Psycho-Babble Medication Thread 95939

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Duloxetine

Posted by Bob on March 2, 2002, at 14:02:48

In reply to When is duloxetine to be approved?, posted by SLS on March 1, 2002, at 9:48:21

What is expected from Duloxetine that we don't already get from Effexor, except possibly a slightly different response profile? Effexor has many problems for many people, and I don't see how Duloxetine will be any better. I don't doubt that the med will produce robust sexual dysfunction, and weight gain in the long run. It may have a severe withdrawal syndrome like that of Effexor too. Nobody will be able to tell you from a short FDA study, though. Why won't this med me subject to poop-out, like so many of the SSRIs, and Effexor? It seems to me that the medical/pharmaceutical community has not addressed the fact that eventually in many cases, the brain adapts to the drug, and effectiveness is lost. I'm not sure the drug companies care, though, as long as a majority of people respond for appreciable amounts of time. The non-responders can be considered a "difficult minority".

I hate to be negative, but I can't really help it anymore.

 

Re: When is duloxetine to be approved?

Posted by Geezer on March 2, 2002, at 14:30:01

In reply to Re: When is duloxetine to be approved?, posted by Bekka H. on March 2, 2002, at 12:46:17

> > Scott - I talked to one of the Eli Lilly reps about duloxetine. They expect it to be released in Canada in 2003. Besides depression they are also trying to get approved for some bladder disorder (stress incontinence? - I can't remember).
>
> Yes, I've heard that, like many other antidepressants, duloxetine causes urinary retention, so instead of seeing this as a potentially dangerous adverse reaction (it's not healthy to retain your urine), Lilly is trying to capitalize on it and exploit it for marketing purposes.
>
> > I have a feeling that it's going to be SSDD (same s**t different day).
>
> I agree about the SSDD. Just what the world needs -- yet another "me too" lipogenic, impotence-ogenic, wimpogenic SSRI.

I called Lilly customer service a couple of months ago. They said they expected US release in late 2002 - understand the FDA is in there messing around with the company computers and recording keeping (standard operating procedure for the FDA Nazis). The only difference between Duloxetine and Effexor I have read about has something to do with a more 50/50 split in the SE NE effect.....apparently you don't have to wade thru as much SE before you get to the NE.

Also was aware Lilly was turning "Lemons Into Lemonade" with the urinary retention hype - another promotional claim has something to do with releiving the physical aches and pains of depression.

Bekka......the "lipogenic, impotence-ogenic, wimpogenic SSRI" almost gave me laughter induced urinary incontinence!

Geezer

 

Re: Amoxapine » SLS

Posted by TSA West on March 2, 2002, at 16:38:06

In reply to Re: When is duloxetine to be approved?, posted by SLS on March 2, 2002, at 8:46:10

I'm interested in your trial of amoxapine. How long did you take it and what was your final dose? Did you have any ExtraPyramidal Symptoms?

>>When it exerts an antidepressant effect, the quality of the improvement it produces is the best of the tricyclics I have yet tried (imipramine, desipramine, amitriptyline, nortriptyline, protriptyline, and amoxapine).

 

Re: Duloxetine

Posted by SLS on March 2, 2002, at 17:15:51

In reply to Duloxetine, posted by Bob on March 2, 2002, at 14:02:48

> What is expected from Duloxetine that we don't already get from Effexor, except possibly a slightly different response profile?

I don't know about the rest of the world, but I expect duloxetine to get some people well whom had not previously responded to anything else. I would like to avail myself of the opportunity to try it. Some people have responded to Zoloft whom had not responded to Prozac; Paxil to Zoloft; Celexa to Paxil; Prozac to Celexa etc. Duloxetine might not appear especially novel with respect to monoamine reuptake inhibition in test-tubes, but I'm not sure that anyone understands the brain and actions of psychotropics well enough to draw firm conclusions about a drug's worth based upon what little is assumed to be understood. Laboratory test paradigms using rats are currently more reliable than deduction, although far from infallible.


