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Dr Charles Shepherd, Hon. Medical Adviser, ME Association.

At present there is no diagnostic blood test for ME/CFS – but testing your blood is essential to rule out other illnesses that can cause similar symptoms.

Dr Shepherd talks about what blood comprises, the kind of tests employed by researchers, what clinical tests should be taken to rule out misdiagnosis and what those tests can reveal.

This latest medical information leaflet has been made available in full to members of the ME Association in the Summer (July) issue of ME Essential magazine.

It can be also now be downloaded from the website shop, or ordered by phone to head office, or via order form:

Extract…

Introduction: What does a blood test measure?

Human blood contains red cells, white cells, platelets and plasma:

  • Red blood cells carry oxygen around the body – so a deficiency or abnormality here will probably cause anaemia.
  • White blood cells help the body to fight off infections and respond to allergies. White cells are sub-divided into cells called basophils, eosinophils, lymphocytes and neutrophils. Each cell has a slightly different function and an increase in a specific cell type can indicate than an allergic or infective reaction is taking place.
  • Platelets help to form blood clots and prevent bleeding. So, a platelet deficiency can cause excessive or prolonged bleeding from a wound site.
  • Plasma is the fluid component that contains a wide variety of substances produced by the immune system (e.g. antibodies, cytokines, natural killer cells) as well as enzymes, hormones and proteins that are made by or excreted by various organs and tissues in the body. The plasma also contains all the other chemicals and substances – vitamins, minerals, sugars and fats – that are carried around the body.

The use of new investigative technologies means that scientists can now also look at specific proteins (proteomics), metabolites – the remains of chemical reactions that have taken place (metabolomics) – and genetic factors that may predispose people to developing specific diseases (genomics).

These tests are increasingly being employed by researchers who are looking for the cause of ME/CFS. They are also being used to try and find diagnostic blood markers (biomarkers), or markers for sub-groups, such as people with severe ME/CFS.

Laboratory analysis of a small sample of blood can, therefore, reveal a great deal of basic information about your state of health and the function of various organ systems.

Is there a diagnostic blood test for ME/CFS?

While minor blood test abnormalities can occur in ME/CFS, none of them are sufficiently consistent or robust enough to turn them into diagnostic markers in our current state of knowledge.

So, the simple answer here is ‘no’ and a diagnostic ‘ME blood test’ seems unlikely to be made available in the near future.

The search for a diagnostic biomarker for ME/CFS

Significant progress is however being made in the search for potential diagnostic biomarkers and a number of research groups have been reporting some interesting preliminary findings.

The UK ME/CFS Biobank (which is funded by the MEA Ramsay Research Fund) has found that some people with severe ME/CFS have a lower than normal level of a muscle enzyme called creatine kinase.

They have also published results from a big study on the immunology of ME/CFS that was funded by the National Institutes of Health in America. This study found that some people with ME/CFS have an increased proportion of an immune system component called MAIT cells (mucosal associated invariant T cells).

This is an interesting abnormality that is being linked to neurological and autoimmune conditions such as multiple sclerosis and inflammatory bowel disease, where these cells appear at sites of inflammation in the nervous system and gut lining.

The Stanford research group in America have reported on changes in the shape of red blood cells and more recently observed that when a specific type of immune cell is stressed to increase its energy requirements it reacts in a different way to immune cells from healthy controls.

Before drawing any firm conclusions about these findings, they need to be repeated in larger numbers of people with ME/CFS, and by other independent research groups, and compared to findings in people with autoimmune, infective and neurological conditions, as well as people with unexplained chronic fatigue.

Summaries and reviews of all these recent research studies can be found in the Research section of the MEA website.

Which blood tests should be checked before a diagnosis of ME/CFS is confirmed?

Everyone should have a number of routine blood tests before a diagnosis of ME/CFS is confirmed. The results of all of these tests should be within normal limits. So, the main purpose of arranging all these blood tests is to help the doctor to rule out medical conditions that can also produce fatigue and other ME/CFS-like symptoms.

Continues with a list of appropriate blood tests to aid diagnosis, blood tests for children, when to repeat blood tests, and a detailed explanation of what each blood test means.

Images sources: 123RF/AlexanderRaths/SergiyLukutin

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Charlotte Stephens, Research Correspondent, ME Association.

Introduction

For many years, a leading theory of causation in ME/CFS has been problems with the mitochondria (the part of the cell responsible for generating energy).

However, researchers are now suggesting that this is less likely and that we should be looking for something that is impacting the mitochondria’s ability to function properly – rather than at the mitochondria themselves.

In light of this, we have created an overview of mitochondrial research to date; explaining what mitochondria are, exploring the possibility of mitochondrial dysfunction as the cause of ME/CFS and offering other possible explanations if the mitochondria are not to blame.

Key Points

  • Mitochondria are the part of the cell responsible for producing most of the body’s energy.
  • Problems with energy production have been found in ME/CFS and have been primarily linked to mitochondrial dysfunction.
  • No ‘faulty genes’ or mutations have been discovered in the mitochondria of people with ME/CFS, suggesting it is not a form of classic mitochondrial disease.
  • There is conflicting research on the role of mitochondrial function in ME/CFS; some studies have found increased mitochondrial activity, some have found reduced activity, and some have found no differences between ME/CFS and healthy controls.
  • Recent research is now indicating that there is a problem with something ‘upstream’ of the mitochondria that is impacting their ability to function i.e. it is not a problem with the mitochondria themselves.
  • More research is needed on larger cohorts to identify this upstream factor, but there are already a few theories (and these are discussed in this review).

What are Mitochondria?

Source: Wikipedia

Mitochondria are small structures inside our cells that generate energy and are often referred to as ‘the powerhouse of the cell’.

They are responsible for converting chemical energy from food into a form that’s readily available for use by the cell, called ATP (adenosine triphosphate).

These energy-rich ATP molecules are the fuel for all of the different functions of the body. Mitochondria allow the cell to produce up to 15x more ATP then they would without them (Davidson, 2015).

Mitochondria are found in every cell in the body, except red blood cells, and there can be up to 2000 mitochondria per cell! There are more of them in parts of the body that use a lot of energy, such as the brain, the heart, the muscles and the liver.

But producing energy is not all these ‘powerhouses’ do; they are also involved in a range of other processes, such as cellular defence mechanisms, immune response signalling, cell signalling, cell growth and cell death (McBride et al., 2006).

Production of ATP

ATP (fuel for the cell) is made through the process of ‘cellular respiration’. This is a series of chemical reactions that combines glucose from food with oxygen to make energy.

Water and carbon dioxide are also produced as waste products of this reaction. Special proteins called enzymes are needed to carry out the chemical reactions involved.

Simplified diagram of the reaction that takes place during cellular respiration.

Types of energy production

Although mitochondria are responsible for around 90% of the cell’s energy production, there are other methods of energy production that the cell can use that don’t require mitochondria.

However, these are a lot less efficient processes that either use a limited fuel supply, produce harmful by-products or are a lot slower.

There are 4 main types of energy production. The first two use glucose as the ‘fuel’ source, whereas the second two use fat and protein:

  1. Aerobic (requires oxygen). The classic form of respiration that the mitochondria adopt, as described above. It is the main form of energy production the body uses to carry out basic functions and low-intensity activities. On average, 36 molecules of ATP (energy molecules) are produced from 1 molecule of glucose.
  2. Anaerobic (doesn’t require oxygen). This is what the body switches to during vigorous activity, where your oxygen supply can’t keep up with the energy demand. This reaction produces lactic acid as a by-product, which is harmful and causes muscle fatigue and aching. Only 2 molecules of ATP are produced from 1 molecule of glucose.
  3. Gluconeogenesis (or fat burning!). This is the slowest form of energy production and can’t be used to supply energy for exercise. The body uses this when glucose is not available and fatty acids become the source of fuel. 1 small fatty acid chain can be used to produce 48 ATP molecules! 
  4. ATP Phosphocreatine (Protein breakdown). This is the quickest, most immediate source of energy, used for short quick bursts, such as sprinting. Lots of ATP are produced from a component of muscle called ‘Creatine phosphate’, until the stores of it run out. This is not a good form of energy to be using often as it breaks down muscle.

