Possible New Chronic Fatigue Syndrome Drug Investigated

shannah

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Anybody know anything about this drug?


Possible New Chronic Fatigue Syndrome Drug Investigated
Wednesday August 25, 2010

http://chronicfatigue.about.com/b/2010/08/25/droxidopa-chronic-fatigue-syndrome.htm


A drug called droxidopa is now moving into phase II clinical trials as a treatment for chronic fatigue syndrome.

Droxidopa is a synthetic version of a substance your body uses to make the neurotransmitter/hormone norepinephrine. Norepinephrine performs several important functions, and you body also uses it to produce dopamine, another important neurotransmitter. Studies have shown that this drug can improve fatigue, weakness, concentration, and orthostatic hypotension (blood pressure drop upon standing, which causes dizziness) in several conditions, including Parkinson's disease. These symptoms are also common in chronic fatigue syndrome, and studies show that some people with this condition may have low levels of norepinephrine and dopamine.

The study will take place at the Hunter-Hopkins Center in Charlotte, North Carolina, under the supervision of Dr. Charles Lapp. Lapp has been involved in both the American Association for CFS and the American Fibromyalgia Syndrome Association.

Droxidopa also is being studied as a possible fibromyalgia treatment. It is not yet approved for any use in the U.S. However, its manufacturer, Chelsea Therapeutics, is working toward approval for neurogenic orthostatic hypotension.
 

shannah

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Just a note: Above article states moving into phase 11 clinical trials as of August 25th for CFS. (Dr. Lapp)
This one states phase 11 clinical trials completed as of July 15th for FMS.

(Moderator: So Sorry - very disoriented tonight - Feel free to move this to Clinical Trials if preferred.)

Positive Results Reported in Fibromyalgia Drug TrialThursday July 15, 2010

http://chronicfatigue.about.com/b/2...sults-reported-in-fibromyalgia-drug-trial.htm

Research Brief

Chelsea Therapeutics International says it's completed a Phase II trial of droxidopa for fibromyalgia, and that the results were favorable.

Droxidopa is a man-made precursor of the neurotransmitter norepinephrine, which is believed to be deficient in people with fibromyalgia. Droxidopa currently is approved in Japan for orthostatic hypotension (OH) resulting from several conditions. OH causes a drop in blood pressure when standing, which can result in dizziness, fainting, weakness and other symptoms. OH is common in fibromyalgia; however, in this study researchers looked at how effective droxidopa is against pain.

As research moves forward, the company says it will focus on a combination of droxidopa and a drug called carbidopa, which allows droxidopa to cross the blood-brain barrier. So far, researchers say they're seeing the most pain reduction by using multiple daily doses of this combination. They also report no safety concerns.

Droxidopa currently is not approved for use outside of Asia, but it's currently in clinical trials in the U.S., Canada, Europe and Australia. Some Phase III trials are now underway, meaning it could come on the market within the next couple of years.

Droxidopa has only a few reported side effects that are generally mild. They include rapid heart beat, high blood pressure, nausea and vomiting, and headache/migraine.
 

Hope123

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Droxidopa is a form of norepinephrine and is a psychoactive drug as well. I think it might help with blood pressure issues but not with the overall picture of CFS.
 

alice1

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there are many anti-depressants that target seretonin and norepinephrine and this drug seems to be similar.
it does help with energy when i have good days.if i'm having a bad day it helps keep me from slipping into the abyss but it won't give me energy.
i also take allertec ,which is the canadian name.this helps with concentration and focus more than the effexor at least for me.
 

ahimsa

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Droxidopa currently is approved in Japan for orthostatic hypotension (OH) resulting from several conditions. OH causes a drop in blood pressure when standing, which can result in dizziness, fainting, weakness and other symptoms. OH is common in fibromyalgia; however, in this study researchers looked at how effective droxidopa is against pain.
"OH is common in Fibromyalgia" - I wonder if this is stated correctly? I'd like to quibble a bit if I may. :Retro smile:

I think there is a difference between the more common form of OH (Orthostatic Hypotension), which means the blood pressure drops immediately upon standing, and Orthostatic Intolerance (which includes POTS and NMH), which is a chronic condition where there is usually a delay between first standing up and having symptoms. I think there are various forms of Orthostatic Intolerance or delayed orthostatic hypotension that have been found in patients with ME/CFS and Fibromyalgia. I don't think that the more common OH (stand up too quickly, feel dizzy, see stars, maybe faints, etc.) is all that common in these patients.

