The Hummingbirds' Foundation for M.E.

The Hummingbirds' Foundation for M.E. (HFME) is fighting for the recognition of M.E.,
and for patients to be accorded the same basic human rights as those with similar
disabling and potentially fatal neurological diseases such as M.S.

The CBT and GET database

  • Section 1: Introduction/Overview: Smoke and Mirrors
  • Section 2: Recommended background reading
  • Section 3: Research and articles which expose the lack of scientific legitimacy (and the hidden financial and political motivations) underlying the scientifically unsupportable 'behavioural' paradigm of M.E. and the use of CBT and GET on M.E. patients
  • Section 4: A summary of the available medical research
  • Section 5: Patient accounts of CBT
  • Section 6: Patient accounts of GET
  • Section 7: Conclusion/Summary of key points (Includes Printer-friendly versions/Downloads, Acknowledgments and Future submissions sections)

Section 4

What is known medically and scientifically about M.E. so far?

Despite popular opinion, Myalgic Encephalomyelitis is not ‘medically unexplained’ nor ‘mysterious.’ There simply is no legitimate scientifically motivated debate about whether or not M.E. is a ‘real’ illness or not or has a biological basis. The psychological or behavioural theories of M.E. are no more scientifically viable than are the theories of a ‘flat earth.’ They are pure fiction.

The reality is that there is an abundance of research which shows that M.E. is an organic illness which can have profound effects on many bodily systems and many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research articles; some dating back to the 1950s and earlier.


Myalgic Encephalomyelitis is not the same thing as 'CFS'

When the terms CFS, CFIDS, ME/CFS, CFS/ME, Myalgic Encephalopathy or ME-CFS are used what is being referred to may be patients with/facts relating to any combination of: 1. Miscellaneous psychological and non-psychological fatigue states (including somatisation disorder) 2. A self limiting post-viral fatigue state or syndrome (eg. following glandular fever.) 3. A mixed bag of unrelated, misdiagnosed illnesses (each of which feature fatigue as well as a number of other common symptoms; poor sleep, headaches, muscle pain etc.) including Lyme disease, multiple sclerosis, Fibromyalgia, athletes over-training syndrome, depression, burnout, systemic fungal infections (candida) and even various cancers 4. Myalgic Encephalomyelitis patients.

The terminology is often used interchangeably, incorrectly and confusingly. However, the DEFINITIONS of M.E. and CFS are very different and distinct, and it is the definitions of each of these terms which is of primary importance. The distinction must be made between terminology and definitions.

  • Chronic Fatigue Syndrome is an artificial construct created in the US in 1988 for the benefit of various political and financial vested interest groups. It is a mere diagnosis of exclusion (or wastebasket diagnosis) based on the presence of gradual or acute onset fatigue lasting 6 months. If tests show serious abnormalities, a person no longer qualifies for the diagnosis, as ‘CFS’ is ‘medically unexplained.’ A diagnosis of ‘CFS’ does not mean that a person has any distinct disease (including M.E.). The patient population diagnosed with ‘CFS’ is made up of people with a vast array of unrelated illnesses, or with no detectable illness. According to the latest CDC estimates, 2.54% of the population qualify for a ‘CFS’ (mis)diagnosis. Every diagnosis of ‘CFS’ can only ever be a misdiagnosis.

  • Myalgic Encephalomyelitis is a systemic neurological disease initiated by a viral infection. M.E. is characterised by (scientifically measurable) damage to the brain, and particularly to the brain stem which results in dysfunctions and damage to almost all vital bodily systems and a loss of normal internal homeostasis. Substantial evidence indicates that M.E. is caused by an enterovirus. The onset of M.E. is always acute and M.E. can be diagnosed within just a few weeks. M.E. is an easily recognisable distinct organic neurological disease which can be verified by objective testing. If all tests are normal, then a diagnosis of M.E. cannot be correct.
         M.E. can occur in both epidemic and sporadic forms and can be extremely disabling, or sometimes fatal. M.E. is a chronic/lifelong disease that has existed for centuries. It shares similarities with MS, Lupus and Polio. There are more than 60 different neurological, cognitive, cardiac, metabolic, immunological, and other M.E. symptoms. Fatigue is not a defining nor even essential symptom of M.E. People with M.E. would give anything to be only severely ‘fatigued’ instead of having M.E. Far fewer than 0.5% of the population has the distinct neurological disease known since 1956 as Myalgic Encephalomyelitis.

