FAQ’s

Q1:   What does ME stand for ?

A1:   Myalgic Encephalomyelitis.

ME

ME was recognised as a neurological disorder by the World Health Organisation (section G 93.3 of ICD10) in 1969.

Q2:   What causes it ?

A2:   ME is characterised by damage to the brain stem and nervous system.  Most researchers suggest this is likely to be caused by a virus or bacteria inducing antibodies that react against healthy cells, organs and tissues as if they were invaders, causing severe disruption to normal bodily functions.  This is known as an autoimmune disease.  For instance, rheumatoid arthritis occurs when immune antibodies attack the joints, leading to serious pain and swelling.

There are also research findings by Dr Naviaux that supports there being damage to the mitochondria, the tiny power plants present in every cell which provides energy for the immune system, nervous system, gut function and other major systems.  My view on reading various research papers is that while the initial infection or virus may be the cause of the ME, it’s the damage done by that to the mitochondria and to the nervous system that has the lasting effect, causing this chronic neurological illness to devastate lives.  Other research is looking at whether this virus or bacteria is introduced through the gut.

Q3:   What are the symptoms ?

A3:   Due to the nature of what the virus does in attacking the central nervous system, it can affect multiple areas of your body and how it functions.  Not all ME sufferers will have the same symptoms, making it difficult for the medical world to diagnose easily.

The main symptoms which will define it as ME are set down as follows:

Main Symptoms: (Not applicable to CFS)

  • Post Exertional Amplification of all Symptoms – a delayed reaction to exertion, both physical and mental is possibly the defining feature of ME.
  • Intractable fatigue of 6 months or more.
  • Unrefreshing sleep, pain, and memory issues.
  • Sensory issues.

ME severity is broken down into Mild, Moderate and Severe. Those with severe tend to be house or bed bound, needing a carer to help with their daily needs.  There are many, including children who have to feed through tubes due to the condition. Bright lights and noise, not necessarily loud, can be painful and debilitating to the individual.  Mobility can be a major issue.  With ME affecting the nervous system, it can have a big impact on memory, and following conversations.  Trying to process the words being heard can be very difficult and can be very draining. As your bodily systems no longer work properly, you can feel extreme cold on a warm day, or very hot on a cold one.

Pain is a major issue, from constant dull pain, sharp pains all over, muscle pain when moving, or doing nothing, as well as major head pain.  An example I can give is when I try to read a book, which is difficult, concentrating hard to take something in can cause me severe pain in my legs.  Strange I know, but true.

Sleep is affected in many ways in that some need to sleep most hours of the day, whilst others can’t sleep, or at least don’t get the level of restorative sleep required. Sleep tends not to refresh.

 

The Chief Medical Officer’s Report on the subject of CFS/ME (Chronic Fatigue Syndrome/Myalgic Encephalomyelitis) issued in January 2002 recognises that “CFS/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.

 

Q4:   So what is Chronic Fatigue Syndrome / CFS ?  Is it not the same thing as ME, just under a different name ?

A4:   Chronic Fatigue is a symptom of ME, as it is of other illnesses.  The name and case definition of CFS was created in the United States in the 1980’s by a board of 18 members sent to investigate on outbreak of ME.  None of them either looked at, or examined any patients with the illness party to the outbreak.

The reasons for this are quite in depth and political, and maybe best left to one side for now, but some claim that if the illness was diagnosed as chronic or ongoing fatigue, it would be easier for US insurance companies to deny claims based on just ‘tiredness’.

Q5:   What are the symptoms of CFS ?

A5:   CFS is characterised by chronic and debilitating fatigue, maybe caused by such as a Thyroid issue, but not fatigue that is brought on by the type of symptoms applicable to ME such as sensory issues.

Q6:   Can you explain the nature of the Fatigue felt ?

A6:   It is not fatigue in the way you might be shattered after a hard days work, or returning from a run.  Think it more as your body closing down.  Everything feels very heavy, and usually very sore.  Your legs refuse to operate and your brain processes slow up as if in a vat of mud.  Simple words don’t come to you, and if they do, it’s difficult to get them spoken as your speech slurs and your jaw seizes up in trying to get the words out.  You can’t understand what’s being said to you as words mean nothing.  The fatigue can be brought on by many things.  It could be light, background noise and sounds, unexpected sounds however quiet can shock your system and physically hurt and drain your energy levels.  Recent research suggests ME is similar to the body going into hibernation with major elements closing down.

