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A SMALL SELECTION OF THE PAPERS SHOWING CFS TO BE A PHYSICLA ILLNESS:

HISTORICAL PAPERS ON CFS / ME
1955
Outbreak at The Royal Free. ED Acheson. Lancet 1955:394-395
1956
A New Clinical Entity? Leading Article. Lancet 1956: 789-790
1959
The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia. ED Acheson. American Journal of Medicine: 1959:569-595
1970
Encephalomyelitis Resembling Benign Myalgic Encephalomyelitis. SGB Innes. Lancet 1970:969-971
1976
Benign Myalgic Encephalomyelitis or Epidemic Neuromyasthenia. AM Ramsay. Update 1976:539-542
1977
Icelandic disease (benign myalgic encephalomyelitis or Royal Free disease). AM Ramsay, EG Dowsett JG Parish et al. BMJ 1977: 1350
1978
Postgraduate Medical Journal 1978:54:637: 709-771. Whole issue.
An outbreak of encephalomyelitis in the Royal Free Hospital Group. Nigel Dean Compston. Postgraduate Medical Journal 1978:54:722-724
Epidemic myalgic encephalomyelitis. Leading Article. BMJ 1978:1436-1437
1979
Clinical and biochemical findings in ten patients with benign myalgic encephalomyelitis. AM Ramsay, A Rundle. Postgraduate Medical Journal 1979:856-857
1983
Sporadic myalgic encephalomyelitis in a rural practice. BD Keighley, EJ Bell. Journal of the Royal College of General Practitioners, June 1983:339-341
1984
Myalgic encephalomyelitis and the general practitioner. JC Murdoch. New Zealand Family Physician 1984:127-128
Excessive Intracellular Acidosis Of Skeletal Muscle On Exercise In A Patient With A Post-Viral Exhaustion/Fatigue Syndrome. DL Arnold, GK Radda et al. The Lancet 1984: 1367-1369
1985
Electrophysiological studies in the post-viral fatigue syndrome. Leading Article. Journal of Neurology, Neurosurgery, and Psychiatry 1985:691-694
The postviral fatigue syndrome - an analysis of the findings in 50 cases. PO Behan, WMH Behan et al. Journal of Infection(1985) 10:211-222
1987
The Epstein-Barr Virus and Chronic Fatigue. IE Salit. Clinical Ecology 1987188 V, 3:103-107
Myalgic encephalomyelitis (ME) syndrome - an analysis of the clinical findings in 200 cases. JC Murdoch. The New Zealand Family Physician 1987:51-54
1988
The Myalgic Encephalomyelitis Syndrome. JC Murdoch. Family Practice 1988:302-306
Myalgic Encephalomyelitis, or what? AM Ramsey. The Lancet 1988: 100- 101 The Clinical Identity Of The Myalgic Encephalomyelitis Syndrome. AM Ramsey. Pub. UK ME Association 1988
Postviral Fatigue Syndrome. PO Behan, WMH Behan. CRC Critical Reviews In Neurobiology 1988:157-178
1989
Postviral fatigue syndrome. DO Ho-Yen. British Journal of Hospital Medicine 1989:250
Postviral syndrome - how can a diagnosis be made? A study of patients undergoing a Monospot test. SJ Bowman, J Brostoff et al. Journal of the Royal Society of Medicine 1989:712-716
Treatment of Patients with Chronic Fatigue Syndrome. Leading Article. Nelson M Gantz & Gary P Holmes Drugs 1989 38(6): 855-862
Post-Viral Fatigue Syndrome: Evidence for Underlying Organic Disturbance in the Muscle Fibre. GA Jamal, S Hansen. European Neurology 1989: 273-276
1991
History of Chronic Fatigue Syndrome. SE Straus. Reviews of Infectious Diseases 1991;13(Suppl 1):S2-7
GENERAL PAPERS ON CFS / ME 1990 ONWARDS
1990
Patient management of post-viral fatigue syndrome. DO Ho-Yen. Journal of the Royal College of General Practitioners 1990:40:37-39
Aerobic work capacity in patients with chronic fatigue syndrome. MS Riley, J O'Brien. BMJ 1990.953-956
1991
General practitioners' experience of the chronic fatigue syndrome. DO Ho-Yen. British Journal of General Practice 1991:41:324-326
Chronic Fatigue Syndrome in Northern Nevada. SA Daugherty, BE Henry et al. Reviews of Infectious Diseases 1991:13(Suppl 1):S39-44
Symptoms and Signs of Chronic Fatigue Syndrome. AL Komaroff, D Buchwald. Reviews of Infectious Diseases 1991:13(Suppl 1):S8-11
1992
CFIDS Has An Organic Basis: It is Not a Psychiatric Illness. Dr. W Gunn (CDC). The CFIDS Chronicle 1992.1
Skeletal Muscle Metabolism in the Chronic Fatigue Syndrome. R Wong, G Lopaschuk et al. Chest 1992:102:1716-1722
Plasma and Cerebrospinal Fluid Monoamine Metabolism in Patients with Chronic Fatigue Syndrome: Preliminary Findings. MA Dernitrack, PW Gold et al. Biol Psychiatry 1992.¬32:1065-1077
1993
Clinical presentation of chronic fatigue syndrome. AL Komaroff. Wiley, Chichester (Ciba Foundation Symposium 173) 1993:43-61
1994
Chronic Fatigue Syndrome: What Have We Learned and What Do We Need to Know? AL Komaroff, N Klimas. Clinical Infectious Diseases 1994:18(Suppl 1):S166-167
1995
Outcome and Prognosis of Patients With Chronic Fatigue vs Chronic Fatigue Syndrome. CH Bombardier, D Buchwald. Arch/Intern Med 1995:155:2105-2110
Features of Chronicity in ME/CFS: A Case Series in the UK. R Gibbons, A Macintyre, C Richards. First World Congress on Chronic Fatigue Syndrome and Related Disorders 1995:56
1996
Health Status in Patients with Chronic Fatigue Syndrome and in General Population and Disease Comparison Groups. AL Komaroff, LR Fagioli et al. The American Journal of Medicine 1996:101:281-290
Prognosis in chronic fatigue syndrome: a prospective study on the natural course. JHMM Vercoulen, CMA Swanink et al. Journal of Neurology, Neurosurgery, and Psychiatry 1996:60:489-494
1997
Chronic Fatigue Syndrome - A Challenge to the Clinical Professions. D Pheby. Physiotherapy 1997:83:53-56
A 56-Year-Old Woman With Chronic Fatigue Syndrome. AL Komaroff. JAMA 1997.278:14:1179-1184
Chronic Fatigue Syndrome: A Disorder of Central Cholinergic Transmission. A Chaudhuri, T Majeed et al. Journal of Chronic Fatigue Syndrome 1997,3(l): 3-16
Epidemiologic Advances in Chronic Fatigue Syndrome. PH Levine. J. psychiat. Res 1997.31:1:7-18
1998
Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome. RJM Lane, MC Barrett et al. J Neurol Neurosurg Psychiatry 1998:64:362-367
Chronic Fatigue Syndrome: An Update. AL Komaroff, DS Buchwald. Annu. Rev. Med. 1998:49:1-13
Chronic fatigue in overlap syndromes. A Chaudhuri, P Behan. CNS 1998:1:2:1620
1999
Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. L Paul, L Wood et al. European Journal of Neurology 1999:6:63-69
A Community-Based Study of Chronic Fatigue Syndrome. LA Jason, JA Richman et al. Arch Intern Med 1999:159:2129-2137
Impaired oxygen delivery to muscle in chronic fatigue syndrome. KK McCully, BH Natelson. Clinical Science 1999:97:603-608
2000
A 37 kDa 2-5A Binding Protein as a Potential Biochemical Marker for Chronic Fatigue Syndrome. K De Meirleir, C Bisbal et al. The American Journal of Medicine 2000:108:99¬105
The Biology of Chronic Fatigue Syndrome. AL Komaroff. Am J Med 2000:108:169-171
Pall ML. 2000a. Elevated peroxynitrite as the cause of chronic fatigue syndrome. Medical Hypoth 54:115-125.
Pall ML. 2000b. Elevated peroxynitrite as the cause of chronic fatigue syndrome: Other inducers and mechanisms of symptom generation. J Chronic Fatigue Syndrome 7(4):45-58.
2001
Pall ML. 2001a. Cobalamin used in chronic fatigue syndrome therapy is a nitric oxide scavenger. J Chronic Fatigue Syndrome 8(2):39-44.
Pall ML. 2001b. Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite. Medical Hypoth 57:139-145.
Pall ML and Satterlee JD. 2001. Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity, chronic fatigue syndrome and posttraumatic stress disorder. Ann NY Acad Sci 933:323-329.
LABORATORY FINDINGS IN CFS / ME
1991
Review of Laboratory Findings for Patients with Chronic Fatigue Syndrome. D Buchwald, AL Komaroff. Reviews of Infectious Diseases 1991:13(Suppl 1):S12-18
Laboratory Abnormalities in Chronic Fatigue Syndrome. Dedra Buchwald. In: Postviral Fatigue Syndrome. Ed: Rachel Jenkins & James Mowbray pub: John Wiley & Sons, Chichester, 1991:117-136
1995
Clinical Laboratory Test Findings in Patients With Chronic Fatigue Syndrome. DW Bates, D Buchwald, AL Komaroff et al. Arch Intern Med 1995:155:97-103
NEUROLOGICAL FACTORS IN CFS / ME
1990
Extract from a press-conference held in San Francisco, Sept 1990. Dr P Cheney. CFIDS Chronicle, Sept 1990:7-8
1991
Testing of Vestibular Function: An Adjunct in the Assessment of Chronic Syndrome. JMR Furman. Reviews of Infectious Diseases 1991:13 (Suppl 1):S109¬11
1994
