FM sufferers dont miss this--A really good study

G

Gerwyn

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This is what happens when the real medical profession aknowledge an illness this drug helps to regulate elements of the HPA axis

e A European Multicenter Randomized Double-blind Placebo-controlled Monotherapy Clinical Trial of Milnacipran in the Treatment of Fibromyalgia.
Author(s) Branco JC, Zachrisson O, Perrot S, Mainguy Y
Institution From the Faculdade Cincias Mdicas, Universidade Nova de Lisboa, Servio de Reumatologia, CHLO, EPE-Hospital Egas Moniz, Lisboa, Portugal; Gottfries Clinic AB, Mlndal, Sweden; Service de Mdecine Interne, Hotel Dieu Hospital, Paris Descartes University, Paris; and Pierre Fabre Mdicament, Boulogne, France.
Source J Rheumatol 2010 Feb 15.
Abstract OBJECTIVE: This randomized, double-blind, placebo-controlled, multicenter study investigated the efficacy and safety of milnacipran in the treatment of fibromyalgia (FM) in a European population.
METHODS: Outpatients diagnosed with FM according to 1990 American College of Rheumatology criteria (N = 884) were randomized to placebo (n = 449) or milnacipran 200 mg/day (n = 435) for 17 weeks (4-week dose escalation, 12-week stable dose, 9-day down-titration), followed by a 2-week posttreatment period. The primary efficacy criterion was a 2-measure composite responder analysis requiring patients to achieve simultaneous improvements in pain (>/= 30% improvement from baseline in visual analog scale, 24-hour morning recall) and a rating of "very much" or "much" improved on the Patient Global Impression of Change scale. If responder analysis was positive, Fibromyalgia Impact Questionnaire (FIQ) was included as an additional key primary efficacy measure.
RESULTS: At the end of the stable dose period (Week 16), milnacipran 200 mg/day showed significant improvements from baseline relative to placebo in the 2-measure composite responder criteria (p = 0.0003) and FIQ total score (p = 0.015). Significant improvements were also observed in multiple secondary efficacy endpoints, including Short-Form 36 Health Survey (SF-36) Physical Component Summary (p = 0.025), SF-36 Mental Component Summary (p = 0.007), Multidimensional Fatigue Inventory (p = 0.006), and Multiple Ability Self-Report Questionnaire (p = 0.041). Milnacipran was safe and well tolerated; nausea, hyperhidrosis, and headache were the most common adverse events.
CONCLUSION: Milnacipran is an effective and safe treatment for pain and other predominant symptoms of FM. Registered as trial no. NCT00436033.
 

SeaShel

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I tried this drug, and was thrilled with the pain relief. Unfortunately, even at a low dose I had side effects. The one that I couldn't ignore and "push through" was a constant tingling down the left arm and into my hand.

My doc had no hesitation in my trying it, which is a minor miracle in itself. I hope that many of you have docs that will give it a try, because it really was a large percentage of relief for me (probably 50-60%).

The pharma company that makes Savella has titration packs out to the docs, so you can give it a whirl for the cost of a dr. appointment. Even without the tingling side effect, I would have never gotten to the full dose, so if you're concerned about cost, keep that in mind.

Shelley
 

IntuneJune

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BACK IN MEDIVAL TIMES, long, long ago..........

I tried antidepressants. (We are all different need I say), they did not help the pain. I cared a little less about the pain, but pain never the less continued.

Would not having decreased pain on antidepressants play into the hands of the theorists "CFS/FMS is a psychological/ psychiatric disorder." More fuel for their fires.

Having questioned that, I welcome being educated in HPA axis regulation and how it helps pain.

Thanks. June
 

Martlet

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Don't I wish! But I already have an irregular heartbeat and my BP is already up, which is almost certainly why my doctor didn't suggest this medication, which received FDA approval for the treatment of FM almost a year ago. Good luck to anyone who tries it though! It sounds as if it might be really helpful to many.
 

Lily

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Savella (Milnaciprin) is very similar to Cymbalta, but supposedly has enough subtle differences to make the claims to fame that it does. I do have a friend who's physician provided oversight of the study. She has, after quite a dubious trial reached some improvement. She needed to titrate up even more slowly than the standard titrate. And it did impact her blood pressure, But she thinks now it was worth it.

There would have been a time when I would have tried anything, but I'm past that now, with seeming reactions to everything I've tried for the past 3 years. This being so similar to Cymbalta, would probably not be a good fit for me, but may work for others. I wouldn't worry about playing into the hands of psychiatrists if you get a little relief, even if temporary.

