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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 47 to 71 of 317. Go back in thread:
Posted by SLS on January 1, 2012, at 6:01:53
In reply to Re: Adding Parnate and prazosin. » SLS, posted by sigismund on December 31, 2011, at 15:34:38
> Scott, I am interested as to whether prazosin deepens sleep, reduces early waking and so on.
Those are great questions for which I don't know the answers. I'll see what I can find out. It most certainly suppresses nightmares and is supposed to smooth sleep out in general according to the PTSD studies.
- Scott
Posted by creepy on January 1, 2012, at 10:05:01
In reply to Adding Parnate and prazosin., posted by SLS on December 29, 2011, at 6:55:56
The best med ever for my PTSD symptoms was topamax.
Oddly, NRIs seem to help me a bit.
zoloft and celexa were good on irritability but the apathy was just too much.
Posted by SLS on January 1, 2012, at 11:56:55
In reply to Re: Adding Parnate and prazosin., posted by creepy on January 1, 2012, at 10:05:01
> The best med ever for my PTSD symptoms was topamax.
> Oddly, NRIs seem to help me a bit.
> zoloft and celexa were good on irritability but the apathy was just too much.
The apathy is one of the things I dread most with the SSRIs. Hopefully, I won't have to return to them.Thanks for the information regarding Topamax.
- Scott
Posted by SLS on January 1, 2012, at 15:22:16
In reply to Re: Adding Parnate and prazosin. » creepy, posted by SLS on January 1, 2012, at 11:56:55
Happy New Year to ME!
It looks like it is going to be a good one.
- Scott
Posted by Phillipa on January 1, 2012, at 18:43:54
In reply to Re: Adding Parnate and prazosin., posted by SLS on January 1, 2012, at 15:22:16
Scott does that mean the three day window is over?Jan/P
Posted by SLS on January 2, 2012, at 8:27:55
In reply to Re: Adding Parnate and prazosin. » SLS, posted by Phillipa on January 1, 2012, at 18:43:54
> Scott does that mean the three day window is over?Jan/P
Yes.
:-)
I love how you remember such details about people.
Thanks.
- Scott
Posted by SLS on January 2, 2012, at 20:25:57
In reply to Adding Parnate and prazosin., posted by SLS on December 29, 2011, at 6:55:56
This stuff is still working - robustly. It is as if a light switch was turned on. I haven't felt this well for as long as I can remember - decades. I am not even 1/2 well yet, but I feel that I am on my way to remission. See how optimistic I get? It is a sickness :-).
Please pray for me. I could use all the help I can get.
Currently:Parnate 80 mg
nortriptyline 150 mg
Lamictal 200 mg
Abilify 10 mg
lithium 300 mg
prazosin 6 mg
- Scott
Posted by Phillipa on January 2, 2012, at 21:40:01
In reply to Re: Adding Parnate and prazosin. » Everyone, posted by SLS on January 2, 2012, at 20:25:57
Horray!!!!! Prayers to you and on your way to FULL remission!!!! Jan/P
Posted by SLS on January 3, 2012, at 14:28:16
In reply to Re: Adding Parnate and prazosin. » Everyone, posted by SLS on January 2, 2012, at 20:25:57
Today is day 6 of my positive response to treatment. Still going strong.
Relief. Finally.
My mind is reawakening after 30 years of existing in a vegetative state.
Keep those prayers coming!
- Scott
> This stuff is still working - robustly. It is as if a light switch was turned on. I haven't felt this well for as long as I can remember - decades. I am not even 1/2 well yet, but I feel that I am on my way to remission. See how optimistic I get? It is a sickness :-).
>
> Please pray for me. I could use all the help I can get.
