Co-Cure Weekly Digest of research and medical posts only

Co-Cure Weekly Digest of research and medical posts only - 12 Mar 2007 to 19 Mar 2007

Topics of the week:

1. not,med: Reply -Question to Dr. Peter Manu
2. res: Is HHV-6 a trigger for ME/CFS?
3. RES: Orthostatic Intolerance in Chronic Fatigue Syndrome
4. RES: Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome?
5. RES: Personality styles in patients with fibromyalgia, major depression and healthy controls
6. RES: Management of musculoskeletal pain
7. RES: Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes
8. res: Can submaximal exercise variables predict peak exercise performance in women with ME/CFS?
9. RES: Personality and chronic fatigue syndrome: Methodological and conceptual issues
10. not,med: International ME/CFS Conference 2007
11. NOT, ACT, MED: Compounded medications in danger of prohibitive legislation from Congress
12. RES: Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome
13. med: New Human Cell-Produced Treatment for Anaemia (2)
14. RES: Neuroendocrine Implications of Opioid Therapy
15. RES: Does Aerobic Exercise Improve Pain Perception and Mood? A Review of the Evidence Related to Healthy and Chronic Pain Subjects
16. NOT,MED: Potential new pain killer drug developed by scientists at Leicester and Italy
17. RES: Infection and vaccination in chronic fatigue syndrome: Myth or reality?
18. RES: Use of mind-body therapies in psychiatry and family medicine faculty and residents: attitudes, barriers, and gender differences
19. RES:Speculative theory for ME
20. RES: Hypothesis based research on "the speculative theory for ME"
21. RES: Sense of effort during a fatiguing exercise protocol in chronic fatigue syndrome
22. not,med: Lost to Lyme
23. RES: The Relationship between Psychological Factors and Health Care-Seeking Behavior in Fibromyalgia Patients
24. res: Infection & vaccination in ME/CFS -Myth or reality?
25. RES: The Relationship Between Cytokines and Pain/Depression: A Review and Current Status
26. RES: Evidence for a Mismatch Between the Brains Movement Control System and Sensory System As an Explanation for Some Pain-related Disorders

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                  Co-Cure Research & Medical posts only
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----------------------------------------------------------------------

Date:    Tue, 13 Mar 2007 21:50:45 -0400
From:    "Jan van Roijen <j.van.roijen chello.nl> via Co-Cure Moderator"
Subject: not,med: Reply -Question to Dr. Peter Manu

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
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Reference: *Question to Dr. Peter Manu* - Help ME Circle,
11 March 2007- http://www.me-net.combidom.com/index.htm


Reactions are welcome: j.van.roijen chello.nl


~jvr


``````````


From: Dr. Peter Manu


Attached please find my c.v.



I do not favor a psychiatric explanation for chronic fatigue
syndrome and I explained my position in my book published in
2004 and reviewed by Dr. Komaroff in NEJM. I recognize the
fact that patients diagnosed with CFS suffer and have physical
and psychological symptoms, but there is no proof that CFS, as
currently defined,  is a physical or psychiatric disease.


In general, I try to avoid misinterpretations of my position by
reminding patients and their families that there is a lot of
suffering in this world, but not all suffering is due to a physical or
mental disease.

The fact that such suffering is accompanied by biological
abnormalities does not always constitute proof that a disease
process is present. A good example is grieving after the loss of
a loved one, a state often associated with a dysfunction in the
NK cells activity. This does not mean that grief is an
immunological disorder or disease.

You may also want to know that I'd be much happier to be able to
say that CFS is a mood disorder.  After all, we can achieve
complete, long-lasting remissions in at least  80% of all those
suffering from a depressive disorder, while the remission rate for
CFS is unfortunately only in the range of 10-25%.


Best wishes,

Peter


````````````


Curriculum Vitae
~~~~~~~~~~~~~
Peter Manu, MD



Office Address
````````````````````
Zucker Hillside Hospital
Glen Oaks, NY 11004
(718) 470-8290

License
``````````
1979  New York

Certification
````````````````
1980 American Board of Internal Medicine


Academic Appointments
````````````````````````````````
2000-present    - Professor of Clinical Medicine, Psychiatry and
Behavioral Sciences -  Albert Einstein College of Medicine

1994-1999    - Associate Professor of Medicine and Psychiatry
Albert Einstein College of Medicine

1991-1993    - Associate Professor of Medicine and Psychiatry
University of Connecticut School of Medicine

1990-1991    - Associate Professor of Medicine
University of Connecticut School of Medicine

1983-1989    - Assistant Professor of Medicine
University of Connecticut School of Medicine

1980-1983    - Assistant Professor of Medicine
State University of New York at Syracuse



Clinical and Administrative Positions
````````````````````````````````````````````````
1993-Present    - Director of Medical Services, Hillside Hospital
Long Island Jewish Medical Center

1991-1993    - Medical Director, Alcohol and Drug Abuse
Treatment Center University of Connecticut Health Center

1989-1991    - Physician in Charge, General Medicine Clinic
Newington Veterans Administration Medical Center

Coordinator, Primary Care Residency Program
University of Connecticut Health Center

1986-1988    - Associate Chief of Staff for Ambulatory Care
Newington Veterans Administration Medical Center

1983-1986    - Staff Physician
Newington Veterans Administration Medical Center

Coordinator, Undergraduate Medical Education
Newington Veterans Administration Medical Center

1981-1983    - Director, Primary Care Residency Program
Upstate Medical Center, College of Medicine, State University
of New York at Syracuse

1980-1981    - Staff Physician
Syracuse Veterans Administration Medical Center


Clinical Training
``````````````````````
1977-1980  Medical Resident, Booth - Memorial Medical
Center, New York -  University School of Medicine

1972-1975  Medical Resident, University Hospitals, Bucharest

1970-1972  Rotating Intern, University Hospitals, Bucharest

Medical School
````````````````````
1964-1970  Institute of Medicine and Pharmacy, Bucharest


Honors
``````````
Best Teacher Award 1982-1983  -  Department of Medicine
State University of New York at Syracuse


Societies Membership
`````````````````````````````
American College of Physicians (Fellow)
American Federation for Clinical Research


Reviewer For Scientific Publications
``````````````````````````````````````````````
Acta Psychiatrica Scandinavica
American Journal of Medicine
Annals of Internal Medicine
Biological Psychiatry
International Journal of Psychiatry in Medicine
Journal of the American Medical Association
Journal of Chronic Fatigue Syndrome
Journal of Health Psychology
Journal of General Internal Medicine
Journal of Psychosomatic Research
Medical Care
New England Journal of Medicine
Psychological Medicine
Psychosomatics
Psychotherapy and Psychosomatics


Grant Support
``````````````````

Source    - National Institute on Alcohol Abuse and Alcoholism

Study    - Controlled Trials of Buspirone and Fluoxetine in the
Prevention of Relapse in Alcoholics

Role    - Medical Consultant

Funding Period    - 1991-1992

Source    - National Institute on Drug Abuse
Study    - Carbamazepine Treatment of Cocaine Dependence

Role    - Medical Consultant

Funding Period    - 1991-1993

Source    - National Institute of Alcohol Abuse and Alcoholism

Study    - Matching Alcoholism Treatment to Client
Heterogeneity

Role    - Co-investigator

Funding Period    -  1991-1993



Bibliography
`````````````````


Books
````````
1. Manu P, Suarez RE, Barnett BJ (Editors). Handbook of
Medicine in Psychiatry. American Psychiatric Publishing, Inc.
2006.

2. Manu P. The Psychopathology of Functional Somatic
Syndromes, Haworth Medical Press, 2004.

3. Manu P. The Pharmacotherapy of Common Functional
Syndromes, Haworth Medical Press, 2000.

4. Manu P (Editor). Functional Somatic Syndromes: Etiology,
Diagnosis and Treatment, Cambridge University Press, 1998.



B.  Research Article
```````````````````````````
5. Correll CU, Harris JL, Pantaleon Moya RA, Frederickson AM,
Kane JM, Manu P.  Low-density lipoprotein cholesterol in
patients treated with atypical antipsychotics: Missed targets and
lost opportunities. Schizophrenia Research, 2007 [Epub ahead
of print].

6. Correll CU, Frederickson AM, Kane JM, Manu P. Does
antipsychotic polypharmacy increase the risk of metabolic
syndrome? Schizophrenia Research 89; 91-100, 2007.

7. Correll CU, Frederickson AM, Kane JM, Manu P. Metabolic
syndrome and risk of coronary heart disease in 367 patients
treated with second-generation antipsychotic drugs. Journal of
Clinical Psychiatry 60:575-583, 2006.

8. Straker D, Correll CU, Kramer-Ginsberg E, Abdulhamid N,
Koshy F, Rubens E, Saint-Vil R, Kane JM, Manu P.
Cost-effective screening for the metabolic syndrome in patients
treated with second generation antipsychotic medications.
American Journal of Psychiatry 162:1217-1221, 2005.

9. Manu P.  Long-term disability for chronic fatigue syndrome.
Journal of Chronic Fatigue Syndrome 3:19-30, 1997.

10.  Manu P, Affleck G, Tennen H, Morse PA, Escobar JI.
Hypochodriasis influences quality of life outcomes in patients
with chronic fatigue. Psychotherapy and Psychosomatics
65:76-81, 1996.

11.  Manu P, Lane TJ, Matthews DA, Castriotta R, Watson R,
Abeles M.  Alpha-delta sleep in patients with a chief complaint of
chronic fatigue. Southern Medical Journal 87:465-470, 1994.

12.  Manu P, Burleson JA, Kranzler HR.  Predictors of irregular
discharge from inpatient substance abuse treatment. American
Journal on Addictions 3:122-128, 1994.

13.  Manu P, Matthews DA, Lane TJ.  Food intolerance in
patients with chronic fatigue. International Journal of Eating
Disorders 13:203-209, 1993.

14.  Manu P.  The psychiatric morbidity of patients with chronic
fatigue. Medecine et Hygiene 51:1927-1929, 1993.

15.  Manu P, Lane T, Matthews D.  Chronic fatigue and chronic
fatigue syndrome: Clinical epidemiology and aetiological
classification. In Chronic Fatigue Syndrome, Ciba Symposium
No. 173, John Wiley, London, 23-42, 1992.

16.  Manu P, Matthews DA, Lane TJ.  Panic disorder among
patients with chronic fatigue. Southern Medical Journal
84:451-456, 1991.

17.  Matthews DA, Lane TJ, Manu P.  Antibodies to
Epstein-Barr virus in patients with chronic fatigue. Southern
Medical Journal 84:832-840, 1991.

18.  Kranzler H, Manu P, Hesselbrock V, Lane T, Matthews D.
Substance use disorders in patients with chronic fatigue.
Hospital and Community Psychiatry 42:924-928, 1991.
19.  Lane TJ, Manu P, Matthews DA.  Depression and
somatization in the chronic fatigue syndrome. American Journal
of Medicine 91:335-344, 1991.

20.  Manu P, Lane TJ, Matthews DA.  How much practice makes
perfect?  A quantitative measure of the experience needed to
achieve procedural competence. Medical Teacher 12:367-369,
1990.

21.  Lane TJ, Matthews DA, Manu P.  Low yield of physical
examinations and laboratory investigations in patients with
chronic fatigue. American Journal of Medical Sciences
299:313-318, 1990.

22.  Manu P, Lane TJ, White PP.  Risk-rate neglect in decisions
involving invasive diagnostic procedures. Methods of Information
in Medicine 28:20-23, 1989.

23.  Manu P, Lane TJ, Matthews DA, Escobar JI.  Screening for
somatization disorder in patients with chronic fatigue. General
Hospital Psychiatry 11:294-297, 1989.

24.  Manu P, Matthews DA, Lane TJ, Tennen H, Hesselbrock V,
Mendola R, Affleck G.  Depression among patients with a chief
complaint of chronic fatigue. Journal of Affective Disorders
12:165-172, 1989.

25.  Manu P, Lane TJ, Matthews DA.  Somatization disorder in
patients with a chief complaint of chronic fatigue.
Psychosomatics 30:388-395, 1989.

26.  Renfro L, Feder HM, Lane TJ, Manu P, Matthews DA.
Yeast connection among 100 patients with chronic fatigue.
American Journal of Medicine 86:165-168, 1989.

27.  Escobar JI, Manu P, Matthews D, Lane T, Swartz M, Canino
G.  Medically unexplained physical symptoms, somatization
disorder and abridged somatization: Studies with the Diagnostic
Interview Schedule. Psychiatric Developments 3:235-245, 1989.

28.  Snow SG, Calder EA, Taylor LS, Lane TJ, Manu P, Federici
C.  Screening for cancer and coronary risk factors through a
nurse practitioner-staffed preventive health clinic. Preventive
Medicine 18:817-823, 1989.

29.  Dziadul J, Teague B, Oshinskie L, Manu P.  A comparison
of lens disorders using undilated and dilated biomicroscopy.
New England Journal of Optometry 40:15-18, 1988.

30.  Manu P, Tremml PG, Rippey RM, Voytovich AE.
Interpretation by students of clinical laboratory results. Medical
Teacher 10:219-225, 1988.

31.  Manu P, Louis TA, Gottlieb L, Engel P, Rippey RM.
Unfavorable outcomes of drug therapy: Subjective probability
versus confidence intervals. Journal of Clinical Pharmacy and
Therapeutics 13:213-217, 1988.

32.  Manu P, Matthews DA, Lane TJ.  The mental health of
patients with a chief complaint of chronic fatigue: A prospective
evaluation and follow up. Archives of Internal Medicine
148:2213-2217, 1988.

33.  Manu P, Lane TJ, Matthews DA.  The frequency of chronic
fatigue syndrome in patients complaining of persistent fatigue.
Annals of Internal Medicine 109:554-556, 1988.

34.  Dziadul J, Teague B, Oshinskie L, Manu P.  A comparison
of lens disorders using undilated and dilated biomicroscopy.
New England Journal of Optometry 40:15-18, 1988.

35.  Manu P, Tremml PG, Rippey RM, Voytovich AE.
Interpretation by students of clinical laboratory results. Medical
Teacher 10:219-225, 1988.

36.  Manu P, Louis TA, Gottlieb L, Engel P, Rippey RM.
Unfavorable outcomes of drug therapy: Subjective probability
versus confidence intervals. Journal of Clinical Pharmacy and
Therapeutics 13:213-217, 1988.

37.  Manu P, Matthews DA, Classen DC, Goodspeed RB.
Medical subspecialty training and interest in cost-containment
education.  Journal of General Internal Medicine 2:229-231,
1987.

38.  Matty P, Manu P.  Outpatient use of beta-blocking agents:
Prescribing preferences of physicians in training. Journal of
Clinical Pharmacy and Therapeutics 12:409-414, 1987.

39.  Manu P, Goodspeed RB, Matthews DA.  A quantitative
measure of consumer preference in health care delivery.
Medical Care 24:86-88, 1986.

40.  Manu P, Landaw SA, Williams WJ, Schwartz SE.  Analysis
of publication output of internal medicine faculty members.
Journal of Medical Education  60:860-864, 1985.

41.  Manu P, Runge LA.  Testing stable angina:  Expert opinion
versus decision analysis. Medical Care 23:1381-1390, 1985.

42.  Manu P, Runge LA, Lee JY, Oppenheim AD.  Judged
frequency of complications after invasive diagnostic procedures:
Systematic biases of a physician population. Medical Care
22:366-370, 1984.

43.  Manu P, Runge LA.  Biochemical screening for
pheochromocytoma: Superiority of urinary metanephrines
measurements. American Journal of Epidemiology
120:788-790, 1984.

44. Manu P, Schwartz SE.  Patterns of diagnostic testing in the
academic setting: The influence of medical attendings
subspecialty training. Social Science and Medicine
17:1339-1342, 1983.

45. Manu P, Varade W.  Penicillin therapy for asymptomatic
neurosyphilis: inpatient, intravenous or outpatient, intramuscular?
Lancet 2 (8304): 924-925, 1982

46.  Spinowitz BS, Simpson M, Manu P, Charytan C.  Dialysis
eosinophilia. Transactions of American Society for Artifical
Organs 27:161-165, 1981.

47  Karassi A, Manu P, Chirculescu N.  Prognostic value of the
P wave terminal force in lead V1 at the onset of acute
myocardial infarction. Cor e Vasa 19:291-298, 1977.

48.  Manu P, Macarie C, Karassi A, Dimitriu CG.
Hypercatecholaminuria at the onset of acute myocardial
infarction:  An unfavorable prognostic sign. Medicina Interna
28:27-32, 1976.

49.  Dimitriu CG, Manu P, Karassi A, Draganovici M, Gavrila F.
The effect of propranolol and glucose-insulin-potassium solution
on the course and prognosis of the acute myocardial infarction.
Medicina Interna 28:199-204, 1976.

50.  Macarie C, Sitcai N, Manu P.  Catecholamine addiction, an
iatrogenic complication of the cardiogenic shock in the course of
acute myocardial infarction. Revista Sanitara Militara 2:165-169,
1976.

51.  Manu P, Mogos G, Sitcai N.  Clinical and functional aspects
in a case of Pickwick syndrome. Viata Medicala 22:7, 1975.

52.  Manu P, Karassi A, Chirculescu N, Rotaru M. Clinical and
prognostic implications in 41 cases of left anterior hemiblock at
the onset of acute myocardial infarction. Medicina Interna
27:259-264, 1975.

53.  Constantineanu M, Manu P.  Nonparoxysmal junctional
tachycardia. Medicina Interna 26:11-21, 1974.

54.  Manu P, Karassi A, Cazan V, Sitcai N, Dimitriu CG.  Value
of the glucose, insulin, potassium and magnesium treatment in
acute myocardian infarction.  Medicina Interna 26:565-576,
1974.

55.  Karassi A, Nicolau V, Manu P, Ticmeanu F, Draganovici M,
Dimitriu CG.  The contribution of the heart rhythm and
electrocardiogram surveillance to an improved prognosis of
major arrhythmias complicating the course of myocardial
infarction. Archives Union Medicale Balkanique 11:315-322,
1973.

56.  Karassi A, Manu P, Ticmeanu F, Dimitriu CG.  Intensive
therapy  unit for coronary patients.  II.  Analytical considerations
with reference to 155 patients with acute myocardial infarction.
Medicina Interna 25:809-826, 1973.

57.  Dimitriu CG, Karassi A, Lack S, Zeana C, Dimitriu M, Manu
P, Cazan V, Ghinea A.  Ruptures of the ventricular wall in
myocardial infarction. Medicina Interna 24:1103-1116, 1972.

58.  Burnea D, Manu P.  Scanning, X-Ray, and clinical aspects
of  pulmonary tuberculosis associated with carcinoma of the
lung. Probleme de Tuberculoza 11:213-231, 1972.

59.  Dimitriu CG, Karassi A, Tumaian A, Gavrila F, Manu P,
Sava S, Russe G, Ticmeanu F.  Electronic surveillance during
the intensive care of the coronary patient. Archives Union
Medicale Balkanique 10:609-616, 1972.

60.  Karassi A, Manu P, Erena R. Urinary catecholamines
excretion in acute myocardial infarction. Medicina Interna
23:1209-1224, 1971.



C. Review Articles and Book Chapters
``````````````````````````````````````````````````