I wonder if this is a similar problem to people thinking that "chronic fatigue" is the same thing as "Chronic Fatigue Syndrome"? Or maybe even doctors and researchers disagree over how to categorize all the different ways that blood pressure and heart rate can be messed up.

I did notice that in post #1 in this thread the term "neurogenic orthostatic hypotension" is used in the description of the drug trial. I'm not familiar with that particular combination of terms. I've heard of NCS (neurocardiogenic syncope), NMH (neurally mediated hypotension), Vasovagal Syncope, Vasodepressor Syncope, POTS (Postural Orthostatic Tachycardia Syndrome), Chronic Orthostatic Intolerance, and maybe a few others that I've forgotten. I'm not a doctor (nor do I play one on TV!) but after years of trying to treat my problems regulating blood pressure and heart rate I've done a fair amount of reading about the autonomic system.

So, I googled "neurogenic orthostatic hypotension" just to see what came up. Here's one of the links showing one doctor's view of how to categorize different blood pressure problems (I've seen different ways listed by different doctors):

http://www.dizziness-and-balance.com/disorders/medical/orthostatic.html

Anyway, back to this new drug, droxidopa --

Now that the FDA may be withdrawing approval in the USA for midodrine (brand name ProAmatine), even generic versions (see http://www.theheart.org/article/1113069.do and http://www.theheart.org/article/1110411.do) it would be nice to have an alternative drug for patients (not just ME/CFS patients) who have various forms of orthostatic intolerance.

If I can't keep getting midodrine, which seems to be helpful in reducing my NMH symptoms, I'll be looking for other options. I usually prefer to take an older drug (more testing has been done and it's available in cheaper generic forms) than a new one. But if midodrine disappears suddenly the options will be fairly limited.
 

August59

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How does droxidopa differ from Cymbalta and Savella (other than I know that these to affect serontonin and norepinephrine in different ratios)? Isn't carbidopa already used in Alzheimers or Parkinson's to boost and prolong the effects of another drug?
 

Dolphin

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"OH is common in Fibromyalgia" - I wonder if this is stated correctly? I'd like to quibble a bit if I may. :Retro smile:

I think there is a difference between the more common form of OH (Orthostatic Hypotension), which means the blood pressure drops immediately upon standing, and Orthostatic Intolerance (which includes POTS and NMH), which is a chronic condition where there is usually a delay between first standing up and having symptoms. I think there are various forms of Orthostatic Intolerance or delayed orthostatic hypotension that have been found in patients with ME/CFS and Fibromyalgia. I don't think that the more common OH (stand up too quickly, feel dizzy, see stars, maybe faints, etc.) is all that common in these patients.

I wonder if this is a similar problem to people thinking that "chronic fatigue" is the same thing as "Chronic Fatigue Syndrome"? Or maybe even doctors and researchers disagree over how to categorize all the different ways that blood pressure and heart rate can be messed up.

I did notice that in post #1 in this thread the term "neurogenic orthostatic hypotension" is used in the description of the drug trial. I'm not familiar with that particular combination of terms. I've heard of NCS (neurocardiogenic syncope), NMH (neurally mediated hypotension), Vasovagal Syncope, Vasodepressor Syncope, POTS (Postural Orthostatic Tachycardia Syndrome), Chronic Orthostatic Intolerance, and maybe a few others that I've forgotten. I'm not a doctor (nor do I play one on TV!) but after years of trying to treat my problems regulating blood pressure and heart rate I've done a fair amount of reading about the autonomic system.

So, I googled "neurogenic orthostatic hypotension" just to see what came up. Here's one of the links showing one doctor's view of how to categorize different blood pressure problems (I've seen different ways listed by different doctors):

http://www.dizziness-and-balance.com/disorders/medical/orthostatic.html

Anyway, back to this new drug, droxidopa --

Now that the FDA may be withdrawing approval in the USA for midodrine (brand name ProAmatine), even generic versions (see http://www.theheart.org/article/1113069.do and http://www.theheart.org/article/1110411.do) it would be nice to have an alternative drug for patients (not just ME/CFS patients) who have various forms of orthostatic intolerance.

