Can simple blood tests help to identify ME/CFS

Health rising forum discussion started by Cort Johnson, 30 April 2016:  Can simple blood tests help to identify Chronic Fatigue Syndrome (ME/CFS)?

How great it would be if a doctor could give a teenager with lingering fatigue after infectious mononucleosis/glandular fever a simple blood test to determine if she had chronic fatigue syndrome (ME/CFS).

She and her parents might not like that result but at least they’d have an answer to their daughters health issues and they could chart their course from there. The doctor, of course, would be quite relieved to have an answer his patients mysterious problems. He or she could study up on how to treat ME/CFS or (hopefully) send her on her way to a doctor who could (instead of a psychiatrist who can’t.)

Significant amounts of stress would be relieved on both ends and both ME/CFS as a disease and the patient would be validated.

That’s what this Renee Taylor/Nancy Klimas group (Broderick, Klimas, Fletcher) and Suzanne Vernon recent study tried to achieve. They tracked almost 300 adolescents diagnosed with infectious mononucleosis in the Chicago area for 24 months and gave the ones who got sick and a handful of the ones who recovered very simple blood, saliva and urine tests.

This study was definitely a gamble; nobody has ever found that standard blood tests tell us anything about chronic fatigue syndrome.

Harvey JM, Broderick G, Bowie A, et al. Tracking post-infectious fatigue in clinic using routine Lab tests. BMC Pediatrics. 2016;16:54 doi:10.1186/s12887-016-0596-8.

Results

There’s nothing like consistency in research. This study underscored and validated what the Dubbo studies found some ten years ago; that if you come down with infectious mononucleosis/glandular fever as an adolescent you, unfortunately, have a pretty good chance of coming with ME/CFS.

At six months 13% of them met the criteria for ME/CFS (CCC criteria tweaked by Jason), at 12 months 7% still did, and two years later 4% (@12 adolescents) were still sick. (Compare that with 11% and 9% at six and 12 months in the Dubbo studies).

It’s not clear if females are more likely to get IM than males but they were definitely hit harder by it. At six months 90% of the ME/CFS adolescents were female; at 12 months 100% were.

Blood, Saliva and Urine Test Results

The results of 59 standard laboratory tests in 13 young women with ME/CFS with those of healthy controls indicated that some differences were found and those differences highlighted the HPA axis and hormones. Unfortunately few of the abnormalities found persisted past one time point.

Reduced levels of glucose and ACTH at six months suggested that the HPA axis was sputtering. ACTH triggers the production of cortisol by the adrenal glands and is produced in response to biological stress.

The authors suggested that a cytokine (Il-6) produced during an infection could be promoting hypoglycemia in these young ME/CFS patients. Older ME/CFS and FM patients will remember that hypoglycemia was all the rage in alternative health circles a couple of decades ago.

Levels of estradiol, the primary sex hormone in women, tanked at 12 and 24 months. Those two findings fit somewhat with Broderick’s past modeling work which highlighted the HPA axis and the hormonal system in ME/CFS.

Broderick’s work suggests that female hormones may play an important role keeping female ME/CFS patients stuck in a suboptimal physiological state. His recent model suggested that women with ME/CFS fall into steady state which includes decreased cortisol, increased estradiol and increased anti-inflammatory activity.

The authors noted that an increase in neutrophils at 24 months could also reflect hormonal changes in ME/CFS women. Plus a close but non-significant tendency towards increased thyroxine levels (T4) at six and twelve months (p<.06/ p<.07) suggested thyroid gland involvement. Ultimately the study suggested that immune changes during infection may be effecting the HPA and HPT axes and female hormones.

Conclusion

This study was probably always something of a crap shoot, but it did underscore possble HPA axis and hormonal problems in ME/CFS. If validated in larger studies and with other disease cohorts it could provide the opportunity for doctors to use simple blood tests to quickly tell who has ME/CFS.

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Diagnosing post infectious fatigue in adolescents using routine lab tests

Research 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.

