(This is by Greg Crowhurst and is taken from : “Severe ME : Notes for Carers” :
1. Many world-class clinicians state that ME is either an infectious disease, or an auto-immune disease as a direct result of infectious insult and recognise ME as a complex neuro-immune disorder accompanied by chronic low-grade inflammation, increased levels of oxidative and nitrosative stress.(Maes et al 2014), requiring a skilled biomedical response.
2. ME was recognised as a specific disease entity by The Royal Society of Medicine in 1978 and by the World Health Organisation since 1969 as an organic neurological disease, ME is currently classified under ICD code G93.3. In the USA, ME ranks second only to HIV as the cause of serious, long-term illness. (Hooper 2004)
3. Cycles of severe relapse are common, as are further symptoms developing over time. Around 30% of cases are progressive and degenerative and sometimes ME is fatal. (National CFIDS Foundation). Two reviews have concluded that, “Substantial improvement is uncommon and is less than 6%"(Anderson et al. 2004); and "Full recovery... is rare". (Cairns & Hotopf, 2005)
4. According to the Chief Medical Officer (DH 2002) people with Severe ME in the UK currently receive "seriously inadequate health care”.
5. There is a significant body of compelling published evidence, demonstrating the involvement of the central nervous system, the autonomic nervous system and the peripheral nervous system in the pathogenesis of ME, as well as immunological and vascular disruption. (Williams 2004)
6. There are known to be so many issues with the body’s defence against pathogens, the Immune System, in ME that it has also been called CFIDS, Chronic Fatigue and Immune Dysfunction Syndrome. When the immune system has been seriously disrupted, all kinds of bacteria can no longer be eliminated.
7. ME is not a somatoform, “all in the mind”, psychiatric disorder. The documented biochemical, metabolic, vascular, neurological and muscle abnormalities in ME/CFS patients (Williams 2004) have led to the WHO classification of ME as a neurological illness. The UK Department of Health and the WHO Collaborating Centre at the Institute of Psychiatry have agreed that ME is undoubtedly neurological. There is no published evidence whatsoever, as opposed to opinion, that ME (as distinct from chronic fatigue) is a psychiatric disorder. (Williams 2004)
8. ME is not ‘medically unexplained.’ ME is a multi-system disease with many organ and bodily systems affected, producing a myriad of symptoms [and] many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research. (ME Society of America)
9. Cognitive Behaviour Therapy (CBT) and Graded Exercise Therapy (GET) are potentially harmful to anyone with ME. The Chief Medical Officer (2002) warned that exercise-based regimes advocated for less severely affected patients tend not to have been studied among those most severely affected. Shepherd (2001) warns that as much care should be taken in prescribing exercise as in prescribing pharmaceuticals, for ME patients do not respond to exercise in a manner that is expected of healthy people. (Streeten et al 2001)
10. It is not 'fatigue' or 'tiredness' that is the one essential characteristic of ME/CFS but central nervous system (CNS) dysfunction (Bassett 2006). As leading ME expert Dr Byron Hyde MD (2003) 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”
11. It has been shown that ME, alongside a wide range of seemingly unrelated disorders, such as Alzheimer’s, Diabetes, may have mitochondrial dysfunction in common (Pieczenik and Neustadt 2007); the research appears to be suggesting that blood flow problems are affecting the mitochondria’s ability to produce energy instead of the mitochondria themselves being messed up in ME. (Johnson 2013). It has been estimated that people with ME are about a litre short of blood.
12. Cardiovascular dysfunction in ME patients has been well documented for many years. (Williams 2008)
13. Cardiac output in normal people will vary from 7 litres per min to 5 litres per min between standing and supine. In healthy people this drop is not enough to affect function. But in ME sufferers Peckerman found that the drop may be from 5 litres lying down to 3.5 litres standing up. At this level, people with ME may be in borderline heart and organ failure.(Peckerman et al 2003)
14. Studies have shown that the baroreflex response that regulates blood pressure is under performing, particularly in Severe ME. (Peckerman et al 2003) The heart’s job is to maintain blood pressure. If the blood pressure falls, organs start to fail and are shut down in terms of priority.
