• N&PD Moderators: Skorpio | thegreenhand

Sexual dysfunction on Effexor

You can't really make blanket statements about which AD is more effective for every patient. Effexor ist for people who need just a tiny bit of extra noradrenaline on top of a large serotonin boost. Cymbalta is for people who need a balanced increase in serotonin and noradrenaline levels. Too much noradrenaline causes a different set of side-effects (some of them sexual), but who knows, it might just hit the sweet spot between serotonin and noradrenaline for you (as I wrote in your other thread, there's also Milnacipran and Reboxetine which are even less serotonergic and more noradrenergic, though I don't think they're as widely available as Cymbalta and Effexor).

Cymbalta is also reputed to induce a greater level of fatigue than venlafaxine.


Is this due to it's greater level of noradrenaline reuptake inhibition?


Also I believe both act on norepinephrine.


There's a degree of reuptake of this receptor very greatly in terms of the comparison of venlafaxine and duloxetine?
 
Depending on whether it's purely physical or not, either sildenafil like drugs or dopamine agonists.

There are people taking wellbutrin together with venlafaxine, it's kind of an augmentation strategy, but if you're otherwise satisfied with Effexor I'd rather try the above mentioned drugs. Dopamine agonists are tricky to dose, here others will be able to get more into detail.

Interesting that Cymbalta induces more fatigue than Effexor. I've read too that norepinephrine reuptake inhibitors tend to lower the overall NE level after some time, and there will be more auto receptor activation, but usually NRIs are stimulating (atomoxetine, reboxetine- the latter I've tried and it was very uncomfortable.) About bupropion it does more than just act as an NRI, it's a nicotinergic antagonist (why it helps to stop smoking, you don't get any more effects from smoking, and the stimulation helps with the withdrawal)- it's labelled as a NDRI. Don't know how effective it is at DA, the numbers are quite low on the paper. Well, basically it's a locked down cathinone ...
 
i just read/realized that norepinephrine and noradreniline are the same thing...

If NI's are activating, then why isn't cymbalta considered an activating drug - more so than effexor - given the NorAdrnl reuptake inhibition ratio's, that one poster highlighted earlier??

Given the activation of the NE/NA at higher doses, 225/300, wouldn't that imply that sexual dysfunction would, almost counter intuitively, be mitigated at those higher doses?

Welbutrin has a negligible effect on dopamine??

Is that what's being said?

So it's effectively a noradreniline inhibitor??

Wouldn't that imply that again, a higher dose of effexor would act similarly to a 150mg dose of effexor, combined with a supplementation of welbutrin?

Did any1 watch the video of that creeped out looking "doctor"?
He explains effexors mechanism as being like prozac and welbutrin conceptualized into one pill.

Though perhaps ironically, prozac did less than squat for me, where 150mg effexor (still solely with the seritonergic range of action) has proved much more beneficial??
 
a dopamine agonist - are u referring to wellbutrin?

Is ritalin/methylphenidate a dopamine agonist?

Cause that offered some but only marginal dysfunction relief
 
I got nothing, really nothing out of 40mg of Prozac / fluoxetine while even 75mg venlafaxine are almost instantly mood lifting for me, 150mg are really good stuff. Somehow the things on papers just seem not to fit with everybody. Either it's additional, not yet screened / documented features of the drugs, or due to genetics (P-glycoprotein activity), or whatever. I like the explanation of that venlafaxine has a PEA skeleton and might release dopamine, but this is probably wrong.

Dopamine agonists I have in mind are pramipexole or ropinirole (seems to cause less problems, based on what I read). These are usually prescribed for restless legs or Parkinson's. Think there are studies where one of them or both helped with SSRI sexual dysfunction.

Curiously I don't get any problems from venlafaxine, it diminishes the wish for sexuality (thankfully) but no dysfunction while paroxetine- a horrible drug - caused the opposite. A benefit you get with dopamine agonists is that you probably will be able to perform longer and have less refraction time.

Methyphenidate is a DAT (inverse) agonist and releases dopamine. Through that dopamine it's an indirect agonist. What dose did you take?

