Is my ED physical, psychological or hormonal?

Dopamine is probably the most important neurosteroid for libido. You could ask you doctor to try Pramipexole.

When it comes to libido let alone erectile function its much more complex!

The main neurosteroids involved in stimulating libido would be dopamine, norepinephrine, and estrogen.

The main neurosteroids involved in stimulating arousal would be nitric oxide, dopamine, NE, estrogen and testosterone, oxytocin, acetylcholine, and melanocortin.

The main neurosteroids involved in stimulating D1 and D5 receptors promoting erections would be T and it's metabolites (DHT and estradiol), allopregnanolone, pregnenolone sulfate, and dehydroepiandrosterone/ DHEA Sulfate.





* When we discuss the sexual cycle and the role of antidepressants in altering it, it becomes useful to first understand the physiology of the sexual cycle and the neurotransmitters affecting it. Among the neurotransmitters concerned with psychiatry, the following have a role to play in the sexual response cycle as well. In chronological order, desire is promoted by dopamine, norepinephrine (NE), and estrogen, while it is inhibited by serotonin and prolactin. When it comes to arousal, nitric oxide, dopamine, NE, estrogen and testosterone, oxytocin, acetylcholine, and melanocortin enhance it, while serotonin brings down the arousal. In the stage of orgasm, dopamine and nitric oxide help in enhancing the orgasm while serotonin dampens it. When D1 and D5 receptors are stimulated, they help in facilitating sexual arousal in the form of erection in males and receptivity in females. On stimulation of D2 receptors, orgasm comes to fruition, while serotonin reduces sexual activity by blocking dopamine.7
 
Dopamine is probably the most important neurosteroid for libido. You could ask you doctor to try Pramipexole.
Thank you for your suggestion. I will try to convince my doctor to prescribe it. In the meantime, I am trying L Tyrosine, which should be a weaker version
 
When it comes to libido let alone erectile function its much more complex!

The main neurosteroids involved in stimulating libido would be dopamine, norepinephrine, and estrogen.

The main neurosteroids involved in stimulating arousal would be nitric oxide, dopamine, NE, estrogen and testosterone, oxytocin, acetylcholine, and melanocortin.

The main neurosteroids involved in stimulating D1 and D5 receptors promoting erections would be T and it's metabolites (DHT and estradiol), allopregnanolone, pregnenolone sulfate, and dehydroepiandrosterone/ DHEA Sulfate.





* When we discuss the sexual cycle and the role of antidepressants in altering it, it becomes useful to first understand the physiology of the sexual cycle and the neurotransmitters affecting it. Among the neurotransmitters concerned with psychiatry, the following have a role to play in the sexual response cycle as well. In chronological order, desire is promoted by dopamine, norepinephrine (NE), and estrogen, while it is inhibited by serotonin and prolactin. When it comes to arousal, nitric oxide, dopamine, NE, estrogen and testosterone, oxytocin, acetylcholine, and melanocortin enhance it, while serotonin brings down the arousal. In the stage of orgasm, dopamine and nitric oxide help in enhancing the orgasm while serotonin dampens it. When D1 and D5 receptors are stimulated, they help in facilitating sexual arousal in the form of erection in males and receptivity in females. On stimulation of D2 receptors, orgasm comes to fruition, while serotonin reduces sexual activity by blocking dopamine.7
Thanks a lot for this valuable information. Will research more about this and read the post you linked.
 
To be honest I was never aware of dopamine agonists. From what I am understanding, these mimick the effects of dopamine, which plays a role in sexual function.

I guess these can only be purchased using a prescription? What kind of doctors usually prescribe them, psychiatrists?

What are some of the best dopamine agonists? If I'm not able to purchase them in case the doctor refuses to prescribe them, do you know of any supplements that do a similar job?

