![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 15 to 39 of 39. Go back in thread:
Posted by Geezer on March 2, 2002, at 20:14:03
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by JohnX2 on March 2, 2002, at 19:55:11
John your spelling was not a problem - mine is worse. Alas, your new drug sent me into hysterics for the second time today. Mind you.....at my age stool softeners are at least as important SSRIs. Think I better get off this thread - I can feel a "redirect" coming.
Geezer
Posted by Geezer on March 2, 2002, at 20:59:06
In reply to Re: When is duloxetine to be approved?, posted by Bekka H. on March 2, 2002, at 17:59:05
> > Bekka......the "lipogenic, impotence-ogenic, wimpogenic SSRI" almost gave me laughter induced urinary incontinence!
> > Geezer
>
> Hello, Geezer, I'm glad I gave you a chuckle. After I posted that, I thought maybe I shouldn't have been so negative because as SLS said, it may help some people, but I'm feeling very discouraged and cynical these days. I'm getting really fed up with pharmaceutical companies, and I think their marketing is a disgrace.Hi Bekka-don't get feeling bad about a comment like that, that's just a "little shootin from the hip". Last Tues. I met with a lady pdoc while in a mixed state (got over-juiced on Remeron), she didn't recognize it, d*** near took her head off when she insisted I needed to undertake cognative therapy. Now that would have been inconsiderate!
Have to agree about the drug companies. Medicine has been commercialized, we are the consumers - we have to be better informed than they are commerical. You keep fighting!
Geezer
Posted by Bob on March 2, 2002, at 21:10:54
In reply to Re: Duloxetine, posted by SLS on March 2, 2002, at 17:15:51
I have no intention of preventing "me too" drugs from hitting the market. I'm just tired of trying drugs. It's almost too much effort now for me to get off one drug and go on another - it's taking too much out of me, and my condition is getting worse and worse. I can't hang my hat on something like duloxetine.
Posted by Bekka H. on March 2, 2002, at 23:47:09
In reply to Re: When is duloxetine to be approved?, posted by Geezer on March 2, 2002, at 20:59:06
Geezer, thank you for the encouragement. By the way, I like your screen name.
Posted by SLS on March 3, 2002, at 12:43:06
In reply to Re: Amoxapine » SLS, posted by TSA West on March 2, 2002, at 16:38:06
Hi TSA.
I tried amoxapine when it first came out in 1982. I don't recall any of the details regarding dosage or length of trial. Sorry. It didn't help at all. In fact, it made my depression worse, particularly with regard to psychomotor-retardation, reduced libido, and a feeling of mental slowing or numbness. I attribute the DA antagonist properties of amoxapine for this.
Your question involving EPS (ExtraPyramidal Symptoms = parkinsonian involuntary movements and akathisia) is a good one. It can be debated as to whether amoxapine should ever been approved as an antidepressant. While working as a research assistant for Baron Shopsin, I investigated the FDA approval process and the ethics practiced by its administrators. In the original trial of 10 subjects, I believe three developed unequivocal EPS. I'd have to go back and find my old notebooks to detail what symptoms developed. Regardless, a 30% incidence of EPS in a trial should have received more focus. It seems that Lederle had a friend in the FDA, for these results were swept under the rug and the approval process allowed to continue.
Amoxapine is derived from the antipsychotic loxapine (Loxitane). Many people would argue that any incidence of EPS is unacceptable in an antidepressant, even if the risk were substantially lower than that of the typical neuroleptic antipsychotics. There were already quite a few effective tricyclics available without the liability of producing EPS and tardive-dyskinesia. However, some people do very well on amoxapine whom had not found success with any of the others. If I were one of those people, I would have quite a different view as to what is unacceptable. I would find it unacceptable to remove amoxapine from the market and applaud everyone who were responsible for it getting there in the first place.
Clomipramine (Anafranil) had at one time been considered the most effective antidepressant available. Although its side effects are generally greater than the other tricyclics, I think its use should be considered in light of your partial response to the others. Clomipramine combines the reuptake inhibitions of both norepinephrine with serotonin. In addition to the anticholinergic side effects common to tricyclics, it can also produce sexual side effects that are similar to those of the SSRIs.
I guess the knee-jerk reaction to your query is, "have you tried an MAOI yet?"
Good luck. It might make sense to first try augmenting amoxapine with things like lithium or Wellbutrin.
