NICE guidelines for ME/CFS:

Tina Writes…

I am one of the stakeholders on the NICE guidelines for ME/CFS committee. I represented over 25,000 children that have ME in the UK and their parents. We were all told that NICE were going to “rip up” the old guidelines and start afresh. We were all shocked when the first few members were announced. Trust in the stakeholders has been shaken, and although I have not been blamed, I am responsible. So, for clarity:

  • I explained at the engagement and scoping meetings experiences of those parents, and that of their very sick children, when forced with no informed consent to enter into a treatment regime of CBT and GET (other names are being used for the same approach) as a rehabilitation. We needed to change this, and NICE appeared to agree.
  • I told of how most, if not all of the children are not diagnosed properly, are given the wrong treatment based on flawed science, a fact that the world and the UK Parliament is now waking up to.
  • I said that all too many parents get accused of fabricating or Inducing Illness (FII) in some way. That FII is used as a weapon to either shut parents up, or to push them to leave a service.
  • I explained the trauma of the methods used by the ME/CFS centres to convince both patient and parent that there is nothing wrong, no harm can be done by activity, and that PEM is not explained or accepted.
  • I told them “NHS Hospital trust websites, that some of your committee members work in, using CBT and GET, give false and misleading information.” NICE are fully aware of this.
  • I explained how draconian measures were used, such as taking away wheelchairs from those children that desperately need them, or changing/denying diagnosis or treatment put forward by those eminent and world respected doctors in the field of ME, Lyme and EDS. NICE said it understood.
  • I explained how induced Post Traumatic Stress Disorder in our children occurs when their reality, experience and understanding is denied. NICE said this would change.
  • I also told that once you have been accused of FII, you cannot clear your name and that treatment then follows a pattern that victimises the children and their families further. That there is no way of recording false allegations of FII, and that the GMC have not held those accusing doctors to account on this matter. Decades of families whose children have been put through CBT and GET and now are severe adults – bear witness to the harm. That there is no way for parents to record this harm in our children.
  • We are not talking about small numbers here, and although Tymes Trust record the most severe cases and those that reach court, parents such as myself have no way of recording our experiences. Furthermore, the courts silence those that have gone through the system, so that the truth is never known, and all sorts of harms are being hidden by the courts. Family courts are held in secret, and evidence is only produced to protect the child. Judges are relying on doctors to be honest and true, and to know their field of expertise. Courts and the Judges expect NICE to be evidence based, and if a treatment of CBT and GET is offered then the parent should trust that evidence and doctors’ advice – based on NICE guidelines.

NICE have a duty of Candour here. Over 200 cases of false accusations is testament to how the diagnosis, treatment and lack of understanding of ME fails our children. We have no idea how many children like the autistic community have been inappropriately put into Metal Health Hospitals and given hostile and harmful treatment. We do know it happens. We know children taken into care are not looked after, as their illness is misunderstood by Social Workers who have been fed the wrong information on ME, POTS, EDS, vEDS, Mast Cell, Lyme, Gastro-paresis, severe pancreatitis, autoimmune, after sepsis, after cancer treatment, Celiac, Thyroid, Colitis and pernicious anaemia. These are a few of the conditions where parents – mostly/all mothers have been accused of fabricating or inducing illness, with some children having life threatening consequences leading to more disability or death. These children were taken into care and given no treatment, or pushed beyond their limits both physically and psychologically by those who believe in CBT and GET.

Doctors that understand ME have also been victimised.
The guidelines belong to NICE. NICE is accountable and in authority. The staff who put all their efforts into making these guidelines and services are being let down by the system that operates within NICE, due to funding bias it would seem. Having members that still use/believe in CBT and GET forming a large part of the committee goes against all scientific evidence. I have a belief in NICE as a system, and can see how this can work for both doctor and patient. Tuesday 13th November 2018, I spent with those at the NICE IT department. We went through how a layperson such as me uses and can use your website with a doctor, commissioning groups and care and quality commission. How to find pathways so that patients or parents like me can find the information they need to understand and to access the NHS, and support their doctors. However, trust in the information NICE offers is of paramount importance, and that the information given is true, honest, unbiased, robust and does no harm. This will not be the case if the CBT and GET lobby remain.