>
>
> Currently:
>
> Parnate 80 mg
> nortriptyline 150 mg
> Lamictal 200 mg
> Abilify 10 mg
> lithium 300 mg
> prazosin 6 mg
>
>
> - Scott
Posted by Phillipa on January 3, 2012, at 21:49:59
In reply to Re: Adding Parnate and prazosin., posted by SLS on January 3, 2012, at 14:28:16
Scott congrats. What are you now doing during the days? Keeping active? Important I think as new habits will help the meds continue to work. No scientific data to support this!!! Jan/P
Posted by SLS on January 4, 2012, at 1:18:25
In reply to Re: Adding Parnate and prazosin. » SLS, posted by Phillipa on January 3, 2012, at 21:49:59
> Scott congrats. What are you now doing during the days? Keeping active? Important I think as new habits will help the meds continue to work. No scientific data to support this!!! Jan/P
I am in total agreement with you. No scientific data to support this.
:-)
- Scott
Posted by SLS on January 4, 2012, at 1:48:02
In reply to Re: Adding Parnate and prazosin. » Phillipa, posted by SLS on January 4, 2012, at 1:18:25
This is an interesting abstract that reports a downregulation of NE alpha-1 (prazosin) binding with antidepressant use.
- Scott
-----------------------------------------
J Neural Transm. 2010 Dec;117(12):1423-30. Epub 2010 Dec 7.Differential modulation of a-1 adrenoceptor subtypes by antidepressants in the rat brain.
Ramakrishna D, Subhash MN.
SourceKamineni Institute of Medical Sciences, Sreepuram, Narketpally, Nalgonda 508254, Andhra Pradesh, India. drramakrishna@klsindia.com
AbstractThe aim of the present study was to examine the effect of chronic antidepressants treatment on the density of a1-adrenoceptor (AR) subtypes in rat brain. Density of total a1 and a(1A)- and a(1?)-ARs was measured in cortex and cerebellum of rats treated with amitriptyline (AMI), desipramine (DMI) and fluoxetine (FLX), (10 mg/kg body wt), for 30 days, using [³H]prazosin in presence and absence of WB-4101. The density of cortical total a1-ARs was significantly decreased with AMI (54%) and DMI (25%) treatment, without altering the affinity of the receptor. Fluoxetine did not alter the density of cortical a1-ARs. The density of cortical a(1A)-ARs was also significantly decreased with AMI (85%) and DMI (50%) treatment, without affecting the affinity. The density of cerebellar total a1-ARs was significantly decreased with AMI (37%), DMI (50%) and FLX (70%) treatment, without affecting the affinity for [³H]prazosin. The density of a(1A)-ARs was significantly decreased with AMI (67%), DMI (59%) and FLX (92%) treatment. a(1B)-AR density was decreased only with FLX (47%) and DMI (47%) treatment. Correspondingly the basal IP3 and NE (10 µM) stimulated IP3 levels were significantly decreased in AMI (47%), DMI (22%) and FLX (48%) treated rat cortex. The results suggest that chronic antidepressant (AD) treatment down-regulates the cortical and cerebellar total a1-ARs in rat brain. However, a(1A) subtype is predominantly down-regulated by AMI and DMI, where as FLX affects cerebellar a(1A)-ARs. The region-specific and subtype specific down-regulation of a1-ARs density, which occurs after prolonged AD treatment, may underline the therapeutic mechanism of action.
PMID:
21136124
[PubMed - indexed for MEDLINE]
Posted by Bob on January 4, 2012, at 3:39:20
In reply to Re: Adding Parnate and prazosin., posted by SLS on January 4, 2012, at 1:48:02
> This is an interesting abstract that reports a downregulation of NE alpha-1 (prazosin) binding with antidepressant use.
>
>
> - Scott
>
>
> -----------------------------------------
>
>
> J Neural Transm. 2010 Dec;117(12):1423-30. Epub 2010 Dec 7.
>
> Differential modulation of a-1 adrenoceptor subtypes by antidepressants in the rat brain.
>
> Ramakrishna D, Subhash MN.