There are now more than nine different definitions of ‘CFS.’ All each of these flawed CFS definitions ‘define’ is a heterogeneous (mixed) population of people with various misdiagnosed psychiatric and miscellaneous non-psychiatric states which have little in common but the symptom of fatigue. The fact that a person qualifies for a diagnosis of CFS, based on any of the CFS definitions (a) does not mean that the patient has Myalgic Encephalomyelitis, and (b) does not mean that the patient has any other distinct and specific illness named ‘CFS.’ A diagnosis of CFS – based on any of the CFS definitions – can only ever be a misdiagnosis.

There is no such disease/s as ‘CFS’ – the name CFS and the bogus disease category of CFS must be abandoned (along with the use of other vague and misleading umbrella terms such as ‘ME/CFS’ ‘CFS/ME’ 'CFIDS' and 'Myalgic Encephalopathy' and others), for the benefit of all the patient groups involved. Myalgic Encephalomyelitis is a distinct neurological disease, it is not the same thing as 'CFS.'

What does the term ICD-CFS mean?

The various definitions of ‘CFS’ do not define M.E. Myalgic Encephalomyelitis is an organic neurological disorder as defined at G.93.3 in the World Health Organization’s International Classification of Diseases (ICD). The definitions of ‘CFS’ do not reflect this. The ‘CFS’ definitions are not ‘watered down’ M.E. definitions, as some claim. They are not definitions of M.E. at all.

However, ever since an outbreak of M.E. in the US was given the label ‘CFS,’ the name/definition ‘CFS’ has prevailed for political reasons. ‘CFS’ is widely though wrongly applied to M.E. as well as to other diseases.

The overwhelming majority of ‘CFS’ research does not involve M.E. patients and is not relevant in any way to M.E. patients. However, a very small amount (a minuscule percentage) of research published under the name ‘CFS’ clearly does involve a significant number of M.E. patients as it details those abnormalities which are unique to M.E. Sometimes the term ‘ICD-CFS’ is used in those studies and articles which, while they use the term ‘CFS,’ do relate to some extent to authentic M.E. 

In addition to its use in relation to research, some people use the term ‘ICD-CFS’ to refer to the disease generally. The term is usually used by people who are aware of the psychological paradigm of ‘CFS,’ and who want to indicate a real, biological disease rather than a psychological one.  However, which exact disease or diseases are being referred to with this term varies considerably from one author to another. As with terms such as ‘ME/CFS’ the term ‘ICD-CFS’ only increases confusion as it has no agreed definition and many different groups use it to refer to very different, often very mixed, patient groups.


Problems with ‘CFS’ or so-called ‘ICD-CFS’ research

The overwhelming majority of ‘CFS’ research does not involve M.E. patients and is not relevant in any way to M.E. patients. A small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. Unless studies are based on an exclusively M.E. patient group, results cannot be interpreted and are meaningless for M.E. Thus while it is important to be aware of the small amount of research findings that do hold some value for M.E. patients, using the term ‘ICD-CFS’ to refer to this research is misleading and in many ways just damaging as using terms and concepts like ‘ME/CFS’ or ‘CFS/ME.’

For further details of the WHO ICD classifications of M.E. and ‘CFS’ worldwide (and why terms such as ‘ICD-CFS,’ ‘ME/CFS’ and Myalgic Encephalopathy’ must be avoided) please see the new paper by patient advocate Lesley Ben entitled: The World Health Organization’s International Classification of Diseases (WHO ICD), ME, ‘CFS,’ ‘ME/CFS’ and ‘ICD-CFS’ 

  • Virtually all of the research which does relate to M.E. (at least in part) but which uses the term/concept of ‘CFS’ (or ME/CFS, or CFIDS etc.) is also contaminated in some way by ‘CFS’ misinformation. Most often these papers contain a bizarre mix of facts relating to both M.E. and ‘CFS.’ For more information on some of the most common inaccuracies and ‘CFS’ propaganda included in this research, see the paper: Putting Research and Articles on Myalgic Encephalomyelitis into Context


