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    Strijd om erkenning
    23-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12-tekort - Een mogelijke oorzaak van Chronische vermoeidheid ? - Deel II
    Klik op de afbeelding om de link te volgen


     

    Vitamine B12-tekort
    - Een mogelijke oorzaak van Chronische vermoeidheid ? -

    Deel II

    1. Het belang van orale B12
      The Health Connection
      Sinds tientallen jaren injecteren mensen zich met vitamine B12 omdat ze dachten dat dit de beste manier was om het in de bloedbaan op te nemen.
      Nieuw onderzoek heeft aangetoond dat orale B12- supplementen beter zijn dan injecties.
      Mensen die tekorten hebben aan B12 in hun bloed zijn al heel lang aangewezen op de oncomfortabele en pijnlijke toedieningsvorm d.m.v. injecties met deze essentiële B-vitamine.
      Nieuwe onderzoeken tonen dat orale B12 net zo goed, zoniet beter, werkt als injecties, volgens een studie welke gepubliceerd werd in het gezaghebbende blad "Blood".
      Recente gegevens melden dat de orale absorptie net zo goed werkt als injecties en met een toegevoegde waarde van behoud van hoge bloedwaarden over langere tijd.
      De studie toont aan dat de bloedwaarde van mensen die injecties kregen na een maand daalde en zich daar stabiliseerde, terwijl de bloedwaarden van hen die de orale spray gebruikten stegen.
      Om B12 in het lichaam te kunnen opnemen wordt in de maag een stof (een proteïne) uitgescheiden welke essentieel is voor dit opnameproces.
      Dit wordt de 'intrinsieke factor' genoemd.
      Oudere mensen produceren minder van deze intrinsieke factor en zijn hierdoor gevoeliger voor B12 tekorten.
      In de eerder genoemde studie werden hoge doseringen orale B12 even goed opgenomen dan de geïnjecteerde dosering (verstoring van afgifte van intrinsieke factor wordt meestal geassocieerd met een chronisch B12-tekort ook bekend als pernicieuze anemie).
      Iedereen met verhoogde homocysteïne-gehalten, psychiatrische stoornissen, eetstoornissen, slaapstoornissen, alsmede als gevolg van het verouderingsproces, heeft mogelijk een tekort aan B12.
      Het is onderzocht dat het niveau aan B12 elk jaar daalt naarmate je ouder wordt.
      Leeftijdsgerelateerde B12 tekorten worden in verband gebracht met gehoorsvermindering, concentratieproblemen, geheugenvermindering, psychiatrische stoornissen, slaapstoornissen, alsmede hartklachten.
      "U kunt geen of onvoldoende B12 innemen via tabletten als u problemen heeft met de intrinsieke factor"
      De snelle opkomst van obesitas en de vele daaruit voorvloeiende chirurgische ingrepen, zoals maagverkleining en maagbypass, hebben een drastisch gevolg voor de productie van intrinsieke factor en de daardoor ontstane verstoringen.
      Voldoende vitamine B12-toediening "buiten het maagdarmkanaal om" is ook voor deze groep absolute noodzaak.
      Onze voeding en leeftijd en medische ingrepen zijn de belangrijkste boosdoeners bij het ontwikkelen van B12 tekorten.
      Vlees is een uitstekende bron voor onze B12.
      Toch is het niet zo dat een vleesrijk dieet garandeert dat iemand geen tekort heeft.
      Bijvoorbeeld oudere mensen, deze kunnen grote hoeveelheden vlees eten en toch een tekort aan vitamine B12 hebben omdat ze niet genoeg intrinsieke factor meer kunnen produceren als gevolg van veroudering van de maagfunctie en het maagslijmvlies waarin de intrinsieke factor geproduceerd wordt.
      B12 tekorten komen voor bij ruim 30% van de senioren en oudere mensen die regelmatig last hebben van een verstoorde spijsvertering / maag-darmfunctie.
      Het schijnt dat er nog een andere oorzaak is voor tekorten aan vitamine B12 bij ouderen maar dit moeten de onderzoekers nog verklaren.
      In een Nederlandse studie hebben onderzoekers ontdekt dat maar 28% van de mensen die een B12 tekort hebben, problemen hebben met hun intrinsieke factor.
      De overige 72% is, nog steeds, een raadsel.
      Wel weten de medici dat ook foliumzuur een grote rol in dit opnameproces speelt.
      Onderzoekers weten wel dat veel meer mensen tekorten hebben dan tot nu toe werd aangenomen.
      Toen onderzoekers aan het Veterans Hospital in Oklahoma standaard bijgestelde criteria gebruikten bij het testen van B12 tekorten, ontdekten ze dat B12 tekorten twee keer zo vaak voorkwam als bij voorgaande testen.
      "B12 tekort komt zo vaak voor dat het bij de artsen al standaard voorgedrukt staat op de formulieren voor bloedonderzoek"
      Diegenen met slaapproblemen, hebben mogelijk vitamine B12 nodig.
      Studies hebben laten zien dat B12 een vroegere vrijmaking van melatonine veroorzaakt tijdens de nacht, welke zorgt voor de juiste instelling van de natuurlijke slaap-waak-cyclus.
      B12 beïnvloed direct de pijnappelklier voor de prikkeling van een snellere productie van melatonine.
      Aan het eind van de cyclus zorgt B12 ervoor dat de productie van melatonine sneller stopt.
      B12 helpt je sneller in te slapen en kan helpen sneller te ontwaken als het daar tijd voor is.
      B12 activeert je systeem voor de zon 's morgens opkomt en het daglicht helpt je verder wakker te worden.
      Vele serieuze slaap-waak stoornissen zijn succesvol behandeld met orale B12.
      De opmerking dat B12 geïnjecteerd moet worden om effectief te zijn is in verschillende studies steeds weerlegd.
      Een factor waar velen het mee eens zijn is dat B12-supplementatie noodzakelijk is in deze tijden van snelle vergrijzing.
      De keuze is nu aan u : oncomfortabele injecties of een gemakkelijke en smakelijke spray.
      Cfr. : http://www.vitaminespray.nl/cms/index.php?option=content&task=view&id=35&Itemid=61
    2. Het nut van vitamine B12 supplementen
      Diëtiste Tina de Vries – Animalfreedom – Bron : Lyra Alves in het magazine van EVA, zomer 2004
      Cfr. : http://www.animalfreedom.org/paginas/informatie/B12.htmlAnimalfreedom
    3. How I treat cobalamin (vitamin B12) deficiency
      Carmel R, Department of Medicine, New York Methodist Hospital, Brooklyn, and Weill Medical College, Cornell University, New York, NY 11215, USA : rac9001@nyp.org - Blood. 2008 Sep 15;112(6):2214-21. Epub 2008 Jul 7 - PMID: 18606874
      The challenges in medical management of cobalamin deficiency lie in attention to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of therapy.
      The central physiologic principles are that clinically important deficiency is more likely to occur (and progress) when intrinsic factor-driven absorption fails than when diet is poor and that most causes take years to produce clinically obvious deficiency.
      Transient defects have little clinical impact.
      The key management principle is the importance of follow-up, which also requires knowing how the deficiency arose.
      The virtues of these principles are not always fully appreciated.
      Recent developments have made diagnosis and management more difficult by diminishing the ability to determine cobalamin absorption status.
      Clinicians must also grapple with premature medicalization of isolated, mild biochemical changes that added many asymptomatic cases of still undetermined medical relevance to their caseload, often expanded by inflated cobalamin level criteria.
      The potential for misattribution of cobalamin-unrelated presentations to nongermane cobalamin and metabolite abnormalities has grown.
      Pathophysiologically based management requires systematic attention to each of its individual components : correctly diagnosing cobalamin deficiency, reversing it, defining its underlying cause, preventing relapse, managing the underlying disorder and its complications and educating the patient.
      Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/18606874?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Disco
      veryPanel.Pubmed_Discovery_PMC&linkpos=3&log$=citedinpmcarticles&logdbfrom=pub
      med
      Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome
      Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CG. Scand - J Rheumatol. 1997;26(4):301-7
      Cfr. : http://lib.bioinfo.pl/pmid:9310111
    4. ME, daar doen we iets aan ! - Multi dimensionele behandeling bij elf patienten met chronische moeheid en het chronisch vermoeidheidssyndroom
      Th.J. Wijlhuizen, M. Hamerslag (e-mail : TIVAT@worldaccess.nl -) - ME/CVS Documentatiecentrum - Bron : Arts & Bedrijf, 1997/6/7
      Myalgische Encephalitis (afgekort 'ME') of correcter, het chronisch vermoeidheidssyndroom ('CVS' – cfr. :
      http://www.gezondheid.be/INDEX.cfm?fuseaction=art&art_id=57 -) .../... staat de laatste jaren volop in de belangstelling.
      Hoewel het syndroom onder andere door de WHO is erkend, stuiten veel patienten in het dagelijks leven en in het contact met allerlei instanties nog op veel onbegrip rond deze aandoening.
      Omdat voor CVS nog geen aantoonbare lichamelijke oorzaak is gevonden wordt patienten dikwijls voorgehouden dat het allemaal tussen de oren zit .../...
      We staan nog maar aan het begin van een lang proces van onderzoek naar de oorzaken en behandeling van CVS .../...
      In dit artikel presenteren we een behandelmethode waarmee we een bijdrage willen leveren aan het onderzoek naar do oorzaken van en mogelijke oplossing voor CVS .../...
      B12-suppletie
      Vitamine-B12-suppletie in de vorm van intramusculaire injecties wordt in Nederland vooral toegepast ter behandeling pernicieuze anaemie.
      Oorzaken hiervan kunnen zijn : hypo-en achloorhydie, intrinsic-factor-deficientie, bacteriele overgroei en parasitaire infecties, ziekten of resectie van het distale ileum en een enkele keer voedingsdeficientie bij veganisten.
      Door een opnametekort ontstaat een te lage bloedspiegel van vitamine B12.
      Uit onderzoeken blijkt dat een tekort aan vitamine B12, ondanks een (laag) normale bloedspiegel, geruime tijd kan bestaan zonder anaemie en neurologische verschijnselen.
      Waarschijnlijk is het beter vitamine B12 op celniveau te meten.
      Twee nieuwe bloedparameters, het plasma homocysteine- en het methylmalonzuurgehalte, geven een beter beeld van de functionele vitamine-B12-status.
      Vitamine B12 is noodzakelijk voor enzymen die deze twee metabolieten omzetten.
      Het heeft er overigens alle schijn van dat hoge spiegels van genoemde metabolieten het risico op hart- en vaatziekten significant verhogen.
      Bij een normale B12-spiegel en verhoging van plasmagehaltes van deze metabolieten, is sprake van een functioneel tekort.
      Een B12-tekort kan dus zelfs bestaan bij een normaal serum-cobalamine, normaal Hb en MCV.
      Meestal zit de B12-spiegel dan in de laag-normale rangen (150-300 mcg/L).
      De neurologische schade die een langere periode van B12-tekort teweeg kan brengen, kan dus optreden zonder de klassieke haematologische afwijkingen die hieraan worden geacht vooraf te gaan.
      Ook kunnen hierbij allerlei neuropsychologische stoornissen zijn.
      Vitamine B12-tekort kan overigens zelfs samen gaan met een normaal resultaat van de Schilling-test.
      Hypothese ten aanzien van de werking van vitamine B12 bij CVS-patienten
      In orthomeleculaire kringen en bij topsporters is het al geruime tijd bekend dat vitamine B12 het herstel van vermoeidheid en overbelasting kan bevorderen.
      Volgens informatie van de fabrikant wordt door artsen in Belgie B12 regelmatig voorgeschreven bij pijn-klachten en vermoeidheid, in hogere doses dan wij gewend zijn. (tot 5000 microgram i.m. per twee dagen).
      In tegenstelling tot sommige andere vitamines zijn er geen schadelijke bijwerkingen van een hoge dosis bekend.
      Vitamine B12 is wel toegepast bij CVS-patienten, in de relatief lage doses die men in Nederland gewoon is (oplaaddoses van drie tot zes maal 1000 microgram en daarna een onderhoudsdosering van 1000 microgram per maand).
      Mogelijk is dit voortgekomen uit het gebruik van zogenaamde lever-injecties uit de tijd dat het mechanisme van pernicieuze anaemie en vermoeidheid nog niet opgehelderd is.
      Voor dit alternatieve gebruik van een regulier geneesmiddel is vooralsnog geen rationeel bewijs.
      Bij 1000 microgram i.m. injecties wordt door CVS-patienten wel vaak een geringe verlichting van de klachten ervaren.
      De mogelijke werkingen van hoge dosis vitamine B12 zijn
      1. Een metabole werking, namelijk het faciliteren van biochemische reacties voor de omzetting van methylmalonzuur en homocysteine in andere, minder schadelijke stoffen.
      2. Een overschot aan vitamine B12, dat snel via de urine wordt uitgescheiden, bindt de schadelijke stof X, die daarmee uit het lichaam wordt verwijderd.
      3. Moleculen die zich hechten op receptoren van zenuwbanen die daardoor (onterechte) sensaties van pijn en vermoeidheid doorgeven, kunnen daarvan worden verdreven door hoge doses B12.
      4. Hoge dosis vitamine B12 beinvloedt een te lage intracellulaire B 12-spiegel gunstiger dan een lage dosis.
      .../...
      Cfr. :
      http://www.me-cvs.nl/index.php?pageid=825&printlink=true&highlight=borreliose
    5. Myalgic encephalomyelitis – Letter
      Simpson LO - J R Soc Med 1991;84:633
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1295578/pdf/jrsocmed00119-0075a.pdf
    6. Oral cyanocobalamin supplementation in older people with vitamin B12 deficiency - A dose-finding trial
      Simone J. P. M. Eussen, MSc; Lisette C. P. G. M. de Groot, PhD; Robert Clarke, MD; Jörn Schneede, MD; Per M. Ueland, MD; Willibrord H. L. Hoefnagels, MD, PhD; Wija A. van Staveren, PhD - Author affiliations : Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands (Ms Eussen and Drs de Groot and van Staveren); Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford, England (Dr Clark); LOCUS of Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway (Drs Schneede and Ueland); and Department of Geriatrics, Hospital St Radboud, Nijmegen, the Netherlands (Dr Hoefnagels) - Arch Intern Med. 2005;165:1167-1172
      Background - Supplementation with high doses of oral cobalamin is as effective as cobalamin administered by intramuscular injection to correct plasma markers of vitamin B12 deficiency, but the effects of lower oral doses of cobalamin on such markers are uncertain.
      Methods - We conducted a randomized, parallel-group, double-blind, dose-finding trial to determine the lowest oral dose of cyanocobalamin required to normalize biochemical markers of vitamin B12 deficiency in older people with mild vitamin B12 deficiency, defined as a serum vitamin B12 level of 100 to 300 pmol/L (135-406 pg/mL) and a methylmalonic acid level of 0.26 µmol/L or greater.
      We assessed the effects of daily oral doses of 2.5, 100, 250, 500 and 1000 µg of cyanocobalamin administered for 16 weeks on biochemical markers of vitamin B12 deficiency in 120 people.
      The main outcome measure was the dose of oral cyanocobalamin that produced 80% to 90% of the estimated maximal reduction in the plasma methylmalonic acid concentration.
      Results - Supplementation with cyanocobalamin in daily oral doses of 2.5, 100, 250, 500 and 1000 µg was associated with mean reductions in plasma methylmalonic acid concentrations of 16%, 16%, 23%, 33% and 33%, respectively.
      Daily doses of 647 to 1032 µg of cyanocobalamin were associated with 80% to 90% of the estimated maximum reduction in the plasma methylmalonic acid concentration.
      Conclusion - The lowest dose of oral cyanocobalamin required to normalize mild vitamin B12 deficiency is more than 200 times greater than the recommended dietary allowance, which is approximately 3 µg daily.
      Cfr. : http://archinte.ama-assn.org/cgi/content/abstract/165/10/1167

    7. Stichting B12 Tekort
      Stichting B12 Tekort is een organisatie die opkomt voor de belangen van mensen met een opnamestoornis van vitamine B12.
      Dit doet zij onder meer door het geven van voorlichting, het bieden van ondersteuning, het organiseren van bijeenkomsten en het bevorderen van lotgenotencontact.
      Op deze website treft u informatie aan die voor u van belang kan zijn, zoals :
      - welke klachten horen bij een tekort aan vitamine B12 ?
      - welke onderzoeken kunnen gedaan worden om de diagnose te stellen ?
      - hoe kan het behandeld worden ?
      - wat kan er in verband met vitamine B12 nog meer belangrijk zijn ?
      Verder kunt u (links naar) wetenschappelijke artikelen vinden over een tekort aan vitamine B12 en alles wat daar mee te maken heeft.
      Dit overzicht wordt voortdurend bijgewerkt.
      Cfr. :
      http://www.stichtingb12tekort.nl/index.html

    8. Studies of biomarker responses to intervention with vitamin B-12 - A systematic review of randomized controlled trials
      Hoey L, Strain JJ, McNulty H, Northern Ireland Centre for Food and Health, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, United Kingdom : l.hoey@ulster.ac.uk - Am J Clin Nutr. 2009 Jun;89(6):1981S-1996S. Epub 2009 Apr 29 - PMID: 19403638
      Background - Mild vitamin B-12 deficiency is common among older adults, but evidence for setting dietary recommendations is limited because most studies have administered vitamin B-12 via nonoral routes or at doses several hundred times higher than current recommendations.
      Furthermore, different biomarkers of vitamin B-12 status have not been systematically reviewed.
      Objective
      - The aim was to assess the effectiveness of biomarkers of vitamin B-12 status through a systematic review of published randomized controlled trials of oral vitamin B-12 supplementation.
      Design
      - Methods included a structured search strategy on Ovid MEDLINE, EMBASE (Ovid) and Cochrane databases; formal inclusion and exclusion criteria; data extraction; validity assessment; and meta-analysis.
      Results
      - Eight randomized controlled trials were included and all studies measured serum and plasma total vitamin B-12, 3 studies measured methylmalonic acid and 6 studies measured total homocysteine response.
      All 3 biomarkers were found to be effective measures of altered vitamin B-12 intake in populations with low and borderline baseline vitamin B-12 status (P < 0.00001); however, in the case of total vitamin B-12, substantial heterogeneity that could not be fully explained by subgroup analysis was observed.
      Insufficient data were available to determine the effectiveness of plasma holotranscobalamin, which was measured in only one randomized controlled trial.
      Conclusions
      - The available evidence suggests that plasma and serum concentrations of total vitamin B-12, methylmalonic acid and total homocysteine are all effective biomarkers of a change in vitamin B-12 intake; however, because the available data were limited, it was not possible to examine fully the factors that could explain the substantial heterogeneity in total vitamin B-12.
      Future trials should include low-dose vitamin B-12 in adults across the entire age spectrum and measure the holotranscobalamin response to supplementation.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/19403638?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Disco
      veryPanel.Pubmed_Discovery_RA&linkpos=4&log$=relatedreviews&logdbfrom=pubmed

    9. The rationale for using high-dose cobalamine
      Lapp CW, Cheney PR - The CFIDS Chronicle Physicians' Forum Fall 1993;19-20
      Cfr. :
      http://www.afme.org.uk/res/img/resources/To%20B12%20or%20not%20to%20B12.txt

    10. Vitamine B12 - Een eenvoudige oplossing
      Is het voor vegetariërs niet moeilijk om voldoende B12 te krijgen ?
      Voeding & Gezondheid, 10/12/98 – Bron : Physicians Committee for Responsible Medicine, U.S.A

      Cfr. : http://users.telenet.be/myprojects/gezondevoeding/voeding/b12.html

    11. Vitamine B12 & een B12 tekort
      Een Gezond Diëet, 19-11-2006
      Volgens Deense onderzoekers zou een tekort aan vitamine B12, ook wel cobalamines genaamd, meer voorkomen dan we denken, vooral bij senioren.
      Vandaar hun voorstel om de aanbevolen dagelijkse hoeveelheid (ADH) te verhogen .../...
      Cfr. :
      http://gezonddieet.skynetblogs.be/post/3890785/vitamine-b12--een-b12-tekort

    12. Vitamine B12 en de relatie met CVS/FM
      Fibromyalgie, 17-12-2007
      Cfr.
      www.jules.be

    13. Vitamine B12 en ouderen
      Stichting B12 Tekort
      Cfr. :
      http://www.stichtingb12tekort.nl/ouderen.htm

    14. Vitamine B12 en veganisme
      Vita Casa plus
      Cfr. : http://www.vitacasa.be/Vit_B12.htm

    15. Vitamine B12 en veganisme – Een literatuurstudie
      Michèl Post - Uitgeverij Den Giraffe, Utrecht 1993 - ISBN: 90-801275-1-5
      Cfr. :
      -
      http://home.hccnet.nl/michel.post/b12voorveganisten/b12voorveganisten.html
      - http://home.hccnet.nl/michel.post/B12/

    16. Vitamine B12 of cobalamine
      Voedingscentrum, 08-08-2008
      Cfr. :
      http://www.voedingscentrum.nl/nl/eten-gezondheid/voedingstoffen/vitamines-en-mineralen/vitamine-b12-of-cobalamine.aspx

    17. Vitamine B12 tekort
      Santé,
      Cfr. :
      http://www.santeonline.nl/medisch-dossier/?titel=Vitamine--B12--tekort

    18. Vitamine B12-tekort bij ouderen
      R.S.v. 55 + - Bron : http://www.voedingscentrum.nl/
      De Wageningen Universiteit plaatste onlangs een advertentie met de boodschap dat ouderen baat kunnen hebben bij grote hoeveelheden vitamine B12.
      Deze stelling geldt nadrukkelijk alleen voor ouderen met maagaandoeningen die de opname van vitamine B12 beperken of belemmeren.
      Alleen in die gevallen is, in overleg met de arts, extra vitamine B12 nodig.
      Ouderen die extra vitamines willen nemen, kunnen een multivitaminesupplement gebruiken met niet meer dan de Aanbevolen Dagelijkse Hoeveelheid (ADH).
      Bij ouderen kan er sprake zijn van een gestoorde aanmaak of werking van de zogenaamde Intrinsic Factor (IF) in het maagdarmkanaal.
      Door deze aandoening kan het lichaam vrijwel geen (minder dan 1%) vitamine B12 meer opnemen.
      Deze zeldzame aandoening komt bij ongeveer 1 tot 2 op de 1000 personen voor.
      Zij moeten hiervoor worden behandeld door een arts.
      Verminderde opname
      Bij een veel grotere groep ouderen, naar schatting 20-25%, wordt wel voldoende Intrinsic Factor geproduceerd, maar de vitamine B12 minder goed opgenomen uit de voeding.
      Dit is mogelijk een gevolg van maagdarminfecties en/of maagaandoeningen met een verminderde maagzuurproductie.
      Omdat het lichaam eerst de vitamine B12-voorraad in de lever gebruikt, leidt de verminderde opname pas na lange tijd tot een vitamine B12-tekort.
      Vitamine B-12 uit supplementen, ook normale doseringen van eenmaal de Aanbevolen Dagelijkse Hoeveelheid, wordt wel goed opgenomen door het lichaam.
      Klachten bij een tekort
      Alleen de arts kan vaststellen of er sprake is van een vitamine B12-tekort.
      Een chronisch tekort aan vitamine B12 leidt uiteindelijk tot een vorm van bloedarmoede.
      Ook neurologische gevolgen zoals tintelingen in de vingers, geheugenverlies, coördinatiestoornissen en spierzwakte in de benen kunnen het gevolg zijn.
      Soms is er bij deze klachten geen sprake van afwijkingen in het bloedbeeld.
      Vitamine B12 en ouderdomsverschijnselen
      Er zijn aanwijzingen dat lage vitamine B12-gehaltes in het bloed leiden tot depressiviteit, vergeetachtigheid en dementie.
      Toch is hiervoor nog onvoldoende bewijs.
      Ook de beschermende werking van het slikken van extra vitamine B12 tegen dit soort ouderdomsverschijnselen is nog onvoldoende aangetoond.
      Het Voedingscentrum adviseert ouderen daarom niet op eigen houtje hoge doseringen vitamine B12 te gebruiken.
      Er is geen bezwaar tegen het gebruik van een multivitaminesupplement met niet meer dan de Aanbevolen Dagelijkse Hoeveelheid.
      Ga met klachten altijd eerst naar de (huis)arts.
      Cfr. :
      http://www.rsv55plus.nl/?Algemeen_Nieuws:Vitamine_B12-tekort_bij_ouderen

    19. Vitamine B12-tekort onderschat
      Arend van Wijngaarden - De Gelderlander, 12-09-2007 (laatst bijgewerkt : 05-10-2009)
      Cfr. :
      http://www.gelderlander.nl/algemeen/gezondheid/article1871560.ece


    23-11-2009 om 00:51 geschreven door Jules

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    Tags:adenosylcobalamine, ataxie, bloedarmoede, cobalamine, CVS, cyanocobalamine, extrinsic factor, foliumzuur, geheugen, homocysteïne, hydrocycobalamine, ileum, maagsap, methylcobalamine, methylmalonzuur, moe, myeline, pernicieuze anemie, vis, vlees
    >> Reageer (1)
    22-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The Guaifenesin Story
    Klik op de afbeelding om de link te volgen




     





    The Guifenesin Protocol
    for
    fibromyalgia patients





    The Guaifenesin Story

    A centuries-old bark extract used for clearing the airways
    Now key to a popular FM symptom-reversal protocol

    ProHealth, Inc., November 20, 2009

    Guaifenesin is a substance that helps loosen and liquefy mucus and as such is a common component of many nonprescription cold and cough remedies (cfr. : http://en.wikipedia.org/wiki/Guaifenesin -).
    It is derived from a tree bark extract called guaiacum (cfr. :
    http://www.botanical.com/botanical/mgmh/g/guaiac42.html -), historically appreciated for its expectorant qualities in the Caribbean region and adopted by European explorers in the 1500’s.

    Guaiacum was approved for use as an expectorant by the Food and Drug Administration some 400 years later, in 1952.
    And 20 years ago the extract was synthesized, pressed into tablets and named 'guaifenesin'.

    How Does Guaifenesin Work ?

    Guaifenesin works by drawing water into the bronchi – the air passages branching into our lungs.
    The released water both thins the mucus and lubricates the airway, facilitating the removal of cold, flu and allergy- associated mucus from the chest by coughing and making it easier to breathe.

    Guaifenesin is also considered helpful for thinning postnasal drainage from the sinuses and reducing nasal congestion (cfr. : 'The Guaifenesin Story - A centuries-old bark extract used for clearing the airways – Now key to a popular FM symptom-reversal protocol' at : http://www.prohealth.com/library/showarticle.cfm?libid=12081 -) and so may relieve sinus pressure/ headache.
    As Dr. Sarah Myhill comments : “
    Whoever designed the human body needs a black mark for putting in sinuses ! They are cavities in the bones of the face with only one entry and exit hole which is easily blocked by catarrh or swollen mucus membranes”.
    When this occurs, less oxygen can enter the sinuses, promoting bacterial overgrowth and causing sinusitis.

    Here again, guaifenesin can help to relieve congestion by increasing the clearance of secretions, helping with the mucus membrane’s natural job of washing away invading viruses, bacteria, pollen and other potential allergens – “the first level of immune defense”.

    Guai also enjoys a popular reputation as ‘the opera singer’s friend'.
    Terming it their ‘wonder drug’ singers have traditionally used guaifenesin to improve the state of their vocal folds in extremes of humidity (very dry or very humid), after flying long distances and during mild allergies, for its ability to promote ‘secondary mucosal secretion’ – the thinner, lubricating mucus that occurs on the vocal folds naturally when they are healthy and well hydrated.

    Patients with chronic obstructive pulmonary disease (COPD) may find guaifenesin’s thinning and lubricating action helpful at times when they experience particular difficulty coughing up the thick or sticky mucus that can block their damaged airways.

    Similarly, guaifenesin can assist by thinning ‘sticky’ mucus to help expel inhaled particles that can exacerbate asthma symptoms.

    Importantly, whether used to ease the congestion of colds, flu or rhinosinusitis or to support healthy vocal folds, guaifenesin works best if one drinks plenty of water, as extra fluids increase the flow of water and mucus.

    As with many complex herbal compounds used in traditional medicine, exactly how guaifenesin encourages healthy mucus flow is not yet completely understood.
    But based on its long history - if taken as instructed on the package or as suggested by a pharmacist or healthcare provider - guai has at most minor side effects and is generally considered safe for use even by youngsters over 12 years of age.

    What is the Guifenesin Protocol for fibromyalgia patients ?

    Guaifenesin is also used in the very popular 'Guaifenesin Protocol for symptoms of Fibromyalgia' conceived by R. Paul St. Amand, MD, Assistant Clinical Professor of Medicine in Endocrinology at UCLA (cfr. : http://www.chronicfatiguerelapse.com/guaifenesin_protocol_by_dr._st._amand.html -).

    Though highly demanding and still considered experimental, the Protocol has been adopted by many FM patients - cfr. : http://www.fibromyalgiatreatment.com/GuaiProtocol.htm -, owing to widespread anecdotal descriptions of quality-of-life benefits.

    Nevertheless, note that Guaifenesin has not been approved by the FDA for this application and should be used as such only with the approval and supervision of a medical doctor familiar with the patient and Protocol.

    What is the Protocol’s underlying theory ?

    Dr. St. Amand explains this in his book written with Claudia Marek : 'What Your Doctor May Not Tell You About Fibromyalgia' and their article on Fibromyalgia symptoms, diagnosis and the Guaifenesin Protocol.

    The theory is that :

    • Excess inorganic phosphate compounds accumulate within the cells of some people rather than being excreted normally, possibly owing to a genetic defect involving a missing enzyme or kidney dysfunction.
    • It is known that excess phosphate in the cells’ mitochondria impedes their formation of adenosine triphosphate (ATP), the body’s energy source - and that muscle pain after exercise is linked with an inorganic phosphate increase.
      Also, researchers have reported a 20 percent average reduction in the level of ATP in muscle biopsies taken from people with FM, notes self-described Guaifenesin Protocol beneficiary Devin Starlanyl in her book : 'Fibromyalgia and Chronic Myofascial Pain: A Survival Manual
      '.
    • When excess phosphate builds up in the cells, excess calcium – the main buffer for phosphate – builds up too.
      Excess calcium in the cells tends to stiffen the body’s tissues.
    • A method of palpating muscles, tendons and ligaments that Dr. St. Amand has described allows a physician to “map” or assess the extent of lesions in the tissues of FM patients, thought to be “contracted cells forming a spastic area caused by an excess of calcium”.
    • A carefully planned, monitored regime of guaifenesin extract supplementation may help the body eliminate the excess calcium and phosphate compounds, supporting improvement of FM symptoms over time in some individuals.

    Dr. St. Amand has reported increases of 60 percent in phosphate excretion and 30 percent in calcium excretion.

    What does the Guaifenesin Protocol involve ?

    Basically, it includes :

    • Adjusting or “titrating” the guaifenesin dosage to the individual’s needs, based on response over time.
    • Strict avoidance of the salicylates in aspirin and other similar pain-relief products, plus a long list of personal care products including plant derivatives such as aloe or mint that are applied to and absorbed through the skin; and many plant extracts taken by mouth.
      These can completely block the action of the guaifenesin.
      Salicylate-containing foods are not a problem, as the digestive process neutralizes their effect.
    • And strict adherence to a low carbohydrate diet, if the individual is hypoglycemic.

    The Protocol also commonly delivers a significant physical impact in the early weeks, including a worsening of the individual’s worst FM symptoms and frequently headaches, burning on urination and/or strong-smelling perspiration and urine.
    These are not considered side effects, but rather “the signs and symptoms of the toxins and wastes being released by the guaifenesin” - and therefore an indication that the Protocol is working.

    So far the Guaifenesin Protocol has not been demonstrated effective in a controlled clinical trial or approved by the FDA for support of Fibromyalgia symptoms.
    An early one-year trial completed at the University of Oregon in June 1995 by Dr. Robert Bennett concluded that “patients in the placebo group compared with patients in the guaifenesin group appeared to improve equally, a finding that suggested a placebo effect
    ,” says Dr. St. Amand.
    But “it is our belief that this study was flawed, due to our own lack of knowledge,” he explains.

    Though Dr. Bennett’s patients were warned to avoid aspirin and aspirin-containing compounds, it wasn’t until after the study was completed that Dr. St. Amand came to understand the immense number of personal products and ingested plant extracts that, even in minute quantities, could reverse patients’ progress.
    Also, in reviewing the patients’ wellness questionnaires, he noted that the study had not screened for hypoglycemic individuals, who therefore were not treated with the necessary diet.
    As a result, he contends, “the study was doomed for lack of knowledge of these pitfalls”.

    What is the status of research ?

    Currently, one of the stated goals of Dr. St. Amand’s not-for-profit Fibromyalgia Treatment Center is to provide supporting research for the Guaifenesin Protocol.

    He is now engaged in a three-year investigation with The City of Hope that involves a cohort of his FM patients (an "Immunological and Genetic Analysis of Autoinflammatory Genes in Fibromyalgia").
    By mid-2008 the research had identified abnormal elevations in a cluster of inflammatory cytokines that appear highly predictive of Fibromyalgia, two of which drop to normal in patients taking guaifenesin (cfr. 'Dr. St. Amand Comments on First Report from City of Hope Fibromyalgia Research
    ' at : http://www.prohealth.com/library/showarticle.cfm?id=8940&t=CFIDS_FM -.
    And in November 2008 Dr. St. Amand issued a call to patients he has diagnosed with FM, to widen the sample of DNA used in the investigation.

    In the meantime, the scores of physicians who employ the Guaifenesin Protocol – as well as many of the individuals, like Devin Starlanyl, who have adopted it – provide personal testimonials indicating that this regime supported significant improvements in their Fibromyalgia symptoms.

    Cfr. : http://www.prohealth.com/library/showarticle.cfm?libid=12081


    22-11-2009 om 23:01 geschreven door Jules

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    Tags:adenosine triphosphate (ATP), allergy, asthma, bacteria, chronic obstructive pulmonary disease (COPD), cold, congestion, fibromyalgia, flu, FM, guaiacum, guaifenesin, Guifenesin Protocol, headache, muscle pain, Rhinosinusitis, sinus, sinusitis, viruses
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.A virus linked to chronic fatigue syndrome - Dr. Nancy Klimas interviews
    Klik op de afbeelding om de link te volgen






























     


     

    A virus linked to chronic fatigue syndrome

    The New York Times, October 15, 2009

    Denise Grady, a science writer for The New York Times, recently explored the link between a recently discovered virus called XMRV and chronic fatigue syndrome, in “Is a Virus the Cause of Fatigue Syndrome ?” (cfr. : http://www.nytimes.com/2009/10/13/health/13fatigue.html?_r=1&ref=health -).
    On the Consults blog, scientists and doctors from the International Association for Chronic Fatigue Syndrome, a society of 500 biomedical and behavioral professionals, took readers’ questions on chronic fatigue syndrome.

    Here, Dr. Nancy G. Klimas, who serves on the board of directors of the organization, answers questions on the recently discovered retrovirus and clinical care of chronic fatigue syndrome.
    Dr. Klimas is a director of the department of immunology of the University of Miami School of Medicine and director of research for clinical AIDS/H.I.V. research at the Miami Veterans Affairs Medical Center. Also read Fred Friedberg’s responses to behavior-related questions in “Behavioral Treatments for Chronic Fatigue Syndrome” (cfr. :
    http://consults.blogs.nytimes.com/2009/10/13/behavioral-treatments-for-chronic-fatigue-syndrome/ -).


    Is chronic fatigue syndrome contagious ?

    I’ve had C.F.I.D.S. for 25 years.
    If it is a virus, is it contagious ?
    How is it transmitted ?
    Now I worry about passing it on to others.
    Thank you.
    Nona

    Dr. Klimas responds :

    In general, retroviruses are not spread by air or droplet but are transmitted sexually, vertically (mother to fetus) and by blood transfusion.
    From what we have learned about other retroviruses, it is clear that the amount of virus matters and people with low amounts of circulating virus are not as infectious as people with high levels of virus in the blood.
    With XMRV, the retrovirus recently found in many patients with chronic fatigue syndrome, we do not have enough information to judge how infectious it might be.

    Whenever the possibility of sexual transmission comes up, people worry that they are in some way responsible for infecting sexual partners.
    While this is possible, it is important to remember that many infections can come from exposures between great-great-grandparents and maintained for generations as latent infections or as infections from early experiences of any sexual partner in a chain of partners.
    We know that it is very unusual for both partners to develop chronic fatigue syndrome or C.F.S. And while mother-to-child C.F.S. can happen, it is unusual.

    It is clear that there are a number of factors that increase the risk for C.F.S. : genetics, immune function, severity of inciting infection — to name a few.
    Just being exposed to or even infected with, a virus does not mean that a person will become ill.
    We don’t even know if infection with the XMRV virus actually causes illness or if it one of several associated reactivated viruses (like HHV-6, EBV and enterovirus).

    It important not to take these new findings about the XMRV virus as anything more than an exciting new development.
    We need confirmatory studies, then studies to see if the virus is contributing to the cause of illness persistence and symptoms.
    The good news is that if XMRV is linked to C.F.S., there are many antiviral drugs that have already been safety tested in H.I.V. that may inhibit viral replication.
    So those studies could be designed very rapidly


    Is there a blood test for the C.F.S. virus ?

    Is there a specific test, blood or other, to determine whether a person is infected with the XMRV virus ?
    Beau Brincefield

    Dr. Klimas responds :

    The test for XMRV that has been reported is currently used only in research settings.
    The research director of the Whittemore Peterson Institute, which was involved in the recent findings, was quoted as saying they were developing a commercial assay that they expected to be available “within weeks”.
    Several other commercial laboratories are also developing assays.

    Some important points :
    First, antibody tests mean you have been exposed to a virus and do not tell you actually have an active infection.
    Second, a technique known as P.C.R. assays measures something called “viral load” and the assay is designed to measure either active replicating virus or latent (inactive) virus.
    Either measure would be helpful with this new virus, but we don’t have access to them except in research settings.

    Another way to see if you are infected is with viral cultures.
    The recent study published in Science used both cultures and P.C.R. Assays.


    Exercise and chronic fatigue syndrome

    I used to be very active and used to love playing sports.
    Then I was hit with some sort of infection.
    Eventually, after going to different doctors and health professionals, I was finally diagnosed with C.F.S.

    I’m finding it easier to cope now.
    I try to have rest periods during the day.
    I would love to play sports again, but I just so feel so ill after I try and my muscles feel so sore.
    Have you any advice ?
    Should I push through and go back to playing sports ?
    I’m finding it tough enough as it is keeping up with college and the normal walking you have to do.
    I don’t want to drop out of college.
    Pat.

    Dr. Klimas responds :

    Most C.F.S. patients do better if they break up their exercise into short segments, take brief rest periods and then try again.
    Certainly pushing through can cause “crashes” and relapses that can last days, even weeks.
    So I tell my patients the five-minute rule : five minutes of exercise, then five minutes lying flat, then five more minutes — increasing their exercise by five-minute increments.

    If you can already tolerate more exercise than this, then try going that far, taking a break, then trying another round.
    Also, C.F.S. patients tolerate flexibility and resistance exercise (stretching and weight training) better than aerobics.
    Because C.F.S. patients are prone to blood pressure drops while exercising, they usually tolerate aerobic training best while in a flat position — swimming, recumbent bicycling, that sort of thing.


    Can I volunteer for a study ?

    I’d like to second Post No. 25 and ask when and how one could volunteer to be part of a drug trial ?
    Please help us.
    Sally.

    Dr. Klimas responds :

    There are drug trials and other studies under way all around the United States and the globe looking at this illness and its possible treatments.
    Investigators at the Whittemore Peterson Institute and elsewhere are already planning antiviral trails based on this exciting research development.
    I would watch three Web sites in particular — the International Association for CFS/ME -
    http://www.iacfsme.org/ -, the CFIDS Association of America - http://www.cfids.org/ - and the Whittemore Peterson Institute for Neuro-Immune Disease - http://www.wpinstitute.org/ - for more developments.


    Was a C.F.S. virus discovered years ago ?

    Back in the early 1990s, Dr. Elaine DeFreitas at the Wistar Institute in Philadelphia discovered a novel human retrovirus (very closely related to HTLV 2, with Spuma-viruslike aspects) in C.F.I.D.S. patients.
    This was subsequently confirmed by two other prominent researchers (and a commercial laboratory).