The guidelines have to be drawn up without a political, or empire agenda. They have to be fit for purpose. The history of ME (well-known and documented) more than any other illness, teaches us what can happen if patients are not listened to, and biomedical research denied. As with AIDS, Shipman, Gosport, Bristol Heart scandal, PACE trial, Autism and many other cases that have drawn negative attention to our healthcare system and show the patient should never be victimised, ‘gas-lighted’ and should be listened to – NICE run the risk of falling causing another medical disaster. Those doctors that make up the committee and use CBT and GET as treatments or in research, show a distinct lack of understanding of ME, and respect for their patient and their families. Those that use CBT and GET on very young children, without logging biomedical changes that happen (that have been well documented), along with not reporting harms, are not only questionable but go against every form of ethical reasoning.  This now jeopardises the trust NICE needs to make the guidelines work and fit for purpose.

It is no good trying to balance out the CBT and GET lobby. Research within CBT is showing flaws in all the different fields it is used in. Dismissing world renowned doctors who deal with FII on a regular basis, and not inviting those that have been formally and falsely accused of FII to be a witness, is a mistake. How can NICE gain the trust that has been lost? Those mothers that have had to live with the consequences of false allegations, or the death of their child as a result of CBT and GET, should be sought out and encouraged to help with the guidelines. Due to the appointment of those that advocate CBT and GET (against the huge amount of data NICE had been given), NICE now run the risk of losing respect from doctors around the world, world renowned researchers, GPs in the UK, and the ME community. All have tried to support NICE, and what NICE and the NHS stands for within the UK. I am asking – where is the respect for the patient in this committee? I sincerely hope NICE can make a difference and keep their promises of making change; supporting doctors to give information to enable informed consent, with duty of candour in mind, protecting those in most need – our children.

I live in hope, Tina.

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Brain differences shown in ME/CFS Fukuda study: by Sasha Nimmo, ME news Australia May 23rd, 2018.

Scientists at Queensland’s National Centre for Neuroimmunology and Emerging Diseases, Griffith University, found obvious differences between the brains of patients with CFS and healthy controls, when examined using magnetic resonance imaging (MRI) during an attention test. The study examined 43 people with CFS (Fukuda criteria) and 26 healthy controls. The people in the study also completed a health survey about the severity of their illness and the MRI findings correlated with the self-reported severity. The participants were all asked to do the ‘Stroop test,’ which tests for brain damage by asking people to read the names of colours, but the words are printed in a different coloured ink. Performance was measured by accuracy and response time. The CFS patients took longer to answer, but were not significantly different in accuracy. Researchers found that CFS patients recruit more regions to accomplish the Stroop task than controls.

This is the first study to investigate BOLD (blood oxygen level dependant) signal SampEn in response to tasks in CFS. The results suggest the brain responds differently to a cognitive challenge in patients with CFS, with recruitment of wider regions to compensate for lower information capacity. Published in ‘NeuroImage: Clinical’, the study’s lead author is Dr Zack Chan, who specialises in neuro-imaging in CFS. He is working on developing objective diagnostic criteria using diagnostic imaging and machine learning. Dr Leighton Barnden, also at the NCNED, has done a lot of work on brain changes and is one of the authors of this study. This study was funded by the Stafford Fox Medical Research Foundation, the Mason Foundation, Douglas Stutt and Blake-Beckett Foundation.

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MillionsMissing 2018

A global campaign for ME health equality

#MillionsMissing 2018

Saturday 12 May, 12-3pm

Queen Square, Bristol, BS1 4LH

#millionsmissing from their careers, schools, social lives and families

#millionsmissing in research funding

Patients, families and allies around the world are gathering on May 12th to demand action for people living with ME. We hope you can join us in Bristol — in person or on social media. There are also several ways in which you can help support the campaign in the lead up to the big day:

  • Send us your shoes with a label attached to: Millions Missing Bristol, 29 Caernarvon Road, Keynsham, BS31 2NY. We will display them on your behalf on the day.



  • Like and share the Millions Missing Bristol Facebook page


  • Follow us on Instagram at millionsmissing_bristol


  • Click “I’m attending” on our Facebook Event


  • Visit and let ME Action know you’ll be attending


  • Invite your local MP to attend on May 12th (a template letter is available on our Facebook page)


  • Volunteer to speak on the day or ask a friend or family member to speak on your behalf

More information:                           Facebook   @millionsmissingbristol

  Instagram   @millionsmissing_bristol

                                                           Tel  07504 989526

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Plea from a fallen doctor on ME/CFS:

I was educated at Baylor and practiced medicine for 30 years. I had a thriving practice, a rich social life, and excellent physical and mental health. I loved what I did and loved my life. I ran marathons, spoke at conferences, and chaired non-profit organisations. I am now completely bedridden from post viral CFS. I am writing this to beg my fellow colleagues to take this disease seriously, understand that it is 100% organic in origin, and that it can happen to anyone. I used to see CFS patients fairly often in my practice. Some of them were quite debilitated and some semi-functional. I always tried to be sympathetic and did what I could to help, but truth be told there was always a voice in my head questioning if their symptoms were psychosomatic. At times I delayed a diagnosis, because the literature told me to wait 6 months. I recommended exercise, antidepressants, and psychotherapy because that had always been the conventional wisdom. And when patients didn’t come back, I subconsciously assumed they had gotten better, and that I was justified in my approach. I feel tremendous guilt about this now.

