Friday, 22 September 2017
By February 2007, I had been receiving daily Nexavir injections (an antiviral) for six months and I was actually starting to see small improvements in my health for the first time in over two years of being acutely ill. But friends and relatives kept sending me newspaper cuttings of articles about the Lightning Process (LP) curing people with ME. I became under enormous pressure to do the LP (“What’s the harm in trying it?” “Don’t you want to get better?” “It has helped others so it’s worth a shot”). I was only 20 years old, vulnerable because of my desperation to get better, and didn’t know much about Myalgic Encephalomyelitis and what the illness actually was (a multi-systemic, neuroimmune illness). By that time, I also had been gaslighted by so many NHS doctors and private doctors about my illness and symptoms, that I was doubting myself. When so many people disbelieve you, you start disbelieving yourself, despite all physical evidence to the contrary. In the end, I buckled and, although sceptical, I agreed to do the LP. I was so ill and I just wanted to get better.
Ironically, I wouldn’t have even been able to get to the LP practitioner’s house (he was an NHS doctor but did the LP privately) even a couple of months previously but because of the small improvements due to the Nexavir injections, I was able to get down the stairs and lie down in the back of our car to get there. There were consequences for my body but I thought that it would be worth it.
I’m not going to go into detail about the “mechanics” of the LP; other people have debunked the methods far better than I’m currently able to. Back then, I decided to throw myself into the LP and be totally committed to doing it properly. The results, however, were nothing less than disastrous for me.
First, the fully-qualified practitioner artfully gaslighted us (a group of four patients) with what I now know is pseudoscience quackery about M.E.; it was done in such a subtle, convincing and skilful way (even experienced scientists have been taken in by it). Using “science” to explain, he told us how we didn’t ‘have’ an illness but that we were ‘doing’ an illness; it was our thoughts, behaviours, and fears about post-exertional symptoms that were causing us to stop ourselves from living normally and causing us to believe that we had symptoms and to believe that we were ill.
He then put mechanisms into place in my brain, via neuro-linguistic programming, that made my own brain automatically gaslight me constantly and stop any thoughts of symptoms dead in their tracks. He added repetitive gestures/movements/phrases that I had to continually apply to my thoughts and body in order to reinforce the programming. This is brainwashing.
It’s hard to describe being brainwashed. The next six months in 2007 after the LP are still a hazy blur to me. Not only did the neuro-linguistic programming in my brain not allow me to ever mention any symptoms to anyone, I was not even allowed to think that I had any symptoms. I wasn’t allowed to be ill anymore. I pushed and pushed myself, even when in the most excruciating pain, even when I was in heart failure or experiencing seizures or passing out, because they didn’t exist. My illness didn’t exist [even though I was extremely ill, I honestly believed that I wasn’t ill anymore, that I was cured]. It sounds ridiculously idiotic but that’s what brainwashing can do. My body was becoming more and more damaged from the enforced gradual Graded Exercise Therapy that the programming in my brain was imposing on myself. It was completely out of my control; I felt glazed over and not with it.
As per what I’d been conditioned and instructed to do during the LP training, I told everyone that I was no longer ill and that I was recovering. I’m pretty sure that I told all my friends and family that I was in recovery, that the Lightning Process had been successful and had worked. I even had a huge 21st birthday/’I’m better now’ party in a village hall, celebrating recovery from illness. Remembering it now is upsetting. I had the biggest smile on my face the whole time and looked fine to everyone but would have to frequently escape into the toilets where I would almost black out and would collapse on the floor for a while. I was in oxygen starvation from being upright and from heart failure. I was very dizzy and everything was spinning around me because of my very low blood pressure. All my muscles were screaming at me. Nobody had any idea that this was happening to me; the LP programming prevented me from being able to tell anyone or from even acknowledging my symptoms to myself. They didn’t exist because I wasn’t ill. It’s just a haze to me now.
In the following months, I kept on pushing myself, doing insane damage to my body (I pushed myself to the point where I was going on a slow 5-minute walk every few days, which was a huge deal for me considering I had been bed-bound for two years) until one day in August 2007, when my parents were away, I pushed myself too far and went on a longer walk. At the end, my body failed and packed in completely; the six months caught up with me and I collapsed. I was never able to get up again. Ever since, I have been bed-bound, unable to sit up and unable to speak, struggling to breathe and swallow. The permanent organ damage that was done during March to August 2007 during the self-imposed GET due to the LP brainwashing, was devastating. I never recovered from it and my health has only deteriorated since. The hold that the brainwashing had over me was broken pretty quickly and thoroughly that August, thank goodness. But I can’t remember much from those six months.
Today it is being reported in the news that an experimental trial of the LP on children and teens with M.E. has been successful. The fact that the results are based on the children and teens themselves saying that they have recovered, is extremely worrying to me. During the six months that I was brainwashed with the LP, I would have said the same: that I was cured, that I was recovering and that the LP was successful. Those poor children. They are even more vulnerable than I was. What they have been subjected to is nothing short of abuse and should never have been allowed to happen in the first place.
Whatever you do, please don’t send news articles about the Lightning Process to anyone with M.E. It’s a dangerous thing. Don’t beckon lightning and invite it in for tea; it will burn your house to the ground with you inside until you’re nothing but ashes.
Monday, 18 September 2017
C H Spurgeon's Evening Devotional for 18th September
"And they follow Me."
C H Spurgeon's Evening Devotional for 18th September
"And they follow Me."