What we know about M.E. so far includes that:

Myalgic encephalomyelitis is a systemic acutely acquired illness initiated by a virus infection which is characterised by post encephalitic damage to the brain stem; a nerve centre through which many spinal nerve tracts connect with higher centres in the brain in order to control all vital bodily functions – this is always damaged in M.E. (Hence the name Myalgic Encephalomyelitis.) The CNS is diffusely injured at several levels, these include the cortex, the limbic system, the basal ganglia, the hypothalamus and areas of the spinal cord and its appendages. This persisting multilevel central nervous system (CNS) dysfunction is undoubtedly both the chief cause of disability in M.E. and the most critical in the definition of the entire disease process.

Myalgic Encephalomyelitis represents an acute change in the balance of neuropeptide messengers, and due to this, a resulting loss of the ability of the CNS (the brain) to adequately receive, interpret, store and recover information which enables it to control vital body functions (cognitive, hormonal, cardiovascular, autonomic and sensory nerve communication, digestive, visual auditory balance etc). It is a loss of normal internal homeostasis. The individual can no longer function systemically within normal limits.

M.E. is primarily neurological, but because the brain controls all vital bodily functions virtually every bodily system can be affected by M.E. Again, although M.E. is primarily neurological it is also known that the vascular and cardiac dysfunctions seen in M.E. are also the cause of many of the symptoms and much of the disability associated with M.E. – and that the well-documented mitochondrial abnormalities present in M.E. significantly contribute to both of these pathologies. There is also multi-system involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs in M.E. Some individuals also have damage to skeletal and heart muscle. Thus Myalgic Encephalomyelitis symptoms are manifested by virtually all bodily systems including: cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage.

M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) – and an associated injury of the immune system – by the chronic effects of a viral infection. There is also transient and/or permanent damage to many other organs and bodily systems (and so on) in M.E. M.E. affects the body systemically. Even minor levels of physical and cognitive activity, sensory input and orthostatic stress beyond a M.E. patient’s individual post-illness limits causes a worsening of the severity of the illness (and of symptoms) which can persist for days, weeks or months or longer. In addition to the risk of relapse, repeated or severe overexertion can also cause permanent damage (eg. to the heart), disease progression and/or death in M.E.

M.E. is not stable from one hour, day, week or month to the next. It is the combination of the chronicity, the dysfunctions, and the instability, the lack of dependability of these functions, that creates the high level of disability in M.E. It is also worth noting that of the CNS dysfunctions, cognitive dysfunction is one of the most disabling characteristics of M.E.

All of this is not simply theory, but is based upon an enormous body of mutually supportive clinical information. These are well-documented, scientifically sound explanations for why patients are bedridden, profoundly intellectually impaired, unable to maintain an upright posture and so on.


What are some of the specific abnormalities that have been found in M.E. patients?

There is an abundance of research which shows that M.E. is an organic illness which can have profound effects on many bodily systems. These are well-documented, scientifically sound explanations for why patients are bedridden, profoundly intellectually impaired, unable to maintain an upright posture and so on. More than a thousand good articles now support the basic premises of M.E. Autopsies have also confirmed such reports of bodily damage and infection.


Many different organic abnormalities have been found in M.E. patients (in peer reviewed research). Patient advocates Margaret Williams and Eileen Marshall explain that:

