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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.How far would you go to find a cure
    Klik op de afbeelding om de link te volgen










     













     

    How far would you go to find a cure

    Lourdes Salvador - The American Chronicle, March 01, 2009
    Source : The MCS America News, March 2009 Issue
    cfr. :
    http://mcs-america.org/March2009.pdf 
    © 2009 Lourdes Salvador & MCS America

    How far would you go to find a cure for your child´s chronic fatigue syndrome (CFS) ?
    Annette Whittemore went $5,000,000 far.

    Expert medical care for chronic fatigue syndrome has been virtually nonexistent.
    Often, patients are left desperate for relief and frustrated at the lack of answers.

    Whittemore, a special education teacher the wife of a Nevada developer and lawyer, Harvey Whittemore, decided to take matters into her own hands when it came to her 31-year-old daughter, Andrea, who has had CFS for 19 years.

    Chronic Fatigue Syndrome (CFS) is an illness primarily characterized by profound, debilitating fatigue which has been ongoing for at least 6 months and is not relieved by rest.
    Other symptoms include :

    • Cognitive difficulties, impaired memory and poor concentration

    • Postexertional malaise (exhaustion and increased symptoms) lasting more than 24 hours following physical or mental exercise

    • Unrefreshing sleep

    • Joint pain (without redness or swelling)

    • Persistent muscle pain

    • Headaches of a new type or severity

    • Tender cervical or axillary lymph nodes

    • Sore throat.

    The dramatic decline in activity level and stamina is often severe enough to result in substantial occupational, educational and social limitations that lead to defining CFS as a major functional impairment.
    At least one quarter of those afflicted are either unemployed or on disability.

    Whittemore hopes to provide care to CFS patients at the Center for Molecular Medicine at the Whittemore Peterson Institute, which she partially funded with $5 million.

    The $86 million Center will be located at the University of Nevada, Reno and is scheduled to open next year.
    Not only will it serve CFS patients, but it will also serve other patients with various neuroimmune and inflammatory diseases, such as myalgic encephalomyelitis, fibromyalgia, atypical multiple sclerosis, autism and other related illnesses.

    The past challenge with obtaining care for CFS was that doctors had no test to confirm whether someone has CFS.

    Now, Judy Mikovits and her colleagues at the Center have developed a diagnostic blood test which measures five cytokines and chemokines that can be used to confirm a diagnose CFS.

    Research projects also uncovered the fact that treating CFS patients with anti-viral drugs has greatly reduced symptoms.

    Patients are calling the center from around the world to inquire.
    Despite their suffering, the prior lack of a clinical test meant that many have been mistreated by the medical community and in some cases disbelieved that anything was wrong at all.

    It is extremely frustrating to be living with a chronic disease and have a doctor dismiss symptoms as "normal" or "all in your head" simply because the medical community has not yet figured out what causes the illness or found a way to confirm it.

    It´s humiliated and degrading for patients.
    Even worse, lack of early treatment frequently leads to disability financial ruin.
    But the Center hopes to change all that.

    In addition to diagnosis, the Center will offer counseling, nutritional advice, supplements and physical therapy.

    For more articles on this topic cfr. : MCS America (MCSA) at : http://mcs-america.org/index.htm -.

    Cfr. : http://www.americanchronicle.com/articles/view/92840


    08-03-2009 om 13:54 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.De biologie van CVS - Tien ontdekkingen
    Klik op de afbeelding om de link te volgen








































     

     

    De biologie van CVS

    - Tien ontdekkingen -

    ME/CVS – Stichting Nederland

    Anthony Komaroff heeft een lijst opgesteld van de belangrijkste ontdekkingen over de biologie van CVS.
    Komaroff is hoogleraar geneeskunde aan Harvard Medical School en een vooraanstaand CVS-onderzoeker.
    Hij heeft meer dan 230 onderzoeks-artikelen en hoofdstukken op zijn naam staan.

    1. Het chronische-vermoedheidssyndroom is geen vorm van depressie, en veel CVS-patiënten hebben geen diagnosticeerbare psychiatrische stoornis. Net zoals patiënten met andere chronische ziekten worden CVS-patiënten soms depressief vanwege de gevolgen van de ziekte voor hun leven. De meeste onderzoeken laten echter zien dat de meerderheid van de patiënten voorafgaand aan de uitbraak van de ziekte geen ervaring had met depressiviteit.

    2. Bij CVS is er sprake van een chronische lichte activering van het immuunsysteem. Er is bewijs van geactiveerde T-cellen, van activering van genen die de activering van het immuunsysteem weerspiegelen,  en van verhoogde niveaus van cytokinen.

    3. Er is overtuigend bewijs dat de natural killer-cellen slecht functioneren – witte bloedlichamen die belangrijk zijn in de strijd tegen virusinfecties. Onderzoekers zijn het niet eens over de vraag of er een toename is van de aantallen T-cellen bij CVS-patiënten.

    4. In de witte stof van de hersenen zijn afwijkingen gevonden bij CVS-patiënten; dat bleek uit MRI-scans. De meest typische vorm daarvan zijn kleine - een fractie van een centimeter grote - gebieden juist onder de cortex, het buitenste gebied van de beide hersenhelften. Ook zijn er verschillen waargenomen in de hoeveelheid grijze stof.

    5. Er zijn afwijkingen ontdekt in de stofwisseling van de hersenen, zoals bleek uit SPECT- en PET-scans. Ander onderzoek doet vermoeden dat er iets mis is met de energiehuishouding van CVS–patiënten en de transportketen van de oxidatieve electronen in de mitochondriën.

    6. CVS-patiënten vertonen afwijkingen in meerdere endocriene systemen binnen de hersenen, in het bijzonder een te lage activiteit van van de HPA-as, maar ook van de hypothalamus-prolactine-as en de hypothalamus-groeihormoon-as.

    7. Cognitieve gebreken komen veel voor bij CVS-patiënten. De afwijkingen die het vaakst gerapporteerd worden zijn problemen met de informatieverwerking, het geheugen en aandacht.

    8. Talloze onafhankelijke onderzoekers hebben afwijkingen gevonden in het autonome zenuwstelsel. Daarbij gaat om het onvermogen van het lichaam om de bloeddruk op peil te houden nadat de persoon is opgestaan, abnormale reacties van het hartritme na het opstaan en een ongewone bloedopeenhoping in de aderen van de benen.

    9. CVS-patiënten hebben een ontregelde expressie van de genen die belangrijk zijn voor de energiehuishouding. Energie komt voort uit natuurlijke chemische stoffen die omgezet worden door enzymen binnen elke cel. Deze enzymen worden aangestuurd door specifieke genen. Ander genomisch onderzoek laat zien dat ook genen die betrokken zijn bij activiteiten van de HPA-as, het sympathische zenuwstelsel en het immuunsysteem, een afwijkende expressie hebben.

    10. Er is bewijs dat een latente actieve infectie met verschillende herpesvirussen en enterovirussen vaker voorkomt. Daarbij gaat het om het Epstein Barr-, HHV-6- en cytomegalovirus. Andere infectueuze actoren, zoals de bacterie die de ziekte van Lyme veroorzaakt, het Ross River-virus en Q-fever, kunnen ook CVS uitlokken.

    Cfr. : http://www.me-cvs-stichting.nl/1694


    Bijlagen:
    http://www.youtube.com/watch?v=O5Z441pe50Q   

    08-03-2009 om 13:27 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Ten discoveries about the biology of CFS
    Klik op de afbeelding om de link te volgen

     







    Ten discoveries about the biology of CFS

    The CFIDS Association of America
    www.cfids.org -


    The summary of CFS research findings below was provided by Anthony Komaroff, MD, a professor of medicine at Harvard Medical School, senior physician at Brigham and Women’s Hospital in Boston and the editor-in chief of Harvard Health Publications.
    Dr. Komaroff has an ongoing research program on chronic fatigue syndrome and has published over 230 research articles and book chapters.

    1. Chronic fatigue syndrome is not a form of depression and many patients with CFS have no diagnosable psychiatric disorder.
      As with most chronic illnesses, some CFS patients become depressed because of the impact of the illness on their lives, but most studies find that the majority haven’t experienced depression before the onset of illness.

    2. There’s a state of chronic, low-grade immune activation in CFS. There is evidence of activated T cells, activation of genes reflecting immune activation and increased levels of immune system chemicals called cytokines.

    3. There’s substantial evidence of poorly functioning natural killer (NK) cells—white blood cells important in fighting viral infections.
      Studies differ as to whether there may be increased numbers of NK cells in CFS patients.

    4. Abnormalities in the white matter of the brain have been found in CFS patients using magnetic resonance imaging (MRI) scans.
      Typically, these are small (fraction of an inch) areas just below the cerebral cortex, the outermost area of the brain hemispheres.
      Differences in gray matter volume are also being observed.

    5. Abnormalities in brain metabolism, as indicated by single photon emission computed tomography (SPECT) and positron emission tomography (PET), have been discovered.
      Other research suggests there’s something wrong with energy metabolism and the oxidative electron transport chain in the mitochondria of CFS patients.

    6. CFS patients experience abnormalities in multiple neuroendocrine systems in the brain, particularly depression of the hypothalamic-pituitary-adrenal (HPA) axis, but also the hypothalamic-prolactin axis and hypothamalmic-growth hormone axis.

    7. Cognitive impairment is common in CFS patients.
      The most frequently documented abnormalities are difficulty with information processing, memory and/or attention.

    8. Abnormalities of the autonomic nervous system have been found by numerous independent researchers.
      These include a failure of the body to maintain blood pressure after a person stands up, abnormal responses of the heart rate to standing and unusual pooling of blood in the veins of the legs.
      Some studies also find low levels of blood volume.

    9. CFS patients have disordered expression of genes that are important in energy metabolism.
      Energy comes from certain natural chemicals that are processed by enzymes inside each cell.
      These enzymes are controlled by specific genes.
      Other genomic research is revealing involvement of genes connected to HPA axis activity, the sympathetic nervous system and immune function.

    10. There’s evidence of more frequent latent active infection with various herpesviruses and enteroviruses.
      The herpesviruses include Epstein Barr, HHV-6 and cytomegalovirus.
      Other infectious agents, like bacterium that cause Lyme disease, Ross River virus and Q fever, can also trigger CFS.

    Cfr. : http://www.cfids.org/cfidslink/2007/062004.pdf


    Bijlagen:
    http://me.startpagina.nl/video/usa-senate-briefing/0/part-3-promising-avenues-in-current-cfs-research-dr-anthony-komaroff-2/   

    08-03-2009 om 13:17 geschreven door Jules

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    07-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The heart of the matter - CFS & cardiac issues - Part I
    Klik op de afbeelding om de link te volgen






































     



    The heart of the matter
    - CFS & cardiac issues -

    Part I


    Dr. Paul R. Cheney :
    "
    This is the best, most important publication in 20 years. - (regarding CFS) -
    This was published the year I left practice, 2003
    .../...
    What this very impressive article says is that,
    without exception,
    every disabled CFS patient is in heart failure.
    "


    Contents :

    1. CFS - Poor heart function could be to blame

    2. CFS - Poor heart function could be to blame - Een reactie

    3. The heart of the matter - CFS & cardiac issues

    4. Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome (cfr. 5 below)

    5. Cardiac Output Linked to Severe CFS Cases - Research Q&A – A discussion on “Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome” (cfr. 4 above)

    6. Cardiovascular Physiology Concepts - Vascular Network



    I. - CFS - Poor heart function could be to blame

    What Doctors Don't Tell You (WDDTY), 14-02-2008
    Source : American Journal of the Medical Sciences, November 27, 2007, February 2008
    © 2006 Copyright Conatus plc.

    Chronic fatigue syndrome (CFS) may be linked to reduced heart activity – but researchers aren’t sure if heart function causes CFS or if it’s the other way round.

    But in a new study, led by Arnold Peckerman, found a link between the two when he analysed 38 CFS patients.
    Of these, 18 had lowered cardiac function and they were also the ones who suffered the most severe symptoms, such as joint pain, headache, swollen lymph glands and sore throat.
    Although the patients’ reduced cardiac functions weren’t clinically significant, Peckerman believes that poor blood circulation may be.
    In a separate study, he found that some CFS patients are more likely to suffer heart failure.

    His study also established that 20 CFS patients didn’t have poor heart function, so why does it affect only some ?
    Peckerman believes that chronic infection can lead to left ventricular dysfunction in a subset of CFS patients, which suggests chronic fatigue symptoms in these people may be the result of poor muscle function in the heart.

    Cfr. :
    -
    http://www.wddty.com/03363800369799468194/cfs-poor-heart-function-could-be-to-blame.html
    - http://www.healthy.net/scr/news.asp?Id=9663



    II - CFS - Poor heart function could be to blame
    - Een reactie -

    Gerard Aalderink : gerard.aalderink@HOME.NL
    ME-PLATFORM Digest – 17-02-2008

    Ik denk dat het bij dit onderzoek van Peckerman nuttig is een paar achtergronden te vermelden :

    • Hij deed dit onderzoek in opdracht van de Amerikaanse overheid

    • De opdracht was om uit te zoeken of er bij mensen met ME een mogelijkheid was om de mate van beperking nauwkeuriger vast te stellen ivm het ervaren onrecht bij mensen met recht op een uitkering.
      Het was dus niet primair de bedoeling om een oorzaak of onderliggend mechanisme te zoeken.
      Alleen vaststellen wat de beperkingen zijn van een individu met ME

    • De conclusie is dus een lage Q.. Cardiac Output..
      Volgens mij te vertalen als een te laag doorstroomvolume.
      Dus er circuleert te weinig bloed door het lichaam

    • Veel symptomen lijken op hartfalen, als er sprake is van een ernstige vorm van ME.
      Echter hartfalen kan niet gediagnostiseerd worden.
      Blijft als conclusie over dat de hartspier vermoedelijk niet goed presteert (net als alle andere spieren in het lichaam)

    • Bij deze link staat een interview met Cheney, die hier verder op ingaat en uitlegt hoe belangrijk dit onderzoek is.

    Ik wou dat er in Nederland (behalve in de CFS-kliniek) artsen te vinden waren die zouden willen meedenken in de richting van dit onderzoek.

    Groeten !
    Gerard.


    III. - The heart of the matter

    - CFS & cardiac issues -

    Carol Sieverling
    © 2005 CFS/FM Support Group of DFW, 04-02-2005

    Contents

    Part 1a

    1. Preface

    2. Peckerman's article

    3. CFS compensates for idiopathic cardiomyopathy

    4. The research

    5. Find an accurate measure of disability

    6. A "Q" problem

    7. The test - Impedance cardiograph

    8. P Value - "Q" correlates with degree of disability

    9. Post-exertional fatigue indicates a "Q" problem

    Part 1b

    1. Top priority - Blood pressure

    2. Nozzles

    3. Sacrificial prioritization

    4. First compromised - Skin and compensatory hypothyroidism

    5. Next up – Muscles

    6. Third system down – Liver/Gut

    7. Fourth affected - The brain

    8. Fifth - Heart—A two-parter
      8.1 - Part A - Manifestation of microcirculatory impairment
      8.2 - Part B - "The event horizon"

    9. Sixth system - Lung & kidney

    Part 2a

    1. The good news - CFIDS prevents us from crossing the event horizon

    2. Recovery takes time

    3. Marshall Protocol & "Q"

    4. Etiology (cause)

    5. Viruses

    6. Heavy metals

    7. The Nexus – Virus, bacteria, toxins, allergies and heavy metals

    8. Pall - Nitric oxide + superoxide = peroxynitrite

    9. A little math

    10. Super oxide - Out of control

    Part 2b

    1. Protection from the death spiral
      1.1 - Klonopin / Neurontin
      1.2 - Avoid Provigil - It stimulates nitric oxide

    2. How to block peroxynitrite
      2.1 - Increase CO2
      -
      Rebreathing
      - Klonopin
      - Barometric Pressure
      2.2 - Uric acid
      -
      Sushi
      - Eggs & raw milk (cheese)
      - Isoprinosine/Imunovir
      - Soy
      - Nuts & seeds
      2.3 - Consume reduced cholesterol

    3. Three ways to block nitric oxide
      3.1 - Hemoglobin
      3.2 - Hydroxycobalalmin injections (B12)
      3.3 - Magnesium sulfate injections
      3.4 - Other Treatments

    4. Physiology - Preload and afterload
      4.1 - Preload - Lying down
      4.2 - Preload chronobiology - Daytime vs. Bedtime
      4.3 - Preload - Hydralate (Gookinaid) / HomeBrew
      4.4 - Preload - Cortisol as licorice root
      4.5 - Afterload Reduction - Magnesium


    Part 1a

    1. - Preface

    The following is my interpretation of transcripts and tapes of conversations that took place between Dr. Paul Cheney and two different patients (including myself) during September and November of 2004.
    Any treatments mentioned are highly individualized and should not be generalized to all CFS patients.
    Dr. Cheney's treatment approach is rapidly evolving as new information and insights unfold.

    Certain broad concepts central to Dr. Cheney's understanding of this illness are generally much more constant (such as decreased cardiac output, HPA axis involvement, the role of glutathione etc.).
    It's essential to note that a set "Cheney protocol" applicable to most patients does not exist, given that his treatment protocol is extremely individualized and constantly evolving.

    Quotes are from Dr. Cheney or, where noted, from a patient.
    Statements in brackets were added by me to provide clarification or context.
    All other comments are statements from Dr. Cheney that have been slightly paraphrased, but, to the best of my knowledge, maintain his original meaning.

    The focus of this article and much of Dr. Cheney's current work is based on the following publication : "Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome" (cfr. I onderaan).

    A synopsis of this article and an interview with Dr. Peckerman was published in the Fall 2003 issue of The CFS Research Review by the CFIDS Association of America : “Cardiac Output Linked to Severe CFS Cases - Research Q&A” (cfr. II onderaan).

    2. - Peckerman's article

    Dr. Cheney stated : "This is the best, most important publication in 20 years." (regarding CFS) : "This was published the year I left practice, 2003. The senior author is Benjamin Natelson and the principal author is Arnold Peckerman. What this very impressive article says is that, without exception, every disabled CFS patient is in heart failure."

    3. - CFS compensates for idiopathic cardiomyopathy

    "Let me first of all define heart failure. There are two kinds of heart failure. There's the kind that any cardiologist can diagnose in about a minute. That you do NOT have. Which is why cardiologists missed this. What you have is Compensated Idiopathic Cardiomyopathy. And your primary means of compensation — now this is the big twist — are you ready ? Have you got your seat belt on ? The primary methodology for compensation for this disorder is in fact CFS itself."
    ['idiopathic' = 'cause unknown' – 'cardiomyopathy' = 'structural or functional disease of heart muscle']

    Patient responds : "I see. So, this is the body's way of saving us from dying of cardiomyopathy."

    Dr. Cheney : “Yes. From dying of cardiomyopathy. What is ironic about this, is that I had Idiopathic Cardiomyopathy (ICM). But I never had CFIDS."

    In the medical literature, at least 35% of those with a diagnosis of ICM will die within 5 years unless they receive a transplant (that was Dr. Cheney's experience — a heart transplant).
    I've been following CFS patients for 20 years and never seen one case of CFIDS go on to transplant or ever even heard of one going on to transplant.

    Now if your diagnosis is ICM, why aren't you dead ?
    Why hasn't one patient in 20 years needed a transplant ?
    It's because you had CFIDS and I didn't.
    "I even suspect the mechanism and that has been published too."

    "The disease [CFS] itself is protecting you from a deeper problem that has been totally missed, including by me. I missed it, too. Because it's so well-hidden."

    4. - The research

    Let's take a closer look at the study, beginning with the researchers.
    This group is at the New Jersey Medical Center, a major medical school.
    Dr. Natelson, a neurologist and professor of neurology, is a very good researcher; quite a bright and accomplished scientist.
    Dr. Peckerman, the lead author, is a cardiac physiologist or cardiopulmonary physiologist.
    About five years ago, the NJ Medical Center received a multi-million dollar grant from the NIH (National Institutes of Health).
    To get the grant, Dr. Natelson wrote a proposal to find a physiological parameter that could be objectively measured and would correlate with disability.

    5. - Find an accurate measure of disability

    Their job was not to find the etiology, pathophysiology or treatment for this disorder.
    "Their job was to find a measurable number that could accurately demarcate those with [CFS] that are disabled vs. those that are not, so that we could resolve some of the disability adjudication problems [that affect so many CFS patients], where people don't believe you have a problem and it's hard for you to get objective proof that will satisfy critics as to your disability."

    As clinicians, we know that not everyone with CFIDS is disabled; yet, there are many people with CFIDS that are disabled.
    "We know these extremes exist. What we know less about is where to draw the line, because that's a harder thing to do. And the government is just nuts about this, because some circles feel that too many people are getting access to SSDI that shouldn't and on the other side there are people who feel that there are some who aren't getting it who deserve it. We need to resolve this in a compassionate and fair manner."

    "That was [Natelson's] proposal and it was funded, fully (The NJMC was named a "CFS Cooperative Research Center). And you can guess why. The government has a vested interest in knowing we're not raiding the treasury unfairly, but they don't want to be accused of knocking people off [SSDI] who later turn out to be disabled."

    6. - A "Q" problem

    So the NJ team looked at many things and they found something : a "Q" problem.
    "Q" stands for 'cardiac output in liters per minute'.
    "Q" in CFIDS patients correlated - with great precision - with the level of disability as judged by validated clinical questionnaires that asked about activities of daily living.
    What can you do (bathe, dress, cook etc.) and how hard is it (no problem, little bit of a problem, moderate problem, lot of problem) ?

    "Question after question after question. Then they have a score and those with the highest score were the most disabled and those with the lowest score were the least disabled. And then they gave the same questionnaire to normal sedentary controls."

    7. - The test - Impedance cardiograph

    "Then they measured Q, using impedance cardiography. This technology allows one to accurately measure the cardiac output using the idea that the resistance a current has, passed through your chest, is a function of the blood flow through it. It's actually inversely proportional. The greater the blood flow, the lower the impedance. The less the blood flow, the greater the impedance [resistance]. Because blood is water, water passes current better. It's a simple idea. Put an electrode on your front and your back and pass the current through. If it goes quickly through, there's a lot of blood going through the chest and if there's resistance, there's less."

    They used a thoracic algorithm, developed at the University of Minnesota some 30 years ago.
    This algorithm allows many factors to be part of determining Q, including chest and body size.
    Using it, you can compare the "Q" of big people to the "Q" of small people and still be comparing apples to apples.

    The University of Minnesota algorithm has been approved by the FDA as a valid measurement of Q.
    The point is that Medicare pays for this.
    It's been clinically validated by a government agency and is not considered experimental or research - as long as you use this algorithm.
    That's important, because whenever this test result filters back to a cardiologist, the first thing many say is, well, but, you know, that's not accurate.
    And indeed, it may not be accurate, depending on the machine and the algorithm it uses.

    "By the way, there's one other important detail. Unlike all other measures of cardiac output, this is the only one that can be done in the upright position. Which, as you'll find out in a second, was a critical step. Absolutely critical. All other cardiac output measurements are done in the supine position - laying down." (to detect the heart problem in CFS patients, it has to be done both lying down and standing up. If you can manage the whole test, it's preferred to take readings in four positions on a tilt table).

    Now, do CFIDS patients prefer to stand up or lie down ?
    Of course, they prefer to lie down.
    Do you know why ?
    "Do you know what your cardiac output does when you stand up ? It drops 30%. In all humans, without exception. So very critical to this technology is that it's the only one that could be done upright [again, four positions on the tilt table are best; standing up and laying down at a minimum]. And what they found is absolutely astonishing, truly astonishing. When [disabled CFIDS patients] stand up, [they're] on the edge of organ failure due to low cardiac output."

    The study involved 38 CFIDS patients and 27 matched sedentary controls - a reasonable sample to get convincing statistics.
    The CFIDS patients were subdivided into 18 severe cases and 20 that were less severe.
    When they looked at the test result statistics, disability correlated with Q !

    8. - P Value - "Q" correlates with degree of disability

    "And this is the relevant number. The correlation coefficient of .46 with P value of 0.0002 suggests that the disability level of those that were disabled was exactly proportional to the severity of their "Q" defect - without exception and with scientific precision by virtue of their most disabling symptom, post-exertional fatigue. WOW. WOW !"

    [Dr. Cheney circles the P value on the copy of the article with great excitement.
    A little research on Google revealed that a P value less than 0.05 means there's a 5% likelihood that the association between the factor and the outcome is due to chance.
    A P value of 0.01 means there's a 1% likelihood that the association is due to coincidence.
    A P value of 0.03 means there's a 3% likelihood that the association is due to chance.
    So, the P value of 0.0002 in this study means there are only 2 chances in 10,000 that the factor and outcome are due to coincidence !
    The factor being severity of CFS (disability) and the outcome being lower cardiac output ("Q" problem)]

    Statin drugs are given to people with high cholesterol due to only a P < 0.05 (they're given - —based on a much weaker P value).

    Dr. Cheney continued : "And I'll tell you, it's profound because no other paper that I know of has been published in 20 years that can give a number which so precisely correlates with the level of disability. There's nothing out there. Believe me—nothing exists. Not RNase L, not immune-activation levels, not SED rates. NOTHING has this sort of correlation with disability that I know of."

    9. - Post-exertional fatigue indicates a "Q" problem

    Next, the NJ team looked to see if there were any symptoms that were 100% observable in the group of disabled cases, but not in the others.
    They found that there was only one symptom (among the loooong list of CFIDS symptoms) that was seen in 100% of the patients with the Q problem.
    Only one.
    Post-exertional fatigue.
    That is, when you push yourself physically, you get worse.

    What distinguishes CFIDS from FM ?
    Post-exertional fatigue.
    Patients who have FM, but not CFIDS, can exercise - it helps them.
    FM patients do not have a Q problem.
    MCS patients do not have a Q problem (unless they also have CFIDS).
    They do have other issues that overlap with CFIDS.
    Martin Pall's conceptual framework allows us to lump these people all together (FM, MCS, GWS, CFIDS).
    However, Q is what separates them.
    CFIDS patients have a big Q problem and post-exertional fatigue is the one symptom that correlates with Q.

    Post-exertional fatigue is the number one symptom reported by people with ICM.
    Among the disabled CFS patients [the severe group], 80% had muscle pain, 75% had joint pain, 72% memory & concentration problems, 70% unrefreshing sleep, 62% generalized weakness, 60% headaches, 60% lymph node swelling, 68% fever and chills and, 50% had sore throat.
    Though some symptoms were certainly more common among the disabled patients, the symptoms varied - with the exception of post-exertional fatigue.
    They all had that.

    This suggests that it is not so much the symptoms that are disabling.
    Rather, "the symptoms are reflecting an interaction (or a nexus) between Q and how you compensate for Q. Depending on the nature of the compensation, which is individually distinct, you will get an array of symptoms that is individually determined. Just like this : ten patients with MS will not have identical symptoms. Any more than ten AIDS patients or ten cancer patients or ten of anything."
    Why ?
    Because the disease process - which they all have - will manifest differently in each person.
    The specific symptoms will arise out of factors unique to each person; those factors will determine how the disease plays out in each.

    "Within the non-disabled [CFS] group they saw pretty much the same thing—it's just that the percentages were a lot lower. For example, fever and chills were found in only 5% of the non-disabled. The highest percent was post-exertional fatigue seen in 60%. But 40% of the CFIDS patients who were not disabled did not have post-exertional fatigue, but did have CFIDS."

    "The reason for that is, of course, if you look at the original case definition, post-exertional fatigue - that is exercise worsens the syndrome, effort-related exacerbation, push-crash phenomenon - is not a major criteria, it's one of the eight minor criteria. It's possible not to have that and still meet the case definition. But all disabled patients have that and 60% of non-disabled have that." (it's possible to not even have post-exertional fatigue and still have CFS; however, all disabled CFS patients have post-exertional fatigue, as do 60% of the non-disabled).

    "More importantly, all disabled CFIDS patients, all of whom have post-exertional fatigue, have low "Q" and are in heart failure."



    Part 1b

    1. - Top priority - Blood pressure

    "Now there is one factor that I want to mention before I get into the data display. Natelson requires, as a rule, before you're allowed into his medical school for study (whether it's this particular study or any other study) that you consider coming off of all medications and all nutraceuticals or he may not see you. Furthermore, his team is not treatment oriented."

    Patient responds : "Well, I certainly wouldn't agree to do that. I'd be a wreck."

    Dr. Cheney continues : "Of course you wouldn't agree. Therefore, the data I'm about to present is not anywhere near as bad as you are."
    You are more severely affected than anyone in this study.
    I'm not sure he has patients from the truly severe end of the spectrum of CFS.
    Those patients don't participate in studies.
    Just reflect on that as I go through this.

    In this study, the normal person and the non-disabled CFIDS patient pump 7 liters a minute through their heart with very little variance : 7 liters plus or minus .5.
    When they stand up, they drop all the way down to 5 liters per minute, a full 30% drop in output.
    That's normal.

    "First of all, why does it go down when you stand up ? Because the heart can only pump as much blood as returns to it. If you drop the return by 2 liters per minute, you will always drop the output by 2 liters per minute. The blood has to go uphill against gravity, so there's an automatic 2 liter per minute drop in return and therefore an automatic 2 liter drop in output even though the heart is completely normal. Where does that extra 2 liters go ? It's pooled in your lower extremities and capacitance vessels. Rapidly, by the way." (capacitance vessels are the larger veins of the body where most of the blood volume is found and where regional blood volume is regulated; for a great explanation of the circulatory system, including the different types of veins and arteries and their respective functions, go to 'Cardiovascular Physiology Concepts - Systemic Circulation' by Richard E. Klabunde, Ph.D. (cfr. III onderaan).

    Why don't normal people sense that 30% drop in output ?
    You might assume that their blood pressure would fall 30% and they'd sense it.
    Nevertheless, their blood pressure either stays normal or goes up when they stand.
    Blood pressure is so vitally important that the body compensates to prevent blood pressure from dropping.

    Think about how significant blood pressure is.
    Physicians are allowed by law to pronounce people dead.
    That's a lot of power.
    And how do we do that ?
    Think about the movies.
    They always check for a pulse—blood pressure.
    No pulse—you're dead.
    And, of course, they check to see if you're breathing.
    However, if you don't have a pulse and aren't breathing, you'll be pronounced dead.
    Doctors don't even have to check for brain activity.

    Why does the law give doctors such power ?
    Because there's never been an exception to this rule.
    No breath, no pulse, you're dead.
    No exceptions - unless you're ice cold.
    "It points to how important blood pressure is to the body, because blood pressure is, in fact, life. And so, your body will defend your blood pressure beyond anything else. Or, to put it another way, it will sacrifice everything—even your brain—to keep the pulse going."

    2. - Nozzles

    "Now, when your Q drops 30%, your pressure will not drop, because your body will defend that pressure, even to the loss of your brain. This is critical to understanding what happens in CFIDS patients." [Let's use an analogy from gardening.] "Here's the hose attached to a spigot at the side of the house. I have the spigot turned fully counterclockwise [on] and it has maximum Q at 7 liters per minute coming out of that hose. Because it's coming out fast enough, there's enough pressure for this water to shoot out of the hose and I can water all the plants out there, all the way out to the 4th row tomato plants, 6 feet beyond this hose. So, I can sit there and water all day long providing sufficient nutrients and stuff to the plants, because I have adequate Q.

    "Now let's take the knob and crank it down so that we drop it down from 7 liters to 5. That would be a normal drop on standing up. The pressure should drop at least 30% or more, but doesn't. Why ?"
    Because, if you turn the flow down, the water can't get out to the tomato plants anymore.
    There's not enough pressure and it's just dribbling out, so what do I do ?
    I take my thumb and I press it on the end to partially block it and create backpressure.
    That builds the pressure back up sufficiently to allow that stream of water to shoot out at sufficient velocity to water the tomato plants in the 4th row—even though
    I had a 30% drop in (cardiac) output.
    Because my thumb gets tired, I put a nozzle on the end of the hose and tighten it down so I can spray all the way out there at a low Q [pressure].
    That's what a nozzle is for.

    And you have a nozzle in you.
    It's called the 'end arteriole' or 'resistance vessel'.
    It regulates the resistance against which flow occurs to keep your pressure within normal range - despite a large fluctuation in Q produced by standing up or laying down.
    Because I can maintain the pressure, I can water the plants all the way out to the tomato plants in the fourth row regardless of the Q, because the pressure is maintained.

    Now, let's crank it to down to 50%, taking it from 7 liters per minute, all the way down to 3.5 liters per minute.
    I still have the same nozzle attached but when I drop the flow to 3.5 liters, I can't reach the tomato plants, unless I really tighten down on the nozzle.
    Moreover, if I tighten it all the way down just a little tiny spray spits out.
    Maybe only a drop or two will reach all the way out to the tomato plants.
    Now I'm sacrificing water perfusion of the plants in order to maintain pressure, because without blood pressure you're dead [perfusion : the injection of fluid into a blood vessel in order to reach an organ or tissues, usually to supply nutrients and oxygen].

    When faced with a low Q, the body sacrifices tissue perfusion in order to maintain blood pressure and that's all you need to know to understand this concept.
    Microcirculation to the tissues of the body is sacrificed to maintain blood pressure so you will not die in the face of a low Q and that is what is going on in the disabled CFIDS patient.

    In Peckerman's study, the data of the disabled CFIDS patients reveals that when they are supine (laying down), their Q is 5 liters per minute.
    So laying down they can perfuse out to the extremities, but admittedly not as much volume gets out there as would occur at 7 [the Q of the controls and mild CFIDS patients when laying down], but there's enough volume that you are really not that badly affected.

    Let's look at what happens when the disabled CFS patients stand up.
    They drop to 3.7 liters per minute, a 50% drop from the normal of 7, and that means they can't water the tomato plants !
    The tomato plants start to shrivel up and experience trouble.
    Big trouble !
    At 3.7 liters per minute, they do not have adequate Q to function.
    There will be a functiovnal contraction [lowering of what you are able to do] determined by the drop in Q.
    The lower the "Q" goes from there, the more in bed you will be, because lying down is the only time you come close to sufficient Q.

    Patient asks : "So basically, the tomato plants are all the organs and tissues in the body ?"

    Dr. Cheney replies : "Yes !"
    And those "severe" patients in the study who dropped to 3.7 liters per minute would be mild or moderately ill patients in my practice.
    How do I know that ?
    I know it by virtue of their pressure changes and their heart rate changes.
    Look particularly at the MAP (mean arterial pressure) - MAP is the average of your systolic and diastolic pressure.
    If your blood pressure is 120 over 80, your MAP is 100.
    All groups in the study had virtually the same MAP when they stood.
    There is no real difference in the MAP of the controls and the patients in this paper.
    That's not true in my practice.
    My patients are virtually always lower than normal.
    Same for their heart rates.

    3. - Sacrificial prioritization

    Now here's an important, critical idea.
    The body does not sacrifice tissue perfusion equally across all organ systems.
    It prioritizes the order of sacrifice and you can see the progression of your disease in this prioritization.

    The heart pumps out blood to the artery and the artery produces blood pressure.
    It pumps down to the smallest arteriole called the resistance vessel, which we will call the nozzle.
    The nozzle then breaks out into a capillary bed that delivers a certain capillary pressure to the tissues.
    In the human body, every cell in your body is within 1 millimeter of a capillary (except in cartilage, periosteal bone and the cornea).
    Then, the blood returns to the heart via the veins, the venous return.

    "There are two organ systems that have a super nozzle in addition to the main nozzle. They have a super built-in nozzle—it's called the 'Renin Angiotension System' or 'RAS'. It's built into two organs : the lung and the kidneys. They have the greatest nozzle in the body. They can spit water out all the way to the tomato plants with practically no Q at all; they just need a little bit. They can sustain the greatest degree of Q problems, because they have this extra fancy nozzle, the Renin Angiotension System."

    Additionally, the heart and the brain also have secondary nozzles.
    Although not as powerful as the RAS, these secondary nozzles protect that tissue even in the face of extremely low Q.
    Therefore, the lung, the brain, the kidneys and the heart are a little bit more protected than the liver, gut, muscles and skin from a drop in Q.

    4. - First compromised - Skin and compensatory hypothyroidism

    Having said this, in what order are things sacrificed and what are the consequences ?
    The first is the skin.
    If you sacrifice the microcirculation of the skin, several problems can arise.
    One is that without adequate microcirculation to the skin, the body cannot thermoregulate anymore [thermoregulate : regulate body temperature].

    You cannot stand heat or cold, although heat will be more difficult at first than cold - in part because if you're too cold you just put on more clothes, but how do you rip your skin off when you get too hot ?
    If your core temperature rises high enough, you will not sleep and your body will activate your immune system.
    In order to regulate that problem, your body will kick in thyroid regulation and you will downregulate [reduce or suppress a response to a stimulus] your thyroid to keep your temperature from going too high and you will develop "compensatory hypothyroidism" !
    Now you will have trouble with cold.

    The second thing your body will not be able to do is get rid of VOCs ('Volatile Organic Compounds'), which are shed in the skin's oil ducts.
    VOCs build up in the fat stores of your body and you become progressively chemically poisoned by whatever is present in your environment and whatever you are genetically susceptible to - different things in different people.
    If that's pretty significant, we call that 'Multiple Chemical Sensitivities' (MCS).
    If all you've got is microcirculatory deficiency of the skin, we'll call that MCS and the treatment is to put you in a sauna to outgas you - to detoxify you - which is in fact the primary treatment of MCS patients.
    We'll also exercise you, which is another MCS treatment.

    5. - Next up – Muscles

    If it gets worse than that, the next thing you'll sacrifice are your muscles.
    You'll have exercise intolerance - you can't go up stairs or climb mountains as easily.
    When you move your muscles, you feel like you got hit by a ten-ton truck.
    Very minor activity on day one produces a day two on which you say, "What did I do, it's almost like I ran a marathon."