Wellbutrin - here I'd like to get to know myself how much or less DA & NE activity it has. It's a strange drug somehow.

I'm really unsure here but I'd say that norepinephrine is more a cause for dysfunction than a relief (NE causes vasoconstriction).
 
I got nothing, really nothing out of 40mg of Prozac / fluoxetine while even 75mg venlafaxine are almost instantly mood lifting for me, 150mg are really good stuff. Somehow the things on papers just seem not to fit with everybody. Either it's additional, not yet screened / documented features of the drugs, or due to genetics (P-glycoprotein activity), or whatever. I like the explanation of that venlafaxine has a PEA skeleton and might release dopamine, but this is probably wrong.

Dopamine agonists I have in mind are pramipexole or ropinirole (seems to cause less problems, based on what I read). These are usually prescribed for restless legs or Parkinson's. Think there are studies where one of them or both helped with SSRI sexual dysfunction.

Curiously I don't get any problems from venlafaxine, it diminishes the wish for sexuality (thankfully) but no dysfunction while paroxetine- a horrible drug - caused the opposite. A benefit you get with dopamine agonists is that you probably will be able to perform longer and have less refraction time.

Methyphenidate is a DAT (inverse) agonist and releases dopamine. Through that dopamine it's an indirect agonist. What dose did you take?

Wellbutrin - here I'd like to get to know myself how much or less DA & NE activity it has. It's a strange drug somehow.

I'm really unsure here but I'd say that norepinephrine is more a cause for dysfunction than a relief (NE causes vasoconstriction).

20mg ritalin.
only marginal dysfunction relief.

that last statement is kind of contradictory, is it not, if wellbutrin has been documented to offer relief, but is primarily a noradrenaline agonist.

From wiki, "as bupropion does not appear to have significant dopaminergic actions in humans under normal clinical circumstances".

Going on your final statement, given Duloxotines inhibition ratio for nor adrenelane, it should prove to induce a greater level of dysfunction, but clinical studies report 40% patient dysfunction of cymbalta, vs 70% on effexor.
Would that not be correct.
I'm no pharmacist and have only fleeting knowledge. I'm just piecing this together on scraps of information and a general application of logic.
 
It's not that easy, reuptake inhibitors are not releasers. Most if not all people partying on amphetamine get strong ED from the released norepinephrine. Release means circumventing the auto receptors which are part of the feedback loop, limiting the amount of chemical getting released. With transporter blockers / reuptake inhibitors, as the blockade level and thus free transmitters rise, the less gets released (but it stays in the synapse for longer). This takes time to achieve a new equilibrium, and different transmitters, if not also different RIs behave different.

Methylphenidate is said to exhibit DAT inverse agonism (don't know about NET, probably too) which makes it more comparable to amphetamines than other NDRIs. Maybe you would have to take it for longer, really can't say. But a dopamine agonist definitely works different, and yo have no NE.

I can't get that statement from a paper out of my mind saying that with one of the NRIs one had in fact less NE activity in the end than before (this may be related to specific parts of the brain though). Don't know the source anymore, unfortunately. Maybe I'll find it again, or someone else knows it, because I'm interested in it too.

Also it's the reason (?) why SSRIs aren't really euphorisant/entheogenic.

Wellbutrin, hm. It also has so different effects in individuals. Maybe it's the nicotinergic antagonism that helps some with ED?
 
Just going to list my experience here. Every SSRI i have ever been on renders my old mate pretty much useless. Either i can get it up but can't keep it up or can't even do so to begin with. Viagra is the obvious option but trying to time that shit to coincide with sexy times can be annoying. So... my doctor put me on the lowest dose of cialis (5mg) to take very day. After about 5 days it has built up in the system enough to make my jolly roger ready whenever called upon. Seriosuly, i was waking up with morning wood which hasn't happened to me since my teen years. I could go multiple rounds with the girlfriend and even knock out a few lazy ones on my own throughout the day. SSRI's also have the side effect of prolonging ejaculation. Some find that frustrating, me? I found it a blessing as i was not exactly the marathon type to begin with. So to recap... Cialis each day keeps the droops away. The only downside i can see is that it is not covered by the concession price (I'm in australia) so costs $186 for a months supply.
p.s, my doc tells me that some research has just uncovered some anti-oxidant properties in cilais as well so may prevent some visible signs of ageing. For a guy with lines around his eyes and a receding hairline at 29, thats another plus for me.
 