Click here to download and read the complete research summary

Please visit our Research section for a complete listing of all the Summaries we have available.

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Russell Fleming, Content Manager, ME Association.

In 1999 I was working and living in Jersey and had been on the island for about two years following a transfer from the UK. I was in my element and twelve years into a career. My role in Jersey was still new and exciting, and any periods of stress were short-lived and resolved without problem.

My health was good, I was exercising regularly, working hard, socialising perhaps too much, and surrounded by people I liked.

We all lived together in a former hotel that my employers had bought and turned into a kind of hostel that housed people around my own age – I was thirty.

Some friends were taking a short break in Greece to relax and play beach volleyball (something we did fairly regularly in Jersey). One of their number dropped out unexpectedly and I took his place.

Diagnosis

Unfortunately for me, during the course of the holiday I picked up a nasty infection, but we all expected it would clear-up quickly once I was back home. The infection did pass but not for some time – time I felt I could not afford – and the symptoms I was experiencing never seemed to resolve.

I tried several times to return to work but each time I struggled and was sent home. Remember, I was surrounded by people who also worked, so being at home and off sick became quite stressful and in ways I had not experienced before.

As the symptoms continued to wear me down and my health deteriorated, I was diagnosed first with PVFS and then M.E. These followed extensive testing, more worry – particularly I recall when a brain tumour was suspected – more waiting… and the only advice from doctors and consultants was to, rest, rest, rest.

Extended Convalescence

I know that for some people with M.E., hearing this advice would be welcome news indeed. How many doctors do we hear about who advise, exercise, exercise, exercise?

But for me and at that time, hearing that repeated advice to rest was more stressful than almost anything else. I was not the sort of person to give up and resting seemed a form of surrender.

Surely there were drugs I could be taking or something other than convalescing? Resting seemed to make not a jot of difference although trying to do more was counterproductive as well. I remember that being asked how I was feeling became a question that I would dread.

There was something particularly difficult about having a medical condition that sapped my vitality. And not knowing what might be causing the symptoms of M.E. further undermined my confidence.

Don’t ask how I feel

I even stopped my parents from asking how I was feeling because the answer was always the same – unless I pretended it wasn’t which was something I often did just to sound positive.

As the stress and uncertainty built, my mental health began to spiral. I had a career to get back to and while Lloyds Private Banking were nothing if not supportive, it was harrowing to keep reporting no positive progress.

In the end my physical and mental health became too much and I couldn’t look after myself. I returned home to Cornwall and my parents.

There is something special about having familial support and understanding. It’s good, don’t get me wrong and I couldn’t have survived without it. But I’d been independent since I was seventeen, and at the time I returned, I saw this as further evidence that I was weak and a failure.

Professional Help

My parents could see how much the combination of M.E. symptoms and mental health problems were crippling me, and we decided that if we couldn’t do very much about the former, we would try to work on improving the latter.

In 2000 getting a referral to a mental health specialist on the NHS was next to impossible. I remember Mum having to pull out all the stops to get me in to see someone.

At the time we knew I was suffering from depression, but we also thought I might be bipolar. My emotions were yo-yoing – one moment I was too positive and the next too negative and suicidal (it transpired that I wasn’t bipolar).

Never for a moment did I consider that speaking to a mental health professional would be unmanly or contribute to my feelings of failure. Things had become so desperate, I needed help and support from someone who knew what they were doing and could relieve some of the pressure from me and from my parents.

While the professionals I saw initially and again some months later, did help me through immediate crises, they didn’t instil in me the ability or confidence to cope with a long-term neurological condition or help me deal with acceptance and with the grieving process.

It was almost a year later, and I’d managed to return to work in the UK. It was tough-going – I had a day-bed set-up in the office, car service to my hotel, and set my own hours – but I thought I had achieved a semblance of control and had learned how to manage M.E. and my mental health.

At the end of nine months and the successful conclusion of the project, I was offered a posting anywhere I wanted. I chose to return to Jersey so that I might vanquish the ghosts of my past. It was to prove a bad decision.

The nine-month project was too much. I was kidding myself that I was coping. And this only became apparent when I got back to Jersey and started a new nine-to-five job. My M.E. came on with a vengeance and was soon followed by worsening mental health.

I think some of my problems in general related to embarrassment and in the grip of depression I would imagine that people had very negative impressions of me and of M.E. I always said that if I could have chosen any medical condition, then M.E. would be my very last choice. It was incredibly hard to explain at the time, and it came with a terrible stigma attached.

The occasional stress I experienced at work before I become ill, was nothing compared to the stress I felt living with M.E.

Getting the right tools

In Jersey while trying to hold down my job once again, I was put in touch with a private counsellor. He happened to also be an actor who had co-starred in a famous and long-running Jersey-based detective show on TV – and he had M.E. Although I didn’t know that before I met him.

He was able to provide me with tools necessary to self-manage my mental health but more importantly for me, he provided a safe space where I could offload, and we could begin to work through my issues and concerns.

He was also blunt and honest. And I needed blunt and honest. His own experiences trying to work and manage M.E. were useful, although he was more hippy-dippy than I cared to be, and he helped me to express some of the mess that was constantly occupying my thoughts.

I coped better I think when I finally returned to the UK and my parents in 2002. I was offered, and I accepted, ill-health retirement from the Bank because of M.E. In fact, by then the end of my career brought with it a sense of relief and I felt better able to cope.

I have had good and bad experiences of mental health professionals just as I have GPs and specialist consultants. When things were really bleak in the early years, I remember having a blazing row with a psychiatrist who claimed that I can’t have been trying hard enough to get better. What a jerk he was!

I still had cause to call on the services of counsellors and a psychologist in later years. And I had a really positive experience from my local NHS ME/CFS specialist service here in Cornwall who provided help in terms of validation, acceptance and illness management.

We all I think need a break at times and whether you can attend in person, by phone or Skype, talking to a professional who is removed from your immediate support network, can bring relief – even if it is just a way to get things off your chest.

It is often a slow process and one you need to keep chipping away at. It’s not a cure for your problems – rather good therapy I think equips you with the right tools to cope better. I learned that I needed to give myself permission to feel sad on occasion and that it was OK to do so. That living with M.E. was difficult, that I did need to adjust but that my life wasn’t over because of it.

It can take some time and effort to find the right counsellor or therapist. Rather like the huge range of antidepressants that your GP might choose from, choosing a therapist can also be rather hit-and-miss. But you have to stick with it until you find the right one for you and at the right dose.

Learning to cope

I have struggled with acceptance of my new life away from the Bank. I struggled accepting disability. I struggled accepting the loss of earnings and with budgeting. And I struggled with the loss of my fiancé and the realisation that I am likely to live alone without any children of my own. But most of all I really struggled finding positivity in my life with M.E.

When anxiety and nerves keep coming at you. When negative thoughts are whirring in your head and preventing sleep. When life seems pointless. When you are constantly battling fear. When you feel you are letting everyone down. When you are still trying to do too much. When you still want to please everyone. When you simply cannot cope. Then I think it’s time to consider reaching out to a professional for help.