  • there is evidence of disrupted biology at cell membrane level
  • there is evidence of abnormal brain metabolism
  • there is evidence of widespread cerebral hypoperfusion
  • there is evidence of central nervous system immune dysfunction
  • there is evidence of central nervous system inflammation and demyelination
  • there is evidence of hypomyelination
  • there is evidence that Myalgic Encephalomyelitis is a complex, serious multi-system autoimmune disorder (in Belgium, the disorder has now been placed between multiple sclerosis and Lupus)
  • there is evidence of significant neutrophil apoptosis
  • there is evidence that the immune system is chronically activated (eg. the CD4:CD8 ratio may be grossly elevated)
  • there is evidence that natural killer (NK) cell activity is impaired (ie. diminished)
  • there is evidence that the vascular biology is abnormal, with disrupted endothelial function
  • there is novel evidence of significantly elevated levels of isoprostanes
  • there is evidence of cardiac insufficiency and that patients are in a form of cardiac failure (which is exacerbated by even trivial levels of physical activity, cognitive activity and orthostatic stress)
  • there is evidence of autonomic dysfunction (especially thermodysregulation; frequency of micturition with nocturia; labile blood pressure; pooling of blood in the lower limbs; reduced blood volume (with orthostatic tachycardia and orthostatic hypotension. Findings of a circulating blood volume of only 75% of expected are common, and in some patients the level is only 50% of expected.)
  • there is evidence of respiratory dysfunction, with reduced lung function in all parameters tested
  • there is evidence of neuroendocrine dysfunction (notably HPA axis dysfunction)
  • there is evidence of recovery rates for oxygen saturation that are 60% lower than those in normal controls
  • there is evidence of delayed recovery of muscles after exercise. (Affecting all muscles including the heart.)
  • there is evidence of a sensitive marker of muscle inflammation
  • there is evidence that the size of the adrenal glands is reduced by 50%, with reduced cortisol levels
  • there is evidence of at least 35 abnormal genes, (these are acquired genetic changes, not hereditary), specifically those that are important in metabolism; there are more abnormal genes in Myalgic Encephalomyelitis than there are in cancer
  • there is evidence of serious cognitive impairment. (Worse than occurs in AIDS dementia)
  • there is evidence of adverse reactions to medicinal drugs, especially those acting on the CNS
  • there is evidence that symptoms fluctuate markedly from day to day and even from hour to hour (2006, [Online])

(Note that this is only a sample of some of the research available, not an exhaustive list.) It is known that Myalgic Encephalomyelitis is:

1.     An acute onset (biphasic) epidemic or endemic infectious disease process


2.     An autoimmune disease (with similarities to Lupus)

3.     An infectious neurological disease, affecting adults and children

4.     A disease which involves significant (and at times profound) cognitive impairment/dysfunction

5.     A persistent viral infection (most likely due to an enterovirus; the same type of virus which causes poliomyelitis and post-polio syndrome)

6.     A diffuse and measurable injury to the vascular system of the central nervous system (the brain)

7.     A central nervous system (CNS) disease (with similarities to MS)

8.     A variable (but always, serious) diffuse (acquired) brain injury

9.     A systemic illness (associated with organ pathology; particularly cardiac)

10.   A vascular disease

11.   A cardiovascular disease

12.   A type of cardiac insufficiency

13.   A mitochondrial disease

14.   A metabolic disorder

15.   A musculo-skeletal disorder

16.   A neuroendocrine disease

17.   A seizure disorder

18.   A sleep disorder

19.   A gastrointestinal disorder

20.   A respiratory disorder

21.   An allergic disorder

22.   A pain disorder

23.   A life-altering disease

24.   A chronic or lifelong disease associated with a high level of disability

25.   An unstable disease; from one hour/day/week or month to the next

26.    A potentially progressive or fatal disease (Hyde 2007, [Online]) (Hooper et al. 2001, [Online]) (Cheney 2007, [video recording]) (Ramsay 1986, [Online])

Myalgic Encephalomyelitis affects every cell in the body. For more information see the General articles and research overviews section. See also articles by: Dr. Elizabeth Dowsett and Byron Hyde MD.



Are there any tests which can be used to confirm a suspected M.E. diagnosis?

Yes. Whilst there is as yet no single, definitive laboratory test for M.E., there are a specific series of tests which enable a M.E. diagnosis to be confirmed. Virtually every M.E. patient will also have various abnormalities visible on physical exam.