When I got the flu that started this, I thought I would be out of work for 10 days. 10 days turned into 10 weeks, and then 10 months. The virus was gone, my labs were clean, and yet I still felt horribly ill. I could barely stand up in the shower, due to orthostatic intolerance. Later my wife would have to install a shower chair. I could not read, or write due to cognitive dysfunction. I could not walk more than 45 steps without extreme lactic build up in my muscles. Any minor exertion would produce an intensifying of symptoms for several days. Add on insomnia, sensitivity to noise and light, and uncharacteristic emotional lability, and you understand the hell my life became. Every type of conventional medical test came back negative, or could not explain symptoms. My own family thought I was crazy (not to mention my friends, cohort, and colleagues).

Of course I tried the standard things I told my patients to do. Antidepressants were hit or miss, as they so often are, and did not touch the core symptoms. Psychotherapy was helpful for coping. Exercise of any kind was a complete unmitigated disaster, that severely and permanently worsened my state. Finally I did find lab abnormalities; Cytokines. Krebs cycle metabolites. Near zero ADH. As I lay bed-bound, I slowly regained the ability to process complex data, and I poured through the research and discovered that yes this is a very real illness, with organic abnormalities documented as early as 1932. Why aren’t we taught this in medical school? I tried antivirals, antibiotics, hormone replacement, and yes I’ll admit, even some more questionable alternative medicine protocols. Nothing worked.

Finally I went into remission using a combination of monoclonal antibodies (Rituxan, Cosyntex, Enbrel). Remission was glorious. I took my wife to Costa Rica, played with my grandchildren, and learned how to sail. And then I relapsed for no good reason, and hell returned. As of yet, I have been unable to reproduce the first remission. I beg other doctors to take this to heart. CFS is a real disease, as bad as end stage AIDS, or cancer. It is also treatable, but only through trial and error, and even then nothing is guaranteed.          i.e.

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Metabolic switch may bring on ME/CFS.

Metabolic switch may bring on CFS: By Andy Coghlan

DAILY NEWS, 13th February 2017.

It’s as if a switch has been flicked. Evidence is mounting that CFS is caused by the body swapping to less efficient ways of generating energy. Also known as ME, CFS affects some 250,000 people in the UK. The main symptom is persistent physical and mental exhaustion that doesn’t improve with sleep, or rest. It often begins after a mild infection, but it’s causes are unknown. Some have argued that CFS is a psychological condition, and that it is best treated through strategies like CBT. But several lines of investigation are now suggesting that the profound and painful lack of energy seen in the condition could in many cases be due to people losing their ability to burn carbohydrate sugars in the normal way, to generate cellular energy. Instead, the cells of people with CFS stop making as much energy from sugar as usual, and start relying more on lower-yielding fuels, such as amino acids and fats. This kind of metabolic switch produces lactate, which can cause pain when it accumulates in muscles. Together, this would explain both the shortness of energy, and why even mild exercise can be exhausting and painful.

Sex differences:

Øystein Fluge of Haukeland University Hospital in Bergen, Norway, and his colleagues studied amino acids in 200 people with CFS, and 102 people without it. The levels of some amino acids in the blood of women with CFS were abnormally low – specifically for the types of amino acid that can be used by the body as an alternative fuel source. These shortfalls were not seen in men with CFS, but that could be because men tend to extract amino acids for energy from their muscles, instead of their blood. And the team saw higher levels of an amino acid, that’s a sign of such a process. “It seems that both male and female CFS patients may have the same obstruction in carbohydrate metabolism to energy, but they may try to compensate differently,” says Fluge. Both sexes had high levels of several enzymes known to suppress pyruvate dehydrogenase (PDH), an enzyme vital for moving carbohydrates and sugars into a cell’s mitochondria – a key step for fully exploiting sugar for energy. Fluge thinks PDH is prevented from working in people with CFS, but that it can spontaneously recover.

