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Clonidine’s a bitter pill for some

The announcement, this week, that a Norwegian team investigating the use of clonidine to treat me/cfs had come up empty handed would not normally be welcome news.But there’s a real positive to come out of this study.

In a randomized study of 120 children with me/cfs, and 68 healthy controls, researchers noted that clonidine had an adverse effect on patients, in terms of lower activity levels (measured as steps per day), lower plasma norepinephrine levels, and lower serum C-reactive protein concentrations, compared with the CFS placebo group.

Surprisingly, the study’s main outcome wasn’t to determine a biophysical cause of me/cfs, rather to prove a long-time, widely-held belief by behavioralists that me/cfs is a conditioned stress response.

So we can probably stop taking clonidine. Not a biggie. You can follow the trail of clonidine failure in patient testimonies across the web.

The study did confirm some of the biology behind me/cfs, noting: “Adolescent CFS is associated with enhanced sympathetic nervous activity, low-grade systemic inflammation, attenuated hypothalamus-pituitary-adrenal axis function, cognitive impairment, and large activity reduction…”

Here’s the kicker

 

Surprisingly, the study’s main outcome wasn’t to determine a biophysical cause of me/cfs, rather to prove a long-time, widely-held belief by some behavioralists that me/cfs is a conditioned stress response.

By making use of clonidine’s ability to tone down sympathetic nervous system activity and ramp up the parasympathetic nervous system, the team hoped to turn off the stress response and effect improvement, if not a cure, thus confirming their behavioralist understanding of me/cfs.

Contrary to expectations, after taking into account the negative effect of clonidine on physical activity, investigators were forced to admit that: “…sympathetic and inflammatory enhancement may be compensatory mechanisms.”

In other words, the observed sympathetic and inflammatory enhancements were not primary, that there might indeed be another cause for me/cfs… a biophysical one?

Dr Vegard Bruun Wyller

Lead researcher Dr Vegard Bruun Wyller is a long-time advocate of using cognitive behavioral therapy to treat me/cfs patients.

In 2007, Dr Wyller signalled his intentions to investigate the use of clonidine: “Cognitive therapy specifically designed to abolish sustained arousal are more effective in the treatment of CFS than unspecific cognitive therapy. To our knowledge, the effectiveness of different cognitive treatment approaches has not been subjected to research. The design should be randomized and controlled.”

He elaborated further: “The alpha2-adrenoceptor agonist clonidine is an effective antihypertensive drug due to central inhibition of sympathetic outflow. Anxiolytic drugs, like benzodiazepines, also exert an inhibitory effect on the relevant brain stem centers.”

Hopes were high.  ” …CFS sustained arousal theory – if proven correct – has implications beyond its present application. Related diseases, such as fibromyalgia, might be fully explicable within the same theoretical framework,” he said.

“Furthermore, similar models seem valuable for providing new insight into totally different areas, for instance hypertension and the mechanisms underlying placebo effects.

“…it might even contribute to a deeper understanding of body-mind interactions in general,” he added.

More on clonidine

Clonidine is used commonly as a sympathetic nervous system suppressant and works by activating alpha 2 adrenergic receptors in the brain and inhibiting norepinephrine release. It reduces blood pressure and heart rate.

It is often used to treat a range of other conditions, including ADHD, alcohol and opioid withdrawal.

It is clonidine’s ability to tone down sympathetic nervous system activity and ramp up parasympathetic nervous system functioning that suggests it could be helpful in alleviating anxiety, neuropathic pain, sleep disorders, night sweats, restless leg syndrome, all symptoms common in me/cfs.

It is somewhat regarded as a front-line treatment for orthostatic intolerance in me/cfs. Not so much now, perhaps.

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Written by Russell Logan

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Russell Logan worked as a magazine publisher and editor until forced into early retirement through ill health with ME. He has battled with moderate to severe ME for 25 years. He now lives in Noosaville, Australia.

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