61. Manu P, Suarez RE, Barnett BJ. Medicine in psychiatry;
What do we need to know? In Manu P, Suarez RE, Barnett BJ
(Editors) Handbook of Medicine in Psychiatry, American
Psychiatric Publishing, Inc, Washington, DC, xxv-xxvii, 2006.

62. Bennett M, Manu P. Pain in extremities. In Manu P, Suarez
RE, Barnett BJ (Editors) Handbook of Medicine in Psychiatry,
American Psychiatric Publishing, Inc, Washington, DC, 127-135,
2006.

63. Frederickson A, Manu P. Risk assessment prior to
electroconvulsive therapy. In Manu P, Suarez RE, Barnett BJ
(Editors) Handbook of Medicine in Psychiatry, American
Psychiatric Publishing, Inc, Washington, DC, 517-524, 2006.

64.  Manu P. Chronic fatigue syndrome: the fundamentals still
apply. American Journal of Medicine 108:172-173, 2000.

65.  Manu P.  Functional somatic syndromes:  definition and
etiological theories.  In Manu P (Editor) Functional Somatic
Syndromes, Cambridge University Press, Cambridge, 1-7,
1998.

66. Manu P.  Functional somatic syndromes:  Exploring common
denominators. In Manu P (Editor) Functional Somatic
Syndromes, Cambridge University Press, Cambridge, 271-292,
1998.

67.  Manu P.  Disability evaluation for chronic fatigue syndrome.
Journal of Chronic Fatigue Syndrome 3:9-15, 1997.

68.  Manu P, Lane TJ, Matthews DA. Idiopathic chronic fatigue:
Depressive symptoms and functional somatic complaints. In
Demitrack MA and Abbey S (Editors) Chronic Fatigue
Syndrome, Guilford Publications, New York, 36-47, 1996.

69.  Worner TM, Manu P.  The pharmacology of gastrointestinal
complications of alcoholism. In Kranzler HR (Editor) The
Pharmacology of Alcohol Abuse, Springer-Verlag, Heidelberg,
395-413, 1995.

70.  Manu P.  Evaluation of patients with chronic fatigue. Primary
Care Update 1:126-129, 1994.

71.  Manu P, Lane TJ, Matthews DA.  Chronic fatigue
syndromes in clinical practice. Psychotherapy and
Psychosomatics 58:60-68, 1992.

72.  Manu P, Lane T, Matthews D.  The pathophysiology of
chronic fatigue syndrome: Confirmations, contradictions, and
conjectures. International Journal of Psychiatry in Medicine
22:395-406, 1992.

73.  Manu P.  Chronic fatigue: Practical guidelines for the
primary caresetting. Consultant 32 (9):71-77, 1992.

74.  Escobar JI, Swartz M, Rubio-Stipec M, Manu P.  Medically
unexplained symptoms: Distribution, risk factors, and
comorbidity.  In Kirmayer LJ, Robbins JM (Eds).  Current
Concepts in Somatization: Research and Clinical Perspectives.
American Psychiatric Press, Washington, 63-78, 1991.

75.  Buchwald D, Gantz NM, Katon WJ, Manu P.  (Gregory T,
Ed). Chronic fatigue syndrome. Patient Care 25 (May 30):45-58,
1991.

76.  Stewart D, Manu P, Wessely S, Straus S, Salit I, Abbey S.
Chronic fatigue syndrome (postinfectious neuromyasthenia).
Annals of the Royal College of Physicians and Surgeons of
Canada 24:509-511, 1991.

77.  Matthews DA, Manu P, Lane TJ.  Evaluation and
management of patients with chronic fatigue. American Journal
of the Medical Sciences 302:269-277, 1991.

78.  Dimitriu CG, Manu P.  Beta adrenergic blocking agents in
the treatment of the ischemic heart disease.  Medicina Interna
28:97-103, 1976.

79.  Karassi A, Manu P.  Summary of the prophylaxis and
therapy of major complications of acute myocardial infarction.
Viata Medicala 21:2-3, 1974.

80.  Dimitriu CG, Zeana C, Karassi A, Manu P.  Immunological
trends in cardiology. Medicina Interna  26:515-522, 1974.

81.  Karassi A, Manu P, Dimitriu CG.  Free fatty acids dynamic
in acute myocardial infarction.  Medicina Interna 26:653-658,
1974.

82.  Karassi A, Manu P, Nicolau V, Cazan V.  The myocardial
consequence of hypovolemia.  Archives Union Medicale
Balkanique 12:721-724, 1974.

83.  Constantineanu M, Manu P.  The electrogram of the bundle
of His in the diagnosis of atrioventricular conduction
disturbances.   Medicina Interna 25:797-808, 1973.

84.  Dimitriu CG, Karassi A, Manu P, Sava S.  Intensive therapy
unit for coronary patients.  I. General considerations.   Medicina
Interna  25:783-795, 1973.

85.  Manu P.  Bioclinical advances in the study of alkaline
phosphatases. Viata Medicala 20:229-234, 1973.

86.  Dimitriu CG, Karassi A, Filipescu Z, Tumaian A, Manu P.
The intensive therapy coronary unit. Viata Medicala 20:393-399,
1973.
87.  Manu P.  Bretylium tosylate:  A major antiarrhythmic drug in
acute myocardial infarction.  Viata Medicala 20:715-717, 1973.

88.  Dimitriu CG, Karassi A, Manu P.  Theoretical and practical
aspects of the treatment of cardiogenic shock in acute
myocardial infarction. Medicina Interna 24:391-399, 1972.

89.  Karassi A, Manu P.  A tentative to integrate hyperglycemia
into the post-aggressive response to acute myocardial infarction
and its complications. Archives Union Medicale Balkanique
10:237-242, 1972.

90.  Karassi A, Manu P, Dimitriu CG.  The sudden coronary
death. Medicina Interna 24:1087-1102, 1972.

91.  Dimitriu CG, Karassi A, Manu P, Gavrila F.  Stress and
catecholamines in cardiovascular pathology.  Medicina Interna
23:1155-1167, 1971.

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 05:57:03 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: res: Is HHV-6 a trigger for ME/CFS?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
       >>>> Help ME Circle  <<<<
 >>>>       14 March 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~


Journal of Clinical Virology
Volume 37, Supplement 1 , December 2006, Pages S39-S46

HHV-6: an underestimated virus - Proceedings of the 5th
International Conference on HHV-6&7 and Abstracts from the
5th International Conference on HHV-6&7

doi:10.1016/S1386-6532(06)70010-5


Is human herpesvirus-6 a trigger for chronic fatigue syndrome?
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Anthony L. Komaroff, a,

a  Division of General Medicine, Department of Medicine,
Brigham and Women's Hospital, Harvard Medical School, 10
Shattuck Street, Suite 602, Boston, MA 02115, USA


Abstract

Chronic fatigue syndrome (CFS) is an illness currently defined
entirely by a combination of non-specific symptoms. Despite this
subjective definition, CFS is associated with objective
underlying biological abnormalities, particularly involving the
nervous system and immune system.

Most studies have found that active infection with human
herpesvirus-6 (HHV-6) - a neurotropic, gliotropic and
immunotropic virus - is present more often in patients with CFS
than in healthy control and disease comparison subjects, yet it is
not found in all patients at the time of testing. Moreover, HHV-6
has been associated with many of the neurological and
immunological findings in patients with CFS.

Finally, CFS, multiple sclerosis and seizure disorders share
some clinical and laboratory features and, like CFS, the latter
two disorders also are being associated increasingly with active
HHV-6 infection. Therefore, it is plausible that active infection
with HHV-6 may trigger and perpetuate CFS in a subset of
patients.