As M.E. expert Dr Byron Hyde MD explains: ‘The one essential characteristic of M.E. is acquired CNS dysfunction, [not] chronic fatigue. A patient with M.E. is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological CNS changes: SPECT, xenon SPECT, PET, and neuropsychological testing.’ Thus it is these tests which are therefore most critical in the diagnosis of M.E., although various other types of tests are also useful. Some of the series of tests which can (in combination) help to confirm a M.E. diagnosis include:

*       SPECT and xenon SPECT scans of the brain

*       MRI and PET scans of the brain

*       EEG brain maps and QEEG brain maps

*       Neurological examination and the Romberg or tandem Romberg test

*       Various tests of the immune system (eg. natural killer cells)

*       Insulin levels and glucose tolerance tests

*       Erythrocyte sedimentation rate (ESR)

*       24 hour Holter monitor

*       Tilt table examination, exercise testing and chemical stress tests

*       Physical exam

While various ‘fatiguing conditions’ with a variety of different aetiology’s may be made up of vague and mild ‘everyday’ type symptoms, have no physical signs and no tests which can aid diagnosis, this is not the case with M.E. M.E. is a distinct neurological illness with a distinct list of symptoms, physical signs and diagnostic (and other) tests – it bears no relationship to such unrelated ‘fatiguing conditions.’ As M.E. authors Verillo and Gellman explain: ‘Contrary to popular belief, ME is a distinct, recognisable entity that can be diagnosed relatively early in the course of he disease, providing the physician has some experience with the illness.’ New clinical guidelines titled The Nightingale Definition of M.E.  also make diagnosis easier than ever before; even for those with no experience with the illness. If all tests are normal, then a diagnosis of M.E. cannot be correct.


Further recommended reading:

Putting Myalgic Encephalomyelitis research and articles into context Because of the politics and financial interests involved in M.E. research it is vitally important that before you read anything about the illness that you read this paper first and first understand the context in which it was written.


For more information about the series of tests which may aid diagnosis see:


The following texts provide overviews of what is known medically about M.E.:

Hundreds of individual research abstracts and articles by some of the world’s leading M.E. experts are also available to view on this site.

The following sections are particularly relevant with regard to GET:

Samples of some of the relevant research in these sections are reproduced below.

Hundreds of individual research abstracts and articles by some of the world’s leading M.E. experts and authors are also available to view; search for articles by topic or by author.

See: Myalgic Encephalomyelitis research and articles

This is a collection of literally HUNDREDS of some of the best M.E. research and articles, from some of the worlds leading researchers, doctors and M.E. advocates. Sections include: M.E. outbreaks, M.E. and children, viral research, cardiac research, the severity of M.E. and many more.


Essential reading on M.E.:

The book: The Clinical and Scientific Basis of Myalgic Encephalomyelitis Edited by Byron Hyde, M.D. is also vital reading for anyone with a real interest in M.E.

This book provides, in one superb 75-chapter source, an up-to-date, comprehensive account of current knowledge concerning the history, epidemiology, children with M.E., investigation, virology, immunology, muscle pathology, host response, food intolerance, brain mapping, neurophysiology, neuropsychology, psychiatry, sleep dysfunction and much more. This is an essential reference book for medical, government and public library reference rooms. This text is a unique vehicle for researchers, physicians and other health education and government officials, and is also easily understandable by the general public. See the Review of this book for more information and for purchasing details.

See the Book Reviews section for more information about thsi (and many other) M.E. books.




Sample articles

Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome. La Manca JJ; Sisto SA; De Luca J; Johnson SK; Lange G; Pareja J; Cook S; Natelson BH C.F.S.

‘We conclude that after physically demanding exercise, CFS subjects demonstrated impaired cognitive processing compared with healthy individuals.’

Vagal tone is reduced during paced breathing in patients with the chronic fatigue syndrome. Sisto SA, Tapp W, Drastal S, Bergen M, DeMasi I, Cordero D, Natelson B. Clinical Autonomic Research 1995; 5(3): 139-43.

‘Using this method, although there was significantly less vagal power in the sitting versus the standing postures for both groups, the overall vagal power was significantly lower (p < 0.034) in the CFS group versus healthy controls. Vagal power was also significantly lower (p < 0.01 to p < 0.05) at all breathing rates in both postures except while standing and breathing at 18 breaths/min.

