![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 21 of 21. This is the beginning of the thread.
Posted by SLS on August 24, 2012, at 11:15:08
Higher dosages of Pristiq (desvenlafaxine) are safe, but is there any clinical advantage to using such dosages compared to 100 mg/day? I recall the days when the average dosage of Effexor (venlafaxine) was 150 mg/day with a maximum of 225 mg/day. Now, it is good practice to use dosages of 300 mg/day and higher of that drug before abandoning it. Could the same be true of Pristiq?
- Scott
------------------------------
CNS Spectr. 2012 Aug 10:1-10. [Epub ahead of print]
High-dose desvenlafaxine in outpatients with major depressive disorder.
Ferguson JM, Tourian KA, Rosas GR.
Source1 University of Utah School of Medicine, Salt Lake City, Utah, USA.
Abstract
OBJECTIVE:
This study investigated the safety and efficacy of long-term treatment with high-dose desvenlafaxine (administered as desvenlafaxine succinate) in major depressive disorder (MDD).
METHODS:
In this multicenter, open-label study, adult outpatients with MDD aged 18-75 were treated with flexible doses of desvenlafaxine (200-400 mg/d) for ≤ 1 year. Safety assessments included monitoring of treatment-emergent adverse events (TEAEs), patient discontinuations due to adverse events, electrocardiograms, vital signs, and laboratory determinations. The primary efficacy measure was mean change from baseline in the 17-item Hamilton Rating Scale for Depression [HAM-D(17)] total score.
RESULTS:
The mean daily desvenlafaxine dose range over the duration of the trial was 267-356 mg (after titration). The most frequent TEAEs in the safety population (n = 104) were nausea (52%) and headache (41%), dizziness (31%), insomnia (29%), and dry mouth (27%). All TEAEs were mild or moderate in severity. Thirty-four (33%) patients discontinued from the study because of TEAEs; nausea (12%) and dizziness (9%) were the most frequently cited reasons. The mean change in HAM-D(17) total score for the intent-to-treat population (n = 99) was -9.9 at the last on-therapy visit in the last-observation-carried-forward analysis and -14.0 at month 12 in the observed cases analysis. Conclusion High-dose desvenlafaxine (200-400 mg/d) was generally safe and effective in the long-term treatment of MDD.
------------------------------------------
Posted by b2chica on August 29, 2012, at 15:20:34
In reply to Pristiq dosages of 200 - 400 mg/day., posted by SLS on August 24, 2012, at 11:15:08
welli upped to 100 about a month ago (my memory is terrible, might be off there)
but i've been crying all mrning and suicidal thoughts. i'mreay to give it all in.
i've over mediated have 2400 gabapentin and 2mg xanax in me.
i'm ready to take more. and i'm sure i will when i have to go home...i'm redy to cave today. no strength to fight. i've been looking for support and help but cant find ita ny where. pdoc txt me back once and said dont take more than rx. ignored other txts.
friendat work is too busy. so i sat in his office and cried.
i assumed this is because of my husband and our issues. but its blown way out of proportion. maybe its an excuse toover medicate. maybe i just want out and using excuese.
maybe i cantor dont want to deal withmy emotions. maybe i'm just not mmeNT TO DEAL WITH LIFE.
God help me.
i've prayed to be a better wife. better mother.
i apparently am not a good wife. and when i exit this earth of myown doing, that would make me a HORRIBLe mother.qustion...better to live as a failyre or
die as a failure...b2c.
ps sorry to steal your thread.
Posted by phidippus on August 31, 2012, at 19:15:05
In reply to Pristiq dosages of 200 - 400 mg/day., posted by SLS on August 24, 2012, at 11:15:08
"the last on-therapy visit in the last-observation-carried-forward analysis and -14.0 at month 12 in the observed cases analysis"
Arg, is -14 good?
HAven't you taken Pristiq?
Eric
Posted by SLS on September 5, 2012, at 8:33:40
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on August 31, 2012, at 19:15:05
> "the last on-therapy visit in the last-observation-carried-forward analysis and -14.0 at month 12 in the observed cases analysis"
>
> Arg, is -14 good?I assumed, perhaps wrongly, that this value represented a reduction in depression scores.
> HAven't you taken Pristiq?