Tracking post-infectious fatigue in clinic using routine Lab tests, by JM Harvey, G Broderick, A Bowie, ZM Barnes, BZ Katz, MR O’Gorman, SD Vernon, MA Fletcher, N Klimas, R Taylor in BMC Pediatr. 2016 Apr 26;16(1):54

 

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The effect of High-intensity interval exercise in CFS

Research abstract:

Purpose: To determine if the typical exacerbation of symptoms in patients with chronic fatigue syndrome (CFS) following a bout of exercise differs between high-intensity interval training (HIIT) or continuous (CONT) aerobic exercise of the same duration and mechanical work.

Methods: Participants with specialist-diagnosed CFS performed two 20-minute bouts of cycling in a randomised crossover study. The bouts were either moderate-intensity-continuous (70% age predicted heart rate max (APHRM)) or high-intensity-interval exercise, separated by at least 2 weeks. Self-report questionnaires capturing fatigue and related symptoms, and actigraphy were collected across 2 days before and 4 days following the exercise. Comparisons between exercise bouts were made using paired sample t-tests.

Results: Fourteen moderately affected participants who were unable to work, but not bed bound, completed the study (9 female, 32 +/- 10 years, 67 +/- 11 kg). Mechanical work was matched successfully between the exercise bouts (HIIT 83,037 vs CONT 83,348 J, p=0.84). Mean heart rate (HIIT 76 +/- 5 vs CONT 73 +/- 6 %APHRM, p<0.05) and RPE (6-20) in the legs (HIIT 15.4 +/- 1.4 vs CONT 13.2 +/- 1.2, p<0.001) were higher for the interval compared to continuous exercise. Mean fatigue scores (0-10) were similar before each exercise challenge (HIIT 4.5 +/- 1.8 vs CONT 4.1 +/- 1.7, p=0.43). Participants reported an increase in fatigue scores following both challenges (Mean difference: HIIT 1.0 +/- 1.3, p<0.01; CONT 1.5 +/- 0.7, p<0.001), but these exacerbations in fatigue were not statistically or clinically different (p=0.20).

Conclusions: High-intensity interval exercise did not exacerbate fatigue any more than continuous exercise of comparable workload. This finding supports evaluation of HIIT in graded exercise therapy interventions for patients with CFS.

Fatigue Exacerbation by Interval or Continuous Exercise in Chronic Fatigue Syndrome, by Carolina X Sandler, Andrew R Lloyd, Benjamin K Barry in Medicine & Science in Sports & Exercise, May 13, 2016 [Published Ahead-of-Print]

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Ubiquinol-10 supplementation improves autonomic nervous & cognitive function in CFS

Research abstract:

The aim of this study was to evaluate the benefit of oral ubiquinol-10 supplementation in CFS patients using an open-label study and a randomized, double-blinded, placebo-controlled (RCT) study.

Twenty patients with CFS were randomly enrolled in an 8-week open-label oral ubiquinol-10 (150 mg ubiquinol-10/day) study. The patients and the attending physicians were not blinded to the supplementation.

Forty-three patients with CFS were randomly assigned to receive either ubiquinol-10 (150 mg/day) or placebo every day for 12 weeks. The patients and the attending physicians were blinded to the supplementation, and a total of 31 patients (N = 17 in the ubiquinol group and 14 in the placebo group) completed the study.

The beneficial effects of ubiquinol-10 were observed in the open-label study we conducted prior to the RCT. The RCT results suggest that supplementation with ubiquinol-10 for 12 weeks is effective for improving several CFS symptoms.

Ubiquinol-10 supplementation improves autonomic nervous function and cognitive function in chronic fatigue syndrome, by S Fukuda, J Nojima, O Kajimoto, K Yamaguti, Y Nakatomi, H Kuratsune, Y Watanabe in Biofactors. 2016 Apr 29. doi: 10.1002/biof.1293. [Epub ahead of print]

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Do anorexia, IBS, CFS share a common cause?

Lancaster University press release, 25 April 2016: Do anorexia, irritable bowel syndrome, chronic fatigue syndrome share a common cause?

Irritable bowel syndrome, chronic fatigue syndrome and anorexia nervosa may all have a common origin according to researchers.

They speculate that all three disorders may be caused by antibodies to the body’s own nerve cells because of a mistake by the immune system following infection.

At the moment, the ultimate cause of these illnesses remains a mystery.