I can’t say my mental health problems don’t return whenever something freaks me out – it can be relatively minor like a phone call, or major like a PIP reassessment or a bad-patch of M.E.

But I am better able to cope and have come to accept my life as a disabled person.

I also know that any periods of acute stress, uncertainty or anxiety will pass – even if they don’t seem like it at the time.

I no longer feel worthless or unable to contribute even if the things I can do might seem small or sporadic. And I know I can re-refer to a counsellor or psychologist if I have the need to talk outside of my immediate support network.

My name is Russell, I am now fifty years old, I have occasional mental health issues and I have M.E.

Additional support from the ME Association

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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The ME Association is indebted to our Welfare Rights Adviser, Ann Innes, for the text of this new 35-page Guide to Employment and Support Allowance.

It can be purchased from the website shop, by phone to head office, or by order form, and will be sent to you in the post:

Extracts…

Introduction

This three-part guide is intended for those making both new claims for ESA or for Universal Credit based on health grounds. People making a renewal claim will also find it helpful.

The rules governing benefits are complex and ever-changing. This guide does not pretend to provide a full list of all them. It’s a general overview only. It is always sensible to seek detailed advice from a welfare rights specialist.

There are three types of ESA: New Style ESA, contribution-based ESA and income-related ESA.

In order to claim any of these, you must be of working age (aged 16 or over but under state pension age) and have an illness or impairment that affects your ability to work.

Part 2: The Work Capability Assessment Questionnaire

The ESA50 / UC50 Questionnaire allows the DWP to score you on a variety of different physical and cognitive tasks to assess your degree of functional impairment and how it affects your ability to work or undertake work-related activity with a view to moving towards work.

These tasks are called descriptors. Each descriptor has a variety of scores, depending on your level of difficulty carrying out that descriptor. In order to pass the Work Capability Assessment at all, you must score at least 15 points across all the descriptors.

To qualify for the “limited capability for work related activity” you must score a full 15 points on any of the “limited capability for work related activity” descriptors, which we will list below.

General Advice on Completing the Questionnaire

  • Get help to complete the ESA50 / UC50 as this plays an important role in the assessment process. People often answer incorrectly unless they are aware of the assessment criteria, which this guide aims to shed some light on.
  • When completing the form, think about the questions in the context of a work setting – working 16 hours or more a week. Remember, the DWP are assessing your ability to carry out any type of work, not just your previous job. In such a context, you would be expected to carry out each descriptor regularly, reliably, repeatedly and safely, within a reasonable timescale, without significant discomfort and to an acceptable standard. It must also apply for either most of the time, or the majority of the occasions that someone attempts that descriptor.
  • Do not complete the form as though it is your worst day. Yes, you do need to focus on what you can’t do rather than what you can do, but explain the variability. The reason I say this is that I have seen clients over the years omit to talk about variability, so that when they either are at their face-to-face assessment or in front of a tribunal panel, they seem “fine” – they can communicate, walk to the assessment room, handle their papers, etc – yet when someone looks at the form it sounds as though they are permanently bedridden and can never communicate. The first thing someone assessing you will think is that you are not credible, or that you have exaggerated your condition.
  • Continues with further advice about completing the questionnaire and with examples of how to respond to the descriptors…

Part 3 – The Face-to-Face Assessment

Preparing for the assessment

  • Try to take someone with you and for someone to support you to get there and back. You will be asked at the assessment how you got there and assumptions will be made if you got there yourself. Don’t forget, you not only have to deal with getting to an assessment centre, but also a potential wait of an hour or more to be seen sat upright in a straight backed chair, possibly without arms, in a potentially busy and noisy assessment centre with strip lighting. You then have to get through the assessment itself, which can last up to an hour (although typically it is usually around half an hour). You then have the journey home.
  • Ask for your assessment to be recorded. This should be done on your claim form but again over the telephone as soon as you receive your appointment. Call the number on your appointment letter to check this is in place.
  • You can change your face-to-face assessment appointment once only. If your request for a home visit is denied, back it up with medical evidence and ask for your request to be looked at again. An experienced welfare rights adviser may be able to assist you in changing the decision.
  • Continues with further advice about what to do in preparation and while at the assessment…

Help with benefits and social care

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Pippa Stacey, Social Media Manager, ME Association.

In the run-up to Severe M.E. Day (8th August), we’re looking for people with Severe M.E. who would like to tell their stories.

We want to talk about the key issues that affect arguably the most neglected section of our community, and plan on raising awareness throughout the week commencing Monday, 5th August.

We’re particularly interested in hearing from people with Severe M.E. and their experiences of the UK benefits system, which might include any problems encountered while trying to obtain the help they deserve.

We’re also keen to share stories of how benefit awards have positively influenced people’s lives or helped them to better manage their condition, to show how much of a lifeline these payments can be.

If you or your carer would like to be involved, you must be comfortable sharing your identity and photographs in either the news-media (newspapers) and on the ME Association website and social media platforms.

If interested, please get in touch by Wednesday 24th July, and provide the following information:

  • Your name, age, where you live, and confirm that you have or have had Severe M.E.
  • A short summary of your story and experiences: in no more than 200 words. 
  • Attach good quality photographs of yourself that you feel best represents your current circumstances. 
  • Title your email ‘Severe ME Campaign’ and send to: feedback@meassociation.org.uk

Even if your story is not selected as a case study for the press, we hope to be able to share it on our website and social media, in a similar way to the successful Real M.E. campaign and reach beyond our immediate community.

Your feedback about welfare benefits will also be used to help inform continuing discussions with the DWP and Minister of State for Disabled People, Health and Work and the future meetings with Atos, Maximus and Capita that we hope will constructively influence the assessment process. 

Thank you in advance.

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Jen Taylor is very kindly raising money for the ME Association by selling her fabulous limited edition animal prints. Here she explains all about her M.E. and how she completes her art mainly from bed.

This lovely squirrel, striking a pose for my camera, is my favourite visitor to my garden, even though he’s only here to raid my bird feeders!  I see him through my window while I’m resting and sometimes it seems like I inspire him to have a rest himself as he has taken to falling asleep on the tree or curling up in the hanging basket.

I’ve had ME for 7 years following a sudden illness (Stevens-Johnson Syndrome).

It took over a year to get my official diagnosis and this was a worrying and lonely time, not understanding what was going wrong with my body and why I couldn’t recover.

When I finally got my diagnosis, the ME Association were there for me with information and support.

Now I want to both give something back to this charity and to support others with ME.

I don’t have any artistic training – it’s only since having ME and needing to give up work that I started getting into art.

So that’s one of the positive things that has come out of my illness. I sketch my designs in bed and then carve a little whenever I have the energy.

It’s really helped me to release some of the frustration of being stuck indoors for so much of my time.

Very Limited Editions

I want to raise money for the ME association by selling some of my lino-cut prints. I make original prints based on my own drawings and photos.  I’ve just a few prints as yet but I’m really excited to keep learning and printing.

Each of my prints is limited edition – VERY limited – there will be just 10 prints of each edition for this sale. 

Each of the prints I’m selling is hand carved and printed. Please understand due to the handmade nature – each print may look a little different from these images here.

This squirrel is priced at £25 (A4 printed on quality acid-free Fabriano paper). And I met this friendly Buffalo in Hoi An Vietnam, many years ago. 
His print (again taken from my photo) is just £15 (again A4 printed on quality acid-free Fabriano paper).

Fundraising manager, Helen Hyland, writes:

“For instructions on how to purchase one of these lovely images, please visit Jen’s JustGiving page – and remember to tick the box that allows her to contact you or she won’t receive your address.”  