Starvation effect:

Several studies have now hinted that defects in sugar burning can cause CFS, but there is still uncertainty over how exactly this is disrupted. However, a picture is emerging. Something makes the body switch from burning sugar, to a far less efficient way of making energy. “We don’t think it’s just PDH,” says Chris Armstrong at the University of Melbourne in Australia, whose research has also uncovered anomalies in amino acid levels in patients. “Broadly, we think it’s an issue with sugar metabolism in general. The result is not unlike starvation,” says Armstrong. “When people are facing starvation, the body uses amino acids and fatty acids to fuel energy for most cells in the body, to keep glucose levels vital for the brain and muscles as high as possible. We think that no single enzyme in metabolism will be the answer to CFS, just as no single enzyme is the ‘cause’ of something like hibernation,” says Robert Naviaux of the University of California at San Diego, who has found depletion of fatty acids in patients, suggesting they were diverted as fuel.

Not psychosomatic:

So what could flick the switch to a different method of metabolism? Fluge’s team thinks that a person’s own immune system may stop PDH from working, possibly triggered by a mild infection. His team has previously shown that wiping out a type of white blood cell called B-cells in CFS patients, seems to relieve the condition. These white blood cells make antibodies, and Fluge suspects that some antibodies made to combat infections may also recognise something in PDH and disable it. The team is now conducting a large trial in Norway of the cancer drug Rituximab, which destroys the cells that make antibodies, in people with CFS. Results are expected next year. Together, these metabolic approaches are suggesting that CFS has a chemical cause. “It’s definitely a physiological effect that we’re observing, and not psychosomatic, and I’ll put my head on the block on that,” says Armstrong. However, he adds that psychological and brain chemistry factors might be involved in some cases.

Journal reference: Journal of Clinical Investigation, DOI: 10.1172/jci.insight.89376


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A response to Professor Esther Crawley’s broadcast on BBC Radio Bristol:

A response to Professor Esther Crawley’s broadcast on BBC Radio Bristol:

By Margaret Williams, 6th November 2016.

It has been said that people like Professor Esther Crawley and those involved in PACE-Gate genuinely don’t understand that the whole endeavour of science is *Predicated on Objective and Reproducible Measurements* (private communication: 5th November
2016). In her broadcast on 5th November 2016 with Dr Phil Hammond on BBC Radio Bristol, in which she promoted her FITNET trial (Fatigue In Teenagers on the interNET), Professor Crawley made some very unscientific statements. The FITNET trial is funded by Health Technology Assessment (HTA) Programme (UK), which claims to fund “independent” research about the effectiveness, costs and broader impact of healthcare treatments. It is the largest of the programmes supported by the National Institute of Health Research (NIHR), which is the research arm of the NHS.

The HTA Programme says: “Our research serves a wide variety of key stakeholders, including decision makers in local government and policy-makers (including NICE)”. It’s Clinical Evaluation and Trials Board includes Professor Michael Sharpe, one of the PACE Principal Investigators, and a staunch supporter of behavioural interventions for ME/CFS. This NHS support presents a major discrepancy, because whilst one arm of the NHS is funding behavioural interventions to be used in the FITNET trial (CBT and GET), another arm of the same NHS (NHS Plus, a Government-funded project) has condemned graded exercise as it may cause (quote): “significant deterioration” (see below).

The “information” leaflets – all headed “Dealing with Chronic Fatigue (CFS/ME) in Young People.. Specialist help for ME” — produced by CFS/NHS/PAEDIATRICS/BATH are lacking in any appreciation of what ME/CFS actually is. The leaflets are deeply concerning because, first and foremost, “Chronic Fatigue” is not “CFS/ME” and they pay no attention to the reality of ME/CFS, for example: The leaflet “Cognitive Behaviour Therapy” starts off by saying: “Hassles and problems are part of everyday life, but sometimes the problems seem to take over, and you may end up feeling unhappy. People with problems often think in unhelpful ways.. CBT will help you find the link between what you think, how you feel and what you do, and how to face and overcome your problems”.

The “Exercise Chart for Severely Affected” requires one specified exercise each hour. The leaflet entitled “Thinking Traps” says: “This leaflet will help you find the negative trap you have fallen into. You will then be able to challenge your negative thoughts and fight back”. The “Thoughts and Feeling Diary” requires that at the end of each day, the young person must write down what they have done that day, naming the time, who was there, where they were, what was happening before, and what happened afterwards. The “Managing Feelings and Emotions” leaflet says: “If we feel angry and frustrated, we might shout or swear at someone.. If we feel anxious and worried about something, we might avoid doing it, and make up excuses.. Don’t worry – the trick is to do just a little bit more each time you do something.” The “Activity, Rest and Sleep Diary” is to “help you use a graded activity programme to record what you do each week. This will help as you gradually increase the amount you do”. The “Energy Management” leaflet says: “We have lots of ways to help you, including charts and cards. When you have managed 2 weeks of the same activity daily, you can start to increase it by 10% a week”.