    If it gets still worse, you begin to get fibromyalgic pain.
    If it affects the joints, it may precipitate pyrophosphoric acid and uric acid crystals and you start to have arthralgias and myalgias linked to this microcirculatory defect.
    Microcirculation problems have been suggested by Fibromyalgia research in Toronto.
    Moldofsky tried to induce FM symptoms by interrupting the sleep of study participants and was successful with a significant number of the women.
    It was harder to induce clinical FM in men and almost impossible in male athletes.
    It came down to microcirculation.
    Men had a higher capillary cross-sectional area (more capillaries) than women.
    Athletes have more than non-athletes.
    Male athletes are therefore more resistant to microcirculatory problems within the muscles, whereas sedentary women are the most vulnerable.
    Microcirculatory problems will be much worse for sedentary women because such problems are modified by the capillary cross-sectional area.
    Low cardiac output further exacerbates microcirculatory problems.

    6. - Third system down – Liver/Gut

    The next thing affected is your liver/gut.
    Probably the very first thing you'll notice is that there are fewer and fewer foods you can tolerate.
    If it gets really bad, there will be only a handful of foods you'll be able to eat - for a lot of odd reasons.
    In part because microcirculation is necessary for proper digestion.
    Also, your body won't secrete digestive juices so you won't digest your food.
    If you can't digest your food you'll get peptides that are only partially digested and highly immune-reactive.
    They'll leak out of your gut [into your bloodstream] and you'll get food allergies and/or sensitivities.

    Your body will also fail to detoxify your gut ecology, so your gut will begin to poison you.
    That's manifested as feeling yucky and a sense of toxic malaise.
    You get diarrhea, constipation, flatulence and all kinds of GI problems, including bacterial overgrowth, yeast overgrowth, parasitic overgrowth.

    It's a problem because you have poor microcirculation.
    If it gets worse, you'll get malabsorption syndromes because the nutrients that are - by some miracle - digested, are not absorbed well because there's no microcirculation.
    At which point, you will begin to become increasingly toxic, which can manifest as a variety of skin disturbances and you don't feel good and other interesting things—particularly in the brain.

    7. - Fourth affected - The brain

    In the brain, there's a devastating effect with respect to liver/gut dysfunction—it can quickly toxify the brain.
    That's perceived initially as, "I only have problems when I have to use my brain."
    Then it becomes a problem even when you don't use your brain that much.
    You have all kinds of cognitive complaints like memory disturbance and processing speed.
    Then you begin to get central brain structures that can destabilize you psychiatrically.
    You can get hypothalamic structures that begin to destabilize you from an autonomic nervous system perspective and/or neuroendocrine response defects [neuroendocrine : the interaction between the nervous system and the hormones of the endocrine glands].
    Whatever the brain does, it doesn't do it as well.

    The brain and the heart probably get hit about the same time, but patients usually notice their brain being affected much earlier than their heart.
    That's because heart muscle cells have the greatest mitochondrial content of any tissue in the body.
    Thus, when mitochondria are impaired, the heart muscle has the greatest reserve and is the least vulnerable.
    Neurons have far less mitochondria and they run out long before the heart, especially if you're sedentary.
    If you're sedentary there's not too much demand on your heart, but you can still think and make great demands on your brain.
    Energy is energy, whether it's being used physically or cognitively.
    The effect on the brain is noticed first because it has less reserve, especially if you're thinking - unless you do meditation.
    Patients who are both sedentary and meditating regularly may actually preserve their brain longer than those who are just sedentary and use their brain a lot.

    8. - Fifth - Heart—A two-parter

    8.1 - Part A - Manifestation of microcirculatory impairment

    The effect on the heart has an "a" part and a "b" part.
    "The initial manifestation of microcirculatory impairment of the heart is arrhythmia. What kind ? You name it, you've got it."

    "You'll also notice, again, exercise intolerance, because the heart is indeed a muscle just like your leg muscle. When you go up flights of stairs or up mountainsides, you need more cardiac output and you can't sustain it. Therefore, you're going to have trouble. As it gets worse, you'll begin to see mitral valve prolapse (MVP) because that inadequate capillary function affects the papillary muscle and results in prolapse of the mitral valve. Finally, when you get even more severe microcirculation problems, you start to get chest pain as you begin to knock off myocardial cells [heart muscle cells] because they can't get adequate oxygen."

    8.2 - Part B - "The event horizon"

    "And finally you get to the 'B' part of the heart and I'll put a line here [on one of many drawings] which I'll call the Event Horizon, after a movie I saw by that name. 'Event Horizon' is a movie in which a group of space explorers discovers a black hole. They park their space vessel outside the event horizon because if they pass that line they can't get back and if they pass it they're drawn down into a vortex into the black hole and vanish from this universe."

    "The Event Horizon with respect to the heart is this: when the microcirculation defect within the heart itself (produced by a low Q), begins to impact Q itself, you enter a vicious cycle. Microcirculation impairment reduces the Q, which produces more microcirculation impairment which produces even more Q problems, and back and forth, zigzagging into a vortex and down you go "through the Event Horizon" to the next phase of cardiac failure, which is the lung."

    9. - Sixth system - Lung & kidney

    "Cardiac failure in the lung produces Congestive Heart Failure (CHF) and Pulmonary Edema. Then comes the kidney - because remember the kidney and lung have the super-duper RAS system. So the last to go turns out to be the kidney which has the biggest RAS system of all buried in its cells, the Renin Angiotension System. When the kidneys go, you go into renal failure, which combined with the liver, is often dubbed hepatorenal failure and that is the requisite cause of death due to Idiopathic Cardiomyopathy." [After crossing the Event Horizon and spiraling down into Congestive Heart Failure]. I've been there and done that. I'm an expert on that particular journey. And this is the exact sequence I went through over a two—to three-year time period."



    Read also : Part II

    07-03-2009 om 21:41 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The heart of the matter - CFS & cardiac issues - Part II
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    The heart of the matter - CFS & cardiac issues

    Part II


    Part 2a

    1. - The good news - CFIDS prevents us from crossing the event horizon

    "You'll notice that the last things afflicted are the lung and the kidney because they have the RAS and therefore you really have to cross the Event Horizon to involve those. I crossed it. One third of all cases of ICM cross it and once you cross it, there's no turning back. You either die or get a transplant. There is no turning back."

    "Now, for some interesting reason, CFIDS patients do not cross the Event Horizon, at least in any significant way. We don't see them in Pulmonary Edema; we don't see them in renal failure; and, we certainly don't see them needing a transplant. Therefore there is something about this disease that keeps you from progressing across the Event Horizon, though you can get cardiac involvement in the milder sense."

    Since no CFIDS patient that I've ever known or heard about has crossed the Event Horizon, I maintain that this means that CFIDS must prevent it from happening in the first place.
    I crossed the Event Horizon and spiraled down because I did not have CFIDS.
    You have CFIDS; therefore, you're very unlikely to cross the Event Horizon, which doesn't mean that you won't over time.
    Peckerman believes that a certain percentage of CFIDS patients are headed right for that.
    However, they may take a long, long time or die of something else before that happens.

    Almost everyone with CFIDS has Compensated Idiopathic Cardiomyopathy [based on the test results he's getting].
    It's the degree of compensation that varies.
    Some compensate very well, others less so.
    How will you know if you eventually lose your ability to compensate and cross the event horizon ?
    You'll know it because you'll lie down and you'll be short of breath.
    When you lie down you'll no longer be able to breathe.
    Rather than lying down and feeling better, you'll lie flat and get short of breath.
    Then you know you've crossed over.

    2. - Recovery takes time

    When I had my heart replaced, one of the first things that came back was my kidneys.
    My brain came back, but slowly.
    Even though my cardiac output was a whopping 10 liters per minute with the transplant, my brain did not come back fully for 6 to 7 months.
    Even then, there was continued progression for about four more months before I reached near 100% or greater.
    In fact, what's interesting is that I now think my brain is functioning at a much higher level than has been present since I was 20.
    That's interesting because age 20 is when you see 10 liters per minute output.
    The point is that, at some interesting level, brain functionality depends on microcirculation and when you have sufficient amounts of it, you have excellent brain function.

    The next thing that came back was my liver/gut; I couldn't stop eating, and my gut functioned perfectly.
    Then, my muscles started to come back and that took 8 months. Interestingly, my skin took a long time.
    So, my body resuscitated in reverse order.
    "It's taken me over a year to fully come back despite an almost instantaneous restoration of Q, which was my only problem in the first place."

    "Which speaks to something very important and that is, fundamental therapy does not instantaneously result in improvement. As a matter of fact, anything that would improve you within a matter of minutes, hours or days is, in fact, not therapy at all. It is palliation—symptom suppression—which in fact may not be helping you at all."

    3. - Marshall Protocol & "Q"

    My hat is off to Trevor Marshall for identifying that the Renin Angiotensin System (RAS) is a key element in the pathology of this disease and pointing out that it acts locally as well as systemically.
    I didn't know that before.
    But I'm concerned that an ARB ('Angiotensin Receptor Blocker') is being used in CFIDS patients without an awareness of its effect on "Q."

    Angiotensin II has two receptors that we know of and we only understand the first, AT1.
    When Angiotensin II binds to AT1, it increases the hormone Aldosterone, which in turn increases blood volume.
    Big issue !
    If you block AT1 with an ARB [like Benicar], down will go your Aldosterone and down will go your blood volume and you could be in a heap of trouble.
    ARBs that bind to AT1 will constrict blood volume.

    I'm also concerned that the other receptor [AT2] is being ignored.
    No one knows what it does.
    Not even Merck !
    I suspect that it has an immune effect.
    An ARB like Benicar selectively binds very tightly to AT1, resulting in a two - to three-fold increase of Angiotensin II, which then binds to the wide-open AT2 receptor.
    And who knows what kind of immune responses that is setting off.
    This is just speculation, but I am concerned.

    "I don't believe that you can block a regulatory pathway, especially tightly, with a rebound upregulation of Angiotensin II, two or three fold, when you leave unblocked an unexplained receptor that you have no idea what that thing is doing and then hope that down the road everything will be rosy."

    4. - Etiology (cause)

    What is the etiology, the cause, of this cardiac output problem ?
    The short version is that cardiac muscles have lost power because their mitochondria are dysfunctional.
    They're not functioning well because of a redox-state problem [Redox : a reversible chemical reaction in which one reaction is an oxidation and the reverse is a reduction. Look for a future article explaining redox states].
    But, what causes the redox-state problem ?
    I don't know.
    I just know that, like MCS and GWS and many other illnesses, we're looking at a redox-state problem.
    But, there's something unique about CFIDS, because this redox problem seems centered on the heart.
    It's not focused on the heart, at least to the extent that we can tell, in these other disorders.
    But there is one big, big clue.
    It ties in to what we know about Idiopathic Cardiomyopathy (ICM), so we need to look at that first.
    It may shed some light on CFIDS-linked cardiomyopathy.

    5. - Viruses

    According to the textbook of medicine, the list of things associated with cardiomyopathy is as long as your arm and covers three pages.
    But most of the things listed are infectious diseases and viruses are at the top of the list.
    ICM appears to be caused, in the minds of most physicians, by a post-viral infectious disorder that evolves following a viral infection, sometimes at a relatively young age.
    Doesn't that sound a little bit like CFIDS ?

    6. - Heavy metals

    The second thing that is mentioned, for which a great deal of evidence now exists in cardiology literature, including recent publications in the Journal of American Cardiology, is heavy metals.
    This is the big, big clue I referred to earlier.
    There's an Italian article published in one of the cardiology journals about a link between ICM and mercury.
    The authors looked at about 13 cases of ICM, 24 cases of other types of heart disease and 4 controls.
    They biopsied the heart muscle of all the participants and radiated it with neutron flux to make any heavy metals radioactive.
    Then they put the tissue in a chromatograph to determine with great precision exactly how many molecules of mercury were in each of the tissues.

    What they found was astounding.
    All 13 cases of ICM had 23,000 times more mercury than the controls and 18,000 times more than the other types of heart disease.
    One hundred percent of the people with ICM were mercury toxic at the tissue level.
    Does that necessarily mean that the cause of ICM is mercury ?
    Or, is mercury linked to some other phenomena ?

    A professor at the University of Kentucky whom I greatly admire analyzed that data.
    He determined that in normal heart muscle there are not enough mercury-binding sites to have that much mercury.
    He said the only way you could load that much mercury into the heart muscle was if something else carried it in.
    There may be a cardiotropic pathogen and/or an immune-system dysregulation associated with a cardiotropic pathogen that is required to load that much mercury into the heart [cardio : heart; tropic : affinity for or influencing].

    I doubt the cardiotropic pathogen by itself can produce ICM.
    I think takes a combination of a pathogen and the presence of a heavy metal like mercury.

    7. - The Nexus – Virus, bacteria, toxins, allergies and heavy metals

    I believe that the proximate etiology of cardiomyopathy is a nexus between an infectious, allergic or toxic experience, as well as heavy metals.
    I'll go through why I think that, but I'm not claiming I know the exact cause.
    I'm just claiming that, based on the medical literature on cardiomyopathy as well as what we know about CFIDS, I would lay my wagers on those two entities and I think they both may be required, not just one.
    That's why I call it a nexus between the two and you'll see why.
    Because the underlying issues for the etiology of a Q loss need those two entities to really get going.

    8. - Pall - Nitric oxide + superoxide = peroxynitrite

    The pathophysiology [functional changes that accompany a disease] at the cellular level that underpins this pathophysiologic state is well elucidated by Martin Pall [a search for "Martin Pall" on immunesupport.com will produce several articles].

    One nitric oxide molecule plus one superoxide molecule equals one peroxynitrite molecule.
    Peroxynitrite is a reactive oxygen species, is deadly and highly damaging.
    At the cellular level, it is the proximate cause of human mortality.
    Even if you are healthy and your body handles peroxynitrite as well as possible, you will still die of old age.

    "These molecules [nitric oxide and superoxide] have to be generated because they are essential for life. They are the end products of a complex scheme of oxidation reactions in the human body; necessary for, among other things, energy generation and their production is inevitable. Indeed, if they weren't produced you would not be alive. But because they are produced, you will die of oxidation. If you live by the sword, you die by the sword. If you live by oxidation then, like any piece of iron set in an oxygen environment, you will eventually rust away and we call that death by old age. This is called 'The Free Radical Theory of Aging.' "

    What do humans die of, usually ?
    The top killer is Coronary Artery Disease [CAD] and the next is cancer.
    It turns out that CAD and cancer are also driven in part by peroxynitrite formation.
    Neurodegenerative diseases like Parkinson's and Alzheimer's are also suspected of being driven by free radical formation.
    Even suicide is increasingly thought to be generated by oxidative stress in the central nervous system.
    And, of course, MS and autoimmune diseases.
    And finally ICM, the path down which you seem to be going, though halted by CFS itself.

    But your path deviated right here, just above the Event Horizon to CFS and you went down the CFS path for a very interesting reason.
    Why didn't you go down the cancer or MS or Parkinson's pathway ?
    For some reason you started down the CFS pathway over those and I think that's a result of preordained genetics and environmental influences that combined in a unique fashion to produce that particular road I went down - the ICM pathway.
    But I could not deviate [from the ICM path] because I never developed CFIDS and I went straight to a near-death experience and came back.

    I want to talk a little bit about these two guys [nitric oxide and superoxide], show you why they're necessary and that you have to make them, and how they can modulate your disease process.
    Especially how they're related to etiology [they cause many, if not most, of our symptoms—directly or indirectly].

    Nitric Oxide is made by iNOS, eNOS and nNOS, so far identified [the small letter in front indicates the source].
    The iNOS is of particular interest because it comes from the immune system.
    When any kind of virus, bacteria, mold, toxin, microbe or allergy activates your immune system, it induces iNOS, which makes copious amounts of Nitric Oxide. iNOS can make far more Nitric Oxide than eNOS and nNOS can ever make.

    eNOS is made by the endothelial cells in the blood vessels and is responsible for regulating microcirculation, basically.

    nNOS is made in neurons and is responsible for memory and learning.
    It is also, when highly activated, very much responsible for MCS, EMR sensitivity [electromagnetic radiation], light and noise sensitivity and can make sleep difficult.
    Over-activation also amplifies pain.

    Your body has to make nitric oxide.
    If you don't make it, you have no immune system, no circulation, no brain.
    The question isn't do you make it; the question is do you make a lot of it.
    If you make a lot of it there can be repercussions downstream.
    What those repercussions are depends on what you're [your body is] doing with superoxide.

    Now superoxide is produced by the act of making energy [ATP].
    It's made in the mitochondria, and for every molecule of ATP generated, you generate one molecule of superoxide - one for one.
    The more energy you make, the more superoxide you make.
    However, superoxide is generally found inside the mitochondria.
    Generally.
    Nitric oxide is found outside the mitochondria.
    As long as superoxide stays in the mitochondria and never leaks out, there's no way you will make peroxynitrite, because it takes one nitric oxide plus one superoxide to make one molecule of peroxynitrite.

    9. - A little math

    Now, let's stop here for a moment to talk about the coupling effect.
    If I have 50 molecules of nitric oxide and five molecules of superoxide have leaked out of the mitochondria, how many peroxynitrite molecules do I generate ?
    Five.
    If I make 10,000 nitric oxide molecules and only 5 superoxide, how many peroxynitrite molecules do I generate ?
    Again, five !
    Do you see what is happening ?
    What dictates peroxynitrite is not the one with the highest amount, but rather the one with the lowest.

    10. - Super oxide - Out of control

    Therefore, the primary driving force behind peroxynitrite is in fact the production of superoxide.
    However, if superoxide is well controlled, peroxynitrite formation is limited.
    However, if superoxide is out of control, there are few limits to the formation of peroxynitrite.
    It's purely a function of energy production.
    The more energy you produce, the higher the peroxynitrite may go, especially if nitric oxide is also out of control.

    If everything worked as intended, the mitochondria would take in oxygen and nutrition and output carbon dioxide, water and ATP (energy).
    You have enzyme systems embedded in the mitochondria that can break superoxide down to water to prevent superoxide from leaking out of the mitochondria.
    One enzyme system is called Superoxide Dismutase (SOD).
    Actually, the enzyme breaks it down to hydrogen peroxide and then down to water, via Glutathione Peroxidase, which depends on selenium and glutathione [without proper amounts of selenium and glutathione, the enzyme cannot do its job].

    For the enzyme [SOD] to break superoxide down properly, selenium is supposed to bind to Glutathione Peroxidase.
    However, if mercury is present in any amount and you have no defense against it [and there are defenses], it competes for that binding site and blocks the selenium.
    When mercury displaces selenium at the binding site, the function of that enzyme is knocked out.
    At that point, you have no way to oxidize superoxide down to water and superoxide starts to leak out contributing to the formation of deadly peroxynitrite.
    How much superoxide leaks out depends on how much energy you're generating [and thus how much superoxide], as well as the presence of other defense mechanisms.
    CoEnzyme Q10 is one and Lipoic Acid is another.

    CoQ10 within the mitochondria and Lipoic Acid in the cytoplasm bind excess superoxide so it's unavailable to couple with nitric oxide to produce peroxynitrite.
    Taking sufficient CoQ10 under certain redox state conditions, would allow you to make more energy and not get creamed with peroxynitrite [Redox will be discussed in another article].
    But, if you keep raising CoQ10 in an inappropriate redox state you may actually generate more superoxide and that's when the CoQ10 bites you [some patients who cannot tolerate CoQ10 find that its analogue, Idebenone, works better].

    Glutathione production is linked to ATP production, because the more ATP (energy) you make, the more Glutathione you need to keep the enzyme breaking the resulting superoxide down to water.
    If you don't, then the lack of Glutathione will actually result in injury to the mitochondrial membrane and a drop in ATP.
    That's the Gibbs Free Energy Equation, which says that Glutathione concentration and ATP generation are intimately linked.

    Which brings me to the most important statement I'll make about this peroxynitrite diagram.
    If you are immune-activated from virus, bacteria, mold and/or toxin exposures, then you're generating an excess amount of nitric oxide.
    And if you also make a significant amount of ATP, it can result in superoxide, which then binds with the nitric oxide to produce large amounts of peroxynitrite.
    Then you're set up for major problems [oxygen transport, microcirculatory impairment, lack of tissue perfusion etc].



    Part 2b

    1. - Protection from the death spiral

    So to protect yourself from going down the death spiral, your body stops making energy - at least to a point.
    That results in significant reduction of superoxide and knocks out peroxynitrite.
    Thus, you cannot and will not advance [toward the event horizon] or, if you do, you will advance very, very slowly.
    I couldn't do that and therefore I crossed the event horizon and almost died.

    By the way, all this is Dr. Pall's model.
    The only added dimension here is the NMDA receptor, which sits on a neuron and when activated, triggers nitric oxide production.
    So blocking NMDA reduces nitric oxide.

    1.1 - Klonopin / Neurontin

    Patient asks :"Klonopin only upregulates the GABA receptor, is that right ?"

    Dr. Cheney responds :"Yes. But that has an indirect effect on the NMDA receptor, through the GABA receptor. By upregulating [increase a response to a stimulus] GABA, you downregulate NMDA and reduce nitric oxide." [Thus, Klonopin and Neurontin can help reduce nitric oxide]

    1.2 - Avoid Provigil - It stimulates nitric oxide

    "Provigil does the opposite. Provigil does several things, but is mostly an NMDA-activator - it's a stimulant similar to cocaine - it will actually stimulate nitric oxide production. It may also stimulate ATP generation, which is the benefit perhaps that one sees. With more nitric oxide, you can think better, your memory improves, you can focus better and you have more energy. But what you're doing is generating more peroxynitrite and this may not be felt for a while, but ultimately it's probably felt - in the brain at least - as Alzheimer's or Parkinson's Disease or worse, ten years from now."

    2. - How to block peroxynitrite

    2.1 - Increase CO2

    Let's turn to peroxynitrite.
    According to the Textbook of Medicine and Dr. Pall himself, what is your primary scavenger of peroxynitrite ?
    The answer is CO2 (carbon dioxide).
    When ATP is generated in the mitochondria, CO2 is produced as a by-product.
    So, when you make energy [ATP], you produce the very thing needed to scavenge peroxynitrite.
    It's a beautiful system !
    When everything works perfectly, you can make a lot of ATP because superoxide is being broken down into water.
    And CO2 is produced which will get rid of any peroxynitrite that accidentally happens to be produced.

    What a great system !
    If that system could be maintained in the state it was in when you were born, you should live to 120 to 140 years of age.
    It's just that things creep in that degrade that operation, that system and we just exit out earlier than we should.

    Now, if you keep lowering ATP production, which then reduces the amount superoxide produced, you also reduce the production of CO2.
    "The result is you have less and less primary defense against peroxynitrite. It's a vicious cycle. And especially in the lowest energy states of all you really have that problem."

    How do you increase CO2 ?
    Well, first let me ask how you decrease CO2, which we definitely don't want !
    Hyperventilation.
    If you hyperventilate, you dramatically decrease CO2, which would be highly damaging.
    It can produce carpal-pedal spasms in some patients ('carpal' : 'wrist'; 'pedal' : 'foot').
    Its most damaging effect is to your brain, however.

    Rebreathing

    You can increase CO2 - and stop hyperventilation - by rebreathing.
    By inhaling your expired CO2, you actually scavenge peroxynitrite [rebreathing involves cupping your hands over your nose and mouth so that when you exhale, your CO2 is trapped there and then you inhale it. Do this for a minute at a time, about once every four or five minutes during a thirty-minute period once or twice a day. You can also do this while breathing oxygen through a nasal cannula. Rebreathing can also help address respiratory alkalosis, extremely common in CFIDS, thereby improving microcirculation by shifting blood pH—thus allowing more oxygen to be transported off the hemoglobin].

    Klonopin

    Taking Klonopin knocks out Nitric Oxide Synthetase (NOS) and that defends against peroxynitrite.
    Klonopin can also slow the breathing and that will raise CO2.

    Barometric Pressure

    Another way to do it is to walk in Death Valley.
    Below sea level, with all the extra oxygen, you hypoventilate and that will increase CO2 [hypoventilate: breathe abnormally slow and shallow].
    The opposite is flying in aircraft at 10K feet, causing you to hyperventilate, so flying in airplanes is not good.

    CFIDS patients often feel bad when low pressure comes through their area and they ache, among other things.
    Low pressures are like climbing to high altitude and you don't do as well, because you tend to hyperventilate more.

    2.2 - Uric acid

    Uric acid is a powerful scavenger of peroxynitrite.
    Uric acid levels in CFIDS patients are among the lowest I've ever measured, in all of medicine [keep in mind that before specializing in CFIDS, Dr. Cheney served as a Major in the Air Force Medical Corps and was Chief of Medicine at Mt. Home Air Force Base hospital in Idaho for several years before moving on to a private practice in Internal Medicine at Incline Village, Nevada. He was also the Chief of Medicine at the Lakeside Community Hospital in Incline Village, Nevada. In Charlotte, before opening his own CFS clinic, he was the Senior Staff Physician in the Department of Internal Medicine at The Nalle Clinic].
    CFIDS patients are the only ones you see at 1 or 2. Everybody else is up at 4, 5 and 6.
    Most CFIDS patients are quite low.
    The lowest I've ever seen as a group [Dr. Cheney currently checks blood levels and 24-hour urine levels of uric acid].

    What do you make uric acid from ?
    You make it from RNA and DNA metabolism and that is produced endogenously [within the body] and exogenously [outside the body].
    Endogenous production is by apoptosis [normal, programmed cell death].
    "Or by fasting in which you lose muscle mass or even by exercise which can produce muscle mass loss. In any event, you can produce your own endogenous RNA and DNA for uric acid production, which then scavenges peroxynitrite."

    Sushi

    Exogenously there are certain foods you can eat that do it [when considering the following foods, take your own food sensitivities and allergies into account !].
    The best foods that produce RNA and DNA are on the meat and the vegetable side.
    On the meat side, the best RNA and DNA production is in sushi.
    Sushi is very high in digestible RNA and DNA.

    Patient asks : "Now what do you mean by sushi ? Is that raw meat ?"

    Dr. Cheney replies :"Yes, raw meat. Raw meat of any kind is better than cooked meat." [Assuming it's safe and not contaminated]
    Cooking destroys the RNA and DNA, depending on how much you cook it.
    If you overcook it, you definitely destroy it.
    But the most efficient way to destroy RNA and DNA is by microwaving.

    Eggs & raw milk (cheese)

    Secondly, young food is better than old because it has a higher RNA and DNA content.
    How young can you go on the meat side before you can't go any younger ?
    The egg.
    Eggs are very rich in RNA and DNA.
    And milk, if it's not pasteurized.
    It has to be raw milk.
    Raw milk has a high content of RNA and DNA.
    It also, interestingly, has a very high proportion of whey protein.

    Moreover, if it's undenatured there's likely to be RNA and DNA embedded in that.
    So I have a sneaky feeling that part of the power of undenatured whey protein may in fact be its RNA and DNA.
    And if you could raise your uric acid level, you would allow yourself to make more energy, which will allow you to raise your Glutathione.
    That could well be the mechanism [of the effectiveness of undenatured whey protein].

    Of course, raw milk is hard to deal in.
    There are laws against it.
    So how can you fix raw milk and make it legal ?
    Make cheese out of it.
    Cheese made from raw milk and stored in caves - which is the traditional European methodology - actually saves raw milk in a form that can be stored for long periods of time and has rich RNA and DNA content.
    You can go to most health food stores and ask for cheeses that are made from raw milk - that's what you want - and ask for the butter that is imported from France or Europe, which is also made from raw milk and is far better for you and is less processed.


    Read also : Part III


    07-03-2009 om 21:38 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The heart of the matter - CFS & cardiac issues - Part III
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    The heart of the matter - CFS & cardiac issues

    Part III

    Isoprinosine/Imunovir

    There's a drug that raises uric acid called 'Isoprinosine' or 'Imunovir'.
    It's a very good immune-modulator; whose only potential side effect is an increase is uric acid levels.
    But that's not a problem for CFIDS patients !
    That "side effect" would have a profound ability to arbitrate this disease at its most fundamental level.

    Soy

    One of the highest RNA and DNA content foods on the vegetable side is soy.
    So, soy could very helpful here.
    Be aware though that soy binds thyroxin [T4] in the gut and is problematic at best if you have hypothyroidism [I buy frozen, shelled soybeans, let them thaw in the refrigerator and eat them raw. Quick, easy and, with or without salt, very good].

    Nuts & seeds

    How young can vegetables be before they can't get any younger ?
    Nuts and seeds !

    Patient asks : "So baby lettuce and things like that ?"

    Dr. Cheney replies : "Yes, exactly like that."
    Young foods are better than old.
    Unprocessed foods are better than processed.
    Uncooked raw vegetables better than cooked.
    What is the best way to prepare raw vegetables ?
    Juice them, especially if you have problems with digestion.
    Juiced raw vegetables, especially organic raw vegetables, would be very high in RNA and DNA content and would be quite easy to digest.
    Definitely, do not microwave them.
    Steam them or juice them.

    2.3 - Consume reduced cholesterol

    HDL cholesterol binds peroxynitrite.
    When it binds peroxynitrite, it produces oxidized LDL.
    So LDL is what's left after having bound peroxynitrite and HDL is what's ready to bind it.
    "So what you're looking at with cholesterol to HDL ratio, is actually how well you are in fact scavenging or capable of scavenging, peroxynitrite."

    It could be that you generate higher levels to protect yourself.
    When Anthony Komaroff looked at cholesterol in CFIDS patients, it was typically elevated.
    Which means, I think, that CFIDS patients may have an enhanced ability to scavenge peroxynitrite via the cholesterol pathway than a normal person does.
    [Reviewing patient's lipid panel lab]
    Good, your HDL is high - 77.6.
    Total cholesterol is not very high at 141.
    But your HDL is high, so this is a mixed picture.

    Patient asks : "Which means ? So what do I need to do ?"

    Dr. Cheney replies : "Well, you need to eat reduced cholesterol. What is reduced cholesterol ? It's found in unprocessed cheeses, butter and raw milk. When you process these things, you oxidize the cholesterol [it's no longer "reduced"].
    If you don't have a source of exogenous cholesterol [i.e. the unprocessed cheese and butter made from raw milk, mentioned earlier], you excessively oxidize your own endogenous cholesterol.
    Both are bad - consuming processed forms of cholesterol and excessively oxidizing your own cholesterol.

    The cholesterol elevation associated with Coronary Artery Disease (CAD) is not the cause of CAD; it's reflective of it.
    That's why treating cholesterol is a misapplication of therapy [statins] to the wrong thing [cholesterol].
    You're treating your defense mechanism [cholesterol], as well as being in big trouble later down the road.
    Why ?
    Because statin drugs lower CoQ10 levels.
    This generates yet even more peroxynitrite; at the very time, you're reducing your defense [cholesterol] against it [peroxynitrite].

    That's a prescription for disaster.
    And you know what that disaster is in the published medical literature ?
    People on statin drugs actually die of many cancers faster than people on placebo.
    The Harvard study said that in the New England Journal of Medicine in 1996.
    This was also reported in animals on statin drugs.
    That's why, although there was a 3% improvement of death rate from CAD in the treated group, the net mortality was identical to the placebo group because those on statin drugs died of cancer more often than the placebo group.
    So there was no net gain.
    You just traded out what you died of.
    And if they'd followed the study out 10 years, they would have seen more Parkinson's disease.
    However, they ended the study at five years.

    They have also seen rhabdomyolysis [destruction or degeneration of skeletal muscle tissue accompanied by the release of muscle cell contents into the bloodstream resulting in hypovolemia (decrease in the volume of the circulating blood); hyperkalemia (the presence of an abnormally high concentration of potassium in the blood); and sometimes acute renal failure] in all the developing statin drugs, resulting in one being recalled.
    I suspect rhabdomyolysis is involved by CoQ10 deficiency produced by the statin drugs.

    3. - Three ways to block nitric oxide

    3.1 - Hemoglobin

    The best endogenous scavenger of nitric oxide is hemoglobin [hemoglobin : the "red" in red blood cells - a protein that transports oxygen from the lungs to the tissues].
    "When hemoglobin scavenges nitric oxide, the nitric oxide bends the hemoglobin, causing the red blood cells to deform. Dr. Les Simpson in New Zealand found that the red blood cells of CFIDS patients were deformed and when they're deformed they can't get through the capillary bed very well and can cause pain."

    "An indication of this [RBC deformation] is it also drops the SED rate. CFIDS patients have the lowest SED rates I've ever recorded and the ones with the lowest SED rate may have the greatest degree of pain" [SED rate refers to sedimentation rate and is listed as ESR on many lab tests].

    "Do you know what your SED rate is by chance ? Normal for you would be 15 plus or minus five. That's according to the British literature. A female your age has a higher SED rate than children and males. And you're probably down around 0 to 3. Which means you have Nitric Oxide binding hemoglobin and therefore you have an induced hemoglobinopathy [a problem with the hemoglobin - nitric oxide bends it] and red cell deformation and a low SED rate on that basis."

    In the Laboratory Textbook of Medicine, there are only three diseases that lower the SED rate to that level.
    One is Sickle Cell Anemia - a genetic hemoglobinopathy.
    The second is CFS - an acquired hemoglobinopathy (acquired by Nitric Oxide binding).
    And guess what the third disease with a low SED rate is ?
    Idiopathic Cardiomyopathy !

    The more deformed red blood cells you have, the more pain you may experience.
    It's bad enough when you don't perfuse your muscles and your joints [because of poor microcirculation], but it's even worse when your red blood cells are so deformed that they can barely get through the capillaries or are blocked entirely.
    Some CFIDS patients have a problem similar to that of Sickle Cell patients in this regard and Sickle Cell patients have unbelievable pain - you have to give them IV morphine and fluids.
    That's how they're treated.

    3.2 - Hydroxycobalalmin injections (B12)

    Another important scavenger of Nitric Oxide is B12 - it binds Nitric Oxide quite vigorously [this form of B12 is available from compounding pharmacies with a script from a doctor. One cc a day is recommended, at a concentration of 10,000 mcg/ml. The injection can be intramuscularly or subcutaneous. Some patients need to work up to this dose slowly since it also detoxifies you. Patients report more energy, less brain fog, better sleep. Some patients report a significant benefit at a higher dose, perhaps 2 cc's. I usually take one cc a day, but if I've done too much and am crashing, I take two cc's. It helps !].

    3.3 - Magnesium sulfate injections

    Magnesium blocks the production of nitric oxide by calcium channel blockade [many patients benefit from magnesium injections, which are virtually painless with the addition of taurine. The Magnesium used by most is Magnesium Sulfate - standard 50% solution - 1/2 cc drawn into the syringe first, followed by 1 1/2 cc's of Taurine. The Taurine is compounded at 50 mg/cc. The taurine makes the injection virtually painless and the ratio eliminates the hard knots many are familiar with. The injection is intramuscular, given in upper, outer quadrant of either buttock. Both require scripts from a doctor].

    3.4 - Other Treatments

    Numerous other treatments are used by Dr. Cheney as appropriate with certain patients.
    Some of the more common ones are zinc and selenium supplements that help block mercury [zinc Picolinate : 50 mg, once a day; Liquid Selenium by Allergy Research Group : 1 tsp a day].

    CoQ10 and/or Idebenone

    Idebenone comes in 40 or 45 mg capsules and one such capsule is roughly equivalent to 200 mg of CoQ10. [600 mg of CoQ10, or an equivalent combination of the two, is highly recommended. There is a lot of poor quality CoQ10 on the market - the cheaper products may not be worth your money. Douglas Lab's "CoQMelt" is a good product and is available from needs.com. Kirkman Labs sells Idebenone, kirkmanlabs.com. It's also available at some local health food stores - 20% off on the first Tuesday of each month at Sunflower Shoppe in Fort Worth and Healthy Approach in Colleyville].

    Proanthocyanidins or bioflavonoids

    The most powerful of these antioxidants are in Grape Skins or Pycnogenol.
    It just makes good sense to supplement with these.

    Essential Fatty Acids, such as Fish Oil, Evening Primrose Oil and Borage Oil.
    "I tend to recommend Fish Oil only. It has certain advantages over the others." [Tyler's Eskimo-3 liquid, one teaspoon a day, manufactured by Cardinova in Sweden]

    4. - Physiology - Preload and afterload

    Turning to physiology, how does a cardiologist treat the heart problem ?
    He uses the Frank-Starling Curve [Dr. Cheney drew a curve for his other patient that I don't have – cfr. :
    http://www.nda.ox.ac.uk/wfsa/html/u10/u1002_02.htm for sample curves].


    Figure 2. – Ventricular end-diastolic volume
    Cfr. : http://www.dfwcfids.org/graphics/vedv.cardiocurves.gif

    To understand this diagram and the rest of this section, the following somewhat simplified definitions may be helpful :
    Stroke Volume (SV) : the amount of blood pumped by one contraction of the heart.
    Cardiac Output : the volume pumped out in one minute (SV x heart rate).
    The ventricle is a lower chamber of the heart.
    Oxygenated blood is ejected from the left ventricle to the body; unoxygenated blood travels from the right ventricle to the lungs.
    Preload is the amount of blood in the left ventricle waiting to be pumped out to the body or - as on the diagram - the volume in the ventricle at the end of diastole.
    It's mainly dependent on the venous return of blood from the body.
    Diastole is when the muscles relax and a chamber of the heart expands and fills with blood; compared with Systole, when the muscles contract and expel blood from the chamber.
    Afterload is the resistance the blood encounters when ejected from the
    heart - remember how arteries constrict like nozzles ?
    The diagram could be seen as plotting the amount of blood waiting in the ventricle to go to the body (horizontal axis) against the amount of blood that is actually ejected from the ventricle (vertical axis).
    Four curves are shown, the highest two (A and B) being healthy hearts with good cardiac output during exercise and at rest.
    The lower two curves (C and D) indicate diseased hearts that cannot produce sufficient cardiac output.
    While they have lower cardiac output, they also have greater ventricular volume - there is more blood in the heart, but the heart muscle isn't strong enough to pump as much out.
    There are also three dotted horizontal lines at increasing heights indicating the necessary cardiac output for rest, walking and maximal activity.