Q7:   How many are affected by ME ?

A7:   Current figures given are:   250,000 in the UK.  (The University of Bristol research in 2011 estimated the number of 11 to 16 year olds with ME at one in 100). Overall there are between 1 and 2 million in the USA, 408,000 in Canada according to self-reported data from Statistics Canada’s 2014 Canadian Community Health Survey,( But according to a Canadian federal review, their condition is all in their minds).  Sweden:  40,000 and approx. 17 million worldwide.  This figure is given by NHS Choices, who interestingly also give the following UK figures: Parkinson’s Disease: 127,000.  MS:  100,000.  Both terrible illnesses, but much more in the public consciousness than ME.

Australia:

Myalgic Encephalomyelitis is estimated to affect between 0.4% and 1% of the population, according to the International Consensus Criteria primer for medical practitioners, endorsed by Australian patient organisations. In Australia, that is between 96,700 and 241,800 people (ABS population figures). Of those, 25% are so severely affected that they cannot leave their homes or even their bed.

Between 24,000 – 60,000 Australians have severe ME.  

Research shows that 4 in every 1,000 in any population suffer from ME, with a quarter of that number being severe and likely bed bound.  By the population of York, that equates to 800 people in York suffering with ME, 200 being severe.

Q8:   Is there a cure ?

A8:   There is no cure.  NICE Guidelines, and therefore the UK Government recommend Cognitive Behaviour Therapy (CBT) and Graded Exercise Therapy (GET).

Graded Exercise has been proved to be harmful to those with ME.

Modern research show abnormalities in ME patients’ energy production systems including research demonstrating that cellular metabolism is dramatically slowed. This indicates that ME patients cannot generate the resources to exercise as MAGENTA and other graded exercise studies recommend. Telling a child with an energy metabolism disorder that if she is more active, she will gain the ability to do so without damage is like telling a diabetic that if she consumes more and more sugar, she will be able to eat cake.  It is like advising someone on the verge of bankruptcy that their problems will be solved if they spend more and more money at a time.

I will add information on the debunked PACE Trial in due course, but in the meantime plenty can be found in various articles on the main page of the site by selecting ‘PACE’ in the Tags box on the right side column.

Q9:   What funding is there for research into ME ?

A9:   UK Government funding into biomedical Research for ME has totalled £1.6m in the last 30 years.  Have a look at our ME Info Videos to see the full story.  This is why the main research is being funded by the likes of Invest in ME, a charity run by ME sufferers who raise funds through family support for the research.  In the US, where they have an estimated figure of between 1 to 2.5 million sufferers, NIH funding is around 5-7 $million.  The US figure for MS suffers is 400,000 people, and MS gets $100 million of the $30 billion NIH budget.  More government funding in the US is given to research into male pattern baldness than towards research into ME. (One report says by 6 times).  We need to get more ‘non-ME’ people involved in fund raising for research as it’s difficult for people with the illness to do what’s required.

A View From The US:

in fiscal year 2015, NIH spent $6,470,000 on ME/CFS grants, an increase of 20% over fiscal year 2014. But even this level of increase is too small to get us to our appropriate funding level any time soon.

ME/CFS is among the 52% of disease categories that saw an increase in spending. We even received more funding than hay fever for the first time since at least 2012. It’s not all good news, though. We were still 249th out of 265, compared to 231st of 244 categories last year. Fibromyalgia (whose funding fell) received 27% more than ME/CFS. Lyme disease research received almost 4 times more, multiple sclerosis received 14.5 times more, and burden of illness research received 12.5 times more than ME/CFS.

What Does It Mean?

A 20% increase is good news. But this does not mean all our problems are solved, by any stretch of the imagination.

This degree of funding increase is highly unusual. Of the 138 categories that received an increase in funding, only 26 categories (19%) saw an increase that was the same or bigger than ME/CFS.

Furthermore, even if a 20% increase could be sustained year after year (something that would also be extremely unusual), it would take ME/CFS a very very long time to reach the level of funding we know is needed now. Even at 20% per year, ME/CFS would not break the $10 million barrier until 2019. It would take until 2023 to break $20 million, and it would be 2032 before we broke $100 million per year.

I don’t know about you, but I can’t wait sixteen years to see ME/CFS receiving the same funding level that multiple sclerosis receives right now. The bottom line is that NIH is going to have to do a lot more than say that they are serious about focusing on ME/CFS. NIH has to prove it. Now.