    Dr. DeFreitas was almost done sequencing its genes and published a meticulous paper in a top journal.
    Then the Centers for Disease Control and Prevention and the National Institutes of Health intentionally destroyed her reputation because it did not mesh with their vigorous assertions that C.F.I.D.S. was psychoneurosis.
    No one else has followed this up for fear that their career might likewise be destroyed.
    This was all detailed in the amazing book “Osler’s Web”.

    Is this the same virus as the “novel” XMRV ?
    Justin Reilly.

    Dr. Klimas responds :

    Dr. DeFreitas was doing exciting work and should be congratulated for her early results suggesting retroviral infection in C.F.S.
    Since that time, technology has advanced in a dramatic way, giving investigators new tools to search for viruses that were yet to be identified in 1990-92, including the XMRV virus.

    New antiviral drugs have also been developed that could potentially be effective in controlling this sort of infection.
    We also have a much stronger understanding of these drugs’ toxicity and safe use.

    I congratulate the Whittemore Peterson Institute researchers for their diligent work.
    I am also very happy for Elaine today.
    I would also ask patients to be patient a little bit longer so that researchers can devise and perform the sort of clinical trials that will let us know if this virus is the linchpin in continued illness.


    Links between H.I.V. and XRMV ?

    I found the comparison to H.I.V. (all because it happens to be another retrovirus) to be alarmist, unnecessary and at worst, the kind of sensualist factoid reporting that’s more typical of a tabloid !
    From what I gather... the link between the two is weak and general at best.

    What angers me is that the comparison to H.I.V. is completely out of context; there are many retroviruses that are not known to cause any pathologies at all – comparing it to the one that is most well known and feared is simplistic and quite simply wrong.
    We should not forget that retroviruses have been common through out human history and while some do not cause disease at all, most are nowhere near as extreme as H.I.V.

    To compare the virus to H.I.V. is to create undue alarm and suffering to people who are already dealing with a difficult disease.
    Not only is the comparison useless outside its context, it does nothing to provide useful information to the reader.

    I ask that you think of the moral consequences of your sloppy comparison — the horror and anguish of those that might have thought that it might be as debilitating as H.I.V., as well as the dread of the thought of potentially passing it on to another person.
    David.

    Dr. Klimas responds :

    You make a good point.
    This is one study, the results needs to be validated, then the next study will look at treatment options.
    And you are right, some retroviruses are seemingly benign, whereas others are pathogens.

    But I hope you are not saying that C.F.S. patients are not as ill as H.I.V. patients.
    My H.I.V. patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested.
    Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families.

    I split my clinical time between the two illnesses and I can tell you if I had to choose between the two illnesses (in 2009) I would rather have H.I.V.
    But C.F.S., which impacts a million people in the United States alone, has had a small fraction of the research dollars directed towards it.

    Despite these limitations, there has been considerable effort to understand the cause and develop effective treatments.
    The Whittemore Peterson Institute should be congratulated for its outstanding work, performed in a brand new center paid for with private donations, state money and N.I.H. collaboration.
    Creative research and creative financing !


    Is sleep a factor in chronic fatigue syndrome ?

    Do you think sleep could be a factor in C.F.S. ?
    Have you heard of Xyrem being used to facilitate Stage 4, deep sleep ?
    Most everyone with fibro and/or C.F.S. report of not being able to sleep deeply — to have restorative sleep.
    We are all anxiously waiting for help in this lifetime.
    So many years have been lost to these illnesses.
    Abot Bensussen.

    Dr. Klimas responds :

    There is a clinical trial under way to study the effects of Xyrem, a medication used to treat sleep disorders like narcolepsy, in fibromyalgia.
    Certainly, getting restorative sleep is a good thing and slow wave sleep is key to restorative sleep.
    A sleep expert can help with this part of treatment, but it is important to have a sleep study done before considering any sleep inducers.

    In a study by my group, we found that about half of C.F.S. patients develop some level of sleep apnea over time, a treatable condition that could be worsened with some sleep medications.


    Cfr. : http://consults.blogs.nytimes.com/2009/10/15/readers-ask-a-virus-linked-to-chronic-fatigue-syndrome/



     
    Watch a Dr. Nancy Klimas interview at :
     
    http://www.youtube.com/watch?v=5ftbsOkYVxE&feature=autofb


    22-11-2009 om 12:57 geschreven door Jules

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    Tags:C.F.S., behavioral treatments, chronic fatigue syndrome, contagious, enterovirus, exercise, fibromyalgia, genetics, immune function, infectious, narcolepsy, restorative sleep, retroviral infection, retroviruses, sleep apnea, sleep, viral load, virus, XMRV
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Don't wait for a cure to appear
    Klik op de afbeelding om de link te volgen















     












       Get on with the hard work of healing yourself !

         
    Don't wait for a cure to appear

    'As someone with chronic fatigue syndrome, I had to change my life to get relief'

    Zachary Sklar, former executive editor of the Nation magazine and co-author of the screenplay for the film "JFK" – Comments : healthscience@washpost.com - Washington Post, October 27, 2009

    So, maybe we're not all slackers.
    Maybe it's not all in our heads, as many employers, psychiatrists, friends and even family members have implied or thought to themselves over the years.
    Maybe the debilitating set of symptoms known as chronic fatigue immune dysfunction syndrome is a legitimate illness, like pneumonia or tuberculosis.
    And maybe, according to a study published recently in the prestigious journal Science, it's actually caused by a virus.

    Many of the millions of people around the world who suffer from chronic fatigue syndrome welcomed the news of this study.
    Not only might it vindicate us, it also offers hope that a cure is possible, if not imminent.

     
    Zachary Sklar

    But as someone who has lived with the syndrome for 23 years, I remain skeptical that this terrible illness is caused by a single virus, identified as the retrovirus XMRV.
    I have no doubt that XMRV was found in many of the 101 chronic fatigue patients in the study.
    But we've been down this road before.
    In the 1990s another retrovirus was announced with fanfare as the culprit.
    Many were disappointed when subsequent studies could not confirm any link between it and the illness.

    And of course nearly everyone with chronic fatigue has been tested for other viruses that were once thought to be the cause : Epstein-Barr, cytomegalovirus, even HIV.
    Often those viruses are found in the blood of those tested.
    But so far, they have not been proved to be the cause of our illness.

    I am not a scientist, I don't have the skills to evaluate the study and I am aware that researchers were only suggesting that XMRV "may be a contributing factor".
    But based on my own experience, I believe that chronic fatigue syndrome is an environmental illness in the broadest sense : an erosion of the immune system that can be caused by any number of factors, including chemicals in our food, pollution in our air and water, exposure to radiation, the stresses of modern life, unhealthful diet, lack of sleep, excessive use of drugs (prescription and recreational), psychological stresses, overwork and, yes, viruses, too.

    I came down with the illness in 1986, when I was 38 years old.
    It hit me suddenly and felt like a severe flu : trembling, nausea, fever, headache, night sweats, digestive problems.
    It just never went away.
    From the blood tests, it's clear that my immune system was so weakened that it was unable to fight off completely whatever attacked it.

    Why was my immune system compromised ?
    I have my own theories.
    I led an extremely stressful life in New York.
    I ate a lot of fast food, high in sugar and low in organics.
    For six years I missed two nights of sleep every week working at Time and Life magazines.
    I once spent my vacation time picking coffee on a peace brigade in Nicaragua and ended up with intestinal parasites.

    But there's something else.
    I grew up in Los Angeles during the 1950s, when nuclear testing in the atmosphere was still permitted.
    As subsequent studies have made clear, a spree of nuclear tests in Nevada in October 1958, called Operation Hardtack II, spread radiation fallout over the L.A. basin.
    When records of those tests were released to the public years later, Linus Pauling, a two-time Nobel laureate for chemistry and for activism against nuclear testing, predicted that over a period of 30 years, 25,000 cancer deaths would result from one of those blasts alone.
    I was 10 years old in 1958 and I got sick 28 years later.
    I don't know if that radiation contributed to my illness.
    But after reading numerous reports of high cancer rates in areas exposed to nuclear fallout, I'm convinced it didn't help.

    My concern about the latest announcement of a possible viral cause is that many people with chronic fatigue syndrome -- and those who become afflicted in the future -- might be misled into waiting for a pill that will instantly cure them.
    Even if such a drug is eventually marketed, I wonder whether chronic fatigue patients will be able to overcome the illness without changing the way they live.

    In my own case, after a miserable year of being treated by a dozen top New York specialists who prescribed medications that made me feel worse, a friend recommended that I see Shyam Singha, an osteopath and naturopath.

    He was the first to zero in on my poorly functioning digestive system.
    He put me on a cleansing fruit fast, then raw food for a month, then a strict vegetarian diet, no sugar, no alcohol, no caffeine.
    I thought he was insane and protested that I was too weak to try such a radical diet.
    "Do it !" he replied.
    I did and after two days on the fruit fast I started to feel better.

    The most important lesson that Singha taught me was that my cure was largely in my own hands.
    Though he offered guidance and knowledge, I had to take responsibility for changing the habits, the diet, the life patterns that contributed to my getting sick in the first place.

    Over nearly 23 years since then, I have tried many approaches to speed my healing : acupuncture, homeopathy, low doses of doxycycline, thyroid supplements, anti-yeast diets and more.
    I've eliminated much of the clutter and stress in my life.
    I feel far better today at the age of 61 than I did at 38.
    Not all those suffering from chronic fatigue syndrome have been so lucky.

    Obviously, my view about the cause of this syndrome is at odds with the notion that people get the illness simply because they are exposed to a particular virus.
    And my belief that we must actively participate in our own healing is not widely accepted, even among chronic fatigue patients.
    The CFIDS Association of America, the biggest chronic fatigue organization, has been lobbying and raising research funds for many years to find a viral cause and then develop a drug to destroy it -- the polio model.

    I hope the group is right, that one day a virus will be identified and there will be a cure or a vaccine, as there was for polio.
    But despite the study published in Science, I am not convinced that such a cure will be here very soon.
    For now, I will continue to do what's worked for me and many others.
    And I will urge anyone who has this illness not to wait passively for doctors and pills to cure them but instead to change their lives and get on with the hard work of healing themselves.

    Cfr. : http://www.washingtonpost.com/wp-dyn/content/article/2009/10/26/AR2009102602405.html


    22-11-2009 om 00:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 5/5 - (1 Stemmen)
    Tags:alcohol, chronic fatigue syndrome, coffee, diet, digestive problems, environmental illness, fast food, flu, immune system, lack of sleep, nuclear fallout, overwork, retrovirus XMRV, sleep, stress, sugar, vaccine, virus, way of live, XMRV
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Gezonde chocoladeletters van Sinterklaas
    Klik op de afbeelding om de link te volgen




     

    Pure chocolade van Sinterklaas


    Gezonde chocoladeletters van Sinterklaas

    Jan Willem Wensink – Dokterdokter.nl, 18-11-2009 – Bronnen : WebMD, Confectionary News, nutraingrediants, Health and Food

    Sinterklaas geeft jaarlijks 22 miljoen chocoladeletters weg.
    Een goed idee, want met name de pure chocoladeletters zijn gezond.

    Een chocoladelettertje oppeuzelen in sinterklaastijd is helemaal niet zo’n grote zonde als je dacht.
    Sterker nog : het is goed voor je.
    Het lijkt te mooi om waar te zijn, maar onderzoeken bevestigen het keer op keer : chocola is gezond – cfr. 'Pure chacolade – Gezonder dan je denkt' op :
    http://www.dokterdokter.nl/man/eten-drinken/article/24047/pure-chocolade-gezonder-dan-je-denkt - , althans in de pure vorm.
    Nog beter, ook voor anderen, zijn de eerlijke 'groene' chocoladeletters, waarbij cacaoboeren een eerlijke prijs krijgen voor hun product (cfr. 'Met de Groene Oxfam Novib Sint en Hyves tegen foute chocola' :
    http://www.marketingfacts.nl/berichten/20091117_met_de_groene_oxfam_novib_sint_en_hyves_te
    gen_foute_chocola/?utm_source=feedburner&utm_medium=feed
    -).

    Goed voor hart en bloedvaten

    De aanhoudend gunstige conclusies van vele onafhankelijke onderzoeken over pure chocola zijn inmiddels zo indrukwekkend, dat veel voedingswetenschappers erkennen dat pure chocola met een hoog cacaopercentage goed is voor hart en bloedvaten.

    Gezond ?

    Wat is er dan zo gezond aan chocolade ?
    Pure chocolade verlaagt bij regelmatig gebruik het slechte ldl-cholesterol in het bloed (cfr. 'Hoog cholesterol' op :
    http://www.dokterdokter.nl/medisch/folder/view/id/1612/hoog-cholesterol -).
    Chocola vermindert de neiging tot vorming van stolsels in het bloed.
    Dagelijks twee blokjes pure chocolade eten dringt hoge bloeddruk iets terug, doordat het de bloedvaten ontspant (cfr. 'De beste remedie tegen hoge bloeddruk' op :
    http://www.dokterdokter.nl/man/psyche/article/24043/de-beste-remedie-tegen-hoge-bloeddruk -).

    Mineralen en aminozuren

    Chocola levert belangrijke mineralen en essentiële aminozuren.
    Het kan bij diabetespatiënten (cfr. 'Diabetes mellitus type 2' op :
    http://www.dokterdokter.nl/medisch/folder/view/id/1563/diabetes-mellitus-type-2 -)de werking van insuline (cfr. : http://www.dokterdokter.nl/medisch/begrippen/view/id/16482/insuline -) verbeteren.
    Chocola bevat meer anti-oxydanten dan bosbessen of groene thee.
    Het beschermt lichaamscellen en werkt ontstekingsremmend.

    Hersenen

    Er zijn aanwijzingen dat chocola de bloedstroom in de hersenen verbetert en de kans op dementie kan verkleinen.
    Chocola werkt volgens sommige onderzoeken goed tegen hoestklachten en helpt diarree voorkomen.
    Vermoed wordt dat chocola ook een anticarcinogene werking heeft (het beschermt tegen kanker), maar bewijs is daarvoor nog niet geleverd.

    Acné

    Sommige mensen zeggen dat chocola bij hen acné bevordert.
    Recente studies geven daarover geen uitsluitsel.
    Chocola reinigt volgens sommige onderzoekers de huid (cfr. 'Hoe mannen hun huid kunnen verzorgen' op :
    http://www.dokterdokter.nl/man/uiterlijk/article/24145/hoe-mannen-hun-huid-kunnen-verzorgen -).
    Als gevolg daarvan zouden volgens hen tijdelijke acnéklachten kunnen ontstaan.

    Vet

    Wetenschappers waarschuwen bij de publicatie van al dat goede nieuws wél steeds dat chocolade ook suiker (cfr. 'Suiker leidt mogelijk toch tot diabetes' op : http://www.dokterdokter.nl/man/eten-drinken/article/5634/suiker-leidt-mogelijk-toch-tot-diabetes -) en verzadigde en onverzadigde vetten (cfr. 'Omega 3 en omega 6 - Belangrijke vetzuren' op : http://www.dokterdokter.nl/man/eten-drinken/article/24062/omega-3-en-omega-6-belangrijke-vetzuren -) bevat.
    Er zijn overigens aanwijzingen dat de verzadigde vetten in pure chocolade helemaal niet slecht zijn.

    Calorie-inname

    Voordat je gezin zich nu enthousiast op een rijtje chocolaletters stort : hou wel rekening met de totale dagelijkse calorie-inname.
    Pure chocola levert per 100 gram ruim 500 calorieën, een kwart van wat vrouwen dagelijks mogen innemen.

    Melkchocola

    De gezondheidsclaims gelden niet of nauwelijks voor melkchocola en witte chocola, waarvan het cacaogehalte veel lager is.
    Ook in cacaopoeder zitten niet zo veel van de goede stoffen uit de cacaoboon.

    Cfr. : http://www.dokterdokter.nl/man/eten-drinken/article/3822/een-gezonde-chocoladeletter-van-sinterklaas


    22-11-2009 om 00:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 5/5 - (1 Stemmen)
    Tags:acné, aminozuren, anti-oxydanten, bloedvaten, calorieën, chocola, chocolade, cholesterol, cholesterolverlager, dementie, diabetes, diarree, hart en bloedvaten, hart- en vaatziekten, hersenen, hoge bloeddruk, insuline, mineralen, omega 3, omega 6, suiker
    >> Reageer (0)
    21-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Oorzaken van puisten
    Klik op de afbeelding om de link te volgen


























     

    Oorzaken van puisten

    Rhijja Jansen – Dokterdokter.nl, 19-11-2009 – Bronnen : Mieke Laarkamp - Schoonheidsinstituut De Schermer

    Puisten heb je niet alleen als je in de pubertijd zit : veel mensen hebben er ook last van als ze volwassen zijn.
    Kijk snel waar ze door veroorzaakt worden en hoe je ze kunt bestrijden.

    Puisten zijn ontstekingen van de talgklieren.
    Deze talgklieren heb je over je hele lichaam, maar ze komen het meest voor op het hoofd en de T-zone van het gezicht (voorhoofd, neus en kin).
    Deze talgklieren produceren talg, waarmee je huid goed gesmeerd wordt en wat je huid tegen uitdroging beschermt.
    Maar als er vuil van buiten in de talgkliertjes terecht komt, kunnen deze gaan ontsteken.
    Wanneer je huid hiervoor gevoelig is, kunnen er puisten ontstaan.

    Oorzaken puisten

    Veel mensen hebben tijdens de pubertijd last van acné: een huidaandoening waarbij je langere tijd last hebt van jeugdpuistjes.
    Tijdens de pubertijd is je hormoonhuishouding enorm door de war, en staan je poriën open, waardoor er gemakkelijker vuil in de huid kan komen waardoor een jeugdpuistje ontstaat.
    Daarnaast produceren je talgklieren in die periode meer talg, waardoor het kliertje verstopt kan raken, gaat ontsteken en er een puistje tevoorschijn komt.

    Voeding

    Maar ook mensen die allang uit de pubertijd zijn, kunnen last van puisten hebben.
    Dit is deels genetisch bepaald : als je ouders een kwetsbare en onrustige huid hebben, is de kans groter dat jij hier ook last van kunt krijgen.
    Maar volgens schoonheidsspecialiste Mieke Laarkamp van Schoonheidsinstituut De Schermer speelt voeding ook een belangrijke rol, al beweren andere gezondheidsdeskundigen wel eens van niet : ‘In mijn praktijk kom ik wel degelijk mensen tegen die bijvoorbeeld door varkensvlees te laten staan, minder last van puisten hebben. Ook hebben veel mensen extra last van puisten als ze chocolade eten. Ik adviseer ze sowieso altijd om voldoende water te drinken, zodat afvalstoffen goed worden afgevoerd.
    Andere oorzaken van puisten kunnen volgens Laarkamp zijn : stress, alcohol drinken, slaaptekort, roken en een slechte doorbloeding.

    Haargel

    Hoe een huid op voeding of invloeden van buitenaf reageert, is volgens Laarkamp voor iedereen verschillend : ‘Ik heb bijvoorbeeld mensen in mijn praktijk die heel gevoelig zijn voor een bepaald merk wasverzachter. Dan zie ik aan de puisten op hun wang op welke kant ze ’s nachts op het kussen liggen. Anderen kunnen slecht tegen bepaalde shampoo en als meiden gel of mousse in hun haar doen en die vette pony op hun voorhoofd hangt, kan dit pukkels ook in de hand werken’.

    Scheren

    De puisten van mannen verschillen overigens vaak met die van vrouwen.
    Laarkamp : ‘Mannen hebben een grovere huidstructuur en meer talgklieren dan vrouwen. Zij zijn daardoor veel bevattelijker voor puisten. Ook scheren kan hieraan bijdragen. Wanneer je de haren beweegt, activeer je de binnenkant van je talgklier en als je daar gevoelig voor bent kan het gaan ontsteken. Bij mannen is ook vaak een kwestie van aanleg, de een krijgt er wel last van en de ander niet. Wel hebben mannen met een gevoelige huid of een hele sterke baardgroei vaak last van puisten. Als je met een scheermes een stukje van de huid afschaaft, wordt hij automatisch kwetsbaarder. Ik adviseer dan ook om met een scheerapparaat te scheren in plaats van met een mesje en schuim, zodat je de huid zo min mogelijk irriteert’.

    Anticonceptiepil

    Vrouwen kunnen bij hevige acne de anticonceptiepil gaan slikken.
    Hiermee worden hormonen onder controle gehouden, waardoor de talgproductie stabiel blijft.
    Voor mannen is dit niet mogelijk, terwijl zij nog meer last kunnen hebben van de puisten.
    Laarkamp : ‘Mannen kunnen ook last van puisten over heel hun lichaam hebben, bijvoorbeeld de rug of de kont. Bij heet douchen gaan de talgklieren ook meer talg produceren, waardoor de puisten op de rug toenemen’.

    Medicijnen

    Voor hen zijn andere ‘sterkere middelen’.
    Bijvoorbeeld het medicijn Roaccutane.
    Laarkamp : ‘Dit zet de gehele talgproductie in het lichaam stil, waardoor de huid uitdroogt. Hierdoor krijgen puisten minder snel een kans. Maar dit soort sterke medicijnen hebben behoorlijk heftige bijwerkingen. Het legt namelijk de talgproductie helemaal stil, waardoor niet alleen de huid uitdroogt, maar mensen die ze gebruiken hebben last van droge lippen, een droge neus, zijn overgevoelig voor de zon en hebben soms zelfs last van depressieve gevoelens of leverfalen’.

    Tandpasta

    Er zijn op internet veel ‘remedies’ te vinden tegen puisten.
    Tandpasta erop smeren is een veelgehoorde oplossing.
    Laarkamp : ‘Hiermee droog je de puist uit, maar het is niet gezond voor de huid. Dit geldt ook voor pure alcohol op de puisten smeren. Ik heb ook een klant gehad die ergens had gelezen dat spruitjes erop leggen nut had. Dat lijkt me niet’.

    Schoonheidsspecialist

    Je huid goed schoonhouden is volgens Laarkamp succesvoller : ‘Je hebt speciale producten op de markt die de overmatige talgproductie van de huid tegengaan. Als je om de zes weken naar de schoonheidspecialist gaat, wordt dit op een professionele manier gedaan. Met een peeling worden dode huidcellen verwijderd. Vervolgens wordt het gezicht gestoomd, waardoor de poriën open gaan staan en de puisten het makkelijkst uitgeknepen kunnen worden. Vervolgens worden de puisten uitgeknepen’.
    Overigens hoef je je geen zorgen te maken over een hoge kostenpost als je naar de schoonheidsspecialist gaat : de meeste behandelingen worden vergoed.

    Lees ook :

    Cfr. : http://www.dokterdokter.nl/man/uiterlijk/article/27298/oorzaken-van-puisten




    21-11-2009 om 00:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:acné, alcohol, anticonceptiepil, baardgroei, haargel, huid, huidaandoening, huidcellen, jeugdpuistjes, poriën, puisten, puistjes, pukkels, roken, scheren, shampoo, slaaptekort, stress, talg, talgklieren, talgproductie, tandpasta, voeding, wasverzachter
    >> Reageer (1)
    20-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Sporten beter dan pauzeren bij RSI
    Klik op de afbeelding om de link te volgen





















     

    Sporten beter dan pauzeren bij RSI

    De Telegraaf, 20-11-2009

    Wie een muisarm wil voorkomen kan beter gaan sporten in de lunchpauze dan telkens kort te stoppen met computerwerk.
    Deze conclusie trekt bewegingswetenschapper Janneke Richter in haar proefschrift, waarop zij is gepromoveerd aan het Erasmus MC.
    Dat maakt het Rotterdamse medisch centrum vrijdag bekend.

    Kantoorwerkers die dagelijks uren achter de computer zitten, worden vaak met speciale software gedwongen te pauzeren : de computer gaat op slot, de werknemer moet even iets anders gaan doen.
    Onderzoek van Richter wijst uit dat de spieractiviteit bij mensen die computerwerk doen nauwelijks verschilt met die van mensen die aan het bureau werkzaam zijn zonder de pc te gebruiken.

    Intensief computerwerk kan leiden tot spierklachten aan de arm, nek of schouders.
    Voorheen stonden deze klachten bekend als 'Repetitive Strain Injury (RSI)'.
    Tegenwoordig zijn ze samengevoegd onder de noemer 'KANS' ('Klachten aan arm, nek of schouder').

    Volgens Richter is het bestuderen van computergebruik niet voldoende om het ontstaan van KANS te verklaren.
    „Het lijkt erop dat ander bureauwerk ook risicofactoren bevat voor het ontstaan van KANS”, stelt ze.
    Uit haar onderzoek blijkt dat mensen die computerwerk (toetsen en muis) verrichten vaak al spontane pauzes nemen, zoals het halen van koffie, een gesprek met een collega of papierwerk.
    Pauzesoftware verandert het werk-pauzepatroon niet noemenswaardig.

    Richter pleit daarom voor meer variatie tijdens de werkdag dan alleen normale- of softwarepauzes om spierkklachten te voorkomen.
    Sporten op het werk is volgens haar beter.

    Cfr. : http://www.telegraaf.nl/binnenland/5374930/__Sporten_beter_dan_pauze_bij_RSI__.html?cid=rss


    20-11-2009 om 23:13 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags: arm, bureauwerk, computer, computergebruik, computerwerk, KANS, klachten aan arm, nek of schouder (KANS), muis, muisarm, nek, papierwerk, pc, repetitive strain injury (RSI), RSI, softwarepauzes, spieractiviteit, spierkklachten, spierklachten, sporten
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Alles voor het goeie doel !!
    Klik op de afbeelding om de link te volgen


      



    Cfr. : http://www.bekendewensen.be/


    20-11-2009 om 20:44 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (1 Stemmen)
    Tags:goede doel
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Gewoon gelukkig zijn...
    Klik op de afbeelding om de link te volgen  



    Gelukkig zijn...

    Studenten, werkenden, werklozen, gepensioneerden, iedereen die dat wil kan nog gewoon gelukkig zijn.
    Juist in deze tijd, waarin de economie en de politiek zo allesoverheersend zijn, is het van belang om nog beslister te kiezen voor gelukkig zijn.
    Geluk is dus zeker niet afhankelijk van wat er in de wereld en rondom jou gebeurt.
    Geluk is iets wat je zélf moet (her)ontdekken en dan nog liefst op een gewone manier.
    Welke zaken kunnen het delicate geluk in de weg staan ?


    Gewoon gelukkig zijn

    Han Koreneef
    (tekst en muziek )
    Bron :
    http://kvk.vara.nl/Songteksten.282.0.html

    Elke dag leer ik op school weer honderdduizend dingen
    Maar nooit krijg ik eens onderwijs in lachen en in zingen
    Geschiedenis en tekenen, handvaardigheid en sport
    Maar hoe je vrolijk op moet staan schrijft niemand op het bord
    Ik weet hoe ik moet rekenen en foutloos zinnen schrijven
    Maar dat geeft geen garantie dat ik altijd blij zal blijven
    En als ik op de blinde kaart haast alle steden ken
    Dan wil dat nog niet zeggen dat ik straks gelukkig ben
    Dus hou nou alsjeblieft een keer je snater
    Met die stomme vraag; wat word je later ?

    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Verdien je een miljoen?
    Ik wil gewoon gelukkig zijn
    Heb je een buitenhuis ?
    Ik wil gewoon gelukkig zijn
    Je chauffeur die brengt je thuis
    Ik wil gewoon gelukkig zijn

    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Verdien je een miljoen ?
    Ik wil gewoon gelukkig zijn
    Heb je een buitenhuis ?
    Ik wil gewoon gelukkig zijn
    Je chauffeur die brengt je thuis
    Ik wil gewoon gelukkig zijn



    Als ik naar grote mensen kijk raak ik geïrriteerd
    Ze hebben op hun eigen school geen malle moer geleerd
    Het kunnen dan wel knappe en geleerde koppen zijn
    Maar heb je daar wat aan wanneer je bol staat van chagrijn ?
    Van mij mogen ze vrolijk zijn als vak verplicht gaan stellen
    Dan ben je beter af dan als je goed tot tien kunt tellen
    Ik wil een tien voor aardig zijn en lol op mijn rapport
    Dan weet ik zeker dat ik later heel gelukkig word
    Dus hou nou alsjeblieft een keer je snater
    Met die stomme vraag; wat word je later ?

    Wat ga je later doen ?
    Ik ga lekker hele dagen paardrijden
    Wat ga je later doen ?
    Ik begin gewoon een eigen snoepfabriek
    Wat ga je later doen ?
    Misschien word ik wel minister van gelukszaken
    Wat ga je later doen ?
    Of beter nog; ik ga de mensen gratis aan het lachen maken

    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn

    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon gelukkig zijn
    Wat ga je later doen ?
    Ik wil gewoon…


    Gelukkige mensen zijn met geluksgenen geboren

    Gezondheid.be, 16-10-2003 - Bron : Nieuwsblad

    Om een leven lang gelukkig te blijven moet je met de juiste genen geboren zijn.
    Wie het met minder goede genen moet stellen, doet er best aan te trouwen.

    Die wijsheid komt uit een onderzoek door het wetenschappelijk tijdschrift New Scientist.

    Sommige mensen hebben nu eenmaal een opgewekt karakter, terwijl anderen van nature eerder zwartkijkers zijn.
    Wetenschappers schrijven dat verschil toe aan de genen.
    Hoe mensen hun leven aanvoelen hangt maar voor de helft af van de omstandigheden.
    We zijn van nature uit geneigd tot optimisme of sombere gedachten.

    Het huwelijk kan aardig helpen om gelukkig te zijn.
    Dat leren tenminste de statistieken.
    Vooral het jaar voor en na de eigenlijke huwelijksceremonie zouden tijden van eindeloos geluk zijn.
    Gehuwde mensen zijn ook op langere termijn meestal gelukkiger dan vrijgezellen.

    Vriendschap levert ook extra geluk op.
    Goede sociale relaties zijn bijzonder waardevol.

    Godsdienst maakt eveneens gelukkig : gelovige mensen voelen zich over het algemeen gelukkiger dan ongelovigen (cfr. ook 'Zonder God is het te eenzaam' op : http://www.hartenziel.nl/artikel/zonder_god_is_het_te_eenzaam -).

    Uiterlijk, rijkdom en intelligentie zijn dan weer van minder belang om gelukkig te zijn.
    Maar dat is al lang bekend.

    Vreemd genoeg rept deze studie met geen woord over het belang van een goede gezondheid voor het geluk.

    Cfr. : http://www.gezondheid.be/index.cfm?fuseaction=art&art_id=1792


    Hoe gelukkig zijn de Belgen ?

    België ontcijferd, 07-09-2007 - In samenwerking met Algemene Directie Statistiek (FOD Economie)

    Tussen maart en juni 2006 ondervroeg de onderzoeksgroep TOR-VUB van de Vrije Universiteit Brussel 4.500 Belgen van 19 tot 81 jaar over hun geluk.
    De respondenten moesten op een schaal van 1 tot 10 aanduiden hoe gelukkig ze zijn.
    Tevens stelden de onderzoekers een twintigtal aanvullende vragen.
    Op basis van al de gezamenlijke antwoorden berekenden Mark Elchardus en Wendy Smits een "
    geluksscore" op een schaal van 100.

    Algemeen

    Het algemeen gemiddelde bedraagt 60,99.
    Dat betekent dat de doorsnee Belg zichzelf een 6 op 10 geeft inzake geluk.
    Mannen zijn met een geluksscore van 61,71 gemiddeld iets gelukkiger dan vrouwen, die een score van 60,26 halen.
    Voor alle leeftijdsgroepen geldt overigens dat mannen gemiddeld gelukkiger zijn dan hun vrouwelijke evenknieën.
    Alleen vrouwen van 36 tot 45 jaar zijn (iets) gelukkiger dan hun mannelijke leeftijdsgenoten.

    Leeftijd

    Het onderzoek toont duidelijk aan dat er een relatie is tussen leeftijd en geluk.
    Jonge volwassenen tussen 19 en 25 zijn gelukkiger dan de doorsnee Belg.
    Daarna daalt het geluk vrij rechtlijnig tot 55 jaar, om daarna opnieuw toe te nemen.
    Het gelukkigst zijn mensen in de leeftijdscategorie van 66 tot 75 jaar.
    Eens boven die leeftijd gekomen, neemt het geluk weer af.

    Opleiding

    Het diploma blijkt een sterk bepalende factor te zijn.
    Hoe hoger het onderwijsniveau, hoe groter de geluksscore.
    Volgens de onderzoekers heeft dat te maken met het feit dat een hoger diploma vaak leidt tot een hoger inkomen, een hogere plaats op de maatschappelijke ladder en meer controle over het eigen leven.
    Heel belangrijk inderdaad is de financiële situatie.

    Geld

    Mensen die in een slechte financiële situatie verkeren rapporteren veel minder vaak dat ze gelukkig zijn, mensen die in een goede financiële situatie verklaren dan weer vaker dat ze (heel) gelukkig zijn.
    Geld maakt dus wel degelijk gelukkig
    ”, zo stellen Elchardus en Smits.
    Lees ook '
    Niet geld, maar slaap maakt gelukkig' van Olav Velthuis op : http://www.hartenziel.nl/artikel/niet_geld_maar_slaap_maakt_gel –.

    Relatie

    Uit de cijfers van de TOR-VUB blijkt dat het al dan niet hebben van een relatie ook een belangrijke factor is.
    Mensen met een relatie zijn door de band gelukkiger dan mensen zonder een relatie.
    Samenwonenden zijn net iets gelukkiger dan gehuwden en een stuk gelukkiger dan mensen met een LAT-relatie.
    Bij mensen zonder relatie valt het op dat gescheiden mensen het ongelukkigst zijn.

    Cfr. ook :

    1. De “verdeling” van geluk over de bevolking
      Cfr. : http://statbel.fgov.be/nl/statistieken/cijfers/index.jsp

    2. Het grootste geluk
      Mark Elchardus en Wendy Smits
      Cfr. : http://www.lannoo.be/content/lannoo/wbnl/listview/1/index.jsp?titelcode=13060&fondsid=8

    Cfr. : http://www.6minutes.be/NL/Artikel.aspx?ArtikelID=8064&RubriekID=10


    Meeste Nederlanders zijn gelukkig
    Nationale Geluksonderzoek

    de Volkskrant, 12-03-2008

    ANP - Ruim 85 procent van de Nederlanders is het eens met de uitspraak 'het glas is half vol'.
    Zij voelen zich vooral tevreden met hun werk en hun uiterlijk.

    Dat bleek woensdag uit het Nationale Geluksonderzoek van onderzoeksbureau Multiscope onder 2800 ondervraagden.

    Nederlanders blijken tevreden over hun geluk en zijn over het algemeen optimistisch ingesteld.
    Het eigen geluk krijgt een 7,4 als rapportcijfer in het online onderzoek.
    Men voelt zich gemiddeld vijf dagen per week gelukkig.

    Ruim 77 procent van de ondervraagden meent dat je zelf invloed hebt op de mate van geluk.
    Volgens de helft van de Nederlanders maakt geld gelukkig.
    Drie op de vier zijn het eens met de stelling : ‘ik word gelukkig van mijn werk’.
    Met het eigen uiterlijk is 62 procent gelukkig.

    Als meest gelukkige BN'ers worden Marco Borsato, Frans Bauer, prinses Máxima, Paul de Leeuw en Jan Smit genoemd.
    Het meest ongelukkig zijn volgens Nederland : Geert Wilders, Gordon, Jan Peter Balkenende, Patty Brard en Linda de Mol.

    Gelukkiger worden ?

    Cfr. : http://www.hartenziel.nl/artikel/meeste_nederlanders_zijn_gelukkig


    Six tips for happiness

    Advice from Tal Ben-Shahar

    1. Give yourself permission to be human
      When we accept emotions -- such as fear, sadness or anxiety -- as natural, we are more likely to overcome them.
      Rejecting our emotions, positive or negative, leads to frustration and unhappiness.

      Geef jezelf de mogelijkheid om mens te zijn
      Aanvaard je emoties in plaats van ze te bestrijden.


    2. Happiness lies at the intersection between pleasure and meaning
      Whether at work or at home, the goal is to engage in activities that are both personally significant and enjoyable.
      When this is not feasible, make sure you have happiness boosters, moments throughout the week that provide you with both pleasure and meaning.

      Geluk ligt tussen plezier en betekenis
      Engageer je in activiteiten die je belangrijk en plezierig vindt, zowel op je werk als thuis.

    3. Keep in mind that happiness is mostly dependent on our state of mind, not on our status or the state of our bank account
      Barring extreme circumstances, our level of well being is determined by what we choose to focus on (the full or the empty part of the glass) and by our interpretation of external events.
      For example : do we view failure as catastrophic or do we see it as a learning opportunity ?

      Geluk is afhankelijk van onze gemoedstoestand, niet van onze bankrekening
      Leer je te focussen op de juiste zaken, het halfvolle glas in plaats van het halflege.


    4. Simplify !
      We are, generally, too busy, trying to squeeze in more and more activities into less and less time.
      Quantity influences quality and we compromise on our happiness by trying to do too much.

      Vereenvoudig !
      Probeer niet te veel in te weinig tijd te doen.

    5. Remember the mind-body connection
      What we do -- or don't do -- with our bodies influences our mind.
      Regular exercise, adequate sleep and healthy eating habits lead to both physical and mental health.

      Denk aan de verbinding tussen lichaam en geest
      Een gezonde geest heeft een gezond lichaam nodig.


    6. Express gratitude, whenever possible
      We too often take our lives for granted.
      Learn to appreciate and savor the wonderful things in life, from people to food, from nature to a smile.

      Laat je dankbaarheid zien
      Neem niet te veel voor vanzelfsprekend aan, maar apprecieer de zaken die je gelukkig maken, een lach, de natuur, lekker eten.

    Cfr. : http://www.npr.org/templates/story/story.php?storyId=5295168


     

    Levenskunst(jes)

    Ad Bergsma

      1. Blijf actief

      2. Kom onder de mensen

      3. Doe betekenisvol werk

      4. Zorg voor een goede organisatie

      5. Stop met piekeren

      6. Verlaag je verwachtingen

      7. Denk Positief

      8. Leef in het hier en nu

      9. Werk aan een gezonde persoonlijkheid

      10. Wees aardig

      11. Wees jezelf

      12. Elimineer negatieve gevoelens

      13. Waar heb je spijt van op je sterfbed ?

      14. Waardeer geluk

    Cfr. : http://www.hartenziel.nl/artikel/levenskunstjes


    Je kan ook gewoon gelukkig zijn
    - 10 Stappen naar geluk -

    Roland Verschaeve (illustraties : D. Demets) - Standaard Uitgeverij, februari 2007 – ISBN 10 : 9002222505 - ISBN 13 : 9789002222504
    - Recensie van Tine Van Puyenbroeck, 05-09-2007 -

    Gelukkig zijn...” Raymond Van Het Groenewoud zong er ook al over...

    Elke verjaardag, elke Nieuwjaar, elk huwelijk, elke geboorte... elke keer wensen we opnieuw en opnieuw geluk voor elkaar.
    Spreekwoorden te over vertellen hoe we gelukkig(er) kunnen zijn : denk maar aan “Geluk zit in de kleine dingen”...
    En toch blijft het bereiken van "het geluk" een zoektocht voor velen.

    Dit dunne boekje van Roland Verschaeve met als ondertitel “10 stappen naar geluk” is een compacte reisgids naar geluk.
    Bewust kort gehouden en vlot leesbaar en met gewoon begrijpbare woorden geschreven, is dit al wat een mens nodig heeft om -mits wat wil en bewustwording- te beseffen dat geluk inderdaad in kleine dingen zit !
    Gewoon bewust zijn van je leven, gewoon blij zijn met kleine gebaren, gewoon genieten van wat je hebt (en niet van wat je zou willen hebben), gewoon gelukkig zijn dat je er bent... meer is volgens de auteur niet nodig om op een hoger niveau van geluk te komen.

    Mijn eigen conclusie ?
    Geluk begint vooral met bewustwording.
    Van zodra je bewust bent van een aantal zaken, ga je er op een andere manier mee om.
    En dat ene woordje “anders” – dus niet “beter” - maakt al een hele wereld van verschil.
    In ieder geval, als iedereen een tiende onthoudt van al wat hier neergeschreven staat, dan is mijn vermoeden groot dat het Bruto Nationaal Geluk er enorm op vooruit zou gaan (waar ik me de vraag stel wat de correlatie zou zijn met het gekende bruto nationaal product ?... een antwoord laat zich raden) !