> Source
>
> Kamineni Institute of Medical Sciences, Sreepuram, Narketpally, Nalgonda 508254, Andhra Pradesh, India. drramakrishna@klsindia.com
> Abstract
>
> The aim of the present study was to examine the effect of chronic antidepressants treatment on the density of a1-adrenoceptor (AR) subtypes in rat brain. Density of total a1 and a(1A)- and a(1?)-ARs was measured in cortex and cerebellum of rats treated with amitriptyline (AMI), desipramine (DMI) and fluoxetine (FLX), (10 mg/kg body wt), for 30 days, using [³H]prazosin in presence and absence of WB-4101. The density of cortical total a1-ARs was significantly decreased with AMI (54%) and DMI (25%) treatment, without altering the affinity of the receptor. Fluoxetine did not alter the density of cortical a1-ARs. The density of cortical a(1A)-ARs was also significantly decreased with AMI (85%) and DMI (50%) treatment, without affecting the affinity. The density of cerebellar total a1-ARs was significantly decreased with AMI (37%), DMI (50%) and FLX (70%) treatment, without affecting the affinity for [³H]prazosin. The density of a(1A)-ARs was significantly decreased with AMI (67%), DMI (59%) and FLX (92%) treatment. a(1B)-AR density was decreased only with FLX (47%) and DMI (47%) treatment. Correspondingly the basal IP3 and NE (10 µM) stimulated IP3 levels were significantly decreased in AMI (47%), DMI (22%) and FLX (48%) treated rat cortex. The results suggest that chronic antidepressant (AD) treatment down-regulates the cortical and cerebellar total a1-ARs in rat brain. However, a(1A) subtype is predominantly down-regulated by AMI and DMI, where as FLX affects cerebellar a(1A)-ARs. The region-specific and subtype specific down-regulation of a1-ARs density, which occurs after prolonged AD treatment, may underline the therapeutic mechanism of action.
>
> PMID:
> 21136124
> [PubMed - indexed for MEDLINE]
>
OK, so in lay terms what does this mean?
Posted by SLS on January 4, 2012, at 5:55:26
In reply to Re: Adding Parnate and prazosin., posted by Bob on January 4, 2012, at 3:39:20
Hi Bob.
It was nice of you to notice my post. It might be an important observation that prazosin has produced such a significant improvement in my condition.
Just to let you know, I performed an experiment to verify that prazosin was the agent responsible for my improvement. I discontinued it for 36 hours and observed that I relapsed pretty hard. I was able to recapture the antidepressant response immediately upon the reintroducton of prazosin. Upon titration, I settled on 6 mg as the dosage. Hopefully, this is the dosage that will bring about a full remission. My instincts tell me that it will.
> OK, so in lay terms what does this mean?
Chronic (long-term) antidepressant treatment with certain drugs causes the norepinephrine NE alpha-1 receptors to downregulate by reducing their numbers. Prazosin blocks these same receptors, thereby producing the same net effect.
I am, of course, extremely interested in the way prazosin might work for others as it now works for me. (Please God, let it continue). Perhaps prazosin has been overlooked in the treatment of TRD.
For now, I would say that prazosin might work best as an adjunct to antidepressants for people who have a history of childhood physical abuse, emotional abuse (including bullying), or neglect. It may be that some people have a backdrop of PTSD acting to drive depression. Does pazosin also work for other subtypes of depression? I don't know.
- Scott
-------------------------------------------------
> > This is an interesting abstract that reports a downregulation of NE alpha-1 (prazosin) binding with antidepressant use.
> >
> > -----------------------------------------
> >
> > J Neural Transm. 2010 Dec;117(12):1423-30. Epub 2010 Dec 7.
> >
> > Differential modulation of a-1 adrenoceptor subtypes by antidepressants in the rat brain.
> >
> > Ramakrishna D, Subhash MN.
