![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 7 of 7. This is the beginning of the thread.
Posted by Diane on November 7, 1999, at 12:20:51
According to that "Listening to Prozac" book (page 147 top) I should just cut my dose in half and continue on.
It doesn't make a lick of sense to me. NONE!..... ZERO!
If one has an immediate bad reaction to an AD (like my overwhelming anger/violence with Prozac), what possible benefit can one derive from continuing it .. at half a dose?
I also don't understand all this delay in kick-in stuff either. I felt that 20mg Of Prozac within hours!
Why does it take some ADs weeks to bloom?
What's it DOING during those weeks?
How can it be doing ANY THING GOOD when it's making you HURT/sick with side-effects?!
According to "Listening..." I shouldn't even of had that reaction. That increasing serotonin levels results in a marked decline in hostility and a decrease in the expression of anger.
The author poopoos the whole idea of people becoming angry/violent off of Prozac.Thanks
Diane
Posted by Adam on November 7, 1999, at 15:39:42
In reply to cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Diane on November 7, 1999, at 12:20:51
There is the way most people respond to a medication, and the way each individual responds to a medication. The
two can be very different. There is a whole new branch of pharmacology emerging, "pharmacogenomics", because of
this. Some day there will be robust diagnotics utilized to predict who may have no response or a paradoxical
response to a drug. Until then, there's only trial and error. If your response doesn't make much sense to you,
don't worry, you're in good company. The best and the brightest have been scratching their heads for years over
just this issue. It is important to remember that because two things occur simultaneously does not necessarily
indicate causality. You might feel angry/hostile because the drug is making you feel sick, not because your
levels of serotonin have been boosted. The side effects may or may not be related to the drug's primary mechanism
of action.Reduced dose usually equals reduced efficacy, but not always. Some people need less of a drug to get a therapeutic
effect, and usually less of the drug means less severe side effects.The antidepressant response to elevated levels of monoamines (the mechanism of action of most antidepressants), is
complex. It is not entirely accurate to say one is antidepressed because they have boosted levels of serotonin.
Rather, changes in the level of serotonin in the synapse (in the case of Prozac, an increase due to inhibition of
reuptake) leads to changes in the pre and/or post-synaptic neurons that take time to develop. One is essentially
made LESS sensitive to serotonergic neurotransmission by Prozac. It is the induced changes in response that are
hypothesized to be the true markers of antidepressant effect, and it can take anywhere from a week to a couple months
before these changes are felt as an improvement in mood. It's safe to say that if you haven't responded after
six weeks or so, you should change doses or change medications.
> According to that "Listening to Prozac" book (page 147 top) I should just cut my dose in half and continue on.
>
> It doesn't make a lick of sense to me. NONE!..... ZERO!
>
> If one has an immediate bad reaction to an AD (like my overwhelming anger/violence with Prozac), what possible benefit can one derive from continuing it .. at half a dose?
>
> I also don't understand all this delay in kick-in stuff either. I felt that 20mg Of Prozac within hours!
>
> Why does it take some ADs weeks to bloom?
>
> What's it DOING during those weeks?
>
> How can it be doing ANY THING GOOD when it's making you HURT/sick with side-effects?!
>
> According to "Listening..." I shouldn't even of had that reaction. That increasing serotonin levels results in a marked decline in hostility and a decrease in the expression of anger.
> The author poopoos the whole idea of people becoming angry/violent off of Prozac.
>
> Thanks
> Diane
Posted by Adam on November 7, 1999, at 19:39:32
In reply to Re: cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Adam on November 7, 1999, at 15:39:42
My last post was based on an explanation of antidepressant action
that I was given by an old psychiatrist a long time ago. While it may
have some validity, some very quick reading I just did (brought on by
reservations I had, given my relationship with the guy), revealed some
possible oversimlifications or inaccuracies in this explanation of
the delayed onset of antidepressant action in relation to serotonin
levels. Perhaps oversimplifications or inaccuracies are inevitable
given the complexity of the changes in neurons caused by antidepressants.
Presynaptic and postsynaptic neurons may indeed undergo certain specific
"desensitizing" changes in response to the increase of serotonin in the
synapse, at least in certain neurons. Overstimulation of 5-HT1A receptors,
for example, can result in lowered rates of firing of both the presynaptic
and postsynaptic neuron, but this effect may be most important, in relation
to depression, when one considers presynaptic neurons in certain regions of
the brain. In one proposed mechanism, increased levels of serotonin (by SSRI)
in the synapse initially leads to a decrease in serotonin synthesis and
release by the serotonergic neuron, a negative feedback response adapted to
maintain normal serotonin levels in the synapse. Initially, this response
remains unmodified, such that serotonin levels in the synapse aren't increased
enough in the short term to bring about a therapeutic response. Over time,
with continued hyperstimulation, 5-HT1A receptor-mediated signalling is inhibited,
and a portion of the negative-feedback loop thus begins to break down. As
neuron firing and serotonin synthesis return to normal levels, and, because
reuptake of serotonin is simultaneously being inhibited, more serotonin is left
in the synapse, and now we are at "therapeutic levels". It is by inhibiting
this specific negative-feedback that 5-HT1A receptor antagonists (ex: pindolol)
are thought to speed up response to SSRIs: They do quickly what must normally
take time to occur (inhibition of 5-HT1A autoreceptor activity), and thus quickly
increase serotonin levels in combination with an SSRI.Perhaps delayed antidepressant onset is largely a "presynaptic" phenomenon. I
wonder if "poop-out" is a "postsynaptic" phenomenon.
