‘As lockdown eases, those of us with chronic illnesses must not be left behind’
[Although not primarily about ME (it is mentioned), I thought that this is an interesting article from The Independent which makes some good points.]
The compassion we’ve learnt in lockdown must be carried through into the post-coronavirus world, says Helen Wilson-Beevers
When Boris announced that pubs, cinemas, hair salons and hotels will reopen from the 4th July, there came collective chatter about reclaimed freedom. There is a palpable feeling holidays and nights out are once again within reach; a new normal is just around the corner. In England, too, shielding for the 2.2 million most vulnerable ends on 1 August.
Tentatively excited talk of lockdown ending joined social media posts about never taking simple daily joys for granted again. I absolutely can’t wait for that day to come too. But as someone who suffers from chronic health conditions, including Hashimoto’s disease and endometriosis, there’s also a degree of pragmatic detachment from this notion. Because for those affected by chronic illnesses, we’re acutely aware our lifelong experience of needing to occasionally shut ourselves away can’t ever be placed in a box marked This Too Shall Pass.
As offices disbanded in mid-March, working from home was suddenly the nation’s new normal. Something which chronic illness sufferers have continuously dreamt of; our unprecedented global circumstances proved that remote working is entirely feasible. For those whose sick days sabotaged careers, will more widespread flexible options finally materialise? Some people have noted that the intense fatigue worsened by their commute pre-pandemic has improved dramatically, they of course dread the return of the old order.
During this pandemic, we have seen a spotlight shone brightly on chronic illness like never before. That those with pre-existing health conditions and the elderly are most likely to be significantly affected by Covid-19, means we have come together to protect people who previously felt invisible. Covid-related messaging that no societal obligation is worth risking your health for was already part of the chronic illness tool kit, and this reality is now finally being seen.
This week in parliament, Conservative MP Sir David Amess asked the Leader of the House about help for endometriosis sufferers, especially those whose treatments and surgeries have been delayed or cancelled during the crisis. I have witnessed first-hand the incapacitating effects endometriosis causes and empathise hugely with people in urgent need of support. Managed out of several jobs during my twenties due to mounting sick days, nobody at work had heard of endometriosis. In one role, after collapsing, paramedics administered a morphine drip to me while I sat at my boss’s desk. The humiliation stays with me until this day.
In this instance, endometriosis was raised directly because of pandemic delays. However, the parliament focus on the disease is a welcome and not insignificant moment. Crushing exhaustion and agony are difficult enough to manage but lack of awareness is something which can be changed- and societal adaptions accordingly made.
The same goes for a major UK study into Myalgic Encephalomyelitis (ME) announced this week, investigating a widely misunderstood and devastating condition. Worryingly, one of the long-term effects of corona is chronic fatigue symptoms, leaving previously healthy people unable to manage simple daily tasks. ME is thought to be triggered by viral infections, yet the extent of its impact remains underreported, highlighting the crucial need for this study.
When quarantine began, comedian Miranda Hart spoke of the seemingly endless nature of this virus holding a mirror up to the emotions of those with chronic illness, tweeting: “As well as dealing with illness there is daily grief on missing out on the simplest things people take for granted. A café. A walk. A bus ride. Views.” As Miranda eloquently outlines, feeling heard makes a massive difference when someone is trapped under the heavy toll living with a chronic illness takes.
A few weeks pre-pandemic, I was in the depths of a debilitating thyroid disease flare and had to skip my good friend’s thirtieth. Lying in bed and aching from head to toe, overwhelming exasperation worsened an already demoralising time. While the familiar sadness about missing out on a fun evening around my favourite people stung, these brilliant friends cocooned me with understanding.
Yet on other occasions, when bailing on plans because my body won’t play ball, I’ve been met with countless unsympathetic comments. After being diagnosed with the auto immune condition Hashimoto’s disease, one person asked if I’d caused the illness myself by taking too many painkillers for endometriosis. Another time someone suggested I wasn’t thinking positively enough, and that daily affirmations or CBD oil could miraculously eradicate pain only improved by morphine. A fellow school mum once sarcastically asked if I “collect illnesses.”
Being pedalled quick fix snake oil ideas is extremely patronising. It invalidates the physical limitations those with chronic illness would do anything not to be held back by. A simple acceptance and understanding that where I’m at today is just part of my ongoing reality would be so much more welcome than an attempt to correct me and make me fit into society like a square peg in a round hole.
For so long, invasive investigations and random symptoms triggered shame and guilt. I’d be caught up in a vicious cycle, apologising about something which wasn’t my fault, and this consumed me. The constant fight to be heard – whether by medical professionals, bosses, or friends – is as crushing as dealing with pain and fatigue itself. No longer willing to be casually gaslit, I’ve learnt the immeasurable value in advocating for myself.
Living with chronic illness doesn’t mean you don’t desperately want to be an active participant. Often boundaries need to be set which won’t always be comprehended. If I had attempted the aforementioned-birthday night out, my already exhausted body wouldn’t have been able to get the kids to school or meet any deadlines that week.
Throughout the pandemic, coronavirus press coverage and Instagram feeds have touched on the daily struggles different health conditions cause. Those without chronic illnesses have been given a brief glimpse into restrictions dictated by uncontrollable health circumstances. And when lockdown does eventually become a distant memory, this overdue focus on our lifelong reality must not disappear either.
UK to launch world’s largest genetic study into chronic fatigue syndrome
Research aims to shine a light on condition that is believed to affect 250,000 people in UK
The world’s largest genetic study into chronic fatigue syndrome is to be launched in the UK after receiving £3.2m of funding from the Medical Research Council and National Institute for Health Research.
The research aims to shine a light on the debilitating long-term condition, about which little is known, by collecting DNA samples from 20,000 people who have CFS, also known as myalgic encephalomyelitis (ME).
CFS is believed to affect about 250,000 people in the UK and has been estimated to cost the economy billions of pounds each year. Individuals experience exhaustion that is not helped by rest, with one in four so severely affected they are unable to leave the house and, frequently, unable to leave their bed. Other symptoms include, pain, mental fogginess, light and noise sensitivities, as well as trouble with memory and sleep. No effective treatment exists.
The DecodeME study is being led by a partnership of scientists and patients including Andy Devereux-Cooke. He said: “As someone living with ME/CFS, I’m well aware that the patient community has waited a long time for a study such as this one that has such a strong, genuine element of patient involvement. All of us involved with this research project hope that it can start to address the totally unwarranted stigma and lack of understanding that so many patients with ME/CFS face on a daily basis.”
The hope is the study will aid development of diagnostic tests and targeted treatments by pinpointing tiny differences in a person’s DNA that may affect their risk of developing CFS and reveal the underlying causes of the condition.
The samples will be compared with a similar number of non-CFS matched controls, which could be drawn from the UK Biobank.
Principal investigator Prof Chris Ponting from the human genetics unit at the University of Edinburgh said: “Our focus will be on DNA differences that increase a person’s risk of becoming ill with ME/CFS. We chose to study DNA because significant differences between people with, and without, ME/CFS must reflect a biological cause of the illness. It is our hope that this study will transform ME/CFS research by injecting much-needed robust evidence into the field.”
People with CFS who are aged 16 and over can volunteer to take part from home by signing up on the study website. When it begins, they will be mailed a collection kit and asked to send back a saliva sample, which will be compared with those from healthy controls.
European ME Coalition: Press release – Scientists call for more European research on ME/CFS
Brussels, 10 June 2020 More than one hundred scientists have signed an open letter calling for more European research into the illness Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). On 17 June, the European Parliament plans to vote on a resolution on ME/CFS research following a popular petition signed by thousands of patients and their loved ones.
ME/CFS is a long-term, debilitating illness that causes extreme exhaustion, poor concentration and memory, unrefreshing sleep, and many other symptoms. “The most characteristic feature is a worsening of symptoms following exertion,” says Evelien Van Den Brink, a Dutch patient who has suffered from ME/CFS for twenty-two years, since the age of fourteen. Because there is no cure for ME/CFS and its pathology remains poorly understood, Evelien submitted a petition to the European Parliament, asking for more scientific research into the condition. “More science is the only way forward,” Evelien says. “I’m almost completely bed-bound and I know fellow patients who are even worse off. We cannot let another generation suffer from this horrible illness.”