- Scott
Posted by SLS on March 3, 2002, at 12:54:07
In reply to Re: Duloxetine » SLS, posted by Bob on March 2, 2002, at 21:10:54
Hi Bob.
> I have no intention of preventing "me too" drugs from hitting the market. I'm just tired of trying drugs. It's almost too much effort now for me to get off one drug and go on another - it's taking too much out of me, and my condition is getting worse and worse.
I know what that's like. I guess we have both been riders on the same train for quite awhile.
> I can't hang my hat on something like duloxetine.
It is sometimes too much to hope. I feel the same way you do. I would rather here that something like a substance-P antagonist were found to be a potent antidepressant.
I hope you find your answer soon.
Sincerely,
Scott
Posted by SLS on March 3, 2002, at 19:33:15
In reply to Re: Duloxetine » Bob, posted by SLS on March 3, 2002, at 12:54:07
Here's a new one (sort of):
http://pharmalicensing.com/news/adisp/982274821_3a8c5305199e4
Excerpts:
"GlaxoSmithKline plc and Merck KGaA have signed a worldwide
development and commercialisation agreement for an antidepressant
with a novel mechanism of action.""The compound, currently known as EMD 68843 or SB 659746-A, is in
Phase II clinical development.""It combines the properties of a selective serotonin- reuptake
inhibitor with those of a 5-HT1A partial agonist."
Does anyone know how long it takes for a drug in phase-II trials to be approved?- Scott
Posted by Bob on March 3, 2002, at 20:50:51
In reply to Re: Duloxetine » Bob, posted by SLS on March 3, 2002, at 12:54:07
> I hope you find your answer soon.
Scott:If you have not found your answer yet, then I hope the same for you.
Bob
Posted by Bob on March 3, 2002, at 21:26:34
In reply to Re: New Glaxo / Merck antidepressant, posted by SLS on March 3, 2002, at 19:33:15
> Here's a new one (sort of):
>
> http://pharmalicensing.com/news/adisp/982274821_3a8c5305199e4
>
> Excerpts:
>
> "GlaxoSmithKline plc and Merck KGaA have signed a worldwide
> development and commercialisation agreement for an antidepressant
> with a novel mechanism of action."
>
> "The compound, currently known as EMD 68843 or SB 659746-A, is in
> Phase II clinical development."
>
> "It combines the properties of a selective serotonin- reuptake
> inhibitor with those of a 5-HT1A partial agonist."
>
>
> Does anyone know how long it takes for a drug in phase-II trials to be approved?
>
> - Scott--------------------------------------------------
Scott:
Forgive me for being obtuse here, but could you explain to me why the drug you described is so unique? What are the advantages of a compound which is an SSRI, yet has a 5HT1A partial agonist property?
Bob
Posted by Ritch on March 3, 2002, at 21:37:46
In reply to Re: New Glaxo / Merck antidepressant, posted by SLS on March 3, 2002, at 19:33:15
> Here's a new one (sort of):
>
> http://pharmalicensing.com/news/adisp/982274821_3a8c5305199e4
>
> Excerpts:
>
> "GlaxoSmithKline plc and Merck KGaA have signed a worldwide
> development and commercialisation agreement for an antidepressant
> with a novel mechanism of action."
>
> "The compound, currently known as EMD 68843 or SB 659746-A, is in
> Phase II clinical development."
>
> "It combines the properties of a selective serotonin- reuptake
> inhibitor with those of a 5-HT1A partial agonist."
>
>
> Does anyone know how long it takes for a drug in phase-II trials to be approved?
>
> - Scott
Gee Scott,That sounds an awful lot like combining Celexa+Buspar. I tried that before and it *did* work fairly well. Maybe others ought to consider that combination in the mean time? Of course, Buspar is relatively "dirty" given its DA receptor affinities, metabolites, etc.