Posted by Tom on November 7, 1999, at 21:44:01
In reply to cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Diane on November 7, 1999, at 12:20:51
> According to that "Listening to Prozac" book (page 147 top) I should just cut my dose in half and continue on.
>
> It doesn't make a lick of sense to me. NONE!..... ZERO!
>
> If one has an immediate bad reaction to an AD (like my overwhelming anger/violence with Prozac), what possible benefit can one derive from continuing it .. at half a dose?
>
> I also don't understand all this delay in kick-in stuff either. I felt that 20mg Of Prozac within hours!
>
> Why does it take some ADs weeks to bloom?
>
> What's it DOING during those weeks?
>
> How can it be doing ANY THING GOOD when it's making you HURT/sick with side-effects?!
>
> According to "Listening..." I shouldn't even of had that reaction. That increasing serotonin levels results in a marked decline in hostility and a decrease in the expression of anger.
> The author poopoos the whole idea of people becoming angry/violent off of Prozac.
>
> Thanks
> DianeYou are not alone. I took 5 mgs of Prozac and had so much anxiety that my stomach hurt. Doc said it's not the Prozac. Increase the dose he said. 10 mgs...20mgs...after one month I was psychotic. It then dawned on me my Pdoc was the one with a screw loose. I immediately stopped the drug and became suicidal. Getting past withdrawl was no piece of cake either. Needless to say that I don't have "Listening to Prozac" on my bookshelf. Just take faith in that you are not alone in your reaction.
Posted by Cindy on November 7, 1999, at 23:29:55
In reply to Re: cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Tom on November 7, 1999, at 21:44:01
> > According to that "Listening to Prozac" book (page 147 top) I should just cut my dose in half and continue on.
> >
> > It doesn't make a lick of sense to me. NONE!..... ZERO!
> >
> > If one has an immediate bad reaction to an AD (like my overwhelming anger/violence with Prozac), what possible benefit can one derive from continuing it .. at half a dose?
> >
> > I also don't understand all this delay in kick-in stuff either. I felt that 20mg Of Prozac within hours!
> >
> > Why does it take some ADs weeks to bloom?
> >
> > What's it DOING during those weeks?
> >
> > How can it be doing ANY THING GOOD when it's making you HURT/sick with side-effects?!
> >
> > According to "Listening..." I shouldn't even of had that reaction. That increasing serotonin levels results in a marked decline in hostility and a decrease in the expression of anger.
> > The author poopoos the whole idea of people becoming angry/violent off of Prozac.
> >
> > Thanks
> > Diane
>
> You are not alone. I took 5 mgs of Prozac and had so much anxiety that my stomach hurt. Doc said it's not the Prozac. Increase the dose he said. 10 mgs...20mgs...after one month I was psychotic. It then dawned on me my Pdoc was the one with a screw loose. I immediately stopped the drug and became suicidal. Getting past withdrawl was no piece of cake either. Needless to say that I don't have "Listening to Prozac" on my bookshelf. Just take faith in that you are not alone in your reaction.Adam, I don't know much about how antidepressants work, but it occurred to me, could the "poop-out" be due to downregulation? At first, antidepressants seem to help (preventing reuptake of neurotransmitters). Could poop out occur when the cell "downregulates" (when sufficient or too much neurotransmitter is present?).
Which mechanism of SSRI's causes the sexual dysfunction in many people? I have read some stuff that suggests that 5HT-2 is affected (?). Why can't they make an SSRI that is even more selective and not cause dysfunction? Thanks!--Cindy
Posted by Adam on November 8, 1999, at 18:03:19
In reply to Re: cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Cindy on November 7, 1999, at 23:29:55
> Adam, I don't know much about how antidepressants work, but it occurred to me, could the "poop-out" be due to downregulation? At first, antidepressants seem to help (preventing reuptake of neurotransmitters). Could poop out occur when the cell "downregulates" (when sufficient or too much neurotransmitter is present?).
> Which mechanism of SSRI's causes the sexual dysfunction in many people? I have read some stuff that suggests that 5HT-2 is affected (?). Why can't they make an SSRI that is even more selective and not cause dysfunction? Thanks!--CindyMaking a more specific SSRI might not help. Citalopram (Celexa) is considered to be highly "specific" in its binding to the 5-HT transporter, but this specificity hasn't translated into
decreased sexual side effects, from what I've heard. I imagine any SSRI, because it boosts synaptic serotonin levels, could lead to stimulation of 5-HT receptors that are responsible for
some or all of the sexual dysfunction. The problem might be solved, rather, by designing more specific receptor agonists and antagonists that have antidepressant effects. I've read that
5-HT2 is involved in sexual dysfunction and that 5-HT1A isn't. I've also read the complete opposite. I'm not sure if there is a definitive explanation for SSRI-induced sexual dysfunction,
though it is probably due, at least in part, to the hyperstimulation of one or more of the 5-HT receptors. It is for this very reason that nefazodone and mirtazapine are thought to have
an antidepressant effect on the serotonergic system without causing sexual side effects. I think this explanation is still unproven, however.
Posted by Elizabeth on November 9, 1999, at 7:46:43
In reply to Re: cont. Prozac after bad reaction WHAT FOR? & misc?, posted by Adam on November 8, 1999, at 18:03:19
> I've read that 5-HT2 is involved in sexual dysfunction and that 5-HT1A isn't.
Well, consider the following two drugs, both of which don't cause sexual dysfunction very much:
* Serzone, a 5-HT reuptake inhibitor and 5-HT2 antagonist
* Buspar, a 5-HT1a partial agonistThat would tend to support the above hypothesis.
> I'm not sure if there is a definitive explanation for SSRI-induced sexual dysfunction,
Oh hell, is there a definitive explanation for any of this stuff?
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.