We should follow our Lord as unhesitatingly as sheep follow their shepherd, for He has a right to lead us wherever He pleases. We are not our own, we are bought with a price-let us recognize the rights of the redeeming blood. The soldier follows his captain, the servant obeys his master, much more must we follow our Redeemer, to whom we are a purchased possession. We are not true to our profession of being Christians, if we question the bidding of our Leader and Commander. Submission is our duty, cavilling is our folly. Often might our Lord say to us as to Peter, "What is that to thee? Follow thou Me." Wherever Jesus may lead us, He goes before us. If we know not where we go, we know with whom we go. With such a companion, who will dread the perils of the road? The journey may be long, but His everlasting arms will carry us to the end. The presence of Jesus is the assurance of eternal salvation, because He lives, we shall live also. We should follow Christ in simplicity and faith, because the paths in which He leads us all end in glory and immortality. It is true they may not be smooth paths-they may be covered with sharp flinty trials, but they lead to the "city which hath foundations, whose builder and maker is God." "All the paths of the Lord are mercy and truth unto such as keep His covenant." Let us put full trust in our Leader, since we know that, come prosperity or adversity, sickness or health, popularity or contempt, His purpose shall be worked out, and that purpose shall be pure, unmingled good to every heir of mercy. We shall find it sweet to go up the bleak side of the hill with Christ; and when rain and snow blow into our faces, His dear love will make us far more blest than those who sit at home and warm their hands at the world's fire. To the top of Amana, to the dens of lions, or to the hills of leopards, we will follow our Beloved. Precious Jesus, draw us, and we will run after Thee.
Saturday, 2 September 2017
By Christina Baltais
This story won’t be particularly unique or shocking to anyone living with ME. Every single one of us has a plethora of stories like this, and far worse than this. It has happened so many times over the last 11 years. What shocks me is the degree to which it still occurs and manages to affect me, no matter how much time I spend trying to advocate for ME.
I was out to eat with extended family members. It was my first outing in weeks, since I had been housebound due to symptoms. An outing after a long period of solitary confinement is a rather momentous occasion. I was so grateful to be out of that bed, out of that bedroom, out of that house. The vibrant world that felt so far away, I now found myself immersed in, taking in everything around me like a grateful sponge. I was basically a bear emerging from a den after a long, long hibernation (minus any refreshing sleep).
When I sat down, the usual catch-up conversation ensued. Updates on my health eventually came up. I said that its been my first outing in quite some time after a rough patch. This statement could have been followed by words that were supportive/empowering/neutral, but it wasn’t. This family member went on to comment that I looked fine, and was sitting up just fine at the table right now. I responded by saying that sitting up was actually very difficult for me because I was experiencing a great deal of weakness, and would need to rest after this outing when I got home. This was followed by a comment indicating that if I was sitting up now, why couldn’t I find a job where all I had to do was sit up and type? Why couldn’t I look for jobs like that? Was I not even going to try? After all that schooling, was I just going to waste my life?
You have got to be kidding me. (And some other words that I can’t say.)
A long uncomfortable silence ensued. I felt the familiar pangs of shame, humiliation, and judgement by someone who not only knew nothing about ME, but who also did not want to listen. No one at the table said anything in my defence, their passive silence feeling like implied agreement. I honestly believe this person’s intent was good, but how disconnected from my experience could they possibly have been to not realize the impact of their words and the implications of their statements. I really embrace the importance of talking about my body and ME as a source of education, but the first caveat always has to be that my voice and experience is heard, valued, and respected. This was another case where it clearly had not been. For if anyone was connected to the experience of ME, they would understand the absolute hell a person goes through. The depths of despair and grief this disease drags you through; it was never a choice. The inner turmoil of having a heart that wants the world everyday, but having a body constantly saying no; you forfeit any control over the direction of your life. I chose ME just as much as the millions of people around the world chose ME; we didn’t. I realize I’m preaching to the choir. The point is, I should not have to spend an outing defending and proving in hopes of understanding. I’m not wasting any precious spoons on that. It just hurts so much, still, even after 11 years.
As human beings we all need to feel love and connection. There is a deep-seated need to feel unified, to have approval, acknowledgement, acceptance—-to feel connected with, intimate and loved by, other human beings. When you are already so physically isolated due to illness, situations that make you feel emotionally and socially isolated take it to an entirely different level. It adds another layer of suffering. As if I didn’t feel disconnected and like an outsider enough already. It’s situations like this that make me realize how much during these 11 years I have not been believed or heard. It’s situations like these that make me realize how exhausting it is to constantly be vying for the understanding of others.
What’s even harder is when it comes from family, as this one did. What’s even more disheartening is that this individual is also a doctor. When I was undergoing medical training myself, some supervisors I highly respected displayed a clear lack of understanding about ME. One spoke of how you have to wonder how much of “the behaviour” is learned as it runs in families. I was told to recommend to an ME patient that they strap on a backpack full of weights and jump on a trampoline to increase bone mineral density. It was explained to me how a new physical symptom could only be psychosomatic “as anxiety is common in that demographic so that is the only plausible explanation for that extreme symptom.” Unbeknownst to them, I had ME and these comments illuminated the presumptions, assumptions, and rampant inaccuracies perpetuated by a lack of knowledge in our medical systems. They were extremely disappointing and painful to hear, as I’ve been on the receiving end of all these assumptions and exacerbating recommendations as a patient myself. The lack of knowledge and understanding is systemic; experiencing and bearing witness to how ME has been relegated to the margins of our medical system has been traumatic.