Writing in Medical Hypotheses, Dr Jim Morris from the University Hospitals of Morecambe Bay NHS Trust, Dr Sue Broughton and Dr Quenton Wessels from Lancaster University say current explanations are unsatisfactory.

“Psychological factors might be important, but are unconvincing as the primary or major cause.

“There might, for instance, be an increased incidence of physical and sexual abuse in childhood in those who go on to manifest functional disorders. It is easy to see how this could influence symptoms in adults but it stretches credulity to imagine abuse as the sole and sufficient cause of the functional disorder.”

It is already well known that women are more at increased risk of autoimmune disease especially ones in which antibodies to the body’s own cells are thought to play a role, like thyroid disease, pernicious anemia and myasthenia gravis.

The researchers said: “The female to male ratio in these conditions is of the order of 10. The female excess in Irritable Bowel Syndrome, Chronic Fatigue Syndrome and Anorexia Nervosa is equally extreme and therefore this fits with the idea that auto-antibodies to nerve cells could be part of the pathogenesis of these conditions.”

The formation of auto-antibodies is found mostly among women and increases with age, which could be why these disorders are more common in midlife. Even with anorexia, which reaches a peak at the age of 30, auto-antibodies have been found in the bodies of patients.

There are also links with infection in that the onset of IBS commonly follows an episode of infectious diarrhea while chronic fatigue syndrome can be triggered by infectious mononucleosis and viral hepatitis.

Even anorexia could be influenced by secretions from bacteria affecting the brain, triggering the production of antibodies which affect mood and motivation.

“Auto-antibodies acting on the (brain’s) limbic system could induce extremes of emotion including disgust and fear. These then become linked, in the minds of adolescent girls, to culturally determined ideas of what is, and what is not, the ideal body shape and size. It is then a small step for disgust and fear to be directed to food and obesity which the fashion industry currently demonizes.”

If their idea is proven, the researchers suggest that these disorders may be amenable to treatment using pooled immunoglobulin from the blood of healthy people, especially in severe cases of anorexia where life is threatened. It should also be possible to identify and eliminate from the gut the bacteria which are triggering auto-antibodies.

Journal Reference: J.A. Morris, S.J. Broughton, Q. Wessels. Microbes, molecular mimicry and molecules of mood and motivation. Medical Hypotheses, 2016; 87: 40

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Effect of acute exercise on fatigue in people with ME/CFS/SEID

Review abstract:

PURPOSE:

A prominent symptom of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, or Systemic Exertion Intolerance Disease (ME/CFS/SEID) is persistent fatigue that is worsened by physical exertion. Here the population effect of a single bout of exercise on fatigue symptoms in people with ME/CFS/SEID was estimated and effect moderators were identified.

METHODS:

Google Scholar was systematically searched for peer-reviewed articles published between February 1991 and May 2015. Studies were included where people diagnosed with ME/CFS/SEID and matched control participants completed a single bout of exercise and fatigue self-reports were obtained before and after exercise. Fatigue means, standard deviations, and sample sizes were extracted to calculate effect sizes and the 95% CI.

Effects were pooled using a random-effects model and corrected for small-sample bias to generate mean [INCREMENT]. Multi-level regression modeling adjusted for nesting of effects within studies. Moderators identified a priori were diagnostic criteria, fibromyalgia comorbidity, exercise factors (intensity, duration, type) and measurement factors.

RESULTS:

Seven studies examining 159 people with ME/CFS/SEID met inclusion criteria, and 47 fatigue effects were derived. The mean fatigue effect was [INCREMENT] = 0.73 (95% CI = 0.24, 1.23). Fatigue increases were larger for people with ME/CFS/SEID when fatigue was measured four or more hours after exercise ended rather than during or immediately after exercise ceased.

CONCLUSIONS:

This preliminary evidence indicates that acute exercise increases fatigue in people with ME/CFS/SEID more than in control groups, but effects were heterogeneous between studies. Future studies with no-exercise control groups of people with ME/CFS/SEID are needed to obtain a more precise estimate of the effect of exercise on fatigue in this population.