Good luck, sure hope it helps.
 
G

Gerwyn

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Savella (Milnaciprin) is very similar to Cymbalta, but supposedly has enough subtle differences to make the claims to fame that it does. I do have a friend who's physician provided oversight of the study. She has, after quite a dubious trial reached some improvement. She needed to titrate up even more slowly than the standard titrate. And it did impact her blood pressure, But she thinks now it was worth it.

There would have been a time when I would have tried anything, but I'm past that now, with seeming reactions to everything I've tried for the past 3 years. This being so similar to Cymbalta, would probably not be a good fit for me, but may work for others. I wouldn't worry about playing into the hands of psychiatrists if you get a little relief, even if temporary.

Good luck, sure hope it helps.
I thought long and hard before posting this Psychiatrists dont claim that FM is caused by depression they claim that this is a somatoform disorder This trial proves that it isnt! dont be taken in by a label this drug produces increased levels of noradenalin much higher than anything I,ve seen before and doesnt prevent the reuptake of seretonin but actually stimulates extra production and boosts the chemicals which are lacking in a dysregulated HPA axis in FM and ME,I dont know what this does to dopamine but I will try to find out.It has been shown in numerous studies is that Me is not depression because depression is associated with an elevated HPA axis and the reverse is true in ME. If ME patients were to get an objective benefit from this drug the somatoform label would also go out of the window.This drug has a similar effect on the HPA axis as pregabalin
 

julius

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Antidepressants are no better than placebo!!

NEJM- "Selective publication of antidepressant trials and its influence on apparent efficacy"!! The title says it all.

The drug companies only published the results that were better than placebo, and even those were only better by a couple of percentage points. Prozac, for instance, (only one of many to do this) took five studies to get two positive results. That's 3 negative and 2 positive!!. Then they don't publish the negative results and publish the positive. And with this, they receive FDA approval.

This information has been available for years. It is published in the highest level of medical journals (NEJM, BMJ) and other respectable sources (Washington Post, Time Magazine).


Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (January 2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". N. Engl. J. Med. 358 (3): 252–60. doi:10.1056/NEJMsa065779. PMID 18199864 Shocking!!



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253608/?tool=pmcentrez Also published in BMJ (I believe)



Against Depression, a Sugar Pill Is Hard to Beat, The Washington Post, May 7, 2002 A copy of original WP article



http://www.time.com/time/health/article/0,8599,1717306,00.html (A good article in Time magazine)


I am aware that the argument here is that they are not working as antidepressants, but by another avenue. However, the study methods are similar, and note that the paper does not compare number of responders vs that on placebo.

I am sure the same tactics are being employed here, and I hope we can stop supporting these criminals.
 
G

Gerwyn

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Antidepressants are no better than placebo!!

NEJM- "Selective publication of antidepressant trials and its influence on apparent efficacy"!! The title says it all.

The drug companies only published the results that were better than placebo, and even those were only better by a couple of percentage points. Prozac, for instance, (only one of many to do this) took five studies to get two positive results. That's 3 negative and 2 positive!!. Then they don't publish the negative results and publish the positive. And with this, they receive FDA approval.

This information has been available for years. It is published in the highest level of medical journals (NEJM, BMJ) and other respectable sources (Washington Post, Time Magazine).


Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (January 2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". N. Engl. J. Med. 358 (3): 25260. doi:10.1056/NEJMsa065779. PMID 18199864 Shocking!!



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253608/?tool=pmcentrez Also published in BMJ (I believe)



Against Depression, a Sugar Pill Is Hard to Beat, The Washington Post, May 7, 2002 A copy of original WP article



http://www.time.com/time/health/article/0,8599,1717306,00.html (A good article in Time magazine)


I am aware that the argument here is that they are not working as antidepressants, but by another avenue. However, the study methods are similar, and note that the paper does not compare number of responders vs that on placebo.