Mitch
Posted by JohnX2 on March 3, 2002, at 23:09:10
In reply to Re: New Glaxo / Merck antidepressant, posted by SLS on March 3, 2002, at 19:33:15
Everything I read about pharmacology of
serotonergic systems seems to indicate that
you want to have an agonist at the 5ht-1a site
while antagonizing or down regulating the 5ht-2a site.Its believed from what I understand that a lot of SSRIs dont
respond because either they don't make it through
the first pass of downregulating the somotodendric
5ht-1a autorecptors (which would then increase
serotonin release, which pindolol is believed
to work at), or the medicine has difficulty
downregulating the postsynaptic receptors.Most SSRIS overtime downregulate 5ht-2 receptors
From "Essential Psychopharmacology" by Stephen
M. Stahl, 2nd edition. (a good book)
Figure 7-19
"Molecular stimulation of the 5ht-2a receptor
will alter the consequence of activating the
serotonin 5ht-1a receptor in a negative way and
reduce the gene expression of the 5ht-1a receptor
acting alone.....blah blah"Figure 7-21
Synergy between 5ht-1a stimulation and 5ht-2a
antagonism:
"The molecular consequence of 5ht-1a receptor
by disinhibition by 5ht-2a blockade is shown here,
namely enhanced gene expression...."So to beat around the bush, Stahl is suggesting
make a direct acting 5ht-1a agonist and combine
it with a 5ht-2a antagonist. i.e. something
like flibanserin. Maybe you can combine it
with a el-cheapo off patent SSRI to get an
enhanced effect.-John
> Here's a new one (sort of):
>
> http://pharmalicensing.com/news/adisp/982274821_3a8c5305199e4
>
> Excerpts:
>
> "GlaxoSmithKline plc and Merck KGaA have signed a worldwide
> development and commercialisation agreement for an antidepressant
> with a novel mechanism of action."
>
> "The compound, currently known as EMD 68843 or SB 659746-A, is in
> Phase II clinical development."
>
> "It combines the properties of a selective serotonin- reuptake
> inhibitor with those of a 5-HT1A partial agonist."
>
>
> Does anyone know how long it takes for a drug in phase-II trials to be approved?
>
> - Scott
Posted by Cam W. on March 5, 2002, at 1:35:24
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by JohnX2 on March 2, 2002, at 19:55:11
John - Actually, Ectris™ (filbanserin) is a "me too" antidepressant. It still is involving neuritransmission, where reseachers should be attacking second-messengers &/or protein - or enzyme-RNA transcription. Or they could try to mess with the hypothalamus or the pituitary. We gotta stop using bandages (neurotransmitter-based antidepressants) and attack a site further upstream, so that eventually we may find a way to target all symptoms via dendrites and neuro-cellular cross-talk.
Just my opinion. - Cam
Posted by JohnX2 on March 5, 2002, at 1:42:31
In reply to Re: what do you think of flibanserin (Ectris)?, posted by Cam W. on March 5, 2002, at 1:35:24
Hi Cam,Thanks for your thoughts. Is your feeling that we ought to be
pushing a bit more down the HPA axis directly in general?-John
> John - Actually, Ectris™ (filbanserin) is a "me too" antidepressant. It still is involving neuritransmission, where reseachers should be attacking second-messengers &/or protein - or enzyme-RNA transcription. Or they could try to mess with the hypothalamus or the pituitary. We gotta stop using bandages (neurotransmitter-based antidepressants) and attack a site further upstream, so that eventually we may find a way to target all symptoms via dendrites and neuro-cellular cross-talk.
>
> Just my opinion. - Cam
Posted by Ponder on March 5, 2002, at 15:04:24
In reply to Re: what do you think of flibanserin (Ectris)?, posted by Cam W. on March 5, 2002, at 1:35:24
I recall the hoopla when info was leaked to the press about Merck's research on Substance P and a new class of ADs. Has this research dead-ended?
Posted by Bob on March 5, 2002, at 16:38:36
In reply to Any word on Substance P from Merck?, posted by Ponder on March 5, 2002, at 15:04:24
> I recall the hoopla when info was leaked to the press about Merck's research on Substance P and a new class of ADs. Has this research dead-ended?
Last I heard, substance-p had less than desireable results in one of the FDA trial phases.
Posted by Cam W. on March 6, 2002, at 8:08:25
In reply to Re: what do you think of flibanserin (Ectris)? » Cam W., posted by JohnX2 on March 5, 2002, at 1:42:31
John - I think we need to take a different view of all biochemical systems that self-check (ie use biofeedback). We need to view them as we do an organ (albeit an ephemeral one). Scientists keep looking at the systems from a bottom-up approach, when perhaps a top-down theory may show us more.
Perhaps we should be looking at simultaneous activity in different brain structures, and how this changes over time and in various emotional states. The flux of the electrical activity in neurons, as it relates to bodily states (eg. moods, reactions, etc.), may be more important than the individual wiring (ie. the type of neurotransmitter a particular neuron uses, and where it "plugs-in").