    Een kleine bedenking bij dit voor de rest absoluut fantastisch boekje : zoveel goede raad in zo weinig bladzijden kan, volgens mij, voor sommige mensen overweldigend zijn, waardoor ze niet ten volle in zich opnemen wat er allemaal staat.
    Vanuit die optie bekeken, scoort dit boekje als aanrader om op je nachtkastje te leggen en af en toe of zelfs regelmatig en al is het slechts voor her en der een stukje, terug vast te nemen.
    Immers, goede raad en vooral herhaling, over hoe we gewoon een ietsje gelukkiger kunnen zijn, wie wil dat niet ?

    Cfr. : http://www.politics.be/recensies/362/?highlight=elke

    20-11-2009 om 15:36 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:baan, geld, gelovig, geluk, gelukkig, gezondheid, godsdienst, huwelijk, intelligentie, ongelovig, opgewekt, optimisme, optimistisch, rijkdom, tevreden, uiterlijk, vriendschap, vrijgezel, werk, zwartkijkers
    >> Reageer (0)
    19-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Chronic Fatigue Syndrome - La bête noire of the Belgian Health Care System
    Klik op de afbeelding om de link te volgen



     



    .../...
    Het is nu duidelijk .../... dat de CVS Centra hebben gefaald in hun primaire missies.
    Het bleek zelfs onmogelijk om vanuit de ervaring van de CVSreferentiecentra gefundeerde wetenschappelijke richtlijnen op te stellen voor de diagnose en behandeling van CVS .../...

    Niettegenstaande de royale financiering van deze Centra, zijn de klinische behandelresultaten van de CVS centra zo goed als onbestaande en is er ook geen wetenschappelijke output .../...

    Duizenden patienten worden nog steeds .../... geoormerkt als zijnde luiaards, hypochonders, hysterica en psychosomatische klagers ofschoon deze patienten lijden aan ernstige, maar toch vaak te behandelen ziektebeelden.

    Nog steeds worden duizenden patienten .../... langdurig behandeld met nonsens therapieen zoals CBT, magnesiumbaxters, rilatine, glucocorticoiden, botox behandelingen, herhaalde operaties, injecties, NSAIDs, psychoanalytische therapieen, morfine pompen etc. .../...

    Dus worden patienten, die eigenlijk ernstig ziek zijn.../... onderworpen aan een ellenlange lijdensweg omdat ze verkeerd behandeld worden met :
    - GET - een training die ze meestal niet aankunnen en soms zelfs schadelijk is.
    - CBT - een psychologische therapie die de biochemische oorzaak van de CVS niet behandeld en die de patient stigmatiseert, namelijk “het zit tussen de oren”.

    Deze onethische aanpak leidt bovendien tot een overconsumptie in de gezondheidszorg.
    .../...

    Cfr. : http://www.ediver.be/ediver/latest%20news/onkelinx-Binder.pdf

    Chronic Fatigue Syndrome
    La bête noire of the Belgian Health Care System

    Michael Maes - crc.mh@telenet.be -, Maes Clinics, Antwerp, Belgium & Frank NM Twisk, ME-de-patiënten Foundation, Limmen, the Netherlands, the Netherlands - Neuroendocrinol Lett Vol 30 issue 3, 2009. pp. 275-420 - © Neuroendocrinology Letters 2006

    The World Health Organization acknowledges Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) to be a medical illness. ME/CFS is characterized by disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways.
    In 2002, the Belgian government started with the development of CFS “Reference Centers”, which implement a “psychosocial” model.
    The medical practices of these CFS Centers are defined by the Superior Health Council, e.g. treatment should be based upon Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) and biological assessments and treatments of ME/CFS should not be employed.
    Recently, the Belgian government has evaluated the outcome of the treatments at the CFS Centers.
    They concluded that a “rehabilitation therapy” with CBT/GET yielded no significant efficacy in the treatment of ME/CFS and that CBT/GET cannot be considered to be curative therapies.
    In case reports, we have shown that patients who were “treated” at those CFS centers with CBT/GET in fact suffered from IO&NS disorders, including intracellular inflammation, an increased translocation of gram-negative enterobacteria (leaky gut), autoimmune reactions and damage by O&NS.
    Considering the fact that these findings are exemplary for ME/CFS patients and that GET may even be harmful, it means that many patients are maltreated by the Belgian CFS Centers.
    Notwithstanding the above, the government and the CFS Centers not only continue this unethical and immoral policy, but also reinforce their use of CBT/GET in patients with ME/CFS treated at those Centers.

    Cfr. : http://node.nel.edu/?node_id=8929

    19-11-2009 om 20:49 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:chronic fatigue syndrome, cognitive behavioral therapy, cytokines, graded exercise therapy, inflammation, leaky gut, myalgic encephalomyelitis, oxidative stress, psychoneuroimmunology
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Persoonlijkheidstests
    Klik op de afbeelding om de link te volgen










     



    Wie zichzelf wil leren kennen heeft altijd ook anderen nodig


    De 'grote acht' persoonlijkheidstest

    Hart en Ziel, 14-09- © 2007 de Volkskrant

    Het eerste wat we van een ander willen weten is of hij te vertrouwen is en daarom is deugdzaamheid de eerste factor.

    De 'Big Eight'' is gebaseerd op de manier waarop mensen over elkaar praten :

    1. deugdzaamheid

    2. comptetentie

    3. extraversie

    4. mildheid

    5. ordelijkheid

    6. neuroticisme

    7. hedonisme en

    8. volgzaamheid.

    Die acht factoren die worden gemeten in de persoonlijkheidstest die door de Groningse psychologen Boele de Raad en Dick Barelds is ontwikkeld, hebben deels zeer herkenbare namen, maar hun betekenis is niet helemaal gelijk aan die van het woordenboek.

    Persoonlijkheidstest

    De persoonlijkheidstest op www.hartenziel.nl vraagt deelnemers zichzelf te beoordelen op grond van een aantal kenmerken, waarvan is aangetoond dat die een sterke samenhang vertonen met de genoemde factoren.
    Het gaat daarbij om zeer concrete gedragingen, waarvan iedereen zich snel een voorstelling kan maken.
    De test vraagt daardoor niet meer dan 10 minuten voor het invullen.
    Daarna heb je een scherp beeld van hoe je je eigen persoonlijkheid waarneemt.

    En als dat nog niet genoeg zelfkennis oplevert, bestaat de mogelijkheid ook anderen te vragen de eigen persoonlijkheid te beoordelen.
    Wie zichzelf wil leren kennen heeft daarvoor immers ook altijd anderen nodig.

    Doe de 'Personlijkheidstest'

    Wilt u in niet meer dan tien minuten inzicht krijgen in uw persoonlijkheid ?
    In deze test krijgt u 120 stellingen voorgelegd waarvan u moet beoordelen in hoeverre die op u van toepassing zijn.
    De stellingen zijn eenvoudig, daarom kost het invullen zo weinig tijd.

    Goede of foute antwoorden bestaan niet

    Het is de bedoeling dat u de uitspraken over zichzelf doet op basis van een vergelijking met anderen.
    Als u aangeeft dat u het helemaal eens bent met de stelling dat u betrouwbaar bent, dan wil dat zeggen dat u vindt dat u in vergelijking met gemiddelde anderen betrouwbaarder bent.

    De test heet 'Big Eight' omdat hij een beoordeling geeft op basis van acht persoonlijkheidskenmerken : deugdzaamheid, competentie, extraversie, mildheid, zorgvuldigheid, neuroticisme, hedonisme en volgzaamheid.

    Cfr. : http://www.hartenziel.nl/artikel/De__grote_acht__persoonlijkheidstest

    Cfr. ook :  

    1. De 'Grote vijf' persoonlijkheidstest
      Cfr. :
      http://nl.outofservice.com/bigfive/
    2. De korte persoonlijkheidstest
      Cfr. :
      http://www.123test.nl/persoonlijkheidtest/
    3. De persoonlijkheidstest
      Cfr. :
      http://www.goodfeeling.nl/persoonlijkheid.html

    19-11-2009 om 00:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (1 Stemmen)
    Tags:karakter, karaktereigenschappen, persoonlijkheidskenmerken, persoonlijkheidstest
    >> Reageer (0)
    18-11-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vaccinatie risicogroepen H1N1
    Klik op de afbeelding om de link te volgen

















     

    Vaccinatie risicogroepen H1N1

    Het is niet de bedoeling om zoveel mogelijk mensen te vaccineren,
    wel om zoveel mogelijk mensen in te enten die echt een risico lopen


    Nederland

    Grensgevallen H1N1-vaccinatie van kastje naar muur

    Gezondheidsnet.nl, 16-11-2009 – Bron : Huisarts Vandaag - http://www.huisartsvandaag.nl/ -

    GROOTEGAST - Zwangeren die binnenkort gaan bevallen en hun huisgenoten willen laten inenten tegen de Mexicaanse griep, worden door de GGD terug naar de huisarts gestuurd.
    De huisarts mag echter geen mensen inenten die buiten de risicogroepen vallen.

    Vaccinatie risicogroepen H1N1 volgende week van start
    LHV – Medischcontact.artsennet.nl, Nr. 45, rubriek 'Federatienieuws', p. 1890 – 04-11-2009
    Deze week ontvangen alle huisartspraktijken in Nederland de vaccins voor de eerste vaccinatieronde tegen het H1N1-virus, de Mexicaanse griep.
    In totaal worden ruim 5 miljoen vaccins afgeleverd bij de huisartsen voor de eerste ronde.
    Een week later kan deze eerste vaccinatieronde beginnen.
    De doelgroep voor deze vaccinatie komt grotendeels overeen met de risicogroepen die de huisarts jaarlijks voor vaccinatie tegen de seizoensgriep oproept.
    Mensen met een medisch risico en gezonde 60-plussers hebben van hun huisarts een uitnodiging gekregen voor de pandemische vaccinatie.
    De vaccinatie wordt ook aangeboden aan mantelzorgers van mensen met een zeer hoog risico op ernstige ziekte en sterfte door griep.
    Onder mantelzorgers wordt verstaan: huisgenoten die contact hebben met genoemde patiëntencategorieën en daarmee vergelijkbare contacten.
    LHV en NHG adviseren hun leden om aan de hand van de lijst met opgeroepen patiënten te bepalen voor welke patiënten het nuttig is om de mantelzorgers te vaccineren.
    De betreffende patiënten kunnen vervolgens hun mantelzorgers vragen naar hun eigen huisarts te gaan.
    Het vaccin wordt ook beschikbaar gesteld aan gezonde zwangeren vanaf de vierde maand, maar de huisarts roept hen niet actief op.
    De Gezondheidsraad heeft bewust gekozen voor de omschrijving van ‘vaccin moet beschikbaar zijn’ in plaats van ‘adviseren om te vaccineren’ voor gezonde zwangeren.
    De reden is dat het vaccin tegen Nieuwe Influenza A (H1N1) nog niet getest is bij zwangeren.
    Onderzoeksresultaten van het vaccin tegen de jaarlijkse seizoensgriep bij zwangeren laat zien dat zich hierbij geen bijzonderheden voordoen.
    Voor de zekerheid is gekozen voor een contra-indicatie in het eerste trimester, omdat dat de meest kwetsbare periode is voor de vrucht.
    Om zwangeren goed te informeren, verstrekt VWS voorlichtingsfolders aan verloskundigen, gynaecologen en verloskundig actieve huisartsen.
    Tot slot heeft ook een deel van het zorgpersoneel recht op vaccinatie.
    Dit gaat bijvoorbeeld om medewerkers van ziekenhuizen, ambulancediensten en verloskundigen.
    Criterium is het risico voor kwetsbare patiënten.
    Vaccinatie van zorgpersoneel loopt via de werkgever.
    De LHV heeft met de KNOV afgesproken dat verloskundigen bij hun huisarts terecht kunnen voor vaccinatie.
    Mensen die niet tot een risicogroep behoren, komen niet in aanmerking voor H1N1-vaccinatie.
    Minister Klink van VWS vroeg de Gezondheidsraad op 19 oktober om de eerdere adviezen over vaccinatie tegen het licht te houden.
    Hij wil weten of deze nog overeenkomen met de nieuwste inzichten over Nieuwe Influenza A.
    Zo vroeg hij onder andere of jongeren in aanmerking moeten komen voor vaccinatie.
    Cfr. :
    http://medischcontact.artsennet.nl/blad/Tijdschriftartikel/Vaccinatie-risicogroepen-H1N1-volgende-week-van-start.htm

    Huisgenoten van zwangeren die gaan bevallen, vallen niet binnen de risicogroepen – cfr. : http://www.gezondheidsnet.nl/de-mexicaanse-griep/nieuws/3708/klink-neemt-vaccinatieadvies-gezondheidsraad-over - en krijgen dus geen oproep van de GGD.
    Het nog niet geboren kind is namelijk nog niet bekend bij de Gemeentelijke Basis Administratie (GBA) van waaruit pasgeboren kinderen en hun huisgenoten opgeroepen worden.

    De GGD verwijst ook mensen die op vakantie zijn tijdens de inentingsdagen naar de huisarts.
    Maar deze kan en mag deze mensen niet inenten.
    Minister Klink heeft zelfs gedreigd met de tuchtrechter als dokters mensen gaan vaccineren die niet in een risicogroep vallen.
    Op dit moment is nog niet bekend hoe deze grensgevallen behandeld gaan worden.

    Huisgenoten van zwangeren die gaan bevallen, vallen niet binnen de risicogroepen en krijgen dus geen oproep van de GGD.
    Het nog niet geboren kind is namelijk nog niet bekend bij de Gemeentelijke Basis Administratie (GBA) van waaruit pasgeboren kinderen en hun huisgenoten opgeroepen worden.

    De GGD verwijst ook mensen die op vakantie zijn tijdens de inentingsdagen naar de huisarts.
    Maar deze kan en mag deze mensen niet inenten.

    Minister Klink heeft zelfs gedreigd met de tuchtrechter als dokters mensen gaan vaccineren die niet in een risicogroep vallen.
    Op dit moment is nog niet bekend hoe deze grensgevallen behandeld gaan worden.

    Cfr. : http://www.gezondheidsnet.nl/de-mexicaanse-griep/nieuws/3724/grensgevallen-h1n1-vaccinatie-van-kastje-naar-muur


                      Michel D'Hooghe

    België

    Vaccinatie Mexicaanse griep bij huisartsen van start

    Knack.rnews.be, 06-11-2009

    Vanaf zaterdag 7 november kunnen risicogroepen zich bij de huisarts laten vaccineren tegen de Mexicaanse griep.
    Er zijn 1,3 miljoen vaccins ter beschikking.

    De tweede vaccinatiecampagne richt zich op een aantal doelgroepen, zoals zwangere vrouwen en ouders van kinderen die jonger zijn dan zes maanden.

    Ook mensen die werken in het onderwijs, de kinderopvang en de gezondheidszorg komen in aanmerking.
    Dat geldt ook voor mensen met medische risicofactoren.

    Het vaccin is niet vrij te koop en dus niet beschikbaar voor mensen die niet tot de risicogroepen behoren.

    Het is niet de bedoeling om zoveel mogelijk mensen te vaccineren, wel om zoveel mogelijk mensen in te enten die echt een risico lopen”, aldus federaal minister van Volksgezondheid Laurette Onkelinx.

    De risicogroepen kunnen vanaf zaterdag een afspraak maken bij hun huisarts om zich te laten vaccineren.

    Het vaccin tegen het A/H1N1-virus is gratis.
    De consultatie bij de dokter wordt volledig terugbetaald”, aldus griepcommissaris Marc Van Ranst.

    Cfr. : http://knack.rnews.be/nieuws/belgie/vaccinatie-mexicaanse-griep-bij-huisartsen-van-start/site72-section24-article42157.html


    18-11-2009 om 16:39 geschreven door Jules

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    Tags:60-plussers, ambulancediensten, gynaecologen, H1N1-vaccinatie, huisarts, inenten, jongeren, kinderopvang, mantelzorgers, Mexicaanse griep, onderwijs, pandemie, risicogroepen H1N1, seizoensgriep, verloskundigen, ziekenhuizen, zorgpersoneel, zwangeren
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Geopereerd Prof. Johann Bauer - Een update (Greta)
    Klik op de afbeelding om de link te volgen




     



     

    Zoals beloofd
    hou ik jullie op de hoogte... 

    Cfr. 'Geopereerd Prof. Johann Bauer' – dit blog dd. 08-11-2009


    Op 16-11-2009 schreef Greta in mijn dagboek :

    Dag Jules en allen die op dit blog een kijkje nemen,

    Zoals beloofd hou ik jullie op de hoogte na mijn operatie van 21-10-2009 door prof. Bauer in Baar (Zwitserland), 4 weken geleden al ondertussen.

    Wat Dr. Bauer me voorspelde qua pijn klopt heel precies : omdat ik in zo'n erge mate fibro heb, had hij gezegd dat ik na de operatie nog veel meer pijn zou kunnen hebben dan ervoor en dat ik die 1ste operatie niet zoveel zou voelen.

    Dat is ook zo, al heb ik in mijn eerste berichtje hier (cfr. 'Geopereerd Prof. Johann Bauer' – dd. 08-11-2009) geschreven dat ik me werkelijk beter voelde...

    Dat wás ook zo - ik zag het weer volkomen zitten - maar vorige week was de hevige pijn er weer.
    Ik ben ondertussen mijn morfine met 12,5 mg ook aan het afbouwen en dat voel ik enorm, dat is weer afkicken...
    Ik ben vorige week echt heel erg ziek geweest.
    Ik kon zelfs mijn bed niet uit en ik kon weer niks meer eten.
    Ik voel maar al te goed dat dit mede komt door de stress hier thuis is : ik kan werkelijk tegen niks meer !

    Ja, als je weer thuis komt...
    We hebben een eigen zaak en ik mag niet meer werken.
    Dat is voor mij niet om aan te zien !
    Al was ik genoeg verwittigd dat ik de eerste weken na de operatie nog niks mocht doen heb ik vorige week weer ietske teveel hooi op de vork genomen.
    Maar wat moet ik doen ?
    Er is niks geregeld, door niemand : ik zorg altijd zélf voor alles...
    Nu voel ik werkelijk dat ik niet meer kán.
    Ik ben gewoon heel erg moe en wil slapen !
    Ik moét afstand nemen, maar dat is heel erg moeilijk voor mij...

    Gisteren zondag 15/11 lag ik hier alweer doodziek in bed.

    Slapen ging heel erg slecht de afgelopen dagen, zelfs na inname van mijn slaapmedicatie.
    De krampen in mijn benen en voeten zijn heel veel verergerd.

    Zoals gezegd had Prof. Bauer dat voorspeld.
    Hij had gelijk, dat geef ik hier eerlijk toe !

    Gisteren hat ik dan ook in een serieuze dip.

    Ik had alweer de pijn aan mijn rechtervoet.
    Daar begint het altijd.
    Maar met de morfinepleisters aan mijn rechtervoet te vernieuwen (om de 2 dagen) ben ik vandaag een stuk beter.

    Als gevolg van een week niet kunnen slapen heb ik een hele grote afte in mijn mond gekregen.
    Vroeger had ik er soms 4 ineens !
    Deze keer had ze de grootte van een 2-eurocentje.
    Ik kan amper iets eten.
    Niet te verwonderen dat ik al bij al zeker nog niet ben verzwaard...

    Vandaag is er toch weer wat hoop, al heb ik nu op het ogenblik alweer ferme krampen in mijn voeten en benen.
    Ik heb boodschappen gedaan met mijn dochter.
    Bovendien was ik gisteren zeer zenuwachtig, want afhankelijk zijn van iemand ligt niet in mijn aard : ik heb altijd ánderen geholpen, ik ben geen vrager, maar een gever, altijd geweest...

    Nu is het uitkijken naar mijn 2de operatie (aan mijn R-been).

    Ik weet het, de prof had me eerlijk gezegd dat het er na die eerste operatie nog niet in zat, maar ik hoop dat ik na deze tweede operatie toch al een beetje verschil zal merken.
    Morgen stuur ik hem een mailtje.

    Ondertussen is de operatiepleister verwijderd.
    Het wondje is nu een heel mooi fijn naadje, echt heel fijn gedaan !
    Ik moet het nu elke dag inwrijven met Johannesolie van A. Vogel (want zalf mag niet op de wonde komen).

    Zo beste allemaal, tot zover mijn verhaal.

    Ik hoop dat ik toch nog iets mag ondervinden van de eerste operatie.

    Het enige wat ik nu precies niet meer voel is de pijn in mijn kaakgewrichten en kaakbeenderen (het gevoel alsof ik slaag gekregen heb in mijn gezicht is verdwenen).
    Dat is toch iets positief.

    Ook mijn darmen zijn wel beter.
    Alleen ben ik ook nog heel misselijk, maar dat is veeleer van de morfine.

    Ik hoop de volgende keer iets positever te kunnen schrijven.
    Maar, nogmaals, de prof had me verwittigd dat ik veel slechter kon worden.
    Hij is eerlijk geweest.

    Ik ben hier nu ook eerlijk geweest, maar ik laat de moed niet zakken !
    Ik moet doorgaan !

    Ik heb al een lange weg afgelegd... door de hel die zo stilaan haar poorten mag sluiten.

    Met geduld kom ik er wel... er zijn nog zóveel mensen die ook heel veel pijn hebben en er óók mee moeten leven.

    Ik wil alle mensen met fibro en cvs hierbij een hart onder de riem steken !

    Met vriendelijke groet, 
    Greta.

    18-11-2009 om 15:16 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 5/5 - (2 Stemmen)
    Tags:aften, Bauer, Dr. Bauer, fibromyalgie, Johann Bauer, krampen, misselijk, moe, morfine, morfinepleisters, operatie, pijn, Prof. Bauer, Prof. Dr. Bauer, Prof. Johann Bauer, slapen
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Weersfactoren oorzaak van hoofdpijn
    Klik op de afbeelding om de link te volgen





















       





     

    Weersfactoren oorzaak van hoofdpijn

    Gezondheidsnet.nl, 16-11-2009 - Bron : Pijnstiller Infocentrum - http://www.pijnstillerinfocentrum.nl/ -

    Weersfactoren die hoofdpijn uitlokken zijn onder andere dalende luchtdruk, toenemende bewolking, stijgende vochtigheid, temperatuurswisselingen en toenemende wind.
    Van al deze factoren is dalende luchtdruk het meest van invloed.

    In het najaar kan de luchtdruk van dag tot dag snel veranderen en worden in de regel de laagste waarden van het jaar gemeten.
    Wanneer de luchtdruk snel daalt, zet de lucht in onder andere bij- en voorhoofdsholten uit, waardoor er meer druk op bloedvaten komt te staan.
    Dit kan hoofdpijn tot gevolg hebben.

    Uiteraard lost het drukprobleem zich uiteindelijk vanzelf op.
    Je lichaam stelt zich erop in of de luchtdruk gaat weer omhoog.

    Cfr. : http://www.gezondheidsnet.nl/medisch/nieuws/3725/weersfactoren-oorzaak-van-hoofdpijn


    18-11-2009 om 15:15 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:bewolking, bloedvaten, hoofdpijn, luchtdruk, temperatuurswisselingen, vochtigheid, weersfactoren, wind
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Infection as one possible cause of fibromyalgia - Part I
    Klik op de afbeelding om de link te volgen

    Dr. Mark J Pellegrino, MD


     





    Infection as one possible cause of fibromyalgia

    Part I


    Though Dr. Pellegrino published these observations before discovery of the XMRV virus,
    the questions they raise are if anything more relevant today
    .


    Infection as one possible cause of fibromyalgia

    Dr. Mark J Pellegrino, MD, October 4, 2009 - © 2009 ProHealth, Inc.
    Excerpted from Chapter 10 of Dr. Pellegrino’s very popular book 'Fibromyalgia - Up close and personal' (cfr. :
    https://www.prohealth.com/shop/product.cfm/product__code/BK90 -).

    Dr. Mark J Pellegrino
    Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center – cfr. : http://www.ohiorehabcenter.com/index.html - and has been a fibromyalgia patient himself since childhood.

    Though Dr. Pellegrino published these observations before discovery of the XMRV virus,
    the questions they raise are if anything more relevant today
    .

    All of us involved with Fibromyalgia, either by treating it or having it, have come to appreciate how complicated this condition is

    Fibromyalgia has different types and subsets (cfr. also Dr. Pellegrino’s articles on “The fibromyalgia spectrum – Part of the Big Picture in Understanding Fibromyalgia” at : http://www.prohealth.com//library/showArticle.cfm?libid=13042 -& “Fibromyalgia – Ultimately a disease of amplified pain” at : http://www.prohealth.com//library/showArticle.cfm?libid=13702 -).
    More than one factor may be involved in causing it.
    Causes may be recognized, but the exact mechanism of how fibromyalgia develops from this cause is not fully known.
    Most importantly, there is more than one way to get fibromyalgia; it is an “end point” condition with multiple ways leading to it.

    I have compiled a list of probable causes of fibromyalgia.
    This list is based on my experiences and understanding of the current literature.
    My opinions on these probable causes may not be shared by everyone.
    My list of probable causes is as follows :

    Like trauma, infection is one of those causes of fibromyalgia that just screams for common sense

    I’ve seen hundreds and hundreds of people whose basic story goes like this : “I was fine, I got a virus, I developed fatigue and pain and I’ve never been the same since”.

    The logical thinking in this scenario is that fibromyalgia was not present before the viral infection.
    There may have been a hereditary predisposition or a vulnerability, but fibromyalgia was not present.
    The virus caused the condition to develop and it has been present since the virus and continues to be present.
    This is a straightforward infectious cause.

    Not all infections are as straightforward

    Many people who have fibromyalgia get a viral infection and find it worsens the fibromyalgia.
    People with active viral infections are at risk for additional infections, particularly bacterial infections which can create additional problems.

    Some people with fibromyalgia are more vulnerable to any type of infection because the fibromyalgia renders them more immunocompromised or more at risk for infection.
    The physician needs to sort out the various possibilities to determine whether an infection is the cause, a consequence or an aggravator of the fibromyalgia.

    The mechanism by which an infection leads to fibromyalgia is probably related to inflammatory or autoimmune changes caused by the infection that starts the fibromyalgia cascade.

    The actual clinical infection resolves and is long gone, yet fibromyalgia symptoms continue :

    • sometimes, the infecting virus or bacteria may hang around and create a persistent low grade infection which activates the autoimmune responses, thereby “triggering” the fibromyalgia

    • many times, though, the infection has long disappeared, but permanent changes occurred in the body and these changes caused fibromyalgia to develop.

    Various viral infections can cause fibromyalgia

    • The Epstein-Barr virus which causes infectious mononucleosis is one;

    • Cytomegalovirus causes a syndrome similar to infectious mononucleosis;

    • Different strains of the influenza virus can also result in fibromyalglia;

    • The adenoviruses, especially Type II, cause common colds, bronchitis and various upper respiratory infections and may lead to fibromyalgia;

    • Human Herpes Virus 6 has also been implicated;

    • Reactive fibromyalgia has been described in patients with AIDS and hepatitis.

    Sometimes viral titers can be directly measured to demonstrate that an acute infection has occurred.
    This concentration can be correlated with the clinical development of fibromyalgia.
    Many times, though, the exact offending virus is not known, but we can still categorize the fibromyalgia as one that was caused by an infection, probably a viral infection, if it fits clinically.

    Bacterial infections can also cause fibromyalgia

    I have seen patients who have developed fibromyalgia after sepsis (blood infection) and salmonella infections and one who, I felt, has gotten it from a Listeria infection.
    Some research studies found Mycoplasma incognitos and Chlamydia pneumoniae (for more on this subject cfr. “Chlamydia pneumoniae in chronic fatigue syndrome and fibromyalgia – An opinion” by Patient Advocate James Kepner (from the Chlamydia pneumoniae Help website) at :
    http://www.prohealth.com//library/showArticle.cfm?libid=127633 -) in patients with fibromyalgia and chronic fatigue syndrome (cfr. “Evidence for bacterial (mycoplasma, Chlamydia) and viral (HHV-6) co-infections in chronic fatigue syndrome patients” by Dr. Garth Nicolson and Dr. Darryl See at : http://www.informaworld.com/smpp/content~db=all?content=10.1300/J092v11n02_02 -).
    These infectious organisms may be causing some of the symptoms.

    Indeed, some of the patients improve with antibiotic therapy.
    Gulf War Syndrome, in part, may have been related to infections from one of these bacteria.
    Symptoms of Gulf War Syndrome include fatigue, headaches, depression, joint and muscle pain, sleep disorders and poor memory (sound familiar ?).

    As of November 2008, a research panel reported their finding that Gulf War illness is real and “is the result of neurotoxic exposures” (cfr. 'Gulf War Syndrome finally declared real - Illness caused by exposure to pesticides and other neurotoxic chemicals' at : http://www.prohealth.com/me-cfs/library/showArticle.cfm?libid=14093 -) as discussed in Chapter 10 under 'Chemical exposure as a probable cause of FM']

    Fibromyalgia can be caused by yeast and parasite infections

    I have seen some patients who developed it following a severe Candida yeast infection and others following parasite infections such as Giardia (cfr. : http://en.wikipedia.org/wiki/Giardia -).
    Most of the time, yeast or parasite infections occur in patients after the fibromyalgia has already developed.
    These infections may aggravate the preexisting fibromyalgia or cause it to flare up.

    Fibromyalgia may predispose us to these infections by interfering with our immune function.
    On the other hand, these infections can sometimes cause the fibromyalgia by “triggering” the fibromyalgia cascade.
    Many of the symptoms of a chronic Candida yeast infection (cfr. also Dr. Pellegrino's article "Candidiasis - Yeast infection and nutritional tepair" at :
    http://www.prohealth.com/library/showArticle.cfm?libid=12385 -) such as fatigue, irritable bowel syndrome, bloating, allergies, altered immune response, and skin conditions - overlap with fibromyalgia symptoms.
    This can make it difficult to “separate” the two conditions and determine cause and effect relationships.

    As I’ve mentioned, some infections come in, do their damage and disappear.
    The infectious agent is no longer present in the body and thus can’t be detected at a later point in time.
    Other infectious agents may hang around in the body and establish a chronic infection; one that perhaps can be detected with blood tests.

    What remains to be seen is whether these chronic infections can be eradicated with antibiotic treatment and, if so, will the fibromyalgia symptoms disappear ?
    Or has the fibromyalgia already established itself as a separate entity which does not disappear with the antibiotic treatment ?

    Hopefully we will have these answers in the near future.
    [But]… one thing is certain : we will continue to learn more about fibromyalgia and understand it better.

    Cfr. : http://www.prohealth.com/fibromyalgia/library/showArticle.cfm?libid=14187&B1=EM110409F


    Cfr. also :

    1. A 37 kDa 2-5A binding protein as a potential biochemical marker for Chronic Fatigue Syndrome
      De Meirleir K, Bisbal C, Campine I, De Becker P, Salehzada T, Demettre E, Lebleu B, Department of Human Physiology and Medicine, Vrije Universiteit Brussels, Belgium - Am J Med. 2000 Feb;108(2):99-105 - PMID: 11126321
      Purpose -
      Recent studies have revealed abnormalities in the ribonuclease L pathway in peripheral blood mononuclear cells of patients with the chronic fatigue syndrome.
      We conducted a blinded study to detect possible differences in the distribution of 2-5A binding proteins in the cells of patients with chronic fatigue syndrome and controls.
      Patients and methods - We studied 57 patients with chronic fatigue syndrome and 53 control subjects (28 healthy subjects and 25 patients with depression or fibromyalgia).
      A radioactive probe was used to label 2-5A binding proteins in unfractionated peripheral blood mononuclear cell extracts and to compare their distribution in the three groups.
      Results - A 37 kDa 2-5A binding polypeptide was found in 50 (88%) of the 57 patients with chronic fatigue syndrome compared with 15 (28%) of the 53 controls (P < 0.01).
      When present, the amount of 37 kDa protein was very low in the control groups.
      When expressed as the ratio of the 37 kDa protein to the 80 kDa protein, 41 (72%) of the 57 patients with chronic fatigue syndrome had a ratio > 0.05, compared with 3 (11%) of the 28 healthy subjects and none of the patients with fibromyalgia or depression.
      Conclusion - The presence of a 37 kDa 2-5A binding protein in extracts of peripheral blood mononuclear cells may distinguish patients with chronic fatigue syndrome from healthy subjects and those suffering from other diseases.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11126321
      Also read the comments on this article :
      - Chronic fatigue syndrome
      Van Houdenhove B, Vanthuyne S, Neerinckx E - Am J Med. 2000 Aug 15;109(3):257-9 - PMID: 11023437
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11023437?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
      - Is there a Gulf War syndrome ?
      Podell RN - Am J Med. 2000 Dec 15;109(9):744 - PMID: 11188785
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11188785?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
      - The biology of chronic fatigue syndrome
      Komaroff AL - Am J Med. 2000 Feb;108(2):169-71 - PMID: 11126311
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11126311?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
      - Chronic fatigue syndrome - The fundamentals still apply
      Manu P - Am J Med. 2000 Feb;108(2):172-3 - PMID: 11126312

      Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11126312?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    2. A family history study of chronic fatigue syndrome
      Walsh CM, Zainal NZ, Middleton SJ, Paykel ES, University Department of Psychiatry, Addenbrooke's Hospital, Cambridge, UK - Psychiatr Genet. 2001 Sep;11(3):123-8 - PMID: 11702053
      Chronic fatigue syndrome (CFS) is characterized by unexplained, disabling fatigue and is associated with high rates of comorbid depression.
      While the aetiology is unknown, findings from recent twin surveys suggest that genetic factors may be relevant to prolonged fatigue states (> 1 month).
      To date, however, there has been no exploration of the role of familial/genetic factors in operationally defined CFS.
      The aims of the present study were: (i) to examine whether CFS is familial by comparing the rates of CFS in the first-degree relatives of CFS cases and medical control subjects; and (ii) to determine whether the high rate of comorbid depression in CFS is reflected in a greater familial loading for affective disorder.
      Twenty-five CFS cases and 36 medical control subjects were assessed for fatigue symptoms based on the Centre for Disease Control (CDC) criteria for CFS and for lifetime psychiatric symptoms using the Schedule for Schizophrenia and Affective Disorders-Lifetime Version.
      Informant family history was obtained regarding first-degree relatives using the CDC criteria and the Family History Research Diagnostic Criteria.
      In addition, informant history was supplemented by sending a questionnaire to first-degree relatives.
      There were significantly higher rates of CFS in the relatives of CFS cases compared with the relatives of control subjects.
      The rate of depression in the CFS cases was similar to previous studies but did not appear to reflect a greater familial loading for depression when compared with control subjects.
      However, these analyses were complicated by higher than expected rates of depression in the control group.
      These findings suggest that familial factors are important in the aetiology of chronic fatigue syndrome.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11702053

    3. Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome
      Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH, Department of Neurosciences, CFS Cooperative Research Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA : apeckerm@njneuromed.org - Am J Med Sci. 2003 Aug;326(2):55-60 - PMID: 12920435
      Background - Findings indicative of a problem with circulation have been reported in patients with chronic fatigue syndrome (CFS).
      We examined this possibility by measuring the patient's cardiac output and assessing its relation to presenting symptoms.
      Methods
      - Impedance cardiography and symptom data were collected from 38 patients with CFS grouped into cases with severe (n = 18) and less severe (n = 20) illness and compared with those from 27 matched, sedentary control subjects.
      Results
      - The patients with severe CFS had significantly lower stroke volume and cardiac output than the controls and less ill patients.
      Postexertional fatigue and flu-like symptoms of infection differentiated the patients with severe CFS from those with less severe CFS (88.5% concordance) and were predictive (R2 = 0.46, P < 0.0002) of lower cardiac output.
      In contrast, neuropsychiatric symptoms showed no specific association with cardiac output.
      Conclusions
      - These results provide a preliminary indication of reduced circulation in patients with severe CFS.
      Further research is needed to confirm this finding and to define its clinical implications and pathogenetic mechanisms.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/12920435

    4. Activation of human monocytes by the pineal hormone melatonin
      Morrey KM, McLachlan JA, Serkin CD, Bakouche O, Department of Molecular Pharmacology and Biologic Chemistry, Northwestern University Medical School, Chicago, IL 60611 - J Immunol. 1994 Sep 15;153(6):2671-80 - PMID: 8077674

      To determine the effects of the pineal hormone melatonin on human monocytes, human monocytes were activated by different concentrations of melatonin.
      Above the activation threshold of 5 x 10(-11) M, melatonin was able to induce the cytotoxicity of human monocytes, the secretion of IL-1 and the production of reactive oxygen intermediates.
      Melatonin and LPS seemed to have a synergistic effect on human monocyte activation.
      Indeed, below their respective monocyte activation threshold (5 x 10(-11) M and 0.625 ng/ml), melatonin (10(-12) M) in association with LPS (0.2 ng/ml) was able to induce cytotoxicity, IL-1 secretion and reactive oxygen intermediates production.
      Melatonin alone at 10(-12) M or LPS alone at 0.2 ng/ml did not activate monocytes.
      Furthermore, melatonin was able to prime the monocytes for a subsequent activation by LPS.
      When monocytes were activated by LPS (0.25 ng/ml) at the time that they were plated and then activated by melatonin (10(-12) M) 8 h later, no IL-1 secretion and no cytotoxicity were detected.
      However, when the cells were first activated by melatonin (10(-12) M) and then 8 h later by LPS (0.25 ng/ml), IL-1 secretion and monocyte cytotoxicity were observed.
      Above its monocyte activation threshold, melatonin induces both cell-associated IL-1 alpha and IL-1 beta activities.
      Below this activation threshold, i.e., at 10(-12) M, melatonin does not induce the cell-associated IL-1 alpha and IL-1 beta activities, but does induce the mRNA for both IL-1 (alpha and beta).
      It seems that melatonin activates monocytes through protein kinase C.
      These data suggest that melatonin activates monocytes and induces their cytotoxic properties, along with the IL-1 secretion.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8077674

    5. Activation of the IFN-inducible RNase L causes apoptosis in animal cells (B. N. FieldsD. M. Knipe, Eds.)
      Margarita Díaz-Guerra1, Carmen Rivas and Mariano Esteban2 -Centro Nacional de Biotecnología, CSIC, Campus Universidad Autónoma, Madrid, 28049, Spain - 1 Current address: Departamento de Bioquímica (UAM) - Instituto de Investigaciones Biomédicas (CSIC), C/Arturo Duperier, 4, 28029 Madrid. Spain - 2 To whom correspondence and reprint requests should be addressed : Fax : 341 5854506 – E-mail :
      MESTEBAN@SAMBA.CNB.UAM.ES – Virology, Volume 236, Issue 2, 29 September 1997, Pages 354-363 - © 1997 Academic Press
      The interferon (IFN)-induced enzyme RNase L produced by a recombinant vaccinia virus (VV) causes death of mammalian cells with morphological and biochemical characteristics of apoptosis. Coexpression of 2-5A-synthetase enhances apoptosis induced by RNase L. Activation of endogenous RNase L by infection with a VV ts mutant (ts22) or with wild-type virus in the presence of the antipoxvirus drug isatin-β-thiosemicarbazone, a treatment known to significantly increase the amount of double-stranded RNA late during infection, also causes pronounced apoptosis of infected cells. The effects observed with recombinant virus-derived RNase L or with the endogenous enzyme are specific, since apoptosis also occurs in cells derived from mice lacking the IFN-induced protein kinase (PKR). The apoptosis antagonist Bcl-2 prevents induction of cell death by RNase L activation. Apoptosis of mammalian cells by RNase L activation could be a mechanism mediating anticellular actions of IFN.
      Cfr. :
      http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WXR-45K15K0-22&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_search
      StrId=1081210930&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion
      =0&_userid=10&md5=ec59327235367bc2e868004cb9b64ac5

    6. Anthrax vaccination and self-reported symptoms, functional status and medical conditions in the National Health Survey of Gulf War Era veterans and their families
      Mahan CM, Kang HK, Dalager NA, Heller JM, Veterans Health Administration, Department of Veterans Affairs, Washington, DC, USA - Ann Epidemiol. 2004 Feb;14(2):81-8 - PMID: 15018879

      Purpose - To evaluate the health status of Gulf War veterans who reported receipt of anthrax vaccination and a small group of Gulf War veterans for whom documentation of anthrax vaccination exists.
      Methods
      - Among the 11,441 Gulf War veterans who completed a health survey, 4601 reported receiving the anthrax vaccine during the war; 2979 veterans reported not receiving it; 3861 were uncertain.
      Also, 352 of these respondents were documented by the Department of Defense as having received anthrax vaccination.
      We compared the medical history of these groups of veterans using multivariate analyses.
      Finally, we analyzed perception of exposure and its relation to reporting bias.
      Results
      - There were statistically significant differences in prevalence for almost all outcomes studied between those who reported having received anthrax vaccination and those who did not so report.
      However, when we compared the veterans for whom vaccination records exist to the group who self-reported that they had not received the vaccine, the significant differences in prevalence for almost all of the outcomes disappeared.
      Conclusions
      - The extent of a reporting bias should be carefully considered when one evaluates the health consequences of anthrax vaccination based on self-reported data.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15018879