Exercise responsive genes measured in peripheral blood of women with Chronic Fatigue Syndrome and matched control subjects. Whistler T, Jones JF, Unger ER, Vernon SD.Journal: BMC Physiol. 2005 Mar 24;5(1):5 PMID: 15790422

‘Exercise-responsive genes differed between CFS cases and controls. These were in genes classified in chromatin and nucleosome assembly, cytoplasmic vesicles, membrane transport, and G protein-coupled receptor ontologies. Differences in ion transport activity/ion channel activity were evident at baseline and were exaggerated after exercise as evidenced by greater numbers of differentially genes in these molecular functions.’

A measure of heart rate variability is sensitive to orthostatic challenge in women with chronic fatigue syndrome. Yamamoto Y, LaManca JJ, Natelson BH.

‘The specificity in differentiating CFS from controls were 90% and 72%, respectively. The data suggest that a decrease in aperiodic fractal component of HRV in response to HUT can be used to differentiate patients with CFS from CON.’

Chronic fatigue syndrome: intracellular immune deregulations as a possible etiology for abnormal exercise response. Nijs J, De Meirleir K, Meeus M, McGregor NR, Englebienne P.

Circulating Blood Volume in Chronic Fatigue Syndrome David H. P. Streeten, MB, DPhil, FRCP, FACP David S. Bell, MD, FAAP

Of the 19 patients reported here, abnormalities in blood volume were very common. The most common, found in 16 of 19 patients, was a reduction in red blood cell mass. Eleven subjects had low plasma volumes, and total circulating blood volume was subnormal in 12 of 19 subjects. In some individuals this abnormality was strikingly severe. Patient #15, for example, had an RBC mass of 12.9 mL/Kg, which is 46% of the expected normal, and a total blood volume of 35.8 mL/Kg, which represents 49.7% of the expected normal value (21).

In general, blood pressure measurements were not predictive of the results of circulating blood volume measurements.

Exercise Capacity in Chronic Fatigue Syndrome Pascale De Becker, PhD; Johan Roeykens, PT; Masha Reynders, PT; Neil McGregor, MD, PhD;

‘This study clearly shows that patients with CFS are limited in their physical capacities. Based on the American Medical Association Guidelines for Impairment Rating,51 our 55.2% of patients who had a VO2max of less than 20 mL/kg per minute correspond to class 3-4 on the disability scale, indicating moderate to severe impairment.51

‘CFS can and does result in prolonged debilitation.3, 4, 51

Respiratory symptoms and lung function testing in Chronic Fatigue Syndrome (CFS) patients P. De Becker, I. Campine, E. Van Steenberge, M. Noppen, A. Leysl, K. De Meirleir

‘CFS patients show a significant decrease in VC, possibly due to a significant increase of RV. The incidence of bronchial hyper-responsiveness in this group is also remarkably high. These observations can, at least partially, explain the respiratory symptoms in these patients.’

Physiological responses to incremental exercise in patients with chronic fatigue syndrome. Inbar O, Dlin R, Rotstein A, Whipp BJ.

‘As a group, the CFS patients demonstrated significantly lower cardiovascular as well as ventilatory values at peak exercise, compared with the control group.’

‘These results could indicate either cardiac or peripheral insufficiency embedded in the pathology of CFS patients.’

‘We conclude that indexes from cardiopulmonary exercise testing may be used as objective discriminatory indicators for evaluation of patients.’

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. Jammes Y, Steinberg JG, Mambrini O, Bregeon F, Delliaux S

‘The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.’

Exercise capacity and immune function in male and female patients with chronic fatigue syndrome (CFS). Snell CR, Vanness JM, Strayer DR, Stevens SR.

‘A significant multivariate main effect was found for immune status (p < 0.01), with no gender effect or interaction. Follow-up analyses identified VO2(peak) as contributing most to the difference. These results implicate abnormal immune activity in the pathology of exercise intolerance in CFS and are consistent with a channelopathy involving oxidative stress and nitric oxide-related toxicity.’

Repetitively negative changing T waves at 24-h electrocardiographic monitors in patients with the chronic fatigue syndrome - left ventricular dysfunction in a cohort. Lerner AM, Lawrie C, Dworkin HS. Chest 1993; 104(5): 1417-21.

‘The patients with CFS all had abnormal Holter readings’

‘We further report the occurrence of mild left ventricular dysfunction in 8 of 60 patients in continuing studies of this population with CFS, younger than 50 years old, and with no risk factors for coronary artery disease. All 60 patients with CFS showed repetitively flat to inverted T waves alternating with normal T waves.’