> > Source
> >
> > Kamineni Institute of Medical Sciences, Sreepuram, Narketpally, Nalgonda 508254, Andhra Pradesh, India. drramakrishna@klsindia.com
> > Abstract
> >
> > The aim of the present study was to examine the effect of chronic antidepressants treatment on the density of a1-adrenoceptor (AR) subtypes in rat brain. Density of total a1 and a(1A)- and a(1?)-ARs was measured in cortex and cerebellum of rats treated with amitriptyline (AMI), desipramine (DMI) and fluoxetine (FLX), (10 mg/kg body wt), for 30 days, using [³H]prazosin in presence and absence of WB-4101. The density of cortical total a1-ARs was significantly decreased with AMI (54%) and DMI (25%) treatment, without altering the affinity of the receptor. Fluoxetine did not alter the density of cortical a1-ARs. The density of cortical a(1A)-ARs was also significantly decreased with AMI (85%) and DMI (50%) treatment, without affecting the affinity. The density of cerebellar total a1-ARs was significantly decreased with AMI (37%), DMI (50%) and FLX (70%) treatment, without affecting the affinity for [³H]prazosin. The density of a(1A)-ARs was significantly decreased with AMI (67%), DMI (59%) and FLX (92%) treatment. a(1B)-AR density was decreased only with FLX (47%) and DMI (47%) treatment. Correspondingly the basal IP3 and NE (10 µM) stimulated IP3 levels were significantly decreased in AMI (47%), DMI (22%) and FLX (48%) treated rat cortex. The results suggest that chronic antidepressant (AD) treatment down-regulates the cortical and cerebellar total a1-ARs in rat brain. However, a(1A) subtype is predominantly down-regulated by AMI and DMI, where as FLX affects cerebellar a(1A)-ARs. The region-specific and subtype specific down-regulation of a1-ARs density, which occurs after prolonged AD treatment, may underline the therapeutic mechanism of action.
> >
> > PMID:
> > 21136124
> > [PubMed - indexed for MEDLINE]
Posted by sigismund on January 4, 2012, at 12:31:23
In reply to Re: Adding Parnate and prazosin. » Bob, posted by SLS on January 4, 2012, at 5:55:26
>Chronic (long-term) antidepressant treatment with certain drugs causes the norepinephrine NE alpha-1 receptors to downregulate by reducing their numbers.
I can see that could easily have happened to you.
>Prazosin blocks these same receptors, thereby producing the same net effect.
I'm lost here.
>For now, I would say that prazosin might work best as an adjunct to antidepressants for people who have a history of childhood physical abuse, emotional abuse (including bullying), or neglect. It may be that some people have a backdrop of PTSD acting to drive depression.
Prazosin is Minipress, right? I was wondering if it blocks overactive NE, or were you saying the reverse?
How has it affected your sleep? I wonder if my sleep is disrupted by too much NE. Certainly something is doing it. I'm not in a hurry to try clonidine.
Posted by sigismund on January 4, 2012, at 12:39:24
In reply to Re: Adding Parnate and prazosin. » SLS, posted by sigismund on January 4, 2012, at 12:31:23
Scott, can you explain simply how prazosin is different to clonidine.
Posted by SLS on January 4, 2012, at 13:58:40
In reply to Re: Adding Parnate and prazosin., posted by sigismund on January 4, 2012, at 12:39:24
> Scott, can you explain simply how prazosin is different to clonidine.
Prazosin (Minipress) was originally developed as a treatment for hypertension. It was discovered by accident at a VA hospital that it was useful to treat PTSD.
Clonidine works the reverse of mirtazapine. It actually stimulates the NE alpha-2 receptors located on the presynaptic membrane. This, in effect, turns off the presynaptic NE neuron. Prazosin, on the other hand, blocks the postsynaptic NE alpha-1 receptor, thereby reducing NE activity.
