A New Decade of ME Research: The 11th Invest in ME International ME Conference 2016
Mark Berry presents the first in a series of articles on the 11th Invest in ME International ME Conference in London ...
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Disease Mechanisms and Clonidine Treatment in Adolescent Chronic Fatigue Syndrome

Discussion in 'Latest ME/CFS Research' started by A.B., Feb 5, 2014.

  1. Dolphin

    Dolphin Senior Member

    Just to be clear, I'm no fan of Dr. Wyller and his views in general. Nor had I anybody else's previous comment in mind when praising the reporting in the trial. I may also have missed important points and there may be problems with the reporting I missed..
  2. anciendaze

    anciendaze Senior Member

    Note that the finding of lower ADH (vasopressin or antidiuretic hormone) goes along with higher rates of excretion, even if it doesn't cross the threshold of polyuria. This is commonly associated with hypovolemia and orthostatic intolerance. This probably affects one patient subgroup more than others.

    As for the finding that there were no more significant adverse events in the clonidine group, this reflects either the insensitivity to adverse events of typical experimental protocols or compensation by patients to avoid adverse events when they felt weak or dizzy. Psychological treatments aim directly at eliminating this compensation.
    NK17 likes this.
  3. leokitten

    leokitten Senior Member

    Guanfacine seems to be a pharmacological improvement over clonidine and I was thinking about taking it but then changed my mind...

    It was recently found that it, as well as a number of other drugs, is a potent agonist of the 5-HT2b serotonin receptor. Long-term use of 5-HT2b agonists are clearly implicated in valvular heart disease (VHD) and pulmonary arterial hypertension (PAD) (which is fatal BTW), remember Phen-Fen being pulled of the market after causing this?

    They have been finding more and more that certain drugs prescribed for other indications are potent 5-HT2b agonists and cause the same problems.

    Serotonin Receptors and Heart Valve Disease – it was meant 2B
    Last edited: May 2, 2014
  4. ramakentesh

    ramakentesh Senior Member

    As Ive been saying all along - most of the sympathetic excess and wired feelings in CFS is compensatory for impaired cerebral autoregulation of neurovascular uncoupling. This supports that hypothesis. Recent cardiopulmonary stress tests in POTS and CFS found consistently that patients had impaired stroke volume from inadequate venous return. Whether this is from venous pooling or hypovolemia Clonidine is probably not the answer.

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