A Comparative Review of Systemic and Neurological Symptomatology in 12 Outbreaks Collectively Described as Chronic Fatigue Syndrome, Epidemic Neuromyasthenia, and Myalgic Encephalomyelitis. NC Briggs, PH Levine. Clinical Infectious Diseases 1994:18 (Suppl 1):S32-42
Chronic Fatigue Syndrome Update - Findings Now Point To Central Nervous System Involvement. DS Bell. Postgraduate Medicine 1994:96:6:73-81
1995
Vestibular Function Test Anomalies in Patients with Chronic Fatigue Syndrome. R Ash¬Bernal, C Wall et al. Acta Otolaryngol (Stockh) 1995:115:9-17
1996
Decreased vagal power during treadmill walking in patients with chronic fatigue syndrome. DL Cordero, WN Tapp et al. Clinical Autonomic Research 1996:6:329-333
Medical Matters: Problems with Balance. UK ME Association Newsletter (Perspectives) September 1996:iv
1997
Does the Chronic Fatigue Syndrome Involve the Autonomic Nervous System? R Freeman, MD Anthony, L Komaroff. The American Journal of Medicine 1997:102:357¬364
1998
Neurally Mediated Hypotension and Chronic Fatigue Syndrome. PC Rowe, H Calkins. The American Journal of Medicine 1998:105(3A):15S-21S
1999
Chronic Fatigue Syndrome is an Acquired Neurological Channelopathy. A Chaudhuri, PO Behan. Hum. Psychopharmacol. Clin. Exp. 1999:14:7-17
2000
Pall ML. 2000b. Elevated peroxynitrite as the cause of chronic fatigue syndrome: Other inducers and mechanisms of symptom generation. J Chronic Fatigue Syndrome 7(4):45-58.
Pall ML. 2001b. Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite. Medical Hypoth 57:139-145.
Pall ML. 2002b. NMDA sensitization and stimulation by peroxynitrite, nitric oxide, and organic solvents as the mechanism of chemical sensitivity in multiple chemical sensitivity. FASEB J 16:1407-1417
EVIDENCE OF DEMYELINATION AND CEREBRAL OEDEMA IN CFS / ME
1988
Anaesthetics and ME / CFS: Anzmes Meeting Place 30:1988:29
Research Workshop, National Institute of Allergy and Infectious Diseases (NIH), University of Pittsburgh, S:Daugherty, le September 1988.
1990
Chronic Fatigue Syndrome and the Psychiatrist: SE Abbey, PE Garfinkel: Can: J: Psychiatry 1990:35:7:625-626
1992
A Chronic Illness Characterized by Fatigue, Neurologic and Immunologic Disorders, and Active Human Herpesvirus Type 6 Infection: D Buchwald, PR Cheney et al: Annals of Internal Medicine 1992:116:2:103
1994
Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome. Comparison of MR Imaging and SPECT: RB Schwartz, BM Garada: American Journal of Roentgenology 1994:162:935-941
1997
A 56 year old woman with chronic fatigue syndrome. AL Komaroff JAMA 1997:278:14:1179-1184
1988 (15th September)
The National Institute of Allergy and Infectious Diseases (NIAID), in cooperation with the University of Pittsburgh, held a large research workshop entitled "Considerations in the Design of Studies of Chronic Fatigue Syndrome":
There were participants from the Centres for Disease Control (CDC) and from the National Institutes of Health (NIH).
At this conference it was recommended that the term CFIDS (pronounced seefids) be used instead of the term CFS, on the basis of the immune dysfunction which has been observed in the disorder.
One of the presentations was by Dr Sandra Daugherty, who reported that MRI scans on patients from Nevada demonstrated abnormalities consistent with demyelination and cerebral oedema in CFS / ME in 57% of patients studied.
RESPIRATORY PROBLEMS IN CFS / ME
1989
Pulmonary Function and the Chronic Fatigue Syndrome. CB Payne, HE Sloan. Ann Intern Med 1989:111(1O):860
Dyspnoea in chronic primary fibromyalgia. Caidahl K, Lurie M et al. J Intern Med 1989:226(4):265-270
1990
Respiratory function in chronic primary fibromyalgia. Lurie M, Caidahl K et al. Scand J Rehabil Med 1990:22(3):151-5
1996
Fibromyalgia syndrome: overnight falls in arterial oxygen saturation. Alvarez LB, Alonso Valdivielso JL. Am J Med 1996:101(f):54-60
Lung function test findings in patients with chronic fatigue syndrome (CFS). F De Lorenzo, J Hargreaves, W Kakkar. Aust NZ J Med 1996:26:563-4
1998
Dyspnoea resulting from fibromyalgia. Weiss DJ, Kreck T, Albert RK. Chest 1998:113(l):246-9
Respiratory Symptoms and Lung Function Testing in Chronic Fatigue Syndrome Patients. P de Becker, K de Meirleir et al. Fourth International AACFS Research & Clinical Conference on CFIDS, Mass. October 1998
NEUROENDOCRINE FACTORS IN CFS / ME
1991
Evidence for Impaired Activation of the Hypothalamic-Pituitary-Ad renal Axis in Patients with Chronic Fatigue Syndrome. MA Demitrack, JK Dale. Journal of Clinical Endocrinology and Metabolism 1991:73:6:1224-1234
1992
Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. AMO Bakheit, PO Behan et al. BMJ 1992:304:1010-1012
1995
Neuroendocrinology of Chronic Fatigue Syndrome. TG Dinan. First World Congress on CFS and Related Disorders, Brussels 1995 (Abstract p 9)
1996
The Neuroendocinology of Chronic Fatigue Syndrome. LV Scott, TG Dinan. Journal of Chronic Fatigue Syndrome 1996:2(4):49-59
Evidence That Abnormalities of Central Neurohormonal Systems Are Key to Understanding Fibromyalgia and Chronic Fatigue Syndrome. LJ Crofford, MA Dernitrack. Rheumatic Disease Clinics of North America 1996:22:2:267-284
Chronic Fatigue Syndrome: a stress disorder? AJ Cleare, SC Wesseley. J. Hosp. Med. 1996:55:9:571-574
1997
Blunted Serotonin-Mediated Activation of the Hypothalamic-Pituitary-Ad renal Axis in Chronic Fatigue Syndrome. TG Dinan, T Majeed et al. Psychoneuroendocrinology 1997:22:4:261-267
Neuroendocrine Correlates of Chronic Fatigue Syndrome: A Brief Review. MA Demitrack. J.Psychiat.Res 1997:31:1:69-82
1998
Salivary Cortisol Profiles in Chronic Fatigue Syndrome. B Wood, S Wessely et al. Neuropsychobiology 1998:37:1-4
Evidence for Pathophysiologic Implications of Hypothalamic-Pituitary-Adrenal Axis Dysregulation in Fibromyalgia and Chronic Fatigue Syndrome. MA Demitrack, LJ Crofford. Ann. NY. Acad. Sci 1998:840:684-697
VIROLOGICAL ASPECTS OF CFS / ME
1986
Medical consequences of persistent viral infection. P Southern, MBA Oldstone. The New England Journal Of Medicine 1986:314:6:359-367
Some problem areas in the interaction between viruses and the immune system. PC Doherty. Immunol. Cell Biol. 1986:65(Pt 4):279-286
1987
Coxsackie B Viruses and the Post-viral syndrome: a prospective study in general practice. BD Calder, PJ Warnock et al. Journal of the Royal College of General Practitioners 1987:37:11¬14
The Epstein-Barr Virus and Chronic Fatigue. IE Salit. Clinical Ecology 1987188:5:103-107
Chronic Enterovirus Infection in Patients with Postviral Fatigue Syndrome. GE Yousef, EJ Bell et al. The Lancet Jan 23 1988:146-150
Chronic Fatigue Syndromes: relationship to chronic viral infections. AL Komaroff. Journal of Virological Methods 1988:21:3-10
1989
Viruses Can Cause Disease in the Absence of Morphological Evidence of Cell Injury: Implication for Uncovering New Diseases in the Future. MBA Oldstone. The Journal of Infectious Diseases 1989:159:3:384-389
1990
Persistence of Enteroviral RNA in Chronic Fatigue Syndrome is Associated with the Abnormal Production of Equal Amounts of Positive and Negative Strands of Enteroviral RNA. L Cunningham, NE Bowles et al. Journal of General Virology 1990:71:1399-1042
Myalgic encephalomyelitis - a persistent enteroviral infection? EG Dowsett, AM Ramsay et al. Postgrad Med J 1990:66:000-000 BU/1991
Reviews of Infectious Diseases. Vol. 13: Supplement 1: Jan-Feb 1991:S1-S140
Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome. JW Gow, WMH Behan et al. British Medical Journal 1991:302:692- 696
Mitochondrial abnormalities in the postviral fatigue syndrome. WMH Behan et al. Acta Neuropathol 1991:83:61- 65
1993
Enteroviruses and postviral fatigue syndrome. PO Behan, WMH Behan et al. Chronic Fatigue Syndrome. Wiley, Chichester (Ciba Foundation Symposium 173) 1993:146 -159
1994
Changes in the 2-5A Synthetase/RNase L Antiviral Pathway in a Controlled Clinical Trial with Poly(I)-Poly(C12U) in Chronic Fatigue Syndrome. RJ Suhadolnik, NL Reichenbach et al. In vivo 1994:8:599 - 604
1997
Evidence for enteroviral persistence in humans. DN Galbraith et al. Journal of General Virology 1997:78:307-312
2000
Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. DV Ablashi, HB Eastman et al. Journal of Clinical Virology 2000:16:179 -191
LIVER INVOLVEMENT IN CFS / ME
1977
Icelandic disease (benign myalgic encephalomyelitis or Royal Free disease) AM Ramsay, EG Dowsett et al BMJ 21st May 1977:1350
1991
Chronic Fatigue Syndrome in Northern Nevada. SA Daugherty, BE Henry et al. Reviews of Infectious Diseases 1991:13 (Suppl 1):S39-44
1997
Chronic Fatigue Syndrome and Depression: Biological Differentiation and Treatment. CM Jorge, PJ Goodnick. Psychiatric Annals 1997:27:5:365-366
2000
Symptom patterns in long duration chronic fatigue syndrome. Fred Friedberg, Lucy Dechene et al J Psychsom Res 2000:48:59-68
IMMUNOLOGICAL ABNORMALITIES IN CFS / ME
1987
Phenotypic and Functional Deficiency of Natural Killer Cells in Patients with Chronic Fatigue Syndrome. M Caligiuri, D Buchwald, P Cheney, D Peterson, AL Komaroff et al. The Journal of Immunology 1987:139:10:3306-3313
1988
What is myalgic encephalomyelitis? AR Lloyd, D Wakefield, C Boughton, J Dwyer. Lancet 1988:1286-1287
IgG subclass deficiency in chronic fatigue syndrome. AL Komaroff et al Lancet 1988:4th June
1989
Interleukin-2 and the Chronic Fatigue Syndrome. PR Cheney, SE Dorman, DS Bell. Ann Int Med 1989 110-4:321
Immunological abnormalities in the chronic fatigue syndrome. AR Lloyd et al Med J Aust. 1989:151:124
Immune function and the chronic fatigue syndrome. Leading Article. W Gin et al Med J Aust 1989:151:117-118
Natural Killer Cell Activity in the Chronic Fatigue-immune Dysfunction Syndrome NL Eby, S Grufferman, RB Herberman et al. In: Natural Killer Cells and Host Defense. Eds: Ades EW, Lopez C. Karger, Basle, 1989: 141-145. Proceedings of 5h International Natural Killer Cell Workshop. Hilton head, SC 1988.
Human IgE Response: Virus-Activated IgE Secretors are Interleukin-2-Dependent Cells. MA Chan, HM Dosch. Int Arch Allergy Appl Immunol 1989: 89:90-97
1990
Myalgic encephalomyelitis: an alternative theory. CWM Wilson. JRSM 1990: 83:8:481¬483
Immunologic Abnormalities in Chronic Fatigue Syndrome. Nancy G Klimas et al J Clin Microbiol 1990:28:6:1403-1410
CD8 Deficiency in Patients with Muscle Fatigue Following Suspected Enteroviral Infections (Myalgia Encephalitica). JR Hobbs, J Mowbray, JE Monroe et al In: Profides of the Biological Fluids, Jan 1990, vol 36:391-398
1991
Immunology of Postviral Fatigue Syndrome. JF Mowbray, GE Yousef. British Medical Journal 1991:4 7.4:886-894
Nervous System-immune System Communication. BGW Arnasonj. Reviews of Infectious Diseases 1991:13(Suppl 1):S134-7
Immunologic Abnormalities Accompanying Acute and Chronic Viral Infections. DE Griffin. Reviews of Infectious Diseases 1991:13(Suppl 1):S129-33
Sources of Confounding in Immunologic Data. RB Herberman. Reviews of Infectious Diseases 1991:13(Suppl 1):S84-6
Natural Killer Cells and the Post Viral Fatigue Syndrome. DO Ho-Yen, RW Billington, J Urquhart. Scand J Infect Dis 1991:23:711-716
Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome. LJA Morrison, WHM Behan, PO Behan. Clin. Exp. Immunol 1991:83:441-446
A Comprehensive Immunological Analysis in Chronic Fatigue Syndrome. S Gupta, B Vayuvegula. Scand. J. Immunol 1991:33:319-327
Chronic Fatigue Syndrome - An Overview. P Cheney.
Chronic fatigue syndrome: clinical condition associated with immune activation. AL Landay, C Jessop et al. The Lancet 1991:338:707-12
1992
A Chronic Illness Characterized by Fatigue, Neurologic and Immunologic Disorders, and Active Human Herpesvirus Type 6 Infection. D Buchwald, PR Cheney et al. Annals of Internal Medicine 1992:116:2:103-111
1993
Chronic Fatigue Syndrome: Is It a State of Chronic Immune Activation Against an Infectious Virus? JA Levy, AL Landay et al. Contemp Issues Infec. Dis. 1993:10:127-146
Immunity and the pathophysiology of chronic fatigue syndrome. AR Lloyd, D Wakefield, I Hickie. Chronic fatigue syndrome 1993. Wiley, Chichester (Ciba Foundation Symposium 173):176-192
1994
Immunological Abnormalities in Patients with Chronic Fatigue Syndrome. U Tirelli, G Marotta et al. Scand. J. Immunol 1994:40:601-608
Simultaneous Measurement of Antibodies to Epstein-Barr Virus, Human Herpesvirus 6, Simplex Virus Types 1 and 2, and 14 Enteroviruses in Chronic Fatigue Syndrome: Is There Evidence of Activation of a Nonspecific Polyclonal Immune Response? FA Marrin. Clinical Infectious Diseases 1994:19:448-53
Decreased Natural Killer Cell Activity Is Associated with Severity of Chronic Fatigue Immune Dysfunction Syndrome. EA Ojo-Amaize, EJ Conley, JB Peter. Clinical Infectious Diseases 1994:18(Suppl 1):S157-9
Association Between HLA Class 11 Antigens and the Chronic Fatigue Immune Dysfunction Syndrome. RH Keller, JL Lane et al. Clinical Infectious Diseases 1994:18(Suppl 1):S154-6
Dysregulated Expression of Tumor Necrosis Factor in Chronic Fatigue Syndrome: Interrelations with Cellular Sources and Patterns of Soluble Immune Mediator Expression. R Patarca, NG Klimas et al. Clinical Infectious Diseases 1994:18(Suppl 1):S147-53
Upregulation of the 2-5A Synthetase/RNase L Antiviral Pathway Associated with Chronic Fatigue Syndrome. RJ Suhadolnik, NL Reichenbach et al. Clinical Infectious Diseases 1994:18(Suppl 1):S96-104
Immunologic Abnormalities Associated with Chronic Fatigue Syndrome. Ebarker, SF Fujimara et al. Clinical Infectious Diseases 1994:18(Suppl 1):S136-41
Part IV: Immunologic Studies of Chronic Fatigue Syndrome. AR Lloyd. Clinical Infectious Diseases 1994:18(Suppl 1):S134-5
Summary: Immunologic Studies of Chronic Fatigue Syndrome. AR Lloyd, N Klimas. Clinical Infectious Diseases 1994:18(Suppl 1):S160-1
Summary and Perspective: Epidemiology of Chronic Fatigue Syndrome. PH Levine. Clinical Infectious Diseases 1994:18(Suppl 1):S57-60
Data Presented at the Dublin International Meeting on CFS 18-20 May 1994 (under the auspices of the World Federation of Neurology). Prof. Dr Rainer.
1995
Immunology. R Patarca. Journal of CFS 1995:1:3-4:195-202
1996
Neuroimmune mechanisms in health and disease: 2. Disease. H Anisman, MG Baines et al. Can Med Assoc J. 1996:155(8):1075-1082
Autoantibodies to Nuclear Envelope Antigens in Chronic Fatigue Syndrome. K Konstantinov, A von Mikecz et al. J. Clin. Invest. 1996:98:8:1888-1896
1997
Biochemical Evidence for a Novel Low Molecular Weight 2-5A-Dependent RNase L in Chronic Fatigue Syndrome. RJ Suhadolink, DL Peterson et al. Journal of Interferon and Cytokine Research 1997:17:377-385
Elevation of Bioactive Transforming Growth Factor-9 in Serum from Patients with Chronic Fatigue Syndrome. AL Bennett, CC Chao et al. Joumal of Clinical Immunology 1997:17:2:160-166
Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal role of protein kinase RNA. A Vojdani, Mghoneum et al. Joumal of Internal Medicine 1997:242:465-478
1998
Immunologic Status Correlates with Severity of Physical Symptoms in Chronic Fatigue Syndrome Patients. S Wagner, L Heider et al. Proceedings of Fourth International AA CFS Research & Clinical Conference on CFIDS 1998.
CD4 Lymphocytes from Patients with Chronic Fatigue Syndrome Have Decreased Interferon-gamma Production and Increased Sensitivity to Dexamethasone. Jvisser, B Blauw et al. Journal of Infectious Diseases 1998:177:451-4
Biochemical Dysregulation of the 2-5A/RNase L Antiviral Defense Pathway in Chronic Fatigue Syndrome. 4h International AACFS Conference 1998.
T-Lymhocytes in CFS: In Vitro Reaction to Mutagens. 4th International AACFS Research & Clinical Conference on CFIDS 1998.
Lymph Node Morphology and Phenotype in Chronic Fatigue Syndrome. 4h International AACFS Research & Clinical Conference on CFIDS 1998.
Fatigue Syndromes and the Aetiology of Autoimmune Disease. A Poteliakhoff. Journal of Chronic Fatigue Syndrome 1998:4(4):31-49
Coincidental Splenectomy in Chronic Fatigue Syndrome. BJ Miller, JL Whiting, AD Clouston. Journal of Chronic Fatigue Syndrome 1998:4(l):37-42
A Study of the Immunology of the Chronic Fatigue Syndrome: Correlation of Immunologic Parameters to Health Dysfunction. IS Hassan, BA Bannister et al. Clinical Immunology and Immunopathology 1998:87:1:60-67
1999
Chronic Immundysfunction. Prof. Dr Rainer.
Vascular problems in CFS / ME

