Disease Mechanisms and Clonidine Treatment in Adolescent Chronic Fatigue Syndrome

[Dolphin]

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..

 

[anciendaze]

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.

 

[leokitten]

I have taken Tenex (guanfacine) for several years. It's a pre-synaptic alpha2A agonist similar to clonidine but it's more centrally acting. It has worked quite well for the "wired" part of the the wired/tired feeling. There is also a lot of research showing how guanfacine can improve working memory circuits in the brain. Shire has actually made an extended release version and it's now FDA approved as a non-stimulant treatment for ADHD.

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
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179857/

 

[ramakentesh]

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.