I am sure the same tactics are being employed here, and I hope we can stop supporting these criminals.
According to the neurobiological perspective anti depressents dont work as they were once thought to do they are now thought to stimulate neurogenesis in the amygdala .The trouble with depression is that it is like CFS, a diagnostic label ,when in fact it covers multiple aetiologies.You can give some people antidepressents untill the cows come home and they will have no effect because the cause is not related to the limbic system.I,m sure the figures you quote are accurate and they dont suprise me.They can be very effective if you chose the right cohort which are suffering cortisol damage to the amygdala. It used to be called reactive depression.They work as HPA regulators but are not very good at it.This one with these effects is intriguing and there may be more here than meets the eye.The word antidepressent is just a label HPA modulators would seem to be a better description if the fairly recent neurobiological research is correct.Certain anticonvulsants appear to act in the same way intreating deep limbic seisures
 

julius

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According to the neurobiological perspective anti depressents dont work as they were once thought to do they are now thought to stimulate neurogenesis in the amygdala .The trouble with depression is that it is like CFS, a diagnostic label ,when in fact it covers multiple aetiologies.You can give some people antidepressents untill the cows come home and they will have no effect because the cause is not related to the limbic system.I,m sure the figures you quote are accurate and they dont suprise me.They can be very effective if you chose the right cohort which are suffering cortisol damage to the amygdala. It used to be called reactive depression.They work as HPA regulators but are not very good at it.This one with these effects is intriguing and there may be more here than meets the eye.The word antidepressent is just a label HPA modulators would seem to be a better description if the fairly recent neurobiological research is correct.Certain anticonvulsants appear to act in the same way intreating deep limbic seisures
There are two problems I see here.

First, these studies measure patient outcome. It doesn't matter the proposed mode of action, if the results are 50/50 with a placebo, then it's no better than a placebo (and probably is a placebo, a toxic one at that!) If you flip a coin 100 times, but only report the times it comes up heads, then you have proven that a coin flip comes up heads 100% of the time (haven't you?)

Second, (I may be assuming here) the studies you are referring to are done after FDA approval. These are subject to no scrutiny at all (as opposed to the tiny bit of scrutiny pre-approval). This post approval work is then what the detailers shop around to the MDs, but is rarely based in reality.

Also, these newer theories started emerging as a response to growing evidence against the 'serotonin hypothesis', and that SSRI's did not in fact increase inter neuronal levels of serotonin. So the manufacturers had to come up with new reasons for why they work (which they DON'T) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1277931/?tool=pmcentrez

However you slice it...they don't work. Whether they don't work by increasing serotonin, or they don't work by acting on the amygdala doesn't matter. They are indisputably ineffective.
 
G

Gerwyn

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There are two problems I see here.

First, these studies measure patient outcome. It doesn't matter the proposed mode of action, if the results are 50/50 with a placebo, then it's no better than a placebo (and probably is a placebo, a toxic one at that!) If you flip a coin 100 times, but only report the times it comes up heads, then you have proven that a coin flip comes up heads 100% of the time (haven't you?)

Second, (I may be assuming here) the studies you are referring to are done after FDA approval. These are subject to no scrutiny at all (as opposed to the tiny bit of scrutiny pre-approval). This post approval work is then what the detailers shop around to the MDs, but is rarely based in reality.

Also, these newer theories started emerging as a response to growing evidence against the 'serotonin theory', and that SSRI's did not in fact increase inter neuronal levels of serotonin. So the manufacturers had to come up with new reasons for why they work (which they DON'T)
i,m sorry you are wrong antidepressents do work for some people depending on the aetiology of their depression.you have the same problem here as you do with cfs namely a heterogenous population under the same subjective linguistic label .The symptoms are very similar but the causes are different.this latest study was in the journal of rheumatology and it is pretty well respected and the peer review process reasonably rigerous.i can see the flaws just as i can see flaws in most studies.That is why science proceeds according to the weight of evidence.The research re the involvement of the amygdala has been in the public domain for some time and is based on cumulative research independent and not at all funded by pharma
.I am very suspicious of pharma companies but the demands on research re new drugs or new applications are much more rigerous than CBT and the like.At the end of the day drs and patients are not fools .If the drugs showed no clinical benefit they would long have fallen out of use----but I reiterate they are not a panacea and as we know results can be fiddled
 

julius

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i,m sorry you are wrong antidepressents do work for some people depending on the aetiology of their depression.
They work for about 25% of people. The same as a placebo. If you have other figures could you please cite them them.

The research re the involvement of the amygdala has been in the public domain for some time and is based on cumulative research
I haven't seen anything convincing. Can you cite please?
All the ones I have seen have made the following error in logic;
antidepressants relieve depression (false) -----> antidepressants modify amygdala function-----> modifying amygdala relieves depression (obviously false)


I am very suspicious of pharma companies
Me too.:Retro mad: (angry face at pharma...not you Gerwyn)


but the demands on research re new drugs or new applications are much more rigerous than CBT and the like
With regards to proving efficacy...no. All you need are two studies showing positive results. And as I pointed out, you can disregard as many negative outcomes as you like, so long as you get two positive. And the positive results were statistically significant, but well below clinically significant.


