@ informahealthcare.com, April 27, 2015:
A critical analysis of the proposal of the Institute of Medicine to replace Myalgic Encephalomyelitis and Chronic Fatigue Syndrome by a new diagnostic entity called Systemic Exertion Intolerance Disease
Posted online on April 27, 2015. (doi:10.1185/03007995.2015.1045472) Frank NM Twisk
ME-de-patiënten Foundation, The Netherlands
Address for correspondence: Frank NM Twisk MBA BEd BEc, Zonnedauw 15, 1905 HB Limmen, The Netherlands. Tel. +31-72-505 4775; frank.twisk@hetnet.nl
Abstract
The Institute of Medicine (IOM) recently published their report in response to an assignment ‘to define diagnostic criteria for Myalgic Encephalomyelitis (ME)/chronic fatigue syndrome (CFS), to propose a process for reevaluation of these criteria in the future, and to consider whether a new name for this disease is warranted’.
The basic preassumption of the IOM committee for the development of evidence-based diagnostic criteria for ME/CFS was that ME and CFS denote conditions with similar symptoms, hence ME/CFS.
The IOM committee recommends
1) that ME/CFS will be renamed “systemic exertion intolerance disease” (SEID); and that a new code should be assigned to SEID in the International Classification of Diseases (ICD), replacing the existing codes for ME (a neurological disease: G93.3) and CFS (“signs, symptoms, and abnormal clinical and laboratory findings, not elsewhere classified”: R53.82).
2) that a diagnosis SEID should be made if the new diagnostic criteria are met;
3) that the Department of Health and Human Services develops a toolkit appropriate for screening and diagnosing patients; and
4) that a multidisciplinary group re-examines the new diagnostic criteria when necessary.
This editorial reviews the working procedure of the IOM and two of the outcomes: the recommendation to introduce a new clinical entity (SEID) and new diagnostic criteria.
Based upon the contents of the report, and the arguments of the IOM, a search of PubMed and the archive of the Journal of Chronic Fatigue using the search terms ME (and old synonyms) and CFS, and a search of PubMed related to the five core symptoms of SEID was conducted.
Reviewing the working method and the recommendations, it is concluded that the new diagnostic criteria for SEID are based upon important methodological shortcomings and that the introduction of SEID to replace both ME and CFS has several profound negative consequences outweighing the advantages.
Keywords
Myalgic Encephalomyelitis, chronic fatigue syndrome, systemic exertion intolerance disease, diagnosis, assessment, methodology
Tuesday, April 28, 2015
Friday, April 10, 2015
Olivia's selfies speak truth about illness
itv player, good morning britain, 8 APR 2015, teenager with ME:
Olivia Cole is a beautiful 16-year-old girl and has lived with Chronic Fatigue Syndrome since she was 10. She has not been to school properly since she was in Year 7 due to her illness and is now in Year 11.
Olivia has taken selfies of herself when she is well and ill to show the two different lives she leads due to CFS. She is encouraging others with the syndrome to do the same to raise awareness - as many do not believe it is real and she has therefore lost many friends to it. More @ ITV player, good morning britain, 8 APR 2015, teenager with ME
Olivia Cole is a beautiful 16-year-old girl and has lived with Chronic Fatigue Syndrome since she was 10. She has not been to school properly since she was in Year 7 due to her illness and is now in Year 11.
Olivia has taken selfies of herself when she is well and ill to show the two different lives she leads due to CFS. She is encouraging others with the syndrome to do the same to raise awareness - as many do not believe it is real and she has therefore lost many friends to it. More @ ITV player, good morning britain, 8 APR 2015, teenager with ME
Saturday, April 4, 2015
Four metabolic changes associated with exercise in cultured skeletal muscle cells in CFS compared to healthy controls
@plosone, April 2, 2015:
RESEARCH ARTICLE
Abnormalities of AMPK Activation and Glucose Uptake in Cultured Skeletal Muscle Cells from Individuals with Chronic Fatigue Syndrome
Audrey E. Brown,David E. Jones,Mark Walker,Julia L. Newton
PLOS
Published: April 2, 2015DOI: 10.1371/journal.pone.0122982
Abstract
Background
Post exertional muscle fatigue is a key feature in Chronic Fatigue Syndrome (CFS). Abnormalities of skeletal muscle function have been identified in some but not all patients with CFS. To try to limit potential confounders that might contribute to this clinical heterogeneity, we developed a novel in vitro system that allows comparison of AMP kinase (AMPK) activation and metabolic responses to exercise in cultured skeletal muscle cells from CFS patients and control subjects.