Effect of Acute Exercise on Fatigue in People with ME/CFS/SEID: A Meta-analysis, by BD Loy, PJ O’Connor, RK Dishman in Med Sci Sports Exerc. 2016 May 17. [Epub ahead of print]

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Does GET & CBT for CFS improve sleep?

Research review:

Cognitive behavioural therapy (CBT) and graded exercise therapy (GET)  are recommended evidence based treatments for chronic fatigue syndrome (CFS), with research supporting their effectiveness in reducing fatigue and functional impairment.

However, little research has focussed on the effect of these treatments on sleep, despite high reported sleep disturbance in CFS. Using a narrative synthesis approach, we aimed to 1)  Systematically identify and summarise the current evidence for the effectiveness of CBT and GET in improving sleep; 2) Consider factors influencing treatment effectiveness, including incorporation of sleep management techniques; and 3) Consider the appropriateness of sleep outcome measures used within evaluations.

Studies evaluating CBT and/or GET for CFS, and including a sleep outcome were eligible for inclusion.  Eight studies were identified. We found that that GET interventions can improve sleep but this effect is inconsistent across studies.

For CBT the evidence is limited with only one of two evaluations demonstrating sleep-related improvements. We conclude from existing research that we know little about the effects of including sleep management components within CBT and GET interventions.

We suggest that future research should explore the effectiveness of sleep components within interventions, and sleep specific interventions, using comprehensive outcome measures that fully capture the range of sleep difficulties experienced in CFS.

Do evidence based interventions for chronic fatigue syndrome improve sleep? A systematic review and narrative synthesis, by C Russell, SD Kyle, AJ Wearden in Sleep Medicine Reviews [Preprint available online 13 May 2016]

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OMF announces an expanded ME/CFS metabolomics study

Open Medicine Foundation newsletter, May 2016: Announcing the Expanded ME/CFS Metabolomics Study

Now that the Severely Ill-BIG DATA Study is fully underway, we want to perform multiple investigations at the same time. Because of the many recent small and large donations, we can start another research project now without waiting.

We are very excited to announce an amazing new collaboration with Dr. Robert Naviaux and our very own Dr. Ronald Davis, director of our ME/CFS Scientific Advisory Board. As previously announced, Dr. Naviaux (of the University of California, San Diego, School of Medicine) joined our Advisory Board and brings remarkable knowledge in metabolomics and mitochrondia.

In addition to Dr. Naviaux and Dr. Davis, the new study is being conducted in collaboration with Dr. Paul Cheney and Dr. Eric Gordon’s team. Dr. Davis will correlate the metabolic findings with genetic results.

What is Metabolomics: Simply put, it’s the study of metabolites, which are chemicals produced as cells carry out their functions. When you know what a body’s cells are producing, you can find out how the cells are functioning, whether normally or abnormally. And if it’s not functioning normally, you can see what aspect of the cells’ activities are defective by measuring the metabolites.

Dr Robert K. Naviaux writes about metabolomics:

Dr Eric Gordon, his team in Northern California and I recently completed a metabolomics study of over 80 patients with ME/CFS and normal controls. The results showed that there was a chemical signature in ME/CFS that might ultimately be used to help physicians diagnose and treat these diseases.

The results were so exciting that we have expanded our pursuit and have launched a validation study in a completely independent group of over 100 ME/CFS patients (already chosen and ready to go) and controls from across the US and Canada. A grant from OMF will make this new study possible.

If the results of the first study are validated in the new study, then both patients and physicians will benefit. The practical application of metabolomics as a research tool in medicine is happening now.

OMF is leading the way to new hope for every patient with complex chronic diseases by collaborating with world-renowned, creative scientists to help search for the molecular causes that underlie the myriad of diverse symptoms. Progress is being made on many fronts. In just a year from now, we should have the science to add NextGen metabolomics to the tool kit needed to crack the mystery of ME/CFS.

Metabolomics

Metabolomics is one of the hottest rising stars in the high tech race to gain a molecular understanding of health and disease. Metabolomics uses a machine called a “mass spectrometer” to measure hundreds of chemicals in our blood.

In our lab, at University of California San Diego, with a single blood specimen, we can measure over 500 of these chemicals from over 60 different biochemical pathways.