Keywords: Human herpesvirus-6; Chronic fatigue syndrome;
Human; Review

Correspondence address: Tel.: +1 617 432 4714; fax: +1 617
432 4719

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 11:31:49 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Orthostatic Intolerance in Chronic Fatigue Syndrome

Orthostatic Intolerance in Chronic Fatigue Syndrome

Journal: The American Journal of Medicine, Volume 120, Issue 3, Page e13
(March 2007)

Authors: Peter C. Rowe, MDa, Katherine E. Lucas, PhDb

Affiliations:
[a] Department of Pediatrics, Johns Hopkins University School of Medicine,
Baltimore, MD USA
[b] Department of Pediatrics, Johns Hopkins University School of Medicine,
Department of Epidemiology, Johns Hopkins University Bloomberg School of
Public Health, Baltimore, MD USA

NLM Citation: PMID: 17349421


To the Editor:

The main outcome measure in Jones and colleagues' study of the prevalence
of orthostatic intolerance in subjects with chronic fatigue syndrome (CFS)1
was a 45-minute head-up tilt test, performed after exclusion of subjects
with other medical conditions and subjects being treated with medications
used to treat orthostatic intolerance. These exclusions were
methodologically necessary to ensure that the observed rate of orthostatic
intolerance was associated with CFS and not with the co-morbid medical
conditions, and that medication use did not partially treat (and therefore
obscure detection of) the underlying circulatory abnormalities.

The exclusions came at a steep methodologic cost to the representativeness
of the sample. After the exclusion of 41 subjects, and refusal to
participate by 23 more, the tilt portion of the study evaluated 10
subjects, just 14% of the original group of 74. The sample was entirely too
small to allow firm conclusions to be drawn about the prevalence of
orthostatic intolerance overall in those with CFS, or about the relative
prevalence of postural tachycardia or neurally mediated hypotension in this
group.

While not the main focus of the article, Table 7 summarizing the literature
on orthostatic intolerance in those with CFS is incomplete. In addition to
the small study by DeLorenzo and colleagues of 5 patients with postural
tachycardia (reference 10 in the Table), the authors may not have known of
a larger study by the same group. That study enrolled 78 subjects with CFS,
22 of whom (28%) developed hypotension during tilt, versus 0 of 38 controls.2
We would also like to clarify the data abstracted in Table 7 from our
randomized trial of fludrocortisone (reference 13). Among 171 with CFS who
underwent tilt testing, the rate of neurally mediated hypotension was 62%;
a further 4% met criteria for postural tachycardia syndrome alone. The
combined prevalence of orthostatic intolerance was 66%, not 62% as reported
in Table 7. Those who did not develop hypotension were excluded from the
treatment portion of the randomized trial, but none of the 171 eligible
subjects was excluded from the data on the prevalence of orthostatic
abnormalities. We therefore are not sure what the authors meant by the
notation "77% excluded." Table 7 also includes some minor typographical
errors: reference 20 appears twice (it should be reference 21 the first
time, then reference 8 the second time), and reference 34 in Table 7 should
be reference 37.

Any debate about the precise prevalence of postural tachycardia syndrome or
neurally mediated hypotension in CFS has the potential to neglect a
critical point. In our studies of orthostatic intolerance, now totaling
over 220 subjects with CFS, quiet upright posture has been a strong and
consistent physiologic stressor in over 95%. Even when not accompanied by
hemodynamic changes, orthostatic stress typically has been associated with
a provocation or exacerbation of characteristic CFS symptoms. Others have
shown that these symptoms and hemodynamic abnormalities with orthostatic
stress can be reversed upon application of external lower-body compression
(reference 37). Whether orthostatic disorders are primary or secondary,
this evidence suggests that they play an important contributing role in the
phenomenology of the illness for a substantial proportion of affected
individuals. In contrast to Jones and colleagues, we would agree with
Freeman that a better understanding of the mechanisms of the disordered
response to orthostatic stress would go a long way toward improving our
understanding of the pathophysiology and treatment of CFS symptoms.3
References

1. Jones JF, Nicholson A, Nisenbaum R, et al.. Orthostatic instability in a
population-based study of chronic fatigue syndrome. Am J Med.
2005;118:1415e19-1415e28. Abstract:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0512D&L=CO-CURE&P=R1014
2. De Lorenzo F, Hargreaves J, Kakkar VV. Pathogenesis and management of
delayed orthostatic hypotension in patients with chronic fatigue syndrome.
Clin Auton Res. 1997;7:185-190.
3. Freeman R. The chronic fatigue syndrome is a disease of the autonomic
nervous system (Sometimes). Clin Auton Res. 2002;12:231-233.


© 2007 Elsevier Inc. All rights reserved.

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 11:45:32 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome?

Can submaximal exercise variables predict peak exercise performance in
women with chronic fatigue syndrome?

Journal: Arch Med Res. 2007 Apr;38(3):350-3. Epub 2007 Jan 30.
doi:10.1016/j.arcmed.2006.10.009

Authors: Nijs J, [a,b], Demol S, [a], Wallman K. [c]

Affiliations:
[a] Department of Human Physiology, Faculty of Physical Education &
Physiotherapy, Vrije Universiteit, Brussels, Belgium
[b] Division of Musculoskeletal Physiotherapy, Department of Health Care
Sciences, University College Antwerp, Antwerp, Belgium
[c] Human Movement & Exercise Science, University of Western Australia,
Perth, Australia

Address reprint requests to: Jo Nijs, Vrije Universiteit Brussel,
MFYS/Sport, KRO-gebouw -1, Laarbeeklaan 101, B-1090 Brussels, Belgium

Received 1 September 2006;
accepted 26 October 2006
published online 31 January 2007.

NLM Citation:  PMID: 17350488


This study aimed at examining whether physiological exercise variables at
the submaximal level, defined as 75% of the age-predicted target heart
rate, are able to predict peak exercise performance in women with chronic
fatigue syndrome (CFS) (n = 222).

Subjects performed a bicycle ergometric test against a graded increase in
workload until exhaustion with continuous monitoring of
electrocardiographic and ventilatory variables.

Oxygen uptake at the submaximal level (VO(2SUBMAX)) correlated strongly
with peak oxygen uptake (VO(2PEAK)) (r = 0.70). For the prediction of
VO(2PEAK), linear regression analysis determined the line of best fit as:
Using this equation, the mean error in the prediction was 14.6 ± 11.2%
(range 0.1-63.7%).

It is concluded that the prediction of VO(2PEAK) based on VO(2SUBMAX) might
be useful for analyzing group differences or treatment effects but not for
individual (clinical) purposes.


Key Words: Submaximal, Exercise test, Prediction, Chronic fatigue syndrome,
Fibromyalgia

© 2007 IMSS. Published by Elsevier Inc. All rights reserved.

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 12:01:01 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Personality styles in patients with fibromyalgia, major depression and healthy controls

Personality styles in patients with fibromyalgia, major depression and
healthy controls.

Ann Gen Psychiatry. 2007 Mar 9;6(1):9 [Epub ahead of print]

Nordahl HM, Stiles TC.

PMID: 17349053


ABSTRACT:
BACKGROUND: The fibromyalgia syndrome (FMS) is suggested to be a
manifestation of depression or affective spectrum disorder. We measured the
cognitive style of patients with FMS to assess personality styles in 44
patients with fibromyalgia syndrome (FMS) by comparing them with 43
patients with major depressive disorder (MDD) and 41 healthy controls (HC).

METHODS: Personality styles were measured by the Sociotropy and Autonomy
Scale (SAS) and the Dysfunctional Attitude Scale (DAS). The Structured
Clinical interview for DSM Axis I was applied to Axis I disorders, while
the Beck Depression Inventory was used to measure depression severity.

RESULTS: Patients with FMS in general have a sociotropic personality style
similar to patients with MDD, and different from HC, but FMS patients
without a lifetime history of MDD had a cognitive personality style
different from patients with MDD and similar to HC.

CONCLUSIONS: These findings suggest that a depressotypic personality style
is related to depressive disorder, but not to FMS.


Trial registration: NCT00184106.

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 15:31:26 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Management of musculoskeletal pain

Management of musculoskeletal pain.

Best Pract Res Clin Rheumatol. 2007 Feb;21(1):153-66.

Bergman S.

Spenshult Hospital, SE 313 92 Oskarstrom, Sweden.

PMID: 17350550


Chronic musculoskeletal pain is a major public health problem affecting
about one third of the adult population. Pain is often present without any
specific findings in the musculoskeletal system and a strictly biomedical
approach could be inadequate. A biopsychosocial model could give a better
understanding of symptoms and new targets for management.

Identification of risk factors for chronicity is important for prevention
and early intervention. The cornerstones in management of chronic
non-specific, and often widespread, musculoskeletal pain are
non-pharmacological. Physical exercise and cognitive behavioral therapy,
ideally in combination, are first line treatments in e.g. chronic low back
pain and fibromyalgia.

Analgesics are useful when there is a specific nociceptive component, but
are often of limited usefulness in non-specific or chronic widespread pain
(including fibromyalgia). Antidepressants and anticonvulsants could be of
value in some patients but there is a need for more knowledge in order to
give general recommendations.

[Return to top]

------------------------------

Date:    Wed, 14 Mar 2007 15:34:11 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes

Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central
Sensitivity Syndromes.

Semin Arthritis Rheum. 2007 Mar 10; [Epub ahead of print]

Yunus MB.

Professor of Medicine, Section of Rheumatology, The University of Illinois
College of Medicine at Peoria, Peoria, Illinois.

PMID: 17350675


OBJECTIVES: To discuss fibromyalgia syndrome (FMS) and overlapping
conditions, eg, irritable bowel syndrome, headaches, and chronic fatigue
syndrome, within the concept of central sensitivity syndromes (CSS).

METHODS: A critical overview of the literature and incorporation of the
author's own views.

RESULTS: The concept of CSS seems viable. It is based on mutual
associations among the CSS conditions as well as the evidence for central
sensitization (CS) among several CSS members. However, such evidence is
weak or not available in other members at this time, requiring further
studies. The biology of CSS is based on neuroendocrine aberrations,
including CS, that interact with psychosocial factors to cause a number of
symptoms.

CONCLUSIONS: CSS is an important new concept that embraces the
biopsychosocial model of disease. Further critical studies are warranted to
fully test this concept. However, it seems to have important significance
for new directions for research and patient care involving physician and
patient education. Each patient, irrespective of diagnosis, should be
treated as an individual considering both the biological and psychosocial
contributions to his or her symptoms and suffering.

[Return to top]

------------------------------

Date:    Thu, 15 Mar 2007 00:34:57 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: res: Can submaximal exercise variables predict peak exercise performance in women with ME/CFS?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
       >>>> Help ME Circle  <<<<
 >>>>       15 March 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~


14 Mar 2007  Fred Springfield posted the abstract of
*Can submaximal exercise variables predict peak exercise
performance in women with chronic fatigue syndrome?*
Nijs J, Demol S, Wallman K. at Co-cure:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703b&L=co-cure&T=0&P=7349


--------------------------------------------------------------
~jvr: as fair use I add the discussion section of this article
--------------------------------------------------------------


Discussion

There is a need for standardized submaximal ergometer tests
not only for patients with CFS but for people with various
disorders that require close monitoring during exercise (4).
Therefore, the present study aimed at examining whether a
standardized submaximal ergometer test was able to predict
peak exercise performance (including peak aerobic work
capacity) in people with CFS.

We utilized an exercise protocol (starting at 10 W with an
increase of 10 W/min) that has previously been used for the
assessment of peak exercise performance in people with CFS
(3,11,12,15,16) and defined the submaximal level in accordance
with the Aerobic Power Index Test (8,9). The results of the study
suggest that exercise variables at the submaximal level are
strongly associated with their corresponding variables at the
peak (maximal) level.

Despite this observation, the associations appeared too weak
to predict peak exercise variables with an error margin <10%.
Both VO2PEAK and body weight-adjusted VO2PEAK can be
predicted from their corresponding submaximal variable with an
error margin of 14.6%. For analyzing group differences or
treatment effects (research purposes), an error margin of 14.6%
might be acceptable and can be taken into account in an a priori
power calculation.

However, for individual (clinical) purposes, the error range (0.1 -
 > 60%) should be taken into account. It is therefore concluded
that, for clinical purposes, the submaximal exercise testing
protocol used here is unable to make an accurate prediction of
peak exercise performance in women with CFS.

The results should be interpreted in light of the study limitations.
Only 71% of the subjects studied here attained the submaximal
exercise level, defined as 75% of the agepredicted target heart
rate. Thus, the results (and the regression equations) are
applicable solely to women attending a specialized chronic
fatigue clinic and able to achieve 75% of the age-predicted
target heart rate during graded exercise tests.

This limits the external validity of the results. Further studies are
warranted, for instance, by using the exercise protocol of the
Aerobic Power Index Test (an increase of 25 W every minute) or
by applying other exercise testing protocols previously used for
studying peak exercise performance in people with CFS.

Fulcher and White used a treadmill walking test at a constant
speed of 5 kph and a gradient increase of 2.5% every 2 min
(17). Sargent et al. applied cycle ergometry starting at 0 W with
incrementing the power output by 25 W every 2 min (10).
Bazelmans and colleagues applied an individually tailored
bicycle ergometer test: the workload was increased every
minute in steps of 10% of estimated maximal workload (5).

In summary, the results of the study suggest that exercise
variables at the submaximal level are strongly associated with
their corresponding variables at the peak level in women with
CFS. VO2PEAK and body weight-adjusted VO2PEAK can be
predicted from their corresponding submaximal variable with a
mean error margin of 14.6%, which might be acceptable for
analyzing group differences or treatment effects. For individual
(clinical) purposes, the submaximal exercise testing protocol
was found inappropriate for predicting peak exercise
performance in women with CFS.

[Return to top]

------------------------------

Date:    Thu, 15 Mar 2007 13:59:01 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Personality and chronic fatigue syndrome: Methodological and conceptual issues

Personality and chronic fatigue syndrome: Methodological and conceptual issues.