Rahter than looking at the HPA axis, we should start looking at the result of what the HPA axis is doing in relation to other bodily "axes" (eg. HPA's interaction between the endocrine system, cardiac system, etc.). In other words, we should be looking a a relative (and perhaps subjective) view of homeostasis, and be studying the overall impact of change on homeostasis through change in one or several of these systems. This is basically using a homeopathic approach, but done in an orderly scientific manner, whose results should be reproduceable and unequivocal (ie. the results should be obvious to everyone).
Just babbling (honestly, the above is not psychotic rambling ... there is a thread of thought in there; it just won't come out in words :^)
Can someone who knows words kinda come to my rescue here? - Cam
Posted by Ritch on March 6, 2002, at 12:03:32
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by Cam W. on March 6, 2002, at 8:08:25
> John - I think we need to take a different view of all biochemical systems that self-check (ie use biofeedback). We need to view them as we do an organ (albeit an ephemeral one). Scientists keep looking at the systems from a bottom-up approach, when perhaps a top-down theory may show us more.
>
> Perhaps we should be looking at simultaneous activity in different brain structures, and how this changes over time and in various emotional states. The flux of the electrical activity in neurons, as it relates to bodily states (eg. moods, reactions, etc.), may be more important than the individual wiring (ie. the type of neurotransmitter a particular neuron uses, and where it "plugs-in").
>
> Rahter than looking at the HPA axis, we should start looking at the result of what the HPA axis is doing in relation to other bodily "axes" (eg. HPA's interaction between the endocrine system, cardiac system, etc.). In other words, we should be looking a a relative (and perhaps subjective) view of homeostasis, and be studying the overall impact of change on homeostasis through change in one or several of these systems. This is basically using a homeopathic approach, but done in an orderly scientific manner, whose results should be reproduceable and unequivocal (ie. the results should be obvious to everyone).
>
> Just babbling (honestly, the above is not psychotic rambling ... there is a thread of thought in there; it just won't come out in words :^)
>
> Can someone who knows words kinda come to my rescue here? - Cam
Hi Cam,I don't know if this is on the same page or not, but here goes...
I believe that most of the problems with depression, bipolar, OCD, etc. have to do with an inability of your brain to orchestrate properly and to process information effectively. I think different brain structures have to have some type of semi-autonomy to function together with the other parts as a whole. I wonder if when you have negative psychic symptoms it may be because parts of your brain stop "cooperating" with the other parts due to some type of "self-preservation" mechanism of sorts?? I liken the whole process to a conference of executives. You have got your VP's in charge of different functions and everybody needs to work together to keep the corporation running smoothly. If somebody gets grouchy (going through a divorce), falls asleep at the wheel, or plainly becomes psychotic, it will affect the ability of the whole group to work together. So what happens? You don't get important information being shared because somebody is asleep, or somebody can't be approached (because they are hostile), or somebody just doesn't make any sense. So, the reaction might be to exclude them from meetings-avoid them at the water cooler, whatever. But, profits are going down and the remaining functional members are getting very worn-out and concerned and start putting in extra hours and they just burn out. Another analogy might be a wacko submarine commander. All of the other officers get together and try to take control away. The commander might try to sink the sub, so the subordinate officers lock themselves in separate water-tight compartments believing they won't drown and they will survive, etc. I think the current spate of psych meds "work" because they are really facilitating information sharing and effective communication between the different structural parts. Unfortunately, they are like a chorus of beginning piano players. They hit the wrong chords often and don't keep time well.
Hope this helps,
Mitch
Posted by jazzdog on March 6, 2002, at 12:19:23
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by Cam W. on March 6, 2002, at 8:08:25
Hi Cam-
I know this is pretty simplistic, but aren't you in essence saying that the bodies' various systems - brain, endocrine, cardiac, digestive, etc - are really part of one holistic system, and complement and regulate (or disregulate) one another? And that a way needs to be found to chemically regulate this system as a whole, thereby bringing its components into balance? A master switch, so to speak? Or am I misreading you completely?
Jane
Posted by Bob on March 6, 2002, at 13:38:08
In reply to Re: what do you think of flibanserin (Ectris)? » Cam W., posted by Ritch on March 6, 2002, at 12:03:32
Wow! That "conference of executives" analogy is something else. Very interesting.