No. I have tried Effexor and Cymbalta, though. I liked Effexor better than Cymbalta. Cymbalta produced fatigue and tiredness. The combination of Effexor and nortriptyline helped - just not enough.What do you think about combining Wellbutrin, Effexor, and Lamictal?
- Scott
Posted by phidippus on September 5, 2012, at 14:28:13
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » phidippus, posted by SLS on September 5, 2012, at 8:33:40
Effexor works as an SNDRI at high doses, so not only does it affect reuptake of seratonin and norepenephrine, it blocks reuptake of dopamine, allowing more dopamine in the system.
Wellbutrin inhibits reuptake of norepenephrine and dopamine, so it might work synergestically with the Effexor, or you may get too much norepenephrine and dopamine acting on the CNS-I don't know what effects this would cause.
Lamictal will of course help keep your mood stable while taking the above mentioned antidepressants, however I can't speculate on how it will react with Effexor and Wellbutrin.
What are you currently taking?
Eric
Posted by SLS on September 5, 2012, at 17:34:38
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 5, 2012, at 14:28:13
Hi Eric.
I was interested to know what you thought of the combination treatment. It is not something that I could use because I react badly to Wellbutrin. It makes me more depressed. However, I know someone who responds robustly to Pristiq + Wellbutrin. My doctor likes to use Wellbutrin and Lamictal together. I was wondering how all three might help someone who is treatment resistant.
I am currently responding to the addition of minocycline to my treatment regime. It looks good.
Currently:
Parnate 80 mg/day
nortriptyline 150 mg/day
Lamictal 200 mg/day
Abilify 10 mg/day
minocycline 200 mg/day
- Scott
Posted by SLS on September 5, 2012, at 17:35:29
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » phidippus, posted by SLS on September 5, 2012, at 17:34:38
> Currently:
>
> Parnate 80 mg/day
> nortriptyline 150 mg/day
> Lamictal 200 mg/day
> Abilify 10 mg/day
> minocycline 200 mg/dayI forgot lithium 300 mg/day
- Scott
Posted by phidippus on September 5, 2012, at 17:48:58
In reply to Re: Pristiq dosages of 200 - 400 mg/day., posted by SLS on September 5, 2012, at 17:35:29
Why do you take the Lithium-its certainly not in a therapeutic range?
So many antidepressants! How do you keep from going manic?
Eric
Posted by jono_in_adelaide on September 15, 2012, at 4:16:35
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 5, 2012, at 14:28:13
Effexor, Cymbalta and Pristique only have a significant effect on noradrenalin reuotake at doses in excess of those commonly used (300mg per day of effexor is a much weaker noradrenalin reuptake inhibitor than 75mg of nortriptyline) - if you want an effective SNRI, take Sertraline along with nortriptyline or bupropion.
Posted by SLS on September 15, 2012, at 7:05:09
In reply to Re: Pristiq dosages of 200 - 400 mg/day., posted by jono_in_adelaide on September 15, 2012, at 4:16:35
> Effexor, Cymbalta and Pristique only have a significant effect on noradrenalin reuotake at doses in excess of those commonly used (300mg per day of effexor is a much weaker noradrenalin reuptake inhibitor than 75mg of nortriptyline) - if you want an effective SNRI, take Sertraline along with nortriptyline or bupropion.
I don't agree with this type of approach. I don't think one can substitute sertraline 200 mg + nortriptyline 150 mg for
venlafaxine 300 mg and guarantee for someone equivalent efficacy.Do you think there are people who respond to clomipramine who do not respond to sertraline + nortriptyline or sertraline + bupropion? If so, how do you account for this?
The point I am making is that things are seemingly not so simple, and I would hate to dissuade someone from trying a potentially effective treatment.
I respond better to nortriptyline + venlafaxine than to nortriptyline + sertraline.
I respond better to nortriptyline + sertraline than to desipramine + sertraline.
I don't respond to nortriptyline + bupropion at all. It makes me feel worse.
I don't think that we can design effective treatments for each individual using theoretical recipes of ingredients we haven't fully characterized yet and without knowing more about the cooking process itself. This becomes obvious when someone responds to one SSRI but not another. Even SNRIs are not interchangeable in the real world. We don't need to know the first thing about pharmacology to make these clinical observations and use them effectively.