“If you want to see more examples of her work, or to make further enquiries, please visit Jen’s Facebook page.”

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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The Journal of the American Medical Association (JAMA), published online July 5, 2019.

By Anthony L. Komaroff, MD, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts.

Viewpoint

When does an illness become a disease? When the underlying biological abnormalities that cause the symptoms and signs of the illness are clarified.

The illness now called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) was first described in the mid-1980s. At that time, nothing was known about its underlying biology.

Indeed, because many standard laboratory test results were normal, some clinicians explained to patients that “there is nothing wrong.”

There was, of course, an alternative explanation: the standard laboratory tests might not have been the right tests to identify the underlying abnormalities.

Over the past 35 years, thousands of studies from laboratories in many countries have documented underlying biological abnormalities involving many organ systems in patients with ME/CFS, compared with healthy controls: in short, there is something wrong. Moreover, most of the abnormalities are not detected by standard laboratory tests.

In 2015, the Institute of Medicine of the National Academy of Sciences concluded that ME/CFS “is a serious, chronic, complex systemic disease that often can profoundly affect the lives of patients,” affects up to an estimated 2.5 million people in the United States, and generates direct and indirect expenses of approximately $17 billion to $24 billion annually (1).

Over the past several years, the National Institutes of Health (NIH) has expanded its research efforts directed toward this disease. It has initiated an unusually comprehensive multisystem study at the NIH Clinical Center, funded 3 extramural ME/CFS research centers and 1 data coordinating center, awarded supplemental support to 7 existing grants, and held regular telebriefings on the illness (as has the Centers for Disease Control and Prevention) (2).

A 2-day conference at the NIH in April 2019 highlighted recent progress. New research was presented that both reinforced and expanded on previous reports. Equally important, several plausible models were proposed that could explain many of the abnormalities that have been described.

The Central and Autonomic Nervous System

Since the early 1990s, multiple studies have compared patients with ME/CFS with healthy age- and sex-matched controls and found abnormalities of the central and autonomic nervous system (3).

  • Neuroendocrine abnormalities were among the first evidence reported and involve impairment of several limbic-hypothalamic-pituitary axes (involving cortisol, prolactin, and growth hormone end products).
    A general downregulation of the hypothalamic-pituitary-adrenal axis is seen in patients with ME/CFS, in contrast to the upregulation of the hypothalamic-pituitary-adrenal axis seen in major depression.
  • Impaired cognition has been found by many investigators, including slowed information processing speed and impaired memory and attention that are not explained by concomitant psychiatric disorders.
  • Magnetic resonance imaging has revealed increased numbers of punctate areas of high signal in white matter. Functional magnetic resonance imaging has demonstrated different responses to auditory and visual challenges and to tests of working memory, as well as altered connectivity between different brain regions.
  • Positron emission tomography and magnetic resonance spectroscopy recently have demonstrated that patients with ME/CFS have a widespread state of neuroinflammation (particularly activation of microglial cells) as well as increased ratios of choline-creatinine and increased levels of lactate that correlate with levels of fatigue (4). Spinal fluid contains increased levels of proteins involved in tissue injury and repair.
  • Autonomic nervous system abnormalities have been repeatedly demonstrated in ME/CFS, particularly altered systemic and cerebral hemodynamics that correlate with symptoms (5). 
    At the NIH conference, it was reported that with prolonged upright posture, abnormal increases in heart rate and decreases in blood pressure are common; even when heart rate and blood pressure responses are normal, substantial cerebral blood flow reductions are noted.

Metabolic Changes

Recently, it has become possible to measure simultaneously thousands of metabolites in a sample of blood or other fluid. Several such metabolomic studies have revealed that in patients with ME/CFS, levels of many metabolites are lower than normal, as occurs in hibernation (6).

Cellular energy generation from all sources is impaired, including energy from oxygen, sugars, lipids, and amino acids. In other words, the human organism may feel that it lacks “energy” because its cells have a problem generating (and possibly using) energy.

In addition, many studies have reported markers of both oxidative stress and nitrosative stress (e.g. increased levels of inducible nitric oxide synthase).

Immunologic Changes

Many phenotypic and functional abnormalities have been reported in lymphocytes. The most consistently reported are increased numbers of activated cytotoxic CD8+ T cells and poorly functioning natural killer cells.

Blood levels of many cytokines are significantly higher in patients with ME/CFS, especially in the first 3 years of illness. Moreover, the levels of many of the circulating cytokines correlate positively with the severity of symptoms. Abnormal levels of several cytokines in spinal fluid also have been reported.

At the NIH conference, new HLA associations with both presence and severity of ME/CFS were reported. In addition, investigators performing single T-cell receptor sequencing reported expansion of CD8+ T-cell clones; characterization of the antigenic targets is under way.

Provocation Studies

In patients with ME/CFS, physical, postural (orthostatic), and cognitive challenges often produce a flare of symptoms, typically after a 12- to 48-hour delay, a condition called postexertional malaise.

Provocation studies seek to clarify whether challenges that make people with ME/CFS feel worse also make a biological abnormality worse. If so, it becomes more likely that the abnormality may be causally connected to the symptoms of the illness.

The NIH conference summarized evidence from multiple studies demonstrating that during exercise, the tissues of patients with ME/CFS have difficulty extracting oxygen, leading to a lower anaerobic threshold; with exercise, patients also have lower heart rate, blood pressure, and preload, several of which become much more prominent during a second exercise test repeated 24 hours after the first (7, 8).

Potential Unifying Models

What if ME/CFS reflects the activation of biologically ancient, evolutionarily conserved responses to injury or potential injury, a pathological inability to turn these responses off, or both?

Several presentations at the NIH conference, citing work in animal models, indicated that low-grade neuroinflammation triggers protective behavioral changes, including reduced activity and appetite and increased sleep; this helps to focus the available energy on preventing or healing the injury.

This stereotyped behavior change is likely triggered by a “fatigue nucleus” (a group of neurons); the nucleus is triggered, in turn, by the cytokines produced by neuroinflammation.

The neuroinflammation could have different triggers in different individuals. In some, it could be induced by brain infection (such as by chronic herpesvirus infection), autoantibodies, neurotoxins, or chronic stress.

In others, inflammation outside the brain may be activating the innate immune system inside the brain, both through humoral signals that breach a porous blood-brain barrier and by retrograde signals sent up the vagus nerve.

Several conference presentations included evidence that gut inflammation may be one peripheral trigger of neuroinflammation: the gut microbiota of patients with ME/CFS often include high numbers of proinflammatory species and low numbers of anti-inflammatory species.

The relatively hypometabolic state seen in patients with ME/CFS might also reflect a second and possibly related biologically ancient response to injury. Such hypometabolism is seen during the state of dauer (i.e. a developmental larval stage) in the worm Caenorhabditis elegans and during hibernation in more complex animals.

Dauer and hibernation allow animals that perceive a vital threat (such as crowding in worms or winter in bears) to throttle down nonessential, energy-consuming metabolic processes to preserve the energy needed for vital functions; i.e. the animal is temporarily sacrificing its ability to function in order to remain alive.

Signals that initiate (and end) dauer and hibernation are known; investigators are pursuing whether they have been activated (or not deactivated) in patients with ME/CFS.

Conclusions

A great deal more is known today than 35 years ago about the underlying biology of ME/CFS. It is clear that many biological measurements clearly distinguish patients with ME/CFS from healthy control individuals.

At the same time, some areas of ME/CFS research remain a challenge, and research has not yet given practicing physicians 2 important tools.