Journal: Clin Psychol Rev. 2007 Jan 27; [Epub ahead of print]

Authors: van Geelen SM [a], Sinnema G [a], Hermans HJ [b], Kuis W. [c]

Affiliations:
[a] Department of Psychology, Wilhelmina Children's Hospital, University
Medical Center Utrecht, The Netherlands
[b] Faculty of Clinical Psychology and Personality, Radboud University
Nijmegen, The Netherlands
[c] Department of Immunology, Wilhelmina Children's Hospital, University
Medical Center Utrecht, The Netherlands

Received 9 December 2005;
revised 29 November 2006;
accepted 19 January 2007.
Available online 27 January 2007.

NLM Citation: PMID: 17350740


Among clinical psychologists, consulting physicians, scientific researchers
and society in general an image has emerged of patients with chronic
fatigue syndrome (CFS) as perfectionist, conscientious, hardworking,
somewhat neurotic and introverted individuals with high personal standards,
a great desire to be socially accepted and with a history of continuously
pushing themselves past their limits.

The aim of this article is to (a) give a concise review of the main recent
studies on personality and CFS, (b) address the major methodological
problems in the study of personality in CFS and (c) discuss some of the
conceptual assumptions that seem to limit the research on personality and CFS.

The results of the reviewed studies range from no evidence of major
differences between the personalities of patients with CFS and controls, to
evidence of severe psychopathology and personality disorder in patients
with CFS. Although personality seems to play a role in CFS, it is difficult
to draw general conclusions on the relation between personality and CFS. It
is argued that this is partially due to the diversity and heterogeneity in
study methods, patient populations, control groups and CFS case
definitions. Personality should be regarded as an important factor to be
studied in CFS. However, additional studies are needed, not focusing
exclusively on personality disorder, or personality considered on a general
trait level.

In recent developments in personality research, the continually evolving
life narrative that makes sense of, and gives direction to, an individual's
life is also regarded as an important aspect of personality. New insights
into personality and CFS might be gained by systematically studying the
self-narratives of patients with the syndrome.

Copyright © 2007 Elsevier Ltd All rights reserved.

[Return to top]

------------------------------

Date:    Thu, 15 Mar 2007 17:31:47 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: not,med: International ME/CFS Conference 2007

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
       >>>> Help ME Circle  <<<<
 >>>>       15 March 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~



International ME/CFS Conference 2007
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Westminster, London



1st May - ME Awareness & Support Day

2nd May - Professionals Conference Day


The International ME/CFS Conference 2007

An Update on Clinical Diagnosis, Treatments, Support and
Research of Myalgic Encephalomyelitis (ME / CFS)

Conference Update:

A reminder of the International ME/CFS conference in London in
May.


News Opening Speech: IiME have pleasure in announcing the
opening speech of the International ME/CFS Conference will be
given by Mr Norman Lamb, Liberal Democrat Shadow Health
Secretary.

As work is underway on the new Whittemore Peterson Nevada
CFS centre for Neuro-Immune disorders it is an opportune time
to remind all that Mrs. Annette Whittemore will be at the London
conference discussing this important new centre.

(See the full list of presenters below)

CPD Accreditation from the Royal colleges has now been given
to the IiME International ME/CFS conference. Twelve credits will
be given for attendance on both days. Six credits are given to
each day and delegates may choose to attend the Professionals
Day (2nd May) or the Pre-Conference Day (1st May) - or both
days.

Discounted rate - Sponsor a Medic:  IiME are offering a
discounted rate for healthcare staff who are recommended to
attend by a local ME Support Group. IiME welcome all
professionals who are working with, or have an interest in,
ME/CFS. We are very pleased that we have received many
enquiries for this scheme.


Background:

Invest in ME is again holding the International ME/CFS
Conference in London in May, 2007. Our ME/CFS conference of
2006 attracted presenters and delegates from eight countries
and our DVD of the conference was distributed to over 20
countries including countries in Europe, USA, Canada, Australia
and New Zealand.

Myalgic Encephalomyelitis (ME) is a serious neurological illness
(classified by the World Health Organisation under ICD-10-93.3)
that causes severe problems for an estimated 250,000 people
in the UK, of whom 25,000 are estimated to be children and
young people.  It is five times more prevalent than HIV/AIDS in
the UK and the leading cause of long term absence of children
from school.

2007 will be a critical year for healthcare staff and ME patients.
The key-note speaker for Professionals' Day is Dr. Ian Gibson,
MP for Norwich North who recently chaired the Parliamentary
Inquiry into ME which reported that ME needed to be treated
with the same urgency as cancer or heart disease. We expect to
have an up-to-date progress report on the status regarding
future research strategy from Dr. Gibson and the Medical
Research Council. This year the NICE Guidelines on ME are
also to be published.

The conference will be a unique opportuniy to be informed of the
latest research and information from some of the leading experts
on ME/CFS in the areas of diagnosis, treatment, epidemiology,
paediatrics and research.


Conference Information:

* The conference takes place over two days
* Either one or both days may be attended.
* Both days carry maximum CPD accreditation.


ME Awareness & Support Day (1st May) is for individuals, ME
Patient Groups and Healthcare staff to discuss important issues
regarding treatment, guidelines and research of ME/CFS.


Professionals Day (2nd May) is for healthcare staff, clinicians,
GPs, Paediatricians, researchers, occupational therapists and
academics who wish to hear the formal lectures on research,
treatments, epidemiology and paediatrics related to ME/CFS.

NOTE: Both days are open to all interested in ME/CFS.

Discounted rates apply for attendance on both days.

Our speakers include some of the foremost experts, researchers
and clinicians working with ME/CFS including -

* Professor Malcolm Hooper - Emeritus Professor of Medicinal
   Chemistry, University of Sunderland
  * Dr. Byron Hyde of the Nightingale Research Foundation,
    Ottawa, Canada
* Dr. Jonathan Kerr - Sir Joseph Hotung Senior Lecturer in
   Inflammation, St George's University of London
* Dr. Kenny de Meirleir - Professor of Physiology and Internal
   Medicine at Free University of Brussels in Belgium
* Dr. Vance Spence Chairman ME Research UK
* Dr. Neil Abbot ME Research UK
* Dr. Abhijit Chaudhuri - Consultant Neurologist at Essex
   Centre of Neurological Science
* Dr. Sarah Myhill - GP and Secretary of the British Society of
   Allergy, Environmental  and Nutritional Medicine
* Dr. Nigel Speight  Consultant Paediatrician at University
   Hospital of North Durham and member of Chief Medical
   Officer's Working Group on ME/CFS
* Professor Basant Puri Consultant at Hammersmith Hospital
* Professor Martin Pall Washington State University
* Annette Whittemore HHV-6 Foundation, Nevada, USA
* Ellen Piro President of Norwegian ME Association
* Dr. Derek Pheby Director Unit of Applied Epidemiology,
   faculty of Applied Sciences, Univ. Western England



Conference Registration:

We welcome everyone who may be interested to attend this
major international conference on ME/CFS.

Bookings may also be made by using the internet web-site at -

http://www.investinme.org/IIME%20International%20ME%20Conference%202007%20Registration.htm

Full details of the conference can be found at ?

http://www.investinme.org/IIME%20International%20ME%20Conference%202007%20Home.htm

Should you have any further questions relating to the conference
please contact us at meconference@investinme.org.

We look forward to welcoming you to the conference,


Yours sincerely,

Invest in ME

UK Registered Charity Nr. 1114035

Tel: 01603 701980 or 02392 252365


http://www.investinme.org/

[Return to top]

------------------------------

Date:    Thu, 15 Mar 2007 14:34:20 -0700
From:    Steven Du Pre <isaiah40 SONIC.NET>
Subject: NOT, ACT, MED: Compounded medications in danger of prohibitive legislation from Congress

Hello,
    A number of you in the US are taking compounded medications,
whether Nexavir, bio-identical hormones, glutathione or vitamin B12
or you are a medical practitioner prescribing compounded medications..
    I learned of this from a member of the Nexavir (Kutapressin)
 newsgroup.

"Now the gel form of Nexavir at least might not be available for long.
I just got an email from a compounder. I looked for more information.

This sentence is from          www.iacprx.org
 -- (go there for more info)


"Senators Kennedy (D-MA), Burr (R-NC) and Roberts (R-MO) have
circulated a copy of proposed draft legislation that would greatly
restrict access to compounded medications. Read more and take action
to prevent this legislation from gaining traction on Capitol Hill!"

It would be helpful for us to do is write or call our
senators, briefly telling why this is a personal threat to our
well-being.

There are links at the website for filling out email forms to your
Senators.
I wrote to both of mine.

Please do not copy this person's letter - use your own - but here is
the meat
of her letter -

"Two medicines that help me much are under threat by this bill. One of
them is something I really cannot live without. The drug is obscure
and the big pharmas, in cooperation with the FDA, are never going to
let it have special privileges. It is more effective, with less
waste, in the compounded form. As it is compounded for me, I can
apply the drug to my skin, instead of injecting it intramuscularly. I
can apply smaller doses as needed over the course of the day.
Expensive--it is our family's largest personal expense, but it is
necessary. It is good to use it well."

Thanks for your help,
Steven Du Pre
Poetry website: http://www.angelfire.com/poetry/soareagle/index.html
"By words the mind is winged."  Aristophanes
Website for National Alliance for Myalgic Encephalomyelitis:
http://www.name-us.org

[Return to top]

------------------------------

Date:    Fri, 16 Mar 2007 11:51:32 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome

Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome.

Journal: Int J Sports Med. 2007 Mar 15; [Epub ahead of print]

Authors: Takken T, Henneken T, van de Putte E, Helders P, Engelbert R.

Affiliation: Pediatric Physical Therapy and Exercise Physiology, UMC
Utrecht, Utrecht, Netherlands.

NLM Citation: PMID: 17357961


The objective of this study was to evaluate exercise capacity in children
and adolescents diagnosed with Chronic Fatigue Syndrome (CFS).

We examined 20 patients (12 girls and 8 boys; mean age 14.9 ± 3.7 years)
diagnosed with CFS. Exercise capacity was measured using a maximal exercise
test on a bicycle ergometer and an expired gas analysis system. Fatigue was
assessed using a questionnaire and a daily activity diary was used to
describe activities for three days. Z-scores were calculated using age- and
sex-matched reference values.

Z-scores in children and adolescents with CFS were - 0.33 ± 1.0 (p =
0.17) for peak oxygen uptake, - 1.13 ± 1.41 (p = 0.002) for relative peak
oxygen uptake [ml/kg/min] and - 0.93 ± 1.29 (p = 0.07) for maximal work
load. Both heart rate and blood pressure at peak performance were
significantly reduced compared to reference values. Fatigue levels were
significantly positively associated with age and negatively with blood
pressure at peak exercise (p < 0.05).

In conclusion maximum exercise testing was feasible in young people with
CFS. Maximal exercise capacity was only reduced in a minority of the
patients and was related to current physical activity levels.

[Return to top]

------------------------------

Date:    Fri, 16 Mar 2007 01:50:27 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: med: New Human Cell-Produced Treatment for Anaemia
[Please note comments from Nancy Klimas, M.D. after the footnotes to this post.]
~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
       >>>> Help ME Circle  <<<<
 >>>>       15 March 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~

In Help ME Circle, 10 March 2007, the article *Anemia drugs
increase death risk* was posted, because these common
anaemia drugs can increase the risk of death and other
serious problems. Procrit, Epogen and Aranesp are used by
some ME/CFS patients (mostly in research) in connection with
low red blood cell volume). See Co-Cure
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703b&L=co-cure&T=0&P=2499

This new human cell-produced treatment for anaemia seems to
be much saver.


