Forum Review: Summary of presentations

Day 1

Professor Kenny De Meirleir,
University of Brussels,
Belgium

ME/CFS RESEARCH OVERVIEW

Professor De Meirleir began by optimistically stating that this condition is now understood at a cellular level, and that this understanding explains the symptoms of the condition. He described CFS as an immunovigilant disorder in which the immune barrier is broken, either from chronic infection or chronic low grade sepsis. He stated that he has data now on a few thousand patients.

Professor De Meirleir presented work that he has presented previously looking at RNase L. He stated that present in CFS and absent in depression, is a low molecular weight (LMW) (37kDa) RNase L. This low molecular weight RNase L correlates with functional capacity, cognitive function deficits, and the number and activity of natural killer cells (NK cells). He stated that this has been confirmed by five groups in the USA, one in Belgium, one in Japan, and one in Spain. He mentioned work by Jo Nijs who looked at 16 CFS patients, and found that the leukocyte elastase activity is universally correlated with exercise activity which is lower in patients. Work by Knox et al showed that 32% of patients vs 4% of controls have deficient STAT1 protein. These proteins mediate cell response to cytokines. Harrison et al showed procoagulent genetic factors play a role in that an abnormality of genes that control coagulability are three times higher in patients (probably related to chronic inflammation). Kuratsume et al showed on PET scans of brains that there is a decrease in serotonin transporter molecules in CFS. Garcia - Quintana et al have shown in CFS a decreased aerobic work capacity on bicycle ergometry. There is also a decrease in upper body work capacity. Professor Dr Meirleir stated clearly that this is not deconditioning, it is a metabolic dysfunction. Work by Strayer et al using ampligen and double blind placebo controlled cross over studies on 234 patients showed that exercise duration was 16.1% greater in the treated group. There is a question which subgroup in particular responds to ampligen.

Also shown was LMW RNase L and an increase in RNase L activity in 90%. PKR activity is activated in about 50%. There is a low intramonocyte nitric oxide. There is peripheral resistance to T3 (one of the thyroid hormones), and there is a switch to the Th2 state in 70% due to a decrease in Th1 immunity. Work by Schwartz et al looking at Lyme diseased questioned whether Lyme disease was a form of CFS, and due to either an unresolved infection or due to immune abnormalities. Kondo et al looking at herpes virus 6 (HHV-6) showed reactivation during work-induced fatigue, which could perhaps be an objective marker for fatigue. Other workers have shown macrophage activation with phagocytosis of apoptotic neutrophils, and that there is a suppression of natural killer cells and alpha T-cell receptors.

Work in Sweden on 60,000 twins showed only a weak genetic trait in CFS (15-30%). Chaudhuri et al showed an abnormality of ion channels and transporter function, which may explain some of the clinical symptoms. Work by Natelson et al showed 20% of patients will have a chronic low grade encephalopathy. Spinal taps have shown increased evidence of infection, such as increased white blood cells and protein. Alegre et al in their work in 74 CFS patients have shown basic antiviral pathways are abnormal. Takahashu et al have shown that turnover of dopamine is high in the amydala and lower in the insula cortex and cingulate gyrus, and that there was a lower uptake of serotonin in the temporal region of the brain. PET scans have shown decreased activity in the frontal and anterior temporal lobes and cingulate cortex, and increased activity in the occipital lobe.

Dr Anthony Komaroff from the Harvard School of Medicine has shown that there is a substantial reduction of function in CFS patients. He showed that CFS symptoms improve in one third during pregnancy, but in one third worsen, and in one third stay about the same. Professor De Meirleir felt that the majority do improve during pregnancy but have a big relapse after. It was also felt that the course in most people waxes and wanes, but only 10% will achieve a complete remission. Central nervous system involvement is evidenced by decreased CRH, ACTH, and cortisol, increased prolactin response to serotonin stimulaters, decreased growth hormone, and the abnormal brain imaging studies. Cognitive studies have shown a decrease in the ability to process complex information, slower speed, difficulties with acquiring new information and learning, and difficulties recalling complex material. There has been shown to be a decrease in blood volume (red cell mass), and a prolonged acetylcholine mediated vasodilation of microcirculation. Sleep has been proven to be less efficient. There are sleep study abnormalities in up to 50%. Activating circulating lymphocytes are increased and can cross the blood-brain barrier to activate other lymphocytes and dendritic cells. This may persist for years. Activated microgliae secrete proinflammatory cytokines and nitric oxide, which cause low level injury. There is increased apoptosis (cell death) in white blood cells. Inflammatory cytokines are increased. At the onset, persistent fatigue correlates with increased gamma interferon in a small subgroup. A large proportion of sufferers have at lease one species of mycoplasma, and this is significantly different to the control group. There are persistent deficiencies in oxidative phosphorylation, glycolysis, and glucose metabolism. There is decreased vitamin D, which correlates with muscle pain. There is increased substance P in fibromyalgia, but not in CFS patients. There are decreased omega 3 fatty acids, which are associated with increased inflammatory mediators and decreased antiviral activity. Overall there is a low grade inflammation with a defective immune system in the gut and blood-brain barrier.