First, there are as yet no US Food and Drug Administration–approved treatments. Second, although various biological measurements distinguish patients with ME/CFS from healthy controls, none yet have demonstrated the high sensitivity and specificity required for a good diagnostic test.

However, 1 small study (20 cases and 20 controls) described at the NIH conference (and recently published (9)) reported perfect sensitivity; the specificity of the test in individuals with other fatiguing illnesses remains to be shown.

With growing international interest in the illness, and increased research support from the NIH, the day is coming when physicians will be able to explain to patients not only that there is something wrong but also that advances in understanding the pathophysiology have led to effective therapy.

Article Information

Corresponding Author: Anthony L. Komaroff, MD, Brigham and Women’s Hospital, 1620 Tremont St, Boston, MA 02120 (komaroff@hms.harvard.edu).

Published Online: July 5, 2019. doi: 10.1001/jama.2019.8312

Conflict of Interest Disclosures: Dr Komaroff reported receiving personal fees from Ono Pharma and Serimmune Inc and grants from the NIH.

Additional Contributions: Peter C. Rowe, MD, Department of Pediatrics, Johns Hopkins University, provided valuable comments for which he received no compensation.

References

1. Institute of Medicine. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness. Washington, DC: National Academies Press; 2015.

2. Koroshetz  W, Collins  F. Moving toward answers in ME/CFS. NIH Director’s Blog. March 21, 2017. https://directorsblog.nih.gov/2017/03/21/moving-toward-answers-in-mecfs/ Accessed June 22, 2019.

3. Komaroff  AL, Cho  TA.  Role of infection and neurologic dysfunction in chronic fatigue syndrome.  Semin Neurol. 2011;31(3):325-337. doi: 10.1055/s-0031-1287654

4. Mueller  C, Lin  JC, Sheriff  S, Maudsley  AA, Younger  JW.  Evidence of widespread metabolite abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy.  Brain Imaging Behav. 2019. doi: 10.1007/s11682-018-0029-4

5. van Campen  CLMC, Rowe  PC, Visser  FC.  Blood volume status in ME/CFS correlates with the presence or absence of orthostatic symptoms: preliminary results.  Front Pediatr. 2018;6:352. doi: 10.3389/fped.2018.00352

6. Naviaux  RK, Naviaux  JC, Li  K,  et al.  Metabolic features of chronic fatigue syndrome.  Proc Natl Acad Sci U S A. 2016;113(37):E5472-E5480. doi: 10.1073/pnas.1607571113

7. Stevens  S, Snell  C, Stevens  J, Keller  B, VanNess  JM.  Cardiopulmonary exercise test methodology for assessing exertion intolerance in myalgic encephalomyelitis/chronic fatigue syndrome.  Front Pediatr. 2018;6:242. doi: 10.3389/fped.2018.00242

8. Nelson  MJ, Buckley  JD, Thomson  RL, Clark  D, Kwiatek  R, Davison  K.  Diagnostic sensitivity of 2-day cardiopulmonary exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome.  J Transl Med. 2019;17(1):80. doi: 10.1186/s12967-019-1836-0

9. Esfandyarpour  R, Kashi  A, Nemat-Gorgani  M, Wilhelmy  J, Davis  RW.  A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).  Proc Natl Acad Sci U S A. 2019;116(21):10250-10257. doi: 10.1073/pnas.1901274116

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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I have no diagnosed mental health condition, but in the same way that we all have a physical health, every single one of us has a mental health too. And recently my mental health hasn’t been as good as it once was.

To put it simply, I have been unwell every single day since September 2010 and no human being can endure what we endure as M.E. sufferers and come away unscathed.

I have experienced incredible ignorance, disbelief, battled with the DWP, and missed out on a lot of life since being ill, but it was the realisation that motherhood would not be something I would experience that ended up being the straw that broke the camel’s back.

Due to the severity of my M.E. and the all-encompassing effects that my health has on my life, I will not be having children (it is not something I am wishing to discuss or justify at this time).

Having reached this devastating conclusion some time ago, I steeled myself for the day my siblings or cousins made a pregnancy announcement.

But I still wasn’t quite ready for it. I will be an aunty for the first time later this month.

The Baby Thing’

With every friend that announced that they were having a baby, there was a huge internal conflict. I was overjoyed for them, but heartbroken for myself.

Every birth announcement left me torn between elation and despair. These feelings were amplified when my sister announced her pregnancy late last year. I have missed out on a lot since being ill, but this sacrifice seemed too cruel a thing to endure.

I have never viewed seeking help for one’s mental health as something to be ashamed of, but I also genuinely never saw myself needing such help.

For nearly nine years I have been okay. More than okay. Happy. Content. Grateful. But it seems you can be all those things and still be sad, angry, frustrated and lost. And feel this searing pain and despair over what I feel is an ultimate loss; not becoming a mother.

The conflicting emotions became overwhelming. I sought help. It took over six months to find the courage to send that first email to my counsellor.

The breaking point came one evening after speaking to my pregnant sister. It was clearly deeply unhealthy to come away from each phone call and cry inconsolably.

Seeking help

When I started to look for a local counsellor online, I became incredibly angry and frustrated to see CFS/ME listed amongst the issues that a counsellor claimed they could offer support with.

I despised the implication that my very physical health condition was something that talking therapy could help. When my appointment came around, I endeavoured to mention my physical health condition as little as possible and just concentrate on The Baby Thing.

I can’t tell you how hard it was to go to that first appointment; to put myself out there when I am so incredibly vulnerable and not nearly as thick-skinned as M.E. sufferers need to be.

To put myself in a situation where another’s views on M.E. could have done such damage to me was a huge risk. But I was desperate. Perhaps the fact that I went highlights how much of a struggle missing out of this milestone has been.

Ever the optimist I though 6-8 sessions, as initially recommended, would be enough. But now, 4 months on, I realise it is more of an ongoing commitment.

It’s opened a can of worms. It’s not that I kept everything in, or hidden away, or bottled up. I have had an incredible support system to lean on. It’s that now I have someone to offload to who has no emotional response to my struggles, and over 8 years of tales to tell.

The emotional impact of ME

While it was The Baby Thing that led to me seeking help, it is the overall subject of long-term illness that has been the main topic of discussion. Afterall, it is M.E. and only M.E. that is the reason behind my husband and I facing a childless future. A condition like M.E. has an incredibly far-reaching effect on the sufferer and those in the sufferer’s life.

While too many medical professionals have inaccurate and outdated views about M.E. being psychological, my person-centred counsellor is in no way trying to cure or help me recover. She is simply supporting me through the emotional impact that M.E. has had. There is a difference.

I think it’s important to note that it is a privilege to be able to seek this help, from both a financial and a health point of view. Just a couple of years ago I would have been too unwell to even contemplate starting this process. Every cloud eh…

Family and friends have offered me support when I have shared my struggles, but there’s something very powerful about getting sympathy and understanding from a health professional. I think that’s something all M.E. sufferers can relate to.

To have coped in any kind of way with the reality of M.E. is commendable. Kicking, screaming, crying, full of hope and optimism, at peace…all responses are valid. I have done them all.

It seems I just needed to hear from someone further removed than my own support network, that it is perfectly okay to be feeling the way I am feeling, particularly around the subject of parenthood.

I can’t stress enough how valuable the experience has been for me so far. It really is good to talk.

Additional support from the ME Association

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Baroness Nicola Blackwood had been misdiagnosed with ME/CFS before it was determined she had Ehlers-Danlos Syndromes (EDS) with migraines and PoTS.

By Johanna Thomas-Corr, The Times, 08 July 2019.