~jvr

````````````


http://www.medadnews.com/News/index.cfm?articleid=423882#


TODAY ON PHARMALIVE.COM



New Human Cell-Produced Treatment for Anaemia
Associated with Chronic Kidney Disease Now Available
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Shire's launch of DYNEPO (epoetin delta) begins across
Europe

LONDON, 15 Mar 2007 - Today, Shire plc (LSE: SHP,
NASDAQ: SHPGY, TSX:SHQ) launched DYNEPO(R)(epoetin
delta) in Germany, completing the initial step of a launch
programme planned for Europe over the coming months.
DYNEPO is a unique erythropoiesis-stimulating agent (ESA), as
it is the only ESA produced in human cells. ESAs are agents
used in the treatment of anaemia to increase the production of
red blood cells. DYNEPO is produced by activating the
erythropoietin (EPO) gene in human cells . All other
commercially available ESAs are presently made in animal
cells.

DYNEPO's entry to the market provides a new, effective and
well-tolerated choice for both physicians and a wide range of
patients who suffer from anaemia as a result of chronic renal
failure (CRF).(i) It is approved for use in patients not yet
requiring dialysis as well as those with end-stage renal disease
(ESRD) on dialysis.(1)

DYNEPO will be available in other European markets in the
coming months. DYNEPO is supported by a comprehensive
clinical efficacy and safety programme and competitive pricing
structures designed to reduce the existing economic burden of
healthcare to providers treating renal anaemia with ESAs.

"This new and different treatment with its proven efficacy and
tolerability is a welcome addition to the options available for
physicians treating anaemia in chronic kidney disease (CKD)
patients," commented Dr Markus Ketteler, Division of
Nephrology, Academic Teaching Hospital, Coburg, Germany.
"Anaemia can be a very compromising condition for patients
suffering with CKD and successfully treating it can improve their
quality of life and may reduce the risk of further complications.
With the growing numbers of patients with kidney failure, we face
a significant challenge to detect, diagnose and treat CKD
across Europe," he added.

Anaemia is a common and serious complication in patients with
CKD, estimated to affect over 180, 000 people in Germany
alone.(2,3) Research has shown that anaemia correction
improves patients' quality of life by reducing fatigue and
increasing both appetite and work capacity.(4) In addition, a
study has shown that treatment with an ESA can reduce the
crude relative risk of mortality by up to 30%.(4) International and
national medical guidelines clearly emphasise the need for
correcting haemoglobin levels in patients with anaemia and then
maintaining them within a pre-specified range.(5,6,7) Two
large-scale Phase III studies have shown that treatment with
DYNEPO can effectively increase and maintain mean average
haemoglobin at target levels (10-12 g/dL) over a period of up to
52 weeks by either subcutaneous or intravenous
administration.(8,9,10)

DYNEPO offers flexibility and ease of use for both healthcare
practitioners and patients. DYNEPO may be administered
intravenously or subcutaneously. It is packaged in pre-filled
syringes for subcutaneous, self administration injection and is
currently available in five presentations. The syringe is designed
for ease of use by patients after training by a medical
professional and features a needle safety guard to reduce
needle stick injury. DYNEPO should be kept in a refrigerator, but
it can be used after a single period of un-refrigerated storage at
25 degrees C or less for up to five days, after which it should be
discarded.

"The launch of DYNEPO is another milestone in Shire's
continuing efforts to focus on improving health outcomes for
patients with renal disease and servicing renal units with
speciality pharmaceuticals," said Mike Cola, President of
Shire's Specialty Pharmaceuticals Business. "DYNEPO's
unique human gene activation origin and comprehensive clinical
efficacy and safety programme provide physicians with an
alternative choice in the management of anaemia. To continue
building on these efforts and supporting DYNEPO's entry into the
market, we have developed pricing structures that are intended
to reduce the economic burden of treating renal anaemia by
reducing the total renal healthcare costs currently consumed by
ESA treatments," he added.

About ERYTHROPOIETIN

Erythropoietin is a glycoprotein hormone; the protein core is a
sequence of 165 amino acids with four attached carbohydrate
residues that make up approximately 40% of the molecular
mass.(11) These carbohydrate residues are important for its
biological activity within the body.(12) Erythropoietin is normally
produced in the kidneys and stimulates the bone marrow to
produce red blood cells. Red blood cells contain haemoglobin
and are vital for oxygen transportation around the body. If the
kidney starts to fail, natural production of erythropoietin declines
leading to lower levels of haemoglobin(anaemia).

About DYNEPO

DYNEPO is the first ESA produced in human cells. This is
accomplished by activating the endogenous human
erythropoietin gene in a human cell line using specialised gene
activating DNA sequences. All other commercially available
ESAs are produced in animal cell lines derived from Chinese
Hamster Ovary cells or Baby Hamster Kidney cells. Anaemic
patients with CKD require treatment with an ESA such as
DYNEPO in order to increase red blood cell production.

DYNEPO is a registered trademark of Sanofi-Aventis.

i) While common terminology is now chronic kidney disease
(CKD), some regulatory agencies have not adopted this
terminology, instead they refer to chronic renal failure (CRF);
these terms are essentially interchangeable. DYNEPO (epoetin
delta) is indicated for the treatment of anaemia in patients with
CRF and may be used in patients on dialysis and in patients not
on dialysis.

Notes to Editors

SHIRE plc

Shire's strategic goal is to become the leading specialty
pharmaceutical company that focuses on meeting the needs of
the specialist physician. Shire focuses its business on attention
deficit and hyperactivity disorder (ADHD), human genetic
therapies (HGT), gastrointestinal (GI) and renal diseases. The
structure is sufficiently flexible to allow Shire to target new
therapeutic areas to the extent opportunities arise through
acquisitions. Shire believes that a carefully selected portfolio of
products with a strategically alignedand relatively small-scale
sales force will deliver strong results.

Shire's focused strategy is to develop and market products for
specialty physicians. Shire's in-licensing and merger and
acquisition efforts are focused on products in niche markets with
strong intellectual property protection either in the US or Europe.

For further information on Shire, please visit the Company's
website: www.shire.com.

"SAFE HARBOR" STATEMENT UNDER THE PRIVATE
SECURITIES LITIGATION REFORM ACT OF 1995

Statements included herein that are not historical facts are
forward-looking statements. Such forward-looking statements
involve a number of risks and uncertainties and are subject to
change at any time. In the event such risks or uncertainties
materialize, Shire's results could be materially affected. The
risks and uncertainties include, but are not limited to, risks
associated with: the inherent uncertainty of pharmaceutical
research, product development, manufacturing and
commercialization; the impact of competitive products,
including, but not limited to the impact of those on Shire's
Attention Deficit and Hyperactivity Disorder (ADHD) franchise;
patents, including but not limited to, legal challenges relating to
Shire's ADHD franchise; government regulation and approval,
including but not limited to the expected product approval dates
of SPD503 (guanfacine extended release) (ADHD), SPD465
(extended release triple-bead mixed amphetamine salts)
(ADHD); Shire's ability to secure new products for
commercialization and/or development; Shire's planned
acquisition of New River Pharmaceuticals announced February
20, 2007; and other risks and uncertainties detailed from time to
time in Shire's and its predecessor registrant Shire
Pharmaceuticals Group plc's filings with the Securities and
Exchange Commission, particularly Shire plc's Annual Report on
Form 10-K for the year ended December 31, 2006.


References

1 DYNEPO, Summary of Product Characteristics, December
2006.

2 The World Factbook.
http://www.cia.gov/cia/publications/factbook/print/gm.html

Accessed 14 March 2007.

3 National Institute for Health and Clinical Excellence. Anaemia
management in people with chronic kidney disease. Costing
report. Implementing NICE guidance in England. September
2006. p15.

4 JFE Mann. What are the short-term and long-term
consequences of anaemia in CRF patients? Nephrol Dial
Transplant 1999; 14 (Suppl 2): 29-36.

5 Kidney Disease Outcomes Quality Initiative. KDOQI Clinical
practice guidelines and clinical practice recommendations for
anemia in chronic kidney disease. Am J Kid Dis 2006: 47(5):
Suppl 3.

6 F Locatelli, P Aljama, P Barany, et al. Revised European best
practice guidelines for the management of anaemia in patients
with chronic renal failure. Nephrol Dial Transplant 2004; 19
Suppl 2: 6-15.

7 National Collaborating Centre for Chronic Conditions.
Published by RCP. Anaemia management in chronic kidney
disease. National clinical guideline for management in adults
and children. 2006. p19.

8 M Smyth, KJ Martin, RD Pratt. Epoetin delta (Dynepo(R)),
erythropoietin produced in a human cell line, is as effective as
epoetin alfa in patients with renal anaemia, including those with
diabetic nephropathy. Poster presented at the 42nd Annual
Meeting of the European Association for the Study of Diabetes
(EASD), 14-17 September 2006, Copenhagen-Malmoe,
Denmark-Sweden.

9 JTC Kwan, RD Pratt on behalf of the Epoetin Delta 3002
Study Group. Epoetin delta, erythropoietin produced in a human
cell line, in the management of anaemia in predialysis chronic
kidney disease patients. Curr Med Res Opin 2007; 23(2):
307-311.

10 JTC Kwan. Subcutaneous epoetin delta for the management
of anaemia in patients with CKD: safety and efficacy in a
one-year study. Poster presented at the American Society of
Nephrology (ASN) Renal Week, 14-19 November 2006, San
Diego, CA.

11 R Deicher and W Horl. Differentiating factors between
erythropoiesis-stimulating agents. Drugs 2004; 64(5): 499-509.

12 V Skibeli, G Nissen-Lie, P Torjesen. Sugar profiling proves
that human serum erythropoietin differs from recombinant human
erythropoietin. Blood 2001; 98(13): 3626-3634.

**********


Date:    Fri, 16 Mar 2007 15:09:56 -0400
From:    Nancy Klimas MD via Co-Cure Moderator <ray CO-CURE.ORG>
Subject: Re: med: New Human Cell-Produced Treatment for Anaemia

 From Nancy Klimas, MD:


[I] would like to comment on the recent email on erythropoietin
products.  I would appreciate if you would widely disseminate this reply,
as I believe CFS patients can be at real risk. [ ... ]   If you know of
other widely read group mails, feel free to send it on.


Erythropoietin warning:

As you know there has been a black box warning added to all of the
erythropoietin products (Procrit, Epogen, and Aranesp), due to two forms of
risk:

1)  The potential for products that stimulate red cell production to
stimulate tumor growth in patients with breast cancer and head and neck
cancer.

2)  The need to monitor very carefully when using red cell production
stimulants in other conditions (including the anemia induced by cancer,
renal failure and HIV medications) due to a risk of blood clots that could
lead to stroke, heart attacks, deep vein thrombosis, and pulmonary
embolism.  The deep vein thrombosis risk and pulmonary embolism risk was
also seen in healthy patients receiving the products to control post
operative anemia.

As you know, the University of Miami CFS research team recently completed a
study of erythropoietin, using Procrit, in a phase 2  double blind placebo
control study.   While we did not have any of these complications in our
study, patients were monitored very closely and the drug was titered to
very low levels when the red cell expansion exceeded the plasma volume
expansion and caused the blood to thicken.    This happened very
frequently, and doses were dropped in many subjects.   Doses anywhere close
to the doses suggested in the PDR would be very dangerous and even life
threatening.  The study's principal investigator, Dr. Barry Hurwitz
recently reported the results of this phase 2 study at the 8th
International IACFS Conference in Ft Lauderdale.    He noted that we were
unable to increase the red cell mass to mid-normal levels with
erythropoietin and salt alone, restricted by safety concerns.   At these
lower than projected levels of RBC mass increase, the tilt table test did
show a longer time until the onset or orthostatic hypotension.   However,
the patients' overall function and quality of life was not significantly
improved.    The results from this phase 2 study are not sufficient to
suggest the use of erythropoietin in CFS patients.  Should the
pharmaceutical world like to review our data, and allow us to design a
study that increased the plasma volume in addition to the RBC mass, we
would consider another clinical trial.     However, I think our data can be
viewed in another way, as it would appear the inflammatory cytokines play a
role in erythropoiesis suppression.    In the future, our studies of
immunomodulators that attempt to quiet the inflammatory cytokines will also
look at the markers of red cell production.

Finally, beware of the new erythropoietin drug, Dynepo, available currently
in Europe.   My reading of the literature suggests that the problem with
the EPO drugs currently on the market is that they do their jobs too
well.  In the end, it is the act of red blood cell stimulation that induced
the tumor growth, or the over production of red cells in relation to the
plasma.    Anything that pushes that button, should, in theory, hold the
same risk.   While the new product is derived from human cell lines, I
don't see why the inherent risk would be different.  As it took many
patient years for this risk to become evident with the current products, I
would not assume that the lack of vast amounts of safety data is the same
as an all out "don't worry this one is safe" reassurance.   Just my take on
a complicated situation!


Sincerely,

Nancy Klimas, MD
Professor of Medicine and
Director CFS/GWI Research Center
University of Miami Miller School of Medicine and the Miami VA Medical Center
Co-PI NIH RO1  HL65668  (the EPO study)


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Date:    Fri, 16 Mar 2007 14:37:05 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Neuroendocrine Implications of Opioid Therapy

Neuroendocrine Implications of Opioid Therapy

Current Pain and Headache Reports 2007, 11:89-92

B. Eliot Cole, MD, MPA, American Society of Pain Educators, 7 Oak Place,
Suite 7, Montclair, NJ 07042, USA.
Email: drcole paineducators.org


Opioid analgesics are given to people with pain. These medications are
highly effective for relieving pain and are generally considered to have
little or no end-organ toxicities.

Although they are generally feared because of their potential for abuse,
diversion, and psychological dependence, little attention is given to their
neuroendocrine consequences.

They are known to have central nervous systems effects and are now
understood to impact the regulation of gonadotropic hormones. Providing
meaningful informed consent requires disclosure about the risks associated
with lowered gonadotropic hormone levels.


Copyright © 2007 by Current Science, Inc.

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Date:    Fri, 16 Mar 2007 14:40:29 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Does Aerobic Exercise Improve Pain Perception and Mood? A  Review of the Evidence Related to Healthy and Chronic Pain Subjects

Does Aerobic Exercise Improve Pain Perception and Mood? A Review of the
Evidence Related to Healthy and Chronic Pain Subjects

Current Pain and Headache Reports 2007, 11:93-97

Martin D. Hoffman, MD and Debi Rufi Hoffman, MA

Corresponding author:
Martin D. Hoffman, MD
Department of Physical Medicine and Rehabilitation (117), Sacramento VA
Medical Center, 10535 Hospital Way, Mather, CA 95655, USA. Email:
martin.hoffman va.gov


Aerobic exercise can cause an acute improvement in mood as well as a
reduction in the perception of pain from a painful stimulus. Regular
exercise training also may offer some protection from depression, is
clinically useful in treating certain psychiatric and chronic pain
conditions, and may allow for an enhancement of the acute improvements in
mood from a single exercise session.

The utility of aerobic exercise training for improving mood disturbances
and pain perception among patients with chronic pain requires further
investigation.


Copyright © 2007 by Current Science, Inc.


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------------------------------

Date:    Fri, 16 Mar 2007 19:37:56 -0400
From:    "Richard Usher <websolutions2 hotmail.com> via Co-Cure Moderator"
Subject: NOT,MED: Potential new pain killer drug developed by scientists at Leicester and Italy


Potential new pain killer drug developed by scientists at Leicester and Italy

Contact: David Lambert
dgl3 le.ac.uk
44-011-625-85291
University of Leicester

A potential new pain-killing drug developed by medical scientists at the
University of Leicester and Ferrara in Italy is to be discussed at a public
lecture on 20th March.

Professor David Lambert, who has been involved in the development the drug
in collaboration with Dr Girolamo Calo in Ferrara Italy, believes the new
drug  called UFP-101 - avoids many of the side effects of morphine,
currently the ‘gold standard’ in pain reduction.

Read the complete press release at
http://fmsglobalnews.wordpress.com/2007/03/16/potential-new-pain-killer-drug-developed-by-scientists-at-leicester-and-italy/


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------------------------------

Date:    Sat, 17 Mar 2007 14:38:32 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Infection and vaccination in chronic fatigue syndrome:  Myth or reality?

Infection and vaccination in chronic fatigue syndrome: Myth or reality?

Autoimmunity. 2007 Feb;40(1):48-53.

Authors: Appel S, Chapman J, Shoenfeld Y.

Affiliation: Department of Neurology, Sheba Medical Center. hashomer. Israel.

NLM Citation: PMID: 17364497

Abstract
Chronic fatigue syndrome (CFS) is characterized by severe disabling fatigue
lasting for more than 6 months associated with physical and mental
disturbances such as headache, arthralgia, myalgia, memory impairment, sore
throat and tender lymph nodes. The exact pathogenesis is still unknown.
Several models were proposed to explain its etiology including chronic
infection, endocrine dysfunction, autonomic imbalance, depression,
decreased immunity states and an aberrant reaction to infection. No
convincing evidence was found to support any of the suggested pathogenic
mechanisms. The current concept is that CFS pathogenesis is a multi
factorial condition in which an infective agent cause an aberrant immune
response characterized by a shift to Th-2 dominant response. When the