Posted by JohnX2 on March 6, 2002, at 13:47:39
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by Cam W. on March 6, 2002, at 8:08:25
Hmm, I kinda see what you are saying...Well, a lot of work has been in trying to analyze things
from ground up and start pushing buttons there. Problem
being things were just too complex and we didn't have the
tools to understand the "big picture" and really think about
how to turn the knobs working from the "top".I do microchip design, and there are a lot of analogies
between the complexity of what makes a microprocessor
with 25+ million transistors that fits on a finger nail
work (would anyone had believed we'd have this 50 yrs ago?),
all the feedback mechanisms, things that need to work
absolutely perfect to get a functional chip, etc. Just blow
1 of those 25 million transistors and we have a dead chip.
We can actually pinpoint which transistor killed the part with
our technology (but this had to be thought out ahead of
time before initiating the design).
We don't build chips by slopping down transistors and then
gluing them together and working are way up into this
elegant 25 million transistor computing device, it would
never work. I understand it from that perspective. Yet
the brain is much more complex, and the transisitors
(neurons, enzymes, whatever) are just being understood and
we really are just exciting them to see how the rest of
the computer (the brain) reacts. Not much to go by.
Need to think about how the body is architected from the
top. Arggh, i almost feel we would need to have the
technology to build a frankenstein monster to really get
a grip on the complexity of the human body/brain though.
But going back to my 25 million transistors on a fingernail,
thats facile today, so maybe getting a grip on the human
system some day is not out of this world. Arggh. Rambling,
don't know if this helps, its how my brain thinks in case
your wondering.-John
> John - I think we need to take a different view of all biochemical systems that self-check (ie use biofeedback). We need to view them as we do an organ (albeit an ephemeral one). Scientists keep looking at the systems from a bottom-up approach, when perhaps a top-down theory may show us more.
>
> Perhaps we should be looking at simultaneous activity in different brain structures, and how this changes over time and in various emotional states. The flux of the electrical activity in neurons, as it relates to bodily states (eg. moods, reactions, etc.), may be more important than the individual wiring (ie. the type of neurotransmitter a particular neuron uses, and where it "plugs-in").
>
> Rahter than looking at the HPA axis, we should start looking at the result of what the HPA axis is doing in relation to other bodily "axes" (eg. HPA's interaction between the endocrine system, cardiac system, etc.). In other words, we should be looking a a relative (and perhaps subjective) view of homeostasis, and be studying the overall impact of change on homeostasis through change in one or several of these systems. This is basically using a homeopathic approach, but done in an orderly scientific manner, whose results should be reproduceable and unequivocal (ie. the results should be obvious to everyone).
>
> Just babbling (honestly, the above is not psychotic rambling ... there is a thread of thought in there; it just won't come out in words :^)
>
> Can someone who knows words kinda come to my rescue here? - Cam
Posted by JohnX2 on March 6, 2002, at 14:03:10
In reply to Re: what do you think of flibanserin (Ectris)? » Cam W., posted by JohnX2 on March 6, 2002, at 13:47:39
>
> Hmm, I kinda see what you are saying...
>
> Well, a lot of work has been in trying to analyze things
> from ground up and start pushing buttons there. Problem
> being things were just too complex and we didn't have the
> tools to understand the "big picture" and really think about
> how to turn the knobs working from the "top".
>
> I do microchip design, and there are a lot of analogies
> between the complexity of what makes a microprocessor
> with 25+ million transistors that fits on a finger nail
> work (would anyone had believed we'd have this 50 yrs ago?),
> all the feedback mechanisms, things that need to work
> absolutely perfect to get a functional chip, etc. Just blow
> 1 of those 25 million transistors and we have a dead chip.
> We can actually pinpoint which transistor killed the part with
> our technology (but this had to be thought out ahead of
> time before initiating the design).Better yet, we have many chips that can run
a good deal of software that can work around those
faulty transistors as they are not always needed.
But pop up a particular game in some bizzare
scenario erratic to duplicate, etc, and "crash".
The events that led to the crash set up a huge cascade
of "states" amongst the other million of transistors that
1 itty bitty transistor was talking too. Sometimes we
go nuts just trying to duplicate these crashes to
have something repeatable and predicable to study.Also a lot of transistors are devoted to making the
chip faster, and they can fail yet the chip can execute
every instruction you give it, just not as fluently as
it would if the transistors were all communicating as
we intended. We don't sell these crummy chips of coarse ;).I see alot of analogies to the body/brain.