The history of ME’s constant invalidation and abhorrent lack of research funding is disturbing. I wish people would listen. I wish they would trust our experiences and accounts of our own bodies, or in some cases, of our children’s bodies. How healing the words, “I believe you,” would would be for all of us. Sometimes, the emotional toll feels worse than the actual disease itself.
We don’t know when the pathological basis of ME will finally be understood. We should not have to wait for that, to be shown the much needed empathy and compassion which we deserve. Why it takes “proof” in order to actually listen to literally millions of voices saying the same thing over decades of time baffles me. When I think of the millions of lives lived, and some ended, in complete suffering—-without voices, it enrages me. If their suffering had been validated and acknowledged, even if treatment was still not available, would it not have made a difference? The injustice of it all enrages me. Anger is often a signal something is not working, and that means something needs to change. Change is possible and can come soon for all of us. Change needs to come especially for those of us who are unable to use their voices, or even read this.
There are many ways to get involved in creating change for health equality and ME awareness. Be a part of the #TimeforUnrest global impact campaign. This campaign advocates for more recognition, education, research, and funding around ME. You can help advocate for our voices to be heard, by hosting a screening of Unrest in your community. You can join the #TimeforUnrest Facebook group, and share and promote the campaign on social media. For more ideas on how to be a part of the change, click here.
Imagine how different the world’s perception of this disease could be; and for an end to the stigma and misconceptions we’ve all experienced. Imagine with research the pathological basis of ME understood, and treatments being offered. We can make this change happen, and we can make this change happen together.
About the author: Christina, 31, lives in Toronto, ON. She holds a Bachelor’s Degree in Science and has a fine arts background. She became ill with ME while completing her Bachelors. This inspired her to become a naturopathic medical doctor in order to better understand how to heal the body. One month before completing her medical degree, her ME progressed. She has been slowly recovering, using writing, music, art, and nature as a means for processing this experience.
Friday, 1 September 2017
(Again, if only they would say ME, Myalgic Encephalomyelitis, instead of CFS)
Posted on: August 25, 2017
by Raeka Aiyar, PhD
Ron Davis, PhD, calls chronic fatigue syndrome (also known as myalgic encephalomyelitis, or ME/CFS) the “last major disease about which we know almost nothing.” That’s because at least a million Americans are debilitated by ME/CFS, and yet no clear cause is known, no treatments are approved; funding, understanding, and awareness are disproportionately limited. Yet thanks in part to a boost in advocacy and fundraising efforts, there is increasing cause for hope, many researchers and patients believe.
Earlier this month, several hundred researchers, doctors, patients and caregivers joined forces for the Open Medicine Foundation’s Community Symposium on the Molecular Basis of ME/CFS chaired by Davis at Stanford University, with another 2,700 worldwide joining online. Known for his contributions in biotechnology and genomics, Davis has rerouted his career to tackle this disease and save his critically ill son. He’s brought together an interdisciplinary team of collaborators, many of whom spoke at the symposium. “The Human Genome Project taught us that we can take on a large project like this and succeed,” Davis said.
The event focused on a new understanding of ME/CFS as a molecular disease. Davis’ team has taken this perspective in an omics and big data study of severely ill patients. Wenzhong Xiao, PhD, Davis’ collaborator at Massachusetts General Hospital and Harvard Medical School, presented a preliminary analysis of this dataset, including efforts to use it to define biomarkers and predict causative factors.
Davis presented his technology-driven approach to unraveling ME/CFS, noting that if sequencing technologies had been available at the time, “we would have figured out AIDS in a couple of weeks.” He presented a nanotechnology developed at the Stanford Genome Technology Center that can successfully distinguish patient blood samples from healthy ones, based on their response to stress in the form of increased salt concentration. This presents the potential for a blood-based diagnostic – a transformative prospect for a field reliant on lengthy, subjective diagnoses.
A core issue in ME/CFS is massive energy depletion, so much research is focused on the mitochondria, the organelles inside cells that are responsible for energy generation. Keynote speaker and mitochondrial physiologist Robert Naviaux, MD, PhD, from the University of California, San Diego, suggested that the ‘cell danger response’ to stressors, which prevents cells from returning to baseline function until healing is complete, is prolonged in ME/CFS, which is consistent with observations of reduced metabolism in patients.
Naviaux’s theory also syncs with reports of common infections triggering the development of ME/CFS. In fact, Davis’ cell-free DNA sequencing revealed no exceptional types or levels of pathogens in patients. “It’s not the stressors themselves, but an inability to resolve them and heal afterwards,” Naviaux said.
Stanford immunologist Mark Davis, PhD, presented evidence suggesting that ME/CFS could be an autoimmune disease: using single-cell sequencing, his lab has observed an increase in patient T cells that share a particular target, a signature of an immune response. He said he is investigating what these T cells are targeting.
Nobel Laureate Mario Capecchi, PhD, from the University of Utah, presented a study in mice that shows a connection between the immune system and the brain in a genetic condition that shares some traits with ME/CFS. He also noted how important patient participation is in studying any disease, and how impressed he was with the ME/CFS patient community.
With so much patient engagement, collaboration, and community spirit – not to mention the many theories and new datasets, researchers say it is an exciting time for the field. Many attendees said they were amazed at how much has been accomplished with such scant resources. The event closed with a standing ovation.
To support ME/CFS research, please donate to OMF today. For more about the symposium, check out the YouTube video of the event or read coverage in The Mercury News.
A version of this post originally appeared on the Stanford Medicine Scope Blog.