These chemicals are the building blocks that cells use to grow and function, to fight and to heal. Like a Hubble telescope for medicine, metabolomics is allowing us to see deeper and with greater clarity into the universe of the cell than has ever been possible before. In a drop of blood, we can “eavesdrop” on the collective conversations of all the cells in the body.

In ME/CFS, as in many complex chronic diseases, many genes interact with many environmental factors encountered at times of vulnerability. Complex diseases are not predestined by our genes alone. Complex diseases are ecogenetic—resulting from the interaction of genes inherited from our ancestors, and environmental factors we encounter in a lifetime. Our metabolism is the real-time readout of the gene-environment interaction. Metabolomics is a new lens that allows us to “see” this inner world of the cell in a new way that lends itself to scientific discovery.

This new vision is leading to breakthroughs in our understanding of why patients with ME/CFS get stuck in a cycle of pain and suffering and disability. But more importantly, metabolomics is also shedding light on how rational therapies designed to trigger a return to health might be just around the corner.

 

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Poor medical care & neglect are major factors in ME/CFS suicide

Shout about ME blog post, by Russell Logan, 14 May 2016: Suicide risk 5 times higher in ME/CFS:  Poor medical care, neglect are major factors

The risk of suicide among ME/CFS patients is a staggering five times higher than the general population, a new Spanish study has found.

Psychologist Juan Jimenez-Ortiz at the Spanish University of Valladolid, and author of the study, pointed to inadequate medical care as a major factor in his findings.

“… the incidence, amongst PWME, of risk of suicide which is 12.75%, compared to the incidence in the general Spanish population which is 2.3%.”

In Depression, hopelessness in people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Risk factors and protection Juan Jimenez-Ortiz also notes that the incidence of depression among patients with me/cfs is 57.25%, compared to that of only 4% in the general Spanish population.

The researcher surveyed 205 Spanish patients with ME/CFS, comprising 187 women and 18 men aged between 27 and 71 years.

A report on the study by Plataforma de Afectadas por los Recortes en Sanidad (PARS) said the findings were “worrisome”.

“The high level of risk of suicide, depression and hopelessness in these patients is much higher than in the rest of the Spanish population due to, mostly, the lack of relevant health care services,” said PARS.

“For several decades, PWME [people with ME] in Spain …live with a great number of social and political factors which, added to their illness, severely reduce their quality of life and put them at risk of suicide…

“These factors include, mainly, a lack of access to relevant medical care and a precarious economic situation due the lack of pensions and other help which people too sick to work are entitled to in Spain. Also the lack of proper care of this illness by the health administrations results in a general lack of social support for PWME.”

Patients let down by the health care system
Some of the reasons which have been found to be associated in a significant manner to depression, hopelessness and risk of suicide amongst PWME, include:

To risk of suicide:

  • Not having medical care
  • Having ME/CFS affect their capacity to earn a living and the worsening of the economic situation of their family unit
  • Having to turn to family members for help with activities of daily life
  • Not being listened to by doctors

To depression and hopelessness:

  • Having been put down and not treated properly by the health care system
  • Not having regular medical follow-up
  • Having been sent for psychological or psychiatric treatment and been labelled as “rebellious patient”
  • Having lost their job
  • Having lost friendships due to the illness
  • Not being believed when mentioning the effects on their health of chemical agents (chemical sensitivities)
  • Having had their intimate (sexual) relationships affected by ME/CFS
  • Having had ME/CFS affect their economic situation

UK report confirms high suicide risk
In 2005, in an article aimed at raising nurses’ awareness of ME, Greg Crowhurst of UK advocacy group The 25% Severe ME Group noted: “Disbelief, especially by GPs and family members, makes it difficult for patients to access services.”