-John
> We don't build chips by slopping down transistors and then
> gluing them together and working are way up into this
> elegant 25 million transistor computing device, it would
> never work. I understand it from that perspective. Yet
> the brain is much more complex, and the transisitors
> (neurons, enzymes, whatever) are just being understood and
> we really are just exciting them to see how the rest of
> the computer (the brain) reacts. Not much to go by.
> Need to think about how the body is architected from the
> top. Arggh, i almost feel we would need to have the
> technology to build a frankenstein monster to really get
> a grip on the complexity of the human body/brain though.
> But going back to my 25 million transistors on a fingernail,
> thats facile today, so maybe getting a grip on the human
> system some day is not out of this world. Arggh. Rambling,
> don't know if this helps, its how my brain thinks in case
> your wondering.
>
> -John
>
>
>
>
>
>
> > John - I think we need to take a different view of all biochemical systems that self-check (ie use biofeedback). We need to view them as we do an organ (albeit an ephemeral one). Scientists keep looking at the systems from a bottom-up approach, when perhaps a top-down theory may show us more.
> >
> > Perhaps we should be looking at simultaneous activity in different brain structures, and how this changes over time and in various emotional states. The flux of the electrical activity in neurons, as it relates to bodily states (eg. moods, reactions, etc.), may be more important than the individual wiring (ie. the type of neurotransmitter a particular neuron uses, and where it "plugs-in").
> >
> > Rahter than looking at the HPA axis, we should start looking at the result of what the HPA axis is doing in relation to other bodily "axes" (eg. HPA's interaction between the endocrine system, cardiac system, etc.). In other words, we should be looking a a relative (and perhaps subjective) view of homeostasis, and be studying the overall impact of change on homeostasis through change in one or several of these systems. This is basically using a homeopathic approach, but done in an orderly scientific manner, whose results should be reproduceable and unequivocal (ie. the results should be obvious to everyone).
> >
> > Just babbling (honestly, the above is not psychotic rambling ... there is a thread of thought in there; it just won't come out in words :^)
> >
> > Can someone who knows words kinda come to my rescue here? - Cam
Posted by klp on December 15, 2002, at 14:39:28
In reply to Re: Duloxetine, posted by Bob on March 3, 2002, at 20:50:51
I'm sorry if this post keeps showing up but I'm not computer literate. I wanted to add some thing,I didn't experience any side effects from duloxetine. Now if they would only approve it
Posted by jaime on December 15, 2002, at 21:03:44
In reply to Re: Duloxetine » Bob, posted by klp on December 15, 2002, at 14:39:28
klp,
That's encouraging to hear that you didn't experience any side effects from duloxetine. How was it (or is it, if you're still on it) as far as effectiveness? Have you been on any other antidepressants, and if so, how did/does duloxetine compare?
Posted by klp on December 16, 2002, at 20:54:27
In reply to Re: Duloxetine » klp, posted by jaime on December 15, 2002, at 21:03:44
> klp,
>
> That's encouraging to hear that you didn't experience any side effects from duloxetine. How was it (or is it, if you're still on it) as far as effectiveness? Have you been on any other antidepressants, and if so, how did/does duloxetine compare?
>
I took part in the trials. The 1st 2 weeks there was no difference. For the remaining 7 weeks I felt so much better. More so than with the other anitdepressants I used(Zoloft, Wellbutran-generic, Remeron also xanax) I also was stress free ( no panic attacks) for a glorious 7 weeks, meaning no tension in my neck or shoulders. It was weird to feel normal. The first two weeks on it I got bad headaches,but only for 2 weeks. They gradually went away. 2 weeks after the trial was over I started feeling bad again. Granted it wasn't long term use so I don't know if there would be side effects a year down the road but other than the 1st two weeks I didn't experience any side effects. I didn't lose the weight I gained on Remeron but I didn't feel anymore hungry either. The shrink who administered it promised he would subscribe for me once it was approved but I stopped pestering him in October. The only negative was that it didn't help me sleep any better.
Posted by usndoc on February 20, 2003, at 14:59:21
In reply to Re: what do you think of flibanserin (Ectris)? » JohnX2, posted by JohnX2 on March 2, 2002, at 19:55:11
My wife saw an advertisement looking for participants in a study of flibanserin for female sexual dysfunction. I am concerned about her being in a drug trial. Was it safe in trials as an AD, but just didn't work well? Or was it unsafe and discontinued?
This is the end of the thread.
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