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Chronic Fatigue Syndrome: HELP
Articles from Los Angeles
Based on 12 articles published since 2010

These are the 12 published articles about Fatigue Syndrome, Chronic that originated from Los Angeles during 2010-2020.
+ Citations + Abstracts
1 Review Mindfulness-based therapies in the treatment of somatization disorders: a systematic review and meta-analysis. 2013

Lakhan, Shaheen E / Schofield, Kerry L. ·Global Neuroscience Initiative Foundation, Los Angeles, California, United States of America. ·PLoS One · Pubmed #23990997.

ABSTRACT: BACKGROUND: Mindfulness-based therapy (MBT) has been used effectively to treat a variety of physical and psychological disorders, including depression, anxiety, and chronic pain. Recently, several lines of research have explored the potential for mindfulness-therapy in treating somatization disorders, including fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome. METHODS: Thirteen studies were identified as fulfilling the present criteria of employing randomized controlled trials to determine the efficacy of any form of MBT in treating somatization disorders. A meta-analysis of the effects of mindfulness-based therapy on pain, symptom severity, quality of life, depression, and anxiety was performed to determine the potential of this form of treatment. FINDINGS: While limited in power, the meta-analysis indicated a small to moderate positive effect of MBT (compared to wait-list or support group controls) in reducing pain (SMD = -0.21, 95% CI: -0.37, -0.03; p<0.05), symptom severity (SMD = -0.40, 95% CI: -0.54, -0.26; p<0.001), depression (SMD = -0.23, 95% CI: -0.40, -0.07, p<0.01), and anxiety (SMD = -0.20, 95% CI: -0.42, 0.02, p = 0.07) associated with somatization disorders, and improving quality of life (SMD = 0.39, 95% CI: 0.19, 0.59; p<0.001) in patients with this disorder. Subgroup analyses indicated that the efficacy of MBT was most consistent for irritable bowel syndrome (p<0.001 for pain, symptom severity, and quality of life), and that mindfulness-based stress reduction (MBSR) and mindfulness-based cognitive therapy (MCBT) were more effective than eclectic/unspecified MBT. CONCLUSIONS: Preliminary evidence suggests that MBT may be effective in treating at least some aspects of somatization disorders. Further research is warranted.

2 Review Fatigue, brain, behavior, and immunity: summary of the 2012 Named Series on fatigue. 2012

Bower, Julienne E. ·UCLA Department of Psychology, 1285 Franz Hall, Los Angeles, CA 90095-1563, USA. jbower@ucla.edu ·Brain Behav Immun · Pubmed #22964543.

ABSTRACT: The focus on fatigue for the 2012 Named Series in brain, behavior, and immunity reflects the growing wave of research examining immune underpinnings of fatigue in healthy and clinical populations. Fatigue is prevalent in the general population and in patients with a variety of medical conditions. However, the etiology of fatigue remains elusive. Psychoneuroimmunological approaches to fatigue have yielded important advances in our understanding of this complex symptom and are represented in the twelve articles included in the Named Series. These articles include animal and human models of fatigue and cross a variety of different medical conditions, including cancer, chronic fatigue syndrome, and diabetes. This review briefly summarizes the articles included in the series and highlights the themes that have emerged from this body of work.

3 Clinical Trial Tracking post-infectious fatigue in clinic using routine Lab tests. 2016

Harvey, Jeanna M / Broderick, Gordon / Bowie, Alanna / Barnes, Zachary M / Katz, Ben Z / O'Gorman, Maurice R G / Vernon, Suzanne D / Fletcher, Mary Ann / Klimas, Nancy G / Taylor, Renee. ·Department of Medicine, University of Miami, Miami, FL, USA. · Department of Medicine, University of Miami, Miami, FL, USA. gbroderick@nova.edu. · Institute for Neuro Immune Medicine, Nova Southeastern University, University Park Plaza, 3440 South University, Fort Lauderdale, 33328, FL, USA. gbroderick@nova.edu. · University of Alberta, Edmonton, AB, Canada. gbroderick@nova.edu. · University of Alberta, Edmonton, AB, Canada. · Ann & Robert H Lurie Children's Hospital of Chicago, Chicago, IL, USA. · Children's Hospital Los Angeles, Los Angeles, CA, USA. · Solve ME/CFS Initiative, Charlotte, NC, USA. · Institute for Neuro Immune Medicine, Nova Southeastern University, University Park Plaza, 3440 South University, Fort Lauderdale, 33328, FL, USA. · University of Illinois at Chicago, Chicago, IL, USA. ·BMC Pediatr · Pubmed #27118537.

