I dont get cymbalta ??????????

[braindead]

A lot of answers on forums are from 2004 ??// would good is that every one seems to take the line that 90-120mg is no better than 60 mg . well why did they make 90-and 120mg tablets if they're no better than 60mg and they're still saying this in 2017 ,i am on 60mg and my depression is better but my anxiety is the same , NNNNNNNNNNow will 90-120mg make my anxiety worse or better i am confused surely there have been enough test on patient to no the answer after 13 years , can anyone tell me if going up helped there anxiety or made it worse because i haven't a clue with this med

[panic_down_under]

every one seems to take the line that 90-120mg is no better than 60 mg

Yeah, you will read learned texts proclaiming that, usually then pontificating that this is because 60mg will block 80% of the serotonin transporters which supposedly is the magic number to produce the therapeutic effect and higher doses don't increase that percentage by much. Sounds really impressive...until you contemplate the French antidepressant tianeptine (Stablon) which not only doesn't block serotonin transporters, it actually increases their efficiency. Yet it seems to be at least as effective as the SSRIs and often works more quickly!

Now will 90-120mg make my anxiety worse or better

Apart from possibly a spike for a week or two, increasing the dose is unlikely to make anxiety worse. Whether it will make it better will only be determined by trying it.

i am confused surely there have been enough test on patient to no the answer after 13 years

There may be a generalized answer, but even if a million others all responded the same way, that's no guarantee you will, unfortunately. Everyone's reaction is unique to them.

[braindead]

Yeah, you will read learned texts proclaiming that, usually then pontificating that this is because 60mg will block 80% of the serotonin transporters which supposedly is the magic number to produce the therapeutic effect and higher doses don't increase that percentage by much. Sounds really impressive...until you contemplate the French antidepressant tianeptine (Stablon) which not only doesn't block serotonin transporters, it actually increases their efficiency. Yet it seems to be at least as effective as the SSRIs and often works more quickly!



Apart from possibly a spike for a week or two, increasing the dose is unlikely to make anxiety worse. Whether it will make it better will only be determined by trying it.



There may be a generalized answer, but even if a million others all responded the same way, that's no guarantee you will, unfortunately. Everyone's reaction is unique to them.

THANKS my man

[MyNameIsTerry]

The thing is, doctors will often keep increasing the dosage hoping to see more improvement. This doesn't always achieve anything and they end up switching people.

SSRI's tend to hit their 80% at minimum therapeutic dosage and increases tend to add around 5%. I think it's debatable just how much benefit that creates and in the case of Citalopram we had the more recent decision it wasn't worth it to go beyond 40mg due to this % increase being so small (as well as the increased risk issue).

Whether their is an advantage in their impact to other neurotransmitters at higher dosages, I would always defer to Ian about.

I suspect doctors know less about SNRI's than they do about SSRI's. It's a confusing classification which I'm starting to believe it's more about drug companies wanting to create something new and your average doctor doesn't look at what the drug really does when compared to some SSRI's.

As far as the age of forum posts goes, just look at this place. Hardly anyone is ever on this med. Ven seems to be used more. Maybe it's more a depression med?

[panic_down_under]

The thing is, doctors will often keep increasing the dosage hoping to see more improvement. This doesn't always achieve anything and they end up switching people.

But it does often enough to make trying higher doses worthwhile, Terry. If my doctors had not explored the upper dose limits I would have been leading the life of what the Japanese call a 'Hikikomori', a recluse imprisoned by agoraphobia, for the last 30 years.

I suspect doctors know less about SNRI's than they do about SSRI's. It's a confusing classification which I'm starting to believe it's more about drug companies wanting to create something new and your average doctor doesn't look at what the drug really does when compared to some SSRI's.

Marketing is probably the major factor, but also most antidepressants were developed before their binding potential could be measured so their supposed effects were based mostly on circumstantial evidence and a fair amount of guessing. Even now binding assays are far from precise, with a 5-10 fold variation quite common even when tested by the same lab. Much of the data is also based on non human receptors and transporters which may reduce its value.

Plus, these are lab results which may or may not reflect what actually happens in a living brain. One of the reason the low serotonin hypothesis gained early credibility is that in test tubes antidepressants do what the hypothesis proposes. It was only dispelled when the invention of microdialysis pipettes allowed researchers to test the hypothesis within living brains. I remember reading a mid 1990s by Chantal Moret and Mike Briley in which they repeated an in vitro experiment they'd done a few years previously, this time using in living rats instead of rat brain slices, and being puzzled by the results failing to replicate the earlier finding. Researchers don't often express surprise in their papers, but they did.

As far as the age of forum posts goes, just look at this place. Hardly anyone is ever on this med. Ven seems to be used more. Maybe it's more a depression med?

Venlafaxine seems to be one of the two most effective antidepressants for pulling the very severely, almost catatonic depressed back from the abyss and has become very popular for general depression because of this. But it really has no advantage in the more usual less severe depressions and given some of its issues such as higher cardio toxicity and the severity of withdrawal is probably best reserved for short-term use to stabilize severe depression before switching to another med for ongpoing maintenance therapy, imho.

