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post #41 of 244 (permalink) Old 02-07-2010, 04:39 PM
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Excuse my ignorance but why would Nardil work better than an SSRI like Lexapro for SA?
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post #42 of 244 (permalink) Old 02-07-2010, 04:50 PM
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Excuse my ignorance but why would Nardil work better than an SSRI like Lexapro for SA?
Because:
Lexapro is garbage
Nardil has a wide mechanism of action, raises dopamine, serotonin, GABA and melatonin.
And I'm sure that you cant achieve the same benefits with adding meds togheter as garbage+garbage = garbage.
Nardil may act on some unknown receptors wich explains its effectiveness.

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post #43 of 244 (permalink) Old 02-07-2010, 05:00 PM
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Because:
Lexapro is garbage
Nardil has a wide mechanism of action, raises dopamine, serotonin, GABA and melatonin.
And I'm sure that you cant achieve the same benefits with adding meds togheter as garbage+garbage = garbage.
Nardil may act on some unknown receptors wich explains its effectiveness.
Ah, I see, thanks.
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post #44 of 244 (permalink) Old 02-07-2010, 07:44 PM
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Originally Posted by crayzyMed View Post
Lexapro is garbage
not true.
lexapro has a very good rating for SAD. it's most prescribed antidepressant in 2008.

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Originally Posted by crayzyMed View Post
Nardil has a wide mechanism of action, raises dopamine, serotonin, GABA and melatonin.
you can make similar mechanism or even better using a combination.

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Originally Posted by crayzyMed View Post
And I'm sure that you cant achieve the same benefits with adding meds togheter as garbage+garbage = garbage.
scientific!!!

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Originally Posted by crayzyMed View Post
Nardil may act on some unknown receptors wich explains its effectiveness.
is nardil the only chemical in the world that hits that unkown receptors!!!!


there are some myths that say nardil abolishes SAD which is completely false. i have lots of user-ratings and meta-analysis which show nardil's improvement size isn't different from other meds.

meta analysis i've collected from different papers:


users rating

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post #45 of 244 (permalink) Old 02-07-2010, 11:19 PM Thread Starter
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Can you provide a source for those studies please Ehsan?

Thing is that it has been well documented that pharmacetical companies run several trials on a given drug, manipulating the time, dose, and methodology and then pic the ones that have the most robust response for publication.

I met a medical student once who ghost wrote research articles for well know professors and the like to sign off on and I don't doubt that Pharmacetical companys would use viral marketing techneiques for any new drug loading up forums with positive reviews.

Antidepressants 'no better than placebo' - February 26, 2008

http://blogs.nature.com/news/thegrea...02/post_3.html

I'm not sure you can take any study at face value with antidepressants being such big business these days
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post #46 of 244 (permalink) Old 02-08-2010, 02:55 AM
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Originally Posted by Ehsan View Post
not true.
lexapro has a very good rating for SAD. it's most prescribed antidepressant in 2008.

Rating from where? revolutionhealth.com? That site cant be taken serieus and the ratings there arent consistent with all the other anecdotal reports.
In short it appears that mostly only ppl that respond to medication post there.

Go read about ssri's for depression, then read this meta analysis.
http://www.plosmedicine.org/article/...l.pmed.0050045
Science baby, you cant beat that.


you can make similar mechanism or even better using a combination.

Then what combination? I asked you that before and you said "i dont know" well go figure it the hell out as so far all combinations of regular antidepressants suck too.

scientific!!!



is nardil the only chemical in the world that hits that unkown receptors!!!!

Then give me the name of that unknown chemical my friend, i'm dying to know. Whats as good as Nardil? Tell us!

there are some myths that say nardil abolishes SAD which is completely false. i have lots of user-ratings and meta-analysis which show nardil's improvement size isn't different from other meds.

Offcourse it doesnt work for everyone, who claimed that? It does work for hell alot more ppl then that ssri's.

meta analysis i've collected from different papers:


Read my meta analysis for some objective information.
....

Disclaimer: I am not a professional, all my advice is based on my own research and experiences.