Extracts:

At 39 the Conservative peer Baroness Nicola Blackwood of North Oxford is 30 years younger than the average member of the Lords. But as well as being the youngest member of the second chamber, she has another distinction — last month she made headlines for fainting at the despatch box.

It happened three weeks ago when, in her capacity as junior health minister, she was answering a question on the outbreak of listeria in hospitals. Looking peaky, Blackwood began to repeat the same phrase about food provisions before alerting other members: “I apologise. I’m going to faint. I’m going to faint.”

Ehlers-Danlos Syndromes

The collapse wasn’t a clever strategy for avoiding a difficult question. Blackwood suffers from a rare genetic condition called Ehlers-Danlos syndromes (EDS), which has made any sort of political career challenging.

Caused by a collagen-production defect, EDS can result in hypermobility, migraines and chronic muscle and joint pain.

As a result of EDS, Blackwood has also been diagnosed with postural tachycardia syndrome (PoTS), an abnormality of the autonomic nervous system, which controls breathing, digestion and the heartbeat.

This time she was “fighting off flu”. Infections play havoc with her blood pressure, meaning she can get “much sicker than everyone else”, but she has learnt how to anticipate and prevent these collapses. However, with such an urgent problem facing the NHS, she had not wanted to call in sick.

“That’s why I conked in the chamber, because I should have taken time off, and I didn’t, and it’s all my own fault,” Baroness Blackwood.

She experienced her first symptoms at seven, when she suffered an asthma attack and had to be rushed to hospital at night by her medic parents. Her father was a consultant cardiologist, her mother a nurse.

Home Schooling

She continued to get weaker throughout her childhood, but no one could diagnose the problem. At school she learnt that “you have to have a stiff upper lip because you don’t want to be perceived as weak. You want to make sure you can still achieve”.

By the age of 17 she was barely able to climb stairs because of severe muscle pain and problems with her heart rate and blood pressure. One doctor told her parents that she wouldn’t be able to go to university or hold down a normal job. But home-schooling helped her through her GCSEs and A levels, and she won a place at St Anne’s College, Oxford, to study music.

No matter how determined she is, she says: “Mind over matter only goes so far and you end up in hospital. Psychologically there were times when I did think, ‘Shall I just give up and accept the fact I shall lie on a bed of pain and never go forward,’ but I wasn’t really brought up like that.”

“I was trying to manage all those moving parts with a fluctuating health condition and hide it from everybody, except my closest family. I realised it wasn’t working particularly well and my health deteriorated,” Baroness Blackwood.

Fluctuating Health

Having had various wrong diagnoses — including chronic fatigue syndrome/ME — Blackwood finally found a doctor, who himself had EDS. Until that point she had always felt “like a hypochondriac”.

But her health “got worse before it got better”. It took a long time to fine-tune her medication and lifestyle regime. At first she was having 32 injections in her head every few months for her migraines.

“You think ‘I’m the unluckiest person in the world’ and then you realise it’s just one thing. It makes perfect sense,” Baroness Blackwood.

She kept the illness secret until she fainted in the presence of Tom Newton Dunn, the political editor of The Sun, in the 2015 general election and was forced to come clean.

Illness Management

She fears that “the trope of weakness” is more readily attached to women. “It’s been instructive how the public have reacted to the prime minister with her diabetes. Some have thought it’s a good thing and others have seen this as a sign of weakness.”

Yet Blackwood is determined to show illness and high-profile jobs are not mutually exclusive. She controls her symptoms with a fine-tuned holistic regime, combining medication, physiotherapy, diet and Pilates (yoga overstretches the ligaments and causes her muscles to go into spasm).

Mercifully, she no longer has to have the injections for her migraines, but she does “titrate” herself daily. She pulls out her phone and shows me the app she uses to monitor her heart rate.

Does she ever get to slow down? After she lost her seat in the last election her Instagram feed was wall-to-wall Mediterranean holidays, trips to Glyndebourne and skiing. However, since she’s been appointed to the Lords, the pictures are of her visiting hospitals.

Westminster, she concedes, is “not a great environment for your mental health or your physical health, especially at the moment. But we are as a government and a parliament trying to solve one of the biggest challenges that we have faced as a nation”.

Nevertheless, she says she couldn’t live with herself if she didn’t try to make it easier for patients with rare diseases to get an early diagnosis and help to create a care system that is easier to navigate.

“Each day I look at what I have in the diary and make a judgment about whether I really have to do it,” she says. “If the person I’m going to see or the speech I’m going to give is something that needs to be done more than I need to have a rest, then I take the hit. That’s what I signed up for and I did it consciously knowing that sometimes it’s not going to work out perfectly for the good of my health.”

The ME Association

Real People. Real Disease. Real M.E.

We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.

If you would like to support our efforts and help ensure we can inform, support, advocate and invest in biomedical research, then please donate today.

Just click the image opposite and visit our JustGiving page for one-off donations, to establish a regular payment or to create your own fundraising event.

Or why not join the ME Association as a member and be part of our growing community? For a monthly (or annual) subscription you will also receive our exclusive ME Essential magazine.

ME Association Registered Charity Number 801279

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Charlotte Stephens, Research Correspondent, ME Association.

ME Association Index of Published ME/CFS Research

The Index of Published ME/CFS Research has now been updated to take account of the research that has been published during the month of June 2019.

The Index is a useful way to locate and then read all relevant research on ME/CFS. It’s free to download and comes with an interactive contents table.

This is an A-Z list of all the most important ME/CFS research studies (and selected key documents and articles), listed by subject matter and author, with links to PubMed or the relevant Journal.

You can also find the index in the Research section of the website together with all the summary reviews that have been published.

ME/CFS research abstracts from studies published in June 2019

1. Ballantine R, et al. (2019)
Gravity-induced exercise intervention in an individual with chronic fatigue syndrome/myalgic encephalomyeltis and postural tachycardia syndrome: a case report.
International Journal of Therapy and Rehabilitation 26 (5).

Abstract
Chronic fatigue syndrome/myalgic encephalomyeltis is a condition of complex nature, characterised by unexplained disabling fatigue and a combination of non-specific accompanying symptoms. Individuals with chronic fatigue syndrome/myalgic encephalomyeltis frequently present with debilitating orthostatic symptoms, which may fall under the umbrella of postural tachycardia syndrome. Postural tachycardia syndrome is underpinned by autonomic nervous system dysfunction.

The gravitational deconditioning that occurs in those severely affected by chronic fatigue syndrome/myalgic encephalomyeltis alongside postural tachycardia syndrome has been suggested as a key focus for interventions in this group. This case report documents the evaluation and rationale behind a novel gravity-induced exercise intervention to improve the symptoms of a 44-year-old female severely affected by chronic fatigue syndrome/myalgic encephalomyeltis and postural tachycardia syndrome, who had been bedbound for 10–15 years.

An exercise intervention was designed to challenge and therefore improve key areas of autonomic nervous system regulation in the presence of gravity. It contained seven different exercises conducted once a month in a class over a 6-month period. Fatigue impact score, activity levels and heart rate upon standing, as detected by an active stand test, improved during the exercise intervention and at follow up.

Gravity-induced exercise intervention can have a positive effect on an individual severely affected by Chronic fatigue syndrome/myalgic encephalomyeltis alongside postural tachycardia syndrome.

