The biopolitics of CFS/ME

The biopolitics of CFS/ME, by Nikos Karfakis, in Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences [Available online 8 June 2018]

Highlights:

  • The diagnosis of CFS/ME is not only a scientific issue nor only contested within the confines of the clinic, but a much broader, biopolitical problem.
  • Attempts at making CFS/ME a stable epistemic object, have so far been only partially successful.
  • CFS/ME advocacy groups have been increasingly active internationally, making various demands on the scientific establishment and the governments.

Abstract:

This paper argues that Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) constitutes a biopolitical problem, a scientific object which needs to be studied, classified and regulated.

Assemblages of authorities, knowledges and techniques make CFS/ME subjects and shape their everyday conduct in an attempt to increase their supposed autonomy, wellbeing and health. CFS and CFS/ME identities are however made not only through government, scientific, and medical interventions but also by the patients themselves, a biosocial community who collaborates with scientists, educates itself about the intricacies of biomedicine, and contests psychiatric truth claims.

CFS/ME is an illness trapped between medicine and psychology, an illness that is open
to debate and therefore difficult to manage and standardise. The paper delineates different interventions by medicine, science, the state and the patients themselves and concludes that CFS/ME remains elusive, only partially standardised, in an on-going battle between all the different actors that want to define it for their own situated interests.

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Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in CFS

Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in CFS by Leighton R. Barnden, Zack Y. Shan, Donald R Staines, Sonya Marshall-Gradisnik, Kevin Finegan, Timothy Ireland, Sandeep Bhuta, in NeuroImage: Clinical Volume 20, 2018, Pages 102-109

Research abstract:
We recruited 43 Chronic Fatigue Syndrome (CFS) subjects who met Fukuda criteria and 27 healthy controls and performed 3T MRI T1 and T2 weighted spin-echo (T1wSE and T2wSE) scans. T1wSE signal follows T1 relaxation rate (1/T1 relaxation time) and responds to myelin and iron (ferritin) concentrations.

We performed MRI signal level group comparisons with SPM12. Spatial  normalization after segmentation was performed using T2wSE scans and applied to the coregistered T1wSE scans.

After global signal-level normalization of individual scans, the T1wSE group comparison detected decreased signal-levels in CFS in a brainstem region (cluster-based inference controlled for family wise error rate, PFWE= 0.002), and increased signal-levels in large bilateral clusters in sensorimotor cortex white matter (cluster PFWE < 0.0001). Moreover, the brainstem T1wSE values were negatively correlated with the sensorimotor values for both CFS (R2 = 0.31, P = 0.00007) and healthy controls (R2 = 0.34, P = 0.0009), and the regressions were co-linear.

This relationship, previously unreported in either healthy controls or CFS, in view of known thalamic projection-fibre plasticity, suggests brainstem conduction deficits in CFS may stimulate the upregulation of myelin in the sensorimotor cortex to maintain brainstem – sensorimotor connectivity.

VBM did not find group differences in regional grey matter or white matter volumes. We argued that increased T1wSE observed in sensorimotor WM in CFS indicates increased myelination which is a regulatory response to deficits in the brainstem although the causality cannot be tested in this study.

Altered brainstem myelin may have broad consequences for cerebral function and should be a focus of future research.

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The expression signature of very long non-coding RNA in ME/CFS

The expression signature of very long non-coding RNA in myalgic encephalomyelitis/ chronic fatigue syndrome, by Chin-An Yang, Sandra Bauer, Yu-Chen Ho, Franziska Sotzny, Jan-Gowth Chang, Carmen Scheibenbogen in Journal of Translational Medicine 2018 16:231 [Published: 17 August 2018]

Research abstract:

Background:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic
debilitating disease with huge social-economic impact. It has been suggested that immune dysregulation, nitrooxidative stress, and metabolic impairment might contribute to disease pathogenesis. However, the etiology of ME/CFS remains largely unclear, and
diagnostic/prognostic disease markers are lacking. Several long noncoding RNAs (lncRNA, > 200 bp) have been reported to play roles in immunological diseases or in stress responses.