Emeritus Professor Barrie Marmion
Q fever Research Group
Institute of Medical and Veterinary Science and Hanson Institute
University of Adelaide,
Adelaide, Australia.

Q FEVER

Professor Barrie Marmion has a huge degree of experience in Q Fever and believes that we have a lot to learn from Q Fever and the fatigue-like state that follows in a subset of patients. Q Fever follows infection with a small intracellular bacteria which grows in the macrophage and works at low pH. Broad spectrum antibiotics are used but the organism is not necessarily eliminated. It is common in Queensland and northern New South Wales. Often people recover from the initial illness and then become ill again, and this can be called “the anniversary syndrome”. There was a letter published in The Lancet in 1996 by John Ayres from Birmingham who discussed an outbreak of 148 cases of patients who were exposed to a wind borne infection from sheep. There was subgroup of patients that did not recover, and Professor Marmion believes that this was due to long term persistence of the organism, and was linked to abnormal cytokine stimulation. In these patients there was an increased liberation of interleuken 6 (Il-6), tumour necrosis factor (TNF) was slightly raised, TGFB was raised, and 12 years later 10% of the group of original patients remained ill. Professor Marmion said that in common with CFS patients there is a failure of homeostasis to infection rather than a particular infection being causative of the illness. Professor Marmion stated that the original cytokine response was not down regulated, and so the organism can persist in the bone marrow. He also stated that organisms could colonise heart muscle even 2 to 5 years after the original infection.

Dr Richard Kwiatek,
Queen Elizabeth and Lyell McEwen Hospitals,
Adelaide, Australia

MRI

Dr Richard Kwiatek has done work looking at structural MRI scans in fibromyalgia. This is a condition in which the symptom is total body pain, and the sign is total body tenderness. He believes that there is biological evidence particular to fibromyalgia, in that there is a deficit in regional cerebral blood flow, particularly a decreased blood flow in the thalami more so on the right. He also found a diffuse area of decreased signal in the orbitofrontal cortex. He stated that the non-dominant hemisphere is more involved in pain processing.

Dr Don Staines
Public Health Physician
Gold Coast Public Health Unit
Queensland, Australia

VASOACTIVE NEUROPEPTIDES

Don presented a novel explanation for chronic fatigue syndrome, questioning whether it is an autoimmune disorder of endogenous vasoactive peptides.

Vasoactive neuropeptides including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP) belong to the secretin/glucagons super family and act as hormones, neurotransmitters, immune modulators, and neurotrophes. They are readily catalysed to smaller peptides fragments by antibody hydrolysis. They and their binding cytes are immunogenic and are known to be associated with a range of autoimmune conditions.

Vasoactive peptides are widely distributed in the body, particularly in the central, autonomic, and peripheral nervous systems, and have been identified in the gut, adrenal gland, reproductive organs, vascularture, blood cells, and other tissues. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory, and concentrations. They are co-transmitters for acetylcholine, nitric oxide, endogenous opioids, and insulin. Are potent immune regulators, with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault, promotion of neural development, and the maintenance of homeostasis.

Dr Staines described a biologically plausible mechanism for the development of CFS based on loss of immunological tolerance to the vasoactive neuropeptides following infection, significant physical exercise, or other assaults. He proposed that the release of these substances is accompanied by a loss of tolerance either to them or to their receptor binding sites in CFS. He believes that all the documented symptoms of CFS are explained by vasoactive neuropeptides compromised, namely fatigue and nervous system dysfunction through impaired acetylcholine activity, myalgia through nitric oxide and endogenous opioid dysfunction, chemical sensitivity through peroxynitrite and adenosine dysfunction, and immunological disturbance through changes in immune modulation. Perverse immunological memory established, against these substances or their receptors, may be the reason for the retractive nature of the condition.