    7. Anthrax vaccine
      © 2009 American Society of Health-System Pharmacists, Inc.
      Cfr. : http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=meds&log$=drug_bottom_one&part=a607013

    8. Anthrax vaccine - Controversy over safety and efficacy
      Garth L. Nicolson and Nancy L. Nicolson, The Institute for Molecular Medicine, Huntington Beach, CA 92649, Meryl Nass, Parkview Hospital, Brunswick, ME 04011, USA & The Institute for Molecular Medicine, Huntington Beach, CA 92649, USA - Antimicrobics and Infectious Diseases Newsletter, Volume 18, Issue 1, January 2000, Pages 1-6 - © 2000 Published by Elsevier Inc.
      Cfr. :
      http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T47-4091G3F-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchS
      trId=1080917228&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=
      0&_userid=10&md5=73fc9588103668a8e5ea1f768122094a

    9. Anthrax vaccine - Historical perspective and current controversy
      Nass M, Nicolson GL - J Nut Environ Med 2002; 14:277-286
      Cfr. :
      http://www.military-biodefensevaccines.org/meryl/resume.html

    10. Antibiotics/antivirals recommended when indicated for treatment of Gulf War illness/CFS/FMS/arthritis
      Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, California 92649-1041 – Tel. : (714) 903-2900 – Fax : (714) 379-2082 – E-mail : gnicolson@immed.org – Website : www.immed.org
      Cfr. :
      http://gulfwarcouncil.com/Nicolson-Consideration%20When%20Undergoing%20Treatment%20for%20Chronic%20and%20Autoimmune%20Diseases.htm

    11. Arthritis in patients with chronic hepatitis C virus infection
      Rivera J, García-Monforte A, Pineda A, Millán Núñez-Cortés J, Instituto Provincial de Rehabilitación, Internal Medicine Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain : fling01@sis.ucm.es - J Rheumatol. 1999 Feb;26(2):420-4 - PMID: 9972979
      Objective - To describe the clinical picture of arthritis in patients with chronic infection by hepatitis C virus (HCV).
      Methods - Two patient populations were studied.
      Patients with arthritis and evidence of serum elevation of alanine aminotransferase (ALT) at the consultation were checked for HCV infection.
      A second group of 303 consecutive patients with rheumatoid arthritis (RA) were also checked for the presence of HCV antibodies.
      All patients attended the outpatient rheumatology unit of a tertiary care teaching hospital.
      Chronic HCV infection was determined by the presence of viral RNA in serum.
      A group of 315 first-time blood donors served as controls.
      Results - Twenty-eight patients with arthritis and chronic HCV infection were identified. Seven fulfilled criteria for RA, psoriatic arthritis was found in one patient, systemic lupus erythematosus in one, gout in 2, chondrocalcinosis in 2, osteoarthritis in 7 and tenosynovitis in one.
      In 7 patients with a clinical picture of intermittent arthritis, a definitive diagnosis could not be made.
      In these patients, mixed cryoglobulinemia was present in 6/7 (86%), whereas mixed cryoglobulinemia was found in 6/21 (28%) of the other patients.
      Among patients with RA, 23 (7.6%) had HCV antibodies and active infection by HCV was found in 7 (2.3%) patients.
      The prevalence of HCV antibodies in a blood donor population was 0.95%, significantly different (p<0.001; 95% CI 0.03, 0.10) compared to patients with RA.
      The distribution of antibodies determined by recombinant immunoblot analysis was similar (p = NS) between RA patients and blood donors with HCV antibodies.
      Conclusion - There is not a single clinical picture of arthritis in patients with chronic HCV infection.
      There is a well defined picture of arthritis associated with the presence of mixed cryoglobulinemia that consists of an intermittent, mono or oligoarticular, nondestructive arthritis affecting large and medium size joints.
      Although a high prevalence of HCV antibodies is suspected in patients with RA, its occurrence may be coincidental and its interpretation is difficult to determine from the data in this study.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9972979?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Single
      ItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed

      Also read the comment on this article :
      Human immunodeficiency virus infection and arthritis
      Rivera J, Garcia-Monforte A - J Rheumatol. 2000 May;27(5):1322-3 - PMID: 10813314
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10813314?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    12. Association of mycoplasma and human immunodeficiency virus infection - Detection of amplified Mycoplasma fermentans DNA in blood
      Hawkins RE, Rickman LS, Vermund SH, Carl M, Department of Internal Medicine, National Naval Medical Center, National Institutes of Health, Bethesda, Maryland - J Infect Dis. 1992 Mar;165(3):581-5 - PMID: 1538164
      A cross-sectional study was undertaken to determine the prevalence of Mycoplasma fermentans infection in patients with human immunodeficiency virus (HIV) infection using polymerase chain reaction methodology.
      Targeted M. fermentans DNA sequences could be amplified from the DNA extracted from the blood of 6 (11%) of 55 HIV-seropositive patients but from none of 26 HIV-seronegative subjects at low risk for HIV infection (P = .17).
      There was no correlation between M. fermentans infection and HIV clinical stage.
      There was a nonsignificant trend toward an association between M. fermentans infection and a history of syphilis.
      Infection with M. fermentans may occur more commonly in HIV-infected patients; however, a role as a copathogen or opportunistic infection was not established in this study.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/1538164

    13. Bacterial and Viral Co-Infections in Chronic Fatigue Syndrome (CFS/ME) Patients
      Bacterial and viral co-infections in chronic fatigue syndrome patients
      Garth L. Nicolson,(1) PhD, Marwan Y. Nasralla,(2) PhD, Kenny De Meirleir,(3) MD, PhD and Jeorg Haier,(4)MD, PhD – (1) The Institute for Molecular Medicine, Huntington Beach, California, USA – (2) International Molecular Diagnostics, Inc., Huntington Beach, California, USA – (3) Department of Internal Medicine, Free University of Brussels, Brussels, Belgium and (4) Department of Surgery, Wilhelm-University, Munster, Germany – Correspondence : Prof. Garth L. Nicolson, Office of the President, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, California 92649. Tel. : 714-903-2900; Fax : 714-379-2082; Email : gnicolson@immed.org - Website : www.immed.org - ProHealth, June 14, 2002
      A majority of Chronic Fatigue Syndrome (CFS) patients have systemic bacterial and viral infections.
      In our study of 200 CFS patients we found a high prevalence (52%) of Mycoplasmal infections.
      Using forensic polymerase chain reaction we also examined whether these same CFS patients showed evidence of co-infections with various Mycoplasmas, Chlamydia pneumoniae and/or Human Herpes Virus-6 (HHV-6).
      We found that 7.5% of the patients had C. pneumoniae and 30.5% had HHV-6 infections.
      Since the presence of one or more infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and HHV-6 infections in Mycoplasma-positive and -negative patients.
      Unexpectedly, we found that the incidence of C. pneumoniae or HHV-6 was similar in Mycoplasma-positive and -negative patients.
      Also, the incidence of C. pneumoniae in HHV-6-positive and -negative patients was similar.
      Control subjects had low rates of Mycoplasmal (6%), HHV-6 (9%) or chlamydial (1%) infections and there were no co-infections in control subjects.
      Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant (P<0.001).
      The results indicate that a very large subset of CFS patients show evidence of bacterial and viral co-infections.
      Full text at :
      -
      http://www.prohealth.com/library/showarticle.cfm?id=3635&t=CFIDS_FM
      - http://www.immed.org/Fatigue%20Illness/Netal_co_MycoAust02%5B1%5D.1.rtf

    14. Bacterial products, cytokines and sleep
      JM Krueger L Johannsen, Department of Physiology and Biophysics, University of Tennessee, Memphis 38163 - J Rheumatol Suppl. 1989 Nov;19:52-7 - PMID: 2691682
      Sleep deprivation, infection and administration of muramyl peptides or certain other immune response modifiers all alter sleep.
      Sleep, temperature and hematologic effects observed after bacterial infection are also elicited after administration of isolated bacterial cell walls.
      Macrophages have the capability to digest bacterial peptidoglycan and in the process produce pyrogenic and somnogenic substances of low molecular weight.
      Activated macrophages also produce cytokines and some of these e.g., interleukin-1 (IL-1), are somnogenic.
      Our results emphasize the close connection of the infection process, fever and sleep.
      Muramyl peptides and/or IL-1 may also be involved in daily regulation of sleep.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/2691682

    15. Baseline mood and psychosocial characteristics of patients developing depressive symptoms during interleukin-2 and/or interferon-alpha cancer therapy
      Capuron L, Ravaud A, Miller AH, Dantzer R, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA : lcapuro@emory.edu - Brain Behav Immun. 2004 May;18(3):205-13 - PMID: 15050647
      It has been suggested that patients with subclinical mood symptoms prior to initiating cytokine treatment (as revealed by elevated baseline scores on depression rating scales) are more likely to become clinically depressed during the course of cytokine therapy.
      The present study was designed to identify which specific preexisting symptoms predict development of depressive symptomatology during treatment with the cytokines, interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha), in patients with cancer.
      Thirty-two patients with renal cell carcinoma or malignant melanoma eligible to receive treatment with IL-2 and/or IFN-alpha were enrolled in the study.
      At baseline and after one month of cytokine therapy (endpoint), depressive symptoms were assessed using the clinician-administered Montgomery-Asberg depression rating scale (MADRS).
      Illness-related coping strategies, social support, somatic complaints, quality of sleep and demographic factors were also assessed as relevant baseline predictive factors.
      MADRS scores significantly increased during cytokine therapy.
      Patients with moderate to marked depressive symptomatology at study endpoint exhibited higher baseline scores in dimensions of the MADRS scale assessing emotional (especially reported sadness), cognitive (especially pessimistic thoughts) and neurovegetative (sleep disturbances) symptoms compared to patients who remained free of depressive symptoms during cytokine therapy.
      Interestingly, only emotional symptoms and sleep disturbance at baseline, along with low social support, predicted severity of depressive symptoms at the end of the first month of therapy.
      By documenting specific behavioral vulnerability factors for cytokine-induced depressive symptoms, these findings may help identify patients at risk for mood disturbances during cytokine treatment and help target specific patient populations and specific symptoms for preventative strategies.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15050647

    16. Biochemical dysregulation of the 2-5A synthetase/RNase L antiviral defense pathway in chronic fatigue syndrome
      Suhadolnik RJ, Peterson DL, Cheney PR, Horvath SE, Reichenbach NL, O’Brien K et al. - Journal of Chronic Fatigue Syndrome 1999; 5:223-42

    17. Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome
      Suhadolnik RJ, Peterson DL, O'Brien K, Cheney PR, Herst CV, Reichenbach NL, Kon N, Horvath SE, Iacono KT, Adelson ME, De Meirleir K, De Becker P, Charubala R, Pfleiderer W, Department of Biochemistry, Temple University School of Medicine, Philadelphia, PA, USA - J Interferon Cytokine Res. 1997 Jul;17(7):377-85 - PMID: 9243369

      Previous studies from this laboratory have demonstrated a statistically significant dysregulation in several key components of the 2',5'-oligoadenylate (2-5A) synthetase/RNase L and PKR antiviral pathways in chronic fatigue syndrome (CFS) (Suhadolnik et al. Clin Infect Dis 18, S96-104, 1994; Suhadolnik et al. In Vivo 8, 599-604, 1994). Two methodologies have been developed to further examine the upregulated RNase L activity in CFS. First, photoaffinity labeling of extracts of peripheral blood mononuclear cells (PBMC) with the azido 2-5A photoaffinity probe, [32P]pApAp(8-azidoA), followed by immunoprecipitation with a polyclonal antibody against recombinant, human 80-kDa RNase L and analysis under denaturing conditions. A subset of individuals with CFS was identified with only one 2-5A binding protein at 37 kDa, whereas in extracts of PBMC from a second subset of CFS PBMC and from healthy controls, photolabeled/immunoreactive 2-5A binding proteins were detected at 80, 42, and 37 kDa. Second, analytic gel permeation HPLC was completed under native conditions. Extracts of healthy control PBMC revealed 2-5A binding and 2-5A-dependent RNase L enzyme activity at 80 and 42 kDa as determined by hydrolysis of poly(U)-3'-[32P]pCp. A subset of CFS PBMC contained 2-5A binding proteins with 2-5A-dependent RNase L enzyme activity at 80, 42, and 30 kDa. However, a second subset of CFS PBMC contained 2-5A binding and 2-5A-dependent RNase L enzyme activity only at 30 kDa. Evidence is provided indicating that the RNase L enzyme dysfunction in CFS is more complex than previously reported.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9243369

    18. British Society for Allergy and Environmental Medicine - Comments on the Gulf-War or human laboratory
      Nicolson GL, Nicolson NL - Med Confl Surviv 1996; 12:260-262
      Cfr. :
      http://www.informaworld.com/smpp/content~db=all~content=a783312384

    19. Candidiasis - Yeast infection and nutritional repair - Causes, symptoms, testing, natural treatments and probiotic strategies, anti-yeast/weight loss diet and trigger avoidance
      Mark J. Pellegrino, MD – ProHealth, December 6, 2006
      What would you say if I told you we had millions of Dr. Jekyll's living in our bodies, each waiting for the opportune time to turn into Mr. Hyde ?
      We all have little round whitish organisms in our body known as Candida albicans that can lose their innocence and become rather vicious creatures that attack our bodies.
      Candida albicans is fungus or yeast that normally thrives in the mouth, gastrointestinal tract, vagina and skin.
      In healthy individuals this yeast is helpful in digestion and vitamin production and it is harmless because it is kept in check by beneficial bacteria and other yeast such as Lactobacillus acidophilus that occupies the same space.
      When the balance of intestinal bacteria and yeast is altered or your immune system becomes compromised, the Candida can overgrow, transforming from a benign yeast into an aggressive fungus that releases numerous toxins and can cause many symptoms.
      When fungal growth exceeds the body’s ability to control it, the friendly Candida becomes unfriendly and cause a yeast infection.
      1. - Causes of Candida
      Various causes of Candidiasis (Candida infection) include :
      - Chronic illnesses or stress
      For example, diabetic patients, hospitalized patients and cancer patients all have low resistance to infection.
      - Antibiotic use
      This destroys normal bacteria and Lactobacillus acidophilus, but spares the Candida.
      - Birth control pills
      The estrogen favors Candida multiplication.
      -
      Cortisone medicine
      - Immunosuppressive drugs
      - Pregnancy

      Hormonal changes favor increased Candida growth.
      - Diets high in sugar and carbohydrates
      Candida loves glucose !
      - Thyroid medicine
      Increases Candida risk.
      - Warm moist areas
      Tight nylons, wet diapers, people who work as dish washers; all this can lead to Candida dermatitis.
      - Alcohol
      Another food for the Candida.
      Those with Fibromyalgia often have multiple risk factors, particularly the altered immune system, the chronic stress and the carbohydrate sensitivity.
      Throw in the woman... who is on birth control pills, thyroid medicine and recently took a course of antibiotics for bronchitis and you have a recipe for “Candisaster”!
      When Candida albicans transforms into an invasive fungal state, it produces rhizoids which are long root-like structures.
      Rhizoids can penetrate the intestinal walls and leave microscopic holes that allow toxins, undigested food particles, bacteria and yeast to enter the blood stream.
      This “invasion” leads to many symptoms.
      2. - Candidiasis symptoms
      -
      Bloating
      - Irritable bowel syndrome (IBS)
      - Chronic heartburn
      - Oral thrush (white spots on the mouth and tongue)
      - Vaginal yeast infection
      - Skin rashes
      - Skin itching
      - Vulvar pain and itching
      - Rectal itching
      - Fatigue
      - Irritability
      - Fibrofog
      - Food cravings (especially carbohydrates)
      - Malnutition (poor nutrient absorption)
      - Food allergies
      - Depression
      - Bad breath.
      As you can see there is much overlap of Candidiasis symptoms with fibromyalgia symptoms.
      These two conditions “feed” into each other where the fibromyalgia makes one have more problems with the Candidiasis and the Candidiasis causes symptoms that can aggravate the fibromyalgia.
      If I suspect Candidiasis, I will treat it separately from the fibromyalgia because this often leads to much improvement of fibromyalgia symptoms as well as correcting the Candida problem.
      3. - Testing for Candida
      A simple home test for Candidiasis can be performed.
      Dr. Kelly Hannigan described a test you can take (Health Points 8 (2) 2003).
      Before you go to sleep at night set a clear glass of water next to your bed.
      When you wake up in the morning (before you clear your throat, swallow or speak), deposit your saliva into the glass of water.
      If within 30 minutes your saliva sinks to the bottom or there are strands of saliva running down into the water or the water turns cloudy, you probably have an abundance of yeast in your body.
      Lab testing can be done for a definitive diagnosis of Candidiasis. Saliva, stool and blood samples can all be tested to look for specific immunoglobulin antibodies against Candida.
      These tests are not routinely covered by insurance companies so the patient has to pay for these tests, which are usually several hundred dollars.
      Since intestinal Candidiasis is so common and easily identified with careful history of symptoms and since treatments are low-risk and well-tolerated, I will usually treat Candidiasis based on the clinical exam (history and physical) and not always order a specific yeast test.
      4. - Candidiasis treatment
      The strategies for treating Candidiasis are focused on rebalancing the intestinal bacteria and yeast.
      Candida that has overgrown needs to be killed and suppressed.
      The “good” yeast and bacterial needs to be replenished and the gastrointestinal tract needs to be rebalanced.
      Here are some strategies used to rebalance the intestinal tract.
      Antiyeast products - Prescribed medicines
      Prescribed medicines to treat Candida include Nystatin (mycostatin) and Fluconazole (Diflucan). Nystatin is available in tablet and liquid form.
      The liquid form is used to treat oral thrush (“swish and swallow”).
      The tablet forms are used for intestinal Candidiasis and they are usually well tolerated, although some people have some nausea or diarrhea with them.
      Patients may need to be on this medicine for several months and some of them need to be on maintenance dose for long-term Candida management.
      Nystatin kills off Candida, but does not harm the Lactobacillus or bacteria.
      Fluconazole is another antifungal medicine that is given to treat Candidiasis.
      Sometimes one tablet or two tablets only are used to treat a vaginal yeast infection.
      However, a vaginal yeast infection or recurring vaginal yeast infections in women are a sign of more widespread Candidiasis; the vaginal yeast infection is actually the “tip of the iceberg”.
      In treating intestinal or more widespread Candidiasis, Diflucan may need to be used for weeks instead of days.
      Antiyeast products - Natural treatments
      Natural antiyeast treatments include herbal products such as enteric coated oregano extract and olive leaf extract (Oleuropein).
      Olive leaf extract has the ability to attack Candida and other potential harmful microorganisms while sparing the helpful ones.
      To treat Candida, two capsules every eight hours on an empty stomach are recommended.
      Olive leaf extract can be used in conjunction with the prescribed antibiotic or can be used as a first line anti-Candida treatment.
      5. - Herxheimer's reaction
      Herxheimer’s reaction can occur when the Candida die off (this reaction typically involves flu-like symptoms and results when infective agents are killed/toxins are released faster than the kidneys and liver can remove them via the natural detoxification process).
      A sudden die-off of Candida can release a lot of toxins and the result may be aggravation of symptoms.
      Whereas this is not necessarily a bad thing, this type of reaction can cause significant discomfort, so we usually back off on the medicine to a lower dose to avoid a rapid die-off and to allow a slower and steadier die-off of Candida.
      To minimize Herxheimer’s reaction when taking Nystatin I have patients start with one Nystatin tablet on the first day and then increase by one tablet a day until the desired dose of six tablets a day is being taken.
      A slow die-off of the Candida is preferred as it allows the gastrointestinal tract to better rebalance and not create sudden changes that a rapid die-off can cause.
      Plus a slower die-off allows the friendly yeast and bacteria to gradually fill the spaces and help rebuild the intestines.
      6. - Friendly replenishers (probiotics & prebiotics)
      Lactobacillus acidophilus and the good bacteria are called probiotics.
      These “friendly” yeast and bacteria help with digestion and vitamin production and when Candida has died off, these friendly probiotics are necessary to help rebuild the gastrointestinal flora by filling the spaces where Candida used to be and restoring proper balance.
      An acidophilus supplement is recommended to help replenish the flora.
      Fructooligosaccharides (FOS) are the food source for healthy bacteria.
      Any good nutrient (FOS) for the probiotics (acidophilus and other friendly bacteria) is called prebiotic.
      I like to use a…prebiotic and probiotic blend that helps counteract Candida buildup and maintain healthy intestinal flora.
      Acidophilus supplements have done an excellent job of treating irritable bowel syndrome, which reinforces the theory that a lot of irritable bowel flare-up can be related to Candidiasis.
      I usually have patient continue the acidophilus on an ongoing basis, especially when fibromyalgia increases their risk of Candidiasis.

    Go to Part II


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    Infection as one possible cause of fibromyalgia

    Part II

    7. - Dietary strategies
    The Candida thrive on high sugar concentrations, so a basic diet strategy is cutting back the number of carbs.
    Fermented foods such as soy sauce, vinegar, pickles, cheese and yogurt have high sugar concentrations that feed yeast so these should be avoided.
    The fibromyalgia diet that I described in Chapter 17 is also a good antiyeast diet (cfr. “Why weight gain is a problem with fibro and what to do about it” at :
    http://www.prohealth.com/library/showarticle.cfm?id=7468&t=CFIDS_FM -).
    In addition to watching the carbohydrates, you should make sure to get enough fiber in your diet because that will help eliminate toxins and unwanted yeast in the bowel.
    Many people can learn to control Candida yeast overgrowth simply by modifying the diet.
    Often a combination of yeast antibiotic and friendly replenishers is also necessary along with dietary changes.
    8. - Avoid aggravating factors
    If possible, avoid drugs, chemicals and foods that can trigger the Candida and its symptoms.
    Since alcohol can aggravate Candida, it should be avoided or used in moderation.
    Obviously it is not practical to stop thyroid medicine, hormone medicines or other necessary prescribed medicines.
    Likewise, if you develop a bacterial infection, you may require an antibiotic.
    If you must take an antibiotic for a bacterial infection, you might want to also take Nystatin or a natural yeast antibiotic to counteract the potential for Candida overgrowth while on the antibiotic.
    Any prescription medication that you have identified as a cause of Candidiasis should be reviewed with your doctor to see if it can be reduced or changed.
    If you have Candidiasis, you can successfully transform the Candida back to Dr. Jekyll where he can live peacefully in the normal flora neighborhood...
    Cfr. :
    -
    http://www.prohealth.com/library/showArticle.cfm?libid=12385
    -
    http://www.prohealth.com/library/showarticle.cfm?id=7553&t=CFIDS_FM

    1. Cardiac insufficiency hypothesis
      M.E. Society of America, (last updated) February 22, 2009
      There is new research from a New Jersey team, authored by Doctors Arnold Peckerman, Benjamin Natelson et al., which found left-ventricular dysfunction following exertion and orthostatic stress in patients with myalgic encephalomyelitis/chronic fatigue syndrome.
      The WedMD article and the press release are available at the link below.
      In an NIH-funded study on impedance cardiography also linked below, Peckerman and Natelson found that low cardiac output correlated with symptom severity in ME/CFS.
      Dr. A. Martin Lerner holds U.S. patents for the diagnosis of ME/CFS in the chronic mononucleosis subset of this disease using 24-hour Holter monitoring.
      He argues that a prominent subset of the disease is a prolonged, chronic mononucleosis following infection with Epstein Barr virus (EBV), Human Cytomegalovirus (HCMV) or both and/or possibly Human Herpes Virus 6 (HHV-6).
      Viral infection persists in the heart, causing left-ventricular dysfunction, producing exercise intolerance.
      Exercise, in turn, worsens the cardiac dysfunction.
      He has also postulated that the disease is an early dilated cardiomyopathy that in later stages might result in progressive, end-stage dilated cardiomyopathy, a type of heart failure.
      Dilated cardiomyopathy is sometimes viewed as "idiopathic" or "Idiopathic Dilated Cardiomyopathy" (IDC).
      In an editorial response titled "Microbial Persistence and Idiopathic Dilated Cardiomyopathy" Dr. Lerner has postulated that these viruses may be the etiological link.
      More recently, physicist, physician, long-time ME/CFS researcher and clinician and heart-transplant recipient Paul Cheney, M.D., Ph.D., has offered an alternative theory that a subset of ME/CFS patients suffer from a diastolic cardiomyopathy, a problem with ventricular filling resulting from mitochondrial dysfunction and low ATP energy in the heart.
      To view a streaming video of a three-hour talk by Dr. Cheney on diastolic cardiomyopathy and ME/CFS, click :
      http://www.cfids-cab.org/MESA/CFS_Dist.htm -.
      This video can be accessed with a broadband connection only.
      The video cannot be properly viewed using a dial-up modem.
      Because there may be many people trying to access the video at once, our server may become temporarily overloaded.
      Please try back again if you encounter this problem or if the video does not play for the full three hours.
      Note that some of the most informative parts of this three-hour talk occur in the second half when Dr. Cheney discusses and shows charts on cardiac output in litres per minute, comparing ME/CFS patients with controls.
      To purchase a videocassette of this seminar by Dr. Cheney from the Dallas-Fort Worth CFS group, click :
      http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0509B&L=CO-CURE&P=R911 -.
      A detailed discussion of Dr. Cheney's views is available below in an interview by Carol Sieverling, and is recommended reading along with the Peckerman/Natelson article on impedance cardiography for those who want to study the insightful issues addressed in the video.
      To purchase a DVD set of another talk by Dr. Cheney illustrating more recent echocardiographic and other objective data on ME/CFS and heart failure, click :
      http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0610E&L=CO-CURE&P=R346 -.
      Some of Dr. Lerner's significant articles, as well as his patent issued in 2002, are linked below in Portable Document File (PDF) format.
      .../...
      Cfr. :
      http://www.cfids-cab.org/MESA/Lerner.html

    2. Causes of death among patients with chronic fatigue syndrome
      Leonard A. Jason, Karina Corradi, Sara Gress, Sarah Williams & Susan Torres-Harding, DePaul University, Chicago, Illinois, USA - Address correspondence to Leonard A. Jason, Center for Community Research, DePaul University, 990 W. Fullerton Ave., Suite 3100, Chicago, IL 60614 : Ljason@depaul.edu - Health Care for Women International, 27:615–626, 2006 - © Taylor & Francis Group, LLC - PMID: 16844674
      Chronic fatigue syndrome (CFS) is a debilitating illness affecting thousands of individuals.
      At the present time, there are few studies that have investigated causes of death for those with this syndrome.
      The authors analyzed a memorial list tabulated by the National CFIDS Foundation of 166 deceased individuals who had had CFS.
      There were approximately three times more women than men on the list.
      The three most prevalent causes of death were heart failure, suicide and cancer, which accounted for 59.6% of all deaths.
      The mean age of those who died from cancer and suicide was 47.8 and 39.3 years, respectively, which is considerably younger than those who died from cancer and suicide in the general population.
      The implications of these findings are discussed.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/16844674
      Full text at : http://www.theoneclickgroup.co.uk/documents/ME-CFS_docs/Causes%20of%20Death%20-%20CFS%20Patients.pdf

    3. Central nervous system manifestations of Mycoplasma pneumoniae infections
      Tsiodras S, Kelesidis I, Kelesidis T, Stamboulis E, Giamarellou H, 4th Academic Department of Internal Medicine and Infectious Diseases, Attikon University Hospital, University of Athens Medical School, 1 Rimini Street, Xaidari, 12462 Athens, Greece : tsiodras@med.uoa.gr - J Infect. 2005 Dec;51(5):343-54. Epub 2005 Sep 19 - PMID: 16181677
      Mycoplasma pneumoniae infection is associated with several manifestations from the central nervous system (CNS) such as encephalitis, aseptic meningitis, acute transverse myelitis, stroke and polyradiculopathy.
      In the current paper epidemiologic, clinical, laboratory and treatment data on these manifestations are reviewed.
      The M. pneumoniae induced immune dysregulation and its contributing role in the pathogenesis of neurological insult is discussed.
      The recent introduction in clinical practice of newer molecular diagnostic techniques has helped in establishing a firmer association between M. pneumoniae infection and CNS disease especially encephalitis.
      Clinicians should be aware of the potential association between M. pneumoniae infection and several CNS manifestations.
      The role of various anti-microbial or immunomodulating therapies in treating such manifestations should be further explored.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/16181677?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleIt
      emSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmed

    4. Central sensitivity syndromes - A new paradigm and group nosology for fibromyalgia and overlapping conditions and the related issue of disease versus illness
      M. Yunus - Seminars in Arthritis and Rheumatism, Volume 37, Issue 6, Pages 339-352 - © 2009 Elsevier B.V.
      Objectives - To discuss the current terminologies used for fibromyalgia syndrome (FMS) and related overlapping conditions, to examine if central sensitivity syndromes (CSS) is the appropriate nosology for these disorders and to explore the issue of disease versus illness.
      Methods - A literature search was performed through PubMed, Web of Science and ScienceDirect using a number of keywords eg, functional somatic syndromes, somatoform disorders, medically unexplained symptoms, organic and nonorganic and diseases and illness.
      Relevant articles were then reviewed and representative ones cited.
      Results - Terminologies currently used for CSS conditions predominantly represent a psychosocial construct and are inappropriate.
      On the other hand, CSS seems to be the logical nosology based on a biopsychosocial model.
      Such terms as “medically unexplained symptoms”, “somatization”, “somatization disorder” and “functional somatic syndromes” in the context of CSS should be abandoned.
      Given current scientific knowledge, the concept of disease–illness dualism has no rational basis and impedes proper patient–physician communication, resulting in poor patient care.
      The concept of CSS is likely to promote research, education and proper patient management.
      Conclusion - CSS seems to be a useful paradigm and an appropriate terminology for FMS and related conditions.
      The disease–illness, as well as organic/non-organic dichotomy, should be rejected.
      Cfr. :
      http://linkinghub.elsevier.com/retrieve/pii/S0049017207001473

    5. Central sensitivity syndromes - A unified concept for Fibromyalgia and other similar maladies
      Muhammad Yunus, Section of Rheumatology, University of Illinois College of Medicine Peoria, Illinois, USA - Journal of Indian Rheumatism Association. 2000 Mar; 8(1): 27-33
      Fibromyalgia syndrome(FMS) and similar other conditions, e.g., myofascial pain syndrome, irritable bowel syndrome, chronic fatigue syndrome, headaches and restless legs syndrome share several characteristics, including pain, poor sleep, fatigue, hyperalgesia and an absence of structural tissue pathology.
      These syndromes are bound by a common pathophysiological mechanism, i.e., neurohormonal dysfunctions, which are generally different from those in psychiatric diseases.
      Central nervous system (CNS) sensitivity, either intrinsic or due to CNS neuroplasticity secondary to peripheral stimuli, results in amplified, widespread and persistent pain.
      This central sensitivity seems to be the most important aberration among the neuroendocrine dysfunctions.
      Thus, FMS and other overlapping syndromes have been called "central sensitivity syndromes" (CSS) as a group.
      Current research suggests that central sensitivity is present among the CSS members and is likely to be the common biopathophysiological glue that binds them.
      Cfr. :
      http://medind.nic.in/imvw/imvw4222.html

    6. Chlamydia pneumoniae antibodies in myalgia of unknown cause (including fibromyalgia)
      Machtey I - Br J Rheumatol. 1997 Oct;36(10):1134 - PMID: 9374940
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9374940
      This article is a comment on :
      Chlamydia pneumoniae--reactive arthritis and persistent infection
      Moling O, Pegoretti S, Rielli M, Rimenti G, Vedovelli C, Pristerá R, Mian P - Br J Rheumatol. 1996 Nov;35(11):1189-90 - PMID: 8948316
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8948316?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    7. Chlamydia pneumoniae in CFS/ME & fibromyalgia / Chronic fatigue syndrome, fibromyalgia & chlamydia pneumoniae
      Cpnhelp.org
      Cfr. :
      http://www.cpnhelp.org/chlamydia_pneumoniae_in_0

    8. Chlamydia pneumoniae in chronic fatigue syndrome and fibromyalgia – An opinion
      Patient Advocate James Kepner from the Chlamydia pneumoniae (Cpn) Help website - http://www.cpnhelp.org - April 23, 2007 - © CpnHelp.org
      Editor's note & introduction
      Does chronic Chlamydia pneumoniae (Cpn) infection play a role in the pathogenesis or symptoms of some patients with chronic fatigue syndrome, fibromyalgia syndrome and other unexplained illnesses ?
      It's a distinct possibility, based on a never-published trial conducted by leading CFS clinical researchers Peterson, Cheney, Bell and Stratton in the late 1990's.
      Here's the story of that research and an opinion on its implications for CFS and FMS patients, written by James Kepner, a leader of the Cpn patient community.
      Who is Jim Kepner ?
      He is an active Chlamydia pneumoniae patient advocate and owner/founder of CpnHelp.org, "a website devoted to the understanding and treatment of Chlamydia pneumoniae, an infectious bacteria implicated in a number of human illnesses".
      It is a non-commercial site "run and supported by volunteers and does not take monetary or other assistance from any other sources".
      In the following article Mr. Kepner refers extensively to the work of Charles W. Stratton, MD,1 Associate Professor and Director of Clinical Microbiology at Vanderbilt University School of Medicine in Nashville, Tennessee.
      Dr. Stratton's research focus is the pathogenesis of Cpn, with a present emphasis on its possible role in Multiple Sclerosis.
      Other researchers at Johns Hopkins, the Mayo Clinic and elsewhere have been similarly focused on investigating Cpn's possible role in a range of illnesses, from Coronary Artery Disease and Rheumatoid Arthritis to Interstitial Cystitis.
      What is Chlamydia pneumoniae ?
      Extensive information about this organism and associated research is offered at the Cpnhelp.org site and in this article.
      Briefly, Chlamydia pneumoniae is a bacterial organism first described in 1988 that is most commonly contracted by breathing droplets floating in the air after a person who carries it has coughed - as with the organism that causes tuberculosis.
      Cpn can then infect the "mucous-moving" cells lining the airways.
      It can paralyze those cells because it survives by stealing their energy, and may cause a serious respiratory infection.
      Then, if the body's immune response is unable to kill the invading Cpn bacteria, they can be disseminated via "mononuclear cells" in the bloodstream to infect other cells in the body, such as those that line the blood vessels, nerve tissues, brain, muscles and even immune cells.
      There again Cpn bacteria metabolize and damage these cells by "stealing" energy. Further, the Cpn bacteria are drawn to newly formed mononuclear blood cells, which tend to be generated where there is inflammation in the body - and where the Cpn can cause a secondary infection.
      And finally, Cpn passes through three forms in its life cycle, so that research indicates a combination of antibiotics may be necessary to kill it off in all forms.
      "If you have inflammation, a spider bite, a viral joint infection, viral meningitis or encephalitis," Dr. Stratton has said, "it doesn't matter what it is, if a Chlamydia-infected cell happens to end up in that inflamed area, you may have just started yourself a Chlamydia farm".
      In which case Chlamydia may not be the cause of the disease, but may play an important role in its progression (cfr. : 'Chlamydia pneumoniae not caught like you thought' - Vanderbilt Medical Center Reporter, April 23, 1999
      Cfr. :
      http://www.mc.vanderbilt.edu/reporter/index.html?ID=779 -).
      2. - Chlamydia pneumoniae in chronic fatigue syndrome and fibromyalgia
      Chronic fatigue syndrome (CFS), also called 'Chronic fatigue immunodeficiency disorder (CFIDS)' or called 'Myalgic Encephalomyelitis (ME)' in Great Britain, affects 1 million Americans, with "tens of millions" more who have a fatigue condition that doesn't meet the strict criteria for CFS (cfr. 'Chronic fatigue syndrome – Basis facts' at :
      http://www.cdc.gov/cfs/cfsbasicfacts.htm#prevalence -).
      According to the Centers for Disease Control and Prevention (CDC), which considers CFS an accepted medical condition
      --- CDC Diagnostic Symptoms