From the very beginning, doctors observed that there are people who respond to Nardil whom do not respond to Parnate and vice versa. They also observed that imipramine and amitriptyline were not interchangeable. They did this without understanding the pharmacology of these drugs. Scientists are still unable to fully account for these observations. Educated guesses are fine, but that's all they are - guesses. Personally, I don't know enough to suggest to someone that a SNRI will be ineffective if they fail to respond to sertraline + nortriptyline.
If I had to guess, I would say that bupropion + venlafaxine will get more people well than bupropion + sertraline. I would also guess that nortriptyline + venlafaxine will get more people well than nortriptyline + sertraline. This should not be true if all that were necessary was to combine serotonin and norepinephrine reuptake inhibition. And what's the deal with clomipramine? Why is this SNRI considered more effective than any other, especially for treating melancholic depression? Calcium channel inhibition? Sodium channel inhibition? Sigma receptor stimulation? 5-HT2a receptor blockade? Muscarinic receptor blockade? NMDA receptor modulation? Opioid kappa and delta receptor stimulation? Glutamate receptor blockade?
I really don't know.
- Scott
Posted by phidippus on September 15, 2012, at 15:57:04
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » jono_in_adelaide, posted by SLS on September 15, 2012, at 7:05:09
One thing you can do is look into the neurotransmitters and the effects they have.
"And what's the deal with clomipramine? Why is this SNRI considered more effective than any other, especially for treating melancholic depression? Calcium channel inhibition? Sodium channel inhibition? Sigma receptor stimulation? 5-HT2a receptor blockade? Muscarinic receptor blockade? NMDA receptor modulation? Opioid kappa and delta receptor stimulation? Glutamate receptor blockade?"
say, for instance, sodium channel inhibition is shown to have negligible effects on mood. Sigma receptor stimulation results in inhibition of ion voltage gated channels-how this effects mood is unknown. NMDA receptor modulation may or may not affect mood, etc.
Of course, all of these chracteristics could add up.
The only thing we can't account for is the individual's reaction to any single medication
In my case, Viibryd proved too be a more powerful anti-obsessional than Clomipramine was. What? Why?
All I know is if a medication has 5ht1a partial agonism, I respond strongly.
Eric
Posted by phidippus on September 15, 2012, at 16:03:30
In reply to Re: Pristiq dosages of 200 - 400 mg/day., posted by jono_in_adelaide on September 15, 2012, at 4:16:35
Or just take Clomipramine. Considered the most effective antidepressant out there.
Eric
Posted by SLS on September 15, 2012, at 19:34:45
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 15, 2012, at 15:57:04
> One thing you can do is look into the neurotransmitters and the effects they have.
>
> "And what's the deal with clomipramine? Why is this SNRI considered more effective than any other, especially for treating melancholic depression? Calcium channel inhibition? Sodium channel inhibition? Sigma receptor stimulation? 5-HT2a receptor blockade? Muscarinic receptor blockade? NMDA receptor modulation? Opioid kappa and delta receptor stimulation? Glutamate receptor blockade?"
>
> say, for instance, sodium channel inhibition is shown to have negligible effects on mood. Sigma receptor stimulation results in inhibition of ion voltage gated channels-how this effects mood is unknown. NMDA receptor modulation may or may not affect mood, etc.
>
> Of course, all of these chracteristics could add up.
>
> The only thing we can't account for is the individual's reaction to any single medication
>
> In my case, Viibryd proved too be a more powerful anti-obsessional than Clomipramine was. What? Why?
>
> All I know is if a medication has 5ht1a partial agonism, I respond strongly.
>
> Eric
Tricyclics are also antiglutamatergic:"Although tricyclic antidepressants have been in existence since the 1940s when they were discovered upon screening iminodibenzyl derivatives for other potential therapeutic uses, their mechanism of action has remained unclear [A. Goodman Gilman, T.W. Rall, A.S. Nies, P. Taylor, Goodman and Gilman's The Pharmacological Basis of Therapeutics, eighth ed., Pergamon Press, New York, 1990]. In addition to their ability to hinder the reuptake of biogenic amines, there is mounting evidence that the tricyclic antidepressants inhibit glutamate transmission. Here, intrinsic tryptophan fluorescence spectroscopy is used to document the binding of desipramine, a member of the tricyclic antidepressant family, to a well-defined extracellular glutamate binding domain (S1S2) of the GluR2 subunit of the amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. The binding is distinct from those of other known effectors of the receptor, including the endogenous sulfated neurosteroids pregnenolone sulfate and 3alpha-hydroxy-5beta-pregnan-20-one sulfate, and is consistent with a conformational change upon binding that is allosterically transmitted to the channel region of the receptor."