    Dr. Cheney states : "This is the normal Starling Curve." [Presumably something like Curve B.]
    This curve is where most CFIDS patients are [I suspect CFIDS curves are between B and C; i.e. - a curve not shown on this diagram].
    The point at the top of that curve is the sweet spot.
    That would give you the most cardiac out output and thus the greatest tissue perfusion and that would be the best.
    On either side of that peak, the cardiac output goes down.
    Most CFIDS patients sit right here [probably somewhere on the left side of the curve].

    Now, here is a Congestive Heart Failure curve [Curve C].
    Those patients are treated with Lasix to make them eliminate the extra volume and then they are able to move up the curve and improve their cardiac output.
    "Most of you, on the other hand, need volume and as we give you more volume you will come up onto the peak and will maximize your cardiac output. But, if we overshoot, you're going to go down the other side and you actually lose volume. And if you keep going down you'll actually go into heart failure."
    It's critical to understand the Frank-Starling Curve of Cardiac Output, where you [the PWC] are and how to manipulate it [notice that the healthy hearts in the diagram (curves A & B) have little to no drop after their peak !].

    4.1 - Preload - Lying down

    How do you augment preload - which is blood volume - to improve cardiac output ?
    You lie down.
    When you lie down, you increase the cardiac output a whopping 2 liters per minute.
    Don't sit, don't recline - lie down.
    Some patients need to lie down and augment volume anytime, all the time.

    But, what if you're one of the ones right near the top of the curve and you increase your volume (preload) 2 liters by lying down ?
    You could actually go over the peak and down the other side.
    Do you know what that means clinically ?
    Some patients can't lie down !
    Some tell me : "When I lay down I cannot rest well or sleep."
    They went right over the top and dropped their cardiac output by lying down !

    4.2 - Preload chronobiology - Daytime vs. Bedtime

    There is a chronobiology to this curve: the time of day affects it.
    In the daytime, patients need to increase blood volume by taking in fluids.
    That allows them to be up more.
    But some can over treat by drinking fluids and lying down in the daytime [some with this problem who can't be up find a semi-recumbent position helpful. Use pillows to raise your torso].

    However, at nighttime, the opposite happens.
    The chronobiology drops your cortisol and aldosterone so you don't hold fluids as well and all that combines to allow this type of patient to lay down without this problem.
    Patients with this problem (lying down makes them feel worse) should only expand volume in the first six or seven hours of their day with the Hydralate (Gookinaid) or Home Brew mentioned below, then switch to water.
    And if they lie down while over-expanding volume with Home Brew or other supplements or drugs, they'll get creamed.
    These patients should not use the Home Brew during the six or seven hours before bedtime.
    If they do, they may not be able to sleep.

    4.3 - Preload - Hydralate (Gookinaid) / HomeBrew

    "Volume loading using appropriate volume expanders can be quite helpful. This can be done in a variety of ways, but falls best under the term of isotonic [same salt concentration as normal cells and blood] volume expansion. Hydralate (Gookinaid) is a well-documented isotonic volume expander and is used in athletic events such as marathon running [Gookinaid.com]. It has an advantage of rapid absorption and is maintained in the intravascular volume far longer than hypotonic [less salt concentration] drinks such as water itself. The disadvantage to Hydralate (Gookinaid) is that it has sugar in it in the form of glucose."

    "Another option would be a HomeBrew mixture of sea salt and "No Salt"” [HomeBrew : one cup of filtered or spring water, 1/8 teaspoon of Sea Salt and 1/8 teaspoon of "No Salt" salt substitute (potassium). Add lime juice or an herbal teabag as well as stevia for taste].
    Four to eight glasses of Hydralate (Gookinaid) or HomeBrew are recommended.

    Why is potassium in these drinks ?
    Potassium induces Aldosterone, a hormone that significantly increases blood volume.

    4.4 - Preload - Cortisol as licorice root

    For those with low blood pressure - most CFIDS patients have low blood pressure - cortisol could also be useful and can be improved adaptogenically using Licorice Root Extract at 1 to 2 tsp every other day [Adaptogenic substances respond to what your body needs. I take licorice root capsules. Only the type with glycyrrhizin works for this purpose].

    4.5 - Afterload Reduction – Magnesium

    The second thing you need to do after increasing your Preload, is reduce your Afterload.
    This means reducing the resistance the blood encounters.
    The best Afterload-reducing agent I know of is Magnesium, an adaptogenic vasodilator [opens up/relaxes the blood vessels as needed].
    Magnesium and taurine injections have been very effective for many patients [cfr. details on these injections in the earlier section].
    You could also use oral Magnesium Glycinate capsules in the form of Magnesium Glycinate Forte 300 to 500 mg at bedtime [I use both the oral and the injectible forms].

    Will implementing these treatment measures cure you ?
    Absolutely not, because none of this is getting at the primary issue.
    It is directed at what is most dysfunctional about this disease.
    If we're trying to get you functional, this is where we start.

    [This concludes the information on CFS and Cardiac Issues. Look for future articles on other topics. Dr. Cheney will speak on this topic on June 18 in Irving, TX. His presentation will also include new information on CFS and Diastolic Cardiomyopathy. Cfr. www.dfwcfids.org/menu.html for details about the seminar and information on ordering a videotape]

    Cfr. :
    -
    http://www.dfwcfids.org/medical/cheney/heart04.part1a.htm
    -
    http://www.dfwcfids.org/videos/video200609cheney_about.shtml



    IV. - 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.cfids-cab.org/MESA/cardiac-1.html
    Full text :
    -
    http://www.cfids-cab.org/MESA/Peckerman.pdf
    - http://www.cfids-cab.org/cfs-inform/Coicfs/peckerman.etal.03.pdf

    Cfr. also : 'Cardiac Output Linked to Severe CFS Cases - Research Q&A' below.



    V. - Cardiac Output Linked to Severe CFS Cases - Research Q&A

    Mark Giuliucci, editor of The CFS Research Review
    The CFIDS Association of America, Fall 2003

    Lead author Arnold Peckerman, PhD discusses the findings of the study :
    Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome

    (cfr. above)

    Synopsis

    While the cause of chronic fatigue syndrome (CFS) remains unknown, researchers have noted circulatory irregularities in many patients.
    These include autonomic nervous system dysfunction, often manifested as orthostatic intolerance; neuroendocrine abnormalities (cfr. : story on p. 4); reduced plasma volume; and low red blood cell mass.
    In combination, some researchers believe, these factors could create deficiencies in blood flow to organs and muscles - with resultant symptoms, such as post-exertional fatigue, that are hallmarks of CFS.

    New research from the CFS Cooperative Research Center at the University of Medicine and Dentistry of New Jersey has tested the possible link between CFS symptoms and cardiac output (the amount of blood pumped by the heart each minute).
    Thirty-eight CFS patients participated in the study, along with 27 matched, sedentary controls.
    All subjects were tested for cardiac output using impedance cardiography, a noninvasive procedure based on the principle that electrical impedance of tissues is proportional to their blood flow.
    Subjects were tested during a 10-minute resting supine period and a five-minute quiet standing period.

    Results showed that patients with severe cases of CFS (those who had more symptoms and rated them as substantial or greater in severity) had significantly lower cardiac output than either controls or patients with less-severe CFS - even though mean arterial blood pressure and heart rate did not vary significantly among the groups.
    Moreover, post-exertional fatigue and flu-like symptoms were predictive of lowered cardiac output (p< 0.0002).

    The authors say their work suggests that “in some patients with CFS, blood pressure is maintained at the cost of restricted flow, possibly resulting in a low flow circulatory state.
    CFS patients with lower cardiac output may not be able to meet the demands of everyday physical activities, leading to fatigue and other symptoms.

    Lead author Arnold Peckerman, PhD, discusses the study’s findings

    Q. : What led to the hypothesis that CFS patients may have reduced cardiac output ?

    Dr. Peckerman : Many of the symptoms of CFS, such as post-exertional fatigue, are also symptoms of low cardiac output.
    A person can have low cardiac output for a number of reasons, but the result is the same — circulation slows down and some organs may not get enough blood flowing through them.
    If cardiac output falls to the point that it is unable to meet metabolic demands, this is called hypoperfusion.
    Clinical signs of hypoperfusion include lowering of pulse pressure, cool extremities, altered mentation, rapid resting heart rate, breathing that alternates between deep and shallow and high blood urea nitrogen relative to creatinine.
    To be sure, most CFS patients do not show clinical signs of hypoperfusion and they couldn’t.
    If you have symptoms like these, you get referred for cardiological evaluation and treated appropriately.
    You would not be diagnosed with CFS.
    The point I am making is that the criteria for defining hypoperfusion are conservative.
    However, if you lower the bar, meaning you entertain a possibility that reduction in blood flow of a lesser degree than that may still be clinically significant and you pull together the many indications from different research and clinical observations in CFS pointing in this direction, it becomes a reasonable question to ask.

    Q. : The gap in cardiac output between controls and severe CFS cases was wider when subjects were supine than when they were standing. Why might that be ?

    Dr. Peckerman : When you are lying down, blood flow to the heart (venous return or preload) is generally higher compared to what it is when you are standing.
    Normally, having high blood flow to the heart is good.
    It helps the heart to work better.
    But if heart muscle is not working properly, if it is compromised and may become overloaded.
    Then you have the opposite effect.
    The more blood goes to the heart, the more the function goes down.

    This is what happens with heart failure patients.
    When they’re lying down, their heart’s pumping capacity is reduced.
    When they stand up, the preload becomes reduced because much of the blood goes to the legs.
    Normal people have reduced cardiac performance when standing.
    In these people, it’s the opposite; it improves.

    In a sense, this is what we found with severe CFS patients.
    When we looked at the lying position, the difference between controls and the severe patients was greater than when they were standing.
    If you start with the presumption that these people have orthostatic intolerance due to low blood volume, you’d expect to see larger deviation from the norm when standing.
    What actually happened was the opposite; it was smaller.

    Q. : Are you saying that some people with severe CFS may have heart failure ?

    Dr. Peckerman : Any such conclusion is really beyond the scope of this study.
    But what we may be seeing here is a more subtle form.
    Present medicine is slowly realizing that there are many people with heart failure that is not clinically evident but which may be progressing in that direction.
    They walk around with an unrecognized disease that is not being treated.
    Unfortunately, when the symptoms appear, it already may be irreversible.

    Of course, there could be many other explanations for what we observed in this study.
    We could not make a statement about heart failure with any certainty based on these preliminary findings.
    More recently we did a follow-up study that included cardiac stress testing and the preliminary data we reported at the Experimental Biology conference in April were consistent with this possibility.
    But much more work still remains to be done.

    Read aslo : Part IV


    07-03-2009 om 21:38 geschreven door Jules

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    The heart of the matter - CFS & cardiac issues

    Part IV


    Q. . Cognitive dysfunction was not found to be predictive of reduced cardiac output ?

    Dr. Peckerman : That’s true, but this does not mean that cardiac output cannot affect cognitive abilities.
    It may very well be happening.
    In fact, patients with severe CFS who had reduced cardiac output rated their problems with memory and concentration quite high.

    What our analysis did show was that reduced cardiac output was more likely to be found in patients whose main symptoms were some combination of post-exertional fatigue and infectious symptoms such as fever and chills.
    This was after controlling for headaches, muscle aches, sleep and other symptoms included in the case definition.

    The same analysis also found that those patients whose main symptoms related to cognitive functioning had less likelihood of having lowered cardiac output.
    The most plausible explanation for this is that primary problem in those people is not with low cardiac output, but may lie elsewhere, possibly in the brain.

    A major stumbling block in studying CFS has been heterogeneity, meaning that different patient groups have different causes for their symptoms — and no reliable means of separating them.
    This study suggested one way it possibly can be done.
    Mind you, we wouldn’t find what we found if we didn’t separate our patients into the severe and less severe subsets.
    However, just looking at symptoms probably would not be sensitive enough.
    One needs to look for combinations of clinical and physiological markers.
    The combination we identified was that of low cardiac output, plus high post-exertional fatigue, high fever-chills and low cognitive problems.
    This approach seems promising.

    Q. : Can you see any treatments for CFS arising from your findings ?

    Dr. Peckerman : Right now, it’s premature to talk about treatments.
    We’re looking at a phenomenon that could have a number of different causes.

    Unless you know the cause, treatment would be a shot in the dark.
    In fact, it can do harm.
    For example, if the problem is with the heart it is one thing, but if the problem is with low blood volume it is another.
    In people with heart failure, blood volume is not low, it is high.
    So if you assume that low cardiac output is due to low blood volume and you give someone treatment to increase their blood volume, this isn’t going to make matters better — it may make it worse.
    Our observations so far have been more consistent with a problem with the heart, but it is too early to tell for sure.

    The good news is that there are ways to treat the problem of reduced cardiac output if the mechanisms are understood.
    If you can identify what’s causing it, it’s certainly possible to treat it.
    Unfortunately, we are nowhere near that point yet in CFS cases.

    Cfr. : http://www.cfids.org/archives/2003rr/2003-rr2-article01.asp



    VI - Cardiovascular Physiology Concepts - Vascular Network

    Richard E. Klabunde, Ph.D.
    Revised 04-06-2007
    © 1999-2007 Richard E. Klabunde

    The left ventricle ejects blood into the aorta, which then distributes the blood flow throughout the body using a network of blood vessels.
    These are illustrated in the following figure – cfr. : http://www.cvphysiology.com/Blood%20Pressure/BP019_network.gif -.

    The relative sizes and functions of different blood vessels are summarized in the following table (Vessel type – Diameter (mm) – Function) – cfr. : http://www.cvphysiology.com/Blood%20Pressure/BP019.htm -.

    The aorta, besides being the main vessel to distribute blood to the arterial system, dampens the pulsatile pressure that results from the intermittent outflow from the left ventricle.
    The actual dampening is a function of the aortic compliance.
    Large arteries branching off the aorta (e.g., carotid, mesenteric, renal arteries) distribute the blood flow to specific organs.
    These large arteries, although capable of constricting and dilating, serve virtually no role in the regulation of pressure and blood flow under normal physiological conditions.
    Once the distributing artery reaches the organ to which it supplies blood, it branches into smaller arteries that distribute blood flow within the organ.
    These vessels continue to branch and become arterioles.
    Together, the small arteries and arterioles represent the primary vessels that are involved in the regulation of arterial blood pressure as well as blood flow within the organ.
    These vessels are highly innervated by autonomic nerves (particularly sympathetic adrenergic) and respond to changes in nerve activity and circulating hormones by constricting or dilating.
    Therefore, these vessels are referred to as resistance vessels.
    As arterioles become smaller in diameter, they lose their smooth muscle.
    Vessels that have no smooth muscle, but are composed of endothelial cells and a basement membrane, are termed capillaries and represent the smallest vessels within the microcirculation.
    Capillaries are the primary exchange vessels within the body.
    Across the capillary endothelium, oxygen, carbon dioxide, water, electrolytes, proteins, metabolic substrates and by-products (e.g., glucose, amino acids, lactic acid) and circulating hormones are exchanged between the plasma and the tissue interstitium surrounding the capillary.
    When capillaries join together, they form postcapillary venules, which also serve as exchange vessels, particularly for large macromolecules as well as fluid.
    As postcapillary venules join together and form larger venules, smooth muscle once again appears.
    These venous vessels, like the resistance vessels, are capable of dilating and constricting and serve an important function in regulating capillary pressure.
    Venules form larger veins that serve as the primary capacitance vessels of the body - i.e., the site where most of the blood volume is found and where regional blood volume is regulated.
    For example, constriction of the veins decreases venous volume and increases venous pressure, which alters cardiac output.
    The final venous vessels are the inferior and superior vena cava, which carry the blood back to the right atrium of the heart.

    Distribution of Pressures and Volumes

    As shown in the figure to the right, the aorta and arteries have the highest pressure.
    The
    mean aortic pressure is about 95 mmHg in a normal individual.
    The mean blood pressure does not fall very much as the blood flows down the aorta and through large distributing arteries.
    It is not until the small arteries and arterioles that there is a large fall in mean blood pressure.
    Approximately 50-70% of the pressure drop along the vasculature occurs within the small arteries and arterioles.
    By the time blood reaches the capillaries the mean pressure may be 25-30 mmHg, depending upon the organ.
    The pressure falls further as blood travels into the veins and back to the heart.
    Pressure within the thoracic vena cava near the right atrium is very close to zero and fluctuates from a few mmHg negative to positive with respiration.

    Regarding the distribution of blood volume within the circulation, the greatest volume resides in the venous vasculature, where 70-80% of the blood volume is found.
    For this reason, veins are referred to as capacitance vessels.
    The relative volume of blood between the arterial and venous sides of the circulation can vary considerably depending upon total blood volume, intravascular pressures and
    vascular compliance.


    Cfr. :
    http://www.cvphysiology.com/Blood%20Pressure/BP019.htm



    Cfr. also :

    1. 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

    2. Baroreceptor reflex and integrative stress responses in chronic fatigue syndrome
      Arnold Peckerman, PhD, John J. LaManca, PhD, Bushra Qureishi, MD, Kristina A. Dahl, MD, Roseli Golfetti, PhD, Yoshiharu Yamamoto, PhD and Benjamin H. Natelson, VA Medical Center, War-Related Illness and Injury Study Center, East Orange, New Jersey 07018, USA : apeckerm@njneuromed.org - Psychosom Med. 2003 Sep-Oct;65(5):889-95 - PMID: 14508037
      Objective -Altered cardiovascular responses to mental and postural stressors have been reported in chronic fatigue syndrome (CFS).
      This study examined whether those findings may involve changes in baroreceptor reflex functioning.
      Methods - Chronotropic baroreceptor reflex (by sequential analysis) and cardiovascular stress responses were recorded during postural (5-minute of active standing) and cognitive (speech task) stress testing in patients with CFS grouped into cases with severe (N = 21) or less severe (N = 22) illness, and in 29 matched control subjects.
      Results - Patients with CFS had a greater decline in baroreceptor reflex sensitivity (BRS) during standing, although only those with severe CFS were significantly different from the controls.
      Systolic blood pressure declined during standing in the control group but was maintained in the CFS patients.
      In contrast, the patients with less severe CFS had blunted increases in blood pressure during the speech task, which could not, however, be explained by inadequate inhibition of the baroreceptor reflex, with all groups showing an appropriate reduction in BRS during the task.
      Conclusions - These results indicate that in CFS, deficiencies in orthostatic regulation, but not in centrally mediated stress responses, may involve the baroreceptor reflex.
      This study also suggests that classifying patients with CFS on illness severity may discriminate between patients with abnormalities in peripheral vs. central mechanisms of cardiovascular stress responses.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/14508037?dopt=Abstract

    3. Cardiac Insufficiency Hypothesis
      M.E. Society of America, (page last updatedà 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" – cfr. :
      http://www.cfids-cab.org/MESA/Microbial.pdf - 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 go to :
      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 go to :
      http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0610E&L=CO-CURE&P=R346 -.
      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.
      Cfr. :
      http://www.cfids-cab.org/MESA/Lerner.html

    4. Cardiac involvement in patients with chronic fatigue syndrome as documented with Holter and biopsy data in Birmingham, Michigan, 1991-1993
      Lerner, A. M., Goldstein, J., O'Neill W. et al. - Inf Dis in Clin Pract, 1997; 6:327-333
      Lerner AM, Goldstein J, Chang CH, Zervos M, Fitzgerald JT et al. - Infectious Diseases in Clinical Practice 1997; 6: 327-33

      We report the prevalence of abnormal oscillating T-waves at Holter monitoring in a consecutive case series of 67 chronic fatigue syndrome (CFS) patients from an infectious diseases center in Birmingham, Michigan, in the years 1991-1993 and compare these abnormal T-waves to similar tests in 78 non-CFS patients matched for age, place, time and the absence of known other confounding medical diseases.
      Patients in both groups had normal resting 12-lead electrocardiograms (ECGs), rest/stress myocardial perfusion studies (thallium 201 or TC-99 sestamibi studies and two-dimensional echocardiograms (except for the incidental nonsignificant aortic stenosis).
      The prevalence of labile T-wave abnormalities by Holter monitoring was greater in CFS patients than in non-CFS patients (P<.01).
      Repetitive T-wave flattening was a sensitive indicator of the presence of CFS.
      The absence of these abnormal T-waves made the diagnosis of CFS unlikely (statistical sensitivity, 0.96).
      The combination (e.g., the presence of both oscillating T-wave flattenings plus T-wave inversions) was an accurate indicator of the possible presence of CFS.
      Right ventricular endomyocardial biopsies in CFS patients showed a single patient with a lymphocytic myocarditis.
      Light and electron microscopic cardiomyopathic changes were present in the others.
      Cfr. :
      https://listserv.surfnet.nl/scripts/WA.EXE?A2=ind0009C&L=me-net&D=0&I=2&P=3964

    5. CFS and Diastolic Cardiomyopathy - A three-hour talk in streaming video
      Dr. Paul Cheney
      Cfr. :
      http://www.dfwcfids.org/videos/video200609cheney.shtml

    6. CFS as Heart Failure Secondary to Mitochondrial Malfunction - A Nutritional Support Protocol
      Dr. Sarah Myhill, MD - November 15, 2006
      (Ed Note
      : Do CFS symptoms stem from a sort of “heart failure” associated with inefficient energy production at the cellular level? UK-based CFS specialist Dr. Sarah Myhill, MD, believes that it is - based on both her own observations treating patients and a careful study of the evolving science.
      Dr. Myhill explains that her focus is on preventive healthcare and patient education.
      In the following patient handout, reproduced here with permission from Dr. Myhill’s patient-information website (DrMyhill.co.uk), she :
      - explains the underlying theory in simple terms
      - details a dietary/supplement protocol for addressing the condition and
      - outlines the baseline tests required to determine the individual patient’s deficiencies in these respects, if any. Dr. Myhill’s handout is specifically based on the groundbreaking research and clinical work of U.S.-based cardiopulmonary physiologists Dr. Arnold Peckerman, PhD and Dr. Stephen T. Sinatra, MD – and presages the continuing work of CFS specialist Dr. Paul Cheney, MD, to further define this condition and test strategies for its treatment (patients interested in these experts’ publications may refer to the footnoted references).
      I think this is one of the most important handouts I have ever produced in terms of my understanding of CFS and what to do in order to recover.
      So please read this very carefully and several times over - because for many sufferers it contains the keys to unlock their illness.
      Two papers have come to my notice recently which make great sense of both my clinical observations and also the idea that CFS is a symptom of mitochondrial failure.
      The two symptoms I am looking for in CFS to make the diagnosis are firstly very poor stamina and secondly, delayed fatigue. I think I can now explain these in terms of what is going on inside cells and the effects on major organs of the body (primarily the heart).
      More importantly, there are major implications for a test for CFS and of course management and recovery.
      If mitochondria (the little batteries found inside every cell in the body) do not work properly, then the energy supply to every cell in the body will be impaired.
      This includes the heart :
      - many of the symptoms of CFS could be explained by heart failure because the heart muscle cannot work properly
      - cardiologists and other doctors are used to dealing with heart failure due to poor blood supply to the heart itself
      - In CFS the heart failure is caused by poor muscle function and therefore strictly speaking is a cardiomyopathy. This means the function of the heart will be very abnormal, but traditional tests of heart failure, such as ECG, ECHOs, angiograms etc, will be normal.
      Thanks to work by Arnold Peckerman, PhD (
      http://www.cfids-cab.org/cfs-inform/Coicfs/peckerman.etal.03.pdf -) we now know that cardiac output in CFS patients is impaired.
      [Note : Dr. Peckerman, a cardiopulmonary physiologist at the VA Medical Center in East Orange, New Jersey, published this groundbreaking article : “Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome,” in 2003. (1) Dr. Paul Cheney, a pre-eminent U.S. researcher now focused on furthering the investigation of CFS heart dysfunction and treatment, has referred to this article as : “The best, most important publication [about CFS] in 20 years." (2)]
      Furthermore, the level of impairment correlates very closely to the level of disability in patients.
      Dr. Peckerman was asked by the U.S. National Institutes of Health to develop a test for CFS in order to help them to judge the level of disability in patients claiming Social Security benefits.
      Dr. Peckerman is a cardiologist, and on the basis that CFS presents with low blood pressure, low blood volume and perfusion defects, he surmised CFS patients were in heart failure.
      To test this he came up with “Q scores”.
      Q Scores
      "Q" stands for 'cardiac output in liters per minute' and this can be measured using a totally non-invasive method called 'Impedance Cardiography' (cfr. :
      http://www.mediboek.nl/Impedance-Cardiography-isbn9789023220664.html -).
      This allows one to accurately measure cardiac output by measuring the electrical impedance across the chest wall.
      The greater the blood flow the less the impedance.
      This can be adjusted according to chest and body size to produce a reliable measurement (this is done using a standard algorithm).
      It is important to do this test in the upright position and again when supine (lying flat on your back).
      This is because cardiac output in healthy fit people will vary from 7 liters per min when supine to 5 liters per min when standing up.
      In healthy people this drop is not enough to affect function, but in CFS sufferers the drop may be from 5 liters lying down to 3.5 liters standing up.
      At this level the sufferer has a cardiac output which causes borderline organ failure.
      This explains why CFS patients feel much better lying down.
      They have acceptable cardiac output lying down, but standing up they are in borderline heart and organ failure.
      CFS is therefore the symptom which prevents the patient developing complete heart failure.
      Actually, everyone feels more rested when they are sitting down with their feet up, not least my daughters !
      The subconscious has worked out that the heart has to work less hard when you are sitting down with your feet up, so we do so because we feel more comfortable.
      Symptoms of CFS explained
      The job of the heart is to maintain blood pressure.
      If the blood pressure falls, organs start to fail.
      If the heart is working inadequately as a pump then the only way blood pressure can be sustained is by shutting down blood supply to organs.
      Organs are shut down in terms of priority - that is, the skin first, then muscles, followed by liver, gut, brain and finally the heart, lung and kidney.
      As these organ systems shut down, this creates further problems for the body in terms of toxic overload, susceptibility to viruses which damage mitochondria further, thus exacerbating all the problems of the CFS sufferer.
      - Effects on the skin
      If you shut down the blood supply to the skin, this has two main effects :
      - The first is that the skin is responsible for controlling the temperature of the body.
      This means that CFS patients become intolerant of heat.
      If the body gets too hot then it cannot lose heat through the skin (because it has no blood supply) and the core temperature increases.
      The only way the body can compensate for this is by switching off the thyroid gland (which is responsible for the level of metabolic activity in the body and hence heat generation) - and so one gets a compensatory underactive thyroid.
      This alone worsens the problems of fatigue.
      - The second problem is that if the micro-circulation in the skin is shut down, then the body cannot sweat.
      Sweating is a major way through which toxins, particularly heavy metals, pesticides and volatile organic compounds, are excreted.
      Therefore the CFS sufferer's body is much better at accumulating toxins, which of course further damage mitochondria.
      - Symptoms in muscles
      If the blood supply to muscles is impaired, then muscles quickly run out of oxygen when one starts to exercise.
      With no oxygen in the muscles the cells switch over to anaerobic metabolism, which produces lactic acid - and it is this that makes muscles ache so much.
      As well as the above problem, muscles in the CFS patient have very poor stamina because the mitochondria which supply them with energy are malfunctioning.
      - Symptoms in the liver and gut
      Poor blood supply to the gut results in inefficient digestion, poor production of digestive juices and leaky gut syndrome.
      Leaky gut syndrome causes many other problems such as allergies, autoimmunity, malabsorption etc., which further compound the problems of CFS.
      If liver circulation is inadequate, this will result in poor detoxification, not just of heavy metals, pesticides and volatile organic compounds, but also toxins produced as a result of fermentation in the gut, again further poisoning the mitochondria.
      - Effects on the brain
      Last October I attended a conference sponsored by the late Dr. John Richardson.
      A Canadian physician - Byron Hyde - showed us some functional scans of the brains of CFS patients.
      If I had not known the diagnosis, I would have diagnosed strokes.
      This is because the blood supply to some area of the brain was so impaired.
      The default is temporary, and with rest, blood supply recovers.
      However, this explains the multiplicity of brain symptoms [that CFS patients] suffer from, such as poor short term memory, difficulty multi-tasking, slow mental processing and so on.
      Furthermore, brain cells are not particularly well stocked with mitochondria and therefore they run out of energy very quickly.
      - Effects on the heart
      There are two effects on the heart :
      - The first effect of poor micro-circulation to the heart is disturbance of the electrical conductivity which causes dysrhythmias. Many patients with Chronic Fatigue Syndrome complain of palpitations, missed heart beats or whatever. This is particularly the case in patients with poisoning by chemicals since the chemicals are also directly toxic to nerve cells.
      - The second obvious result is poor exercise tolerance. Heart muscle fatigues in just the same way that other muscles fatigue. Symptomatically this causes chest pain and fatigue. In the longer term it can cause heart valve defects because the muscles which normally hold the mitral valve open also fatigue.
      The difference between this type of heart failure and medically recognized congestive cardiac failure is that patients with CFS protect themselves from organ failure because of their fatigue symptoms.
      Patients with congestive cardiac failure initially do not get fatigue and often present with organ failures such as kidney failure or overt heart failure.
      At present I do not know why there is this difference.
      So patients with angina, high blood pressure, heart failure, cardiomyopathy, some valve defects, as well as patients with cardiac dysrhythmias, also have mitochondrial problems and will respond in the same way to nutritional therapies and detox therapies.
      This approach to treating heart disease is exactly the same, regardless of the conventional diagnosis.
      - Effects on lung and kidney
      The lung and kidney are relatively protected against poor micro-circulation because they have the largest renin angiotensin system, which keeps the blood pressure up in these vital organs.
      Therefore, clinically one does not see patients with kidney failure or pulmonary hypoperfusion in CFS.
      Explanation of the fatique problems in CFS patients
      Energy to the body is supplied by mitochondria, which produce NAD (nicotinamide adenosine diphosphate) and ATP (adenosine triphosphate).
      These molecules are the “currency” of energy in the body.
      Almost all energy requiring processes in the body have to be “paid for” with NAD and ATP, but largely ATP.
      The reserves of ATP in cells are very small.
      At any one moment in heart muscle cells there is only enough ATP to last about 10 contractions.
      Thus the mitochondria have to be extremely good at re-cycling ATP to keep the cell constantly supplied with energy.
      If the cell is not very efficient at re-cycling ATP, then the cell runs out of energy very quickly and this causes the symptoms of weakness and poor stamina.
      The cell literally has to “hibernate” and wait until more ATP has been manufactured.
      Energy is produced when ATP (three phosphates) is converted into ADP (two phosphates).
      ADP is then re-cycled back through mitochondria to create more ATP for future energy production.
      However, if the cell is pushed when there is no ATP about, then it will start to use ADP instead.
      The body can create energy from ADP to AMP (one phosphate), but the trouble is that AMP cannot be re-cycled.
      The only way that ADP can be regenerated is by making from fresh ingredients, but this takes days to do.
      This explains the delayed fatigue seen in Chronic Fatigue Syndrome.
      To summarize
      The basic pathology in CFS is slow re-cycling of ATP to ADP and back to ATP again.
      If patients push themselves and make more energy demands, then ADP is converted to AMP, which cannot be recycled, and it is this which is responsible for the delayed fatigue.
      This is because it takes the body several days to make fresh ATP from new ingredients.
      When patients overdo things and "hit a brick wall" this is because they have no ATP or ADP to function at all.


    Read aslo : Part V


    07-03-2009 om 21:37 geschreven door Jules

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    The heart of the matter - CFS & cardiac issues

    Part V

    1. Implications for treatment – The concept
      The vast majority of patients I see get well with my standard work-up with respect to vitamins and minerals, diet, pacing, sleep, B12, magnesium, detoxing etc. etc.
      All these things must be put in place to repair and prevent ongoing damage to mitochondria, so allowing them to recover.
      For mitochondria to recover they need all the essential vitamins, minerals, essential fatty acids and amino acids to manufacture the cellular machinery to restore normal function.
      However, despite doing that, I am still left with a hard core of patients whom I struggle with.
      This is where direct micronutrient support for mitochondria may prove to be an extremely useful intervention.
      I have learned what to do through reading '
      The Sinatra Solution - New Hope for Preventing and Treating Heart Disease' (3) Basic Health Publications (1 edition), March 2005 – ISBN-10 : 1591201586 / ISBN-13 : 978-1591201588 - cfr. : http://www.amazon.com/Sinatra-Solution-Preventing-Treating-Disease/dp/1591201586 - a book produced by the American metabolic cardiologist Dr. Stephen T. Sinatra, who has used these techniques for treating patients with heart disease such as congestive cardiac failure, angina, arrhythmias and so on.
      Dr. Sinatra worked initially using entirely conventional techniques - drugs, pacemakers, surgery or whatever.
      However, he realized that cardiac disease was not all about poor blood supply to the heart.
      For many, the problem was heart muscle disease due to mitochondrial failure.
      Once he tackled this aspect, patients made dramatic recoveries, were able to come off medication, avoid surgery and return to their normal jobs and sporting activities.
      To understand his ideas, you need to understand a little bit about how mitochondria work.
      - How Mitochondria Actually Work - CO-Enzyme Q10 : The electron handler
      The job of mitochondria is to get the energy contained inside foods (sugars and fats) and convert it into a form the body can use (NAD and ATP).
      This requires a series of reactions (Krebs citric acid cycle, for the chemists in the audience).
      This process is called oxidative phosphorylation - and chemically speaking needs electrons to move about from one molecule to another, changing their chemical make-up as they go.
      These reactions require enzymes, which are made up of many different vitamins, minerals, fatty acids and amino acids.
      However, one of the most important electron handlers is Co-Enzyme Q10.
      - L-carnitine : The shunter
      Once ATP has been made, it then has to be delivered to where it is needed - out of the mitochondria. This it does with a shunting reaction.
      ATP is made inside mitochondria from ADP, and has to be shunted across the mitochondrial membrane so the cell can use the energy in the ATP by converting it back to ADP.
      ADP then needs to be shunted back across the cell membrane.
      This shunting reaction involves acetyl L-carnitine, which effectively shunts energy in the form of ATP from inside mitochondria, through the mitochondrial cell membrane into the cell, where it gives up its energy and converts to ADP.
      L-carnitine then shunts ADP back through the mitochondrial membrane, where it is reformed into ATP.
      Obviously, if this shunting reaction does not run smoothly, energy supply will be impaired.
      - Magnesium : The spark-plug
      All the molecules involved here are re-cycled.
      There is another essential element, which is magnesium.
      If you think of glucose and short chain fatty acids as the fuel of the engine, acetyl L-carnitine and Co-enzyme Q10 are the oil and magnesium is the spark plug !
      - D-Ribose: Precursor to ATP
      In order to make new ATP, one needs a sugar, namely D-ribose.
      Normally the body can manufacture this for itself from glucose, but if energy levels are very low, then it may be unable to synthesize this essential sugar.
      So when the CFS sufferers push themselves too much, ADP is converted into AMP, which they cannot recycle.
      It usually takes a few days to make new ATP from D-ribose, but the CFS sufferers may be unable to make D-ribose altogether.
      - Vitamin B3

      In order to make new NAD, one needs vitamin B3.
      Implications for treatment – The details
      If the body is functioning normally and has access to all essential minerals, vitamins, essential fatty acids and amino acids, it can make all these essential ingredients, in particular co-enzyme Q 10, acetyl L-carnitine and D-ribose.
      Magnesium must be supplied.
      This explains why most patients get well on my standard work up of treatment because this supplies all the essential ingredients for the body to heal itself.
      However, for those who do not get well, it is likely that there is some sort of metabolic defect which prevents them from manufacturing these essential ingredients.
      I call this “metabolic dyslexia” !
      It may well be that genetically poor mitochondrial function alone is the problem or there may be toxins or pesticides stuck in the system which stop the mitochondria functioning properly.
      It may well be that once the patient has dropped below a certain critical level, all cellular processes are going so slow that the sufferer is unable to manufacture the very things required to restore health.
      With age, our metabolism becomes less efficient anyway and we may need more raw materials in order to maintain the status quo.
      Either way there is a cocktail of micronutrients that could be taken to kick start the system.
      This cocktail is already of tried and tested value.
      It has been used in America by many metabolic cardiologists to treat cardiomyopathy, ischemic heart disease, dysrhythmia, congestive cardiac failure, high blood pressure and angina with great success.
      Not only have patients felt better, but they have come off all their medication and avoided life threatening interventions such as cardiac transplants, arterial surgery, pacemakers and so on.
      Dr. Sinatra has developed several schemes for age management, high blood pressure, arrhythmia, mitral valve prolapse, congestive cardiac failure, syndrome X, for professional and world class athletes, but also for Fibromyalgia, Chronic Fatigue Syndrome and mitochondrial cytopathies.
      Dr. Sinatra recommends the following daily cocktail for CFS (cfr. 'The Sinatra Solution - Metabolic Cardiology. (4)] :
      - Co-enzyme Q 10
      300 - 360 mg (the oil of the engine, this moves electrons from one molecule to another)
      - L-carnitine

      2,000 - 3,000 mg (the oil of the engine, this moves ATP and ADP across mitochondria membranes)
      - D-ribose
      15 grams (the raw material to make new ATP)
      - Magnesium
      400 – 800 mg (the spark plugs, this fires up many enzyme reactions).
      To this I would also add niacinamide 500 mgs daily (the raw material to make NAD).
      I would expect this cocktail of supplements to work best taken together, not as individual supplements.
      I have tried a number of my patients on this cocktail of supplements and have already had some very encouraging feedback.
      Incidentally this helps explain why some CFS sufferers have such problems with drug medication and indeed this may help to point toward treatment.
      All my CFS patients feel much worse on statins because these stop the body from making its own Co Q 10.
      Beta blockers, tricyclic antidepressants and phenothiazines also block Co Q 10 synthesis.
      Practical details

      There is no point taking this cocktail until you have done my standard work up [tests] to treating CFS.
      This is because normally the body is perfectly capable of making its own Coenzyme Q 10 and its own D-ribose so long as it has all the vitamins, minerals, EFAs [essential fatty acids] and amino acids to do so.
      Vitamin B3 and magnesium come from supplements and acetyl L-carnitine from red meat (and mutton specifically is much higher in L-carnitine than any other red meat).
      The supplements in the Sinatra protocol are expensive, so for those who would like to try it I suggest the following : [Note that patients in England and Wales may contact Dr. Myhill’s office to order kits for these tests, which they may receive by mail and provide to their personal healthcare professionals. Contact information and details on sourcing of supplements for patients in the UK are available on the Dr. Myhill website :
      http://www.drmyhill.co.uk/ -]
      - measure levels of Co Q 10 to show there is a deficiency
      - measure NAD levels
      - measure red cell magnesium.
      Treating a deficiency
      - Co-enzyme Q 10
      This must be in a hydrosoluble or oil form or it is not well absorbed.
      Co Q 10 is fairly widely available.
      - Acetyl L-carnitine

      This is an amino acid with highest levels in meat (the word carnitine comes from “
      carne” meaning 'meat').
      This may explain why vegetarians are at risk of CFS.
      It also partly explains why my CFS patients do best on high protein diets.
      Eat red meat daily for acetyl L-carnitine : the best source is mutton.
      Vegetarians will have to take the supplement.
      If you have poor digestion then you may need to supplement with L-carnitine anyway.
      - D-ribose

      Needs to be taken throughout the day.
      - Niacinamide 500 mgs.
      - Magnesium
      Magnesiumt is a
      mineral supplement, but if there is a severe deficiency, then magnesium by injection may be required.
      How long before you see improvement ?