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post #47 of 244 (permalink) Old 02-08-2010, 03:00 AM
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Can you provide a source for those studies please Ehsan?
i've used the following paper for nardil. it's one of the latest papers published considering nardil in SAD by well-known scientist Liebowitz:

Cognitive behavioral group therapy vs phenelzine therapy for social phobia: 12-week outcome.

a comparison between nardil and meclebomide in SAD:
Pharmacotherapy of social phobia. A controlled study with moclobemide and phenelzine

these are papers i've used for Sertraline for example:
MULTIDIMENSIONAL EFFECTS OF SERTRALINE IN SOCIAL ANXIETY DISORDER by Kathryn M. Connor, M.D., Jonathan R.T. Davidson, M.D., Henry Chung, M.D., Ruoyong Yang, Ph.D., and Cathryn M. Clary, M.D.

Sertraline Treatment of Generalized Social Phobia:A 20-Week, Double-Blind, Placebo-Controlled Study
by Michael A. Van Ameringen et al



Quote:
Originally Posted by zendog78 View Post
Thing is that it has been well documented that pharmacetical companies run several trials on a given drug, manipulating the time, dose, and methodology and then pic the ones that have the most robust response for publication.
I met a medical student once who ghost wrote research articles for well know professors and the like to sign off on and I don't doubt that Pharmacetical companys would use viral marketing techneiques for any new drug loading up forums with positive reviews.

Antidepressants 'no better than placebo' - February 26, 2008

http://blogs.nature.com/news/thegrea...02/post_3.html

I'm not sure you can take any study at face value with antidepressants being such big business these days
i know that these methods are already used by many ones(i've seen myself in the field of engineering) to write new papers but we shouldn't suspect all papers.


anyway, many people respond to their firs meds and there isn't any reason for them to come to forums. on the other hand, many few ones try nardil and it isn't available in many countries. i think MAOIs have a higher response rate but they don't abolish SAD. we need better combination

it is known that HPA axis and CRF are highly related to all anxiety and depression disorders but nardil can't affect CRF or many other factors involved in SAD.

Quote:
When an organism is under stress, or perceives itself under stress, the hypothalamus secretes corticotropin-releasing hormone/factor (CRH/CRF). CRH/CRF in turn increases secretion of adrenocorticotrophic hormone (ACTH) from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex. Persistent, uncontrolled physical and psychosocial stress causes excess cortisol secretion from the adrenal glands. Excess cortisol causes dendritic shrinkage in the hippocampus and a contrasting growth of dendrites in the lateral amygdala. These stress-induced changes tend to lower mood; they can cause clinical depression in the genetically vulnerable.
unfortunately, there isn't any miracle drug for SAD. we should separate what one drug can do and what it can't do.

what nardil can do:

1)inhibit MAO-A and MAO-B so increase Dopamine, Serotonin, GABA and trace amines(reduces NE activity)
2) it slightly releases Dopamine which is pleasant and help sociability.

what nardil can't do:

1) to agonize or antagonize receptor subtypes selectively. for example 5-ht2 antagonists are shown to decrease anxiety and depression while 5-ht1 agonists decrease anxiety.
2)to affect many hormones(oxytocin,...), neuropeptides(CRF,...), receptors(NMDA,...), neurotransmitters(Glutamate, ...), enzymes, ... involved in SAD or other mental disorders.

nardil can help many ones who haven't responded to simple selective antidepressants but there is many other combos to try for who want better results or who haven't responded to nardil.
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post #48 of 244 (permalink) Old 02-08-2010, 03:46 AM
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I completely agree that nardil isnt a miracle drug, i never claimed that it is. I however did learn that there's more then just looking at the mechanism of action of a drug.

For example, riluzole was found to be very effective for OCD, but lamictal with the same mechanism of action is NOT.
Reports about emsam seem far more negative then those about Nardil while both have the same mechanism of action.
Buspar is a 5HT1A agonist but its barely effective.

And so one.

I AM convinced that there are combo's that are far better then Nardil, but those would involve benzo's, amphetamine or something else. Combo's with agomelatine, memantine etc could work very well too, i'm just very skeptical of the effectiveness of SSRI's and doubt they would be good in combination with other stuff.
Its just that i read about ppl combining ssri's+wellbutrin with little succes and that often something that looks good on paper isnt good at all, moclobemide and reboxetine being good examples.

Disclaimer: I am not a professional, all my advice is based on my own research and experiences.

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post #49 of 244 (permalink) Old 02-08-2010, 03:51 AM
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Originally Posted by zendog78 View Post
Why do you think there continues to be a market for several new antidepressants every year?
I can think of two reasons:

1. Financial: "new" drug (which often means slight variation on old drug) bring a new patent and piles of money for big pharma which I mock as huge marketing firms with a little chemistry lab out back.