      Unexplained, persistent fatigue that is not due to ongoing exertion, is not substantially relieved by rest, is of new onset (not lifelong) and results in a significant reduction in previous levels of activity - and four or more of the following symptoms are present for six months or more : * impaired memory or concentration - * postexertional malaise (extreme, prolonged exhaustion and exacerbation of symptoms following physical or mental exertion) - * unrefreshing sleep - * muscle pain - * multi-joint pain without swelling or redness adults - * headaches of a new type or severity - * sore throat that’s frequent or recurring - * tender cervical or axillary lymph nodes. ---
      ---
      Other Commonly Observed Symptoms in CFS
      The frequencies of occurrence of these symptoms vary from 20% to 50% among CFS patients .../... include abdominal pain, alcohol intolerance, bloating, chest pain, chronic cough, diarrhea, dizziness, dry eyes or mouth, earaches, irregular heartbeat, jaw pain, morning stiffness, nausea, night sweats, psychological problems (depression, irritability, anxiety, panic attacks), shortness of breath, skin sensations, tingling sensations and weight loss.
      ---
      there is no officially known cause or cure for CFS or for the related and often co-occurring, condition of Fibromyalgia Syndrome (FMS).
      --- Estimated by the American College of Rheumatology to affect 6 million Americans ---
      Despite the CDC's affirmation, the syndrome and its diagnosis is still considered controversial, even in this day and age.
      Some doctors continue to insist that chronic fatigue syndrome is not a "real" disease entity.
      It may be rather a surprise to its sufferers when, naively seeking medical assistance, they find that their doctor doesn't believe that their symptoms are from a "real disease" or merit medical treatment.
      That there is no known "test" for chronic fatigue syndrome that can conclusively demonstrate its existence is one of the difficulties here.
      Perhaps another difficulty is that medical practitioners are socialized to believe that feelings of their own helplessness are a sign of personal failure.
      A solution to this psychological conundrum is to blame the patient by "psychologizing" the problem - that is, "It's in your head".
      Fortunately, acceptance of the legitimacy of the disease has increased in recent years, even if conventional medical treatment for it continues to have little offer of help.
      As the causal factors of CFS are considered unknown, conventional medical treatment for it and for fibromyalgia syndrome are all palliative [addressing symptoms] in nature : antidepressants for mood and pain associated with it, medications for sleep, stimulants for the fatigue, behavioral strategies and so on.
      These can help make life bearable but don't fundamentally change the condition.
      ---
      A popular palliative intervention with “cutting edge” conventional practitioners is Cognitive Behavioral Therapy (CBT). I’m a psychologist by profession and should be fond of my profession’s contributions to a challenging disease. But my personal and professionally informed commentary on the value of CBT as a CFS/FMS treatment is not high. As applied to the condition of chronic fatigue syndrome, CBT may be likened to teaching someone to how to become more relaxed and organized while one is standing upon a sinking ship. Thus, metaphorically, CBT teaches one how to adjust their viewpoint as the horizon tilts; how to stop worrying about the water lapping at their feet, how to counter the emotional responses of impending doom, how to relax so their stress doesn’t add water to the already sinking ship and so on. Like my stubborn friends here at www.cpnhelp.org dealing with Multiple Sclerosis who were often told there’s nothing that can be done but “get comfortable with your disease,” finding comfort in my decline has never been personally attractive to me as a solution.
      Some studies have found CBT “effective” in reducing CFS symptom severity. This makes CBT much beloved by conventional physicians as it, a) is legitimized by scientific research, b) they feel at least they have something to offer these “difficult-to-help-patients” and c) CBT still fits comfortably with the continuing vague suspicion that CFS isn’t really a disease at all but is really “all in their head” after all. I have not spoken a single CFS patient and I have communicated with many, who has found that CBT did anything of significance for them in terms of their disease. This said, CBT does teach highly valuable relaxation, stress management and cognitive strategy skills. These are useful in a disorder highly impacted by stress and which is very cognitively disorganizing. However like all palliative measures, CBT is only helpful at managing the disease and in this it is not even profoundly so.
      ---
      3. - Disease syndromes – More common than you think
      Chronic fatigue syndrome is often disparaged as being a "syndrome", merely a collection of symptoms, not a disease - that is, not a causal entity.
      Of course, a critique applying to one syndrome should apply to them all, yes ?
      A syndrome is a collection of signs and symptoms ('sign' = something you can measure; 'symptom' = patient reports) that appear to have diagnostic consistency.
      A syndrome tells you nothing per se about the cause of the problem.
      Many different causes, and sometimes more than one cause at the same time, can result in a syndrome.
      Interestingly, the diagnosis of "pneumonia", just like chronic fatigue syndrome, is actually a syndrome, though it is not referred to as “pneumonia syndrome".
      The diagnosis of "pneumonia" does not tell what is causing it, which can be variously viral, bacterial, food aspiration and so on.
      Similarly, diagnosing chronic fatigue syndrome doesn't tell you about possible causes until further investigation is done.
      There could be a variety and/or combination of potential causes.
      There are examples of modern, multi-factorial and case-individualized approaches to CFS/FMS that go beyond conventional medical ignorance about CFS.
      These combine both symptomatic treatment and a search for possible causal contributors for each specific patient (cfr. : “Effective treatment of chronic fatigue syndrome and fibromyalgia—A randomized, double-blind, placebo-controlled, intent-to-treat study” - Jacob E. Teitelbaum a; Barbara Bird a; Robert M. Greenfield b; Alan Weiss b; Larry Muenz c; Laurie Gould d - a Annapolis Research Center for Effective FMS/CFIDS Therapies and the Anne Arundel Medical Center, Annapolis, MD, USA - b Anne Arundel Medical Center, Annapolis, MD, USA - c Larry Muenz resides in Gaithersburg, MD, USA - d Annapolis Research Center for Effective FMS/ CFIDS Therapies, Annapolis MD, and also the USDA, Beltsville, MD, USA - Journal Of Chronic Fatigue Syndrome, Volume 8, Issue 2 May 2000 , pages 3 – 15 at :
      http://www.informaworld.com/smpp/content~db=jour~content=a903600733~tab=citations -).
      The various causal factors being looked into are amply discussed elsewhere and can be found in any web search.
      One of the proposed causal mechanisms for at least a sub-set of CFS is that of bacterial or viral infection. Especially "occult infections" - that is, those organisms that are either typically overlooked or difficult to test for or tend to evade the immune system (cfr. “The immune system, atherosclerosis and persisting infection“ - Pigarevskii PV, Mal'tseva SV, Seliverstova VG - Vestn Ross Akad Med Nauk. 2005;(2):17-22 at :
      http://www.cpnhelp.org/?q=node/129 -).
      Within this causal possibility are infectious organisms such as Chlamydia pneumoniae.
      My purpose here will to be present the information that argues for the involvement of Chlamydia pneumoniae in at least a subset of CFS and FMS patients.
      I will outline how Chlamydia pneumoniae's known biology and impact on the body could explain some of the characteristic symptoms and signs of CFS.
      At the outset it should be said that Chlamydia pneumoniae (Cpn) is not the only infectious agent that has been implicated in CFS/FMS.
      We certainly don't know if it is involved in all or in a subset, or is merely a co-condition of such cases.
      But there is good reason to look further at this particular organism's involvement.
      Most of the argument discounting Cpn's involvement in CFS/FMS has been based on ignorance and poor understanding about the organism itself and the difficulties of testing and treatment for it.
      This is an attempt to correct this ignorance and place Chlamydia pneumoniae more clearly in the realm of possible sources for these devastating conditions.
      4. - The early Vanderbilt work – Chlamydia pneumoniae in chronic fatigue syndrome
      The incomplete research
      There is some published work linking Chlamydia pneumoniae to chronic fatigue syndrome/fibromyalgia syndrome in medical research journals (cfr. : “Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients - Association with signs and symptoms” - Nicolson GL, Gan R, Haier J, The Institute for Molecular Medicine, Huntington Beach, California 92649, USA :
      gnicolson@immed.org - APMIS. 2003 May;111(5):557-66 - PMID: 12887507 at : http://www.ncbi.nlm.nih.gov/pubmed/12887507 -&- “Chronic Chlamydia pneumoniae infection - A treatable cause of chronic fatigue syndrome” - Chia JK, Chia LY, Torrance Memorial Medical Center, California, USA : chiasann@pol.net - Clin Infect Dis. 1999 Aug;29(2):452-3 - PMID: 10476765 at : http://www.ncbi.nlm.nih.gov/pubmed/10476765 -).
      But perhaps the most important research in this regard never reached publication.
      This article is the first thorough description in a public information setting.
      The original initial work at Vanderbilt by Dr. Charles Stratton and his lab on Chlamydia pneumoniae was actually not first directed at Multiple Sclerosis, as is more commonly believed, but looked at Cpn in Chronic Fatigue Syndrome.
      The first grant monies received by Dr. Stratton for Cpn research, using the highly sensitive tests they have developed, were from the Massachusetts Chronic Fatigue Foundation in the mid to late 1990s.
      Dr. Stratton was asked to test blood samples submitted by the well-known Chronic Fatigue Syndrome physicians Paul Cheney, MD, Daniel Peterson, MD and David S. Bell, MD to explore the possible involvement of Cpn in their CFS patients.
      As I understand it, the grant was given to these doctors and the determination of patients was by their own diagnostic selection.
      This research was never published, for reasons that will be explained later.
      The lack of publication and follow-through of this work may be one of the great tragedies in a long line of them in the history of chronic fatigue syndrome.
      Many patients may have suffered needlessly from this disease because the strong link between CFS and Cpn has remained largely unknown.
      4.1 - A Remarkable Finding
      In this research, Doctors Cheney, Peterson and Bell sent blood samples from their own CFS patients to Dr. Stratton's Vanderbilt Chlamydia pneumoniae Research Lab for testing.
      According to Dr. Stratton, they tested hundreds if not thousands of such blood samples.
      These were tested using both ELISA-based serologic methods and PCR [polymerase chain reaction] testing using the tests developed by Stratton et al. at the Vanderbilt Cpn lab. Dr. Stratton's lab found that the majority (almost 100%) of CFS patients were PCR positive for Cpn in blood samples.
      That the selected patient group of CFS patients had almost 100% positive PCR tests for Cpn (actual proteins, which means actual presence of the bacterial particles - not only an antigen response, which could be a remnant from prior infection) is an extraordinary finding.
      Further, the majority also had either elevated IgM or IgG antibodies to Cpn major outer membrane protein, cross-confirming the PCR-based findings.
      Of course, this in and of itself does not mean Cpn is the cause of CFS.
      The presence of Cpn could be due to some third factor that is part of CFS (such as immuno-suppression etc).
      But such a high correlation with one specific organism outweighs every other biological finding to date in CFS research.
      No other single variable in the CFS literature even comes close to being found in near 100% of CFS patients.
      Now there are some unknowns here - especially the criterion used to select those patient samples sent to Vanderbilt.
      This remains unknown as of this writing.
      4.2 - The first research problem
      They also discovered that many of the randomly selected "healthy controls" were also Cpn PCR positive.
      This would tend to call into question the tests themselves - that is, suggest that the tests are generating false positives.
      So they tested a random sample of blood donors to have a larger pool of healthy controls from which to get a baseline comparison for the study's original control group.
      They found that, of "healthy blood donors" about 20% were Chlamydia pneumonia positive !
      This percentage was higher than expected at the time, as it was not yet understood how ubiquitous Cpn is.
      However, it turns out that this matches the figures of Cpn [incidence] found in recent research with healthy, young blood donors (cfr. “Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescence microscopy and flow cytometry techniques” - Cirino F, Webley WC, West C, Croteau NL, Andrzejewski C Jr, Stuart ES, Department of Microbiology, University of Massachusetts, Amherst, Massachusetts 01003, USA :
      fcirino@microbio.umass.edu - PMID: 16472397 (erratum in : BMC Infect Dis. 2006;6:165) at : http://www.ncbi.nlm.nih.gov/pubmed/16472397 --- … “Thirteen of 70 donors (18.5%) showed the presence of bacterial transcript in cultured PBMNCs. …Conclusion : The bacterial transcripts in PBMNCs obtained from healthy donors were detected by the RT-PCR method. Viable C. pneumoniae may be present in healthy human PBMNCs…” ---.
      That these earlier Vanderbilt studies found the percentage of Cpn occurring in healthy donors replicating the current accepted findings (which range from 18% to 25%) lends credence to the accuracy and sensitivity of the tests used to study this original CFS sample.
      In other words, post hoc data suggest that their finding of an incidence of Cpn in healthy "controls" was an accurate one, not an artifact from an inaccurate test.
      4.3 - The Next Problem - Treatment
      The obvious next step was to try courses of antibiotics known to be anti-chlamydial and see if reduction of PCR signal for Cpn correlated with reduction in CFS symptoms.
      This was done by Doctors Cheney, Peterson and Bell with a sample of their patients.
      It turned out that no single antibiotic agent eradicated the Chlamydia pneumoniae PCR signal.
      So Dr. Stratton's lab, having laboriously developed the PCR susceptibility tests (described quite elegantly in the patent materials, which can be found linked elsewhere in the CpnHelp.org website) now had to use them to discover which agents or combinations of agents were required to eradicate Cpn completely, such that no PCR signal was evident in blood samples.
      This is called "sensitivity testing".
      This was a greater challenge than most of us would think.
      Along the way to infecting mice and cell cultures with Cpn and looking for effective combinations of antibiotics, they discovered that the available laboratory and commercial cell cultures widely assumed by scientists to be "clean" and thus proper starting points for introducing new variables, were themselves often infected with Chlamydia pneumoniae.
      This could seriously skew the interpretation of their tests.
      So Dr. Stratton's lab had to first develop methods to clear the cell cultures of Cpn and prove such clearance using their sensitive PCR testing.
      This is a remarkable bit of science here.
      Their finding that common biological laboratory materials are contaminated with Cpn appears also to be relatively unknown.
      From all of this they managed to find that only certain combinations of antibiotic agents (described elsewhere in the CpnHelp.org website) would completely eradicate Cpn from tissue cultures and laboratory mice, as indicated by clearance of Cpn PCR signal.
      No single antibiotic treatment, nor any series of antibiotics one at a time, was able to eradicate Cpn.
      Now that they had the combination antibiotic protocol (CAP), they could test the impact of eradicating Cpn on the resulting CFS symptoms and then confirm whether patients were actually clear of Cpn from the blood testing.
      4.4 - And another thing
      As in all research, there is always another problem ahead.
      This time the problem was with the reactions to the clinical treatment itself being tried by Doctors Cheney, Peterson and Bell, as well as by Dr. Stratton with his own CFS patients.
      The treatment was indeed working to kill Cpn, but the toxicity of the Cpn kill was causing existing symptoms to worsen significantly.
      The dropout rate using the combination antibiotic protocol or CAP for CFS was very high.
      Many patients were unable to see it through to the endpoint of the whole treatment process - where PCR signal was absent for Cpn.
      As Dr. Stratton put it to me in an interview, "The cure appeared worse than the disease".
      It was difficult for the treating physicians to keep patients on the protocol long enough to begin to see significant symptomatic improvement.
      This was due to two major difficulties.
      Die-off reactions - When combinations [of antibiotics] were used, the die-off reactions from this potent mix could be as bad as or worse than the CFS itself.
      Little was yet known about how to support patients through these reactions or what exactly their nature was (cfr. : the explanation of “worsening” later in this article).
      Length of treatment - Moreover, the length of treatment of Cpn with these combination antibiotic protocols for CFS was very long.
      It was difficult to get patients to "stay the course" without extraordinary support or dedication on the part of both the patient and the physician.
      It was quite a challenge for the CFS physicians, including Dr. Stratton, to know how to manage these responses and how to support their patients to hang in with a treatment that seemed to have little short term gain (one of the things Dr. Stratton said to me shortly after I started www.cpnhelp.org was that this kind of thing was one of the missing elements in the treatment process : some kind of on-going support community that could help patients through the challenges and confusions of being on a difficult protocol).
      For those patients (a small number) whom Dr. Stratton treated personally and who continued after the end of the study through the full course of the protocol there was, says Dr. Stratton, "100 percent improvement of symptoms".
      Why did the eradication of Cpn cause such a reaction in CFS patients ?
      People treated for actual pneumonia caused by Cpn (community acquired pneumonia) don't appear to have severe reactions to their antibiotics, after all.
      First, the combination antibiotic protocol (CAP) was far more effective than a single antibiotic used in standard treatment of Cpn because it attacked all of the phases of the Cpn life cycle.
      A single antibiotic only kills Cpn in one of its life phases.
      The symptoms of CFS are related to Cpn's toxic and inflammatory impact on the body.
      The more you kill at once, the greater these reactions.
      Second, CFS patients appear to have built up a very high load of Cpn, spread through a large variety of tissues: the bone marrow, the connective tissue, the liver, the spleen, the vascular system, heart and so on.
      When you have a highly toxic organism being killed in large numbers, in a wide variety of tissues, you have more severity of reactions.
      Additionally, the overall Cpn bacterial load appears to be one of the big determining factors in the length of the therapy needed.
      The higher the load, the longer the therapy required.
      Implied in this also is that...
      - the longer one has had the disease
      - the more organ systems affected and
      - the less resilient the patient from age, additional illnesses etc.,
      ...the longer and more challenging is the treatment required.
      As a group, patients with CFS/FMS appear to have higher Chlamydia pneumoniae loads in more different organs and tissues, compared with, say, Multiple Sclerosis patients - making treatment with the CAP more challenging and longer and creating a significant dropout rate, as it took longer to see the beneficial results versus the immediate term die-off reactions.
      But further research into this very promising but challenging treatment process was halted before questions about how to improve the treatment process could be answered.
      4.5 - Research is halted
      At about this point in the research, word was getting out in the medical community that they were testing blood samples from CFS patients.
      There ensued a deluge of protest from medical colleagues who objected to research with CFS being conducted at Vanderbilt. According to Dr. Stratton, the objections were "quite heated".
      Why would microbiological research, as hard-science an aspect of medicine as one could imagine, stir such heated outrage ?
      At that time, the late 1990's, the diagnosis of CFS was hugely controversial.
      Even more than it is today. Despite having a CDC case definition, a significant number of physicians believed that Chronic Fatigue Syndrome did not exist as a real medical entity or diagnosis.
      They believed that it was a false, catchall "syndrome" essentially representing psychiatric problems.
      Therefore it was not considered a legitimate area of serious scientific medical research.
      The expressed concern was that the reputation of Vanderbilt University and by extension the protesting physicians who were associated with Vanderbilt, would be sullied by sponsoring work on such a medical "non-entity" and be seen as fostering specious science.
      This kind of reaction was not just reflective of physicians only associated with Vanderbilt, of course.
      In general at that time, scientists or institutions associated with any kind of Chronic Fatigue Syndrome research were seen as incompetents, and were often made pariahs to conventional medicine.
      CFS research was often a career ender for career scientists.
      The reactions from potential publication journals at this time were similar.
      Please remember that this was only 10 or 12 years ago and these attitudes still exist today in medicine.
      At about this time the grant money for this study ran out.
      As Dr. Stratton was serving only as the testing laboratory, he did not have access to the patient data himself to have adequate controls over patient selection and the like to make for publishable results.
      Vanderbilt itself did not have a CFS clinic to draw from.
      As Dr. Stratton's expertise was in Chlamydia, not in CFS, he turned his research interests toward an area of research on Cpn with less diagnostic controversy and where Vanderbilt did have its own disease-based clinic.
      Dr. Stratton and his colleagues, spearheaded by Dr. Subramaniam Sriram, MD, in neurology, shifted the focus of their research to Multiple Sclerosis.
      This was done in part to have a widely accepted, "legitimate" nosological (diagnostic) entity for research.
      As an accepted neurological disease, no one could call MS a psychological problem.
      As many of us know, this research has turned out to be almost as controversial, although for different reasons than the CFS study.
      While one might wonder at Dr. Stratton's penchant for seeking controversy, the reality is that any research that cuts across accepted conventional viewpoints in medicine is likely to face rejection and derision.
      Anyone who knows Dr. Stratton would know that controversy is not at all a motivator in picking his research areas; Chlamydia is the motivator.
      Dr. David Wheldon, a colleague and friend of Dr. Stratton's, noted Dr. Stratton's avoidance of the limelight by saying that he "tends to hide his considerable light under a bushel".
      There are probably other factors operating here as well.
      Any treatment process requiring a combination of three to four antibiotics for a very long period of time is anathema to most conventionally trained MD's.
      Most physicians have only the rudiments of microbiology in their training and no basis to understand the complexities of treating multiple life-phase infectious agents.
      As well, the development of antibiotic resistant strains of bacteria has created a kind of phobia about the long term use of antibiotics amongst most practicing MD's.
      This attitude is even more true for the use of multiple antibiotics at the same time.
      It is ironic that physicians who see nothing wrong in pumping patients full of multiple chemotoxic agents for cancer treatment will balk at the suggestion of far less harmful multiple antibiotic agents, calling it "polypharmacy".
      Ironically too, it is actually the use of multiple antibiotics in the CAP for Chlamydia pneumoniae that truly minimizes the chance of developing bacterial resistance, while use of repeated courses of single antibiotics, the "conventional medical" approach, creates much higher risk for developing bacterial resistance.
      At any rate, these very interesting findings were never pursued.
      We still don't know what percentage of CFS patients are PCR positive for Chlamydia pneumoniae and exactly how much Cpn is the origin of symptoms in this disease syndrome.
      What we do know is that those of us who have diagnosed CFS/FMS and have positive blood tests for Cpn have benefited, slowly, gradually, but significantly in many of our symptoms from the combination antibiotic protocol for Cpn based on Dr. Stratton's work.
      This improvement is true as well for a number of CFS/FMS patients who, while not testing positive for Cpn using standard tests that are not as sensitive as those used by Dr. Stratton's lab, have evidenced typical die-off reactions to the CAP antibiotics, suggesting Cpn infection.
      Is it the case for all CFS/FMS? No one knows.
      4.6 - Chlamydial persistence and antibiotic response
      Cpn has some unique characteristics which make it both an adaptive parasite and difficult to eradicate.
      While over the years some clinicians treating chronic fatigue syndrome/fibromyalgia syndrome patients have tried the use of monotherapy (single) antibiotics with the notion that there might be an occult (hidden) bacterial infection involved in the disease, response by patients has been inconsistent.
      Some CFS/FMS patients may even have found their own symptoms temporarily improving when on incidental antibiotic treatment, say for ear infections and the like, but improvements not lasting.
      That informal clinical experimenting with antibiotics in CFS/FMS has not resulted in much useful direction of treatment or research that has to do with the unique biology and characteristics of Cpn.
      As these unique characteristics apparently are only known by microbiologists and little understood by treating physicians, treatment of CFS/FMS with antibiotics has yielded conflicting results.
      Curiously, this ignorance of important microbiological facts about Cpn (and other infectious organisms) appears to extend to medical Infectious Disease specialists, whose knowledge of microbiology appears shockingly limited and have not intelligently pursued the possibility of occult infection in these disorders.
      Antibiotics in CFS/FMS have resulted in the whole range of responses :
      - No improvement - leading to the assumption that no bacterial presence is involved.
      - Improvements followed by a return of symptoms after the antibiotic is withdrawn. Since long-term use of antibiotics is discouraged, with the fear of creating resistance, further treatment is often discouraged.
      - Symptoms worsening - leading to the assumption that they are having toxic or allergic effects and leading to halting antibiotic treatment.
      If, in fact, Cpn causes even a subset of CFS/FMS, the lack of consistency to antibiotic treatment has to be explained. This inconsistency becomes understandable if you know some key features about the biology of Chlamydia pneumoniae.
      - No improvement - The antibiotics used may not be effective antichlamydials. Thus a "trial of antibiotics" using the incorrect agent would be expected to yield negative results in the disease symptoms. The sensitivity tests done by Stratton et al. demonstrated clearly that a number of commonly held "high power" antibiotics are not effective against Chlamydia pneumoniae.
      - Temporary improvement - One of the great scientific puzzles about Chlamydia pneumoniae has been its ability to persist and reinfect, even treatment by antibiotics. It does this and evades the immune system and threats such as starvation, by its ability to switch forms and survive in a different life phase that is not affected by the particular threat.
      There are three known phases or forms of Cpn :
      - The infectious, spore-like Elementary Body (EB) : Only killed by cysteine reducing agents like N-acetyl-cysteine and amoxicillin.

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    Infection as one possible cause of fibromyalgia

    Part III

    - Once the EB invades a host cell it converts to the replicating Reticulate Body (RB) : Only antibiotics that interfere with replication, such as protein synthase inhibitors doxycycline or azithromycin, affect it.
    - Finally, Cpn can survive those drugs by converting to the low metabolizing "cryptic" form, which Dr. Stratton's research found is only killed by metronidazole family drugs.
    Thus two weeks, or even two years of a single antibiotic may improve symptoms by suppressing one form of Chlamydia pneumoniae, but symptoms recur as soon as the antibiotic is withdrawn.
    Worsening - Killing Chlamydia pneumoniae liberates significant amounts of bacterial endotoxins which cause widespread cytokine reactions, including inflammation, pain, depression, low energy and so on.
    These are precisely the symptoms of Chronic Fatigue Syndrome/Fibromyalgia Syndrome itself.
    In addition, Stratton's work found that Chlamydia pneumoniae causes a condition of secondary porphyria (as far as I know Dr. Stratton’s group are the only ones to have found the link between Chlamydia pneumoniae infection and secondary porphyria. It remains unpublished in the scientific literature and so virtually unknown to most medical practitioners) that engenders further misery and suffering.
    Reports of strong reactions to antibiotics and particularly to metronidazole, have led the treating clinicians to misinterpret these reactions as allergy or drug reactions and to prematurely withdraw the agent.
    The reality is that it is these bacterial toxins are a great part of what causes the symptoms in CFS/FMS and there is no way to kill Cpn without dumping these toxins into the system and feeling worse.
    The only question is how to pace it, and what measures can be taken to make it more tolerable.
    5. - CFS/DMS symptoms & chlamydia pneumoniae
    When we look at the common symptoms of chronic fatigue syndrome and fibromyalgia, how might they be explained by what we know about chlamydia pneumoniae biology and infection ?
    In this section I will present a list of the major symptoms and look at how chlamydial biology and our own bodily response to this might generate these often puzzling symptoms.
    5.1 - Features of Cpn and Cpn infection
    Multi-organ infection - Cpn crosses from the respiratory system and can infect multiple organ systems including the nervous system, liver, heart, bone marrow, immune cells, skin and so on.
    Intracellular energy parasite - Cpn reproduces by entering the host cell of your body tissue and stealing the ATP energy molecules that your cells function with [ATP or 'Adenosine triphosphate', transports chemical energy within the body’s cells].
    Secondary porphyria - Depletion of host cell ATP by chlamydia pneumoniae means that your cells don't have enough energy to complete their normal biochemical reactions.
    One of these, the production of heme [the deep red iron containing component of hemoglobin], requires lots of ATP to come to completion.
    ATP depletion results in incomplete heme production and a build up of the incomplete byproducts called porphyrins.
    Porphyrins are neurotoxic and have numerous deleterious effects on the nervous system including anxiety, depression, bowel and digestive disturbance and interference with sleep, rapid pulse and even psychosis.
    Chlamydial endotoxins - Chlamydia pneumoniae contains a number of endotoxins in its structure, such as LPSi and HSPi-60.
    These endotoxins cause widespread inflammation (cytokine cascades) and a host of other metabolic disturbances.
    These are released chronically in small amounts in chlamydia pneumoniae infection and in large amounts when Cpn cells are killed.
    Cytokine cascades - Cytokine responses (inflammatory immune reactions) are rampant in Chlamydia pneumoniae infection from a number of sources : to Cpn endotoxins; to the bacterial envelopes left behind by dead Chlamydia pneumoniae bacteria in tissue, which cause a variety of inflammatory reactions; and even the death of neighboring non-infected healthy cells (cfr. “Cell death and inflammation during infection with the obligate intracellulari pathogen, Chlamydia” - Perfettini JL, Hospital V, Stahl L, Jungas T, Verbeke P, Ojcius DM, Laboratoire Apoptose, Cancer et Immunite, CNRS UMR 1599, Institut Gustave Roussy, 39, rue Camille-Desmoulins, 94805 Villejuif cedex, France - Biochimie. 2003 Aug;85(8):763-9 at :
    http://www.cpnhelp.org/?q=cell_death_and_inflammati -).
    Antibodies to Vitamin B-12 - B-12 is an important co-factor in a number of energy and detoxification processes in the body. One of the unique findings of Dr. Stratton's group was that antibodies to vitamin B-12 develop in many chlamydia pneumoniae infected patients. This means that normal blood levels of this vitamin are insufficient, as it is bound to antibodies and useless to body functions affecting energy production and detoxification (methylization).
    With these in mind, let's look at how these and other factors about Cpn, might explain some of the otherwise mysterious symptoms of chronic fatigue syndrome and fibromyalgia.
    5.2 - General, unrelieved fatigue
    - This is the most characteristic feature of CFS and, other than pain, of FMS.
    - ATP depletion from Chlamydia pneumoniae parasitism simply leaves less energy available for body functions.
    - Fatigue is a main symptom of porphyria.
    - Cardiac infection : Cpn infects the cardiac system and is a major culprit being investigated as a source of cardiac disease. Parasitization of cardiac muscle by chlamydia pneumoniae would reduce heart efficiency and contribute significantly to fatigue. A recent paper found evidence of Cpn throughout myocardium, the heart muscle wall. These infected muscles would presumably be functioning at lower efficiency because of ATP depletion, resulting in a chronic cardiac insufficiency. This is consistent with findings of cardiac insufficiency in CFS patients (cfr. Peckerman) (cfr. “Persistent chlamydia pneumoniae infection of cardiomyocytes is correlated with fatal myocardial infarction” - Spagnolie LG et al., Cattedra di Anatomia ed Istologia Patologica, Dipartimento di Biopatologia e Diagnostica per Immagini, Universita di Roma Tor Vergata, Rome, Italy (e-mail :
    spagnoli@uniroma2.it -) - Am J Pathol. 2007 Jan;170(1):33-42 at : http://www.ncbi.nlm.nih.gov/pubmed/17200180?dopt=Abstract -&- “Causes of death among patients with chronic fatigue syndrome” - Jason LA, Corradi K, Gress S, Williams S, Torres-Harding S, DePaul University, Chicago, IL 60614, USA : Ljason@depaul.edu - Health Care Women Int. 2006 Aug;27(7):615-26 - PMID: 16844674
    at :
    http://www.ncbi.nlm.nih.gov/pubmed/16844674 -&- http://www.theoneclickgroup.co.uk/documents/ME-CFS_docs/Causes%20of%20Death%20-%20CFS%20Patients.pdf -).
    --- “… in response to postural stress, 81% of patients with CFS, but none of controls, experienced ejection fraction decreases (suggesting left ventricular dysfunction in the heart) and those with more severe symptoms had greater decreases (Peckerman, Chemitiganti, et al., 2003)” ---
    --- “Patients with CFS might have lower cardiac output and the resulting low flow circulatory state could make it difficult for patients to meet the demands of everyday activity and it could also lead to fatigue and other symptoms (Peckerman, LaManca et al., 2003)…” ---
    - Cytokine cascade in CFS (cfr. “Cytokines and chronic fatigue syndrome” - Patarca R, Department of Medicine, University of Miami School of Medicine, Florida 33101, USA :
    rpatarca@pol.net - Ann N Y Acad Sci. 2001 Mar;933:185-200 - PMID: 12000020 at : http://www.ncbi.nlm.nih.gov/pubmed/12000020 -).
    The typical malaise and fatigue of a cold or flu is caused by the flood of cytokines that are generated in the innate immune response.
    Chlamydia pneumoniae infection tends to stimulate a chronic innate immune response and this chronic cytokine cascade is an additional source possible in CFS fatigue.
    This has been called "sickness behavior" - i.e., the behavioral responses to an immune cascade (cfr. “Cytokine dysregulation, inflammation and well-being” - Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP, Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, Washington, D.C., USA. - Neuroimmunomodulation. 2005;12(5):255-69 - PMID: 16166805 - © 2005 S. Karger AG, Basel at :
    http://www.ncbi.nlm.nih.gov/pubmed/16166805 -).
    5.3 - Tender axillary or cervical lymph nodes
    One of the main routes by which Cpn is carried through the body is the lymphatic system via infected immune cells.
    Chlamydia pneumoniae infected lymphocytes and/or infection of the lymphatic system itself would easily account for this clinical finding in CFS ((cfr. “The immune system, atherosclerosis and persisting infection” - Pigarevskii P V; Mal'tseva S V; Seliverstova V G, Vestnik Rossiiskoi akademii meditsinskikh nauk - Rossiiskaia akademiia meditsinskikh nauk 2005;(2):17-22 at :
    http://www.biomedexperts.com/Abstract.bme/15776961/The_immune_system_atherosclero
    sis_and_persisting_infection
    -&- “Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature” - Gieffers J, van Zandbergen G, Rupp J, Sayk F, Krüger S, Ehlers S, Solbach W, Maass M, Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany : jens.gieffers@hygiene.ukl.mu-luebeck.de - Eur Respir J. 2004 Apr;23(4):506-10 - PMID: 15083745 at : http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=15083745&cmd=showdetailview&indexed=google -).
    These lymph nodes in particular drain the upper respiratory system (sinuses, throat etc) and these areas are a major entry point for Cpn into the body via sinus infection, laryngitis and so on.
    6. - Immune deficiency
    (cfr. “Causes of death among patients with chronic fatigue syndrome” - Leonard A. Jason, Karina Corradi, Sara Gress, Sarah Williams & Susan Torres-Harding, DePaul University, Chicago, Illinois, USA - Address correspondence to Leonard A. Jason, Center for Community Research, DePaul University, 990 W. Fullerton Ave., Suite 3100, Chicago, IL 60614 :
    Ljason@depaul.edu - Health Care for Women International, 27:615–626, 2006 - © Taylor & Francis Group, LLC at : http://www.ncbi.nlm.nih.gov/pubmed/16844674 -&- http://www.theoneclickgroup.co.uk/documents/ME-CFS_docs/Causes%20of%20Death%20-%20CFS%20Patients.pdf -).
    -
    Chlamydia pneumoniae can infect bone marrow
    (cfr. : “Detection of Chlamydophila pneumoniae in the bone marrow of two patients with unexplained chronic anaemia” - Nebe CT, Rother M, Brechtel I, Costina V, Neumaier M, Zentgraf H, Böcker U, Meyer TF, Szczepek AJ, Central Laboratory, University Hospital Mannheim, Mannheim, Germany :
    thomas.nebe@ikc.ma.uni-heidelberg.de - Eur J Haematol. 2005 Jan;74(1):77-83 - PMID: 15613113 at : http://www.ncbi.nlm.nih.gov/pubmed/15613113 -).
    That is where our immune cells (macrophages, monocytes, neutrophils) are produced.
    Infected bone marrow will produce infected and thus poorly functioning immune cells, resulting in a low-grade immunodeficiency.
    - Co-infections resulting from poor immune functioning from opportunistic organisms - viruses, bacteria, mycoplasms, fungi & yeasts and such - are more likely gain a foothold. These further confuse the clinical picture as to what is cause and what is effect or co-factor and add to further immune burden and further reduced immune function. The more organisms the immune system (already infected itself) has to deal with, the less resources available for any one thing.
    6.1 - Cardiac Insufficiency
    Cardiac insufficiency has been identified in CFS patients as a significant correlate to symptom severity (cfr. “Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome“ - Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH, Department of Neurosciences, CFS Cooperative Research Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA : apeckerm@njneuromed.org - Am J Med Sci. 2003 Aug;326(2):55-60 - PMID: 12920435 at : http://www.ncbi.nlm.nih.gov/pubmed/12920435 -) – so much so that Dr. Paul Cheney (yes, the same one who participated in the CFS/CPN study) has focused on this as his cause celebre for CFS recently (cfr. “Cardiac insufficiency hypothesis” - M.E. Society of America, (last updated) February 22, 2009 at :
    http://www.cfids-cab.org/MESA/Lerner.html -).
    As we have noted, Cpn is parasitic and steals ATP, the energy molecule, from the infected host cell to subvert it for its own replication process.
    Heart muscle is one of the most ATP demanding cells.
    Cp infection of heart muscle as discussed previously is likely to result in reduced heart efficiency, explaining the results of the Peckerman study and giving a causal element to Dr. Cheney’s observations of cardiac dysfunction in CFS.
    Why Dr. Cheney has ignored the earlier work he participated in, which implicates an organism that is becoming well known for its involvement in cardiac disease, is a real curiosity.
    6.2 - Exercise intolerance and post-exertional fatigue
    - Cardiac insufficiency – Cfr. cardiac infection comments previously noted. Impaired performance on treadmill commonly noted in CFS/FMS could be similarly explained by this as well as other factors.
    - Muscle and general ATP depletion - Chlamydia pneumoniae is an ATP parasite in infected cells, leaving of this energy molecule for host cells. In a broad based Chlamydia pneumoniae infection stores of ATP would be generally depleted, such that high output exercise would leave a significant ATP deficit in some systems such as the muscular system.
    - Porphyrins - Porphyrin load increases after exercise or exertion because ATP stores, already in short supply because of Cpn parasitism, are used up at rapid rate by muscle activity. This makes even less ATP available for heme production resulting in incomplete heme and its byproducts, porphyrins. An inadequate supply of ATP means that only the amount of exercise up to the ATP limit at that particular moment can be tolerated. The increased porphyrin byproducts result in post-exertional fatigue and long recovery time. This is the "over-exert one day, payback for three days" report common to many CFS patients.
    6.3 - Gastrointestinal problems
    - CFS and FMS patients often have concomitant gastrointestinal problems, ranging from Irritable Bowel Syndrome, poor nutrient absorption and other problems.
    - Cpn infects endothelial tissues, as its preferred home, including the endothelial tissues of the gut. Some of the micrographs of Cpn infected cells which can be viewed on this website are of stained intestinal endothelial tissues (cfr. “Cpn in GI tract tissue 1” at :
    http://www.cpnhelp.org/cpn_in_gi_tract_tissue_1 -&- “Cpn in GI tract tissue 2” at : http://www.cpnhelp.org/cpn_in_gi_tract_tissue_2 -&- “Cpn in GI tract tissue 3” at :http://www.cpnhelp.org/cpn_in_gi_tract_tissue_3 -).
    - Porphyria is notorious for causing chronic gut distress: nausea, intestinal cramping, etc. Chlamydia pneumoniae infection of gut endothelial tissue.
    - Gut co-infections from fungi, bacteria, or yeast resulting from general immunosuppression, or specific Cpn infected gut-immune system will further add to gastrointestinal problems.
    6.4 - Sleep disorder
    - Porphyrins block GABA receptors, a main cause of anxiety and agitation in porphyria and likely to interfere with sleep.
    - Melatonin serves a number of functions that are related to protecting cells from oxidation as well as binding inflammatory endotoxins and activating immune functions (cfr. “Melatonin as antioxidant under pathological processes” - Cristina Tomás-Zapico, Ana Coto-Montes, Departamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, 33006 Oviedo, Spain - Recent Patents on Endocrine, Metabolic & Immune Drug Discovery 2007, 1, 63-82 63 - © 2007 Bentham Science Publishers Ltd. at :
    http://www.bentham.org/emi/samples/emi1-1/Tom%E1s-Zapico.pdf - &- “Melatonin inhibits expression of the inducible NO synthase II in liver and lung and prevents endotoxemia in lipopolysaccharide-induced multiple organ dysfunction syndrome in rats” – Elena Crespo,* Manuel Maci´as,* David Pozo,† Germaine Escames,* Miguel Marti'n,* Francisco Vives,* Juan M. Guerrero,† and Dari'o Acun˜ A-Castroviejo*,1 - *Departamento de Fisiologı´a, Instituto de Biotecnologı´a, Universidad de Granada, Spain - †Departamento de Bioquı´mica Me´dica y Biologı´a Molecular, Facultad de Medicina, Universidad de Sevilla, Spain - FASEB J. 13, 1537–1546 (1999) at : http://www.fasebj.org/cgi/reprint/13/12/1537.pdf -&- “Activation of human monocytes by the pineal hormone melatonin” - Morrey KM, McLachlan JA, Serkin CD, Bakouche O, Department of Molecular Pharmacology and Biologic Chemistry, Northwestern University Medical School, Chicago, IL 60611 - J Immunol. 1994 Sep 15;153(6):2671-80 - PMID: 8077674 at : http://www.ncbi.nlm.nih.gov/pubmed/8077674 ).
    Melatonin depletion from it being used up for antioxidant and other metabolic purposes resulting from Cpn infection could result in inadequate amounts left for neurotransmitter production and its influence on inducing sleep.
    - Hypothalamic infection and disturbance by Chlamydia pneumoniae could be a contributing factor.
    - Cytokine disturbance of sleep regulation (cfr. : “The Role of Cytokines in Physiological Sleep Regulation / The Role of Neural Plasticity in Chemical Intolerance”” - Kruegera JM et al. - Annals of the New York Academy of Sciences, 933 (1), 211–221 -&- “The Chlamydia Pneumoniae Handbook” at :
    http://www.cpnhelp.org/book/export/html/408 -& “Chlamydia pneumoniae in CFS/ME & fibromyalgia / Chronic fatigue syndrome, fibromyalgia & chlamydia pneumoniae” at : http://www.cpnhelp.org/chlamydia_pneumoniae_in_0 -).
    6.5 - Anxiety & depression
    - Porphyrins- noted previously for causing anxiety, depression, even psychosis.
    - Depletion of melatonin noted above causes depletion of serotonin in the brain. Inadequate serotonin results in depression, as well as increased pain sensitivity.
    - Cytokine depression - cytokines are clearly linked to causing depressive symptoms (cfr. “Is there a biologic connection between inflammatory disease and depression ?” -
    Colby Stong - NeuroPsychiatry Reviews, September 2004, Vol. 5, No.7 – at :
    http://www.neuropsychiatryreviews.com/sep04/sep04_npr_inflammatory.html -).
    6.6 - Endocrine disturbance (thyroid, periods etc.)
    - Infection of endocrine gland cells: thyroid, pancreas islet cells, pituitary, pineal etc.
    - Glucose disturbance - Chlamydia pneumoniae steals ATP that requires the host cell to absorb and metabolize more glucose. This disturbs glucose homeostasis. "Hypoglycemic" symptoms (must have food now, worsening of inflammatory and porphyric symptoms when get depleted of glucose or during fasting, etc.) are common in CFS/FMS and are quite notable in those suffering from disseminated Chlamydia pneumoniae infection. Anecdotally, Chlamydia pneumoniae patients on the CAP report significant lessening of episodes of these hypoglycemic symptoms over the course of treatment.
    6.7 - Headaches
    - Porphyrins - One of the neurotoxic effects of porphyrins is headaches.
    - Vascular disturbance direct and indirect - Cpn infects the vascular system leading to high blood pressure (from rigidified vascular walls), headaches, inflammation of blood vessels (including those in the brain) etc.
    - Sympathetic nervous system over activation from chronic upregulated innate immune response caused by infection (cfr. : “Migraine - A chronic sympathetic nervous system disorder“ - Perouta SJ - Headache. 2004 Jan;44(1):53-64 - © 2004 Blackwell Publishing at :
    http://www.medscape.com/viewarticle/466937 -).
    6.8 - “Sickness behavior”
    Mentioned earlier, sickness behaviors are the innate, the behavioral responses to cytokines that have been stimulated by infection: feeling lousy, withdrawal, depression, movement avoidance and energy conserving etc. (cfr. “Illness, cytokines and depression” - Yirmiya R, Pollak Y, Morag M, Reichenberg A, Barak O, Avitsur R, Shavit Y, Ovadia H, Weidenfeld J, Morag A, Newman ME, Pollmächer T, Department of Psychology, Hebrew University, Hadassah Hospital, Jerusalem, Israel :
    msrazy@mscc.huji.ac.il - Ann N Y Acad Sci. 2000;917:478-87 - PMID: 11268375 at : http://www.ncbi.nlm.nih.gov/pubmed/11268375 -&- “Cytokine dysregulation, inflammation and well-being” - Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP, Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, Washington, D.C., USA - Neuroimmunomodulation. 2005;12(5):255-69 - PMID: 16166805 at : http://content.karger.com/ProdukteDB/produkte.asp?doi=10.1159/000087104 -).
    6.9 - Cognitive dysfunction ('brain fog')
    This is one of the most frustrating features of CFS/FMS and one with little explanation in the domain, despite its being one of the most life-impacting symptoms for the sufferer.
    Cpn infection explains this very well.
    - Secondary porphyria induced by it and the impact of porphyrins on brain functioning.
    - Cerebral inflammation from circulating cytokines.
    - Brain infection.
    - Endotoxins.
    7. - Fibromyalgia symptoms
    All of the above plus…
    7.1 - Musculoskeletal pain and inflammation
    - Soft tissue infection by Chlamydia pneumoniae and subsequent inflammation.
    - Fibromyalgia syndrome often starts after injury/accident. In the normal response to tissue repair, injured and inflamed areas attract macrophages. Chlamydia pneumoniae infected macrophages can leave Chlamydia pneumoniae behind in injured/inflamed area. Infection then becomes progressive gradually spreading from that area. As generalized inflammation increases (from free circulating cytokines) these sites are further infected by parasitized macrophages drawn to increasingly inflamed sites etc. (cfr. “How chlamydia pneumoniae causes such a plethora of diseases” - Cpnhelp.org, 2006-2-24 at :
    http://www.cpnhelp.org/how_chlamydia_pneumoniae_ -).
    - Porphyrins blocking GABA receptors will also lower pain tolerance.
    - Generalized cytokine load causes broad based "feels lousy all over".
    --- In 1990, the American College of Rheumatology, the official body of doctors who treat arthritis and related conditions, finally legitimized Fibromyalgia in the medical community by presenting its criteria for diagnosing it. It is diagnosed when you display the following symptoms : 1) a history of widespread pain (pain on both sides of the body and above and below the waist) that is present for at least three months and 2) pain in at least 11 of 18 tender-point sites – cfr. : “Fibromyalgia” - Arthritis Foundation at : http://ww2.arthritis.org/conditions/diseasecenter/fibromyalgia/fibromyalgia.asp --- An excellent review of infectious issues – “Fibromyalgia - Is there an infectious connection ?” – can be found at : http://www.roadback.org/index.cfm/fuseaction/education.display/display_id/135.html ---
    8. - Summary conclusion
    The case for Cpn in CFS does not prove that Cpn is always the causal element.
    As a syndrome, CFS may originate from a variety of causal factors and these could be different for different patients.
    But in a disease where modern medicine has had no curative treatment to offer, it is clearly a causal factor worth looking into.
    Even with negative blood tests for Cpn, an empirical trial of the CAP for Cpn is worth exploring.
    In future articles I hope to discuss some of the potential complexities of treating Cpn in CFS/FMS patients with the Combination Antibiotic Protocol and some considerations that make treating this different from other Cpn related diseases.
    Cfr. :
    http://www.prohealth.com//library/showArticle.cfm?libid=12763