      Not sure at the moment.
      Heart transplant patients whose cardiac output is improved overnight can take up to a year before they start to feel fully well again.
      However, I would expect sufferers to see improvements after a few weeks of supplements.
      What is important is that these interventions be done in combination with all my other recommendations with respect to diet, micronutrients, pacing, sleep, detoxing etc.
      First get the regime tight, then start to feel better and then start to increase activity.
      Cfr. :
      http://www.prohealth.com/me-cfs/library/showarticle.cfm?id=7495&t=CFIDS_FM

    2. Chronic fatigue is not all in the mind
      Rowan Hooper - New Scientist magazine, issue 2509 of, 21 July 2005, page 9 – Source : Journal of Clinical Pathology (vol 58, p 823, 860)
      At lang last, we are beginning to get to grips with chronic fatigue syndrome.
      Differences in gene expression have been found in the immune cells of people with the disease, a discovery that could lead to a blood test for the disorder and perhaps even to drugs for treating it.
      The symptoms of chronic fatigue syndrome have been compared to those of a really bad hangover : extreme weakness, inability to think straight, disrupted sleep and headache.
      But unlike a hangover, the symptoms linger for years, devastating people's lives.
      While nobody doubts CFS exists, just about every aspect of it is controversial.
      Some say it is the same as myalgic encephalomyelitis (ME), others disagree.
      Many specialists are convinced it does have a biological basis, but pinning down physical abnormalities common to all patients has proved tough.
      People with CFS have often received little sympathy from doctors who dismiss it as "
      all in the mind
      ".
      The study shows some aspects of chronic fatigue syndrome may be understood in molecular terms. It is not a 'made-up' illness

      Now Jonathan Kerr's team, which is moving to St George's University of London, has compared levels of gene expression in the white blood cells of 25 healthy individuals with those in 25 patients diagnosed as having CFS according to strict criteria.
      The researchers found differences in 35 of the 9522 genes they analysed using DNA chip technology.
      The few similar studies done in the past have produced conflicting results, so the team double-checked their results using a more accurate method called real-time PCR.
      That confirmed that 15 of the genes were up to four times as active in people with CFS, while one gene was less active.
      The results will appear in the Journal of Clinical Pathology next month.
      Kerr is repeating the study in 1000 CFS patients and healthy controls, this time looking at 47,000 gene products.
      So far, the larger study backs up the earlier results
      ,” he told New Scientist.
      If Kerr really has succeeded where many have failed and identified clear physical changes in people with CFS, the lingering opinion that it is "
      all in the mind
      " could finally be laid to rest.
      "
      This exciting new work shows that some aspects of this complex illness may be understandable in molecular terms and that CFS is not a 'made up' illness
      ," says Russell Lane, a neurologist at Charing Cross Hospital in London.
      It should also be possible to develop a blood test for CFS
      .
      The team has already discovered differences in blood proteins related to the changes in gene expression.
      Kerr hopes the work might even lead to treatments.
      "
      We have shown that a significant part of the pathogenesis resides in the white blood cells and in their activity," he says : "It will open the door to development of pharmacological interventions.
      "
      Several of the genes identified by the team in CFS play important roles in mitochondria, the power factories of our cells.
      "
      The involvement of such genes does seem to fit with the fact that these patients lack energy and suffer from fatigue
      ," Kerr says.
      One of these gene products, EIF4G1, is involved in protein production in mitochondria.
      It is hijacked by some viruses, so cells may compensate by ramping up gene expression.
      "
      I am excited by the paper," says Basant Puri, a CFS expert at Hammersmith Hospital in London : "The group's finding of upregulation of EIF4G1 is consistent with subclinical persistent viral infection.
      "
      This fits in with the idea that CFS is sometimes triggered by viruses such as Epstein-Barr, Q fever, enteroviruses and parvovirus B19.
      "
      CFS often begins with a flu-like illness which never goes away
      ," Kerr says.
      Of the other genes whose expression varies in CFS patients, some are involved in regulating the activity of the immune system.
      Others play important roles in nerve cells, including a gene called '
      NTE
      ' which codes for an enzyme affected by organophosphates and nerve gases.
      Cfr. : http://www.newscientist.com/channel/health/mg18725093.700

    3. Chronic heart failure and the immune system
      Mari D, Di Berardino F, Cugno M, Department of Internal Medicine, University of Milan, Maggiore Hospital IRCCS, Via Pace 15, 20122 Milan, Italy : daniela.mari@unimi.it - Clin Rev Allergy Immunol. 2002 Dec;23(3):325-40 - PMID: 12402415
      Several lines of evidence support a role of immune mechanisms in the pathogenesis of chronic heart failure (CHF).
      Proinflammatory cytokines (interleukin-1, -2, -6, and tumor necrosis factor) and chemokines are involved in cardiac depression and in the progression of heart failure.
      Other components believed to be relevant to the pathogenesis of CHF are adhesion molecules, autoantibodies, nitric oxide (NO) and endothelin-1.
      The origin of the immune activation in patients with CHF is still unknown, however two hypotheses have been proposed on the basis of experimental and clinical data.
      One suggests that the bowel wall edema leads to bacterial translocation with subsequent endotoxin release and immune activation.
      The second suggests that the heart in CHF is the main source of cytokines, as is shown by the fact that TNF alpha is produced by the failing myocardium but not by a normal one.
      No single source of cytokine production (gut or heart) seems sufficient to fully explain the multiple organ involvement and the systemic inflammation of CHF, which is probably related to systemic hypoxia, a potent stimulus for activation of the immune system and for cytokine production.
      The effort of define the immune system's role has opened new perspectives of therapeutic strategies, such as anti-cytokine drugs, to treat CHF.
      Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12402415?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Disco
      veryPanel.Pubmed_Discovery_RA

    4. Diastolic Heart Failure - A Common and Lethal Condition by Any Name
      Gerard P. Aurigemma - N Engl J Med. 2006 Jul 20;355(3):308-10 - PMID: 16855273
      Cfr. : http://www.cfids-cab.org/MESA/Aurigemma.pdf

    5. Diminished Cardiopulmonary Capacity During Post-Exertional Malaise
      VanNess JM, Snell CR, Stevens SR - Journal of Chronic Fatigue Syndrome, Vol. 14, No. 2, 2007, pp. 77-85
      Cfr. : http://www.prohealth.com/library/showarticle.cfm?id=8661&t=CFIDS_FM

    6. Fibromyalgia and costochondritis
      Adrienne Dellwo, About.com 'Chest & Ribcage Pain', October 9, 2008 – Source : Flowers, LK. "Costochondritis"10 eMedicine. Aug 9, 2007 - ©2009 About.com, Inc., a part of The New York Times Company
      Fibromyalgia and costochondritis frequently go together, but a lot of people with costochondritis don't realize it's actually a separate condition that requires its own treatment.
      Because any other sources of pain can make your fibromyalgia1 (FMS) symptoms worse, it's important for you to treat costochondritis.
      Costochondritis causes chest and ribcage pain that
      can make you think you're having cardiac problems
      .
      This pain is actually what signaled the beginning of my fibromyalgia pain, after non-pain symptoms had crept up for months.
      I was sitting calmly at work when I suddenly thought I was having a heart attack.
      I ended up in the emergency room and that's when I began the long series of negative tests that eventually led to my FMS diagnosis. (2)
      If you have fibromyalgia and get chest pains, don't assume it's costochondritis.
      You should always get immediate treatment for chest pain in case it's heart-related.
      What is Costochondritis ?

      Costochondritis is an inflammation of the cartilage that connects your ribs to your breast bone.
      Depending on how much inflammation there is, it can range from a mild annoyance to extremely painful.
      The causes of costochondritis aren't clear, but may include :
      - chest trauma, such as from a car accident
      - repetitive trama or overuse
      - viral infections, especially upper respiratory infections.
      Some experts believe FMS may actually be a cause as well.
      Regardless of the cause, fibromyalgia generally makes costochondritis much more painful.
      People with costochondritis describe the pain as stabbing, aching or burning.
      Why Do Fibromyalgia & Costochondritis Go Together ?
      Estimates are that 60% to 70% of us with FMS have symptoms very similar to costochondritis.
      No one is exactly sure whether it is costochondritis or why it occurs with FMS, especially since FMS doesn't cause inflammation.
      The fibromyalgia tender points3 just beneath the collar bone may play a role.
      Myofascial pain syndrome4, which is common in people with fibromyalgia, also could be a cause.
      Costochondritis is typically a minor injury that heals within days.
      If costochondritis symptoms don't clear up, they could be a sign that something else, such as fibromyalgia, is going on.
      Symptoms of Costochondritis
      Pain in the chest wall and ribcage is the chief symptom of costochondritis.
      Generally, it will get worse with activity or exercise.
      Taking a deep breath can also cause more pain, because it stretches the inflamed cartilage.
      Sneezing and coughing can increase pain as well.
      Costochondritis pain can also radiate to your shoulder and arms as well, transferred there by the many nerves that branch away from the chest (this is another way in which the condition mimics a heart attack).
      Sometimes, costochondritis pain is accompanied by redness and/or swelling in the most painful areas.
      This is when it's called Tietze's Syndrome (when my chest pain is bad, I get a lump on my breast bone that looks like half a golf ball).
      Diagnosing Costochondritis
      Your doctor can diagnose costochondritis by pressing on the area where the ribs and breast bone come together.
      If it's tender and sore there, costochondritis is the most likely cause of pain.
      Doctors generally will perform other test to rule out heart problems and other causes of pain before diagnosing costochondritis.
      Costochondritis Treatment vs. Fibromyalgia Treatment
      You can treat costochondritis the way you'd treat any inflammation -- ice and anti-inflammatory drugs, including Aleve (naproxen) (5) and ibuprofen-based drugs such as Advil (6) and Motrin (7).
      This treatment runs counter to most FMS treatments (8), which generally include other types of pain relievers and heat.
      If you have both, you might find yourself with an ice pack on your chest and a heating pad on your back at the same time.
      Be sure to check with your doctor or pharmacist about any possible interactions between anti-inflammatories and your other medications.
      Living With Costochondritis & Fibromyalgia
      It's bad enough to live with one source of chronic pain.
      The more you heap on, the more pain you'll have and the more it can impact your life.
      Fortunately, costochondritis is fairly easy and inexpensive to treat, and managing it will keep it from exacerbating your fibromyalgia symptoms. (9)
      Cfr. :
      http://chronicfatigue.about.com/od/whyfmscfsarelinked/a/costochondritis.htm

    7. Fibromyalgia and Low Thyroid Function
      Amazines.com, 09/23/2008
      Over 20 million Americans suffer from thyroid dysfunction.
      And over 500,000 new cases of thyroid disease occur each year.
      However, as staggering as those numbers appear, millions more go undiagnosed.
      It’s estimated that more than 10 million women have a low-grade thyroid dysfunction, which isn’t treated.
      And almost another 8 million people with low thyroid go undiagnosed.
      Like my patient Allison, many individuals with low or hypothyroid simply fall through the cracks.
      Allison K. I really felt terrible most of the time.
      I had no energy at all. I’d gained 40 pounds over the last year even though I ate very little and tried to follow my Weight Watcher’s program.
      I kept cutting my calorie intake and even started skipping meals in an attempt to lose weight.
      The less I ate the worse I felt.
      I had numerous sinus infections, which I had never had before.
      My hair was falling out, I had tingling pain in my hands and feet and always felt cold even in the summer.
      I had this constant ringing in my ears.
      I was depressed or anxious a good deal of the time.
      Every doctor I consulted said that my blood tests were normal and it must be my fibromyalgia that was causing me to feel so bad.
      I knew something was wrong with me, but I couldn’t find anyone who could help me.
      One doctor said I had all the symptoms of low thyroid.
      But, the endocrinologist she referred me to, said all my tests were normal.
      How could my thyroid be normal when I have all the symptoms of hypothyroid ?
      Allison’s story is a typical one.
      I routinely have new fibromyalgia and CFS patient’s who present with all the symptoms of hypothyroid including fatigue, headaches, dry skin, swelling, weight gain, cold hands and feet, poor memory, hair loss, hoarseness, nervousness, depression, dry skin, constipation, joint and muscle pain and burning or tingling sensations in the hands or feet.
      The symptoms associated with hypothyroid are after all very similar to those of fibromyalgia and CFS.
      And in fact, up to 63% of patient’s with fibromyalgia and CFS have been shown to have hypothyroid.
      I estimate that as many as 40% of my FMS and CFS patients are suffering from low or hypothyroid function.
      Your Thyroid Gland
      The thyroid gland is shaped like a butterfly and is located in the lower front part of your neck (just above the breastbone).
      The thyroid gland is responsible for secreting thyroid hormones.
      A hormone is a chemical substance formed in the body and carried in the bloodstream to affect another part of the body.
      Thyroid hormones travel through the bloodstream and help cells convert oxygen and calories to energy.
      Thyroid hormones control a person’s metabolism.
      Metabolism is defined as the sum of all physical and chemical changes that take place within the body; it’s all the energy and material transformation that occur within living cells.
      Every cell in the body depends on having enough thyroid hormone.
      If your thyroid gland becomes dysfunctional, every cell in the body suffers.
      This is why thyroid disorders can cause so many problems.
      When your thyroid gland produces too much thyroid hormone, this is known as hyperthyroid.
      When your thyroid doesn’t produce enough thyroid hormone, it's called 'hypothyroid'.
      As you can see below, hypothyroid can cause many of the symptoms of FMS/CFS.
      Symptoms Associated with Hypothyroid
      - fatigue (the most profound symptom)
      - headache
      - dry skin
      - swelling
      - weight gain
      - cold hands and feet
      - poor memory
      - hair loss
      - hoarseness
      - nervousness
      - depression
      - joint and muscle pai
      - burning or tingling sensations in the hands and/or feet (hypothyroid neuropathy)
      - yellowing of skin from a build up of carotene (conversion of carotene to vitamin A is slowed by hypothyroidism)
      - carpal tunnel syndrome • problems with balance and equilibrium (unsteadiness or lack of coordination)
      - constipation (from slowed metabolism)
      - edema around the ankles, below the eyes and elsewhere
      - observation of delayed Achilles tendon reflex test
      - hypertension (high blood pressure)
      - angina (chest pain)
      - atherosclerosis (hardening of the arteries)
      - hypercholesterolemia (high cholesterol)
      - menstrual irregularities
      - infertility
      - PMS
      - fibrocystic breast disease
      - polycystic ovary syndrome
      - reactive hypoglycemia
      - psoariasis
      - urticaria
      - allergic rhinitis.
      Understanding Thyroid Hormones, T3, T4 and TSH
      The hypothalamus stimulates the pituitary gland to produce thyroid-stimulating hormone (TSH).
      TSH then stimulates the thyroid gland to produce and release the hormone, thyroxine (T4).
      T4 hormone is then converted into the more active, triiodothyronine (T3).
      T3 hormone is essential for life and four times more active than T4.
      You can live without T4 but not without T3.
      A thyroid gland that functions normally produces T4 and T3.
      Twenty percent of the T3 circulating in the body comes directly from the thyroid gland and the remaining 80 percent comes from conversion of T4. This conversion of T4 to T3 takes place in the cells (T4 can also be converted into reverse T3, which is physiologically inactive).
      The enzyme 5-deiodinase converts T4 into T3 and reverse T3. The 5-deiodinase enzyme, can be inhibited by prolonged stress, steroids (stress hormones or cortisol), poor nutrition, acute and chronic illnesses. If T4 doesn’t convert into active T3, symptoms of low thyroid start to show up.
      This can happen in spite of a normal TSH blood test reading.
      Chronic Stress Leads to Low Thyroid
      The symptoms of low thyroid tend to come on or become worse after a major stressful event.
      Childbirth, divorce, death of a loved one, job or family stress, chronic illness, surgery, trauma, excessive dieting and other stressful events can all lead to hypothyroidism.
      Under significant physical, mental, or emotional stress the body slows down the metabolism by decreasing the amount of raw material (T4) that is converted to the active thyroid hormone (T3).
      This is done to conserve energy.
      However, when the stress is over, the metabolism is supposed to speed up and return to normal.
      This process can become derailed by a buildup of reverse T3 (rT3) hormone.
      Reverse T3 can build to such high levels that it begins to start using up the enzyme that converts T4 to T3.
      The more stress the more likely rT3 can block T4 from converting into T3.


    Read also : Part VI


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    The heart of the matter - CFS & cardiac issues


    Part VI


    Blood Test may be Inaccurate
    Blood tests for thyroid function measure the amount of TSH, T4 and T3 in the bloodstream.
    But thyroid hormones don’t operate within the bloodstream; the action takes place in the cells themselves.
    What good is a blood test that only shows what is racing around the bloodstream one second out of one minute, out of one hour, out of a one day ?
    Blood tests are measuring how much thyroid hormone is swimming around in the blood stream, but not what is in the cell.
    Blood tests are an educated guess based on the bell curve theory.
    Sixty percent of patients will have thyroid levels between the usual testing parameters, twenty percent will be above and twenty percent will fall below these parameters.
    Traditional medical professionals know that thyroid blood tests are less than perfect.
    The Journal of Clinical Psychiatry has reported that “laboratory blood tests for thyroid may be inaccurate for many who get tested for hypothyroid disorder”.
    Compounding the problem of using standard blood tests to diagnose hypothyroid is the inability of doctors to agree on the laboratory parameters.
    According to the American Association of Clinical Endocrinologists (AACE) guidelines, doctors have typically been basing their diagnoses on the "normal" range for the TSH test.
    The typical normal TSH levels at most laboratories, has fallen between the 0.5 to 5.0 range.
    Those with a TSH below 5 are considered to have too much thyroid hormone (hyperthyroid).
    Those whose test results are above 5 are considered to have too little thyroid (hypothyroid).
    However, it’s not uncommon to find doctors including endocrinologists (thyroid specialist) who withhold the diagnoses and treatment of hypothyroid until a patient's TSH tests considerably above 10.
    While some doctors believe that anyone who has a TSH above 2 and complains of hypothyroid symptoms (depression, fatigue, brain fog etc.) should be placed on thyroid hormone.
    While doctors often debate which parameters or numbers are correct, millions of low thyroid patients are not properly diagnosed and treated.
    Patients often relate that they and sometimes their doctors, suspected a thyroid problem only to have their blood work return normal.
    Most physicians, in this case, won’t recommend thyroid replacement therapy.
    Doctors are typically reluctant to prescribe thyroid replacement therapy, without a definitive test that reveals true hypothyroid.
    They’re afraid that doing so would jeopardize the health of the patient.
    And true, excess thyroid can cause several unwanted health problems including elevated heart rate, rapid pulse and accelerated bone loss.
    However, millions suffer with symptoms far worse then these when prescription therapy is withheld.
    Certainly the dangers of thyroid replacement therapy should be a concern.
    But if you weight the pro’s and con’s of administering thyroid replacement therapy to a patient with normal blood tests, yet all the symptoms of hypothyroid, fatigue, anxiety, depression, achy diffuse pain, weight gain etc., its’ easy to see that withholding therapy should be considered malpractice.
    This is especially true in light of the fact that most of my fibromyalgia and CFS patients are taking numerous drugs to cover-up the symptoms of hypothyroid; Provigil or Aderall to increase energy, antibiotics for chronic sinus infections, a laxative for constipation, NSAIDs for pain, SSRI medication for depression and perhaps a benzodiazepine like Ativan or Xanax for anxiety.
    All of these drugs may in turn cause side effects that may cause further symptoms (poor sleep, fatigue, depression etc.).
    It’s not uncommon for my patient’s to be able to drastically reduce or eventually wean off these very medications once their thyroid disorder is corrected.
    New Developments
    To complicate matters, the parameters for determining who has a thyroid disorder and who doesn’t has recently been changed.
    The new guidelines narrow the range for acceptable thyroid function; the AACE is now encouraging doctors to consider thyroid treatment for patients who test the target TSH level of 0.3 to 3.04, a far narrower range.
    The AACE believes the new range will result in proper diagnosis for millions of Americans who suffer from a mild thyroid disorder but have gone untreated until now.
    At a press conference in 2004, Hossein Gharib, MD, FACE and president of AACE, said : "This means that there are more people with minor thyroid abnormalities than previously perceived."
    I still routinely get test results that use the old numbers and unfortunately many doctors continue to misdiagnose their patient’s based on these outdated lab parameters.
    The AACE estimates that the new guidelines actually double the number of people who have abnormal thyroid function, bringing the total to as many as 27 million, up from 13 million thought to have the condition under the old guidelines.
    Euthyroid Syndrome Euthyroid is a medical term for patients who have normal thyroid blood tests but have all the symptoms associated with hypothyroidism: fatigue, low metabolism, headache, etc. Many doctors don’t know about (or they choose to ignore) well documented studies that show that low body temperature is indicative of euthyroid hypothyroidism.
    Body Temperature, Metabolism and Thyroid Hormones
    Self-test for Low Thyroid Dr. Broda Barnes was the first to show that a low basal body temperature was associated with low thyroid.
    His first study was published in 1942 and appeared in JAMA.
    This study tracked 1,000 college students and showed that monitoring body temperature for thyroid function was a valid if not superior approach to other thyroid tests.
    The test for low thyroid function, according to Dr. Barnes’s protocol, starts first thing in the morning.
    While still in bed, shake down and place the thermometer (preferably mercury; digital thermometers are not as accurate) under your arm and leave it there for 10 minutes.
    Record your temperature in a daily log.
    Women who are still having menstrual cycles should take their temperature after the third day of their period.
    Menopausal women can take their temperature on any day.
    A reading below the normal 97.8° strongly suggests hypothyroid.
    A reading above 98.2° may indicate hyperthyroidism (overactive thyroid).
    Treatment for Hypothyroid - The Barnes Method
    Dr. Barnes recommends patients take a desiccated glandular (derived from pigs) prescription medication known as Armour Thyroid, which was used before synthetic medications such as Synthroid were introduced.
    Armour Thyroid and other prescription thyroid glandulars (including Westhroid), contain both T4 and T3.
    Synthroid and other synthetic thyroid medications contain T4 only.
    Since some individuals have a difficult time converting inactive T4 to active T3, these medications may not work at the cellular level.
    Individuals may take T4 medications for years and never notice much improvement.
    Their blood tests look good, but mean time they’re falling apart; gaining weight, having more aches and pains, battling one sinus infection after another and becoming more and more fatigued, depressed and withdrawn.
    Low Thyroid and Depression
    Several studies demonstrate that a combination of T4, T3 or T3 therapy alone may provide welcomed relief from a number of symptoms commonly associated with depression.
    Studies show that T3 therapy is more effective in reducing the symptoms associated with depression than SSRI antidepressants.
    Over All Well Being
    A study by the New England Journal of Medicine showed that patients who received a combination of T4 and T3 were mentally sharper, less depressed and feeling better overall than a control group who received T4 only.
    The addition of T3 often helps with many symptoms of hypothyroidism that may not disappear with supplemental T4 only.
    It has improved or eliminated depression, brain fog, feeling cold, constipation, chronic fatigue, headaches, insomnia, muscle and joint pain and chronic sinus infections.
    Weight Loss
    For some people it has helped them finally lose weight.
    Fibromyalgia
    One study showed that all the symptoms associated with FMS could be eliminated while the patient was taking high-doses (120 mcg.) of T3. (6)
    Over the Counter Glandular Thyroid Supplements
    Since I no longer employ medical doctors in my practice I have to rely on natural supplements instead of prescription medications.
    I used to refer my patient’s back to their medical doctor in an attempt to get them on prescription.
    Armour thyroid medication
    I prefer my patients take Armour thyroid.
    However, most doctors are so reluctant to treat patient’s with normal thyroid blood tests or to use Armour thyroid medication, that I’ve been forced to use over the counter thyroid glandular replacement therapy.
    Fortunately I’ve found a reliable manufacturer of high quality thyroid glandular and I’m getting great results with my hypothyroid patient’s.
    Thyroid bovine glandular supplements have been used since the beginning of thyroid treatment.
    Dr. Barnes used Armour Thyroid (available by prescription).
    However, over-the-counter thyroid glandular supplementations are also available.
    The over the counter thyroid glandulars come from pig glands just as the prescription drug Armour thyroid.
    However, unlike Armour Thyroid, over the counter thyroid glandulars contain no T4, only T3.
    By removing the T4 manufacturers can then legally sell the glandular extract with out a prescription.
    Since these raw thyroid tissue concentrates contain the active thyroid hormone T3, they can be used as a first line of treatment for low to moderate hypothyroid dysfunction.
    I’ve been using thyroid glandular supplements for almost 2 years.
    My patient’s report they feel better on these supplements.
    They often notice improved energy, better moods, increased mental clarity and weight loss on these thyroid glandular replacement supplements.
    If you have fibromyalgia I encourage you to check for low body temperature it could a sign you're suffering from undiagnosed hypothyroid.
    About Dr. Murphree
    Dr. Murphree is a board certified nutritional specialist and chiropractic physician who has been in private practice since 1990.
    He is the founder and past clinic director for a large integrated medical practice located on the campus of Brookwood Hospital in Birmingham Alabama.
    The clinic was staffed with medical doctors, chiropractors, acupuncturists, nutritionists and massage therapists.
    The clinic combined prescription and natural medicines for acute and chronic illnesses.
    He is the author of 5 books for patients and doctors, including /
    - Treating and Beating Fibromyalgia and Chronic Fatigue Syndrome - The Definitive Guide For Patients and Physicians
    - Rodger H. Murphree - Harrison & Hampton Publishing (2 edition), March 2004 – ISBN-10 : 0972893806 / ISBN-13 : 978-0972893800 - cfr. : http://www.amazon.com/Treating-Beating-Fibromyalgia-Chronic-Syndrome/dp/0972893806
    -
    Heart Disease - What Your Doctor Won't Tell You - Rodger H., II, Dr. Murphree - Harrison & Hampton Publishing (2 edition), October 2008 – ISBN-10 : 0972893830 / ISBN-13 : 978-0972893831 - cfr. : http://www.amazon.com/Heart-Disease-What-Your-Doctor/dp/0972893830/ref=sr_1_1?ie=UTF8&s=books&qid=1236451139&sr=1-1
    - Treating and Beating Anxiety and Depression with Orthomolecular Medicine -
    cfr. :
    http://www.amazon.com/Treating-Beating-Anxiety-Depression-Orthomolecular/dp/0972893814/ref=sr_1_1?ie=UTF8&s=books&qid=1236451349&sr=1-1 -.
    In 2002 Dr. Murphree sold his medical practice and now maintains a busy solo practice specializing in fibromyalgia, chronic fatigue syndrome, heart disease, mood disorders and other chronic illnesses.
    For more information about Dr. Muphree and fibromyalgia go to :
    http://www.treatingandbeating.com/index.html -.
    Cfr. :
    https://www.amazines.com/article_detail.cfm/620973?articleid=620973

    1. Hawthorn extract for treating chronic heart failure - Meta-analysis of randomized trials
      Pittler MH, Schmidt K, Ernst E, Complementary Medicine, Peninsula Medical School, Universities of Exeter and Plymouth, 25 Victoria Park Road, Exeter EX2 4NT, United Kingdom : M.H.Pittler@exeter.ac.uk - Am J Med. 2003 Jun 1;114(8):665-74 - PMID: 12798455

      The aim of this meta-analysis was to assess the evidence from rigorous clinical trials of the use of hawthorn extract to treat patients with chronic heart failure.
      We searched the literature using MEDLINE, EMBASE, the Cochrane Library, CINAHL, CISCOM and AMED.
      Experts on and manufacturers of commercial preparations containing hawthorn extract were asked to contribute published and unpublished studies.
      There were no restrictions about the language of publication.
      Two reviewers independently performed the screening of studies, selection, validation, data extraction and the assessment of methodological quality.
      To be included, studies were required to state that they were randomized, double-blind and placebo controlled and used hawthorn extract monopreparations.
      Thirteen trials met all inclusion criteria. In most of the studies, hawthorn was used as an adjunct to conventional treatment.
      Eight trials including 632 patients with chronic heart failure (New York Heart Association classes I to III) provided data that were suitable for meta-analysis.
      For the physiologic outcome of maximal workload, treatment with hawthorn extract was more beneficial than placebo (weighted mean difference, 7 Watt; 95% confidence interval [CI] : 3 to 11 Watt; P < 0.01; n = 310 patients).
      The pressure-heart rate product also showed a beneficial decrease (weighted mean difference, -20; 95% CI : -32 to -8; n = 264 patients) with hawthorn treatment.
      Symptoms such as dyspnea and fatigue improved significantly with hawthorn treatment as compared with placebo.
      Reported adverse events were infrequent, mild and transient; they included nausea, dizziness and cardiac and gastrointestinal complaints.
      In conclusion, these results suggest that there is a significant benefit from hawthorn extract as an adjunctive treatment for chronic heart failure.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/12798455

    2. IgM serum antibodies to Epstein-Barr virus are uniquely present in a subset of patients with the chronic fatigue syndrome
      Lerner AM, Beqaj SH, Deeter RG, Fitzgerald JT, Department of Medicine, William Beaumont Hospital and Wayne State University School of Medicine, Royal Oak, Michigan, USA : lerner@cdimed.com - In Vivo. 2004 Mar-Apr;18(2):101-6 - PMID: 15113035
      Background - A unique subset of patients with chronic fatigue syndrome (CFS) and IgM serum antibodies to cytomegalovirus (HCMV) non-structural gene products p52 and CM2 (UL 44 and UL 57) has been described.
      Patients and methods - Fifty-eight CFS patients and 68 non-CFS matched controls were studied.
      Serum antibodies to EBV viral capsid antigen (VCA) IgM and EBV Early Antigen, diffuse (EA, D) as well HVCMV(V), IgM and IgG; VP (sucrose, density purified V); p52 and CM2 IgM serum antibodies were assayed.
      Results - Mean age of CFS patients was 44 years (75% women).
      Control patients were 9 years older (73% women).
      Serum EBV VCA IgM positive antibody titers were identified in 33 CFS patients (Group A subset EBV VCA IgM 62.3+/-8.3, neg. <20), but were not present in other CFS patients, (Group B subset EBV VCA IgM 6.8+/-0.7) controls (p<0.0001).
      EBV VCA IgM titers remained positive in CFS patients from Group A for 24-42 months.
      Conclusion - Serum antibody to EBV VCA IgM may be a specific diagnostic test for a second subset of CFS patients.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15113035

    3. IgM serum antibodies to human cytomegalovirus nonstructural gene products p52 and CM2(UL44 and UL57) are uniquely present in a subset of patients with chronic fatigue syndrome
      Lerner AM, Beqaj SH, Deeter RG, Fitzgerald JT, Department of Medicine, William Beaumont Hospital, Wayne State University School of Medicine, Royal Oak, Michigan, USA : lerner@cdimed.com - In Vivo. 2002 May-Jun;16(3):153-9 - PMID: 12182109
      Human cytomegalovirus (HCMV) IgM serum antibodies to two nonstructural gene products UL44 and UL57 (p52 and CM2) were assayed in patients with the diagnosis of the chronic fatigue syndrome (CFS) according to criteria established by the US Centers for Disease Control and Prevention.
      A subset of 16 CFS patients demonstrated HCMV IgG, but no HCMV IgM serum antibodies to conformational structural HCMV antigens (designated, V).
      By convention, these findings are interpreted to indicate only a remote HCMV infection.
      However, HCMV IgM p52 and CM2 antibodies were uniquely present in these 16 CFS patients.
      Other CFS patients with similar HCMV (V) IgG antibodies (18 patients), non-fatigued HCMV (V) IgG-positive control patients (18 patients), random HCMV (V) IgG-positive control patients from a clinical laboratory (26 patients) and non-fatigued HCMV (V) IgG-negative control patients (15 patients) did not have HCMV, IgM p52 or CM2 serum antibodies (p < 0.05).
      Control HCMV (V) IgG-positive patients had no serum IgM HCMV (V) antibodies to conventional structural HCMV (V) antigen.
      Thus, 77 various control patients did not contain IgM p52 or CM2 serum antibodies.
      The presence of IgM p52 and/or CM2 HCMV serum antibodies in this subset of CSF-specific patients may detect incomplete HCMV multiplication in which a part of the HCMV protein-coding content of the HCMV genome is processed, but remains unassembled.
      These findings suggest that the presence of HCMV IgM p52 and CM2 serum antibodies may be a specific diagnostic test for the diagnosis of a subset of CFS patients.
      Further, these data suggest an etiologic relationship for HCMV infection in this group of CFS patients.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/12182109

    4. Left Ventricular Function in Chronic Fatigue Syndrome (CFS): Data From Nuclear Ventriculography Studies of Response to Exercise and Postural Stress - Information on the study
      Arnold Peckerman, Rahul Chemitiganti, Caixia Zhao, Kristina Dahl, Benjamin H. Natelson, Lionel Zuckier, Nasrin Ghesani, Samuel Wang, Karen Quigley and S. Sultan Ahmed – Presentation at the American Physiological Society conference, Experimental Biology, April 11–15, 2003. San Diego Convention Center, San Diego, CA.
      This study found that the heart failed to pump enough blood following exertion and upright posture in the CFS patients that were studied.
      Although abnormalities to autonomic function, plasma volume and circulation are being increasingly observed in people with ME/CFS, a new study — presented at the conference of the American Physiological Society (Experimental Biology) April, 2003 in San Diego, California — reports reduced cardiac function in some patients.
      Arnold Peckerman and colleagues at University of Medicine and Dentistry of New Jersey, Newark, NJ and the VA Medical Center, East Orange, NJ, studied 16 CDC-1994 defined patients and 4 matched control subjects.
      The radioisotopic multiple gated acquisition (MUGA) blood pool method of ventriculography was used to perform a series of dynamic studies of the heart to assess myocardial function, including resting ejection fraction (EF).
      Subjects were studied under maximal exercise and an “active postural change” since some patients report worsening of symptoms during standing.
      Overall, during maximal exercise, EF declined in CFS patients but increased in controls and decreases in EF tended to be greater in patients with more severe symptoms.
      The authors conclude that these results represent preliminary indications of “reduced cardiac function in some patients with CFS” and that “further studies capable of defining more precisely the causes of altered cardiac stress responses are required”.
      Cfr. :
      http://www.meresearch.org.uk/archive/lvfunction.html

    5. Method for Diagnosing and alleviating the symptoms of chronic fatigue syndrome - Patent
      U.S. Patent issued to A. Martin Lerner on June 4, 2002 - Appl. No. : 971291 – Filed : October 3, 2001 - Current U.S. Class : 514/263.38; 514/49 - Intern'l Class : A61K 031/505; A61K 031/70 - Field of Search : 514/258,259,260,49
      A method for alleviating chronic fatigue syndrome with the administration of antiviral agents.
      Based on clinical tests, chronic fatigue syndrome is a persistent herpes virus infection including incomplete virus multiplication and thus administration of antiviral agents are shown to alleviate the symptoms associated with the disorder.
      Based on therapeutic trials, patients receiving the recommended antiviral treatment, have experienced significant reduction or elimination of the symptoms associated with chronic fatigue syndrome.
      A method of diagnosis of the chronic fatigue syndrome is further disclosed.
      Cfr. :
      http://www.cfids-cab.org/MESA/Lerner%20Patent%20Oct%202001.pdf

    6. Microbial Persistence and Idiopathic Dilated Cardiomyopathy - Editorial Response
      Lerner, A.M. - Clinical Infectious Diseases (1999):29:526-7 - PMID: 10530440
      Cfr. :
      http://www.cfids-cab.org/MESA/Microbial.pdf