15. A study showing that the mean age of ME patients dying from heart failure is significantly lower than the age of those dying from heart failure in the general US population, implies that ME is a risk factor to cardio-vascular disorder.( Maes and Twisk 2009 )
16. Maes et al (2009) found that Coenzyme Q10 deficiency in ME is related to fatigue, autonomic and neurocognitive symptoms and is a risk factor explaining the early mortality in ME due to cardiovascular disorder.
17. Neurocognitive problems, strikingly similar to those of patients presented with D-lactic acidosis (linked to Short Bowel Syndrome) reported to be made worse by physical or mental exertion, are one of the most frequent and disabling symptoms associated with ME. (Sheedy et al 2009)
18. In 2009 a study found vitamin D levels to be considerably lower in ME patients than in healthy people. Soon after an investigation at the University of Dundee discovered an association between lower vitamin D levels and arterial stiffness, dysfunction of the endothelium (the lining of blood vessels) and inflammation, in ME patients. (Breakthrough Spring 2015)
19. ME is not depression. Research, for example, shows that ME patients show more alpha electroencephalographic activity during non-REM sleep, but this is not seen in dysthymic or major depressive disorder (Whelton, Salit, & Moldofsky, 1992). There are five major clinical tests of depression, all related to disturbances of the HPA (Hypothalamic-Pituitary-Adrenal) axis; they are, increased levels of Overnight Cortisol, 24-hour urinary cortisol, Corticotropin-releasing hormone, Arginine vasopressin and Adrenocorticotropin hormone (ACTH), ACTH is a hormone that is often released in response to stress, high ACTH levels can be an indicator of depression. ME patients, generally, show none of these signs, that is because ME, contrary to what many doctors wrongly believe, is not depression. (cf. Komaroff 2015)
20. SPECT cerebral blood flow studies of persons with ME show decreased blood flow in several key areas such as frontal lobes and brain stem which are different from both healthy controls (Barnden et al, 2001Costa et al, 1995) and depressed subjects (Schwartz et al, 1994, Fischler et al, 1996). PET scan studies have reached similar conclusions. (Tirelli et al, 1998)
21. The neurocognitive impairment in ME has been found to be rooted in physical dysfunction, not maladaptive thinking, related to decreased cerebral blood flow velocity. (Ocon et al 2011)
22. Hickie (1991) found that general characteristics of depression: anhedonia (lack of pleasure in life); weight loss; suicidal ideation; severe psychomotor change; pathological guilt; and severe anxiety, are not typical in ME.
23. ME is not deconditioning. The predominant psychiatric paradigm, still seems to be that patients have medically unexplained chronic fatigue, and that their problems derive from deconditioning consequent on physical inactivity at best and simple avoidance behaviour (underpinned by abnormal illness beliefs) at worst. (Scottish Cross Party Submission 2005).
24. What happens in ME has little to do with cardiovascular deconditioning (Spence & Stewart 2004) and is more related to chronic orthostatic intolerance/postural tachycardia syndrome (POTS), caused by vascular dysfunction.