response fails to be switched-off, a chronic immune activation occurs and
clinically expressed as the symptomatology of CFS.

Vaccinations are used in order to stimulate the immune system to induce a
persistent immunity against the favorable antigens. Several syndromes that
contain chronic fatigue as one of their symptoms, such as "Gulf war
syndrome" and macrophagic myofasciitis were related to vaccinations.

Can vaccinations induce the aberrant immune response of CFS? Little is
known about this issue. There are some reports on CFS occurring after
vaccination, but few prospective and retrospective studies failed to find
such an association.

A working group of the Canadian Laboratory Center for Disease Control
(LCDC) that was founded in order to examine the suspected association
between CFS and vaccinations concluded that there is no evidence that
relates CFS to vaccination. Further studies are requested to examine this
issue since it is very conceivable that if infection can lead to CFS,
vaccination may also lead to it in the same immune-mediated pathogenesis.

Keywords
Chronic fatigue syndrome, infection, vaccination, Th-2 immune response


References
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Koppel man, M and Reeves, WC. (1998) The epidemiology of chronic fatigue in
San Francisco Am J Med, 105, pp. 83S - 90S.

Straus, SE. (1988) The chronic mononucleosis syndrome J Infect Dis, 157,
pp. 405 - 412.

Fukuda, K and Straus, S and Hickie, I and Sharpe, M and Dobbins, J and
Komaroff, A. (1994) The chronic fatigue syndrome: A comprehensive approach
to its definition and study Ann Intern Med, 121, pp. 953 - 959.

Sharpe, M and Archard, LC and Banatvala, JE. (1991) A report chronic
fatigue syndrome: Guidelines for research J R Soc Med, 84, pp. 118 - 121.

Poteliakhoff, A. (1981) Adrenocortical activity and some clinical findings
in chronic fatigue J Psychosom Res, 25, pp. 91 - 95.

Moorkens, G and Berwaerts, J and Wynants, H and Abs, R. (2000)
Characterization of pituitary function with emphasis on GH secretion in the
chronic fatigue syndrome Clin Endocrinol (Oxf), 53, pp. 99 - 106.

Cleare, AJ and Blair, D and Chambers, S and Wessely, S. (2001) Urinary free
cortisol in chronic fatigue syndrome Am J Psychiatry, 158, pp. 641 - 643.

Cleare, AJ and Miell, J and Heap, E and Sookdeo, S and Young, L and Malhi,
GS and O'Keane, V. (2001) Hypothalamopituitaryadrenal axis function in chronic
fatigue syndrome, and the effects of low-dose hydrocortisone therapy J Clin
Endocrinol Metab, 86, pp. 3545 - 3554.

Cleare, AJ and Heap, E and Malhi, GS and Wessely, S and O'Keane, V and
Miell, J. (1999) Low-dose hydrocortisonee in chronic fatigue syndrome: A
randomised crossover trial Lancet, 353(6), pp. 455 - 458.

Scott, LV and Svec, F and Dinan, T. (2000) A preliminary study of
dehydroepiandrosterone response to low-dose ACTH in chronic fatigue
syndrome and in healthy subjects Psychiatry Res, 97, pp. 21 - 28.

Kuratsune, H and Yamaguti, K and Sawada, M and Kodate, S and Machii, T and
Kanakura, Y and Kitani, T. (1998) Dehydroepiandrosterone sulfate deficiency
in chronic fatigue syndrome Int J Mol Med, 1, pp. 143 - 146.

Moorkens, G and Wynants, H and Abs, R. (1998) Effect of growth hormone
treatment in patients with chronic fatigue syndrome: A preliminary study
Growth Horm IGF Res, 8, pp. 131 - 133.

Kennedy, G and Spence, V and Underwood, C and Belch, JJ. (2004) Increased
neutrophil apoptosis in chronic fatigue syndrome J Clin Pathol, 57, pp. 891
- 893.

Patarca, R. (2001) Cytokines and chronic fatigue syndrome Ann N Y Acad Sci,
933, pp. 185 - 200.

Gerrity, TR and Bates, J and Bell, DS and Chrousos, G and Furst, G and
Hedrick, T and Hurwitz, B and Kula, RW and Levine, SM and Moore, RC and
Schondorf, R. (2002/2003) Chronic fatigue syndrome: What role does the
autonomic nervous system play in the pathophysiology of this complex
illness? Neuroimmunomodulation, 10, pp. 134 - 141.

Naschitz, JE and Yeshurun, D and Rosner, I. (2004) Dysautonomia in chronic
fatigue syndrome: Facts, hypotheses, implications Med Hypotheses, 62, pp.
203 - 206.

Zachrisson, O and Colque-Navarro, P and Gottfries, CG and Regland, B and
Mollby, R. (2004) Immune modulation with a staphylococcal preparation in
fibromyalgia/chronic fatigue syndrome: Relation between antibody levels and
clinical improvement Eur J Clin Microbiol Infect Dis, 23, pp. 98 - 105.
Epub 2004 January 20

Prins, JB and Bleijenberg, G and Bazelmans, E and Elving, LD and de Boo, TM
and Severens, JL and van der Wilt, GJ and Spinhoven, P and van der Meer,
JW. (2001) Cognitive behaviour therapy for chronic fatigue syndrome: A
multicentre randomised controlled trial Lancet, 357(9259), pp. 841 - 847. 17

Gold, D and Bowden, R and Sixbey, J and Riggs, R and Katon, WJ and Ashley,
R and Obrigewitch, R and Corey, L. (1990) Chronic fatigue: A prospective
clinical and virologic study JAMA, 264, pp. 48 - 53.

Natelson, BH and Haghighi, MH and Ponzio, NM. (2002) A review of the
evidence on the presence of immune dysfunction in chronic fatigue syndrome
Clin Diagn Lab Immunol, 9, pp. 747 - 752.

Lerner, AM and Dworkin, HJ and Sayyed, T and Chang, CH and Fitzgerald, JT
and Beqaj, S and Deeter, RG and Goldstein, J and Gottipolu, P and O'Neill,
W. (2004) Prevalence of abnormal cardiac wall motion in the cardiomyopathy
associated with incomplete multiplication of Epstein-barr virus and/or
cytomegalovirus in patients with chronic fatigue syndrome In Vivo, 18, pp.
417 - 424.

Ablashi, DV and Eastman, HB and Owen, CB and Roman, MM and Friedman, J and
Zabriskie, JB and Peterson, DL and Pearson, GR and Whitman, JE. (2000)
Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue
syndrome (CFS) patients J Clin Virol, 16, pp. 179 - 191.

Soto, NE and Straus, SE. (2000) Chronic fatigue syndrome and herpesviruses:
The fading evidence Herpes, 7, pp. 46 - 50.

Lane, RJ and Soteriou, BA and Zhang, H and Archard, LC. (2003) Enterovirus
related metabolic myopathy: A postviral fatigue syndrome J Neurol Neurosurg
Psychiatry, 74, pp. 1382 - 1386.

Galbraith, DN and Nairn, C and Clements, GB. (1997) Evidence for
enteroviral persistence in humans J Gen Virol, 78, pp. 307 - 312.

Straus, SE. (1996) Chronic fatigue syndrome BMJ, 313(5), pp. 831 - 832.

Swanink, CM and Melchers, WJ and van der Meer, JW and Vercoulen, JH and
Bleijenberg, G and Fennis, JF and Galama, JM. (1994) Enteroviruses and the
chronic fatigue syndrome Clin Infect Dis, 19, pp. 860 - 864.

Kerr, JR and Bracewell, J and Laing, I and Mattey, DL and Bernstein, RM and
Bruce, IN and Tyrrell, DA. (2002) Chronic fatigue syndrome and arthralgia
following parvovirus B19 infection J Rheumatol, 29, pp. 595 - 602.

McGhee, SA and Kaska, B and Liebhaber, M and Stiehm, ER. (2005) Persistent
parvovirus-associated chronic fatigue treated with high dose intravenous
immunoglobulin Pediatr Infect Dis J, 24, pp. 272 - 274.

Nijs, J and Nicolson, GL and De Becker, P and Coomans, D and De Meirleir,
K. (2002) High prevalence of Mycoplasma infections among European chronic
fatigue syndrome patients. Examination of four Mycoplasma species in blood
of chronic fatigue syndrome patients FEMS Immunol Med Microbiol, 34(15),
pp. 209 - 214.

Endresen, GK. (2003) Mycoplasma blood infection in chronic fatigue and
fibromyalgia syndromes Rheumatol Int, 23, pp. 211 - 215. Epub 2003 July 16

MacDonald, KL and Osterholm, MT and LeDell, KH and White, KE and Schenck,
CH and Chao, CC and Persing, DH and Johnson, RC and Barker, JM and
Peterson, PK. (1996) A case-control study to assess possible triggers and
cofactors in chronic fatigue syndrome Am J Med, 100, pp. 548 - 554.

Schutzer, SE and Natelson, BH. (1999) Absence of Borrelia
burgdorferi-specific immune complexes in chronic fatigue syndrome
Neurology, 53(6), pp. 1340 - 1341. October 12

Gustaw, K. (2003) Chronic fatigue syndrome following tick-borne diseases
Neurol Neurochir Pol, 37, pp. 1211 - 1221. NovemberDecember
Grayston, JT and Grayston, JT. (1992) Infections caused by Chlamydia
pneumoniae strain TWAR Clin Infect Dis, 15(5), pp. 757 - 761. November

Chia, JK and Chia, LY. (1999) Chronic Chlamydia pneumoniae infection: A
treatable cause of chronic fatigue syndrome Clin Infect Dis, 29, pp. 452 - 453.

Nicolson, GL and Gan, R and Haier, J. (2003) Multiple co-infections
(Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue
syndrome patients: Association with signs and symptoms APMIS, 111, pp. 557
- 566.

Komaroff, AL and Wang, SP and Lee, J and Grayston, JT. (1992) No
association of chronic Chlamydia pneumoniae infection with chronic fatigue
syndrome J Infect Dis, 165, pp. 184.

Rottem, M and Shoenfeld, Y. (2004) Vaccination and allergy Curr Opin
Otolaryngol Head Neck Surg, 12, pp. 223 - 231.

Molina, V and Shoenfeld, Y. (2005) Infection, vaccines and other
environmental triggers of autoimmunity Autoimmunity, 38, pp. 235 - 245.

Schattner, A. (2005) Consequence or coincidence? The occurrence,
pathogenesis and significance of autoimmune manifestations after viral
vaccines Vaccine, 23(10), pp. 3876 - 3886.

Haley, R and Kurt, T. (1997) Self-reported exposure to neurotoxic chemical
combinations in Gulf war JAMA, 277, pp. 231 - 237. [CrossRef]
Rook, G and Zumla, A. (1997) Gulf war syndrome: Is it due to a systemic
shift in the cytokine balance towards a Th 2profile? Lancet, 349, pp. 1831
- 1833.

Hotopf, M and David, A and Hull, L and Ismail, K and Unwin, C and Wessely,
S. (2000) Role of vaccinations as risk factor for ill health in veterans of
the Gulf war: Cross sectional study BMJ(320), pp. 1363 - 1367.

Gherardi, RK and Authier, FJ. (2003) Aluminum inclusion macrophagic
myofasciitis: A recently identified condition Immunol Allergy Clin North
Am, 23, pp. 699 - 712.

Alleged link between hepatitis B vaccine and chronic fatigue syndrome CMAJ,
1461 1992. p 1145.

Duclos, P. (2003) Safety of immunisation and adverse events following
vaccination against hepatitis B Expert Opin Drug Saf, 2, pp. 225 - 231.

Zuckerman, JN. (2006) Protective efficacy, immunotherapeutic potential, and
safety of hepatitis B vaccines J Med Virol, 78, pp. 169 - 177.

Sleigh, KM and Marra, FH and Stiver, HG. (2002) Influenza vaccination: Is
it appropriate in chronic fatigue syndrome? Am J Respir Med, 1, pp. 3 - 9.


Copyright ©2007, Taylor & Francis Group. All Rights Reserved.

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Date:    Sat, 17 Mar 2007 22:05:50 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Use of mind-body therapies in psychiatry and family  medicine faculty and residents: attitudes, barriers, and gender  differences

Use of mind-body therapies in psychiatry and family medicine faculty and
residents: attitudes, barriers, and gender differences.

Explore (NY). 2007 Mar-Apr;3(2):129-35.

Sierpina V, Levine R, Astin J, Tan A.

University of Texas Medical Branch, Galveston, TX.

PMID: 17362848


BACKGROUND: Mind-body medicine (MBM) approaches to many health problems
have been well documented in the literature, including through multiple
meta-analyses. Efficacy has been well demonstrated in conditions such as
headache, irritable bowel syndrome, anxiety, fibromyalgia, hypertension,
low back pain, depression, cancer symptoms, and postmyocardial infarction.
However, an apparent disconnect (ie, translational block) prevents more
widespread adoption of such therapies into practice. Biofeedback,
relaxation therapy, hypnosis, guided imagery, cognitive behavioral therapy,
and psychoeducational approaches are the domain of MBM we examined in
assessing physician attitudes, beliefs, and practices.

METHODS: Using a Web-based survey, we obtained responses from 74 faculty
and resident physicians in the Department of Family Medicine and the
Department of Psychiatry. Our response rate was 69%. We conducted
descriptive statistics, bivariate analysis, and multivariate analysis using
a logistic regression model. Various statistics were chosen depending on
the nature of analyzed variables. Synoptic tables are presented.

RESULTS: Comparing these cohorts, we found little difference between
physicians in the two specialties, but substantial reports that barriers to
the use of MBM were largely based on lack of training, inadequate
expertise, and insufficient clinic time. Lack of expertise and insufficient
clinic time were higher among family physicians than among psychiatrists.
There was a high interest in both groups in learning relaxation techniques
and meditation and lower interest in biofeedback and hypnosis. Female
physicians were significantly more likely to use MBM, both with patients
and for their own self-care, and were less likely to be concerned that
recommending these therapies would make patients feel that their symptoms
were being discounted. Female physicians also had significantly higher
beliefs about the benefits of MBM on health disorders in several of the
conditions examined, with a consistent though nonsignificant trend in others.

[Return to top]

------------------------------

Date:    Sun, 18 Mar 2007 11:19:15 -0400
From:    "ME/CFS" <me_cfs glocalnet.net> [via Co-Cure Moderators]
Subject: RES:Speculative theory for ME

Speculative theory for ME

Here a speculative theory for an explanation of myalgic enecephalomyelitis
(ME) will be presented. The text will be presented as if everything is true,
but it is all speculation. The text or the ideas may be used, but only if
the author is cited and credited.


Speculative understanding of human body:

When a healthy individual (person without ME) get an infection it protects
itself by several physiological actions. The immune system releases
cytokines that influences the CNS in order to change the behaviour of the
person.

The person shall optimally lie down and rest during an infection. How is
this achieved? The person get orthostatic intolerance, so he will feel
discomfort when standing up. He looses motivation and so on. This is
achieved by an interaction between immune system and CNS. Probably basic
mechanisms at several levels collaborate to achieve this change of
behaviour. Also pain occurs in order to give the individual discomfort and
motivate to rest.

The brain is important to protect, therefore the "gates are closed" to the
CNS compartment. The CNS compartment is protected by dura mater, but the
brain is highly perfused with capillary blood vessels, and this is a "weak
point" of the CNS compartment protection. In order to counter this "entry"
for pathogens to the CNS compartment, the body has a strategy. The brain has
to be highly perfused and nourished during normal function, so it adopts a
strategy to "close the gates" when there is a threat. When the immune system
signals that there is an infection, the capillaries in the CNS decreases its
permeability. This means for example that the brains receives less blood
during infection.

Certain regions of the brain have their metabolism highly decreased, this
can be in order to change the behaviour of the person and/or because some
regions are particularly important to keep intact.


Speculative theory of ME:

The immune system is locked in a dysfunctional mode. This could be due to a
combination of effects as for example: inheritance, gene expression
(epigenetics), pathogens, toxins and stress.

The immune system communicates with the CNS with cytokines and other
signals. The CNS changes its mode of function in order to change the
behaviour of the individual. Also the blood capillaries of the brain reacts
to the immune system response, and they become less permeable.

Kasper Ezelius

[Return to top]

------------------------------

Date:    Sun, 18 Mar 2007 16:50:19 +0100
From:    ME/CFS <me_cfs@GLOCALNET.NET>
Subject: RES: Hypothesis based research on "the speculative theory for ME"

Hypothesis based research on "the speculative theory for ME"

Earlier, 2007-03-16, a speculative theory for ME was presented in Co-Cure
(http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703c&L=co-cure&T=0&O=D&P=24
49). Here a design of hypothesis based research will be presented with that
theory as basis.

Compare cerebral blood flow, activity and metabolism for healthy individuals
(controls) in their healthy condition and in a condition with infection.
Compare this with ME patients. Do controls with infection show any
similarities in brain state with ME patients?

Check with brain imaging, if any cytokines, interleukines, interferons or
other signal from immune system injected in an healthy human or other mammal
provoke any change in brain state (cerebral blood flow, activity and
metabolism). Observe that the effects may be time dependent and therefore
data should be collected as a function of time.

Check if capillaries in the brain react (change of dilatation or change of
permeability) to any cytokines, interleukines, interferons or other signal
from immune system. The permeability should be checked to different
molecules and cells. Could be performed in vivo and/or in vitro for humans
and other mammals.

The ideas and text in this message may be used under the condition that the
author is mentioned.

/Kasper Ezelius


[Return to top]

------------------------------

Date:    Sun, 18 Mar 2007 13:32:17 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Sense of effort during a fatiguing exercise protocol in chronic fatigue syndrome

Sense of effort during a fatiguing exercise protocol in chronic fatigue
syndrome.

Journal: Res Sports Med. 2007 Jan-Mar;15(1):47-59.

Authors: Karen E. Wallman [a]; Paul Sacco [b]

Affiliations:
[a] School of Human Movement & Exercise Science, The University of Western
Australia. Crawley. Western Australia
[b] Rehabilitation Neurosciences, University of East London. London. England

NLM Citation: PMID: 17365951


The purpose of this study was to determine whether chronic fatigue syndrome
(CFS) subjects would produce greater force production in their matching
limb during a fatiguing contralateral limb-matching task of the elbow
flexors, compared with healthy, matched controls.

Eight CFS subjects and 8 healthy, matched control subjects participated in
a fatiguing task that consisted of intermittent submaximal contractions
(30% maximal voluntary contraction) of the nondominant arm performed over a
45 min duration. Each minute, the subject attempted to match the force of
the nondominant arm with their dominant arm (without visual feedback for
the dominant arm).

Results showed that average matching force and ratings of perceived effort
values were significantly higher in the CFS group during the fatiguing task
(P = 0.04, P = 0.02, respectively).

This study demonstrated objectively that CFS subjects experienced a greater
sense of effort in the elbow flexors while performing a fatiguing task.


[All costs associated with this study were incurred by Edith Cowan
University.]

Keywords: contralateral limb matching task; fatigue; matching force

[Return to top]

------------------------------

Date:    Mon, 19 Mar 2007 00:34:25 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: not,med: Lost to Lyme

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Send an Email for free membership
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
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Outgoing mail scanned by Norton AV
~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~


Quote from below:

*....Lyme can mirror other illnesses and is sometimes
misdiagnosed as arthritis, Lou Gehrig's disease (ALS),
fibromyalgia, chronic fatigue syndrome and multiple
sclerosis....*

~jvr