    7. New Cardiomyopathy - Pilot Study of Intravenous Ganciclovir in a Subset of the Chronic Fatigue Syndrome
      A. Martin Lerner, Marcus Zervos, Howard J. Dworkin, Chug-ho Chang, James T. Fitzgerald, James Goldstein, Claudine Lawrie-Hoppen, Barry Franklin, Steven M. Korotkin, Marc Brodsky, Daniel Walsh and William O'Neil - Infectious Disease in Clinical Practice, 1997;6:110-117 - © 1997 by Willaims and Wilkins - Address for reprints : A. Martin Lerner M.D., 31000 Lahser Road, Birmingham,MI 48025 – Fax : 810-540-0139
      We describe a subset of patients with chronic fatigue syndrome (CFS) as defined by the CDC, a duration of overwhelming fatigue for <2 years and oscillating repetitively abnormal aberrant T-waves at 24-hour electrocardiogram (ECG) recordings (Holter monitors).
      Baseline 12-lead ECF, 2-D echocardiogram, rest/stress myocardial perfusion (thallium 201 or TC-99 sestamibi) and rest/stress multiple-gated acquisition studies, as well as coronary angiography excluded coronary artery disease.
      Patients in this CFS subset had significant Ig (with or without positive IgM) human cytomegalovirus enzyme-linked immunoassay antibody titers.
      They had little or no evidence of concurrent Epstein-Barr virus (EBV) multiplication, corroborated by negative viral capsid antigen IgM antibody titer and an EBV total early antigen antibody of 40.
      Patients were given intravenous ganciclovir (5 mg/kg 1 12 h for 30 days).
      Before this treatment, none of 18 patients could work or manage a household.
      At evaluations, 24 weeks after ganciclovir, 13 patients (72%) returned to their premorbid health states (P<.05).
      There were no adverse effects from ganciclovir in these nonimmunosuppressed patients.
      Introduction

      Chronic Fatigue Syndrome (CFS) is a disorder the natural history, clinical characteristics, pathologic physiology and treatment of which remain uncertain [1].
      Various hypotheses propose neuroendocrine or immunologic abnormalities or viral infections, including epstein-barr virus (EBV), human herpesvirus 6 and several enteroviruses and retroviruses [2].
      There have been several studies of treatments [3-5].
      Since the fatigue of the mononucleosis syndrome [6-8] resembles that of the CFS [9], we assayed antibodies to human cytomegalovirus (HCMV) and Epstein-Barr virus.
      High antibody titers to toxoplasmosis, an occasional cause of the mononucleosis syndrome [10], are unusual in CFS patients.
      Rowe and colleagues [11] described seven nonsyncopal adolescents presenting with fatigue an lightheadedness and demonstrated abnormal responses to upright tilt.
      They followed this work with a prospective, nonselected, nonblinded study confirming a strong association between neurally mediated hypotention and CFS [12].
      An abnormal response to upright tilt was observed in 22 of 23 patients with CFS vs. four of 14 controls (P<.001).
      Open, nonblinded therapy directed at this abnormal reflex with fludrocortisone, B-adreniergic blocking agents and disopyramide appeared beneficial in this nonblinded trial.
      The authors concluded that neurally mediated hypotension is a cause of the symptoms of CFS or that it is strongly associated with another important etiologic factor.
      We reported in 1993 that repetitively oscillating abnormal T-waves inversions and/or T-wave flats during 24-hour electrocardiogram (ECG) monitoring are present in patients with CFS, ECG abnormalities that are nonspecific but seen less frequently in non-CFs patients (P-<.01) [13].
      Abnormal left ventricular myocardial dynamics are present in a cohort of patients with CFS.
      Decreased and /or flat ejection fractions with stress, abnormal wall motion at rest and stress, dilatation of the left ventricle and segmental wall motion abnormalities in CFS patients[14].
      We now report a subset of CFS patients with (1) high human cytomegalovirus (HCMV) IgG enzyme-linked immunoassay antibody titers (ELISA), (2) minimal or no serologic evidence of concurrent EBV multiplication and (3) oscillating ECG abnormalities at Holter monitoring.
      We performed a pilot study to assess the possible efficacy of ganciclovir, an antiviral nucleoside useful in the treatment of several HCMV infections in immunosuppressed patients.
      .../...
      Discussion
      This preliminary open trial of IV ganciclovir in patients with CFS, abnormal T-wave oscillations at Holter monitoring and significant HCMV ELISA antibody titers was conducted to identify a possible subset of patients who may benefit from this therapy.
      A significant HCMV ELISA IgG antibody titer (>120 U) with or without the presence of an HCMV IgG antibody titer, plus an absence of EBV VCA IgM antibody titer, along with an EBV EA antibody titer of <40 may help describe a CFS cohort of patients who may derive benefit from ganciclovir.
      This study as not blinded, randomized or placebo-controlled and the efficacy of ganciclovir has not been determined.
      The use of a single 30-day course of intravenous ganciclovir is arbitrary.
      During the EBV infectious lytic cycle, antigen is expressed and can be divided into a diffuse (EA-D) complex and a cytoplasmic restricted (EA-R) complex.
      Here, we assayed EA-D. The 52/50 kDa EA-D protein complex neutralizes EBV-encoded DNA polymerase activity.
      Elevated EBV VCA IgM and EBV EA antibody titers indicate recent EBV multiplication (e.g., within 90 days).
      Buffy coats from blood samples, urine samples and cardiac biopsies did not contain infectious HCMV.
      It appears that we report a nonlytic, nonpermissive, persistent HCMV infection [24].
      Cfr. :
      -
      http://www.ncf-net.org/library/ganciclovir.htm
      -
      http://www.ahummingbirdsguide.com/wlerner.htm

    8. Outcome of heart failure with preserved ejection fraction in a population-based study
      Bhatia RS, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, Gong Y, Liu PP, Heart & Stroke/Richard Lewar Centre of Excellence, University of Toronto, and the Division of Cardiology, Toronto General Hospital, University Health Network, Toronto, ON, Canada - N Engl J Med. 2006 Jul 20;355(3):260-9 - PMID: 16855266 - © 2006 Massachusetts Medical Society
      Background
      - The importance of heart failure with preserved ejection fraction is increasingly recognized.
      We conducted a study to evaluate the epidemiologic features and outcomes of patients with heart failure with preserved ejection fraction and to compare the findings with those from patients who had heart failure with reduced ejection fraction.
      Methods - From April 1, 1999, through March 31, 2001, we studied 2802 patients admitted to 103 hospitals in the province of Ontario, Canada, with a discharge diagnosis of heart failure whose ejection fraction had also been assessed.
      The patients were categorized in three groups : those with an ejection fraction of less than 40 percent (heart failure with reduced ejection fraction), those with an ejection fraction of 40 to 50 percent (heart failure with borderline ejection fraction) and those with an ejection fraction of more than 50 percent (heart failure with preserved ejection fraction).
      Two groups were studied in detail: those with an ejection fraction of less than 40 percent and those with an ejection fraction of more than 50 percent.
      The main outcome measures were death within one year and readmission to the hospital for heart failure.
      Results - Thirty-one percent of the patients had an ejection fraction of more than 50 percent.
      Patients with heart failure with preserved ejection fraction were more likely to be older and female and to have a history of hypertension and atrial fibrillation.
      The presenting history and clinical examination findings were similar for the two groups.
      The unadjusted mortality rates for patients with an ejection fraction of more than 50 percent were not significantly different from those for patients with an ejection fraction of less than 40 percent at 30 days (5 percent vs. 7 percent, P=0.08) and at 1 year (22 percent vs. 26 percent, P=0.07); the adjusted one-year mortality rates were also not significantly different in the two groups (hazard ratio, 1.13; 95 percent confidence interval, 0.94 to 1.36; P=0.18).
      The rates of readmission for heart failure and of in-hospital complications did not differ between the two groups.
      Conclusions - Among patients presenting with new-onset heart failure, a substantial proportion had an ejection fraction of more than 50 percent.
      The survival of patients with heart failure with preserved ejection fraction was similar to that of patients with reduced ejection fraction.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/16855266


    Read also : Part VII


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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The heart of the matter - CFS & cardiac issues - Part VII
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    The heart of the matter - CFS & cardiac issues


    Part VII



    1. Prevalence of abnormal cardiac wall motion in the cardiomyopathy associated with incomplete multiplication of Epstein-barr Virus and/or cytomegalovirus in patients with chronic fatigue syndrome
      Lerner AM, Dworkin HJ, Sayyed T, Chang CH, Fitzgerald JT, Beqaj S, Deeter RG, Goldstein J, Gottipolu P, O'Neill W, Department of Medicine, William Beaumont Hospital, Royal Oak, Michigan, USA : lerner@cdimed.com - In Vivo. 2004 Jul-Aug;18(4):417-24 - PMID: 15369178
      We reported unique incomplete herpesvirus (Epstein-Barr Virus (EBV) and/or nonstructural (HCMV) cytomegalovirus) multiplication in 2 distinct subsets of CFS patients.
      The CFS subsets were identified by :
      a) presence of IgM serum antibodies to HCMV nonstructural gene products p52 and CM2 (UL44 and UL57) and/or
      b) IgM serum antibodies to Epstein-Barr virus viral capsid antigen (EBV, VCA IgM).
      Diagnostic IgM serum antibodies were found in two independent blinded studies involving 49 CFS patients, but the same antibodies were absent in 170 control patients (p<0.05).
      Abnormal 24 Hr-electrocardiographic monitoring, tachycardias at rest and, in severe chronic cases, abnormal cardiac wall motion (ACWM) were seen in these same CFS patients.
      We now report a prospective consecutive case control study from 1987--1999 of cardiac dynamics as measured by radionuclide ventriculography in 98 CFS patients from 1987—1999.
      Controls were patients with various malignancies who were evaluated in protocols requiring radionuclide ventriculography before initiation of cardiotoxic chemotherapeutic agents.
      The prevalence of abnormal cardiac wall motion (ACWM) at rest in CFS patients was 10 out of 87 patients (11.5%).
      With stress exercise, 21 patients (24.1%) demonstrated ACWM. Cardiac biopsies in 3 of these CFS patients with ACWM showed a cardiomyopathy.
      Among the controls, ACWM at rest was present in 4 out of 191 patients (2%) (p=0.0018).
      A progressive cardiomyopathy caused by incomplete virus multiplication of EBV and/or HCMV in CFS patients is present.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15369178

    2. Systolic and Diastolic Heart Failure in the Community
      Francesca Bursi, MD, MSc; Susan A. Weston, MS; Margaret M. Redfield, MD; Steven J. Jacobsen, MD, PhD; Serguei Pakhomov, PhD; Vuyisile T. Nkomo, MD; Ryan A. Meverden, BS; Véronique L. Roger, MD, MPH – JAMA 2006;296:2209-2216
      Context
      - The heart failure (HF) syndrome is heterogeneous.
      While it can be defined by ejection fraction (EF) and diastolic function, data on the characteristics of HF in the community are scarce, as most studies are retrospective, hospital-based and rely on clinically indicated tests.
      Further, diastolic function is seldom systematically assessed based on standardized techniques.
      Objective - To prospectively measure EF, diastolic function and brain natriuretic peptide (BNP) in community residents with HF.
      Main outcome measures - Echocardiographic measures of EF and diastolic function, measurement of blood levels of BNP and 6-month mortality.
      Design, setting and participants - Olmsted County residents with incident or prevalent HF (inpatients or outpatients) between September 10, 2003 and October 27, 2005, were prospectively recruited to undergo assessment of EF and diastolic function by echocardiography and measurement of BNP.
      Results - A total of 556 study participants underwent echocardiography at HF diagnosis.
      Preserved EF (≤ 50%) was present in 308 (55%) and was associated with older age, female sex and no history of myocardial infarction (all P<.001).
      Isolated diastolic dysfunction (diastolic dysfunction with preserved EF) was present in 242 (44%) patients.
      For patients with reduced EF, moderate or severe diastolic dysfunction was more common than when EF was preserved (odds ratio, 1.67; 95% confidence interval [CI], 1.11-2.51; P = .01).
      Both low EF and diastolic dysfunction were independently related to higher levels of BNP.
      At 6 months, mortality was 16% for both preserved and reduced EF (age- and sex-adjusted hazard ratio, 0.85; 95% CI, 0.61-1.19; P = .33 for preserved vs reduced EF).
      Conclusions - In the community, more than half of patients with HF have preserved EF and isolated diastolic dysfunction is present in more than 40% of cases.
      Ejection fraction and diastolic dysfunction are independently related to higher levels of BNP.
      Heart failure with preserved EF is associated with a high mortality rate, comparable to that of patients with reduced EF.
      Cfr. :
      http://jama.ama-assn.org/cgi/content/full/296/18/2209

    3. Systolic blood pressure at admission, clinical characteristics and outcomes in patients hospitalized with acute heart failure
      Mihai Gheorghiade; William T. Abraham; Nancy M. Albert; Barry H. Greenberg; Christopher M. O’Connor; Lilin She; Wendy Gattis Stough; Clyde W. Yancy; James B. Young; Gregg C. Fonarow; for the OPTIMIZE-HF Investigators and Coordinators - JAMA. 2006;296:2217-2226 - PMID: 17090768
      Context : The association between systolic blood pressure (SBP) at admission, clinical characteristics and outcomes in patients hospitalized for heart failure who have reduced or relatively preserved systolic function has not been well studied.
      Objective - To evaluate the relationship between SBP at admission, clinical profile and outcomes in patients hospitalized for acute heart failure.
      Design, setting and patients - Cohort study using data from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry and performance-improvement program for patients hospitalized with heart failure at 259 US hospitals between March 2003 and December 2004.
      Patients were divided into quartiles by SBP at hospital admission (<120, 120-139, 140-161 and >161 mm Hg).
      In-hospital outcomes were based on 48,612 patients aged 18 years or older with heart failure.
      Of the 41,267 patients with left ventricular function assessed, 21,149 (51%) had preserved left ventricular function.
      Postdischarge outcomes were based on a prespecified subgroup (n = 5791, 10% of patients) with follow-up data assessed between 60 and 90 days.
      Main outcome measures - In-hospital and postdischarge mortality.
      Results - Patients with higher SBP were more likely to be female and black and to have preserved systolic function.
      Fifty percent of the patients had SBP higher than 140 mm Hg at admission.
      Patients with lower SBP at admission had higher in-hospital and postdischarge mortality rates.
      Higher SBP at admission was associated with lower in-hospital mortality rates : 7.2% (<120 mm Hg), 3.6% (120-139 mm Hg), 2.5% (140-161 mm Hg), and 1.7% (>161 mm Hg) (P<.001 for overall difference).
      Postdischarge mortality rates in the follow-up cohort by SBP at admission were 14.0%, 8.4%, 6.0%, and 5.4%, respectively (P<.001 for overall difference).
      Conclusions - Systolic hypertension is common in patients hospitalized for heart failure.
      Systolic blood pressure is an independent predictor of morbidity and mortality in patients with heart failure with either reduced or relatively preserved systolic function.
      Low SBP (<120 mm Hg) at hospital admission identifies patients who have a poor prognosis despite medical therapy.
      These findings may have important therapeutic implications because characteristics and outcomes differ greatly among patients with heart failure with varying SBP.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17090768

    4. The Heart of the Matter - CFS & Cardiac Issues
      Carol Sieverling - Dr. Paul Cheney's theoretical insights on ME/CFS and heart failure. Pamphlet
      Cfr. :
      http://www.dfwcfids.org/medical/cheney/heart04.htm

    5. The importance of the gastrointestinal system in the pathogenesis of heart failure
      Krack A, Sharma R, Figulla HR, Anker SD, Clinical Cardiology, NHLI, Imperial College School of Medicine, London, UK : andreas.krack@med.uni-jena.de - Eur Heart J. 2005 Nov;26(22):2368-74. Epub 2005 Jun 24 - PMID: 15980032
      Chronic heart failure (CHF) is a multi-organ disease with increasing evidence for the involvement of the gastrointestinal (GI) system in this syndrome.
      In recent research, the gut has received very little attention from cardiologists as its role in the pathogenesis of cardiovascular disease is poorly understood.
      Intestinal ischaemia may play an important role in bacterial translocation by increasing bowel permeability.
      Decreased cardiac function can reduce bowel perfusion and so clearly impairs the function of the intestinal barrier.
      There is an increasing evidence to suggest that a 'leaky' bowel wall may lead to translocation of bacteria and/or endotoxin, which may be an important stimulus for inflammatory cytokine activation in CHF.
      Impaired functioning of the GI system may also contribute to malnutrition and cachexia in CHF.
      It is hoped that by improving our understanding of the role of the gut in cardiac disease will lead to the development of novel therapeutic strategies in the future.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15980032?dopt=AbstractPlus

    6. Usefulness of an abnormal cardiovascular response during low-grade head-up tilt-test for discriminating adolescents with chronic fatigue from healthy controls
      Wyller VB, Due R, Saul JP, Amlie JP, Thaulow E, Department of Pediatrics, Rikshospitalet-Radiumhospitalet Medical Centre, and Department of Physiology, University of Oslo, Oslo, Norway : brwylle@online.no - Am J Cardiol. 2007 Apr 1;99(7):997-1001. Epub 2007 Feb 16 - PMID: 17398200
      Hemodynamic dysfunction is documented in chronic fatigue syndrome (CFS).
      This study was conducted to investigate cardiovascular responses to orthostatic stress in adolescents with CFS, using a novel procedure for tilt-table testing.
      A total of 27 adolescents with CFS and 33 healthy control subjects with equal age and gender distribution underwent 15 minutes of 20 degrees head-up tilt testing.
      Heart rate, systolic blood pressure (BP), mean BP, diastolic BP, stroke index, total peripheral resistance index, end-diastolic volume index and acceleration index were continuously and noninvasively recorded.
      At rest, patients with CFS had higher total peripheral resistance index values (p<0.01) and lower stroke index and end-diastolic volume index values (p<0.05) than controls.
      During 20 degrees head-up tilt testing, patients with CFS had greater increases in heart rate, diastolic BP (p<0.001), mean BP (p<0.01) and total peripheral resistance index (p<0.05) than controls and greater decreases in stroke index (p<0.05).
      Syncope or near syncope was not observed.
      In conclusion, this study found that adolescents with CFS have significant abnormalities of cardiovascular regulation in response to mild orthostatic stress, differentiating them from healthy controls.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17398200

    Bijlagen:
    http://www.cfids-cab.org/MESA/CFS_Dist.htm   

    07-03-2009 om 00:00 geschreven door Jules

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    06-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The SHINE approach and treatment protocol
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    From Fatigued to Fantastic !
    - A Clinically Proven Program to Regain Vibrant Health and Overcome
    Chronic Fatigue and Fibromyalgia -
    Jacob Teitelbaum - Avery Publishing Group Inc.,U.S. (3rd revised edition)
    oktober 2007
    ISBN10 : 1583332898 / ISBN13 : 9781583332894
    Cfr. :
    -
    http://www.endfatigue.com/store/products/publications/from-fatigued-to-fan/
    -
    http://www.bol.com/nl/p/boeken-engels/from-fatigued-to-fantastic/1001004005646947/index.html


    The SHINE approach and treatment protocol

     S H I N E
    SleepHormonesInfectionsNutritonal supplements - Exercise



    A chiropractic treatment flared her CFS

    Dr. Teitelbaum
    © The Annapolis Chronic Fatigue and Fibromyalgia Research Center


    Question

    Joanne asks :

    I had one spinal manipulation and now I feel I am having a CFS flair

    Hello Dr. T, How are you ?
    I am a former patient of yours.
    I saw you in 2006.
    You saved me !
    Although I have yet to fully recover, I will say that I recovered about 75%.
    Which I'll gladly take !
    I'm just a little scared.
    I developed some back problems, which I wouldn't associate with my CFS, but more from having a 2 year-old son.
    I began massage therapy and my therapist recommended I see a chiropractor because of the abnormal spacing of my shoulders.
    I had one spinal manipulation about three days ago and now I feel I am having a CFS flair (brain fog, nausea, disorientation) !

    What are your thoughts on this ?


    Answer

    In your case, I would hold off and treat with SHINE instead

    Dear Joanne,
    It will pass.
    Sometimes spinal manipulation (especially in the neck) can flare autonomic dysfunction because of spinal cord stimulation if the space in the spinal cord is tight.
    I suspect the muscle tightness you were being treated for reflected that the CFS was beginning to act up again as well just a little—even before the manipulation.

    This is not a big deal and simply requires a tune up.
    Begin with taking (or continuing) the Energy Revitalization System vitamin powder

    End Fatigue Energy Revitalization (powder) & B-Complex (caps) Berry Splash
    Cfr. :
    http://www.endfatigue.com/store/products/supplements/berry-splash/

    and Ribose (Corvalen)

    CORvalen (D-Ribose)
    Cfr. :
    http://www.endfatigue.com/store/products/supplements/corvalen-d-ribose/

    and add natural remedies or medications (Ambien – cfr. : http://www.drugs.com/ambien.html -, Desyrel – cfr. : http://www.drugs.com/cdi/desyrel.html -, Klonopin – cfr. : http://www.drugs.com/cdi/klonopin.html -) as needed to get your eight hours sleep a night.
    Ask your doctor to increase your thyroid dose to see if it helps and if spastic colon or nasal congestion symptoms are present, re-treat for candida.
    Add in vitamin B6 at 200 mg a day for 6-12 weeks as it can help recovery from the chiropractic manipulation.

    Usually chiropractic can be very helpful—especially when combined with SHINE ('sleep-hormones-infection- nutritional supplements-exercise') – cfr. : http://www.endfatigue.com/treatment_options/Shine_treatment_protocol.html - to treat the metabolic issues (discussed in my book).
    In your case though, I would hold off and treat with SHINE instead.
    Also, ask your therapist or chiropractor to check to see if your hip heights are even.
    If not, a $15 heel lift can do wonders (if it is the right size heel lift, you'll feel better and more balanced immediately when you use it; if not, it is not the right size).

    Love & Blessings,
    Dr. Teitelbaum (-
    http://www.endfatigue.com/about-dr-t/Index.html -).

    Cfr. : http://www.endfatigue.com/qa/Questions_and_answers_0808.html



    The SHINE Approach and Treatment Protocol
    Understanding The SHINE Approach to CFS/FM Treatment


    In his 30 years of clinical experience and in his landmark study on Effective Treatment of CFS/FM, Dr. Teitelbaum has found that his SHINE approach to treating CFS/FM is successful in the vast majority of patients.

    The SHINE Treatment Protocol is a list of the more common treatments for CFS/FM.
    SHINE represents five areas of health issues that need to be addressed when creating a treatment program.
    These health issues and their roles in treating CFS/FM are as follows :

    • S = SLEEP
      Get adequate sleep, preferably eight to nine hours a night.
      Sleep replenishes the body's energy and heals its muscles.
      Inadequate sleep will leave you exhausted and in pain.

    • H = HORMONES
      Get tested for hormone deficiency and treated if needed.
      Hormone deficiencies can contribute to fibromyalgia and chronic fatigue syndrome.

    • I = INFECTIONS
      Get treatment when symptoms of infections occur.
      The lack of restorative sleep in CFS/FM leads to dysfunctional immune systems.
      Underlying viral, bacterial, bowel, sinus and yeast infections are common and can be a contributing cause or result of CFS/FM.

    • N = NUTRITONAL SUPPLEMENTS
      Optimal nutritional supplementation is essential.
      Many nutrients can be depleted as a result of CFS/FM. B-12, magnesium, Acetyl L Carnitine and glutathione, as well as your basic A, B, C and D vitamins need to be supplemented at a level that your average over the counter multivitamin cannot provide.

    • E = EXERCISE
      Exercise as able.

    After 10 weeks on the 4 steps above, you will be able to slowly increase your exercise-without being wiped out the next day !

    'SHINE Treatment Protocol for CFIDS/Fibromyalgia' that Dr. Teitelbaum used in his own practice and his study is available at : http://www.endfatigue.com/treatment_options/Shine_protocol_document.html -.
    This protocol is used worldwide by practitioners who want to effectively treat CFS/FM, as well as patients who want to start natural remedies on their own.
    You can download, print and use this as a guide with your practitioner to tailor your treatment regimen to your specific symptoms.

    Het protocol van dokter Teitelbaum
    Deel I & II

    Cfr. : www.jules.be – dd. 07-08-2007


    What to expect

    It takes an average of six weeks to begin to feel the benefits of your treatment.
    During this time, you should chart important information about your treatment progress, such as dates when you start or stop individual treatments and their effects.

    For most of you, CFS/FM took months to fully manifest.
    It can also take several months to get well.
    Although the SHINE protocol gives you the fastest path to healing, keep in mind that total recovery can take several months to over a year.
    You should remain on the treatment program until you are feeling consistently well for six months or more (with no back-sides).
    After that, you can taper off the program by discontinuing one treatment every one to two weeks.

    The gradual tapering is recommended so that you can make sure a particular treatment is no longer needed.
    Although it isn't usually necessary, any or all of the treatments can be used forever without harm.
    Many patients choose to continue several treatments long term after stopping the majority of them.
    Reading your body’s signals and taking your practitioner’s advice are your best tools in determining which treatments should be continued to remain well.

    Cfr. : http://www.endfatigue.com/treatment_options/Shine_treatment_protocol.html

     

    Read all about
    chronic fatigue syndrome and fibromyalgia
    at :
    http://www.endfatigue.com/resources/




    06-03-2009 om 20:31 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Innerlijke onrust
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    Innerlijke onrust

    Gezondheidsplein.nl

    Wanneer je zenuwstelsel te veel onder druk komt te staan
    - bijvoorbeeld door ander of te moeilijk werk, meer verantwoordelijkheden, relatieproblemen, een sterfgeval, een trauma of een ongeluk -
    kun je flink uit balans raken.
    Nu is het onmogelijk om stressvolle situaties altijd uit de weg te gaan,
    maar je kunt bepaalde factoren wel degelijk beïnvloeden.
    Hoe ?
    Dat en meer over evenwicht in je leven lees je in de special 'In balans met jezelf'
    Cfr. :
    http://www.gezondheidsplein.nl/thema/34/In-balans-met-jezelf.html


    Soms herken je bij jezelf een periode dat je lichaam en geest niet meer met elkaar in balans zijn.
    Je voelt je onrustig vanbinnen en het lukt je niet meer om te ontspannen.
    Dat kan verschillende oorzaken hebben.
    Té veel druk op het werk, een lang ziektebed van een dierbare of een overvolle agenda, bijvoorbeeld.
    Toch hoeft innerlijke onrust – ook wel spanning genoemd – zeker niet problematisch zijn.
    Sterker nog, misschien ga je juist wel beter presteren door een beetje spanning.
    Pas wanneer je innerlijke onrust en nerveuze gevoelens een lange periode aanhouden en/of té heftig worden, wordt het een ander verhaal.


    Prestatiemaatschappij

    Helaas leven we in een maatschappij waar (tijds)druk een zeer grote rol speelt.
    We rennen letterlijk van hot naar her om onze vrienden, familie, sportmaatjes, leraren en werkgever tevreden te stellen.
    Overal verwachten mensen dat we optimaal presteren en dat begint al van kinds af aan.
    Je moet goede cijfers halen op school, populair zijn bij je vriendengroep, perfect werk afleveren voor je baas, beter (of de beste) worden in sport of een andere hobby, de ideale (schoon)zoon of (schoon)dochter zijn, een goede ouder zijn, een goed kind zijn en ga zo maar door.
    Door al dat presteren kan er flink wat druk op je lichaam en geest ontstaan.
    En wanneer die druk te hoog wordt, kan dat leiden tot een behoorlijk onrustig gevoel vanbinnen.


    Innerlijke onrust

    - Het ontstaan van innerlijke onrust
    Het is je zenuwstelsel dat centraal staat in het proces van onrustige gevoelens en nervositeit.
    Wanneer je jezelf ‘gewoon goed’ voelt, doen de cellen in je zenuwstelsel hun werk zonder dat je dat merkt.
    Pas wanneer je zenuwstelsel overbelast raakt – door aanhoudende spanningen bijvoorbeeld – seint het signalen door je lichaam en geest die aangeven dat het allemaal teveel wordt.
    Je kan daar behoorlijk van uit balans raken, met alle gevoelens van onrust en nervositeit vandien.

    - Klachten als gevolg van innerlijke onrust
    Waar je het gevoel van innerlijke onrust en nervositeit vaak vooral zelf merkt, is een aantal symptomen wel degelijk merkbaar voor je directe omgeving.
    De meest voorkomende, hinderlijke verschijnselen zijn :
    - overmatig transpireren
    - trillen en beven
    - prikkelbaarheid
    - neerslachtigheid
    - hoofdpijn
    - duizeligheid
    - hartkloppingen
    - concentratieproblemen.
    Je kunt je voorstellen dat – wanneer zo'n spanningstoestand té lang duurt – je misschien wel overspannen kunt raken.
    Het kan zélfs zo ver komen dat je met een burnout geconfronteerd wordt.

    Burnout
    Burnout is een specifieke stressreactie of toestand van overspannenheid die voornamelijk voorkomt bij mensen in sociale of contactuele beroepen zoals het welzijnswerk, de gezondheidszorg, het onderwijs.
    Werkende vrouwen en managers hebben er vaker last van dan anderen.
    In het algemeen worden bij burnout drie reacties onderscheiden, die niet gelijktijdig hoeven voor te komen : emotionele uitputting, depersonalisatie (het gevoel buiten je eigen lichaam of geest te staan) en verminderde persoonlijke bekwaamheid.
    Specifieke symptomen zijn :
    - niet meer met plezier naar je werk gaan (als gevolg van vermoeidheid)
    - slaapstoornissen
    - te lang en te veel over het werk piekeren
    - niet meer kunnen genieten van dingen
    - geen zin meer in seks
    - chaotisch denken en handelen (niet meer kunnen organiseren)
    - hoofd- en nekpijn
    - verlies van eetlust.
    Neurotische klachten zoals schuldgevoelens, angsten, depressies of obsessies manifesteren zich meestal in een latere fase.
    De risicofactoren voor burnout zijn : hoge werkdruk, slechte werksfeer, beperkte controlemogelijkheden (zoals beslissen over vrije dagen en pauzes) en lage beloning.
    Uit onderzoek blijkt dat één op de tien Nederlanders zich 'opgebrand' voelt.
    Met name werknemers in het onderwijs en de horeca hebben hier last van.
    Daarnaast komt werkstress in het bijzonder voor bij mensen tussen de 35 en 55 jaar.
    Er is ook een verband tussen opleiding en werkdruk.
    Hoe hoger opgeleid, hoe groter de kans op werkstress.




    Passiebloem (Passiflora incarnata)

    - Hulp bij innerlijke onrust
    Om de kans op innerlijke onrust en nervositeit te verkleinen, bestaan er verschillende voedings- en leefadviezen die je kunt opvolgen.
    Maar ook een aantal krachtige planten uit de natuur - passiebloem, valeriaan en citroenmelisse bijvoorbeeld – kunnen je de broodnodige rust brengen.

    Ontspannen gevoel
    Ontspannen, wat is dat nou eigenlijk ?
    In feite betekent het niets meer dan tot rust komen.
    Geestelijk en lichamelijk
    Voor de een is een avond sporten de ultieme manier van ontspannen en voor de ander is dat een avondje uit met vrienden.
    En misschien vind jij het juist wel weer heerlijk om zo af en toe eens een boswandeling te maken om tot rust te komen.
    Bovendien kan jij wel veel meer ontspanning nodig hebben dan je beste vriend of vriendin.
    Zo zie je maar weer, ontspannen is iets heel persoonlijks.
    Maar het is wél voor iedereen even belangrijk.
    Ontspanning zorgt er namelijk voor dat je in balans blijft en je de drukte van alledag goed aankunt.
    Toch is het soms ontzettend moeilijk om te relaxen in een maatschappij waar (tijds)druk een grote rol speelt.
    Gezonde spanning versus ongezonde spanning
    Een beetje spanning is natuurlijk ook helemaal niet slecht voor je.
    Het kán zelfs zijn dat je door 'gezonde spanning' beter presteert.
    Pas wanneer je té veel of té lang gespannen bent en het je niet meer lukt om het ontspannen gevoel terug te krijgen, wordt spanning een probleem.
    Bijvoorbeeld bij een té hoge werkdruk die ook nog eens heel lang aanhoudt, een lang ziektebed van een dierbare of continu een overvolle agenda.
    Dán is het belangrijk tijdig naar je lichaam te luisteren.
    Langdurige spanning kan immers makkelijk leiden tot lichamelijke en psychische klachten.
    En uiteindelijk kan het zelfs je complete leven negatief beïnvloeden.
    Daarnaast zijn er diverse tips en technieken om tot rust te komen.
    Als je te veel gespannen bent, nemen je reserves af en ben je gevoeliger voor allerlei factoren die stress kunnen veroorzaken.
    Voorkomen is beter dan genezen
    Overmatige spanning voorkomen, het klinkt bijna te mooi om waar te zijn.
    Maar door goed te luisteren naar je eigen lichaam is het wel degelijk mogelijk.
    Door wat vaker 'nee' te zeggen, kun je bijvoorbeeld veel stressfactoren vermijden.
    Sta je op het punt om promotie te maken op het werk ?
    Houd dan rekening met meer verantwoordelijkheid en meer taken.
    En vraag jezelf af of je deze verantwoordelijkheid aan kunt.
    Twijfel je daaraan ?
    Zeg dan 'nee' tegen de promotie.
    Want een hoger salaris wint het écht niet van een ontspannen gevoel en ordelijke gedachten.
    Maar zeg ook eens 'nee' tegen een privé-afspraak als je weekend al bijna vol zit.
    Of geef bij een collega aan dat je écht geen ruimte meer hebt voor een extra taak.
    De rol van voeding en sporten
    Natuurlijk voorkom je stress niet alléén door wat vaker 'nee' te zeggen.
    Er zijn veel meer zaken die kunnen bijdragen aan een ontspannen leven.
    Evenwichtige voeding en regelmatig sporten, bijvoorbeeld.
    Maar wat verstaan we nou onder evenwichtige voeding ?
    Een sterk zenuwstelsel is erg belangrijk om stress minder kans te geven.
    Dit stelsel draait onder andere op voldoende brandstof en verschillende hulpstoffen die je via je eten binnenkrijgt.
    Vooral vitamine B - uit volkoren producten en biergist - is zo'n belangrijke hulpstof.
    Maar ook mineralen zijn essentieel.
    Daarom passen (biologische) groenten, fruit en volkoren producten zeer goed in een verantwoord voedingspatroon.
    Geraffineerde producten - gemaakt van witmeel - kun je beter zoveel mogelijk vermijden.
    Ook sporten kan je ondersteunen bij een ontspannen gevoel.
    Wanneer je sport, maken je hersenen namelijk van nature een chemische stof aan.
    Deze stof heet 'endorfine' en zorgt ervoor dat je je rustig en goed voelt.
    Niet voor niets hebben mensen het vaak over 'even de stress eruit werken'.
    Belangrijk is wel om een sport te kiezen waar je plezier in hebt, anders zal je plan nooit slagen.
    Overige leefadviezen
    Natuurlijk zijn er nog veel meer manieren om je ontspannen gevoel te behouden of te herwinnen.
    - Praat problemen uit : daardoor blijf je er niet mee zitten én het voorkomt piekeren.
    - Vermijd overmatige fysieke, psychische en emotionele druk
    - Zoek gezelschap van goede vrienden : zij helpen jou je gedachten op leuke dingen te richten.
    - Ga iedere dag lekker naar buiten : frisse buitenlucht heeft een ontspannende werking.
    - Verbeter je ademhalingstechniek : langzaam en diep ademhalen, zorgt voor de toevoer van meer zuurstof in je lichaam. Het resultaat is vaak een rustiger gevoel. Wat je moet doen om op deze manier adem te halen ? Leg je hand op je buik en adem diep in. Probeer bij het inademen je hand op je buik weg te drukken. Zo adem je via je buik en kan de zuurstof zijn werk beter doen. Oefen dit dagelijks.
    - Dagelijks een warm bad met citroen : citroen heeft namelijk een kalmerend effect op je lichaam.

    - De kracht van de natuur
    Ook de natuur kan je op weg helpen om een ontspannen gevoel te behouden of te herwinnen.
    Er zijn namelijk tal van planten en kruiden die een rustgevende werking op je lichaam hebben.
    De passiebloem, bijvoorbeeld, werkt kalmerend en ontspannend.
    Valeriaan heeft een kalmerende invloed op het centrale zenuwstelsel en vermindert beven als gevolg van nerveuze gevoelens.
    En citroenmelisse kalmeert en werkt krampopheffend op maag en darmen.
    A.Vogel combineerde deze drie ingrediënten tot één krachtig zelfzorgmiddel dat 100% natuurlijk is : 'A.Vogel Passiflora forte met valeriaan' – cfr. :
    http://www.gezondheidsplein.nl/topic/3457/Passifloraforte.html -.
    Passiflora forte met valeriaan helpt je op gezonde en verantwoorde wijze te ontspannen als het jou niet meer wil lukken.
    En dat terwijl je wél fris en alert blijft.
    Lijnrecht tegenover een ontspannen gevoel staat innerlijke onrust.

    Stress bij kinderen

    Het nieuwe schooljaar is voor sommige kinderen een groot plezier, voor andere kinderen echter een grote stressfactor.
    Net als volwassenen kunnen kinderen gespannen zijn en uit hun evenwicht raken.
    Daar kunnen diverse oorzaken voor zijn, zoals een te druk leven of spanningen thuis.
    Maar ook school kan de oorzaak zijn; problemen op school, een overstap naar een nieuwe school, niet goed in een groep passen of niet aan de verwachtingen kunnen voldoen.
    Allemaal factoren die tot stress kunnen leiden.

    - Een geval apart : stress bij kinderen
    Net als volwassenen kunnen ook kinderen gespannen zijn en uit hun evenwicht raken.
    Dat kan verschillende oorzaken hebben.
    Denk maar eens aan spanningen in het gezin, een nieuw schooljaar of zelfs een nieuwe school, problemen bij het leren, een spannende sinterklaasperiode en niet aan de verwachtingen van ouders en leraren kunnen voldoen.
    Het zijn stuk voor stuk factoren die een kind behoorlijk uit zijn evenwicht kunnen halen.