References to vasomotor instability / vasculitis in ME (CFS) in the obtained Authorities
A most cursory glance at the medical Authorities reveals the following:
A. From the earliest reports of ME, autonomic vasomotor instability has been noted:
e.g. A.M. Ramsay: Benign Myalgic Encephalomyelitis: Update: September 1976:539-541
e.g. A.M.Ramsay: A Baffling Syndrome with a Tragic Aftermath: / November 1981:
“A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder"
B. Reference to impaired blood flow in the micro-circulation:
e.g. L.O. Simpson et al: Myalgic Encephalomyelitis: New Zealand Medical Journal: 1984: 10th October: 698-699:
"Much of the symptornatology of ME is explicable on the expected consequences of impaired blood flow in the micro-circulation"
C. Reference to vasculopathy in ME found in the major textbook on ME edited by Dr Byron Hyde:
1. page 42 (chapter 5 / Hyde)
" We routinely observe patients with severely cold extremities and a visible line demarcating the cold from the area of normal skin temperature…….. The fact that the loss of normal blood flow may be persistent has been indicated by Gilliam (ref. 18, 1938)"
2. page 62
"Patients will ... complain of severe blanching of their extremities, nose, ears, lower arms and hands as well as lower legs and feet. Observation will often reveal a blanched clearly demarcated line separating warm from icy cold tissue. The whitened extremities may persist for hours and can be extremely painful"
3. page 70:
Hyde quotes from Wallis (ref. 25,1957): "The hemorrhages are mostly around small vessels, but some are also to be seen in the free tissue"
4. page 73:
Hyde discusses the occurrence of Raynaud's Disease in ME. “This is common in ME / CFS. These acute Raynaud's Disease changes are visible"
5. paqe 87:
Dr John Richardson (Chapter 8) Re the Central Nervous System involvement in ME: "Is it myelin, is it cellular, or is it vasonervorum, i.e.. vascular?"
6. page 89:
" A liver biopsy showed ... a vasculitis of the liver"
7. paqe 91:
"Liver Function Tests are sometimes abnormal and signify sometimes a
vasculitis of the liver"
8. page 250: Dr Jay Goldstein (Chapter 23)
"SPECT scanning... may justify vasodilator therapy with calcium channel
blockers..."
9. page 268:
Dr Betty Dowsett (Chapter 28) "ME is a multisystem syndrome including nervous, cardiovascular, endocrine and other involvement .... Symptoms and Signs (table 2): Vasculitic skin lesions-, autonomic dysfunction, especially circulation and thermoregulation"
10. page 376: Drs Hyde and Jain (Chapter 42)
Referring to the findings of Dr John Richardson: "frequent vasomotor abnormalities"
11. re: 1934 epidemic:
"vasomotor ... disturbances were almost constant findings ... with coldness and cyanosis. It was the impression of most observers that a generalised disturbance of vasomotor control occurred in these patients"
12. re: 1965 Galveston epidemic:
Dr Leon-Sotomayer: "vascular headaches"
note that these were classed as "long-term residuals" in 100% of ME patients.
13. re: Professor Behan's lecture to CIBA, 1988:
his team was regularly able to demonstrate micro-capillary perfusion defects in the cardiac muscle of ME patients
14. re: Nightingale Clinic cardiovascular observations on over 6,000 patients with ME:
“vascular headaches"; "autonomic system dysfunction with vasomotor instability"
15. page 427: Dr R. Biddle (Chapter 48)
"... lymphocytes in the CFS congregate in the perivascular (Virchow Robin) spaces of the brain... these findings do suggest that the disease may involve the perivascular spaces of the brain"
16. page 428-9:
"Dilatation of the Virchow Robin spaces ... could also suggest intracranial arterial or periarterial pathology... in particular, one would expect to find a congregation of lymphocytes in the perivascular spares around the Central Nervous System arteries ... (the literature about the Cumberland epidemic in 1955 has revealed) "an artefact that is in an anatomical position similar to that suggested by MRI studies (see ref. Wallis, idem)
17. page 430:
re: the Los Angeles 1934 epidemic- "The blood vessels throughout the nervous system were distended with red blood cells... the most characteristic change was infiltration of the blood vessel walls"
18. page 433: Dr Ismael Mena (Chapter 49)
"most probably temporal lobe perfusion defects may fingerprint primary inflammatory changes or secondary vascular impairment in these patients………the diminished uptake of this oxime can be interpreted as due to
a) diminished rCBF,
b) inflammatory regional changes .... (present in 71% of patients studied)
19. page 597: Dr L.O.Simpson (Chapter 65)
"The presence of increased percentages of nondiscocytic erythrocytes ... will impair flow in capillaries smaller than the diameter of the cells. (and) may initiate stasis in the smallest capillaries"
20. page 598:
"if the stasis did not resolve, focal lesions of ischemic necrosis would develop"
21. page 601:
"The impaired capillary flow in tissues or organs with secretory functions may result in reduced secretory activity (which) could reach pathological levels"
22. page 604:
"More attention should be paid to means of improving microcirculatory blood flow, to alleviate symptoms"
23. page 677: Dr Jon Russell (Chapter 75)
NOTE: On page 645, Professor Hugh Fudenberg, (one of the pioneers of clinical immunology and twice nominated for the Nobel Prize) states "Those (ME) patients who presented with severe muscle pains as the predominant symptoms were initially given a diagnosis of fibromyalgia": Dr Russell is the world expert on fibromyalgia (which is a component of ME).
re: the prevalence of vasculitis: "It is apparent that some patients with ... fibromyalgia also exhibit RA / SLE / vasculitis ... with a frequency that has caught the attention of clinicians"; the general prevalence of vasculitis is stated as being 0.14
D. Other Papers
24. Enterovirus infections and systemic clinical manifestations with prolonged inflammatory syndrome: association with a persistence of specific IgM antibodies.
Cathebras, P. et al. Rev Med Interne: 1993:14:10:961
Abstract: "We report 9 Gases of enteroviral infection associated with systemic inflammatory disease, including 4 cases of vasculitis .....We then reviewed 36 cases of enteroviral infection ... among them 11 cases were found to present with sub acute or chronic inflammatory disease. We conclude that enteroviruses might be important triggers of systemic inflammatory disease".
25. Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome: comparison of MR Imaging and SPECT.
Schwartz, R. B.,Garada,B.M., Komaroff A. L. et al: American Journal of Roentgenology 1994:162:935-941
"in addition to CNS lupus, other inflammatory vascular.. conditions can appear similar to CFS (ME) clinically and radiologically……As with any chronic inflammatory condition affecting the CNS, the T2-bright foci on MR in CFS (ME) may represent perivascular cellular infiltrate and / or reactive demyelination of the surrounding white matter. Alternatively, these abnormalities may reflect the result of a vasculopathy specifically involving the small vessels of the cerebral white matter; indeed, the distribution of lesions on MR in CFS (ME) is similar to that observed in occlusive arteriolar disease of any origin. The cortical defects measured with SPECT likewise may result from decreased flow through cortical arterioles owing to vasculitis. Specifically, on the basis of our observations, the white matter abnormalities seen on MR images may represent ... chronic demyelination, which appears to be irreversible".
26. SPECT Imaging of the Brain: Comparison of Findings in Patients with Chronic Fatigue Syndrome, AIDS Dementia Complex (ADC) and Major Unipolar Depression
Richard B. Schwartz, Anthony L Komaroff et al: Am. J. Roentgenology: 1994:162:943¬-951
"This study shows that CFS (ME) shares some similarities on SPECT imaging with AIDS Dementia Complex acute changes in radionuclide uptake in the younger population may be caused by inflammatory processes at the cellular or micro vascular level .... the findings in CFS (ME) are consistent with the hypothesis that CFS (ME) ... results from a viral infection of neurons, glia or vasculature .....viral infection can provoke neurological dysfunction by interfering with intra-cellular mechanisms or membrane transport systems .... or by cerebral hypo perfusion due to vasculitis".
Quotes (verbatim) from Dr Betty Dowsett (Past President of the United Kingdom ME Association) on 11th October 1998:
a) "Most ME patients have vasculitis" (Note that Dr Dowsett distinguishes
between patients with ubiquitous chronic fatigue syndrome and those with
true, defined ME, and that she was referring ONLY to patients with
true, defined ME).
b) “13% of ME patients are indistinguishable from multiple sclerosis".
HEART PROBLEMS IN CFS / ME
1989
Myalgic encephalomyelitis: postviral fatigue and the heart. NR Grist. BMJ 1989:299:12-19
1991
Post-viral Fatigue Syndrome and the Cardiologist. RG Gold. In: Postviral Fatigue Syndrome Eds: Rachel Jenkins & James Mowbray, pub.- John Wiley & Sons, Chichester 1991:227-231
1992
Cardiac and Cardiovascular Aspects of ME / CFS that may be secondary to Neurological or Psychological Involvement -- A Review. B Hyde, A Jain. In: The Clinical and Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome. Ed.- BM Hyde, Pub. The Nightingale Research Foundation, Ottawa,1992
1997
Arguments for a role of abnormal ionophore function in chronic fatigue syndrome (Syndrome X). A Chaudhuri et al. In: Chronic Fatigue Syndrome. Ed: Yehuda and Mostotsky pub. Plenum Press, New York 1997
Cardiac Involvement in Patients with Chronic Fatigue Syndrome as Documented With Holter and Biopsy Data in Birmingham, Michigan, 1991-1993. AM Lerner, J Goldstein et al. Infectious Diseases in Clinical Practice 1997:6:327-333
1998
Chronic Fatigue Syndrome. A Chaudhuri, WMH Behan et al. Proc. R. Coll. Physicians Edinb 1998:28:150-163
Cardiovascular Responses During a Cognitive Stressor Before and After Exercise in Chronic Fatigue Syndrome vs Sedentary Healthy Subjects. SA Sisto, B. Natelsonetal Fourth Intemational AACFS Research & Clinical Conference on CFIDS, Mass. October 1998
CFS Severity is Related to Reduced Stroke Volume and Diminished Blood Pressure Responses to Mental Stress. A Peckerman, BH Natelson et al Fourth International AA CFS Research & Clinical Conference on CFIDS, Mass. October 1998
1999
Chronic Fatigue Syndrome is an Acquired Neurological Channelopathy. A Chaudhuri, PO Behan. Hum. PsychopharmacoL Clin. Exp 1999:14:7-17
Cardiovascular response during head-up tilt in chronic fatigue syndrome. La Manca JJ, Natelson BH et al Physiol 1999:19:2:111-120
NUCLEAR MEDICINE FINDINGS IN CFS / ME
1992
Assessment of regional cerebral perfusion by 99-rcm-HMPAO SPECT in chronic fatigue syndrome. M Ichise, IE Salit. Nuclear Medicine Communications 1992:13:767-772
1994
SPECT Imaging of the Brain: Comparison of Findings in Patients with Chronic Fatigue Syndrome, AIDS Dementia Complex, and Major Unipolar Depression. RB Schwartz, AL Komaroff et al. 951
Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome: Comparison of MR Imaging and SPECT. RB Schwartz, BM Garada et al. AJR:1994:162:935-941
1995
Brainstem perfusion is impaired in chronic fatigue syndrome. DC Costa, C Tannock, J Brostoff. Q J Med 1995:88:767-773
1998
Brain SPET in Chronic Fatigue Syndrome. D DiGiuda, D Racciatti et al Fourth International AACFS Research & Clinical Conference on CFIDS 1998
1999
Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome. G Lange, J Deluca et al. Journal of the Neurological Sciences 1999:171:3-7