In her interview, Crawley said about ME/CFS: “we know very little about it,” and this was endorsed by Hammond: “We certainly know very little about it”. Such statements are untrue: Although the cause remains unknown, much is known about significant pathology in ME/CFS:

*) Abnormalities of the central nervous system: include abnormalities of brain cognition, brain perfusion, brain metabolism and brain chemistry; there is evidence of low blood flow in multiple areas of the brain; neuro-imaging has revealed lesions in the brains of approximately 80% of those tested, and according to the researchers, these lesions are probably caused by inflammation. There is a correlation between the areas involved and the symptoms experienced. Abnormalities on SPECT scans provide objective evidence of central nervous system (CNS) dysfunction. There is evidence of a chronic inflammatory process of the CNS, with oedema, or demyelination in 78% of patients tested. There is evidence of a significant and irreversible reduction in grey matter volume (especially in Brodmann’s area 9), which is related to physical impairment and may indicate major trauma to the brain (which could also explain the low recovery rate). There is evidence of seizures; a positive Romberg is frequently seen in authentic ME/CFS patients.

*) Abnormalities of the autonomic and peripheral nervous systems: There is evidence of dysautonomia in ME/CFS patients.

*) Cardiovascular dysfunction: There is evidence of
haemodynamic instability and aberrations of cardiovascular reactivity (an expression of autonomic function). There is evidence of diastolic cardiomyopathy. There is evidence of endothelial dysfunction. There is evidence of peripheral vascular dysfunction, with low oxygenation levels and poor perfusion and pulsatilities. There is evidence of abnormal heart rate variability, and evidence of abnormal orthostasis. There is evidence of abnormally inverted T-waves and of a shortened QT interval, with electrophysiological aberrancy. There is evidence of abnormal oscillating T-waves and of abnormal cardiac wall motion (at rest and on stress). There are indications of dilatation of the left ventricle and of segmental wall motion abnormalities. There is evidence that the left ventricle ejection fraction – at rest and with exercise – is as low as 30%. There is evidence of reduced stroke volume.

*) Respiratory system dysfunction: there is evidence of significant reduction in many lung function parameters, including a significant decrease in vital capacity. There is evidence of bronchial hyper-responsiveness.

*) A disrupted immune system: there is evidence of an unusual and inappropriate immune response. There is evidence of very low levels of NK cell cytotoxicity. There is evidence of low levels of autoantibodies (especially antinuclear and smooth muscle). There is evidence of abnormalities of immunoglobulins, especially sIgA and IgG3 (the latter having a known linkage with gastrointestinal tract disorders). There is evidence of circulating immune complexes. There is evidence of a Th1 to Th2 cytokine shift. There is evidence of abnormally diminished levels of intracellular perforin. There is evidence of abnormal levels of interferons and interleukins. There is evidence of increased white blood cell apoptosis, and there is evidence of the indisputable existence of allergies and hypersensitivities, and positive mast cells, among many other anomalies, with an adverse reaction to pharmacological substances being virtually pathognomonic.

*) Virological abnormalities: there is evidence of persistent enterovirus RNA in ME/CFS patients. There is evidence of abnormalities in the 2-5 synthetase / RNase L antiviral pathway, with novel evidence of a 37 kDa binding protein not reported in healthy subjects, or in other diseases. There is evidence of reverse transcriptase, an enzyme produced by retrovirus activity, with retroviruses being the most powerful producers of interferon. There is evidence of the presence of HHV-6, HHV-8, EBV, CMV, Mycoplasma species, Chlamydia species and Coxsackie virus in the spinal fluid of some ME/CFS patients – the authors commenting that it was surprising to find such a high yield of infectious agents on cell free specimens of spinal fluid that had not been centrifuged.

*) Evidence of muscle pathology: this includes laboratory evidence of delayed muscle recovery from fatiguing exercise, and evidence of damage to muscle tissue. There is evidence of impaired aerobic muscle metabolism. There is evidence of impaired oxygen delivery to muscle, with recovery rates for oxygen saturation being 60% lower than in normal controls. There is evidence of prolonged EMG jitter in 80% of ME/CFS patients tested. There is evidence of greater utilisation of energy stores. There is evidence that total body potassium (TBK) is significantly lower in ME/CFS patients (and abnormal potassium handling by muscle in the context of low overall body potassium may contribute to muscle fatigue in ME/CFS).  There is evidence that creatine (a sensitive marker of muscle inflammation) is excreted in significant amounts in the urine of ME/CFS patients, as well as choline and glycine. There is evidence of type II fibre predominance, of scattered muscle fibre necrosis and of mitochondrial abnormalities.