Thank you so much for your assistance
I get my selegiline prescribed by Defy, my HRT clinic, but u can purchase it without a prescription as well. Here’s one of the most popular websites that members here use

 
Does it help for your libido?
I don’t think I’ve personally seen any improvement in libido while on it. My libido is pretty healthy tho. So maybe it would be less if I stopped taking it. I don’t take a lot tho. Right now I’m just taking 1.25mg sublingually every three days

Theoretically tho there’s a pretty good chance it can improve libido, due to increased dopamine levels tending to improve libido, and lowering prolactin can also improve libido. Here’s a couple anecdotes I have saved where they mentioned a libido boost


Energizer
Member
I took 5mg Selegeline Hydrochloride Capsules USP daily for 2 months. Noticed a bit of a mood / energy boost and definitely a libido boost.


(thread that comments below are from)
genericshitaccount
-How much do you even take? Doubt it is the Selegiline causing it because if anything it should suppress and reduce prolactin as long as you keep it at MAO-B selective dosages. Also if you have a genetic predisposity for hyperprolactinoma and have also used exogenous testosterone in the past then these are more than anything the actual causes for your breast issues.. what happened now is probably just a coincidence.
-Also not sure what you are expecting as for effects from sublingual selegiline? They are all very subtle in my opinion, except the increased libido which is almost a bit annoying at times. The improved memory recall and learning and motivation increases and improved deeper sleep that I have gotten took a while to get. You need to give it some time for sure, and like I said it is all very subtle. It took several trials of coming on and off for me to realize the beneficial nootropical effects it was giving me. And yes there is an immediate acute feeling/rush that you can get and feel from dosing Selegiline that is unrelated to its MAO inhibiting effects and that is because it is a CAE (catecholamine activity enhancer) which increases dopaminergic and noradrenergic transmission and release acutely which makes it have noticable stimulating properties for many people. This feeling is nothing spectacular however but it is still there and like I said, it is an immediate effect exerted on the brain completely unrelated to Selegiline's MAO inhibiting properties.
 
Here’s another post from the same guy

genericshitaccount
5y ago
Well for me the libido boost took a while to become really apparent. For me that effect has sort of accumulated over time too. I think your dose may be a little bit too high, if you take it daily there's no need to go over 1.25~ mg. At 2.5 mg daily you will most likely inhibit MAO-A to some degree and the increase in serotonin and norepinephrine can have the opposite effects on libido, especially serotonin. The prolactin reducing effect from Selegiline disappears when you start crossing into MAO-A territory a lot as serotonin has the opposite effect on prolactin compared to dopamine. I take like 1/4 of a pill now (about 1.25 mg) sublingually every 5th-6th day or so and this alone has a really big almost annoying increase in libido and sexual desire for me. Also orgasms feel so much better with MAO-B inhibited and for me they seem to last longer too, and when I was taking 1.25 mg daily it was really crazy as I would be getting multiple orgasms after coming once and it could last for like half a minute or so if not more. But if I take too much like 5 mg sublingual daily I in fact get greatly reduced libido and the complete opposite effects, and from what I remember when I was trying 2.5 mg/day I also had less libido than I had from 1.25 mg/day or the regime I am on now until my body maybe later adapted after a couple of weeks due to the increased serotonin I am guessing.

So try a lower dose imo, don't go over 1.25 mg/day and give it some time to see if it will have any "positive" effects on libido as the brain and body needs some time to adapt to these changes. In fact Selegiline seems to have made my testicles noticably bigger after some months of use now and that is a direct effect due to the lowered prolactin and increased dopamine (which in turn makes the testes produce more testosterone). Selegiline actually has this ability in male rats and mice too, where their testicles grew to a quite noticable level on measurements. So with this change made to testicles in mind and the effects I have had personally with a slowly increase in libido it sort of makes sense imo to give the brain and body some time to adapt and give it some time to see if it affects your libido or not.

And yeah when you start crossing into MAO-A inhibition territory that is also where you start crossing into the insomnia side-effect territory due to all the increase serotonin, noradrenaline and trace amines broken down by MAO-A greatly affecting and promoting wakefulness. Also this may suppress things like REM sleep and dreams, another huge downside in my own opinion. I would probably take selegiline daily if it were not for potentially crossing into MAO-A territory and getting many of these unwanted effects, also too much MAO-B inhibition just increases histamine too much for me personally.