Permission to Repost

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Evidence that ME/CFS is not a somatisation disorder

Margaret Williams 26th April 2009

Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) is not a
somatisation disorder. That ME/CFS is not a somatisation disorder is not
simply a matter of belief or opinion but is a matter of substantive fact.

ME has been internationally classified since 1969 by the World Health
Organisation (WHO) as a disease of the Nervous System. There are now over
5,000 peer-reviewed published scientific papers which demonstrate
unequivocally that it is not a somatisation disorder. To assert otherwise
signifies either a serious failure to keep up-to-date with medical science
(as NHS Consultants are - or used to be - contractually required to do), or
a perverse and irrational denial of a large body of biomedical evidence that
shows ME/CFS to be a complex neuroimmune disorder affecting every major
bodily system and that recovery is rare.

The wealth of scientific biomarkers that distinguish ME/CFS from "chronic
fatigue" (which may indeed be a somatisation disorder) include the
following:

. abnormal brain scans (SPECT & PET scans) and MRI scans that are
consistent with organic brain syndrome, showing focal demyelination and/or
oedema in the sub-cortical area

. a dysregulated HPA axis

. a dysregulated antiviral pathway (RNase-L)

. cardiac abnormalities

. abnormal capillary flow

. low circulating blood volume

. abnormal ergometry test (indicating immediate anaerobic threshold)

. haemodynamic instability

. abnormal immune profile

. gene profiling (in one US study, Sorensen et al demonstrated that
expression of several complement genes remains at a higher level in ME/CFS
subjects before and post-exercise, which may lead to uncontrollable
inflammation-mediated tissue damage. In the UK, Kerr has demonstrated
differential expression in 88 genes [85 up-regulated and 3 down-regulated]
indicating haematological disease and function, immunological disease and
function, cancer, cell death, and infection [J Infect Dis
2008:197(8):1171-1184], all of which are seen in ME/CFS but not in states of
psychiatric fatigue).

All the above investigations are specifically not recommended by NICE in its
Clinical Guideline 53 on CFS that was published on 22nd August 2007. This
means that they are effectively proscribed in the UK, as no Primary Care
Trust (PCT) will fund them if NICE does not recommend them (and NICE
Guidelines are to become legally enforceable in 2009).

As long ago as 18th February 1993, Dr Paul Cheney (Professor of Medicine at
Capital University) testified before the US FDA Scientific Advisory
Committee that:

" I have evaluated over 2,500 cases. At best, it is a prolonged post-viral
syndrome with slow recovery. At worst, it is a nightmare of increasing
disability with both physical and neurocognitive components. The worst
cases have both an MS-like and an AIDS-like clinical appearance. We have
lost five cases in the last six months. The most difficult thing to treat is
the severe pain. Half have abnormal MRI scans. 80% have abnormal SPECT
scans. 95% have abnormal cognitive-evoked EEG brain maps. Most have
abnormal neurological examination. 40% have impaired cutaneous skin test
responses to multiple antigens. Most have evidence of T-cell activation.
80% have evidence of an up-regulated 2-5A antiviral pathway. 80% of cases
are unable to work or attend school. We admit regularly to hospital with an
inability to care for self".

Signs and symptoms seen in ME/CFS are legion (signs are observable by
clinicians and symptoms are reported by patients).

Documented and observable physical signs include a typically swinging
low-grade temperature, nystagmus; sluggish visual accommodation; abnormality
of vestibular function with a positive Romberg test; abnormal tandem or
augmented tandem stance; abnormal gait; hand tremor; incoordination;
cogwheel movement of the leg on testing; muscular twitching or
fasciculation; hyper-reflexia without clonus; facial vasculoid rash;
vascular demarcation which can cross dermatomes with evidence of Raynaud's
syndrome and / or vasculitis; mouth ulcers; hair loss; a markedly labile
blood pressure (sometimes as low as 84/48 in an adult at rest); flattened or
even inverted T-waves on 24 hour Holter monitoring (a standard 12 lead ECG
is usually normal); orthostatic tachycardia; shortness of breath (patients
show significant reduction in all lung function parameters tested);
abnormal glucose tolerance curves; liver involvement (an enlarged liver or
spleen may not be looked for in ME/CFS, so missed) and destruction of
fingerprints (atrophy of fingerprints is due to perilymphocytic vasculitis
and vacuolisation of fibroblasts).

Well-documented symptoms include: frequency of micturition, including
nocturia (bladder and bowel control may be insecure); abdominal pain and
diarrhoea (there are usually chronic problems with diarrhoea); persistent
headache (vascular headaches are common and recurring); generalised myalgia,
described as intense and burning; muscles are tender to palpation and muscle
spasm is not uncommon; there may be severe, intractable pain in particular
groups of muscles, most notably in the neck and in the shoulder and pelvic
girdles; the more severely affected patients are unable to stand unsupported
for more than a few minutes; there is sometimes segmental pain in the chest
wall.

In the more severely affected patients, dizziness is a particularly striking
and chronic feature, as is persisting dysequilibrium and ataxia, with
patients frequently bumping into things and becoming bruised. Attacks of
vertigo may be incapacitating. There is impaired neuromuscular coordination,
particularly with fine finger movements. In the severely affected, there may
be difficulty with swallowing; choking fits are not infrequent. There may be
difficulty with voice production, particularly if speaking is sustained.

There may be seizures, although these are found only in the most severe
cases.

In the most severe cases, photophobia and hyperacusis are common, as is
tinnitus; often there is parasthesia.

Hypersomnia is prevalent, especially in the early stages of the disorder;
this may be replaced by reversed sleeping patterns, with vivid and
disturbing dreams; unrefreshing sleep is common.

Cardiac arrythmias are very common, with pronounced tachycardia and an
uncomfortably pounding heart; there may be paroxysmal attacks of angina-like
chest pain. Cardiac pain is a recognised feature: patients may be convinced
they are suffering a heart attack. Myocarditis was a common symptom in an
analysis of 1,000 ME/CFS patients seen in Glasgow, where clinicians were
struck by the often-occurring association of patients with ME/CFS with acute
chest pain resembling coronary thrombosis.

In the more severely affected, palindromic arthropathies regularly recur;
spontaneous periarticular bleeds are frequent, especially in the fingers,
which become swollen and painful, making the patient appear even more
clumsy.

Pancreatitis is not uncommon and may cause acute, severe pain and illness:
pancreatic exocrine insufficiency leads to malabsorption, which is a
well-recognised feature found in the more severely affected; some patients
have almost non-existent pancreatic exocrine function. Some patients have
been shown to have achlorhydria.

Food intolerance is a prominent feature across all degrees of severity:
multiple sensitivities to normal foods and household chemicals (including
perfumes, chemical treatments of furniture and carpets such as
flame-retardants and glues in chipboard), petrol and agricultural chemicals
are frequent.

Intolerance to alcohol and to medicinal drugs, particularly to
antidepressants, is virtually pathognomonic. Patients have to be cautious
about all drugs but especially those acting on the central nervous system
(ie. anaesthetics), as there is an increased occurrence of adverse reaction.

ME/CFS affects not only the central nervous system but the autonomic and
peripheral nervous systems as well. Sympathetic nervous system dysfunction
is integral to ME/CFS pathology and includes blurred and double vision, with
difficulty in focusing and visual accommodation; eyes may be dry and eyelids
are often swollen and painful. Typical autonomic symptoms include alternate
sweating and shivering, with marked thermodysregulation. Patients experience
orthostatic hypotension and symptoms of hypovolaemia, with blood pooling in
the legs and insufficient blood flow to the brain: patients may feel faint,
shaky and nauseous; they can be tearful and observably pale and they may
experience severe distress. Patients are often understandably anxious and
afraid.

In the more severely affected, commonly there is difficulty with breathing,
with sudden attacks of breathlessness and dyspnoea on minimal effort; the
administration of oxygen may be necessary.