At the end of the day drs and patients are not fools
Not fools, but fooled. after graduation, doctors get nearly all their new information from 'detailers' (drug reps.) And patients get nearly all their information from doctors.

Characteristics and Impact of Drug Detailing for Gabapentin - http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0040134

and

http://www.nytimes.com/2008/04/28/us/28doctors.html?_r=2&ref=health&oref=slogin


If the drugs showed no clinical benefit they would long have fallen out of use
Obviously not. I don't mean this to sound confrontational, but did you read the studies I cited. If not, at least read the NEMJ one. The other study I cited states clearly that they don't have a clinical benefit.

I think this is a very important topic, and if anyone thinks it's not suitable for this thread, feel free to move it. But I would like to continue. We talk about the insurance industry getting in our way. But with a cash cow like antidepressants, Big Pharma is certainly also playing a role in psychologising us.

Please, raise your hand if you are reading this and have been prescribed an antidepressant.
Now, raise your hand if you think an antidepressant was the correct medication given the symptoms you presented to your doctor.
 

spindrift

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Savella Sucks

Tried it because my really nice doc talked me into it. Bad side effects, no improvement.
My doc is so nice I felt really bad to tell him that it is NOT helping.

Doing the Myhill protocol now. Slow improvent over the last six months. No side effects :)
 
G

Gerwyn

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They work for about 25% of people. The same as a placebo. If you have other figures could you please cite them them.



I haven't seen anything convincing. Can you cite please?
All the ones I have seen have made the following error in logic;
antidepressants relieve depression (false) -----> antidepressants modify amygdala function-----> modifying amygdala relieves depression (obviously false)




Me too.:Retro mad: (angry face at pharma...not you Gerwyn)




With regards to proving efficacy...no. All you need are two studies showing positive results. And as I pointed out, you can disregard as many negative outcomes as you like, so long as you get two positive. And the positive results were statistically significant, but well below clinically significant.




Not fools, but fooled. after graduation, doctors get nearly all their new information from 'detailers' (drug reps.) And patients get nearly all their information from doctors.

Characteristics and Impact of Drug Detailing for Gabapentin - http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0040134

and

http://www.nytimes.com/2008/04/28/us/28doctors.html?_r=2&ref=health&oref=slogin




Obviously not. I don't mean this to sound confrontational, but did you read the studies I cited. If not, at least read the NEMJ one. The other study I cited states clearly that they don't have a clinical benefit.

I think this is a very important topic, and if anyone thinks it's not suitable for this thread, feel free to move it. But I would like to continue. We talk about the insurance industry getting in our way. But with a cash cow like antidepressants, Big Pharma is certainly also playing a role in psychologising us.

Please, raise your hand if you are reading this and have been prescribed an antidepressant.
Now, raise your hand if you think an antidepressant was the correct medication given the symptoms you presented to your doctor.
If you are asking if you should prescribe an antidepressent at anything like a standard dose to anyone with ME then the answer is categorically no--we cant detoxify--I had horrendous side effects at the very lowest dose1If we are talking about the studies you referenced then it is a different matter.you can use different analytical tools in the same meta analysis and reach different conclusions they have even used unpublished studies!If someone published an anti ME study of this quality we would all be up in arms.It is early AM for me so cognitively the mists havent cleared but I will come back later and we can continue the thdiscussion I will try and dig up the references.These studies were really looking at low mood.I think if anyone prescribes anti depressents here questions should certainly be asked
 
G

Gerwyn

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They work for about 25% of people. The same as a placebo. If you have other figures could you please cite them them.



I haven't seen anything convincing. Can you cite please?
All the ones I have seen have made the following error in logic;
antidepressants relieve depression (false) -----> antidepressants modify amygdala function-----> modifying amygdala relieves depression (obviously false)




Me too.:Retro mad: (angry face at pharma...not you Gerwyn)




With regards to proving efficacy...no. All you need are two studies showing positive results. And as I pointed out, you can disregard as many negative outcomes as you like, so long as you get two positive. And the positive results were statistically significant, but well below clinically significant.




Not fools, but fooled. after graduation, doctors get nearly all their new information from 'detailers' (drug reps.) And patients get nearly all their information from doctors.

Characteristics and Impact of Drug Detailing for Gabapentin - http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0040134

and

http://www.nytimes.com/2008/04/28/us/28doctors.html?_r=2&ref=health&oref=slogin




Obviously not. I don't mean this to sound confrontational, but did you read the studies I cited. If not, at least read the NEMJ one. The other study I cited states clearly that they don't have a clinical benefit.