25. Studies have shown that most patients do not avoid minimal activity and that lack of fitness is not related to the fatigue in ME (Bazelmans et al 2001 ). Moreover, deconditioning cannot explain the documented delay between the end of exertion and the exacerbation of symptoms, the upregulated immune system etc. (De Merlier et al 2000)
26. Although, as with lupus, multiple sclerosis and ovarian cancer for example, there is no medical test available to confirm a diagnosis of ME, it is absurd to claim no objective or quantifiable abnormalities can be found in patients with Severe ME. (Bassett 2006) “Tests will only all be normal in M.E. patients – as with all illnesses – if completely the wrong tests are done, or if those tested do not in fact have M.E. in the first place.” (Bassett 2006)
27. A 2015 study at Stanford University, comparing brain MRI images, found that the brains of people with ME differ from healthy subjects in at least three distinct ways: white-mater content was reduced by about 7%, a consistent abnormality in the right arcuate fasciculus was identified with links to the severity of illness and there was a thickening of grey matter, where the two areas of the brain connect at the right arcuate fasciculus. These results, showing strong evidence for Central Nervous System defects, were reported widely around the world. (Breakthrough Spring 2015)
28. Certain aspects of immune system dysfunction, dysregulation of the RNase L pathway, hyperactive NF-kappaB leading to disturbed apoptotic mechanisms and oxidative stress or excessive nitric oxide, for example, appear to be present in both Cancer and in ME and may play a role in the two diseases and in the physiopathology of the common symptom fatigue. (Meeus et al 2009)
29. There is evidence that ME is characterised by increased oxidative stress (Maes et al 2011). Researchers at the University of Dundee have found that people with ME have high levels of reactive oxygen molecules which can harm blood vessels and muscles. (Breakthrough Spring 2015)
30. There is good evidence that ME patients have a generalised hyperalgesia (an increased sensitivity to pain throughout the body which increases after stressors and following exercise – this is unusual because sensitivity to pain normally decreases in people during physical activity. (Breakthrough Spring 2012)
31. Problems with eyes and vision are common feature of ME, including eye pain (which is severe or very severe in one third of cases), prominent eye movement dysfunction and visual processing issues. (ME Research 2015)
32. Studies examining the microecology of the gastrointestinal (GI) tract have identified specific microorganisms whose presence appears related to ME, which is associated with marked alterations in the gut microbiota, with lower levels of Bifidobacteria and higher levels of aerobic bacteria. A CFIDS Association of America pilot study, for example, found greatly increased ratios of Firmicute/Bacteriodetes bacteria before and after exercise in ME. (CIFDS 2013)
33. It has been found that a significant subset of ME patients may have a chronic, non-cytolytic form of enteroviral infection which could be diagnosed by stomach biopsy. (Chia 2008)
34. Reports also suggest that ME patients may have a major drop in all E.Coli species - in contrast to Crohn’s Disease where over 95% of the invasive species are E.Coli. (Lassesen 2013)
35. One of the most consistently observed abnormalites in ME is hypocortisolism (low cortisol levels); there is evidence for reduced cortisol and ACTH production/responsiveness in ME, alongside evidence of reduced adrenal gland productivity. A mutation in the cortisol binding globulin gene (CBG) has also been found in people with ME, this impaired CBG functioning would exacerbate any cortisol deficiencies already present. (Torpy et. al. 2001)
36. New Scientist magazine reported in July 2015 that nearly two thirds of people, diagnosed with “ME/CFS” who have taken Rituximab, a drug normally used to knock out white blood cells in people with lymphoma and rheumatoid arthritis, have experienced a major remission of their symptoms. We are not sure, however, if Rituximab really is a potential treatment for ME; it could be that the two thirds of patients it helped have “CFS”, not ME, for “ME/CFS” is an umbrella term, subject to many different interpretations, incorporating a wide range of meaning and poorly identified conditions. If you have ME, caused by an enterovirus, the John Richardson Group (2013) warn, it could be very dangerous indeed to take Rituximab, which suppresses the immune/virus balance.
It should be stressed that any registered medical practitioner, consultant or GP, in the UK, who chooses to dismiss or ignore widely available biomedical evidence for ME, may be in breach of the legal requirement for doctors to keep up to date with developments in medicine and medical science and this consequently raises issues of medical indemnity.(Hooper 2010 )
In the UK, there is no act of parliament setting out patient’s rights, however the NHS must take account of law made by parliament (e.g. Human Rights Act etc.) or by court judgements. Health professionals must use reasonable care and skill and patients are entitled to receive care of a standard which a “responsible body of medical opinion” considers to be appropriate to their condition. If the duty of care is breached, the patient may be able to sue for negligence.(NHS 2006)
Greg Crowhurst (c) 2016
From : Severe ME : Notes for Carers