Prazosin seems to be particularly successful at treating the disturbed sleep and nightmares associated with PTSD. I guess you are already aware that clonidine can produce or make worse depression. I find prazosin to be extremely clean. I noticed that I don't remember my dreams as much as I had before starting prazosin.
Good luck with whatever you decide to do.
- Scott
Posted by sigismund on January 4, 2012, at 14:14:09
In reply to Re: Adding Parnate and prazosin. » sigismund, posted by SLS on January 4, 2012, at 13:58:40
> Prazosin, a highly lipophilic α1-adrenergic receptor blocker that is traditionally used to treat hypertension and benign prostatic hyperplasia,
Maybe two birds with one stone?
Posted by SLS on January 4, 2012, at 14:24:30
In reply to Re: Adding Parnate and prazosin., posted by sigismund on January 4, 2012, at 14:14:09
> > Prazosin, a highly lipophilic α1-adrenergic receptor blocker that is traditionally used to treat hypertension and benign prostatic hyperplasia,
>
> Maybe two birds with one stone?
Poor birds. :-(Is PTSD involved in your case?
If it were me, and PTSD were suspected, I would try the prazosin first. Also, Topamax is good for PTSD.
- Scott
Posted by Bob on January 4, 2012, at 14:50:31
In reply to Re: Adding Parnate and prazosin. » Bob, posted by SLS on January 4, 2012, at 5:55:26
>
> Chronic (long-term) antidepressant treatment with certain drugs causes the norepinephrine NE alpha-1 receptors to downregulate by reducing their numbers. Prazosin blocks these same receptors, thereby producing the same net effect.
>
> - Scott
>
I'm still lost. Is causing NE alpha-1 receptors to downregulate a desired effect or something that that we are trying to offset? Logically it would seem to me that if you are blocking the receptors it would reduce the available NE to the brain?Bob
Posted by Bob on January 4, 2012, at 14:51:41
In reply to Re: Adding Parnate and prazosin. » Bob, posted by SLS on January 4, 2012, at 5:55:26
> Hi Bob.
>
> It was nice of you to notice my post. It might be an important observation that prazosin has produced such a significant improvement in my condition.
>
> Just to let you know, I performed an experiment to verify that prazosin was the agent responsible for my improvement. I discontinued it for 36 hours and observed that I relapsed pretty hard. I was able to recapture the antidepressant response immediately upon the reintroducton of prazosin. Upon titration, I settled on 6 mg as the dosage. Hopefully, this is the dosage that will bring about a full remission. My instincts tell me that it will.
>
> > OK, so in lay terms what does this mean?
>
> Chronic (long-term) antidepressant treatment with certain drugs causes the norepinephrine NE alpha-1 receptors to downregulate by reducing their numbers. Prazosin blocks these same receptors, thereby producing the same net effect.
>
> I am, of course, extremely interested in the way prazosin might work for others as it now works for me. (Please God, let it continue). Perhaps prazosin has been overlooked in the treatment of TRD.
>
> For now, I would say that prazosin might work best as an adjunct to antidepressants for people who have a history of childhood physical abuse, emotional abuse (including bullying), or neglect. It may be that some people have a backdrop of PTSD acting to drive depression. Does pazosin also work for other subtypes of depression? I don't know.
>
>
> - Scott
>
>
> -------------------------------------------------
>
>
> > > This is an interesting abstract that reports a downregulation of NE alpha-1 (prazosin) binding with antidepressant use.
> > >
> > > -----------------------------------------
> > >
> > > J Neural Transm. 2010 Dec;117(12):1423-30. Epub 2010 Dec 7.
> > >
> > > Differential modulation of a-1 adrenoceptor subtypes by antidepressants in the rat brain.
> > >
> > > Ramakrishna D, Subhash MN.