Methods:
In our study, we examined the expression signature of 10 very long lncRNAs (> 5 kb, CR933609, His-RNA, AK124742, GNAS1-AS, EmX2OS, MIAT, TUG1, NEAT1, MALAT1, NTT) in the peripheral blood mononuclear cells of 44 ME/CFS patients.

Results:
LncRNAs NTT, MIAT and EmX2OS levels were found to be significantly elevated in ME/CFS patients as compared with healthy controls. Furthermore, NTT and EmX2OS levels increased with disease severity.

Stimulation of human monocytic cell line THP-1 and glioma cell line KALS1 with H2O2 (oxidative stress) and poly (I:C) (double strand RNA, representing viral activation) increased the expression levels of NTT and MIAT.

Conclusions:
Our study revealed a ME/CFS-associated very long lncRNA expression signature, which might reflect the regulatory response in ME/CFS patients to oxidative stress, chronic viral infection and hypoxemia.

Further investigations need to be done to uncover the functions and potential diagnostic value of these lncRNAs in ME/CFS…

In conclusion, although the pathogenic mechanisms of very large lncRNAs in ME/CFS remains to be elucidated, we have first evidence that a lncRNA expression signature could be of diagnostic value in ME/CFS.

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Metabolic features & regulation of the healing cycle – a new model for chronic disease pathogenesis & treatment

Metabolic features and regulation of the healing cycle – a new model for chronic disease pathogenesis and treatment, by Robert K Naviaux in Mitochondrion [Available online 9 August 2018]

This article presents a hypothesis of chronic diseases including ME/CFS

Highlights for Mitochondrion:

  • Four stages of the healing cycle are defined in bioenergetic and metabolic terms.
  • Progression through the healing cycle is controlled by metabokines and mitochondria.
  • Three differentiation states of polarized mitochondria are described. These include anti-inflammatory M2, pro-inflammatory M1, and uncommitted M0 organelles.
  • The pathophysiology of chronic disease is reframed as a problem resulting from abnormalities in metabokine signaling that cause the normal stages of the cell danger response (CDR) to persist abnormally, creating blocks in the healing cycle.

Abstract:
Without healing, multicellular life on Earth would not exist. Without healing, one injury predisposes to another, leading to disability, chronic disease, accelerated aging, and death.

Over 50% of adults and 30% of children and teens in the United States now live with a chronic illness. Advances in mass spectrometry and metabolomics have given scientists a new lens for studying health and disease.

This study defines the healing cycle in metabolic terms and reframes the pathophysiology of chronic illness as the result of metabolic signaling abnormalities that block healing and cause the normal stages of the cell danger response (CDR) to persist abnormally. Once an injury occurs, active progress through the stages of healing is driven by sequential changes in cellular bioenergetics and the disposition of oxygen and carbon skeletons used for fuel, signaling, defense, repair, and recovery.

>100 chronic illnesses can be organized into three persistent stages of the CDR. One hundred and two targetable chemosensory G-protein coupled and ionotropic receptors are presented that regulate the CDR and healing. Metabokines are signaling molecules derived from metabolism that regulate these receptors.

Reframing the pathogenesis of chronic illness in this way, as a systems problem that maintains disease, rather than focusing on remote trigger(s) that caused the initial injury, permits new research to focus on novel signaling therapies to unblock the healing cycle, and restore health when other approaches have failed.

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Dry eye syndrome & the subsequent risk of CFS

Dry eye syndrome and the subsequent risk of chronic fatigue syndrome—a prospective population-based study in Taiwan, by Chih-Sheng Chen, Hui-Man Cheng, Hsuan-Ju Chen, Shin-Yi Tsai, Chia-Hung Kao, Hui-Ju Lin, Lei Wan, and Tse-Yen Yang in Oncotarget 2018 Jul 17; 9(55): 30694–30703 [Published online 2018 Jul 17]

Research abstract:

Background and Aim
The clinical association between dry eye syndrome (DES) and chronic fatigue syndrome (CFS) remain unclear with less evidences. We aimed to investigate the relationship between CFS and DES using a national insurance and prospective cohort study.

Methods
Data from the Longitudinal Health Insurance Database 2000 was applied to estimate the incidence of CFS among patients with DES, and their age- and sex-matched controls without DES over a long-term follow-up period. All participants were CFS free at baseline, before the interval (2005–2007), but were later diagnosed with CFS. DES patients and its relative matched controls were excluded prevalent CFS before the same interval.