Dr Staines also discussed the role of vasoactive neuropeptides in thermoregulation, and postulated a novel theory in sudden infant death syndrome, that vasoactive neuropeptides may be involved. He commented that babies had no shivering response until they are one year, and that probably sudden infant death syndrome is not in fact “sudden” but that it is an impaired immune response happening over a few days.

He also commented at the end of his presentation that perhaps new vaccines may be able to be discovered to protect against vasoactive neuropeptide disorders.

Dr Richard Schloeffel,
General Practitioner
Sydney, Australia

5 CASE HISTORIES

Dr Schloeffel has had a vast experience treating CFS, stating that he has seen over 2500 patients. He has a number of patients at the severe end of the spectrum, and presented 5 patients who are so severely ill he believes that some of them may be at risk of dying.

Dr Schloeffel discussed MNGIE (Mitochondrial Neurogastrointestinal Encephalomyopathy), this being a disorder of mitochondria and he believes although rare should be excluded in severe cases of CFS. (MNGIE will be discussed in Dr Duley’s presentation).

Dr John Duley,
Senior Scientist Chemical Pathology,
Misericodiae Hospital,
Brisbane, Australia

ME/CFS AND METABOLIC DISORDERS

Dr Duley has an interest in mitochondria (the energy factories of cells), and stated that mitochondrial disorders can be inherited, for example MNGIE, or acquired, for example environmental pollutants.

He stated that there were three main ways to look for metabolic diseases. Firstly you could look for a mutation in the gene, but this is difficult if it is not known. Secondly you can measure the activity of a protein (enzyme), for this you need a blood sample or a biopsy, and usually a muscle biopsy is the best way to do this. Thirdly he stated you could look for an accumulation or loss of metabolic chemicals in body fluids. He spoke about MNGIE (mentioned previously in Dr Schloeffel’s talk), this being an inherited mitochondrial disorder. MNGIE is diagnosed by the following symptoms: loss of eye muscle control, droopy eyelids, limb weakness, cramps, gastrointestinal and digestive problems including chronic diarrhoea and constipation and abdominal pain. In this condition, which is a recessive condition and inherited from both parents, there is a blockage in one of the metabolic pathways, leading to a build up of abnormal metabolites (d urid and d thymid), and this build up leads to damage in the DNA in the mitochondria, causing a mitochondrial deficiency. This can be diagnosed by seeing a build up in the urine of two abnormal pryimidine metabolites.

In ME/CFS Dr Duley believes there is a problem with adenosine which is a purine metabolite. This is a powerful alarm signal in the body, and signal breakdown of the energy molecule ATP. When oxygen is low or mitochondrial function is compromised, ATP gets converted to adenosine. Adenosine is multifunctional in the body, it regulates sleep, blood pressure, heart rate, immune response, kidney function, and wound healing. He stated that high adenosine levels have been found in some CFS families in the UK, possibly due to adenylate deaminase deficiency (there are two forms of this enzyme, one in the muscle, and one in the blood).

Dr Richard Burnet,
Endocrine and Metabolic Unit,
Royal Adelaide Hospital,
Adelaide, Australia

GASTRIC EMPTYING

He also looked at lower GI symptoms, looking at the number of bowel motions a day, their consistency, whether constipation was there, and also symptoms of nocturnal diarrhoea and faecal urgency, and CFS patients did show some differences here as well with increased numbers of bowel motions and increased nocturnal diarrhoea.

In summary Dr Burnet has found a marked delay in CFS patients in gastric emptying, markedly seen with the emptying of liquids, a less dramatically delay seen with solids. There was no difference in oesophageal symptoms, and no significant differences in oesophageal clearance.