ABSTRACT: BACKGROUND: While biomarkers for chronic fatigue syndrome (CFS) are beginning to emerge they typically require a highly specialized clinical laboratory. We hypothesized that subsets of commonly measured laboratory markers used in combination could support the diagnosis of post-infectious CFS (PI-CFS) in adolescents following infectious mononucleosis (IM) and help determine who might develop persistence of symptoms. METHODS: Routine clinical laboratory markers were collected prospectively in 301 mono-spot positive adolescents, 4 % of whom developed CFS (n = 13). At 6, 12, and 24 months post-diagnosis with IM, 59 standard tests were performed including metabolic profiling, liver enzyme panel, hormone profiles, complete blood count (CBC), differential white blood count (WBC), salivary cortisol, and urinalysis. Classification models separating PI-CFS from controls were constructed at each time point using stepwise subset selection. RESULTS: Lower ACTH levels at 6 months post-IM diagnosis were highly predictive of CFS (AUC p = 0.02). ACTH levels in CFS overlapped with healthy controls at 12 months, but again showed a trend towards a deficiency at 24 months. Conversely, estradiol levels depart significantly from normal at 12 months only to recover at 24 months (AUC p = 0.02). Finally, relative neutrophil count showed a significant departure from normal at 24 months in CFS (AUC p = 0.01). Expression of these markers evolved differently over time between groups. CONCLUSIONS: Preliminary results suggest that serial assessment of stress and sex hormones as well as the relative proportion of innate immune cells measured using standard clinical laboratory tests may support the diagnosis of PI-CFS in adolescents with IM.

4 Article Unexplained exertional intolerance associated with impaired systemic oxygen extraction. 2019

Melamed, Kathryn H / Santos, Mário / Oliveira, Rudolf K F / Urbina, Mariana Faria / Felsenstein, Donna / Opotowsky, Alexander R / Waxman, Aaron B / Systrom, David M. ·Division of Pulmonary and Critical Care Medicine, David Geffen School of Medicine at UCLA, University of California at Los Angeles, 10833 Le Conte Avenue, 43-229 CHS, Los Angeles, CA, 90095, USA. kmelamed@mednet.ucla.edu. · Division of Pulmonary and Critical Care Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA, USA. · Heart and Vascular Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. · Division of Respiratory Diseases, Dept of Medicine, Federal University of São Paulo (Unifesp), São Paulo, Brazil. · Infectious Disease Unit, Medical Services, Harvard Medical School, Massachusetts General Hospital, Boston, MA, USA. · Boston Adult Congenital Heart Service, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. ·Eur J Appl Physiol · Pubmed #31493035.

ABSTRACT: PURPOSE: The clinical investigation of exertional intolerance generally focuses on cardiopulmonary diseases, while peripheral factors are often overlooked. We hypothesize that a subset of patients exists whose predominant exercise limitation is due to abnormal systemic oxygen extraction (SOE). METHODS: We reviewed invasive cardiopulmonary exercise test (iCPET) results of 313 consecutive patients presenting with unexplained exertional intolerance. An exercise limit due to poor SOE was defined as peak exercise (Ca-vO RESULTS: Prevalence of impaired SOE as the sole cause of exertional intolerance was 12.5% (32/257). At peak exercise, poor SOE and HV had less acidemic arterial blood compared to NL (pHa = 7.39 ± 0.05 vs. 7.38 ± 0.05 vs. 7.32 ± 0.02, p < 0.001), which was explained by relative hypocapnia (PaCO CONCLUSIONS: We identified a cohort of patients whose exercise limitation is due only to systemic oxygen extraction, due to either an intrinsic abnormality of skeletal muscle mitochondrion, limb muscle microcirculatory dysregulation, or hyperventilation and left shift the oxyhemoglobin dissociation curve.

5 Article Genome-epigenome interactions associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. 2018

Herrera, Santiago / de Vega, Wilfred C / Ashbrook, David / Vernon, Suzanne D / McGowan, Patrick O. ·a Centre for Environmental Epigenetics and Development , University of Toronto , Scarborough , Canada. · b Department of Biological Sciences , University of Toronto , Scarborough , Canada. · c Department of Cell and Systems Biology , University of Toronto , Toronto , Canada. · d Solve ME/CFS Initiative , Los Angeles , CA , USA. · e Department of Psychology , University of Toronto , Toronto , Canada. · f Department of Physiology, Faculty of Medicine , University of Toronto , Toronto , Canada. ·Epigenetics · Pubmed #30516085.

