Tag: critique

Contesting oppressive regimes of truth: A critical feminist re-examination of (bio)psychosocial hegemony in the field of myalgic encephalomyelitis / chronic fatigue syndrome

Abstract:

Myalgic encephalomyelitis / chronic fatigue syndrome, a disabling condition disproportionately affecting women, is predominantly clinically managed through a (bio)psychosocial lens with psychosocial-inspired therapies, criticised for facilitating social and epistemic injustice, psychological and physical harms. Whilst most literature contesting (bio)psychosocial practices espouses a mainstream scientific perspective, politics and power relations undergirding psychosocial hegemony are better explicated through a critical lens. This article re-examines the ascendancy of psychosocial therapies and related practices through a critical feminist psychology and Foucauldian lens, with a view to locating oppressive practices in their socio-political and cultural context and promoting dialogue on possibilities for positive social change.

Source: Hunt, J. E. (2023, August 10). Contesting oppressive regimes of truth: A critical feminist re-examination of (bio)psychosocial hegemony in the field of myalgic encephalomyelitis / chronic fatigue syndrome. https://doi.org/10.31235/osf.io/3g7kp https://osf.io/preprints/socarxiv/3g7kp/ (Full text)

A Concerning Display of Medical Indifference: Reply to ‘Chronic Fatigue Syndrome and an Illness-Focused Approach to Care: Controversy, Morality and Paradox’

Abstract:

In ‘Chronic fatigue syndrome and an illness-focused approach to care: controversy, morality and paradox’, authors Michael Sharpe and Monica Greco begin by characterising myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) as illness-without-disease. On that basis they ask why patients reject treatments for illness-without-disease, and they answer with a philosophical idea. Whitehead’s ‘bifurcation of nature’, they suggest, still dominates public and professional thinking, and that conceptual confusion leads patients to reject the treatment they need. A great deal has occurred, however, since Whitehead characterised his culture’s confusions 100 years ago.

In our time, I suggest, experience is no longer construed as an invalid second cousin of bodily states in philosophy, in medicine or in the culture at large. More importantly, we must evaluate medical explanations before we reach for philosophical alternatives. The National Institutes of Health and the Institute of Medicine have concluded that ME/CFS is, in fact, a biomedical disease, and all US governmental health organisations now agree.

Although it would be productive for Sharpe and Greco to state and support their disagreement with the other side of the disease debate, it is no longer tenable, or safe, to ignore the possibility of disease in patients with ME/CFS, or to recommend that clinicians should do so. When we find ourselves in a framework that suggests the possibility of medical need is somehow beside the point for medical providers, it is time to reconsider our conceptual foundations.

Source: O’Leary D. A concerning display of medical indifference: reply to ‘Chronic fatigue syndrome and an illness-focused approach to care: controversy, morality and paradox’ [published online ahead of print, 2020 Jun 29]. Med Humanit. 2020;medhum-2019-011743. doi:10.1136/medhum-2019-011743 https://pubmed.ncbi.nlm.nih.gov/32601171/

Conceptualising illness and disease: reflections on Sharpe and Greco (2019)

Abstract:

In a recent paper, Sharpe and Greco suggest that chronic fatigue syndrome/myalgic encephalomyelitis (MECFS) can be viewed as an instance of “illness without disease”, and consequently, treatment should be directed towards altering the patient’s experience of, and response to, their symptoms. We discuss two broad issues that arise from Sharpe and Greco’s article, one relating to the assumptions they make about MECFS and its treatment specifically, and the other relating to their conceptualisation of the illness/disease dichotomy.

We argue that the term “illness without disease”, in the sense that Sharpe and Greco use it, is problematic because it can lead to unwarranted causal assumptions. Following these critical comments, we present a new framework for conceptualising the relationship between explanatory disease models and the experience of illness.

© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.

Source: Wilshire C, Ward T. Conceptualising illness and disease: reflections on Sharpe and Greco (2019). Med Humanit. 2019 Dec 11. pii: medhum-2019-011756. doi: 10.1136/medhum-2019-011756. [Epub ahead of print] https://www.ncbi.nlm.nih.gov/pubmed/31826926 (Abstract) https://sci-hub.se/10.1136/medhum-2019-011756 (Full article)

Tenuous link between chronic fatigue syndrome and pyruvate dehydrogenase deficiency

Abstract:

Researchers studying the energy metabolism of patients with chronic fatigue syndrome have reached the conclusion that these patients have impaired pyruvate dehydrogenase function, but their measurements are not consistent with the changes we see in patients with primary genetic pyruvate dehydrogenase deficiency.

A cross-sectional study published in December 2016 found a change in the pattern of amino acids in the plasma of patients with chronic fatigue syndrome. Gene expression in white blood cells and energy metabolism in muscle cells was also found to have changed (1). The authors interpret the results as an expression of functional inhibition of the enzyme pyruvate dehydrogenase, and they postulate dysregulation of the enzyme complex as a possible key factor in the pathogenesis associated with chronic fatigue syndrome.