> Effexor has many problems for many people, and I don't see how Duloxetine will be any better.

During a consultation, Patrick McGrath of Columbia-Presbyterian stated to me that for every new drug that appears, a certain percentage of people whom had previously been refractory to treatment responds well to it.

> I hate to be negative, but I can't really help it anymore.

Of course I'm frustrated that there are so few new drugs with novel mechanisms of action available or in development. It's obvious to me that the mechanisms of those that are currently available ain't hitting my target.

How does it hurt me to allow the drug companies and the FDA to release hundreds of drugs that are similar to each other? Capitalism just about insures that drug companies will still be working feverishly to develop novel drugs to break away from the pack. I don't think it is at all negative to be frustrated with the limitations of the current pharmacopeia and want to see drugs with very different mechanisms of action appear. I do, however, think it is negative to prevent drugs of only slightly differing mechanisms of action be brought to market. Slightly different might be different enough for some people. I have a vested interest in seeing duloxetine make it to the pharmacist's shelves. It's one more tool to work with.


- Scott

 

Re: When is duloxetine to be approved?

Posted by Bekka H. on March 2, 2002, at 17:59:05

In reply to Re: When is duloxetine to be approved?, posted by Geezer on March 2, 2002, at 14:30:01

> 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.

 

what do you think of flibanserin (Ectris)?

Posted by JohnX2 on March 2, 2002, at 19:45:42

In reply to Re: Duloxetine, posted by SLS on March 2, 2002, at 17:15:51


What do you guys think about the possibility
of this medicine: flibanserin (Ectris)?

I've been following it for quite a while.
When I tryed to dig up info from the company,
they wouldn't let me pry anything from there hands,
but I saw they applied for trademark name in the
US at the time (Ectris, this was a year or 2 ago).
Its gotton almost NO marketing hype or fanfare,
its just sorta secretly moved along phase I,II,III
clinical trials.

Its not another "me too" medicine. It does something new.
Its a direct acting 5ht-1a agonist combined with a 5ht-2a antagonist
Rumored to be fast acting.

-John


> > What is expected from Duloxetine that we don't already get from Effexor, except possibly a slightly different response profile?
>
> I don't know about the rest of the world, but I expect duloxetine to get some people well whom had not previously responded to anything else. I would like to avail myself of the opportunity to try it. Some people have responded to Zoloft whom had not responded to Prozac; Paxil to Zoloft; Celexa to Paxil; Prozac to Celexa etc. Duloxetine might not appear especially novel with respect to monoamine reuptake inhibition in test-tubes, but I'm not sure that anyone understands the brain and actions of psychotropics well enough to draw firm conclusions about a drug's worth based upon what little is assumed to be understood. Laboratory test paradigms using rats are currently more reliable than deduction, although far from infallible.
>
>
> > Effexor has many problems for many people, and I don't see how Duloxetine will be any better.
>
> During a consultation, Patrick McGrath of Columbia-Presbyterian stated to me that for every new drug that appears, a certain percentage of people whom had previously been refractory to treatment responds well to it.
>
> > I hate to be negative, but I can't really help it anymore.
>
> Of course I'm frustrated that there are so few new drugs with novel mechanisms of action available or in development. It's obvious to me that the mechanisms of those that are currently available ain't hitting my target.
>
> How does it hurt me to allow the drug companies and the FDA to release hundreds of drugs that are similar to each other? Capitalism just about insures that drug companies will still be working feverishly to develop novel drugs to break away from the pack. I don't think it is at all negative to be frustrated with the limitations of the current pharmacopeia and want to see drugs with very different mechanisms of action appear. I do, however, think it is negative to prevent drugs of only slightly differing mechanisms of action be brought to market. Slightly different might be different enough for some people. I have a vested interest in seeing duloxetine make it to the pharmacist's shelves. It's one more tool to work with.
>
>
> - Scott

 

Re: what do you think of flibanserin (Ectris)? » JohnX2

Posted by JohnX2 on March 2, 2002, at 19:55:11

In reply to what do you think of flibanserin (Ectris)?, posted by JohnX2 on March 2, 2002, at 19:45:42


my spelling is so bad. how can I have a college
degree, much less a grade school diploma? sorry for the distraction, it just depresses
me when I re-read my posts and count all my typos.