Tuesday, 22 August 2017
From the ME Association website -
The 2017 Invest In ME Research Conference Report – Dr Charles Shepherd | 22 August 2017
The Invest in ME Research conference took place on Friday, 2nd June, 2017.
This year’s conference was held at One Great George Street, an impressive Edwardian building located opposite St James’s Park, London. There was an excellent mixture of people with ME/CFS, carers and parents, charity representatives, health professionals and researchers from all over the world.
- There was an emphasis on immunology and new approaches to research that are aimed at increasing our understanding of the underlying disease process in ME/CFS and research to potentially deliver more effective forms of treatment.
- Presentations covering treatment were largely focused on the clinical trials taking place in Norway into the use of rituximab and cyclophosphamide.
* This is a copy of the conference summary that was published in the Autumn issue of ME Essential magazine
* We have made Dr Shepherd’s full (16-page) conference report available as a download, which might make it easier for people with M.E. to read at their own pace
Chairman, Dr Ian Gibson opened the meeting with some quotes from a letter written by Sir Bruce Keogh, National Medical Director at NHS England, relating to discussions that are currently taking place at NICE. Current NICE guideline recommendations relating to CBT and GET were referred to in this letter.
Professor Ian Charles of the Quadram Institute of Food Health, University of Norwich: Prof. Charles spoke about the important overlap between food and health and the role of the microbiome in helping to regulate the body’s immune system and the signalling systems that link the brain and gut. He explained how research is starting to provide new insights about possible causal mechanisms in diseases such as diabetes and obesity.
Dr Vicky Whittemore, Programme Director, National Institutes of Neurological Disorders and Stroke at NIH, USA: Dr Whittemore explained how the NIH (National Institutes of Health) operates and talked about how it funds research. There are 27 separate institutes and centres at NIH, each with a specific research agenda focused on diseases or body systems and, as ME/CFS is an illness that covers a wide range of symptoms and body systems, it now has 24 different homes at NIH! NIH is also setting up a ME/CFS Data Management Co-ordinating Centre and arranging educational seminars on ME/CFS.
Professor Donald Staines, National Centre for Neuroimmunology and Emerging Diseases, Griffiths University, Australia: The presentation focused on the work that Professor Staines and his team have been doing at a molecular level on calcium ion channels and cellular signalling mechanisms that involve calcium ions. This is a process that could link in with some of the immune system disturbances found in ME/CFS. It is possible that disturbances in the way that calcium ions are behaving in ME/CFS could form part of the underlying disease process.
Professor Nancy Klimas, Director, Institute for Neuroimmune Medicine, Nova Southeastern University, USA, has put together a large multidisciplinary team, led by two ‘Blue Ribbon Fellowship’ medical students, who are concentrating on the genetic component, aiming to understand the genetic risk in ME/CFS and the possible role of gene mutations. This global study could help to provide a ‘genetic signature’ for ME/CFS and explain why some people recover from ME/CFS and others do not.
From the Karolinska Institute, Sweden, Dr Jakob Theorell’s research focuses on people who have immunodeficiency syndromes. In relation to ME/CFS, he has been looking at a specific part of the immune system orchestra called cytotoxic lymphocytes. These are cells that combat intracellular infections with dysfunctional abnormalities being reported in previous research studies.
Fane Mensah, PhD student at University College London presented a summary of key points from a paper which has reviewed the immunology of ME/CFS. The most consistent abnormality to be reported in ME/CFS is a decrease in number and function of NK (natural killer) cells. Studies that have looked at cytokines (immune system chemicals) have produced inconsistent results. However, there is some evidence of changes in the cytokine make up in relation to illness duration.
Dr Jo Cambridge, Professorial Research Assistant at University College London, belongs to a well established research group at UCL that has a particular interest in drug treatment (rituximab in particular) relating to the depletion of a component of the immune system orchestra called B cells. The group has also been exploring how B cell depletion helps to modify the disease process in rheumatoid arthritis through removing immune complexes and reducing inflammation in the joints.
Professor Simon Carding, Leader in Gut Health and Food Safety Programme a the Institute of Food Research, Norwich Research Park introduced four PhD students who are looking at components of a research hypothesis that involves the gut.
Professor Mady Hornig, Associate Professor, Centre for Infection and Immunity, Columbia University Mailman School of Public Health, New York: Professor Hornig’s research focuses on infective, immune and toxic stimuli relating to conditions that range from autism to ME/CFS. She has a particular interest in establishing how genes and maturational factors can interact with environmental triggers, leading to various brain disorders. Her ME/CFS research has concentrated on establishing whether there are immune system profiles/signatures that are characteristic of the disease and identifying infections that are linked to ME/CFS.
Professor Olav Mella, Dept. Director, Oncology, Haukeland University Hospital, University of Bergen, Norway: Professor Mella spoke on the current state of two separate clinical trials in Norway involving rituximab and cyclophosphamide, looking back at how rituximab, a drug that is normally used in cancer treatment, became a possible treatment for ME/CFS. As an oncologist, his interest in the use of this drug in ME/CFS occurred after three patients with lymphoma, who also had ME/CFS, noticed that their ME/CFS significantly improved whilst receiving rituximab.
Dr Ingrid Rekeland, Dept of Oncology, Haukeland University Hospital, University of Bergen, Norway: Dr Rekeland is investigating whether there is a metabolic obstruction in the pathway that creates glucose into energy inside the mitochondria and whether this could help to explain some of the key symptoms of ME/CFS and the rise in lactic acid production on exertion in some people with ME/CFS.