And once again yeah, a lot of people just expect too much from Selegiline and think it will be some kind of strong amphetamine-like stimulant. People even like to talk about its amphetamine metabolites as if they could actually have any particular positive effects when they are the levo isomers which are pretty much only unpleasant and have so little affinity for anything else than norepinephrine that they are proven to have 0 abuse potential and addiction liabilites in animal studies lol.

Also I have never noticed any withdrawal symptoms from Selegiline. The effects from it are already very subtle and since the MAO-B enzyme is slowly and steadily recovered it is like a small self-taper is already built into the substance when you discontinue it(the dopamine and not to mention trace amine and PEA levels will slowly be going down as MAO-B activity increases). So I wouldn't worry about this. Almost nobody on the net has ever said that they experienced withdrawals from discontinuing it, and from what I remember animal and human studies showed that there was zero dependence developed on the substance.
 
I don’t think I’ve personally seen any improvement in libido while on it. My libido is pretty healthy tho. So maybe it would be less if I stopped taking it. I don’t take a lot tho. Right now I’m just taking 1.25mg sublingually every three days

Theoretically tho there’s a pretty good chance it can improve libido, due to increased dopamine levels tending to improve libido, and lowering prolactin can also improve libido. Here’s a couple anecdotes I have saved where they mentioned a libido boost


Energizer
Member
I took 5mg Selegeline Hydrochloride Capsules USP daily for 2 months. Noticed a bit of a mood / energy boost and definitely a libido boost.


(thread that comments below are from)
genericshitaccount
-How much do you even take? Doubt it is the Selegiline causing it because if anything it should suppress and reduce prolactin as long as you keep it at MAO-B selective dosages. Also if you have a genetic predisposity for hyperprolactinoma and have also used exogenous testosterone in the past then these are more than anything the actual causes for your breast issues.. what happened now is probably just a coincidence.
-Also not sure what you are expecting as for effects from sublingual selegiline? They are all very subtle in my opinion, except the increased libido which is almost a bit annoying at times. The improved memory recall and learning and motivation increases and improved deeper sleep that I have gotten took a while to get. You need to give it some time for sure, and like I said it is all very subtle. It took several trials of coming on and off for me to realize the beneficial nootropical effects it was giving me. And yes there is an immediate acute feeling/rush that you can get and feel from dosing Selegiline that is unrelated to its MAO inhibiting effects and that is because it is a CAE (catecholamine activity enhancer) which increases dopaminergic and noradrenergic transmission and release acutely which makes it have noticable stimulating properties for many people. This feeling is nothing spectacular however but it is still there and like I said, it is an immediate effect exerted on the brain completely unrelated to Selegiline's MAO inhibiting properties.
Awesome.

I'm looking for the best dopamine agonist. What do you think about pramipexole? I have PFS and libido problems
 
Awesome.

I'm looking for the best dopamine agonist. What do you think about pramipexole? I have PFS and libido problems
So pramipexole and cabergoline are the two dopamine agonists that are used in the bodybuilding community, and I’ve always heard that they come with some worrying sides. More so cabergoline. Think the sides were related to the heart. But maybe I’ve always heard those two have sides because of the dosages bodybuilders would use, when using both medications. So maybe neither have any negatives when using them in appropriate dosages. Really not sure. I just know I personally would never take either of those medications long term

As far as I know, if ur going to take a dopamine agonist indefinitely, and overall health/ longevity is a priority, selegiline is the best dopamine agonist out there. Again, not only is it the only dopamine agonist, that I know of, that actually can increase longevity, it’s one of the few medications out there in general, that have studies done on it showing that it can increase longevity

Here’s a vid about it from Sam Robbins, who’s channel is all about health/ longevity

 

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Lakshman KM, Kaplan B, Travison TG, Basaria S, Knapp PE, Singh AB, LaValley MP, Mazer NA, Bhasin S. The effects of injected testosterone dose and age on the conversion of testosterone to estradiol and dihydrotestosterone in young and older men. J Clin Endocrinol Metab. 2010 Aug;95(8):3955-64.

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