````````


http://www.sunjournal.com/story/203796-3/MaineNews/Lost_to_Lyme/


Sun Journal


Lost to Lyme
~~~~~~~~~~


By Lindsay Tice, Staff Writer

Sunday, March 18, 200


Bill Chinnock's suicide means Maine's Lyme
disease community has lost a champion ... and so
much more. But they hope his death will bring
help and maybe a cure.


When Jodi Ireland heard last week that Bill Chinnock had died,
she was stunned.
When she learned he'd killed himself, she was devastated.

As neighbors in Fairfield, Chinnock had helped her find a
diagnosis - Lyme disease - for the crushing fatigue, headaches
and numbness that plagued her.

Chinnock, a well-known Maine rock musician, an
Emmy-award-winning composer and a founding member of
what became Bruce Springsteen's E Street Band, was waging
his own battle with Lyme. The little-understood tick-borne illness
can leave patients debilitated, in pain, confused and forgetful.
Still, he encouraged Ireland. He was hopeful.

"I don't know how he did it, but he always stayed so positive,"
Ireland said.

Like many Lyme patients, Chinnock - a husband and father - had
his ups and downs. But he always seemed eager to help others,
eager to tell them they'd be all right. In Maine, he was the Lyme
disease community's champion. He was its rock.

And then, late last week, police were called to Chinnock's home.
His manager said he committed suicide. In the press, his sister
blamed it on the disease.

The news sent the Lyme community reeling.

"I just lost it. I kept saying 'I can't believe he did that,'" said
Ireland, a dance teacher now struggling with a Lyme relapse. "I
can't believe he gave up."

'Survive and rise above'

Over 23,000 new cases of Lyme disease were reported in the
U.S. in 2005, nearly 250 of those in Maine, according to the
National Centers for Disease Control. But because testing isn't
always accurate and because Lyme can mirror other diseases,
experts say there were likely many more new cases than that.

Lyme can cause myriad symptoms, including exhaustion, joint
pain and a generally "foggy" feeling. If caught early, experts say,
the disease can be cured with antibiotics. But some people
aren't diagnosed for years. When that happens, despite
long-term antibiotics, their symptoms are chronic and severe,
turning them from healthy to bed-ridden without warning.

"It's almost like a death every time you get sick again," Ireland
said.

Many Lyme patients go from doctor to doctor, getting diagnosed
with every disease but Lyme. Some lose their jobs because they
can't keep up with the workload. Others lose relationships
because friends and family don't understand the illness.

In Maine, the Lyme disease community is particularly close.

A handful of support groups meet every month, trading help and
advice. An online Yahoo group has 175 members who post
hundreds of messages each month. For some, it's the only place
they can find real understanding.

"Other people say 'Well, you look good.' I hate that expression.
Never mind that it took me all day to take a shower. Maybe I can
put on mascara by the time my husband gets home," said Gail
Richard, a former special education teacher who lives in
Livermore Falls.

Chinnock and Ireland both became sick in the late 1990s. They
lived down the road from each other and he worked out at a gym
she owned with her husband, she said.

"We realized we were both having a lot of the same symptoms,"
Ireland said.

Exhaustion. Headaches. Heart palpitations. Numbness. They
checked for chemicals in the water. He went to doctors out of
state. She went to doctors locally.

"Basically his doctors told him he was crazy and mine told me I
had fibromyalgia and to go home and cope," Ireland said.

Chinnock eventually saw a doctor in Connecticut, where Lyme
was named (after the town of Lyme, Conn.) and diagnosed in the
1970s. He called Ireland, excited, urging her to be tested for
Lyme disease, too.

They both had it.

"I will always feel that I owe him so much. He helped save my
life," Ireland said.

Chinnock and Ireland went through treatment, including
antibiotics, but some symptoms persisted. After Chinnock
moved to Yarmouth several years ago, the pair kept in touch.

They each had their ups and downs. Sometimes Chinnock felt
well enough to put in a 17-hour day producing a new album.
Sometimes he couldn't work at all. But no matter what was going
on with his own health, Chinnock sought out others to help.

"So many people are so sick and so few doctors know enough,"
Ireland said.

He advocated for greater Lyme disease public education. He
met with Lyme sufferers, recommending doctors and suggested
treatments. Sometimes he simply commiserated, a blessing to
patients who felt unheard for so long.

He was constantly upbeat, unfailingly positive.

Already a music legend as a songwriter and guitarist, Chinnock
soon became a legend in the Lyme community as well.

"A lot of people knew Bill. He helped a lot of people get
diagnosed," said Constance Dickey of Hampden, founder of the
MaineLymeDisease support group on Yahoo and chairwoman
of the International Lyme and Associated Diseases Society.

Stacey Cimino, a southern Maine resident, met Chinnock after
learning she had Lyme. She'd been dealing with the symptoms -
headaches, seizures, tremors, breathing and heart problems -
for a decade. Doctors told her she had everything from Lou
Gehrig's disease to stress. By the time Cimino was diagnosed
with Lyme, she was sick and tired of being sick and tired.

Chinnock sent her an e-mail.

"He said 'God has a plan for people. You'll get through this,'" she
said.

He offered advice in his letters, telling her about his own
experience with a new treatment. He encouraged her, like he
encouraged so many people, to keep fighting.

"You will survive and rise above," he wrote.

Grief and hope

In 2004 and 2005, Chinnock seemed to be doing well. He'd
found an herbal supplement that helped and he was working
long hours on a new album, the first in years.

But when Chinnock called to check in with Ireland last year, he
told her he wasn't feeling well again. That was the last time she
heard from him.

On March 2, Chinnock's live-in caretaker called police to his
Yarmouth home. His manager said he committed suicide.

Chinnock was 59.
"This has been a huge emotional blow," said Dickey, the support
group founder. "It has rocked the community."

Some now wonder how they can possibly be strong enough to
handle the waves of pain and fatigue if Chinnock, their
champion, couldn't.

"It broke my heart because I know what he goes through, I know
what he went through," said Richard, the former special
education teacher. "There are some days you don't want anyone
to talk to you or touch you, the pain is so bad. I walk from window
to window and look outside. I'm 52 years old and I feel 80."

For a week, online message boards have buzzed with news of
Chinnock's death.

"I'm sure many of us here have had thoughts similar on our very
worst days. How bad must he have been to take that last final
step? My heart breaks for him," wrote one person on
Lymenet.org.

"I pray that he has found peace at last," wrote another.

LymeMemorial.org now lists Chinnock among 230 people who
have died from Lyme or other tick-borne diseases.

But even as they grieve, Lyme patients say they also have hope:
that Chinnock's death will not be in vain.

"I hope someone in Augusta is paying attention," said Dickey.

They want publicity. They want Lyme disease education for
doctors and the public. They want passage of a federal bill
earmarking $100 million for Lyme disease research and
prevention. They want passage of a state bill that forces
insurance companies to cover Lyme patients, requires
employers to educate workers about Lyme if they work in a high
risk area and creates a study of Lyme disease issues.

It's all been missing, they say. And maybe now, with Chinnock's
death, it will come.

"I bet that's what he would have wanted, too," Ireland said.


Lyme disease facts
~~~~~~~~~~~~~~~~~~

  * Nearly 250 new cases were reported in Maine in 2005, the last
year data is available.
  * Disease comes from deer ticks.