Professor Warren Tate, Group Leader, Biochemistry Department, School of Biomedical Sciences, University of Otago, New Zealand, opened his presentation by explaining that his research interest in ME/CFS research resulted from his daughter developing the illness at the age of 14. This followed an episode of Epstein-Barr infection/glandular fever almost 20 years ago. He likened the cause of ME/CFS to a large jigsaw puzzle where we had only some of the pieces in place.
Professor Ron Davis, Professor of Biochemistry and Genetics, Stanford School of Medicine, California, USA, is also involved in ME/CFS research as a result of having a seriously ill son. He updated the meeting on his research that is looking at the molecular basis to ME/CFS, how this should help to increase both our understanding of the underlying disease process and how this information can then be used to provide effective forms of treatment.
We have made Dr Shepherd’s full (16-page) conference report available as a download, which might make it easier for people with M.E. to read at their own pace.
Thursday, 17 August 2017
C H Spurgeon's Morning Devotional for 17th August
"The mercy of God”
Meditate a little on this mercy of the Lord. It is tender mercy. With gentle, loving touch, He healeth the broken in heart, and bindeth up their wounds. He is as gracious in the manner of His mercy as in the matter of it. It is great mercy. There is nothing little in God; His mercy is like Himself-it is infinite. You cannot measure it. His mercy is so great that it forgives great sins to great sinners, after great lengths of time, and then gives great favours and great privileges, and raises us up to great enjoyments in the great heaven of the great God. It is undeserved mercy, as indeed all true mercy must be, for deserved mercy is only a misnomer for justice. There was no right on the sinner's part to the kind consideration of the Most High; had the rebel been doomed at once to eternal fire he would have richly merited the doom, and if delivered from wrath, sovereign love alone has found a cause, for there was none in the sinner himself. It is rich mercy. Some things are great, but have little efficacy in them, but this mercy is a cordial to your drooping spirits; a golden ointment to your bleeding wounds; a heavenly bandage to your broken bones; a royal chariot for your weary feet; a bosom of love for your trembling heart. It is manifold mercy. As Bunyan says, "All the flowers in God's garden are double." There is no single mercy. You may think you have but one mercy, but you shall find it to be a whole cluster of mercies. It is abounding mercy. Millions have received it, yet far from its being exhausted; it is as fresh, as full, and as free as ever. It is unfailing mercy. It will never leave thee. If mercy be thy friend, mercy will be with thee in temptation to keep thee from yielding; with thee in trouble to prevent thee from sinking; with thee living to be the light and life of thy countenance; and with thee dying to be the joy of thy soul when earthly comfort is ebbing fast.
Monday, 7 August 2017
When it comes to my illness, I've learned to listen to my symptoms, trust my body, and give it the one thing it really needs: rest.
Posted on August 6, 2017, at 10:46 a.m.
It took 11 medical appointments across 20 weeks of pain and despair before I finally got a diagnosis.
For months, I’d been suffering from exhaustion so extreme that bit by bit, I’d had to let my whole life drop away. For a long time I tried to ignore it – after all, who stops doing anything just because they're tired? – but life became simply impossible. So first I cut down on my activities – like going for a run or seeing my friends – then, as my condition got worse, I cut them out completely. As for my job, I tried working from home, and I tried working half days. But my body just wouldn't play ball, and I had to stop working completely.
The tiredness was on a par with the worst flu you've ever had: Remember trying to drag yourself to the bathroom, or being hungry but barely strong enough to make food? As well as the fatigue, there were all sorts of aches and pains: a soreness in my spine, headaches and heavy limbs.
But this had lasted way longer than any flu. And now, here I was. After many fruitless discussions with GPs and inconclusive tests, I was finally in front of a specialist. He’d been able to put a clear label on my illness: a diagnosis of chronic fatigue syndrome. And he was now telling me that he had a track record of helping patients to recover. I nearly wept at my good fortune.
The doctor gave me an exercise program. “We’ll start small and build up from there,” he told me. “Stick to the routine and you'll see results.” He also said it was important that I stayed positive and didn't get too "lost" in my symptoms. “Try not to give them too much space in your mind, because you run the risk of magnifying them.”
The exercise started at a level I was comfortable with: five minutes of walking each day for the first week. At week two, five minutes became six, and so on. But by week four the nonstop walking had gotten to be too much. Weirdly, I was OK while doing the actual walk itself; it would hit me afterwards and I'd have to lie down, and I'd wake the next day feeling as though I'd run a marathon.
I discussed it with the doctor. “You're deconditioned,” he said. “You've been resting too much. Don't be afraid of exercise – it's good for you.”
I knew this made sense; exercise is good for you, isn't it? Besides, the doctor was a specialist – he'd seen it all before and he was assuring me this was the way to get better.
“I'll keep going,” I said.
“That's the right attitude,” said the doctor. He also reminded me not to dwell on my symptoms.
I didn't think I was dwelling. But when you have to lie down for days on end, it's hard to stay positive and upbeat, and it's hard not to think about the pain you're in. So I carried on walking, and hurting, and trying not to think about the hurting, and walking some more.
By week six, I had fallen behind on the programme and was feeling worse than ever. But the doctor told me that I wasn't trying hard enough. So I kept trying, and I kept paying the penalty. I didn't know what else to do, and it didn't occur to me that a doctor could consistently deny a patient’s reality. I thought maybe if I just tried a little harder, pushed a little further, I could prove the doctor right – and my own body wrong.
Going into week eight, I knew that I needed to stop. But I didn't want to give up. I held on and on to the hope of improvement – I didn't want to let my chance of recovery go. And I didn't want to stop and admit, even though by now it was clear, that not only was I not going to recover this way, but the treatment to which I'd so diligently applied myself had been making me worse.