I think this is a very important topic, and if anyone thinks it's not suitable for this thread, feel free to move it. But I would like to continue. We talk about the insurance industry getting in our way. But with a cash cow like antidepressants, Big Pharma is certainly also playing a role in psychologising us.

Please, raise your hand if you are reading this and have been prescribed an antidepressant.
Now, raise your hand if you think an antidepressant was the correct medication given the symptoms you presented to your doctor.
They have not included any data in the last ten years because they felt the data in the really big studies were biased! Pleeeaase! yet they saw fit to include phase three studies used to establish safety not efficacy already seen by the FDA---As for gaba pentin I would hesitate in suggesting for anyone, other than those having otherwise intractable seisures where other anticonvulsants have failed.This is literally a life or death situation because the chance of status eplilepticus is so high.Antidepressants would only be potentially useful for what used to be called endogenous depression and not exogenous where causation is myriad.I think big pharma have clouded this issue for profit.The patients I,m talking about cant dress communicate use any cognitive function and sit into a corner staring into space with almost no awareness of the outside world dont eat drink etc and need full time care-Low mood does not come close.I,m nevertheless intrigued by the effect of the production of these doses of neurotransmitters of normalising the dissociation inherent in a disregulated hypothalamic pituatary adrenax axis.I,m also intrigued that such large numbers of objectivel diagnosed FM patiets appeared to tolerate it
 

natasa778

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There is an in vitro study showing inhibition of retrovirus by SSRI's. I cannot find the study right now but here is something related:

Antiretroviral activity of SSRIs and statins?
Earlier research offered conflicting evidence on whether statins have anti-HIV activity. A Retrovirus Conference report by Scott Letendre (University of California, San Diego) and CHARTER cohort colleagues suggested statins help lower HIV levels in CSF, but mainly in people already taking antiretrovirals [13]. On the other hand, selective serotonin reuptake inhibitors (SSRIs, the popular antidepressants) seemed to have antiretroviral activity in CSF mainly in people not taking antiretrovirals.

Among 659 CHARTER members studied, 467 (71%) used antiretrovirals, 195 (30%) SSRIs, and 63 (10%) statins when they made their study visit. CHARTER clinicians measured HIV RNA in plasma of 383 people (58%) and in CSF of 230 (35%). The group had a median CD4 count of 402, and 64% had AIDS.

Not surprisingly, people taking SSRIs reported more severe depression symptoms than people not taking these antidepressants (P < 0.001). SSRI users also were more likely to be taking antiretrovirals (77% versus 70%, P = 0.06) and had higher CD4 counts (median 433 versus 389 cells, P = 0.07) and lower viral loads (median 1.9 versus 2.4 log, P = 0.07).

An unadjusted analysis determined that people taking SSRIs were about 30% less likely to have detectable HIV in CSF (29% versus 37%, odds ratio 0.69, P = 0.05). Three of seven SSRIs used appeared to have the biggest impact on HIV in CSF: citalopram (Celexa), trazodone (Desyrel), and sertraline (Zoloft). Combining these three antidepressants into a single "antiretroviral" category strengthened their apparent anti-HIV activity in CSF.

People who took one of these three SSRIs also had better global deficit scores on neuropsychological testing (median 0.37 versus 0.47, P = 0.04), and a lower proportion had evidence of neuropsychological impairment (55% versus 64%, P = 0.05). Logistic regression analysis determined that these three "antiretroviral" SSRIs correlated with lower HIV RNA levels in CSF (odds ratio 0.72, P < 0.05), as did antiretroviral use, lower CD4 counts, undetectable HIV RNA in plasma, and Caucasian race.

One might speculate that SSRI use correlates with lower viral loads in plasma and CSF because less depressed people taking these drugs are more likely to adhere to antiretroviral therapy. But Letendre found that "antiretroviral" SSRI users not taking licensed antiretrovirals had the best chance of reaching an undetectable HIV load in CSF. Compared with people not taking SSRIs, this group had about a 70% lower chance of detectable HIV in CSF (odds ratio 0.31, P = 0.01).