2. Bohne V and Bohne O (2019)
Suggested Pathology of Systemic Exertion Intolerance Disease: Impairment of the E3Subunit or Crossover of Swinging Arms of the E2 Subunit of the Pyruvate Dehydrogenase Complex Decreases Regeneration of Cofactor Dihydrolipoic Acid of the E2 Subunit.
Medical Hypothesis [Epub ahead of print]

Abstract
Systemic Exertion Intolerance Disease (SEID) or myalgic encephalomyelitis (ME) or chronic fatigue syndrome (CFS) has an unknown aetiology, with no known treatment and a prevalence of approximately 22 million individuals (2%) in Western countries. Although strongly suspected, the role of lactate in pathology is unknown, nor has the nature of the two most central symptoms of the condition – post exertional malaise and fatigue.

The proposed mechanism of action of pyruvate dehydrogenase complex (PDC) plays a central role in maintaining energy production with cofactors alpha-lipoic acid (LA) and its counterpart dihydrolipoic acid (DHLA), its regeneration suggested as the new rate limiting factor. Decreased DHLA regeneration due to impairment of the E3 subunit or crossover of the swinging arms of the E2 subunit of PDC have been suggested as a cause of ME/CFS/SEID resulting in instantaneous fluctuations in lactate levels and instantaneous offset of the DHLA/LA ratio and defining the condition as an LA deficiency with chronic instantaneous hyperlactataemia with explicit stratification of symptoms.

While instantaneous hyperlactataemia has been suggested to account for the PEM, the fatigue was explained by the downregulated throughput of pyruvate and consequently lower production of ATP with the residual enzymatic efficacy of the E3 subunit or crossover of the E2 as a proposed explanation of the fatigue severity.

Functional diagnostics and visualization of instantaneous elevations of lactate and DHLA has been suggested. Novel treatment strategies have been implicated to compensate for chronic PDC impairment and hyperlactataemia.

This hypothesis potentially influences the current understanding and treatment methods for any type of hyperlactataemia, fatigue, ME/CFS/SEID, and conditions associated with PDC impairment.

3. Castro-Marrero J et al. (2019)
Unemployment and work disability in individuals with chronic fatigue syndrome/myalgic encephalomyelitis: a community-based cross-sectional study from Spain.
BMC Public Health 19: 840.

Abstract
Background: Few reports have examined the association between unemployment and work disability in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). This study explored the key determinants of work disability in a CFS/ME cohort.

Methods: A community-based prospective study included 1086 CFS/ME patients aged 18–65 years. Demographic and clinical characteristics and outcome measures were recorded. Multiple linear regression analysis was performed to identify key risk indicators of work disability.

Results: Four hundred and fifty patients with CFS/ME were employed (41.4%) and 636 were unemployed (58.6%). Older age at pain onset (OR: 1.44; 95% CI: 1. 12–1.84, autonomic dysfunction (OR: 2.21; 95% CI: 1.71–2.87), neurological symptom (OR: 1.66; 95% CI: 1. 30–2.13) and higher scores for fatigue (OR: 2.61; 95% CI: 2.01–3.39), pain (OR: 2.09; 95% CI: 1.47–2.97), depression (OR: 1.98; 95% CI: 1. 20–3.26), psychopathology (OR: 1.98; 95% CI: 1.51–2.61) and sleep dysfunction (OR: 1.47; 95% CI: 1. 14–1.90) were all associated with a higher risk of work disability due to illness.

Conclusions: Using an explanatory approach, our findings suggest that unemployment is consistently associated with an increased risk of work disability due to CFS/ME, although further more rigorous research is now needed to help in targeting interventions at the workplace.

4. Dibnah B et al. (2019)
Investigating the role of TGF-B and fatigue in Chronic Fatigue Syndrome.
Annals of the Rheumatic Diseases 78 (2).

Abstract
Background: Chronic fatigue syndrome (CFS) is estimated to affect up to 5% of people in Europe and is more common in women than men. It is characterised by unexplained fatigue, post-exertional malaise and a range of other symptoms. Recent studies indicate potential immune dysfunction in CFS, specifically regarding cytokines and the adaptive behavioural response.

Objectives: This study aims to investigate serum transforming growth factor-beta (TGF-β) and the expression of the TGF-β Receptor 1 (TGFBR1) and TGF-β Receptor 2 (TGFBR2) genes, in relation to the fatigue associated with CFS.

Methods: Serum active and total TGF-β concentrations were measured in 117 CFS patients and 40 HCs using a TGF-β responsive luciferase bioassay. Expression levels of TGFBR1 and TGFBR2 were analysed using quantitative PCR. Fatigue was measured using the fatigue impact scale (FIS)1. FIS was categorised into three groups; ‘mild’ (0-80), ‘moderate’ (81-120) and ‘severe’ (121-160). Linear and ordinal regressions were performed on the continuous FIS and FIS categories respectively.

Results: Serum TGF-β concentrations in the CFS group did not differ significantly compared with the HC group (p=0.58). TGF-β concentrations showed no correlation with disease duration but there was a trend towards decreased TGF-β with increasing symptom duration. There were no significant differences between the levels of TGFBR1 and TGFBR2 in any of the fatigue groups, or between HCs. Active TGF-β concentrations were significantly elevated in the ‘severe’ FIS group compared to the ‘mild’ FIS group (p=0.04). Active/total TGF-β levels were significantly higher in the ‘severe’ FIS group than the ‘mild’ and ‘moderate’ FIS groups (p=0.02, p=0.03 respectively).

Conclusion: These data suggest no differences in serum concentrations of TGF-β or expression of TGFBR1 and TGFBR2, between the HC and CFS groups. It also suggests no differences in expression levels of TGFBR1/2 between any of the CFS fatigue groups. However, active/total TGF-β levels were increased in more severely fatigued patients based on FIS. This finding could be due to higher levels of circulating TGF-β, or increased amounts of TGF-β activation. Further work is necessary to confirm this finding in a larger cohort of CFS patients, and to explore how this increase in TGF-β relates to fatigue.

5. Garner R and Baraniuk J (2019)
Orthostatic intolerance in chronic fatigue syndrome.
Journal of Translational Medicine 17: 185.

Abstract
Background: Orthostatic intolerance (OI) is a significant problem for those with chronic fatigue syndrome (CFS). We aimed to characterize orthostatic intolerance in CFS and to study the effects of exercise on OI.

Methods: CFS (n = 39) and control (n = 25) subjects had recumbent and standing symptoms assessed using the 20-point, anchored, ordinal Gracely Box Scale before and after submaximal exercise. The change in heart rate (ΔHR ≥ 30 bpm) identified Postural Orthostatic Tachycardia Syndrome (POTS) before and after exercise, and the transient, exercise-induced postural tachycardia Stress Test Activated Reversible Tachycardia (START) phenotype only after exercise.

Results: Dizziness and lightheadedness were found in 41% of recumbent CFS subjects and in 72% of standing CFS subjects. Orthostatic tachycardia did not account for OI symptoms in CFS. ROC analysis with a threshold ≥ 2/20 on the Gracely Box Scale stratified CFS subjects into three groups: No OI (symptoms < 2), Postural OI (only standing symptoms ≥ 2), and Persistent OI (recumbent and standing symptoms ≥ 2).

Conclusions: Dizziness and Lightheadedness symptoms while recumbent are an underreported finding in CFS and should be measured when doing a clinical evaluation to diagnose orthostatic intolerance. POTS was found in 6 and START was found in 10 CFS subjects. Persistent OI had symptoms while recumbent and standing, highest symptom severity, and lability in symptoms after exercise.

6. Groven N et al. (2019)
Patients with Fibromyalgia and Chronic Fatigue Syndrome show increased hsCRP compared to healthy controls.
Brain, Behaviour and Immunity [Epub ahead of print]

Abstract
Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are both chronic disorders that have a devastating effect on the lives of the affected patients and their families. Both conditions have overlapping clinical features that partly resemble those of inflammatory disorders. The etiology is still not understood, and it is suggested that the immune system might be a contributing factor. So far, the results are inconclusive.