The study received extensive media coverage (2, 3), and the link to pyruvate dehydrogenase is published without reservations as an established fact (4, 5). At our laboratory we are now receiving samples for metabolic screening from patients with suspected fatigue syndrome. On the basis of my own experience with biochemical diagnostic workup for pyruvate dehydrogenase deficiency, I would like to point out weaknesses in the study that should have prompted much greater caution in the conclusions.

Source: Bliksrud YT. Tenuous link between chronic fatigue syndrome and pyruvate dehydrogenase deficiency. Tidsskr Nor Laegeforen. 2017 Nov 28;137(23-24). doi: 10.4045/tidsskr.17.0948. Print 2017 Dec 12. [Article in English, Norwegian] http://tidsskriftet.no/en/2017/12/debatt/tenuous-link-between-chronic-fatigue-syndrome-and-pyruvate-dehydrogenase-deficiency (Full article)

Comment on Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Toxins 2013, 5, 605-617

Abstract:

The paper by Brewer et al. entitled “Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Toxins 2013, 5, 605–617” is so methodologically flawed that it should never have been published in the scientific literature [1].

In this paper, the authors measure the presence of mycotoxins in the urine of 112 patients suffering from chronic fatigue syndrome (CFS). These finding are then compared to urine samples from 55 healthy control subjects “… with no history of exposure to WDB (water damaged buildings) or moldy environment…” (sic). Not surprisingly, there were more people from the CFS group with mold exposure than in the comparison group. These results are not surprising because, BY DEFINITION, the control group had no history of exposure to mold. By purposely choosing a control group with no history of mold exposure, the authors have statistically rigged their results in such a way that only a positive relationship will be found when compared to the CFS group.

Using the same approach, the authors could test urine from their CFS patients for the presence of caffeine metabolites and compare the results to urine from a group not exposed to caffeinated beverages; they would find more caffeine metabolites in the CFS group for the same methodological reasons, the control group having been purposely selected to be not exposed. The same would be true for nicotine metabolites in the CFS patients’ urine using urine from non-smokers as a comparison group or comparing urinary animal protein metabolites from the CFS group to animal protein metabolites in urine from vegetarians. The results from these studies would show a positive but erroneous association between CFS and caffeine, nicotine and animal protein. The same is true for the relationship that Brewer et al. purportedly found in this study of CFS and mold. The findings from this study are misleading and meaningless.

This study is an example of extreme selection bias and is akin to showing that men are shorter than women by comparing the height of an average group of men to that of women on the national basketball team!

Given the mountain of “junk” science on the Internet, I feel that a credible on-line scientific journal must ensure rigorous methodological standards for the papers it publishes. Such was not the case for this paper.

 

Source: Osterman JW. Comment on Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Toxins 2013, 5, 605-617. Toxins (Basel). 2016 Nov 7;8(11). pii: E322. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5127119/ (Full article)

 

Is chronic fatigue syndrome truly associated with haplogroups or mtDNA single nucleotide polymorphisms?

Letter to the Editor:

With interest we read the article by Billing-Ross et al. [1] about 193 patients with chronic fatigue syndrome (CFS) diagnosed according to the Fukuda or Canadian Consensus criteria and undergoing sequencing of the mtDNA, the DePaul Symptom questionnaire and the Medical Outcome Survey Short Form-36. The study showed that CFS is associated with mtDNA haplogroups J, U and H, that 8 mtDNA single nucleotide polymorphisms (SNPs) were associated with 16 symptom categories, and that three haplogroups were associated with six symptom categories [1]. We have the following comments and concerns.

The main limitation of this study is that only the mtDNA was investigated for sequence variants. Since it is well-known that mitochondrial disorders (MIDs) may be also caused by mutations in nDNA-located genes, particularly in children [2], disease-causing mutations or SNPs facilitating the development of CFS may have been missed. Furthermore, MIDs may not only be due to respiratory chain dysfunction but also due to disruption of other mitochondrial pathways, such as the beta-oxidation, the hem synthesis, the calcium handling, the coenzyme-Q metabolism, or the urea cycle. There is also consensus that investigations of mtDNA mutations or SNPs in mtDNA from lymphocytes may not be constructive since some mutations may not be present or heteroplasmy rates may be lower than in more severely affected tissues [3].

You can read the rest of this letter here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4912808/

 

Source: Finsterer J, Zarrouk-Mahjoub S. Is chronic fatigue syndrome truly associated with haplogroups or mtDNA single nucleotide polymorphisms? J Transl Med. 2016 Jun 18;14(1):182. doi: 10.1186/s12967-016-0939-0. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4912808/ (Full article)

 

Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity

Dear Editor:

We have closely read the article published by Isasi et al.1 in Reumatologia Clínica presenting a case of fibromyalgia (FM) and chronic fatigue syndrome (CFS) caused by non-celiac sensitivity to gluten (NGCD). We would like to comment our experience with this attractive topic regarding patients with FM/CFS, which I hope will contribute to an improved knowledge of this association. The authors have reasonably ruled out celiac disease (CD) and have hypothesized that NGCD is the cause of FM and CFS in their patient; upon complete remission (CR) of symptoms, both digestive and musculoskeletal, with a gluten-free diet (GFD).