    - Hoe herken je stress bij kinderen
    Vaak is het heel moeilijk om stress bij je kind te herkennen.
    Toch is er wel degelijk een aantal symptomen die je als ouder kunt oppikken als alarmsignaal.
    Het kan bijvoorbeeld zijn dat je kind ineens slecht slaapt en veel buikpijn heeft.
    Maar ook angstig zijn, veel huilen of niet buiten willen spelen zijn bekende verschijnselen.
    Gelukkig is stress bij kinderen relatief makkelijk te verhelpen door de ouders zelf.
    Open staan voor de problemen van je kind en goed luisteren zijn hierbij sleutelwoorden.

    - Hoe uit stress bij kinderen zich ?
    Stress bij kinderen uit zich op verschillende manieren, bijvoorbeeld door slaapproblemen, buikpijn, angstig zijn, veel huilen of niet buiten willen spelen.
    Gelukkig is stress bij kinderen vaak op te lossen door de ouders zelf.
    Open staan voor de problemen van je kind en goed luisteren zijn hierbij sleutelwoorden.

    - Eerste hulp bij kinderstress
    Natuurlijk wil je als ouder alleen het beste voor je kind.
    En je hoopt natuurlijk dat je kind op jonge leeftijd nog niet wordt geconfronteerd met vervelende spanningen.
    Hieronder vind je een aantal tips die je op weg kunnen helpen om de spanningen bij je kind te voorkomen of te verminderen :
    - Realiseer je dat het ene kind meer aan kan dan het andere. Kijk daarom goed naar alle activiteiten van je kind. Vindt hij het allemaal wel leuk ? En – misschien wel belangrijker - is het eigenlijk niet te veel ?
    - Stressgevoelige kinderen denken eerder negatief. ‘Ik kan het niet’ is daarom een logische reactie van een kind dat spanningen heeft. Zorg er daarom als ouder voor dat je ze juist de andere kant laat zien. Zeg bijvoorbeeld : ‘Wat kan jij mooie verhalen schrijven’. Positieve boodschappen maakt je kind sterk.
    - Kijk kritisch naar je eigen gezinsleven. Is er voldoende ruimte voor spontane gezinsmomenten ? En maken jullie tijd voor rustige gesprekjes met elkaar ?
    - Let op het mediagebruik van je kind. Het is voor jou en voor hen verleidelijk om ze na een lange schooldag achter de televisie of computer te zetten, omdat ze al zo moe zijn.
    Het probleem is alleen dat hij dan volop met prikkels in aanraking komt en eigenlijk geen rust krijgt.
    - Een goede lichaamsconditie bepaalt mede de weerstand tegen stress. Zorg er daarom voor dat je kind gezond eet, genoeg lichaamsbeweging krijgt en voldoende lang slaapt.
    Ook jouw kind kan baat hebben bij de kracht van de natuur.
    Passiebloem, valeriaan en citroenmelisse staan bekend om hun rustgevende werking en kunnen daarmee stress verminderen.
    Je vindt een krachtige combinatie van deze planten in Passiflora forte van A.Vogel.


    Gelukkig kun je zelf innerlijke onrust voorkomen en verminderen.
    Dat kan via voeding, leefstijl en behandeling met natuurlijke geneesmiddelen.


    Cfr. : http://www.gezondheidsplein.nl/topic/3442/Innerlijke-onrust.html


    06-03-2009 om 19:42 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 1/5 - (1 Stemmen)
    >> Reageer (0)
    05-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Fibromyalgie anders bekeken - Deel I
    Klik op de afbeelding om de link te volgen







     






    Fibromyalgie anders bekeken
     
    Deel I

    Een paradigma
    Een paradigma is een theoretisch denkkader, een samenhangend stelsel van modellen en theorieën die een invalshoek vormen waarmee de 'werkelijkheid' geanalyseerd en beschreven wordt.

     Medici zijn zich vaak niet bewust
    van het paradigma dat zij in de praktijk hanteren
    of staan er niet bij stil hoe hun denk- en handelwijze is
    t.o.v. een bepaald ziektebeeld en de patiënt die eraan lijdt.
    Dat geldt zeker ook voor fibromyalgie !


    Fibromyalgie anders bekeken

    Dr. H.L.S.M. Busard, zenuwarts, afdeling Psychiatrie Isala Klinieken Zwolle : h.l.s.m.busard@isala.nl - Stichting Corv – Bron : Medisch Contact : redactie@medischcontact.nl -, 06-07-2007 - Publicatie : Nr. 27, 1168-1170


    Paradigmawisseling biedt frisse blik op diagnostiek en behandeling

    Artsen benaderen hun patiënten meestal vanuit een biologisch onderzoeksparadigma : klachten vaststellen en de fysieke oorzaak aanpakken.
    Maar bij stressaandoeningen levert die benadering vaak weinig op.
    Diagnosticeren en behandelen vanuit het relationele communicatieve paradigma kan dan uitkomst bieden.

    Een paradigma is een set van regels en procedures, die wordt gehanteerd om de werkelijkheid in kaart te brengen. (1)
    Medici zijn zich vaak niet bewust van het paradigma dat zij in de praktijk hanteren.
    Door de realiteit vanuit een ander perspectief in kaart te brengen, verandert het beeld.
    Een voorbeeld van zo’n paradigmawijziging in de praktijk komt hier aan bod.
    Het betreft de benaderingswijze van fibromyalgie, die frequent voorkomt, maar waarbij inzicht in de pathofysiologie ontbreekt.
    Ook een effectieve aanpak mist nog.


    Spieren en pezen - Het biologische onderzoeksparadigma

    Fibromyalgie wordt geclassificeerd als een reumatologische aandoening omdat de klachten grotendeels bestaan uit pijn van spieren en pezen.
    Richt de reumatoloog zijn aandacht op de ziekte fibromyalgie, dan verwacht de patiënt een causale ordening en behandeling van de fysieke klachten.
    Daarbij hanteren patiënt en medicus beiden impliciet het causaal biologische onderzoeksparadigma, met biologische tijd als centraal ankerpunt (cfr. : tabel 1). (2)(3)

    • Het klinische beeld is in dit geval dat van een patiënte die dagelijks bijna continu wisselend gelokaliseerde pijnklachten heeft aan alle gewrichten.
      Zij is steeds moe, ook al omdat ze slecht doorslaapt.
      Haar activiteiten moet ze plannen om qua energie in balans te blijven.
      In de huishouding heeft ze veel steun van haar partner nodig.
      Hobby’s heeft ze niet meer.
      De patiënt is lichamelijk zeer gespannen.
      Dit gaat gepaard met verhoogde prikkelbaarheid.
      De patiënte is snel emotioneel en gemakkelijk negatief gestemd.
      Zij kan zich maar moeizaam concentreren en de geheugenfunctie is duidelijk teruggelopen.

    • Uit lichamelijk onderzoek komen geen duidelijke afwijkingen, behoudens de bekende pijn op drukpunten.
      Globaal psychiatrisch onderzoek laat geen duidelijke afwijkingen zien, anders dan stemmingsschommelingen en disregulatie van de externe prikkel- en informatieverwerking.
      Laboratoriumonderzoek toont evenmin afwijkingen.

    • Diagnose en behandeling : de ziekteverschijnselen zijn in hun samenhang als fibromyalgie te classificeren.
      De pathofysiologie wordt binnen dit paradigma niet opgelost, want er wordt geen oorzaak gevonden.
      Om die reden is er ook geen zicht op een effectieve behandeling.
      De patiënte krijgt van haar reumatoloog leefregels aangereikt en wordt terugverwezen.
      Zij doet regelmatig een beroep op haar huisarts, die haar een luisterend oor biedt en haar symptomatisch begeleidt.
      Bij pijn schrijft hij pijnstillers voor.
      Ook verwijst hij haar af en toe voor fysiotherapie en/of zwemmen in warm water.


    Contact en houding - Het relationele communicatieve paradigma

    De arts kan patiënten behalve vanuit het biologische ook vanuit het relationele communicatieve paradigma beschouwen.
    Dit perspectief is gebaseerd op de theorie van het communicatieve handelen en focust op de wijze waarop de patiënt zichzelf presenteert door middel van communicatie met de omgeving. (4)(5)
    Binnen de psychiatrie is deze manier van diagnosticeren bekend, zeker met betrekking tot het in kaart brengen van de achterliggende betekenis van onbegrepen gedrag.
    Wordt het relationeel communicatieve paradigma gebruikt om het klinische beeld weer te geven, dan betreft het een beschrijving van het interactieve proces van het psychosociaal communiceren van de patiënt met de onderzoeker.
    Verondersteld wordt dat dit contact in hoge mate representatief is voor hoe de patiënt in zijn of haar leefwereld staat.
    Terug naar ‘onze’ patiënte.

    • Het contact : de patiënte houdt zich nadrukkelijk aan de vraagstelling, het tempo en de regie van de onderzoeker.
      Zij gaat uit van de ‘onderpositie’ en neemt nooit de vrijheid om de structuur van het contact te veranderen.
      De patiënte maakt het gesprek niet persoonlijk en toont zich weinig open.
      Er ontstaat geen relatie.

    • Het denken : de patiënte ordent haar leven vooral cognitief.
      Ze vormt haar antwoorden niet associatief in het hier-en-nu door uit te gaan van haar eigen lichaamssignalen en gevoel, maar baseert zich onbewust op verwachtingen van anderen.
      Als het gaat om eigenwaarde en zelfregie, overheersen in haar denken negatieve en belemmerende overtuigingen.

    • Emoties en gevoelens : de patiënte gebruikt haar emoties niet actief in de communicatie met anderen.
      Ze houdt emoties als boosheid in en blokkeert de expressie ervan.
      Hierdoor is zij weinig in staat tot het reguleren van een ontspannen contact.
      De patiënte maakt ook nauwelijks contact met haar lichamelijke signalen : het lichaamsbewustzijn is weinig ontwikkeld.
      Zij schat haar fysieke grenzen niet goed in en forceert zichzelf hierdoor.

    • Handelen : de patiënte blijft erg concreet.
      Ze spreekt bijna alleen als reactie op vragen van de onderzoeker.
      De patiënte geeft niet aan dat haar grens is bereikt, terwijl non-verbaal wel toenemende lichamelijke gespannenheid en motorische onrust waarneembaar zijn.

    • Houding tegenover de wereld : het op eigen benen staan heeft patiënte onvoldoende ontwikkeld.
      Ze blijft ambivalent/symbiotisch afhankelijk van de ander voor veiligheid, sociale regie en betekenis.


    Eigen regie

    Binnen het relationeel communicatieve paradigma wordt gefocust op de zieke zelf.
    Het is een aanvulling van het biologische paradigma met betekenisgeving aan het eigen leven, leidend tot levenskwaliteit en met de sociale ruimte die alle mensen met elkaar verbindt als ankerpunt (cfr. : tabel 2). (4)(5)

    Bij het relationele communicatieve paradigma gaat het niet om het ordenen van oorzaak en gevolg van de ziekteverschijnselen, maar om de relationele betekenis, gecommuniceerd door psychosociale interactie.
    Het is de wijze waarop de patiënt door middel van eigen regie en verantwoordelijkheid zijn leven in relatie tot zijn directe omgeving betekenis geeft. (6)(7)
    Symptomen worden daarbij gezien als tekenen van disfunctionele psychosociale communicatie, die door de patiënt zelf (on)bewust worden ingezet om voor zichzelf relationele betekenis te creëren.

    Onderzoek richt zich op het niet uitdrukken van emoties en dan vooral de boosheid over het verlies aan betekenis met verlies van levenskwaliteit als gevolg.
    Fysiologisch stemt het niet tot expressie brengen van boosheid bovendien goed overeen met klachten van het bewegingsapparaat : bij uitstek de weg waarlangs emoties worden uitgedrukt.

    De zieke wordt in dit aanvullende paradigma beschouwd als een levend en lerend systeem op de niveaus van ervaren c.q. voelen, emoties en cognities. (8)(9)
    Binnen dit paradigma is niet langer sprake van een medische expert die een oplossing aanreikt : de patiënt zal zelf met coachende ondersteuning een antwoord op de vraag naar betekenis (her)formuleren.


    Onderpositie

    Het klinische beeld van het psychosociale script dat de patiënte zelf onbewust hanteert, verheldert haar gedrag.
    Ziekteverschijnselen zijn daarbij te duiden als de negatieve output van haar disfunctionele communicatie.
    Het relationeel communicatieve paradigma maakt duidelijk hoe weinig de patiënte in staat is om een eigen plaats in te nemen in de sociale ruimte.
    Ze gebruikt haar mogelijkheden tot zelfregie niet, kiest onbewust steeds voor een ‘onderpositie’ en ontkent negatieve emotionele feedback (boosheid).
    Het gebruik van dit paradigma verheldert dat de patiënte moet leren om verantwoordelijkheid te nemen voor de betekenisgeving aan haar leven.
    Een beroep doen op medische zorg is om die reden oneigenlijk en zal haar daarbij ook niet helpen.

    De beoogde gedragsverandering kan worden bereikt door het volgen van een gestructureerd en effectief interventieprogramma, gebaseerd op het relationeel communicatieve paradigma en de multidimensionaliteit van communicatie (cognities, emoties en lichamelijke gevoelens).
    Een dergelijk programma volgt patiënte dan ook. (10)
    Zij leert hierin te ervaren wat lichamelijke signalen voor haar betekenen en haar emoties te uiten, zodat ze zich bewust wordt van wat ze nodig heeft en hoe ze eigen keuzes kan maken om haar leven te regisseren.
    Door de training ontwikkelt de patiënte zich tot iemand die weet heeft van zichzelf, haar eigen wensen en behoeften kent en zichzelf durft te laten zien.
    Ze is niet langer gefocust op haar klachten, maar op de vraag hoe ze vanuit haar eigen verantwoordelijkheid betekenis kan geven aan haar leven.


    Medisch beroep

    Thomas S. Kuhn, auteur van 'The structure of Scientific Revolutions' (University Of Chicago Press (1 edition), December 15, 1996 – ISBN-10 : 0226458083 / ISBN-13 : 978-0226458083 – cfr. : http://www.amazon.com/Structure-Scientific-Revolutions-Thomas-Kuhn/dp/0226458083 -), introduceerde het concept paradigma in de wetenschappelijke wereld. (11)
    Kuhn postuleerde dat wetenschappelijke paradigma’s aanvaarde voorbeelden uit de wetenschappelijke traditie zijn.
    Deze voorbeelden bevatten wetten, theorieën, toepassingen en instrumenten, die modellen representeren waarop een bepaalde samenhangende praktijk van het wetenschappelijk onderzoek is gebaseerd.
    Professionals die hun onderzoek baseren op gedeelde paradigma’s, hanteren gelijke normen en regels voor de beoefening van wetenschap.
    Dit gaat ook op voor het medische beroep.
    Men moet zich als het ware steeds weer bewust zijn van het feit dat men een model van de wereld hanteert dat niet de wereld zelf is.
    Als eigen paradigma’s op die manier worden gehanteerd, is het mogelijk flexibel en vrij naar de wereld te kijken.
    Een ander paradigma biedt immers een nieuw perspectief, dat mogelijk verhelderend kan zijn, bijvoorbeeld wat betreft diagnosestelling.
    Diagnosticeren is immers niets anders dan het in kaart brengen van verschijnselen tot een samenhangend en betekenisvol geheel, vanuit een ander paradigma dan dat van de patiënt, namelijk het medische.


    Samenspraak

    De vraag bij de hier beschreven paradigmawisseling is welke betekenis die heeft voor de diagnosestelling en begeleiding bij fibromyalgie.
    Beide paradigma’s, zowel het biologische als het relationeel communicatieve paradigma zijn betekenisvol en vullen elkaar aan.
    Het biologische paradigma maakt het mogelijk om een ziektebeeld gericht te classificeren, het communicatieve paradigma biedt een nieuw pathofysiologisch inzicht en een wezenlijk effectief therapeutisch perspectief met meer begrip en respect voor de ‘fibromyalgie-mens’.
    Dit begrijpen en respecteren is noodzakelijk om in samenwerking en samenspraak, passend bij het relationele paradigma, tot een gerichte behandeling te komen.
    De patiënt zelf dient daar gemotiveerd en vanuit eigen verantwoordelijkheid aan deel te nemen.
    De verschuiving naar het relationeel communicatieve paradigma kan worden gezien als het begin van een nieuwe aanpak, waarbij de zieke mens en diens mogelijkheden om nieuw en effectief gedrag te leren centraal staan. (12)
    De beschreven paradigmawisseling kan een stimulans zijn om deze innoverende aanpak uit te breiden naar patiënten met andere humane stressaandoeningen, zoals chronische vermoeidheid en postwhiplash.
    Ook die kunnen op basis van het nieuwe paradigma worden beschreven.


    Samenvatting

    Het causaal biologische onderzoeksparadigma voldoet niet bij de behandeling van fybromyalgie.
    Uitgangspunt voor een nieuw en aanvullend pathofysiologisch model voor fibromyalgie is het relationele communicatieve paradigma.
    Dit paradigma helpt om tot een betekenisvolle diagnose te komen, gebaseerd op een functionele stoornis in de psychosociale interactie.
    Paradigmawisseling is mogelijk ook van nut om te komen tot een effectievere behandeling van patiënten met humane stressaandoeningen als chronische vermoeidheid en postwhiplash.


    Literatuur

    1. Paradigma’s - Mentale modellen voor de toekomst
      Barker JA - . Schiedam, Scriptum Books, 1996 – ISBN-13 : 9789055940547 / ISBN-10 : 9055940542
      De laatste dertig jaar hebben wij veranderingen meegemaakt wat betreft de regels die ons leven bepalen.
      Wat als u of uw bedrijf enkele van deze veranderingen had kunnen zien aankomen ?
      Wat als u of uw onderneming één van deze veranderingen met zekerheid had kunnen voorspellen ?
      Wat had uw organisatie met deze informatie kunnen doen ?
      Wie u ook bent of wat u ook doet, het zou heel wat hebben uitgemaakt.
      Op zijn minst zou u minder verrast zijn door de ontwikkelingen en minder last hebben van een 'toekomstschok'.
      In het gunstigste geval zou u miljoenen hebben kunnen verdienen - als u de kennis had gehad.
      Goed anticiperen en innoveren is het resultaat van strategische verkenningen aan de hand waarvan u toekomstscenario's kunt ontdekken.
      Strategische verkenningen bestaan uit vijf onderdelen :
      1/ Inzicht in invloeden - Het vermogen te begrijpen wat uw percepties beïnvloedt.
      2/ Divergent denken - De vaardigheid meerdere goede antwoorden te ontdekken.
      3/ Convergent denken - De vaardigheid gegevens doelgericht te integreren en keuzemogelijkheden te rangschikken.
      4/ Routeplanning - Het vermogen de paden aan te geven waarmee u van het heden in de toekomst komt.
      5/ Weergeven - De vaardigheid om de resultaten van de toekomstverkenningen in woorden, figuren of modellen te vangen.
      Dit boek concentreert zich vooral op het inzicht in invloeden.
      Immers, als je niet begrijpt hoe je percepties van de toekomst beïnvloed worden, zijn alle onderdelen nutteloos.
      Barker begint dus bij inzicht in invloeden in de hoop de lezer op weg te helpen naar een verbeterd anticiperend vermogen.
      Inhoudsopgave
      Dankbetuigingen
      Woord vooraf
      1. Met het oog op de toekomst
      2. Het belang van anticiperen
      3. Definitie van een paradigma
      4. Waneer duiken nieuwe paradigma's op ?
      5. Wie verandert het paradigma ?
      6. Wie zijn de paradigmapioniers ?
      7. Het paradigma-effect
      8. Tweeëntwintig voorbeelden
      9. De belangrijkste paradigmaverschuiving van de twintigste eeuw
      10. Terug naar af
      11. De belangrijkste eigenschappen van paradigma's
      12. Managers, leiders en paradigma's
      13. Verschuivingen - Het dozijn van Barker
      14. De wereld draait verder
      Nawoord
      Bibliografie
      Register
      Cfr. :
      http://www.managementboek.nl/boek/9789055940547/paradigmas_mentale_modellen_voor
      _de_toekomst_joel_barker

    2. Values and psychiatric diagnosis
      John Z. Sadler, Professor and Director Undergraduate Psychiatric Education, Department of Psychiatry, University of Texas Southwestern, Dallas - Oxford University Press, Dec 2004 – ISBN13 : 9780198526377 / ISBN10 : 0198526377
      The public, mental health consumers, as well as mental health practitioners wonder about what kinds of values mental health professionals hold and what kinds of values influence psychiatric diagnosis.
      Are mental disorders socio-political, practical or scientific concepts ?
      Is psychiatric diagnosis value-neutral ?
      What role does the fundamental philosophical question "How should I live ?" play in mental health care ?
      In his carefully nuanced and exhaustively referenced monograph, psychiatrist and philosopher of psychiatry John Z. Sadler describes the manifold kinds of values and value judgements involved in psychiatric diagnosis and classification systems like the DSM.
      Professor Sadler takes the reader on a fascinating conceptual tour of the inner workings of psychiatric diagnosis, considering the role of science, culture, sexuality, politics, gender, technology, human nature, patienthood and professions in building his vision of a more humane psychiatric diagnostic process.
      Cfr. :
      http://www.oup.com/us/catalog/general/subject/Medicine/PsychiatryPsychology/~~/dmlldz11
      c2EmY2k9OTc4MDE5ODUyNjM3Nw
      ==

    3. Of Time, passion and Knowledge - Reflections on the Strategy of Existence
      J. T. Fraser - Princeton University Press (2e Edition), April 1990 – ISBN10 : 0691024375 / ISBN13 : 9780691024370
      Only a wayfarer born under unruly stars would attempt to put into practice in our epoch of proliferating knowledge the Heraclitean dictum that 'men who love wisdom must be inquirers into very many things indeed.'
      Thus begins this remarkable interdisciplinary study of time by a master of the subject.
      And while developing a theory of time as conflict, J. T. Fraser does offer many things indeed --an enormous range of ideas about matter, life, death, evolution and value.
      Cfr. :
      http://www.bol.com/nl/p/boeken-engels/of-time-passion-and-knowledge/1001004000604299/index.html

    4. Habermas’ theorie van het communicatieve handelen - Een samenvatting
      Kunneman H, 22-11-2007 - Meppel, Boom, 1983, 1984, 1885
      In korte tijd is 'Theorie des kommunikativen Handelns' van Jürgen Habermas – cfr. :
      http://de.wikipedia.org/wiki/Theorie_des_kommunikativen_Handelns -&- http://www.hypothesis.nl/argumentatietheorie/habermas.htm - uitgegroeid tot een monument.
      Het vormt niet alleen een mijlpaal in Habermas eigen intellectuele groei, maar eveneens in de ontwikkeling van het moderne denken over mens en maatschappij.
      Omdat het werk door zijn omvang (circa 1200 paginas) en zijn abstractieniveau moeilijk toegankelijk is, groeide onder studenten en docenten een sterke behoefte aan een samenvatting van het zware werk.
      Harry Kunneman, verbonden als medewerker sociale filosofie aan de Universiteit van Amsterdam, heeft zo'n samenvatting gemaakt.
      Deze tekst, die het betoog van Habermas op de voet volgt, kan gebruikt worden als leeswijzer bij de bestudering van het boek, maar kan ook dienen als eerste kennismaking met Habermas kritische maatschappijtheorie.
      Habermas biedt een indringende diagnose van de belangrijkste problemen waarmee westerse maatschappijen te kampen hebben.
      In onze alledaagse leefwereld, waar discussie en argumentatie de boventoon zouden moeten voeren, zijn economie (geld, monetaire dwang) en staat (macht, bureaucratische dwang) als destructieve krachten binnen gedrongen.
      Deze kolonialisering van levensgebieden is volgens Habermas de belangrijkste oorzaak van de ziekelijke verschijnselen in onze moderne samenleving.
      Cfr. :
      https://www.booksonboard.com/index.php?BODY=viewbook&BOOK=182920&v=synopsis
      Samenvatting
      In 1981 heeft Jürgen Habermas (1929) voorlopig een lange denkweg afgesloten met zijn "Theorie des kommunikativen Handelns".
      Zijn ideeën hebben veel weerklank gevonden, ook in de theologie.
      Dat is enerzijds bevreemdend, omdat hij meent te kunnen aantonen, dat het godsdienstige, althans in rationele, wetenschappelijke zin, heeft afgedaan.
      Anderzijds is zijn handelingstheorie z.i. een voortzetting van de tradities van joden en christenen.
      Het doel van deze theologische studie is dan ook, na te gaan of en in hoeverre de handelingstheorie van Habermas verenigbaar is met de christelijke geloofsovertuiging en bruikbaar is voor het handelen vanuit deze overtuiging, in het bijzonder voor de praktische theologie (Hoofdstuk 1).
      Habermas wil de Kritische Theorie van de Frankfurter Schule – cfr. :
      http://nl.wikipedia.org/wiki/Frankfurter_Schule - een nieuwe, rationele grondslag geven.
      Hij neemt in plaats van het conceptuele kader van de bewustzijnsfilosofie, dat uitgaat van het subject-object-model van kennis en handelen, het kader van taal en van communicatief handelen.
      Hij onderscheidt drie gelijkwaardige momenten van rationaliteit, te weten :
      - het objectieve,
      - het normatieve en
      - het expressieve.
      Deze rationele symmetrie ligt in de menselijke taal zelf besloten.
      Men kan in de arbeid zeer wel instrumenteel, objectiverend handelen.
      Maar via taal kan dat niet.
      Uitspraken, proposities, het objectieve (b.v. "de bal is rood"), verwijzen niet uit zichzelf naar de werkelijkheid.
      Dat is pas het geval als men bedenkt, dat de volledige taalhandeling eigenlijk luidt : "Ik beweer tegen jou, dat de bal rood is".
      Habermas onderscheidt drie typen van taalhandelingen, nl. constatieve als bovengenoemde, regulatieve (b.v. "Ik verzoek u niet te roken") en expressieve (b.v. "Ik ben bang, dat ...").
      Wie in het alledaagse handelen zo'n taalhandeling uit, handelt, als hij -veelal impliciet- aanspraak wil maken op de geldigheid van zijn uitspraken, d.w.z. op de waarheid resp. de juistheid of de waarachtigheid van zijn woorden, communicatief.
      Habermas maakt onderscheid tussen dergelijk communicatief handelen, waarbij men uit is op gedeeld begrip ("Verständigung") en eventueel tot overeenstemming ("Einverständnis") komt en het diskurs, de formele argumentatievorm, die "begrifflich fundamental" is.
      Hij weet aannemelijk te maken, dat in het argumentatieproces zelf de motivatie ontstaat om drievoudig rationeel te gaan handelen.
      Daardoor is z.i. het denken en handelen van de moderne mensheid in principe transparant geworden.
      Men kan en hoeft zich niet meer achter religieuze normen en waarden te verschuilen.
      Het sacrale is "versprachlicht".
      Indien mensen uit zijn op "Verständigung", kunnen zij de leefwereld 'symbolisch reproduceren', d.w.z. tegelijkertijd zichzelf verwerkelijken, hun eigen persoonlijkheid vormen en solidair zijn in de opbouw van een rechtvaardige samenleving.
      De Nederlandse filosoof en kenner van het werk van Habermas, Kunneman,corrigeert hem.
      Z.i. is de reproductie ook mogelijk via andere vormen van sociaal handelen, maar dan wordt de leefwereld niet 'ververst'.
      Nu is echter in onze tijd deze symbolische reproductie van de werkelijkheid losgekoppeld van de materiële reproductie.
      Habermas meent, dat men economie en staat het beste kan bestuderen als systemen.
      Want daar wordt het gebruik van taal overheerst door andere communicatiemedia, met name geld en macht.
      We moeten niet proberen daar verandering in te brengen, want deze ontwikkeling is het gevolg van de differentiaties die in de moderne samenleving hun beslag hebben gekregen en waar we op zichzelf veel goeds aan te danken hebben.
      Problematisch is echter, dat economie en staat hun invloedssfeer steeds verder uitbreiden over de leefwereld en deze koloniseren.
      In tegenstelling tot Parsons en Luhmann denkt Habermas, dat het juist omgekeerd zou moeten zijn : geld en macht moeten worden teruggekoppeld aan en verankerd worden in de communicatief gestructureerde leefwereld.
      Systeem-integratie veronderstelt vormen van sociale integratie en een legitimatie door middel van wetten en instituties (Hoofdstuk 2 en 3.3).
      Habermas wordt van allerlei kanten bestookt met kritiek, maar hij weet, vanuit zijn eigen vooronderstellingen, telkens aan te tonen, dat zijn theorie zeer consistent in elkaar zit.
      Wel stuiten we steeds op twee punten van kritiek, die van groot belang zijn voor onze theologische vraagstelling :
      - ten eerste : overtrekt Habermas niet de betekenis van -zij het ook drievoudige- rationaliteit ?
      - ten tweede : heeft Habermas zijn vooronderstellingen wel afdoende verdedigd ?
      Hij gaat uit van de menselijke mogelijkheid van "Verständigung", met als Telos de ideale communicatiegemeenschap.
      Habermas weet wel, dat dit ideaal onbereikbaar is en wijst de utopie af, maar meent dat deze intuïtie toch wel als een quasi-transcendentaal gegeven kan dienen.
      Kunneman betwijfelt, of Habermas deze idee voldoende onderbouwd heeft.
      Ten aanzien van de eerste vraag is hij van mening, dat Habermas deze rationaliteit goed kan verdedigen tegenover opponenten, maar zijn eigen theore- tisch kader niet voldoende uitbouwt.
      Kunneman komt tot de slotsom, dat de integriteit van de leefwereld en dus de mogelijkheid van symmetrische communicatie van de handelenden de voorrang moet krijgen boven objectieve waarheid.
      Wellmer voegt daar aan toe : “Ook boven de logica van een rationaliseringsproces, gebaseerd op systeemtheorie”.
      Bovendien ontvouwt Kunneman de diskurstheorie op zo'n wijze, dat de levensbehoeften van elke mens van het grootste gewicht worden voor resp. het identiteitsdiskurs (waar de expressieve rationaliteit centraal staat), het praktische diskurs (normatieve rationaliteit) en zo zelfs voor het theoretische diskurs (objectieve rationaliteit).
      Het bijzondere van deze ontvouwing van Habermas' theorie is, dat aan het primaat van de drievoudige rationaliteit alle recht wordt gedaan, terwijl ze niet meer heerst over het niet-rationele (Hoofdstuk 3).
      Reeds in 1976 heeft de theoloog Helmuth Peukert aangegeven, dat de wetenschapstheorie zichzelf moet relativeren en dat de status van theorieën mede afhankelijk is van de vooronderstellingen van de mensen die er gebruik van maken.
      Hij meent, dat de school waartoe Habermas behoort, de meest bruikbare wetenschapstheorie van dit moment vertegenwoordigt.
      Deze is, zoals hierboven is beschreven, gebaseerd op het solidaire, normatieve communicatieve handelen.
      Peukert wijst echter op een aporie in deze handelingstheorie.
      De solidariteit gaat niet verder dan de levenden : aan hen die onschuldig gestorven zijn voor de gerechtigheid wordt geen recht gedaan.
      Door het christelijk geloof kan men echter wel spreken van anamnetische (‘zich herinnerende’) solidariteit met de gestorvenen.
      Want in deze traditie gaat het om de werkelijkheid, die ervaren wordt in de grond- en grenservaringen van het communicatieve handelen.
      Zij vraagt om een fundamentele theologie die theorie is van dit communicatieve, anamnetisch-solidair op de dood afgaande handelen en van de in dit handelen ervaren en ontsloten werkelijkheid.
      Deze werkelijkheid, die exemplarisch zichtbaar werd in het gebeuren van de opstanding van Jezus, bewaart de ander die in de geschiedenis gehandeld heeft voor het grotere geluk van de anderen, voor de vernietiging.
      Pas door deze vorm van interactie, communicatief handelen in herinnerende solidariteit met anderen die onschuldig vernietigd zijn, krijg ik de mogelijkheid van mijn eigen identiteit in een op de dood afgaande existentie.
      Het probleem van een dergelijke strikt intersubjectieve theorie is, dat er geen plaats in kan worden aangewezen voor de openbaring van God, voor het werk van de Heilige Geest. Geloven, het godsdienstige, wordt wel volkomen plausibel gemaakt door Peukert, maar de inhoud van het godsdienstige blijft uitwisselbaar (Hoofdstuk 4).
      In de volgende hoofdstukken wordt dan ook een andere theologische weg bewandeld.
      Eerst wordt beschreven, dat een theorie waarin een intersubjectieve -immanente- metafysica convergeert met de openbaring weliswaar aanlokkelijk is, vooral voor de godsdienstpedagogiek, maar toch moet worden afgewezen, voorzover ze suggereert, dat de openbaring op de één of andere manier menselijk bepaald kan worden.
      We kunnen vanaf de menselijke kant niet verder gaan dan de constatering, dat de werkelijkheid niet volledig vastligt, maar poreus is.
      Religiositeit is een seculiere menselijke mogelijkheid, die ook door christenen gebruikt wordt.
      Maar met Jüngel wijzen we vervolgens dergelijke vormen van metafysika af en gaan uit van de openbaring van God in Jezus Christus.
      Waar de Heilige Geest door mensen heen zijn werk kan doen, zijn hemel en aarde het eens met elkaar.
      Er is dus meer dan de werkelijkheid via taal, al zullen mensen telkens juist via taal dit meerdere in hun leven en handelen uitdrukken.
      Daarmee is het eerste doel van deze studie bereikt : de theologie kan de theorie van het communicatieve handelen tot op grote hoogte aanvaarden en gebruiken.
      Maar ze wijst de visie van Habermas af, dat de ideale communicatiegemeenschap het laatste quasi-transcendentale Telos is van het menselijk handelen.
      De theologie kan, ook wetenschappelijk gezien, blijven vasthouden aan de openbaring van God.
      Zij kan "God" niet rationeel bewijzen, noch zijn openbaring, maar de mogelijkheid van ervaring van openbaring, van geloofservaringen, is wel plausibel (Hoofdstuk 6).
      De theorie van Habermas en met name de toespitsing van de diskurstheorie door Kunneman worden zo omgewerkt, dat de kleur, die het christelijk geloof geeft aan de werkelijkheid, de handelingstheorie gaat kenmerken.
      De verandering van handelingstheorie komt mede tot stand doordat de geloofservaringen, die de -seculiere- werkelijkheid zijn binnengegaan, de motivatie geven voor de "Verständigung".
      We maken daarbij gebruik van de studie van Grözinger over religieuze (esthetische) ervaringen.
      Via Seel is duidelijk te maken, dat geloofservaringen wezenlijk twee kanten hebben, nl. een cognitief aspect, dat in taal is uit te drukken en een gevoelsaspect, dat het specifieke van de geloofservaringen uitmaakt : én het anders zien door wat ons geopenbaard wordt (de kleur van de werkelijkheid verandert) én de verandering van de gelovige instelling zelf.
      Hieruit zijn de volgende thesen afgeleid, waar Habermas zelf mee kon instemmen :
      a. - “Der Mensch sollte lernen, nur human leben zu können, wenn man sich rational verständigt”;
      b. - “Religion kann -muss leider nicht-, neben anderen Formen, als externe Motivation für den Verständigungsprozess dienen”;
      c. - “Religion kann auch dienlich sein für die Motivation in der Praxis des Alltags". (Hoofdstuk 7).
      De eerdergenoemde inzichten van Kunneman worden gebruikt om duidelijk te maken, hoe deze motivatie vanuit het christelijk geloof bruikbaar wordt binnen de diskursen.