You can't really make blanket statements about which AD is more effective for every patient. Effexor ist for people who need just a tiny bit of extra noradrenaline on top of a large serotonin boost. Cymbalta is for people who need a balanced increase in serotonin and noradrenaline levels. Too much noradrenaline causes a different set of side-effects (some of them sexual), but who knows, it might just hit the sweet spot between serotonin and noradrenaline for you (as I wrote in your other thread, there's also Milnacipran and Reboxetine which are even less serotonergic and more noradrenergic, though I don't think they're as widely available as Cymbalta and Effexor).

Is there an article somewhere someone can link in terms of examining the inhibition ratios for these two different drugs?


Effexor is working reasonably well, but in terms of it's potency regarding noradrenaline reuptake in contrast to cymbalta, I'm curious as to whether that might be a better option for me, not to mention possibly lessening these hideous sexual effects.

I don't study pharmacology, but am interested in the finer details regarding this specific case.

Do I actually have to buy a book off amazon or something to gain access to the pertinent information??
 
too young to have to take viagra under reasonable circumstances.

anyone with serious useful input?

got 4 10mg cialis tabs from my gp.
it works... but taking it long term?

Yup -- effexor causes hyperprolactinemia --higher levels of prolactin than normal -- the mechanism is not clearly known but likely due to the influence of serotonin on prolactin directly or by way of oxytocin involvement.

Prolactin release after orgasm causes Mr softy, and non-response to stimulation. Cialis may help with erection and help you satisfy your partner, but you may be left -- err.. unfulfilled.

Regardless, this can be fixed by increasing dopamine. Dopamine lowers prolactin by directly inhibiting prolactin production by the pituitary. Cabergoline (a potent dopamine agonist) is commonly prescribed in concert with SSRIs in patients that experience lack of libido, erection, or anorgasmia.

An interesting effect of cabergoline is that it can help men achieve multiple orgasms by eliminating or reducing the refractory period after orgasm. Anecdotal reports of multiple serial orgasms (seemingly without end) by users of MDMA and other potent dopamine releasing recreational drugs supports the likely mode of action.

Ask your doc for some cabergoline.
 
Alright.

Good news.

doses above 150mg - 225, which I started on a week ago, in some cases, alleviate sexual problems.

I fall into this catagory.

I can now nut within normal frequency.

I can't express the relief to not have to induce a hernia trying to nut.

This is so super awesome!!


Now, effexor is good so far.
I just hope it clears up the rest of my symptoms and gets me back functioning fully.

one week in on 225, and I believe it can go up to 375, right??
 
Alright.

Good news.

doses above 150mg - 225, which I started on a week ago, in some cases, alleviate sexual problems.

I fall into this catagory.

I can now nut within normal frequency.

I can't express the relief to not have to induce a hernia trying to nut.

This is so super awesome!!


Now, effexor is good so far.
I just hope it clears up the rest of my symptoms and gets me back functioning fully.

one week in on 225, and I believe it can go up to 375, right??

At higher doses effexor acts as amild dopamine reuptake inhibitor.
 
Yup -- effexor causes hyperprolactinemia --higher levels of prolactin than normal -- the mechanism is not clearly known but likely due to the influence of serotonin on prolactin directly or by way of oxytocin involvement.

Prolactin release after orgasm causes Mr softy, and non-response to stimulation. Cialis may help with erection and help you satisfy your partner, but you may be left -- err.. unfulfilled.

Regardless, this can be fixed by increasing dopamine. Dopamine lowers prolactin by directly inhibiting prolactin production by the pituitary. Cabergoline (a potent dopamine agonist) is commonly prescribed in concert with SSRIs in patients that experience lack of libido, erection, or anorgasmia.