The petition has been signed fourteen thousand times and resulted in the first-ever resolution on ME/CFS in the European Parliament. “These patients have been ignored for far too long,” says Pascal Arimont, one of the members of Parliament who strongly supports the resolution. “There is currently no diagnostic test for ME/CFS because we know so little about the underlying pathology. In the US, Australia, and Canada, governments have invested substantial funds in ME/CFS research. Europe is running behind, so we urgently need to take action.” An estimated two million European citizens suffer from ME/CFS.
Today, the upcoming resolution received support from an open letter signed by 115 researchers and scientists worldwide. The letter stresses that ME/CFS “has long been a neglected area in medicine” despite its high societal burden and economic costs. “ME/CFS is not rare and it is highly debilitating,” says Professor Jonas Bergquist, who recently formed the ME/CFS Collaborative Research Center at Uppsala University, Sweden. “It often starts after a viral infection and we don’t really know what the mechanisms are for post-viral fatigue. Neuroinflammation and potentially autoimmune reactions may be parts of the explanation. More research is needed so that we get a better understanding of the disease.”
“A key priority is to develop a diagnostic test for ME/CFS to increase the accuracy of diagnosis,” Dr. Carmen Scheibenbogen, a Professor at Universitätsklinik Charité Berlin and one of the first signees of the letter, explains. “We hope to get a better understanding of the disease mechanism and eventually, an effective treatment. ME/CFS is one of the great challenges for modern medicine but I’m confident that a scientific breakthrough is possible.”
The open letter and full list of signees is available in the link below. For more info contact email@example.com
Physiotherapists taught three little words for the care of people with Post-Viral Fatigue Syndrome
Rest, Nutrition and Sleep should be the new normal when working with patients with Post Viral Fatigue Syndrome. The ‘Physios for ME’ group were asked for their views in the June edition of Frontline, journal of the Chartered Society of Physiotherapy.
As we enter the next phase of pandemic response, physiotherapy services are looking to support people recovering from Covid-19. One of the most prevalent problems is fatigue. Fatigue following a viral infection is common, but for some people the symptoms may persist for months and impact on their quality of life. We asked Physios for ME (Karen Leslie, Dr Michelle Bull, Natalie Hilliard and Dr Nicola Clague-Baker) for the low-down on post viral fatigue syndrome.
What is post viral fatigue syndrome (PVFS), and how do I recognise it?
PVFS is a persistent state of ill health following a viral infection. Symptoms include fatigue, loss of energy, muscular aches and pains, intermittent flares of viral symptoms and an inability to return to previous levels of activity. PVFS is not the same as being deconditioned. Ignoring or exacerbating the symptoms may worsen them.
If there has been a sustained change to daily life and if rehabilitation isn’t progressing as you think it should, consider PVFS.
Where, say, a person may have returned to work but uses their weekends to recover, or is struggling even with basic daily tasks, it’s worth considering PVFS.
With PVFS there is a possibility of development into Myalgic Encephalomyelitis (ME – often known as chronic fatigue syndrome or CFS). The link between severe viral infection and ME is clear. Previous outbreaks of SARS and Epstein Barr saw a 10 per cent rise in the number of patients diagnosed with ME1,2. ME affects approximately 250,000 people in the UK, more than multiple sclerosis and Parkinson’s disease combined. Around 25 per cent of patients are completely bedbound.
If I suspect someone recovering from Covid-19 is developing PVFS, what should I do?
Adapt to provide pacing strategies to work within energy levels, rather than push beyond limits. And make sure you are clearly communicating your concerns with the multidisciplinary team for ongoing monitoring and support.
The best approach is to ensure adequate:
How do I know if a person with PVFS has developed ME?
The hallmark feature of ME is post-exertional malaise (PEM), which is characterised by a set of symptoms including fever, muscle ache, headache, sensitivities, fatigue and dizziness. PEM is triggered by physical or cognitive exertion, which can be as simple as taking a shower or talking to a relative, and it can last days, weeks, or even months. PEM can manifest up to 24-48 hours after exertion, so it is not always apparent what activity was the trigger.
Clinical signs to look for include:
* post exertional malaise
* persistent reported fatigue that substantially reduces activity levels
* tiredness after sleep
* muscle and/or joint pain
* cognitive disturbances (memory, attention, information processing)
* sensory disturbances (photophobia, sound sensitivity)
* orthostatic intolerances (inability to tolerate anti-gravity positions)
* ongoing flu-like symptoms, swollen lymph glands, sore throat.
Research into the exercise physiological processes behind PEM is ongoing, so far finding 3:
* increased intracellular acidosis in exercising muscles and reduced post-exercise recovery from exercise
* abnormally low anaerobic threshold during maximal testing
* reduced maximum heart rate, maximum oxygen consumption, cardiac output and blood pressure on maximal exertion.
Such adverse physiological processes can be temporary, but for many they can result in a progression of the severity of their condition.
What should physiotherapists do?
The challenge for physiotherapists who are working to rehabilitate people recovering from Covid-19 is to identify those who start to display symptoms of ME so that they can adapt their approach to avoid triggering PEM and worsening the condition.
Careful questioning and an awareness of their history may help to identify potential new ME patients. It may be several months before their symptoms are accurately identified.
A standard physiotherapy programme of graded exercise, no matter how gentle it begins, always hinges on the principle of progression, and will therefore always end up at a level that triggers PEM. Up to 80 per cent of ME patients who have attempted some form of graded exercise have reported a deterioration in their condition4, and NICE Guidelines are currently under review after a campaign to remove graded exercise from any recommendations.
So physiotherapy that might work for one group of post Covid-19 patients may end up worsening another group who have gone on to develop ME. This is why we need to continually evaluate our treatments and monitor patients closely, as well as update our knowledge base around this condition and its management.
1. Hickie, I., Davenport, T., Wakefield, D., Vollmer-Conna, U., Cameron, B., Vernon, S. D., Lloyd, A. (2006). Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study. BMJ, 333(7568), 575.
2 . Moldofsky, H., & Patcai, J. (2011). Chronic widespread musculoskeletal pain, fatigue, depression and disordered sleep in chronic post-SARS syndrome; a case-controlled study. BMC neurology, 11(1), 37.
The CSP’s Professional Advice Service gives advice and support to members on complex and specialist enquiries about physiotherapy practice, including professional practice issues, standards, values and behaviours, international working, service design and commissioning, and policy in practice.
* Frontline is the Journal of the Chartered Society of Physiotherapists – the professional, educational and trade union body for the UK’s 59,000 chartered physiotherapists, physiotherapy students and associates.
New Video: Severe ME and Very Severe ME
This video [which is just under 15 minutes long] is from the project ‘Dialogues from a Neglected Illness’ – supported by a Wellcome Public Engagement Fund Award 2018 / 21. The project addresses different aspects of ME/CFS and includes interviews and input from doctors, researchers, patients, carers and advocates.
Produced by Natalie Boulton, with cameraman and editor Josh Biggs.
Please go to the project website dialogues-mecfs.co.uk for more information and to see other videos
To watch the video on Severe ME and Very Severe ME, please go to https://vimeo.com/422742593
Explaining ME/CFS? Prusty / Naviaux Study Ties Infections to Energy Breakdowns
by Cort Johnson
Unexpected synchronies are always a good sign. Many, of course, are familiar with Bob Naviaux, MD, PhD from the University of California, San Diego (UCSD). Naviaux’s metabolomic work and his Cell Danger Response (CDR) hypothesis have opened up new possible ways of understanding ME/CFS, autism and other diseases.
Bhupesh Prusty, PhD of the University of Würzburg in Germany, is newer on the scene but has been raising eyebrows with his proposal that herpesviruses like HHV-6 (and other viruses as well) may be knocking the mitochondria in ME/CFS patients for a loop.
The two authors – Prusty and Naviaux were the co-senior authors who conceived the project – teamed together to attempt to answer a question that’s been plaguing patients, doctors and researchers for years: how to tie together the energy problems in ME/CFS with the infectious onset that so many patients experience. Coming from two separate fields, Bhupesh Prusty and Bob Naviaux may have come up with a way.
They chose, what else, herpesviruses (HHV-6, HHV-7) to test their hypothesis.
Herpes viruses form a large and diverse group. Epstein-Barr virus (EBV), cytomegalovirus (CMV), and Herpes simplex viruses (HSV-1 and 2) have the ability to remain latent in the body and then explode into activity during times of stress or immunodeficiency. That has always made them a clear target in a disease largely defined by symptoms associated with infections.