*) Neuroendocrine abnormalities: there is evidence of HPA axis dysfunction, with all the concomitant implications. There is evidence of abnormality of adrenal function, with the size of the glands being reduced by 50% in some cases. There is evidence of low pancreatic exocrine function. There is evidence of an abnormal response to buspirone challenge, with a significant increase in prolactin release, that is not found in healthy controls or in depressives. There is evidence of abnormal arginine – vasopressin release during standard water-loading test. There is evidence of a profound loss of growth hormone. Even when the patient is euthyroid on basic screening, there may be thyroid antibodies and evidence of failure to convert T4 (thyroxine) to T3 (tri-iodothyronine), which in turn is dependent upon the liver enzymes glutathione peroxidase and iodothyronine deiodinase, which are dependent upon adequate selenium in the form of selenocysteine (which may be inactivated by environmental toxins).

*) Defects in gene expression profiling: there is evidence of reproducible alterations in gene regulation, with an expression profile grouped according to immune, neuronal, mitochondrial and other functions, the neuronal component being associated with CNS hypomyelination.

*) Abnormalities in HLA antigen expression: Teraski, from UCLA, found evidence that 46% of ME/CFS patients tested were HLA-DR4 positive, suggesting an antigen presentation.

*) Disturbances in oxidative stress levels: there is mounting evidence that oxidative stress and lipid peroxidation contribute to the disease process in ME/CFS. Circulating in the bloodstream are free radicals, which if not neutralised can cause damage to the cells of the body, a process called oxidative stress. In ME/CFS there is evidence of increased oxidative stress, and of a novel finding of increased isoprostanes, not seen in any other disorder. These raised levels of isoprostanes precisely correlate with patients’ symptoms (isoprostanes being abnormal prostaglandin metabolites that are highly noxious by-products of the abnormal cell membrane metabolism). There is evidence that incremental exercise challenge (as in graded exercise regimes) induces a prolonged and accentuated oxidative stress. There is evidence of low GSHPX (glutathione peroxidase, an enzyme that is part of the antioxidant pathway. If defective, it causes leakage of magnesium and potassium from cells).

*) Gastro-intestinal dysfunction: There is evidence of objective changes, with delays in gastric emptying and abnormalities of gut motility. There is evidence of swallowing difficulties and nocturnal diarrhoea. There is evidence going back to 1977 of hepatomegaly, with fatty infiltrates. On administration of the copper response test, there is evidence of post-viral liver impairment – an increase of at least 200 in the copper level is the expected response, but in some severely affected ME/CFS patients the response is zero. There is evidence of infiltration of splenic sinuses by atypical lymphoid cells, with reduction in white pulp, suggesting a chronic inflammatory process. There is evidence that abdominal pain is due to unilateral segmental neuropathy. There is significant evidence that people with ME/CFS have increased serum levels of IgA and IgM against the LPS of gram-negative enterobacteria, indicating the presence of increased gut permeability, resulting in the autoimmunity seen in many ME/CFS patients. This indicates that the symptoms of irritable bowel seen in ME/CFS reflect a disorder of gut permeability, rather than psychological stress as most psychiatrists believe (gastro-intestinal problems are a serious concern in ME/CFS, and 70% of the body’s immune cells are located in the GI tract).

*) Reproductive system: There is clinical evidence that
some female patients have an autoimmune oophoritis. There is evidence of endometriosis. There is evidence of polycystic ovary syndrome. In men with ME/CFS, prostatitis is not uncommon.

*) Visual dysfunction: There is evidence of latency in accommodation, of reduced range of accommodation and of decreased range of duction (ME patients being down to 60% of the full range of eye mobility). There is evidence of nystagmus. There is evidence of reduced tracking. There is evidence of problems with peripheral vision. There is evidence that the ocular system is very much affected by, and in turn affects, this systemic condition.