If I can't keep getting midodrine, which seems to be helpful in reducing my NMH symptoms, I'll be looking for other options. I usually prefer to take an older drug (more testing has been done and it's available in cheaper generic forms) than a new one. But if midodrine disappears suddenly the options will be fairly limited.
I think the delayed point you make is probably relevant in ME/CFS. However, whether it is more relevant for blood pressure and not POTS, I'm not sure.

This study tested for POTS from two minutes of standing. This is possibly the best testing place for POTS and the like in Europe (I think they claim to be).

QJM. 2008 Dec;101(12):961-5. Epub 2008 Sep 19.

Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome.
Hoad A, Spickett G, Elliott J, Newton J.

Northern CFS/ME Clinical Network, Equinox House, Silver Fox Way, Cobalt Business Park, Newcastle upon Tyne.

Abstract
BACKGROUND: It has been suggested that postural orthostatic tachycardia syndrome (POTS) be considered in the differential diagnosis of those with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). Currently, measurement of haemodynamic response to standing is not recommended in the UK NICE CFS/ME guidelines.

OBJECTIVES: To determine prevalence of POTS in patients with CFS/ME.

DESIGN: Observational cohort study.

METHODS: Fifty-nine patients with CFS/ME (Fukuda criteria) and 52 age- and sex-matched controls underwent formal autonomic assessment in the cardiovascular laboratory with continuous heart rate and beat-to-beat blood pressure measurement (Task Force, CNSystems, Graz Austria). Haemodynamic responses to standing over 2 min were measured. POTS was defined as symptoms of orthostatic intolerance associated with an increase in heart rate from the supine to upright position of >30 beats per minute or to a heart rate of >120 beats per minute on standing.

RESULTS: Maximum heart rate on standing was significantly higher in the CFS/ME group compared with controls (106 +/- 20 vs. 98 +/- 13; P = 0.02). Of the CFS/ME group, 27% (16/59) had POTS compared with 9% (5) in the control population (P = 0.006). This difference was predominantly related to the increased proportion of those in the CFS/ME group whose heart rate increased to >120 beats per minute on standing (P = 0.0002). Increasing fatigue was associated with increase in heart rate (P = 0.04; r(2) = 0.1).

CONCLUSION: POTS is a frequent finding in patients with CFS/ME. We suggest that clinical evaluation of patients with CFS/ME should include response to standing. Studies are needed to determine the optimum intervention strategy to manage POTS in those with CFS/ME.
 

ahimsa

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I think the delayed point you make is probably relevant in ME/CFS. However, whether it is more relevant for blood pressure and not POTS, I'm not sure.
I think you're right that POTS symptoms are not necessarily delayed and may appear within a couple minutes of standing. So I should have left out that particular category when talking about delayed symptoms.

My biggest issue with the statement "OH (orthostatic hypotension) is common in Fibromyalgia" is that it seemed to imply that these patients have the more common form of hypotension. My understanding of the term is that OH means the form of hypotension that is easily diagnosed by measuring blood pressure while standing in a doctor's office. This is less likely to cause disability than Orthostatic Intolerance. I'm not as familiar with Fibromyalgia patients but the research studies that I have read for ME/CFS patients talk about finding NMH and POTS, forms of Orthostatic Intolerance, quite different from the more simple form of OH.

So, I guess my question is this - does the phrase Orthostatic Hypotension include forms of chronic Orthostatic Intolerance such as NMH or POTS? I've never seen the term OH used in this way. It was just a bit confusing to me because my doctors, and the medical studies that I've read, don't use the term OH to include Orthostatic Intolerance.

A few links on Orthostatic Intolerance:

http://www.cfids.org/about-cfids/orthostatic-intolerance.asp

http://www.ndrf.org/orthostat.htm

http://www.nymc.edu/fhp/centers/syncope/orthostatic_intolerance.htm
 
C

Cloud

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Nor-epi re-uptake inhibitors make me horribly sick. Since inhibiting the re-uptake is the same as adding more to the synapses, I would guess that taking synthetic nor-epi, would cause the same bad reaction. Nothing makes me more sick that Nor-Epi re-uptake inhibitors....I'm amazed they are saying that this drug can help CFS.