Statins, on the other hand, exerted their greatest anti-HIV activity in people already taking antiretrovirals. Cohort members combining statins with antiretrovirals had about a 90% lower chance of detectable HIV in CSF than non-statin users (odds ratio 0.09, P < 0.001). Among all statin users, regardless of antiretroviral use, 16% had detectable HIV in CSF compared with 37% of people not taking statins (odds ratio 0.32, P < 0.001). The apparently stronger anti-HIV activity of statins with antiretrovirals led Letendre and colleagues to speculate that statins' apparent anti-HIV activity "may be mediated by modifying antiretroviral metabolism or distribution."

Next the CHARTER researchers compared HIV CSF levels in four groups--people taking neither SSRIs nor statins, people taking only SSRIs, people taking only statins, and people taking both SSRIs and statins. SSRIs and statins appeared to have additive antiretroviral activity in this analysis. Rates of detectable HIV in CSF measured 39% in the no-SSRI/no-statin group, 27% in the SSRI-only group, 17% in the statin-only group, and 12% in the SSRI-plus-statin group (P = 0.001).

Unlike SSRIs, statins had no neurocognitive benefit in this cohort. Such benefits, Letendre and coworkers surmised, may be negated by concomitant PI therapy, statins themselves, or the lipodystrophy syndrome suffered by many people taking statins. The researchers also caution that some evidence ties statins to brain injury, such as memory loss.

from http://www.natap.org/2007/CROI/croi_64.htm
 

Jenny

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There are over 200 FM and CFS patients reporting their experiences with milnacipran over on patientslikme http://www.patientslikeme.com/home. Most said they found it to some degree effective for pain. If you register you can see what they say about other benefits and side effects.

Also a lot of people saying whether they got any benefits from other anti-depressants.

I was given sertraline by a stupid pain clinic doctor some years ago. No improvement.

Jenny
 

julius

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They have not included any data in the last ten years because they felt the data in the really big studies were biased! Pleeeaase! yet they saw fit to include phase three studies used to establish safety not efficacy already seen by the FDA
I'm not sure what you mean here. It has nothing to do with anything I brought up. Perhaps you are commenting on another post...not sure.



As for gaba pentin I would hesitate in suggesting for anyone, other than those having otherwise intractable seisures where other anticonvulsants have failed.This is literally a life or death situation because the chance of status eplilepticus is so high
.

Again, nothing to do with what I said. The paper I quoted was about Detailing, gabapentin just happened to be the drug in the study because there was abundant documentation available resulting from an FOI request(re detailing...not the drug per se). Of course that is made very clear in the paper, so I'm sure you picked that up when you read it[?]


Antidepressants would only be potentially useful for what used to be called endogenous depression
No. They are not. That is the point.

Please read the papers I cited. Otherwise I don't see the point in commenting.

Here are the salient points;

Of approx 70 applications for FDA approval studies, all were completed but less than half were published. The only ones published were the ones in which the antidepressant performed better than placebo. More than 50%, which were not published had placebo outperforming the antidepressant.

It was based on these studies that next gen. antidepressants have been approved. It is also the basis on which the more recent theories you are bringing up are founded.

This is a very simple synopsis, the complete story is quite a bit worse.
 

julius

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Hi Julius,

FWIW - more information re efficacy of anti-depressants.

http://www.drugawareness.org/ssri-facts/kauffman-ssri-study

Take care,


Hysterical :Retro smile:
Thanks, he says it a lot better than I can. I guess not having brain fog can be helpful.

This is the point I have been trying to make, but in better writing;

"Analyses of datasets including unpublished as well as published clinical trials reveal smaller effects that fall well below recommended criteria for clinical effectiveness. Specifically, a meta-analysis of clinical trial data submitted to the U.S. Food and Drug Administration (FDA) revealed a mean drug–placebo difference in improvement scores of 1.80 points on the Hamilton Rating Scale of Depression (HRSD), whereas the National Institute for Clinical Excellence (NICE) used a drug–placebo difference of three points as a criterion for clinical significance when establishing guidelines for the treatment of depression in the United Kingdom. Kirsch et al. concluded that the updated findings from 35 carefully vetted trials suggest that, compared with placebo, the four new- generation antidepressants ( fluoxetine, venlfaxine, nefazodone, and paroxetine) do not produce clinically significant improvements in depression in patients who initially have moderate or even severe depression."


Also, this is interesting;

"Even these unimpressive findings exaggerated the benefits of antidepressants. In three fluoxetine trials and in the three sertraline trials for which data were reported, the protocol allowed replacement of patients who, in the investigators’ judgment, were not improving after 2 weeks. The trials also included a 1–2 week washout period, during which patients were given a placebo prior to randomization. Those whose scores improved 20% or more were excluded from the study."


There's nothing too sleazy for these guys!