> > > Source
> > >
> > > Kamineni Institute of Medical Sciences, Sreepuram, Narketpally, Nalgonda 508254, Andhra Pradesh, India. drramakrishna@klsindia.com
> > > Abstract
> > >
> > > The aim of the present study was to examine the effect of chronic antidepressants treatment on the density of a1-adrenoceptor (AR) subtypes in rat brain. Density of total a1 and a(1A)- and a(1?)-ARs was measured in cortex and cerebellum of rats treated with amitriptyline (AMI), desipramine (DMI) and fluoxetine (FLX), (10 mg/kg body wt), for 30 days, using [³H]prazosin in presence and absence of WB-4101. The density of cortical total a1-ARs was significantly decreased with AMI (54%) and DMI (25%) treatment, without altering the affinity of the receptor. Fluoxetine did not alter the density of cortical a1-ARs. The density of cortical a(1A)-ARs was also significantly decreased with AMI (85%) and DMI (50%) treatment, without affecting the affinity. The density of cerebellar total a1-ARs was significantly decreased with AMI (37%), DMI (50%) and FLX (70%) treatment, without affecting the affinity for [³H]prazosin. The density of a(1A)-ARs was significantly decreased with AMI (67%), DMI (59%) and FLX (92%) treatment. a(1B)-AR density was decreased only with FLX (47%) and DMI (47%) treatment. Correspondingly the basal IP3 and NE (10 µM) stimulated IP3 levels were significantly decreased in AMI (47%), DMI (22%) and FLX (48%) treated rat cortex. The results suggest that chronic antidepressant (AD) treatment down-regulates the cortical and cerebellar total a1-ARs in rat brain. However, a(1A) subtype is predominantly down-regulated by AMI and DMI, where as FLX affects cerebellar a(1A)-ARs. The region-specific and subtype specific down-regulation of a1-ARs density, which occurs after prolonged AD treatment, may underline the therapeutic mechanism of action.
> > >
> > > PMID:
> > > 21136124
> > > [PubMed - indexed for MEDLINE]
>
I thought you were attributing your response to the Parnate, not the Prazosin.Bob
Posted by Phillipa on January 4, 2012, at 19:59:28
In reply to Re: Adding Parnate and prazosin. » Bob, posted by SLS on January 4, 2012, at 5:55:26
Scott does this mean it could also help someone with anxiety ocd with emotional abuse? Jan/P
Posted by Phillipa on January 4, 2012, at 20:07:14
In reply to Re: Adding Parnate and prazosin. » SLS, posted by Bob on January 4, 2012, at 14:51:41
What if your blood pressure runs low? Jan/P
Posted by SLS on January 4, 2012, at 22:44:12
In reply to Re: Adding Parnate and prazosin. » SLS, posted by Phillipa on January 4, 2012, at 19:59:28
> Scott does this mean it could also help someone with anxiety ocd with emotional abuse? Jan/P
I really don't know what other conditions prazosin will demonstrate efficacy in treating. It is certainly a benign drug to try. A friend of mine uses it for sleep. It has been studied for PTSD.
How do you sleep? Do you ever have nightmares?
Prazosin often causes dizziness when you first start taking it. Mine went away for the most part.
- Scott
Posted by SLS on January 4, 2012, at 23:39:33
In reply to Re: Adding Parnate and prazosin. » SLS, posted by Bob on January 4, 2012, at 14:50:31
> I'm still lost. Is causing NE alpha-1 receptors to downregulate a desired effect
Apparently, it is. It should reduce NE activity, thereby reducing anxiety.
> Logically it would seem to me that if you are blocking the receptors it would reduce the available NE to the brain?
Prazosin does not reduce the amount of norepinephrine neurotransmitter in the brain.
When NE attaches to a receptor, that receptor is stimulated to perform a function (either excitatory or inhibitory). Blocking this receptor using an antagonist or using an inverse agonist serves to prevent this function. Prazosin is an antagonist at excitatory NE alpha-1 receptors, thus reducing the number of receptors available for stimulation.
I hope this helps. Maybe I'm confusing things.
- Scott
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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
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