Recently, Naviaux et al reported that targeted, broad-spectrum metabolomics of plasma revealed a characteristic chemical signature, and showed that ME/CFS  is a highly concerted hypometabolic response to environmental stress that traces to the mitochondria (PNAS 2016:113:7). As world expert Professor Anthony Komaroff said at the IACFSME conference in Fort Lauderdale in October 2016, we know that genes involved in signal transduction are hypomethylated, but that genes involved in apoptosis are hypermethylated; that exercise triggers a characteristic gene expression signature involving 15 cytokines/adipokines/growth factor; that there is lower oxygen consumption, leading to earlier conversion to anaerobic metabolism, and that lactate levels are higher at all work effort, that most of the dysfunctional cytokines are pro-inflammatory and that there is chronic low-level inflammation. We know there is altered heart rate variability, due to reduced cardiac vagal activity.

As a paediatrician with an interest in ME/CFS, why does Professor Crawley ignore this large body of science and persist in testing – yet again – a theory that has comprehensively and unarguably failed, and why did she make such insupportable assertions on BBC radio, demonstrating once again a fundamental lack of understanding of basic scientific principles? Data from the FINE and PACE trials do not support Crawley’s assertions, in fact they vitiate them and, as Komaroff also pointed out, it has been shown in a study of 990 ME/CFS patients that their belief about the cause of the illness did not explain their level of activity, a result that does not support the use of CBT, but Crawley said on air: “the evidence for CBT and GET is good. It’s good in adults, and if you’re a child with CFS, you have a two-thirds chance of recovery at six months, with treatment. I’ll just say that again – two thirds at six months with treatment”.

When Hammond mentioned that in the Dutch study, upon which Crawley’s FITNET trial is based, recovery was not sustained over time, Crawley’s response was immediate: “Oh people have really made a mistake on this. The recovery was still very high.” This appears to demonstrate Crawley’s inability to accept that in the Dutch study in question, there was no difference between the active and control groups at long-term follow-up, which is consistent with every other trial of CBT. Despite many trials that have attempted to cure ME/CFS by incremental physical exercise, none of these has demonstrated sustained objective improvement, let alone a cure for the disease. Of importance is that by promising even a two-thirds recovery in her FITNET trial, Crawley is in breach of the General Medical Council Regulations as set out in “Good Medical Practice”: “You must not make unjustifiable claims about the quality or outcomes of your services in any information you provide to patients. It must not offer guarantees of cures”

Furthermore, Crawley is introducing bias into her own trial by declaring that the active therapy has already been shown to work. Given that the trial relies on subjective endpoints and is un-blinded, this is particularly egregious. In her broadcast, Crawley said of the PACE trial that: “It was a GREAT, great trial.” Even though the PACE trial has been debunked beyond dispute, she seems to be blinkered, as evidenced by the fact that she co-authored a paper which claimed up to 40% recovery in the PACE trial participants (BMC Health Services Research 2011, 11:217 doi:10.1186/1472-6963-11-217), with which even the PACE trial authors disagreed, as they published a 22% recovery rate.

Crawley was dismissive about the biological studies that have produced ground-breaking results, including evidence of hypometabolism, saying: “We have to stop doing these really small studies, because I think they’re just confusing. They don’t end up being what’s called ‘replicated’, so they’re not reproduced a second time, and I don’t think they’re adding, at the moment, to the world literature.” Crawley went on to say about graded exercise therapy: “the best evidence that you can ever get is what’s called the systematic review – and the largest systematic review, of over 1,500 people was absolutely clear, there was no evidence of harm”. The “evidence” from a systematic review of the literature cannot be taken in isolation (for example, Professor Peter White, whose life’s work has been spent on proclaiming the benefits of behavioural interventions in ME/CFS, was involved in the Cochrane Database of Systematic Reviews 2014, Issue 4: “Exercise therapy for chronic fatigue syndrome”: Larun L, Odgaard-Jensen J, Brurberg KG, Chalder T, Dybwad M, Moss-Morris RE, Sharpe M, Wallman K, Wearden A, White PD, Glasziou PP, thus potentially compromising the independence of the Review).

Over the years, there is abundant evidence from numerous surveys by ME/CFS charities of almost 5,000 patients, that in such patients CBT is ineffective and that GET is unacceptable and sometimes positively harmful. Those surveys include one sponsored jointly by the ME Association and Action for ME (“Report on a Survey of Members of Local ME Groups”. Dr Lesley Cooper, 2000). Cooper found that “Graded exercise was felt to be the treatment that made more people worse than any other, and that it had actually harmed patients.” Another survey of 2,338 ME/CFS sufferers (“Severely Neglected: M.E. in the UK”) was carried out in 2001 by Action for ME; it’s preliminary report stated: “Graded exercise was reported to be the treatment that had made most people worse.” In the final report, this was changed to stating that graded exercise had made 50% of patients worse. The 25% ME Group for the Severely Affected carried out a further survey in 2004, which found that 93% of respondents found GET to be unhelpful, with 82% reporting that their condition was made worse. In 2005, a report (“Our Needs, Our Lives”) published by The Young ME Sufferers Trust found that 88% had been made worse by exercise.