Crowhurst cited a 2001 report by Action for ME (AfME), another UK me/cfs charity, which found that:

  • 77 per cent of patients experienced severe pain; and more than 80 per cent had felt suicidal as a result of the illness
  • 70 per cent were either never able, or sometimes too unwell, to attend a doctor’s clinic
  • 65 per cent received no advice from the GP on managing the illness
  • 80 per cent of those who were bedridden with ME reported that a request for a home visit by a doctor had been refused
  • Many people do not receive the state benefits to which they are entitled

AFME SURVEY RESULTS
>SUICIDAL FEELINGS 80%
>SEVERE PAIN 77%
>TOO ILL TO VISIT A GP 70%
>RECEIVED NO GP ADVICE 65%
>REFUSED HOME VISIT BY GP 80%

Average age of suicide is much lower among CFS patients
A study by Leonard Jason found that the average age of death by suicide among CFS patients is 39, compared to the US national average of 48. The full text of the study is available here.

Jason analyzed a memorial list tabulated by the National CFIDS Foundation of 166 deceased individuals who had had CFS.

The three most prevalent causes of death were heart failure, suicide, and cancer, which accounted for 59.6% of all deaths.

Jason also found that while the median age of death from cancer in the US population is 72, for CFS patients, it’s 48. Also, the average age at death from heart failure is 83, compared to 59 in CFS patients who die of heart failure.

Russell Logan
Russell Logan worked as a magazine publisher and editor until forced into early retirement through ill health with ME. He has battled with moderate to severe ME for 25 years. He now lives in Noosaville, Australia.

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MEGA: new UK research alliance announces ‘big data’ study

MEGA: ME/CFS Epidemiology and Genomics Alliance:
On the 13th and 14th of April 2016, experts from multiple fields came together for a ‘grand challenge’ workshop to discuss how to advance research in understanding CFS/ME.

It was agreed that:

Very large numbers of people would need to be involved to conduct the necessary genomic studies. This is likely to need at least 10,000 adults and 2,000 children and young people plus many more others who would act as controls. The patients would need to be well described (phenotyped) with more detail than has previously been collected on characteristics such as pain and sleep patterns.

Blood and urine samples

In this big data study, the first of its kind in the UK, each patient will be asked to provide blood and urine samples which would then allow researchers to investigate, in terms of DNA, RNA and other molecules, what distinguishes individuals with CFS/ME from controls. In other words, what are the distinctive genetics, epigenetics, proteomics and metabolomics of CFS/ME?

Aim of research

Doing this will allow us to understand more about the causes and underlying biology of CFS/ME but also about the different types (sub-phenotypes) which may be caused by different underlying mechanisms. This may eventually enable us to develop new diagnostic tests and new treatments for each sub-phenotype.

Worldwide collaboration

The researchers involved in MEGA will actively engage with researchers world-wide to further replicate and investigate findings. This very large collection of samples and data will be of interest to researchers from a wide range of disciplines.

Funding

We anticipate applying for funding at the end of 2016. If successful, data and sample collection will start late in 2017. Work is now being undertaken to further develop the collaboration and application. A study of this scale will require considerable funding and may need a two-phase approach.

Patient involvement

The group discussed how engagement of people with ME/CFS and participation during development of the study will be essential. This will include establishing advisory groups, for adults as well as for children and young people with CFS/ME. The group also considered the importance of maintaining good two-way communication with the wider community and providing updates on the progress being made.

Researcher blogs

Each of the workshop participants agreed to contribute blog posts about the roles of their respective field and the benefit this could bring to the CFS/ME research. These are being prepared and will be published over the next few months.

Genomics

Prof George Davey-Smith (Bristol), Prof Chris Ponting (Edinburgh), Prof Chris
Smith (Brighton)

Epigenetics – Prof Caroline Relton (Bristol)

Proteomics (Mr Tony Bartlett, Somalogic)

Metabolomics (Dr Rick Dunn, Birmingham)

Routinely collected data

Prof Andrew Morris (Edinburgh) and Prof David Ford (Swansea)

Infection – Prof Paul Moss (Birmingham)

Sleep – Prof Jim Horne (Loughborough)

Pain – Prof Maria Fitzgerald (UCL)

Primary care – Prof Paul Little (Southampton)

Joining them at the workshop was Sonya Chowdhury (Action for M.E., representing the patient charity members of the UK CFS/ME Research Collaborative Board) and CFS/ME researchers:
 Prof Julia Newton (Newcastle)
 Prof Peter White (QMUL)
 Dr Esther Crawley (Bristol)
 Dr Simon Collin (Bristol).

 

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