ABSTRACT: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disease of unknown etiology. Multiple studies point to disruptions in immune functioning in ME/CFS patients as well as specific genetic polymorphisms and alterations of the DNA methylome in lymphocytes. However, potential interactions between DNA methylation and genetic background in relation to ME/CFS have not been examined. In this study we explored this association by characterizing the epigenetic (~480 thousand CpG loci) and genetic (~4.3 million SNPs) variation between cohorts of ME/CFS patients and healthy controls. We found significant associations of DNA methylation states in T-lymphocytes at several CpG loci and regions with ME/CFS phenotype. These methylation anomalies are in close proximity to genes involved with immune function and cellular metabolism. Finally, we found significant correlations of genotypes with methylation modifications associated with ME/CFS. The findings from this study highlight the role of epigenetic and genetic interactions in complex diseases, and suggest several genetic and epigenetic elements potentially involved in the mechanisms of disease in ME/CFS.

6 Article Epigenetic modifications and glucocorticoid sensitivity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). 2017

de Vega, Wilfred C / Herrera, Santiago / Vernon, Suzanne D / McGowan, Patrick O. ·Department of Biological Sciences, University of Toronto, Scarborough, 1265 Military Trail, Toronto, ON, M1C 1A4, Canada. · Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada. · Present affiliation: Department of Biological Sciences, Lehigh University, Bethlehem, PA, USA. · Solve ME/CFS Initiative, Los Angeles, CA, USA. · Present affiliation: The Bateman Horne Center of Excellence, Salt Lake City, UT, USA. · Department of Biological Sciences, University of Toronto, Scarborough, 1265 Military Trail, Toronto, ON, M1C 1A4, Canada. patrick.mcgowan@utoronto.ca. · Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada. patrick.mcgowan@utoronto.ca. · Department of Psychology, University of Toronto, Toronto, ON, Canada. patrick.mcgowan@utoronto.ca. · Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. patrick.mcgowan@utoronto.ca. ·BMC Med Genomics · Pubmed #28231836.

ABSTRACT: BACKGROUND: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating idiopathic disease characterized by unexplained fatigue that fails to resolve with sufficient rest. Diagnosis is based on a list of symptoms and exclusion of other fatigue-related health conditions. Despite a heterogeneous patient population, immune and hypothalamic-pituitary-adrenal (HPA) axis function differences, such as enhanced negative feedback to glucocorticoids, are recurring findings in ME/CFS studies. Epigenetic modifications, such as CpG methylation, are known to regulate long-term phenotypic differences and previous work by our group found DNA methylome differences in ME/CFS, however the relationship between DNA methylome modifications, clinical and functional characteristics associated with ME/CFS has not been examined. METHODS: We examined the DNA methylome in peripheral blood mononuclear cells (PBMCs) of a larger cohort of female ME/CFS patients using the Illumina HumanMethylation450 BeadChip Array. In parallel to the DNA methylome analysis, we investigated in vitro glucocorticoid sensitivity differences by stimulating PBMCs with phytohaemagglutinin and suppressed growth with dexamethasone. We explored DNA methylation differences using bisulfite pyrosequencing and statistical permutation. Linear regression was implemented to discover epigenomic regions associated with self-reported quality of life and network analysis of gene ontology terms to biologically contextualize results. RESULTS: We detected 12,608 differentially methylated sites between ME/CFS patients and healthy controls predominantly localized to cellular metabolism genes, some of which were also related to self-reported quality of life health scores. Among ME/CFS patients, glucocorticoid sensitivity was associated with differential methylation at 13 loci. CONCLUSIONS: Our results indicate DNA methylation modifications in cellular metabolism in ME/CFS despite a heterogeneous patient population, implicating these processes in immune and HPA axis dysfunction in ME/CFS. Modifications to epigenetic loci associated with differences in glucocorticoid sensitivity may be important as biomarkers for future clinical testing. Overall, these findings align with recent ME/CFS work that point towards impairment in cellular energy production in this patient population.

7 Article Increased prevalence of two mitochondrial DNA polymorphisms in functional disease: Are we describing different parts of an energy-depleted elephant? 2015

Boles, Richard G / Zaki, Essam A / Kerr, Jonathan R / Das, Kingshuk / Biswas, Sawona / Gardner, Ann. ·Division of Medical Genetics and the Saban Research Institute, Children's Hospital Los Angeles, CA USA; Department of Pediatrics, Keck School of Medicine at the University of Southern California, Los Angeles, CA USA. Electronic address: richard.boles@courtagen.com. · Division of Medical Genetics and the Saban Research Institute, Children's Hospital Los Angeles, CA USA. · Division of Clinical Sciences, St. George's University of London, Cranmer Terrace, London United Kingdom. · Department of Clinical Neuroscience, Division of Psychiatry, Karolinska Institutet, Stockholm Sweden. ·Mitochondrion · Pubmed #25934187.