  * Symptoms often begin within days or weeks and sometimes
come with a red rash that can look like a bull's-eye.

  * More severe symptoms include joint pain, fatigue, muscle
aches, headaches, nervous system problems, facial paralysis
and a general "foggy" feeling.

  * Lyme can mirror other illnesses and is sometimes
misdiagnosed as arthritis, Lou Gehrig's disease (ALS),
fibromyalgia, chronic fatigue syndrome and multiple sclerosis.

  * Treatment is a course of antibiotics, although doctors debate
how long treatment should last.
Deer tick facts

  * Both baby deer ticks and adult deer ticks can transmit Lyme
disease.

  * Baby deer ticks are about the size of a pinhead.

  * Adult deer ticks are often shiny, reddish brown with black
heads.

  * Deer ticks favor trees and leaves, although they can be found
on the coast or in grass.

  * They must feed on someone for 24 to 48 hours in order to
transmit Lyme disease.

  * They can also transmit ehrlichiosis, a rare disease with flu-like
symptoms, and babesiosis, a malaria-like disease that affects
red blood cells.

  * Use insect repellents with DEET and protective clothing to
prevent tick bites. For pets, use only repellents OK'd by a vet.

  * To remove a tick, grasp it with fine tweezers as close to the
skin as possible. Pull gently but firmly. It could take several
minutes. Do not handle ticks with your bare hands.
What you can do

  * Several U.S. centers test ticks for Lyme disease, including
those listed below. Contact each for information on price,
response time and proper procedure for mailing.

North American Laboratory

New Britain, CT
(203) 826-1140

800-866-NALG

New Jersey Laboratories

New Brunswick, NJ

(732) 249-0148

IgeneX

Palo Alto, California

http://www.igenex.com/

(415)424-1191

800-832-3200

Tick Research Laboratory

Kingston, Rhode Island

(401)874-2650

  * The Vector-borne Disease Laboratory at Maine Medical
Center identifies ticks and can tell whether they have fed long
enough to transmit Lyme. It is free.

Ask your doctor or veterinarian to send the tick or do it yourself
by sealing the tick in a small, crush-proof container with alcohol.
Include the form found at www.mmcri.org/lyme/lymehome.html
and mail it to:

Vector-Borne Disease Laboratory

Maine Medical Center Research Institute

75 John Roberts Road, Suite 9B

South Portland, ME 04106



Sources: Maine CDC, the Vector-Borne Disease
Laboratory, Lymenet.org, International Lyme and
Associated Diseases Society

[Return to top]

------------------------------

Date:    Mon, 19 Mar 2007 15:23:06 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: The Relationship between Psychological Factors and Health Care-Seeking Behavior in Fibromyalgia Patients

[The Relationship between Psychological Factors and Health Care-Seeking
Behavior in Fibromyalgia Patients.]
[Article in Turkish]

Turk Psikiyatri Derg. 2007 Spring;18(1):22-30.

Gulec H, Sayar K, Yazici Gulec M.

PMID: 17364265


OBJECTIVE: The aim of this study was to examine whether cognitive factors,
such as attributions, expectations, and anger management style, contribute
to the decision to seek medical care for fibromyalgia syndrome (FMS).

METHOD: We recruited 3 groups of subjects; patients from a FMS tertiary
care setting, community residents with FMS who had not sought medical care
for their FMS symptoms (nonpatients), and healthy controls. In all, 38 FMS
nonpatients were compared to 37 FMS patients and 41 healthy controls on
measures of anxiety, depression, anger, locus of control (LOC),
attributions, pain intensity, and disability, as well as demographic
characteristics.

RESULTS: The prevalence of FMS non-patients was 2%. There was a significant
difference between the 3 groups on the measures of anxiety, depression,
LOC, and somatic and normalizing subscale scores of the symptom
interpretation questionnaire (SIQ). FMS nonpatients, relative to FMS
patients and healthy controls, were characterized by a significantly higher
measure of both LOC and normalizing subscale score on the SIQ. There were
no differences between the 2 FMS groups in demographical percentage and
other psychometric measures. A hierarchical logistic regression model
showed that the number of tender points, normalizing attribution style, and
depression were independent predictors of help-seeking behavior.

CONCLUSION: The rate of psychiatric and medical history is not related to
the FMS syndrome. Expectations and a normalizing attribution style may
contribute to help-seeking behavior for FMS.

[Return to top]

------------------------------

Date:    Mon, 19 Mar 2007 04:31:53 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: res: Infection & vaccination in ME/CFS - Myth or reality?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


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~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~
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Sat, 17 Mar 2007 Fred Springfield posted the abstract of
*Infection and vaccination in chronic fatigue syndrome: Myth or
reality?* - Appel S, Chapman J, Shoenfeld Y - Autoimmunity.
2007 Feb;40(1):48-53. -  at Co-cure:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703c&L=co-cure&T=0&P=2067


--------------------------------------------------------------
~jvr: as fair use I add the *discussion* (*Can vaccinations
induce CFS?* section of this article
--------------------------------------------------------------


Can vaccinations induce CFS?


As discussed above, the exact pathogen of CFS in unknown, but
the leading theory is that an aberrant immunological response to
infection causes a chronic activation biased toward a Th-2
dominant reaction.

This theory raises the suspicion that vaccinations that are given
in order to trigger an immunological defense reaction, may
cause in distinct cases an aberrant reaction that will be
expressed as CFS by the mechanism discussed above.

The main adverse reactions to vaccinations are usually local at
the site of injection (erhythema and pruritus) but systemic
flue-like reaction (fever, myalgia, fatigue and lymph nodes
tenderness) and allergy may occur [39]. Those adverse
reactions are usually mild and self-limited.

Several reports associate distinct vaccinations with the induction
of autoimmune disease [40,41]. Rheumatoid arthritis, reactive
arthritis, vasculitis, encephalitis, thrombocytopenia and multiple
sclerosis relapse have been documented after hepatitis B virus
(HBV) vaccination. Acute arthritis or arthralgia, chronic arthritis
and thrombocytopenia appeared after mumps and rubella
vaccine (MMR). Guillain–Barre syndrome (GBS) and vasculitis
after influenza, and GBS that appeared after polio-immunization.

Several syndromes that are related to vaccinations contain
chronic fatigue as a part of the syndrome. The Gulf war
syndrome was described in 4–8% of the soldiers who
participated in the Gulf war and few months–years later suffered
from illness that included impaired cognition (distractibility,
memory problems), fatigue, arthromyoneuropahy (joints and
muscle pains) and post-traumatic stress disorder [42].

The syndrome was related to chronic Th-2 biased immune
response. Rook and Zumla [43] raised the hypothesis that the
multiple vaccinations given to the troops during their deployment
induced a systemic Th-1 to Th-2 switched immune response and
cause to the symptoms above. Four features of the vaccination
protocol used in this war led them to this theory:

(1) The vaccination against anthrax that was given to the soldiers
used Pertussis derivate as an adjuvant agent, which is known to
induce a Th-2 dominant response.

(2) The soldiers were exposed to large burden of vaccinations
which tend to shift the immune response to a Th-2 dominant
response.

(3) The vaccinations were given after the deployment of the
troops, while being in stressful condition. Under this condition
the cortisol level is reduced, the DHEA level is increased and
the immune response is shifted to Th-2 dominant profile.

(4) The troops were exposed to carbamate and
organophosphate insecticides which inhibits IL- 2—a pivot
cytokine of Th-1 response.

Support for this theory came from a cross sectional study of 923
UK Gulf war veterans who still had their vaccinations records
[44]. The study found an association between multiple
vaccinations given during the conflict and later evolution of Gulf
war syndrome.


Another syndrome that was related to vaccinations is
macrophagic myofasciitis. This syndrome is a postvaccination
disorder characterized by stereotypic lesion on the deltoid
muscle (site of injection) associated with prominent fatigue that
fulfills the CFS criteria. Electron microscopy and experimental
studies show that the lesion is due to persistent immune reaction
to aluminum hydroxyl used in different vaccination as an adjuvant
agent including HAV, HBV and toxoid vaccinations. The
aluminum hydroxyl is known to induce a shift of the immune
response toward a Th-2 profile reaction and if it persists—a
chronic inflammatory activation may occur. The persistent
elevated levels of the Th-2 cytokines induce the systemic
symptoms of chronic fatigue, muscle and joints pain [45].


An association between vaccination and CFS is much less
documented. In 1992 several reports claimed that CFS was
evolved after immunization to HBV was published in Canada. A
working group of the Laboratory Center for Disease Control
(LCDC) of the Canadian National Health andWelfare (NHW)
was founded in order to examine the suspected association
between anti-HBV vaccination and CFS.

The working group gathered 30 cases of patients with CFS that
appeared within 3 month after immunization against HBV—the
great majority after the first dose of the vaccine [46].The working
group examined several studies dill with this question. A
retrospective study on 134 CFS patients found that 2.2% of
them received anti-HBV vaccine within the 3 month before the
beginning of the disease. When they compared this figure to the
occurrence of anti-HBV vaccination in the matched Canadian
population (1.9%), no significant different was found.

A prospective study followed after 700 students who were
vaccinated with anti-HBV vaccine. About 12% of the students
complained on tiredness that was self limited and none of them
evolved to CFS. Those studies brought the members of the
working group to a conclusion that there is no evidence that
show an association between CFS and anti-HBV vaccine.
Updated studies that checked the relationship between CFS
and vaccination came to the same conclusion [47,48].

The use of vaccinations in CFS patients did not exacerbate their
symptoms. A study that examined CFS patients vaccinated with
anti-influenza vaccination found no significant difference
between the CFS patients and the control healthy group.
Although CFS patients reported on adverse affects four times
more then the healthy vaccines, those adverse effects were
related to common post-influenza vaccination symptoms and to
constitutional CFS symptoms [49].


We can summarize carefully that except for several
case-reports, there is no study that found induction of CFS by
vaccination, but only few studies concerning this issue have
been published. Further studies examining this question should
be carried out and the physician's index of suspicion should be
raised because this possibility of vaccination-induced CFS is
reasonable in view of the ability of vaccinations to cause Th-2
dominant response.

[Return to top]

------------------------------

Date:    Mon, 19 Mar 2007 20:05:48 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: The Relationship Between Cytokines and Pain/Depression: A  Review and Current Status

The Relationship Between Cytokines and Pain/Depression: A Review and
Current Status

Current Pain and Headache Reports 2007, 11:98-103

Thomas B. Strouse, MD, UCLA Department of Psychiatry and Biobehavioral
Sciences, Outpatient Cancer Center at the Samuel Oschin Comprehensive
Cancer Institute, UCLA and Cedars-Sinai Medical Centers, 8700 Beverly
Boulevard, Los Angeles, CA 90048, USA. Email: thomas.strouse@cshs.org


Cytokines are small protein molecules secreted in response to immune
stimuli. Recent research has outlined important roles for proinflammatory
cytokines in the cascade of normal physiologic responses to environmental
stresses, encompassing so-called sickness behavior that is thought to be an
adaptive response to infection and other illnesses.

Cytokines are involved in signaling that activates central nervous system
glial cells. This activation is part of a poorly understood interaction
between immune challenge or injury and host that can lead to the
development or facilitation of persistent mood symptoms or pathologic pain.

This article reviews evidence that may enhance our understanding of how
pathologic symptoms, such as mood disorders and neuropathic pain, may
emerge from proinflammatory cytokine activation. Possible
conceptualizations of these illnesses and potential treatment implications
are explored.


Copyright © 2007 by Current Science, Inc.

[Return to top]

------------------------------

Date:    Mon, 19 Mar 2007 20:18:47 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Evidence for a Mismatch Between the Brains Movement  Control System and Sensory System As an Explanation for Some  Pain-related Disorders

Evidence for a Mismatch Between the Brain's Movement Control System and
Sensory System As an Explanation for Some Pain-related Disorders

Current Pain and Headache Reports 2007, 11:104-108

Candida S. McCabe, PhD, RGN and David R. Blake, MB, FRCP

Corresponding author:Candida S. McCabe, PhD, RGN, The Royal National
Hospital for Rheumatic Diseases and School for Health, University of Bath,
Upper Borough Walls, Bath BA1 1RL, United Kingdom.
Email: candy.mccabe rnhrd-tr.swest.nhs.uk


The motor-control system usually operates below our conscious level, and we
only become aware of the complex interaction between desired movements and
actual movements when an irregularity in the system occurs. Recently, it
has been proposed that such discordances in sensorimotor function may
generate pain and other somaesthetic disturbances.

This article describes this model of pain and determines how it may be
applied to a range of chronic pain conditions in which there is a lack of
obvious causal pathology, including complex regional pain syndrome. In
addition, we discuss the clinical implications of such a theory and examine
how enhancing sensory feedback may reduce chronic pain.


Copyright © 2007 by Current Science, Inc.


[Return to top]

------------------------------

End of Co-Cure Weekly Digest of research and medical posts only - 12 Mar 2007 to 19 Mar 2007

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