Methods
Skeletal muscle cell cultures were established from 10 subjects with CFS and 7 age-matched controls, subjected to electrical pulse stimulation (EPS) for up to 24h and examined for changes associated with exercise.
Results
In the basal state, CFS cultures showed increased myogenin expression but decreased IL6 secretion during differentiation compared with control cultures. Control cultures subjected to 16h EPS showed a significant increase in both AMPK phosphorylation and glucose uptake compared with unstimulated cells. In contrast, CFS cultures showed no increase in AMPK phosphorylation or glucose uptake after 16h EPS. However, glucose uptake remained responsive to insulin in the CFS cells pointing to an exercise-related defect. IL6 secretion in response to EPS was significantly reduced in CFS compared with control cultures at all time points measured.
Conclusion
EPS is an effective model for eliciting muscle contraction and the metabolic changes associated with exercise in cultured skeletal muscle cells. We found four main differences in cultured skeletal muscle cells from subjects with CFS; increased myogenin expression in the basal state, impaired activation of AMPK, impaired stimulation of glucose uptake and diminished release of IL6. The retention of these differences in cultured muscle cells from CFS subjects points to a genetic/epigenetic mechanism, and provides a system to identify novel therapeutic targets.
RESEARCH ARTICLE
Abnormalities of AMPK Activation and Glucose Uptake in Cultured Skeletal Muscle Cells from Individuals with Chronic Fatigue Syndrome
Audrey E. Brown,David E. Jones,Mark Walker,Julia L. Newton
PLOS
Published: April 2, 2015DOI: 10.1371/journal.pone.0122982
Abstract
Background
Post exertional muscle fatigue is a key feature in Chronic Fatigue Syndrome (CFS). Abnormalities of skeletal muscle function have been identified in some but not all patients with CFS. To try to limit potential confounders that might contribute to this clinical heterogeneity, we developed a novel in vitro system that allows comparison of AMP kinase (AMPK) activation and metabolic responses to exercise in cultured skeletal muscle cells from CFS patients and control subjects.
Methods
Skeletal muscle cell cultures were established from 10 subjects with CFS and 7 age-matched controls, subjected to electrical pulse stimulation (EPS) for up to 24h and examined for changes associated with exercise.
Results
In the basal state, CFS cultures showed increased myogenin expression but decreased IL6 secretion during differentiation compared with control cultures. Control cultures subjected to 16h EPS showed a significant increase in both AMPK phosphorylation and glucose uptake compared with unstimulated cells. In contrast, CFS cultures showed no increase in AMPK phosphorylation or glucose uptake after 16h EPS. However, glucose uptake remained responsive to insulin in the CFS cells pointing to an exercise-related defect. IL6 secretion in response to EPS was significantly reduced in CFS compared with control cultures at all time points measured.
Conclusion
EPS is an effective model for eliciting muscle contraction and the metabolic changes associated with exercise in cultured skeletal muscle cells. We found four main differences in cultured skeletal muscle cells from subjects with CFS; increased myogenin expression in the basal state, impaired activation of AMPK, impaired stimulation of glucose uptake and diminished release of IL6. The retention of these differences in cultured muscle cells from CFS subjects points to a genetic/epigenetic mechanism, and provides a system to identify novel therapeutic targets.
Thursday, April 2, 2015
Simon Wessely in The Lancet: "being too stupid to know how stupid you are"
Quote from Wessely in The Lancet, 21st of march 2015 ..... (I wonder if he noticed the hysterical absurdity ...)
.... "to introduce something new to me. This is the Kruger-Dunning effect—the state of being too stupid to know how stupid you are being."
Simon Wessely in The Lancet: "being too stupid to know how stupid you are".pdf
Find by LYN.
.... "to introduce something new to me. This is the Kruger-Dunning effect—the state of being too stupid to know how stupid you are being."
Simon Wessely in The Lancet: "being too stupid to know how stupid you are".pdf
Find by LYN.
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