Rashes may occur; mouth ulcers may be recurrent and may be painful and
severe to the extent that speaking and eating may be affected.

Hands and feet are frequently cold, blanched and / or purple, with painful
vascular spasms seen in the fingers.

In females, ovarian-uterine dysfunction is not uncommon; in males,
prostatitis and impotence may occur.

Many patients can walk only very short distances and require a wheelchair.
There is difficulty with simple tasks such as climbing stairs and dressing.

Problems with short-term memory are common: cognitive impairment is
significant and includes difficulty with memory sequencing, processing
speed, word searching; dyslogia, spatial organisation, calculation
(dyscalculia), and particularly with decision-making. In relation to the
degree of cognitive impairment, American researchers found that:

"the performance of the (ME/CFS) patients was sevenfold worse than either
the control or the depressed group. These results indicated that the memory
deficit in (ME/CFS) was more severe than assumed by the CDC criteria. A
pattern emerged of brain behaviour relationships supporting neurological
compromise in (ME/CFS)".

Uncharacteristic emotional lability is very common; there may be an
increased irritability.

There may be significant and permanent damage to skeletal or cardiac muscle
as well as to other end-organs including the liver, pancreas, endocrine
glands and lymphoid tissues, with evidence of dysfunction in the brain stem.
Injury to the brain stem results in disturbance of the production of
cortisol (required for stress control) via damage to the hypothalamus and to
the pituitary and adrenal glands, and patients react extremely adversely to
stress.

Cycles of severe relapse are characteristic and common, together with the
evolution of further symptoms over time. ME/CFS is rarely listed as the
cause of death, although after decades of illness, death from end-organ
damage (mainly cardiac or pancreatic failure) is known to occur.

Suicide rates are high and are said to be the most common cause of death in
ME/CFS and to be related to the current climate of disbelief and rejection
of welfare support.

A major Report by the charity Action for ME (2001) found that 77 % of
sufferers experienced severe pain; over 80% had felt suicidal as a result of
the illness; 70% are either never able, or are sometimes too unwell to
attend a doctor's clinic; 65% (nearly two out of three) have received no
advice from their GP on managing this illness; 80% of those who are
currently bedridden by ME report that a request for a home visit by a doctor
has been refused; many people do not receive state benefits to which they
are clearly entitled.

Despite all the verifiable and authenticated international research, much of
the current perception of ME/CFS, both medical and lay, is beset by
confusion and misinformation.

A (documented) major cause of death in ME/CFS is heart failure.

International ME/CFS expert Paul Cheney's focus is based on the paper by Dr
Ben Natelson (neurologist and Professor of Neurology) and Dr Arnold
Peckerman (cardiopulmonary physiologist) at New Jersey Medical Centre (ref:
"Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic
Fatigue Syndrome": Peckerman et al: The American Journal of the Medical
Sciences: 2003:326:(2):55-60).

Cheney says that, without exception, every disabled CFIDS (Chronic Fatigue
Immune Dysfunction Syndrome ie. ME/CFS) patient is in heart failure.

The New Jersey team looked at many things in CFIDS patients and they found
something: a "Q" problem. "Q" stands for cardiac output in litres per
minute. In CFIDS patients, Q values correlated -- with great precision -
with the level of disability. Q was measured using impedance cardiography,
a clinically validated and Government agency-recognised algorithm that is
not experimental.

Normal people pump 7 litres per minute through their heart, with very little
variance, and when they stand up, that output drops to 5 litres per minute
(a full 30% drop, but this is normal). Those two litres are rapidly pooled
in the lower extremities and capacitance vessels. Normal people do not
sense that 30% drop in cardiac output when they stand up because their blood
pressure either stays normal or rises when they stand up -- the body will
defend blood pressure beyond anything else in order to keep the pulse going.

However, what the New Jersey team found in people with CFIDS was astonishing
-when disabled CFIDS patients stand up, they are on the edge of organ
failure due to extremely low cardiac output as their Q drops to 3.7 litres
per minute (a 50% drop from the normal of 7 litres per minute). These
patients do not have adequate Q to function. The lower the Q, the more time
the patient will spend lying down because lying down is the only time they
come close to having sufficient cardiac output to survive.

The disability level was exactly proportional to the severity of their Q
defect, without exception and with scientific precision.

The New Jersey team then looked to see if there were any symptoms that were
observable in disabled CFIDS patients but not in others and they found that
there was only one such symptom that was seen in patients with a Q problem:
post-exertional fatigue. To quote Cheney: "That is, when you push yourself
physically, you get worse".

CFIDS patients have a big Q problem; to quote Cheney again: "all disabled
CFIDS patients, all of whom have post-exertional fatigue, have low Q and are
in heart failure".

Post-exertional fatigue (long documented as the cardinal feature of ME/CFS
but not of other, non-specific, states of chronic fatigue) is the one
symptom that correlates with Q. Among disabled CFIDS patients, 80% had
muscle pain; 75% had joint pain; 72% had memory and concentration problems;
70% had unrefreshing sleep; 68% had fever and chills; 62% had generalised
weakness; 60% had headaches, but 100% had post-exertional fatigue.

Cheney posits that when faced with a low Q, the body sacrifices tissue
perfusion in order to maintain blood pressure: ie. microcirculation to the
tissues of the body is sacrificed to maintain blood pressure so that the
person does not die in the face of too a low Q (Q being cardiac output in
litres per minute). This compensation is what is going on in the CFIDS
(ME/CFS) patient.

(ME)CFS patients have a high heart rate but a low cardiac output. In
(ME)CFS there is a cardiac dimension

that is independent of (but not excluding) autonomic function or blood
volume.

82% of patients have abnormal cardiac impedance.

Cheney states that it is important to note that the body does not sacrifice
tissue perfusion equally across all organ systems: instead, it prioritises
the order of sacrifice and one can observe the progression of ME/CFS by
noting this prioritisation.

Order of sacrifice in cases of declining microcirculation: first is the
skin; second is the muscles and joints;

third is the liver and gut (patients can usually only tolerate a few foods);
fourth is the brain; fifth is the heart;

sixth is the lung and lastly is the kidney.

The first is the skin: if the microcirculation of the skin is compromised,
several problems can arise. One is that without adequate microcirculation
to the skin, the body cannot thermoregulate anymore: the patient cannot
stand heat or cold and if the core temperature rises, the patient will not
be able to sleep and the immune system will be activated. In order to
regulate that problem, the body will kick in thyroid regulation which will
down-regulate in order to keep the body temperature from going too high.
The result of this is that the patient develops compensatory hypothyroidism,
which means that now the patient will have trouble with feeling cold. Also,
the body will not be able to eliminate VOCs (volatile organic compounds),
which are shed in the skin's oil ducts, so VOCs build up in the body's fat
stores and the patient becomes progressively chemically poisoned by whatever
is present in the environment -- in other words, the patient develops
Multiple Chemical Sensitivity.

The second effect: if things get worse, the next microcirculation to be
sacrificed is that to the muscles and the patient will have exercise
intolerance and s/he cannot go upstairs. If things get still worse, the
patient begins to get fibromyalgic pain in the muscles. Cheney posits that
if microcirculation to the joints becomes compromised, it may precipitate
pyrophosphoric acid and uric acid crystals and the patient starts to have
arthralgia linked to this circulatory defect.

The next system to be compromised is the liver and gut. One of the first
things the patient may notice in this stage of disease progression is that
there are fewer and fewer foods s/he will be able to tolerate, partly
because microcirculation is necessary for proper digestion. Also the body
will not secrete digestive juices so whatever food is tolerated will not be
digested: if food cannot be digested, there will be peptides that are only
partially digested and therefore are highly immune-reactive; they will leak
out of the gut into the bloodstream, resulting in food allergies and / or
sensitivities. The body will be unable to detoxify the gut ecology, so the
gut will begin to poison the patient, who will feel a sense of toxic
malaise, with diarrhoea, constipation, flatulence and all kinds of gut
problems. If this gets worse, a malabsorption syndrome will develop,
resulting in increasing toxicity in which the patient feels "yucky" and
which can manifest as a variety of skin disturbances (for instance, a rash),
as well as problems in the brain.

The fourth affected system is the brain: Cheney posits that there is a
devastating effect in the brain as a result of liver / gut dysfunction,
which can quickly toxify the brain, resulting in disturbances of memory and
of processing speed. Also, the hypothalamus begins to destabilise the
patient from the autonomic nervous system perspective. In all probability,
the brain and heart suffer simultaneous compromise, but patients usually
notice the brain being affected much earlier than the heart - this is
because heart muscle cells have the greatest mitochondrial content of any
tissue in the body, so when the mitochondria are impaired, the heart muscle
has the greatest reserve. Even if the patient is sedentary with not too
much demand on the heart, s/he can still think and make great demands on the
brain, and energy is energy, whether it is being used physically or
cognitively.

The fifth affected system is the heart: Cheney posits that the effect of
compromised microcirculation upon the heart has an "a" part and a "b" part:
part "a" is the manifestation of microcirculation impairment and part "b" is
"the event horizon".

Part "a": manifestation of microcirculation impairment: the initial
manifestation of microcirculatory impairment of the heart is arrhythmia with
exercise intolerance: when the patient goes upstairs, more cardiac output is
needed but the patient cannot sustain it. As it gets worse, there will be
mitral valve prolapse (MVP) because of inadequate capillary function.
Finally, when there are even more severe microcirculatory problems, the
patient starts to get chest pain as the myocardial cells die because they
cannot get adequate oxygen.

Part "b": the event horizon: (once this line is passed, there is no going
back): Cheney's view is that the "event horizon" with respect to the heart
is this: when the microcirculation defect within the heart itself begins to
impact Q itself, a vicious circle begins - microcirculation impairment
reduces the Q, which produces more microcirculation impairment, which
produces even more Q problems, so down goes the patient into the next phase
of cardiac failure, which is the lung.