    Lees verder : Deel II


    05-03-2009 om 22:21 geschreven door Jules

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    Fibromyalgie anders bekeken
     
    Deel II

    Vanuit christelijk standpunt gezien is God -zelf niet rationeel weer te geven- de Bron van het rationele.
    Zo blijkt, dat wat "begrifflich fundamental" is, nl. de formele pragmatiek, niet het meest fundamentele van het bestaan is.
    We moeten er van af, dat het cognitief-instrumentele, de doelrationaliteit, het één en het al is.
    De Verlichting kan pas positief gewaardeerd worden, zegt Habermas terecht, indien we uitgaan van een drievoudige rationaliteit.
    Maar christenen weten (drievoudig rationeel !) vanuit hun geloof (niet-rationeel) dat het rationele op haar beurt slechts een -zij het essentieel- onderdeel is van de antropologische gaven en mogelijkheden.
    Zij geloven dat God door zijn Geest mensen aanzet om liefdevol en rechtvaardig te handelen.
    Natuurlijk vervangt de theologie daarmee de seculiere wetenschappen niet.
    Enerzijds werkt ze er mee samen en heeft als authentieke inbreng in seculiere taal weergegeven handelingsintenties, die een niet-rationele oorsprong hebben en gevoed worden door eerbied en liefde voor de Schepper en zijn schepping.
    Want een christen leeft van de nieuwe zin, die het hele leven anders maakt, waardoor we in de kosmos schepping zien.
    Anderzijds kunnen zo 'geloof, hoop en liefde' niet langer misbruikt worden als ideologische dekmantel voor macht en beïnvloeding.
    Deze zuivering, die gelukkig allang op gang is gekomen binnen het christendom, wordt ondersteund en geanalyseerd door de theorie van Habermas.
    Zo is ook het tweede doel van deze studie bereikt, nl. het nagaan van de mogelijkheden die de theorie van Habermas biedt om haar te gebruiken voor het handelen vanuit de christelijke geloofsovertuiging.
    Tenslotte gaan we na, hoe de praktische theologie gebruik kan maken van de theorie van het communicatieve handelen.
    We kijken vooral naar de school van Van der Ven uit Nijmegen (NL), die de praktische theologie heeft omgedoopt in "theorie van het religieus communicatief handelen".
    Zij wil een empirische theologie ontwerpen, die zich zowel kwalitatieve als kwantitatieve onderzoeksmethoden uit de sociale wetenschappen eigen maakt en aldus 'intra-disciplinair' kan worden genoemd.
    Van der Ven hecht grote waarde aan de nomothetische methodologie van A.D.de Groot, die expliciet cognitief- instrumenteel van opzet is.
    Terecht meent Kunneman, dat deze methode een schoolvoorbeeld is van de werking van de waarheidstrechter in de sociale wetenschappen, een zeef, die alleen objectiverende momenten van sociale problemen doorlaat en normatieve en subjectieve elementen elimineert.
    Operationalisering van theologische concepten binnen de empirische theologie van Van der Ven leidt aldus tot vervorming van de problemen omdat het objectieve de beide andere rationaliteitsaspecten geheel gaat overheersen.
    De conclusie luidt dan ook dat communicatief handelen en een dergelijke empirische theologie niet kunnen samengaan.
    Ik stel voor om een model van praktische theologie te ontwerpen dat begint met het stimuleren van de mogelijkheden van christenen om open te staan voor geloofservaringen en dat hen leert deze ervaringen te gebruiken binnen de gemeente en in het seculiere handelen.
    Op deze manier proberen we binnen allerlei vormen van gemeenten van Christus tot "Verständigung" te komen over de christelijke leefwijze.
    Hoewel praktische theologie dus niet moet vergeten, systeemtendenzen en andere vormen van sociaal handelen te bestuderen, b.v. strategisch handelen, zal haar eigen methode bij voorkeur het communicatieve handelen zijn.
    Deze vorm van handelen zou vanzelfsprekend moeten zijn binnen de gemeente van Christus.
    Waarbij ieder die dat wil, deel kan nemen aan het open ‘diskurs’.
    N.B. - Vgl. voor een recent bijgewerkt standpunt :
    Morgen… in de verte - Een kerk van mensen
    A.K. Ploeger & J.J.Ploeger-Grotegoed – Kok, Kampen juli 2007 - ISBN/EAN : 9789043513432
    De auteurs - Albert Ploeger en Joke Ploeger-Grotwgoed hebben beiden zowel praktische theologie gedoceerd als predikantswerk verricht.
    Sinds 1960 zijn zij betrokken bij verbanden tussen rooms-katholieken en protestanten, die in vieringen en bezinning gemeenschappelijk zoeken naar spirituele vernieuwing.
    Het boek - Een blauw kader met een groot wit vlak- wat wil dat zeggen ?
    Dit boek gaat over een kerk van mensen die zichzelf willen zijn.
    Mensen die zelf uitmaken wat ze geloven en hoe ze zich willen verhouden tot de kerk.
    In de gemeenten en parochies die de auteurs voor ogen hebben, bepalen niet de instituties en hun gezagsdragers de regels, maar de kerkeden zelf.
    De auteurs bieden wel een kader en geven hun vaak uitgesproken meningen, maar dat verwachten ze ook van de lezers.
    Zij hebben hun eigen invulling aan het ‘blauwe kader’ gegeven en gaan ervan uit dat ieder kerklid voor zichzelf het grote witte vlak gaat invullen.
    Dat kan met behulp van de open voorstellen die in dit boek geboden worden.
    Vroeger zei men dat het geloof ‘uit het gehoor’ was, maar in het multimediale tijdperk wil ieder graag geloven met alle zintuigen, naar lichaam en geest.
    Waarnemen en kunst spelen in dit boek dan ook een belangrijke rol.
    De auteurs schetsen een kerk met een spiritueel aanbod, waar bidden en recht doen, eredienst en diaconaat, samen de kern uitmaken.
    Een kerk die na Auschwitz anders gelooft, waar de angst voor het terrorisme serieus wordt genomen en waar het beleven centraal staat.
    Een kerk waar men geborgenheid vindt en tegelijk waakzaamheid leert, op weg naar 'Morgen… in de verte'.
    Cfr. :
    https://www.webshopboekhandel.nl/Webshop/Product.aspx?MemberGroupID=6&MemberNr=7307&tl=Morgen&pid=756264&rm=False&oa=True&
    max=50&ProductID=756264

    Cfr. :
    -
    http://theol.eldoc.ub.rug.nl/FILES/root/Ploeger/Habermas1/HabermasSamenvatting.pdf
    -
    http://arno.uvt.nl/show.cgi?fid=57293
    Habermas' theorie van het communicatieve handelenden
    Hypothesis.nl
    De centrale stelling van Habermas luidt: maatschappijen vormen netwerken van communicatief handelen en communicatief handelen is erop gericht begrip tot stand te brengen.
    De communicatietheorie moet de structuren blootleggen, die kenmerkend zijn voor het vermogen deel te nemen aan communicatie.
    Het tot stand brengen van begrip analyseert Habermas in termen van taalhandelingen.
    Habermas stelt dat bij iedere taalhandeling die een actor verricht, tegelijkertijd een aanspraak gemaakt wordt op :
    - begrijpelijkheid van hetgeen gezegd wordt
    - waarheid van wat beweerd wordt
    - waarachtigheid van de intentie
    - juistheid van de houding tegenover de hoorder.
    Communicatieve handelingen worden door Habermas begrepen als het maken van een viervoudige aanspraak op geldigheid : nl. de geldigheidsaanspraken begrijpelijkheid, waarheid, waarachtigheid en juistheid.
    Het communicatieve handelen kan slechts ongestoord doorgang vinden zolang de betrokkenen wederzijds de vier aanspraken erkennen.
    Wanneer die erkenning er niet meer is,zijn er nog 2 mogelijkheden :
    - óf we kiezen een andere vorm van handelen
    - óf we kiezen voor een ander niveau van communicatie.
    De vier geldigheidsaanspraken
    Linguïstische competentie: het geheel van regels op basis waarvan volwassen sprekers in staat zijn grammaticaal correcte, welgevormde zinnen te vormen en uit te spreken.
    Naar aanleiding van de linguïstische competentie definieert Habermas een communicatieve competentie, m.a.w. : hoe kunnen we begrijpen dat een mens in staat is om succesvol te communiceren met anderen.
    De communicatieve competentie moet het vermogen tot uitdrukking brengen van een spreker om:
    - zinnen zo te kiezen dat deze een ervaring of een feit weergeven
    - zijn intenties adequaat weer te geven
    - zinnen zo te uiten dat ze overeenstemmen met geaccepteerde normen.
    De communicatieve competentie brengt teweeg dat :
    - informatie overgebracht kan worden - de toehoorder de spreker kan vertrouwen
    - de toehoorder met de spreker overeen kan stemmen met betrekking tot de geldigheid van bepaalde normen.
    Taalhandelingen
    Overdragen van informatie, het tot stand brengen van vertrouwen en het tot stand brengen van normatieve overeenstemming gebeurt in de vorm van taalhandelingen.
    Er zijn twee belangrijke groepen van taalhandelingen : constatieve en regulatieve taalhandelingen.
    De aanspraken : geldigheid, waarheid, waarachtigheid en juistheid nader bekeken [p.118].
    1/ - Begrijpelijkheid is verbonden met de linguïstische competentie.
    2/ - Waarheid - In iedere taalhandeling waarin iets beweerd wordt, zitten twee dingen opgesloten :
    (a) de spreker laat weten dat hij, wat hij beweert voor waar houdt
    (b) dit voor waar houden kan desgewenst gerechtvaardigd worden.
    Verder geldt voor iedere taalhandeling, dat er een propositionele inhoud mee verbonden is, die de spreker voor waar houdt.
    Van de zin : 'Ik beweer....' kan niet gezegd worden of ie waar is.
    3/ - Juistheid - De aanspraak op juistheid kan duidelijk gemaakt worden aan de hand van regulatieve taalhandelingen.
    De juistheid van een taalhandeling kan uiteindelijk alleen gerechtvaardigd worden, door te verwijzen naar de juistheid van normen. "Ik veroordeel u hierbij tot 10 jaar celstraf.... “.
    4/ - Waarachtigheid - Communicatief handelen kan slechts doorgang vinden zolang de hoorder ervan overtuigd is dat de spreker inderdaad de intenties heeft die hij met zijn taalhandelingen tot uitdrukking brengt.
    Conclusie : De structuur van het communicatieve handelen: door de wederzijdse acceptatie van geldigheidsaanspraken komt een achtergrondconsensus tot stand, die het communicatieve handelen draagt.
    Indien de achtergrondconsensus ophoudt te bestaan dan vervalt de communicatie en zijn de genoemde twee mogelijkheden nog over om voort te gaan.
    Door wederzijdse acceptatie van geldigheidsaanspraken komt een achtergrondconsensus tot stand, die het communicatieve handelen draagt.
    Indien de achtergrondconsensus ophoudt te bestaan, kan het communicatief handelen geen voortgang meer vinden.
    Dan moet in een theoretische of praktische discussie een beslissing genomen worden over de geldigheid van de betreffende aanspraak.
    Objectiviteit en waarheid
    Een feit is wat gegrond over een stand van zaken in de werkelijkheid gezegd kan worden.
    Feiten beweer ik, ze zijn zelf geen stand van zaken in de werkelijkheid, ander dan mijn bewering over iets anders.
    Over de waarheid van uitspraken : Deze staat vast totdat de waarheid van een uitspraak betwijfeld kan worden [p.128].
    Dan is er een theoretische discussie nodig over de waarheid van de uitspraak.
    Waarheid wordt vervolgens omschreven als een geldigheidsaanspraak waarover in een discussie op goede gronden overeenstemming is bereikt.
    Hoe stel je echter vast of de overeenstemming op goede gronden is.
    Deze beslissing kan op zijn beurt niet weer van consensus afhangen.
    In discussies kan volgens Habermas overeenstemming bereikt worden op grond van 'dwang' die uitgeoefend wordt door de argumenten die ingebracht worden.
    Conclusie : Waarheid is een geldigheidsaanspraak waarover in een theoretische discussie op goede gronden overeenstemming is bereikt.
    De 'dwang' houdt verband met de logica van de discussie.
    Dit is een pragmatische logica, die de samenhang van argumentaties onderzoekt.
    De ideale gesprekssituatie
    De volgende stap is te formuleren waaraan een theoretische discussie moet voldoen opdat in ieder geval de mogelijkheid bestaat tot een gefundeerde consensus te komen.
    In de theoretische discussie zijn er vier stappen :
    (a) thematisering van de geldigheidsaanspraken
    (b) mogelijkheid tot argumenteren
    (c) het moet mogelijk zijn het gekozen taalsysteem te wijzigen
    (d) bezinning moet mogelijk zijn.
    Een consensus die in een discussie tot stand is gekomen, is slechts dan een consensus op goede gronden, indien binnen die discussie de mogelijkheid bestond desgewenst alle vier de stadia van radicalisering te doorlopen.
    Hierop berust de consensus genererende kracht van de argumentatie.
    Wanneer is er sprake van een discussie waarin aan al deze voorwaarden is voldaan ?
    In een ideale gesprekssituatie.
    De vier grondnormen voor een ideale gesprekssituatie:
    1. gelijke kansen voor de potentiële gespreksdeelnemers om een discussie te beginnen
    2. alles moet bekritiseerd kunnen worden
    3. gelijke kansen voor representatieve handelingen
    4. gelijke kansen voor regulatieve taalhandelingen.
    De praktische hypothese die met de anticipatie op de ideale gesprekssituatie gegeven is, betreft mogelijke realisering van een machtsvrije samenleving.
    Juistheid van normen
    Zowel voor de waarheid van uitspraken als voor de juistheid van normen geldt hetzelfde criterium : een redelijk gefundeerde consensus.
    De consensus wordt in principe bereikt op dezelfde manier als de consensus in het geval van waarheidsaanspraken.
    Gold echter in de theoretische discussie de logische dwang van de argumenten, in de praktische discussie moeten we het principe van universaliasering toepassen.
    De veredelde versie van : wat gij niet wilt dat u geschied, doe dat ook een ander niet.
    Ook in praktische discussies moet een stapsgewijze radicalisering van normatieve kritiek mogelijk zijn.
    Cfr. :
    http://www.hypothesis.nl/argumentatietheorie/habermas.htm
    Lees ook :
    - Het Communicatieve Paradigma - Mogelijkheden En Beperkingen Van Habermas' Theorie Van Het Communicatieve Handelen - Michiel Korthals & Harry Kunneman – Boom - 905352018X / 9789053520185 / 90-5352-018-X
    Cfr. :
    http://www.recensie.eu/cgi-bin/boek.cgi?boek=1017931
    - Geld in de context van leefwereld en systeem - Cobben, P.G. (1992) – In : 'Het communicatieve paradigma - Mogelijkheden en beperkingen van Habermas' theorie van het communicatieve handelen' (pp. 171-190) - M. Korthals & M. Kunneman (Eds.) - Meppel : Boom.
    Cfr. :
    http://arno.uvt.nl/show.cgi?fid=75601
    - Habermas' theorie van het kommunikatieve handelen - Cobben, P.G. (1984) - Tijdschrift voor filosofie, 46(2), 216-268.
    Cfr. :
    http://www.narcis.info/dare/RecordID/oaiwouvtnl198371/repository_id/uvtwo

    1. Logica van het gevoel - Filosofie van de stabiliteitslagen in de cultuur als nesteling der emoties
      Arnold Cornelis - Uitgeverij Boom, oktober 2000 – ISBN10 : 9072258029 / ISBN13 : 9789072258021
      In dit originele en baanbrekende werk in de filosofie en de sociale theorie van de kennis worden de kaarten van de werkelijkheid grondig geschud en opnieuw gelegd door de meesterhand.
      Achter dit werk gaan meer dan twintig jaar onderzoek en onderwijs schuil.
      Arnold Cornelis is niet slechts een meester in het denken, maar ook in de communicatie.
      Zijn filosofie maakt de brokstukken van het wereldbeeld tot een geheel.
      Terwijl de wereld steeds complexer wordt streeft zijn theorie van de kennis het omgekeerde na, eenvoud als wijsgerige levenskunst van zelfherkenning.
      Ontwikkelingen in de afzonderlijke wetenschappen, in de technologie en in de sociale vragen van beleid worden verweven tot een nieuw denkmodel dat ons niet loslaat en fascineert door herkenbaarheid, bruikbaarheid en inzichtelijkheid.
      Cfr. :
      http://www.bol.com/nl/p/boeken/logica-van-het-gevoel/666880352/index.html
      Logica van het gevoel
      Arnold Cornelis - Amsterdam, Brussel, Middelburg, Stichting Essence – Editie 1993
      Cfr. :
      http://www.kapaza.be/Boeken/Diversen/6103620/Logica_van_het_gevoel_Arnold_Cornelis
      _ed_1993.html

    2. Social Intelligence - The New Science of Human Relationships
      Daniel Goleman – Bantam (1 edition), september 26, 2006 – ISBN-10 : 0553803522 / ISBN-13 : 978-0553803525
      Review by Rick Lipkin, From Scientific American : We all recognize a special capacity that humans have - some more so than others - to connect with others in a deep and direct way.
      We see this quality expressed by a performer revving a crowd, a doctor healing a patient or a mother putting a child to sleep.
      To orchestrate these tasks, a person must sense and stimulate the reactions and mood of another.
      In 1995 Daniel Goleman, a Harvard University–trained psychologist and writer for the New York Times, published Emotional Intelligence, in which he discussed the human ability "to manage our own emotions and inner potential for positive relationships".
      Now he goes a step further.
      In 'Social Intelligence' he enlarges his scope to encompass our human abilities to connect with one another.
      "We are wired to connect," Goleman says : "Neuroscience has discovered that our brain’s very design makes it sociable, inexorably drawn into an intimate brain-to-brain linkup whenever we engage with another person. That neural bridge lets us affect the brain - and so the body - of everyone we interact with, just as they do us".
      Each encounter between people primes the emotions.
      This neurological pas de deux stimulates our nervous systems, affecting hormones, heart rate, circulation, breathing and the immune system.
      Goleman peppers his discourse with anecdotes to illustrate the power of social intelligence.
      From the countertop of Rosie Garcia, a multitasking baker in New York’s Grand Central Terminal, to the tantrum-tainted class of a Texas teacher, he shows how social sensitivity and wisdom can profoundly reshape conflicts.
      In one encounter in Iraq, a quick-witted U.S. commander turned a Muslim mob’s threats into laughter when he ordered his soldiers to kneel, lower rifl es and smile - averting a potentially fatal clash.
      Goleman deftly discusses relevant neural pathways, including the thalamus and amygdala, which together regulate sensory and arousal stimuli.
      He speaks of
      - spindle cells, which rapidly process social decisions;
      - mirror neurons, which sense another’s movements;
      - dopamine neurons, which react to pleasure-inducing neurotransmitters that flow freely while two lovers gaze.
      The author’s introductory tour through this emerging research landscape helps readers grasp core concepts of social neuroscience, illustrating abstractions with poignant anecdotes, without excessive jargon.
      Goleman also explains how such research may influence our lives.
      Given our socially reactive brains, we must "be wise" he says and be aware of the ways that our moods influence the biology of each life we touch.
      Cfr. :
      http://www.amazon.com/Social-Intelligence-Science-Human-Relationships/dp/0553803522

    3. Natural Conflict Resolution
      Filippo Aureli & FMD van Waal - University of California Press (1 edition), August 7, 2000 – ISBN-10 : 0520223462 / ISBN-13 : 978-0520223462
      Aggression and competition are customarily presented as the natural state of affairs in both human society and the animal kingdom.
      Yet, as this book shows, our species relies heavily on cooperation for survival as do many others - from wolves and dolphins to monkeys and apes.
      A distinguished group of fifty-two authors, including many of the world's leading experts on human and animal behavior, review evidence from multiple disciplines on natural conflict resolution, making the case that reconciliation and compromise are as much a part of our heritage as is waging war.
      Chimpanzees kiss and embrace after a fight.
      Children will appeal to fairness when fighting over a toy.
      Spotted hyenas, usually thought to be a particularly aggressive species, use reconciliation to restore damaged relationships.
      As these studies show, there are sound evolutionary reasons for these peacekeeping tendencies.
      This book also addresses the cultural, ecological, cognitive, emotional and moral perspectives of conflict resolution.
      Cfr. :
      http://www.amazon.com/Natural-Conflict-Resolution-Filippo-Aureli/dp/0520223462

    4. Laat de chaos los - Paralellen tussen kosmos en psyche
      Stephen H Wolinsky (vertaling : Ananto Dirksen) - Altamira, Heemstede, 1999 / Gottmer/H.J.W. Becht, 01-11-1999 - EAN : 9789069634449
      Cfr. :
      http://www.bol.com/nl/p/boeken/laat-de-chaos-los/666840664/index.html

    5. De eenheid van leven - De ontdekking van de verborgen overeenkomsten tussen het biologische, het psychologische en het sociale leven
      Fritjof Capra (vertaling : Gerard Grasman) – Utrecht/Antwerpen : Servire, oktober 2002 - ISBN10 : 9021532492 / ISBN13 : 9789021532493
      In zijn nieuwste boek 'De eenheid van leven' presenteert Fritjof Capra, de wereldberoemde auteur van o.m. 'De tao van fysica' – cfr. :
      http://www.bol.com/nl/p/boeken/de-tao-van-fysica/1001004002401282/index.html -, een nieuw begrip van wat leven eigenlijk is.
      De mens moet zich deel weten van het grote geheel en daarnaar handelen.
      Globalisering, biotechnologie en ecologische bewustwording zijn trends die ingrijpen in de levende netwerken waarvan ook de mens onderdeel is.
      Capra laat zien hoe het biologische en het sociale leven samenhangen.
      Vanuit zijn wetenschappelijk én spiritueel gedreven visie, schildert hij een indrukwekkend panorama van de eenheid van leven.
      Capra heeft uiteindelijk een positieve boodschap : de mensheid als geheel, maar ook elk individu, kan keuzes maken tussen de kansen en bedreigingen die de toekomst brengt.
      Wij kunnen tegengestelde ontwikkelingen met elkaar verzoenen om het leven op deze planeet te behouden en te versterken.
      Cfr. :
      http://www.bol.com/nl/p/boeken/de-eenheid-van-leven/1001004001712389/index.html  

    6. Werken aan balans - Een geïntegreerd traject gericht op zelfsturing bij stressgerelateerde klachten - Evaluatie van de pilootfase
      Kuiper D, Dijkstra GJ, Groothoff JW - Noordelijk Centrum voor Gezondheidsvraagstukken, Sectie Toegepast Onderzoek, (NCG/TO), Universitair Medisch Centrum Groningen, maart 2006 - ISBN: 90 77113 43 6

    7. De structuur van wetenschappelijke revoluties
      T. Kuhn (vertaling : Bastiaan Willink) - Uitgeverij Boom, mei 2003 – ISBN10 9053528008 / ISBN13 9789053528006
      Recensie – NBD|Biblion : De Amerikaanse auteur(1922-1996), aanvankelijk fysicus, later wetenschapshistoricus, constateert in de geschiedenis een voortdurende neiging om de vooruitgang van de wetenschap lineair/cumulatief te verklaren : ontwikkeling door aanwas.
      Naast de normale ontwikkeling komen er in de geschiedenis echter radicale keerpunten voor, die de bestaande wetenschappelijke traditie omverwerpen : wetenschappelijke revoluties.
      De auteur verduidelijkt deze revoluties door middel van illustraties (Copernicus, Newton) en tracht de structuur ervan nader te verklaren.
      In de wetenschapstheorie een standaardwerk, bedoeld voor historiografen, wetenschapsfilosofen en geinteresseerde intellectuelen.
      Herziene en geactualiseerde vertaling met een informatief voorwoord.
      Cfr. :
      http://www.bol.com/nl/p/boeken/de-structuur-van-wetenschappelijke-revoluties/1001004001647560/index.html

    8. De boom der kennis - Hoe wij de wereld door onze eigen waarneming creëren
      'The Tree of Knowledge - The Biological Roots of Human Understanding
      ' - Shambhala, Boston & London, 1987
      H.R. Maturana en F.J.Varela, beiden neuroloog - Amsterdam : Contact, 1989

      De auteurs zien de hele evolutie als een complex adaptief systeem.
      Recensie door G.J.C. Lokhorst onder de titel 'De mens als duikboot' in NRC Handelsblad, Zaterdags Boekenbijvoegsel, p. 3, September 30, 1989 - ISSN 0002-5259 : Humberto R. Maturana (RCH) is neurobioloog en doceert aan de Universiteit van Chili.
      Naar aanleiding van de vraag naar de aard van het leven en de aard van cognitie formuleerde hij een antwoord : 'autopoiese' (het Griekse 'auto' betekent 'zelf' en 'poiein' 'maken').
      Samen met Francisco J. Varela schreef hij "Autopoiesis and Cognition - The Realization of the Living" (D. Reidel Publishing Company, 1980 & Springer (1 edition), August 31, 1991 – ISBN-10 : 9027710163 / ISBN-13 : 978-9027710161 – cfr. :
      http://www.amazon.com/Autopoiesis-Cognition-Realization-Studies-Philosophy/dp/9027710163 -) en "The Tree of Knowledge - The biological roots of human understanding" (Shambhala, 1987, vert. "De Boom der Kennis. Hoe wij de wereld door onze eigen waarneming creëren", Contact 1988 – cfr. : http://www.amazon.com/Tree-Knowledge-Biological-Roots-Understanding/dp/B001U0WY6W/ref=sr_1_1?ie=UTF8&s=books&qid=1236280832&sr=1-1 -), waarin hij deze verandering van de kentheorie ontvouwt, die een nieuwe grondslag vormt voor de biologistische systeemtheorie.
      Hij onderzocht de ideeën over cognitie en perceptie en heeft het begrip "mens-zijn" en de psychotherapie uitgebreid door het blootleggen van de biologie van de waarnemer.
      Maturana"s systemische kijk op menselijke ervaringen heeft geleid tot een veranderd begrip van het mens-zijn, met als belangrijkste gevolg dat er een herwaardering heeft plaatsgevonden van emoties als het fundament van het menselijk leven en zelfs van de rationaliteit.
      Cfr. :
      http://framework.v2.nl/archive/archive/leaf/other/.xslt/nodenr-70123
      De meeste mensen denken dat onze kennis ergens in ons hoofd ligt opgeslagen.
      De hersenen zouden afbeeldingen van de buitenwereld bevatten, die ons in staat stellen onze weg in de wereld te vinden.
      In de loop van ons leven stellen we onze `cognitieve landkaarten' steeds bij, zodat ze de werkelijkheid steeds accurater weerspiegelen en we ons steeds beter kunnen oriënteren.
      Volgens de uitgeweken Chileense neurobioloog Maturana en zijn leerling Varela is deze populaire visie volstrekt onjuist.
      Uit hun onderzoek naar de visuele systemen van verscheidene diersoorten trekken zij de conclusie dat de hersenen helemaal geen plaatjes bevatten van de wereld om hen heen.
      De hersenen verkeren in dezelfde positie als de kapitein van een onderzeeboot die zijn schip nooit heeft verlaten, maar wel precies weet hoe hij moet reageren op de standen van de meters aan boord.
      Stel dat hij zijn schip ergens heeft laten opduiken en we hem complimenteren met zijn stuurmanskunst : "Uitstekend, u heeft alle klippen vermeden en bent sierlijk boven water gekomen."
      Hij zou perplex staan : "Wat kletst u over klippen en boven water komen ? Ik heb alleen maar wat wijzerplaten afgelezen en wat hendels overgehaald, in een vaste volgorde waarmee ik vertrouwd ben. Ik heb geen bijzondere manoeuvre gemaakt en ik weet niet wat u bedoelt met een onderzeeboot. Maakt u soms een grapje ?"
      Onze hersenen zijn even geïsoleerd als deze kapitein.
      Het enige dat tot hen doordringt, zijn de signalen die binnenkomen via de zintuigen, maar deze geven niet meer informatie over de omgeving dan de wijzers in de duikboot.
      De zintuigen zijn bovendien geen passieve doorgevers van informatie.
      Ze zijn uiterst actief, selecteren, misvormen en interpreteren dat het een lieve lust is en bepalen zo in feite zelf een groot deel van de boodschap.
      Kennis is `autopoëtisch', zoals Maturana het noemt : zij schept zichzelf, in een voortdurende dynamische wisselwerking met de omgeving.
      Iedereen creëert zijn eigen wereld.
      Wij zijn geen lijdzame ontvangers van informatie die al bestaat, geen fototoestellen die alleen maar registreren.
      Als kennis geen weerspiegeling van de werkelijkheid is, wat is ze dan wel ?
      Volgens Maturana en Varela is kennis gelegen in de wisselwerking tussen een organisme en zijn omgeving.
      Kennis is een bepaalde vorm van `structurele koppeling' van deze twee : "We spreken van kennis wanneer we in een bepaalde context effectief gedrag waarnemen."
      Kennis zit niet binnen in een organisme.
      Het organisme is in zichzelf opgesloten, net zoals de kapitein in zijn schip en kan daarom onmogelijk bepalen of het een geslaagde `structurele koppeling' met zijn omgeving heeft.
      Alleen een waarnemer, een buitenstaander, kan zeggen of een dier of mens ergens verstand van heeft.
      Het is moeilijk om een oordeel over de filosofisch-biologische visie van Maturana en Varela te vellen.
      Af en toe hullen zij banale waarheden in wollige en quasi-diepzinnige woorden, soms lijken zij toch ook weer een echt nieuw gezichtspunt te presenteren.
      Veel lezers zijn de laatste mening toegedaan : Maturana en Varela hebben een grote schare van bewonderaars.
      Het is het beste om zelf te oordelen.
      Het boek bevat niet louter en alleen theorie, maar ook smeuïge verhalen zoals die over de mentale vermogens van twee Indiase `wolfsmeisjes' die temidden van een wolvenfamilie waren opgegroeid.
      Bovendien bevat het tientallen aardige afbeeldingen, zoals een grafiek waarin de maximumsnelheden van moleculen, dieren en melkwegen met elkaar worden vergeleken.
      Wat men er uiteindelijk ook van mag vinden, het is in ieder geval aangenaam toeven in 'De boom der kennis'.
      Cfr. :
      http://homepages.ipact.nl/~lokhorst/maturana.html
      Cfr. :
      http://www.amazon.com/Tree-Knowledge-Biological-Roots-Understanding/dp/B001U0WY6W/ref=sr_1_1?ie=UTF8&s=books&qid=1236280832&sr=1-1


    Twee reacties :

    1/ - Maarten de Boo

    Fibromyalgie anders bekeken
    Publicatie: Nr. 37 - 14 september 2007
    Maarten de Boo : “
    In het artikel van Bert Busard over fibromyalgie en de mogelijkheden die een paradigmashift biedt (MC 27/2007 : 1168) zitten enkele onwenselijke tegenstrijdigheden.
    Ik bestrijd niet dat het gebruik van een relationeel communicatief paradigma in diagnostiek en behandeling bij deze aandoening geen gunstig therapeutisch resultaat kan hebben.
    Ik meen dat deze aandoeningen vergrote stressreactiviteit en veranderingen in centrale pijngewaarwording inderdaad met meer dan alleen aandacht voor een fysiologische causaliteit moeten worden benaderd. (1)
    Het gaat hier bij uitstek om systemische aandoeningen die slechts te begrijpen zijn als in de verschijningsvorm de biologische, psychologische en sociale aspecten worden herkend en in de uitleg en het behandelvoorstel worden betrokken.
    Om niet de indruk te wekken dat het daarmee aandoeningen zijn die alleen door psychiaters en psychologen kunnen worden behandeld, meen ik dat niet een nieuw of aanvullend paradigma wordt aangedragen.
    Het dualisme in de gezondheidszorg en de onfortuinlijke scheiding tussen de behandeling van somatische en mentale aspecten van ziekten, van zieke mensen, moet worden geslecht door het in ere herstellen van het biopsychosociaal model.
    Dit kan eenzijdigheid, reductionisme of eclecticisme voorkomen.
    Het model kan verder worden uitgewerkt aan de hand van de meest recente neurobiologische en epidemiologische inzichten over de relatie tussen deze aspecten. (2)
    Ik sta een pragmatisch model voor waarbij niet een scheiding maar een overbrugging, een verbinding tussen de aspecten van ons functioneren wordt gebruikt.
    Bij fibromyalgie is beide waar of beter gezegd alles : er is een ondragelijke pijn en vermoeidheid (die terug te brengen is op een sensitisatie in het centraal zenuwstelsel), weinig contact met lichamelijke signalen en weinig veiligheid in het contact met anderen.
    Niet een tweede paradigma, maar een samenhangend medisch model voor alle facetten van ons functioneren is nodig om ook mensen met complexe ziekten een behandeling te bieden die groei en herstel kan brengen.
    Dan kan de arts als coach optreden in de zoektocht naar het eigen relationele antwoord : de verhouding naar jezelf, je lichaam en de verhouding naar de ander
    .
    Delft, juli 2007
    Maarten de Boo, psychiater.

    Literatuur

    1. Narrative review - The pathophysiology of fibromyaligia
      Abeles AM, Pillinger MH, Solitar BM, Abeles M, New York University School of Medicine, New York University Hospital for Joint Diseases and New York Harbor Healthcare System, New York, New York 10003, USA - Ann Intern Med. 2007 May 15;146(10):726-34 - PMID: 17502633
      Primary fibromyalgia is a common yet poorly understood syndrome characterized by diffuse chronic pain accompanied by other somatic symptoms, including poor sleep, fatigue and stiffness, in the absence of disease.
      Fibromyalgia does not have a distinct cause or pathology.
      Nevertheless, in the past decade, the study of chronic pain has yielded new insights into the pathophysiology of fibromyalgia and related chronic pain disorders.
      Accruing evidence shows that patients with fibromyalgia experience pain differently from the general population because of dysfunctional pain processing in the central nervous system.
      Aberrant pain processing, which can result in chronic pain and associated symptoms, may be the result of several interplaying mechanisms, including central sensitization, blunting of inhibitory pain pathways, alterations in neurotransmitters and psychiatric comorbid conditions.
      This review provides an overview of the mechanisms currently thought to be partly responsible for the chronic diffuse pain typical of fibromyalgia.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/17502633
    2. The end of the biopsychosocial model ? - An assessment and alternatives
      Waterman GS en Brendel DH. (2005) - Symposium on de 158th Annual Meeting of the APA, Atlanta, GA
      Cfr. :
      -
      http://www.psychiatrictimes.com/display/article/10168/54761?pageNumber=2
      -
      http://www.critpsynet.freeuk.com/Pilgrim.htm
      -
      http://en.wikipedia.org/wiki/Biopsychosocial


    2/ - Hanneke van Lier

    Fibromyalgie anders bekeken
    Publicatie: Nr. 37 - 14 september 2007
    Hanneke van Lier : “
    Complimenten aan Bert Busard voor de heldere beschouwing door middel van paradigma’s (MC 27/2007: 1168).
    Het expliciet maken van het perspectief van waaruit men kijkt en handelt, beleef ik als zeer positief.
    De volgende vraag blijft na lezing echter bij mij bestaan : hoe komt een patiënt of cliënt zo snel mogelijk uit bij de volgens recente inzichten beste behandeling ?
    Paradigmawisselingen kosten tijd en soms moet nogal een omweg worden afgelegd voordat de behandeling wordt aangeboden die empirisch gezien het effectiefst is.
    Zou het niet klantvriendelijk zijn om als beroepsgroep een meer integrerend paradigma naast of tussen de genoemde paradigma’s te presenteren ?
    Graag maak ik u hierbij deelgenoot van een vingeroefening paradigmaontwerpen, waarbij ik uitzie naar een discussie.
    Als derde paradigma stel ik het onderstaande schema voor.

    Den Haag, juli 2007
    Hanneke van Lier, verpleeghuisarts

    Cfr. : http://www.corv.nl/Forum/topic.asp?ARCHIVE=true&TOPIC_ID=6267&whichpage=4


    05-03-2009 om 22:01 geschreven door Jules

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Largest-ever chronic fatigue syndrome research initiative
    Klik op de afbeelding om de link te volgen
























     







    Largest-ever chronic fatigue syndrome research initiative

    Announced by CFIDS Association of America (www.cfids.org -) on December 3, 2008


    The four million Americans who suffer from chronic fatigue syndrome (CFS) have new reason for hope today with the announcement of an unprecedented research program to help identify biomarkers to improve diagnosis and treatment of CFS.
    The announcement was made by the CFIDS Association of America, which is funding the program, called the Accelerate CFS Research Initiative.

    The initiative was made possible by the successful completion of a yearlong, million-dollar fundraising campaign, the largest research campaign for CFS to date in the United States.
    The CFIDS Association has funded more than $5.4 million in research since 1987, making it second only to the federal government in CFS research spending.

    The campaign is enabling us to develop a revitalized research program for CFS,” said Kimberly McCleary, president and CEO of the CFIDS Association : “Today, the Accelerate CFS Research Initiative has already resulted in research grants totaling $647,940 to six research teams in the U.S. and Canada. This will lead to an international network of scientists who routinely collaborate and communicate to accelerate the pace of CFS research.

    The grants were awarded following a rigorous process that included a review of proposals by 44 independent experts for scientific merit and by CFIDS Association board members for strategic merit.
    We were very impressed with the number and caliber of grant proposals we received this year, which signals a heightened level of interest in CFS research,” said Suzanne Vernon, PhD, the CFIDS Association’s scientific director : “And most of the grant recipients, while experts in their respective fields, are new to CFS research. It’s critical to attract new investigators to CFS research in order to propel the field forward.

    The grant recipients are :

    • Gordon Broderick
      Gordon Broderick
      , PhD, associate professor in the Department of Medicine at the University of Alberta in Canada. Broderick, a chemical engineer and leader in bioinformatics, will lead a cross-disciplinary team from four institutions to study adolescent patients who became ill with CFS after contracting infectious mononucleosis, which is caused by the Epstein-Barr virus.
      By studying the immune and endocrine response in patients from the time they get infectious mononucleosis to the development of CFS and through the first 24 months of illness, the researchers hope to identify biomarkers for early disease and for disease progression.
      These markers are essential for early detection and diagnosis and may point to novel treatment courses.

    • Kathleen Light
      Kathleen Light, PhD, a research professor at the University of Utah Health Sciences Center and her team will try to uncover the mechanisms involved in the chronic pain that afflicts 40%-70% of CFS patients.
      This study will confirm or negate preliminary evidence Light gathered during an NIH-funded study demonstrating that receptors located on blood cells are increased and overactive in people with CFS, causing increased pain sensitivity.
      Light theorizes that increases in specific receptors following exercise may be blood-based biomarkers for CFS and could lead to a medical test to identify CFS patients.
      The study will also examine a combination of blood receptors to help identify subtypes of CFS and guide treatment of specific patient subgroups.

    • Marvin Medow
      Marvin Medow, PhD, associate director of the Research Division of the Department of Pediatrics at New York Medical College and his colleagues will investigate whether increased pooling of blood in the abdomen of CFS patients results in reduced cerebral blood flow.
      Medow will examine physiologic and oxidative stress changes associated with disturbance in blood flow.
      These results will help determine if alterations in blood flow affect brain metabolism.

    • Bhubaneswar Mishra
      Bhubaneswar Mishra, PhD, a computational biology expert and professor at the Courant Institute of Mathematical Sciences at NYU will use state-of-the-art bioinformatics and computational biology tools to create an agnostic computational model of CFS - a kind of “Google for CFS” that will be part database, part knowledge-base, part research network.
      This new resource will provide a “systems view” of CFS that accumulates published CFS literature and experimental data to disentangle complex relationships among reported findings and discover causes of CFS.

    • Sanjay Shukla
      Sanjay Shukla, PhD, a microbiologist and research scientist at Marshfield Clinic Research Foundation and his team are using metagenomics to determine if the ratio of good to bad intestinal bacteria in CFS patients is altered and whether this imbalance in gut bacteria may be responsible for triggering CFS symptoms.
      Recent advances in metagenomics have demonstrated the significance of altered gastrointestinal bacteria in illnesses like HIV, diabetes, Crohn’s disease, inflammatory bowel disease and ulcerative colitis.
      Shukla theorizes that CFS patients also have an imbalance of good and bad intestinal bacteria, resulting in enhanced intestinal permeability - called 'leaky gut' - allowing bacteria to move across the protective intestinal barrier and causing chronic inflammation and immune activation in CFS patients.
      The study will rigorously examine these issues and investigate whether exercise may worsen this bacterial translocation, helping contribute to postexertional malaise in CFS.
      This study will contribute to our understanding of the relationship between the human microbiome and CFS.
      It may also produce evidence for new treatments, including the use of probiotics.