You can read the rest of this letter here: http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/

 

Source: Qanneta R, Fontova R, Castel A. Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity. Reumatol Clin. 2015 May-Jun;11(3):185. doi: 10.1016/j.reuma.2014.09.008. Epub 2014 Nov 7. http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/ (Full article)

A definition of recovery in myalgic encephalomyelitis and chronic fatigue syndrome should be based upon objective measures

Abstract:

INTRODUCTION: Adamowicz and colleagues recently proposed to use “a consistent definition of recovery that captures a broad-based return to health with assessments of both fatigue and function as well as the patients’ perceptions of his/her recovery status” for patients with chronic fatigue syndrome (CFS).

METHODS: A qualitative analysis of case definitions for Myalgic encephalomyelitis (ME) and CFS and methods to assess the symptoms and clinical status of ME and CFS patients objectively.

RESULTS: The criteria of CFS define a heterogeneous disorder. ME, often used interchangeably with CFS, is principally defined by muscle weakness, cognitive impairment etc., but above all post-exertional “malaise”: a long-lasting increase in symptoms, e.g. muscle pain and cognitive deficits, after a minor exertion. The principle symptom of CFS however is “chronic fatigue”. Since post-exertional “malaise” is not obligatory for CFS, only part of the CFS patients meet the diagnostic criteria for ME, while not all ME patients qualify as CFS patients. There are several accepted methods to assess characteristic symptoms and the clinical status of ME and CFS patients using objective measures, e.g. (repeated) cardiopulmonary exercise tests.

CONCLUSION: To resolve the debate about the clinical status, proposed effectiveness of therapies and recovery in ME and CFS, it is crucial to accurately diagnose patients using well-defined criteria for ME and CFS and an objective assessment of various typical symptoms, since subjective measures such as “fatigue” will perpetuate the debate.

Comment in

Comment on

 

Source: Twisk FN. A definition of recovery in myalgic encephalomyelitis and chronic fatigue syndrome should be based upon objective measures. Qual Life Res. 2014 Nov;23(9):2417-8. doi: 10.1007/s11136-014-0737-1. Epub 2014 Jun 17. https://www.ncbi.nlm.nih.gov/pubmed/24935018

 

Rebuttal to Ickmans et al. association between cognitive performance, physical fitness, and physical activity level in women with chronic fatigue syndrome

Dear Editor:

In a study recently published in Journal of Rehabilitation Research and Development, Ickmans et al. [1] found a substantially deteriorated physical exercise capacity in myalgic encephalopathy/chronic fatigue syndrome (ME/CFS), as established by a cardiopulmonary exercise test (peak oxygen uptake [VO2max]: 19.1 ± 4.6 mL/min/kg, peak heart rate: 145.1 ± 22.4 beats per minute [bpm], peak workload: 114.2 ± 31.3 W, compared with 27.2 ± 5.6 mL/min/ kg, 170.0 ± 36.2 bpm, and 114.2 ± 31.3 W, respectively, in sedentary controls). Ickmans et al. Also observed various cognitive deficits in ME/CFS, e.g., prolonged choice and simple reaction times in various Stroop subtests and the psychomotor vigilance task test (PVT), more errors of omission in the PVT, and worse letter recall scores on the operation span task test, indicative for working memory impairment and reduced psychomotor speed.

You can read the rest of this letter here:  http://www.rehab.research.va.gov/jour/2013/509/pdf/pagevii.pdf 

Comment on: Association between cognitive performance, physical fitness, and physical activity level in women with chronic fatigue syndrome. [J Rehabil Res Dev. 2013]

 

Source: Twisk F. Rebuttal to Ickmans et al. association between cognitive performance, physical fitness, and physical activity level in women with chronic fatigue syndrome. J Rehabil Res Dev. 2013;50(9):vii-viii. http://www.rehab.research.va.gov/jour/2013/509/pdf/pagevii.pdf (Full article)

 

Article on CFS does not reflect current best treatment practices

TO THE EDITOR: We feel that the overview of the diagnosis and treatment of chronic fatigue syndrome (CFS) was incomplete and did not reflect current best treatment practices. The discussion of current CFS research omitted key studies, such as evidence from prospective cohort studies indicating that up to 10 percent of patients with postinfectious syndromes develop CFS, regardless of the type of infectious agent.1 Biomarker research has shown distinct patterns of gene expression correlating with cytokine, adrenergic, and sensory receptor changes after modest exercise in patients with CFS compared with healthy sedentary patients.2 Indeed, many peer-reviewed publications support a physiologic etiology of CFS.

You can read the rest of this comment here: http://www.aafp.org/afp/2013/0401/ol1.html

Comment on: Chronic fatigue syndrome: diagnosis and treatment. [Am Fam Physician. 2012]

 

Source: Bateman L, Spotila J. Article on CFS does not reflect current best treatment practices. Am Fam Physician. 2013 Apr 1;87(7):Online. http://www.aafp.org/afp/2013/0401/ol1.html (Full article)