OH is typically caused by meds, and even something as benign as dehydration....but can also be caused by disease such as Addison's, or Adrenal Insufficiency. The symptoms of OH correct quickly after remaining upright for a brief period allowing blood distribution in the body to correct. OI is almost the opposite with symptoms worsening the longer we are upright. OH corrects itself......OI does not, and the autonomic nervous system symptoms worsen until we lay down. I don't usually see OH included as part of the OI seen in ME/CFS. They are by definition not the same.
 

Impish

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Given how long it takes a drug to go through the process to stage II they would have started this long before the evidence of a virus started to show up. It could very well be that the recent findings will make this totally pointless.

Hmmm... I wonder if I should short their stock :)
 

Wonko

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i have to agree with Cloud - medication that mucks around with norepinephrine levels makes me very ill - not the sickest I've been but really quite ill
 

pictureofhealth

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The last thing on God's earth anyone with ME/CFS needs, I would have thought, is Norepinephrine. This acts on the body in a similar way to Adrenaline (epinephrine) and sends the body into 'Fight & Flight' mode. (Even the psychs should agree with this - if CFS patients have repressed childhood trauma - why risk reigniting it by stimulating the sympathetic nervous system?)

When will medics get that we are NOT depressed patients in need of stimulation, but neuro-immune dysfunction patients in a state of hyper stimulation already? Why do they think we have hypersensitivities to sound, light, touch, movement, chemicals, allergies to certain foods, insomnia and exhaustion, and crave peace, quiet and minimal exertion? Could it be because our systems are permanently in an hyper alert state due to constant stimulation of the immune and nervous systems (presumably from the chronic presence of a stealthy retrovirus)?

I was prescribed Venlafaxine early on in the illness, (a stimulating anti depressant), due to the flawed but essentially kind thinking processes of a Consultant who assumed I had depression because he couldn't find anything else. "Its state of the art." he said. If I had your symptoms, if my wife had your symptoms, I'd advise this." Poor doctors - they are so easily impressed by magic pill companies.

I had been just about to take a shower but once the chemicals hit, I was utterly poleaxed and could do nothing for the first hour or so except lie on the bed in the dark in a drug induced stupor. I had no idea how to get into the bathroom let alone use the equipment once in there - the concept of 'taking a shower' became utterly meaningless.

I cannot overstress how powerful these drugs of the stimulating variety are, especially to patients with ME already sensitive to medication. My shoulders tensed up to my ears and I couldn't get them down. My jaw froze. My body was rigid as if I had Parkinson's disease. I felt weird and wired beyond belief. My mum had to drive me around in the car for several hours until the effects wore off - I could barely talk - I certainly couldn't smile.

The next day she insisted on driving me to the doctor to change the prescription to something else - she had to make the appointment herself on my behalf, the day before, as I couldn't use the phone or explain myself. Luckily, once there, it was a locum medic, not my regular GP. He took one look at me - "How bad is it?" he asked. "Its bad." I said. He stopped the prescription instantly. That was just one tablet and I utterly refused to take any more after that.

I've said it before, but it bears repeating again. When will (the majority of) doctors start listening to their patients instead of the sound of their own opinions? Patients with ME have a neuro-immune dysfunction - they DO NOT HAVE PRIMARY DEPRESSION. This is my view based on my own experience - if norepinephrine helps anyone - I would delighted be for you. Personally I think its more likely to bring about heart failure in people with ME.
 

Dolphin

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Off-topic?

pictureofhealth - you might be interested in the following.
By the way, I know one woman with ME/CFS who had terrible diarrhoea for months because of an SSRI. She was an inpatient in hospital I think for weeks as they did lots of tests. Once they took her off, the problem disappeared - it was a "simple" case of serotonin/similar excess:

RES: Heterogeneity of serum tryptophan concentration and availability to the brain in patients with the chronic fatigue syndrome

Journal: J Psychopharmacol. 2005 Dec;19(4):385-91.

Authors: Badawy AA, Morgan CJ, Llewelyn MB, Albuquerque SR, Farmer A.

Affiliation: Cardiff & Vale NHS Trust, Biomedical Research Laboratory,
Whitchurch Hospital, Cardiff, Wales, UK.

We assessed the serotonin status of patients with the chronic fatigue
syndrome (CFS).

Tryptophan (Trp) availability to the brain, expressed as the ratio of
concentration of serum Trp to the sum of those of its five competitors
(CAA), and other parameters of Trp disposition were compared in 23 patients
with the CFS and 42 healthy controls.