2. Antidepressants tend not to work very well, leaving plenty of patients to try the next "wonder drug." Even in clinical trials designed by the company that produces the drug where they make the trial to present their drug in the most positive light possible they still typically only get it to be effective in about twice as many as respond to sugar pills. They'll crow about how 70% responded to their drug, leaving out that 35% responded to a sugar pill! They don't lie, they just leave out the truth.
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post #50 of 244 (permalink) Old 02-08-2010, 03:59 AM
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Originally Posted by Ehsan View Post

what nardil can do:
1)inhibit MAO-A and MAO-B so increase Dopamine, Serotonin, GABA and trace amines(reduces NE activity)
2) it slightly releases Dopamine which is pleasant and help sociability.

what nardil can't do:
1) to agonize or antagonize receptor subtypes selectively. for example 5-ht2 antagonists are shown to decrease anxiety and depression while 5-ht1 agonists decrease anxiety.
2)to affect many hormones(oxytocin,...), neuropeptides(CRF,...), receptors(NMDA,...), neurotransmitters(Glutamate, ...), enzymes, ... involved in SAD or other mental disorders.
Doesn't anything that increases serotonin (ie SSRI's, MAOIs) inadvertantly also raise oxcytocin levels to an extent?
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post #51 of 244 (permalink) Old 02-08-2010, 05:10 AM
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Doesn't anything that increases serotonin (ie SSRI's, MAOIs) inadvertantly also raise oxcytocin levels to an extent?
i've read somewhere that some of TCAs(anfranil) increase CSF level of oxytocin and decrease CRF but further research needed.

Changes in cerebrospinal fluid neurochemistry during treatment of obsessive-compulsive disorder with clomipramine.
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This study examined the effect of long-term (mean, 19 months) treatment with clomipramine hydrochloride on cerebrospinal fluid (CSF) levels of several neuropeptides and monoamine metabolites in children and adolescents with obsessive-compulsive disorder. METHODS: The CSF levels of corticotropin-releasing hormone, vasopressin, somatostatin, and oxytocin and of the monoamine metabolites 5-hydroxyindoleacetic acid, homovanillic acid, and 3-methoxy-4-hydroxyphenylglycol were measured in 17 children and adolescents with obsessive-compulsive disorder before and after long-term treatment with clomipramine. RESULTS: Treatment resulted in significant decreases in CSF levels of corticotropin-releasing hormone (mean +/- SD, 175 +/- 32 vs 152 +/- 25 pmol/L, P < .03) and vasopressin (mean +/- SD, 1.30 +/- 0.57 vs 0.86 +/- 0.54 pmol/L, P < .02) and a trend toward a decrease in somatostatin levels (mean +/- SD, 21.3 +/- 8.5 vs 15.3 +/- 9.8 pmol/L, P < .06). Treatment also significantly increased CSF oxytocin levels (mean +/- SD, 6.05 +/- 1.60 vs 6.70 +/- 1.44 pmol/L, P < .01). Significant changes in CSF monoamine metabolite levels with treatment included significant decreases in CSF levels of 5-hydroxyindoleacetic acid (mean +/- SD, 109 +/- 31 vs 77 +/- 23 pmol/mL, P < .001), CSF homovanillic acid (mean +/- SD, 273 +/- 111 vs 237 +/- 101 pmol/mL, P < .04), and 3-methoxy-4-hydroxyphenylglycol (mean +/- SD, 42.4 +/- 10.2 vs 36.1 +/- 4.8 pmol/L, P < .02) and a significant increase in the homovanillic acid-5-hydroxyindoleacetic acid ratio (mean +/- SD, 2.44 +/- 0.46 vs 3.42 +/- 0.84, P < .0001). CONCLUSIONS: These neuropeptide results coupled with evidence that central administration of corticotropin-releasing hormone, vasopressin, and somatostatin to laboratory animals increases arousal and acquisition of conditioned behaviors whereas central administration of oxytocin has opposite behavioral effects are consistent with a role for these neuropeptides in the pathophysiologic processes and pharmacologic treatment of obsessive-compulsive disorder.
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post #52 of 244 (permalink) Old 02-08-2010, 05:19 AM
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When I said combinations I means combos of different types of drugs to affect different systems, not SSRI + SSRI.

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Originally Posted by crayzyMed View Post
Buspar is a 5HT1A agonist but its barely effective.
But it's a very weak agonist, with other undesirable effects (D2/a2 blockade).