Professor Kenny De Meirlier

APPROACH TO MANAGEMENT

Professor De Meirleir spoke about the significance of the herpes virus (HHV6) in CFS. He stated that this is a virus we all contract between 0-18 months. HHV6B gives a short-lived illness with a high fever and a rash for 3 days, and if you get B this protects you from A. A infects you when you are older than 18 months. He stated that in an animal model, if you get A, which was infected into 11 Macaque monkeys, 5 of these monkeys developed multiple sclerosis, and 6 developed symptoms of CFS. The B strain is latent and can be reactivated when there is damage to the immune system, whereas A is lytic which destroys cells and causes scar tissue. He did state than in cerebrospinal fluid in a number of CFS patients studied, that there has been a positive viral culture and that you see an increase in opening pressure in a lumbar puncture, increased protein, and lymphocytosis (increased white blood cells).

Professor De Meirleir then went on to talk about anti-viral treatment and mentioned that ampligen is an immune modulating treatment, but that there are also anti-viral treatments. He mentioned several, but stated that there are currently no good anti-virals to treat HHV6A but that there has been an anti-viral studied called Cidovar (Vistide) in which T and natural killer cell function seems to improve in studied patients. Professor De Meirleir mentioned Dan Peterson in the USA who has a large experience with this particular virus.

Professor De Meirleir went on to also talk about other infections. He mentioned mycoplasma and stated that antibiotics must be continued for 36 weeks to 1 year. In Gulf War Syndrome, in which mycoplasma has been thought to play a role, he mentioned 2 studies in which 78-80% of people were “cured” with antibiotics. In 3 studies of CFS patients, with a total example of more than 700, there was improvement in 60-80%, with a cure in 47-50%. The treatment of choice for chlamydia pneumonii is azithromycin.

He also about rickettsia, bartonella, and coxiella, seen in 8-10% of CFS patients, and went on to discuss Cecile Jadin’s work on rickettsia using antibiotics over a 12-18 month period.

He also spoke about looking for heavy metals with a metal ELISA test (MELISA). This tests for metals in the tissues.

He spoke about mycotoxins which are neurotoxins, and mentioned aspergillus niger requiring antifungal treatment if high antibody levels (IgG) are found. He also mentioned Candida for which antifungal treatment and diet is used, if high antibody levels (IgG) are found. He did mention that Candida is found in the digestive tract as part of a normal immune system. He also briefly mentioned leaky gut, peripheral resistance to thyroid hormone treated with low dose T3 (Cynomel) starting with 25mcg and titrating the dose up every 2-3 weeks to 37.5mcg.

Dr John Graham,
Physician,
Adelaide, Australia

THE MARSHALL PROTOCOL

Dr Graham stated that of his 611 CFS patients, 337 were found positive for rickettsia (mainly spotted fever). Dr Graham spoke about the Marshall protocol, which is considered a therapy for Th1 inflammatory diseases. The pleomorphic intracellular bacteria which cause Th1 diseases seem to be resistant to most antibiotics. Only the immune system can kill these bacteria. The Marshall protocol weakens the bacteria so that the immune system can then kill them. The killing of these bacteria always elicits an inflammatory cytokine release from the cells they have parasitized. This results in a temporary exacerbation of the symptoms, a phenomenon often referred to as the Herxheimer reaction. This will continue until all the bacteria are eliminated. The Marshall protocol minimises this reaction by allowing the patient to control the severity of the Herxheimer reaction by controlling the antibiotic dose.

As this protocol is quite complicated, if anybody is interested in looking into this further I suggest they do their own research. Most of the work has been done in the area of sarcoidosis and involves restricting vitamin D.

Dr Nicole Philips,
Psychiatrist,
Melbourne, Australia

PSYCHIATRIC ASSESSMENT IN CFS

My presentation was divided into three sections. Firstly I introduced a paper by a Canadian psychiatrist, Dr Eleanor Stein. This looked at differentiating depression and anxiety from Chronic Fatigue Syndrome. Dr Stein spoke about the difficulty in using a number of diagnostic instruments in diagnosing depression in physically ill people, and suggested the HAD (Hospital and Anxiety Depression Scale), which is a self-screening questionnaire for depression and anxiety, be used in CFS as it tends not to focus so much on the importance of somatic symptoms. Her paper suggested that a diagnosis of co-morbid depression in CFS be considered when the depressive symptoms pre-dated the physical disorder, when pessimism in generalised beyond health and illness related issues, and when the patient seems stuck in depression and it is having a negative effect on treatment. She listed the DSM IV criteria to diagnose major depression, and importantly as there are a number of somatic or physical symptoms in the diagnostic list, it is important to have either depressed mood or loss of interest or pleasure as a must before depression is diagnosed with all the other physical symptoms. This does seem to be forgotten in things like sleep disturbance, fatigue, and cognitive disturbance, as seen in both illnesses. When diagnosing anxiety she stated that a co morbid anxiety disorder should be considered when anxiety pre-dated the physical disorder, and anxiety is generalised and not limited to health and healthcare related issues, and when the patient is unable to cope with or resolve anxiety over the long term. Importantly with the DSM IV diagnostic criteria it clearly states that symptoms of anxiety should not be due to direct physiological effects of a medical condition.