The Human herpes viruses (HHV-6 and HHV-7) are a little different. Over 90% of people are infected by 3 years of age, usually through their mother’s saliva. The virus then leaves a copy of its DNA in a chromosome of a few cells, then becomes dormant. For most people, we never know if HHV-6 is reactivated or not.
Prusty and Naviaux believe this is because when HHV-6 is reactivated, it triggers cells to produce a protective factor that helps prevent other cells from getting infected (superinfected) with other viruses. This protective mechanism comes at a cost, though: mitochondrial fragmentation and a decrease in cellular energy production.
In people who don’t have ME/CFS, this phenomenon is normal and only lasts a few days at the beginning of a new infection or after exposure to certain environmental chemicals, or after physical injury. However, in ME/CFS, they believe HHV-6 infected cells continue to secrete a substance which inhibits cellular energy production, leading to fatigue, and all the other symptoms of the disease.
The very low viral loads of HHV-6 found in past ME/CFS studies have suggested that active reinfection with the virus is not an issue. A 2019 HHV-6 antibody study that turned up mostly subtle issues didn’t inspire further interest, either. (That study, it should be noted, focused mostly on late antibodies which would miss the smoldering infection that some believe may be happening.) Plus all HHV-6 serological studies to date suffer from the inability to differentiate between the more difficult to assess, and possibly more dangerous, HHV-6A and HHV-6B.
In 2018, though, Prusty, produced a controversial paper that roiled the HHV-6 research world. His cell line study suggested he’d identified very small non-coding RNA’s (sncRNA) produced by the virus in the earliest stages of reactivation, but before any virus replication occurred. The production of this sncRNA produced a signal which altered mitochondrial activity in the infected cells and caused the mitochondria to fragment. The study suggested that HHV-6 might be powering down the energy motors of the cells even as it was sitting mostly quietly in the cell. It was as if the virus was putting the cells in stasis.
If Prusty was right, you could throw the viral load data in ME/CFS right out the window: HHV-6 didn’t need to be replicating to cause something like ME/CFS – it simply needed to be a little active.
Nobody in the HHV-6 field had come up with that idea before, but Bob Naviaux in San Diego had developed a similar paradigm which proposed that the cells of ME/CFS patients had responded to infections and other stressors by getting stuck in a hypometabolic state (aka a state of hibernation or dauer, the German word for persistence).
Naviaux proposed that the stricken cells used what he called a “cell danger response” to power down their motors and redirect all energy toward cellular defense and survival, at the cost, though, of not having enough energy left over for normal cellular activity and function.
The metabolic system, in particular the mitochondria, he believed, were working hand in hand to repel invaders. In fact, in Naviaux’s paradigm, it was the metabolic or energy producing system that alerted the immune system to trouble, not the other way around.
A 2015 Nature article, which has been cited over 500 times, agreed. The study found that it only took moderate mitochondrial stress to send the cell’s antiviral defenses skyrocketing. It suggested the first goal of a pathogen was to damage, knock off, or disrupt the mitochondria of the cell it infected. Once the signs of mitochondrial damage presented themselves, however, the cell – now knowing that a pathogen was present – turned on its antiviral batteries.
Just last year, a French team showed that bacteria attempt to quickly knock out the engines powering immune cells as well. The cellular immune defense, it seems, starts with the mitochondria.
To read the rest of the article, please go to –
Oxford Health leaflet – a United Response
Leading ME charities, including ME Research UK, have joined in a Physios for ME led initiative which includes the All-Party Parliamentary Group on ME, the Forward-ME Group and other notable signatories in a united response to Oxford Health NHS Foundation Trust’s leaflet entitled ‘Coping with the Coronavirus‘.
The publication is one a series prepared by the Psychosocial Response Group in the context of Coronavirus and mental health. However, immediately it focuses upon the possible longer-term effects of the virus and elaborates the theme over a number of pages linking specifically to CFS and ME –
Some people may go on to develop Chronic Fatigue Syndrome (CFS), sometimes also called Myalgic Encephalitis (ME), which is a condition which affects people in different ways. The main symptom is persistent fatigue (tiredness) and exhaustion which can be severe and disabling.
Anyone can be affected by CFS, but there may be common themes for those with persistent problems. We know that there are both helpful and unhelpful ways to manage symptoms following a virus:
* Resting too much, for example spending most of the day in bed or doing very little, will lead to loss of fitness and muscle strength. When you then try to resume normal activities, you may find that you cannot do as much as you expect to do, and then rest more, causing further loss of fitness in a vicious cycle.
* Sleeping for hours during the day can lead to general malaise and problems sleeping at night. This in turn leads to more daytime fatigue and more resting, which in turn leads to more problems sleeping at night.
* Not allowing yourself time to recuperate and get better, such as going back to work too soon or resuming normal activities before you are fully well. People who have very high standards, like to do things well and do not like to let other people down, can push themselves very hard and do not allow themselves time to rest.
Three main ways you can improve the management of chronic fatigue are:
Pacing, and activity management, Graded exercise
In reply, the signatories, representing a broad sweep of charities, groups and informed individuals rebutted the most egregious assertions in the leaflet and the letter begins
Opposition to Oxford Health NHS Foundation Trust: “Coping with Coronavirus: Fatigue”
We, the undersigned, request immediate withdrawal of the Oxford Health NHS Foundation Trust leaflet “Coping with Coronavirus: Fatigue” for the following reasons;
The leaflet conflates post viral fatigue with myalgic encephalomyelitis (“ME”)
The leaflet purports to provide information for post-COVID-19 rehabilitation but is predominantly comprised of rehabilitation advice for ME/CFS
The information provided is incorrect or misleading.
The advice provided is potentially detrimental to patients and may result in deterioration and exacerbation of disability.
An e-mail copy of the letter was sent to Stuart Bell, Chief Executive of Oxford Health NHS Foundation Trust, and, in copy to Professor Chris Whitty – Chief Medical Officer for England, earlier today (20th April).
The full text of the letter signed by 24 representatives and individuals includes detailed rebuttals with citations to relevant studies, reports etc. is available in full here .
ME and PEM
This film will give you an introduction to PEM (Post Exertional Malaise).
Once you’ve understood what PEM is about, you’ll know a lot more about the debilitating chronic disease ME.
The film is made by the Norwegian ME Association – Rogaland County with professional support from psychologist Ketil Jakobsen and paediatric neurologist Kristian Sommerfelt.
God’s Love in a Pandemic
From the Metropolitan Tabernacle (“Spurgeon’s”), London: God’s Love in a Pandemic
These are momentous days when we find ourselves in the midst of a worldwide ‘discipline’ or warning from God, calling us to acknowledge and seek Him. And although we shrink from the thought, this is the reason for all unexpected catastrophes whether HIV, MERS, SARS, floods or vast fires. The Bible says these things will come more often in the ‘last days’.
A warning from God is not like the last judgement, because it is an expression of God’s love, urging people to turn to Him, whereas the last judgement will finally close the door of mercy for those who turn away from Him.
A warning is not permanent, and God has also given mankind the skill to control it, eventually. But a warning catastrophe pulls us up and humbles us, reminding us that we are only people, and that we are in God’s hands and accountable to Him.
Coronavirus has certainly shaken us more than any other catastrophe of recent generations. The relatively gentle approach of our UK scientific elite soon gave way to radical measures as the virus defied all predictions. Mighty China shook with alarm; the grim regime of Iran was stunned; Europe was soon sent scurrying to lock-down, and the all-powerful USA is now cowering like everyone else.
As the pandemic proceeds, significant features become apparent. It is the elderly (like the writer of this) who are most at risk – those who have had a lifetime of opportunity to honour their Creator (and may have refused). The virus seems to say to the younger people – ‘you have some opportunity left: don’t despise the longsuffering of the Lord.’ Remember that while God is love, He is also holy and just.
This may not be the last warning or discipline, although its full ‘indignation’ has not yet unfolded. Christians are praying for relief and healing for those suffering, and we are witnessing many acts of kindness among people, but it is vital that we heed the message and meaning of this pandemic. Its purpose is to call us to forgiveness and reconciliation with God, by coming to the Saviour, Jesus Christ our Lord, who has opened a way of salvation by suffering and dying for sinful people on Calvary’s cross. To trust in Him, repent of sin, and yield your life to Him, is to receive from Him a new and eternal life.