Quote:
Its just that i read about ppl combining ssri's+wellbutrin with little succes and that often something that looks good on paper isnt good at all, moclobemide and reboxetine being good examples.
Most of the reports I've seen of SSRIs with Wellbutrin were good. Moclobemide and reboxetine aren't very good, I agree.


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post #53 of 244 (permalink) Old 02-08-2010, 05:26 AM
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I can think of two reasons:

1. Financial: "new" drug (which often means slight variation on old drug) bring a new patent and piles of money for big pharma which I mock as huge marketing firms with a little chemistry lab out back.

2. Antidepressants tend not to work very well, leaving plenty of patients to try the next "wonder drug." Even in clinical trials designed by the company that produces the drug where they make the trial to present their drug in the most positive light possible they still typically only get it to be effective in about twice as many as respond to sugar pills. They'll crow about how 70% responded to their drug, leaving out that 35% responded to a sugar pill! They don't lie, they just leave out the truth.
ok,
but i think introducing SSRIs was only a try to make antidepressant more safe not more effective.
they are really selective for serotonin transporter.
this is enough for many ones but someone need more potent meds so it's almost impossible that one respond differently to two different SSRI other than when some drug has some unknown mechanism of action.

i agree that pharmaceutical companies are making huge benefit while their meds does not work for many ones but they need some motivation to continue their work
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post #54 of 244 (permalink) Old 02-08-2010, 05:39 AM
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When I said combinations I means combos of different types of drugs to affect different systems, not SSRI + SSRI.



But it's a very weak agonist, with other undesirable effects (D2/a2 blockade).

Most of the reports I've seen of SSRIs with Wellbutrin were good. Moclobemide and reboxetine aren't very good, I agree.
Okay..., if your right i'l change my mind, still not convinced it would match the effectiveness of MAOI's tough :P.

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post #55 of 244 (permalink) Old 02-08-2010, 05:40 AM
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ok,
but i think introducing SSRIs was only a try to make antidepressant more safe not more effective.
they are really selective for serotonin transporter.
this is enough for many ones but someone need more potent meds so it's almost impossible that one respond differently to two different SSRI other than when some drug has some unknown mechanism of action.

i agree that pharmaceutical companies are making huge benefit while their meds does not work for many ones but they need some motivation to continue their work
They are working on some interesting things, if only research could go a little faster.

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post #56 of 244 (permalink) Old 02-08-2010, 05:45 AM
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Most of the reports I've seen of SSRIs with Wellbutrin were good. Moclobemide and reboxetine aren't very good, I agree.
i've just started selegiline+fluoxetine+wellbutrin+inderal and i will report my experiences soon.
however i don't need miracle drugs anymore coz my SAD has turned to a mild one after three years of medication.
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post #57 of 244 (permalink) Old 02-08-2010, 06:06 AM
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i've just started selegiline+fluoxetine+wellbutrin+inderal and i will report my experiences soon.
however i don't need miracle drugs anymore coz my SAD has turned to a mild one after three years of medication.
It might be wise to check your blood pressure regularly when on that combo, as you are combining stimulant + beta blocker.


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post #58 of 244 (permalink) Old 02-08-2010, 06:34 AM
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It might be wise to check your blood pressure regularly when on that combo, as you are combining stimulant + beta blocker.
thanks, i'll do that.
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post #59 of 244 (permalink) Old 02-08-2010, 06:36 AM
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i've just started selegiline+fluoxetine+wellbutrin+inderal and i will report my experiences soon.
however i don't need miracle drugs anymore coz my SAD has turned to a mild one after three years of medication.
Okay, i hope the combo works for you, this is the first time ive seen anyone come up with this combo, it makes sense pharmacology wise.
If you want to replicate a MAOI i would add in melatonin as its been suggested that the increase in melatonin contributes to the antidepressant effect.[1].

Maybe some gabatril to counteract any possible increase in anxiety caused by deprenyl and wellbutrin and this combo could have some major potential.

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post #60 of 244 (permalink) Old 02-08-2010, 08:44 AM
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Okay, i hope the combo works for you, this is the first time ive seen anyone come up with this combo, it makes sense pharmacology wise.
If you want to replicate a MAOI i would add in melatonin as its been suggested that the increase in melatonin contributes to the antidepressant effect.[1].

Maybe some gabatril to counteract any possible increase in anxiety caused by deprenyl and wellbutrin and this combo could have some major potential.
thanks,
i take melatonin every night however i'm not going to make a complete regime now.
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