My presentation went on to emphasise that depression is a major medical illness, and by the year 2020 is estimated to be the second major cause of disability world wide under ischaemic heart disease. I emphasised that physical signs and symptoms in major depression are the norm, with tiredness and lack of energy being described in at least 85% of patients with depression, headache and head pains in 64%, dizziness or faintness in 60%, parts of the body feeling weak in 57%, muscle aches and pains in 53%, stomach pains in 51%, and chest pains in 46%. When depression is being treated most of the residual symptoms are physical, and I also made the point that most physical complaints that people experience are not ever linked to an identifiable cause. With this understanding it is easy to see how Chronic Fatigue Syndrome and depression could be easily confused. I felt that in differentiating the conditions, the following eight points were important.

1. Fatigue should be considered secondary rather than primary. It is secondary to many other symptoms, for example chronic inflammation. When we de-emphasise the importance of fatigue we will actually progress much further in this condition.
2. CFS has been seen in epidemics. I believe there has been at least 30 epidemics between 1934 and 1977. This does not occur in depression.
3. As Dr Stein mentioned, it is important to consider the temporal order of psychiatric and physical symptoms, and what you see in CFS is that depression usually follows the illness rather than pre-dates it.
4. There are differences in the somatic symptoms between the two. In particular, the relationship to activity is important in that it is not just the fatigue that worsens after activity, other symptoms are also made worse, as exercise-induced fatigue is also seen in depression.
5. Although the somatic symptoms are similar, the cognitive symptoms do differentiate the two conditions. In CFS you see less low self esteem, less suicidal ideation, less hopelessness, less loss of pleasure. In depression you get loss of pleasure both in anticipation of the act and after its fulfilment vs CFS where there is more a frustration that things can’t be done. Also in depression there is often a worse mood in the morning.
6. It is important to focus in CFS on the early symptoms vs the chronic symptoms. These are often infective in nature, for example night sweats, enlarged glands and sore throat. These symptoms may not be seen in the latter stages of the illness.
7. It is important to focus on the variability of the symptoms, both within and between episodes of CFS. This does differ to what is seen in depression.
8. It is important to focus on the biology that we do understand that is clearly different to depression, for example in CFS we see neurally mediated hypotension, this is not seen in depression. In CFS we see a disturbance of the HPA axis but it is opposite to what is seen in depression. In CFS you see a decrease in CRH leading to a decrease in cortisol and there is no abnormality of the dexamethasone suppression test. In depression you see an increased CRH leading to an increased ACTH and an increased cortisol and a failure of suppression with dexamethasone.

I also gave an update on what is currently the thinking in psychiatry about CFS. The previous week to the forum, the Royal Australian and New Zealand College of Psychiatry Congress. I attended a lecture given by Professor Ian Hickey, who spoke about chronic fatigue as opposed to Chronic Fatigue Syndrome. He used this term interchangeably with neurasthenia, fatigue states, and neuropsychiatric disorders, and stated that chronic fatigue was “a culture bound syndrome” which was becoming international. He stated that in cross cultural studies of “somatic syndromes”, Sydney and Manchester seemed to have the highest incidence. He presented a slide looking at the prevalence of these conditions but did not compare “apples with apples”. He stated that a WHO primary test study of neurasthenia showed a 5.4% incidence. An Indian study presented in the British Medical Journal this year by Patel et al showed a 12.1% incidence in women (of what I am not sure). He then went on to state that the USA, using CDC criteria for “chronic fatigue” with “limited psychiatric input”, showed a 0.5-2.5% incidence (this is much closer to the Chronic Fatigue Syndrome incidence that we would expect world wide). He also commented on the fact that cognitive behaviour therapy trials have shown that they are a “highly effective” treatment.