The sixth affected system is the lung and kidney: cardiac failure in the
lung produces Congestive Heart Failure (CHF) and pulmonary oedema, then the
kidney is affected (the kidney is the last to go because it has the RAS
back-up system). Combined with liver impairment, this stage is known as
hepatorenal failure, which is the requisite cause of death due to
Compensated Idiopathic Cardiomyopathy.

The message from Professor Cheney is clear: in order to stay relatively
stable, it is essential for the

ME/CFS patient not to create metabolic demand that the low cardiac output
cannot match.

Cheney states that the cardiac index of ME/CFS patients is so severe that it
falls between the value of patients with myocardial infarction (heart
attack) and those in shock.

According to Cheney, it is difficult to talk about a low cardiac output
without talking about the involvement

of the brain and the adrenal glands.

If the cardiac output goes down, in order not to die, there is a rise in
noradrenergic tone (also involving the

adrenal glands) to bring the output back up. In ME/CFS, this is a serious
problem, because when the adrenals

are exhausted, there will be low cardiac output.

There is no such thing as an ME/CFS patient who is NOT hypothyroid: this
has nothing to do with thyroid

failure, but everything to do with matching metabolic demand and cardiac
output.

A mismatch between metabolic demand and cardiac output, even very briefly,
will kill.

Given the significant body of published international evidence that ME/CFS
is a complex chronic multi-system disorder, it is disturbing that there are
still doctors who dismiss the condition as non-existent or as a somatisation
disorder. Such a view does not accord with the evidence of experts in
ME/CFS, for example:

1988

"Any kind of muscle exercise can cause the patient to be almost
incapacitated for some days afterward. In severe cases, the patient is
usually confined to bed. What is certain is that when one reviews (the)
clinical features and laboratory results, it becomes plain that this is an
organic illness in which muscle metabolism is severely affected".
(Postviral fatigue syndrome PO Behan WMH Behan Crit Rev Neurobiol
1988:4:2:157-178)

1989

"Our investigations suggest that (ME)CFS is characterized by objective
laboratory abnormalities and that the currently used names for the syndrome
are inappropriate. A more appropriate name for this syndrome would be
chronic fatigue-immune dysfunction syndrome (CFIDS), since immune
dysfunction appears to be the hallmark of the disease process". (Natural
Killer Cell Activity in the Chronic Fatigue-Immune Dysfunction Syndrome.
Nancy Eby, Seymour Grufferman et al. In: Natural Killer Cells and Host
Defense. Ed: Ades EW and Lopez C. 5th International Natural Killer Cell
Workshop. Pub: Karger, Basel, 1989:141-145)

1989

"Many of the immunological and physical features of ME/CFS cannot be
explained by mental illness" (Stephen E Straus of the National Institutes
for Allergy and Infectious Diseases, USA, Progress toward an answer to
Chronic Fatigue: an interview with "USA Today", 13th April, 1989: reported
in CFIDS Chronicle, Spring 1989, pp77-78)

1989

"The abnormalities we found provide evidence for central nervous system and
neuromuscular involvement" (Carolyn L Warner: Neurology, March 1989:39:3:
Suppl 1: 420; Presentation at the American Academy of Neurology Conference,
Chicago, April 1989)

1990

"Patients with the chronic fatigue syndrome have reduced aerobic work
capacity compared with normal subjects. We found that patients with the
chronic fatigue syndrome have a lower exercise tolerance than either normal
subjects or patients with the irritable bowel syndrome. Previous studies
have shown biochemical and structural abnormalities of muscle in patients
with the chronic fatigue syndrome" (Aerobic work capacity in patients with
chronic fatigue syndrome MS Riley DR McClusky et al
BMJ:1990:301:953-956)

1992

"57% of patients were bed-ridden, shut in or unable to work. Immunologic
(lymphocyte phenotying) studies revealed a significantly increased CD4 / CD8
ratio. Magnetic resonance scans of the brain showed punctate, subcortical
areas of high signal intensity consistent with oedema or demyelination in
78% of patients. Neurologic symptoms, MRI findings, and lymphocyte
phenotyping studies suggest that the patients may have been experiencing a
chronic, immunologically-mediated inflammatory process of the central
nervous system". (A chronic illness characterized by fatigue, neurologic and
immunologic disorders, and active human herpes Type 6 infection. Dedra
Buchwald, Paul Cheney, Robert Gallo (co-discoverer of the HIV virus),
Anthony L Komaroff et al Ann Intern Med 1992:116:2:103-113)

1992

"CFIDS has an organic basis; it is not a psychiatric illness. Our
Surveillance Study does not support the notion that (ME)CFS is a psychiatric
illness, and in fact, suggests that it has an organic basis" (Dr Walter
Gunn, Principal Investigator of (ME)CFS studies at the US Centres for
Disease Control: CFIDS Chronicle, February 1992, page 1)

1994

"Abnormalities of immune function, hypothalamic and pituitary function,
neurotransmitter regulation and cerebral perfusion have been found in
patients with (ME/CFS). Recent research has yielded remarkable data. The
symptoms of (ME)CFS have long been viewed as a neurologic pattern, as
confirmed by other names such as myalgic encephalomyelitis. A link is being
forged between the symptoms pattern of (ME)CFS and objective evidence of
central nervous system dysfunction. The view that (ME)CFS is a primary
emotional illness has been undermined by recent research" (Dr David S Bell:
Instructor in Paediatrics, Harvard Medical School: Chronic fatigue syndrome
update: Findings now point to CNS involvement: Postgraduate Medicine
1994:98:6:73-81)

1995

"In my experience, (ME/CFS) is one of the most disabling diseases that I
care for, far exceeding HIV disease except for the terminal stages" (Dr
Daniel L Peterson: Introduction to Research and Clinical Conference, Fort
Lauderdale, Florida, October 1994; published in JCFS 1995:1:3-4:123-125)

1997

"The findings suggest that quality of life is particularly and uniquely
disrupted in (ME)CFS. 90% of the sample group experienced frequent feelings
of isolation, alienation and inadequacy due to (ME)CFS. All participants
stated that (ME)CFS had had a profound impact on every aspect of their lives
in ways they had never imagined possible. All participants related profound
and multiple losses, including the loss of jobs, relationships, financial
security, future plans, daily routines, hobbies, stamina and spontaneity,
and even their sense of self because of (ME)CFS. Activity was reduced to
basic survival needs in some subjects. Symptoms were reported to be
multiple, diverse, variable and pervasive. Symptom variability also made it
impossible for those with (ME)CFS to predict their level of functioning,
which interfered with efforts to plan activities. For this reason, symptom
variability was regarded as an especially frustrating aspect of (ME)CFS, and
the uncertainty was one of the most difficult aspects to deal with. All
participants (100%) felt that (ME)CFS had devastated social relationships
and activities. The extent of the losses experienced in (ME)CFS was
devastating, both in number and in intensity. Participants described a sense
of hopelessness that was integral to the illness due to symptom variability,
length of illness and repeated relapses. Over time, those who were initially
optimistic became emotionally exhausted. The impact of (ME)CFS on patients'
life was so total and so devastating that participants had difficulty in
accepting their illness and its consequences. (ME)CFS is a poorly understood
and often trivialized illness, which in reality causes marked disruption and
devastation". (The Quality of Life of Persons with Chronic Fatigue
Syndrome. JS Anderson CE Ferrans. The Journal of Nervous and Mental
Disease l997:185:5:359-367)

1998

"The results showed that in (ME)CFS patients, a lower stroke volume was
highly predictive of illness severity: across three different postures, the
most severely affected (ME)CFS patients were found to have a lower stroke
volume and cardiac output compared with those with more moderate illness.
These findings suggest a low flow circulatory rate in the most severe cases
of (ME)CFS; this may indicate a defect in the higher cortical modulation of
cardiovascular autonomic control. In the most severely affected, situations
may arise where a demand for blood flow to the brain may exceed the supply,
with a possibility of ischaemia and a decrement of function". (CFS severity
is related to reduced stroke volume and diminished blood pressure responses
to mental stress. Arnold Peckerman Benjamin Natelson et al. Presented at
the Fourth International AACFS Research & Clinical Conference on CFIDS,
Mass. USA 1998: Abstract page 47)

1999

"Complaints of muscle weakness and pain are common, and abnormal muscle
metabolism has been reported to occur in (ME)CFS. (ME)CFS patients had
recovery rates for oxygen saturation that were 60% lower than those for
recovery of oxygen saturation in normal subjects. The present study has
demonstrated direct impairments in oxygen delivery in (ME)CFS patients
compared with normal controls. These impairments were more clearly seen
after exercise". (Impaired oxygen delivery to muscle in chronic fatigue
syndrome. Kevin K McCully Benjamin H Natelson Clinical Science
1999:97:603-608)

1999

"The use of 31 P-nuclear magnetic resonance (31 P-NMR) has now provided
positive evidence of

defective oxidative capacity in (ME)CFS. Patients with (ME)CFS reach
exhaustion more rapidly than normal subjects, in keeping with an abnormality
in oxidative metabolism and a resultant acceleration of glyolysis in the
working skeletal muscles. When the rate of resynthesis of phosphocreatinine
(PCr) following exercise is measured, this abnormality is confirmed. (This)
provides a conclusive demonstration that recovery is significantly delayed
in patients with (ME)CFS. The results demonstrate that patients with (ME)CFS
fail to recover properly from fatiguing exercise and that this failure is
more pronounced 24 hours after exercise". (Demonstration of delayed
recovery from fatiguing exercise in chronic fatigue syndrome. Lorna Paul
Leslie Wood Wilhemina M.H.Behan William M.Maclaren European Journal of
Neurology 1999:6:63-69)