From the 25% ME Group: 25 year anniversary of the 25% ME Group
by Simon Lawrence
This year marks the 25 year anniversary of the 25% ME Group, the only charity concerned specifically with the needs of the severely affected.
From the downloadable document –
This year marks the 25 year anniversary of the 25% ME Group, the only charity concerned specifically with the needs of the severely affected.
They have a wealth of experience and as such are generally seen as an authority on Severe ME. The charity has been active in campaigning for better diagnosis, treatment and care of people with Severe ME including being a stakeholder in the NICE review, supporting use of ICC, undertaking surveys about various aspects of Severe ME, disseminating information, etc, and being a respected voice for people who are the most affected by ME. https://25megroup.org/about-us
As part of their 25 year celebrations, and to mark Severe ME Awareness Day on 8 August, 25% ME Group have invited members of the charity and the 25% ME Facebook group to participate in a project to make Severe ME visible. They have been asked to submit Stories and Images of their lives with Severe ME. https://25megroup.org/severe-me-day-2020
For further information, go to –
Cerebral blood flow is reduced in ME/CFS during head-up tilt testing
Cerebral blood flow is reduced in ME/CFS during head-up tilt testing even in the absence of hypotension or tachycardia: A quantitative, controlled study using Doppler echography
- Doppler imaging to measure cerebral blood flow is feasible during tilt testing.
- Cerebral blood flow in ME/CFS patients is reduced during tilt testing.
- 90% of ME/CFS patients show abnormal cerebral blood flow reduction on tilt testing.
- Cerebral blood flow reduction correlates with symptoms of orthostatic intolerance.
The underlying hypothesis in orthostatic intolerance (OI) syndromes is that symptoms are associated with cerebral blood flow (CBF) reduction. Indirect CBF measurements (transcranial Doppler flow velocities), provide inconsistent support of this hypothesis. The aim of the study was to measure CBF during a 30 min head-up tilt test (HUT), using Doppler flow imaging of carotid and vertebral arteries, in individuals with chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), a condition with a high prevalence of OI.
429 ME/CFS patients were studied: 247 had a normal heart rate (HR) and blood pressure (BP) response to HUT, 62 had delayed orthostatic hypotension (dOH), and 120 had postural orthostatic tachycardia syndrome (POTS). We also studied 44 healthy controls (HC). CBF measurements were made at mid-tilt and end-tilt. Before mid-tilt, we administered a verbal questionnaire to ascertain for 15 OI symptoms.
End-tilt CBF reduction was 7% in HC versus 26% in the overall ME/CFS group, 24% in patients with a normal HR/BP response, 28% in those with dOH, and 29% in POTS patients (all P < .0005). Using a lower limit of normal of 2SD of CBF reduction in HC (13% reduction), 82% of patients with normal HR/BP response, 98% with dOH and 100% with POTS showed an abnormal CBF reduction. There was a linear correlation of summed OI symptoms with the degree of CBF reduction at mid-tilt (P < .0005).
During HUT, extracranial Doppler measurements demonstrate that CBF is reduced in ME/CFS patients with POTS, dOH, and even in those without HR/BP abnormalities.
This study shows that orthostatic intolerance symptoms are related to CBF reduction, and that the majority of ME/CFS patients (90%) show an abnormal cerebral flow reduction during orthostatic stress testing. This may have implications for the diagnosis and treatment of ME/CFS patients.
What is ME?
Video produced by A Broken Battery
From the description on the webpage –
ME is “a life-altering debilitating disease affecting the brain, the immune system and energy metabolism. The defining symptom of ME is that even minimal exertion can cause a flare in symptoms (a crash) that can last for days, weeks or even months.
Severity ranges from mild to very severe. Around 25% are house or bedbound, unable to properly care for themselves, sometimes for many years or decades at a time. The majority of severely affected patients are unable to access any services and are not offered home visits or specialist inpatient care. People with ME have a lower quality of life than people with Stroke, Cancer, Heart disease, Multiple Sclerosis, Rheumatoid arthritis. ME is not taught in most medical schools despite it affecting 15-30 million worldwide.
The WHO classified ME as neurological in 1969 but 80% of doctors still believe its psychosomatic. Many doctors still don’t know that over the last 35 years there have been over 9000 scientific publications that compared people with the illness to healthy people and they find a whole variety of abnormalities, like energy metabolism.
Dr Nina Muirhead ME Patient and Specialist Surgeon in Dermatology – The NICE guidelines “do not fit” with the patient experience and “perpetuated my misunderstanding” of ME by recommending Cognitive Behavioural Therapy and Graded Exercise. NICE is currently updating its guidance, which is expected in October 2020. The Centers for Disease Control and Prevention (CDC) in the US dropped Graded Exercise and Cognitive Behavioural Therapy as treatments for ME in 2017.
Patient surveys consistently report that Graded Exercise makes over 50% of patients worse. “In the absence of effective treatments, patients who are given a period of enforced rest from the onset have the best prognosis”. Pacing was consistently shown to be the most effective, safe, acceptable and preferred form of activity management”.
(See the webpage at the address above for references.)
From the ME Research UK website –
A revised version of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) is due to be implemented in January 2022.
The ICD is the diagnostic classification standard for all clinical and research purposes, and is therefore highly influential. Its many uses include identifying health trends, and monitoring and reporting diseases, resource allocation, safety and quality.
ICD-11 will include a new classification, Bodily Distress Disorder, which is defined as “characterized by the presence of bodily symptoms that are distressing to the individual and excessive attention directed toward the symptoms, which may be manifest by repeated contact with health care providers”.
There have been understandable concerns that ME/CFS would be grouped under this diagnosis of Bodily Distress Disorder in the new revision, which might mean that individuals with the illness would be directed through psychiatric care.
However, thanks to the sterling efforts of campaigners over many years, ICD-11 will NOT include Postviral Fatigue Syndrome, Chronic Fatigue Syndrome or Benign Myalgic Encephalomyelitis under the new classification.
At the moment, ICD-10 lists Benign Myalgic Encephalomyelitis in the ‘Diseases of the nervous system’ heading, under PostViral Fatigue Syndrome (Block 93.3, ICD 10th revision, 2007), as follows:
- Diseases of the nervous system
- Other disorders of brain
- Other disorders of the nervous system
- G93.3 Postviral fatigue syndrome
- Benign myalgic encephalomyelitis
ICD-11 will list both Benign Myalgic Encephalomyelitis and Chronic Fatigue Syndrome separately, but still under ‘Diseases of the nervous system’ and Postviral Fatigue Syndrome (Block 8E49, ICD 11th revision, 2019), as follows:
- Diseases of the nervous system
- Other disorders of the nervous system
- 8E49 Postviral fatigue syndrome
- Benign myalgic encephalomyelitis
- Chronic fatigue syndrome
From the 25% ME Group – Diagnostic Tests 4 Myalgic Encephalomyelitis
This is a summary of a highly detailed, sourced text describing measurable organic abnormalities that researchers and specialists have identified in testing of Myalgic Encephalomyelitis patients.
For various reasons, many of the articles on Myalgic Encephalomyelitis in the mainstream media (and even some of the medical texts on the illness) unequivocally proclaim not only that there are no tests which can be utilized to help confirm an ME diagnosis, but that despite extensive testing no objective or quantifiable abnormalities have ever been found in any patients with ME whatsoever. Despite their popularity, these are simply absurd claims. The reality is that objective evidence of quantifiable organic abnormalities in Myalgic Encephalomyelitis patients has existed since the 1950’s.
Not only are there a series of tests which readily allow an ME diagnosis to be confirmed, but more than 1,000 medical studies have shown a variety of measurable and in some cases extremely severe abnormalities in many different bodily systems of ME patients.