    1. Chronic Chlamydia pneumoniae infection - A treatable cause of chronic fatigue syndrome
      Chia JK, Chia LY, Torrance Memorial Medical Center, California, USA : chiasann@pol.net - Clin Infect Dis. 1999 Aug;29(2):452-3 - PMID: 10476765
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10476765

    2. Chronic fatigue illness and Operation Desert Storm
      Nicolson GL, Nicolson NL - J Occup Environ Med 1996; 38:14-16
      Cfr. :
      http://journals.lww.com/joem/Citation/1996/01000/Chronic_Fatigue_Illness_and_Operation_
      Desert_Storm.3.aspx

    3. Chronic fatigue illnesses - Chronic fatigue syndrome, fibromyalgia syndrome and other fatigue conditions
      Prof. Garth L. Nicolson
      Chronic fatigue is reported by 20% of all patients seeking medical care and is considered as a nonspecific sign that is associated with many well known medical conditions.
      Chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME) and fibromyalgia syndrome (FMS) patients suffer from complex overlapping signs and symptoms (cfr. : 'Signs/Symptoms' Questions, above) CFS is primarily characterized by persisting or relapsing fatigue without previous history of comparable symptoms that does not resolve with rest.
      In these patients other clinical conditions are absent that can explain the signs and symptoms such as malignancies or autoimmune diseases.
      In contrast, FMS patients have overall muscle pain, tenderness and weakness as primary complaints, but they have most if not all of the commonly found signs and symptoms for CFS.
      We previously proposed that CFS/ME patients might be suffering from chronic infections that can cause, in part, their complex signs and symptoms.
      For example, systemic mycoplasmal infections can cause chronic fatigue, muscle pain and a variety of additional signs and symptoms, some of which are related to dysfunctional immune responses and in extreme cases autoimmune-like disorders.
      Some mycoplasmas can invade virtually every human tissue and can compromise the immune system, permitting opportunistic infections by other bacteria, viruses, fungi and yeast.
      When mycoplasmas exit certain cells, such as synovial cells, nerve cells, among others that can be infected, they can stimulate autoimmune response.
      Our recently published studies demonstrated a possible link between mycoplasmal infections and CFS and FMS, since we found high frequencies of mycoplasmal infections in these patients.
      Previously we examined patients with chronic illnesses for the presence of mycoplasmal infections.
      We found that about one half of patients with Gulf War Illness and two third of patients with CFS/ME and FMS were positive for mycoplasmal infections in their blood.
      The Gulf War Veterans suffer from signs and symptoms similar to patients diagnosed with CFS and FMS.
      They can be treated using antibiotics effective against mycoplasmal infections and once they recover, their blood is no longer positive for the presence of mycoplasmal infections.
      Our recent results indicate that Rheumatoid Arthritis is also associated with mycoplasmal infections (cfr. 'Autoimmune Diseases').
      Recent reports and publications indicate that in addition to mycoplasmal infections, CFS/ME and FMS patients have other chronic infections caused by other intracellular bacteria and viruses.
      For example, patients with Lyme Disease, caused by intracellular Borrelia infections, have been diagnosed with CFS/ME.
      Also, CFS/ME and FMS patients can have intracellular Chlamydia species infections.
      These patients can also have infections by other bacteria that enter their bodies through 'leaky gut' problems.
      Chronically ill patients often have inflammatory bowel syndrome and other gut problems and this can allow pathogenic bacteria to enter their systems.
      Patients with CFS/ME and FMS can also have viral infections that complicate their conditions and cause morbidity.
      Such infections can occur with or without the bacterial infections described above.
      Viruses that have been associated with CFS/ME and FMS are Human Herpes Virus-6 (HHV-6) and Cytomeglovirus (CMV).
      These viruses have been found at high incidence in chronically ill patients and especially those with CFS/ME.
      Patients with CFS/ME or FMS can have predominantly intracellular bacterial infections, predominantly viral infections or a combination of intracellular bacterial and viral infections.
      This may be one reason why the underlying causes of these chronic illnesses are so difficult to determine and effectively treat.
      The other reason could be the persistent nature of the infections and their ability to hide inside cells where they are essentially refractory to immune system responses, their slow growing natures and their relative insensitivity to therapeutic drugs (see references below).
      A new direction at the Institute is studying the role of decreased cellular energy in causing fatigue.
      Cellular energy is mainly produced by the mitochondria, subcellular organelles that contain the machinery that converts fats and sugars to energy in the form of the high-energy molecules, such as ATP.
      Mitochondrial function requires an intact inner membrane where the electron transport chain or energy machinery is located.
      When the inner mitochondrial membrane is damaged, the efficiency of the electron transport chain is reduced along with the ability of cells to produce the energy that they need for vital functions—thus fatigue becomes a problem.
      Various environmental insults and even aging produce excess oxidation molecules that can damage the mitochondrial membrane, including chronic infections of the type mentioned above.
      At the Institute for Molecular Medicine clinical studies have shown the benefits of dietary membrane lipids (Lipid Replacement Therapy) in replacing damaged mitochondrial membrane lipids, increasing the efficiency of the electron transport chain, increasing energy and reducing fatigue.
      A number of non-pharmaceutical approaches to decreasing fatigue are being investigated at the Institute.
      Cfr. :
      http://www.immed.org/illness/fatigue_illness_research.html

    4. Chronic fatigue illnesses associated with service in Operation Desert Storm - Were biological wWeapons used against our forces in the Gulf War ?
      Nicolson GL, Nicolson NL - Townsend Lett Doctors 1996; 156:42-48
      Cfr. :
      http://www.all-natural.com/part-1.html

    5. Chronic fatigue syndrome - A working case definition
      Holmes GP, Kaplan JE, Gantz NM, Komaroff AL, Schonberger LB, Straus SE, Jones JF, Dubois RE, Cunningham-Rundles C, Pahwa S et al., Division of Viral Diseases, Centers for Disease Control, Atlanta, Georgia - Ann Intern Med. 1988 Mar;108(3):387-9 - PMID: 2829679
      The chronic Epstein-Barr virus syndrome is a poorly defined symptom complex characterized primarily by chronic or recurrent debilitating fatigue and various combinations of other symptoms, including sore throat, lymph node pain and tenderness, headache, myalgia and arthralgias.
      Although the syndrome has received recent attention and has been diagnosed in many patients, the chronic Epstein-Barr virus syndrome has not been defined consistently.
      Despite the name of the syndrome, both the diagnostic value of Epstein-Barr virus serologic tests and the proposed causal relationship between Epstein-Barr virus infection and patients who have been diagnosed with the chronic Epstein-Barr virus syndrome remain doubtful.
      We propose a new name for the chronic Epstein-Barr virus syndrome--the chronic fatigue syndrome--that more accurately describes this symptom complex as a syndrome of unknown cause characterized primarily by chronic fatigue.
      We also present a working definition for the chronic fatigue syndrome designed to improve the comparability and reproducibility of clinical research and epidemiologic studies and to provide a rational basis for evaluating patients who have chronic fatigue of undetermined cause.
      Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2829679

    6. Chronic fatigue syndrome and myalgic encephalomyelitis
      Chaudhuri A - Lancet. 2002 May 11;359(9318):1698-9 - PMID: 12020562

      Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12020562?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleI
      temSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed

    7. Chronic fatigue syndrome patients subsequently diagnosed with lyme disease borrelia burgdorferi - Evidence for mycoplasma species co-infections
      Garth L. Nicolson a; Nancy L. Nicolson a; Joerg Haier b - a Institute for Molecular Medicine, Huntington Beach, CA - b Department of Surgery, University Hospital, Munster, Germany - Journal Of Chronic Fatigue Syndrome, Volume 14, Issue 4 June 2008 , pages 5 – 17
      Objective - We examined the blood of 48 North American chronic fatigue syndrome (CFS) patients subsequently diagnosed with Lyme disease (Borrelia burgdorferi infection) and compared these with 50 North American CFS patients without evidence of Borrelia burgdorferi infections for presence of Mycoplasma species coinfections using forensic polymerase chain reaction.
      Results - We found that 68.75% of CFS/Lyme patients show evidence of mycoplasma coinfections (odds ratio [OR] = 41.8; confidence limits [CL] = 11.3-155; and p < .001) compared with controls, whereas 50% of CFS patients without a diagnosis of Lyme disease show Mycoplasma coinfections (OR = 19.0; CL = 5.3-69; and p < .001) compared with controls.
      Because CFS patients without a diagnosis of Lyme disease have a high prevalence of one of four Mycoplasma species and a majority show evidence of multiple infections, we examined CFS/Lyme patients' blood for various Mycoplasma species.
      We found that CFS patients with Lyme disease mostly had single species Mycoplasma infections (OR = 31.7; CL = 8.6-116; and p < .001) with a preponderance of Mycoplasma fermentans infections (50% of patients; OR = 59.0; CL = 7.6-460; and p < .001), whereas the most commonly found Mycoplasma species in CFS patients without Lyme disease was Mycoplasma pneumoniae(34% of patients; OR = 14.94; CL = 3.3-69; and p < .001).
      Conclusions - The results indicate that a subset of CFS patients show evidence of infection with Borrelia burgdorferi, and a large fraction of these patients were also infected with Mycoplasma fermentans and to a lesser degree with other Mycoplasma species.
      Cfr. :
      http://www.informaworld.com/smpp/content~content=a903736316~db=all~jumptype=rss

    8. Chronic infections as a common etiology for many patients with Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses
      Nicolson GL - Intern J Med 1998; 1:42-46
      Cfr. :
      www.immed.org/GulfWarIllness/GLNpubl%5B1%5D.GWI_CFS06.rtf

    9. Chronic Infections in Fibromyalgia Syndrome - Sources of morbidity and illness progression
      Prof. Garth Nicolson, The Institute for Molecular Medicine 16371 Gothard St. H, Huntington Beach, CA 92647 - Fibromyalgia Survivor 2000
      Fibromyalgia Syndrome (FMS) is characterized by muscle pain and tenderness at specific sites, but there are also a number of other less specific chronic signs and symptoms.
      Among these are disabling fatigue, impairments in short-term memory, headaches, gastrointestinal and vision problems and sometimes intermittent low-grade fevers, joint pain and other signs and symptoms.
      In many patients the diagnosis of FMS is accompanied by other secondary diagnoses, such as Chronic Fatigue Syndrome (CFS), Rheumatoid Arthritis (RA), Inflammatory Bowel Diseases and other syndromes, which can also present with overlapping signs and symptoms.
      This suggests that although the exact causes of these illnesses are not known and may be different in each patient, there are similarities in these conditions that may be important in patient morbidity (sickness) or in illness progression (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176).
      Instead of concentrating on possible causes of FMS, we have been interested in the progression of chronic illnesses like FMS and in the potential role that chronic infections may play in FMS.
      The complex signs and symptoms that evolve in many FMS, CFS and RA patients may be due, in part, to systemic chronic infections (bacteria, viruses, fungi).
      Such infections can follow acute or chronic chemical, environmental or other insults (trauma, chemical exposures, acute viral illness etc.) that have the potential to suppress the immune system and cause metabolic imbalances (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176).
      Illness progression in FMS patients
      Illnesses like FMS evolve over time, probably in a multistep process that may require multiple toxic exposures, including infections that could be causative for the illness in a few patients, cofactors for the illness (not causative but important in patient morbidity) in others or more likely in most patients, opportunistic infections that cause morbidity.
      Such infections need not be present at the onset of illness to be important.
      Because of their dysfunctional metabolic and immune systems, many FMS patients may be particularly susceptible to chronic infections that worsen their illness.
      Of course, illness progression in FMS patients could also be caused by other factors, psychological stress, physical trauma, other illnesses and many other factors (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21).
      Chronic infections are usually held in check by our immune systems, but they can take hold if they can avoid immune surveillance and penetrate and hide in various tissues and organs, including muscle cells and nerve cells.
      When such “stealth” viral and bacterial infections occur, they can cause many of the complex signs and symptoms seen in FMS, CFS, RA and GWI, including enhanced immune dysfunction and metabolic imbalances (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21 -&- “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21).
      Changes in environmental responses as well as increased titers to various endogenous viruses that are commonly found to be expressed in these patients have been seen in FMS, CFS and GWI patients.
      If infectious agents are involved, few can produce the complex chronic signs and symptoms found in these patients.
      One that can is represented by a small, primitive class of bacteria called mycoplasmas (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32).

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    Infection as one possible cause of fibromyalgia

    Part IV

    Mycoplasmas and other bacteria (Chlamydia, Coxiella, Brucella, Borelia etc.), although not as well known as other agents in causing various diseases, are now considered important emerging pathogens in various chronic illnesses.
    As chronic illnesses such as FMS, CFS and RA progress, there are a number of accompanying clinical problems, and in some patients show increases in autoimmune signs and symptoms.
    This suggests that they do not have classical autoimmune diseases but they may have incomplete diagnoses for these diseases.
    Although it is certainly not proven,  this pattern is consistent with certain chronic infections, such as mycoplasmal infections, that penetrate into nerve cells, synovial cells in joints, muscle cells and other cell types.
    Microorganisms like mycoplasmas can incorporate into their own surface structures pieces of host cell membranes that contain important host membrane antigens that can trigger autoimmune responses (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176) and they can also mimic host cell antigen structures (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32).
    Thus patients with such infections may respond immunologically to microorganism antigens as well as their own membrane antigens, producing unusual autoimmune signs and symptoms.
    This could explain why such patients do not have all of the clinical characteristics expected in these usually rare autoimmune diseases.
    Microorganisms can cause morbidity in FMS patients
    Microorganisms like Mycoplasmas are not considered important human pathogens when they are found at superficial sites, such as the oral cavity or gut, but some species, such as M. fermentans, M. penetrans, M. pneumoniae, M. genitalium, M. Pirum and M. hominis, among others, have the capacity to penetrate into the blood circulation and colonize various tissues and these cell-penetrating microorganisms have been closely associated with various human diseases (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32).
    Do such infectious agents actually cause FMS, CFS or RA ?
    Probably not on their own, but some bacteria and viruses appear to be an important element in causing chronic illness progression, patient morbidity or exacerbating the major signs and symptoms seen in patients with chronic illnesses.
    We have found that ~70% of FMS, ~60% of CFS and ~50% of RA and Gulf War Illness patients have mycoplasmal blood infections that can explain many of the chronic signs and symptoms found in these patients.
    In the majority of FMS and CFS patients we have found multiple pathogenic mycoplasmas in their white blood cells but these infections are only found in 0-9% of controls (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients” - Nasralla, M., Haier, J. and Nicolson, G.L. - Eur. J. Clin. Microbiol. Infect. Dis. 1999; 18:859-865).
    Interestingly, the majority of CFS and FMS patients had multiple mycoplasmal infections but none were found in controls (cfr. “Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients” - Nasralla, M., Haier, J. and Nicolson, G.L. - Eur. J. Clin. Microbiol. Infect. Dis. 1999; 18:859-865); however, single infections are found in some nonsymptomatic subjects (0-9%).
    The tests that we use to identify mycoplasmal infections, Forensic Polymerase Chain Reaction, are very sensitive and highly specific.
    These tests are a dramatic improvement over the relatively insensitive serum antibody and other tests that have been used to assay for systemic infections.
    New treatments for FMS and other chronic illnesses
    When microorganism infections are identified in the blood of patients, they should be treated as medical not psychiatric patients, just like any other patients with blood infections.
    This does not mean that psychological or psychiatric problems are not important in chronic illness patients.
    But if such infections are important in these disorders, then appropriate treatments with antibiotics or other medications that suppress chronic infections should result in improvement and even recovery.
    This is exactly what has been found (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21).
    The majority of patients with confirmed pathogenic mycoplasmal infections eventually recover from 50-100% of their premorbid health on therapies that are directed specifically against their chronic infections not against possible psychological problems (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21).
    The recommended treatment for confirmed mycoplasmal blood infections is long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline (200-300 mg/day), ciprofloxacin or Cipro (1,500 mg/day), azithromycin or Zithromax (500 mg/day) or clarithromycin or Biaxin (750-1,000 mg/day).
    Multiple cycles are required, because few patients recover after only a few cycles, possibly because of the intracellular locations of the infections, the slow-growing nature of these microorganisms and their inherent insensitivity to antibiotics.
    We now recommend that patients who have been diagnosed with blood infections receive continuous oral antibiotics for at least 6 months before using the 6-week cycles of treatment.
    Although patients starting such therapy usually have Herxheimer reactions and feel initially worse due to die-off or release of toxic materials from damaged microorganisms, they eventually stabilize within days to a few weeks and then slowly begin to recover.
    Unfortunately, the treatment requires long-term therapy, and recovery is usually very slow.
    Patients that have been sick for many years are unlikely to recover within a year of therapy (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128).
    The clinical responses that are seen are not due to placebo effects, because administration of some antibiotics, such as penicillins, resulted in patients becoming more not less symptomatic.
    In addition, they are not due to immunosuppressive effects of some of the antibiotics, because other antibiotics that do not cause immune suppression are also effective but only if they suppress the chronic infections.
    If they don’t have these infections, then antibiotics should not work (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21).
    Some patients recover to a certain point and then fail to continue to respond to the recommended antibiotics, suggesting that other problems, such as viral infections, environmental exposures and other toxic events and even stress, also play an important role in these illnesses, and may even play a predominant role in some patients.
    What results have been obtained with antibiotics for chronic illnesses like FMS ?
    Although a majority of patients diagnosed with chronic blood infections appear to benefit from antibiotic therapy, many patients respond and have some alleviation of most signs and symptoms but do not fully recover.
    A 3-year follow-up of antibiotic therapy in Northern California indicates that a majority (~80%) of FMS/CFS) patients from Shasta County that were confirmed with mycoplasmal infections recovered from 50-100% of their pre-illness health within this time period and even some patients who did not test positive showed benefit from antibiotics, suggesting other bacterial infections.
    Similar to other therapies for chronic illnesses, not every patient benefited from antibiotic therapy and the time required for recovery was quite variable in different patients (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32).
    In some patients oxygen therapy has proved useful.
    Oxygen suppresses the anaerobic chronic infections like mycoplasmas.
    In addition to antibiotics, patients must take vitamins, minerals, immune enhancement and other supplements to help boost immunity.
    For example, these patients are often depleted in vitamins B complex, C and E, among others and certain minerals (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128).
    Amino acids, fish oils, probiotic bacteria (Lactobacillus acidophillus) and a number of natural remedies have proven useful during therapy (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128).
    Complex causes of chronic illnesses
    Do chronic infections explain illnesses like FMS ?
    It is unlikely that there is only one or even a few explanations for complex chronic illnesses like FMS or CFS.
    Rather, these illnesses are probably due to a combination of multiple toxic exposures, chemical and biological, in combination with genetic susceptibility (immune systems and/or detoxification systems, cellular metabolism) that determines whether a person becomes chronically ill.
    These considerations probably also play an important role in determining who will recover to various extents on different types of therapy.
    In addition, recovery can be complicated by patients’ over-dependence on drugs, such as certain antidepressants or other drugs that can suppress portions of the immune system.
    Interestingly, those patients that slowly recover after several cycles of antibiotics are generally less environmentally sensitive, suggesting that their immune systems may be returning to pre-illness states.
    If such patients had illnesses that were solely caused by psychological or psychiatric problems or by environmental or chemical exposures, they should not respond to the recommended antibiotics and recover their health.
    In addition, if such treatments were just reducing the autoimmune responses, then patients should not maintain recovery after the treatments are discontinued.
    For further information
    Contact : Prof. Garth L. Nicolson, The Institute for Molecular Medicine 16371 Gothard St. Bld H, Huntington Beach, CA 92647 – Tel. : 714-596-6636 – Fax : 714-596-3791 – E-mail :
    gnicolson@immed.org – Website : www.immed.org -.
    Cfr. :
    www.immed.org/Fatigue%20Illness/.../FMSurvivorNewslett00.rtf

    1. Chronic Lyme Disease" as the incorrect diagnosis in patients with Fibromyalgia
      VM Hsu, SJ Patella, LH Sigal, Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019 - Arthritis Rheum. 1993 Nov;36(11):1493-500 - PMID: 8240427
      Objective - To evaluate a large number of patients referred with persistent symptoms thought to represent chronic Lyme disease.
      Methods - We retrospectively reviewed the charts of nearly 800 patients referred with persisting nonspecific musculoskeletal and/or neurologic symptoms thought to represent chronic Lyme disease.
      Results - Seventy-seven patients were found to have fibromyalgia, not ongoing Lyme disease, as the explanation of their chronic symptoms.
      Many had received multiple courses of antibiotic therapy for symptoms of fibromyalgia mistakenly attributed to chronic Lyme disease.
      No patient reported permanent and/or total resolution of fibromyalgia symptoms following antibiotic therapy.
      Appropriate therapy for fibromyalgia in those who remained compliant, however, was often effective in improving some if not all of the chronic symptoms.
      Conclusion - Fibromyalgia is a treatable and potentially curable disorder and should be considered in the evaluation of patients with "refractory Lyme disease".
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8240427
      Also read the comment on this article :
      Do infections trigger fibromyalgia ?
      Goldenberg DL - Arthritis Rheum. 1993 Nov;36(11):1489-92 - PMID: 8240426
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8240426?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    2. Chronic mycoplasmal infections in Gulf War veterans’ children and autism patients
      Garth L. Nicolson, PhD, 1 Paul Berns, MD, 1 Robert Gan, MD, 1 and Jeorg Haier, MD, PhD2 – 1 The Institute for Molecular Medicine, Huntington Beach, California, USA 16371 Gothard Street H, Huntington Beach, California 92647 – Phone : +1 714 596-6636 Fax : +1 714 596-3791; Email : gnicolson@immed.org - Website : www.immed.org - 2 Department of Internal Medicine, and Department of Surgery, Wilhelm-University, Munster, Germany - ©2009 Wellsphere
      Autism patients have systemic bacterial, viral and fungal infections that may play an important part in their illnesses.
      We found that immediate family members of veterans diagnosed with Gulf War Illnesses (GWI) often complain of fatigue and other problems and upon analysis they report similar signs and symptoms as their veteran family members, except that their children are often diagnosed with Autism.
      Since a relatively common finding in GWI patients is a bacterial infection due to Mycoplasma fermentans, we examined military families (149 patients : 42 veterans, 40 spouses, 32 other relatives and 35 children with at least one family complaint of illness) selected from a group of 110 veterans with GWI who tested positive (~42%) for mycoplasmal infections.
      Consistent with previous results, over 80% of GWI patients who were positive for blood mycoplasmal infections had only one Mycoplasma species, M. fermentans.
      In healthy control subjects the incidence of any mycoplasmal infection was ~8.5% and none were found to have multiple mycoplasmal species (P <0.001).
      In 107 family members of mycoplasma-positive GWI patients there were 57 patients (53%) that had essentially the same signs and symptoms as the veterans and were diagnosed with Chronic Fatigue Syndrome (CFS/ME) and/or Fibromyalgia Syndrome.
      The majority of children (n=35) in this group were diagnosed with Autism.
      Most of these CFS or Autism patients also had mycoplasmal infections compared to the few non-symptomatic family members (P <0.001), and the most common species found was M. fermentans.
      In contrast, in the few non-symptomatic family members that tested mycoplasma-positive, the Mycoplasma species were usually different from the species found in the GWI patients.
      The results suggest that a subset of GWI patients have mycoplasmal infections and these infections can be transmitted to immediate family members who subsequently display similar signs and symptoms, except for their children who are often diagnosed with Autism.
      In a separate study in Central California we examined a group of Autism patients and also found a high incidence of mycoplasmal infections, but in contrast to the military families a variety of Mycoplasma species were detected.
      Cfr. :
      http://stanford.wellsphere.com/autism-autism-spectrum-article/chronic-mycoplasmal-infections-in-gulf-war-veterans-children-and-autism-patients/739902
      Full text at : http://www.immed.org/GulfWarIllness/CMIGWVC%20AutismPatients.pdf

    3. Clinical experiences with post-traumatic fibromyalgia syndrome
      Romano TJ, Department of Medicine, West Virginia University School of Medicine - W V Med J 1990;86(5):198-202
      Fibromyalgia syndrome (FS) is a musculoskeletal problem that has become more and more widely recognized.
      There are three types : primary (PFS idiopathic), secondary (associated with another disorder) and post-traumatic (PTFS).
      The latter condition, PTFS, is especially intriguing since quite often litigation is involved and doubt is cast as to whether the patient is actually suffering.
      Accusations of malingering have been made.
      A retrospective chart review of 14 PTFS patients was made in an effort to ascertain the likelihood of malingering.
      Over the past two years, 14 patients (three male, 11 female) were treated for PTFS.
      The mean age was 37 years for both men and women.
      All had classic PTFS with a chronic musculoskeletal problem that started immediately after a traumatic event, classic myofascial tender points, poor sleep and normal standard laboratory tests.
      Twenty-three per cent went to trial; 77 per cent settled out of court.
      All were given a monetary award.
      The vast majority (77 per cent) returned to a rheumatologist for continued treatment, suggesting that patients who meet strict FS criteria are not malingering and are indeed in need of medical help.
      Cfr. :
      http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19921926

    4. Cloning and characterization of a RNAse L inhibitor - A new component of the interferon-regulated 2-5A pathway
      Bisbal C, Martinand C, Silhol M, Lebleu B, Salehzada T, Institut de Génétique Moléculaire-UMR 9942, CNRS-Université de Montpellier I et II, France - J Biol Chem. 1995 Jun 2;270(22):13308-17 - PMID: 7539425
      The 2-5A/RNase L system is considered as a central pathway of interferon (IFN) action and could possibly play a more general physiological role as for instance in the regulation of RNA stability in mammalian cells.
      We describe here the expression cloning and initial characterization of RLI (for RNase L inhibitor), a new type of endoribonuclease inhibitor.
      RLI cDNA codes for a 68-kDa polypeptide whose expression is not regulated by IFN.
      Its expression in reticulocyte extracts antagonizes the 2-5A binding ability and the nuclease activity of endogenous RNase L or the cloned 2DR polypeptide.
      The inhibition requires the association of RLI with the nuclease and is dependent on the ratio between the two proteins.
      Likewise RLI is coimmunoprecipitated with the RNase L complex by a nuclease-specific antibody.
      RLI does not lead to 2-5A degradation or to irreversible modification of RNase L.
      The overexpression of RLI in stably transfected HeLa cells inhibits the antiviral activity of IFN on encephalomyocarditis virus but not on vesicular stomatitis virus.
      RLI therefore appears as the first described and potentially important mediator of the 2-5A/RNase L pathway.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/7539425

    5. Co-Infections in Fibromyalgia Syndrome, Chronic Fatigue Syndrome and Other Chronic Illnesses
      Prof. Garth Nicolson - Fibromyalgia Frontiers 2002; 10(3):5-9, 27-28

    6. Considerations when Undergoing Treatment for chronic and autoimmune diseases Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 16371 Gothard St. H, Huntington Beach, California 92647 USA – Tel. : (714) 596-6636 – Fax : (714) 596-3791 – E-mail : gnicolson@immed.org - Website: www.immed.org - Reprinted from Intern. J. Medicine 1998; 1:123-128 - Plus Supplemental Suggestions : Prof. Nicolson 11/15/05
      Several people have asked me for instructions on a cost-effective way to remove heavy metals like uranium without weekly clinic visits.
      Also, I have received questions on our Lipid Replacement Therapy protocol to restore mitochondrial function and restore cellular energy.
      I have attached our updated treatment information on these topics as a MS Word 9 rich text format doc.
      The Institute for Molecular Medicine is a nonprofit research organization and does not make any money on any of the products listed in the information.
      This is provided only as a public service.
      Antibiotic therapy for chronic infections
      Please consult “Antibiotics/antivirals recommended when indicated for treatment of Gulf War illness/CFS/FMS/arthritis - Prof. Garth L. Nicolson, The Institute for Molecular Medicine at :
      http://gulfwarcouncil.com/Nicolson-Consideration%20When%20Undergoing%20Treatment%20for%20Chronic%20and%20Autoimmune%20Diseases.htm - for general information.
      We are finding that subsets of GWI (~45%) and FMS/CFS (~60%) patients have chronic mycoplasmal infections and probably other infections as well.
      We usually recommend several 6-week cycles of doxycycline, ciprofloxacin, azithromycin, clarithromycin or minocycline etc. with 2-week cycles of Augmentin in between or concurrently, if needed.
      To overcome Herxheimer reactions or die-off that cause chills, low grade fever, night sweats, muscle aches, joint pain, short term memory loss and fatigue or adverse responses i.v antibiotics have been used and a whole lemon/olive drink is useful (1 blended whole lemon, 1 cup fruit juice, 1 tbs olive oil--strain and drink liquid).
      This period usually passes within 1-2+ weeks.
      Some physicians add the antiviralFamvir (500 mgX3/day) for first 2 weeks in each 6-week cycle of antibiotics.
      The rational is that mycoplasmas have some characteristics of viruses, and antivirals can have a useful effect.
      Alternatively, viral infections may also be important in these illnesses.
      Other therapies for chronic infections
      One therapy that appears to be useful is oxidative therapy.
      This can be done at home with peroxide baths(2-4X 16 oz. bottles of 3% hydrogen peroxide in 20 inch bath (or Jacuzzi) with 2 cups of Epsom salt.
      Soak in hot water + salt until pores open (about 5 min), then add peroxide solution.
      Repeat daily or 3X per week at bedtime; no vitamins 8 hr before bath.
      Peroxide (3%, one 16 oz. bottle) can also be directly applied to skin after a work-out or hot shower/tub (for better effect apply Swedish Beauty type A tanning accelerator for 5 min before peroxide).
      Leave peroxide on for 5 min and then wash off.
      For oral irrigation, mix 1 part 3% peroxide with 2 parts water 3X per day and use like a mouth wash.
      General nutritional considerations
      GWI/CFS/FMS patients are often immunosuppressed and could be susceptible to a variety of opportunistic infections, so proper nutrition is important.
      You should not smoke or drink alcohol or caffeinated products.
      Drink as much fresh fluids as you can, lots of fruit juices or pure water are best.
      Try to avoid high sugar and fat foods, such as military (MRE) or other fast foods and acid-forming, allergen-prone and stressing foods or junk foods.
      Increase your intake of fresh vegetables, fruits and grains and decrease your intake of fats and eliminate simple or refined sugars that can suppress your immune system.
      To build up your immune system cruciferous vegetables, soluble fiber foods, such as prunes and bran, wheat germ, yogurt, fish and whole grains are useful.
      In some patients exclusive use of 'organic' foods have been beneficial.
      Vitamins and minerals
      GWI/CFS/FMS patients are often depleted in vitamins (especially B, C and E) and certain minerals.
      Unfortunately, illnesses like GWI result in poor absorption.
      Therefore, high doses of some vitamins must be used and others, such as vitamin B complex, cannot be easily absorbed by the gut (oral capsules).
      Sublingual (under the tongue) natural B-complex vitamins in small capsules or liquids (such as Total B, Real Life Research, Norwalk, CA, 310-926-5522) should be used instead of oral capsules that are swallowed.
      General vitamins plus extra C, E, CoQ-10, beta-carotene, folic acid, bioflavoids and biotin are best. L- cysteine, L-tyrosine, L-carnitine and malic acid are reported by some to be useful.
      Certain minerals are also often depleted in GWI/CFS/FMS patients, such as zinc, magnesium, chromium and selenium.
      Some recommend doses as high as 300 mg/day sodium selenite for a few days, followed by lower maintenance doses.
      Minerals should not be taken at the same time of day that antibiotics are taken because the minerals can affect the absorption of certain antibiotics.
      Replacement of natural gut flora
      GWI/CFS/FMS patients are often undergoing treatment with antibiotics and other substances that can destroy the normal gut flora.
      Antibiotic use that depletes normal gut bacteria and can result in over-growth of less desirable bacteria.
      To supplement bacteria in the gastrointestinal system yogurt and especially Lactobacillus acidophillus tablets are recommended.
      One product is a mixture of Lactobacillus acidophillus, Lactobacillus bifidus and FOS (fructoologosaccharides) to promote growth of these “friendly” bacteria in the gut (example, DDS-Plusor Multi-Flora ABF, UAS Labs (800-422-3371); Intestinal Care-DF, Ethical Nutritionals (Vitamin Park, 714-251-1800).
      L. acidophillus or mixtures above should be taken 3X daily to restore gut flora.
      Natural immunoenhancers or immunomodulators
      A number of natural remedies, such as ginseng root, herbal teas, whole lemon/olive extract drink or an extract of olive leaves with antioxidants are available and are potentially useful, especially during or after antibiotic therapy has been completed.
      Some examples are Eden, Echinacea-C (NF Formulas, 800-547-4891), Super-Immunotone (Phyto Pharmica, 800-553-2370), Immunocal (800-337-2411) olive leaf extract (Immuno-screen, 818-966-1610), NSC-100 (Nutritional Supply, 888-246-7224), Nu-Life Formula (Sophista-Care, 760-837-1908), Tahitian Noni (Morinda, 800-445-8596) or Super Defense Plus (BioDefense Nutritionals, 800-669-9205).
      These have been used to boost immune systems.
      Although these products appear to help many CFS/FMS patients, their clinical effectiveness in GWI/CFS/FMS patients has not been evaluated.
      They appear to be useful during therapy to boost the immune system or after antibiotic therapy in a maintenance program to prevent relapse of illness.
      Yeast/fungal or bacterial overgrowth
      Yeast overgrowth can occur, especially in female patients (vaginal infections).
      Gynecologists recommend Nizoral, Diflucan, Mycelex or anti-yeast creams for women on antibiotics.
      In some cases, use of metronidazole (Flagyl, Prostat) have been used to prevent fungal or parasite overgrowth or other antifungals (Nystatin, Amphotericin B, Fluconazole, Diflucan) have been administered for fungal infections that can occur while on antibiotics.
      As described above, L. acidophillus should be taken daily to restore gut flora.
      Bacterial overgrowth can also occur, for example, in between cycles of antibiotics or after antibiotics have been stopped.
      This can be controlled with 2 week courses of Augmentin (3 X 500 mg/day) in between cycles or concurrent with other antibiotics.
      Flying and exercise
      Flying, especially in unpressurized aircraft, excessive exercise and lack of sleep can make signs/ symptoms worse.
      Some exercise is essential (don’t over do it ! A common problem !).
      Adjust your exercise level to help the recovery process without causing a relapse.
      Dry saunas help rid the system of contaminating chemicals and saunas should be taken at least 3-5X per week--moderate exercise, followed by 15-20 min of dry sauna and tepid shower.
      The sauna can be repeated, by not more than 2X per day.
      The idea is to work up a good sweat, eliminating chemicals without placing too much stress on your system.
      During exercise GWI/CFS/FMS patients should always try to avoid pollutant and allergen exposures.
      For recovery after exercise and to decrease muscle soreness, some use a Jacuzzi or hot tub, but only after a sufficient cool-down period.
      Don’t get overheated in the process.
      Cfr. :
      -
      http://gulfwarcouncil.com/Nicolson-Consideration%20When%20Undergoing%20Treatment%20for%20Chronic%20and%20Autoimmune%20Diseases.htm
      - http://compkarori.com/arthritis/pi16007.htm

    7. Controversies in neurological infectious diseases
      Greenlee JE, Rose JW, Neurology Service, Veterans Affairs Medical Center and Department of Neurology, University of Utah Health Science Center, Salt Lake City 84148-001, USA - Semin Neurol. 2000;20(3):375-86 - PMID: 11051301
      The past several years have seen major advances in our understanding of neurological infectious diseases, their diagnosis, and their treatment.
      Along with these advances, however, new information about infectious agents and new therapeutic options have also introduced both uncertainty and controversy in the approach and management of patients with diseases of the central nervous system.
      Here, we discuss six such areas: the long-term efficacy of HAART therapy in treatment of HIV infection; the role of viral infection in chronic fatigue syndrome; Rasmussen's encephalitis as an infectious or autoimmune disease; the spectrum of neurological diseases caused by rickettsial infection; the role of Mycoplasma pneumoniae in human central nervous system disease; and the possible association of Chlamydia pneumoniae and human herpesvirus 6 with multiple sclerosis.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/11051301

    8. Cytokine dysregulation, inflammation and well-being
      Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP, Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, Washington, D.C., USA. - Neuroimmunomodulation. 2005;12(5):255-69 - PMID: 16166805 - © 2005 S. Karger AG, Basel
      Cytokines mediate and control immune and inflammatory responses.
      Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health and well-being.
      Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time.
      A full-fledged systemic inflammatory reaction results in stimulation of four major programs : the acute-phase reaction, the sickness syndrome, the pain program and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system.
      Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance.
      Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances.
      During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines.
      Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis.
      Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression and atherosclerosis.
      These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health.
      These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/pubmed/16166805
      - http://content.karger.com/ProdukteDB/produkte.asp?doi=10.1159/000087104

    9. Cytokines and chronic fatigue syndrome
      Patarca R, Department of Medicine, University of Miami School of Medicine, Florida 33101, USA : rpatarca@pol.net - Ann N Y Acad Sci. 2001 Mar;933:185-200 - PMID: 12000020
      Chronic fatigue syndrome (CFS) patients show evidence of immune activation, as demonstrated by increased numbers of activated T lymphocytes, including cytotoxic T cells, as well as elevated levels of circulating cytokines.
      Nevertheless, immune cell function of CFS patients is poor, with low natural killer cell cytotoxicity (NKCC), poor lymphocyte response to mitogens in culture and frequent immunoglobulin deficiencies, most often IgG1 and IgG3. Immune dysfunction in CFS, with predominance of so-called T-helper type 2 and proinflammatory cytokines, can be episodic and associated with either cause or effect of the physiological and psychological function derangement and/or activation of latent viruses or other pathogens.
      The interplay of these factors can account for the perpetuation of disease with remission/exacerbation cycles.
      A T-helper type 2 predominance has been seen among Gulf War syndrome patients and this feature may also be present in other related disorders, such as multiple chemical sensitivity.
      Therapeutic intervention aimed at induction of a more favorable cytokine expression pattern and immune status appears promising.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/12000020