The purpose of this study was to compare the two conditions and investigate the level of the inflammatory marker high-sensitivity CRP (hsCRP) in CFS and FM patients compared to healthy controls. Female participants aged 18–60 years were enrolled in this study. The group consisted of 49 CFS patients, 57 FM patients, and 54 healthy controls.

hsCRP levels were significantly higher for both the CFS and the FM groups compared to healthy controls when adjusting for age, smoking, and BMI (p < .001). There was no difference between the two patient groups. The level of hsCRP was affected by BMI but not by age and smoking.

Patients with CFS and FM have higher concentrations of hsCRP compared to healthy controls. This remains significant even after adjusting for BMI. CFS and FM cannot be distinguished from each other on the basis of hsCRP in our study.

7. Lien K et al. (2019)
Abnormal blood lactate accumulation during repeated exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome.
Physiological Reports 7 (11).

Abstract
Post‐exertional malaise and delayed recovery are hallmark symptoms of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Studies on repeated cardiopulmonary exercise testing (CPET) show that previous exercise negatively affects oxygen uptake (VO2) and power output (PO) in ME/CFS. Whether this affects arterial lactate concentrations ([Laa]) is unknown.

We studied 18 female patients (18–50 years) fulfilling the Canadian Consensus Criteria for ME/CFS and 15 healthy females (18–50 years) who underwent repeated CPETs 24 h apart (CPET1 and CPET2) with [Laa] measured every 30th second.

VO2 at peak exercise (VO2peak) was lower in patients than in controls on CPET1 (P < 0.001) and decreased in patients on CPET2 (P < 0.001). However, the difference in VO2peak between CPETs did not differ significantly between groups. [Laa] per PO was higher in patients during both CPETs (Pinteraction < 0.001), but increased in patients and decreased in controls from CPET1 to CPET2 (Pinteraction < 0.001). Patients had lower VO2(P = 0.02) and PO (P = 0.002) at the gas exchange threshold (GET, the point where CO2production increases relative to VO2), but relative intensity (%VO2peak) and [Laa] at GET did not differ significantly from controls on CPET1. Patients had a reduction in VO2 (P = 0.02) and PO (P = 0.01) at GET on CPET2, but no significant differences in %VO2peak and [Laa] at GET between CPETs. Controls had no significant differences in VO2, PO or %VO2peak at GET between CPETs, but [Laa] at GET was reduced on CPET2 (P = 0.008).

In conclusion, previous exercise deteriorates physical performance and increases [Laa] during exercise in patients with ME/CFS while it lowers [Laa] in healthy subjects.

8. McPhee G et al. (2019)
Monitoring treatment harm in myalgic encephalomyelitis/chronic fatigue syndrome: A freedom-of-information study of National Health Service specialist centres in England.
Journal of Health Psychology [Epub ahead of print].

Abstract
The use of graded exercise therapy and cognitive behavioural therapy for myalgic encephalomyelitis/chronic fatigue syndrome has attracted considerable controversy. This controversy relates not only to the disputed evidence for treatment efficacy but also to widespread reports from patients that graded exercise therapy, in particular, has caused them harm.

We surveyed the National Health Service-affiliated myalgic encephalomyelitis/chronic fatigue syndrome specialist clinics in England to assess how harms following treatment are detected and to examine how patients are warned about the potential for harms. We sent 57 clinics standardised information requests under the United Kingdom’s Freedom of Information Act. Data were received from 38 clinics.

Clinics were highly inconsistent in their approaches to the issue of treatment-related harm. They placed little or no focus on the potential for treatment-related harm in their written information for patients and for staff. Furthermore, no clinic reported any cases of treatment-related harm, despite acknowledging that many patients dropped out of treatment.

In light of these findings, we recommend that clinics develop standardised protocols for anticipating, recording, and remedying harms, and that these protocols allow for therapies to be discontinued immediately whenever harm is identified.

9. Murga I and Lafuente JV (2019)
From neurasthenia to post-exertion disease: Evolution of the diagnostic criteria of chronic fatigue syndrome/myalgic encephalomyelitis.
Atencion Primaria [Epub ahead of print]

Abstract
Changes in the terminology and diagnostic criteria for chronic fatigue syndrome/myalgic encephalomyelitis are explained in this paper. This syndrome is a complex and controversial entity of unknown origins. It appears in the medical literature in 1988, although clinical pictures of chronic idiopathic fatigue have been identified since the nineteenth century with different names, from neurasthenia, epidemic neuromyasthenia, and benign myalgic encephalomyelitis up to the current proposal of disease of intolerance to effort (post-effort). All of them allude to a chronic state of generalised fatigue of unknown origin, with limitations to physical and mental effort, accompanied by a set of symptoms that compromise diverse organic systems.

The International Classification of Diseases (ICD-10) places this syndrome in the section on neurological disorders (G93.3), although histopathological findings have not yet been found to clarify it. Multiple organic alterations have been documented, but a common biology that clarifies the mechanisms underlying this disease has not been established. It is defined as a neuro-immune-endocrine dysfunction, with an exclusively clinical diagnosis and by exclusion. Several authors have proposed to include CFS/ME within central sensitivity syndromes, alluding to central sensitisation as the common pathophysiological substrate for this, and other syndromes.

The role of the family doctor is a key figure in the disease, from the detection of those patients who present a fatigue of unknown nature that is continuous or intermittent for more than 6 months, in order to make an early diagnosis and establish a plan of action against a chronic disease with high levels of morbidity in the physical and mental sphere.

OBJECTIVE: To carry out a bibliographic review of the terminology and diagnostic criteria of the chronic fatigue syndrome/myalgic encephalomyelitis, in order to clarify the pathology conceptually, as a usefulness in the diagnosis of Primary Care physicians.

10. Neale FK et al. (2019)
Illness duration, mood and symptom impact in adolescents with chronic fatigue syndrome/myalgic encephalomyelitis?
Archives of Disease in Childhood [Epub ahead of print].

Abstract
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disabling condition that affects 0.4% to 2.4% of adolescents in the UK. Previous studies have reported high levels of anxiety, depression and worry among adolescents with CFS/ME. In adult studies, concerns have been raised about delays in accessing specialist CFS/ME services and the impact of delays on patients’ health and well-being.

In this study, we aimed first to assess the prevalence of self-reported anxiety/depression, worry and degree of symptom impact among our patient population of adolescents with CFS/ME. We then investigated whether longer illness duration was associated with higher prevalence of self-reported anxiety/depression, worry and symptom impact at initial assessment.

11. Pederson M (2019)
Chronic Fatigue Syndrome and chronic pain conditions – vitally protective systems gone wrong.
Scandinavian Journal of Pain [Epub ahead of print]

Abstract
Chronic Fatigue Syndrome (CFS) and chronic pain syndromes represent major health problems in society. These conditions are disabling and strongly associated with low quality of life. Even though CFS and chronic pain are separate conditions, they have strikingly much in common.

Both pain and fatigue are important sensations with protective value in an acute situation. It can be life-threatening not to be aware of them. However, as these symptoms become chronic, their protective roles decrease and instead they become health problems.

Our understanding of the perception of pain and fatigue has shifted through the years, from a dualistic biomedical point of view to a holistic biopsychosocial understanding. This combined with the increasing evidence of how our brain works in a predictive/anticipatory manner, gives a deeper understanding of why treatments like cognitive behavior therapies and stress relief therapies can..

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