In Australia, the figure given by ME Australia is $120,000 per year being given to ME Research.  This equates to just 40 cents per sufferer per year.  The majority of that fund in recent years is accounted as being given to a CBT/GET Researcher.  There are lots of articles on this site about CBT, GET as treatments for ME.  You may wish to look into the ‘PACE Trial’ to get the full picture.

 

Q10.  OK, ME is debilitating, but it isn’t fatal is it ?

A10.  Just through my minimal connections, I’m aware of 15 deaths from ME from Jan – Aug 2016.  These include cancer patients who couldn’t undergo normal cancer treatment due to the ME, organ failures and suicides as a direct consequence of ME.

A study by Dr Leonard Jason of Chicago found:

McManimen, S. L., Devendorf, A. R., Brown, A. A., Moore, B. C., Moore, J. H., & Jason, L. A. (2016) Mortality in patients with Myalgic Encephalomyelitis and Chronic Fatigue Syndrome. Fatigue: Biomedicine, Health & Behavior. Published online Oct. 12, 2016 doi: 10.1080/21641846.2016.1236588

ABSTRACT
Background: There is a dearth of research examining mortality in
individuals with myalgic encephalomyelitis (ME) and chronic
fatigue syndrome (CFS). Some studies suggest there is an elevated
risk of suicide and earlier mortality compared to national norms.
However, findings are inconsistent.
Objective: This study sought to determine if patients are reportedly
dying earlier than the overall population from the same cause.
Methods: Family, friends, and caregivers of deceased patients were
recruited. This study analyzed data including cause and age of death for 56 individuals.
Results: The findings suggest patients in this sample are at a
significantly increased risk of earlier all-cause (M = 55.9 years) and
cardiovascular-related (M = 58.8 years) mortality, and they had a
directionally lower age of death for suicide (M = 41.3 years) and
cancer (M = 66.3 years) compared to the overall U.S. population
[M = 73.5 (all-cause), 77.7 (cardiovascular), 47.4 (suicide), and 71.1
(cancer) years of age].
Conclusions: Results suggest there is an increase in risk for earlier
mortality in patients. Due to sample size and over-representation
of severely ill patients, the findings should be replicated to
determine if the directional differences for suicide and cancer
mortality are significantly different from the overall population.

 

Q11.  What research is currently happening ?

A11.  The following is in a constant process of being updated as worldwide changes are ongoing and therefore may seem a little ‘untidy’ at times !  All research articles published on the site can be found via our index of ‘Posts by Topics’, on the right hand column of the front page of the site.

CANADA

In March 2006, the Canadian Institute of Health Research (CIHR) agreed and asked scientists to submit proposals for up to $600,000 in funding to study ME/CFS. It then used an independent panel of experts in the field to evaluate the submitted applications.

A team of Canadian ME/CFS specialists submitted a proposal for that grant, with the aim of creating a research network, establishing standards of care for CFS patients, and educating doctors and other clinicians.

But their proposal – the only one from CFS researchers — was rejected. The reason? The reviewers felt “there is no evidence that Chronic Fatigue Syndrome is a disease.” It also said there was evidence that “psychosocial factors” are “both a cause and perpetuating factor for CFS.”

In other words, ME/CFS is likely all in sufferers’ heads.

AUSTRALIA

September 2016:

Gene differences found in severe Myalgic Encephalomyelitis patients

Queensland scientists looked at blood samples from patients with moderate and severe Myalgic Encephalomyelitis (International Consensus Criteria). In the severe ME patients, they found 37 genes were significantly upregulated and 55 genes were significantly downregulated compared with nonfatigued controls. However, there was no difference in expression of protein kinase genes between moderate ME patients and controls.

“This current paper reports novel results of far reaching importance for CFS/ME diagnosis and possible pathology. The paper describes world first discoveries of kinase gene dysregulation associated with changes in calcium ion function. This research leads from previous significant papers we have recently published involving research into calcium ion channels in CFS/ME,” the scientists said on their Facebook page.

The paper by Chack, Staines, Johnston and Marshall-Gradisnik, Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients, was published in Gene Regulation and Systems Biology, July 2016.  (The authors refer to CFS/ME in the paper but the criteria they use, ICC, “recommends that only the name ‘myalgic encephalomyelitis’ be used to identify patients meeting the ICC because a distinctive disease entity should have one name. Those who fulfill the criteria have ME; those who do not would remain in the more encompassing CFS classification.”)