The serum [free Trp]/[CAA] ratio was 43% higher in CFS patients, due to a
48% higher [free Trp]. [Total Trp] was also significantly higher (by 19%)
in CFS patients, and, although the [total Trp]/[CAA] ratio did not differ
significantly between the control and patient groups, the difference became
significant when the results were co-varied with age and gender. [CAA] was
not significantly different between groups, but was significantly lower in
females, compared to males, of the CFS patient group.

We have established normal ranges for Trp disposition parameters and
propose criteria for defining the serotonin-biosynthetic status in humans.
We have provisionally identified two subgroups of CFS patients, one with
normal serotonin and the other with a high serotonin status.

The relevance of our findings to, and their implications for, the
pharmacological and other therapies of the chronic fatigue syndrome are
discussed.
The discussion section of this paper has some interesting comments:

"If the present results are confirmed, our proposals should have important
implications for the pharmacotherapy of the CFS. Serotonin- modifying and
other antidepressants are prescribed to CFS patients to treat depression (if
present), pain and/or fatigue. However, CFS patients with serotonin excess
should not be exposed to, and are unlikely to benefit from,
serotonin-modifying antidepressants, particularly selective
serotonin-re-uptake inhibitors (SSRIs), to avoid a potential excessive
serotonin hyperactivity. Similarly, in view of the well known TrpSSRI
interaction, the latter should not be prescribed to CFS patients with high
Trp levels or increased availability to the brain. By contrast, as suggested
by a meta-analysis of previous pharmacological trials (OMalley et al.,
1999) and a survey of psychiatrists (Hickie et al., 1999), tricyclic
antidepressants have a greater likelihood of effi- cacy than SSRIs, are
preferred by patients with chronic pain, and have superior antinociceptive
properties in fibromyalgia (McQuay et al., 1996). Also, our clinical
impression suggests that tricyclic antidepressants improve sleep
disturbances in, and are better tolerated than SSRIs by, CFS patients.


A high level of brain serotonin may also be important in relation to other
therapies, which influence this indolylamine, such as exercise and diet.
Exercise is a recognized therapy of the CFS (McCully et al., 1996), but it
is also known to increase serum [free Trp] and the [free Trp]/[CAA] ratio in
normal subjects (Newsholme et al., 1991) by a mechanism involving
NEFA-mediated release of serum albumin-bound Trp. In CFS patients, however,
exercise fails to increase Trp availability to the brain (Castell et al.,
1999). In this latter study, only one exercise session was conducted, and it
is therefore important to establish if a repeated exercise programme in CFS
patients is associated with normalization of the above Trp response and
whether such a potential normalization is related to, or indeed predictive
of, therapy outcome. Food can also have profound effects on Trp disposition,
with carbohydrate increasing (Madras et al., 1973), and protein decreasing
(Mller, 1985), brain [Trp] and hence serotonin synthesis and turnover. If
our results are confirmed, CFS patients with excess serotonin could be
advised to avoid eating carbohydrate-rich foods and targeted to adjunctive
nutritional strategies aimed at reducing their high central serotonin
levels.

The present results suggest that further research on the serotonin status of
patients with the CFS should yield important information for the appropriate
management of, and advice and ultimately a better service provision to
sufferers from, this condition, in accord with the aims of recent
recommendations (Clark et al., 2002)."
 

urbantravels

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I've never had much problem in the seven months or so I've been on venlafaxine, but then my dose is pretty low (75 mg). I never found it to be stimulating.

The pharmacist who dispensed it told me: It will either wake you up or make you sleepy. If it wakes you up, take it in the morning. If it makes you sleepy, take it at night. The first week or so I was taking it in the morning, and constantly found myself nodding off during the day. (Not normally part of my CFS symptoms, I don't normally nap or have daytime sleepiness.) So I switched to taking it at night, and gradually the daytime sleepiness/yawning tapered off. Still gives me hella dry mouth, though.

I should make clear that I'm on venlafaxine for depression and anxiety, not CFS, and don't plan to stay on it long term since the major depression (secondary to CFS and the disruption of my life it caused) has mostly resolved. I'll be interested to see what effect, if any, going off it will have on my CFS - for the better, worse, or no effect. (And yes, I've been warned about how hellish withdrawal is.)
 