Results
We identified 884 patients with DES and 3,536 matched controls in baseline and estimated the hazard ratios for incident CFS in the follow-up period. Patients with DES had a 2.08-fold considerably increasing risk of developing CFS, compared to non-DES group. An elevated risk of developing CFS remained (1.61-fold risk) even after adjusting for age, sex, and comorbidities.

There was a presence of increasing risk in DES-related CFS when CFS-related comorbidities existing (adjusted hazard ratio, 1.98, 95% confidence interval, 1.19–3.29; p < 0.01). The subsequent risk for CFS between DES and non-DES patients was significant increased with three or more annual medical visits, the adjusted risk for CFS was 4.88-fold risk (95% CI, 2.26–10.58, p < 0.001).

Conclusion
We recommended that physicians should be aware of the increased risk of CFS among DES patients and adequately assess the health impacts among these patients.
Keywords: fatigue, dry eye syndrome, national health insurance research database (NHIRD), prospective cohort study

Dr Charles Shepherd gives more information: Dry eye symptoms and M.E 

Excerpt:

Having a persistent problem with dry eyes should always prompt a visit to either your doctor or optician – just to make sure that it is not linked to either eye disease or another medical condition.

As far as treatment is concerned, it is usually pretty straightforward.

You can purchase what are called artificial tears in the form of drops, lubricants or ointment from a pharmacy or on prescription from your GP.

These can all be very helpful, providing immediate lubrication and relief – although they may need to be used for some time, even indefinitely.

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ME/CFS – Metabolic disease or disturbed homeostasis?

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-Metabolic Disease or Disturbed Homeostasis? by Erifili Hatziagelaki, Maria Adamaki, Irene Tsilioni, George Dimitriadis and Theoharis C Theoharides in Journal of Pharmacology and Experimental Therapeutics August 3, 2018, jpet.118.250845

Research article abstract:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disease characterized by debilitating fatigue, lasting for at least 6 months, with severe impairment of daily functioning and associated symptoms. A significant percentage of ME/CFS patients remains undiagnosed, mainly due to the complexity of the disease and the lack of reliable objective biomarkers.

ME/CFS patients display decreased metabolism and the severity of symptoms appears to be directly correlated to the degree of metabolic reduction that may be unique to each individual patient. However, the precise pathogenesis is still unknown preventing the development of effective treatments.

The ME/CFS phenotype has been associated with abnormalities in energy metabolism, mostly with mitochondrial dysfunction, resulting in reduced oxidative metabolism. Mitochondrial dysfunction may be further contributing to the ME/CSF symptomatology by extracellular secretion of mitochondrial DNA, which could create an “innate” inflammatory state in the hypothalamus, thus disrupting normal homeostasis.

We propose that stimulation of hypothalamic mast cells activates microglia leading to focal inflammation in the brain and disturbed homeostasis.

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Multidisciplinary rehabilitation treatment is not effective for ME/CFS: a review of the FatiGo trial

Multidisciplinary rehabilitation treatment is not effective for myalgic encephalomyelitis/chCronic fatigue syndrome: A review of the FatiGo trial, by Mark Vink and Alexandra Vink-Niese in Health Psychol Open. 2018 Jul-Dec; 5(2): 2055102918792648 [Published online 2018 Aug 6]

 

Research abstract:
The FatiGo trial concluded that multidisciplinary rehabilitation treatment is more effective for chronic fatigue syndrome/myalgic encephalomyelitis in the long term than cognitive behaviour therapy and that multidisciplinary rehabilitation treatment is more cost-effective for fatigue and cognitive behaviour therapy for quality of life.

However, FatiGo suffered from a number of serious methodological flaws. Moreover, it ignored the results of the activity metre, its only objective outcome. This jeopardizes the validity of FatiGo. Its analysis shows that there was no statistically significant difference between multidisciplinary rehabilitation treatment and cognitive behaviour therapy and neither are (cost-)effective.

FatiGo’s claims of efficacy of multidisciplinary rehabilitation treatment and cognitive behaviour therapy for chronic fatigue syndrome/myalgic encephalomyelitis are misleading and not justified by their results.