1999

"Within the homogenous group of severe (ME)CFS patients, the prognosis for
recovery was poor". (Natural History of Severe Chronic Fatigue Syndrome.
NF Hill, LA Tiersky, BH Natelson et al. Arch Phys Med Rehab
1999:80:1090-1094)

2000

"Our patients with (ME)CFS had an average VO2 max just below 20 mL/kg per
minute, representing significant impairment relative to the controls.
Comparing the exercise capacity in our patients with data from other studies
shows a functionality similar to that of individuals with chronic heart
failure, patients with chronic obstructive pulmonary disease, and those with
skeletal muscle disorder". (Exercise Capacity in Chronic Fatigue Syndrome.
Pascale de Becker Neil McGregor Kenny De Meirleir et al. Arch Intern
Med 2000:160:3270-3277)

2001

"In ME, there are chronic sequelae and the effects may be neurological,
hormonal, autoimmune and myalgic, which may affect the myocardium" (Dr John
Richardson: Enteroviral and Toxin Mediated Myalgic Encephalomyelitis /
Chronic Fatigue Syndrome and Other Organ Pathologies. The Haworth Press
Inc, New York, 2001)

2001

"In ME/CFS, convincing evidence of cardiovascular impairment can be
demonstrated". ("Research Update on ME/CFS". Behan WHM. Professor of
Pathology, Glasgow. Extracts from Over-view of the Alison Hunter Memorial
Foundation ME/CFS Clinical and Scientific Meeting, December 2001, Sydney,
Australia. For the complete over-view, see
http://listserv.nodak.edu/cgi-bin/...
3579> &L=co-cure&T=0&F=&S=&P=3579

2002

"Several cardiopulmonary and neurological symptoms in the present
investigation occurred with higher frequency and uniquely differentiated the
(ME)CFS group from the controls. Shortness of breath, chest pain, dizziness
after standing, skin sensations, general dizziness, dizzy moving the head,
and alcohol intolerance uniquely differentiate those with (ME)CFS from
controls. Results of the current investigation also indicated that muscle
weakness differentiated the (ME)CFS group from controls. Furthermore, it
appeared that the muscle weakness in the (ME)CFS group occurred at multiple
sites, with weak legs being the most frequently reported form of weakness.
These findings concur with those of Hartz et al (1998), and therefore
provide further support for the inclusion of muscle weakness in the case
definition of (ME)CFS". (Symptoms occurrence in persons with chronic
fatigue syndrome. LA Jason et al. Biological Psychology 2002:59:1:15-27

2003

"The patients with (ME)CFS (indicated) profound physical impairment. These
scores tended to be below the published norm for patients with Type II
diabetes, cancer, congestive heart failure and myocardial infarction"
(Functional Status, Neuropsychological Functioning and Mood in Chronic
Fatigue Syndrome. LA Tiersky, Benjamin Natelson et al. J Nerv Ment Dis
2003:191:324-331)

2003

"ME in adults is associated with measurable changes in the central nervous
system and autonomic function and injury to the cardiovascular, endocrine
and other organs and systems. The patient with the diagnosis of ME/CFS is
chronically and potentially seriously ill. These ME/CFS patients require a
total investigation and essentially a total body mapping to understand the
pathophysiology of their illness and to discover what other physicians may
have missed. A patient with ME is a patient whose primary disease is
central nervous system change, and this is measurable. The belief that
ME/CFS is a psychological illness is the error of our time". (The
Complexities of Diagnosis. Byron Hyde. In: Handbook of Chronic Fatigue
Syndrome. Leonard A Jason et al. John Wiley & Sons, Inc. 2003)

2004

"In comparison with other chronic illnesses such as multiple sclerosis,
end-stage renal disease and heart disease, patients with (ME)CFS show
markedly higher levels of disability" (Quality of Life and Symptom
Severity for Individuals with Chronic Fatigue Syndrome: Findings from a
Randomised Clinical Trial. RR Taylor. American Journal of Occupational
Therapy 2004:58:35-43)

2005

"Our patients are terribly ill, misunderstood, and suffer at the hands of a
poorly informed medical establishment and society" (Professor Nancy
Klimas, University of Miami, AACFS In-coming Presidential Address: Co-Cure,
21 March 2005: http://www.co-cure.org )

2006

"There is evidence that the patients with this illness experience a level of
disability that is equal to that of patients with late-stage AIDS, patients
undergoing chemotherapy (and) patients with multiple sclerosis" (Professor
Nancy Klimas, University of Miami, speaking at the launch of the US CDC
campaign to raise awareness of ME/CFS, 3 November 2006, National Press Club,
Washington DC)

The book PROZAC BACKLASH Overcoming the Dangers of
Prozac, Zoloft, Paxil, and Other Antidepressants with
Safe, Effective Alternatives by JOSEPH GLENMULLEN, M.D. discusses the evidance based research as to why people with CFS shouldn't be prescribed with SSRI antidepressants.
Sharon you could have done more harm than good with your article here.
Check out other sources like CFIDS.com
Incedently your statment "the approach to the treatment of fatigue is the same if the fatigue is fairly recent the treatment for fatigue lasting , a month or so, or is more chronic lasting six months or more" is absolutly wrong now that there is an objective mitacondreal dysfunction test.
http://www.ijcem.com/IJCEM812001
Someone who has Mitacondreal dysfunction an is in the initial stages of CFS but who cant yet be diagnosed acording to CDC , Canadian of Holmes Myer criteria will suffer moresevere and more devistating results if prescribed GET . There is an abundance of evidance to support this and CFS specialists have known this for about 10 years, especially in adolescants.
CFS always starts as Fatigue. You need to wrap your head around this fact. Fatigue that leads to CFS can be avoided but not by any of your recomended treatments. CBT, GET and Anti Depressants dont work.
Sleep Hygiene is sensible but when your Pineal gland is damaged and your natural Melatonin levels are altered, your TNF-a and your IL-6 levels are out of wack then 'Sleep' and stable sleep cycle can be beyond your control.
Early in 2009 the first specific test for CFS (Mitacondrial Dysfunction)was published worldwide.
This test has resulted from the brilliant and pioneering work of the internationally recognised Dr John McLaren-Howard of Acumen laboratories and Dr Sarah Myhill who gatehered the original data from her patients, and from the biochemical tests she conducted and noticing a relationship between the two which has enebled Dr McLaren-Howard to design a specific test.

This test can help distinguish between those people fatigued because of a biochemical problem in their mitochondria and those who are fatigued for other reasons. Other reasons include dietary causes (allergy and carbohydrate intolerance), hormonal reasons (such as borderline thyroid and adrenal function), poor antioxidant status, chronic insomnia, psycho-social causes such as anxiety and other causes.

In paragraph 6 of the article at http://cfsfm.org/index.php?option=...
Dr Myhill, one of the authors of the paper, says "This test represents a huge breakthrough in the diagnosis and management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. This illness has already been classified as a neurological disease by the World Health Organisation under ICD 10 G93.3, but many doctors continue to treat CFS/ME as if it were a psychological condition. This has been enshrined in NICE Guidelines for treating CFS/ME because their recommendations are for psychological treatments including antidepressants, cognitive behaviour therapy and graded exercise therapy. This is completely inappropriate for patients who have mitochondrial pathology and indeed is likely to make the mitochondrial pathology even worse.

http://cfsfm.org/index.php?option=...

Sharon you really need to come to grips with this infomation before you write such generic and potentially harmful advice.
Any well meaning person with fatigue issues (undiagnosed Mitacondrial Dysfunction issues) who read your post could have decided to persue a path on your advice which will most probably harm them.
Please write an amendment to your post for the patients sake.
Sincerely
Ali5tair

Dear Dr Sharon Orrange, I have CFS and have had it for 5 years. So much of your infomation here is generic and outdated according to contempory research. Dr Sarah Myhills research on Chronic fatigue syndrome and mitochondrial dysfunction published in the
International Journal of Clinical Expimental Medicine (2009) 2, 1-16 (which is one of the most prestigeous Medical Journals on the planet comments on both the relivance or not of both CBT and GET with respect to Fatigue and CFS.
She sais "Graded exercise - this is positively harmful when CFS is active. I find it quite extraordinary that so many doctors seem to advocate this as a treatment. It is as if they are unable to distinguish between CFS and lack of fitness! Let's face it, if graded exercise worked then the diagnosis could not possibly be CFS. The only possible explanation I can think of as to why this has stuck in the medical folklore is that after a physician has recommended this to the CFS patient, the latter never bothers to attend again for useless advice. The doctor then believes he has cured the patient because they don't come back. Has anybody else got any better explanation?

Cognitive behaviour therapy - The idea behind this is that the CFS patient does not exercise because he is afraid to because it makes him ill. CBT is all about getting round this fear."

Please note that in 35 years of Research it is Dr Sarah Myhill who made the breakthrough with the tst for Mitacindreal function which is the first scientific measure of fatigue. I expected better from you.
Ali5tair


www.ijcem.com/IJCEM812001

Kimistry: you can find a therapist to do CBT (cognitive behavioral therapy) with you..they can be a PhD, MSW (masters in social work), etc
Dr O.

What kind of health care professional should you seek out for cognitive behavioral therapy? One of the big reasons my sleep is affected is because of the pain. The pain in my joints-hips and shoulders makes it very difficult to stay in one position long enough to fall asleep, and if I do fall asleep, it wakes me up.

what about a yeast free diet?. . its my understanding that people who have excess candida (yeast) in their bodies can suffer from extreme fatigue. . look up the benefits of Grapefruit Seed Extract (GSE).

Have you ever tried unsulfered blackstrap molasses?