Natural killer (NK) cell dysfunction, in particular reduced NK cytotoxic activity, is a consistent finding in patients with ME, say the scientists from the National Centre for Neuroimmunology and Emerging Diseases and Menzies Health Institute at Griffith University, Australia

The rest of this story is available in a post on the our site.

August 2016: 

USA

“The publication, “Metabolic Features of Chronic Fatigue Syndrome” by Naviaux RK, et al. is a landmark in ME/CFS research. It is the most important and groundbreaking study of ME/CFS to date.
Extending recent indications of metabolic alterations in ME/CFS, this study provides the first comprehensive, quantitative demonstration of the metabolomic deficiencies that characterize the disease. They define a clear metabolic ‘signature’ that accurately distinguishes patients from healthy individuals.
This signature was consistent even among patients with different symptoms or disease-initiating events. These findings are exciting news for both patients and researchers. Not only do they substantiate the biological reality of this stigmatized disease, but they also point to the most promising ME/CFS biomarker candidate the field has seen. An ME/CFS biomarker – long awaited by scientists – would allow the precise and objective diagnostics that have never been possible for this disease. In addition, it would accelerate the search for treatments.
Dr. Naviaux’s study suggests that both of these endeavours could be designed in a way that will benefit all patients, regardless of their symptoms and initiating events (which are not always known).
In addition to a common metabolomic response, patients show a variety of individual responses. These individual responses may contribute to the symptomatic differences, and may be caused in part by genetic differences. Similarly, effectively treating ME/CFS might require two components: a common treatment for all patients and a personalized treatment. Interestingly, this might explain the plethora of treatments that have helped individual patients but only rarely work on other patients.
Another important finding from this study is that the metabolomic response observed in ME/CFS is opposite to the pattern seen in acute infection and metabolic syndrome. This result supports the controversial idea that while infection is often the initiating event for ME/CFS, it does not contribute to the ongoing illness. What is important to note is that in the absence of evidence of an active infection, it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good.
This breakthrough study thus presents several new findings of great importance to the ME/CFS patient, medical, and research communities – and perhaps most importantly, to the search for treatments. For these findings to have an impact on patient care, further investigation and validation via independent studies are crucial. Because of this, the Open Medicine Foundation has funded the next study of a larger patient cohort, in which Dr. Naviaux will validate the ME/CFS metabolomic signature in a larger, geographically diverse sample, and I will explore the role of genetics in the individual responses. These studies are already underway. We appointed Dr. Naviaux to the Scientific Advisory Board of OMF earlier this year, and we are grateful for his expertise in helping to unravel the metabolic mysteries of this debilitating disease.
We are finally on the right path to understanding ME/CFS. We and many of our collaborators are working hard to translate this new understanding into general and personalized treatments. ”

USA

A team from Cornell University reports finding biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In 2014, a study from Stanford University found abnormalities in the white matter of patients with ME/CFS, while research published the following year by Columbia University researchers showed distinct differences in the immune systems of people with the disease, compared to healthy controls.

 

OTHER AREAS OF ON-GOING RESEARCH

Mitochondrial – Damage to the energy producing part of body cells.

 

NORWAY

Rituximab – Use of this cancer drug has had some success in Norway.

Dr Fluge and Professor Mella’s work is bringing hope to millions of ME/CFS sufferers, worldwide. Their research into the use of rituximab to treat ME/CFS is considered a real breakthrough after the success of an earlier trial, and they are currently undertaking a large phase III trial of rituximab on 152 ME patients running over over three years.

Mella and Fluge believe that ME/CFS is a form of autoimmune illness where the body comes under attack from its own defence system.

Norwegian researchers have commenced phase II trials of the anti-cancer drug cyclophosphamide on ME/CFS patients.

Led by senior consultant Dr Øystein Fluge and Prof Olav Mella, the team is focusing on non-responders and those patients who have relapsed after treatment with rituximab, a B-cell depleting drug.

Forty patients with moderate to serious myalgic encephalomyelitis (ME) (sometimes referred to as me/cfs or chronic fatigue syndrome) are taking part in the cyclophosphamide trial, which began in March this year and is scheduled for completion by September 2016.

Twenty-five participants have not received previous treatment with rituximab, are either rituximab non-responders, or have relapsed following rituximab treatment.

Exercise / Heart – evidence to show that a body affected by ME can be damaged further by even minimal exercise….update to follow.

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