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System reset? Study suggests Pro-Inflammatory / Autoimmune reset in ME/CFS

Simmaron Research blog post, by Cort Johnson, 4 August 2018: System Reset? Study Suggests Pro-Inflammatory / Autoimmune Reset Occurred in Chronic Fatigue Syndrome (ME/CFS)

Epigenetics research holds the fascinating possibility of figuring out what shifted at the very beginning of chronic fatigue syndrome (ME/CFS). For many with ME/CFS a sudden change occurred – some sort of biological reset quickly happened – which never relinquished itself.

Finding out what “reset” occurred is what epigenetics is all about. Epigenetics identifies changes in the expression of our genes that occur after we meet up with biological stressors such as pathogens, drug, toxin or even foods.

Most of our genes that produce proinflammatory cytokines, for instance, have a kind of a lock on them. Removing that lock leaves them free to express themselves and leaves us open to poor health.

Epigenetics explores how the biological challenges we encounter in life can remove those locks (or add to them) resulting in an entirely new genetic landscape – one that could perhaps cause something like ME/CFS.

Many people’s ME/CFS/FM starts with an infection, and viruses can exert major epigenetic changes to our genome. Herpes simplex virus (the virus Dr. Pridgen is targeting in fibromyalgia) engineers changes to our genome which help the virus avoid destruction and enhance its replication. Those changes include a suppression of our immune system, which can result in an increased risk of cancer.

What goes around comes around, though. Epigenetic News recently reported that an epigenetic modifying cancer drug was able to return the parts of the immune system that the herpes simplex virus had disturbed to normal. The drug was able to effectively fill in the immune hole created by the herpes virus by boosting a number of immune factors (IFN-a, IL-8, IL-6, transcription factors, stress response factors). Mouse studies revealed that the drug also reduced reactivation of the virus.

That suggests that some similar drugs now in clinical trials could help in the fight against

Unleashing the IL2R gene could contribute to inflammation (including neuroinflammation), thyroid disease and autoimmunity

herpes and other viruses or could perhaps simply return to normal epigenetically modified genes that have suppressed immune functioning.

“A new class of antivirals based on this study might be useful for patients who are resistant to existing antivirals like acyclovir and ganciclovir….. (or in) viral infections for which there aren’t pharmaceuticals to boost an individual’s immune response.” Dr Kristie

If epigenetics turns out to play the major role in ME/CFS that it does in cancer and other diseases, a cancer drug could someday be in store for ME/CFS treatment.

Read more about epigenetics and ME, & the research of Dr Klimas’ group

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M.E.: ‘an insane idea’ – an animation by Alexandra Hohner

M.E. – ‘an insane idea’ – an animation by Alexandra Hohner

An award winning short animation by Alexandra Hohner uses interviews with a young man who developed ME/CFS following a giardia infection.

She says ” The experiment is based on the idea to create a simulation of Olly’s photophobia (sensitivity to light)”

The animation’s character, Olly, talks about the cognitive issues of ME and after describing how it feels to overdo things and relapse, he laughs and says: “It’s crazy. The whole idea of it is insane”

 

 

“I can’t keep talking to you, because I can’t get the words out. I can’t think of the right words and when you have that kind of a crash, it’s like 30 points being knocked off your IQ. Basically you go stupid and emotional.”

“I never realised that a noise could feel painful”

Watch the 3 minute video

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Visual aspects of reading performance in ME

Visual aspects of reading performance in Myalgic Encephalomyelitis (ME), by Rachel Wilson, Kevin B. Paterson, Victoria A. McGowan, Claire Hutchinson in Frontiers in Psychology [Preprint July 26, 2018]

Research abstract:

People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) report vision-related reading difficulty, although this has not been demonstrated objectively.

Accordingly, we assessed reading speed and acuity, including crowded acuity and acuity for isolated words using standardised tests of reading and vision, in 27 ME/CFS patients and matched controls.

We found that the ME/CFS group exhibited slower maximum reading speed, and had poorer crowded acuity than controls.

Moreover, crowded acuity was significantly associated with maximum reading speed, indicating that patients who were more susceptible to visual crowding read more slowly.

These findings suggest vision-related reading difficulty belongs to a class of measureable symptoms for ME/CFS patients.

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