"Linking tricyclic antidepressants to ionotropic glutamate receptors" - Stoll, Gentile 2005
- Scott
Posted by phidippus on September 16, 2012, at 14:08:30
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » phidippus, posted by SLS on September 15, 2012, at 19:34:45
"Excessive glutamate, or excitotoxins acting on the same glutamate receptors, overactivate glutamate receptors (specifically NMDARs), causing high levels of calcium ions (Ca2+) to influx into the postsynaptic cell. High Ca2+ concentrations activate a cascade of cell degradation processes involving proteases, lipases, nitric oxide synthase, and a number of enzymes that damage cell structures often to the point of cell death. Ingestion of or exposure to excitotoxins that act on glutamate receptors can induce excitotoxicity and cause toxic effects on the central nervous system.
In the case of traumatic brain injury or cerebral ischemia (e.g. cerebral infarction or hemorrhage), acute neurodegeneration caused by excitotoxicity may spread to proximal neurons through two processes. Hypoxia and hypoglycemia trigger bioenergetic failure; mitochondria stop producing ATP energy. Na+/K+-ATPase can no longer maintain sodium/potassium ion concentration gradients across the plasma membrane. Glutamate transporters (EAATs), which use the Na+/K+ gradient, reverse glutamate transport (efflux) in affected neurons and astrocytes, and depolarization increases downstream synaptic release of glutamate"
Eric
Posted by jono_in_adelaide on September 16, 2012, at 21:55:28
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » jono_in_adelaide, posted by SLS on September 15, 2012, at 7:05:09
What I am saying is that in clinicaly used doseages, the SNRI's dont inhibit noradrenalin reuptake as much as nortriptyline or desipramine
Of course there are some people who will respont spiffingly to effexor or cymbalta, however, more would respond to an SSRI + nortriptyline/bupropion/desipramine
In commonly used doseages, Effexor is just an overpriced SSRI
Posted by jono_in_adelaide on September 16, 2012, at 21:57:11
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » jono_in_adelaide, posted by phidippus on September 15, 2012, at 16:03:30
Agree, clomipramine is virtualy the gold standard, the 5HT2 effect is the crowning glory ontop of the reuptake inhibition.... but the side effects can be rough
Posted by SLS on September 17, 2012, at 7:06:15
In reply to Re: Pristiq dosages of 200 - 400 mg/day., posted by jono_in_adelaide on September 16, 2012, at 21:55:28
> What I am saying is that in clinicaly used doseages, the SNRI's dont inhibit noradrenalin reuptake as much as nortriptyline or desipramine
That's hard to say. At high but clinically relevant dosages (300 - 375 mg/day), absolute occupancy of NET at full saturation in the brain might be quite high. I have never seen assays comparing venlafaxine to TCA in this regard. That's too bad. Even if desipramine inhibits NET more potently, the potency of venlafaxine is probably more than adequate to generate a therapeutic effect. Assays of venlafaxine alone demonstrate NET inhibition at dosages as low as 75 mg/day.
http://jop.sagepub.com/content/15/1/9.abstract
> Of course there are some people who will respont spiffingly to effexor or cymbalta, however, more would respond to an SSRI + nortriptyline/bupropion/desipramine
Can you cite any scientific evidence to support this statement?
> In commonly used doseages, Effexor is just an overpriced SSRI
It would be difficult to explain this to someone who responds to venlafaxine who does not respond to SSRIs.
Even if your opinion reflected reality pharmacodynamically, it does not reflect clinical observation. My opinion is that venlafaxine will get more people well than any SSRI. Another opinion of mine is that paroxetine will get more people well than any other SSRI. Lexapro comes close. Both of these opinions are based upon my impressions rather than scientifically arrived at statistics, so they aren't terribly significant. Some meta-analyses show venlafaxine to be unequivocally superior to SSRIs. Some show these drugs to be almost equally effective, usually with a slight advantage to venlafaxine. In my opinion, the bottom line is that venlafaxine is different enough from all other antidepressants to justify its continued availability. I would say the same thing about any antidepressant. I would have to reach a bit to include moclobemide and maprotiline, but as long as there are people who respond preferentially to these drugs, it is difficult to regard them as equivalent to any other drug.
