, 30(4), 470-476. Abstract conclusion: The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population. Since statins significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation.

14.  Booth, N. E., Myhill, S., & McLaren-Howard, J. (2012). Mitochondrial dysfunction and the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). International journal of clinical and experimental medicine, 5(3), 208. Abstract conclusion: We find that all patients tested have measureable mitochondrial dysfunction which correlates with the severity of the illness. The patients divide into two main groups differentiated by how cellular metabolism attempts to compensate for the dysfunction. Comparisons with exercise studies suggest that the dysfunction in neutrophils also occurs in other cells. This is confirmed by the cell-free DNA measurements which indicate levels of tissue damage up to 3.5 times the normal reference range. The major immediate causes of the dysfunction are lack of essential substrates and partial blocking of the translocator protein sites in mitochondria. The ATP Profile is a valuable diagnostic tool for the clinical management of ME/CFS.

 
 
 
 
 
 
 

 

 
 
 
 

2 comments

  • Jon Kaiser, MD - Medical Director, Hope for Fatigue
    Jon Kaiser, MD - Medical Director, Hope for Fatigue Tuesday, 02 February 2016 19:59 Comment Link

    The use of antiviral medication in the setting of CFS/ME is controversial. I have always believed that one should know exactly what bacteria or virus one is treating before prescribing an antibacterial or antiviral medication. Therefore, unless there are clearly documented increases in viral titers (such as HHV6), I would discourage the experimental use of antiviral medications that might have unexpected side effects and toxicities.

  • James Branscom
    James Branscom Tuesday, 02 February 2016 15:20 Comment Link

    Do you all believe there's a place for antivirals?

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