ABSTRACT: About 20% of the population suffers from "functional syndromes". Since these syndromes overlap greatly in terms of co-morbidity, pathophysiology (including aberrant autonomic activity) and treatment responses, common predisposing genetic factors have been postulated. We had previously showed that two common mitochondrial DNA (mtDNA) polymorphisms at positions 16519 and 3010 are statistically associated with the functional syndromes of migraine, cyclic vomiting syndrome and non-specific abdominal pain. Herein, among individuals with mtDNA haplogroup H (HgH), the presence of these two mtDNA polymorphisms were ascertained in additional functional syndromes: chronic fatigue syndrome, complex regional pain syndrome, sudden infant death syndrome, and major depressive disorder. Polymorphic prevalence rates were compared between disease and control groups, and within each disease group in participants with and without specific clinical findings. In all four conditions, one or both of the polymorphisms was significantly associated with the respective condition and/or co-morbid functional symptomatology. Thus, we conclude that these two mtDNA polymorphisms likely modify risk for the development of multiple functional syndromes, likely constituting a proportion of the postulated common genetic factor, at least among individuals with HgH. Pathophysiology likely involves broad effects on the autonomic nervous system.

8 Article Association of C-reactive protein and interleukin-6 with new-onset fatigue in the Whitehall II prospective cohort study. 2013

Cho, H J / Kivimäki, M / Bower, J E / Irwin, M R. ·Cousins Center for Psychoneuroimmmunology, UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA. hjcho@mednet.ucla.edu ·Psychol Med · Pubmed #23151405.

ABSTRACT: BACKGROUND: Although basic research on neuroimmune interactions suggests that inflammatory processes may play a role in the development of fatigue, population-based evidence on this association is limited. This study examined whether plasma C-reactive protein (CRP) and interleukin-6 (IL-6), biomarkers of systemic inflammation, predict fatigue onset. METHOD: The Whitehall II study is a large-scale cohort study conducted in 20 civil service departments in London. Plasma CRP and IL-6 were measured in 4847 non-fatigued participants at phase 3 (1991-1993, aged 39-63 years). Fatigue was assessed using the Vitality subscale of the 36-item Short Form Health Survey (SF-36) at phase 3 and phase 4 (1995-1996). RESULTS: During a mean follow-up of 3.1 years, 957 new fatigue cases (19.7%) were identified using the pre-established cut-off score of ≤ 50 on the Vitality subscale. CRP values were dichotomized as low (<1.0 mg/l ) or high (≥ 1.0 mg/l) using the Centers for Disease Control/American Heart Association recommendations. Similarly, IL-6 values were also dichotomized as low (<1.5 pg/ml) or high (≥ 1.5 pg/ml). After full adjustment for sociodemographic and biobehavioral covariates, the odds ratios for new-onset fatigue were 1.28 [95% confidence interval (CI) 1.09-1.49, p = 0.003] for high CRP and 1.24 (95% CI 1.06-1.45, p = 0.008) for high IL-6. Similar results were found when CRP and IL-6 were treated as continuous variables. CONCLUSIONS: Plasma CRP and IL-6 were prospectively associated with new-onset fatigue, supporting the hypothesis that low-grade inflammation has a role in the development of fatigue.

9 Article Biology and pathophysiology of the new human retrovirus XMRV and its association with human disease. 2010

Rusmevichientong, Alice / Chow, Samson A. ·Department of Molecular and Medical Pharmacology, Molecular Biology Institute, 650 Charles E. Young Drive, Los Angeles, CA 90095, USA. ·Immunol Res · Pubmed #20717743.

ABSTRACT: Xenotropic murine leukemia virus-related virus (XMRV) is a new human retrovirus originally identified in prostate cancer patients with a deficiency in the antiviral enzyme RNase L. XMRV has been detected with varying frequencies in cases of prostate cancer and chronic fatigue syndrome (CFS), as well as in a small proportion of healthy individuals. An etiologic link between XMRV infection and human disease, however, has yet to be established. Here, we summarize existing knowledge regarding the characteristics of XMRV replication, association of XMRV with prostate cancer and CFS, and potential mechanisms of XMRV pathophysiology. We also highlight several areas, such as the establishment of standardized assays and the development of animal models, as future directions to advance our current understanding of XMRV and its relevance to human disease.