[braindead]

THANKS PANIC DOWN UNDER, I had a word with my shrink nurse this morning about my 60mg CYMBALTA and the good way it stunted my depression but seems to leave sleep patterns and anxiety still lingering, and she said straight away go up to 90mg to see if thats the missing link.If tolerated and still not working after a week we try 120mg has a final push , has she and you said all brains work differently. EFFEXOR to me is the spawn of the devil and swore i would never try a SNRI again after my experience, it took me to the brink of suicide with it famed bad start up this was 30 years ago on tablet form venlafaxine, I was given it in mental hospital and the doses were lifted to fast turned me into a space cadet first class nut job. they sent me home and i fired the meds in the bin and did a detox no person should ever go through.there was even a web site called venlafaxine .org to help people get off the med. I have had a lot smoother ride with Cymbalta apart from a split arse Fisher from constipation so hear is hoping 90mg dont hold no gremlins

[panic_down_under]

EFFEXOR to me is the spawn of the devil and swore i would never try a SNRI again after my experience

...I have had a lot smoother ride with Cymbalta

You shouldn't judge other SNRIs by venlafaxine. It is a different beast than the others. Really a SNRI in name only as most of the SSRIs are more potent noradrenaline/norepinephrine inhibitors than it is. That said, the way it was administered didn't do you any favours and may have been at least as big a contributor to what happened as the med.

this was 30 years ago on tablet form venlafaxine

Were they the weird shield shaped tablets? I only took one because it had the same immediate mania effect on me as all the SSRIs I've tried despite the protestation of the shrink that it was a completely different type of med. Not his fault as there was no data to prove otherwise back then.

[braindead]

A guy who live just across the road from me was on 75mg Effexor for years, he became ill and was raised to 150mg , he said he felt great and after a few months had the notion that he didn't need it anymore looking on himself has some kind of middle-class junkie . I think you can guess the next bit he crashed big time . he was put back on 75mg then 150mg he was off work 12 weeks before he went back 6 weeks of that was under the blanket syndrome and 10 week before the Effexor trickled back into his system, all this because he thought he new best. NEVER EVER stop a med thats working , he was lucky it gave him a second chance. I doubt he will make that mistake again.

---------- Post added at 14:00 ---------- Previous post was at 13:54 ----------

You shouldn't judge other SNRIs by venlafaxine. It is a different beast than the others. Really a SNRI in name only as most of the SSRIs are more potent noradrenaline/norepinephrine inhibitors than it is. That said, the way it was administered didn't do you any favours and may have been at least as big a contributor to what happened as the med.



Were they the weird shield shaped tablets? I only took one because it had the same immediate mania effect on me as all the SSRIs I've tried despite the protestation of the shrink that it was a completely different type of med. Not his fault as there was no data to prove otherwise back then.

No weird shape they were round and a dirty brown colour. in hospital when the med nurse got to my bed she said its a long time since i gave anyone this med , soon has she said that i had a bad feeling

[MyNameIsTerry]

But it does often enough to make trying higher doses worthwhile, Terry. If my doctors had not explored the upper dose limits I would have been leading the life of what the Japanese call a 'Hikikomori', a recluse imprisoned by agoraphobia, for the last 30 years.



Marketing is probably the major factor, but also most antidepressants were developed before their binding potential could be measured so their supposed effects were based mostly on circumstantial evidence and a fair amount of guessing. Even now binding assays are far from precise, with a 5-10 fold variation quite common even when tested by the same lab. Much of the data is also based on non human receptors and transporters which may reduce its value.

Plus, these are lab results which may or may not reflect what actually happens in a living brain. One of the reason the low serotonin hypothesis gained early credibility is that in test tubes antidepressants do what the hypothesis proposes. It was only dispelled when the invention of microdialysis pipettes allowed researchers to test the hypothesis within living brains. I remember reading a mid 1990s by Chantal Moret and Mike Briley in which they repeated an in vitro experiment they'd done a few years previously, this time using in living rats instead of rat brain slices, and being puzzled by the results failing to replicate the earlier finding. Researchers don't often express surprise in their papers, but they did.

I don't disagree, Ian. For many that extra helps greatly, it's just that for some the med is a dud and they switch and maybe even increase with that until they find what works. But GP's can also be a bit over zealous upping doses far too quickly or even when the patient is responding well already.

I can understand the drugs companies trialling, getting licenced and then never caring as the watch their reps pull the cash in for them. But the medical professionals you would think would be altering the status of drugs where needed. It just seems led by the companies with often little interest from the docs in changing things because the drugs are plastering over problems in patients.

[panic_down_under]

I can understand the drugs companies trialling, getting licenced and then never caring as the watch their reps pull the cash in for them. But the medical professionals you would think would be altering the status of drugs where needed. It just seems led by the companies with often little interest from the docs in changing things because the drugs are plastering over problems in patients.

A lot of the medical professions, psychiatrists included, have only limited understanding of receptor affinities, etc. The number of posters here on both mirtazapine and quetiapine, which are very *similar in their action is evidence of this.

* mirtazapine: H1: 1.6 Ki, 5-HT2a: 69.0 Ki, D2: 1000 Ki
* quetiapine : H1: 6.9 Ki, 5-HT2a: 118. Ki, D2: 500. Ki

As for the drug companies, they lose interest as soon as thr patent expires and their market share begins evaporating. That is assuming they cared in the first place. The big players that created the antidepressants most of us are taking have pretty much abandoned psych meds generally, and antidepressants particularly in recent years. Small startups are doing what antidepressant drug development there is, though this may change given recent excitement about ketamine.