Complement activation in a model of chronic fatigue syndrome. Sorensen B, Streib JE, Strand M, Make B, Giclas PC, Fleshner M, Jones JF. Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA.

‘Exercise challenge induced significant increases of the complement split product C4a, but not C3a or C5a, at 6 hours after exercise only in the CFS group (P <.01), regardless of allergy status. Mean symptom scores were significantly increased after exercise through the use of a daily diary (P <.03) and a weekly diary (P <.01) for the CFS group only.’

‘Exercise challenge may be a valuable tool in the development of diagnostic criteria and tests for CFS.’

CFS severity is related to reduced stroke volume and diminished blood pressure responses to mental stress Arnold Peckerman, John J. LaManca, Sharon L. Smith, and Benjamin H. Natelson; NJ CFS Research Center, University of Medicine and Dentistry of New Jersey

‘An observation was made that in patients with CFS, a lower stroke volume was highly predictive (r = -.72, p < .001) of illness severity. When divided into severe (N = 11) and less-than-severe (N = 10) groups, the severe CFS patients were found to have a lower stroke volume and cardiac output (p < .05) relative to a more moderate CFS group across three different postures.’

‘These findings suggest the possibility of a low flow circulatory state in the most severe cases of CFS. In patients with a less severe form of CFS, a diminished blood pressure response to a cognitive-behavioral (speech presentation), but not to an aversive-sensory (the cold pressor test) stressor may indicate a defect in the higher cortical modulation of cardiovascular autonomic control. In this latter group, situations may arise where a demand for blood flow to the brain may exceed the supply with a possibility of ischemia and a decrement of function.’

[Note that the so-called 'severe' patients in this study are in reality only mildly or possibly moderately ill]

Evaluating Blood Volume Studies - Some Thoughts David S. Bell, MD, FAAP Published in Lyndonville News, March 2000

'So far in our office we have measured the circulating blood volume in nearly fifty patients using the Chromium 51 method. It is essential that this method be employed (done in the nuclear medicine department of large University hospitals) as it is the only reliable method of assessing blood volume. There are two components of blood: the red blood cells and the plasma (fluid); everything else doesn't contribute much to the volume. The results are expressed as a function of body weight. Normal red blood cell mass should be between 23 and 28 ml/Kg, and the plasma volume should be between 40 and 52 ml/Kg. The total circulating blood volume is the sum of the two parts, and should lie between 60 and 80 ml/K.

Overall, about eighty percent of our patients with CFS have had either a low red blood cell mass, plasma volume, or both. Some patients have been extremely low, less than 50% of normal blood volume. To put this in perspective, if a healthy person were to bleed 40% of their volume out in a car accident it would likely be fatal. The loss in CFS is presumably gradual. The finding of decreased blood volume in CFS first came from Dr. David Streeten, and I am convinced it is accurate and will serve as a marker for the illness in some regard.'

Alterations in muscles of CFS patients at morphological, biochemical and molecular level. Pizzigallo E, Di Girolamo A, Montanari G, Dragani L, Vecchiet J, Calella G.

‘Our results agree with those of other AA (Behan et al., 1991; Gow et al., 1994). The alterations are compatible with a myopathy of probable mitochondrial origin. This could explain the drop in the functional capability of the muscle as a reduction in potency but, above all, as a reduction in resistance. In conclusion, even if CFS seems to be attributable to mitochondrial and/or muscular alterations, a damage in the central nervous system cannot be excluded. This could explain the neurophychological, behavioral, and neuroendocrinological alterations often found in these patients.

Mitochondrial abnormalities in the postviral fatigue syndrome. Behan WM, More IA, Behan PO.

'We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected.'

In vivo magnetic resonance spectroscopy in chronic fatigue syndrome. Chaudhuri A, Behan PO.

'Cell membrane oxidative stress may offer a common explanation for the observed MRS changes in the muscles and brain of CFS patients and this may have important therapeutic implications. As a research tool, MRS may be used as an objective outcome measure in the intervention studies. In addition, regional brain 1H MRS has the potential for wider use to substantiate a clinical diagnosis of CFS from other disorders of unexplained chronic fatigue.'