    10. Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with Chronic Fatigue Syndrome
      W. J. Martin, L. C. Zeng, K. Ahmed and M. Roy, Department of Pathology, USC School of Medicine, Los Angeles 90033 - American Journal of Pathology 1994; 145: 440-51
      An atypical virus, cytopathic for human and animal fibroblasts, was repeatedly cultured from a patient with chronic fatigue syndrome.
      Viral particles, suggestive of cytomegalovirus (CMV) were seen by electron microscopy.
      Infected cells did not, however, stain with antisera specific for CMV, herpes, simplex virus or human herpes-virus-6.
      Polymerase chain reaction (PCR) assays for these viruses were also negative.
      Two distinct products of approximately 1.5 kilobase pairs were amplified from virally infected cells using the human T lymphotropic virus-II tax gene reactive primer, SK44, in low stringency PCR.
      Sequencing of one of the amplified products showed a region of highly significant partial homology with the UL34 gene of CMV.
      The sequence of the other PCR product did not correspond with CMV or any other virus.
      DNA was extracted from the material pelleted by ultracentrifugation of filtered culture supernatants.
      It migrated in agarose gels as a single band of approximately 20 kpb.
      The banded DNA was digested with EcoRI and cloned.
      A 2.2 kbp plasmid containing the CMV-related sequence identified within the PCR product was recovered.
      Sequencing of this plasmid extended the region of partial sequence homology with CMV to include a portion of the UL35 gene of CMV.
      Initial sequencing of additional plasmids has confirmed the partial relatedness to CMV.
      The data indicate a novel type of CMV-related "stealth" virus that is able to establish a clinically persistent human infection.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1887390/

    11. Deregulation of the 2.5A synthetase RNase L antiviral pathway by mycoplasmas in subsets of Chronic Fatigue Syndrome
      Nijs J, De Meirleir K, Coomans D, De Becker P, Nicolson GL - J Chronic Fatigue Syndr 2003; 11(2):37-50
      The deregulation of the 2.5A synthetase RNase L antiviral pathway and the prevalence of Mycoplasma spp. in subsets of Chronic Fatigue Syndrome [CFS] have been separately reported in the scientific literature.
      We hypothesised that a co-morbid pathophysiological mechanism involving infection by Mycoplasma spp. and the deregulation of the 2,5A synthetase / RNase L antiviral pathway may exist in CFS.
      Therefore, 186 consecutive CFS patients were enrolled.
      Mycoplasma detection was performed using forensic polymerase chain reaction.
      For RNase L determination, a radioactive probe was used to label 2,5A binding proteins in unfractionated peripheral blood mononuclear cell extracts.
      Mycoplasmainfected CFS patients presented with significantly elevated RNase L-ratio, compared to noninfected age- and sex-matched patients [p = 0.016].
      These results suggest that Mycoplasma infections may cause deregulation of the 2,5A synthetase RNase L antiviral pathway in patients with CFS.
      Cfr. :
      http://www.name-us.org/ResearchPages/ResearchArticlesAbstracts/ImmuneArticles/Nijsi2003RNaseLMyco
      Full.pdf

    12. Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescence microscopy and flow cytometry techniques
      Cirino F, Webley WC, West C, Croteau NL, Andrzejewski C Jr, Stuart ES, Department of Microbiology, University of Massachusetts, Amherst, Massachusetts 01003, USA : fcirino@microbio.umass.edu - PMID: 16472397 (erratum in : BMC Infect Dis. 2006;6:165)
      Background - Chlamydia trachomatis (Ct) and Chlamydia pneumoniae (Cp) are medically significant infectious agents associated with various chronic human pathologies.
      Nevertheless, specific roles in disease progression or initiation are incompletely defined.
      Both pathogens infect established cell lines in vitro and polymerase chain reaction (PCR) has detected Chlamydia DNA in various clinical specimens as well as in normal donor peripheral blood monocytes (PBMC).
      However, Chlamydia infection of other blood cell types, quantification of Chlamydia infected cells in peripheral blood and transmission of this infection in vitro have not been examined.
      Methods - Cp specific titers were assessed for sera from 459 normal human donor blood (NBD) samples.
      Isolated white blood cells (WBC) were assayed by in vitro culture to evaluate infection transmission of blood cell borne chlamydiae.
      Smears of fresh blood samples (FB) were dual immunostained for microscopic identification of Chlamydia-infected cell types and aliquots also assessed using Flow Cytometry (FC).
      Results - ELISA demonstrated that 219 (47.7%) of the NBD samples exhibit elevated anti-Cp antibody titers.
      Imunofluorescence microscopy of smears demonstrated 113 (24.6%) of samples contained intracellular Chlamydia and monoclonals to specific CD markers showed that in vivo infection of neutrophil and eosinophil/basophil cells as well as monocytes occurs.
      In vitro culture established WBCs of 114 (24.8%) of the NBD samples harbored infectious chlamydiae, clinically a potentially source of transmission, FC demonstrated both Chlamydia infected and uninfected cells can be readily identified and quantified.
      Conclusion - NBD can harbor infected neutrophils, eosinophil/basophils and monocytes.
      The chlamydiae are infectious in vitro and both total and cell type specific Chlamydia carriage is quantifiable by FC.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/16472397

    13. Detection of Chlamydophila pneumoniae in the bone marrow of two patients with unexplained chronic anaemia
      Nebe CT, Rother M, Brechtel I, Costina V, Neumaier M, Zentgraf H, Böcker U, Meyer TF, Szczepek AJ, Central Laboratory, University Hospital Mannheim, Mannheim, Germany : thomas.nebe@ikc.ma.uni-heidelberg.de - Eur J Haematol. 2005 Jan;74(1):77-83 - PMID: 15613113
      Anaemia of chronic disease (ACD) is a common finding involving iron deficiency and signs of inflammation.
      Here, we report on two patients with ACD where a persistent infection with Chlamydophila (Chlamydia) pneumoniae (CP) was detected in bone marrow (BM) biopsies.
      Infection was suspected by routine cytology and confirmed by immunofluorescence, electron microscopy, polymerase chain reaction (PCR) including different primer sets and laboratories and sequencing of the PCR product.
      This is a first report of chlamydial presence in the BM of anaemic patients.
      The cases are presented because persistent chlamydial infection may contribute more frequently to chronic refractory anaemia than previously suspected.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15613113

    14. Detection of Mycoplasma genus and Mycoplasma fermentans by PCR in patients with Chronic Fatigue Syndrome
      Vojdani A, Choppa PC, Tagle C, Andrin R, Samimi B, Lapp CW, Immunosciences Laboratory, Beverly Hills, CA 90211, USA : immunsi@ix.netcom.com - FEMS Immunol Med Microbiol. 1998 Dec;22(4):355-65 - PMID: 9879928
      Mycoplasma fermentans and other Mycoplasma species are colonizers of human mucosal surfaces and may be associated with human immunodeficiency virus infection.
      While many infectious agents have been described in different percentages of patients with Chronic Fatigue Syndrome (CFS), little is known about the prevalence of mycoplasmas and especially M. fermentans in CFS patients.
      A polymerase chain reaction (PCR)-based assay was used to detect Mycoplasma genus and M. fermentans genomes in peripheral blood mononuclear cells (PBMC) of CFS patients.
      Blood was collected from 100 patients with CFS and 50 control subjects.
      The amplified products of 717 bp of Mycoplasma genus, and 206 bp of M. fermentans were detected in DNA purified from blood samples in 52% and 34% of CFS samples, respectively.
      In contrast, these genomes were found in only 14% and 8% of healthy control subjects respectively (P < 0.0001).
      All samples were confirmed by Southern blot with a specific probe based on internal sequences of the expected amplification product.
      Several samples, which were positive for Mycoplasma genus, were negative for M. fermentans indicating that other Mycoplasma species are involved.
      A quantitative PCR was developed to determine the number of M. fermentans genome copies present in 1 microg of DNA for controls and CFS patients.
      Mycoplasma copy numbers ranging from 130 to 880 and from 264 to 2400 were detected in controls and CFS positive subjects, respectively.
      An enzyme immunoassay was applied for the detection of antibodies against p29 surface lipoprotein of M. fermentans to determine the relationship between M. fermentans genome copy numbers and antibody levels.
      Individuals with high genome copy numbers exhibited higher IgG and IgM antibodies against M. fermentans specific peptides.
      Isolation of this organism by culture from clinical specimens is needed in order to demonstrate specificity of signal detected by PCR in this study.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9879928

    15. Detection of Mycoplasma pneumoniae by using the polymerase chain reaction
      C Bernet, M Garret, B de Barbeyrac, C Bebear, and J Bonnet, Institut de Biochimie Cellulaire et Neurochimie du Centre National de la Recherche Scientifique, Bordeaux, France - J Clin Microbiol. 1989 November; 27(11): 2492–2496
      The polymerase chain reaction (PCR) technique was used to detect Mycoplasma pneumoniae.
      A specific DNA sequence for M. pneumoniae was selected from a genomic library and two oligonucleotides were chosen in this sequence to give an amplified fragment of 144 base pairs.
      We show that DNA from different M. pneumoniae strains can be detected by PCR, with DNA from other Mycoplasma species giving negative results.
      Analysis of biological samples (throat swabs) obtained from hamsters that were experimentally infected with M. pneumoniae showed that PCR was more sensitive and reliable than conventional culture techniques for the detection of M. pneumoniae.
      Initial experiments on artificially seeded human bronchoalveolar lavages showed that PCR can be used to detect 10(2) to 10(3) organisms.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC267064/

    Go to Part V


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    Infection as one possible cause of fibromyalgia

    Part V

    1. Detection of Mycoplasma pneumoniae in the airways of adults with chronic asthma
      Monica Kraft, Gail H. Cassell, Jan E. Henson, Harold Watson, Jan Williamson, B.P. Marmion, Charlotte A. Gaydos and Richard J. Martin, Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colorado; Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama; Royal Hobart Hospital, University of Tasmania, Hobart, Tasmania; Institute of Medical and Veterinary Science, University of Adelaide, Australia; and Department of Medicine, The Johns Hopkins University, Baltimore, Maryland - Am. J. Respir. Crit. Care Med., Volume 158, Number 3, September 1998, 998-1001
      Infection with Mycoplasma pneumoniae has been shown to exacerbate asthma in humans.
      However, the role of M. pneumoniae in the pathogenesis of chronic asthma has not been defined.
      Eighteen asthmatics with chronic, stable asthma and 11 nonasthmatic control subjects underwent evaluation of the upper and lower airways and serologic analysis to determine the presence of M. pneumoniae, Chlamydia pneumoniae and seven respiratory viruses through culture, enzyme-linked immunoassay (EIA) and polymerase chain reaction (PCR).
      M. pneumoniae was detected by PCR in 10 of 18 asthmatics and one of 11 control subjects (p = 0.02).
      In nine of the 10 patients, the organism was detected in bronchoalveolar lavage or bronchial biopsies.
      Seven of 18 asthmatics and one of 11 control subjects were also positive for M. fermentans and M. genitalium by PCR.
      All patients' cultures, EIAs and serology were negative for M. pneumoniae.
      All PCR and cultures were negative for C. pneumoniae and all EIAs for respiratory viruses were negative in all subjects.
      Nine asthmatics and one control subject exhibited positive serology for C. pneumoniae (p = 0.05).
      M. pneumoniae was present in the lower airways of chronic, stable asthmatics with greater frequency than control subjects and may play a role in the pathogenesis of chronic asthma.
      Cfr. :
      http://ajrccm.atsjournals.org/cgi/content/abstract/158/3/998

    2. Detection of mycoplasmal infections in blood of 565 chronic illness patients detected by polymerase chain reaction
      Nasralla M, Haier J, Nicolson GL - Intern J Med Biol Environ 2000; 28(1):15-23
      Garth L. Nicolson, PhDb, a, f1, Marwan Y. Nasralla, PhDc, a, Joerg Haier, MD, PhDd, a and John Pomfret, PhDb - a Molecular Biology Laboratory, Department of General Surgery, University Hospital Muenster, Muenster, Germany - b Gulf War ALS Research Project, Parsons Walk, Wigan, UK - c International Molecular Diagnostics, Inc. Huntington Beach, California, USA - d Department of Surgery, Wilhelm University, Muenster, Germany - f1 Correspondence to : Prof. Garth L. Nicolson, Molecular Biology Laboratory, Department of General Surgery, University Hospital Muenster, Waldeyerstrasse 1, 48149 Muenster, Germany – Tel. : +1-714-903-2900; Fax : +1-714-379-2082 - Website :
      www.immed.org – E-mail : gnicolson@immed.org - Journal of Clinical Neuroscience, Volume 9, Issue 5, September 2002, Pages 525-529 - © 2002 Elsevier Science Ltd.

      The presence of systemic mycoplasmal infections in the blood of Gulf War veterans (n=8) and civilians (n=28) with Amyotrophic Lateral Sclerosis (ALS) and age matched controls (n=70) was investigated by detecting mycoplasma gene sequences with forensic
      Polymerase Chain Reaction (PCR) and back hybridization with a radiolabeled internal oligonucleotide probe.
      Almost all ALS patients (30/36 or not, vert, similar83%) showed evidence of Mycoplasma species in blood samples, whereas <9% of controls had blood mycoplasmal infections (P<0.001).
      Using PCR ALS patients with a positive test for any mycoplasmal infection were investigated for the presence of M. fermentans, M. pneumoniae, M. hominis and M. penetrans in their blood.
      All Gulf War veterans with ALS were positive for M. fermentans, except one that was positive for M. genitalium.
      In contrast, the 22/28 civilians with detectable mycoplasmal infections had M. fermentans (13/22, 59%) as well as otherMycoplasama species in their blood and two of the civilian ALS patients had multiple mycoplasma species (M. fermentans plus M. hominis).
      Of the few control patients that were positive, only two patients (2/70, 2.8%) were positive for M. fermentans (P<0.001).
      The results support the suggestion that infectious agents may play a role in the pathogenesis and/or progression of ALS or alternatively ALS patients are extremely susceptible to systemic mycoplasmal infections.
      Cfr. :
      http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHP-46W191P-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchSt
      rId=1081260880&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0
      &_userid=10&md5=d97f94b9749fc8a1c440a560f53d47d9

    3. Detection of Mycoplasmal infections in blood of patients with rheumatoid arthritis
      Haier J. (1), Nasralla M. (1), Franco A. R. (2), Nicolson G. L. (1) - (1) Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041, Etats-Unis - Arthritis Center of Riverside, Riverside, CA 92501,Etats-Unis - Rheumatol 1999; 38:504-509
      Objective - Mycoplasmal infections are associated with several acute and chronic illnesses.
      Some mycoplasmas can enter a variety of tissues and cells and cause system-wide or systemic signs and symptoms.
      Methods - Patients (14 female, 14 male) diagnosed with rheumatoid arthritis (RA) were investigated for mycoplasmal infections in their blood leucocytes using a forensic polymerase chain reaction (PCR) procedure.
      Amplification was performed with genus- and species-specific primers and a specific radiolabelled internal probe was used for Southern hybridization with the PCR product.
      Patients were investigated for the presence of Mycoplasma spp. and positive cases were further tested for infections with the following species : M. fermentans, M. hominis, M. pneumoniae and M. penetrans.
      Results - The Mycoplasma spp. sequence, which is not entirely specific for mycoplasmas, was amplified from the peripheral blood of 15/28 patients (53.6%) and specific PCR products could not be detected in 13 patients (46.4%).
      Significant differences (P < 0.001) were found between patients and positive healthy controls in the genus test (3/32) and in the specific tests (0/32).
      Moreover, the incidence of mycoplasmal infections was similar in female and male patients.
      Using species-specific primers, we were able to detect infections with M. fermentans (8/28), M. pneumoniae (5/28), M. hominis (6/28) and M. penetrans (1/28) in RA patients.
      In 36% of the patients, we observed more than one Mycoplasma species in the blood leucocytes.
      All multiple infections occurred as combinations of M. fermentans with other species.
      Conclusions - The results suggest that a high percentage of RA patients have systemic mycoplasmal infections.
      Systemic mycoplasmal infections may be an important cofactor in the pathogenesis of RA and their role needs to be explored further.Cfr. :
      http://rheumatology.oxfordjournals.org/cgi/reprint/38/6/504.pdf

    4. Detection of RNA sequences in cultures of a stealth virus isolated from the cerebrospinal fluid of a health care worker with Chronic Fatigue Syndrome - Case report
      Martin JW, Center for Complex Infectious Diseases, Rosemead, Calif., USA - Pathobiol ogy1997; 65: 57-60 - © 1997 S. Karger AG, Basel
      A cytopathic stealth virus was cultured from the cerebrospinal fluid of a nurse with chronic fatigue syndrome.
      Reverse transcriptase-polymerase chain reaction (RT-PCR) performed on the patient's culture yielded positive results with primer sets based on sequences of a previously isolated African green monkey simian-cytomegalovirus-derived stealth virus.
      The same primer sets did not yield PCR products when tested directly on DNA extracted from the cultures.
      The findings lend support to the possibility of replicative RNA forms of certain stealth viruses and have important implications concerning the choice of therapy in this type of patient.
      Cfr. :
      http://content.karger.com/ProdukteDB/produkte.asp?Doi=164104

    5. Development of an amplification and hybridization assay for the specific and sensitive detection of Mycoplasma fermentans DNA
      Berg S, Lüneberg E, Frosch M, Institut für Medizinische Mikrobiologie, Medizinische Hochschule, Hannover, Germany - Mol Cell Probes. 1996 Feb;10(1):7-14 - PMID: 8684379
      A polymerase-chain-reaction-based detection system for Mycoplasma fermentans was established.
      The highly conserved tuf gene, which encodes elongation factor Tu of prokaryotes, served as target sequence for the PCR.
      With two PCR oligodeoxynucleotides, which were selected from M. fermentans specific sequences of the tuf gene, we amplified a 850 base pair DNA fragment.
      Via the biotin-moiety of one primer the PCR fragments were immobilized on streptavidin-coated microtitre plates.
      After alkaline denaturation a digoxigenin-labelled M. fermentans specific DNA probe was hybridized to the single stranded immobilized PCR fragment.
      Detection was performed by addition of an alkaline phosphatase conjugated anti-digoxigenin antibody. 4-methyl-umbelliferyl-phosphate was used as a fluorogenic substrate.
      Amplification of 10 fg chromosomal target DNA was detected by this 'DNA enzyme immuno assay (DEIA)' technique, corresponding to seven genome copies.
      Our study supports the presumption that the tuf gene proves to be a suitable target sequence for the PCR based detection of any bacterial species.
      Furthermore, hybridization of PCR fragments with radio-labelled DNA probes should no longer be necessary, because a very sensitive non-radioactive test system can easily be established with the 'DEIA' technique.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8684379

    6. Diagnosis and integrative treatment of intracellular bacterial infections in Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness, Rheumatoid Arthritis and other chronic illnesses
      Nicolson GL, Nasralla M, Franco AR, Nicolson NL, Erwin R, Ngwenya R, Berns PA - Clin. I'racl. Ail.Med, 2000; 1:92-102
      Cfr. : http://www.immed.org/

    7. Diagnosis and treatment of chronic infections in chronic fatigue syndrome, fibromyalgia syndrome and Gulf War illness
      G.L. Nicolson and N.L. Nicolson - International Journal of Occupational Medicine, Immunology and Toxicology 1996 ; 5 : 69-78
      Cfr. : http://www.immed.org/

    8. Diagnosis and treatment of chronic mycoplasmal infections in Fibromyalgia and Chronic Fatigue Syndromes - Relationship to Gulf War Illness
      Nicolson GL. Nasralla M. Haier and Nicolson NL - Biomed. Ther, 1998;16:266-71
      Cfr. : http://www.immed.org/

    9. Diagnosis and treatment of mycoplamsmal infections in Persian Gulf War Illness – CFIDS patients
      Nicolson GL, Nicolson NL - International Journal of Occupational Medicine, Immunology and Toxicology 1996; 5: 67-78
      Veterans of Operation Desert Storm returned from the Persian Gulf Theater of Operations and developed multiple signs and symptoms characterized by disabling fatigue, arthralgia, intermittent fever, myalgia, impairments in short-term memory, headaches, skin rashes, diarrhea and additional symptoms that have defied a disease case definition but has been called Gulf War Illness (GWI).
      In a sampling of GWI patients and symptomatic family members (n=30) we have used the technique of Gene Tracking and have found evidence of mycoplasmal infections in the blood leukocytes of approximately one-half of these cases.
      Mycoplasma-positive patients can be successfully treated with several 6 week courses of doxycycline (200 mg/d) or other antibiotics.
      Of the 14/30 patients that were mycoplasma-positive, 11/14 completely recovered after multiple cycles of antibiotics and 3/14 are still undergoing antibiotic therapy and relapsing.
      Cfr. :
      www.immed.org/Fatigue%20Illness/_GWI_IJO.rtf

    10. Dietary supplement Healthy Curb for reducing weight, girth, body mass, appetite and fatigue while improving blood lipid values with NTFactor Lipid Replacement Therapy
      Garth L Nicolson, PhD, Rita Ellithorpe, MD, Robert Settineri, MS - J. IiME 2009; 3(1): 39-48 – Source : Journal of IiME, May 28, 2009 (note : the full text of this article with charts is available free online in the Spring 2009 issue of the Journal of IiME - http://bit.ly/3PvOQ -; dr. Nicolson presented the results at the recent International IiME Conference]
      Often Chronic Fatigue Syndrome (CFS) patients have weight issues and weight reduction regimens can increase fatigue.
      Therefore, we initiated a weight loss clinical trial using an all natural oral supplement mixture containing an FDA-approved amylase inhibitor plus NTFactor®, which is known to safely reduce fatigue in aged subjects, chronic fatigue and CFS.
      The objective was to see if subjects could safely lose weight without increasing appetite and fatigue and without changing eating or exercise patterns or using drugs, herbs or caffeine.
      A 2-month open label clinical trial was initiated with 30 patients who used an oral mixture (Healthy Curb™) of amylase inhibitor (500 mg white kidney bean extract) plus 500 mg of NTFactor 30 min before each meal.
      Weight and measurements were taken weekly, appetite was assessed and fatigue was determined using the Piper Fatigue Scale.
      - Sixty-three percent of the participants lost an average of 3 pounds, with average reductions of 1.5 and 1 inch waist and hip circumference, respectively.
      - Participants experienced gradual and consistent weight loss along with waist and hip, body mass index (BMI) and basal metabolic rate (BMR) reductions during the entire trial.
      - There was a 44% reduction in overall hunger with reduced cravings for sweets; therefore, notable appetite suppression occurred.
      - Using the Piper Fatigue Scale the entire test group showed an average of 23% decrease in overall fatigue.
      - Blood lipid profiles generally improved, suggesting improved cardiovascular health and
      - no adverse effects were noted clinically or found in blood chemistries.
      Conclusions - The vast majority of the subjects in this trial lost weight, showed decreased waist and hip measurements and overall body mass.
      Their overall fatigue was reduced and they experienced marked appetite suppression.
      The product was completely safe and void of any side effects and was extremely well tolerated.
      Healthy Curb appears to be a safe and effective means for CFS patients to manage weight without changes in eating or exercise patterns.
      Cfr. :
      http://www.prohealth.com/alzheimers/library/showarticle.cfm?libid=14581

    11. Do infections trigger fibromyalgia ?
      DL Goldenberg - Arth & Rhu, 1993; 36: 1489-92
      Cfr. :
      http://www.roadback.org/index.cfm/fuseaction/education.display/display_id/135.html

    12. Doxycycline treatment and Desert Storm
      Garth L. Nicolson, PhD, The University of Texas M. D. Anderson Cancer Center Houston - Nancy L. Rosenberg-Nicolson, PhD, Rhodon Foundation for Biomedical Research Kingwood, Tex – JAMA 1995;273(8):618-619
      Cfr. :
      http://jama.ama-assn.org/cgi/content/summary/273/8/618-a

    13. Effective treatment of chronic fatigue syndrome and fibromyalgia—A randomized, double-blind, placebo-controlled, intent-to-treat study
      Jacob E. Teitelbaum a; Barbara Bird a; Robert M. Greenfield b; Alan Weiss b; Larry Muenz c; Laurie Gould d - a Annapolis Research Center for Effective FMS/CFIDS Therapies and the Anne Arundel Medical Center, Annapolis, MD, USA - b Anne Arundel Medical Center, Annapolis, MD, USA - c Larry Muenz resides in Gaithersburg, MD, USA - d Annapolis Research Center for Effective FMS/ CFIDS Therapies, Annapolis MD, and also the USDA, Beltsville, MD, USA - Journal Of Chronic Fatigue Syndrome, Volume 8, Issue 2 May 2000 , pages 3 – 15
      Cfr. :
      http://www.informaworld.com/smpp/content~db=jour~content=a903600733~tab=citations

    14. Emerging concepts in the neurobiology of chronic pain - Evidence of abnormal sensory processing in fibromyalgia
      Bennett RM, Division of Arthritis and Rheumatic Diseases, Oregon Health Sciences University, Portland 97201, USA - Mayo Clin Proc. 1999 Apr;74(4):385-98 - PMID: 10221469
      Chronic pain often differs from acute pain.
      The correlation between tissue pathology and the perceived severity of the chronic pain experience is poor or even absent.
      Furthermore, the sharp spatial localization of acute pain is not a feature of chronic pain; chronic pain is more diffuse and often spreads to areas beyond the original site.
      Of importance, chronic pain seldom responds to the therapeutic measures that are successful in treating acute pain.
      Physicians who are unaware of these differences may label the patient with chronic pain as being neurotic or even a malingerer.
      During the past decade, an exponential growth has occurred in the scientific underpinnings of chronic pain states.
      In particular, the concept of nonnociceptive pain has been refined at a physiologic, structural and molecular level.
      This review focuses on this new body of knowledge, with particular reference to the chronic pain state termed "fibromyalgia".
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10221469
      Aslo read the comment on this article :
      Fibromyalgia and pain management
      Sartin JS - Mayo Clin Proc. 2000 Mar;75(3):316-7 - PMID: 10725965
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10725965?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    15. Empiric parenteral antibiotic treatment of patients with fibromyalgia and fatigue and a positive serologic result for Lyme disease - A cost-effectiveness analysis
      Lightfoot RW Jr, Luft BJ, Rahn DW, Steere AC, Sigal LH, Zoschke DC, Gardner P, Britton MC, Kaufman RL, Division of Rheumatology, Kentucky Clinic J515, University of Kentucky Medical Center, Lexington 40536-0284 - Ann Intern Med. 1993 Sep 15;119(6):503-9 - PMID: 8357117
      Purpose -
      To examine the cost-effectiveness of empirical, parenteral antibiotic treatment of patients with chronic fatigue and myalgia and a positive serologic result for Lyme disease who lack classic manifestations.
      Data sources - Peer-reviewed journals, opinion of experts in the field and published epidemiologic reports.
      Study selection - Consensus by authors on articles that indicated methods for patient selection; on criteria used for diagnosis; on immunologic methods used for classifying patients; on the dose and duration of therapy; and on criteria by which responses to therapy were ascertained.
      Data extraction - In a cost-effectiveness model, the costs and benefits of empirical parenteral therapy for patients seropositive for Lyme disease were compared with a strategy in which only patients having classical symptoms of Lyme disease were treated.
      Data synthesis - In areas endemic for Lyme disease, the incidence of false-positive serologic results in patients with nonspecific myalgia or fatigue exceeds by four to one the incidence of true-positive results in patients with nonclassical infections.
      Treatment of the former group of patients costs $86,221 for each true-positive patient treated.
      The empirical strategy causes 29 cases of drug toxicity for every case in the more conservative strategy.
      If patients were willing to pay $3485 to eliminate anxiety about not treating possible true Lyme disease, the empirical strategy would break even.
      Conclusion - For most patients with a positive Lyme antibody titer whose only symptoms are nonspecific myalgia or fatigue the risks and costs of empirical parenteral antibiotic therapy exceed the benefits.
      Only when the value of patient anxiety about leaving a positive test untreated exceeds the cost of such therapy is the empirical treatment cost-effective.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8357117
      Also read the comments on this article :
      - Appropriateness of parenteral antibiotic treatment for patients with presumed Lyme disease - A joint statement of the American College of Rheumatology and the Council of the Infectious Diseases Society of America
      Ann Intern Med. 1993 Sep 15;119(6):518 - PMID: 8357119
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8357119?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
      - Simplifying the diagnosis of obstructive sleep apnea
      Pack AI - Ann Intern Med. 1993 Sep 15;119(6):528-9 - PMID: 8204127
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8204127?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract

    16. Established fibromyalgia syndrome and parvovirus B19 infection
      Berg AM, Naides SJ, Simms RW, Arthritis Section, Boston University, MA - J Rheumatol. 1993 Nov;20(11):1941-3 - PMID: 8308782
      Objective - To determine the seroprevalence of prior and persistent parvovirus B19 (B19) infection in a group of patients with fibromyalgia (FS) compared with controls.
      Methods - Fifteen female patients with FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and eleven patients with FS who did not recall any such illness (-VP) were selected from a referral practice.
      We excluded patients with FS who described a history of trauma prior to the onset of FS symptoms.
      Twenty-six female medical workers served as controls.
      Serum IgM and IgG anti-B19 antibodies were measured by ELISA.
      Polymerase chain reaction (PCR) products from serum were analyzed by dot blot hybridization for B19 DNA.
      Fisher's 2-tailed exact test was used to compare the proportion of positive serologies in each group.
      Results - No patient or control had positive IgM levels.
      For all patients with FS, the prevalence of prior B19 infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00) and that of the general population.
      No significant difference was found in the prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11, p = 0.25).
      None of the patients or controls showed evidence for persistent B19 viremia, as determined by PCR analysis.
      Conclusion - Our data do not suggest that B19 plays a pathogenic role in this population of patients with FS.
      Testing for IgM against B19 within 2-3 months of symptom onset may prove more helpful in further defining the role of B19 in FS.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/8308782

    17. Evidence for bacterial (mycoplasma, Chlamydia) and viral (HHV-6) co-infections in chronic fatigue syndrome patients
      Garth L. Nicolson a; Marwan Y. Nasralla b; Kenny De Meirleir c; Robert Gan b; Joerg Haier - a Institute for Molecular Medicine, Hunting-ton Beach, CA, USA - b International Molecular Diagnostics, Inc., Huntington Beach, CA, USA - c Department of Internal Medicine, Free University of Brussels, Brussels, Belgium - Journal Of Chronic Fatigue Syndrome, Volume 11, Issue 2 March 2003 , pages 7 - 19
      Cfr. :
      -
      http://www.informaworld.com/smpp/content~db=all?content=10.1300/J092v11n02_02
      - http://www.informaworld.com/smpp/content~db=all~content=a902686227~tab=citations

    18. Evidence for Brucella spp. and Mycoplasma spp. co-infections in blood of chronic fatigue syndrome patients
      Nicolson GL, Gan R, Haier J - J Chronic Fatigue Syndr 2005; 12(2):5-17
      Cfr. :
      http://www.informaworld.com/smpp/content~db=all~content=a902981759~tab=citations

    19. Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders
      Nicolson GL, Gan R, Nicolson NL, Haier J, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA : gnicolson@immed.org - J Neurosci Res. 2007 Apr;85(5):1143-8 - PMID: 17265454 - © 2007 Wiley-Liss, Inc.
      We examined the blood of 48 patients from central and southern California diagnosed with autistic spectrum disorders (ASD) by using forensic polymerase chain reaction and found that a large subset (28/48 or 58.3%) of patients showed evidence of Mycoplasma spp. infections compared with two of 45 (4.7%) age-matched control subjects (odds ratio = 13.8, P < 0.001).
      Because ASD patients have a high prevalence of one or more Mycoplasma spp. and sometimes show evidence of infections with Chlamydia pneumoniae, we examined ASD patients for other infections.
      Also, the presence of one or more systemic infections may predispose ASD patients to other infections, so we examined the prevalence of C. pneumoniae (4/48 or 8.3% positive, odds ratio = 5.6, P < 0.01) and human herpes virus-6 (HHV-6, 14/48 or 29.2%, odds ratio = 4.5, P < 0.01) coinfections in ASD patients.
      We found that Mycoplasma-positive and -negative ASD patients had similar percentages of C. pneumoniae and HHV-6 infections, suggesting that such infections occur independently in ASD patients.
      Control subjects also had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 (4/48 or 8.3%) infections, and there were no coinfections in control subjects.
      The results indicate that a large subset of ASD patients shows evidence of bacterial and/or viral infections (odds ratio = 16.5, P < 0.001).
      The significance of these infections in ASD is discussed in terms of appropriate treatment.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17265454

    20. Examination of Mycoplasmas in blood of 565 chronic illness patients by polymerase chain reaction
      Marwan Y. Nasralla, Jörg Haier, Nancy L. Nicolson and Garth L. Nicolson.*, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel. : 1-714-903-2900 – Fax : 714-379-2082 - *Correspondence to: Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel: 1-714-903-2900, Fax: 1-714-379-2082 – Website : www.immed.org – E-mail : gnicimm@ix.netcom.com - International Journal Medicine Biology Environment 2000; 28(1):15-23
      Mycoplasmal infections are associated with several acute and chronic illnesses.
      Patients with Chronic Fatigue Syndrome (CFS), myalpic encepthalomyelitis (ME) and/or Fibromyalgia Syndrome (FMS) were examined for systemic mycoplasmal infections by analysis of blood specimens.
      Using an optimized protocol for forensic polymerase chain reaction (PCR) blood samples from 565 CFS or FMS patients (401 female, 164 male) and 71 healthy controls were investigated for presence of Mycoplasma spp. and M. fermentans infections.
      The Mycoplasma spp. sequence was amplified from the peripheral blood of 300/565 patients (53.1 %).
      Specific PCR products could not be detected in 265 patients (46.9 %).
      A significant difference (p<0.001) was found between mycoplasma-positive patients and healthy controls (7/71; 9.9%).
      The prevalence of M. fermentans infections (24.6%) was also significantly (p<0.001) higher in CFS/FMS patients than in controls (2/71; 2.8%).
      Moreover, the prevalence of mycoplasmal infections was similar in female and male CFS patients.
      The data indicate that mycoplasmas can be detected in blood specimens from a high proportion of CSF/FMS patients.
      M. fermentans can be an opportunistic infection, cofactor or causative agent resulting in morbidity in these patients.

    21. Fibromyalgia - Is there an infectious connection ?
      The Road Back Foundation
      Fibromyalgia (FM) is a commonly misunderstood, sometimes misdiagnosed rheumatic disease.
      The main symptoms are achiness, pain (more in the muscles than in the joints), stiffness, fatigue, accompanied by headaches, depression, sleep disorders, Raynaud's and irritable bowel syndrome.
      The sites of pain are located in specific areas call-ed tender or trigger points.
      The painful tender points are located where the ligament attaches the muscle to the bone.
      There are 18 tender point locations. Sensitivity at 11 points defines a diagnosis of fibromyalgia.
      FM is not life threatening nor does it cause physical deformities.
      Many lab tests are within normal range.
      In fact, most patients look extremely well and fit, making it difficult to account for the degree of clinical suffering they are experiencing, yet 10-30% of fibromyalgia patients are disabled to some degree because of their disease symptoms.
      It is 9 times more common among women than men, usually between the ages of 40 and 60, is more common in Caucasians than other races and is the second or third most common disorder treated by rheumatologists.
      Potential Pathogens As is the case of most forms of "arthritis", no known cause has been established, but a number of possibilities are mentioned in the medical literature.
      Like many forms of arthritis, the cause of FM is probably not limited to one single factor.
      55% of patients identify a "flu-like" or viral type illness, 33% physical trauma/injury and 14% emotional stress as a precursor to the onset of symptoms.
      The connection of FM to infections is well documented in the literature, especially in relation to Lyme disease, mycoplasma, Chlamydia pneumoniae., Hepatitis C, Parvovirus B19, HIV and Epstein-Barr.
      It is believed as many as 25-40% of long-term Lyme patients develop fibromyalgia-like symptoms, particularly pain and fatigue; as many as 25% of HIV patients, 57% of RA patients and 24% of Psoriatic Arthritis patients also have FM symptoms.
      A 1993 Annals of Internal Medicine article (Lightfoot et al) found 10% of patients with Lyme Disease would have arth-ritis develop as a result of the spirochete infection.
      Because this organism (like mycoplasma) is difficult to culture, the diagnoses is based on the occurrence of (1) one or more of the classical features and (2) serum antibodies to the etiologic spirochete after the first 4 to 6 weeks of illness.
      Some Lyme/FM patients do not respond to courses of antibiotics, causing researchers to dismiss the possibility of an organism as a trigger for the disease and antibiotics as a therapy.
      This might be a misleading assumption as explained by Garth Nicholson, PhD, in a recent article (Environmental Phys, 1997).
      "Are chronic, systemic mycoplasmal infections the answer to CFS, FMS, GWI* and other disorders ? Of course not ! This is likely to be an appropriate explanation for a rather large subset of CFS, FMS, GWI* and some arthritis patients, but certainly not every patient will have the same chronic infections. Some patients may have chemical exposures or other environmental problems as the underlying reason for their chronic signs and symptoms. In these patients, antibiotics should have no effect whatsoever".
      Nicholson has found mycoplasma infections in approximately one half of patients with FM as well as arthritis.
      "The identification of mycoplasma infections in the leukocyte blood fractions of a rather large subset of CFS, FMS and arthritis patients suggests that mycoplasmas and probably other chronic infections as well, may be an important source of morbidity in these patients. If such infections are important in these disorders, then appropriate treatment with antibiotics should result in improvement and even recovery. This is exactly what has been found" (Nicholson JAMA 1995).
      "Only antibiotics that are effective against the pathogenic mycoplasmas result in recovery, and some antibiotics, such as penicillins, can worsen the condition" (Nicholson, 1996, & 1997).
      Goldenberg suggests two possibilities for an infectious cause :
      1) the infectious agent would either directly invade tissues such as the joints or central nervous system or
      2) "trigger" factors that would cause the chronic myalgias, fatigue, headaches, sleep disturbances and mood disturbances...
      Infectious agents are capable of activating cytokines which may in turn cause severe myalgias, fatigue and neurocognitive disturbances...
      The potential role of a microbial agent as a trigger to fibromyalgia remains tenable.
      Antibodies to Chlamydia pneumoniae have been found in 78.3% of FM patients tested or 67.4% for unselected rheumatic patients.
      These high numbers point to a possible connection between Chlamydia pneumoniae and fibromyalgia.
      In a Spanish study, Rivera et al found 15% of 112 FM patients had Hepatitis C viral Infection (HCV) and among HCV patients, 10% had FM.
      The incidence of FM in the control group was less than 2%; the prevalence of FM in the general population was 2%.
      "The presence of active infection by HCV is more likely to trigger FM than the stress and anxiety produced by the disease" (Rivera et al, 1997).
      Other researchers have described HCV infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992).
      "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997).
      Parvovirus B19 infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992).
      "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997).
      Parvovirus B19 has been implicated as a cause in cases of chronic arthritis and may mimic rheumatoid arthritis.
      Berg et al identified patients with established FM who had symptoms consistent with recent or distant B19 infection.
      In fact, 30-60% of the general population test positive for Parvovirus B19 and the incidence increases with age.
      The timing of testing for PV B19 appears to be critical.
      Testing too early or too late will yield negative results.
      25% of HIV patients experience fibromyalgia symptoms, adding additional discomfort and anxiety.
      Epstein Barr Virus (EBV) has been considered a possible cause of FM or CFS because of similarity of symptoms, but so far, a connection has not been proven.
      Most observers currently believe that no single infectious agent is likely to be the cause of CFS (or FM).
      Yet it has been shown that chronic persistent viruses may often be reactivated during this illness.
      Is this merely an epiphenomenon ?
      Or, once reactivated, do these viruses go on to produce many of the symptoms of the disease ?
      And what reactivates these viruses ?
      If it is some defect in immunologic containment, what causes the defect ?
      Could it be stress ? Genetics ? infection with other viruses ?
      In the view of Komaroff et al, it is reasonable to speculate that all these factors are capable triggers, with different factors playing different roles in different individuals.
      Common FM symptoms
      - Chronic, widespread pain - most fatigue : 70-90%
      - morning stiffness : 80%
      - migraine headaches : 50%
      - depression : 25-50%
      - sleep disturbances : 70%
      - anxiety : 25%
      - Raynaud's-like syndrome : 33%
      - numbness, tingling : 75%
      - irritable bowel syndrome : 50%
      - positive ANA : 10%.
      Organisms that might be connected to FM
      -
      Borellia borgdorferi (Lyme)
      - Hepatitis C
      - Epstein-Barr Virus
      - Mycoplasma
      - Chlamydia pneumoniae
      - Parvovirus B19
      - HIV
      References
      .../...
      Cfr. :
      http://www.roadback.org/index.cfm/fuseaction/education.display/display_id/135.html