I didn’t want to admit that, but eventually I had no choice. And when, one morning, I couldn't even make it to the kitchen to make my cup of coffee – let alone shower or dress – it was a relief to let it all go. Relief not simply because I could stop hurting, but because I could stop hurting myself. And with that I could cease the huge mental effort of trying to convince myself, in the face of all evidence, that I had been doing the right thing.
It soon became clear just how much I’d been fooling myself, as the payback for my efforts set in. Even now, even when I’ve experienced that same state of body and mind many times, it’s hard to convey what it’s like to be that sick. Hard to convey the crushing weight on my chest and limbs. Hard to convey the soreness, the shivers and the burning, the headaches, the other aches; the inability to concentrate on anything other than the feeling that every atom of my being was somehow spewing poison.
For several weeks, I was too sick to make it to the clinic, so my last conversation with the doctor was by telephone. And he didn’t seem particularly surprised or concerned to hear I’d decided not to return in person.
“I really urge you to have another go at some point,” were his parting words, as though it was simply a matter of my mustering the motivation. “That is,” he added, “if you really do want to get better.”
I hung up with the impression that, contrary to what I'd been told at the start, failures weren't so uncommon. I felt I was being shunted off the books, like a low-achieving pupil being excluded so that the school could maintain its high pass rate.
It turns out that the only thing more scary than developing a life-changing disease is finding that there is no effective help available. Reality drops away from you. Nothing in your previous life carries any weight any longer; nothing can give you strength or sense; all is swallowed into an enormous void, and the void is waiting for you, and it says: You’re on your own, and there is no resisting me.
After the worst phase of physical punishment for my efforts had passed, I also found that I'd lost the little function that I'd had before starting the exercise program. And when you get as bad as I was then, you become unable to advocate for yourself. You can’t leave your bed, and even if you could, you can’t hold a conversation in real time, because your brain won’t process things quickly enough.
There I lay, abandoned by the medical establishment – or had I abandoned it? Either way, I was full of fear, and the self-doubt instilled in me by the doctor remained. Should I try again, at some point? And what was going to become of me?
It was at that point, lost, alone, that I decided to do my own research. Sure, I’d done some light googling before, enough to find out that graded exercise was the only real option open to me (it was either that or cognitive behavioural therapy, designed to persuade me that I should think more positively and get active again – sound familiar?). But now I took a different approach, going beyond the official literature. I joined discussion forums, I started asking questions on social media, and, eventually, I learned to make sense of scientific papers.
As I dug deeper, I found that I wasn't alone in finding the exercise programme damaging. Around the world there were hundreds of thousands – possibly millions – of people stuck in their beds like me, and in the UK a sizeable proportion believed they had been put there by exercise therapy. And the rest of the world kept on spinning, and nobody knew.
From my bed, I learned that chronic fatigue syndrome, or CFS, is sometimes also known as myalgic encephalomyelitis, or ME. And I learned that the history of ME/CFS is a story of people bewildered, in pain, and often severely disabled, and suffering the even greater cruelty of being told their symptoms are only in their mind.
On the internet I met people who had been told they were “sick, not ill”. I met people who had been informed that “you must want to die, then”. (And I spoke to several who at times had felt that death would indeed be preferable.) I read the stories of children who had been removed from their families due to their parents’ refusal to force them to exercise.
I also met – online of course – several sufferers who had lived for months or years in darkness, unable to speak or interact, just strong enough to drink liquidised meals and drag themselves to the bathroom when necessary. But in this darkness I also found hope, support, and a sense of community.
On the scientific side of things, I learned that outside the UK, postexertional malaise, a flu-like delayed response to exertion, is known to be the hallmark of the disease (in fact, the US Institute of Medicine recommended renaming it on this basis). I read studies that showed that people with ME/CFS have restricted cardiovascular ability, and that they experience an overwhelming buildup of lactic acid with exertion.
I learned also that scientists had started to unpick the biological foundations of ME/CFS. Research groups in the US and Norway have now identified the disease as a sort of restricted metabolic state where the body can't manufacture energy in the normal way. No wonder exercise made me and so many others worse.
The science hasn't reached most doctors yet, but it will do. This means that help will, eventually, be on the way. Although there aren't yet any drug treatments for ME/CFS, some approaches have shown early promise.
Am I angry that I was given the wrong advice? Of course. And my heart breaks every time I read another story of how graded exercise put another person with ME/CFS in bed. More than this, though, I'm angry at how needlessly we have suffered. Why was biomedical research not begun earlier? Why were psychiatrists allowed to squash exploration in this field, by taking it and calling it their own? Why, even now, are people being told to undertake exercise programmes without being informed of the risks?
As for me, I am improving slowly, but it will be a long time before I can travel anywhere or work again. I've learned great patience, and even greater compassion for others; I'm truly thankful for that. These are qualities that will stay with me for life, because I have seen the cruelty and the grace of the world that we each experience, and the love that holds it all together.
And when it comes to my illness, I've learned to listen to my symptoms, trust my body, and give it the one thing it really needs: rest.
Wednesday, 2 August 2017
(If only they would say ME, Myalgic Encephalomyelitis, instead of CFS)
By Andy Coghlan
Inflammation biomarkers may help doctors diagnose chronic fatigue syndrome (CFS), a poorly-understood condition in which people feeling continually exhausted. These biomarkers could also give new clues to what causes the condition, and how to treat it.