- Scott
Posted by phidippus on September 17, 2012, at 15:56:22
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » jono_in_adelaide, posted by SLS on September 17, 2012, at 7:06:15
>paroxetine will get more people well than any >other SSRI. Lexapro comes close
Actually, a recent study showed Zoloft and Lexapro to be most efficacious.
http://www.healthyplace.com/lexapro/patient-center/lexapro-zoloft-best-of-newer-antidepressants/
http://www.washingtonpost.com/wp-dyn/content/article/2009/01/29/AR2009012901774.html
http://depressionintrospection.wordpress.com/2009/02/16/antidepressant-rankings-zoloft-and-lexapro-considered-best-overall/ - this one places Remeron first.
Eric
Posted by SLS on September 17, 2012, at 16:51:53
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 17, 2012, at 15:56:22
> >paroxetine will get more people well than any >other SSRI. Lexapro comes close
>
> Actually, a recent study showed Zoloft and Lexapro to be most efficacious.
>
> http://www.healthyplace.com/lexapro/patient-center/lexapro-zoloft-best-of-newer-antidepressants/
>
> http://www.washingtonpost.com/wp-dyn/content/article/2009/01/29/AR2009012901774.html
>
> http://depressionintrospection.wordpress.com/2009/02/16/antidepressant-rankings-zoloft-and-lexapro-considered-best-overall/ - this one places Remeron first.
>
> Eric
I don't buy it. I question the methods of this study."The Italian researchers reviewed 117 studies that included more than 25,000 patients with major depression to come to this conclusion."
What dosages were used? This is the part that is often ignored when comparing drugs. 100 - 200 mg of Zoloft will always be more effective than 75 - 150 mg of Effexor. This type of bias in the dosages used occurs all the time. The study you refer to was a retrospective analysis, and not a prospective investigation. The dosages used were likely not controlled for through a selection process of 25,000 patients. We would need to see the study itself as it was published in The Lancet in 2009.
The study said that venlafaxine was as efficacious as Zoloft and Lexapro, but that it was not tolerated as well. I would agree that venlafaxine is generally not as tolerable, but I still believe that it is more efficacious than SSRIs. Escitalopram comes pretty close, though.
Maybe the actual 2009 study can be located?
-------------------------------------------------------
Same year 2009: What do you think?
http://www.ncbi.nlm.nih.gov/pubmed/19165525Eur Arch Psychiatry Clin Neurosci. 2009 Apr;259(3):172-85. Epub 2009 Jan 22.
The effect of venlafaxine compared with other antidepressants and placebo in the treatment of major depression: a meta-analysis.
Bauer M, Tharmanathan P, Volz HP, Moeller HJ, Freemantle N.
SourceDepartment of Psychiatriy and Psychotherapy, University Hospital Carl Gustav Carus, Technical University Dresden, Fetscherstr. 74, Dresden 01307, Germany.
AbstractOBJECTIVE:
Meta-analysis of all available trials of Venlafaxine in the treatment of major depressive disorders, including treatment resistant depression and long-term relapse prevention.
METHODS:
We conducted a meta-analysis comparing venlafaxine and tricyclics, or selective serotonin reuptake inhibitors (SSRIs), in major depression. We also included trials comparing venlafaxine and alternative antidepressants in subjects with treatment resistant depression, or compared with placebo in long-term relapse prevention. Trials were identified through searches of Medline, Embase, Cochrane Library and through accessing unpublished trials held by the manufacturer. Results based on intention to treat analyses where available, were pooled using theoretically exact conditional maximum likelihood methods for fixed effects (primary analyses), and numerical simulation using a Gibbs sampler for full random effects.
RESULTS:
Compared to all SSRIs for the treatment of major depression (fluoxetine, paroxetine, sertraline, citalopram, escitalopram and fluvoxamine), venlafaxine was associated with a greater response [odds ratio 1.15 (95% CI 1.02-1.29)] and remission [odds ratio 1.19 (95% CI 1.06-1.34)]. Overall drop out rates appeared similar for SSRIs and venlafaxine. Compared to tricyclics, response to venlafaxine was estimated to be greater by exact method, odds ratio 1.21 (95% CI 1.03-1.43), but not statistically significantly different, using a full random effects method odds ratio 1.22 (95% CI 0.96-1.54). We observed no difference in remission rates (odds ratio 1.06 (95% CI 0.74-1.63)). Tricyclics were less well tolerated with higher overall drop out rates. Compared to alternative antidepressants in treatment resistant depression (trials included comparison with sertraline, bupropion, fluoxetine, citalopram, and one with a range of agents-mostly SSRIs), the odds ratio for response was 1.35 (95% CI 1.19-1.54). The odds ratio for remission was 1.35 (95% CI 1.20-1.52). Compared to placebo the odds ratio for relapse prevention with venlafaxine was 0.37 (95% CI 0.27-0.51).