10 Article Fidelity of target site duplication and sequence preference during integration of xenotropic murine leukemia virus-related virus. 2010

Kim, Sanggu / Rusmevichientong, Alice / Dong, Beihua / Remenyi, Roland / Silverman, Robert H / Chow, Samson A. ·Biomedical Engineering Interdepartmental Program, University of California Los Angeles, Los Angeles, California, United States of America. ·PLoS One · Pubmed #20421928.

ABSTRACT: Xenotropic murine leukemia virus (MLV)-related virus (XMRV) is a new human retrovirus associated with prostate cancer and chronic fatigue syndrome. The causal relationship of XMRV infection to human disease and the mechanism of pathogenicity have not been established. During retrovirus replication, integration of the cDNA copy of the viral RNA genome into the host cell chromosome is an essential step and involves coordinated joining of the two ends of the linear viral DNA into staggered sites on target DNA. Correct integration produces proviruses that are flanked by a short direct repeat, which varies from 4 to 6 bp among the retroviruses but is invariant for each particular retrovirus. Uncoordinated joining of the two viral DNA ends into target DNA can cause insertions, deletions, or other genomic alterations at the integration site. To determine the fidelity of XMRV integration, cells infected with XMRV were clonally expanded and DNA sequences at the viral-host DNA junctions were determined and analyzed. We found that a majority of the provirus ends were correctly processed and flanked by a 4-bp direct repeat of host DNA. A weak consensus sequence was also detected at the XMRV integration sites. We conclude that integration of XMRV DNA involves a coordinated joining of two viral DNA ends that are spaced 4 bp apart on the target DNA and proceeds with high fidelity.

11 Article Comorbidities associated with the increasing burden of hepatitis C infection. 2010

Basseri, Benjamin / Yamini, David / Chee, Grace / Enayati, Pharm D Pedram / Tran, Tram / Poordad, Fred. ·Hepatology Section, Division of Gastroenterology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. ·Liver Int · Pubmed #20408945.

ABSTRACT: BACKGROUND: Hepatitis C virus (HCV) infection is implicated in an increasing number of liver transplantations, hospitalizations and healthcare costs. AIMS: We present an updated assessment of comorbidities associated with HCV in comparison to the general US population. METHODS: Cross-sectional retrospective review of data from 800 patients with HCV evaluated between January 1998 and November 2007. Patient data were prospectively collected using a standardized questionnaire completed at the first encounter and was compared with general US epidemiological data. Odds ratios and 95% confidence intervals (CI) are reported. RESULTS: HCV conferred a 44% (CI 1.16-1.78) and 25% (CI 1.01-1.54) increased risk of diabetes (12.5 vs. 7.3-8.4%; P=0.001) and obesity (23.9 vs. 19.8-33.1%; P=0.041), respectively, compared with the US population. Human immunodeficiency virus (HIV) (5.3 vs. 0.3%; P<0.001) and end-stage renal disease (ESRD) (4.5 vs. 0.2%; P<0.001) were 16- and 13-fold more prevalent in HCV. Interestingly, HCV bestowed 90% decreased odds (CI 0.09-0.15) for hyperlipidaemia (12.3 vs. 53.2-56.1%; P<0.001). The HCV population had a higher prevalence of significant alcohol consumption (41.5 vs. 4.7%; P<0.001), current smoking (57.7 vs. 18.8-20.8%; P<0.001), drug use (46.8 vs. 14.6-15.6%; P<0.001), incarceration (6.6 vs. 2.7%; P<0.001) and tattoos (20.3 vs. 14%; P=0.011), as well as chronic fatigue (44.6 vs. 11.3-19%; P<0.001) and depression (29.3 vs. 5.0-10.3%; P<0.001). CONCLUSION: HCV poses an increasing healthcare burden associated with increased prevalence of diabetes, obesity, HIV, ESRD, maladaptive lifestyle habits and poor quality of life. Practitioners should be cognizant of these trends in order to appropriately manage these comorbidities.

12 Minor Anti-neural antibody response in patients with post-treatment Lyme disease symptoms versus those with myalgic encephalomyelitis/chronic fatigue syndrome. 2015

Ajamian, Mary / Cooperstock, Michael / Wormser, Gary P / Vernon, Suzanne D / Alaedini, Armin. ·Department of Medicine, Columbia University Medical Center, New York, NY, USA. · Division of Infectious Diseases, Department of Child Health, University of Missouri Health System, Columbia, MO, USA. · Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla, NY, USA. · Solve ME/CFS Initiative, Los Angeles, CA, USA. · Department of Medicine, Columbia University Medical Center, 1130 Saint Nicholas Ave., Room 937, New York, NY 10032, USA. Electronic address: aa819@columbia.edu. ·Brain Behav Immun · Pubmed #25866194.

ABSTRACT: -- No abstract --