Wayne

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When will medics get that we are NOT depressed patients in need of stimulation, but neuro-immune dysfunction patients in a state of hyper stimulation already? Why do they think we have hypersensitivities to sound, light, touch, movement, chemicals, allergies to certain foods, insomnia and exhaustion, and crave peace, quiet and minimal exertion? Could it be because our systems are permanently in an hyper alert state due to constant stimulation of the immune and nervous systems (presumably from the chronic presence of a stealthy retrovirus)?
Hi Pictureofhealth,

Your above paragraph: VERY, VERY Good.

Thank you.

Wayne
 

pictureofhealth

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Wayne -
thank you! You made my day.

Urbantravels -
thank you for posting your experience on the Venlafaxine. It did make me feel a lot better to know that other people have been able to get some benefit from this type of medicine. (I'm just sorry it wasn't me!)

Dolphin's article (1 or 2 posts above) indicated that people with ME/CFS do seem to divide into different groups in terms of response to some anti depressant medications. Many do well on the older types such as Amitryptiline too I know from talking to friends who have tried, but probably not everyone.

btw - I hear that sometimes doctors can prescribe SSRI's to help with the Venlafaxine withdrawal.
When coming off the SSRI's I gave myself several weeks and had tablets I could halve, but V doesn't work in quite the same way as a 'simple' SSRI.
Venlafaxine apparently has a v short half life in the body (which was v lucky for me!) which is what makes the difference.
(There is also a slow release variety which can reduce some of the gastro-i effects I hear during medication, but not sure if that helps when you are trying to come off the medication).

In any case, I wish you all good luck & wishes with your progress back to health recovery.
 

pictureofhealth

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Dolphin - Thanks for posting the v interesting information & article above.

I have only come across 'serotonin syndrome/toxicity' recently and the details you have posted were v helpful.
So can serotonin excess also cause depression/anxiety, or mainly neuro overload effects?

I have heard from a friend who has ME that Amitryptiline suited her better and helped with sleep and that it can be better tolerated by ME patients than SSRI's.

Venlafaxine is for moderate to severe depression so I've no idea why I was prescribed it apart from a mis-diagnosis. Its chemical make up and the way it acts in the body is different to usual anti depressant SSRI medications. It is a combination of a Serotonin reuptake inhibitor and a Noradrenaline reuptake inhibitor and the end result is in effect more akin to Amphetamine (according to Wikipedia). If I had known this prior to taking it I would not have agreed and would have asked for something milder.

The Parkinsons' like symptoms I experienced are probably due to the over abundance of norepinephrine, which I did not need. I already have enough adrenaline & related neuro boosters thank you.

After my x1 tablet Venlafaxine episode, the locum GP prescribed Citoprolam (another SSRI) for 6 months. This didn't really suit me either but I tolerated it much better. I really only agreed to take the stuff to shut everyone up. Most people around me at the time seemed convinced I was having some kind of depressive episode - which of course only increased my isolation, anxiety - I know - we've all gone through this. Anyway, 'What the hell' I thought. 'Do I want to be right or do I want to be better? Anyway, it might help ..'

The Citoprolam worsened my sleep and I couldn't check my bank statements or information process at all for 6 months (previously with brain fog I could do it v slowly - on Citoprolam it became impossible). It helped my mood, but did nothing to help my underlying illness/'brain & body inflammation'/inability to exercise/ etc etc. Frankly I think I'd have been better off with Valium.

[btw Off topic but relevant here - I have done the Lightning Process (which claims to stop thoughts which give rise to an overabundance of adrenaline and cortisol) and which did help hugely with fatigue - but once again has not been remotely curative of my underlying medical condition or any of the other huge list of symptoms I have - especially the inability to walk far or exercise without increasing aching all over and fatigue and feeling ill). I gave this feedback to my LP tutor and she did not seem surprised. I do not want to comment a lot more on this thread as it is off topic - but suffice to say - she said in her experience of teaching the LP, she could NOT in all honesty claim for herself the alleged 95% 'cure' rate which is claimed by the founder of this technique.]

In my view - something other than 'thoughts' is maintaining the overactivation of the sympathetic nervous system & the immune system. I have had depression, anxiety and viral meningitis, amongst other more minor ailments in my life. Viral agents feel different in the body to the other illnesses. I would say that the ME/CFS is much more like the Meningitis than anything else.
 

