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Metabolic Abnormalities, Antioxidant Capacity and Toxic Exposures in ME/CFS

Grant Winners

  • Irina Rozenfeld, M.S.N., ARNP, CCRC – College of Osteopathic Medicine
  • Violetta Renesca, M.S. – College of Osteopathic Medicine
  • Nancy Klimas, M.D. – College of Osteopathic Medicine
  • Maria Vera Nunez, M.D. – College of Osteopathic Medicine
  • Ana Maria Castejon, Ph.D. – College of Pharmacy
  • Christiana Okwaraji, BSN – College of Nursing

Deans

  • Elaine Wallace, D.O., M.S., M.S., M.S. – College of Osteopathic Medicine
  • Lisa Deziel, Pharm.D., Ph.D., BCPS, FASHP – College of Pharmacy

Abstract

Award Winners

​Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), is a chronic physical disorder characterized by unexplained debilitating fatigue lasting for at least six months with an accompanying range of constitutional symptoms including: post-exertional malaise and fatigue, sleep dysfunction, cognitive dysfunction, chronic pain, exertional dyspnea, irritable bowel symptoms, heat/cold intolerance, increased/decreased appetite, fever, chills, night sweats, and immune symptoms such as recurrent sore throat. ME/ CFS is classified by the Institute of Medicine (IOM) as systemic exertion intolerance disease (SEID). Between 836,000 and 2.5 million Americans suffer from ME/ CFS (National Academy of Sciences, 2016). It is a highly prevalent condition and is more common in females (Afrin, 2016). The 2010 Canadian Community Health Survey showed that 20% of patients with ME/CFS had food insecurity with no access to adequate healthy foods (Bested & Marshall, 2015). ME/CFS patients are often severely disabled and bedridden and this can contribute to nutritional deficiencies observed in these patients. Armstrong et al. (2015) regarded physical fatigue and post-exertional malaise as the cornerstones of this illness which are typically implicated in energy metabolism within the body. Recent studies by Naviaux et al. (2016) demonstrated abnormalities in energy metabolism that affected mitochondrial function in patients with ME/CFS. Oxidative stress markers have been reported as abnormal in ME/CFS with finding showing reduced antioxidants levels and increased markers of oxidative damage (Maes et al. 2011; Kennedy et al. 2005). The proinflammatory cytokines produced during chronic inflammation in ME/CFS was found to trigger the production of reactive oxygen species linking the chronic inflammatory response to oxidative stress (Morris & Maes 2014). Toxic exposures, metabolic abnormalities, and nutritional deficiencies decrease antioxidative capacities in the body and may contribute to the severity of the health status in patients with ME/CFS (Vecchiet et al., 2003). In this study, we propose to measure a very comprehensive panel of biomarkers that evaluates biochemical nutritional and metabolic indicators, markers of oxidative stress, environmental exposures and anti-oxidative activity in 30 patients diagnosed with ME/CFS to assess how nutritional deficiencies correlate with the severity of ME/CFS symptoms. After this study is completed, reliable biomarkers of disease severity may be identified creating an opportunity for personalized interventions to correct nutritional deficiencies and improve clinical symptoms.

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