Abnormalities are also visible on physical exam. Tests will only all be normal in ME patients – as with all illnesses – if the completely wrong tests are done, or if those tested do not in fact have ME. Contrary to much of the propaganda surrounding the illness, it is also not “fatigue” or “tiredness” that is the one essential characteristic of ME, but central nervous system (CNS) dysfunction. As ME expert Dr. Byron Hyde, explains: “The one essential characteristic of ME is acquired CNS dysfunction, [not] chronic fatigue. A patient with ME is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological CNS changes: SPECT, xenon SPECT, PET, and neuropsychological testing.” Thus it is these tests which are most critical in the diagnosis of ME, although various other types of tests are also useful. Tests That Can Aid Diagnosis Some of the series of tests which can (in combination) help to confirm a suspected ME diagnosis include:
SPECT and xenon SPECT scans of the brain
SPECT scans have demonstrated decreased cerebral blood flow most frequently in the frontal, parietal, temporal, occipital, and brain stem areas of the brain. Eighty percent of ME-ICC patients will have abnormal SPECT scans. These abnormalities have also correlate with clinical status. Dr. Hyde adds that “I do not describe a patient as having ME unless there is an abnormal SPECT. If the SPECT is normal, I repeat it along with xenon SPECT. If the brain scans remain normal, I conclude it is unlikely to be ME.”
MRI scans of the brain
Punctate, subcortical areas of high signal intensity consistent with edema or demyelination were identified by MRI in 78 percent of ME patients (similar to those seen in MS). Research has shown that 50 percent to 80 percent of ME patients will have abnormal MRI scans. ME patients with abnormalities on MRI have been reported as being more severely impaired than those without such abnormalities.
PET scans of the brain
PET scans have shown decreased metabolism of glucose in the right mediofrontal cortex and generalized hypoperfusion of the brain with a particular pattern of decreased neuronal metabolism in the brain stem.
Of the CNS dysfunctions that make up ME, cognitive dysfunction is easily one of the most disabling characteristics of the illness. Neuropsychological testing can be used to identify cognitive dysfunction and/or to confirm a ME diagnosis. It should focus on the abnormalities known to differentiate ME from other causes of organic brain dysfunctions.
EEG brain maps and QEEG brain maps
Ninety-five percent of ME patients have been found to have abnormal cognitive-evoked EEG brain maps. But Dr. Hyde argues that QEEG brain maps are far more accurate, and that they “have been able to demonstrate not only lack of normal activity in ME patients but migration of the normal activity centers from injured areas to different parts of the brain.”
Neurological examination and the Romberg or tandem Romberg test
Most ME patients have abnormal neurological examination. The Romberg test is a useful test of brain stem function. It involves standing with eyes open and then with eyes closed with feet together or one behind the other for a minute or more. A patient tests positive for “Romberg’s sign,” or abnormal, if he or she can stand with the eyes open but falls when the eyes are closed. Professor Malcolm Hooper ME specialist at the University of Sunderland, England, explains that “In his 1995 Australian Workshop, Dr. Paul Cheney said that more than 90 percent of ME patients have an abnormal Romberg, versus 0 percent of controls.”
Tests of the immune system
The immune system abnormalities in ME patients mimic the immune pattern seen in viral infections. Specific findings include (but are not limited to):
- Increased numbers of activated cytotoxic T cells (most patients have evidence of Tcell activation)
- Low natural killer cell numbers/percentage and function (cytotoxicity)
- Elevated immune complexes
- Atypical lymphocyte count
- Significantly reduced CD8 suppressor cell population and increased activation marker (CD38, HLA-DR) on CD8 cells
- Abnormal CD4/CD8 ratio
- Elevations of circulating cytokines
- Immunoglobulin deficiencies (most often IgG 1 and IgG 3).
A more specific immune system abnormality has been discovered in MEICC of increased activity and dysfunction of the 2-5A RNase L antiviral pathway in lymphocytes. The dysregulation of the RNase L pathway strongly supports the hypothesis that viral infection plays a role in the pathogenesis of the illness. Between 80.0 percent and 94.7 percent of ME patients have evidence of an up-regulated 2-5A antiviral pathway. The degree of elevation of 37 kDa RNase L has also been shown to correlate with symptom severity. This test is as yet not widely available but will be one of the most useful tests in helping to diagnose ME in the future.
Erythrocyte sedimentation rate (ESR)
This is a common blood test used to detect and monitor inflammation based on the rate at which red blood cells settle in a test tube.] An unusually low ESR of < 5mm/hr is common in ME
Insulin levels and glucose tolerance tests
Derangement of insulin response is a frequent finding in ME patients. Glucose tolerance curves are often abnormal.
24-Hour Holter monitor
A 24-hour Holter monitor (a type of heart monitor) may show repetitively oscillating T-wave inversions, and/or a flat T-wave may be found. Holter monitors may also show heart rates as high as (or higher than) 150 beats per minute as an immediate or delayed response to the patient maintaining an upright posture, or at rest. Heart rates as low as 40 beats per minute may also be observed (during sleep).
Tilt table examination
Orthostatic intolerance is very common in ME patients, and may manifest as one of, or a combination of, the following: neurally mediated hypotension (NMH), postural orthostatic tachycardia syndrome (POTS), or delayed postural hypotension.
Exercise testing and chemical stress tests
Cardiopulmonary exercise testing (CPX) is widely used for the diagnosis (and functional assessment) of various cardiac and metabolic disorders and can also be used in the diagnostic evaluation of ME patients. Heart rate and blood pressure responses during the exercise test may reveal abnormalities specific to ME, including: lower cardiovascular and ventilatory values at peak exercise (patients only being able to attain half the expected maximal workload and oxygen uptake compared to sedentary controls), elevated resting heart rates, and an inability to reach maximum age-predicted heart rates. Some ME patients can be tested via nuclear medicine (no treadmill) in Hospital.
As exercise tests are not appropriate for many ME sufferers, Dr. Byron Hyde, writes: “Patients with ME frequently cannot do exercise tests, so chemical testing as an option.”
There are also a variety of abnormalities visible on physical exam in ME patients. These abnormalities are not usual in healthy patients, but they are also found in people with other organic illnesses (so they are not specific to ME). The post-exertional paralytic muscle weakness unique to ME should also be tested for; a diagnosis of ME should never be made without this characteristic being present.
ME shares no characteristics of various “fatiguing conditions” with a variety of different etiologies made up of vague & mild “everyday” type symptoms and have no physical signs or no tests which can’t show abnormalities to aid diagnosis.
Myalgic Encephalomyelitis is a distinct organic neurological disorder (which can occur in both epidemic and sporadic forms) that has been recognized as such by the World Health Organization (WHO) in their International Classification of Diseases since 1969 with the code G93.3. It bears no relationship to any unrelated, vague, and hard-to-diagnose “fatiguing illnesses.”
“Unlike Somatization Disorder, Medically Unexplained Symptoms (MUS), Functional Neurological Disorder (FND), and Munchausen Syndrome, ME is not ‘medically unexplained.’ ME is a disease which, like lupus, has no single marker. ME is a multisystem disease with many organ and bodily systems affected, producing a myriad of symptoms, and many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research. These are well-documented, scientifically sound explanations for why patients are often bedridden and unable to maintain an upright posture.”
- See the full-length, fully-sourced article, “Testing for ME,” at Jodi Bassett’s Australia-based Website, A Hummingbirds’ Guide to ME, at https://www.hfme.org/ provides more information on the tests listed here as well as on many other aspects of diagnosis, plus a list of references.
- Dr. Byron Hyde, MD, is an internationally recognized ME specialist, and chairman of the Nightingale Research Foundation for the study and treatment of ME in Ontario, Canada. https://liberationislife.files.wordpress.com/2017/03/definitionofme_nrf_print.pdf
- Myalgic Encephalomyelitis: International Consensus Criteria
- GAME Website: https://artzstudios1.wixsite.com/globaladvocatesmeicc
From Let’s Do It For ME: New Total £960,000!
Invest in ME Research announced in their Christmas and New Year Funding Appeal that £960,000 has been raised and pledged to support the charity’s Centre of Excellence for Myalgic Encephalomyelitis projects.
The Let’s Do It for ME campaign is run by severely ill patients supporting the charity’s Centre of Excellence programme of biomedical research and medical education projects. Our original crowdfunding goal of £100,000 enabled this work to get underway in 2013 (patient samples for the lab work obtained since 2014) and we would love to reach £1,000,000!
So to start off the new year, we have created a grid with 40 vacant slots with a funding target of £1,000 each and invite you to contact us if you’d like to aim to raise £1,000 whether as an individual or group, private or business. Read more on the page for Our 40 x £1k Fundraisers Challenge.
Many thanks to everyone helping Invest in ME Research to achieve their goals relating to maintaining a programme of high quality biomedical reseach with international collaboration focused on establishing diagnostic tests and medical treatments for this disease.