    • Dikoma Shungu
      Dikoma Shungu, PhD is a physics professor and research scientist at Weill Medical College of Cornell University.
      Using a brain scanning technique called magnetic resonance spectroscopy, which not only provides a picture of the brain but also detects and measures various brain chemicals, Shungu and his team will build on a preliminary study showing that brain fluid of CFS patients contains significantly elevated levels of lactic acid or lactate, a substance important in metabolism (results from this preliminary study, also funded by the CFIDS Association, were published in October 2008 in the journal NMR in Biomedicine).
      The investigators will also determine whether lactate levels are higher in CFS patients because their brains contain high levels of toxic compounds that cause a condition called oxidative stress, which could implicate chronic inflammation or because mitochondrial dysfunction is causing their brain energy production to malfunction.
      If this study is successful, brain lactate levels could provide an objective diagnostic biomarker for CFS and evidence of a metabolic problem in these patients.

    The research studies being funded this year are interconnected in many ways.
    Not only will several of the investigators collaborate directly, all of them will be sharing their data with each other and with other scientists,” Vernon said : “This is essential if we are to make rapid progress in unraveling the complexities of a multisystem illness like CFS and in providing medical professionals with better diagnostic and treatment tools to improve patients’ lives.

    Cfr. : http://www.cfids.org/about-cfids/research-release12-08.pdf



    05-03-2009 om 01:18 geschreven door Jules

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    04-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.In de kenniseconomie lopen de Hazen anders
    Klik op de afbeelding om de link te volgen

    Mathieu Weggeman




     

    In de kenniseconomie
    lopen de Hazen anders

    Mathieu Weggeman, Hoogleraar innovatie aan de Technische Universiteit Eindhoven - NRC van 11 mei 2004 - © 2007 Managementissues.com

    Max Herold : “Ik vroeg Mathieu Weggeman me de electronische versie van dit artikel toe te sturen.
    De reden voor dit verzoek was een discussie die ik enige tijd geleden meemaakte over een doelstelling zoals die op de Europese top in Lissabon werd geformuleerd.
    Daar werd het doel gesteld Europa binnen tien jaar tot dé kenniseconomie van de wereld te maken.

    Tijdens deze interdepartementale discussie viel me op dat velen van de aanwezigen die als een typisch beleidsprobleem zagen.
    Een doel dat met het bestaande beleidsmatige en/of economische denken kan worden aangepakt.
    Weer anderen zagen het als een gewone hype die wel weer over zou gaan.
    Maar in mijn ogen was/is het meer een (macro)organisatorisch probleem.
    Als je die gedachte koppelt aan het begrip economische 'ordening', dan zou je wel eens kunnen stellen dat er enkele vooronderstellingen, zoals die decennia lang zijn gehanteerd m.b.t. die economische ordening, langzaam aan het veranderen zijn...
    Welnu Mathieu heeft op die kenniseconomie en de kennis van het kabinet daaromtrent, zo zijn eigen kijk dus laten we hem snel het woord geven
    ”.

    De Haagse plannen om medewerkers langer aan het werk te houden omdat dat geld oplevert, bewijst eens te meer dat dit kabinet nog steeds niet goed weet wat het betekent om een kenniseconomie te besturen.
    In zo'n economie lopen de hazen anders dan in de fabrieken en kantoren van de industriële economie.
    Voor de werknemers van die traditionele organisaties zijn ervaring en technische vaardigheden het belangrijkst en hoe langer je werkt, hoe meer ervaring je opdoet.
    Dat geldt ook voor de vaardigheden.
    Als je ze maar blijft toepassen, ontwikkelen ze zich, want er zijn immers heel weinig mensen die al twee jaar lang elke dag een uur piano studeren en steeds slechter gaan spelen.

    Hou je de medewerkers van die kantoren en fabrieken langer aan het werk, dan kunnen ze ook langer kapitaliseren op hun steeds grotere ervaring en op hun voortdurend toenemende vaardigheid.
    De kans dat hun productiviteit stijgt naarmate hun leeftijd toeneemt, is dan inderdaad groot.
    Alleen hebben we in Nederland steeds minder van die fabrieken en kantoren waar mensen min of meer routinematig bezig zijn om hetzelfde werk steeds beter en efficiënter uit te voeren.
    Slechts in sectoren als de landbouw, de horeca, het transport, de bouw en de thuiszorg en achter de loketten van banken en gemeentehuizen, kan het langer doorgaan met werken mogelijk meer geld opleveren dan momenteel het geval is.
    En dan nog zal de vreugde van korte duur zijn, omdat dat werk - waarbij het vooral draait om de productiefactor fysieke arbeid - in toenemende mate geautomatiseerd wordt.

    Een dergelijke redenering gaat echter niet op voor de moderne kennisintensieve organisatie.
    Daar treffen we werknemers aan waarvoor de productiefactor kennis tenminste even belangrijk is als ervaring en vaardigheid.
    Veel van die beroepen beginnen met een 'a': artsen, architecten, adviseurs, accountants, advocaten, apothekers, amerikadeskundigen en dergelijke.
    Dat type medewerkers heeft in onze kenniseconomie ruim de overhand.
    Geschat wordt dat op dit moment in Nederland meer dan 70% van alle werkenden tot de categorie kenniswerkers behoort en er komen er in snel tempo steeds meer bij.
    Voor hen geldt dat zij voortdurend relatief veel moeten leren om goed in hun vak te blijven, relatief ten opzichte van bijvoorbeeld buschauffeurs, voetballers, ambachtslieden en productiemedewerkers.
    Dat vereist het bijhouden van vakliteratuur, het bezoeken van congressen en symposia, het deelnemen aan opleidingen en studiedagen, het willen werken in meester-gezel relaties en het kunnen plaatsen van innovaties die klanten , burgers en patiënten op internet gevonden hebben.

    Uit onderzoek blijkt dat de motivatie om voortdurend vakinhoudelijk vooraan te blijven lopen, bij het overgrote deel van de kenniswerkers afneemt naarmate de leeftijd vordert.
    Het is niet zo dat dan de leervaardigheden als vanzelf minder worden.
    Wél treedt er bij het vorderen der jaren een soort mentale moeheid op : "Moet het nu wéér anders, wanneer stopt het nu eens met die vernieuwingen !?".
    En omdat kennis steeds sneller veroudert, slaat die moeheid steeds eerder toe.
    Voor ontwerpers van internet-gerelateerde software en voor nano- en biotechnologen kan dat al rond de 35 gebeuren; voor elektrotechnisch ingenieurs en fiscaal-juristen zo'n vijf tot tien jaar later.

    Dat betekent dat veel kenniswerkers op veel jongere leeftijd dan vroeger aan het eind van hun professionele Latijn geraken.
    Het tot op hogere leeftijd laten doorwerken van kenniswerkers leidt er dus uiteindelijk toe dat een groter deel van de beroepsbevolking aan de gang is met verouderde kennis.
    Tel uit je winst.
    De chirurg die niet geleerd heeft endoscopisch te behandelen, blijft grote incisies maken.
    Dat levert meer trauma's en een langere hersteltijd op voor de patiënt, een groter beslag op voorzieningen en meer inzet van ondersteunend personeel.
    Allemaal zaken die kostenverhogend werken.

    Een ander voorbeeld speelde zo'n twaalf jaar geleden.
    Ik had ergens gelezen dat er uit amalgaamvullingen minivoltjes kunnen ontsnappen die onder bepaalde omstandigheden de elektrische stroompjes in de hersenen beïnvloeden.
    Daarom vroeg ik mijn tandarts het nieuwe gaatje in mijn kies te willen vullen met keramiek of porselein.

    Die bemoeienis van een bijdehante leek met zijn vak, stelde hij geenszins op prijs : "Meneer, die techniek staat nog in de kinderschoenen. Het krimpen en uitzetten van het materiaal hebben we nog niet onder controle".
    Pas veel later begreep ik wat er eigenlijk aan de hand was.
    Mijn tandarts was toen 54 en meer bezig met zijn tweede huis in Spanje dan met het bijhouden van de vernieuwingen in zijn vak.
    Hij had al 30 jaar kiezen met amalgaam gevuld en zag niet in waarom hij dat de laatste jaren voor zijn pensioen niet zou kunnen blijven doen.

    Het langer laten doorwerken van professionals, kan er in onze kenniseconomie toe leiden dat ook op andere gebieden dit soort situaties nog vaker voor gaat komen dan nu al het geval is.
    Met de vergrijzing zullen we steeds meer kenniswerkers krijgen die 'uitdieselen' op de methoden en technieken die ze al beheersen en die de innovaties in hun vak laten voor wat ze zijn.
    Het gevolg daarvan is dat steeds meer patiënten, klanten en burgers producten en diensten geleverd krijgen waarvoor inmiddels alternatieven bestaan die goedkoper, sneller, preciezer, veiliger, effectiever, gezonder, makkelijker of gebruiksvriendelijker zijn.
    De maatschappelijke kosten van dat professioneel conservatisme zijn hoog.
    Het financiële saldo van de door Den Haag voorgestelde arbeidsduurverlenging, zou daarom wel eens eerder negatief dan in de buurt van de nul uit kunnen komen.
    In het beste geval zijn de plannen van het kabinet op dit punt dus lood om oud ijzer.

    De hooggeleerde Paul Scheffer sprak over 'vernietiging van sociaal kapitaal' als mensen boven de 55 niet meer zouden werken.
    Dat klopt voor ambachtelijk werk zoals glas blazen, schapen scheren en violen bouwen en ook voor die paar koekjesfabrieken die we nog in Nederland hebben, maar dat klopt helemaal niet voor het overgrote deel van onze organisaties waar de vloer bevolkt wordt door kenniswerkers.

    Kenniswerkers verplichten langer door te werken, is alleen verantwoord als zij ook verplicht worden om state of the art in hun vak te blijven.
    Dat impliceert blijven studeren tot op hoge leeftijd en het beschikbaar stellen van tijd voor deskundigheidsbevordering.
    Ik heb destijds het ministerie van van Volksgezondheid, Welzijn en Sport mogen adviseren over een mid-life studie voor medisch specialisten waarbij ze rond hun veertigste weer voor een of twee jaar teruggaan naar de universiteit.
    Dat was zo'n slecht idee nog niet, te meer daar dankzij de wachtlijsten de gedateerde kennis van de oudere specialist in ons land niet zo'n issue is.

    Ook het door Hans Weijers in zijn tijd als minister van Economische Zaken geïntroduceerde T-profiel voor professionals – cfr. : http://www.carrieretijger.nl/carriere/profiel/t-profiel -, is een goed voorstel.
    Kern daarvan is dat de kenniswerker in de tweede fase van de loopbaan zijn professioneel repertoire aanzienlijk verkleint door te kiezen voor een specialistisch deelgebied dat hij diepgaand wil blijven beheersen (de poot van de T).
    Daarnaast houdt hij één tot drie aanpalende gebieden op appreciatie niveau bij, teneinde met collega's over de breedte van het vak te kunnen communiceren.
    De kans dat je een klein repertoire tot in lengte van dagen state of the art kunt bijhouden, is immers groter dan geldt voor een breed repertoire.
    Bovendien is de 'man of all seasons' en de 'Jack of all trades' in de kenniseconomie van vandaag een ongeloofwaardige figuur.

    Heel goed weten waar je het over hebt zolang je in functie bent, dat is wat nu nodig is.
    Kenniswerkers langer in dienst houden, zonder hen terug naar school te sturen, levert daar geen enkele bijdrage aan en kost maatschappelijk meer dan het oplevert.
    Het is 'penny wise, pound foolish' (= kosten besparen lijkt nuttig, maar kan op termijn duurder uitvallen).

    Cfr. : http://www.managementissues.com/kennismanagement/kennismanagement/in_de_kenniseconomie_
    lopen_de_hazen_anders_20050203106.html




    04-03-2009 om 00:36 geschreven door Jules

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    03-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.The 3rd Meeting of the International Advisory Group (AG) for the Revision of ICD-10 Mental and Behavioural Disorders
    Klik op de afbeelding om de link te volgen

     



    ICD-10
    International Statistical Classification of Diseases
    and Related Health Problems
    - 10th Revision -

    Fibromyalgia

    The ICD-10 lists fibromyalgia under M79.7

    Chapter XIII - Diseases of the musculoskeletal system and connective tissue (M00-M99) - Soft tissue disorders (M60-M79) - Other soft tissue disorders (M70-M79)
    Cfr. : http://www.who.int/clas
    sifications/apps/icd/icd10
    online/?gm70.htm+m797

    Chronic fatigue syndrome

    The Chronic Fatigue Syndrome Advisory Committee (CFSAC) has recommended CFS to be placed under G93.3

    The International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) - cfr. : http://www.cdc.gov/nchs/about/otheract/icd9/abticd
    10.htm
    - lists CFS under the R53 code ('
    Malaise and Fatigue') and chronic fatigue syndrome, post viral under G93.3 (which implies sudden onset following a virus, but excludes gradual or undetermined onset, placing CFS under R53.82 ('Chronic fatigue, unspecified').
    But the ICD-10-CM is not yet implemented and still subject to revision.
    The Chronic Fatigue Syndrome Advisory Committee (CFSAC) has recommended CFS to be placed under the same neurological code as Myalgic Encephalomyelitis (ME) and Post-Viral Syndrome (PVS) namely
    G93.3.


    The 3rd Meeting of the International Advisory Group (AG) for the Revision of ICD-10 Mental and Behavioural Disorders
    - Held in Geneva Switzerland, 11/12 March, 2008 -

    World Health Organization, Department of Mental Health and Substance Abuse

    First meeting
    - 11 – 12 January 2007 -
    Cfr. : http://www.who.int/mental_health/evidence/icd_advisory_group_meeting_jan_%202007_summary.pdf

    Second meeting
    - 24 – 25 September 2007 -
    Cfr. : http://www.who.int/mental_health/evidence/icd_summary_report_sept_2007.pdf


    Meeting Summary Report

    The AG was constituted by the World Health Organization (WHO) with the primary task of advising WHO on all steps leading to the revision of the mental and behavioural disorders classification in ICD-10 in line with the overall revision process.
    A list of participants in this meeting is provided in the Annex.
    This Summary Report provides a summary of the conclusions reached during the meeting.


    1. - Opening Remarks

    The meeting was opened by Dr. Ala Alwan, Assistant Director General, Noncommunicable Diseases and Mental Health.
    Dr. Alwan emphasized the importance of the revised ICD Mental and Behavioural Disorders classification as a tool for improving services for people with mental disorders and to encourage accountability among governments for their efforts to reduce the substantial disease burden associated with them.


    2. - Large groups of diagnoses and entities and spectra
    Introduced by Dr. Gavin Andrews
    Presentations by Dr. Robert Krueger, Dr. William Carpenter, Dr. David Goldberg and Dr. Gavin Andrews

    The purpose of this series of presentations was to introduce a proposed re-conceptualization of the

    large groups of mental disorders currently found in ICD-10.
    This re-conceptualization relates to how disorders are grouped together into classes and not to the criteria for individual diagnoses.
    This conceptual schema was offered as a basis for discussion by the AG and not as a completed project.
    The proposed grouping is based on several factors, including symptom presentation, risk factors, treatment response and other biological, cognitive and emotional characteristics.
    Based on the available information, four large clusters of disorders were proposed, which were the focus of the subsequent presentations.
    It is important to note that the names used in this report to refer to these clusters are simply for the purpose of clarity and with the AG’s awareness that a more complete discussion of terminology would be needed.

    Dr. Krueger reviewed evidence from a variety of studies indicating that common mental disorders separate into two correlated clusters, which have been labelled Internalizing and Externalizing.
    He also presented data suggesting that the Internalizing Disorders cluster further separates in to Distress (e.g., depression, dysthymia, generalized anxiety disorder) and Fear (e.g., phobias, panic disorder).
    The evidence for the coherence of the Externalizing cluster includes genetic effects, course in early adulthood and neural correlates, in addition to phenomenological similarities.
    Prototypic examples of disorders in the Externalizing cluster are those related to alcohol and substance use, conduct disorder, adult antisocial personality disorder and possibly the hyperactivity component of ADHD.

    Dr. Carpenter argued that the current classificatory structure for psychotic disorder fails to define similarities and differences among disorders that result in specific and discrete classification.
    The Summary Report of the 3rd Meeting of the International Advisory Group for the Revision of ICD-10 Mental and Behavioural Disorders current over-specification and arbitrary grouping of disorders has contributed to problems in both research and practice.
    The conceptualization of treatments at a cluster level and the identification of key similarities and differences among disorders within clusters would help to refine the research and therapeutic issues.
    Evidence for the coherence of the Psychotic Disorders cluster comes from research on biomarkers, environmental and genetic influences on psychotic disorders, family studies of schizophrenia spectrum, neural substrates, cognitive and emotional factors, co-morbidity and treatment response.
    The disorders in this cluster include those that are currently classified as psychotic disorders, as well as bipolar disorder and some forms of personality disorder.

    Dr. Goldberg presented evidence for common features within the cluster of Internalizing Disorders.
    These disorders are characterized by distress experienced inwardly and related to the emotions of anxiety, depression and fear.
    Although diagnostic criteria are specific to each disorder, many symptoms are shared so that a wide range of common disorders may be identified by superficial screening.
    As symptom severity increases, the symptoms that differentiate among the disorders appear.
    Disorders in this cluster share common environmental risk factors and substantial similarities in cognitive and emotional processes (e.g., high negative affectivity or “neuroticism”).
    Available treatments are generally effective across disorders within the cluster (e.g., SSRIs, cognitive behaviour therapy).
    Internalizing disorders include generalized anxiety, panic disorder, specific phobias, social phobias, obsessional states, dysthymic disorders, neurasthenia, somatoform disorders, post-traumatic stress disorder and non-psychotic forms of depression.

    Dr. Andrews presented findings relevant to a cluster of disorders characterized by neurocognitive deficit, usually associated with permanent neural loss.
    Dr. Andrews argued that clustering these disorders together can help to facilitate diagnosis, improve treatment processes, improve prognosis by facilitating early identification and treatment and inform research.
    Disorders in this cluster share some genetic and environmental risk factors.
    Treatments that are effective for disorders within this cluster are not disorder-specific and also typically effective for other disorders within the cluster (e.g., anticholine esterase inhibitors, antipsychotic medications, cognitive behaviour therapy).
    At the same time, this cluster was recognized as the most disparate of the four presented.
    The AG acknowledged that this approach would represent a major change in classification, but viewed the proposed approach as a potential basis for the development of a more clinically useful system, both for multidisciplinary mental health professionals and in primary care settings.
    The approach is intuitively appealing, easily understandable, roughly corresponds to the way in which mental health care is often organized and provides a useful correction to the over-pecification that characterizes current classification systems.
    At the same time, the AG noted several limitations and reservations about the proposed approach, in particular regarding the coherence of a single cluster of neurocognitive disorders.
    The AG discussed the idea of a separate cluster for disorders that can be considered under the rubric of developmental disorders.
    There was also considerable discussion about the names for the clusters.

    Based on the AG’s discussion, Drs. Andrews and Goldberg were asked to prepare a more complete

    straw man” grouping as a basis for further discussion.
    This second iteration, presented on the second day, included the notable addition of a category for Bodily Disorders (e.g., eating disorders, sleep disorders, sexual disorders) and the separation of developmental disorders and mental retardation from neurocognitive disorders such as delirium and depression.
    A number of additional issues were raised regarding the revised proposal, but there was not sufficient time for the AG to discuss them thoroughly.
    Further development of the proposal will be reported at the AG’s next meeting.


    3. - Progress in the overall ICD revision
    Introduced by Dr. Bedirhan Üstün and Mr. Can Celik

    Dr. Üstün reminded the AG that the goals of the revision are to develop a multi-purpose and coherent classification with logical linkages to available health-related terminologies and ontologies. ICD-11 should function seamlessly in an electronic health records environment and serve as an international Summary Report of the 3rd Meeting of the International Advisory Group for the Revision of ICD-10 Mental and Behavioural Disorders and multilingual reference standard for scientific comparability and communication purposes.
    Specific challenges for this revision include: to achieve comparable and consistent data across health information systems; to managing the transition from legacy systems and to involve multiple stakeholders on a large scale to capture and synthesize information.
    Web-based tools are available for enhanced communication among individuals involved in the revision process, via three primary methods :

    1. The ICD Update and Revision Platform is a web-based application that allows any user to post proposals or comments and to review other proposals and comment on them.

    2. The ICD-11 draft will be a WIKI-like joint authoring tool, designed for use by ICD-11 Technical Advisory Group (TAG) and WHO editors in the specification of taxonomic rules, definitions and diagnostic criteria.

    3. The ICD terminology provides the basis of the information model linking between ICD and SNOWMED-CT, other ontology and terminologies and clinical interface algorithms.

    The timeline for the revision process is as follows : the Alpha draft version of ICD-11 should be completed in 2010, followed by 1 year for commentary and consultation.
    The Beta draft version should be completed in 2011, followed by field trials, analysis of field trial data and revision during the subsequent 2 years.
    The final version for public viewing should be completed in 2013, with approval by the World Health Assembly in 2014.


    4. - Progress on Coordinating Groups

    Reports from three Coordinating Groups established by the AG were presented and discussed.
    The AG noted that these groups had been appointed for the 2-year period of 2007 – 2008.

    A. - Global Scientific Partnership Coordination Group
    Introduced by Dr. Norman Sartorius
    The Global Scientific Partnership Coordination Group was established to assist the AG in ensuring continued involvement of and input from scientists around the world during the revision process.
    The group has created a Global Scientific Partnership Network that is intended as an important scientific resource for the AG.
    This network will facilitate identification and use of key scientific papers, particularly from countries mainly using languages other than English.
    Its tasks also include identification and evaluation of country-level or regional adaptation of ICD Mental and Behavioural Disorders.
    The AG commended Dr. Sartorius for the group’s progress and plans and expects that Dr. Sartorius will be in close communication with the AG Chair and the Secretariat as the group’s work proceeds.

    B. - Stakeholder Input and Partnership Coordination Group
    Introduced by Dr. Juan Mezzich and Dr. Benedetto Saraceno
    The purpose of this group was to stimulate input, collaboration, and commitment to implementation among the three primary groups of WHO constituents :
    1) users/consumers of mental health services and their families;
    2) multidisciplinary mental health professionals and other relevant health professionals and
    3) governments of WHO member states.
    The AG recognized the important and valuable resources represented by World Psychiatric Association (WPA), its Section on Classification and Diagnostic Assessment and the WPA Global Network of Classification and Diagnostic Groups.
    The AG also believes that it is important to develop relationships with other groups of relevant professional associations, beginning with those represented on the AG.
    These organizations should be encouraged to develop infrastructures to Summary Report of the 3rd Meeting of the International Advisory Group for the Revision of ICD-10 Mental and Behavioural Disorders enable participation, such as WPA has done.
    In terms of service users and family members, the WHO Secretariat will identify groups who may be in a position to participate constructively in the revision process and a plan for communicating with them about the revision.
    In relation to governments, the Secretariat has already initiated communication with a number of member states, as evidenced by the participation of their representatives at AG meetings.
    In view of the current nature and range of tasks related to stakeholder coordination and input, the Terms of Reference and composition of this group will be reviewed at the Fall AG meeting.

    C. ICD-DSM Harmonization Group
    Introduced by Dr. Shekhar Saxena
    The task of this group is to facilitate the achievement of the highest possible extent of uniformity and harmonization between ICD-11 mental and behavioural disorders and DSM-V disorders and their diagnostic criteria.
    Dr. Saxena emphasized the genuine desire of both organizations to achieve harmonization of the two systems.
    He described a variety of specific issues related to differences between the DSM and the ICD-10 that are important areas of discussion by the Harmonization Group.
    The AG endorsed the following statement intended to guide the WHO representatives in their activities as part of the ICD-DSM Harmonization Group : “WHO and APA should make all attempts to ensure that in their core versions, the category names, glossary descriptions and criteria are identical for ICD and DSM. Adaptations of the ICD should be directly translatable into the core version.


    5. - Contributions of epidemiology - Report from the ad-hoc group
    Introduced by Dr. Somnath Chatterji

    At its September, 2007 meeting, the AG appointed Dr. Oye Gureje, Dr. Maria Elena Medina-Mora, Dr. Andrews and Dr. Goldberg to work with Dr. Chatterji to consider the needs to epidemiological data and analyses as a part of the AG’s work.
    Dr. Chatterji provided a discussion of ways in which epidemiological data would make an important contribution to decisions about the classification system.
    For example, using available epidemiological datasets, from the World Mental Health Survey as well as other studies, the effects on or proposed changes on parameters such as case identification and prevalence.
    The AG was in full agreement regarding the relevance and importance of epidemiological data in the revision process.
    The AG recommended that an open call be issued for epidemiological information relevant to series of specific questions based on the information presented by Dr. Chatterji.
    This may help to distribute the resource demands of time-intensive reanalyses of epidemiological datasets.
    The AG recommended formalization of this ad-hoc group as a Coordinating Group reporting to the AG.


    6. Report on progress and plans on public health aspects of diagnoses and classification
    Introduced by Dr. Norman Sartorius

    The WHO/APIRE Conference on Public Health Aspects of Diagnosis and Classification of Mental Disorders was held during 26 – 27 September, 2007, immediately following the most recent AG meeting.
    As Co-Chair of that conference, Dr. Sartorius provided a summary to the AG.
    The conference produced the following outcomes :
    1) Ten background papers regarding the public health implications of diagnosis and classification of mental disorders were developed;
    2) A series of recommendations from a public health perspective regarding the revision of mental disorders diagnosis and classification systems and
    3) Summary recommendations from the previous conferences in the APIRE series on diagnosis, reviewed and revised in order to best serve public health needs.
    The background papers developed for the conference will be finalized for publication as part of a joint WHO/APIRE publication and the recommendations considered as they relate to both DSM and ICD.


    7. - Research versus clinical diagnoses
    Introduced by Dr. Shekhar Saxena and Dr. Norman Sartorius

    Dr. Saxena provided a brief overview of the history of the development of the different versions of the ICD-10 Chapter V and the DSM-IV.
    In the case of ICD-10, the Clinical Descriptions and Diagnostic Guidelines for mental and behavioural disorders were developed first and the Diagnostic Criteria for Research were published a year later.
    The AG decided to devote more of its time to discussion of the “large groups” or categories of disorders, so the series of presentations that had been planned for this item was truncated.
    The AG has already established its intention to develop a comprehensive ICD-11 that can be viewed at different levels of detail for different purposes.
    These “views” would be developed simultaneously and in integrated form, rather than being based on different conceptualizations.
    The question of how the disorders are aggregated in large groups is a fundamental part of this process.

    The AG placed a priority on the development of a user-friendly classification system for clinical applications, including for use in primary care.
    It would also be important to develop a version with more specific criteria to meet the requirements of researchers, in close collaboration with the DSM group.
    The AG will need to have additional discussion of the need for different versions as the revision process proceeds.


    8. - Reports from representatives of federations/associations

    A. - WONCA
    Comments by Dr. Michael Klinkman
    Dr. Klinkman provided a discussion of relationship between ICD-10 and mental health concepts included in the International Classification of Primary Care (ICPC), which has been accepted by WHO as a related classification.
    A revision of the ICPC is currently underway, with its completion planned within two and a half year.

    B. - International Council of Nurses
    Comments by Dr Amy Coenen
    Dr Coenen presented an overview about the International Council of Nurses (ICN).
    Members of the ICN include 129 national associations of nurses, each representing one country.
    The ICN’s mission is “to represent nursing worldwide, advancing the profession and influencing health policy.
    The pillars of ICN programmatic activity are professional practice, social and economic welfare of nurses and nursing regulation.
    Dr Coenen also described the International Classification of Nursing Practice (ICNP), which is a standard ontology that includes nursing diagnoses, nursing interventions and outcomes of nursing care.
    Dr Coenen recommended that the ICD revision be examined for compatibility with the ICNP, in addition to other structured terminologies.

    C. - International Union of Psychological Science
    Comments by Dr. Geoffrey Reed
    Dr. Reed presented an overview of the International Union of Psychological Science (IUPsyS), which is an umbrella organization of national or regional associations representing psychologists in more than 70 countries.
    IUPsyS’s mission is to support “the development of psychological science, whether biological or social, normal or abnormal, pure or applied”.
    In characterizing psychological practice as it relates to the ICD revision, a challenge is presented by the major international differences in professional requirements.
    The authorization of psychologists to make diagnoses and therefore their use of a diagnostic classification system and capacity to participate in the ICD revision process will differ from country to country in relation to the standard of training for practice.
    Dr. Reed suggested that there is a need for more involvement of multidisciplinary mental health Summary Report of the 3rd Meeting of the International Advisory Group for the Revision of ICD-10 Mental and Behavioural Disorders professionals in specifying use requirements, establishing the development process and conducting field trials.
    To accomplish this, international associations of health professionals must develop an infrastructure that enables such participation.

    D. - World Psychiatric Association
    Comments by Dr. Juan Mezzich
    Dr. Mezzich presented the perspective of the World Psychiatric Association (WPA) on the ICD

    revision.
    WPA is committed to full collaboration with the WHO in developing the ICD-11 and related classifications.
    WPA will engage its Section on Classification and Diagnostic Assessment, other scientific sections, member societies and members of the WPA Global Network of Classification and Diagnosis Groups in this process.
    Dr. Mezzich presented recent publications and additional contributions of WPA that are relevant to the ICD revision, such as the organization of symposia on international classification and diagnostic systems and the WPA Institutional Program on Psychiatry for the Person.

    E. International Federation of Social Workers
    Comments by Mr. Rolf Blickle-Ritter
    Mr. Blickle-Ritter described the perspective of the International Federation of Social Workers (IFSW) related to the ICD revision process.
    The profession of social work defines itself on the basis of acting for and with the person, emphasizing the characteristics of the person instead of the diagnosis, including strengths as well as deficits and viewing the person within his or her social context.
    The Federation is establishing a reference group in relation to the ICD revision process in order to raise awareness and to solicit input on the questions of relevance to the AG.
    The Federation believes that the revision process should emphasize the public health purposes of diagnosis, helping to improve access to treatment all over the world, to educate the public about mental disorders and to involve more people in the treatment and recovery process.
    The Federation believes that a version of the ICD-11 for use in primary care would be more attractive to social workers and therefore result in wider training, dissemination and implementation of the system.
    The AG requested that the representatives of professional organizations to the AG develop methods for soliciting comments from their groups regarding the issues that are under discussion.
    Representatives should provide summary feedback from these comment processes to the AG, with specific and individual comments submitted through the ICD Update and Revision Platform.
    Professional association representatives were asked to disseminate information about the platform to their members and to obtain as much input as possible over the next year.
    This will increase the active involvement of the organizations, but also help to ensure input from a range of mental health professionals.


    9. - Future plans for coordinating and working groups
    Introduced by Benedetto Saraceno

    As noted, the existing coordinating and working groups of the AG were established at the beginning of 2007 and intended to have a life of two years.
    At its Fall 2008 meeting, the AG will review the need for, Terms of Reference and composition of existing groups and propose changes it views as necessary at that time.
    The AG itself was also appointed for a 2-year period through the end of 2008,and the Chair and Secretariat will review its composition in relationship to the ongoing needs of the revision effort.
    It would be helpful for more member states to designate representatives and support their participation.
    The AG recommended that two new working groups be established with immediate effect : a working group on epidemiology and one on the “large groups” to provide input to the AG and to inform the work of the ICD-DSM Harmonization Group.


    Annex

    List of participants

    1. Gavin Andrews
      Clinical Research Unit for Anxiety Disorders, St. Vincent's Hospital, 299 Forbes Street, Darlinghurst, NSW 2010, Australia
      Email : gavina@unsw.edu.au

    2. Rolf Blickle-Ritter
      International Federation of Social Workers, Psychiatrizentrum Münsingen, Leitung Sozialdienst, 3110 Münsingen, Switzerland
      Email : rolf.blickle@gef.be.ch

    3. Amy Coenen
      International Council of Nurses, University of Wisconsin - Milwaukee, College of Nursing, PO Box 413, Milwaukee WI 53201-0413, USA
      Email : coenena@uwm.edu

    4. David Goldberg
      Institute of Psychiatry, King's College, London, United Kingdom
      Email : spjudpb@hotmail.com

    5. Oye Gureje
      Department of Psychiatry, University College Hospital, PMB 5116 Ibadan, Nigeria
      Email : ogureje@comui.edu.ng

    6. Steven Hyman (Chairman)
      Harvard University, Massachusetts Hall, Cambridge, MA 02138, USA
      Email : steven_hyman@harvard.edu

    7. Michael Klinkman
      The World Organisation of Family Doctors (Wonca), University of Michigan Depression Center, 1500 E Medical Center Drive, F6321 MCHC Ann Arbor, MI 48109-0295, USA
      Email : mklinkma@med.umich.edu

    8. Maria Elena Medina-Mora
      Instituto Nacional de Psiquiatria Ramon de la Fuente, Calzada Mexico-Xochimilco, Col. San Lorenzo Huipulco, México, D.F. 14370, Mexico
      Email : medinam@imp.edu.mx

    9. Juan Mezzich
      World Psychiatric Association, International Center for Mental Health, Mount Sinai School of Medicine of New York University, Fifth Avenue & 100th Street, Box 1093 New York, NY 10029-6574, USA
      Email : juanmezzich@aol.com

    10. Geoffrey Reed
      International Union of Psychological Science, Glorieta de Bilbao, 5, 4º 428004 Madrid, Spain
      Email : gmreed@mac.com

    11. Karen Ritchie
      Institut National de la Santé et de la Recherche Médicale, E 361 Pathologies of the Nervous System Epidemiological and Clinical Research, Hôpital La Colombière, 34093 Montpellier Cedex 5, France
      Email : ritchie@montp.inserm.fr

    12. Khaled Saeed
      H. No: B-18, St: 02, Rawalpindi Medical College Staff Colony, Rawal Road, B-18, St. 02, Rawalpindi, Pakistan
      Email : saeedsh1993@yahoo.co.uk

    13. Norman Sartorius
      14 chemin Colladon, 1209 Geneva, Switzerland
      Email : sartorius@normansartorius.com

    14. Rangaswamy Thara
      Schizophrenia Research Foundation (SCARF), R/7A, North Main Road, West Anna Nagar Extension, Chennai- 600 101, India
      Email : scarf@vsnl.com

    15. Xin Yu
      Institute of Mental Health, Peking University, Huayuanbeilu 51, Haidian District, 100083, Beijing, China
      Email : yuxin@bjmu.edu.cn

    Special invitees

    1. William Carpenter
      University of Maryland School of Medicine, Maryland Psychiatric Research Center, Baltimore, USA
      Email : wcarpent@mprc.umaryland.edu

    2. Toshimasa Maruta
      Department of Psychiatry, Tokyo Medical University,6-7-1 Nishi-Shinjuku, Shinjuku-Ku, Tokyo 160-0023, Japan (representative of the Government of Japan)
      E-mail : maruta@tokyo-med.ac.jp & t-maruta@bd5.so-net.ne.jp

    3. Graham Mellsop
      University of Auckland, P O Box 128469, Remuera, Auckland New Zealand (representative of the Government of New Zealand)
      Email : Mellsopg@waikatodhb.govt.nz

    4. Robert Krueger
      Department of Psychology, University of Minnesota,75 E. River Rd.,Minneapolis, MN 55455, USA
      Email : krueg038@umn.edu

    5. Kimmo Kuoppasalmi
      National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland (representative of the Government of Finland)
      Email : kimmo.kuoppasalmi@ktl.fi

    Observers

    1. David Kupfer
      Department of Psychiatry, University of Pittsburgh, Western Psychiatric Institute & Clinic, 3811 O'Hara Street, Pittsburgh, PA 15213-2593, USA
      Email: kupferdj@upmc.edu

    2. Darrel Regier
      American Psychiatric Association, 1000 Arlington Blvd, Suite 1825, Arlington, VA 22209-390, USA
      Email : dregier@psych.org

    Who secretariat

    1. Can Celik
      Classifications and Terminology, Department of Measurement and Health Information Systems, WHO
      Email : celikc@who.int

    2. Somnath Chatterji
      Country Health Information, Department of Measurement and Health Information Systems, WHO
      Email : chatterjis@who.int

    3. Tarun Dua
      Management of Mental and Brain Disorders, Department of Mental Health and Substance Abuse, WHO
      Email : duat@who.int

    4. Samy Egli
      Mental Health: Evidence and Research, Department of Mental Health and Substance Abuse, WHO
      Email : eglis@who.int

    5. Robert Jakob
      Classifications and Terminology, Department of Measurement and Health Information Systems, WHO
      Email : jakobr@who.int

    6. Vladimir Poznyak
      Management of Substance Abuse, Department of Mental Health and Substance Abuse, WHO
      Email : poznyakv@who.int

    7. Benedetto Saraceno
      Director, Department of Mental Health and Substance Abuse, WHO.
      Email : saracenob@who.int

    8. Shekhar Saxena
      Mental Health: Evidence and Research, Department of Mental Health and Substance Abuse, WHO
      Email : saxenas@who.int

    9. Bedirhan Ustun
      Classifications and Terminology, Department of Measurement and Health Information Systems, WHO
      Email : ustunb@who.int

    10. Rosemary Westermeyer
      Mental Health: Evidence and Research, Department of Mental Health and Substance Abuse, WHO
      Email : westermeyerr@who.int


    Cfr. : http://www.who.int/mental_health/evidence/icd_summary_report_march_2008.pdf

    03-03-2009 om 22:04 geschreven door Jules

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