Dr Kathy Rowe,
Paediatrician,
Royal Childrens Hospital,
Melbourne, Australia

CHILDREN AND ADOLESCENTS

Dr Rowe’s experience is with CFS and adolescents. She has concerns that the symptoms may be different to those experienced by adults, and stated that the symptoms experienced by more than 80% of the clinic group are the following: fatigue, headaches, sleep disturbance, myalgia after activity, and “lost for the word”. She stated that prolonged fatigue and headache are nearly universal, and divided groups of symptoms into: a) muscle pain and fatigue, which involves muscle pain after activity and muscle pain after doing nothing, b) neurocognitive, which includes poor concentration, speech problems, memory loss, vivid dreams, and nightmares, c) abdominal and chest pain, and d) neurophysiological, which involves recurrent chest pain and the need to sleep longer, e) immunological symptoms. She stressed that there were no abnormalities in parental bonding, as parents of CFS children and adolescents have often been considered to be over protective. She stated that parental bonding is identical to that of the control group. She found 28% of her adolescents with CFS had depression vs 20% seen in “normal” adolescents. Depression is associated with the severity of the CFS, a delay in diagnosis, not being believed, school difficulties, and family problems, and sexual abuse. She found that 80% of her sample had an onset following a viral or febrile illness. Others followed immunisation, surgery, or perhaps had a subclinical infection.

Day two

The second day of the forum revolved around discussing diagnostic criteria, and also the establishment of a tissue bank. Professor De Meirleir stated that if symptoms were present in more than 80% of patients that they should be included in diagnostic criteria. The following diagram, which Professor De Meirleir drew, I personally found to be one of the most exciting outcomes from the forum, because this then leads the way for some kind of battery of diagnostic testing and a possibility to subgroup different groups of CFS patients.

This diagram shows that there is a very severe group (number 3) who are likely to have significant bowel problems and to have almost no natural killer cell activity, very low uric acid, a very high PKR, a lot of fragmentation with a high amount of elastase and a very high nitric oxide. A less severe group (number 2), which is probably the largest CFS group, have decreased natural killer cell activity, average or a bit low uric acid, increased PKR, some fragmentation of RNase L, and a slightly increased nitric oxide. Both of these groups had Th2 illnesses. On the other side of the line are Th1 illnesses like multiple sclerosis. This group are immune activated, they have high natural killer cell activity, high uric acid, low nitric oxide, low PKR activity, and high low molecular weight Rnase L.

Other than uric acid, these tests are not standard tests done in Australia, so Professor De Meirleir is currently in discussions with a laboratory in Australia to perhaps get these tests off the ground.

The group as a whole discussed the pros and cons of the different diagnostic criteria that have been used currently. Obviously because of the differences in diagnostic criteria, different groups of research subjects are being studied making a lot of the research quite meaningless. Although the Fukuda criteria are primarily used in Australia, we reviewed the more comprehensive Canadian criteria which Professor De Meirleir was involved in putting together. The Canadian guidelines were developed by a committee following input from invited world leaders in the research and clinical management if ME/CFS. It was felt that the Canadian guidelines represent evidence-based clinical practice guidelines developed from the best available research evidence. The forum agreed unanimously to propose that the Canadian criteria be used in world wide discussions of this illness. See below.

Although it is unlikely that a single disease model will account for every case of ME/CFS, there are common clusters of symptoms that allows a clinical diagnosis.

Clinical Working Case Definition of ME/CFS is available at the National ME/FM Action Network. See Overview pp 2–3.

TISSUE BANK

With respect to the establishment of a tissue bank, Christine Hunter gave a heart rendering story of what she personally went through with her daughter Alison when Alison died as she tried to get tissue saved for future study. It was felt that electron microscopy must be done in order to see the mitochondria. Someone commented that when autopsies are performed there is only a 30% concordance with what the clinical diagnosis was. Someone else mentioned that even tissue done from such procedures as endoscopies could be used positively to look for clues in this difficult illness.

CONCLUSIONS

Simon Molesworth concluded the forum by stating that he had felt that this had been a great coming together, and that the crisis of credibility that he has always spoken of has “come a hell of a long way”. We spoke about how important it was to disseminate the information from the forum to wide reaching areas medically and politically, and that hopefully such forums will be repeated bi-annually.

First printed in "Emerge", Journal of ME/Chronic Fatigue Syndrome Society of Victoria.

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