Impaired oxygen delivery to muscle in chronic fatigue syndrome. McCully KK, Natelson BH

'In conclusion, oxygen delivery was reduced in CFS patients compared with that in sedentary controls. This result is consistent with previous studies showing abnormal autonomic control of blood flow.'

Post-viral fatigue syndrome: evidence for underlying organic disturbance in the muscle fibre. Jamal GA, Hansen S.

'Ten patients with post-viral fatigue syndrome and abnormal serological, virological, immunological and histological studies were examined by the single-fibre electromyographic (EMG) technique after excluding concurrent problems in the neuromuscular system. No abnormality of fibre density was noted but all patients had abnormal jitter values. Very high jitter values were not associated with impulse or concomitant blocking. The findings confirm the organic nature of the disease.'

'This muscle membrane defect may be due to the effects of a persistent viral infection.'

Enteroviruses and postviral fatigue syndrome. Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S.Department of Neurology, University of Glasgow, UK.

'Postviral fatigue syndrome (PFS) occurs both in epidemics and sporadically. Many of the original epidemics were related to poliomyelitis outbreaks which either preceded or followed them. The core clinical symptoms are always the same.'

'We have detected enteroviral genome sequences in muscle biopsies from cases of PFS, using specific enteroviral oligonucleotide primers in the polymerase chain reaction (PCR). In addition, whole virus particles can be demonstrated in PCR-positive muscle, using solid-phase immuno-electron microscopy. An increase in the number and size of muscle mitochondria was found in 70% of PFS cases, suggesting an abnormality in metabolic function. Evidence of hypothalamic dysfunction was present, particularly involving 5-hydroxytryptamine metabolism. A putative model of PFS, based on persistent enteroviral infection in laboratory mice, revealed resolving inflammatory lesions in muscle with, however, a marked increase in the production of certain cytokines in the brain. This model may help to explain the pathogenesis of PFS.'

Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome Stefania Fulle (a), Patrizia Mecocci (b), Giorgio Fano (c), Iacopo Vecchiet (d), Alba Vecchini (e), Delia Racciotti (d), Antonio Cherubini (b), Eligio Pizzigallo (d), Leonardo Vecchiet (c), Umberto Senin (b) and M. Flint Beal (f)

'From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia.'

'These data support an organic origin of CFS, in which muscle suffers oxidative damage.'

Important note

Before reading the research/advocacy information given in the above external links or excerpts, please be aware of the following facts:

1. Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms. The overwhelming majority of research on ‘CFS’ or ‘CFIDS’ or ‘ME/CFS’ or ‘CFS/ME’ or ‘ICD-CFS’ does not involve M.E. patients and is not relevant in any way to M.E. patients. If the M.E. community were to reject all ‘CFS’ labelled research as ‘only relating to ‘CFS’ patients’ (including research which describes those abnormalities/characteristics unique to M.E. patients), however, this would seem to support the myth that ‘CFS’ is just a ‘watered down’ definition of M.E. and that M.E. and ‘CFS’ are virtually the same thing and share many characteristics.

A very small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. The
A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy paper is recommended reading and includes a checklist to help readers assess the relevance of individual ‘CFS’ studies to M.E. (if any) and explains some of the problems with this heterogeneous and skewed research.

In future, it is essential that M.E. research again be conducted using only M.E. defined patients and using only the term M.E. The bogus, financially-motivated disease category of ‘CFS’ must be abandoned.

2. The research referred to on this website varies considerably in quality. Some is of a high scientific standard and relates wholly to M.E. and uses the correct terminology. Other studies are included which may only have partial or minor possible relevance to M.E., use unscientific terms/concepts such as ‘CFS,’ ‘ME/CFS,’ ‘CFS/ME,’ ‘CFIDS’ or Myalgic ‘Encephalopathy’ and also include a significant amount of misinformation. Before reading this research it is also essential that the reader be aware of the most commonly used ‘CFS’ propaganda, as explained in A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy and in more detail in Putting research and articles on Myalgic Encephalomyelitis into context.