    22. Fibromyalgia - Up close and personal
      Mark J. Pellegrino, MD - Anadem Publishing; 2 edition (January 2005) - ISBN-10: 1890018503 - ISBN-13: 978-1890018504
      'Fibromyalgia - Up close & personal' is packed with 43 chapters of "inside" medical information and "hands-on" practical advice for everyday living.
      Dr. Mark J. Pellegrino brings readers up-to-date with the newest drug and physical treatments for fibromyalgia.
      He also presents the latest thinking on diet and exercise to help people with this condition lead a full life.
      Recognized by fibromyalgia sufferers for understanding what they are going through, Dr. Pellegrino is a welcoming and encouraging presence for everyone with this condition and this quality comes through very clearly in his writing.
      It’s as if each person reading his book is having a private consultation about their shared disease.
      In 'Up close & personal' Dr. Pellegrino has enlisted two leading attorneys to bring readers much needed insight into disability and personal injury issues.
      Also, he asked a knowledgeable physician to contribute a chapter on common pain problems.
      Cfr. :
      -
      https://www.prohealth.com/shop/product.cfm/product__code/BK90
      - http://www.amazon.com/Fibromyalgia-Personal-Mark-J-Pellegrino/dp/1890018503

    23. Fibromyalgia – Ultimately a disease of amplified pain
      Mark J. Pellegrino, MD, May 26, 2008 - © 2009 ProHealth, Inc.
      ---
      Excerpted with permission from Chapter 9 of Dr. Mark Pellegrino’s very popular book 'Fibromyalgia - Up close and personal' and reproduced with permission (this book may now be purchased from the ProHealth.com store – cfr. : https://www.prohealth.com/shop/product.cfm/product__code/BK90 -).
      Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center and has been a Fibromyalgia patient himself since childhood ---
      Many conditions can lead to permanent changes in the pain transmission mechanism and result in chronic pain that overwhelms the body’s pain defense mechanisms.
      One such condition is Fibromyalgia.
      Fibromyalgia may not cause destruction along the pain pathways as other conditions I have mentioned can [rheumatoid arthritis, carpal tunnel syndrome, shingles, multiple sclerosis, for example].
      However, Fibromyalgia does cause chronic abnormal changes along all the pathway components and this results in chronic pain via both peripheral (from skin, muscles and nerves) and central (from spinal cord and brain) neurological mechanisms.
      The end result of Fibromyalgia’s abnormal changes appears to be a state of pain amplification that cause severe generalized pain.
      Fibromyalgia is ultimately a disease of amplified pain.
      Dr. Robert Bennett has written and presented excellent information that explains why we hurt with Fibromyalgia (e.g. “Emerging Concepts in the Neurobiology of Chronic Pain - Evidence of Abnormal Sensory Processing in Fibromyalgia” - Mayo Clinic Proceedings at :
      http://www.ncbi.nlm.nih.gov/pubmed/10221469 -).
      If we trace the pain signals through the various parts of the pain pathway (from the nociceptors - or specialized pain nerve endings – to the nerves to the spinal cord to the brain) in people with Fibromyalgia, we find various abnormalities along the way.
      Many studies have shed light on different points along the complete pain pathway.
      I want to briefly summarize some of these different abnormalities and possible problems encountered by Fibromyalgia pain signals on the path to the brain.
      Nociceptors - Pain originates from the nociceptors
      Trauma is a common trigger of Fibromyalgia.
      Tissue injury - damage to the muscles and soft tissues – activates the nociceptors.
      Some studies have suggested that microscopic injury occurs in specific parts of the muscles (for those who want the medical names: muscle spindles, intrafusal fibers and calcium pumps).
      Localized tissue injury probably activates arachidonic acid (a biological protein), which turns into “bad” prostaglandans (called Cox-II prostaglandins) and cause inflammation and pain.
      In addition to trauma, autoimmune factors may be another pain nerve activator.
      Perhaps autoimmune processes create compounds which act as irritants and activate the nociceptors chronically to the point where they become “permanently” sensitized and irritated.
      As a result, biochemical, hormonal, and red blood cell changes occur that interfere with the cells’ ability to receive adequate supplies of oxygen, glucose and other nutrients.
      Blood flow, energy formation and the cells’ electrical and neurological harmonies are all disrupted.
      Since the nociceptors remain “faulty” the electrical and neurological balance remains abnormal and nociceptors continue to be activated.
      Pain-producing neurotransmitters are released and accumulate as long as the nociceptors stay activated at the peripheral level (skin and muscles, especially).
      These persistent pain signals we experience may be interpreted as an itching, burning, swelling, or tingling at one end of the spectrum or – at the other end – knife-stabbing, burning or throbbing.
      One nociceptor can signal different pain signals and sensations depending on its level of irritation – the more irritated it is, the more severe the pain.
      These changes can become permanent and cause the nerves to become sensitized to the point where they are easily activated to send pain, even in the absence of any noxious stimulus.
      In other words, persistent pain signals can spontaneously arise from peripheral nerve endings and bombard the rest of the pain pathway.
      So, instead of waiting for outside stimulation such as trauma, pressure, temperature or touch to signal the nociceptors, these nociceptors send pain signals on their own, without any outside help.
      This “spontaneous” pain is what we complain about the most !
      Nerves
      The nerves, especially the sensory nerves and the autonomic nerves, “wonder what is happening” because they are getting bombarded by all of these signals from the nociceptors.
      At first, they try to diminish these painful signals by using accommodation and gate mechanisms.
      However, the signals persist and they, too, undergo a sensitization process.
      They become hypersensitized and react with an exaggerated response instead of a normal or diminishing response (accommodation).
      Now we get even more pain, numbness, swelling, burning and other sensations.
      Some of the hypersensitization may be mediated by nerve growth factor, which has been found in higher levels in Fibromyalgia.
      A high nerve growth factor may indicate the nerves are trying to regenerate or repair themselves.
      But instead of repairing the nerves so they act normal again, the opposite seems to happen.
      Nerve growth factor is probably enhancing the nerves’ abilities to transmit pain to the spinal cord.
      More pain results, not less.
      Spinal cord - Amplification, wind-up, allodynia, Substance P, generalization
      At the spinal cord level, the Fibromyalgia begins to take control.
      It is here that additional changes occur to perpetuate the pain and spread it to different levels.
      When pain generators first start firing, the spinal cord pain processing centers may act at first like a dry sponge and easily soak up all the signals.
      Our bodies may have many pain generators at any given time, but if they are slowly and intermittently firing, drug sponges can soak up the signals and not cause any bothersome symptoms.


    Go to Part VI


    18-11-2009 om 02:17 geschreven door Jules

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    Infection as one possible cause of fibromyalgia

    Part VI

    From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain.
    In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more.
    The additional oncoming continuous signals will spill over the wet sponge and this leads to persistent pain.
    The two main changes that occur at the spinal cord include :
    - pain amplification (by specialized nerves called NMDA receptors) and
    - loss of pain filtering (by the diffuse noxious inhibitory control system).
    Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain.
    This phenomenon is called “wind-up” and is the neurological mechanism for the amplification of pain.
    Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified and be sent to the brain as pain.
    The spinal cord becomes more sensitized to sending pain, lots of it.
    Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals.
    As a result, different sensory signals such as touch, pressure, temperature and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature or joint motion signals.
    This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia.
    Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain !
    We can still appreciate touch, pressure, temperature, joint movement and other non-pain signals, but pain contaminates these signals and we feel the pain.
    Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters.
    Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain.
    When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal.
    As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “generalization” of the Fibromyalgia.
    This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain.
    A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured.
    Over time, the pain begins to involve the mid-back, low back and ultimately the whole body, even though these areas were never injured.
    The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body.
    Brain
    Our poor brains have no chance, do they ?
    Any pain memory stored in the past will be re-awakened by this process.
    Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops.
    This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive.
    Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated.
    The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord.
    Changes occur :
    - serotonin levels decrease,
    - brain waves change,
    - sleep stages are affected,
    - blood flow and glucose [blood sugar] metabolism are affected.
    The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain.
    Fibrofog occurs.
    Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness and helplessness, which can further amplify the pain.
    In patients with Fibromyalgia, functional reorganization (brain plasticity) in both sensory and motor portions of the brain has been observed and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003).
    These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses.
    The brain makes these changes to enhance its ability to perceive pain – brain amplified pain.
    This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs.
    This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain.
    Fibromyalgia pain summary
    To summarize, Fibromyalgia changes our pain pathways.
    It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain.
    The main problem, in a nutshell, is amplified pain.
    The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain.
    What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia.
    Our pain signal of a “1” gets amplified and magnified and by the time it reaches our brain, it is a “10” !
    Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals.
    Even tiny subconscious pain signals can get amplified or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain.
    These are not your everyday aches and pains, these are severe pains that cannot be ignored.
    This severe, chronic pain can completely disrupt one’s life.
    And by the way, while all of this is happening, we continue to look completely normal on the outside.
    Cfr. :
    -
    http://www.prohealth.com//library/showArticle.cfm?libid=13702
    - http://www.prohealth.com/library/showarticle.cfm?id=8892&t=CFIDS_FM
    -
    http://www.prohealth.com/library/print.cfm?libid=13702

    1. Fibromyalgia among central sensitivity syndromes
      Adrienne Dellwo, About.com Guide to Fibromyalgia & CFS, Wednesday June 27, 2007
      Fibromyalgia syndrome (cfr. :
      http://arthritis.about.com/od/fibromyalgia/Fibromyalgia_Syndrome_Cause_Diagnosis_Sympto
      ms_Treatment.htm
      -) is a chronic condition characterized by widespread pain, sleep problems, fatigue and depression, among other symptoms.
      Tender points (cfr. :
      http://arthritis.about.com/od/fibromyalgia/g/tenderpoints.htm -) have been used to diagnose the condition.
      Muhammad B. Yunus, M.D. and colleagues published the first controlled study of the clinical characteristics of fibromyalgia 25 years ago in Seminars in Arthritis and Rheumatism.
      That article is credited for leading to formal recognition of fibromyalgia by the medical community.
      In the June 2007 issue of Seminars in Arthritis and Rheumatism (cfr. :
      http://www.semarthritisrheumatism.com -), Dr. Yunus again is being credited for contributing to the understanding of chronic pain and fatigue syndromes.
      Dr. Yunus, through a review of 225 publications and his own experience studying fibromyalgia and related diseases, describes 13 separate conditions that are related to "central sensitization".
      The 13 conditions related to central sensitization, which occurs when the central nervous system (brain and spinal cord) becomes hypersensitive to stimuli which normally would not cause pain, include :
      - Chronic fatigue syndrome – cfr. :
      http://chronicfatigue.about.com/od/treatingfmscfs/a/treating_CFS.htm
      - Depression – cfr. : http://depression.about.com/
      - Fibromyalgia syndrome – cfr. : http://arthritis.about.com/od/fibromyalgia/Fibromyalgia_Syndrome_Cause_Diagnosis_Sympto
      ms_Treatment.htm
      -&- http://chronicfatigue.about.com/od/whatisfibromyalgia/a/fibrofactsheet.htm -&- http://arthritis.about.com/od/fibromyalgia/l/blfibroquiz.htm -&- http://arthritis.about.com/library/quiz/blfibroknowledge.htm -&- http://arthritis.about.com/od/fibromyalgia/a/fibro_facts.htm
      - Interstitial cystitis – cfr. : http://adam.about.com/encyclopedia/infectiousdiseases/Interstitial-cystitis-IC.htm
      - Irritable bowel syndrome – cfr. : http://ibdcrohns.about.com/od/irritablebowelsyndrome/Irritable_Bowel_Syndrome.htm
      - Migraines – cfr. : http://headaches.about.com/
      - Multiple chemical sensitivity – cfr. : http://allergies.about.com/b/2007/03/17/multiple-chemical-sensitivity-syndrome.htm
      - Myofascial pain syndrome / Regional soft-tissue pain syndrome – cfr. : http://emedicine.medscape.com/article/334141-overview
      - Post-traumatic stress disorder – cfr. : http://panicdisorder.about.com/od/?once=true&
      - Primary dysmenorrhea – cfr. : http://adam.about.com/reports/Menstrual-disorders.htm
      - Restless legs syndrome – cfr. : http://arthritis.about.com/od/rls/Restless_Legs_Syndrome_Causes_Diagnosis_Symptoms_Tre
      atment.htm

      - Temporomandibular disorders – cfr. : http://arthritis.about.com/od/tmj/ss/guidetotmdtmj.htm
      - Tension-type headaches – cfr. : http://headaches.about.com/
      Dr. Yunus concludes that central sensitivity syndromes involve a "biopsychosocial" model of disease.
      Read the full article "Fibromyalgia and Overlapping Disorders - The Unifying Concept of Central Sensitivity Syndromes" from Dr. Yunus at :
      http://www.semarthritisrheumatism.com -(you'll find an abstract at : http://www.prohealth.com/library/showarticle.cfm?libid=12658 -).
      Cfr. :
      http://chronicfatigue.about.com/b/2007/06/27/fibromyalgia-among-central-sensitivity-syndromes.htm

    2. Fibromyalgia and its relation to chronic fatigue syndrome, viral illness and immune abnormalities
      Goldenberg DL, Newton-Wellesley Hospital, Department of Medicine, Tufts University School of Medicine, MA 02162 - J Rheumatol Suppl. 1989 Nov;19:91-3 - PMID: 2607516
      Fibromyalgia and chronic fatigue syndrome have similar clinical and demographic features.
      We found that most patients with chronic fatigue syndrome have a tender point examination similar to patients with fibromyalgia.
      Similar pathophysiologic mechanisms are also being explored in each syndrome, including a potential role for viral induced immune dysfunction.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/2607516

    3. Fibromyalgia and other chronic fatigue syndromes - Is there evidence for chronic viral disease ?
      Goldenberg DL, Department of Medicine, Boston University School of Medicine, MA 02118 - Semin Arthritis Rheum. 1988 Nov;18(2):111-20 - PMID: 3064302
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/3064302

    4. Fibromyalgia and overlapping disorders - The unifying concept of central sensitivity syndromes
      Yunus MB, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, One Illini Drive, Peoria, IL 61605, USA - Semin Arthritis Rheum. 2007 Jun;36(6):339-56. Epub 2007 Mar 13 - 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.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17350675

    5. Fibromyalgia and parvovirus infections
      Lawrence J. Leventhal, MD *, Stanley J. Naides, MD, Bruce Freundlich, MD, From the Section of Rheumatology, Department of Medicine, University of Pennsylvania School of Medicine and the Presbyterian Medical Center, Philadelphia, Pennsylvania and the Division of Rheumatology, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City - * Correspondence to : Lawrence J. Leventhal, Address reprint requests to Lawrence J. Leventhal, MD, 570 Maloney Building, Hospital of the University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA 19104
      An infectious cause of fibromyalgia (FM) has been hypothesized based upon the observed similarity of this entity and chronic fatigue syndrome.
      Three patients developed symptoms of FM after documented episodes of acute parvovirus B19 infections.
      B19 antibody determinations were obtained approximately 1 month after the symptoms began; both IgM and IgG titers were positive at that time.
      All 3 patients met criteria for FM. Polysomnography performed on 2 of the patients revealed profound alpha-wave intrusion throughout non-rapid eye movement sleep.
      A more careful search for viral infections in FM patients whose symptoms appear following a flu-like illness appears warranted.
      Cfr. :
      http://www3.interscience.wiley.com/journal/112208394/abstract

    6. Fibromyalgia and related central sensitivity syndromes - Twenty-five years of progress
      John B. Winfield, MD, University of North Carolina School of Medicine - Seminars in Arthritis and Rheumatism, Volume 36, Issue 6, Pages 335-338
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17303220

    7. Fibromyalgia and the therapeutic domain - A philosophical study on the origins of fibromyalgia in a specific social setting
      I. Hazemeijer and J. J. Rasker1, Department of Military Forensic and Social Psychiatry, PO Box 3003, 3800 DA Amersfoort and 1 Department of Rheumatology, Hospital Medisch Spectrum Twente and Department of Communication Studies, Faculty of Philosophy and Social Sciences, University of Twente, Enschede, The Netherlands - Rheumatology 2003; 42: 507-515 - © 2003 British Society for Rheumatology
      Objectives - Fibromyalgia has always attracted controversy. Wolfe states that fibromyalgia will always exist regardless of the name given to the syndrome. Hadler describes fibromyalgia as a form of illness behaviour escalated by labelling. However, we believe that fibromyalgia, as other functional somatic syndromes, is not waiting below the surface until it becomes manifest by labelling.
      Methods - We developed our hypothesis on the relationship between a specific social setting (called the therapeutic domain) and fibromyalgia using empirical philosophical arguments based on Foucault and Hacking.
      A therapeutic domain is a real and heterogeneous medical domain in which people, their thoughts and practices and medical technology in any form coexist and communicate.
      In this domain blood is aspirated, radiographs are taken and classification criteria are made and applied.
      It is a domain where patient and therapist have initiated a relationship, which is influenced by the media and political pressure.
      This results in a looping effect where classification criteria and images give structure to perceptions and form the description for human behaviour; the person thus diagnosed (!) constantly has to grow into the conformity of these classification criteria, which also have to be constantly revised.
      The fibromyalgia concept becomes manifest in an individual as non-specific aches and pains along with other features.
      Results - In other times and settings this resulted in analogue syndromes like railway spine, telegraph wrists, neurocirculatory asthenia or perhaps repetitive strain injury.
      In the application of American College of Rheumatology fibromyalgia classification criteria, labels and medical technology it is possible that invisible experiences manifest themselves in a therapeutic domain.
      It is not only a phenotype induced by the physician, but in this domain a certain power creates reality making the ‘disease’ become manifest.
      Conclusion - The only certainty in fibromyalgia is that it is still being diagnosed.
      For prevention and treatment of fibromyalgia, doctors as well as politicians and media have to start by fundamentally changing the therapeutic domain.
      In such a renewed setting, fibromyalgia cannot become manifest in an individual and thus fibromyalgia syndrome can no longer exist.
      A firm public message that symptoms can be psychological in origin to prevent their spread, as Wessely recently stated in the comparable case of mass psychogenic illness, is only a part of the answer.
      Cfr. :
      http://rheumatology.oxfordjournals.org/cgi/content/full/42/4/507

    8. Fibromyalgia as a complication of injuries
      Dr. Mark J. Pellegrino, MD, October 7, 2009 - © ProHelath
      --- Dr. Pellegrino is a specialist in Physical Medicine & Rehabilitation who sees many people with chronic pain including Fibromyalgia. This information is excerpted with permission from Dr. Pellegrino’s book 'Fibromyalgia - Up close & personal' which includes chapters on trauma, the whiplash injury and specific types of whiplash, the evaluation and treatment of injuries and the legal aspects of post-traumatic fibromyalgia ---
      The pain started after the car accident, and it has never gone away. Before the accident I was perfectly healthy, and now I hurt all over and nothing has helped”.
      This is a typical story I hear from patients who have chronic pain after a whiplash injury.
      Some of the treatments may have helped reduce the pain, but it didn’t disappear.
      Many times, the pain is localized at first to the neck, shoulders and upper back areas, but over time, other areas of the body begin to hurt just as bad.
      Eventually, the person may say the classic four-word sentence that practically epitomizes Fibromyalgia : “I hurt all over”.
      Fibromyalgia caused by trauma is called post-traumatic Fibromyalgia (PTF)
      Trauma to the body causes tissue damage.
      Whereas healing is the expected outcome for trauma, it doesn’t always happen and PTF can develop.
      PTF does not occur immediately after an injury; it takes time to evolve and fully develop the characteristic tender points in distinct locations.
      Just as trauma other than motor vehicle accidents can cause whiplash-type injuries, trauma other than whiplash-related ones can lead to PTF.
      Lifting injuries, falls, work injuries, sports injuries and repetitive-type injuries are examples of other kinds of non-whiplash trauma.
      The medical literature has numerous examples of persistent pain following trauma.
      Since fibromyalgia criteria were established by the American College of Rheumatology study published in 1990, various articles have appeared in the medical literature about PTF.
      • Dr. T.J. Romano wrote in 1990 about patients with PTF who continued to require treatment for their condition years after settlement of litigation (cfr. “Clinical experiences with post-traumatic Fibromyalgia syndrome” - Romano TJ, Department of Medicine, West Virginia University School of Medicine - W V Med J 1990;86(5):198-202 at :
      http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19921926 -).
      - In 1992 Dr. S. Greenfield published a paper describing reactive Fibromyalgia syndrome in patients who report trauma as a precipitating event (cfr. “Reactive Fibromyalgia Syndrome” zt :
      http://www.ncbi.nlm.nih.gov/pubmed/1599521 -).
      - Dr. G.W. Waylonis published a paper entitled “Post-traumatic Fibromyalgia, a long term follow-up” (cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/7993614 -) in 1994 that described a follow-up of 176 patients with PTF.
      - Dr. F. Wolfe wrote a paper “Post-traumatic Fibromyalgia - A case report narrated by the patient” in 1994 (cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/7727557 -).
      - Dr. D. Buskila’s 1997 study showed a higher rate (about 22%) of fibromyalgia following trauma to the cervical spine (neck) (cfr. “Increased rates of fibromyalgia following cervical spine injury - A controlled study of 161 cases of traumatic injury” at :
      http://www.ncbi.nlm.nih.gov/pubmed/9082932 -).
      A study by Dr. H.R. Walen (cfr. “Traumatic events, health outcomes and health care use in patients with fibromyalgia” - Journal of Musculoskeletal Pain, 2001 at :
      http://www.informaworld.com/smpp/content~db=all?content=10.1300/J094v09n02_03 -) showed a remarkably high prevalence of over 90% of patients reporting at least one traumatic event prior to the onset of fibromyalgia symptoms.
      More and more researchers seem to be reporting on the importance of physical trauma as a factor in the development of fibromyalgia.
      Among doctors in private practice, many (including me) have reported over half of fibromyalgia patients attribute the onset of their symptoms to a traumatic event.
      In my own private practice, about 65% of patients report a traumatic injury as the cause of their fibromyalgia...
      Diagnosing PTF
      Trauma-related fibromyalgia, or PTF, is a specific medical condition that exists regardless of individual physician’s beliefs or opinions.
      This diagnosis is never assumed before a patient is seen or from the patient’s history alone.
      In order for a physician to diagnose PTF, information from the overall clinical evaluation needs to be analyzed.
      This evaluation includes the patient’s history and physical exam, supplemented by any diagnostic testing and review of any previous medical records.
      The final diagnosis of PTF is made if the total clinical picture “fits”.
      PTF can be diagnosed if these features are present :
      1/ No previous pain complaints before the trauma similar to those experienced since the trauma. That is, the person didn’t already have a pre-existing fibromyalgia diagnosis or fibromyalgia-like symptoms before the trauma.
      2/ History of a trauma that led to the pain.
      3/ Pain resulting from the trauma that has persisted ever since the trauma. I call this the “unbroken chain of pain”.
      4/ Widespread pain persisting for at least 6 months after the injury, well beyond the usual soft tissue healing time.
      5/ The presence of characteristic painful tender points as defined by the American College of Rheumatology criteria; i.e., at least 11 of 18 positive tender points. If consistent reproducible tender points are present only in an injured region and not widespread, a subset of fibromyalgia – post-traumatic regional fibromyalgia – may be considered.
      A person can be diagnosed with PTF after one evaluation with an experienced physician.
      The physician does not have to order specific tests first, or reevaluate the patient over time, to conclude PTF is present.
      The tender points are the key findings on exam, but muscle spasms and trigger points may be helpful to the physician to clarify the diagnosis.
      The physician’s exam will provide clues if something other than fibromyalgia (e.g., inflammation or neurological disorder) or in addition to fibromyalgia is present.
      Conditions in addition to PTF are often present
      They can include, but are not limited to, post-concussive syndrome, disc disease, facet dysfunction and reflex sympathetic dystrophy.
      After the initial diagnosis of PTF, the patient may visit the physician for subsequent evaluations to review the condition and effects of any treatment.
      Re-demonstrating the initial tender points upon follow-up examination is a reliable and supportive physical finding of PTF.
      The exam abnormalities are expected to persist over time in PTF and the physician can confirm this expectation upon re-evaluation at a later date.
      The ability to diagnose PTF is not dependent upon the person being seen immediately after the trauma.
      PTF takes time to develop, and once it does, it leaves telltale puzzle clues.
      If the pieces of the puzzle fit and form the “big picture”, a diagnosis of PTF can be made...
      Mechanisms of PTF
      There is a difference between cause and mechanism.
      The cause is WHY something developed.
      Trauma is the cause of PTF.
      The mechanism is HOW something developed or the pathological events that led to the problem.
      If you fall on the ground and break your hip, trauma is the cause of the broken hip (WHY you have a hip fracture).
      The pathological mechanism of injury (the HOW) is that high amounts of compressive forces (momentum) impacted the hip and resulted in a fracture.
      Many times it is difficult to determine if an abnormal research finding is part of the cause or the mechanism of fibromyalgia.
      Changes occur after fibromyalgia has developed, so an abnormality can be one of the consequences of fibromyalgia.
      It’s like asking the famous question : “What came first, the chicken or the egg ?”.
      Onjury pain mechanisms
      Damage to body tissues from an injury can occur from muscle strains, ligament sprains, disc tear or herniation, joint impaction, direct nerve trauma, swelling and inflammation.
      A combination of injuries activates the normal pain cascades from multiple locations, bombarding the spinal cord and brain with pain signals.
      Dr. Rajesh Munglani recently published a good review article on the neurobiologic mechanisms that can occur with whiplash injuries (cfr. “Neurobiological mechanisms underlying chronic whiplash associated pain” - Journal of Musculoskeletal Pain, 2000 at :
      http://www.spirehealthcare.com/Cambridge/Our-Facilities-Treatments-and-Consultants/Our-Consultants/Dr-Rajesh-Munglani/ -).
      His descriptions help explain how some people develop chronic pain and others do not.
      The road to PTF travels first through acute pain and then chronic pain.
      As noted, PTF does not happen immediately after the accident.
      It takes time to fully evolve.
      Presently, we have no way to determine which injured people will get PTF and which ones will heal and not develop chronic pain.
      Complete healing without residual pain is attempted in all with injuries and expected in most.
      If chronic pain persists several months after an injury, complete healing is not likely to occur and the risk for getting PTF increases.
      Let’s review the neurobiological mechanisms that lead to fibromyalgia after an injury.
      • Nerve injuries, tissue inflammation, soft tissue damage and scarring activate the nociceptors (specialized nerve endings where pain originates) and signal pain. Localized injuries to the muscle components (spindles, intrafusal fibers, calcium pumps) can create biochemical, hormonal and red blood cell changes that interfere with cells’ ability to receive oxygen, glucose and other nutrients.
      • Blood flow, energy formation and bioelectrical harmony are all disrupted. In those who ultimately develop PTF, the nociceptors probably remain “faulty” and continue to signal pain. Like faulty electrical short-circuits, the nociceptors continue to release pain-producing neurotransmitters.
      • Hypersensitization of the nociceptors also occurs, so they respond more dramatically to any stimulation (called allodynia). The nerves cannot “turn off” these continuous painful signals and undergo profound functional changes. Pain arises spontaneously from the nerves, causing the person to hurt “for no obvious reason”. Instead of waiting to be signaled from outside sources such as trauma, pressure, touch or temperature changes, the nerves signal spontaneous pain without any outside help.
      • Furthermore, permanent nerve changes cause outside sensory signals to be misinterpreted as pain. Instead of feeling ordinary touch, movement or pressure, one feels painful touch, throbbing movement and stabbing pressure. This exaggerated painful interpretation of ordinarily non-painful sensations is known as allodynia.
      --- For a detailed plain-language explanation of the mechanisms by which trauma and tissue injury may trigger persistent activation step-by-step throughout the pain pathway from nociceptors to brain cfr. Dr. Pellegrino’s article “Fibromyalgia – Ultimately a Disease of Amplified Pain” at : http://www.prohealth.com/library/showarticle.cfm?id=8892&t=CFIDS_FM ---
      Persistent triggers
      Ongoing peripheral input that feeds into the centrally sensitized “fibromyalgia pain cascade” comes from different injured tissues.
      These areas are known as “triggers” or “pain generators” and can occur wherever there is residual damager or instability from injury.
      A number of pain generators exist and include :
      1/ Muscle triggers
      Ongoing muscle spasms and restrictive muscle scars are examples of persistent triggers that can exist in muscles.
      Muscle bundles may go into protective spasms whenever there is inflammation or potential irritation in the region.
      For example, someone with a low back disc herniation may have spasms in the low back muscles as an involuntary attempt to protect or guard from movements of the back.
      Any back movement could cause further damage or inflammation from the already damaged disc.
      In PTF, muscles have a double whammy effect on the pain-generating cascade.
      The injury itself caused muscle damage and persistent localized spasms, causing ongoing pain signals.
      But the muscles may be forced to work harder because tother tissues (e.g., discs, facets, ligaments) were permanently damaged and cannot do their jobs of stabilizing the spine.
      Hence, the muscles tighten and spasm up to assist in the stabilization and more persistent pain signals are sent… the double whammy effect.
      2/ Facet joint dysfunctions
      Australian researcher Nikolai Bogduk and his colleagues have demonstrated how the cervical facet joints (joints in the vertebra of the neck) especially are a major trigger of chronic pain ( cfr. “Chronic whiplash and whiplash-associated disorders: an evidence-based approach” at :
      http://lib.bioinfo.pl/pmid:17916783 -).
      The facet joints may be unstable because the capsular ligaments were damaged or overstretched from the whiplash.
      Loose ligaments cannot hold the joints together as tightly as needed to stabilize them and any “extra” movement in the facet joints triggers pain.
      The facet joints may be too restricted or tight, leading to instability.
      Muscle spasms can tighten or restrict the facet joints, causing pain from immobility.
      3/ Intervertebral discs
      These areas can become chronic pain generators if the whiplash trauma caused tears or defects in the disc’s annular ligament.
      Dr. Bogduk’s work noted up to 50% of chronic whiplash patients have problems with these discs.
      4/ Nerve injuries
      Direct injuries to nerves can result in chronic pain generation, as opposed to indirectly signaling chronic pain through normal uninjured nerves.
      Nerve roots, brachial plexus and sympathetic nerves can all be bruised, stretched or damaged from the whiplash trauma and never heal properly, causing chronic pain signals.
      All of the above sources can feed into the sensitized central nervous system (spinal cord and brain) and maintain, aggravate, and permanently worsen the PTF’s chronic pain state.
      Treatment of post-traumatic fibromyalgia (PTF)
      Just as in nontraumatic fibromyalgia, no one single treatment eliminates the symptoms of PTF.
      Currently there is no cure for this disorder.
      However, various treatments can help those with PTF even if the condition is not cured.
      Each person’s treatment program needs to be individualized and what works for some may not work for others.
      Hopefully each patient will find some treatment that helps to deal with the chronic pain.
      --- Other chapters on medications, therapeutic injections and physical medicine treatments review in detail the various treatments for fibromyalgia. The treatments for PTF are really the same, since fibromyalgia is fibromyalgia regardless of the cause ! ---
      Treatment goals
      Overall, six main treatment goals can be identified for each person with PTF :
      1/ Decrease pain
      The ideal goal is to eliminate pain altogether, but this rarely happens because PTF has no known cure at this time.
      Many treatments can reduce the pain, however, even if it is still present.
      Sometimes a remission occurs where the pain is hardly noticed although painful tender points are still palpable on exam.
      2/ Improve function
      The ability to perform everyday activities such as dressing oneself, driving, moving about and eating is the basis for “quality of life” issues.
      If pain interferes with basic daily activities, the patient with PTF usually reports a poorer quality of life.
      Pain can interfere with work abilities, especially if the job requires a lot of reaching, bending or lifting.
      Optimizing job functions is an important treatment goal.
      3/ Promote healing of any residual injuries
      If residual damage to tissues is still present and contributing to pain, instability, ongoing irritation or inflammation, then treatments to promote healing of this damage should help.
      4/ Prevent worsening or complications
      If residual damage to tissues is present and cannot be healed, then the goal becomes avoiding further damage or complications.
      5/ Decrease the risk of re-injury or flare-up
      If PTF is chronic and permanent, than a goal is to keep it at a stable baseline or a level where the pain can be successfully managed.
      A stable baseline free from annoying flare-ups may sound boring, but is exactly what is hoped for.
      6/ Find a successful home program to control symptoms
      This goal is the ultimate prize. One hopes the therapy program works and learns to do the program on his/her own to maintain a stable baseline.
      In PTF, various types of treatments are prescribed in order to achieve as many individual treatment goals as possible.
      Some treatments may work better than others, and usually the combination of all the different treatments can lead to overall improvement.
      Cfr. :
      http://www.prohealth.com//library/showArticle.cfm?libid=14010

    9. Fibromyalgia in human immunodeficiency virus infection
      Buskila D, Gladman DD, Langevitz P, Urowitz S, Smythe HA, University of Toronto Rheumatic Disease Unit, Wellesley Hospital, ON, Canada - J Rheumatol. 1990 Sep;17(9):1202-6 - PMID: 2290162
      Tenderness was assessed by point count and by scored palpation in 51 patients with human immunodeficiency virus (HIV) infection as well as 51 patients with rheumatoid arthritis (RA) and 50 patients with psoriatic arthritis (PsA).
      Fifteen of 51 (29%) patients with HIV infection met criteria for fibromyalgia, based on the presence of 10 tender (of 14) "fibrositic" points.
      Similar results were observed among patients with PsA (24%).
      The prevalence of fibromyalgia was higher among patients with RA (57%).
      Patients with HIV and PsA were less tender than patients with RA. Fibromyalgia in patients with HIV was significantly associated with myalgia and arthralgia, but not with age, duration of HIV infection, stage of HIV disease or zidovudine therapy.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/2290162

    10. Fibromyalgia-associated hepatitis C virus infection
      Rivera J, de Diego A, Trinchet M, García Monforte A, Rheumatology Unit, Hospital General Universitario Gregorio Marañón, Madrid, Spain - Br J Rheumatol. 1997 Sep;36(9):981-5 - PMID: 9376995
      The objective was to determine whether there might be an association between hepatitis C virus (HCV) chronic infection and fibromyalgia (FM).
      We determined the prevalence of HCV infection in 112 FM patients, in comparison with matched rheumatoid arthritis (RA) patients from the out-patient clinic of a teaching tertiary care general hospital.
      Furthermore, we looked for evidence of FM in 58 patients diagnosed with chronic hepatitis due to HCV, compared with matched surgery clinic patients, HCV antibodies were determined by enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA).
      Serum RNA of HCV (HCV-RNA) was determined by polymerase chain reaction.
      In the group of FM patients, HCV antibodies were found by ELISA in 17 (15.2%) patients and in six (5.3%) of the RA controls (P < 0.05).
      RIBA was positive in 16 and indeterminate in one of the FM patients.
      Serum HCV-RNA was found in 13 of these FM patients.
      In eight (47%) FM patients, alanine aminotransferase (ALT) was normal, although HCV-RNA was detected in four (50%) of them.
      In the group of patients with chronic hepatitis due to HCV, all patients had HCV antibodies and the presence of HCV-RNA in serum.
      Within these patients, 31 (53%) had diffuse musculoskeletal pain, while six (10%) fulfilled FM diagnostic criteria.
      In the control group, 13/58 (22%) had diffuse musculoskeletal pain (P < 0.001), whereas only one female patient (1.7%) fulfilled FM criteria (P < 0.05).
      Serum ALT was 51.7 +/- 38.4 in FM patients, whereas it was 122 +/- 76.3 in patients with HCV chronic hepatitis but without FM (P < 0.001).
      There were no statistical differences in autoimmune markers between patients with and without FM.
      These data suggest that there exists an association between FM and active HCV infection in some of our patients.
      FM is not associated with liver damage or autoimmune markers in these patients.
      HCV infection should be considered in FM patients even though ALT elevations were absent.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9376995

    11. Fibromyalgia, chronic fatigue syndrome and myofascial pain syndrome
      Goldenberg DL, Newton-Wellesley and Tufts University School of Medicine, Massachusetts, USA - Curr Opin Rheumatol. 1995 Mar; 7(2):127-35 - PMID: 7766493

      Two important studies in which nuclear magnetic resonance spectroscopy was used convincingly demonstrated that muscle is not the primary pathologic factor in fibromyalgia.
      There were further studies reporting that fibromyalgia-chronic fatigue syndrome may follow well treated Lyme disease or mimic Lyme disease.
      The longest therapeutic trial to date in fibromyalgia demonstrated an initial modest effect of tricyclic medications, but at 6 months that efficacy was no longer evident.
      Investigation in both fibromyalgia and chronic fatigue syndrome now focuses on the central nervous system.
      The use of new technology, eg, neurohormonal assays and imaging such as single-photon emission computed tomography scan, may be important in understanding these elusive conditions.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/7766493?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleI
      temSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmed

    12. Fibromyalgia, infection and vaccination - Two more parts in the etiological puzzle
      Jacob N. Ablina, Yehuda Shoenfeldb and Dan Buskilac - aDepartment of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, 6 Weizman St., 64239 Tel-Aviv, Israel - bDepartment of Medicine ‘B’ and Center for Autoimmune Diseases, Sheba Medical Center Tel-Hashomer and Sackler Faculty of Medicine, Tel-Aviv University, Israel - cRheumatic Disease Unit, Department of Medicine, Soroka Medical Center, Beer Sheba, Israel
      As the pathogenesis of fibromyalgia continues to raise debate, multiple putative triggers have been implicated.
      The current review summarizes the available data linking fibromyalgia to either infection or vaccination.
      Multiple infectious agents have been associated with the development of either full-blown fibromyalgia (e.g. hepatits C) or with symptom complexes extensively overlapping with that syndrome (e.g. chronic Lyme disease).
      The cases of Lyme disease, mycoplasma, hepatits C and HIV are detailed.
      Despite the described associations, no evidence is available demonstrating the utility of antibiotic or anti-viral treatment in the management of fibromyalgia.
      Possible mechanistic links between fibromyalgia and HIV are reviewed.
      Associations have been described between various vaccinations and symptom complexes including fibromyalgia and chronic fatigue syndrome.
      The case of Gulf War syndrome, a functional multisystem entity sharing many clinical characteristics with fibromyalgia is discussed, with emphasis on the possibility of association with administration of multiple vaccinations during deployment in the Persian Gulf and the interaction with stress and trauma.
      Based on this example a model is proposed, wherein vaccinations function as co-triggers for the development of functional disorders including fibromyalgia, in conjunction with additional contributing factors.
      Cfr. :
      http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHC-4M7CDJ5-1&_user=10&_coverDate=11%2F30%2F2006&_alid=1081388956&_rdoc=3&_fmt=high&_orig=search&_cdi=6847&_docancho
      r=&view=c&_ct=134&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md
      5=7cd5ea72fb8f7bab0830aa8998b5326d

    13. Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients
      DV Ablashi, HB Eastman et al. Journal of Clinical Virology 2000:16:179 -191
      Cfr. :
      http://www.prohealth.com/me-cfs/library/showarticle.cfm?id=1439&t=CFIDS_FM

    14. Gulf War Illnesses - Causes and treatments
      Nicolson GL - Armed Forces Med Dev 2001; 2:41-44
      Cfr. :
      http://74.125.77.132/search?q=cache:RpUILVKKMdcJ:www.immed.org/illness/gulfwar_illness_research.html+Gulf+War
      +Illnesses+-+Their+causes+and+treatment&cd=1&hl=nl&ct=clnk&gl=be

    15. Gulf War Illnesses - Chemical, radiological and biological exposures resulting in chronic fatiguing illnesses can be identified and treated
      Nicolson GL, Berns P, Nasralla M, Haier J, Nicolson NL, Nass M - J Chronic Fatigue Syndr 2003; 11(1):135-154
      Cfr. : http://www.informaworld.com/smpp/content~db=all~content=a903290769

    16. Gulf War Illnesses - Chemical, radiological and hiological exposures resulting in chronic l'aliQuing illnesses can be idemificd and treated
      Nicolson GL, Berns P, Nasralla M, Haicr J, Nicolson NL, Nass M - Chronic tigne Syndr. 2003; ll(l):21-36

    17. Gulf War Illnesses - Role of chemical, radiological and biological exposures
      Nicolson GL, Nasralla M, Haier J, Nicolson NL – In : 'War or Health' - H. Tapanainen, Ed., 431-446, Zed Press, Helinsiki, 2001
      Cfr. :
      http://www.immed.org/illness/gulfwar_illness_research.html


    Go to Part VII


    18-11-2009 om 02:16 geschreven door Jules

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    Tags:adenoviruses, antibiotic therapy, autoimmune responses, bacterial infection, blood infection, bronchitis. catastrophic stress, chemical exposure, Chlamydia pneumoniae, chronic fatigue syndrome, common colds, connective tissue disease, cytomegalovirus
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