CONCLUSION:
This meta analysis provides evidence of the clinical efficacy of venlafaxine in achieving therapeutic response and remission in patients with major depression. Venlafaxine appears more effective than SSRIs, and at least as effective as tricyclic antidepressants, in the treatment of major depressive episode. Venlafaxine appeared more effective than comparators in treatment resistant depression. In addition, venlafaxine effective in reducing relapse when given long term after major depressive episode.
PMID:
19165525
[PubMed - indexed for MEDLINE]-------------------------------------------------------
- Scott
Posted by phidippus on September 17, 2012, at 18:09:50
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » phidippus, posted by SLS on September 17, 2012, at 16:51:53
Here's the original study from The Lancet:
Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis
Dr Andrea Cipriani PhD a d Corresponding AuthorEmail Address, Toshiaki A Furukawa MD b, Georgia Salanti PhD c, John R Geddes MD d, Julian PT Higgins PhD e, Rachel Churchill PhD g, Norio Watanabe PhD b, Atsuo Nakagawa MD h, Ichiro M Omori PhD b, Hugh McGuire MA f, Michele Tansella MD a, Corrado Barbui MD a
Summary
Background
Conventional meta-analyses have shown inconsistent results for efficacy of second-generation antidepressants. We therefore did a multiple-treatments meta-analysis, which accounts for both direct and indirect comparisons, to assess the effects of 12 new-generation antidepressants on major depression.
Methods
We systematically reviewed 117 randomised controlled trials (25 928 participants) from 1991 up to Nov 30, 2007, which compared any of the following antidepressants at therapeutic dose range for the acute treatment of unipolar major depression in adults: bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirtazapine, paroxetine, reboxetine, sertraline, and venlafaxine. The main outcomes were the proportion of patients who responded to or dropped out of the allocated treatment. Analysis was done on an intention-to-treat basis.
Findings
Mirtazapine, escitalopram, venlafaxine, and sertraline were significantly more efficacious than duloxetine (odds ratios [OR] 1·39, 1·33, 1·30 and 1·27, respectively), fluoxetine (1·37, 1·32, 1·28, and 1·25, respectively), fluvoxamine (1·41, 1·35, 1·30, and 1·27, respectively), paroxetine (1·35, 1·30, 1·27, and 1·22, respectively), and reboxetine (2·03, 1·95, 1·89, and 1·85, respectively). Reboxetine was significantly less efficacious than all the other antidepressants tested. Escitalopram and sertraline showed the best profile of acceptability, leading to significantly fewer discontinuations than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine.
Interpretation
Clinically important differences exist between commonly prescribed antidepressants for both efficacy and acceptability in favour of escitalopram and sertraline. Sertraline might be the best choice when starting treatment for moderate to severe major depression in adults because it has the most favourable balance between benefits, acceptability, and acquisition cost.
The Venlafaxine study is compelling. The above study seems barebones and lacks details.
Eric
Posted by jono_in_adelaide on September 17, 2012, at 19:09:18
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 17, 2012, at 18:09:50
SLS, I'm not trying to get into a pissing contest with you, or say that effexor is useless, what I am saying is that
- It is only marginaly more effective that the best of the SSRI's for most patients 9statisticalsignificance doesnt equal clinical significance) and that the marginal increase in effeciency
- That if you need an SNRI response, Sertaline or Citralopam with desipramine/nortriptyline/bupropion will generaly give a more robust response than Effexor in a majority of patients, mainly those with endrogenous features
- That if you take cost effectiveness i to account, generic sertaline + generic nortriptyline (at about $8 per month using Walmart) is a lot more cost effective that 300mg/day of Effexor.
Of course Effexor is the ideal drug for some, and of course it should still be marketed, I just think that Wyeth Labs over sold it quite significantly
This is the end of the thread.
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