The biomarkers were discovered when a team of researchers screened the blood of 192 people with chronic fatigue syndrome for cytokines – substances used by the immune system to control inflammation. The team compared the levels of 51 different cytokines in the people with CFS and 392 people who didn’t have the condition, and found that 17 cytokines rose in tandem with how bad a person’s CFS was.
“These 17 go up by various degrees in a straight line with severity,” says José Montoya, of Stanford University.
Overall, only one cytokine was consistently higher in people with CFS. But when severity was taken into account, the other 16 emerged from the analysis as being linked to the condition. For example, three-times as much of the appetite hormone leptin, which is part of the cytokine family, was present in people with very bad cases of CFS.
It is not yet clear whether the increase in inflammation markers could be a cause or result of the condition.
However, Montoya says the results support mounting evidence that CFS is a physiological condition, not a psychosomatic disorder. “There’s no question this is something that’s biologically based,” he says. “This is a disease that does not get cured with psychological treatments, counselling or anti-depression drugs.”
Montoya’s team want to use the biomarkers to develop ways to diagnose CFS, also known as myalgic encephomyelitis, and monitor its severity. These cytokines may also help identify new CFS treatments that dampen inflammation, Montoya says.
“The results and how they were obtained are encouraging, as finding markers for subsets and categorisations within the illness is much needed for future research and treatments,” says Chris Armstrong, of the University of Melbourne, Australia.
Armstrong’s own team have found that the fatigue of CFS may be caused by disrupted metabolism and energy production in the body. “The metabolic changes we found suggest a physiological stressor in the body is affecting the cells,” he says. “The cause of that stress is unknown, but is likely to be immune-based given the mounting evidence in that direction – this new study included.”
A team in Norway has had some early success in treating CFS by targeting the immune system and reducing inflammation. They have been using a drug called rituximab to wipe out the white blood cells that may make inflammatory antibodies.
Montoya says it’s unclear what causes the increase in cytokines they have seen in CFS, but he thinks something is triggering inflammation in the body – possibly an infection like the herpes virus.
Journal reference: PNAS, DOI: 10.1073/pnas.1710519114
Tuesday, 1 August 2017
By Greg Crowhurst
27th July 2017
Sir Andrew Dillon,
Dear Andrew Dillon,
Re : Myalgic Encephalomyelitis
I have cared full time, for 25 years, for my wife who has a diagnosis of Very Severe ME, my Nursing Standard article "Supporting people with severe myalgic encephalomyelitis" is referenced by NICE in the original 2007 guidelines. In 2015 I was third place finalist, BJN, Nurse of the Year, for which I received an award specifically for my work in raising awareness of and advocating for people with Severe ME. I was Secretary of the 25% Severe ME Group charity for many years and represented the Group at the Gibson Parliamentary Inquiry.
In February the Joint Commissioning Panel for Mental Health document published Guidance for Commissioners of services for people with medically unexplained symptoms – practical mental health commissioning, which misinformed Commissioners that Myalgic Encephalomyelitis is a Somatoform, mental health disorder.
The response, in a letter to me, dated March 2nd, from the Co-Chairs of the Expert Reference Group for JCPMH Guide on Commissioning for MUS and the Co-Chairs of the JCPMH claimed that the: "The content of the MUS guide is fully in line with NICE guidelines and with current practice. Should the relevant NICE guidelines alter, or the evidence in this area change, then we will revise the guide accordingly."
On March 15, NICE assured me that CG53 does not list ME as a somatoform disorder. Therefore the MUS guidelines cannot be correct.
I raised the misinformation in the JCPMH Report with the Department of Health, who confirmed that the Government recognises the WHO classification of ME as a neurological disease. They advised me to take the issue up personally with you.
I am interested to know what you can do to correct the misinformation that the JCPMH has given to Commissioners, especially given the serious potential implication in regard to the current consultation on CG53?
I also have the following questions, given that NICE has confirmed that it does not consider ME to be a Somatoform Disorder:
1. Can you tell me why NICE itself lists ME under "Depression and anxiety disorders" on the IAPT webpage and can you reassure me that it will be removed? That surely is as great a misrepresentation of ME as the JCPMH document, especially given the recognition in CG53 that “the physical symptoms can be as disabling as multiple sclerosis, systemic lupus erythematosus and congestive heart failure .”
2. Can you explain the nature of IAPT’s involvement in ME, especially in light of the the CDC’s recent decision not to recommend CBT and GET? http://www.meassociation.org.uk/2017/07/cdc-removes-cbt-and-get-as-recommended-treatments-for-mecfs-11-july-2017/
3. Can you tell me what role, if any, IAPT played in the drafting of the recent CG53 Surveillance Document, which has been heavily criticised by all major ME Charities and thousands of patients for:
* its adherence to the widely disputed CBT/GET paradigm, which has been shown to make patients, especially the most severely affected, much worse. http://stonebird.co.uk/psurvey.pdf
* its many references to the universally discredited PACE Trial
* its reliance upon vague diagnostic criteria that do not clearly identify or separate ME from mental health Chronic Fatigue (WHO F48). A wide definition helps no one; surely it is time to acknowledge that ?
* its scant regard for biomedical evidence
* its extraordinary decision not to update the 10 year old guidance which not only was condemned as “unfit for purpose” at the time, but continue to deny patients, like my profoundly physically ill wife, equal access to health care
* its failure to accurately represent international clinical practice
* its failure to remove outdated treatment recommendations and its pronounced self-circular psychiatric bias.