An interesting effect of cabergoline is that it can help men achieve multiple orgasms by eliminating or reducing the refractory period after orgasm. Anecdotal reports of multiple serial orgasms (seemingly without end) by users of MDMA and other potent dopamine releasing recreational drugs supports the likely mode of action.

Ask your doc for some cabergoline.

If I get my prolactin levels done, and they come in high, is that the indicator that effexor is (was) inducing the dysfunction??

How do you guys know this stuff??

And how come my doctor knows less that squat about this??
 
If I get my prolactin levels done, and they come in high, is that the indicator that effexor is (was) inducing the dysfunction??

How do you guys know this stuff??

And how come my doctor knows less that squat about this??

I wouldn't waste the money -- you said you can nut now. Either your body has adjusted and is not over-producing prolactin due to the increased serotonin, -- OR -- the higher dose keeps enough extra dopamine around that it supresses the release of prolactin, either way empirically you can orgasm.

Medical research journals are fascinating -- and chock full of information. When several studies/papers by different researchers and institutions corroborate each other it gives one confidence regarding the results.

Most doctors want to treat symptoms by pill, and side effects of that pill with another pill. Most don't want to find the cause.
 
Okay - up and down.

I could nut, but now I can't again, two days or so later.
So.... I've read sometimes it can take several weeks for sexual function to return when tuitrating to higher doses.

That's curious to me though, how it was regulated, then goes wonky again.
But the fact that it did return, albeit temporarily, is encouraging at least.

I spoke to the consultant - he seemed bemused at how cialis didn't have a rectifying effect on the dysfunction.
He said oftentimes 5mg can do the trick.
For me, 10mg didn't work, n my pharmacist said try 20, so that's the next step I guess.

Either way - I'm hoping time will tell.

It doesn't cost to get prolaction done for me as, I'm on disability and the government covers my medical costs.


If I want to educate myself better regarding the pharmacology of AD's and what might be most suitable for myself - where would be a good place to start?
Just a regular pharmacology book from the college library of which?
 
Okay - up and down.

I could nut, but now I can't again, two days or so later.
So.... I've read sometimes it can take several weeks for sexual function to return when tuitrating to higher doses.

That's curious to me though, how it was regulated, then goes wonky again.
But the fact that it did return, albeit temporarily, is encouraging at least.

I spoke to the consultant - he seemed bemused at how cialis didn't have a rectifying effect on the dysfunction.
He said oftentimes 5mg can do the trick.
For me, 10mg didn't work, n my pharmacist said try 20, so that's the next step I guess.

Either way - I'm hoping time will tell.

It doesn't cost to get prolaction done for me as, I'm on disability and the government covers my medical costs.


If I want to educate myself better regarding the pharmacology of AD's and what might be most suitable for myself - where would be a good place to start?
Just a regular pharmacology book from the college library of which?


Like I said before, cabergoline is the " go to" dopamine agonist for ed issuers related to ssri treatment.

Cabergoline has issues (potential cardiotoxicity) -- discuss with your doc.

Honestly, if it is because of high prolactin -- NOTHING will work other than a dopamine agonist.
 
Just out of curiosity, this Cabergoline, is used as a dopamine agonist.

Would that not mean it carries anti-depressant properties in some sense also?
 
Dopamine agonists as a counter to sexual dysfunction.... wouldn't it stand to reason that in general, parkinsons agents, perhaps at a lower dose, would be a suitable treatment for SNRI induced dysfunction.

L-Dopa could be effective, no?

And just my hyperbola'ing here but, wouldn't parkinsons agents, in theory, act as AD's in and of themselves?
But certainly, given the dopamine agonizm, serve to counter the dysfunction side effect?
 
Wellbutrin is a NE releaser not a NRI with neglible da activity, 20& reuptake inhibition to be exact, which MAY be sufficient for some people, that said NRIS are usually sedating by activating one of the ne receptors which decreases NE, i forgot which kind it was, as an example reboxetine a pure nri is sedating initially.

That said from reports it seems that bupropion has unique prosexual effects which may be unrealted to its NE release but that is just speculation.

In the worst cases the addition of amphetamine or another strong dopaminergic would be needed, but that depends on your individual case.
 
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