Dolphin

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(OT?) Serotonin, SSRIs, etc

Dolphin - Thanks for posting the v interesting information & article above.

I have only come across 'serotonin syndrome/toxicity' recently and the details you have posted were v helpful.
So can serotonin excess also cause depression/anxiety, or mainly neuro overload effects?
I'm not an expert. And I forgot some stuff I read. So will pass on trying to answering that.

I have heard from a friend who has ME that Amitryptiline suited her better and helped with sleep and that it can be better tolerated by ME patients than SSRI's.

Venlafaxine is for moderate to severe depression so I've no idea why I was prescribed it apart from a mis-diagnosis. Its chemical make up and the way it acts in the body is different to usual anti depressant SSRI medications. It is a combination of a Serotonin reuptake inhibitor and a Noradrenaline reuptake inhibitor and the end result is in effect more akin to Amphetamine (according to Wikipedia). If I had known this prior to taking it I would not have agreed and would have asked for something milder.

The Parkinsons' like symptoms I experienced are probably due to the over abundance of norepinephrine, which I did not need. I already have enough adrenaline & related neuro boosters thank you.

After my x1 tablet Venlafaxine episode, the locum GP prescribed Citoprolam (another SSRI) for 6 months. This didn't really suit me either but I tolerated it much better. I really only agreed to take the stuff to shut everyone up. Most people around me at the time seemed convinced I was having some kind of depressive episode - which of course only increased my isolation, anxiety - I know - we've all gone through this. Anyway, 'What the hell' I thought. 'Do I want to be right or do I want to be better? Anyway, it might help ..'

The Citoprolam worsened my sleep and I couldn't check my bank statements or information process at all for 6 months (previously with brain fog I could do it v slowly - on Citoprolam it became impossible). It helped my mood, but did nothing to help my underlying illness/'brain & body inflammation'/inability to exercise/ etc etc. Frankly I think I'd have been better off with Valium.
Some doctors recommend one or more drugs from the Valium family e.g. Rivotril/Klonopin

I think some SSRIs, etc may help some people.
But I definitely think lots of ordinary doctors give them out too often for people with ME/CFS when the activating effect is often not suitable, like you say.

Randomised, double-blind, placebo-controlled study of fluoxetine in chronic fatigue syndrome.

Lancet. 1996 Mar 30;347(9005):858-61.

Vercoulen JH, Swanink CM, Zitman FG, Vreden SG, Hoofs MP, Fennis JF, Galama JM, van der Meer JW, Bleijenberg G.

Department of Medical Psychology, University Hospital, Nijmegen, The Netherlands.
Abstract

BACKGROUND: No somatic treatment has been found to be effective for chronic fatigue syndrome (CFS). Antidepressant therapy is commonly used. Fluoxetine is recommended in preference to tricyclic agents because it has fewer sedative and autonomic nervous system effects. However, there have been no randomised, placebo-controlled, double-blind studies showing the effectiveness of antidepressant therapy in CFS. We have carried out such a study to assess the effect of fluoxetine in depressed and non-depressed CFS patients.

METHODS: In this randomised, double-blind study, we recruited 44 patients to the depressed CFS group, and 52 to the non-depressed CFS group. In each group participants were randomly assigned to receive either fluoxetine (20 mg once daily) or placebo for 8 weeks. The effect of fluoxetine was assessed by questionnaires, self-observation lists, standard neuropsychological tests, and a motion-sensing device (Actometer), which were applied on the day treatment started and on the last day.

FINDINGS: The two groups were well matched in terms of age, sex distribution, employment and marital status, and duration of CFS. There were no significant differences between the placebo and fluoxetine-treated groups in the change during the 8-week treatment period for any dimension of CFS. There was no change in subjective assessments of fatigue, severity of depression, functional impairment, sleep disturbances, neuropsychological function, cognitions, or physical activity in the depressed or the non-depressed subgroup.

INTERPRETATION: Fluoxetine in a 20 mg daily dose does not have a beneficial effect on any characteristic of CFS. The lack of effect of fluoxetine on depressive symptoms in CFS suggests that processes underlying the presentation of depressive symptoms in CFS may differ from those in patients with major depressive disorder.

PMID: 8622391 [PubMed - indexed for MEDLINE]