The charity wrote in December,
“To our supporters we owe great thanks – you helped create something that was thought unachievable. A sustainable Centre of Excellence for ME is now harnessing the benefits of a strategy of collaborative international biomedical research in modern facilities with world-class researchers.”
With very best wishes to you for 2020 and the new decade ahead and grateful thanks for supporting Invest in ME Research.
In case you missed it, your input is needed to inform the agenda for an upcoming public engagement meeting at Quadram Institute.
A very Happy New Year to readers of my website, your families and friends.
A couple of weeks ago I was given a Christmas card containing a separate little tract with the following poem, which I trust may be an encouragement to you as we start another new year –
Throughout the New Year, and each step of the way,
May Christ be your portion, your joy and your stay.
With God’s precious precepts your daily delight
To lead and encourage in paths that are right.
“The Lord is my Shepherd,” how precious the word!
He’ll lead in green pastures, His promise is heard.
“Beside the still waters,” what comfort and rest!
What peace there is found upon Jesus’ breast.
His “goodness and mercy,” each day may you prove,
His comforting presence, His infinite love!
With richest compassions, each morning anew,
May multiplied mercies be showered on you!
“My cup runneth over,” His grace so abounds,
That fullest enjoyment in Jesus is found.
“The Lord is my portion,” this may your soul say,
And you will be happy each step of the way.
– Lois Beckwith (1896-1958)
A Holiday Message from Dr Ron Davis, 21 December 2019
Dr Ron Davis shares an update on research at the OMF-funded ME/CFS Collaborative Research Center at the Stanford Genome Technology Center. He shares holiday greetings and hope with the entire ME/CFS community.
Press Release from Invest in ME Research
for Immediate Release
UK Charity Pledges £500,000 for Research into ME in Norwich Research Park
UK Charity Invest in ME Research is pledging £500,000 for continued research into the disease myalgic encephalomyelitis (ME or ME/CFS) in Norwich Research Park, UK (NRP).
This major investment builds on the foundations already made for a UK/European Centre of Excellence for ME research hub in Norwich Research Park.
The pledge covers joint funding of a PhD position in partnership with University of East Anglia and over 70% of the required funding for a clinical trial of Faecal Microbiota Transplantation (FMT) being performed alongside other high-quality biomedical research at the Quadram Institute (QI).
QI’s world-class facility has seen four PhDs already employed on research into ME, focusing specifically on the gut microbiota and links to ME.
Invest in ME Research Chairman Kathleen McCall said: “This is a massive undertaking for a small charity but it underlines our confidence in the quality and direction of research at Quadram Institute. This research offers an opportunity to test a new form of treatment for ME in well-designed clinical trial. On top of the other initiatives being created in partnership with QI we believe this has the potential to change the face of research into this disease.”
Professor Simon Carding, Head of Gut Microbes and Health Research Programme at Quadram Institute Bioscience said: “We are incredibly grateful for the ongoing support from Invest in ME Research and their supporters. We are very excited at the prospect of undertaking the FMT clinical trial, as part of our ongoing investigations into the links between ME and the gut microbiome.”
This research news comes after recent meetings of the European ME Research Group (EMERG) and European ME Clinicians Council (EMECC) in which QI and UEA played major roles and which will form European collaborations and coordination of research into ME and clinical expertise development for this disease.
The continuing and developing research in Norwich Research Park holds out great hope for the future for ME patients and their families.
ME commonly presents with hugely diverse and debilitating symptoms including post-exertional malaise, unrefreshing sleep, cognitive dysfunction and widespread pain. ME has been estimated to affect around 250,000 people in the UK and direct and indirect economic costs have been estimated in the USA to be $20 billion annually. The severity of symptoms varies. Around 25% of sufferers may be classed as severely affected – often bed bound at some point in their lives with periods of relapse and remission common and only 6% returning to full health.
The pledge brings to five the number of PhD positions that the charity has funded/part-funded.
Notes for editors
About Invest in ME Research
Invest in ME Research (charity nr 1153730) is an independent UK charity finding, funding and facilitating biomedical research into ME.
Invest in ME Research is run by volunteers – patients or parents of children with ME – with no paid staff. Overheads are kept to a minimum to enable all funds raised to go to promoting education of, and facilitating and funding biomedical research into ME. The charity organises an annual International ME Conference Week in London which includes a two day research Colloquium, young/early career researcher conference and a public international conference that regularly has delegates from twenty countries attending.
The charity’s efforts are on developing the Centre of Excellence for ME to maintain a strategy of high-quality biomedical research into the disease and encouraging European collaboration in research and development of clinical expertise.
For more information visit www.investinme.org/pr01-Dec19
Contact details [Chairman Kathleen McCall, Invest in ME Research, PO BOX 561, Eastleigh SO50 0GQ, UK email: firstname.lastname@example.org]
About the Quadram Institute
The Quadram Institute (quadram.ac.uk) is an interdisciplinary research centre at the forefront of a new era of food and health research. It brings together researchers and clinicians under one roof and houses one of Europe’s largest endoscopy units and a clinical research facility.
Based on the Norwich Research Park, The Quadram Institute is a partnership between Quadram Institute Bioscience, the Norfolk and Norwich University Hospitals NHS Foundation Trust, the University of East Anglia and the Biotechnology and Biological Sciences Research Council (BBSRC).
Its mission is to deliver healthier lives through innovation in gut health, microbiology and food and its vision is to understand how food and microbes interact to promote health and prevent disease.
Four interconnected research themes in Quadram Institute Bioscience deliver a pipeline of research in plants, microbes, food and health: microbes in the food chain; the gut and the microbiome; food innovation and population health.
For media enquiries please contact:
Andrew Chapple, email@example.com, 01603 251490, 07713087883
About University of East Anglia
The University of East Anglia (UEA) is a UK Top 25 university and is ranked in the top 50 globally for research citations. Known for its world-leading research and good student experience, it was awarded Gold in the Teaching Excellence Framework and is a leading member of Norwich Research Park, one of Europe’s biggest concentrations of researchers in the fields of environment, health and plant science. www.uea.ac.uk
For media enquiries please contact:
Penny Powell, P.Powell@uea.ac.uk: 01603 591238
Ron Davis talks ME/CFS at Columbia and Princeton
Written by Janet Dafoe, PhD
Ron Davis spent the last week on the East Coast giving talks and talking individually to scientists and doctors about ME/CFS. First, he spent two days at Princeton University. He talked to individuals, groups of graduate students, and groups at lunches and dinners. He gave a talk in the huge Molecular Biology Department (includes immunology, microbiology, genetics, biochemistry, et al) in a big lecture hall with about 300 scientists. He sensed that they were surprised and shocked by how many people are affected and how severe the disease is. They were impressed by the progress Dr. Davis has made with such minimal NIH funding and relying on donations from patients.
Then Dr. Davis went to the Einstein Medical Center at Columbia University and gave a similar talk to 100 doctors and scientists in person and 184 more who logged in online. Again, they were surprised and shocked by the information he presented. He knew it was being Livestreamed so he didn’t take questions, but talked for 1 1/2 hours and incorporated questions that he is commonly asked. Nobody left. Ron really emphasizes the prevalence and severity of ME/CFS, the need for medical care, the urgent need for research, the growing group of great scientists that are working on it and the fact that none of them have enough funding from NIH.
The week before this, Dr. Davis gave the keynote address at Synchrony 2019, a large Autism conference in Pleasanton, California. Again, he had a large audience of researchers, doctors, and caregivers. They were really impressed by his research and were struck by some of the similarities between Autism and ME/CFS. OMF Scientific Advisory Board Member Robert Naviaux, MD, talked just before Ron. They are going to collaborate with Ron, sending some patients to his lab so they can investigate similarities and differences. The Autism group will be funded by one of the Autism Foundations since Ron only uses Open Medicine Foundation funds on ME/CFS.
Altered cardiac autonomic regulation
From the ME Research UK website –
Published in the journal, Medicine, last month was a systematic review looking at “evidence of altered cardiac autonomic regulation in ME/CFS”.
Simply put, “cardiac autonomic regulation” refers to the body’s control system that acts unconsciously to regulate the functions of the heart such as heart rate. This has been a recurring topic in projects funded by ME Research UK, and several of the studies referenced in this new review are from research supported by the charity, including those involving Prof. Julia Newton (Aug 2007, Apr 2009 and Aug 2011) and Prof. Jo Nijs.