-John

>
> What do you guys think about the possibility
> of this medicine: flibanserin (Ectris)?
>
> I've been following it for quite a while.
> When I tryed to dig up info from the company,
> they wouldn't let me pry anything from there hands,
> but I saw they applied for trademark name in the
> US at the time (Ectris, this was a year or 2 ago).
> Its gotton almost NO marketing hype or fanfare,
> its just sorta secretly moved along phase I,II,III
> clinical trials.
>
> Its not another "me too" medicine. It does something new.
> Its a direct acting 5ht-1a agonist combined with a 5ht-2a antagonist
> Rumored to be fast acting.
>
> -John
>
>
>
>
>
>
> > > What is expected from Duloxetine that we don't already get from Effexor, except possibly a slightly different response profile?
> >
> > I don't know about the rest of the world, but I expect duloxetine to get some people well whom had not previously responded to anything else. I would like to avail myself of the opportunity to try it. Some people have responded to Zoloft whom had not responded to Prozac; Paxil to Zoloft; Celexa to Paxil; Prozac to Celexa etc. Duloxetine might not appear especially novel with respect to monoamine reuptake inhibition in test-tubes, but I'm not sure that anyone understands the brain and actions of psychotropics well enough to draw firm conclusions about a drug's worth based upon what little is assumed to be understood. Laboratory test paradigms using rats are currently more reliable than deduction, although far from infallible.
> >
> >
> > > Effexor has many problems for many people, and I don't see how Duloxetine will be any better.
> >
> > During a consultation, Patrick McGrath of Columbia-Presbyterian stated to me that for every new drug that appears, a certain percentage of people whom had previously been refractory to treatment responds well to it.
> >
> > > I hate to be negative, but I can't really help it anymore.
> >
> > Of course I'm frustrated that there are so few new drugs with novel mechanisms of action available or in development. It's obvious to me that the mechanisms of those that are currently available ain't hitting my target.
> >
> > How does it hurt me to allow the drug companies and the FDA to release hundreds of drugs that are similar to each other? Capitalism just about insures that drug companies will still be working feverishly to develop novel drugs to break away from the pack. I don't think it is at all negative to be frustrated with the limitations of the current pharmacopeia and want to see drugs with very different mechanisms of action appear. I do, however, think it is negative to prevent drugs of only slightly differing mechanisms of action be brought to market. Slightly different might be different enough for some people. I have a vested interest in seeing duloxetine make it to the pharmacist's shelves. It's one more tool to work with.
> >
> >
> > - Scott

 

Re: what do you think of flibanserin (Ectris)?

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

 

Re: When is duloxetine to be approved?

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

 

Re: Duloxetine » SLS

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.

 

Re: When is duloxetine to be approved?

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.

 

Re: Amoxapine » TSA West

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

 

Re: Duloxetine » Bob

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

 

Re: New Glaxo / Merck antidepressant

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

 

Re: Duloxetine

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

 

Re: New Glaxo / Merck antidepressant » SLS

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

 

Re: New Glaxo / Merck antidepressant » SLS

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

 

Re: New Glaxo / Merck antidepressant

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

 

Re: what do you think of flibanserin (Ectris)?

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

 

Re: what do you think of flibanserin (Ectris)? » Cam W.

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

 

Any word on Substance P from Merck?

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?

 

Re: Any word on Substance P from Merck? » Ponder

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.

 

Re: what do you think of flibanserin (Ectris)? » JohnX2

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

 

Re: what do you think of flibanserin (Ectris)? » Cam W.

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

 

Re: mind and body » Cam W.

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


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