4. I am very curious to know the composition of the Topic Experts and their knowledge base and impartiality. What biomedical representation, if any, did you have? What clinical input, outside of the biopsychosocial school, was involved for unbiased appraisal of the biopsychosocial content? Can you tell me who the Topic Experts were? Were any of the Royal College’s involved?
5. Can you tell me why NICE only gave stakeholders two weeks to respond to the 56 page Surveillance document, making it incredibly difficult for those people who have ME themselves or full time carers, to have enough time to contribute adequately or at all.
6. Can you explain why NICE has relied heavily on an unfounded psychiatric theory of ME that is nothing more than that, with no real evidence itself, while ignoring the more than 9000 published papers that have been published world wide, detailing the biomedical abnormalities in ME?
7. Can you explain, given the statement in 2014 by Professor Mark Baker, Director of the Centre for Clinical Practice, at a Forward- ME meeting, that the Guideline failed to address the real issues in ME/CFS, does not promote innovation and has had a disappointing impact on specialist care and commissioning issues, why NICE has continued to stick to its outmoded, inappropriate, dangerous guidance?
The Surveillance document does nothing, in my opinion, to challenge the misperception that ME is a mental illness, in fact it's decision to come off the static list, not for medical reasons, but because of the FITNET CBT/GET Trial reinforces the apparent psychosocial bias of the whole document and attitude of NICE.
If CG53 continues to contribute to a situation where people with ME are:
* misinterpreted as having a mental health issue
* where biomarkers are not sought for and relevant tests are proscribed
* where health professionals of every level are misinformed and their awareness skewed wrongly towards a biopsychosocial interpretation of a serious physical disease with ignored multi-system dysfunction, endangering lives and leading to mistreatment, misinterpretation, neglect and harm
* where the guidance on Severe ME fails to recognise the terrible suffering and multiple physical symptoms patients experience, making it dangerously irresponsible. http://www.stonebird.co.uk/principles%20of%20care.pdf
* where ME is still not separated from and confused with mental health Chronic Fatigue and other poorly diagnosed diseases
* where services are geared towards a psychiatric diagnosis of wrong illness thought and deconditioning
* where patients are offered treatments that are inhuman, cruel, inappropriate and dangerous, because they are in direct denial of their physical reality- the potential for harm is enormous and terrifying in ME
then surely that is in contravention of your obligations under the Human Rights Act and the Equality Act?
The ME Community has been insisting for years that CG53 is not and never has been appropriate for patients with Myalgic Encephalomyelitis; the way forward is for ME to have its own biomedical Guideline and pathway, categorically without psychiatric interpretation and involvement.
Tuesday, 25 July 2017
24 July 2017
By David Tuller, DrPH
The Countess of Mar, a well-known advocate for ME/CFS patients in the House of Lords, has received a negative response to her request for the names of the experts involved in the review of the NICE guideline for CFS/ME. The ME Association has not yet received a response related to the same question, nor have I. But the response to the countess indicates that the process is proceeding with a lack of full transparency.
Here’s the response from the Department of Health:
“The National Institute for Health and Care Excellence (NICE) routinely consults a range of topic experts as part of its surveillance review process. NICE is currently consulting on a review proposal for its clinical guideline on the diagnosis and management of chronic fatigue syndrome and myalgic encephalomyelitis. NICE does not routinely publish the names of topic experts as they are not part of the decision making [sic] process for the surveillance review.”
This answer is of course unsatisfactory. The last sentence is the operative one, so let’s deconstruct it. In the first part of the sentence, NICE is telling us that it does not routinely publish the names of topic experts. But just because it doesn’t routinely do something is not necessarily relevant to whether it should take this step now. Perhaps no one has asked for these names before. Presumably the development or review of most guidelines is not so controversial as this particular one for CFS/ME. (The patient-preferred name for the illness, and the most appropriate one, is of course just ME, without the CFS tacked on.)
It is also not routine that more than 15,000 people sign petitions expressing serious dissatisfaction with existing clinical guidelines. But that’s how many have put their names to the petition launched by the ME Association. That’s a huge number of unhappy patients and advocates; NICE would be well-advised not to ignore them. Perhaps the strict adherence to routine measures—like not disclosing the names of topic experts involved in the process—should be reconsidered in the current urgent context. (The petition drive closed today to coincide with the deadline for the stakeholder comments on the NICE guidelines.)
The second part of the sentence explains the purported reason for not sharing the topic expert names: they are not part of the decision-making process. First of all, what does that mean? Given that topic experts have been consulted in this instance, it is bizarre to read that they are “not part of the decision-making process”? Is their advice then ignored completely? Are they just a fig leaf to create the appearance of consultation while NICE does what it wants? If their advice is reviewed and considered rather than tossed right in the trash, why does the statement declare that they are not part of the decision-making process?
Perhaps the statement means that the topic experts are not officially in the room or on the conference call when the final approval is made. But even if that were the case, why would that mean their names should be kept from the public? Is the development process of NICE guidelines an official state secret that demands utmost protection?
And if the topic experts are not involved in the decision-making, as the statement asserts, then what exactly is their function? And who are the people involved in making the decision? Are they themselves experts, or just functionaries listening to others? Is it the group that originally developed the 2007 guideline? That group includes Professor Esther Crawley [Correction–see below], a close colleague of the PACE authors-—so that’s not a particularly good sign. Given the enormous impact of these guidelines, it is imperative that the process be conducted as openly as possible—which, given the response to the Countess of Mar’s question, is so far not the case.
Correction, July 24th: In the initial post, I mistakenly wrote Professor Trudie Chalder.