The review included 64 publications looking at a number of different measurements in people with ME/CFS and healthy control subjects, including resting heart rate, maximal heart rate during exercise, heart-rate response to head-up tilt testing, and resting heart-rate variability.
A meta-analysis combining the results of multiple studies found that these parameters and more were significantly abnormal in ME/CFS patients compared with controls, indicating that the illness is associated with altered autonomic cardiac function. Although the differences were not sufficiently consistent for any of these parameters to be useful on their own for diagnosis.
These findings are not news if you have been following ME Research UK-funded studies over the last few years, but it is good to see the conclusions confirmed in a meta-analysis that includes results from many other researchers.
WE ME – a Community and ME
A new booklet from Invest in ME Research –
A condition such as ME presents not only a challenge to the patient who receives the diagnosis, nor only to the family where a child or partner contracts the illness. It tests the values and the fabric of a community. How does the community react?
The reactions and experiences describe how prepared or willing it is to overcome the challenges and support the patient with ME.
A condition such as ME presents not only a challenge to the patient who receives the diagnosis, nor only to the family where a child or partner contracts the illness.
Thanks to funding from an Awards for All grant Invest in ME Research have been able to have printed a small booklet that the team has produced giving an overview of how ME affects a community.
The booklet can be downloaded as a pdf file by clicking here.
From page 3 –
What is ME?
ME is a multisystem, complex, acquired illness with symptoms related mainly to the dysfunction of the brain, gastro-intestinal, immune, endocrine and cardiac systems. ME has been classified as a neurological disorder in the World Health Organisation’s International Classification of Diseases since 1969.
The Chief Medical Officer’s Report issued in January 2002, recognised that ME “should be classed as a chronic condition with long term effects on health, alongside other illnesses such as multiple sclerosis and motor neurone disease”. Similarly the Institute of Medicine report of 2015 stated that ME is “a serious, chronic, complex, multisystem disease that frequently and dramatically limits the activities of affected patients.”
The Third Annual Community Symposium on the Molecular Basis of ME/CFS
The Third Annual Community Symposium on the Molecular Basis of ME/CFS, sponsored by the Open Medicine Foundation, took place on September 7, 2019 at Stanford University.
All of the individual talks are now available to watch on YouTube –
Individual talks –
01 Ron Davis – Opening Remarks https://youtu.be/jWlJ0Clv6pw
02 Linda Tannenbaum and Chris Armstrong – Welcome https://youtu.be/2GSKnDE0biw
03 Janet Dafoe – Greetings https://youtu.be/mAnCWhEzNGg
04 Ashley Haugen – Symposium Logistics https://youtu.be/kEnS_d7q0u4
05 Raeka Aiyar – Revolutionizing Disease Research with Stem Cells https://youtu.be/gilWemHSI1k
06 Robert Harrington – Video from the Stanford Chair of Medicine https://youtu.be/jMApmri1YDI
07 Maureen Hanson – Thoughts and Data about ME/CFS https://youtu.be/2BZnL-ZKta4
08 Alain Moreau – Let’s Talk About You and ME https://youtu.be/AY5yrva1zYY
09 Oystein Fluge – Lessons from clinical trials in ME/CFS https://youtu.be/fGsqjx-N9yI
10 Q & A Panel Discussion – Morning Speakers https://youtu.be/T0VhJw2Fh-c
11 Ron Tompkins – OMF ME/CFS Collaboration at the Harvard Affiliated Hospitals https://youtu.be/hY6rpd4yf2M
12 Jonas Bergquist – A short video update https://youtu.be/mmIKU1OQH58
13 Juan Santiago – High-Resolution and High-Throughput Quantification of RBC Deformability https://youtu.be/LnG0TM88tes
14 Mike Snyder – Big Data, Wearables, and Health https://youtu.be/YoccazReqgU
15 Robert Phair – Metabolic Traps in ME/CFS https://youtu.be/d9oVHDh8rjk
16 Ron Davis – What’s Next? https://youtu.be/YdR6ujHxloo
17 Q & A Panel Discussion – Afternoon Speakers https://youtu.be/j5H8u4FXcHo
18 Ron Davis – Closing Remarks https://youtu.be/1wvw-idPRSQ
The PACE trial – Series Highlights
MPs, experts and patients discuss the harm and flaws of the controversial trial of Graded Exercise on ME patients. “One of the biggest scandals of the 21st century” Carol Monaghan MP.
Children with ME – Highlights
Highlights (~1 min) of the Children with ME video. 1 in 5 parents face child protection proceedings, in extreme cases parental rights have been removed. MPs, experts, charities and patients discuss some of the reasons this is happening and the impact it has had.
Watch the series –
Ron Davis discusses his research at Stanford and An Exciting Week for Advancing ME/CFS Research
Ronald W. Davis is a Professor of Biochemistry and Genetics at Stanford University and Director of the Stanford Genome Technology Center. He also has a personal connection to ME/CFS — his son was diagnosed almost 10 years ago.
In this interview with Llewellyn King, Ron discusses his research at Stanford.
The interview was posted on YouTube on September 13th 2019.
An Exciting Week for Advancing ME/CFS Research
I’m pleased to share with the OMF community that the OMF sponsored Stanford ME/CFS Working Group and Third Annual Community Symposium on the Molecular Basis of ME/CFS once again is helping to advance urgently needed research on this disease.
During the three days prior to the Community Symposium, 60 scientists from all over the world, including OMF Scientific Advisory Board members, actively participated in the Working Group. They gathered behind closed doors to brainstorm and openly discuss new ideas to move this field forward.
It was wonderful to see that this year there were new faces and early-career participants, including talented engineers, contributing to the discussions. From my conversations during the meetings, it struck me again how much kindness, passion and collaborative spirit all the participating scientists have.
At the lovely pre-symposium dinner on Friday evening at Dr. Ron Davis’s home, I had the pleasure to thank Dr. Davis as well as Dr. Ron Tompkins, Dr. Wenzhong Xiao, and Dr. Jonas Bergquist for the initiative they’ve taken in leading the OMF-funded Collaborative Research Centers, as well as the many scientists, donors, leaders and OMF staff for all their hard work.
On Saturday, the Community Symposium provided our outstanding panel of speakers an opportunity to share updates with the international ME/CFS community as well as those attending in person. Nearly 300 people were present, mostly from the U.S. but also from Sweden, Norway, Canada, Korea, Japan and Italy, and the Livestream broadcast and Facebook Live reached thousands more around the world.
In between presentations, patients, scientists and clinicians exchanged insights and ideas. It’s always inspiring to see how the scientists and clinicians in this field are personally invested in finding answers for patients fast, and how much they’re interested in learning from patients and using these events to interact with the community as much as possible.
Paolo Maccallini, a patient-expert who traveled from Italy to attend, described the experience perfectly: “Meeting all these top-notch scientists, gathered to share their perspectives on the latest advancements in the knowledge of ME/CFS, was thrilling. You deeply perceived the collaborative spirit and the professional trust they have for each other. This, along with the information they shared, made me confident for a hopeful future for patients.”
The Symposium ended on a very encouraging note, when all six speakers who were on stage for the closing panel discussion agreed, “We are very hopeful for the near future!”
In the years I’ve been working to end ME/CFS, I’ve never felt more hopeful and inspired. Our talented research collaborators have the expertise to figure this out, and the generous support of the community continues to grow so we can accelerate the pace of discovery.
With that in mind I want to emphasize to patients, keep hope alive; there’s light at the end of the tunnel, now more than ever!
Thank you all for being a part of this unique community effort, and I look forward to keeping you updated on the exciting ME/CFS research that you help make possible. We will share an overview of the Symposium from Dr. Chris Armstrong soon.
With hope for all,
Founder & CEO/President
Tribute paid to Professor Peter Behan – M.E. expert and ME Association patron
On the ME Association website –
Dr Charles Shepherd, Hon. Medical Adviser, ME Association.
I knew Peter Behan as a friend and colleague for almost 40 years.
I first met him when the late Dr Melvin Ramsay, who originally diagnosed my own M.E. following an episode of chickenpox encephalitis, suggested that I should go and see Peter at the Institute of Neurological Sciences at the University of Glasgow to help with the research that he was doing into the condition.