In October 2006, the ME Association secured an acknowledgement by NHS Plus – a Government-funded project – that GET (recommended in the NICE Guideline as part of CBT) can be harmful to people with ME/CFS. The NHS Plus Guidance leaflets now say: “Although some RCTs show evidence of improved functional capacity for work, and reduced fatigue, some patients experience a significant deterioration in symptoms with this intervention”. The ME Association noted: “This is a significant acknowledgment by the NHS that GET has dangers to people with ME/CFS”. In 2008, Action for ME published a survey of over 2,760 patients (“M.E. 2008: What progress?”), which found that one third had been made worse by GET and that at their worst, 88% were bed/housebound, being unable to shower, bathe or wash themselves, and that 15% were unable to eat unaided. The Press Release of 12th May was unambiguous: “Survey finds recommended treatment makes one in three people worse”. Professor Crawley, a member of the GDG that drew up the NICE Guideline, dismissed the AfME/AYME report’s findings, saying the survey was unreliable: “This survey is based on a biased sample of people who have had an issue with treatment, and we cannot deduce who had graded exercise therapy delivered by a specialist, as NICE recommends”. Her dismissal was notable, given that she was – and still is – Medical Adviser to the charity AYME.

On 15th May 2008, a Joint Statement about CBT and GET by the ME Association and The Young ME Sufferers’ Trust, noted their “serious concern for the safety of patients given this controversial approach to management. Put simply, the illness worsens as a result of physical and mental effort. Advocating progressive exertion is to show a worrying lack of knowledge about the nature of the illness. Any treatment that causes an adverse reaction in 33% – 50% of those using it, cannot be recommended as a blanket form of treatment. We consider this is likely to result in iatrogenic damage to some patients”. In 2009, the Norfolk and Suffolk ME Patient Survey of 225 respondents stated: “Respondents found the least helpful and most harmful interventions were Graded Exercise Therapy and Cognitive Behavioural Therapy”. Hence there is an abundance of patient reports of harm (which are analogous to Yellow Card reporting of adverse drug reactions) from ME/CFS patients and charities (and indeed from NHS Plus), confirming that GET makes people with ME/CFS, including children, worse.

Regarding the economic value of CBT/GET, if an intervention has been shown to fail, how can it possibly be cost-effective? Prior to the failed PACE trial and the 2012 paper by McCrone et al on the alleged cost-effectiveness flowing from it, as far as GET is concerned, there is no evidence at all of cost-effectiveness. The single study which attempted to demonstrate that GET is more (or indeed less) effective than CBT was unable to show any difference between CBT and GET (McCrone P et al: Psychological Medicine 2004:34:991-999), and there were only two studies that considered the cost-effectiveness of CBT: One was the flawed (Dutch) study by Prins et al (Lancet 2001:357:841-847), and the other was a study by Wessely et al (BJGP 2001:51:15-18); It showed no cost-effective benefit from CBT. Given the existing evidence, how can yet more trials of behavioural interventions be justified? Will anyone ever be held accountable for such a significant failure of regulatory and ethical oversight in supporting trials of disproven interventions on children? Why do those with responsibility continually deny and disregard so much evidence and authorise the waste of public money on trials of interventions that have been shown to be ineffective? Surely it is time to stop.

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Vitamin D supplements:

MEA comment on new public health advice about Vitamin D supplements: 21 July 2016

The BBC and other media outlets are reporting new official guidance, issued by Public Health England today, urging everyone to take a vitamin D supplement during the autumn and winter, to compensate for all those dreary days without sunshine. This is music to the ears of ME Association medical adviser, Dr Charles Shepherd, who comments: “We often flag up the fact that people with ME/CFS, especially those who are partially or totally housebound, are at increased risk of developing vitamin D deficiency – mainly due to the lack of exposure to sunlight (which helps with vitamin D production). This may also be compounded by lack of foods that are good sources of vitamin D in their diet (i.e. oily fish, eggs, fortified breakfast cereals). This new advice from Public Health England – that everyone should consider taking a vitamin D supplement during the autumn and winter months – is therefore very relevant, as vitamin D is essential for good muscle and bone health. Any deficiency of vitamin D in ME/CFS could add to the problems of muscle weakness that is already occurring.

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