It was immediately obvious that Peter was a very kind and caring physician who knew all about ME.
Peter was also an outstanding neurologist who, along with his wife Professor Mina Behan and virologist Professor John Gow, was carrying out important research into brain, muscle and immune system function, along with the role of infection, in people with M.E.
Unlike most of his neurology colleagues he had no doubt that M.E. was a serious neurological illness and that the patients were being badly let down by both clinicians and the research community.
The papers that were published from his research group at the time played a significant role in helping to change medical opinion about M.E. and the whole situation regarding research.
The fact that M.E. was firmly on the medical curriculum at the Southern General Hospital also meant that a succession of neurologists working in Peter’s team gained a solid knowledge of the condition – Dr Abhijit Chaudhuri in particular, who now advises the ME Association on neurology.
Peter continued with his research interest well into retirement and helped to develop the research strategy for the MEA Ramsay Research Fund and made personal donations to the fund.
In recognition of his contribution to both clinical and research work he was invited to become a Patron of the ME Association – a position he held until his death at the end of August.
Peter was excellent and amusing company – either in Glasgow, or up in Denkeld where he was an accomplished fisherman with an encyclopaedic knowledge of salmon fishing. Each year at Christmas we would receive one of Peter’s whole smoked salmon from the Tay!
I kept in touch with Peter following his move to Edinburgh where, despite failing health in the past few years, he was always keen to know what was happening to research into M.E.
We all owe an enormous debt of gratitude to Peter. He will be sadly missed and I will be attending his funeral on Friday 13th September in Edinburgh on behalf of the ME Association.
BEHAN Professor Peter Oliver Professor Emeritus of Neurology, MD DSc FACP FRCP FLS, University of Glasgow Died peacefully at home, in Edinburgh on 31st August 2019, aged 84. Husband of the late Professor Wilhelmina Behan. Loving father to Charlotte, Miles and Edmund and devoted grandfather. Very dear friend to Dr Valerie Cairns. A service will be held at Warriston Crematorium, Lorimer Chapel, Edinburgh on Friday, 13th September at 1pm, to which all are welcome. Family flowers only. The Herald
Investigating sensory processing and cognitive function in people with ME: a pilot study
From the ME Research UK website –
Dr Sanjay Kumar and Dr Farzaneh Yazdani
Oxford Brookes University, Oxford, UK
Background and aim
Our senses are constantly being bombarded with information from our surroundings – the sights, sounds, sensations and smells around us, as well as the tastes in our mouths.
The brain has to work hard to process all this information simultaneously, and filter out what’s irrelevant so we can concentrate on what’s important at any given moment. But this ability can be impaired in people with certain clinical conditions, leading to a disabling hypersensitivity to the stimuli around them.
The resulting physical and mental overload can lead to poor coordination, dizziness, clumsiness, numbness, tingling and nausea, and may affect individuals’ ability to take in information and make decisions.
Dr Sanjay Kumar, Dr Farzaneh Yazdani and colleagues at Oxford Brookes University have previously looked at this phenomenon in people with post-concussion syndrome following head injury. And we recently awarded funding to the team to investigate the problem in ME/CFS.
Although hypersensitivity is not considered a primary factor in the diagnosis of ME/CFS, it is a common finding in people with the condition. This was borne out when the team met with people from a local ME support group, many of whom identified with the issue and said that it interfered with their daily life.
This prompted a series of investigations to understand the nature and impact of the sensory problems experienced by people with ME/CFS, and to determine whether they are associated with any functional or electrical changes in the brain.
The team aims to recruit 40 patients with ME/CFS and 40 healthy control subjects, and will begin their investigations by using a self-report questionnaire to assess patterns of sensory processing and how they affect functional performance.
The participants will then complete a series of neuropsychological tests (see below) to investigate a range of cognitive processes, followed by some simple computer-based tasks, while the electrical activity of the brain is measured non-invasively using electroencephalography.
The investigators’ hope is that the results of this preliminary work will help in our understanding of the brain mechanisms that underlie the abnormal sensory experiences of people with ME/CFS, and also lead to the development of interventions to help manage these problems.
Motor Screening Task – Participants are introduced to the format of the tests and responding via a touchscreen, and are asked to select on-screen crosses as they appear. Measures speed of response and accuracy, and tests for sensorimotor deficits or lack of comprehension.
Rapid Visual Information Processing – Assesses how well someone can keep attention on a task, in this case pressing an on-screen button when they see a predefined sequence of numbers (e.g. 2-4-6) within a random stream of numbers. Measures speed of responses and number of false alarms.
Delayed Matching to Sample – Assesses visual recognition and short-term visual memory by asking participants to match a pattern to one of four options shown below it. Measures speed of responses and number of correct patterns selected.
Stop Signal Task – Assesses how well someone can control their impulses. Participants are presented with an arrow and asked to press an on-screen button corresponding to whether it points left or right, but they must not respond if they also hear a beep. Measures reaction time and number of errors.
Two new videos about the PACE Trial
The PACE trial – Part 1: Moving the goalposts
The PACE trial – Part 2: Harm
Apparently there are more videos in the pipeline – you can look out for them on the YouTube playlist by clicking here.
The IDO Metabolic Trap
From the Open Medicine Foundation website –
By Christopher Armstrong, PhD
Dr. Robert Phair has recently published a paper detailing his “metabolic trap” hypothesis underlying ME/CFS, a theory that combines engineering and physiology put together by a man adept in both fields. Dr. Phair is co-founder and Chief Science Officer of Integrative Bioinformatics, Inc, a small company built around a unique software capable of modeling human biochemistry and theories of disease. Development of this theory was funded by Open Medicine Foundation (OMF). The paper, published in the open access journal, Diagnostics, is co-authored by Alex Kashi and Dr. Ron Davis, OMF Scientific Advisory Board Director and Director of the Stanford Genome Technology Center (SGTC).
Interestingly, understanding the theory of the “metabolic trap” opens the eyes to some unique elements of ME/CFS.
Like most chronic diseases, ME/CFS can be triggered by various factors and can run in families indicating a genetic element. Unlike other chronic diseases, ME/CFS can occur in outbreaks or epidemics. For outbreaks to exist, the genetic element of ME/CFS must be common enough for a large proportion of exposed people to get the disease. This thought process led Dr. Phair to look for damaging genetic mutations that were common in the broader population but present in 100% of ME/CFS patients. A search of public genome databases including the OMF-funded ME/CFS Severely ill Big Data Study led to IDO2. The IDO2 gene stood out because it has four common damaging mutations, and every ME/CFS patient in the Severely ill Big Data Study has at least one of them.
This story isn’t solely about IDO2 though, it’s also about its brother, IDO1. The IDO1 and IDO2 genes are named so similarly because they each encode for enzymes that transform an essential amino acid (tryptophan) into an important regulator of the immune system (kynurenine). The main difference is that when tryptophan is at high levels in a cell, the IDO2 enzyme increases its production of kynurenine while, surprisingly, the IDO1 enzyme decreases its production of kynurenine. If you have a problem with IDO2 (mutations in the gene) then you must rely solely on IDO1 to produce kynurenine from tryptophan. If for any reason the tryptophan levels in a cell rise too high, then IDO1 will stop making kynurenine and tryptophan levels will remain high. This is the IDO metabolic trap.
When we think of ME/CFS we often break the disease down into predisposing, triggering and maintaining factors. In this case, the predisposing factors are the damaging mutations in IDO2, the triggering factor is an elevation in tryptophan and the maintaining mechanism is that the IDO1 enzyme can’t convert tryptophan to kynurenine when tryptophan is high, therefore maintaining a high level of tryptophan and the low level of kynurenine in the cell. Mutations in IDO2 are common in the human population but it is unlikely that many would get ME/CFS. This is because the triggering is unlikely. Apparently, it is difficult to increase tryptophan enough to trigger the trap. That trigger likely requires an overlay of many factors, including pathogens, stressors and the environment.
This paper is avowedly theoretical; it elucidates the biochemical and mathematical foundations of the “IDO metabolic trap” as well as the experimental tests required to test the theory. Currently, these experimental tests are funded by OMF and ongoing at Stanford University in collaboration with Dr. Davis and his colleagues at the SGTC.
Read the full paper The IDO Metabolic Trap Hypothesis for the Etiology of ME/CFS.Back to top